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YEAR4 Mod B cards for quizlet

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In what age group do hip fractures typically occur?Elderly- risk increases significantly with age
What is most commonly associated with hip fractures?- Low-energy falling (e.g. fall from standing height)<div>- Osteoporosis</div><div>- Osteopenia</div>
How is a hip fracture defined?"Fracture of femur distal to femoral head, and proximal to level a few cms below lesser trochanter. <div><div><br></div><div><img src=""204799.jpg""><br></div></div>"
What is the definition of <b>osteoporosis</b>?Compromised bone strength predisposing a person to increased risk of fracture (describes what?)
Compromised bone strength predisposing a person to increased risk of fracture (describes what?)What is the definition of <b>osteoporosis</b>?
What are the two main features which determine bone strength?- Quality<div>- Density</div>
How does the WHO define osteoporosis and osteopenia?<b>Bone mineral density:</b><div><b><br></b></div><div><u>Osteoporosis</u><b>: </b> ≥2.5 s.d. below normal peak values for young adults</div><div><u>Osteopenia:</u>  Between 1 and 2.5 s.d. below normal peak values</div>
What are risk factors for hip fractures?- Osteoporosis/osteopenia<div>- Age >65</div><div>- Falls</div><div>- Female sex</div><div>- Low BMI</div>
What might you find on physical examination of a hip fracture?- Leg on affected side may be shortened and externally rotated<div><br></div><div>(Finding may also be seen with other fractures of femur/pelvis/lower leg)</div>
How can hip fractures be diagnosed radiologically?"<b>X-rays</b>, using AP pelvis and lateral hip<div><br></div><div>- Trace <b>Shenton's line</b>- if disrupted, likely hip fracture (or developmental dysplasia of the hip)</div><div>- Assess for symmetry- note lesser trochanter</div><div>- Bone trabeculae</div><div>- Sclerosis</div><div>- Smudge</div><div><img src=""387-4_default.jpg""><br></div>"
How are hip fractures generally classified anatomically?<b>Intra-capsular:</b> Within hip capsule (femoral neck fractures)<div><b>Extra-capsular: </b>e.g. inter-trochanteric fractures</div>
What are your differentials for a hip fracture, and how do you exclude them?<b>Acetabular fracture</b>: Leg is rarely shortened/externally rotated; X-ray should differentiate<div><b>Pubic rami fracture: </b>Leg rarely shortened/externalyl rotated; X-ray should differentiate. MRI pelvis may be needed</div><div><b>Femoral shaft/sub-trochanteric femur fracture: </b>Often thigh is deformed; X-Ray</div><div><b>Femoral head fracture:</b> Often associated with hip dislocation; X-Ray and pelvic CT</div><div><b>Septic Hip: </b>Fever + Chills; hip aspiration may revela pus; laboratory isolation in fluid; elevated WBC<br><div><br></div></div>
"How do you draw Shenton's line? What is it used for?""Draw a curved line from inferior border of superior pubic ramus, along inferior border of neck of femur- line should be continuous and smooth.<div><img src=""shenton_line-e1478309207389.jpg""><br></div><div><br></div><div>Disruption indicates:</div><div>- <b>Hip fracture (fractured neck of femur)</b></div><div>- <b>Developmental dysplasia of the hip</b></div>"
What muscles insert onto the greater and lesser trochanters?Lesser: Iliopsoas<div>Greater: Abductors (stabilise pelvis when walking)</div>
What does the <b>Trendelenburg test </b>assess?Function of <b>hip abductors</b> + ability to support pelvis when standing on one leg (is assessed by what test?)
Function of <b>hip abductors</b> + ability to support pelvis when standing on one leg (is assessed by what test?)What does the <b>Trendelenburg test </b>assess?
"What is a ""positive"" Trendelenburg test?""Pelvis falls on side of lifted leg (indicates weakness of muscles on weight-bearing leg)<div><img src=""ClutteredBlondBagworm-max-1mb.gif""><br></div>"
What complication must be considered with an intracapsular fracture of the femoral neck?Blood supply to femoral neck compromised- <b>avascular necrosis of the femoral head</b> likely
For what type of hip fractures is blood supply to femoral head a concern?Intracapsular fractures (extracapsular are unlikely to have this)
How are extracapsular femoral fractures managed?"Internal fixation with dynamic hip screw (a) , or intramedullary nail (b)<div><img src=""mplants-for-the-screw-group-a-Dynamic-hip-system-DHS-screw-b-Gamma-nail.png""><br></div><div>DHS are generally preferred, but cephalomedullary nail more used for 4-part fractures</div>"
Discuss the prognosis of hip fractures- 30% risk of mortality at 1 year.<div>- 25-75% of adults may not regain previous level of function. </div><div>- Operating within <b>48hrs </b>shown to be beneficial  </div>
How can femoral neck fractures be differentiated from dislocations?"<b>Fracture: </b>Shortened leg and <font color=""#0000ff"">externally rotated</font><div><b>Dislocation (commonly posterior): </b>Shortened leg and <font color=""#0000ff"">internally rotated</font></div>"
What are the different types of trochanteric fractures?"<b>Pertrochanteric</b>: Through greater and lesser trochanters. <font color=""#0000ff"">Trauma history: sharp twisting injury.</font><div><b>Intertrochanteric: </b>Between trochanters. <font color=""#0000ff"">Trauma history: sharp twisting injury</font></div><div><b>Subtrochanteric: </b>Below trochanters. Pathological, often due to <font color=""#0000ff"">Paget's or metastases</font></div><div><b>Avulsion: </b>Fragment of bone tears away from main mass. <font color=""#0000ff"">Violent adduction</font></div>"
"Identify the pathology:<div><img src=""paste-856ddab41481777bf5eb306cea76171acdd17c4a.jpg""><br></div>"Avulsion fracture of greater trochanter
"Identify the pathology:<div><img src=""it.jpg""><br></div>""Intertrochanteric fracture<div><img src=""paste-8b2a82704fcad9e1bae8604b74175d7cb7e022e4.jpg""><br></div>"
"Identify the pathology:<div><img src=""bisphos fx.jpg""><br></div>"Subtrochanteric fracture 
What is the importance of bone remodelling?-<b> Repair microfractures</b><div>- Allows<b> modification in response to stress</b> + biochemical forces</div>
What cells mediate bone remodelling?<b>Osteoblasts</b>: Bone formation<div><b>Osteoclasts: </b>Bone resorption</div><div><br></div><div>(note osteocytes are simply osteoblasts trapped in the bone matrix, so matured osteoblasts)</div>
What membrane component can differentiate osteoblasts and osteoclasts?"<b>Osteoclasts </b>have <font color=""#ff0000"">acid <b>phosphatase</b> </font>(think because release acid alongside hydrolytic enzymes to resorb bone)<div><br></div><div><b>Osteoblasts </b>have <font color=""#0000ff""><b>alkaline phosphatase</b></font> (used as a marker for bone formation)</div>"
How is calcium stored in our bodies?99% of Calcium is stored in bone as <b>hydroxy apatite</b>
Describe Calcium Balance across different ages<b>Childhood</b>: Ca<sup>2+</sup> balance is positive (as growing bones + bodies)<div><b>Post-puberty</b>: Ca<sup>2+</sup> balance is neutral</div><div><b>In post menopausal women</b>: Ca<sup>2+</sup> is negative (hence older female populations more at risk of osteoporosis, hip fractures etc.)</div>
What are the main hormones involved in calcium homeostasis?- Parathyroid hormone PTH)<div>- Calcitriol (active Vitamin D)</div><div>- Calcitonin</div>
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9e9b5045ddec4623ac47f07cd1a660ce-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmp3byjcgqb.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9e9b5045ddec4623ac47f07cd1a660ce-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmp3byjcgqb.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9e9b5045ddec4623ac47f07cd1a660ce-ao-2-Q.svg"" /></div> <div id=""io-original""><img src=""tmp3byjcgqb.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9e9b5045ddec4623ac47f07cd1a660ce-ao-2-A.svg"" /></div> <div id=""io-original""><img src=""tmp3byjcgqb.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9e9b5045ddec4623ac47f07cd1a660ce-ao-3-Q.svg"" /></div> <div id=""io-original""><img src=""tmp3byjcgqb.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9e9b5045ddec4623ac47f07cd1a660ce-ao-3-A.svg"" /></div> <div id=""io-original""><img src=""tmp3byjcgqb.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
How is calcium homeostasis maintained when blood calcium rises or falls?<b>Rises</b>: <b>Thryoid</b> gland release<b> calcitonin</b><div><b>Falls</b>: <b>Parathyroid </b>gland releases <b>PTH </b>(which in turn increases calcitriol)</div>
What is the effect of <b>PTH </b>on calcium homeostasis?<b>Bone: </b><div>- Promotes recruitment + differentiation of <b>osteoclasts</b> --> Increased <b>resorption</b> --> increases Ca<sup>2+</sup> </div><div><br></div><div><b>Kidney: </b></div><div>- Increases renal tubular calcium <b>reabsorption</b></div><div>- Increases <b>phosphate excretion</b></div><div>- Increases renal <b>calcitriol production</b></div><div><br></div><div><br></div><div><b>GI tract:</b></div><div>- Stimulates <b>production of 1,25 dihydroxyvitamin D</b> which <b>increases GI absorption of Calcium and Phosphate</b></div>
How is PTH release controlled?-<b> High Ca<sup>2+</sup></b><div><b>- Calcitriol (active VitD)</b></div><div><b>- Low phosphate levels</b></div><div><br></div><div>All act via negative feedback on PTH gland</div>
How does calcitonin affect Calcium homeostasis?- <b>Inactivates osteoclasts </b>--> prevents bone resorption <div><br></div><div><br></div><div>(though this is at pharmacologic doses: in reality at physiological levels, its role is minmal)</div>
Describe how active vitamin D is produced?- <b>Chole calciferol</b> formed in <b>skin </b>on exposure to UV radiation. <div>- Cholecalciferol, and <b>ergo calciferol</b> (from food) are converted into 2,5 hydroxyvitamin D<b> (calcidiol) </b>in liver and stored</div><div>- Calcidol then hydroxylated in kidney to form 1,25 dihydroxyvitamin D (calcitriol)</div>
What is the effect of calcitriol (activated vitamin D) on calcium homeostasis?-Increases intestinal calcium and phosphate absorption<div>(can also increase bone resorption under conditions of calcium and phosphate deficiency)</div><div><br></div><div>Has <b>negative feedback effects on PTH secretion</b> </div>
What are signs and symptoms of<b> hyper</b>calcaemia?<b>Stones, Bones, Groans, Thrones, and Psychiatric Overtones</b><div><br></div><div><br></div><div>Kidney stones</div><div>Bone pain</div><div>Groans (abdominal pain, nausea and vomiting)</div><div>Polyuria</div><div>Depression, anxiety, cognitive dysfunction</div><div><br></div>
How might hypercalcaemia be seen on an ECG?<b>Decreases heart rate</b> but <b>increases contractility</b> --> <b>short QT</b> interval on ECG
How might <b>hypercalcaemia</b> lead to GI problems?<b>Increases gastrin </b>production --> increased acidity --> <b>peptic ulcers</b>
What are signs of <b>hypo</b>calcaemia?"<b>CATS</b><div><br><b>Cramps</b>/ convulsions: <b>Trousseau's sign</b></div><div><b>Arrhythmias</b></div><div><b>Tetany</b></div><div><b>Spasms</b>/stridor (Chvosteks' sign)</div>"
What are clinical signs of <b>hypo</b>calcaemia on examination?"<div><b>Chvostek's sign</b>: Tapping of facial nerve causes twitch on side of face.</div><div><img src=""SandySmoothChameleon-size_restricted.gif""><br></div><b>Trousseau's sign</b>: Inflating pressure cuff to 20mmHg for 3-5 mins causes hand to form specific shape<div><img src=""maxresdefault_1567497790841.jpg""><br><div><br></div></div>"
What causes <b>osteoarthritis?</b>Mechanical/biological/metabolic events which destabilise process of degradation + synthesis of articular cartilage chondrocytes, ECM + subchondral bone (exact aetiology not known)
Where does osteoarthritis affect?Entire joint:<div>- Articular cartilage</div><div>- Subchondral bone</div><div>- Pericapsular muscles</div><div>- Capsule</div><div>- Synovium</div>
What happens to the joint in osteoarthritis?- Loss of articular cartilage<div>- Sclerosis and eburnation of subchondral bone</div><div>- Osteophytes and subchondral cysts form</div>
What is meant by sclerosis in the context of OA?Hardening of bone below cartilage surface 
What is meant by eburnation of bone?Exposed subchondral bone becomes dense and has smooth surface 
What are osteophytes?"Bony projections associated with degeneration of cartilage <div><img src=""4453-4463-5494-12674tn.jpg""><img src=""paste-0c7ad3fe3349a5578d24cded4cfa450ed6edf17a.jpg""><br></div>"
What is the clinical characterisation of osteoarthritis?- Joint pain<div>- Stiffness</div><div>- Functional limitation</div>
What are risk factors for Osteoarthritis?- Age > 50years<div>- Female gender (especially post meno-pause)</div><div>- Obesity</div><div>- Genetic factors</div><div>- Physical/manual occupation</div><div>- High bone mineral density (negative correlation with osteoporosis)</div><div>- Knee malalignment</div>
What might you see on examination of a patient with osteoarthritis?"- Pain and crepitus on movement<div>- Joint swellings: Heberden's and Bouchard's nodes</div><div>- Pain gets worse with prolonged activity (ask about this). </div><div><br></div><div><img src=""h9991469_003.jpg""><br></div><div><br></div>"
What is <b>nodal osteoarthritis</b><b>?</b>Osteoarthritis of the hands:<div><br></div><div>- Typically in DIP, PIP and CMC joints</div>
What is the archetypal patient with nodal osteoarthritis?Post-menopausal female
In osteoarthritis <span class=cloze>[...]</span> nodes are found at the DIP and <span class=cloze>[...]</span> nodes are found at the PIP"In osteoarthritis <span class=cloze>Heberden's</span> nodes are found at the DIP and <span class=cloze>Bouchard's</span> nodes are found at the PIP<br> "
"In osteoarthritis Heberden's nodes are found at the <span class=cloze>[...]</span> and Bouchard's nodes are found at the <span class=cloze>[...]</span>""In osteoarthritis Heberden's nodes are found at the <span class=cloze>DIP</span> and Bouchard's nodes are found at the <span class=cloze>PIP</span><br> "
"What is seen here?<div><img src=""osteoarthritismi01b0w3n6_1525989.jpg""><br></div>"Heberden Nodes
"What is seen here?<div><img src=""bce26ff346ffba76bfbb93d557467a_gallery.jpeg""><br></div>""Bouchard's nodes"
What is 1st line and 2nd line management for Osteoarthritis?"<div><b>Non-pharmacological approaches: </b></div><div>- Weight loss</div><div>- Encourage exercise to improve local muscle strength (reassure exercise is not harmful)</div><div>- Provide supports and braces</div><div><b><br></b></div><div><b>Analgesia</b></div><font color=""#0000ff"">1st line</font>: Paracetamol + Topical NSAIDs<div><font color=""#0000ff"">2nd line</font>: Oral NSAIDs (+PPI), opioid, capsaicin cream and intra-articular corticosteroids</div>"
What is septic arthritis?Infection of one or more joints, caused by <b>pathogenic inoculation of microbes</b>
What are key diagnostic features of septic arthritis?"Joints which are: <div>- Hot</div><div>- Swollen</div><div>- Tender</div><div>- Restricted </div><div><br></div><div><img src=""images_1567497790841.jpg""><br></div>"
What are risk factors of septic arthritis?<div><b>PMH:</b></div><div>- Pre-existing joint disease (particularly RA)<br></div><div>- History of diabetes</div><div>- Immunosuppression</div><div>- Recent joint surgery</div><div>- Prosthetic joints</div><div><br></div><div><b>Social:</b></div><div>- IV drug abuse</div><div>- Alcohol use disorder</div>
What is the key investigation for suspected septic arthritis?- Joint aspiration --> synovial fluid microscopy and culture<div>- Blood culture </div>
How are joints inoculated in septic arthritis?<b>Directly</b>: e.g. surgery, trauma<div><b>Haematogenous</b>: pathogen travels in blood ciruclation</div>
What are the most common causative organisms of septic arthritis?<b>Staph</b> and <b>strep</b> account for 91% of cases (staph 60%):<div>- <i>Staph aureus </i></div><div><i>- Strep</i></div><div><i><br></i></div><div><i>+ Neisseria gonococcus </i>(in sexually active patients)</div><div>+ gram neg bacteria (in older and immunocompromised)<br></div>
What are contraindications to aspirations (e.g. in the case of suspected septic arthritis?)- Presence of a joint prosthesis (should be undertaken under sterile conditions- refer to orthopaedic surgeon)<div>- Suspected tuberculous arthritis</div><div><br></div><div>(overlying cellulitis/anticoagulation are not <b>absolute contraindications</b>) </div>
Describe treatment of septic arthritis?- Empirical antibiotic therapy (before causative agents determined) <div>- Give antibioitics IV for 2 weeks, followed by 4 weeks oral therapy (flucloxacilin, or clindamycin if pen allergic)</div><div>- Aspirate affected joints to dryness</div>
What are examples of monoarthritic conditions?- Septic arthritis<div>- Crystal arthritis (gout, Calcium pyrophosphate deposition disease)</div><div>- Osteoarthritis</div><div>- Trauma: Haemarthrosis</div>
What is meant by <b>oligoarthritis?</b>Joint pain in ≤5 joints<br>
What are examples of oligoarthritic conditions?- Crystal arthritis (gout, CPPD)<div>- Psoriatic arthritis</div><div>- Reactive arthritis</div><div>- Ankylosing spondylitis</div><div>- Osteoarthritis</div>
Which polyarthritic conditions present symmetrically?- Rheumatoid arthritis<div>- Osteoarthritis</div><div>- Viral arthritis ( Hep A-C, mumps)</div>
What polyarthritic conditions present asymetrically?- Reactive arthritis<div>- Psoriatic arthritis</div>
What are the key rheumatological investigations?"-<b> Joint aspirations</b>: key in monoarthritis. Assess <font color=""#0000ff"">appearance</font>, and <font color=""#0000ff"">measure WCC</font>, <font color=""#0000ff"">gram stain/culture</font>, <font color=""#0000ff"">polarised light microscopy</font><div>- <b>Bloods: </b></div><div>Basic: FBC, Urea +Electrolytes, ESR, CRP, urate.</div><div>Culture: Septic arthritis</div><div>Abs: RF, ANA etc.</div><div>HLA-B27 (ankylosing spondylitis)</div><div>Viral serology, PCR </div>"
What is the appearance of rheumatoid arthritis in X-rays?"- Loss of joint space<div>- Soft tissue swelling</div><div>- Peri-articular osteopenia</div><div>- Deformity</div><div>- Subluxation (partial dislocation)</div><div><img src=""h9991226.jpg""><br></div>"
What is the appearance of gout in X-ray?"- Normal joint space<div>- Soft tissue swelling</div><div>- Periarticular erosions</div><div><img src=""19893tn.jpg""><br></div>"
Where is the liver located?Predominantly right hypochondrium + epigastric areas, but extends into left hypochondrium 
Describe the diaphragmatic surface of the liver"<b>Anterosuperior </b>surface of liver:<div>- Smooth and convex- fits snugly beneath curvature of diaphragm. </div><div>- <b>Posterior aspect</b> of diaphragmatic surface <b>not covered</b> by visceral peritoneum, and in direct contact with diaphragm- <font color=""#0000ff"">""bare area""</font></div>"
Describe the visceral surface of the liver?<b>Posteroinferior </b>surface:<div><br></div><div>- Covered with peritoneum (apart from fossa of gallbladder, and porta hepatis)</div><div>- Lies in contact with right kidney (and adrenal gland), right colic flexure, transverse colon, first part of duodenum, gallbladder, oesophagus and stomach</div>
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What does the falciform ligament connect?Anterior surface of liver to anterior abdominal wall
What does the <b>falciform ligament </b>separate?Right and left lobes of the liver (are separated by what?)
Right and left lobes of the liver (are separated by what?)What does the <b>falciform ligament </b>separate?
What does the coronary ligament connect?Superior surface of liver to inferior surface of diaphragm 
What does the <b>coronary ligament </b>demarcate on the liver?Bare area of the liver (is demarcated by what ligament?)
Bare area of the liver (is demarcated by what ligament?)What does the <b>coronary ligament </b>demarcate on the liver?
What do the triangular ligaments connect?Left triangular ligament: Left lobe of liver to diaphragm<div>Right triangular ligament: Right lobe of liver to diaphragm</div>
Where are the hepatic recesses found?"<b>Subphrenic</b>: Between diaphragm and anterior/superior aspects of liver. <div><b>Subhepatic</b>: Peritoneal space between inferior surface of liver and transverse colon</div><div><b>Morison's pouch</b>: Potential space between visceral surface of liver and right kidney</div>"
Pathological abdominal fluid (blood/ascites) is most likely to collect in <span class=cloze>[...]</span> in a bedridden patient."Pathological abdominal fluid (blood/ascites) is most likely to collect in <span class=cloze>Morison's pouch</span> in a bedridden patient.<br> Deepest part of peritoneal cavity when supine<br><br>(morisons collects fluid)"
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What and where are the accessory lobes of the liver?"<div>Both arise from right lobe, on visceral (postero-inferior) surface of liver</div><b><div><b><br></b></div>Caudate</b>: Lies between inferior vena cava, and fossa produced by <b>ligamentum venosum.</b><div><b>Quadrate</b>: Lies between gallbladder and fossa produced by l<b>igamentum teres.</b></div><div><br></div><div><img src=""Anatomical-Lobes-of-the-Liver-1024x335.jpg""><br></div>"
The accessory lobes of the liver arise from the <span class=cloze>[...]</span>The accessory lobes of the liver arise from the <span class=cloze>right lobe</span><br> What separates the <b>caudate and quadrate </b>lobe?<b>Porta hepatis</b>, which transmits all vessels, nerves and ducts entering/leaving the liver (apart from hepatic veins)
Describe the microscopic structure of the liver"Hepatocytes arranged into<b> lobules</b>: hexagonal-shaped, and drained by<b> central vein.</b> <div><img src=""paste-14169196f45979d50edfaa06f81ed6ae0f5fbd77.jpg""><br></div>"
What makes up a portal triad, and where are they found?"<div>Found at periphery of lobules:</div><div><br></div><div>Made up of three structures:<br></div><div><br></div><div><b>Arteriole: </b>Branch of hepatic artery</div><div><b>Venule: </b>Branch of hepatic <b>portal </b>vein</div><div><b>Bile duct: </b>Branch of bile duct leaving the liver</div><div><br></div><div><img src=""paste-b1d075ca31248a63b5144abf046d1b1cb06bc5e7.jpg""><br></div>"
What provides the liver with blood?<b>Hepatic artery (25%):</b> Supplies non-parenchymal structures of liver, derived from coeliac trunk.<div><br></div><div><b>Hepatic portal vein (75%):</b> Supplies liver with blood carrying nutrients absorbed from small intestine. Allows liver to perform gut-related functions</div>
What is the source of the hepatic portal vein?"- Splenic vein<div>- Superior and inferior mesenteric vein</div><div><img src=""Venous-Drainage-of-the-Spleen.jpg""><br></div>"
What is the <b>porta hepatis?</b>"Region where hepatic artery and portal vein enter the liver, and the common hepatic duct exits. <div><br></div><div><img src=""liver-porta-hepatis.png""><br></div>"
How are hepatocytes arranged in the lobule?"Arranged in trabeculae 1-2 cells thick. <div><br></div><div>Each trabecula surrounded by sinusoids, which have fenestrae facilitating fluid + molecular exchange. </div><div><br></div><div><img src=""paste-d50103ed986d861b1a7c4386db77ba18e257515c.jpg""><br></div>"
What is the space of Disse?"Space between the sinusoids and the hepatocytes<div><img src=""hsinus2.gif""><br></div>"
What is the source of the blood feeding into the sinusoids?Hepatic artery and portal vein branches
Discuss the heirachy of vessels which drain bile in the liverCanaliculi --> Bile ductules (+ canals of Hering) --> Portal bile ducts --> Septal ducts --> Segmental ducts --> right/left hepatic ducts
Aside from hepatocytes and epithelial cells, what other cells reside in the liver?<b>Kupffer cells: </b>Macrophages attached to sinusoidal epithelium<div><b>Lymphocytes e.g pit cells: </b>Natural Killer cells, also attached to sinusoidal epithelium</div><div><b>Hepatic stellate cells</b>: Lie in space of Disse. </div>
What is the physiological role of hepatic stellate cells, and what happens in pathology?<b>Physiological</b>: Store vitamin A<div><b>Pathology</b>: In response to hepatic injury, transform into myofibroblast-like cells + lay collagen.</div>
Describe the layout of a liver acinus"Area of liver parenchyma centred on two portal tracts, extending to terminal hepatic venule. Can be divided into 3 zones, from portral tract to central venule<div><br></div><div><img src=""051.jpg""><br></div>"
With reference to the liver acinus, which area is most prone to damage, and why?"Zone 3 of liver acinus (around central venule), as it is least perfused<div><img src=""A-schematic-drawing-of-simple-liver-acinus-grouped-around-the-portal-tract-PT-with.png""><br></div>"
What are the basic functions of the liver?- Bilirubin and bile acid metabolism<div>- Lipid metabolism (cholesterol, triglyceride, phospholipid etc.)</div><div>- Protein metabolism (albumin, clotting factors; synthesis +degradation of amino acids and proteins)</div><div>- Carbohydrate metabolism (glucose and glycogen formation)</div><div>- Xenobiotic metabolism (drugs + toxins)</div><div><br></div>
What is the distinction between acute and chronic hepatitis?<b>Acute: </b>Inflammation and necrosis of hepatocytes lasting <6 months<div><b>Chronic: </b>Lasting >6 months</div><div><br></div><div>Acute hepatitis may resolve or become chronic</div><div>Chronic hepatitis may progress to fibrosis and cirrhosis</div>
What is hepatitis?Inflammation of the liver
Discuss the aetiology of hepatitis- Alcohol<div>- Viral </div><div>- Drugs </div><div>- Autoimmune</div><div>- Metabolic </div>
What are the autoimmune causes of hepatitis?- Autoimmune hepatitis<div>- Primary biliary cholangitis</div><div>(Primary sclerosing cholangitis)</div>
What are metabolic causes of hepatitis?"- Alpha-1-antitrypsin deficiency<div>- Wilson's disease</div>"
What common change to the liver is often reversible?"Fatty liver:<div>- Hepatocytes accumulate lipid droplets in cytoplasm. </div><div><img src=""LIVER007.jpg""><br></div><div>Usually reversible on removal of stimulus</div>"
What are the macroscopic and microscopic changes in fatty liver disease?"<b>Macroscopic: </b>Liver is enlarged, soft, yellow and greasy<div><b>Microscopic: </b>Lipid accumulates in hepatocytes in <font color=""#0000ff"">macrovesicles </font>of varying size. </div>"
"What is the significance of hepatocytes with microvesicular vesicles?<div><img src=""Figure3_1_9.jpg""><br></div>""Microvesicular steatosis: rare, but indicates severe metabolic derangement (e.g. acute fatty liver of pregnancy, Reye's syndrome, mushroom poisoning)<div><br></div><div><br></div>"
What are the causes of steatohepatitis?- <b>Alcohol</b><div>- NASH (non-alcoholic steatohepatitis): usually obesity or diabetes</div>
What are the microscopic changes in steatohepatitis?- Inflammatory infiltrate, with neutrophil polymorphs<div>- Hepatocytes show ballooning</div><div>- Mallory bodies form: cytoplasmic filaments aggregate</div><div>- Fatty change</div><div>- Fibrosis (particularly in zone 3)</div>
What is steatosis?Fatty change- abnormal retention of lipids within a cell
What are the microscopic changes in acute hepatitis?"- Inflammatory cell infiltrate of portal tracts, parenchyma + interface. <font color=""#0000ff"">(parenchymal most infiltrated)</font><div>- Hepatocyte damage: swelling, acidophils, apoptotic heaptocytes (Councilman bodies)</div><div>- In severe cases, necrosis can join- <b>bridging necrosis</b></div>"
What is fulminant hepatitis, and how is it characterised?Severe and sudden hepatitis, characterised by massive necrosis of liver parenchyma + acute yellow atrophy of liver
What types of hepatitis viruses cause acute and chronic hepatitis?<b>Acute</b>: HAV, HBV +/- HDV, HEV<div><b>Chronic</b>: HBV, HCV</div>
What are the microscopic changes typically seen in chronic hepatitis?- Chronic inflammatory cell infiltrate (mainly lymphocytes), found mainly in portal tracts and interface. <div><br></div><div>- Accompanying portal tract fibrosis + architectural disruption </div>
Define cirrhosis?A diffuse process characterised by <b>fibrosis </b>and conversion of normal architecture into abnormal <b>nodules. </b>
What are some common complications resulting from <b>decompensated hepatitis?</b>- Hepatocellular failure (Jaundice, hypoalbuminaemia, coagulopathy)<div>- Portal hypertension </div><div>- Ascites</div><div>- Porto-systemic shunting of blood </div><div>- Encephalopathy </div><div>- Hepatocellular carcinoma </div><div>- Increased risk of systemic infections </div>
Why is consideration of the CVS important in pre-op patients?- CVD most common co-morbidity in surgical pts<div>- Anaesthesia stresses the cardiovascular system</div>
What is the relevance of cardiac failure in pre-op patients?Limits ability of heart to respond under stress, during anaesthesia/surgery. <div><br></div><div><b>More dangerous than Ischaemic heart disease in this context</b></div>
What is the relevance of ischaemic heart disease in pre-op patients?"Pts with unstable angina/recent MI are at<font color=""#0000ff""> increased risk of peri-operative MI</font> (w/ mortality of >30%). <div><br></div><div>Revascularisation before surgery does little to reduce mortality</div>"
What are the guidelines for pre-op pts with hypertension?Persistent uncontrolled HTN should be treated for a month or more before elective surgery
What valvular heart disease in particular can lead to significant perioperative risk?Aortic stenosis
When is an ECG recommended in pre-op patients?"<font color=""#0000ff"">>55y/o</font>: <b>All </b>patients (due to risk of silent MI)<div><font color=""#0000ff""><55y/o</font>: Pts with cardiac symptoms/signs (including HTN)</div>"
What drugs affecting the Cardiovascular system should be continued/stopped before operations?"<b><font color=""#0000ff"">Continue</font>:</b><div>- Anti-anginal </div><div>- Anti-hypertensives</div><div><br></div><div><b><font color=""#ff0000"">Stop:</font></b></div><div>- ACE inhibitors</div><div>- Angiotensin-II Receptor antagonists</div><div><br></div><div>(associated with severe hypotension after anaesthesia)</div>"
How can a cardiopulmonary exericise test be used pre-operatively?"Assess pt fitness: measure gas exchange of pt exercising on a cycle ergometer. <div><br></div><div><font color=""#ff0000"">- Low peak VO<sub>2</sub></font></div><div><font color=""#ff0000"">- Low VO<sub>2</sub> at anaerobic threshold</font></div><div><font color=""#ff0000"">- High VE/VCO<sub>2</sub> (Amount of breathing to breath off 1L of CO<sub>2</sub>) </font></div><div><br></div><div>Are associated with <font color=""#ff0000"">poor outcome</font></div>"
Patients undergoing what type of surgery need to be particularly optimised with regard to their respiratory system?Upper abdominal surgery- has a greater impact on respiratory function
What is <b>tenesmus?</b>Feeling of incomplete evacuation of the bowels (describes what symptom?)
Feeling of incomplete evacuation of the bowels (describes what symptom?)What is <b>tenesmus?</b>
What is <b>melaena?</b>Blood passed in faeces, with characterstic offensive smell and black, tar-like appearance (describes what?)
Blood passed in faeces, with characterstic offensive smell and black, tar-like appearance (describes what?)What is <b>melaena?</b>
What is the common cause of septic arthritis in <b>young, fit, sexually active patients</b>?Neisseria gonorrhoeae (is the most common causative agent of septic arthritis in which patient group?)
Neisseria gonorrhoeae (is the most common causative agent of septic arthritis in which patient group?)What is the common cause of septic arthritis in <b>young, fit, sexually active patients</b>?
What is typically associated with ankylosing spondylitis?<b>8 As</b><div><b><br></b></div><div>Atlanto-axial subluxation</div><div>Anterior uveitis</div><div>Apical lung fibrosis</div><div>Aortic regurgitation</div><div>Amyloidosis</div><div>Autoimmune bowel disease (ulcerative colitis)<br>Atrioventricular block</div><div>Achilles tendon enthesitis</div>
What is the action of <b>alendronic acid?</b>"Bisphosphonate- prevents loss of bone density, to treat osteoporosis (+Paget's disease, osteogenesis imperfecta etc.)<div><br></div><div><font color=""#0000ff"">Acts to encourage osteoclast apoptosis</font></div>"
Give an example of a bisphosphonate?Alendronate/Alendronic Acid
What is the <b>Garden classification?</b>Classification of subcapital femoral neck fractures, predicts development of avascular necrosis (Uses what classification?)
Classification of subcapital femoral neck fractures, predicts development of avascular necrosis (Uses what classification?)What is the <b>Garden classification?</b>
Outline the Garden classification. "<font color=""#0000ff"">Garden Stage I</font>: Incomplete fracture, undisplaced<div><font color=""#0000ff"">Garden Stage II</font>: Complete fracture, undisplaced</div><div><font color=""#0000ff"">Garden Stage III</font>: Complete fracture, partially displaced</div><div><font color=""#0000ff"">Garden Stage IV</font>: Complete fracture, completely displaced</div><div><img src=""paste-8c6e7441ebf3d39d8acbd24c9b5364802f17dd93.jpg""><br></div>"
How do the Garden classifications correlate with management options?"<font color=""#0000ff"">Garden I and II:</font> Dynamic Hip Screw- as minimal displacement of femoral head --> blood supply to femoral head likely intact. <div><br></div><div><font color=""#0000ff"">Garden III, IV</font>: Higher risk of avascular necrosis, so Total hip arthroplasty or hemiarthroplasty best option. </div>"
For a #NOF Garden IV, how would one decide between a hemiarthroplasty and a total hip replacement?"<font color=""#0000ff"">Hemiarthoplasties useful in pts with poor pre-op mobility</font>. Much less extensive, but have <b>high rate of wear + lead to rapid joint pain and erosion of acetabulum</b> (less of a problem in immobile pts). <div><br></div><div><font color=""#0000ff"">Otherwise use THR</font>: fast return to mobility- most pts mobilise within 48hrs. <div><br></div></div>"
What is <b>compartment syndrome?</b>Elevated interstitial pressure in a closed compartment, resulting in microvascular compromise 
What can cause compartment syndrome?- Fracture<div>- Compartment haemorrhage</div><div>- Direct soft-tissue injury</div><div>- Direct muscular injury</div>
Describe the pathophysiology of compartment syndrome?Elevated interstitial pressure in a closed compartment restricts capillary flow. <div><br></div><div>Causes tissue necrosis secondary to oxygen deprivation</div>
What are the common characteristics of acute compartment syndrome?"<b>6 Ps:</b> <div><br></div><div><font color=""#0000ff"">Pain</font></div><div><font color=""#0000ff"">Paraesthesia</font></div><div>Paralysis</div><div>Pallor</div><div>Pulselessness (though some cases can still have pulselessness)</div><div>Pressure</div><div><br></div><div><font color=""#0000ff"">Pain and paraesthesia are early symptoms of compartment syndrome</font></div>"
What are the symptoms of chronic compartment syndrome?Numbness + tingling<div>Pain (burning, cramping, sharp/stabbing), over months, relieved by rest. </div><div><br></div><div><b>Symptoms brought on by exercise</b></div>
What is a sensitive, early clinical feature for acute compartment syndrome, which can be elicited on examination?Pain out of proportion to injury aggravated by <b>passive stretching </b>of muscle groups involved in compartment. <div><br></div><div>e.g. More pain on assessing tone than power of an examination</div>
What is the preferred treatment for compartment syndrome?"<font color=""#0000ff"">Acute</font>: <b>Fasciotomy</b>- fascia is cut to relieve tension or pressure. Important to act within 6 hr window- decreases risk of significant muscle necrosis, requiring amputation<div><br></div><div><font color=""#0000ff"">Chronic</font>: Conservative management (prolonged rest, modify offending activities, NSAIDS), fasciotomy second line</div>"
<span class=cloze>[...]</span> = Calcium pyrophophate deposition (CPPD)<span class=cloze>Pseudogout</span> = Calcium pyrophophate deposition (CPPD)<br> Pseudogout = <span class=cloze>[...]</span>Pseudogout = <span class=cloze>Calcium pyrophophate deposition (CPPD)</span><br> How do crystals differ between pseudogout and gout in polarised light microscopy?<b>Pseudogout</b>:<div>- Positively birefringent (blue and pink)</div><div>- Rhomboid-shaped</div><div><br></div><div><b>Gout</b>:</div><div>- Negatively birefringent (orange/yellow, red)</div><div>- Needle-shaped </div>
In <span class=cloze>[...]</span> crystals are made up of calcium pyrophosphate whereas in <span class=cloze>[...]</span> crystals are made up of monosodium urate crystalsIn <span class=cloze>pseudogout</span> crystals are made up of calcium pyrophosphate whereas in <span class=cloze>gout</span> crystals are made up of monosodium urate crystals<br> In pseudogout crystals are made up of <span class=cloze>[...]</span> whereas in gout crystals are made up of <span class=cloze>[...]</span>In pseudogout crystals are made up of <span class=cloze>calcium pyrophosphate</span> whereas in gout crystals are made up of <span class=cloze>monosodium urate crystals</span><br> "Polarised light microscopy of synovial fluid from a joint is shown below. What is the most likely diagnosis?<div><img src=""o-Sh-N7iJzDZJZ3A77iUOknjHIBZR2sw34ADiUAIZCYHaF6-2KVfsEcvKQScMMwrgAHPsD1os7debz3conQ-M0Ewh3A3tK_XDAW6ixFVEpk3gFppcgw4DrO6IoeV=w740.png""><br></div>""<div>Crystals are <b>rhomboid </b>and <b>positively birefringent </b>(blue/pink)</div><div><br></div><font color=""#0000ff"">Pseudogout/ acute calcium pyrophosphate deposition arthritis</font>"
"Polarising light microscopy of synovial fluid from a joint shows the following. What is the most likely diagnosis?<div><img src=""goutdiagnost.jpg""><br></div>"<b>Needle shaped crystals</b>, <b>negatively </b>birefringent (red/orange)<div><br></div><div>Gout</div>
What pts does pseudogout typically occur in?- Older patients (often women)<div>- Younger patients with associated metabolic conditions (hyperparathyroidism, haemochromatosis)</div>
How can pseudogout be seen radiographically?"Often causes chondrocalcinosis: deposition of calcium in cartilage and soft tissue<div>(typically occurs in pts already with osteoarthritis, so this can be seen too)</div><div><br></div><div><img src=""60ec4y5YFKnU-N_m94arSXpZaRxamXOXZHioIRo4Bxb9SzIgn6WJyBPtpQckEfFu4lYoaRph5a-ugvuOq-ZxcAasPnvWymGX8oDPPLWE3W3qIen3Ysamnn7p0EZH=w477.png""><br></div>"
Where and how does CPP arthritis typically manifest?Usually joints not commonly affected by osteoarthritis (wrists, or shoulders)<div><br></div><div>Most common form of disease presents as chronic degenerative arthritis, which <b>resembles osteoarthritis</b> </div>
What are key diagnostic factors of Calcium Pyrophosphate Deposition arthritis?"- Painful + Tender joints<div>- Osteoarthritis-like involvement of joints <font color=""#0000ff"">(wrists, shoulders)</font></div><div>- Sudden worsening of osteoarthritis</div><div>- Risk factors: Older age, FHx, previous injury/surgery, <font color=""#0000ff"">metabolic disorders</font></div>"
What is the management of acute CPPD?- NSAIDs (or intrarticular corticosteroids if joint is accessible)<div>- Colchicene if pt has (low eGFR or Hx of Upper GI Bleed)</div>
In what patient populations is SLE most common in?- Women (12x than men)<div>- Asian and <b>African </b>descent</div>
What are some genetic associations with SLE?- More common in those with complement deficiency (esp. C2-def homozygotes, and C4 heterozygotes)<div>- Associations with genes in the MHC region. </div>
What some environmental factors in aetiology of SLE?<b>Drugs </b>(strongest causative agents):<div>- Procainamide</div><div>- Hydralazine</div><div>- Isoniazid</div><div>- Phenytoin</div><div>- Anti-convulsants (Carbamazepine, chlorpromazine) </div><div><br></div><div>- Sulfasalazine, sulphonamides, penicillin, oral contraceptives rarer</div><div><br></div><div>Some hypotheses about viruses- EBV</div>
What mediates the pathophysiology of SLE?High affinity IgG Ab to ds-DNA and nuclear proteins
What are some common features of SLE?"<div><b>General </b></div>- Fatigue<div>- Fever</div><div>- Weight loss</div><div><br></div><div><b>Mucocutaneous</b></div><div>- Skin manifestations- malar (butterfly) rash, due to photosensitivity</div><div>- Mouth ulcers </div><div><br></div><div><b>Musculoskeletal:</b></div><div>- Inflammatory pain (worse in mornings w/ stiffness)</div><div>- Acute polyarthritis</div><div><br></div><div>- Raynaud's</div><div><br></div><div>Multisystemic, can can also produce GI, Haematological, CNS, and cardiopulmonary symptoms </div>"
Describe the possible renal involvement in SLE?Lupus nephritis common (particularly in those with Ab to dsDNA)<div><br></div><div>Presentations include:</div><div>- HTN</div><div>- Nephrotic syndrome</div><div>- Renal failure </div><div><br></div><div>Urinalysis may have haematuria, casts, or proteinuria</div>
What are common findings from blood in SLE?- Raised ESR, normal CRP<div>- Thrombocytopaenia (low platelets)</div><div>- High creatine + low GFR --> lupus nephritis</div>
What antibodies are associated with Systemic Lupus Erythematosus?"<b>ANA</b> (antinuclear antibodies) and anti-dsDNA<div><br></div><div>(Anti-Smith's too- specific but not common)</div><div>Most SLE pts have ANA, but this is present in many conditions, so not diagnostic, unless with clinical picture</div>"
A pt with positive results for ANA and anti-dsDNA is suggestive of what?SLE
In what age group does SLE typically emerge?15-45 y/o
Discuss the management of SLE?<b>General measures:</b><div>- High-factor sunblock</div><div>- Hydroxychloroquine: cornerstone as it reduces disease flares + improves survival</div><div><br></div><div><b>Maintenance:</b></div><div>- NSAIDs + hydroxychloroquine for joint + skin symptoms</div><div>- Azathioprine, methotrexate, mycophenolate as steroid sparing agents. </div><div>- Belimumab (inhibits BAFF) in auto-ab +ve disease with high activity</div><div><br></div><div>- Corticosteroids if other symptom-relieving measure have failed</div>
What is the blood supply to the femoral head?- <b>Medial</b> (main supply) and lateral circumflex arteries (from profunda femoris)<div>- Artery to the ligamentum teres (from obturator)</div><div>- Ascending cervical branches</div>
SLE is often associated with <span class=cloze>[...]</span> syndromeSLE is often associated with <span class=cloze>antiphospholipid</span> syndrome<br> <span class=cloze>[...]</span> is often associated with antiphospholipid syndrome<span class=cloze>SLE</span> is often associated with antiphospholipid syndrome<br> What are the antibodies associated with antiphospholipid syndrome?"<font color=""#0000ff"">- Lupus anticoagulant</font><div>- Anti cardiolipin antibodies<div><div>- Anti-beta2-glycoprotein I antibodies</div></div></div>"
What occurs in antiphospholipid syndrome?<b>CLOT</b><div><b><br></b></div><div>Coagulation defect (arterial/venous)</div><div>Livedo reticularis (pink-blue mottling from capillary dilation, and stasis in skin)</div><div>Obstetric (recurrent miscarriage)</div><div>Thrombocytopenia</div><div><br></div>
How might you differentiate between SLE and Rheumatoid Arthritis?Difficult clinically as SLE presents with similar inflammatory arthritis, though in SLE tends to be less symmetrical. <div><div><br></div><div>SLE tends to be <b>correctable</b>- ask to make a fist. RA cannot move</div><div><br></div><div>RA tends to have Anti-CCP and RF, whereas SLE will likely have ANA and anti-dsDNA</div></div>
What antibodies are closely associated with Sjogren syndrome?Anti-Ro and anti-La Abs
"What is the Simmonds' triad used to assess?"Achilles tendon rupture
"How is <b>Thompson's test </b>carried out?""Ask pt to kneel on chair with feet hanging off the edge, then squeeze calves. <div><br></div><div>+ve result: Foot will not move- achilles tendon rupture</div><div>-ve result: Foot will plantarflex</div><div><br></div><div><img src=""tenor.gif""><br></div><div>(+ve result shown here)</div><div><br></div><div>(describes what test?)</div>"
What are the main serious side effects of NSAIDs?- GI bleeding<div>- Cardiovascular events (MI + stroke)</div><div>- Renal injury</div>
What factors increase the risk of ulcers, cardiovascular side effects etc associated with NSAIDs?- Old age<div>- Polypharmacy</div><div>- Hx of peptic ulcers</div><div>- Renal impairment</div>
How can you reduce the risk of GI side effects with prescribing NSAIDs?<b>- </b>Co-prescribe PPIs if >45 or other risk factors. <div>- Avoid prescribing NSAIDs with anti-coagulants, anti-platelet agents, SSRI, spironolactone, steroids + bisphosphonates</div><div>- Consider using coxibs instead of non-selective NSAIDs</div>
Which NSAIDs should be considered or avoided wrt Cardiovascular side effects?"<div><font color=""#00aa00"">+ Naproxen </font>(lowest CVD risk)</div><div><br></div><div>- <font color=""#ff0000"">Coxibs and diclofenac </font>higher risk, <b>contraindicated </b>if prior history of CVD</div>"
In what pts prescribed NSAIDs are renal risks higher?Pts already on:<div>- Diuretics</div><div>- ACE inhibitors</div><div>- ARB (angiotensin II Receptor blockers)</div>
What are the safest NSAIDs to give wrt to avoiding renal risks?- Naproxen<div>- Ibuprofen plus PPI</div>
Where does gout typically occur?Metatarsophalangeal joint of the big toe (50% of cases)<div><br></div><div>Other common joints are: </div><div>- Ankle</div><div>- Foot</div><div>- Small joints of hand</div><div>- Wrist</div><div>- Elbow</div><div>- Knee</div>
Where is the cauda equina found?"Lumbar cistern- a gap between the arachnoid and pia mater<div><br></div><div><img src=""Distal-End-of-the-Spinal-Cord-The-Lumbar-Cistern.jpg""><br></div>"
What typically causes cauda equina syndrome?Massive disc herniation in lumbar region, which causes pressure on nerve roots in cauda equina
What are common signs in a patient with <b>cauda equina?</b>- Saddle <b>(perineal) anaesthesia</b><div>- <b>Bladder retention</b> (often presents earlier as difficulty starting/stopping a stream of urine)</div><div>- <b>Leg weakness</b></div>
How is Cauda Equina Syndrome treated?Decompressive <b>Laminectomy</b> (removal of the lamina of vertebra, to relieve pressure on nerves)<div><br></div><div><b>Early treatment </b>may significantly reduce risk of long-term damage. </div><div><br></div><div>Some pts may not recover complete function</div>
How is cauda equina diagnosed?o/e:<div>- Lumbar loss of pain sensation</div><div>- <b>Perineal altered sensation</b></div><div>- <b>Paraplegia</b></div><div><br></div><div>Confirmed with an MRI/CT</div><div><br></div>
"What is seen on this MRI?<div><img src=""f7a8adca63efae788f621869cc21e8_big_gallery.jpg""><br></div>"Cauda equina syndrome: Slipped disc pushing on cauda equina
What is the most common hip disorder in adolescents?Slipped capital femoral epiphysis
"This is an X-ray of an 11 year old, complaining of hip pain. What is seen here?<div><img src=""xrb011.jpg""><br></div>""Slipped capital femoral epiphysis on the left hand side: Epiphysis looks smaller, and drawing Klein's line does not intersect the femoral head<div><img src=""Kleins-line-in-normal-situation-versus-in-slipped-capital-femoral-epiphysis-13.png""><br></div>"
What can cause weakening of the growth plate in slipped capital femoral epiphysis?- Stress on growth plate (obesity)<div>- Endocrine disorders: panhypopituitarism, hypothyroidism, renal osteodystrophy</div><div>- Rapid growth in adolescence may also weaken the plate</div>
"What is Klein's line and what is it used for?""Line drawn parallel to upper edge of femoral neck- if line does not intersect femoral head, confirms diagnosis of slipped capital femoral epiphysis. <div><br></div><div><img src=""757-5_default.jpg""><br></div>"
What is meant by development dysplasia of the hip?Spectrum of conditions affecting proximal femur and acetabulum 
How is developmental dysplasia of the hip picked up in examination?"Barlow/Ortolani's test are positive<div><br></div><div>Barlow: Hip flexed to 90° and <b>adducted</b>. Hand placed on knee, and posterior pressure placed, to identify dislocatable hips. </div><div><br></div><div>Ortolani: Hip flexed to 90° and <b>abducted. </b>Hand placed on greater trochanter/hip joint. Anterior pressure placed to identify a dislocated hip that is relocatable</div><div><br></div><div><img src=""UADwIN.gif""><br></div>"
"How is <b>Barlow's</b> test carried out?""Hip flexed to 90° and <b>adducted</b><div>Posterior pressure applied with hand on knee</div><div><br></div><div><img src=""nhN261.gif""><br></div>"
"How is Ortolani's test performed?"Hip flexed to 90° and <b>abducted</b>, with fingers placed over greater trochanter/hip joint. Anterior pressure applied over the trochanter<div><br></div>
Aside from positive findings on Barlow and Ortolani tests, what additional findings can be made in congenital hip dislocation?Asymmetrical gluteal folds and <b>limb-length inequality. </b>
What investigations may be taken to investigate Developmental Dysplasia of the Hip?<b>6 weeks- 6 months</b>: Ultrasound (X-ray not helpful as insufficient ossification of hip). Not before 6 weeks to reduce false positives.<div><br></div><div><b>>6 months:</b> Hip X-Ray</div>
How can DDH be detected on an X-Ray?"Drawing Hilgenreiner and Perkin lines:<div><br></div><div><font color=""#0000ff"">Hilgenreiner</font>: Horizontally through superior aspect of both triradiate cartilages. </div><div><font color=""#0000ff"">Perkin</font>: Perpendicular to Hilgenreiner line, intersecting lateral most aspect of acetabular roof. </div><div><br></div><div>Femoral epiphysis should be seen in inferomedial quadrant (below hilgenreiner and medial to perkin line)</div><div><img src=""Pelvis-X-Ray-AP-view-showing-left-sided-dysplastic-hip-with-femur-head-lying-in-the.png""><br></div><div><br></div><div>Left side DDH</div>"
Where is the triradiate cartilage found on X ray?"Y-shaped epiphyseal plate at junction of ischium, ilium and pubis<div><br></div><div><img src=""A273344_1_En_11_Fig8_HTML.jpg""><br></div><div><br></div>"
What is <b>teratological hip dysplasia?</b>Antenatal fixed dislocation of the hip. 
Antenatal fixed dislocation of the hip. What is <b>teratological hip dysplasia?</b>
What are management options for patients with developmental dysplasia of the hip?"<b>Monitor: </b>Many pts will achieve spontaneous resolution, so no need. <div><b>Pavlik Harness: </b>Given to pts <6 months, if dysplasia worsens/persists after 3 weeks. </div><div><b>Closed Reduction: </b>With spica cast- given to most children aged 6-18 months. </div><div><b>Open Reduction: </b>With spica cast- given to pts 18months- 6 years. </div><div><br></div><div><img src=""paste-471996b7c41a7ab0edad7e3aa47ab5ff10a08c4e.jpg""> <img src=""15aec41e1887c0f57b54e88ca509f615.jpg""><br></div><div>Pavlik harness                                         Spica Cast</div>"
At what age is there little potential for remodelling following developmental dysplasia of the hip? >6 years old. Salvage osteotomies are recommended for symptomatic hips instead
What is the most common cause of hip pain in children?Transient synovitis (typically affects 2-12 y/o)
What is thought to be the aetiology of transient synovitis of the hip?Temporary inflammation secondary to a viral URTI
What is the most sensitive test for transient synovitis of the hip?"<b>Log roll:</b> Pt lies supine and leg rolled gently from side to side. Positive test is <font color=""#0000ff"">involuntary muscle guarding in affected limb</font>"
How do you differentiate between transient synovitis of the hip and spetic arthritis in children?<b>Septic: </b><div>- Pain is more severe- child often cannot walk. <div>- Fever >38.5°C, Non-weight bearing, ESR >40, and WBC >12,000 good predictors</div></div>
"What are the stages of Perthes' disease?"- Avascular necrosis<div>- Collapse</div><div>- Repair</div><div>- Re-modelling<br><div><br></div></div>
What are features of Perthes Disease?- Hip pain- develops progressively over a few weeks<div>- Limp</div><div>- Limited range of hip movement</div><div>- X ray shows widening of joint space + decreased femoral head size</div>
"What is seen in this X-Ray?<div><img src=""xrb089.jpg""><br></div>"Perthes disease: Femoral epiphyses show extensive destruction, acetabulae are deformed
In osteomyelitis, what is the causative agent typically associated with <b>malaria and homzogyous sickle cell disease?</b>Non-typhi Salmonella (often cause osteomyelitis in which patients?)
Non-typhi Salmonella (often cause osteomyelitis in which patients?)In osteomyelitis, what is the causative agent typically associated with <b>malaria and homzogyous sickle cell disease?</b>
"What are the signs of <b>flexor tendon sheath infection</b> (Kanavel's signs)?"- Fixed flexion<div>- Fusiform swelling</div><div>- Tenderness</div><div>- Pain on passive extension</div><div><br></div><div>(suggest what?)</div>
" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-2-Q.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-2-A.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-3-Q.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-3-A.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-4-Q.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-4-A.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-5-Q.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-5-A.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-6-Q.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header"">Hip X-Ray Lateral</div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e1f9b39dba154a8aa85fe54d18d656cd-ao-6-A.svg"" /></div> <div id=""io-original""><img src=""tmpcg83kwm0.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
What typically causes hip dislocation?Direct trauma: Road Traffic Accidents + significant falls from height
In what direction are most hips dislocated?Posteriorly (90%): Affected leg is shortened, adducted and internally rotated
"What is seen here?<br><img src=""swan_neck_deformity_2.jpg""><br>"Swan-neck deformity of index finger
What are common causes of swan-neck and boutonniere deformities?- Inflammatory conditions (RA)<div>- Genetic conditions e.g. Ehlers-Danlos</div><div>- Injury</div>
"What is seen here?<br><div><img src=""Boutonniere_Fig1.jpg""><br></div>"Boutonniere deformity
"What is seen here?<div><img src=""maxresdefault (1).jpg""><br></div>"Hyperextension of interphalangeal joint, <b>fixed flexion </b>and <b>subluxation</b> of <b>MCP<br></b>- <b>Z-thumb</b> (associated with RA)
"What is seen here?<div><img src=""B3AHW0.2e16d0ba.fill-920x613.jpg""><br></div>"Psoriatic Plaques (salmon coloured, with silvery scales)<div><br></div><div>Psoriasis and psoriatic arthritis closely associated</div>
"What is seen here?<div><img src=""642x361_Slide_2_Nail_Pitting.jpg""><br></div>"Nail <b>p</b>itting- indicative of <b>p</b>soriasis
"What is seen here?<div> <img src=""paste-527dc090485b61ff523187e2f19d94487be2a18a.jpg""></div>"<b>Onycholysis- </b>nails separates from skin underneath. 
What is onycholysis suggestive of?- Psorisis (+ psoriatic arthritis)<div>- Fungal infections</div>
"What is seen here, and what does it indicate?<div><img src=""paste-42dcbed7fdbf93b1eda01901b3968548b730faa6.jpg""><br></div>""<b>Gouttron's</b> papules- suggests <b>dermatomyositis</b>"
"What is seen here?<br><div><img src=""Gouty_tophi_5_800_580_70.jpg""><br></div>"<b>Gouty tophi</b>
"In what rheumatological conditions is raynaud's associated?""- Dermato myositis<div>- Poly <b>myositis</b></div><div>- Sclero derma</div><div><br></div><div>Though note,<font color=""#0000ff""> often found in young healthy people </font>(particularly thin pts)</div>"
"What is seen here, and what does it suggest?<div><img src=""paste-2358b0fe2c07516d793784e37f09d1a8eec348a5.jpg""><br></div>"<b>Sclerodactyly</b>- suggestive of scleroderma
What is sclerodactyly?Localised thickening and tightness of skin of fingers or toes<div><br></div><div>Often leads to ulceration of skin </div>
"What is seen here, and what is it suggestive of?<div><img src=""mechanics-hand-menu.jpg""><br></div>""Dry, cracked fingers, predominantly affecting index finger: <b>mechanic's hand</b>- suggestive of myositis"
"If these feel rubbery, what are they likely?<div><img src=""rheumatoid nodules.jpg""><br></div>"Rheumatoid nodules
"What is this?<br><img src=""7361-dystrophic_calcification-1296x728-slide1.jpg"">"Calcinosis (typically on pressure points, so fingers and elbows)
"What is Tinel's test?"Lightly tapping over a nerve- should elicit sensation of tingling in the distribution of the nerve.<div><br></div><div>Ask if this tingling sensation mimics symptoms pt has been describing- if so, then Positive sign</div>
What features should be used to describe the distal radius in radiographs?- Radial height<div>- Radial inclination</div><div>- Volar tilt</div>
What is the <b>radial height </b>and how long should it be?"Distance between 2 parallel lines drawn perpendicular to radial shaft:<div>- From tip of radial styloid</div><div>- From ulnar corner of lunate fossa</div><div>- Should be 11mm</div><div><br></div><div><img src=""ee465ccc1e22a74da6db96db98a0a87f.jpg""><br></div>"
What is the <b>radial inclination </b>and how much should it be?"Angle between one line connecting styloid tip and ulnar aspect of radius, and line drawn perpendicular to longitudinal axis. <div><br></div><div>Should be 22°</div><div><br></div><div><img src=""7826a1e171cf1e76a42e26f21f1dafb8.jpg""><br></div>"
What is the <b>volar tilt</b> and how much should it be?"Angle between line along distal radial articular surface, and line perpendicular to longidutinal axis. Should be 11°<div><br></div><div><img src=""0aaee788cd2f9d990510ffa8752a85b9.jpg""><br></div>"
On what radiographs can radial length, radial inclination and volar tilt be measured?"<font color=""#0000ff"">AP</font>: Radial length and inclination<div><font color=""#0000ff"">Lateral</font>: Volar Tilt</div>"
What should you discuss when talking through fractures?- Skeletally mature/immature bone?<div>- What bone?</div><div>- Where in the bone?</div><div>- Intra-articular/ extra-articular fracture?</div>
What are the different parts of a bone?<b>Diaphysis</b> (shaft)<div><b>Metaphysis</b> (zone on diaphyseal line adjacent to growth plate)</div><div><b>Physis </b>(growth plate)<br><div><div><b>Epiphysis </b>(end)</div></div></div>
What is a sesamoid bone?Bone which ossifies within a tendon 
"In this diagram below, where is the cortex and where is the medulla?<div><img src=""paste-006c38bd5ca9d80238456aacb6e74bd5d9aea5b6.jpg""><br></div>""<img src=""paste-d1dbab3af6a544ff81e7d2b5d25c71d4c2543a24.jpg"">"
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-2-Q.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-2-A.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-3-Q.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-3-A.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-4-Q.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""78c4c2fd7c934d8e82acc80da4c78dd3-ao-4-A.svg"" /></div> <div id=""io-original""><img src=""tmprlynqp9j.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
"Describe the fracture seen below?<div><img src=""paste-15ea71aa32ed16b6d88d474f294d5694b5efef8f.jpg""><br></div>"Transverse fracture in the diaphysis of long bone
"Describe the fracture? <div><img src=""paste-4476bdfe13f29c91df43e59f3314bc771e7838ac.jpg""><br></div>"Oblique fracture in metacarpal bone
"Describe the pathology seen here?<div><img src=""paste-bc92a1660c5f70e8679456bf2a808c175754ebe2.jpg""><br></div>"Spiral fracture in long bone (caused by twisting injury)
"What type of fracture is seen below?<div><img src=""paste-21ad327cb3d661299104cffeaf8489b35b157d61.jpg""><br></div>"Comminuted fracture- injury which results in more than 2 separate bone components
"Describe what is seen here?<div><img src=""images (1).jpg""><br></div>"Displaced and shortened femur
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e9fa9f99bea84ea7b6b6e6fe25e3f02e-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmp63obgyz3.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""e9fa9f99bea84ea7b6b6e6fe25e3f02e-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmp63obgyz3.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
"What is the pathology seen here?<div><img src=""paste-4ff6482fa22cb6ec2d7dcb933fe6bfe785fbbce9.jpg""><br></div>""Transverse fracture caused by multiple myeloma in bone- bone appears moth-eaten. <div><br></div><div><img src=""paste-4ba41a5e643ba0abffd5683af49c98562b98aa01.jpg""><br></div>"
"What is seen here?<div><img src=""paste-97cc5c1c931829948ba2867d6a82e094457fd869.jpg""><br></div>"<b>Diastasis </b>(separation) of the pubic symphysis
"Describe what is seen here?<div><img src=""paste-f0113b7de769a46c6d964ec09c48559b6bfb9ea3.jpg""><br></div>""- Inferior surfaces of clavicle and acromion not in line- disruption of acromioclavicular ligaments<div>- Coracoclavicular distance is wide --> coracoclavicular ligament injury</div><div><br></div><div><img src=""paste-1a01f8e4b50dc0c695c67e2feff952594adc2cd2.jpg""><br></div><div><br></div>"
In what direction is the shoulder most commonly dislocated?Anteriorly
"What is seen here?<div><img src=""paste-323bd8865f358170be8e83015f00976e43681a10.jpg""><br></div>""Anterior shoulder dislocation:<div>- Humeral head and glenoid surface not aligned</div><div>- Head lies below coracoid</div><div><img src=""paste-f3696a19c267a2647751cd60cfb13f9f70e780df.jpg""><br></div>"
"What is seen here?<div><img src=""paste-8bcdcb9c6adfb4f8fe6ade0a9fd70eb92c9fa2b8.jpg""><br></div>"Posterior shoulder dislocation:<div><br></div><div>- Glenohumeral joint is widened</div><div>- Humerus held in internal rotation- head shaped like a light bulb</div>
What most commonly causes posterior shoulder dislocations?- Electric shocks<div>- Epileptic fits</div>
"What is seen here?<div><img src=""paste-4686815f8c401ea1cdf90dc7cafdf98107c5dadd.jpg""><br></div>"Displaced fracture of scapula
"What is seen here?<div><img src=""paste-f1718df30e37ec9689a58407a46609bd09c8abeb.jpg""><br></div>""- Transverse fracture through surgical neck<div>- Fracture causing separation of greater tubercle</div><div><img src=""paste-5cb2b573a1681fbe90b50046b98244a7e0fdacd4.jpg""><br></div>"
What neurovascular structures are at risk in fractures of the surgical neck of humerus?- Axillary nerve<div>- Posterior circumflex humeral artery </div>
What are the consequences of damage to axillary nerve?Loss of function of teres minor and deltoid:<div>- Loss of abduction (from 15-90°)</div><div>- Weak flexion, extension and rotation of shoulder</div><div><br></div><div>- Loss of sensation over lateral arm- <b>regimental badge </b>region</div>
In what type of fractures do you fear <b>radial nerve injury?</b>Mid-shaft fractures of humerus (as radial nerve runs in radial groove of humerus)
What nerve is frequently damaged in mid-shaft fractures of the humerus?Radial nerve
What nerve is frequently damaged in <b>supracondylar fractures</b>?Ulnar nerve (is most frequently damaged in what type of fractures?)
Ulnar nerve (is most frequently damaged in what type of fractures?)What nerve is frequently damaged in <b>supracondylar fractures</b>?
What is a <b>greenstick fracture?</b>"Fracture in children's bones:<div>- Visible fracture in cortex on one side, with buckling on the other</div><div><img src=""paste-fcd1a7b443c37f6dc9e714a116641bb9073b15d9.jpg""><br></div><div>(describes what?)</div>"
"Fracture in children's bones:<div>- Visible fracture in cortex on one side, with buckling on the other</div><div><img src=""paste-fcd1a7b443c37f6dc9e714a116641bb9073b15d9.jpg""><br></div><div>(describes what?)</div>"What is a <b>greenstick fracture?</b>
What is a <b>torus fracture?</b>"Fracture commonly in children:<div>- Buckled bone with no visible fracture line</div><div><img src=""paste-565b475b3aeeb5f6d6ce02043e778ffea2776d72.jpg""><br></div><div>(describes what?)</div>"
"Fracture commonly in children:<div>- Buckled bone with no visible fracture line</div><div><img src=""paste-565b475b3aeeb5f6d6ce02043e778ffea2776d72.jpg""><br></div><div>(describes what?)</div>"What is a <b>torus fracture?</b>
What is the management of ankylosing spondylitis?- Exercise regime <div>- NSAIDs</div><div><br></div><div>- Anti-TNF therapy only to patients with persistently high disease activity <b>despite </b>conventional treatments</div><div><br></div><div>Local steroid injections can provide temporary relief. </div><div>Surgery: THR if hips are involved, spinal osteotomy (rare)</div><div><br></div>
A man presents with pain in anatomical snuffbox, but X-rays 2hrs after fall show no fracture. There is persistent pain for 10 days after the injury.<div><br></div><div>What is the cause and why?</div>Scaphoid fracture- fracture line often present several days after fall. <div><br></div><div>Pain in anatomical snuffbox= Scaphoid fracture</div>
What is a common complication of scaphoid fractures?- Avascular necrosis of proximal part of scaphoid
What is the <b>Salter-Harris </b>system used to describe?Paediatric fractures involving the growth plate (is described with what system?)
Paediatric fractures involving the growth plate (is described with what system?)What is the <b>Salter-Harris </b>system used to describe?
Outline the Salter-Harris classification"<font color=""#0000ff"">I</font>: Fracture through physis only (often normal X-ray)<div><font color=""#0000ff"">II</font>: Fracture through physis and metaphysis</div><div><font color=""#0000ff"">III</font>: Fracture through physis and epiphysis including joint</div><div><font color=""#0000ff"">IV</font>: Fracture involving physis, metaphysis and epiphysis</div><div><font color=""#0000ff"">V</font>: Crush injury involving physis (may resemble I)</div><div><img src=""paste-e67e0411f3847297bd21c71d1cfdacbfa76ac844.jpg""><br></div>"
What are signs which would arouse concerns about non-accidental injury?- Delayed presentation<div>- Delay in attaining milestones</div><div>- Lack of concordance between proposed and actual mechanism of injury</div><div>- Multiple injuries, at sites not commonly exposed to trauma</div><div>- Children on the at risk register</div>
"What is the first-line treatment for a man who presents with inflammatory pain and an X-Ray shown below?<div><img src=""xrb085.jpg""><br></div>"Squaring of vertebral bodies + syndesmophytes (bony growth from supraspinous ligament) --> Anklyosing spondylitis<div><br></div><div>First-line treatment is NSAIDs</div>
What is <b>fibromyalgia?</b>Syndrome characterised by widespread pain throughout body with tender points at specific anatomical sites<div><br></div><div>(describes what?)</div>
Syndrome characterised by widespread pain throughout body with tender points at specific anatomical sites<div><br></div><div>(describes what?)</div>What is <b>fibromyalgia?</b>
What is the typical presentation of someone with fibromylagia?- Chronic, widespread body pain<div>- Accompanying comorbid symptoms e.g. fatigue, memory difficulties + sleep/mood difficulties. </div>
Discuss the pathophysiology of patients with fibromyalgia?Pathology in the CNS:<div>- Diffuse hyperalgesia </div><div>- Allodynia. </div><div><br></div><div>CNS-mediated symptoms other than pain (fatigue, memory loss) often frequent comorbidities</div>
What are the clinical classifications of fibromyalgia?<b>Primary fibromyalgia</b>: Most common form, cause for pain not found<div><b>Secondary fibromyalgia</b>: Fibromyalgia which accompanies another painful disorder, or an inciting event. </div>
How can fibromyalgia be diagnosed?Purely clinical:<div>- Pain should be chronic (>3 months) + widespread (in 4 out of 5 regions). </div><div>- Diagnosis is valid irrespective of other diagnoses. Does not exclude presence of other illnesses</div>
How should fibromyalgia be managed?"- Explanation: emphasise fibromyalgia can be managed but not cured + encourage to take active role in therapy. <div>-<font color=""#0000ff""> Aerobic exercise</font>:</div><div>- Cognitive Behavioural Therapy</div><div>- Medication: Low* dose of TCAs (amitriptyline) helps relieve pain and improve sleep. Pregabalin if TCAs fail. Duloxetine (SNRI) or SSRIs if fibromyalgia with comorbid anxiety/depression</div>"
What are the DMARDs? List someDisease-modifying Anti-Rheumatic Drugs:<div><br></div><div>- Methotrexate</div><div>- Sulfasalazine</div><div>- Leflunomide</div><div>- Hydroxychloroquine</div>
What is the mechanism of action of methotrexate as a DMARD?- Inhibition of enzymes involved in purines --> accumulation of adenosine (immunosuppresive)<div>- Inhibition of T cell activation + suppression of intercellular adhesion molecules </div><div>- Down-regulation of B Cells</div>
If a patient is put on methotrexate, what must be monitored?FBC and LFTs:<div>- Risk of myelosuppression</div><div>- Risk of liver cirrhosis</div>
What are some side effects of methotrexate?- Pneumonitis<div>- Oral ulcers</div><div>- Cirrhosis</div><div>- Teratogenic</div><div>- Myelosuppression</div>
In what patients is Rheumatoid Arthritis most common?- Females: 2x<div>- Higher in smokers</div><div>- Linked to HLA DR4/DR1 (also associated w/ increased severity)</div>
What are early signs of RA?"<font color=""#0000ff"">Inflammation, but no joint damage</font>. Swollen MCP, PIP, wrist or MTP joints (often symmetrical). Tenosynovitis/bursitis. <div><br></div>"
What are late signs of RA?"<div><font color=""#0000ff"">Joint damage --> deformity</font>. </div><div>- Ulnar deviation</div><div>- Subluxation of wrist and fingers </div><div>- Boutonniere and swan-neck deformities, or z-deformity of thumb.</div><div>- Hand extensor tendons may rupture. <br></div><div><br></div><div>- Rare, but atlanto-axial joint subluxation can threaten spinal cord</div>"
How can Rheumatoid Arthritis be diagnosed?<div>- Clinical diagnosis</div><div>- Laboratory tests: Rheumatoid factor (+ve in 60-70% cases), and anti-CCP (more sensitive)</div><div>- Radiographs</div>
How is rheumatoid arthritis managed?"- Early and aggressive treatment to prevent irreversible destruction. <div><font color=""#0000ff"">1st line:</font></div><div>- DMARDs: Methotrexate, leflunomide, hydroxychloroquine</div><div>- Corticosteroids + NSAIDs</div><div><br></div><div><font color=""#0000ff"">2nd line:</font></div><div>- Add second DMARD</div><div><br></div><div>If high disease activity despite dual DMARD thearpy give biologics</div>"
Discuss the biologicals that can be used to treat RA?<b>TNFalpha inhibitors: </b>Infliximab, etanercept, adalimumab. <div><b>B-cell depletion: </b>Rituximab, used in combination with methotrexate, where DMARD and TNFalpha inhibitor has failed</div><div><b>IL-1 and IL-6 inhibition: </b>Tocilizumab (IL-6R antagonist)</div><div><b>Inhibition of T-cell co-stimulation: </b>Abatacept, used in active RA where patients have not responded to DAMRDs or TNFalpha blocker</div>
What are common side effects in the use of biologics to treat RA?- Serious infection (as many are immunosuppressive)<div>- Reactivation of TB (screen, and consider prophylaxis) and hep B</div><div>- Worsening heart failure</div><div>- Hypersensitvity</div><div>- Injection site eactions, and blood disorders </div>
What are the TNF-inhibitors used to treat RA?"- <font color=""#0000ff"">Etanercept</font>: TNF-α Receptor, acts as decoy receptor for TNFα. Subcutaneous administration<div>- <font color=""#0000ff"">Infliximab</font>: Monoclonal antibody, binds to TNF-α and prevents it binding to receptors. Intravenous administration. </div><div>- <font color=""#0000ff"">Adalimumab</font>: Monoclonal antibody, subcutaneous administration. </div>"
What is the action of Rituximab?Anti-CD20 monoclonal antibody --> B-cell depletion
What is the action of abatacept?CTLA4 Fusion protein- modulates a key signal required for activation of T Lymphocytes --> decreased T-cell proliferation and cytokine production
"What is seen here, and what is it commonly caused by?<div><img src=""paste-bdf93eec0151f9f74ebe4ea68a048cb13b694e5b.jpg""><br></div>"Dactylitis- Swelling of a finger. <div><br></div><div>Caused by:</div><div>- Spondyloarthropathies e.g. psoriatic and reactive arthritis (sarcoidosis + Juvenile RA)</div><div>- Sickle-cell disease</div><div>- Rarely caused by certain infections: TB, Sarcoidosis, Syphilis</div><div><br></div>
What is meant by <b>seronegativity </b>with regard to rheumatological conditions?Rheumatoid factor -ve
What are the different spondyloarthropathies?- Axial spondylo-arthritis<div>- Enteric arthropathy</div><div>- Psoriatic arthritis</div><div>- Reactive arthritis</div><div>- Undifferentiated spondyloarthropathy</div>
What are the shared features of the spondyloarthropathies?- Seronegativity<div>- HLA B27 association</div><div>- Axial arthritis (pathology in spine + sacroiliac joints)</div><div>- Asymmetrical large-joint oligoarthritis, or monoarthritis</div><div>- Enthesitis</div><div>- Dactylitis</div><div>- Extra-articular manifestations (e.g. uveitis, rashes, ulcers, aortic valve incompetence etc.)</div>
What is <b>enthesitis?</b>Inflammation at site of insertion of tendon/ligament into bone<div><br></div><div>(describes what?)</div>
Inflammation at site of insertion of tendon/ligament into bone<div><br></div><div>(describes what?)</div>What is <b>enthesitis?</b>
In what populations is ankylosing spondylitis more common?- Men (men often present earlier: 6x more common at 16, then 2x more common at 30)<div>- Patients with HLA B27</div>
Where does ankylosing spondylitis typically manifest?Sacroiliac joints, and axial spine
What are key diagnostic hallmarks of ankylosing spondylitis?<div><b>Diagnosis is clinical, supported by imaging</b></div>- Chronic inflammatory back pain (early morning stiffness, improvement with exercise, resolution with NSAIDs, alternating buttock pain, waking up in night with back pain)<div>- Often emerges in younger people (<20)</div><div>- Iritis/uveitis</div><div>- Enthesitis</div><div><br></div><div>- Pelvic x-ray should show sacroiliitis</div>
"This is an X-Ray taken from a 21 year old man complaining of back pain. What is the likely diagnosis?<div><img src=""x-ray-of-ankylosing-spondylitis-with-sacroiliac-joints-fused-wellcome-images.jpg""><br></div>"X-ray shows sacroiliitis- suggestive of ankylosing spondylitis
What is a <b>syndesmophyte?</b>Bony growth originating inside a ligament (describes what?)
Bony growth originating inside a ligament (describes what?)What is a <b>syndesmophyte?</b>
What causes syndesmophytes in anklyosing spondylitis?Enthesitis between ligaments and vertebrae cause outgrowth of bone
When managing <b>ankylosing spondylitis</b>, what drug may be given prophylactically?- <b>Bisphosphonates</b> as Ank spond has increased risk of osteoporotic spinal fractures 
What is enteric arthropathy?"Acute/sub acute arthritis in association with: <div>- Inflammatory Bowel Disease</div><div>- GI Bypass</div><div>- Coeliac</div><div>- Whipple's Disease</div><div><br></div><div>(describes what?)</div>"
How can enteric arthropathy be managed?- Treatment of underlying bowel symptoms (<b>beware not to give NSAIDs)</b><div>- DMARDs can be used for resistant cases</div>
How often does <b>psoriasis </b>cause psoriatic arthritis?Occurs in 10-40% of psoriasis patients (can present before skin changes)
What are the different presenting patterns of psoriatic arthritis?<div>Psoriatic arthritis known as the great mimic:</div><div><br></div>- Symmetrical polyarthritis (like RA)<div>- Asymmetrical oligoarthritis </div><div>- Spinal (like Ank spond)<br><div>- DIP joints (like OA)</div></div><div>- Psoriatic arthritis mutilans</div>
How is polyarticular psoriatic arthritis distinguished from RA?- Presence of dactylitis<div>- Absence of anti-CCP antibodies</div>
How is psoriatic arthritis managed?- NSAIDs<div>- DMARDs: Sulfasalazine, methotrexate</div><div>- Anti-TNFα agents also effective</div>
What is <b>reactive arthritis?</b>Condition where arthritis occurs as an autoimmune response to infection elsewhere (though the infection may have resolved/asymptomatic when arthritis presents)
What infections typically trigger reactive arthritis?GI or GU infections 
"What is this?<div><img src=""Feet-Reiters_syndrome.jpg""><br></div>"Keratoderma blenorrhagica 
How is reactive arthritis managed?<div><br></div>"<font color=""#0000ff"">If acute, symptomatic relief:</font><div>- NSAIDs</div><div>- Local corticosteriod injections</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If chronic (>6 months)</font></div><div>- DMARDs: sulfasalazine or methotrextae</div><div><b><br></b></div><div><b>Treating original infection may make little difference to arthritis</b></div>"
Where are the most common sites of osteomyelitis in children and adults who have otherwise suffered no trauma/surgery?"<div>Haematogenous osteomyelitis</div><div><br></div><font color=""#0000ff"">Children: Metaphysis of long bones (as good blood supply)</font><div><font color=""#0000ff"">Adults</font>: Vertebrae </div>"
Most pts with dermatomyositis have what antibody present?ANA (whilst Jo/Mi are more specific, minority of patients actually have this. ANA is not specific for dermatomyositis however)
"What are the classic triad of symptoms in <b>Behcet's syndrome?</b>"- Oral ulcers<div>- Genital ulcers</div><div>- Anterior uveitis </div><div><br></div><div>(commonly present together in what disease?)</div>
- Oral ulcers<div>- Genital ulcers</div><div>- Anterior uveitis </div><div><br></div><div>(commonly present together in what disease?)</div>"What are the classic triad of symptoms in <b>Behcet's syndrome?</b>"
"What is seen here?<div><img src=""xrb015.jpg""><br></div>"Loss of joint space, distributed in the DIP and the CMC joints, + some sclerosis --> OA
7-year-old boy presents to hospital with a suspected fracture of his right humerus. His parents do not know how this occurred and deny any injury. On examination, you notice widespread dental caries, a blueish tinge to the sclera and on X-ray, multiple fractures at varying stages of healing are reported.<br><div><br></div><div>What is the most likely diagnosis?</div>Blue sclera --> Osteogenesis imperfecta
What are features of osteogenesis imperfecta?- Presents in childhood<div>- Fractures following minor trauma</div><div>- Blue sclera</div><div>- Deafness secondary to otosclerosis</div><div>- Dental imperfections</div>
What is the pathophysiology underlying osteogenesis imperfecta?- Abnormality in type 1 collagen due to decreased synthesis of pro-collagen polypeptides
What is the most marked restriction in adhesive capsulitis of the shoulder?External rotation
What should clinicians do to assess the risk of a fracture in their patient?- FRAX tool<div>- DEXA scan if FRAX tool results are intermediate. </div>
In DEXA scans, what is the Z score adjusted for?- Age<div>- Gender</div><div>- Ethnic factors</div>
What should occur before a patient begins long-term course of hydroxychloroquine?Examination by an ophthalmologist: hydroxychloroquine often causes retinopathy, so baseline examination required
<span class=cloze>[...]</span> and <span class=cloze>[...]</span> are common symptoms of meniscal injury<span class=cloze>Locking</span> and <span class=cloze>giving away</span> are common symptoms of meniscal injury<br> Locking and giving away are common symptoms of <span class=cloze>[...]</span>Locking and giving away are common symptoms of <span class=cloze>meniscal injury</span><br> What are the motor + sensory functions, and the nerve roots of the <b>musculocutaneous </b>nerve?"<div><font color=""#0000ff"">Motor</font>: Elbow flexion + supination (supplies biceps brachii)<br></div><div><font color=""#0000ff"">Sensory</font>: Lateral part of forearm</div><div><font color=""#0000ff"">Nerve roots</font>: <b>C5-C7</b></div>"
What are the motor + sensory functions of the <b>radial nerve</b>, and what is its nerve supply?"<font color=""#0000ff"">Motor</font>:<b> Extension</b> of forearms, wrist, fingers and thumb<div><font color=""#0000ff"">Sensory</font>: Dorsal aspect of 1st and 2nd metacarpals (but not nailbeds)</div><div><font color=""#0000ff"">Nerve roots</font>: <b>C5-C8</b></div>"
What is the motor + sensory functions of the <b>median</b> nerve, and its nerve roots?"<font color=""#0000ff"">Motor</font>: LOAF muscles (thumb etc), <b>flexors</b> of the wrist + <b>pronator teres</b><div><font color=""#0000ff"">Sensory</font>: Palmar aspect of lateral 3.5 fingers (+ nail beds)</div><div><font color=""#0000ff"">Nerve roots</font>: <b>C6, C8, T1</b></div>"
What are motor defects expected in median nerve laceration at the wrist and elbow?<b>Wrist:</b> Paralysis of <b>thenar</b> muscles, opponens pollicis<div><b>Elbow: </b>Loss of <b>pronation</b> of forearm, and <b>weak wrist flexion</b> + paralysis of thenar and opponens muscles</div>
What are the motor + sensory functions and the nerve roots of the <b>ulnar nerve</b>?"<font color=""#0000ff"">Motor</font>: <b>Intrinsic </b>hand muscles <b>except</b> LOAF + flexor carpus <b>ulnaris</b> (+ part of flexor digitorum profundus)<div><font color=""#0000ff"">Sensory</font>: Medial 1.5 fingers, both surfaces</div><div><font color=""#0000ff"">Nerve roots</font>: <b>C8, T1</b></div>"
What are the motor + sensory functions and nerve roots of the long <b>thor</b>acic nerve?"<font color=""#0000ff"">Motor</font>: Serratus anteri<b>or</b><div><font color=""#0000ff"">Sensory</font>: None</div><div><font color=""#0000ff"">Nerve roots</font>: C5-C7</div>"
How is the long thoracic nerve often damaged?- During sport (e.g. following blow to <b>ribs</b>)<div>- Damaged in<b> masectomies</b></div>
What is the result following damage to the<b> long thoracic</b> nerve? Supplies <b>serratus anterior</b>- damage results in<b> winged scapula</b>
What are the motor + sensory functions and nerve roots of the femoral nerve?"<font color=""#0000ff"">Motor</font>: Knee extension, thigh flexion (L 2, 4, kick door)<div><font color=""#0000ff"">Sensory</font>: Anterior + medial aspect of thigh and lower leg (inner thigh)</div><div><font color=""#0000ff"">Nerve roots</font>:<b> L2-L4</b></div><div><img src=""Sensory-Branches-of-the-Femoral-Nerve-Anterior-Cutaneous-and-Saphenous.jpg""><br></div>"
How is the <b>femoral nerve</b> frequently damaged?- <b>Hip + pelvic fractures</b><div>- Stab/ gunshot wounds</div>
What are the motor + sensory functions and the nerve roots of the obturator nerve?"<font color=""#0000ff"">Motor</font>: Thigh adduction (medial)<div><font color=""#0000ff"">Sensory</font>: Medial thigh</div><div><font color=""#0000ff"">Nerve roots</font>: <b>L2-L4</b> (like femoral)</div><div><img src=""Obturator-and-Femoral-Nerve-Cutaneous-Innervation-of-the-Thigh.jpg""><br></div>"
How is the <b>obturator nerve</b> frequently damaged?<b>Anterior hip dislocation</b> (threatens which nerve in particular?)
<b>Anterior hip dislocation</b> (threatens which nerve in particular?)How is the <b>obturator nerve</b> frequently damaged?
What are the motor + sensory and nerve roots of the <b>lateral cutaneous nerve of the thigh?</b>"<font color=""#0000ff"">Motor</font>: <b>None</b><div><font color=""#0000ff"">Sensory</font>: Lateral + posterior surfaces of the thigh</div><div><font color=""#0000ff"">Nerve roots:</font> L2-L3 (la2ral)</div><div><img src=""Gray826-LFC.png""><br></div>"
What frequently causes disruption to innervation by the lateral cutaneous nerve of the thigh?<b>Compression</b> of the nerve near ASIS --> Meralgia paraesthetica 
<b>Meralgia paraesthetica</b> arises from compression of what nerve?<b>Lateral cutaneous </b>nerve of the <b>thigh</b>
What is the motor + sensory function and nerve roots of the tibial nerve?"<font color=""#0000ff"">Motor</font>: Foot plantarflexion + inversion (down & in)<div><font color=""#0000ff"">Sensory</font>: Sole of foot</div><div><font color=""#0000ff"">Nerve roots</font>: L4-S3</div>"
What typically causes damage to the <b>tibial nerve</b>?Not usually injured as deep + well protected, but:<div>- <b>Popliteal </b>lacerations</div><div>- <b>Posterior knee dislocation </b></div>
What are the motor + sensory functions and nerve roots of the common peroneal nerve?"<font color=""#0000ff"">Motor</font>: Foot dorsiflexion + eversion; extensor hallucis longus (up & out)<div><font color=""#0000ff"">Sensory</font>: Dorsum of foot + lower lateral part of leg</div><div><font color=""#0000ff"">Nerve roots</font>: <b>L4-S2</b></div><div><br></div>"
What typically causes damage to the <b>common peroneal nerve?</b>- Injury to<b> neck of fibula</b><div>- <b>Tightly applied</b> lower limb plaster <b>cast</b></div><div><br></div><div>(Frequently damages which nerve?)</div>
- Injury to<b> neck of fibula</b><div>- <b>Tightly applied</b> lower limb plaster <b>cast</b></div><div><br></div><div>(Frequently damages which nerve?)</div>What typically causes damage to the <b>common peroneal nerve?</b>
What are the motor + sensory functions and nerve root supply of the<b> superior gluteal </b>nerve?"<font color=""#0000ff"">Motor</font>: Hip abduction (glutes abduct)<div><font color=""#0000ff"">Sensory</font>: None</div><div><font color=""#0000ff"">Nerve roots</font>: Sacral plexus L4-S1 (quite low)</div>"
Injury to the <span class=cloze>[...]</span> nerve results in a <b>Positive Trendelenburg sign</b>Injury to the <span class=cloze><b>superior gluteal</b></span> nerve results in a <b>Positive Trendelenburg sign</b><br> Superior gluteal nerve supplies <b>hip abductors (glut med &min)<br></b>(glut max is more extensor)
Injury to the <b>superior gluteal</b> nerve results in a <span class=cloze>[...]</span>Injury to the <b>superior gluteal</b> nerve results in a <span class=cloze><b>Positive Trendelenburg sign</b></span><br> Superior gluteal nerve supplies <b>hip abductors (glut med &min)<br></b>(glut max is more extensor)
What frequently causes damage to the <b>superior gluteal nerve</b>?- Misplaced intramuscular <b>injection</b><div>- <b>Hip surgery </b></div><div>- <b>Pelvic fracture</b></div><div>-<b> Posterior </b>hip dislocation </div><div><br></div><div>(risks damage to what nerve?)</div>
- Misplaced intramuscular <b>injection</b><div>- <b>Hip surgery </b></div><div>- <b>Pelvic fracture</b></div><div>-<b> Posterior </b>hip dislocation </div><div><br></div><div>(risks damage to what nerve?)</div>What frequently causes damage to the <b>superior gluteal nerve</b>?
What is the motor + sensory functions + nerve root supply of the inferior gluteal nerve?"<font color=""#0000ff"">Motor</font>: <b>Hip extension</b> and lateral rotatin<div><font color=""#0000ff"">Sensory</font>: None</div><div><font color=""#0000ff"">Nerve roots</font>: Sacral plexus: <b>L5-S2.</b> </div><div><br></div><div><br></div>"
What are common adverse effects of bisphophonates?- Oesophageal reactions: Oesophagitis, ulcers<div>- Osteonecrosis of the jaw</div><div>- Increase in atypical stress fractures of proximal femoral shaft</div><div>- Acute phase response (fever, myalgia, arthalgia)</div><div>- Hypocalcaemia</div>
A patient experiencing clawing of the 4th and 5th digits notices the deformity worsens before eventually resolving. What is the cause of this and why?Damage to ulnar nerve at elbow:<div>- Ulnar clawing worsens as flexor digitorum profundus re-innervated, causing further flexion. </div><div><br></div><div>Ulnar paradox, as deformity appears more mild in more severe injury</div>
What is the action of raloxifene?Selective oestrogen receptor modulator<div><br></div><div>Particularly useful in post-menopausal women</div>
What are the advantages and disadvantages of using raloxifene for osteoporotic patients?Raloxifene is a SERM:<div><br></div><div>+ Increases bone density in spine and proximal femur</div><div>+ May decrease risk of breast cancer</div><div><br></div><div>- May worsen menopausal symptoms</div><div>- Increased risk of thromboembolic events</div><div>- Increased risk of ovarian cancer </div>
What is the action of strontium ranelate?Dual action bone agent;<br>- Increases differentiation of osteoblasts<div>- Inhibits osteoclasts</div>
When is strontium ranelate indicated to treat osteoporosis?- Only used by patients where all other treatments have failed. <div><br></div><div>Should only be prescribed by a specialist in secondary care </div>
What are the risks of strontium ranelate?"- <font color=""#0000ff"">Increased risk of cardiovascular events:</font> CVD or risk of CVD is a contraindication<div>- <font color=""#0000ff"">Increased risk of Thromboembolic events</font>: Hx of VTE contraindicated</div><div>- <font color=""#0000ff"">Serious skin reactions</font> e.g. Stevens Johnson syndrome</div>"
What is the action of denosumab?Human monoclonal antibody, inhibits RANK-ligand, which inhibits maturation of osteoclasts. <div><br></div><div>Initial data suggests it is effective + well tolerated</div>
What is the action of teriparatide?Recombinant form of PTH. <div><br></div><div>Increases bone mineral density (though role in management of osteoporosis yet to be clearly defined)</div>
When is Hormone Replacement Therapy indicated for osteoporosis?- No longer recommended for 1° or 2° prevention, unless woman is <b>suffering from vasomotor symptoms</b><div>- Increased rates of CVD and breast cancer</div>
What are the vasculitides and how are they categorised?Inflammatory disorders of blood vessels: commonly classified by size of blood vessels affected
What are the vasculitides which affect <b>large blood vessels?</b>"- Giant cell arteritis<div>- Takayasu's arteritis</div><div><br></div><div>(affect what blood vessels?)</div>"
"- Giant cell arteritis<div>- Takayasu's arteritis</div><div><br></div><div>(affect what blood vessels?)</div>"What are the vasculitides which affect <b>large blood vessels?</b>
What are the vasculitides which affect <b>medium sized blood vessels</b>?- Polyarteritis nodosa<div>- Kawasaki disease</div><div><br></div><div>(affect what blood vessels?)</div>
- Polyarteritis nodosa<div>- Kawasaki disease</div><div><br></div><div>(affect what blood vessels?)</div>What are the vasculitides which affect <b>medium sized blood vessels</b>?
What are the vasculitides which affect <b>small blood vessels?</b>"- ANCA- associated (microscopic polyangiitis, Wegener's granulomatosis, Churg Strauss syndrome)<div>- Immune complex vasculitis (Goodpastures, cryoglobulinaemic vasculitis, IgA vasculitis)</div><div><br></div><div>(affect which blood vessels?)</div>"
"- ANCA- associated (microscopic polyangiitis, Wegener's granulomatosis, Churg Strauss syndrome)<div>- Immune complex vasculitis (Goodpastures, cryoglobulinaemic vasculitis, IgA vasculitis)</div><div><br></div><div>(affect which blood vessels?)</div>"What are the vasculitides which affect <b>small blood vessels?</b>
Which rheumatic disease present with variable vessel vasculitis?"- Behcet's <div>- Cogan's syndrome</div>"
How might vasculitis present if it is <b>systemic?</b>- Fever<div>- Malaise</div><div>- Weight loss</div><div>- Arthalgia</div><div>- Myalgia</div>
How might vasculitis present if it affects the skin?- Fever<div>- Malaise</div><div>- Livedo reticularis</div><div>- Nail bed infarcts</div><div>- Digital gangrene</div>
"What is seen here?<div><img src=""Livedo-Reticularis-on-legs.jpg""><img src=""skinEruption.jpg""><br></div>"Livedo reticularis<div><br></div><div>(note the very different appearance on black skin!)</div>
What is livedo reticularis?- Pink-blue mottling caused by capillary dilatation and stasis in skin venules<div><br></div><div>Can be physiological, caused by cold or vasculitis</div>
How does vasculitis present if it affects the eyes?<div><br></div>- Episcleritis<div>- Scleritis</div><div>- Visual loss</div>
How does vasculitis present if it affects the ENT?- Epistaxis<div>- Nasal crusting</div><div>- Stridor</div><div>- Deafness</div>
How does vasculitis present if it affects the pulmonary system?- Haemoptysis + dyspnoea (due to pulmonary haemorrahge)
How does vasculitis present if it affects the cardiac system?-- Angina/MI (coronary arteritis)<br><div>- Heart failure</div><div>- Pericarditis</div>
How does vasculitis present if it affects the GI system?- Pain or perforation (infarcted viscus)<div>- Malabsorption (chronic ischaemia)</div>
How does vasculitis present if it affects the renal system?- Hypertension<div>- Haematuria</div><div>- Proteinuria</div><div>- Casts</div><div>- Renal failure </div>
How does vasculitis present if it affects the neurological system?- Stroke<div>- Fits</div><div>- Chorea</div><div>- Psychosis</div><div>- Confusion</div><div>- Imparied cognition</div><div>- Altered mood</div>
What occurs in arteritis of the vasa nervorum?Vasculitis of the arteries supplying peripheral nerves --> can causes sensorimotor polyneuropathy or mononeuritis mulitplex
How does vasculitis often present?Overwhelming fatigue with raised ESR/CRP
How are vasculitides managed?<b>Large vessels: </b>Steroids, + steroid sparing agents later<div><b>Medium/small: </b>Immunosuppression (steroids + another ageent if severe)</div>
<span class=cloze>[...]</span> arteritis= Temporal arteritis <span class=cloze>Giant cell</span> arteritis= Temporal arteritis <br> Giant cell arteritis= <span class=cloze>[...]</span> arteritis Giant cell arteritis= <span class=cloze>Temporal</span> arteritis <br> <span class=cloze>[...]</span> is commonly associated with polymyalgia rheumatica<span class=cloze>Giant cell arteritis</span> is commonly associated with polymyalgia rheumatica<br> 50% of GCA pts have PMR
Giant cell arteritis is commonly associated with <span class=cloze>[...]</span>Giant cell arteritis is commonly associated with <span class=cloze>polymyalgia rheumatica</span><br> 50% of GCA pts have PMR
What are typical features of temporal arteritis?"- Rapid onset, in an older pt> 55 (<font color=""#0000ff"">only affects in older than 55)</font><div>- Headache</div><div>- Jaw claudication</div><div>- Visual disturbances (2° to anterior ischaemic optic neruopathy)</div><div>- Tender, palpable temporal artery</div><div>- Associations with PMR</div>"
What investigations could confirm giant cell arteritis?- Raised ESR and CRP<div>- Temporal artery biopsy (though skip lesions may occur)</div>
What is the prognosis of giant cell arteritis?Typically 2 year course of steroids leads to remission<div><br></div><div>Main cause of death + morbidity is due to long-term steroid treatment so balance risks. </div>
How is antiphospholipid syndrome managed?"<div>Give aspirin (to inhibit platelet activation) + warfarin. Typically lifelong<font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If initial VTE</font>: Warfarin with target INR 2-3</div><div><font color=""#0000ff"">If recurrent VTE:</font> Lifelong, if occured when on warfarin increase INR to 3-4</div><div><font color=""#0000ff"">If arterial thrombosis</font>: Target INR 2-3</div><div><br></div><div><b>If pregnant, consider using heparin instead</b></div><div><br></div><div><br></div><div><b>NOTE NOACs (apixiban) aren't useful in Antiphospholipid syndrome</b><br><div><br></div><div>Woman with antiphospholipid syndrome able to have successful birth w/ anticoagulation</div></div>"
In pre-op assessment, what should be noted wrt drugs in asthmatic patients?NSAIDs can sometimes provoke asthma attacks- check in pre-op assessment of asthmatic patients. If in doubt find alternatives
What are factors that should be considered in pre-op assessment of patients?<b>Patient factors: </b>PMH, are they <b>fit</b> and well (2 flights of stairs), consent etc.<div><b>Drug factors: Allergies</b>, reactions w/ anaesthetic medication, side effects<br></div><div><b>Anaesthetic factors: </b>Ease of intubation? Ease of introducing spinal etc.<br></div><div><b>Surgical factors: </b>Type of surgery, correct<b> position</b></div>
What are common presentations of someone with fibromyalgia?- Chronic pain diffuse across body<div>- Fatigue unrelieved by rest (non-refreshing sleep)</div>
What are strong risk factors for fibromyalgia?- Female <div>- 20-60y/o</div><div>- FHx of fibromyalgia</div><div>- Rhuematological conditions</div>
What investigations can be done for fibromyalgia?"- ESR, CRP should be normal<div>- Thyroid function tests should be normal</div><div>- FBC should be normal</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Everything normal biochemically</font></div>"
What conditions tend to cause a raised ESR?- Infection<div>- Autoimmunity</div><div>- Malignancy</div>
"What is <b>Ponset's disease?</b>"Reactive arthritis in tuberculosis
What is the main fear of prescribing large doses of hydroxychloroquine for prolonged periods?Chloroquine retinopathy- causes apoptosis of cone cells around the fovea
What might you be looking out for on a CVS examination of a pt with antiphospholipid syndrome?Heart sounds:<div><br></div><div>Heart valve disease common complication- appears in 30% of antiphospholipid syndrome patients. </div>
Why might patients with rheumatic disease be closely monitored in terms of blood pressures/cholesterol levels etc?Higher risk of atherosclerosis (as endothelium constantly exposed to inflammatory signals)
Decreased C3, C4 levels is associated with what conditions?<b>Immune complex diseases</b><div>- SLE</div><div>- Cryoglobulinaemias</div><div>- Immune complex deficiency</div><div>- Infective endocarditis</div>
If a pt has anti-Glutamic acid decarboxylase (GAD) antibodies, what is this suggestive of?- Stiff person syndrome (rare neurological conditions causing stiffness + rigidity)<div>- T1DM (autoimmune diabetes)</div>
"What is <b>Schober's test?</b>""Measures ability to flex lower back. Useful in suspected <font color=""#0000ff"">ankylosing spondylitis</font><div><br></div><div>Tell pt to touch their toes while keeping knees straight and measure the increase in distance between a point 5cm below and 10cm above L5. </div><div><br></div><div>If distance increase is less than 5cm, sign of restriction in lumbar flexion</div><div><img src=""6738467dcf1ad9a5d167f14b14a5b5f2.jpg""><br></div>"
Reflexes tend to be reduced in the <span class=cloze>[...]</span> population Reflexes tend to be reduced in the <span class=cloze>Afro-Carribean</span> population <br> So slower/absent reflexes not necessary pathology
What is an additional concern for women with Ro/La autoantibodies present?<div>If women are pregnant, risk that these antibodies will cross the placenta and cause congenital heart block (5%)<br></div>
What is serum sickness?Type III hypersensitivity reaction in reaction to proteins in antiserum (e.g. rituximab/infliximab)
What proportion of the population have HLA B27?8% of caucasians (lower in other ethnicities e.g. HLA-B27 a better discriminator for spondyloarthropathies in afro-carribeans)
What measurements are useful to make on clinical examination of suspected ankylosing spondylitis?"- Schober's test: lumbar extension<div>- Thoracic expansion</div><div><br></div><div>Both will be reduced in Ank spondylitis as <b>progressive loss of all spinal movement</b></div>"
What other conditions are associated with ankylosing spondylitis?- Acute iritis (1/3) of patients<div>- Osteoporosis (60%)</div><div>- Aortic valve incompetence (<3%)</div><div>- Pulmonary apical fibrosis </div>
What level are vertebral syndesmophytes initially seen in ankylosing spondylitis?T11-L1
"What is responsible for the 'bamboo spine' appearance seen in late stage ankylosing spondylitis?"Calcification of supraspinous ligaments following syndesmophyte formation 
What factors are associated with a worse prognosis in ankylosing spondylitis?- ESR >30<div>- Onset <16 y/o</div><div>- Early hip involvement </div><div>- Poor response to NSAIDs</div>
Aside from arthropathy, what are other clinical features of Reactive arthritis?"- Iritis<div><font color=""#0000ff"">- Keratoderma blenorrhagica</font></div><div><font color=""#0000ff"">- Circinate balanitis </font></div><div>- Mouth ulcers</div><div>- Enthesitis</div><div>- Dactylitis</div><div><br></div>"
What is <b>circinate balanitis?</b>Painless penile ulceration secondary to Chlamydia (describes what?)
Painless penile ulceration secondary to Chlamydia (describes what?)What is <b>circinate balanitis?</b>
What is the typical manifestation of <b>polymyalgia rheumatica?</b>"<div>- >50 y/o</div>- Pain/ morning stiffness in neck, shoulders, hips or proximal limb muscles<div><font color=""#0000ff"">- No weakness</font></div><div> - Sometimes accompanied by fatigue, fever, weight loss, anorexia and depression</div><div><br></div><div>(Describes a typical presentation of what?)</div>"
"<div>- >50 y/o</div>- Pain/ morning stiffness in neck, shoulders, hips or proximal limb muscles<div><font color=""#0000ff"">- No weakness</font></div><div> - Sometimes accompanied by fatigue, fever, weight loss, anorexia and depression</div><div><br></div><div>(Describes a typical presentation of what?)</div>"What is the typical manifestation of <b>polymyalgia rheumatica?</b>
What are risk factors for having polymyalgia rheumatica?- Female<div>- >50</div><div>- PMH of Giant Cell Arteritis</div>
What findings from investigations would suggest polymyalgia rheumatica?- Raised CRP<div>-  ESR typically >40</div><div><br></div><div>- Alkaline phosphate sometimes raised</div><div><b>Creatinine kinase levels are normal </b>(differentiates from myositis/ myopathies)</div>
What is the management of Polymyalgia rheumatica?- Corticosteroids (prednisolone 15mg/d PO- <b>dramatic response within 1 week). </b><i>Consider alternative diagnosis if not.</i><div><br></div><div>Many need steroids for >2yrs, so slowly decrease dose and give bone protection.</div><div><br></div><div>Methotrexate may be considered for patients at risk of relapse/ prolonged therapy.</div><div><br></div><div><b>NSAIDs not effective</b></div>
Rheumatoid arthritis increases the risk of <span class=cloze>[...]</span> by 2-3 foldRheumatoid arthritis increases the risk of <span class=cloze>CVD</span> by 2-3 fold<br> What is the peak onset of RA?5th-6th decade
What is <b>palindromic rheumatoid arthritis?</b>Subset of RA with recurring mono/poly arthritis of various joints which seem to affect different joints.<div><br></div><div>Between attacks, joints return to normal</div><div><br></div><div> (describes what?)</div>
Subset of RA with recurring mono/poly arthritis of various joints which seem to affect different joints.<div><br></div><div>Between attacks, joints return to normal</div><div><br></div><div> (describes what?)</div>What is <b>palindromic rheumatoid arthritis?</b>
If rheumatoid arthritis presents systemically, what symptoms may occur?- Fatigue<div>- Fever</div><div>- Weight loss</div><div><br></div><div>- Pericarditis</div><div>- Pleurisy</div><div><br></div>
A systemic extra articular presentation of RA is more common in which gender?Male 
"What is <b>Felty's syndrome?</b>"Triad of:<div>- RA </div><div>- Splenomegaly </div><div>- Neutropenia </div>
What percentage of RA patients have extra articular manifestations?40%
"How is Felty's syndrome treated?"DMARDs (+ rituximab if refractory)
What are high titles of RF associated with in Rheumatoid arthritis?- Severe disease<div>- Erosions</div><div>- Extra-articular disease</div>
Why might someone with RA have a decreased Hb?Anaemia of chronic disease
What blood vessels are typically affected in Giant Cell Arteritis?"<font color=""#0000ff"">Temporal</font>: causes claudication of temporalis muscles (jaw pain)<div><font color=""#0000ff"">Ophthalmic</font>: retinal ischaemia and visual loss</div>"
What must always supplement treatment with methotrexate?Folate tablets (as methotrexate works by inhibiting purine synthesis, anti-folate)
What considerations should be made to patients given long term steroids?- Bone protection<div>- PPI (as gastric ulcers are common)</div>
Describe the idiopathic inflammatory myopathies?Heterogeneous group of sub-acute and chronic (rarely acute) diseases of skeletal muscle which present with:<div>- Moderate to severe proximal muscle weakness</div><div>- Inflammation on muscle biopsy</div>
What are the conditions which make up the idiopathic inflammatory myopathies?- Polymyositis <div>- Dermatomyositis</div><div>- Inclusion Body Myositis</div>
What are some clinical signs caused by muscle weakness in polymyositis and dermatomyositis?- Dysphagia<div>- Dysphonia (poor phonation)</div><div>- Respiratory weakness</div>
How can malignancy cause myositis (esp in dermatomyositis)?Paraneoplastic phenomenon, particularly in lung, pancreatic, ovarian or bowel malignancies 
Why might you screen for cancers in polymyositis or dermatomyositis?Myositis can have paraneoplastic causes.
What additional signs might you see in<b> dermato</b>myositis (as opposed to myositis)?"- Macular<b> rash </b>(shawl sign +ve if over back and shoulders)<div>- Heliotrope <b>rash on eyelids</b>, often with oedema</div><div>- Nailfold erythema (dilates capillary loops)</div><div>- Gottron's papules</div>"
What are extra-articular signs in polymyositis and dermatomyositis?"- Fever<div>- Raynaud's</div><div>- Interstitial lung fibrosis </div><div>- Myocardial involvement (myocarditis, arrhythmias)</div>"
What tests may you carry out in suspected polymyositis/dermatomyositis?"- Muscle enzymes (ALT, AST, LDH, CK and aldolase) <b>raised </b>in plasma<div>- Antibodies: anti-Jo1 and anti-Mi2<br><div>- <b>EMG: </b>characteristic fibrillation potentials</div><div>- <b>Muscle biopsy CONFIRMS diagnosis</b></div><div><font color=""#0000ff""><b>- </b>Malignancy screen (dermatomyositis is a common paraneoplastic phenomenon)</font></div><div><br></div></div>"
What autoantibodies are associated with <b>polymyositis/dermatomyositis?</b>- Anti-Jo1<div>- Anti-Mi2</div><div>(ANA)</div><div><br></div><div>(are associated with what rheumatological condition?)</div>
- Anti-Jo1<div>- Anti-Mi2</div><div>(ANA)</div><div><br></div><div>(are associated with what rheumatological condition?)</div>What autoantibodies are associated with <b>polymyositis/dermatomyositis?</b>
In polymyositis/dermatomyositis, the presence of anti-Jo and anti-Mi antibodies are associated with what?- Acute onset of disease<div>- Interstitial lung fibrosis which should be treated aggressively </div>
What is the management of polymyositis/ dermatomyositis?- Prednisolone<div>- Immunosuppressives and cytotoxics in resistant cases</div><div><br></div><div>- Hydroxychloroquine/ topical tacrolimus helps skin diseases </div>
How are ANA titres expressed?Dilutions at which antibodies can be detected (e.g. 1:160 means Ab still detected after 160 dilutions)<div><br></div><div>1:40, 1:80 may not be significant </div>
How is smoking thought to be related to RA?Increases risk of RA, particularly CCP +ve RA.<div><br></div><div>Thought to cause epigenetic changes which increases the risk of developing the autoantibodies</div>
What are environmental factors which increase the risk of developing RA?- Smoking<div>- Silica exposures</div><div>- Infectious agents</div><div>- Vitamin D deficiency</div><div>- Changes in microbiota</div>
What is the pathophysiology underlying preclinical RA?"<b>Asymptomatic autoimmunity</b>:<div>- Increased levels of cytokines, chemokines and CRP<div>- Post-translational modifications (e.g. citrullination)</div><div>- Loss of immune tolerance at mucosal sites</div><div><br></div><div><font color=""#0000ff"">Then autoantibodies formed, which cause early symptomatic autoimmunity</font></div></div>"
What joints are typically affected by Rheumatoid arthritis?"- MCPs, PIPs and MTPs (90%)<div>- Knees, wrists and ankles (80%)</div><div>- Hip, elbow (50%)</div><div>- Cervical spine (40%)</div><div>- Tempormandibular and acromioclavicular joints (30%)</div><div><br></div><div><b>Very rarely affects the DIPs (think OA)</b></div><div><b><br></b></div><div><font color=""#0000ff"">Bilateral and symmetrical</font></div>"
What are the different patterns of presentation of Rheumatoid Arthritis?- Insidious, slow progression, small joints 70%<div>- Abrupt acute polyarthritis 20%</div><div>- Acute monoarthritis</div><div>- Palindromic rheumatism with variable episodes of polyarthritis 10%</div>
What are the most frequeunt areas affected by extra-articular manifestations of RA?- Skin<div>- Eyes </div><div>- Lungs</div>
What are eye complications seen in RA?"- <font color=""#0000ff"">Keratoconjunctivitis sicca</font> (most common)<div>- Episcleritis</div><div>- Scleritis</div><div>- Scleromalacia</div><div>- Scleromalacia perforans (occurs after progression of scleritis/episcleritis, melting of the sclera)</div>"
Discuss the lung involvement seen in RA?"- Pleuritis → chest pain, pleural effusions<div>- Pulmonary nodules- peripheral, may cavitate and cause effusions</div><div>- Basal Pulmonary fibrosis- usually mild, non progressive. </div><div>- Caplan's syndrome</div>"
"What is Caplan's syndrome?"Combination of Rheumatoid Arthritis, Pneumoconiosis and  pulmonanary rheumatoid nodules in the lung<div><br></div><div>- Typically in people who breathe in dust (e.g. miners)</div>
How can the cardiac system be affected by RA?- Pericarditis (most common)<div>- Myocardial disease from nodular granulomatous lesions</div>
If the renal system is affected by RA, what can occur?- Amyloidosis
How can RA affect the neurological system?- Cervical cord compression (subluxation of cervical spine at AA joint)<div>- Entrapment neuropathies (carpal tunnel)</div><div>- Peripheral neuropathy (glove and stocking sensation loss)</div><div>- Mononeuritis multiplex</div>
What inflammatory rheumatological disease typically causes a raised ESR, but normal CRP?- SLE<div>- Sjogrens</div>
Why might a patient with Rheumatoid Factor be labelled as seronegative from testing?Testing only detects IgM antibody, but patient may have other subtype (IgA) of immunoglobulin against F<sub>c</sub> in IgG 
What are the targets of NSAIDs?COX-1 (real target) and COX-2 (peptic ulcers)
How does sulfasalazine work?- Inhibits lymphocyte function and neutrophil migration
In what type of RA is sulfasalazine most effective in?Seronegative RA
What patients should you <b>absolutely avoid </b>giving sulfasalazine?SLE patients- produces very bad side effects
What is the action of hydroxychloroquine as a DMARD?- Inhibits microtubules<div>- Stabilises lysosomes in neutrophils</div>
What rheumatological conditions is hydroxychloroquine used in?- Skin in SLE<br>- RA<div>- Sjogrens</div>
What are side effects of azathioprine?- Bone marrow suppression<div>- Malignancy (lymphoma)</div><div><br></div><div>(safe in pregnancy however)</div>
Patients on long-term corticosteroids should be regularly monitored for what at GP?- Diabetes (suppression of insulin)<div>- Hypertension</div>
Nowadays, how are corticosteroids used to treat RA?- Give dose of corticosteroids alongside DMARDs<div>- Gradually decrease dose as DMARDs begin to take affect</div>
What is the effect of leflunomide?- Inhibits pyrimidine synthesis
What are side effects of <b>leflunomide</b>?- Diarrhoea<div>- Alopecia</div><div>- Rash</div><div>- Abnormal liver function tests</div><div>- Hypertension</div><div><br></div><div>(are side effects caused by which DMARD?)</div>
What is the only biologic approved for RA in pregnancy?Certolizumab (anti-TNF)- it is pegylated, so cannot cross the placenta 
What is the order of preference of biologic treatment in RA?"<font color=""#0000ff"">1st line</font>: Anti-TNF<div><font color=""#0000ff"">2nd line</font>: Rituximab (combined with methotrexate) <b>but not in seronegative</b></div><div><font color=""#0000ff"">3rd line:</font> Toclizumab (anti IL-1 and IL-6)</div>"
What should patients be screened for before starting biologics?- Hepatitis/ TB (as can cause reactivation)<div>- Pulmonary function tests: as biologics can cause fibrosis</div>
When can biologics be used in RA?When DAS28 is >5.1 despite treatment with 2 DMARDs (inc. Methotrexate) 
What is meant by <b>seronegative </b>in seronegative spondyloarthropathy?Does not have RF, or anti-CCP antibodies
What is the most common seronegative spondyloarthropathy?- Psoriatic Arthritis
Where do rashes typically manifest in psoriatic arthritis?<div>- Hairline</div><div>- Behind the ear</div><div>- Outside of knees and elbows</div><div>- Lower back</div><div>- Palms and soles of feet</div><div><br></div>
What are classical features of Psoriatic Arthritis clinically<b>Nail: </b>Pitting, onycholysis, yellow-pink discoloration, ridging<div><b>Dactylitis</b></div><div><b>Enthesopathy: </b>Inflammation at sites of ligamentous and tendinous insertions</div><div><b>DIP joint involvement</b></div><div><b>Psoriatic plaques</b></div>
What are features of psoriatic arthritis on X Ray?"- Periarticular Erosions<div>- Joint space thinning<br><div>- Dactylitis</div><div>- Sacroilitis</div><div>- <b>Pencil in Cup</b></div><div>- Plantar spur</div><img src=""Psorxray.gif""></div>"
What are the two subgroups of axial spondyloarthritis?"- <font color=""#0000ff"">Ankosing spondylitis</font>: When x-ray changes are clearly present<div>- <font color=""#0000ff"">Non-radiographic axial spondyloarthritis:</font> Clinical symptoms, but no x-ray changes present (70% of this group can bes een on MRI)</div>"
What are characteristics of inflammatory back pain?- Age at onset < 40 years<div>- Insidious onset</div><div>- Improvement with exercise</div><div>- No improvement with rest</div><div>- Pain at night (w/ improvement on getting up)</div><div>(Buttock pain + achilles enthesitis additional suggestion of ank spond)</div>
What is the <b>question mark posture?</b>"- Thoracic kyphosis<div>- Loss of cervical lordosis </div><div><br></div><div><img src=""paste-9e959567e68ab7a2c2eae180e252f8156a87966f.jpg""><br></div>"
"Aside from Schober's test, what are other tests that can be used to investigate ankylosing spondylitis?""- Measure chest expansion (<2.5cm)<div>- <font color=""#0000ff"">Cervical test</font>: Have pt stand straight against wall, and measure distance from occiput/tragus to wall. Distance > 5cm is positive. </div><div>- <font color=""#0000ff"">FABERs test:</font> Testing sacroiliac joint- felxion, abduction, external rotation</div>"
What is the prognosis of reactive arthritis?"Most people's symptoms will get better within 3-12 months without treatment. <div><br></div><div>30% of cases can progress to chronic arthritis</div>"
"What is <b>Reiter's triad?</b>"- Arthritis (reactive)<div>- Urethritis</div><div>- Conjunctivitis</div>
What are common extra-articular areas affected in reactive arthritis?- Eye (50%)<div>- GUM (20-40%)</div><div>- Aortic valve (10%)</div><div>- Pericarditis</div>
What joints are typically affected in enteropathic arthritis?"Any joint but often affects:<div>- Feet</div><div>- Ankles</div><div>- Knees</div><div><br></div><div>(Axial joints more likely with Crohn's)</div>"
What is the action of <b>ustekinumab?</b>Anti-IL-12, IL-23 antibody<div><br></div><div>(describes what?)</div>
Anti-IL-12, IL-23 antibody<div><br></div><div>(describes what?)</div>What is the action of <b>ustekinumab?</b>
What seronegative spondyloarthropathy is ustekinumab typically used (2nd line)?- Psoriatic Arthritis
When is etanercept contraindicated?- If patient has eye issues: etanercept can cause damage to eye<div>- If pregnant: Etanercept can cross placenta </div><div>- If TB/HepB: can cause reactivation</div>
What is the most likely cause of anterior knee pain in a young adult?"Patello-femoral pain syndrome: particularly if Q angle of patella is more than 20°<div><img src=""maxresdefault (2).jpg""><br></div>"
When does serum sickness occur?Around 5-10 days after receiving protein-based treatments
What are clinical signs and symptoms of serum sickness?- Rashes<div>- Itching</div><div>- Arthralgia (especially in fingers and toes)</div><div>- Fever</div><div>- Lymphadenopathy</div><div>- Splenomegaly </div><div>- Protein/blood in urine</div>
What are some adverse effects of PPIs such as omeprazole?"- Decrease renal tubule function --> decreased phosphate , Na + Mg<div><div>- Osteoporosis<div><font color=""#0000ff"">- Microscopic colitis</font><br><div>- Increase in c.diff and TB infections</div></div></div></div>"
What is <b>mononeuritis multiplex?</b>Progressive motor + sensory deficits in distribution of specific peripheral nerves 
What are key diagnostic factors of mononeuritis multiplex?- Numbness<div>- Weakness</div><div>- Pain</div><div>- Sicca symptoms (dry conjunctiva, oral membranes)</div><div>- Wheeze, cough</div><div>- Fever, weight loss and malaise</div>
What is the most common cause of mononeuritis multiplex?Vasculitis
What is optic neuritis?Inflammation of the optic nerve 
What are clinical features of optic neuritis?- Peri-orbital/retro-ocular pain (exacerbated by eye movements)<br><div>- Loss of visual acuity with scotoma</div><div>- Colour desaturation (not as bright as before)</div><div>- RAPD</div>
What is scotoma?"Partial loss of vision/blind spot in an otherwise normal visual field<div><img src=""1-s2.0-B9780444529039000169-f10-03-9780444529039.jpg""><br></div>"
What nerve roots are most commonly affected in sciatica?- L5-S1<div><br></div><div>Causes pain to radiate from buttock to back of calf</div>
<span class=cloze>[...]</span> = Granulomatosis with polyangiitis "<span class=cloze>Wegener's granulomatosis</span> = Granulomatosis with polyangiitis <br> "
"Wegener's granulomatosis = <span class=cloze>[...]</span> ""Wegener's granulomatosis = <span class=cloze>Granulomatosis with polyangiitis</span> <br> "
What is the classic triad of involvement in granulomatosis with polyangiitis?- Upper Respiratory Tract<div>- Lower Respiratory Tract</div><div>- Pauci-immune Glomerulonephritis</div>
Why might the nasal septum be examined on MRI in <b>Granulomatosis with Polyangiitis?</b>Nasal septum often perforated due to granulomatous destruction of nasal cartilage (occurs in what condition?)
Nasal septum often perforated due to granulomatous destruction of nasal cartilage (occurs in what condition?)Why might the nasal septum be examined on MRI in <b>Granulomatosis with Polyangiitis?</b>
What does ANCA stand for?Anti-neutrophil cytoplasmic antibodies
How can acquired haemophilia A occur, and what is the treatment?- Autoantibodies formed against factor VIII<div>- Steroids + Rituximab</div><div><br></div>
What acquired conditions can lead to depleted vWF?"<font color=""#0000ff"">Hades syndrome</font>: Sclerotic aortic valve<div><font color=""#0000ff"">Thrombotic Thrombocytopenic Purpura</font>: Antibody against enzyme ADAMTS13</div>"
Why is adalimumab more favoured over inflixmab?Adalimumab= Subcut<div>Infliximab= IV</div><div><br></div><div>Patients can inject themselves with adalimumab, so do not need to regularly go to the hospital </div>
"What arteries are particularly affected by Takayasu's arteritis?"Primarily affects aorta and its branches (subclavian, carotid, right brachiocephalic)
"What are typical symptoms of Takayasu's arteritis?"- Limb claudication on exertion (often absent limb pulses)<div>- Chest pain</div><div>- Systemic symptoms: Weight loss, fatigue, fever and myalgia </div>
"How is Takayasu's arteritis diagnosed?""<div>- Vascular imaging: should show vessel wall thickening, occlusion and oedema<br></div><div><img src=""1064-3_default.jpg""><br></div><div>(Bruits may be heard)</div>"
"What is seen here?<div><img src=""cow60.jpg""><br></div>"Pencil in cup deformity in both thumb PIPs- suggestive of <b>Psoriatic Arthritis</b>
"What is this, and if it presents with polyarticular symmetrical arthalgia, what is the likely cause?<div><img src=""1057-16_default.jpg""><br></div>""Erythema infectiosum- erythematous ""slapped cheeks""<div><br></div><div>Caused by Parvovirus B19 infection</div>"
"What is seen here, and what does this indicate?<div><img src=""F2.large (1).jpg""><br></div>"Romanus lesions: shiny corner sign from healing to early inflammatory erosions. <div><br></div><div>Finding in inflammatory spondyloarthropathies (e.g. ankylosing spondylitis, enteropathic arthritis)</div>
What disease is often associated with adhesive capsulitis?Diabetes mellitus: up to 20% of diabetics may have an episode of frozen shoulder
What types of movements are affected in adhesive capsulitis?- Both active <b>and </b>passive movement affected<div>- External rotation affected most</div>
What are the different phases of adhesive capsulitis?- Painful freezing phase (1 year)<div>- Adhesive phase (0.5-1 year)</div><div>- Recovery phase (1-3 years)</div>
What imaging should be performed pre-op for patients with RA?"<b>Atlantoaxial subluxation </b>can occur in RA --> cervical cord compression. Need to screen to ensure patient goes into surgery in a C-spine collar. <div><br></div><div><font color=""#0000ff"">AP and lateral cervical spine radiographs</font> would help here</div>"
What are medications that may worsen osteoporosis?- Glucocorticoids<div>- SSRIs</div><div>- Antiepileptics</div><div>- PPIs</div><div>- Glitazones (Diabetes)</div><div>- Long term heparin</div><div>- Aromatase inhibitors</div>
What would you expect the heart rate and resp rate to be in compartment syndrome?Both should be raised, due to increased sympathetic response from pain
What should be done with children/young people presenting with unexplained bone swelling or pain?"<font color=""#ff0000"">Red Flag:</font> <font color=""#ff0000"">Osteosarcoma</font><div><br></div><div>Urgent X-Ray (<48hrs) to assess.</div>"
"What is Sjogren's syndrome?"Chronic inflammatory autoimmuen disorder, with lymphocytic infiltration + fibrosis of exocrine glands (particularly lacrimal and salivary)
"In what populations is primary Sjogren's syndrome most common?"- Women (9x)<div>- 40-50y/o</div>
Secondary Sjogrens syndrome is typically linked to what diseases?Connective tissue disease:<br>- RA<div>- SLE<br>- Systemic sclerosis</div>
What type of Sjogrens is most common?Secondary Sjogrens
What HLA markers are linked with susceptibility to <b>Sjogrens syndrome</b>?HLA-A1, B8, or DR2/3
"What are clinical features of Sjogren's syndrome?"- Decreased tear production (dry eyes, keratoconjunctivitis sicca)<div>- Decreased salivation (xerostomia- dry mouth, dental caries)<br>- Parotid swelling </div>
"How can Sjogren's syndrome be investigated?""- Positive Schirmer's Test<div>- Anti-Ro (SSA) and Anti-La antibodies (SSB) antibodies may be present </div>"
"What is Schirmer's test?""Quantitatively measures tears: place filter paper in lower conjunctival sac. Test is positive if <5mm of paper is wetted after 5 minutes<div><br></div><div><img src=""schirmers.jpg""><br></div>"
"How is Sjogren's syndrome treated?"Treat symptoms:<div>- Give hypromellose (artificial tears)</div><div>- Encourage frequent drinks + sugar free gum etc. (salivary substitutes)</div><div>- Pilocarpine, M<sub>3</sub> agonist shown to be useful for mouth and eye dryness</div>
"People with Sjogren's syndrome have a marked increased risk of developing <span class=cloze>[...]</span>""People with Sjogren's syndrome have a marked increased risk of developing <span class=cloze>Non-Hodgkin B Cell Lymphoma</span><br> "
"What antibodies can be found in patients with Sjogren's syndrome?"- Rheumatoid Factor<div>- ANA</div><div>- Anti-Ro</div><div>- Anti-La </div>
What is a <b>Monteggia </b>fracture?Fracture of proximal ulna + dislocation of proximal head of radius (describes what type of fracture?)
Fracture of proximal ulna + dislocation of proximal head of radius (describes what type of fracture?)What is a <b>Monteggia </b>fracture?
What is a <b>Galeazzi </b>fracture?Fracture of distal radius + dislocation of distal radioulnar joint (describes what type of fracture?)
Fracture of distal radius + dislocation of distal radioulnar joint (describes what type of fracture?)What is a <b>Galeazzi </b>fracture?
What is a <b>Colles </b>fracture?Distal radius fracture with dorsal displacement (describes what?)
Distal radius fracture with dorsal displacement (describes what?)What is a <b>Colles </b>fracture?
"What is a <b>Smith's </b>fracture?"Distal radius fracture with volar displacement (describes what?)
Distal radius fracture with volar displacement (describes what?)"What is a <b>Smith's </b>fracture?"
"What is a <b>Bennett's </b>fracture?"Fracture of base of first metacarpal which extends into CMC joint (describes what?)
Fracture of base of first metacarpal which extends into CMC joint (describes what?)"What is a <b>Bennett's </b>fracture?"
What causes a Smiths fracture?- Falling backwards onto palm of outstretched hand<div>- Falling with wrists flexed</div>
"What is seen here?<div><img src=""swb135.jpg""><br></div>""Bennett's fracture: intra-articular fracture of first carpometacarpal joint"
"What is seen here?<div><img src=""paste-95b8ca8179b7d6ec3313366dbf8292c4b2220140.jpg""><br></div>""Colles' fracture: Fracture of distal radius, with dorsal displacement (loss of volar angle)"
"What is seen here?<div><img src=""300px-11751_2012_127_Fig1_HTML.jpg""><br></div>""Smith's fracture: Fracture of distal radius with increased volar angulation "
"What is seen here?<div><img src=""swb134.jpg""><br></div>""Monteggia's fracture: Fracture of ulna with dislocation of proximal radioulnar joint "
"What is seen here?<div><img src=""86bc033b86310ef27328c4b723226a_gallery.jpeg""><br></div>"Galeazzi fracture: Radial shaft fracture with dislocation of distal radioulnar joint
"What causes a Monteggia's fracture?"Fall on outstretched hand with forced pronation
"What is a Pott's Fracture?"Bimalleolar ankle fracture
"What causes a Pott's fracture?"Forced foot eversion
"What is a Barton's fracture?"Distal radius fracture with associated radiocarpal dislocation<div><br></div>
What is the main side-effect of colchicine?Diarrhoea
When should urate-lowering therapy be considered in gout?- ≥2 attacks in 12 months<div>- Tophi</div><div>- Renal disease</div><div>- Uric acid renal stones</div><div>- As prophylaxis if on cytotoxics/diuretics</div>
What is the first line drug used in Urate lowering therapy?- Allopurinol
What lifestyle modifications should you suggest to a patient with gout?- Reduce alcohol intake<div>- Lose weight (if obese)</div><div>- Avoid food high in purines e.g. liver, kidneys, seafood, oily fish </div>
What are risk factors (not including age) for developing pseudogout?"- Haemochromatosis<div>- Hyperparathyroidism</div><div>- Acromegaly </div><div>- Low Mg, Low Phosphate</div><div>- Wilson's disease</div>"
"What is Morton's neuroma?"A benign neuroma affecting the intermetatarsal plantar nerve, most commonly in the 3rd inter-metatarsophalangeal space 
"What are features of Morton's neuroma?""- Forefoot pain (commonly in 3rd inter-metatarsophalangeal space)<div>- Worse on walking</div><div>- Loss of sensation distally</div><div>- Positive Mulder's click</div>"
"What is Mulder's click?""Test to investigate Morton's neuroma:<div>- One hand tries to hold neuroma, other squeees metatarsals together. </div><div>- Click is heard, as neuroma moves between metatarsal heads</div>"
"What investigation may aid diagnosis of Morton's Neuroma?"- Ultrasound
"What is the management of Morton's neuroma?"- Avoid high heels<div>- Metatarsal pad</div><div>- Corticosteroid injection/ neurectomy of involved nerve + neuroma</div>
What antibiotic should be avoided with use of methotrexate?Trimethoprim: both inhibit dihydrofolate reductase<div><br></div><div>Increased risk of bone marrow suppression + pancytopaenia</div>
Where does Buergers disease affect?- Small + medium sized vessels: proximal pulses usually present, but distal pulses lost<div><br></div><div>(can affect both upper and lower limb)</div>
What may be seen in angiography of Buergers disease?- Tortuous corkscrew shaped collateral vessels
What are symptoms associated with fat embolism?"- Cardio/resp: Tachycardia, tachypnoea, dsypnoea, Hypoxia, pyrexia<div>- Neurological: Agitation, confusion</div><div>- Petechial rash</div><div>- Retinal haemorrhages</div><div><br></div><div><img src=""578 (1).jpg""><br></div>"
What genetic condition is frequently associated with gout?Lesch-Nyhan syndrome (x-linked recessive only seen in boys): HGPRTase deficiency 
What is a key investigation following diagnosis of temporal arteritis?Vision testing
If there are visual defects in patients with temporal arteritis, what drug should be given?"<b>IV Methyl</b>prednisolone- stronger than prednisolone and want to ensure patient's sight is maintained"
<span class=cloze>[...]</span> nerve compression may cause referred pain in the hip<span class=cloze>Femoral</span> nerve compression may cause referred pain in the hip<br> How can referred lumbar spine pain be investigated clinically ?Femoral nerve stretch test:<div><br></div><div>- Lie pt prone, then extend hip joint with straight leg then bend the knee --> stretches femoral nerve + causes pain if trapped</div>
<span class=cloze>[...]</span> = Trochanteric bursitis<span class=cloze>Greater trochanteric pain syndrome</span> = Trochanteric bursitis<br> Greater trochanteric pain syndrome = <span class=cloze>[...]</span>Greater trochanteric pain syndrome = <span class=cloze>Trochanteric bursitis</span><br> What causes greater trochanteric pain syndrome?Repeated movement of the iliotibila band 
Where is pain felt in greater trochanteric pain syndrome?- Lateral side of thigh
In what population is greater trochanteric bursitis most common in?Women aged 50-70 y/o
For which particular patients would you suspect avascular necrosis as being a cause of hip pain?- Pts following previous #NOF<div>- Pts on high dose steroids</div><div>- Pts on chemotherapy</div>
What occurs in pubic symphysis dysfunction?- Ligament laxity increases due to hormonal changes in pregnancy<div>- Pain over pubic symphysis which radiates to groins + medial aspects of thigh</div><div>- May cause a waddling gait</div>
What occurs in <b>transient idiopathic osteoporosis?</b>- Groin pain with limited range of movement in hip. <div>- Pts may be unable to weight bear</div><div>- ESR may be elevated</div>
When does transient idiopathic osteoporosis occur?Third trimester of pregnancy
Which antibodies are associated with limited cutaneous systemic sclerosis?Anti-centromere
Which antibodies are associated with diffuse cutaneous systemic sclerosis?Anti-scl-70 (Also known as anti-topoisomerase)
What typically causes a fracture of the radial head?Falling on outstretched hand 
What are clinical signs of a fracture of the radial head?- Local tenderness over head of radius<div>- Impaired movements at the elbow</div><div>- Sharp pain at lateral side of elbow at extremes of rotation (pronation + supination)</div>
How does <b>spinal stenosis</b> present?- Unilateral/bilateral leg pain<div>- Numbness + weakness</div><div>- Worse on walking</div><div>- Resolved by sitting down, leaning forwards and crouching down</div><div>(describes what?)</div>
- Unilateral/bilateral leg pain<div>- Numbness + weakness</div><div>- Worse on walking</div><div>- Resolved by sitting down, leaning forwards and crouching down</div><div>(describes what?)</div>How does <b>spinal stenosis</b> present?
How is a diagnosis of spinal stenosis made?- MRI required to confirm diagnosis as clinical examination often normal
How does peripheral arterial disease present?- Pain on walking, relieved by rest<div>- Absent/weak foot pulses </div><div>- Past history may include smoking + other vascular diseases</div>
What are causes of gout?DART:<div><br></div><div><b>D</b>iuretics</div><div><b>A</b>lcohol</div><div><b>R</b>enal disease</div><div><b>T</b>rauma</div>
What would you expect to see from arthrocentesis of an affected joint in reactive arthritis?- Cloudy yellow colour<div>- Culture negativity</div><div>- No crystals </div>
What does a turbid grey coloured joint aspirate indicate?Septic arthritis
In what fractures of the femur are intramedullary devices typically recommended?- Reverse oblique<div>- Transverse</div><div>- Subtrochanteric </div>
What typically causes an anterior cruciate ligament rupture?- Twisting force applied to flexed knee
A patient with an anterior cruciate ligament might describe what at the time of injury?- Loud crack<div>- Pain</div><div>- <b>Rapid </b>joint swelling (haemarthrosis)</div>
What typically causes a ruptured posterior cruciate ligament?Hyperextension injuries
What typically causes a rupture of the medial collateral ligament?- Leg forced into valgus via force outside the leg
What patients does chondromalacia patellae typically occur in?Teenage girls, following injury to knee
What are characteristic features of chondromalacia patellae?- Pain on going downstairs/ or at rest<div>- Tenderness, quadriceps wasting</div>
How does dislocation of the patella occur?- Traumatic primary event (direct trauma or severe contraction of quadriceps with knee stretched in valgus + ER)
How does a tibial plateau fracture occur?- Knee forced into valgus/varus, but knee fractures before ligaments rupture
"What are causes of Dupuytren's contracture?"- Manual labour<div>- Phenytoin treatment</div><div>- Alcoholic liver disease</div><div>- Diabetes mellitus</div><div>- Trauma to the hand</div>
"What is Dupuytren's contracture, and where is it most commonly seen?"Thickening of palmar fascia, particularly around the ring and little fingers
"When should Dupuytren's contracture be surgically treated?"- If MCP joints cannot be straightened and<b> hand cannot be placed flat on table</b>
A FRAX score of <span class=cloze>[...]</span> or more warrants a DEXA scanA FRAX score of <span class=cloze>10%</span> or more warrants a DEXA scan<br> FRAX score is 10 year risk  
<span class=cloze>[...]</span> = Lateral epicondylitis<span class=cloze>Tennis elbow</span> = Lateral epicondylitis<br> Tennis elbow = <span class=cloze>[...]</span>Tennis elbow = <span class=cloze>Lateral epicondylitis</span><br> What are the features of lateral epicondylitis?- Pain + tenderness localised to lateral epicondyle<div>- Pain worse on wrist extension/supination against resistance with extended elbow </div>
What are management options of lateral epicondylitis?- Avoid muscle overload<div>- Simple analgesia</div><div>- Steroid injection</div><div>- Physiotherapy</div>
What is the most common reason total hip replacements need to be revised?Aseptic loosening
"What bones does Paget's most commonly affect?"- Skull (can cause hearing loss)<div>- Spine/pelvis</div><div>- Long bones of lower extremeties</div>
"What would you expect to see from blood tests of Paget's disease?"- Raised ALP<div>- Normal Calcium and phosphate</div>
What is the most appropriate imaging modality to diagnose meniscal tears?- MRI 
"What is the clinical presentation of De Quervain's tenosynovitis?"- Pain over radial styloid process on forced abduction or flexion of thumb
What nerve (and root) is largely responsible for the triceps reflex?Radial nerve, C7
What is osteoarthritis?"<font color=""#0000ff"">Degenerative </font>condition of joints, characterised by progressive <font color=""#0000ff"">loss of articular cartilage </font>in association with <font color=""#0000ff"">pain and stiffness</font>"
What is the difference between primary and secondary osteoarthritis?"<b>Primary</b>: No other underlying cause- more common<div><b>Secondary</b>: Secondary to other condition e.g. trauma, Paget's, acromegaly</div>"
What are the stages of degeneration in osteoarthritis?- Fibrillation and flaking of articular cartilage<div>- Eburnation and sclerosis of underlying bone</div><div>- Formation of subchondral cysts</div><div>- Osteophyte formation </div>
What features of osteoarthritis may be elicited on Hx?- Pain (Mechanical, Resting pain in severe OA)<div>- Stiffness</div><div>- Instability of joint</div><div>- Deformity (varus/valgus) </div><div>- Decreases in ADL</div>
How might gait be affected in osteoarthritis?<b>Antalgic gait: </b><div><b><br></b></div><div>Affected leg spends less time in stance phase. </div><div>[anki:play:a:0]<br></div>
Why is physiotherapy helpful in OA?Pressure and movement from physiotherapy forces synovial fluid into joint --> provides nutrients in synovial fluid to the cartilage: allows healing and repair
Where do mature bones get their nutrients from?No blood supply- get it from <b>synovial fluid</b>
When measuring someone for a walking stick, what measurement should be made?Measure from ground to radial styloid 
What are the different surgical options for OA?- <b>Arthroplasty</b><div>- <b>Osteotomy </b>(remove some bone to improve weight distribution at joint)</div><div>- <b>Arthrodesis</b>: Fuses the bones together and stiffens the joint</div>
What antibody in Scleroderma is associated with a better prognosis?<b>Anti-centromere</b> antibodies: associated with limited cutaneous systemic sclerosis
What antibodies in Scleroderma are associated with renal crisis?Anti-RNA Polymerase III
What drugs are particularly good at treating renal crisis in scleroderma?ACE Inhibitors
"What dermatological signs are associated with Behcet's syndrome?"- Aphthous ulcer (mouth)<div>- Genital ulcer</div><div>- Erythema nodosum </div>
What are erythema nodosum, and where do they commonly arise?Painful red lesions due to inflammation of subcutaneous fat, typically in shins
"What is seen here?<br><img src=""at029g00a.jpg""><br>"Erythema <b>nodosum</b>
What dermatological sign is associated with <b>rheumatic fever?</b><b>Erythema</b> marginatum (is associated with which condition?)
<b>Erythema</b> marginatum (is associated with which condition?)What dermatological sign is associated with <b>rheumatic fever?</b>
What does erythema marginatum look like?"Pink rings on extensor surfaces<div><img src=""26d5bf9ee7c6eb66ed2d96086bc7bdb5.jpg""><br></div>"
What conditions are associated with <b>asteatotic eczema?</b>- Hypothyroidism<div>- Lymphoma </div><div><br></div><div>(have what associated dermatological sign?)</div>
- Hypothyroidism<div>- Lymphoma </div><div><br></div><div>(have what associated dermatological sign?)</div>What conditions are associated with <b>asteatotic eczema?</b>
"What is seen here?<div><img src=""Asteatotic_eczema_1_DW_600_450_70.jpg""><br></div>"Asteatotic eczema
"What is seen here?<div><img src=""642x361_Gallery_2_Guttate_Psoriasis.jpg""><br></div>"Guttate <b>psoriasis</b>- tear-drop lesions
What precipitates <b>guttate psoriasis?</b><b>Strep</b>tococcal throat infections (can cause what dermatological sign?)
<b>Strep</b>tococcal throat infections (can cause what dermatological sign?)What precipitates <b>guttate psoriasis?</b>
According to the Ottawa rules, when is an ankle X-ray required?"<font color=""#0000ff"">Pain in malleolar zone</font>, <b>and </b>one of the following:<div><br></div><div>- Bony tenderness at lateral malleolar zone</div><div>- Bony tenderness at medial malleolar zone</div><div>- Inability to walk four weight bearing steps immediately after the injury and in the emergency department</div>"
What are side effects of <b>sulfasalazine</b>?- Oligospermia<div>- Lung fibrosis</div><div>(are side effects of which DMARD?)</div>
"What is seen here?<div><img src=""C0110412.2e16d0ba.fill-320x213.jpg""><br></div>""Baker's Cyst"
Morning stiffness which lasts more than <span class=cloze>[...]</span> suggests inflammatory painMorning stiffness which lasts more than <span class=cloze>30mins</span> suggests inflammatory pain<br> Morning stiffness which lasts more than 30mins suggests <span class=cloze>[...]</span> painMorning stiffness which lasts more than 30mins suggests <span class=cloze>inflammatory</span> pain<br> - Oligospermia<div>- Lung fibrosis</div><div>(are side effects of which DMARD?)</div>What are side effects of <b>sulfasalazine</b>?
"What is <b>Buerger's disease?</b>"Non-atherosclerotic smoking related inflammation + thrombosis of veins & middle-sized arteries, causing thrombophlebitis and ischaemia. (describes what?)
Non-atherosclerotic smoking related inflammation + thrombosis of veins & middle-sized arteries, causing thrombophlebitis and ischaemia. (describes what?)"What is <b>Buerger's disease?</b>"
What is <b>thrombophlebitis?</b>Inflammatory process causing blood clot to form and block veins, typically in legs. <div><br></div><div>(Describes what?)</div>
Inflammatory process causing blood clot to form and block veins, typically in legs. <div><br></div><div>(Describes what?)</div>What is <b>thrombophlebitis?</b>
"What is a classic patient with Buerger's disease?"- Male<div><div>- 20-45 y/o<div><div><b>- Smoker</b></div></div></div></div><div>- Typically from south-east Mediterranean or Middle/Far Eastern origin</div>
"How should Buerger's disease be managed?"Stopping smoking 
What is polyarteritis nodosa?Necrotising vasculitis which affects medium-sized arteries 
<span class=cloze>[...]</span> is a vasculitis associated with hepatitis B<span class=cloze>Polyarteritis nodosa</span> is a vasculitis associated with hepatitis B<br> Polyarteritis nodosa is a vasculitis associated with <span class=cloze>[...]</span>Polyarteritis nodosa is a vasculitis associated with <span class=cloze>hepatitis B</span><br> What is the main cause of death in polyarteritis nodosa?Renal involvement: narrowing of renal artery --> glomerular ischaemia, insufficiency 
What organ system is typically spared in polyarteritis nodosa?Lungs 
How is polyarteritis nodosa managed?- Control BP (renal issues)<div>- Steroids for mild cases, steroid-sparing agents for more severe.</div>
What are the symptoms of <b>microscopic polyangiitis</b>?- Rapidly progressive glomerulonephritis<div>- Pulmonary haemorrhage (in 30%)</div><div><br></div><div>(occurs in which vasculitis?)</div>
- Rapidly progressive glomerulonephritis<div>- Pulmonary haemorrhage (in 30%)</div><div><br></div><div>(occurs in which vasculitis?)</div>What are the symptoms of <b>microscopic polyangiitis</b>?
<span class=cloze>[...]</span> syndrome = Eosinophilic granulomatosis with polyangiitis<span class=cloze>Churg-Strauss</span> syndrome = Eosinophilic granulomatosis with polyangiitis<br> Churg-Strauss syndrome = <span class=cloze>[...]</span>Churg-Strauss syndrome = <span class=cloze>Eosinophilic granulomatosis with polyangiitis</span><br> What is <b>hypocomplementaemic urticarial vasculitis?</b>Lupus-like illness with urticaria and antibodies to complement (C1q)<br><br><div>(describes what?)</div>
Lupus-like illness with urticaria and antibodies to complement (C1q)<br><br><div>(describes what?)</div>What is <b>hypocomplementaemic urticarial vasculitis?</b>
<span class=cloze>[...]</span> = Hives<span class=cloze>Urticaria</span> = Hives<br> Urticaria = <span class=cloze>[...]</span>Urticaria = <span class=cloze>Hives</span><br> "<div>What is seen here?</div><img src=""paste-cb3d12058d4fb7aeecc3bab2f7c5650246f8eef7.jpg"">"<b>Urticaria (hives)</b>
What are cryoglobulins?Immunoglobulins which reversibly precipitate at temperatures below 37°C
What are the most common autoimmune conditions associated with mixed cryoglobulinaemias?- Sjogrens syndrome<div>- SLE</div><div>- Systemic sclerosis</div><div>- Undifferentiated connective tissue disease</div><div>- Vasculitis</div>
What is the classic clinical presentation of cryoglobulinaemias?- Purpura<div>- Weakness</div><div>- Arthralgia</div><div>(though may have multiple organ involvement)</div>
What vessels does cryoglobulinaemia vasculitis affect? What organs are typically affected?Small vessels:<div>- Skin</div><div>- Joints</div><div>- Peripheral nervous system</div><div>- Kidneys</div>
If granulomas are seen in the lung, what diseases should be suspected?- Sarcoidosis <div>- Tuberculosis</div><div>- Histoplasmosis</div><div>- Granulomatosis with polyangiitis</div><div>- Non-small cell lung cancer</div><div>- Lymphoma</div>
Where does Sarcoidosis typically affect?- Lung (in 90% of pts)<div>- Skin</div><div>- Eyes </div>
What is the characteristic pathophysiology in Sarcoidosis?Non-caseating granulomas with multinucleated giant cells in centre. 
In cutaneous sarcoidosis, what might be seen?"- Plaques<div>- Lupus pernio</div><div><br></div><div><img src=""6486tn.jpg""><img src=""1-s2.0-S0012369209601379-gr1.jpg""><br></div>"
What is the most common sign in ocular sarcoidosis?- Anterior uveitis
How is sarcoidosis diagnosed?Diagnosis of exclusion of granulomatous lung diseases (ing. tuberculosis and histoplasmosis)
What is the most common cause for elbow symptoms in patients with elbow pain?Lateral epicondylitis
"<span class=cloze>[...]</span> epicondylitis = Golfer's elbow""<span class=cloze>Medial</span> epicondylitis = Golfer's elbow<br> "
Medial epicondylitis = <span class=cloze>[...]</span>"Medial epicondylitis = <span class=cloze>Golfer's elbow</span><br> "
"<span class=cloze>[...]</span> = Student's elbow""<span class=cloze>Olecranon bursitis</span> = Student's elbow<br> "
Olecranon bursitis = <span class=cloze>[...]</span>"Olecranon bursitis = <span class=cloze>Student's elbow</span><br> "
What causes olecranon bursitis?Pressure on the elbows causes inflammation and swelling of the bursa 
How is olecranon bursitis treated?Bursa aspirated: fluid sent for MC&S, and microscopy for crystals
What nerve root mainly mediates the bicep reflex?C6
What movement tests <b>C5?</b>Shoulder abduction (tests what nerve root?)
Shoulder abduction (tests what nerve root?)What movement tests <b>C5?</b>
What movement tests <b>C6?</b>Elbow flexion (tests what nerve root?)
Elbow flexion (tests what nerve root?)What movement tests <b>C6?</b>
What movement tests <b>C7?</b>Elbow extension (tests which nerve root?)
Elbow extension (tests which nerve root?)What movement tests <b>C7?</b>
What movement tests <b>C8?</b>Finger flexion (tests what nerve root?)
Finger flexion (tests what nerve root?)What movement tests <b>C8?</b>
What movement tests <b>T1?</b>Finger abduction (tests which nerve root?)
Finger abduction (tests which nerve root?)What movement tests <b>T1?</b>
What are the muscles which make up the rotator cuff? What movements do they regulate?<div>- Subscapularis (internal rotation)</div><div>- Supraspinatus (abduction)<br></div><div>- Infraspinatus (external rotation)</div><div>- Teres minor (external rotation and extension)</div>
What percentage of pts suffering from recurrent shoulder dislocation are atraumatic?5%: Atraumatic indicates joint laxity without history of injury (born loose)
What are characteristics of atraumatic recurrent shoulder dislocations?- Multidirectional<div>- Bilateral</div>
How is atraumatic recurrent shoulder dislocation treated?- Rehabilitation<div>- Inferior capsular shift surgery, if rehab fails</div><div><br></div><div>(AMBRI)</div>
What is a Bankart lesion?"Injury of anterior glenoid labrum from shoulder dislocation<div><img src=""220px-Shoulder_dislocation_with_Bankart_and_Hill-Sachs_lesion,_before_and_after_reduction.jpg""><br></div>"
What is the Hill-Sachs lesion?"Posterolateral dent in humeral head, from impaction of humeral head into glenoid rim<div><img src=""220px-Shoulder_dislocation_with_Bankart_and_Hill-Sachs_lesion,_before_and_after_reduction.jpg""><br></div>"
How is traumatic recurrent shoulder dislocation managed?- Surgery: (open repair may have better results than arthroscopic)
What is the Apprehension test of the shoulder?With elbow flexed at 90°, abduct and externally rotate arm to 90°<div><br></div><div>Feeling of apprehension = anterior joint stability</div>
How is frozen shoulder treated?- NSAIDs<div>- Intra-articular steroid</div><div>- Phsyiotherapy</div><div>- Manipulation under anaesthesia</div>
What is the most common cause of shoulder pain?Subacromial impingement 
What is the spectrum of rotator cuff injuries?"- <font color=""#0000ff"">Impingement</font>: inflammation from overuse<div>- <font color=""#0000ff"">Tendinopathy</font>: Irreversible changes within the tendon</div><div>- <font color=""#0000ff"">Tear</font></div>"
What are the risks if a patient has a tear in a rotator cuff muscle?- Instability of shoulder joint<div>- Larger risk of osteoarthritis (2°)</div>
What is the difference in surgical management of normal osteoarthritis of the shoulder and cuff tear arthritis?"<font color=""#0000ff"">Normal osteoarthritis</font>: Anatomical shoulder replacements<div><font color=""#0000ff"">Cuff-tear arthritis</font>: Reverse shoulder arthroplasty (as joint capsule disrupted)</div>"
What is the first line imaging technique to investigate rotator cuff injury?- Ultrasound
In what patients is frozen shoulder more common?- Diabetics<div>- Middle aged</div><div>- Women</div>
What is the prognosis of septic arthritis?- 50% cases have permanent joint damage<div>- Up to 11% mortality </div>
What joint is most commonly affected in septic arthritis?Knee
What is the pathophysiology of septic arthritis?- Microbes form biofilm on joint, which offers protection<div>- Microbes cause acute synovitis with proliferative hyperplasia</div><div>- Cartilage degradation by bacterial/leucocyte proteases/cytokines etc. </div><div>- Subchondral bone loss</div>
What are the most common origins for haematogenous spread of septic arthritis?- Skin <div>- Genitourinary</div><div>- Respiratory </div>
What are the typical causative agents for septic arthritis in infants, children, adults and the elderly?<b>Infants</b><div>- Gram neg bacilli</div><div>- Haemophilus influenza</div><div><br></div><div><b>Children</b></div><div>- Staph aureus</div><div><br></div><div><b>Adults</b></div><div>- Staph aureus</div><div>- Lancefield Group A streptococcus</div><div><br></div><div><b>Elderly</b></div><div>- Gram neg. bacilli</div>
What is the typical patient profile of gonococcal arthritis?- Young, sexually active female
What is the initial presentation of gonococcal arthritis?- Migratory polyarthralgia<div>- Tenosynovitis</div><div>- Dermatitis</div>
What is the response of gonococcal arthritis to antibiotics?Treated within a few days, excellent outcome
"If a pt presents with migratory joint pains and these skin signs, what do you suspect?<div><img src=""paste-27a9b02756f1cb3dca9660bad25ab37d3c8e8b58.jpg""><br></div>"Gonogoccal pustular skin lesions --> Gonococcal arthritis
What is the management of septic arthritis?- Empirical Abx against staph and strep (penicillin and flucloxacillin) Modify based on culture and serology from investigations.<div>- IV Abx for 2-4 weeks</div><div>- Joint drainage</div><div>- Early joint mobilisation to prevent contractures</div>
How is gonococcal arthritis distinct from reactive arthritis?- Reactive arthritis typically occurs across axial joints<div>- Reactive arthritis less acute- over course of weeks</div><div>- Reactive arthritis does not have dermatitis (pustules)</div><div>- Reactive arthritis does not respond to antibiotic therapy</div>
What is the most typical cause of hyperuricaemia?"<font color=""#0000ff"">Underexcretion (rather than overproduction):</font><div>- Chronic renal failure</div><div>- Drugs (CAN'T LEAP)</div>"
What drugs can cause hyperuricaemia?"CAN'T LEAP<br><div><br></div><div>Cyclosporin</div><div>Alcohol</div><div>Nicotinic acid</div><div>Thiazides</div><div>Lasix (furosemide)</div><div>Ethambutol</div><div>Aspirin (low dose)</div><div>Pyrazinamide</div>"
When would you not use allopurinol in patients with gout?In acute gout- will prolong attack, or precipitate it due to large shifts in intra/extracellular urate gradients
How does colchicine work?Inhibits intracellular microtubule formation- impairs neutrophil chemotaxis and degrandulation
The symptoms of <span class=cloze>[...]</span> are similar to lateral epicondylitisThe symptoms of <span class=cloze>radial tunnel syndrome</span> are similar to lateral epicondylitis<br> The symptoms of radial tunnel syndrome are similar to <span class=cloze>[...]</span>The symptoms of radial tunnel syndrome are similar to <span class=cloze>lateral epicondylitis</span><br> What differentiates the pain felt in radial tunnel syndrome from lateral epicondylitis?- Pain tends to be 4-5cm distal to the lateral epicondyle
<span class=cloze>[...]</span> arises from compression of the ulnar nerve<span class=cloze>Cubital tunnel syndrome</span> arises from compression of the ulnar nerve<br> Cubital tunnel syndrome arises from compression of the <span class=cloze>[...]</span> nerveCubital tunnel syndrome arises from compression of the <span class=cloze>ulnar</span> nerve<br> <span class=cloze>[...]</span> arises from compression of the posterior interosseous branch of radial nerve<span class=cloze>Radial tunnel syndrome</span> arises from compression of the posterior interosseous branch of radial nerve<br> Radial tunnel syndrome arises from compression of the <span class=cloze>[...]</span> nerveRadial tunnel syndrome arises from compression of the <span class=cloze>posterior interosseous branch of radial</span> nerve<br> Patients with documented allergies to co-trimoxazole should avoid taking which DMARD?Sulfasalazine<div><br></div><div>(sulfa allergy)</div>
What are stress fractures?Small hairline fractures caused by repetitive activity and loading of normal bone 
<span class=cloze>[...]</span> seen on radiographs may suggest stress fractures"<span class=cloze>Callus formation</span> seen on radiographs may suggest stress fractures<br> <img src=""e751cb87f9b416562d6b6c77a7a8ffac.jpg"">"
Callus formation seen on radiographs may suggest <span class=cloze>[...]</span>"Callus formation seen on radiographs may suggest <span class=cloze>stress fractures</span><br> <img src=""e751cb87f9b416562d6b6c77a7a8ffac.jpg"">"
How are stress fractures typically treated?Immobilisation may not be required:<div><br></div><div>- Early stage presentation: Immobilisation</div><div><br></div><div>(Immobilisation unlikely to be beneficial at late-stage)</div>
What is the main neurovascular structure compromised in a scaphoid fracture?Dorsal carpal branch of the radial artery
What fractures are most commonly associated with compartment syndrome?- Supracondylar<div>- Tibial shaft</div>
What type of hypersensitivity mediates allergic contact dermatitis?Type IV
What anti-clotting medication should be stopped/can be given in surgeries?- Clopidogrel should be stopped<div>- Aspirin is okay </div>
How should patients on warfarin be managed for operations?- Stopped at least 5 days before surgery; INR< 1.4<div>- Bridge with LMWH (which should also be stopped 24h prior to surgery)</div>
What GI symptoms are worrying in pre-op assessment?"<font color=""#0000ff"">Hiatus hernia</font>: <div>- Increases risk of regurgitation and aspiration of stomach contents at induction of anaesthesia</div>"
How might hiatus hernia be managed pre-operatively?- Pt should be started on metoclopramide (anti-emetic) and H<sub>2</sub> receptor antagonist (e.g. ranitidine) <b>or</b> PPI<div><br></div><div>(as worried about risk of regurgitation and aspiration)<br><div><br></div></div>
When should LFTs be done on a pre-op patient? What other tests should be done?Hx of jaundice or hepatic dysfunction.<div><br></div><div>- Also do a coagulation screen and platelet count</div>
What CNS issues are particualrly worrying for pre-op assessment?TIA/Stroke: Pts are at risk of further cerebrovascular events perioperatively 
How should patients with diabetes mellitus be managed pre-operatively?<div>- ECG, U&E analysis necessary</div><div>- Should try and schedule diabetic patients at start of operating list where possible </div><div>- 2 hourly blood glucose analysis<br></div>
When should VTE prophylaxis be considered?- Prolonged surgeyr<div>- Abdominal/pelvic surgery</div><div>- Prolonged bedrest</div><div>- Obese</div><div>- Oncological surgery </div>
What VTE prophylaxis may be given peri-operatively?- Thromboembolic deterrent stockings<div>- Subcutaneous heparin <br></div>
When is sickle cell testing carried out in pre-op assessment?- All Afro-Caribbean, east Indian and central South American descent 
In terms of fluid and food restriction pre-op, what rules apply?- Solids stopped 6hrs before surgery<div>- Breast milk stopped at 4hrs before surgery</div><div>- Water stopped 2hrs before surgery </div>
What diabetic medication should be stopped on the morning of surgery?- Short acting s.c. insulin<div>- Oral hypoglycaemics </div>
According to NICE recommendations, what pre-op investigations should be given to pts >60 who are otherwise fit?- FBC<br>- U&E<br><div>- ECG</div>
What are the risks of a pt with liver disease undergoing surgery?- Reduced production of clotting factors --> increased bleeding risk<div>- Possible portal hypertension --> varices, ascites</div><div>- Electrolyte abnormalities</div>
How should epilepsy be managed peri-operatively?- Continue all anti-epileptics during perioperative period<div>- Full seizure history/type of epilepsy</div><div>- If seizures becoming more frequent, <b>refer </b>for optimisation of medication</div>
"What are issues with Parkinson's patients undergoing surgery?"- Autonomic dysfunction (e.g. postural hypotension)<div>- Neck sitffness may lead to difficult intubation</div><div>- Exacerbation of condition</div><div>- Some anti-emetics worsen symptoms + cause extrapyramidal side effects</div><div>- Increased risk of post-op delirium</div>
"What considerations should be made with parkinson's patients peri-operatively?"- PD drugs should be continued peri-operatively<div>- Avoid metoclopramide and prochlorperazine (anti-emetics that work by antagonism of dopamine, will worsen Extra-pyramidal symptoms)</div><div>- Have nurse in side room to avoid delirium </div><div>- Put early on list</div><div><br></div>
What are the risks of diabetic patients peri-operatively?- Poor control --> high glucose levels --> poor outcome<div>- Increase rate of infection</div><div>- Increased rate of Major Adverse Cardiovascular Events (MACE)</div>
What are the guidelines for optimising diabetics before elective surgery?HbA1c < 8.5% (69mmol/mol)<div><br></div><div>Refer back to GP if target not achieved. </div><div><br></div><div>ECG + U&Es</div><div><br></div>
What are the risks of thyroid disease peri-operatively?- If uncontrolled, risk of thyrotoxic crisis or myxoedema coma<div>- Palpitations/arrhythmias</div><div>- If pt has goitre, risk of airway comrpomise</div>
What are considerations to be made for renal disease pts undergoing surgery?-<b> Avoid dehydration</b><div>- No NSAIDs</div><div>- Careful fluid management</div><div>- Check FBC, U&E, Calcium and Phosphate levels</div>
What is the difference between Group & Save, and Crossmatch?"<font color=""#0000ff"">Group and Save</font>: Processing blood sample to determine ABO group and Rh status of blood<div><br></div><div><font color=""#0000ff"">Crossmatch</font>: Final phase- confirms donor blood is compatible with pt's samples</div>"
What are risk factors for VTEs?<b>Patient factors:</b><div>- Obesity</div><div>- Pregnancy</div><div>- Hx of DVT/PE</div><div>- Inherited pro-clotting disorders</div><div>- Immobility</div><div>- Cancer</div><div>- SMoking</div><div><br></div><div><b>Surgical factors:</b></div><div>- Lower limb/pelvic surgery</div><div>- Surgery > 90 mins</div><div><br></div><div><b>Drug factors:</b></div><div>- Oral contraceptive pill </div>
What are the triad of drugs used in general anaesthesia?- Hypnotic<div>- Analgesia</div><div>- Neuromuscular Paralysis</div>
What are the three stages of general anaesthesia?- Induction<div>- Maintenance</div><div>- Neuromuscular paralysis</div>
Describe the airways of an unconscious patient?- Reduced/no airway protective reflexes<div>- Possible airway obstruction</div><div>- Reduced/no cough reflexes</div>
Describe the circulation of an unconscious patient?Reduced peripheral vascular tone (so reduced b.p.)
Why can anaesthesia predispose to post-operative chest infections?- Reduced respiratory <b>drive</b><div>- Fall in Functional <b>Residual Capacity</b></div><div>- Decreased <b>mucocilliary clearance</b></div><div>- Reduced <b>laryngeal competence</b></div>
What are patients at high risk of respiratory complications peri-operatively?COUPLES<div><br></div><div><b>C</b>OPD</div><div><b>O</b>besity</div><div><b>U</b>pper abdominal surgery</div><div><b>P</b>rolonged bed rest</div><div><b>L</b>ong surgery</div><div><b>E</b>lderly</div><div><b>S</b>mokers</div>
What are signs of respiratory distress?- Increased RR and HR<div>- Signs of CO<sub>2</sub> retention (sweating, tremor, increased b.p.)</div><div>- Abnormal respiratory pattern</div>
During anaesthesia, patients receive a minimum of <span class=cloze>[...]</span> oxygenDuring anaesthesia, patients receive a minimum of <span class=cloze>30%</span> oxygen<br> What are the limitations of pulse oximetry?- Performs poorly on poorly perfused peripheries (if hypoperfusion/cold fingers)<div>- Need to see reliable wave form</div><div>- Measures oxygenation not ventilation</div><div>- Can read falsely high in presence of carboxyhaemoglobin </div>
What is the advice for stopping methotrexate in terms of pregnancy?- Women should avoid pregnancy for at least 6 months after treatment has stopped<div>- Men using methotrexate should use effective contraception for at least 6 months after treatment </div>
What is the differentiation between osteomalacia and rickets?Osteomalacia is decreased mineral content in bone <b>after epiphysis fusion</b><div>Rickets is in growing bone </div>
What blood results suggest osteomalacia?- Raised ALP<div>- Low calcium, phosphate </div><div>- Low Vitamin D</div>
What is seen on X-Ray in osteomalacia?"Translucent bands- Looser's Zones (stress fractures) <div><img src=""6f6f7bcb446c3bb4b3c6864d717406_big_gallery.jpg""><br></div>"
What is seen on X ray in rickets?Cupped, ragged metaphyseal surfaces
What are features of rickets?- Genu varus/valgus<div>- Features of hypocalcaemia</div>
What are features of <b>osteomalacia</b>?<div>- Axial pain- vague and poorly located</div>- Bone tenderness<div>- Fractures</div><div>- Muscle tenderness</div><div>- Proximal myopathy (may result in waddling gait)</div><div><br></div><div>(describes what?)</div>
Why is APTT extended in Anti-Phospholipid syndrome?<b>Not because of thrombocytopenia</b>: as APTT solely looking at clotting factors<div><br></div><div>Anti-phospholipid antibodies react against phospholipids in the reagents, which impair the clotting in the test</div>
What is <b>discitis?</b>Infection in the intervertebral disc space (describes what?)
Infection in the intervertebral disc space (describes what?)What is <b>discitis?</b>
What is the standard therapy for discitis?6-8 weeks of IV antibiotics
In patients with discitis, what should be further investigated?ECHO to assess for endocarditis: <div><br></div><div>Discitis most commonly from haematagenous spread from elsewhere, and commonly arise from endocarditis</div>
In <span class=cloze>[...]</span> pain is exacerbated by walking on tip toes unlike <span class=cloze>[...]</span>In <span class=cloze>plantar fasciitis</span> pain is exacerbated by walking on tip toes unlike <span class=cloze>subcalcaneal bursitis</span><br> In plantar fasciitis pain is exacerbated by <span class=cloze>[...]</span> unlike subcalcaneal bursitisIn plantar fasciitis pain is exacerbated by <span class=cloze>walking on tip toes</span> unlike subcalcaneal bursitis<br> What occurs in <b>trigger finger?</b>- Initial stiffness and snapping, when extending a flexed digit<div>- Nodule may be felt at base of affected finger</div><div><br></div><div>(describes what?)</div>
- Initial stiffness and snapping, when extending a flexed digit<div>- Nodule may be felt at base of affected finger</div><div><br></div><div>(describes what?)</div>What occurs in <b>trigger finger?</b>
What are the associations of trigger finger?<div>- More common in women</div>- Diabetes mellitus<div>- Rheumatoid arthritis</div><div>- HTN, Hypercholesterolaemia</div>
How is trigger finger managed?"<b>1st line</b>: <font color=""#0000ff"">Steroid injection + finger splint:</font> Steroids reduce swelling and size of tendon nodule<div><br><div><b>2nd line</b>: <font color=""#0000ff"">Surgery if no response to injections:</font> cut flexor sheath ('pulley') at MCP joint, to prevent trapping</div><div><br></div><div>Diabetics tend not to respond to steroid injections- lower threshold for operation</div></div>"
Patients with <span class=cloze>[...]</span> often get relief from shaking their handsPatients with <span class=cloze>carpal tunnel syndrome</span> often get relief from shaking their hands<br> Patients with carpal tunnel syndrome often get relief from <span class=cloze>[...]</span>Patients with carpal tunnel syndrome often get relief from <span class=cloze>shaking their hands</span><br> In young fit patients with intracapsular hip fractures (Garden III), what is the most appropriate treatment option?"- Reduction and fixation with cannulated screws<div><img src=""hum4.jpg""><br><div><br></div><div>LIfespan of hip prosthesis means young patients are likely to require more revisions in the future</div></div>"
Patients with allergies to what drugs should be carefully considered before starting sulfasalazine?- Sulphonamides<div>- Aspirin</div>
What are the classical symptoms of <b>Leriche syndrome</b>?- Claudication of buttocks and thighs<div>- Atrophy of musculature of legs</div><div>- Impotence (due to paralysis of L1)</div><div><br></div><div>(are classic signs of what condition?)</div>
What is Leriche syndrome?Form of peripheral arterial disease, affecting the aortic bifurcation (or common iliac vessels)
How is Leriche syndrome managed?- Correcting underlying risk factors (hypercholsterolaemia, smoking)
What are the risk factors for osteoporosis (used by FRAX)?- Hx of glucocorticoid use<div>- Rheumatoid arthritis</div><div>- Alcohol Excess</div><div>- History of parental hip fracture</div><div>- Low BMI</div><div>- Current smoking</div>
In cases of suspected temporal arteritis, what is the most appropriate next step?Start on high-dose oral prednisolone (start before taking biopsy results, as this is an emergency)
"If these are painful to touch, what are they?<div><img src=""What-is-Osler-Nodes-300x202.jpeg""><br></div>"<b>Oslers nodes</b>- indicative of<b> infective endocarditis</b>
<span class=cloze>[...]</span> often has cANCA whereas <span class=cloze>[...]</span> often has pANCA antibodies<span class=cloze>Granulomatosis with polyangiitis</span> often has cANCA whereas <span class=cloze>Eosinophilic granulomatosis with polyangiitis</span> often has pANCA antibodies<br> Granulomatosis with polyangiitis often has <span class=cloze>[...]</span> whereas Eosinophilic granulomatosis with polyangiitis often has <span class=cloze>[...]</span> antibodiesGranulomatosis with polyangiitis often has <span class=cloze>cANCA</span> whereas Eosinophilic granulomatosis with polyangiitis often has <span class=cloze>pANCA</span> antibodies<br> What might you see on Chest X-Ray in late stage ankylosing spondylitis?Apical fibrosis
What are common complications of a posterior hip dislocation?- Sciatic nerve injury (10-20%)<div>- Avascular necrosis (6%)</div><div>- Osteoarthritis</div><div>- Recurrent dislocation</div>
What is suggestive of metastatic tumour to bone?- Increasing pain at rest<div>- Increased serum calcium and ALP</div>
What is the recommended calorie intake for men and women?"<font color=""#0000ff"">Men</font>: 2500 calories a day<div><font color=""#0000ff"">Women</font>: 2000 calories a day</div>"
What is an appropriate BMI to aim for?18.5-25
What is the advice regarding taking folic acid for women attempting to conceive?Take 400µg/a day of folic acid from (pre) conception to at least 12 weeks
"What is seen here?<div><img src=""BPG54A1.2e16d0ba.fill-320x213.jpg""><br></div>"Leucoplakia- oral mucosal white patch which will not rub off 
"What is seen here and what causes it?<div><img src=""3-s2.0-B9780323552257000075-f007-026-9780323552257.jpg""><br></div>"Oral hairy leucoplakia, caused by EBV, in HIV+ individuals
"What is seen here?<div><img src=""paste-d77416c58ae9c352ade2046e78b91f200c6bd93b.jpg""><br></div>"Aphthous ulcer
What are causes of severe aphthous ulcers?"<font color=""#0000ff"">- Crohn's</font><div><font color=""#0000ff"">- Coeliac disease</font></div><div><font color=""#0000ff"">- Behcets</font></div><div><font color=""#0000ff"">- Trauma</font></div><div><font color=""#0000ff"">- Infections (HSV, syphyilis, Vincent's angina)</font><br></div><div>- Erytheme multiforme</div><div>- Lichen planus</div><div>- Pemphigus</div><div>- Pemphigoid</div>"
How can minor aphthous ulcers be managed?"<font color=""#0000ff"">Conservative</font>:<div>- Avoid oral trauma (e.g. hard toothbrushes, hard foods like toast)</div><div>- Avoid acidic foods and drinks </div><div><br></div><div><font color=""#0000ff"">Treatment</font>:</div><div>- Tetracycline or antimicrobial mouthwashes</div><div>- Topical steroids (triamcinolone)</div><div>- Topical analgesia</div>"
How can severe aphthous ulcers be managed?- Systemic corticosteroids<div>- Thalidomide (contraindicated in pregnancy)</div>
"What is a <font color=""#ff0000"">red flag</font> in aphthous ulcers?"If ulcer not healed after 3 weeks, biopsy to excluse malignancy
"What is seen here?<div><img src=""800.jpg""><br></div>"Candidiasis 
What are risk factors for candidiasis?- Extremes of age<div>- Diabetes mellitus</div><div>- Antibiotics</div><div>- Immunosuppression (corticosteroids, including inhalers)</div><div>- Cytotoxics</div><div>- Malignancy</div><div>- HIV</div>
What is the management for oral candidiasis?- Nystatin suspension<div>- Fluconazole (for oropharyngeal thrush)</div>
<span class=cloze>[...]</span> in an apparently fit patient may suggest underlying HIV infection<span class=cloze>Oropharyngeal candidiasis</span> in an apparently fit patient may suggest underlying HIV infection<br> Oropharyngeal candidiasis in an apparently fit patient may suggest underlying <span class=cloze>[...]</span>Oropharyngeal candidiasis in an apparently fit patient may suggest underlying <span class=cloze>HIV infection</span><br> "What is seen here?<div><img src=""paste-e7af872d75102cfc8af1af376fa72b8afafe80bb.jpg""><br></div>"Cheilitis (angular stomatitis)
What causes cheilitis?- Denture problems<div>- Candidiasis</div><div>- Deficiency of iron or vitamin B2</div>
<span class=cloze>[...]</span> = Angular stomatitis<span class=cloze>Cheilitis</span> = Angular stomatitis<br> Cheilitis = <span class=cloze>[...]</span>Cheilitis = <span class=cloze>Angular stomatitis</span><br> "What is seen here?<div><img src=""300px-Gingivitis_(crop).jpg""><br></div>"Gingivitis
What is gingivitis?"Gum inflammation and hypertrophy<div><img src=""300px-Gingivitis_(crop).jpg""><br></div>"
What drugs can cause <b>gingivitis</b>?- Phenytoin<div>- Cyclosporin</div><div>- Nifedipine</div><div><br></div><div>(can cause what side effect in common?)</div>
What can cause gingivitis?"<div>- <font color=""#0000ff"">Scurvy- </font>Vitamin C deficiency<br></div>- Drugs<div>- Pregnancy</div><div>- Acute myeloid leukaemia (particularly APML)</div><div>- Vincent's Angina</div>"
"What is Vincent's angina?""<font color=""#0000ff"">Necrotising ulcerative gingivitis: </font>Mouth infection with ulcerative gingivitus"
"What organisms cause Vincent's angina>"- Borrelia vincentii (a spirochaete)<div>- Fusiform bacilli </div>
"What patients are typically prone to Vincent's angina?"- Young male smokers, with poor oral hygiene
"How is Vincent's angina managed>"- Amoxicillin (500mg/8hrs)<br>- Metronidazole (400mg/8hrs)<div>- Chlorhexidine (anti-microbial) mouthwash</div>
What is <b>microstomia</b>?"Mouth is too small<div><img src=""paste-4aea09195cc827e40b5147b8f096732b9d805442.jpg""><br></div><div><br></div><div>(describes what?)</div>"
"Mouth is too small<div><img src=""paste-4aea09195cc827e40b5147b8f096732b9d805442.jpg""><br></div><div><br></div><div>(describes what?)</div>"What is <b>microstomia</b>?
What are causes of microstomia?- Thickening + tightening of perioral skin (after burns)<div>- Peidermolysis bullosa</div><div>- Systemic sclerosis</div>
"What does this suggest?<div><img src=""peutz-jeghers04_600_399_70.jpg""><br></div>""Peutz-Jeghers' syndrome"
"What causes <b>Peutz-Jeghers</b>' syndrome?"Dominant germline mutations of TSG STK11 (causes which eponymous syndrome?)
Dominant germline mutations of TSG STK11 (causes which eponymous syndrome?)"What causes <b>Peutz-Jeghers</b>' syndrome?"
"What are features of Peutz-Jeghers' syndrome?"- Characteristic brown freckles on lips, oral mucosa, palms and soles<div>- Multiple GI Polyps, causing obstruction, intussusception or bleeds</div><div>- 15 fold increased risk of developing GI Cancer </div>
"What is seen here, and what disease could it suggest?<div><img src=""paste-a3c9d3c58e9b5398eabce1b0ce1db65dd76f94ff.jpg""><br></div>"Telangiectasia:<div>- Systemic sclerosis</div><div>- Osler-Weber-Rendu syndrome</div>
"What is seen here, and what could cause it?<div><img src=""28650tn.jpg""><br></div>""Pigmentation in mouth:<div>- Addison's disease</div><div>- Drugs e.g. antimalarials</div>"
"What are seen here?<div><img src=""256918_1100.jpg""><br></div>"Fordyce glands: sebaceous cysts, common and benign
"What is seen here, and what does it suggest?<div><img src=""41415_2009_Article_BFsjbdj2009524_Fig1_HTML.jpg""><br></div>"Blue line at gum-tooth margin --> lead poisoning 
"What i seen here?<div><img src=""AtrophicGlossitis.jpg""><br></div>"Glossitis: smooth red sore tongue
What causes glossitis?"<font color=""#0000ff"">Deficiencies in:</font><div>- Iron</div><div>- Folate</div><div>- B12</div>"
What are causes of macroglossia?- Myxoedema (advanced hypothyroidism)<div>- Acromegaly</div><div>- Amyloidosis</div>
"What is seen here?<div><img src=""Ranula_human_09.jpg""><br></div>"A ranula: salivary retention cyst to one side of the fenulum 
"What is seen here?<div><img src=""squamous-cell-carinoma-of-the-tongue.jpg""><br></div>"Raised ulcer with firm edges- could be tongue cancer
Cancers in the tongue spread to what nodes?"<font color=""#0000ff"">Anterior 1/3:</font> Submental nodes<div><font color=""#0000ff"">Middle 1/3:</font> Submandibular nodes</div><div><font color=""#0000ff"">Posterior 1/3:</font> Deep cervical nodes</div>"
Discuss the differences in bone mass between genders?- Women have lower peak bone mass (as oestrogen in puberty causes bone plates to close quicker; and less anaerobic exercise)<div>- Women have larger bone loss at menopause</div>
What is the most common cell in bone?Osteocytes (Osteoblasts embedded in hydroxyapatite)
<span class=cloze>[...]</span> bone is found in the outer shell whereas <span class=cloze>[...]</span> is found in the inner bone <span class=cloze>Cortical</span> bone is found in the outer shell whereas <span class=cloze>trabecular</span> is found in the inner bone <br> Cortical bone is found in the <span class=cloze>[...]</span> whereas trabecular is found in the <span class=cloze>[...]</span>Cortical bone is found in the <span class=cloze>outer shell</span> whereas trabecular is found in the <span class=cloze>inner bone </span><br> What is the difference between a T-score and Z-score for DEXA scans?"<font color=""#0000ff"">T-Score:</font> Compared to a young healthy person of the same gender (for older post-menopausal women)<div><font color=""#0000ff"">Z-Score:</font> Compared to healthy person of the <b>same age and gender</b> </div>"
What is <b>osteopetrosis?</b>Autosomal recessive condition causing dense and brittle bones
What is <b>osteomalacia?</b>Defect of bone mineralisation secondary to vitamin D deficiency
<div>- Axial pain- vague and poorly located</div>- Bone tenderness<div>- Fractures</div><div>- Muscle tenderness</div><div>- Proximal myopathy (may result in waddling gait)</div><div><br></div><div>(describes what?)</div>What are features of <b>osteomalacia</b>?
"What is <b>Paget's Disease</b>"Localised disorder of bone metabolism with osteoblastic and osteosclerotic hyperactivity
"How does Paget's disease present?"Most commonyl asymptomatic (just raised ALP with normal LFTs)<div><br></div><div>If symptomatic:<br>- Pain</div><div>- Deformity</div><div>- Fracture</div><div>- Nerve compression</div><div>- High output cardiac failure </div><div>- Loss of hearing (ossicles)</div>
"What are long term risks of Paget's Disease?"<1% chance of osteosarcoma
What are most common sites of cancers which spread to bone?- Breast<div>- Lung</div><div>- Prostate</div><div>- Kidney </div><div>- Thyroid</div><div><br></div><div>(5Bs- Breast, Brostate, Bung, Bidney and Byroid)</div>
What findings may you find from blood tests in metastatic bone disease?- Raised ALP<div>- Raised Calcium (though can be normal in osteosclerotic diseases)</div>
Where are common areas of osteonecrosis?- Femoral head<div>- Distal femur</div><div>- Scaphoid</div><div>- Proximal humerus</div><div>- Talus</div>
What imaging is best to pick up osteonecrosis?- MRI
What are the Ottawa rules with regards to foot X-Rays?"X-rays are only required if <font color=""#0000ff"">any pain in midfoot zone </font>and <b>one of the following:</b><div><br></div><div>- Bony tenderness at base of fifth metatarsal</div><div>- Bone tenderness at navicular</div><div>- Inability to bear weight both immediately and in the ED for four steps</div>"
"What is seen here?<div><img src=""MyPortalFiles.png""><br></div>""Plantar ecchymosis: <font color=""#ff0000"">could indicate Lisfranc tarsometatarsal injuries</font>"
What do the Lisfranc ligaments connect?"Medial cuneiform with the 2nd and 3rd metatarsal base<div><img src=""260px-Lisfranc_ligaments.jpg""><br></div>"
What are complications of Lisfranc injuries if not managed?Instability --> Posttraumatic arthritis<div><br></div>
Which vertebrae are affected in osteomyelitis?"Depends on causative organism:<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Staph aureus</font>: Cervical spine</div><div><font color=""#0000ff"">TB</font>: Thoracic spine</div><div><font color=""#0000ff"">Other causes</font>: Lumbar spine</div>"
What cardiac problems can you see in Ehler-Danlos syndrome?- Aortic <b>regurgitation</b><div>- Mitral valve<b> prolapse</b></div><div>- Aortic<b> dissection</b></div>
What is the relevance of the grading for acromioclavicular joint injuries?"<font color=""#0000ff"">I-II:</font> Common, and managed conservatively, by resting the joint using a sling<div><font color=""#0000ff"">III</font>: under debate- depends on individual circumstances<br></div><div><font color=""#0000ff"">IV-VI</font>: Rare + require surgical intervention</div>"
What is the <b>Stimson Manouevre</b> used for?Reduction of dislocated shoulders (is achieved by what?)
Reduction of dislocated shoulders (is achieved by what?)What is the <b>Stimson Manouevre</b> used for?
What structure is divided in surgical management of carpal tunnel syndrome?Flexor retinaculum
<span class=cloze>[...]</span> fracture = Torus fracture<span class=cloze>Buckle</span> fracture = Torus fracture<br> Buckle fracture = <span class=cloze>[...]</span> fractureBuckle fracture = <span class=cloze>Torus</span> fracture<br> Vitamin <span class=cloze>[...]</span> is teratogenicVitamin <span class=cloze>A</span> is teratogenic<br> What is a charcot joint?Neuropathic joint: joints disrupted and damaged secondary to loss of sensation 
What are the features of a charcot joint?Progressive degeneration of weight bearing joint, due to loss of sensation (individuals will continue to damage joint, but unable to feel pain and so continue)
What are the common causes of charcot joint?"<font color=""#0000ff"">- Diabetic neuropathy (most common)</font><div>- Alcoholic neuropathy</div><div>- Syphyilis</div><div>- Cerebral palsy</div>"
What special tests might you do for a hip examination? Describe them."<b>Trendelenburg test: </b>Hold patients hands and ask them to flex their knee behind. Observe any sagging- if hip falls on one side suggests<font color=""#0000ff""> pathology in abductors on opposite side</font><div><b><br></b></div><div><b>Thomas test: </b>Place hand under back (isolate the lumbar spine), and ask pt to<b> bring knee to chest</b> (flex a flexed knee), and hold it with both hands. Examine the other leg, to see if there is loss of extension.<font color=""#0000ff""> Suggests fixed flexion deformity</font></div>"
How do you assess the function of <b>supraspinatus </b>in a shoulder examination?<b>Empty can test:</b><div><b><br></b></div><div><div>- Abduct arm to 90°, and angle arm forward 30°, then internally rotate arm, as if pouring liquid from a can. </div><div>- Push down on arm and ask patient to resist the movement</div></div>
How do you test for impingement of<b> supraspinatus</b>?<b>Painful arc</b><div><b><br></b></div><div>- <b>Passively abduct</b> arm to maximum point of abduction. </div><div>- Ask pt to slowly lower arm back to neutral position</div><div><br></div><div>Impingement/supraspinatus tendonitiys typically causes pain between 60-120° of abduction </div>
How do you test the function of <b>infra</b>spinatus?Test <b>external rotation </b>against resistance (with elbow flexed at 90° and in slight abduction)
How do you test the function of <b>subscap</b>ularis?<b>Internal </b>rotation against resistance:<div><br></div><div>- Get patient to place dorsum of hand on lower back</div><div>- Apply resistance to hand, pressing it towards back, and ask pt to oppose this resistance</div>
What type of osteoporosis is predominant in men and women?"<font color=""#0000ff"">Women</font>: Primary (80%)<div><font color=""#0000ff"">Men</font>: Secondary (80%)</div><div><br></div><div>As women naturally have a lower bone mass peak, and higher loss post-menopause</div>"
How can osteoporosis be conservatively managed?- Aerobic exericse<div>- Calcium and vitamin D supplements (Adcal D3)</div>
How are bisphosphonates taken orally?Alendronate- once a week<div>Ibandronate- once a month. </div><div><br></div><div>Pt has to starve overnight, and must eat tablet first thing, sitting up for 30 minutes. </div>
How long can patients be on bisphosphonates for? Why?"Only for 5-7 years: bisphosphonates can cause <font color=""#0000ff"">atypical fractures</font>.<div><br></div><div>Risk of atypical fractures increases with increased duration of use.</div>"
Why is teriparatide not commonly given?- Very expensive<div>- Has to be given every day</div>
What are the two main drugs used for osteoporosis?- Bisphosphonates<div>- Sub-cut RANK-L inhibitor (denosumab)</div>
"How is Paget's disease managed?""<font color=""#0000ff"">If asymptomatic</font>: Observe, regular follow up + preventative measures<div><font color=""#0000ff"">Symptomatic</font>: Bisphosphonate (risedronate) /calcitonin, physiotherapy </div>"
"What is seen here? What could this represent?<div><img src=""tumblr_n04rfkqznM1ru4rx5o1_640.jpg""><br></div>""Pepper pot skull/raindrop skull: <div><br></div><div>- Could be cause by resorption of trabecular bone in<b> </b><font color=""#0000ff"">hyperparathyroidism</font></div><div>- Could be multiple lytic lesions of <font color=""#0000ff"">multiple myeloma</font></div>"
What blood test reading can provide information whether a raised ALP is due to liver or bone pathology?"<font color=""#0000ff"">GGT (gamma-glutamyltransferase):</font><div><br></div><div>If GGT is raised, suggests liver pathology rather than bone.</div>"
What are skeletal surveys commonly used for?Multiple myeloma- detect where tumour deposits in bones<div><br></div><div>(outdated now, MRI whole body more commonly done)</div>
"What are the features of <b>Still's disease</b>?"- Arthralgia<div>- Elevated serum ferritin </div><div>- Salmon pink rash, macropapular</div><div>- Pyrexia: Rises in early evening in daily pattern and accompanies worsening of joint symptoms and rash.</div><div>- Lymphadenopathy</div><div>- RF and ANA negative</div><div><br></div><div>(Describes what?)</div>
- Arthralgia<div>- Elevated serum ferritin </div><div>- Salmon pink rash, macropapular</div><div>- Pyrexia: Rises in early evening in daily pattern and accompanies worsening of joint symptoms and rash.</div><div>- Lymphadenopathy</div><div>- RF and ANA negative</div><div><br></div><div>(Describes what?)</div>"What are the features of <b>Still's disease</b>?"
"How is Still's disease managed?"- NSAIDs for fever, joint pain and serositis<div>- Steroids (for symptoms but no improvement in prognosis)</div><div><br></div><div>If symptoms persist:</div><div>- Methotrexate</div><div>- anti- IL-1 (anakinra) or anti-TNF therapy</div>
"What is <b>De Quervain's tenosynovitis?</b>""Inflamed sheath containing extensor policis brevis and abductor pollicis longus (describes what?)<div><br></div><div><img src=""de-quervains-tenosynovitis-8col-3746063-001-0.jpg""><br></div>"
"Inflamed sheath containing extensor policis brevis and abductor pollicis longus (describes what?)<div><br></div><div><img src=""de-quervains-tenosynovitis-8col-3746063-001-0.jpg""><br></div>""What is <b>De Quervain's tenosynovitis?</b>"
"What are features of De Quervain's tenosynovitis?"- Painful abduction of thumb against resistance<div>- Positive finkelsteins test</div>
What is Finkelsteins test?"Test for de Quervain's tenosynovitis: with thumb flexed across palm, pain reproduced by flexing and ulnar deviation of wrist."
<span class=cloze>[...]</span> is caused by a mutation in fibrillin-1<br>"<span class=cloze>Marfan's syndrome </span> is caused by a mutation in fibrillin-1<br><br> Autosomal Dominant condition"
"Marfan's syndrome is caused by a mutation in <span class=cloze>[...]</span><br>""Marfan's syndrome is caused by a mutation in <span class=cloze>fibrillin-1</span><br><br> Autosomal Dominant condition"
What hand signs can you look for in an abdominal examination?"- Clubbing<div>- Koilonychia</div><div>- Leukonychia</div><div>- Palmar erythema</div><div>- Dupuytren's contracture</div>"
What are gastro causes of clubbing?- Inflammatory Bowel Disease<div>- Cirrhosis</div><div>- Coeliac Disease</div>
What causes <b>Koilonychia?</b>Chronic iron deficiency (causes what hand sign?)
Chronic iron deficiency (causes what hand sign?)What causes <b>Koilonychia?</b>
"What is seen here?<div><img src=""642x361_Spoon_Nails.jpg""><br></div>"Thin nails, which have lost shape- koilonychia
What are gastro causes of leukonychia?Hypoalbuminaemia- liver failure/enteropathy
"What is seen here?<div><img src=""CAPD_leukonychia_striata.jpg""><br></div>"Leukonychia- sign of hypoalbuminaemia
What are abdo related causes of palmar erythema?- Liver disease<div>- Pregnancy</div>
"What are causes of the sign seen below?<div><img src=""uopi_P.gif""><br></div>"Flapping:<div><br></div><div>- Hepatic encephalopathy</div><div>- Uraemia</div><div>- CO<sub>2</sub> retention</div>
"What is seen here? What could this be caused by?<div><img src=""Excoriations2+copy.jpg""><br></div>"Excoriations: cholestasis
"What are gastro causes of the sign seen below?<div><img src=""S_0318_Acanthosis_nigricans_C03739.2e16d0ba.fill-320x213.jpg""><br></div>""<div><font color=""#0000ff"">Acanthosis nigricans</font>:</div>- GI adenocarcinomas<div>- Obesity</div>"
"What is seen below? How many is required for this to be a significant finding, and what does it suggest?<div><img src=""spidernaevus.gif""><br></div>""Spider naevi- >5 to be significant. <div><br></div><div>Suggestive of<font color=""#0000ff""> chronic liver disease</font></div>"
"What is seen below?<div><img src=""Cullen's_sign.jpg""><br></div>""Bruising surrounding umbilicus: <b>Cullen's sign</b>"
"What is Cullen's sign suggestive of?"Retroperitoneal bleed (e.g. pancreatitis/ruptured AAA)
What can cause abdominal distension?5 Fs:<div><br></div><div>Fluid (ascites)</div><div>Fat (obesity)</div><div>Faeces (constipation)</div><div>Flatus </div><div>Foetus (pregnancy)</div>
"What is seen here?<div><img src=""4174-Caput_Medusae_642x361.jpg""><br></div>"Caput medusae- indicative of portal hypertension 
Where are colostomy, ileostomy and urostomy bags found?"<font color=""#0000ff"">LIF</font>: Colostomy<div><font color=""#0000ff"">RIF</font>: Ileostomy and urostomy</div>"
"What is Murphy's sign?""Place hand in right costal margin, mid-clavicular line, and ask pt to take deep breath. <div><br></div><div>Patient may stop inspiring halfway through, as gallbladder is pushed into your hand. If so, <font color=""#0000ff"">suggestive of cholecystitis</font></div>"
What are further investigations you may wish to do following an abdominal examination?HELP US<div><br></div><div>Hernial orifices</div><div>External genitalia</div><div>Lymphadenopathy</div><div>PR</div><div><br></div><div>Urine dipstick</div><div>Stool sample</div>
A <b>mosaic pattern of lamellar bone</b> found on biopsy suggests what disease?"Paget's disease (presents with what on biopsy?)"
"Paget's disease (presents with what on biopsy?)"A <b>mosaic pattern of lamellar bone</b> found on biopsy suggests what disease?
Pain on flexing a hip on a straight leg suggests what?Positive straight leg test: suggestive of sciatic nerve problem
What predisposes people to azathioprine toxicity?Thiopurine methyltransferase deficiency
"What is seen here?<div><img src=""xrb117b.jpg""><br></div>"Calcification of the supraspinatus tendon- suggests supraspinatus tendonitis
When should the FRAX tool be used/Assess fracture risk?- In all women > 65y/o, or men > 75y/o<div>- Younger patients (50 and above) with risk factors</div><div><br></div><div>(note FRAX is valid for pts aged 40-90)</div>
For what ages is FRAX valid?40-90
How should clubfoot be corrected?Manipulation and progressive casting starting soon after birth
What is antisynthetase syndrome?Subtype of dermatomyositis, characterised by myositis and interstitial lung disease
Which antibody is responsible for antisynthetase syndrome?Anti-Jo1
Patients with myositis and +ve anti-Jo1 antibodies are at particular risk of what?Developing interstitial lung disease
What are characteristic features of antisynthetase syndrome?"- Myositis<div>- Interstitial lung disease</div><div>- Thickened and cracked skin of the hands (mechanic's hands)</div><div>- Raynaud's</div>"
What antibiotic is often linked with achilles tendon disorders?Ciprofloxacin
What muscle is needed for the first 20° of shoulder abduction?Supraspinatus
What are key features of acromioclavicular joint dislocation?- Loss of shoulder contour<div>- Prominent clavicle</div>
What is the action of secukinumab?Anti-IL-17 monoclonal antibody<div><br></div><div><br></div><div>(used in ank spond and psoriatic arthritis)</div>
Although secukinumab are typically second-line biologics after anti-TNF therapy for ank spond, why might they be favoured?Anti-TNF therapy may have increased risk of lymphomas + leukemias
What antibodies may be associated with cutaneous lupus erythematosus?- ANA<br>- Anti-Ro
"What is seen here?<div><img src=""Crohnie_Pyoderma_gangrenosum.jpg""><br></div>"Pyoderma gangrenosum often associated with systemic inflammation- (RA, IBD in 50% of cases)
If you see an increased Q angle on the knee examination, what else should you look for?<b>Pronated flat feet</b>- often predispose to <b>knee pain </b>
"What do Baker's cysts often present with?""Red swelling down leg/bruising low down on limb, caused by leak of cystic fluid down leg. <div><br></div><div><img src=""iotwbakercystca071601_1020999.jpg""><br></div><div><br></div>"
"A patient presents with repeated blood-stainned effusions of their knee. An MRI scan is shown below. What is the most likely diagnosis?<div><img src=""02b.jpg""><br></div>"Pigmented vilonodular synovitis
What are signs of a medial meniscus tear that can be elicted on examination?"- Medial joint line tenderness (feeling around from tibial plateau, medial to patellar tendon)<div>- <b>McMurray's test</b></div>"
"How is McMurray's test carried out?"<b>Bend knee</b>, then <b>continually invert/evert</b> foot <b>as you extend</b> it. <div><br></div><div>Will cause popping of the meniscus and severe pain</div>
Tenderness over lumbar spine, pain worsened on leaning back, with normal straight leg raising suggests what condition?Facet joint pain (disc prolapse will also have pain on leaning back, but pain on lifting of straight leg)
"What is seen on this X-Ray?<div><img src=""xrb013.jpg""><br></div>""- Thickened skull<div>- Sclerotic and radiolucent areas</div><div><br></div><div><b>Paget's disease of bone</b></div>"
<span class=cloze>[...]</span> = Parsonage-Turner Syndrome<span class=cloze>Brachial neuritis</span> = Parsonage-Turner Syndrome<br> Brachial neuritis = <span class=cloze>[...]</span>Brachial neuritis = <span class=cloze>Parsonage-Turner Syndrome</span><br> What does <b>Parsonage-Turner Syndrome present with?</b>Brachial neuritis:<div><br></div><div>- Peripheral nerve disorder causing severe pain typically in shoulder and arm, followed by subsequent weakness</div><div>(can follow viral infection)</div>
What is a useful sign of psoas irritation (e.g. from abscess) on examination?- Patient may be lying on back with flexed knees (laxes the psoas muscle). <div>- Inability to weight bear, pain moving the hip</div>
What is the <b>Beighton score </b>used for?Assess hypermobility (is assessed by what score?)
Assess hypermobility (is assessed by what score?)What is the <b>Beighton score </b>used for?
What is the <b>Galeazzi test </b>used for?Tests unilateral developmental dysplasia of the hip (describes what test?)
Tests unilateral developmental dysplasia of the hip (describes what test?)What is the <b>Galeazzi test </b>used for?
What drug does <b>allopurinol</b> interact with to cause bone marrow suppression?Azathioprine (interacts with what drug to cause bone marrow suppression?)
Azathioprine (interacts with what drug to cause bone marrow suppression?)What drug does <b>allopurinol</b> interact with to cause bone marrow suppression?
How does taking both azathioprine and allopurinol cause bone marrow suppression?Both inhibit xanthine oxidase
What are the diagnostic inidcations for upper GI endoscopy?- Haematemesis/melaena<div>- Dysphagia</div><div>- Dyspepsia (>55y/o OR alarm symptoms, or treatment refractory)</div><div>- Persistent vomiting</div><div>- Iron deficiency (?cancer)</div><div>- Dudoenal biopsy (?coeliac)</div>
What are therapeutic indications of upper GI endoscopy?- Treatment of bleeding lesions<div>- Variceal banding + sclerotherapy</div><div>- Argon plasma coagulation for suspected vascular abnormality</div><div>- Stent insertion, laser therapy</div><div>- Stricture dilatation, polyp resection</div>
What are pre-procedure considerations for Upper GI endoscopy?- Stop PPIs 2 weeks pre-op (to prevent masking of pathology)<div>- NBM for 6hrs before</div><div>- No driving for 24 hrs if sedation used</div>
What sedation might be used for Upper GI endoscopy?<div>- Pharynx sprayed with local anaesthetic </div>- Midazolam 1-5mg slowly IV (remains conscious)<div>- Fentanyl<br><div>- Propofol via anaesthetist (if deeper sedation)</div><div><b>Important to have continuous suction, to prevent aspiration </b></div></div>
What are complications of upper GI endoscopy?- Sore throat<div>- Amnesia from sedation</div><div>- Perforation (<0.1%)</div><div>- Bleeding (aspirin, clopidogrel, warfarin or DOACs only need to be stopped if therapeutic procedure)</div>
"What is the gold standard test for coeliac's disease?"Duodenal biopsy
What does sigmoidoscopy view?Views rectum + distal colon (to roughly the splenic flexure)
How are patients prepared for sigmoidoscopy?Phosphate enema PR<div><br></div><div>(hyperosmolar, which causes water to move into bowels →diarrhoea + clearing of bowels)</div>
When is diagnostic colonoscopy indicated?- Rectal bleeding<div>- Iron-deficiency anaemia</div><div>- Persistent diarrhoa</div><div>- Positive FOBT/FIT</div><div>- Assessment or suspicion of IBD</div><div>- Colon cancer surveillance</div>
What is the preparation required for a colonoscopy?- Stop iron 1 week prior<div>- Bowel preparation day before</div>
What are complications of colonoscopy?- Abdominal discomfort<div>- Incomplete examination</div><div>- Haemmorhage after biopsy/polypectomy</div><div>- Perforation (<0.1%)</div>
What are the therapuetic indications for colonoscopy?- Haemostasis (by clipping vesesls)<br>- Bleeding angiodysplasia lesion (argon beamer photocoagulation)<div>- Colonic stent deployment (cancer)</div><div>- Volvulus decompression (in sigmoid colon)</div><div>- Psuedo-obstruction</div><div>- Polypectomy</div>
How does Video Capsule Endoscopy (VCE) work?Capsule is like a pill: swallowed, which transmits video wirelessly to device worn by pt. <div><br></div><div>Pt can carry out normal activity </div>
When is video capsule endoscopy used?- Evaluate obscure GI bleeding<div>- Detect small bowel pathology (as this is missed in OGD and Colonoscopy)</div>
What are complications for video capsule endoscopy?- Capsule retention (1%)- requires endoscopy or surgical removal<div>- Obstruction</div><div>- Incomplete exam (slow transit, achalasia) </div>
What investigation is contraindicated in patients who have recently undergone a VCE?Video capsule endoscopy:<div>- No MRI, as video capsule may contain magnetic parts- must confirm capsule has been cleared via AXR first. </div>
Through what route would you take a liver biopsy?"<font color=""#0000ff"">If INR is in normal range</font>: Percutaneous<div><font color=""#0000ff"">If INR is high</font>: Transjugular with FFP</div>"
What are the pre-op considerations for a liver biopsy?<div>- Aim for INR < 1.5</div><div>- Aim for platelets >50 x 10<sup>9</sup></div>- NBM for 8Hrs. <div>- Analgesia </div>
What are important questions to ask about a pt with dysphagia?1. Difficulty swallowing solids <b>and </b>liquids at the start? <div><div>2. Difficult to initiate a swallowing movement?</div><div>3. Is swallowing painful?</div><div>4. Is dysphagia intermittent or constant and getting worse?</div><div>5. Does neck bulge or gurgle on drinking?</div></div>
Why is it useful to ask a pt with dysphagia whether there was difficulty with swallowing solids and liquids from the start?"<font color=""#0000ff"">If difficulty swallowing both:</font> suggests motility disorder (achalasia, CNS, or pharyngeal causes)<div><br></div><div><font color=""#0000ff"">If first difficult swallowing solids, and then liquids</font>: Suggests stricture</div>"
Why is it useful to ask a pt with dysphagia whether <b>initiating swallowing </b>movement is difficult?If yes, suggests bulbar palsy (esp. if pt coughs on swallowing)
What is <b>odynophagia?</b>Painful swallowing (describes what?)
Painful swallowing (describes what?)What is <b>odynophagia?</b>
If swallowing is painful in a pt with dysphagia, what does this suggest?-  Ulceration<div>- Spasm</div>
Intermittent dysphagia suggests what?Oesophageal spasm 
Constant and worsening dysphagia suggests what?Malignant stricture
A bulging or gurgling neck on drinking in a pt with dysphagia suggests what?Pharyngeal pouch
What test may be used to identify suspected pharynegal pouch?Contrast swallow
What are mechanical causes of dysphagia?<b>Malingant stricture</b><div>- Pahryngeal, oesophageal, gastric cancers</div><div><b>Benign stricture</b></div><div>- Oesophageal web or ring</div><div>- Peptic stricture</div><div><b>Extrinsic pressure</b></div><div>- Lung cancer</div><div>- Enlarged mediastinal lymph nodes</div><div>- Retrosternal goitre</div><div>- Aortic aneurysm</div><div>- Left atrial enlargement</div><div><b>Pharyngeal pouch</b></div>
What are motility related causes of dysphagia?- Achalasia<div>- Diffuse oesophageal spasm</div><div>- Systemic sclerosis</div><div>- Neurological bulbar palsy </div>
What is <b>achalasia?</b>"Loss of co-ordinated peristalsis, <font color=""#0000ff"">causing lower oesophageal sphincter to fail to relax</font> (describes what condition?)"
"Loss of co-ordinated peristalsis, <font color=""#0000ff"">causing lower oesophageal sphincter to fail to relax</font> (describes what condition?)"What is <b>achalasia?</b>
How does achalasia present?- Dysphagia<div>- Regurgitation</div><div>- Heart burn</div><div>- Weight loss</div><div><br></div><div>(pt may also adopt certain positions to ease swallowing)</div>
How is achalasia diagnosed?"<div>-<font color=""#0000ff""> 1st line: Oesophageal manometry</font>: Incomplete relaxation of lower oesophageal sphincter + oesophageal aperistalsis (<b>gold standard)</b></div><div>- <font color=""#0000ff"">2nd line:</font> <font color=""#0000ff"">Barium swallow</font>: in advanced disease, will show dilated oesophagus which tapers to a beak-like narrowing. <b><br></b></div>"
What is oesophageal manometry used to assess?Test motor function of upper and lower oesophageal sphincters and oesophageal body
"What is seen from the barium swallow seen below:<div><img src=""22419f406cdcbde969f2e69b729b21_jumbo.jpeg""><br></div>"Widened oesophagus tapering to a beak-like narrowing: suggests <b>achalasia</b>
What is the first line investigation for pts with dysphagia?Endoscopy to exclude malignancy
How is achalasia managed?"<div><font color=""#0000ff"">Invasive interventions</font></div>- Endoscopy balloon dilation: mechanical dilation of LOS.<div>- Heller's cardiomyotomy: Removal of muscles of the LOS.</div><div><font color=""#0000ff"">Pharmacological (if not good candidate)</font></div><div>- Calcium channel blockers(nifedipine, verapamil)/nitrates (isosorbide dintirate(</div><div>- Injection of botulinum toxin (repeat every few months)</div><div><br></div>"
What causes benign oesophageal strictures?- GORD<div>- Corrosives</div><div>- Surgery</div><div>- Radiotherapy</div>
How are benign oesophageal strictures treated?Endoscopy balloon dilatation 
What are associations of oesophageal cancer?"- Male<div>- GORD</div><div>- Tobacco</div><div>- Alcohol</div><div>- Barrett's oesophagus</div><div>- Tylosis</div><div>- Plummer-Vinson syndrome</div>"
"A 5 y/o boy presents with 3 day history of achy joints and diffuse abdominal pain. He noticed a rash on his legs, seen below:<div><img src=""Pcic3wG8DtFpDwczh6HTWhdd39WGDXnajcWEf5m70MwMbtVE6v7OF2almvrVlB6DZpl7VfLcswOmvDeq3uLujW7DkvNOQBpZCNWrutmKsLi0pPBGrXm_yZL7SsL1=w672.jpg""><br></div><div><br></div><div>What is the most likely diagnosis?</div>"Henoch-Schonlein purpura- a small vessel vasculitis
What are the characteristic features of Henoch-Schonlein purpura?Tetrad of:<div><br></div><div>1. Polyarthritis</div><div>2. Abdominal pain (w/ haematemesis and melaena)</div><div>3. Glomerulonephritis (can be life-threatening)</div><div>4. Extensor-surface purpura limited to legs and buttocks</div>
In what patients is Henoch-Schonlein purpura most common in?Boys between 3 and 10 years old (often recently following URTIs)
<span class=cloze>[...]</span> vasculitis = IgA vasculitis<span class=cloze>Henoch-Schonlein</span> vasculitis = IgA vasculitis<br> Henoch-Schonlein vasculitis = <span class=cloze>[...]</span> vasculitisHenoch-Schonlein vasculitis = <span class=cloze>IgA</span> vasculitis<br> What is the pathogenesis of SLE?B cells produce autoantibodies, which forms immune complexes which can deposit across the body, causing inflammation 
What is serositis?Inflammation of a serous membrane (pericarditis, pleural lining inflammation)
What abnormalities in blood are common in SLE?- Decreased Hb (anaemia of chronic disease)<div>- Decreased lymphocytes </div><div>- Decreased platelets</div><div>- Raised ESR, normal CRP</div><div>- Low complement C3, C4</div>
How are joints involved in SLE?"Causes<font color=""#0000ff""> arthralgia and tendinopathy</font>, but not genuine arthritis<div><br></div><div>(There may be Rheumatoid overlap with SLE- Rupus!)</div>"
What group of SLE patients will have <b>both raised ESR, and CRP</b>?- SLE Pts w/ concurrent infection<div>- SLE Pts w/ serositis (often a complication of SLE)</div>
What antibodies have high specificity for SLE?"- Anti-dsDNA (found in 60%)<div>- Anti-Smith's antibody (Found in 20%?)</div>"
A malar rash in SLE will not cross the <span class=cloze>[...]</span> foldA malar rash in SLE will not cross the <span class=cloze>naso-labal</span> fold<br> What are the mucocutaneous features of SLE?- Rashes: malar, discoid<div>- Ulcers: Mouth, genital</div><div>- Scarring alopecia </div>
What is the frequency of renal manifestations in SLE patients?50% of caucasians<div>75% in black patients (and more aggressive)</div><div><br></div><div>(though renal failure is rare- 5%)</div>
What are common neurological manifestations of SLE?"<font color=""#0000ff"">- Headaches</font><div>- Epilepsy</div><div>- Hemiparesis</div><div>- Cranial nerve lesions</div><div>- Brain stem lesions</div><div>- Aseptic meningitis</div><div>- Psychoses</div><div><br></div><div>- Peripheral neuropathy</div>"
What is <b>Libman-sacks endocarditis?</b>Nonbacterial endocarditis associated with SLE
What are the different types of obstetric complications in Antiphospholipid Syndrome?- Recurrent early miscarriages before 12 weeks<div>- Late foetal loss/ late miscarriage (2nd trimester/early 3rd trimester)</div><div>- Pre-eclampsia</div>
What are the biggest causes of death in SLE?"<font color=""#0000ff"">- Infection (as immunocompromised)</font><div>- Renal disease</div><div>- Cardiovascular disease (atherosclerosis etc.)</div><div>- Malignancy (associated with SLE, and treatments e.g. cyclophosphamide, methotrexate)</div>"
How might Drug-Induced Lupus present differently to SLE?Tends to only have mucocutaneous involvement- does not affect internal organs 
How does discoid lupus present differently to SLE?Only mucocutaneous- more severe rash, but no internal organ involvement. <div><br></div><div>Prognosis not affected, but morbidity may be severe</div>
What antibodies are associated with drug induced lupus?- Anti-Histone<div><br></div><div>(often can be ANA negative)</div>
"In what patients are Baker's cysts more likely?"- Patients with arthritis/gout<div>- Following minor trauma to knee </div>
"What is <b>Foucher's sign?</b>""Increase in tension of cyst on extension of knee- suggestive of Baker's cyst "
What is the initial management of open fractures?-  Administration of IV antibiotics<div>- Photography of wound</div><div>- Application of sterile soaked gauze and impermeable film </div><div><br></div><div>(then likely to require definitive skeletal and soft tissue reconstruction)</div>
Discuss the management of open fractures?- Image wound, establish distal neurovascular status, give IV antibiotics and cover with dressing. <div>- Early debridement- remove foreign material and devitalised tissue</div><div>- Irrigate wound</div><div>- Stabilise fracture (often using external fixator)</div>
What would you expect of calcium, phosphate, ALP and PTH levels in a patient with osteoporosis?Everything normal
What is the advice for patients on allopurinol with acute episodes of gout?"<font color=""#0000ff"">If already prescribed,</font> continue to take at same dose. <div><br></div><div>(though only start patients on allopurinol after acute attack has settled)</div>"
"In what age group is Still's disease most common?"Bimodal age distribution:<div>- 15-25y/o</div><div>- 35-46y/o</div>
"How is Adult-onset Still's disease diagnosed?"Diagnosis of exclusion <b>and </b>only diagnosed if Rheumatoid Factor and ANA are negative
What is the most appropriate treatment for benign back pain?- Paracetamol<div>- Codeine</div><div><br></div><div>Enables mobility and helps reduce stiffness. </div><div><br></div><div>(Bed rest not recommended for back pain as it worsens recovery)</div>
What is the most effective method of anlagesia for patients with a #NOF?Iliofascial nerve block 
What nerves are affected by iliofascial nerve block?- Femoral<div>- Obturator</div><div>- Lateral femoral cutaneous nerve</div><div><br></div>
What is the measure of disease activity in <b>Rheumatoid Arthritis</b>?DAS28 (measures disease activity in what disease?)
DAS28 (measures disease activity in what disease?)What is the measure of disease activity in <b>Rheumatoid Arthritis</b>?
What are the clinical findings of clubfoot?"Inverted and plantar flexed foot, which is not passively correctable<div><img src=""paste-3c2a5c4c9e409a8a66811d875c4e377b79010480.jpg""><br></div>"
<span class=cloze>[...]</span> = Clubfoot<span class=cloze>Talipes equinovarus</span> = Clubfoot<br> Talipes equinovarus = <span class=cloze>[...]</span>Talipes equinovarus = <span class=cloze>Clubfoot</span><br> "How does Golfer's elbow present?"- Tenderness over medial epicondyle<div>- Medial wrist pain on resisted wrist pronation</div>
Patients with ankylosing spondylitis tend to have decreased <span class=cloze>[...]</span> and increased <span class=cloze>[...]</span>Patients with ankylosing spondylitis tend to have decreased <span class=cloze>lumbar lordosis</span> and increased <span class=cloze>thoracic kyphosis</span><br> Patients with ankylosing spondylitis tend to have <span class=cloze>[...]</span> lumbar lordosis and <span class=cloze>[...]</span> thoracic kyphosisPatients with ankylosing spondylitis tend to have <span class=cloze>decreased</span> lumbar lordosis and <span class=cloze>increased</span> thoracic kyphosis<br> Why are open fractures typically initially managed with an external fixation device as opposed to surgical correction?Must have sufficient soft tissue coverage before surgery
What are red flags for back pain?TUNA FISH<div><br></div><div>Trauma/thoracic back pain</div><div>Unexplained weight loss (& loss of appetite</div><div>Neuro sx</div><div>Age (<20, >55)</div><div><br></div><div>Fever (&night sweats)</div><div>IVDU/ immunocompromised</div><div>Steroid use</div><div>Hx of cancer/HIV</div>
What is an appropriate response for patients with back pains, presenting with red flag symptoms?Blood tests:<div>- FBC<br>- ESR</div><div>- Calcium, phosphate, ALP</div><div>- PSA</div><div><br></div><div>X Rays</div>
What are the risks factors of congenital hip dislocation?- Female gender<div>- Breech presentation</div><div>- FHx</div><div>- Firstborn</div><div>- Oligohydramnios</div>
What side is congenital hip dislocation more common on?Left side
How is subluxation of the radial head managed?Reduction: Passive supination of the elbow joint whilst flexed to 90°
Chemotherapy patients are at an increased risk of <span class=cloze>[inflammatory arthritis]</span>Chemotherapy patients are at an increased risk of <span class=cloze>gout</span><br> Due to increased urate production
In terms of walking aids, how do you decide whether to carry out a THR, or hemi-arthroplasty for intracapsular #NOF?<div>If frail, and uses walking aids more serious than a walking stick- Hemi-arthroplasty<br></div>
What are the weight bearing instructions you should give to a pt having received a dynamic hip screw?Full weight bearing immediately post-op:<div>- Reduces length of stay + complications</div><div>- DHS requires weight bearing so compression is achieved across fracture site</div>
"What does ""Coffee-ground"" vomit suggest?"Upper GI bleeding 
Vomiting occurring in the <span class=cloze>[...]</span> suggests pregnancyVomiting occurring in the <span class=cloze>morning</span> suggests pregnancy<br> Vomiting occurring in the morning suggests <span class=cloze>[...]</span>Vomiting occurring in the morning suggests <span class=cloze>pregnancy</span><br> Vomiting occuring <span class=cloze>[...]</span> suggests gastric stasis/gastroparesisVomiting occuring <span class=cloze>1hr post food</span> suggests gastric stasis/gastroparesis<br> Vomiting occuring 1hr post food suggests <span class=cloze>[...]</span>Vomiting occuring 1hr post food suggests <span class=cloze>gastric stasis/gastroparesis</span><br> Vomiting that <span class=cloze>[...]</span> suggests peptic ulcerVomiting that <span class=cloze>relieves pain</span> suggests peptic ulcer<br> Vomiting that relieves pain suggests <span class=cloze>[...]</span>Vomiting that relieves pain suggests <span class=cloze>peptic ulcer</span><br> Vomiting <span class=cloze>[...]</span> suggests GI obstructionVomiting <span class=cloze>preceded by loud gurgling</span> suggests GI obstruction<br> Vomiting preceded by loud gurgling suggests <span class=cloze>[...]</span>Vomiting preceded by loud gurgling suggests <span class=cloze>GI obstruction</span><br> What tests might you carry out to investigate nausea and vomiting?<b>Bloods: </b>FBC, U&Es, LFT, Ca<sup>2+</sup>, Glucose, Amylase<div><b>ABG: </b>Alkalosis suggests severe vomiting</div><div><b>Plain AXR</b>: Investigates bowel obstruction</div><div><b>Upper GI endoscopy</b>: If suspicion of bleed or persistent vomiting</div>
On top of giving anti-emetics, what else should you provide to a patient with persistent vomiting?- Give IV fluids and K<sup>+</sup> replacement 
What are the different types of anti-emetic drugs?- H<sub>1</sub> antagonists (e.g. cyclizine)<div>- D<sub>2</sub> antagonists (e.g. metoclopramide, domperidone, prochlorperazine)</div><div>- 5HT<sub>3</sub> antagonists (e.g. Ondansetron)</div><div><br></div><div>Others: hyoscine, dexamethasone, midazolam</div>
What are the common H<sub>1</sub> antagonists used as anti-emetics and their indications?- Cyclizine: used for GI causes<div>- Cinnarizine: Used for vestibular disorders</div>
What D<sub>2</sub> antagonist is used for <b>chemical induced vomiting</b> (e.g. opioids)?Haloperidol (is used as an anti-emetic in which specific scenario?)
Haloperidol (is used as an anti-emetic in which specific scenario?)What D<sub>2</sub> antagonist is used for <b>chemical induced vomiting</b> (e.g. opioids)?
How does hyoscine act as an anti-emetic?Antimuscarinic (though therefore also anti-spasmodic and antisecretory)
Which anti-emetics are also pro-kinetic?- Metoclopramide<div>- Domperidone </div>
- Claudication of buttocks and thighs<div>- Atrophy of musculature of legs</div><div>- Impotence (due to paralysis of L1)</div><div><br></div><div>(are classic signs of what condition?)</div>What are the classical symptoms of <b>Leriche syndrome</b>?
What is Gastro-oesophageal reflux disease?Symptoms or complications resulting from reflux of gastric contents into oesophagus or beyond 
What are potential complications if GORD is prolonged?"- Oesophagitis<div>- Benign oeosphageal stricture</div><div>- Barrett's oesophagus </div><div>- Ulceration</div><div>- Iron deficiency</div>"
How might a pt describe heartburn symptoms in a Hx?- Burning<div>- Retrosternal discomfort after meals, lying, stooping or straining</div><div>- Relieved by antacids</div>
What are oesophageal symptoms of GORD?- Heartburn<div>- Belching</div><div>- Acid brash (acid/bile regurgitation)<br>- Waterbrash (increased salivation)</div><div>- Odynophagia </div>
What are extra-oesophageal signs of GORD?"- Nocturnal asthma<div>- Chronic cough</div><div>- Laryngitis</div><div><font color=""#0000ff"">- Sinusitis </font></div>"
What are causes of GORD?- Lower oesophageal sphincter hypotension<div>- Hiatus hernia</div><div>- Oesophageal dysmotility (e.g. systemic sclerosis)</div><div>- Obesity</div><div>- Pregnancy</div><div>- Gastric acid hypersecretion</div><div>- Delayed gastric emptying</div><div>- Smoking, alcohol</div><div>- Drugs</div><div>- <i>Helicobacter pylori</i></div>
What drugs can cause GORD?- Tricyclic antidepressants<div>- Anticholinergics</div><div>- Nitrates</div>
What investigations are required for a diagnosis of GORD?None- diagnosis can be clinical
"What changes occur in Barrett's Oesophagus?"Distal oesophageal epithelium undergoes metaplasia:<div><br></div><div>From stratified squamous → non-ciliated columnar</div>
What are common symptoms of <b>dyspepsia?</b>- Epigastric <b>pain </b>(related to hunger, foods, or time of day)<div>- <b>Heartburn</b></div><div>- Tender epigastrium</div><div><div>- (<b>Fullness</b> after meals?)</div><div><br></div></div>
When is urgent endoscopy indicated in gastro?- <b>All </b>with dysphagia<div>- >55 y/o with upper abdominal pain, reflux or dyspepsia</div><div>- Treatment-refractory dyspepsia</div>
If a patient with dyspepsia is +ve for <i>H. pylori</i>, what should be given?- PPI<div>- 2 antibiotic combination (e.g. clarithroymycin + amoxicillin) </div>
What are causes of dyspepsia?- Non-ulcer dyspepsia<div>- Oesophagitis/GORD</div><div>- Duodenal/gastric ulcer</div><div>- Gastric malignancy</div><div>- Duodenitis</div><div>- Gastritis</div>
<span class=cloze>[...]</span> ulcers are 4 times more common than <span class=cloze>[...]</span> ulcers <span class=cloze>Duodenal</span> ulcers are 4 times more common than <span class=cloze>gastric</span> ulcers <br> Duodenal ulcers are <span class=cloze>[...]</span> more common than gastric ulcers Duodenal ulcers are <span class=cloze>4 times</span> more common than gastric ulcers <br> What are risk factors for duodenal ulcers?<div><b>Major</b></div>- <i>H. pylori</i><div>- Drugs (NSAIDs, steroids, SSRI)</div><div><br></div><div><b>Minor</b></div><div>- Increased gastric secretion</div><div>- Increase gastric emptying (decreases duodenal pH)</div><div>- Blood group O</div><div>- Smoking</div>
In which population are gastric ulcers more common?Elderly 
What are risk factors for gastric ulcers?- <i>H. pylori</i><div><i>- </i>Smoking</div><div>- NSAIDs</div><div>- Reflux of duodenal contents</div><div>- Delayed gastric emptying</div><div>- Stress (neurosurgery or burns)</div>
What are treatment options for dyspepsia?Lifestyle<div>- Decrease alcohol and tobacco</div><div>- <i>H. pylori </i>eradication</div><div>- Drugs to reduce acid (PPIs, H<sub>2</sub> blockers)</div><div>- Stop drugs may have caused drug-induced ulcers </div>
What lifestyle changes could improve GORD?- Weight loss<div>- Smoking cessation</div><div><br></div><div>- Small, regular meals</div><div>- Reduce: hot drinks, alcohol, citrus, tomatoes, onions, fizzy drinks, spicy foods, caffeine, chocolate</div><div><br></div><div>- Avoid eating <3hr before bed. </div><div>- Raised bed head</div>
What drugs can be used to help GORD?"- Antacids (e.g. magnesium trisilicate mixture) / Alginates (Gaviscon) relieve symptoms<div>- PPI </div><div><br></div><div>If refractory symptoms:</div><div>- Add H<sub>2</sub> blocker <font color=""#0000ff"">(these are not made anymore) </font>and/or try twice-daily PPI </div>"
What is the typical dose of lansoprazole you would give for dyspepsia/GORD?- 30mg/24hr PO 
What drugs should you avoid in GORD patients?"<font color=""#0000ff"">Affect oesophageal motility:</font><div>- Nitrates</div><div>- Anticholinergics</div><div>- Ca<sup>2+</sup> channel blockers (relax oesophageal sphincter)</div><div><br></div><div><font color=""#0000ff"">Damage mucosa:</font></div><div>- NSAIDs</div><div>- K<sup>+</sup> salts</div><div>- Bisphophonates</div>"
What are surgical options to treat GORD?All aim to increase resting lower oeosphageal sphincter pressure:<div><br></div><div>- Laparoscopic Nissen Fundoplication </div><div>- Laparoscopic insertion of a magnetic bead band</div><div>- Radiofrequency induced hypertrophy</div>
What is the most common type of hiatus hernia?Sliding hiatus hernia (80%)
What occurs in a sliding hiatus hernia?Gastro-oesophageal junction slides up into chest --> Lower oesophageal sphincter becomes less competent --> acid reflux 
What occurs in a rolling hiatus hernia?- Gastro-oesophageal jucntion remains in abdomen, but bulge of stomach herniates up into chest alongside oesophagus<div>- GORD less common as gastro-oesophageal junction remains intact </div>
"What does this diagram show?<div><img src=""paste-a2cf74d49e582616fcdb3e4f3253fac3071cdc25.jpg""><br></div>"Rolling hiatus hernia
"What does this diagram show?<div><img src=""paste-0c691ea8d951ce7a471b3f7f380f4f84fdfc2f3c.jpg""><br></div>"Sliding hiatus hernia
<span class=cloze>[...]</span> = Rolling hiatus hernia<span class=cloze>Paraoesophageal hernia</span> = Rolling hiatus hernia<br> Paraoesophageal hernia = <span class=cloze>[...]</span>Paraoesophageal hernia = <span class=cloze>Rolling hiatus hernia</span><br> What are key risk factors of hiatus hernia?- Obesity<div>- Elevated intra-abdominal pressure</div><div>- Previous gastro-oesophageal procedure</div><div>- Large hernias</div><div>- Older (30% are >50)</div>
What is the management for hiatus hernia?- Lose weight<div>- Treat GORD symptoms </div>
When might surgery be considered for hiatus hernia?Intractable symptoms despite aggressive medical therapy
Patients undergoing hysterectomy and oophorectomy are at higher risk of developing what bone disease?Osteoporosis- likely to have lower oestrogen levels 
How should osteopenia be treated?<div>- Lifestyle advice: Diet, <b>weight-bearing </b>exercise, drinking/smoking cessation, stop certain drugs</div>- 800-1000 units of vitamin D (cholecalciferol) a day <div>- 1.5g Calcium </div><div><br></div><div>(Adcal D3, two tablets a day)</div>
Discuss the management of osteoporosis?Main goal is to avoid fractures:<div><br></div><div>- Lifestyle advice </div><div>- Calcium + Vitamin D</div><div>- Bisphosphonates</div><div>- Denosumab </div>
What advice should you give to patients taking bisphosphonates?- Avoid dental work when taking bisphosphonates (sort it out before starting)<div>- Take first thing on day, 30 mins sitting up</div><div>- Still need Vitamin D and Calcium supplements, required for bone formation.</div>
What bisphosphonate is given IV, and how often is it given?Zolendronate, given once a year
What are issues of denosumab?- Rebound osteoporosis: When stopping denosumab, improvements in bone density likely to quickly be lost<div>- Also carries risks of osteonecrosis of jaw and atypical femoral fracture</div>
How is topical capsaicin useful in OA?Gives burning sensation, but blocks pain receptors
Which DMARDs are safe in pregnancy?- Hydroxychloroquine<div>- Sulfasalazine (w/ folic acid)</div><div>- Azathioprine</div><div><br></div>
What is the action of <b>tocilizumab?</b>Anti-IL6 monoclonal antibody (describes what?)
Anti-IL6 monoclonal antibody (describes what?)What is the action of <b>tocilizumab?</b>
What is the action of <b>tofacitinib?</b>JAK2 inhibitor (describes what?)
JAK2 inhibitor (describes what?)What is the action of <b>tofacitinib?</b>
What is anti-RNA Polymerase antibody associated with in systemic sclerosis?- Diffuse cutaneous systemic sclerosis<div>- Scleroderma Renal Crisis</div>
What is anti-pm-scl associated with in systemic sclerosis?- Overlap with polymyositis, dermatomyositis; arthritis overlap; Pulmonary fibrosis
<b>Homogenous ANA </b>antibodies may suggest what?SLE (has what pattern of ANA staining?)
SLE (has what pattern of ANA staining?)<b>Homogenous ANA </b>antibodies may suggest what?
<b>Speckled </b>ANA staining suggests what disease?Mixed connective tissue disease (has what pattern of ANA staining?)
Mixed connective tissue disease (has what pattern of ANA staining?)<b>Speckled </b>ANA staining suggests what disease?
<b>Nucleolar </b>ANA staining indicates what disease?Systemic sclerosis (has what pattern of ANA staining?)
Systemic sclerosis (has what pattern of ANA staining?)<b>Nucleolar </b>ANA staining indicates what disease?
What are the anti-ENAs?Anti Extractable Nuclear Antigen antibodies:<div><br></div><div>- Anti-Ro, Anti-La</div><div>- Anti-Sm</div><div>- Anti-RNP</div><div>- Anti Jo-1; Anti-Mi-2</div><div>- Anti-Scl70</div>
What is chondromalacia patellae?Inflammation of underside of patella, and softening of the cartilage 
Whilst chondromalacia patellae is often used interchangeably with patellofemoral pain syndrome, how are they distinct?Patellofemoral pain syndrome applies to individuals without cartilage damage
- Diarrhoea<div>- Alopecia</div><div>- Rash</div><div>- Abnormal liver function tests</div><div>- Hypertension</div><div><br></div><div>(are side effects caused by which DMARD?)</div>What are side effects of <b>leflunomide</b>?
If allopurinol is not well tolerated, what could be used as second line?- Febuxostat: also inhibits xanthine oxidase (though has a small risk of heart attacks)
What should be given alongside urate lowering therapy such as allopurinol?Prophylactic colchicene, to prevent acute attacks of gout
Which antihypertensives also lowers urate levels?- ARBs<div>- Calcium channel blockers</div>
Ultrasound shows <b>synovial thickening and increased vascularity of a joint.</b> What does this indicate?Acute synovitis (appears as what on ultrasound?)
Acute synovitis (appears as what on ultrasound?)Ultrasound shows <b>synovial thickening and increased vascularity of a joint.</b> What does this indicate?
How is sciatica treated?Conservative: Encourage exercise w/ physiotherapy<div><br></div><div>Medical: Paracetamol and/or oral NSAIDs (topical, opioid analgeisa adjuncts)</div><div><br></div><div>Surgical: Neural decompression</div>
"How is De Quervain's tenosynovitis managed?""<font color=""#0000ff"">1st line:</font> NSAIDs + Splinting<div><font color=""#0000ff"">2nd line:</font> Injection into first dorsal compartment</div><div><font color=""#0000ff"">3rd line:</font> Surgery to incise first dorsal compartment</div>"
What are the main subtypes of juvenile idiopathic arthritis?- Oligoarticular: Affects ≤5 joints<div>- Polyarticular: Affects >5 joints within 6 months<br><div>- Oligoarticular extended: Affects >5 joints across longer than 6 months</div></div><div>- Systemic</div>
How is juvenile idiopathic arthritis managed?- Intra-articular corticosteroids if only a few joints affected. <div>- Methotrexate</div><div>- Biologics (TNFalpha, IL-1, IL-6 inhibitors)</div>
What is a regular complication of juvenile idiopathic arthritis?Anterior uveitis (10-20% develop)
What are signs of upper GI bleeding?- Haematemesis (bright red/coffee ground vomit)<div>- Melaena</div>
What are common causes of upper GI bleeding? "<font color=""#0000ff"">- Peptic ulcers (26%)</font><div><font color=""#0000ff"">- Oesophagitis (17%)</font></div><div>- Mallory-Weiss tear</div><div>- Oesophageal varices</div><div>- Gastritis/gastric erosions</div><div>- Drugs</div><div>- Duodenitis</div><div>- Malignancy</div>"
What drugs can cause upper GI bleeding?- NSAIDs<div>- Aspirin</div><div>- Steroids</div><div>- Thrombolytics</div><div>- Anticoagulants </div>
What are useful questions to ask a patient with suspected upper GI bleeding?- Past GI bleeds<div>- Dyspepsia/known ulcers</div><div>- Known liver disease/oeosphageal varices</div><div>- Dysphagia</div><div>- Vomiting</div><div>- Weight loss</div><div>- Drugs (medical and recreational) and alcohol use</div><div><br></div>
What is the <b>Rockall score</b> used for?Calculates risk of <b>rebleeding </b>and <b>death</b> from upper GI bleeds (describes what?)
Calculates risk of <b>rebleeding </b>and <b>death</b> from upper GI bleeds (describes what?)What is the <b>Rockall score</b> used for?
What parameters are used for the Rockall score?<b>Pre-endoscopy:</b><div>- Age</div><div>- Shock: systolic b.p. and pulse rate</div><div>- Comorbidity</div><div><br></div><div><b>Post-endoscopy: </b></div><div>- Diagnosis </div><div>- Signs of recent haemorrhage on endoscopy</div>
What is the distinction between upper and lower GI bleeding?"<font color=""#0000ff"">Upper</font>: Proximal to ligament of Treitz at the duodenojejunal junction <div><font color=""#0000ff"">Lower</font>: Distal to ligament of Treitz.</div><div><br></div><div><img src=""paste-b3dbdfbe331e31caecdeeef0de169b6a8048ceb7.jpg""><br></div>"
What is the mortality rate of upper GI bleeding, and how does this occur?10%- mortality secondary to hypovolaemic shock 
What should be the action if the cause of upper GI bleeding is suspected to be varices?<div><b>First give:</b></div>- Terlipressin IV (1-2mg/6h for ≤3 days): reduces relative risk of death by 34%. <div>- Initate broad spectrum IV antibiotic cover </div><div><b>Then do:</b></div><div>- Endoscopy to band/clip the vessel<br></div>
What should occur if endoscopic control of upper GI bleeding fails?<div>- Emergency mesenteric angiography/embolisation (carried out by Interventional Radiologists)</div><div>- Surgery</div>
What is a <b>Sengstaken-Blakemore tube </b>used for?"Tube used to compress varices in uncontrolled oesophageal variceal bleeding<div><img src=""Photograph-shows-a-Sengstaken-Blakemore-tube.png""><br></div>"
On endoscopic findings, what are high and low-risk for peptic ulcer bleeds?"<font color=""#0000ff"">High risk</font>: Active bleeding, adherent clot, or non-bleeding visible vessel<div><font color=""#0000ff"">Low risk</font>: Flat, pigmented spot, or clean base</div>"
What is the appropriate management for a high-risk peptic ulcer bleed from endoscopic findings?- Endoscopic haemostasis (clips, cautery, adrenaline)<div>- Admit to monitored bed; and start PPI (omeprazole 40mg/12hrs IV/PO)</div><div>- If haemodynamically stable, start oral intake of clear liquids 6hrs after endoscopy</div><div>- Treat if positive for <i>H. pylori</i></div>
What is the appropriate management for a low-risk peptic ulcer bleed from endoscopic findings?- No need for endoscopic haemostasis<div>- Consider early discharge if pt otherwise low risk</div><div>- Give oral PPI</div><div>- Regular diet 6hrs after endoscopy if stable</div><div>- Treat if positive for <i>H. pylori</i></div>
What are gastro-oesophageal varices?Abnormally enlarged submucosal veins, secondary to portal hypertension(e.g. from liver disease) 
Why might bleeding from gastro-oesophageal varices be particularly quick?Gastro-oesophageal varices often occur 2° to liver disease, which may also cause decreased clotting components
What are intra-hepatic causes of portal hypertension?"<font color=""#0000ff"">- Cirrhosis (80% in UK)</font><div><font color=""#0000ff"">- Schistosomiasis (commonest worldwide)</font></div><div>- Sarcoid</div><div>- Myeloprolifeartive disease</div><div>- Congenital hepatic fibrosis</div><div><br></div>"
What are post-hepatic causes of portal hypertension?- Budd-Chiari syndrome<div>- Right heart failure</div><div>- Constrictive pericarditis</div><div>- Veno-occlusive disease </div>
What causes Budd-Chiari syndrome?Hepatic vein obstruction by thrombosis or tumour --> Congestive ischaemia + hepatocyte damage
What are clinical features of Budd-Chiari syndrome?- Abdominal pain<div>- Hepatomegaly</div><div>- Ascites</div><div>- ↑ALT </div><div><br></div><div>- Portal hypertension if chronic </div>
What are causes of Budd-Chiari syndrome?Anything causing hepatic vein obstruction by thrombosis/tumour:<div><br></div><div>- Hypercoagulable states (Combined Oral Contraceptive pill, pregnancy, thrombophilia etc)</div><div>- TB</div><div>- Liver, renal or adrenal tumour </div>
What tests are used to investgate Budd-Chiari syndrome?- USS + dopplers<div>- CT</div><div>- MRI</div>
What is the management of Budd-Chiari syndrome?- Angioplasty/ transjugular intrahepatic portosystemic shunt may be needed <div>- Anticoagulation lifelong (unless varices)</div><div>- Consider liver transplant if cirrhosis or fulminant hepatic necrosis </div>
"What are differences in the features of Crohn's disease vs Ulcerative colitis?""<font color=""#0000ff"">Crohn's</font>: <div>- Diarrhoea usually non-bloody</div><div>- Weight loss more prominent</div><div>- Upper GI symptoms (mouth ulcers)</div><div>- Abdominal mass palpable in right iliac fossa</div><div><br></div><div><font color=""#0000ff"">UC</font>:</div><div>- Bloody diarrhoea more common</div><div>- Abdominal pain in left lower quadrant</div><div>- Tenesmus</div>"
In which inflammatory bowel disease are you more likely to see gallstones?"Crohn's: oxalate renal stones<div>- Reduced bile acid reabsorption --> increases loss of calcium in bile. (calcium usually binds oxalate)</div>"
What is the most common extra-intestinal feature of ulcerative colitis?Primary sclerosing cholangitis
Risk of colorectal cancer is higher in <span class=cloze>[type of IBD]</span> than <span class=cloze>[type of IBD]</span>"Risk of colorectal cancer is higher in <span class=cloze>ulcerative colitis</span> than <span class=cloze>Crohn's disease</span><br> "
"What are common complications of Crohn's disease"- Obstruction<div>- Fistula</div><div>- Colorectal cancer</div>
"<span class=cloze>[pathology]</span> are more common in Crohn's disease than Ulcerative colitis""<span class=cloze>Skip lesions</span> are more common in Crohn's disease than Ulcerative colitis<br> "
Skip lesions are more common in <span class=cloze>[subset of IBD]</span> than <span class=cloze>[subset of IBD]</span>"Skip lesions are more common in <span class=cloze>Crohn's disease</span> than <span class=cloze>Ulcerative colitis</span><br> "
"Where is pathology found in Crohn's disease?"From mouth to anus (skip lesions may be present)
Where is pathology found in Ulcerative Colitis?Inflammation starts at rectum and limited to ileocaecal valve (continuous disease)
"In what layers can inflammation be found in Crohn's vs UC?""Crohn's: Inflammation in all layers from mucosa to serosa<div>UC: No inflammation beyond submucosa (unless fulminant disease)</div>"
"Describe the histology of Crohn's disease?"- Increased goblet cells<div>- Granulomas</div>
Describe the histology found in Ulcerative Colitis?"- Neutrophils migrate through walls of glands to form crypt abscesses<div>- Depletion of goblet cells and mucin from gland epithelium</div><div>- Granulomas more infrequent (c.f. Crohn's)</div>"
"How does Crohn's compare with Ulcerative Colitis on endoscopy?""Crohn's:<div>- Deep ulcers</div><div>- Skip lesions ""Cobble-stone appearance""</div><div><br></div><div>Ulcerative Colitis</div><div>- Widespread ulceration with preservation of adjacent mucosa, has appearance of polyps (pseudopolyps)</div>"
"What is seen here?<div><img src=""871581-Figure1.jpg""><br></div>""Deep ulcers, skip lesions- Cobble-stone appearance: <b>Crohn's disease</b>"
"What is seen here?<div><img src=""image2 (1).jpeg""><br></div>"Widerspread ulceration, with preservation of adjacent mucosa- <b>Ulcerative Colitis</b>
What is a stereotypical history of <b>pancreatic cancer</b>?70 y/o man presents with:<div>- Anorexia</div><div>- Weight loss</div><div>- Painless jaundice </div><div><br></div><div>(is a classic Hx of what disease?)</div>
70 y/o man presents with:<div>- Anorexia</div><div>- Weight loss</div><div>- Painless jaundice </div><div><br></div><div>(is a classic Hx of what disease?)</div>What is a stereotypical history of <b>pancreatic cancer</b>?
<span class=cloze>[...]</span> ulcers have epigastric pain relieved by eating whereas <span class=cloze>[...]</span> ulcers have epigastric pain worsened by eating<span class=cloze>Duodenal</span> ulcers have epigastric pain relieved by eating whereas <span class=cloze>gastric</span> ulcers have epigastric pain worsened by eating<br> Beware, Q stem may have pain worsened several hours after eating- this is duodenal as immediately after eating, pain was relieved, but then gets worse
Duodenal ulcers have epigastric pain <span class=cloze>[...]</span> by eating whereas gastric ulcers have epigastric pain <span class=cloze>[...]</span> by eatingDuodenal ulcers have epigastric pain <span class=cloze>relieved</span> by eating whereas gastric ulcers have epigastric pain <span class=cloze>worsened</span> by eating<br> Beware, Q stem may have pain worsened several hours after eating- this is duodenal as immediately after eating, pain was relieved, but then gets worse
What is <b>gastroparesis?</b><b>Delayed emptying</b> of solids by stomach in the <b>absence </b>of any mechanical <b>obstruction </b>(describes what?)
<b>Delayed emptying</b> of solids by stomach in the <b>absence </b>of any mechanical <b>obstruction </b>(describes what?)What is <b>gastroparesis?</b>
What extrinsic pressures can cause dysphagia?<div>- Lung cancer</div><div>- Enlarged mediastinal lymph nodes</div><div>- Retrosternal goitre</div><div>- Aortic aneurysm</div><div>- Left atrial enlargement</div>
What is <b>ulcerative colitis?</b>Chronic relapsing + remitting inflammatory disorder of the colonic mucosa 
Where does Ulcerative colitis typically affect first? Where might it extend next?<b>Rectum</b>: it may:<div>- Remain localised (ulcerative proctitis, 30%)</div><div>- Extend proximally to part of colon (left sided colitis, 40%) or whole colon (pancolitis, 30%)</div>
What is <b>ulcerative proctitis?</b>Ulcerative colitis which remains in the rectum (describes what?)
Ulcerative colitis which remains in the rectum (describes what?)What is <b>ulcerative proctitis?</b>
How does <b>toxic/fulminant colitis </b>occur?Transmural extension of ulceration (into muscularis) results into localised ileus and peritonitis. <div><br></div><div>Colon loses muscular tone and begins to dilate. Colonic perforation may occur </div><div><br></div><div>Tends to occur spontaneously in very severe colitis, but can be precipitated by opioid or anti-cholinergic antidiarrhoeal drugs</div>
What is the cause of ulcerative colitis?- Inappropriate immune response against (?abnormal) colonic flora in genetically susceptible individuals 
Describe the pathology in ulcerative colitis?Hyperaemic/haemorrhagic colonic mucosa + pseudopolyps formed by inflammation. 
What are local symptoms of Ulcerative colitis?- Episodes of diarrhoea (± blood &mucus) w/ asymptomatic intervals<div>- Abdominal cramps </div><div>- Increased urgency to defecate </div>
What are systemic symptoms in ulcerative colitis attacks?- Fever <div>- Malaise</div><div>- Anorexia</div><div>- Weight loss</div><div>- Anaemia </div><div>- Extraintestinal manifestations (joint + skin complications) </div>
What is the clinical manifestation of toxic/fulminant colitis?- Sudden violent diarrhoea<div>- Fever to 40°C</div><div>- Abdominal pain</div><div>- Signs of peritonitis (rebound tenderness)</div><div>- Profound toxaemia</div>
What are signs of Ulcerative colitis?<div>- Fever, tachycardia, tender + distended abdomen</div><div>- Extraintestinal signs: Clubbing, aphthous oral ulcers, erythema nodosum, pyoderma gangrenosum, conjuncitvits, episcleritis, iritis, sacrioilits, ankylosing spondylitis</div><div><br></div><div>May be none (if in asymptomatic phase)</div>
What investigations could be carried out for Ulcerative colitis?"<div>- <font color=""#0000ff"">Bloods </font>(FBC, ESR, CRP, U&Es, LFT, blood culture)<br></div><div>- <font color=""#0000ff"">Negative Stool MC&S</font>: To rule out infection </div><div>-<font color=""#0000ff""> Faecal calprotectin</font>: Stool inflammatory test, should be elevated. </div><div>- <font color=""#0000ff"">Lower GI endoscopy:</font> Assess + biopsy </div><div>(<font color=""#0000ff"">AXR</font>: Reserved for severe colitis, to rule out toxic megacolon/perforation) <br></div>"
What is the minimum required for a diagnosis of Ulcerative Colitis to be made?Requires negative stool culture + sigmoidoscopy/colonoscopy
How might different methods of endoscopy be carried out to investigate Ulcerative Colitis?"<font color=""#0000ff"">If acute</font>: carry out limited flexible sigmoidoscopy to assess + biopsy<div><font color=""#0000ff"">Once controlled</font>: Full colonoscopy to define disease extent</div>"
What are acute and chronic complications of Ulcerative colitis?"<div><font color=""#0000ff"">Acute</font>:</div>- Toxic dilatation of colon w/ risk of perforation<div>- VTE<br>- Hypokalemia</div><div><br></div><div><font color=""#0000ff"">Chronic</font>:</div><div>- Colorectal cancer (risk related to amount of colon affected and duration of disease)</div><div>- PSC</div>"
What is the prognosis of Ulcerative colitis?- 10% have complete recovery after a single attack<div>- 10% have fulminant colitis w/ <b>haemorrhage, perforation or sepsis</b> + toxaemia</div><div><br></div><div>Patients with localised ulcerative proctitis have best prognosis </div>
"What antibodies are typically present in UC and Crohn's Disease?""UC: Perinuclear ANCA<br>Crohn's: Anti-<i>saccharo myces cerve visiae</i>"
What is typically used to treat Ulcerative Colitis?"<div>- <font color=""#0000ff"">Loperamide</font>: for symptom relief (opioid receptor agonist) (loper amide agonist)</div>- <font color=""#0000ff"">Mesalazine </font>(5-ASA): Anti-inflammatory, for remission-induction/maintenance<div>- <font color=""#0000ff"">Corticosteroids </font>(if moderate-severe)</div><div>- <font color=""#0000ff"">Anti-cytokine</font> drugs</div><div>- <font color=""#0000ff"">Surgery </font>(if failure of medical therapy, or fulminant colitis)</div>"
How is mild UC treated?- Mesalazine (5-ASA) <div>- <b>Topical steroid</b> foams or retention enemas (can be given as adjunct)</div>
How is <b>mesalazine </b>delivered in Ulcerative Colitis?"<font color=""#0000ff"">PR </font>(suppositories or enemas): For distal disease (1g daily)<div><font color=""#0000ff"">PO</font>: Extensive disease (2g daily)</div><div><br></div><div>Combine both routes if flare. </div>"
"How can Ulcerative Colitis be classified as <font color=""#00aa00"">mild</font>, <font color=""#ffaa00"">moderate </font>or <font color=""#ff0000"">severe</font>?""<b>Bowel movements</b>: <font color=""#00aa00"">≤4</font>, <font color=""#ffaa00"">5</font>, <font color=""#ff0000"">≥6</font><div>Rectal bleeding: <font color=""#00aa00"">Small</font>, <font color=""#ffaa00"">Moderate</font>, <font color=""#ff0000"">Large</font></div><div>Temperature: <font color=""#00aa00"">Apyrexial</font>,<font color=""#ffaa00""> 37.1-37.8°C</font>, <font color=""#ff0000"">>37.8°C</font></div><div>Resting Pulse: <font color=""#00aa00""><70bpm</font>, <font color=""#ffaa00"">70-90bpm,</font> <font color=""#ff0000"">>90bpm</font></div><div>Haemoglobin: <font color=""#00aa00"">>110g/L,</font> <font color=""#ffaa00"">105-110g/L</font>, <font color=""#ff0000""><105g/L</font></div><div>ESR/CRP: <font color=""#00aa00""><30</font>,      ,<font color=""#ff0000""> >30 (or CRP>45)</font></div>"
How should moderate UC be managed?- INduce remission w/ oral prednisolone 40mg/d for 1 wk (then taper by 5mg/week over 7 weeks)<div>- Maintain on 5-ASA</div><div><br></div><div>Important to monitor FBC + U&E at start, then at 3 months, then annually</div>
How should osteomalacia be treated?Calcium + Vitamin D Supplements
How should severe Ulcerative Colitis be managed?Admit for:<div>- IV hydration/electrolyte replacement</div><div>- IV Steroids </div><div>- Rectal steroids</div><div>- Thromboembolism prophylaxis</div><div>- Ensure multiple stool MC&S/CDT to exclude infection </div>
On a patient admitted with severe UC, when should rescue therapy be considered?If on day 3-5, CRP>45, >6 stools/day, consider cyclosporin or infliximab.<div><br></div><div>If fails to improve then urgent colectomy required </div>
If a patient with severe UC is responding to IV corticosteroid regime, what should happen?Transfer to prednisolone 40mg/24hrs PO
When should immunomodulation be considered in UC?- Patients flare on steroid tapering<div>- Require<b> ≥ </b>2 courses of steroids a year </div>
How can treatment be escalated in UC?1. 5-ASA<div>2. Topical steroids --> PO --> IV (in severe) </div><div>3. Immunomodulation e.g. azathioprine, cyclosporine </div><div>4. Biologic (Anti-TNF, or vedolizumab)</div><div>5. Surgery</div>
What is the action of <b>vedolizumab?</b>Anti-integrin: targets adhesion molscules in gut lymphocyte trafficking (describes what monoclonal antibody?)
Anti-integrin: targets adhesion molscules in gut lymphocyte trafficking (describes what monoclonal antibody?)What is the action of <b>vedolizumab?</b>
"How is immunomodulation tolerated in treatment of Crohn's? What occurs if not tolerated?"30% of patients develop side effects requiring cessation e.g. abdominal pain, nausea, pancreatitis, leucopenia, abnormal LFTs. <div><br></div><div>- If untolerated, try on biologics</div>
What proportion of Ulcerative Colitis patients will require surgery, and in what cases are these?20%, when:<div>- Failure of medical therapy</div><div>- Fulminant colitis with toxic dilation/perforation</div>
What is IBD-U, and in what patients is it more common?"Unclassified colonic IBD, when IBD is not obviously Crohn's or Ulcerative Colitis. <div><br></div><div>More common in children than adults</div>"
What are classic signs of haemochromatosis?"- <font color=""#0000ff"">Endocrinological dysfunction (iron deposition in glands)</font>: Hypothyroidism, hypogonadism<div>- <font color=""#0000ff"">Joint pain (intra-articular iron deposition)</font>: Typically 2nd, 3rd fingers</div><div>- <font color=""#0000ff"">Cutaneous deposition:</font> Hyperpigmentation</div><div>- <font color=""#0000ff"">Cerebral deposition</font>: Depression</div><div>-<font color=""#0000ff""> Cardiac issues</font>: Heart-block, restrictive cardiomyopathy</div><div>- <font color=""#0000ff"">Pancreatic</font>: Diabetes</div><div>- <font color=""#0000ff"">Parathyroid</font>: Hypercalcaemia</div>"
What iron study results would you expect in haemochromatosis?- Reduced haptoglobin<div>- Increased ferritin</div><div>- Increased serum iron </div>
How can joint pain be caused by malignancies?Hypertrophic osteoarthropathy: paraneoplastic syndrome in lung malignancies
What causes lumbar spinal stenosis?Narrowing of spinal canal by either tumour, ankylosing spondylitis, disc prolapse or other degenerative changes 
What is produced from the breakdown of <b>haem?</b>Bilirubin and other bile pigments (are produced from what?)
Bilirubin and other bile pigments (are produced from what?)What is produced from the breakdown of <b>haem?</b>
What are the 5 steps of bilirubin excretion?"1. <font color=""#0000ff"">Formation</font>: 70-80% formed from breakdown of RBCs, 20-30% from other haem products. <div>2. <font color=""#0000ff"">Plasma transport</font>: Unconjugated bilirubin not water soluble so t<b>ransported bound to albumin. </b></div><div>3. <font color=""#0000ff"">Liver uptake</font>: Liver takes up bilirubin but not albumin</div><div>4. <font color=""#0000ff"">Conjugation</font>: Bilirubin conjugated to form bilirubin diglucuronide (now water soluble)</div><div>5. <font color=""#0000ff"">Biliary excretion</font>: Conjugated bilirubin secreted into bile canaliculus --> secreted as bile into duodenum</div>"
How is haemoglobin degraded?- Hb --> Iron + Protoporphyrin (converted into biliverdin, and then bilirubin)<div>- Globin --> Amino acids</div>
What weakens albumin binding of bilirubin?- Acidosis<div>- Competition from other substances (e.g. salicylates, certain antibiotics)</div>
What enzyme carries out conjugation of bilirubin?Uridine Glucuronyl transferase
Where does the common bile duct drain into the GI tract?Joined by the pancreatic duct to form the ampulla of vater, emptying in the duodenum
<span class=cloze>[...]</span> implies irreversible liver damage<span class=cloze>Cirrhosis</span> implies irreversible liver damage<br> Cirrhosis implies <span class=cloze>[...]</span> liver damageCirrhosis implies <span class=cloze>irreversible</span> liver damage<br> How is bilirubin mostly excreted? What happens to it in this process?<div>In faeces:</div><div><br></div>Bacteria metabolise bilirubin --> urobilinogen --> stercobilins, which render the stool brown 
Why do you get pale stools in biliary obstruction?Brown colour from stools is from stercobilins, which arise from metabolism of bilirubin in bile<div><br></div>
How is bilirubin recycled in the enterohepatic ciruclation?Bacteria convert bilirubin --> urobilinogen. <div><br></div><div>Urobilinogen is reabsorbed + delivered to hepatocytes via portal vein + sinusoids.</div><div><br></div><div>Then extracted by hepatocytes + re-excreted in bile</div>
Patients with steatorrhea are at risk of deficiencies of vitamins <span class=cloze>[...]</span>Patients with steatorrhea are at risk of deficiencies of vitamins <span class=cloze>A, D, E and K</span><br> <b>Fat-soluble</b> vitamins (ADEK)
Where is pain felt typically in liver disorders, and how?Right upper quadrant pain:<div><br></div><div>- Typically from<b> distention </b>or <b>inflammation</b> of the liver capsule </div>
What is the most common cause of <b>ascites</b>?<b>Portal hypertension</b>
What is <b>ascites</b>?Free fluid in the peritoneal cavity (describes what?)
Free fluid in the peritoneal cavity (describes what?)What is <b>ascites</b>?
What are the hepatic causes of ascites?- Portal hypertension (90%), usually 2° to cirrhosis<div>- Chronic hepatitis</div><div>- Severe alcoholic hepatitis without cirrhosis</div><div>- Budd-Chiari syndrome </div>
What are non-hepatic causes of ascities?- Generalised fluid retention associated with systemic diseases (e.g. heart failure, nephrotic syndrome, hypoalbuminaemia, constrictive pericarditis)<div>- Peritoneal disorders</div><div><br></div><div><br></div><div>Rare causes include renal dialysis, pancreatitis, SLE + endocrine disorders</div>
How does portal hypertension 2° to cirrhosis lead to ascites?"Altered Starling's forces:<div>- ↑ Portal venous pressure (hydrostatic)</div><div>- ↓Oncotic pressure from hypoalbuminaemia</div><div><br></div><div><img src=""Starling-and-osmotic-forces-affect-fluid-flow-into-and-out-of-capillaries-From-305.png""><br></div>"
What are symptoms of ascites?<b>Minor</b>: No Symptoms<div><b>Moderate</b>: Increased abdmonial girth + weight gain</div><div><b>Massive</b>: Non-specific diffuse abdominal pressure</div><div><br></div><div>If results in elevation of diaphragm, dyspnoea may occur</div><div><br></div><div><b>Pain is uncommon</b> (typically suggests another cause of abdominal pain)</div>
What are signs of ascites?Shifting dullness on abdominal percussion 
What is <b>sponteaneous bacterial peritonitis</b>?Infection of ascitic fluid, presents with abdominal discomfort and fever (describes what?)
Infection of ascitic fluid, presents with abdominal discomfort and fever (describes what?)What is <b>sponteaneous bacterial peritonitis</b>?
How is ascites treated?"<div><b>Conservative</b>:</div>- Bed-rest<div>- Dietary Na<sup>+</sup> restriction</div><div><br></div><div><b>Medical</b>:</div><div>- Spironolactone</div><div>- Furosemide (added if spironolactone ineffective)</div><div><br></div><div>- Sometimes <font color=""#0000ff"">therapeutic paracentesis </font>(removal of 4L/day is safe)</div>"
What are the most common bacteria causing spontaneous bacterial peritonitis?- Gram negatives: <i>E. coli, Klebsiella pneumoniae</i><div>- Gram positive: <i>Strep pneumoniae</i></div>
How can spontaneous bacterial peritonitis be diagnosed?- Diagnostic paracentesis: look for levels of PMNs (culture is not as sensitive)
What is the pathophysiolgoy of non-alcoholic steatohepatitis?"- <font color=""#0000ff"">Steatosis (fat accumulation)</font>: Possible from ↓synthesis of VLDL and ↑hepatic triglyceride synthesis<div>- <font color=""#0000ff"">Inflammation</font>: From Lipid peroxidative damage to cell membranes</div><div>- <font color=""#0000ff"">Fibrosis (variable)</font>: If inflammation stimulates stellate cells</div>"
If advanced, what can Non-alcoholic steatohepatitis develop into?Cirrhosis + Portal hypertension
What are symptoms and signs of non-alcoholic steatohepatitis?<b>Most are asymptomatic</b><div>- Hepatomegaly (in 75%)</div><div>- Some may have fatigue, malaise, or right upper quadrant discomfort</div><div><br></div><div>- Splenomegaly if advanced fibrosis (suggests portal hypertension has developed)</div>
Patients with cirrhosis due to <span class=cloze>[...]</span> can be asymptomatic + may lack the usual signs of chronic liver diseasePatients with cirrhosis due to <span class=cloze>NASH</span> can be asymptomatic + may lack the usual signs of chronic liver disease<br> Non-alcoholic steatohepatitis
What are the common laboratory abnormalities in NASH?- Elevations in aminotransferase levels (though AST/ALT is usually <1)<div>- ALP and GGT sometimes increased </div>
How can NASH be differentiated from alcoholic liver disease from laboratory findings?In NASH, AST/ALT ratio is <1
How can NASH be diagnosed?<div>- Liver biopsy showing similar findings to alcoholic hepatitis (e.g. macrovesicular fatty infiltration) </div>- Strong evidence that alcohol intake is not excessive<div>- Absence of Hep B/C infection</div>
What is the prognosis of NASH?<div>Typically good uness complications develop:</div>- Most patients do not develop hepatic insufficiency/cirrhosis<div> </div><div>(though some drugs e.g. cytotoxic drugs and metabolic disorders may accelerate NASH)</div>
How is NASH managed?- Eliminate causes + control of risk factors (T2D, dyslipidaemia, obesity)
Jaundice becomes visible when bilirubin levels are around <span class=cloze>[...]</span>Jaundice becomes visible when bilirubin levels are around <span class=cloze>2-3mg/dL</span><br> What are causes of conjugated hyperbilirubinaemia?- Dysfunction of hepatocytes (hepatocellular dysfunction)<div>- Slowing of bile egress from liver (intrahepatic cholestasis)</div><div>- Obstruction of extrahepatic bile flow (extra-hepatic cholestasis)</div>
What symptom indicates onset of conjugated hyperbilirubinaemia more accurately than onset of jaundice?- Dark urine 
"What is seen here?<div><img src=""Fig-1.-K-F-ring.png""><br></div>""Kayser-Fleischer rings, indicative of Wilson's disease <div><br></div><div>(Greenish gold rings)</div>"
What are complications that may arise in recovery post-op- Airway compromise<div>- Nausea and vomiting</div><div>- Pain</div><div>- Hypotension/hypertension</div>
What are causes of hypoxia post-op?"<div><font color=""#0000ff"">- Basal atelectais</font></div>- Inadequate reversal of muscle relaxants<div>- Low RR 2° to opiates</div><div>- Exacerbation of asthma/COPD<br>- Pulmonary oedema</div><div>- Pneumothorax</div><div>- PE</div>"
What are the main causes of hypotension post surgery?- Residual anaesthesia<div>- Hypovolaemia</div><div>- Sepsis </div>
What are the main causes of hypertension post-op?"- Pain<div>- Anxiety</div><div>- CO<sub>2</sub> retention</div><div>- Pre-existing hypertension</div><div>- Withdrawal of anti-hypertensives (i.e. didn't take them before surgery)</div>"
"What is seen here?<div><img src=""1041-hudson-mask-medium-concentration-elongated-with-7ft-oxygen-tubing-adult.jpg""><br></div>"Hudson mask
"What is seen here?<div><img src=""Venturi-Mask-Colours.jpg""><br></div>"Venturi Mask
"What is seen here?<div><img src=""61B3SO4uHZL._SL1200_.jpg""><br></div>"Non-Rebreathe Mask
"What is seen here?<div><img src=""guedel-pattern-airway-500x500.jpg""><br></div>"Guedel- oropharyngeal airway adjunct
In an acute patient with a stable airway who is desaturating, what would you give them?Oxygen: 15L/min through a non-rebreathe mask (85%)
What is the FiO<sub>2</sub> of Oxygen through nasal cannulas?- 1L/min - 24%<div>- 2L/min- 28% etc. </div><div><br></div><div>up to 6L/min- 44%</div>
What is a fixed method of giving oxygen?"Venturi mask- not dependent on patient's own respiratory drive"
What can be given peri-op to reduce the risk of VTEs?- Intermittent pneumatic compression devices<div>- Low-weight molecular heparins post-op (tinseparin) </div>
Urine output less than <span class=cloze>[...]</span> is typically defined as oliguriaUrine output less than <span class=cloze>0.5ml/kg/hr</span> is typically defined as oliguria<br> What are causes of oliguria?- Dehydration/hypovolaemia<div>- AKI</div><div>- Urinary retention/obstruction</div>
What are signs of sepsis?- Hypotension<div>- Temperature</div><div>- Warm peripheries</div><div>- Tachycardia</div><div><br></div>
In an acute upper GI bleed, what must be done/prepared for the patient?<div>- IV Fluids</div>- 2 Cannulas (wide-bore)<div>- 4 Blood tests: FBC, Biochemistry, INR and Group & Save</div><div>- 4 Units of Cross-matched blood</div>
What is measured by a U&E?- Urea<div>- Creatinine</div><div>- eGFR?</div><div>- Na<sup>+</sup></div><div>- K<sup>+</sup></div>
What are the two different types of fluids you can give?"<font color=""#0000ff"">Crystalloids</font>: e.g. Hartmann's, saline<div><font color=""#0000ff"">Colloids</font>: Albumin, Fresh Frozen Plasma</div>"
How should a diabetic patient be managed if they are NBM?- Take off oral hypoglycaemics (reduce the risk of hypoglycaemia)<div>- Give IV insulin as required on sliding scale, alongside glucose </div>
Why are PPIs useful in acute upper GI bleeds?Formation of first clot is by platelets, and more stable in alkaline conditions. <div><br></div><div>PPI aids formation of alkaline condition</div>
How do you decide whether to carry out an urgent endoscopy or not in acute upper GI bleed?If suspected oesophageal varicoele bleed, do ASAP. <div><br></div><div>Otherwise, make sure endoscopy done in 12-24hrs of presenting to hospital </div>
What is the lower limit of Hb before you consider transfusing?70g/dL (for both men and women)
When would you consider giving a blood transfusion to a patient even if their Hb was higher than 70g/dL?- Very symptomatic patients (out of breath, very tired)<div>- Underlying Coronary Heart Disease (aim to maintain Hb around 90-100)</div>
What causes high urate in GI bleeding?- Hypotension --> underperfusion of kidney --> less excretion of urea<div>- Hb breakdown --> breakdown of protein --> Increased urea </div>
What is the expected increase in Hb with blood transfusions?1 unit= 10g/dL increase
If a patient is NBM, how much fluids should they be given?2L per day
What is meant by <b>PR negative</b>If normal brown stool found on glove (in a PR examination, how should this be described?)
If normal brown stool found on glove (in a PR examination, how should this be described?)What is meant by <b>PR negative</b>
How should your examination be described if no residue/faecal matter found on PR examination?PR non-diagnostic (empty rectum)
"What characterises Crohn's disease?"<div>Transmural granulomatous inflammation affecting any part of gut from mouth to anus</div>
"Where is most commonly affected in Crohn's disease?"Terminal ileum (in 70%)
"At what age do Crohn's and UC typically present?"20-40
"What is the prevalence and incidence of Crohn's/UC?""<font color=""#0000ff"">Prevalence</font>: 100-200/100,000<div><font color=""#0000ff"">Incidence</font>: 10-20/100,000</div>"
What is an <b>enterocutaneous fistula</b>?Abnormal communication between small/large bowel and the skin, which allows its contents to leak through an opening in the skin (describes what?)
Abnormal communication between small/large bowel and the skin, which allows its contents to leak through an opening in the skin (describes what?)What is an <b>enterocutaneous fistula</b>?
"What are associations with Crohn's disease?"- Smoking (increases risk x3-4)<div>- NSAIDs may exacerbate disease </div>
"What are symptoms of Crohn's disease?"- Diarrhoea<div>- Abdominal pain</div><div>- Weight loss/failure to thrive</div><div><br></div><div>Systemic: Fatigue, fever, malaise, anorexia</div>
"What are common complications of Crohn's disease?"- <b>Bowel obstruction</b>: Extensive inflammation --> hypertrophy of muscle wall, fibrosis + stricture formation<div>- <b>Abscesses</b></div><div>- <b>Fistulas</b></div><div>- <b>Perforation</b></div><div>- <b>Colorectal cancer</b> (though lower risk than in UC)</div><div>- <b>Primary Sclerosing Cholangitis </b>(though lower risk than in UC)</div><div>- <b>Malnutrition</b></div>
"What are the different presentations of Crohn's (in terms of areas affected)?""<font color=""#0000ff"">Ileitis</font>: Ileum alone (35%)<div><font color=""#0000ff"">Ileocolitis</font>: Ileum and colon (45%)</div><div><font color=""#0000ff"">Granulomatous colitis</font>: Colon alone (20%)</div><div><br></div><div>Note most spare the rectum</div>"
What is <b>jejunoileitis?</b>"Crohn's disease involving the entire small bowel (describes what?)"
"Crohn's disease involving the entire small bowel (describes what?)"What is <b>jejunoileitis?</b>
"How might Crohn's present differently in children?"Extraintestinal manifestations predominante:<br>- Arthritis<div>- Fever of Unknown origin</div><div>- Anaemia</div><div>- Growth retardation</div><div><br></div><div>Abdomainl pain + diarrhoea may be absent</div>
"What is the most common initial manifestation of Crohn's disease?"Chronic diarrhoea with abdominal pain, fever, anorexia + weight loss
What is a <b>colicky </b>pain?Pain which comes and goes (describes what?)
Pain which comes and goes (describes what?)What is a <b>colicky </b>pain?
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""1f4dfefc6ea54c47ba6449d23cf46110-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmp35nxqjpa.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""1f4dfefc6ea54c47ba6449d23cf46110-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmp35nxqjpa.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
Patients with bowel obstruction may have what symptoms?"<font color=""#0000ff"">- Colicky pain</font><div>- Distention</div><div>- Obstipation (severe/complete constipation)</div><div>- Vomiting</div>"
"What are the three principal patterns of Crohn's disease according to the Vienna Classification?""<font color=""#0000ff"">1.</font> Primarily inflammatory <div><b>which after several years commonly develops into:</b><div><div><font color=""#0000ff"">2.</font> Primarily stenotic/obstructing</div><div><b>or</b></div><div><font color=""#0000ff"">3.</font> Primarily penetrating/fistulizing</div></div></div>"
"What blood tests should be done in suspected Crohn's Disease?"- FBC<div>- U&E</div><div>- LFT: Elevated ALP + GGT levels w/ major colonic involvement suggests PSC</div><div>- INR</div><div>- ESR + CRP: Monitor disease activity</div><div>- Screen for anaemia: Ferritin, TIBC, B12, Folate</div>
"What stool tests should be done in suspected Crohn's?"- MC&S: Exclude Campylobacter, e.coli <div>- C difficile toxin test</div><div>- Faecal calprotectin: GI Inflammation </div>
In patients with suspected bowel obstruction, how do you avoid the risk of a stuck VCE?Use dummy patency capsule, which will disintegrate if it gets stuck, to test if VCE will get through 
"What are characteristic findings of Crohn's on MR/CT enterography?"Characteristic strictures/fistulas with accompanying separation of bowel loops
"What symptoms in a Crohn's patient might suggest they could be admitted for IV steroids?"- ↑ Temp<div>- ↑ Pulse</div><div>- ↑ ESR and ↑CRP</div><div>- ↑WCC</div><div>- ↓ Albumin </div>
"How can symptoms be generally managed in Crohn's?""<font color=""#0000ff"">Cramps + Diarrhoea</font>: Oral administration of loperamide (2-4mg) or antimuscarinics 4 times/day<div><br></div><div><font color=""#0000ff"">Anal irritation</font>: Hydrophilic mucilloids (e.g. methylcellulose) increases stool firmness to prevent irritation </div><div><br></div><div><font color=""#0000ff"">Diet</font>: Avoid dietary fibre to reduce stricutring disease/active colonic inflammation</div><div><br></div><div><font color=""#0000ff"">Stop smoking</font></div>"
"How do we attempt to induce remission in Crohn's disease?""<font color=""#0000ff"">1st line</font>: Glucocorticoids (budesonide an alternative) <div><div><font color=""#0000ff"">2nd line:</font> 5-ASA drugs (mesalazine) </div><div><br></div><div><font color=""#0000ff"">Add-on:</font></div><div>- Azathioprine or mercaptopurine-  but not used as monotherapy</div><div><br></div><div><br></div><div>- Enteral feeding with elemental diet (can be used instead of or on top of management- esp if worry about steroidns in younger children)</div></div>"
"What methods are used to maintain remission in Crohn's?""- Stopping smoking<div><font color=""#0000ff"">1st line</font>: <b>Azathioprine/mercaptopurine </b></div><div><font color=""#0000ff"">2nd line</font>: Methotrexate</div><div><br></div><div>(Consider mesalazine if pt has had previous surgery)</div>"
"What is the treatment for fistulising perianal disease in Crohn's?""- Oral antibiotics (metronidazole)<div>- Immunosuppressant therapy ± anti-TNFα</div><div>- Local surgery ± seton insertion</div><div><img src=""seton-diagram2.jpg""><br></div>"
"How should perianal involvement in Crohn's disease be investigated?"- MRI<div>- Examination under anaesthetic </div>
What are common side effects of azathioprine?"<div><div><font color=""#0000ff"">- Leucopenia</font></div><div><font color=""#0000ff"">- Abnormal LFTs </font></div></div>- Abdominal pain<div>- Nausea</div><div>- Pancreatitis</div>"
"How long do immunomodulators such as azathioprine take to work in Crohn's disease?"6-10 weeks 
"When are the use of anti-TNFα agents contraindicated in the management of Crohn's?"- Sepsis<div>- Active/latent TB</div><div>- ↑LFTs >3fold above top end of normal </div><div>- Underlying malignancy </div>
"What biologics are being used in Crohn's and what are their targets?""<font color=""#0000ff"">Anti-TNFα:</font> Infliximab, adalimumab<div><font color=""#0000ff"">Anti-integrin</font>: Vedolizumab</div><div><font color=""#0000ff"">Anti-IL-12/IL-23:</font> Ustekinumab</div>"
What is TPN in the context of gastro patients?Total parenteral nutrition: feeding nutritional products to a patient IV (nutrition is not obtained by any other route)
What is enteral nutrition?Feeding through the GI system: tube placed down through nose into stomach or bowel to provide nutrition
What is a <b>polymeric diet?</b>Liquid only diet but carbohydrates etc in complex forms (refers to what?)
Liquid only diet but carbohydrates etc in complex forms (refers to what?)What is a <b>polymeric diet?</b>
What is an elemental diet?"Liquid nutrients in an easily assimilated form: contains amino acids (which can give remission in Crohn's)"
"What percentage of Crohn's patients require surgery?"50-80%
"When is surgery indicated in Crohn's disease?""<font color=""#0000ff"">- Failure of medical management (most common)</font><div>- GI obstruction </div><div>- Intractable fistulas/abscesses</div><div>- Perforation</div>"
"What percentage of patients receiving surgery for Crohn's require further surgery?"Almost 50% of cases 
"What is the risk of operating on the small intestines in Crohn's?"Risk of <b>short gut syndrome</b>: malabsorption due to insufficient residual small bowel:<div>- Diarrhoea + malabsorption (particularly of fats)</div><div>- Deficiency in vitamins ADEK and B12</div><div>- Hyperoxaluria (--> renal stones)<br>- Bile salt depletion (gallstones)</div>
Adults with less than <span class=cloze>[...]</span> of <span class=cloze>[...]</span> are at risk of developing short gut syndromeAdults with less than <span class=cloze>150cm</span> of <span class=cloze>small intestines</span> are at risk of developing short gut syndrome<br> "What are signs of poor prognosis in Crohn's disease?"- Age <40<div>- Steroids needed at 1st presentation</div><div>- Perianal disease</div><div>- Isolated terminal ileitis</div><div>- Smoking</div>
"What are cutaneous manifestations of Crohn's disease?"<div><b>Skin: </b></div>- Erythema nodosum<div>- Pyoderma gangrenosum</div><div><br></div><div><b>Mouth: </b></div><div>- Aphthous ulcers</div><div>- Granulomatous nodules </div>
"Smoking <span class=cloze>[...]</span> Crohn's disease but <span class=cloze>[...]</span> Ulcerative Colitis""Smoking <span class=cloze>worsens</span> Crohn's disease but <span class=cloze>improves</span> Ulcerative Colitis<br> "
Smoking worsens <span class=cloze>[subtype of IBD]</span> but improves <span class=cloze>[subtype of IBD]</span>"Smoking worsens <span class=cloze>Crohn's disease</span> but improves <span class=cloze>Ulcerative Colitis</span><br> "
What is the <b>Forrest classification </b>used for?Identifies patients with upper GI haemorrhage who are at increased risk for bleeding, rebleeding and mortality, from endoscopic findings. (describes what?)
Identifies patients with upper GI haemorrhage who are at increased risk for bleeding, rebleeding and mortality, from endoscopic findings. (describes what?)What is the <b>Forrest classification </b>used for?
Broadly speaking, what are the three main categories of the Forrest classification?"<font color=""#0000ff"">Forrest I:</font> Acute haemorrhage<div><font color=""#0000ff"">Forrest II:</font> Signs of recent haemorrhage</div><div><font color=""#0000ff"">Forrest III:</font> Lesions without active bleeding </div>"
What are the sub categories of Forrest I?"<font color=""#0000ff"">Forrest Ia:</font> Spurting <div><img src=""forrest-klassifikation-01.jpg""><br><div><font color=""#0000ff"">Forrest Ib:</font> Oozing</div><div><br></div><div><img src=""forrest-klassifikation-02a.jpg""><br></div></div>"
What are the sub-categories of Forrest II?"<font color=""#0000ff"">Forrest IIa</font>: Non-bleeding visible vessel<div><img src=""forrest-klassifikation-03a.jpg""><br><div><font color=""#0000ff"">Forrest IIb:</font> Adherent clot</div><div><img src=""forrest-klassifikation-03b-I.jpg""><br></div><div><font color=""#0000ff"">Forrest IIc:</font> Flat pigmented haematin on ulcer base</div></div><div><img src=""forrest-klassifikation-5.jpg""><br></div>"
How does the Forrest classification dictate management?Forrest I (A and B) and Forrest IIA should be for endoscopic therapy (+ IV PPI bolus and infusion)<div><br></div><div>Forrest IIB can consider endoscopic therapy (+ IV PPI bolus and infusion)<br></div><div><br></div><div>Forrest IIC or Forrest III does not require endoscopic therapy (+ Oral PPI)</div>
<span class=cloze>[...]</span> = Jaundice<span class=cloze>Icterus</span> = Jaundice<br> Icterus = <span class=cloze>[...]</span>Icterus = <span class=cloze>Jaundice</span><br> What is the fate of urobilinogen formed from bilirubin?<div>- 80% excreted as stercobilins in faeces<br></div><div>- 20% absorbed back into blood (90% of this returns to liver, in enterohepatic circulation, 10% to kidneys, where excreted in urine)</div>
Why are the eyes often affected before the skin in jaundice?Scleral tissue is high in elastin, which has high affinity for bilirubin
Why are newborns vulnerable to physiological jaundice of the newborn?- Newborn hepatocytes have low uridine glucoronyl transferase levels<div>- Macrophages break down foetal RBCs, causing rise in serum [unconjugated bilirubin]</div>
What is a consequence of phyisological jaundice of the newborn if left untreated?Unconjugated bilirubin collects in basal ganglia, causing <b>kernicterus</b>: <div>- Brain damage</div><div>- Death</div>
How is phototherapy useful in physiologic jaundice of the newborn?UV light encourages structural changes in unconjugated bilirubin, allowing it to be more soluble and excreted in urine
"What causes <b>Gilbert's syndrome?</b>"Low levels of uridine glucorynl transferase in hepatocytes (causes what disease?)
Low levels of uridine glucorynl transferase in hepatocytes (causes what disease?)"What causes <b>Gilbert's syndrome?</b>"
"How can Gilbert's syndrome lead to jaundice?"Hepatocytes have low levles of uridine glucuronyl transferase:<div><br></div><div>- Infection, stress, starvation --> <b>↑</b>haemolysis --> ↑Unconjugated bilirubin in blood, which hepatocytes are unable to deal with</div>
What causes <b>Crigler Najjar </b>syndrome?Lack of Uridine glucuronyl transferase enzymes in hepatocytes (causes what?)
Lack of Uridine glucuronyl transferase enzymes in hepatocytes (causes what?)What causes <b>Crigler Najjar </b>syndrome?
How does Gilbert syndrome present?"Asymptomatic, mild <font color=""#0000ff"">unconjugated</font> hyperbilirubinaemia<div><br></div><div>(often detected in young adults serendipitously, by finding elevated bilirubin levels)</div>"
What is the prognosis of (type 1) Crigler-Najjar syndrome?Poor- most die of kernicterus at 1y/o due to severe hyperbilirubinaemia
What is the inheritance pattern and prognosis of the two different subtypes of Crigler-Najjar syndrome?"<font color=""#0000ff"">Type I</font>: Autosomal recessive (complete lack of glucuronyl transferase- poor prognosis, most die at 1)<div><font color=""#0000ff"">Type II</font>: Autosomal dominant (partial loss of glucuronyl transferase- less severe hyperbilirubinaemia and usually live into adulthood w/o neurological damage)</div>"
What causes <b>Dubin-Johnson syndrome?</b>"Deficient MRP2 → impaired excretion of bilirubin into bile canaliculi<br><div><img src=""paste-e253d0335af45a928126a369cffba5899194ef2e.jpg""> </div>"
What type of hyperbilirubinaemia do you get in Dubin-Johnson syndrome?Conjugated hyperbilirubinaemia:<div><br></div><div>- Conjugated bilirubin is not transported into bile canilculus due to deficienct MRP2, but MRP3 is upregulated instead, transporting it to blood </div>
How is Dubin-Johnson syndrome usually diagnosed?Liver biopsy: liver will be deeply pigmented but otherwise histologically normal
Which of the eponymous metabolic disorders causing hyperbilirubinaemia will have a dark urine?"Ones which cause conjugated hyperbilirubinaemia (as conjugated are soluble):<div><br></div><div>- Dubin-Johnson and Rotor's Syndrome</div>"
"What occurs in Rotor's syndrome?"Conjugated hyperbilirubinaemia --> jaundice<div><br></div><div>Similar to Dubin-Johnson but liver not pigmented</div>
<span class=cloze>[...]</span> = Cancer of the bile ducts<span class=cloze>Cholangiocarcinoma</span> = Cancer of the bile ducts<br> Cholangiocarcinoma = Cancer of the <span class=cloze>[...]</span>Cholangiocarcinoma = Cancer of the <span class=cloze>bile ducts</span><br> What type of hyperbiliurbinaemia occurs in obstructive jaundice?"Conjugated hyperbilirubinaemia:<div><br></div><div>- Block in the common bile duct, causes increased pressure, causing bile contents to enter blood</div><div><img src=""paste-448b0c5deee836751df31c1ac4ff482751be8a05.jpg""><br></div>"
What type of hyperbilirubinaemia is caused by viral hepatitis and why?Both conjugated, and unconjugated hyperbilirubinaemia:<div><br></div><div>- Infected hepatocytes will have ↓ ability to conjugate bilirubin --> ↑ Unconjugated</div><div>- Death of hepatocytes causes leak of bile from canaliculi into blood --> ↑ Conjugated</div>
What are red flags to establish in Jaundice?- Marked abdominal pain and tenderness<div>- Altered mental status (hepatic encephalopathy)</div><div>- GI bleeding/Petechiae + purpura (Coagulopathy)</div>
What are the main causes of unconjugated hyperbilirubinaemia?"<font color=""#0000ff"">Overproduction</font>: Haemolysis, ineffective erythropoiesis<div><font color=""#0000ff"">Impaired hepatic uptake</font>: Drugs (paractemol, rifampicin), Ischaemic Hepatitis</div><div><font color=""#0000ff"">Impaired Conjugation</font>: Gilbert's, Crigler-Najjar</div><div><font color=""#0000ff"">Physiological neonatal jaundice</font></div>"
What causes pruritus in jaundice?Deposit of bile salts in the skin
Pruritus is not typically caused by <span class=cloze>[...]</span> hyperbilirubinaemiaPruritus is not typically caused by <span class=cloze>unconjugated</span> hyperbilirubinaemia<br> What drugs can cause hepatitis?- Paracetamol overdose<div>- Halothane</div><div>- Methyldopa</div><div>- Isoniazid, rifampicin, pyrazinamide (anti-TB)</div><div>- MAO- Inhibitors</div><div>- Sodium valproate</div><div>- Statins</div>
What drugs may give an unconjugated hyperbilirubinaemia?"- Unconjugated = Excess production of unconjugated production --> haemolysis:<div><br></div><div>Antimalrials e.g. dapsone (can cause ↑ haemolysis)</div><div><br></div><div>- Rifampicin and paracetamol- reduce liver's ability to take in unconjugated bilirubin</div>"
What drugs may cause cholestasis?Abx:<div>- Flucloxacillin</div><div>- Fusidic acid, co-amoxiclav, nitrofurantoin, ceftriaxone.</div><div><br></div><div>- Sulphonylureas</div><div>- Prochlorperazine</div><div>- Chlorpromazine</div><div>- Steroids (anabolic, the pill)</div>
What is <b>cholestasis</b>?Reduction or stoppage of bile flow (describes what?)
Reduction or stoppage of bile flow (describes what?)What is <b>cholestasis</b>?
What causes post-hepatic jaundice?Obstruction of biliary drainage
What are different causes of post-hepatic jaundice?<b>Intra-luminal: </b>Gallstone in common bile duct<div><b>Mural</b>: Cholangiocarcinoma, stricutres, drug-induced cholestasis</div><div><b>Extra-mural: </b>Pancreatic cancer or abdominal passes (push to cause obstruction)</div>
"What is <b>Mirrizi's syndrome?</b>"Obstructive jaundice from common bile duct compression by gallstone impacted in cystic duct (causes what?)
Obstructive jaundice from common bile duct compression by gallstone impacted in cystic duct (causes what?)"What is <b>Mirrizi's syndrome?</b>"
"What is <b>Courvoisier's Law?</b>"If gallbladder is palpable but with painless jaundice, cause is not gallstones
What might the urine reveal about jaundice?"<font color=""#0000ff"">If pre-hepatic</font>: Bilirubin absent<div><font color=""#0000ff"">If post-hepatic:</font> Urobilinogen is absent </div>"
Why is urine dark in obstructive jaundice?Obstructive jaundice → bile is being releated into duodenum + pressure builds:<div><br></div><div>Increased pressure causes conjugated bilirubin + other bile salts to enter blood circulation + excreted out in urine. </div><div><br></div><div>Excess Bilirubin in urine makes it look dark </div>
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""c04f5d876adf45d7a4288461507bea72-oa-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmptj32t15y.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""c04f5d876adf45d7a4288461507bea72-oa-1-A.svg"" /></div> <div id=""io-original""><img src=""tmptj32t15y.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
What are causes of jaundice in a previously stable patient with cirrhosis?- Sepsis<div>- Malignancy</div><div>- Alcohol; drugs</div><div>- GI Bleeding (large protein meal)</div><div>- HCC</div><div>- Constipation</div>
Acute jaundice in the young + healthy typically suggests <span class=cloze>[...]</span>Acute jaundice in the young + healthy typically suggests <span class=cloze>acute viral hepatitis</span><br> Paracetamol overdose could also give this presentation
A personal or family Hx of recurrent mild jaundice without findings of hepatobiliary dysfunction suggests <span class=cloze>[...]</span>A personal or family Hx of recurrent mild jaundice without findings of hepatobiliary dysfunction suggests <span class=cloze>a hereditary disorder e.g. Gilbert sydrome</span><br> Gradual onset of jaundice with pruritus, weight loss and clay-coloured stools suggests <span class=cloze>[...]</span>Gradual onset of jaundice with pruritus, weight loss and clay-coloured stools suggests <span class=cloze>cholestasis</span><br> Why might blood tests of bilirubin, aminotransferases and ALP be useful in jaundiced patients?Help differentiate cholestasis from hepatocellular dysfunction:<div><br></div><div>- Useful as pts with cholestasis tend to require imaging tests</div>
How can blood tests in jaundiced patients differentiate between hepatocellular dysfunction and cholestasis?"<font color=""#0000ff"">Hepatocellular dysfunction</font>: Marked aminotransferase elevation (>500 U/L) and moderate ALP elevation (<3x normal)<div><br></div><div><font color=""#0000ff"">Cholestasis</font>: Moderate aminotransferase elevation (<200) and marked alkaline phosphatase elevation (>3x normal)</div><div><br></div><div><br></div><div>ALP production increased in response to cholestasis</div>"
What imaging can be used in jaundice?- Abdominal ultrasonography<div>- CT/MRI</div><div>- ERCP </div>
What is TIPS used for, and how does it work?Transjugular intrahepatic portosystemic shunting:<div><br></div><div>Creates a stent between portal and hepatic veins. Used to reduce portal hypertension (+ therefore useful in ascites)</div>
What processes lead to portal hypertension?"<font color=""#0000ff"">Increased resistance to flow</font>:<div>- Increased resistance within liver (e.g. in cirrhosis)</div><div>- Blockage of splenic/portal vein </div><div>- Impaired hepatic venous outflow  </div>"
How does cirrhosis cause portal hypertension?"Tissue <font color=""#0000ff"">fibrosis + regeneration</font> increases resistance in <b>sinusoids + terminal portal venules. </b>"
How can encephalopathy arise as a result of portal hypertension?Portal hypertension creates portal-systemic venous collaterals which decreases portal vein pressure (e.g. oesophageal varices, visible abdominal wall collaterals, caput medusae)<div><br></div><div>- This shunts blood away from liver --> more toxic substances in portal vein shunted directly to systemic circulation --> <b>encephalopathy</b></div>
What causes splenomegaly in portal hypertension?↑Blood flow through splenic vein 
What forms the hepatic portal vein?- Splenic vein<div>- Superior and inferior mesenteric vein</div>
How can portal hypertension be confirmed?- Direct pressure measurement through transjugular catheter (invasive so not usually done)<div><br></div><div>- USS, or CT can reveal dilated intra-abdominal collaterals + Doppler ultrasonography on portal vein patency and flow</div>
How is portal hypertension treated?Treat underlying disorder where possible<div><br></div><div>Medical: </div><div>- β-blockers </div><div>- Isosorbide mononitrate</div><div><br></div><div>Surgical: </div><div>- TIPS</div>
What can cause hepatic encephalopathy?<div>- Cirrhosis</div>- Portal-systemic collaterals 2° to portal hypertension<div>- Fulminant hepatitis (caused by viruses, drugs/toxins)</div>
What typically precipitates hepatic encephalopathy in patients with chronic liver disease?- Metabolic stress (e.g. infection, electrolyte imbalance, dehydration, use of diuretics)<br>- Disorders which increase gut protein (high-protein diet, GI bleeding)<br>- Nonspecific cerebral depressants (alcohol, sedatives, analgesics)
What is the pathophysiology of hepatic encephalopathy?As liver fails, nitrogenous waste builds up (as ammonia) in circulation<div>- Cleared by astrocytes, causing conversion of glutamate to glutamine</div><div>- Excess glutamine causes osmotic imbalance and shift of fluid into these cells → cerebral oedema </div>
What are symptoms of hepatic encephalopathy?"- Constructional apraxia (patients cannot reproduce simple designs)<font color=""#0000ff"">- early sign</font><div>- Asterixis (flapping tremor) </div><div>- Symmetrical neurological deficits</div><div><br></div><div>- Agitation + mania are rare</div><div>- musty sweet breath odor?</div>"
How can hepatic encephalopathy be managed?- Treatment of underlying cause (usually reverses mild cases)<div>- Bowel cleansing (using lactulose, or enemas) </div><div>- Antibiotics: Neomycin, rifaximin</div><div>- Dietary protein restriction</div>
What causes a raised CEA?Carcinoembryonic antigen:<div><br></div><div>- Certain colorectal cancers (+ benign masses)</div><div>- Smoking</div>
What are pre-hepatic causes of portal hypertension?- Thrombosis in the splenic/portal veins
What laboratory investigations might reveal whether a jaundiced patient is cholestatic or hepatitic in origin?"<font color=""#0000ff"">Cholestatic</font>: ↑ALP, ↑GGT<div><font color=""#0000ff"">Hepatitic</font>: ↑AST + ALT </div>"
What does the AST:ALT ratio inform about aetiology of hepatitis?AST:ALT >2 suggests alcoholic liver disease<div>AST:ALT <1 suggests non-alcoholic steatoheaptitis</div>
What is <b>hepatic fibrosis</b>?Overly exuberant wound healing where excessive conective tissue builds up in the liver (describes what?)
Overly exuberant wound healing where excessive conective tissue builds up in the liver (describes what?)What is <b>hepatic fibrosis</b>?
What are complications of hepatic fibrosis?- Portal hypertension (scarring distorts blood flow through liver) <br><div>- Cirrhosis (scarring results in disruption of normal hepatic architecture + liver dysfunction) </div>
What triggers hepatic fibrosis?Chronic injury (particularly if there is an inflammatory component)
<span class=cloze>[...]</span> cells = Stellate cells<span class=cloze>Ito</span> cells = Stellate cells<br> Ito cells = <span class=cloze>[...]</span> cellsIto cells = <span class=cloze>Stellate</span> cells<br> What is the pathophysiology underlying hepatic fibrosis?- Stellate cells are activated, proliferate + become myofibroblasts. <div>- Myofibroblasts produce abnormal matrix, which cause Kupffer cells, injured hepatocytes, platelets + leukocytes to aggregate</div><div>- These cells release reactive O<sub>2</sub> species + inflammatory mediators (PDGFs, TGFs etc)</div>
Typically how long does it take for cirrhosis to develop?>6 months of liver disease 
How is hepatic fibrosis detected?Liver biopsy currently the only means. <div><br></div><div>Helps clarify the diagnosis + stage its progress </div>
What are the most common causes of cirrhosis around the world?"<font color=""#0000ff"">Developed countries:</font> Chronic alcohol abuse (or chronic Hep C)<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">In parts of Asia & Africa</font>: Chronic hepatitis B</div>"
What are complications of liver cirrhosis?<b>Portal hypertension</b><div>- GI bleeding from varices</div><div>- Ascites (w/ risk of SBP)</div><div>- Splenic congestion w/ hypersplenism </div><div><br></div><div><b>Hepatic insufficiency:</b></div><div>- Coaguloapthy</div><div>- Encephalopthy</div><div>- Hypoalbuminaemia (oedema)<br>- Sepsis</div><div><br></div><div><b>Hepatocellular carcinoma</b></div>
What causes hepatorenal syndrome?<div>- Portal Hypertension in liver failure triggers arterial vasodilation.<br></div><div>- Drop in b.p. activates Renin-Angiotensin-Aldosterone axis, which causes increase in renal vascular resistance --> <b>hypoperfusion </b>of kidneys </div><div><br></div>
What is hepatorenal syndrome?Progressive oliguria + azotemia in the absence of structural damage to the kidney, often occuring in patients with fulminant hepatitis or advanced cirrhosis <div><br></div><div>(Cirrhosis + Ascites + Renal failure)</div>
What is <b>azotemia</b>?High levels of nitrogen-containing compounds (urea, creatinine) in the blood (describes what?)
High levels of nitrogen-containing compounds (urea, creatinine) in the blood (describes what?)What is <b>azotemia</b>?
What is <b>cholethiasis?</b>Uncomplicated gallstones (is described by what?)
Uncomplicated gallstones (is described by what?)What is <b>cholethiasis?</b>
What is <b>biliary colic?</b>Gallstones obstructing the cystic duct during contraction of gallbladder (describes what?)
Gallstones obstructing the cystic duct during contraction of gallbladder (describes what?)What is <b>biliary colic?</b>
What is the typical presentation of biliary colic?Right upper quadrant pain following fatty meal, as gallstones obstruct the cystic duct during contraction of gallbladder
What is <b>cholecystitis?</b>Inflammation of the gall bladder (is described by what?)
Inflammation of the gall bladder (is described by what?)What is <b>cholecystitis?</b>
What is <b>choledocholithiasis?</b>Gallstone within the common bile duct (is described by what?)
Gallstone within the common bile duct (is described by what?)What is <b>choledocholithiasis?</b>
What is <b>cholangitis?</b>Infection of the common bile duct secondary to choledocholithiasis (describes what?)
Infection of the common bile duct secondary to choledocholithiasis (describes what?)What is <b>cholangitis?</b>
"What is Charcot's triad and what does it typically present in?""Presents in <font color=""#0000ff"">cholangitis</font>, featuring:<div><br></div><div>- Right upper quadrant pain</div><div>- Fever</div><div>- Jaundice</div>"
Where is the gallbladder found?"<b>Right hypochondrial region</b>, in <font color=""#0000ff"">fossa </font>between<font color=""#0000ff""> inferior aspects</font> of the <font color=""#0000ff"">right </font>and <font color=""#0000ff"">quadrate </font>lobes of the liver<div><img src=""Anatomical-Position-of-the-Gallbladder.png""><br></div>"
What are the three parts of the gallbladder?"- Fundus<div>- Body</div><div>- Neck</div><div><img src=""Parts-of-the-Gallbladder-and-Proximal-Biliary-Tree.jpg""><br></div>"
What lies posteriorly to the gallbladder?- Transverse colon<div>- Proximal duodenum</div>
Where are gallstones typically lodged in the gallbladder?"<b>Hartmann's pouch</b>, a mucosal fold in the neck of the gallbladder<div><img src=""paste-220a27a6a3e0ddc47aa0fd48c70585548f87795e.jpg""><br></div>"
What drains from the neck of the gallbladder?Cystic duct
What forms the common bile duct?Cystic duct and common hepatic duct
What forms the hepatopancreatic ampulla of Vater?- Common bile duct <div>- Pancreatic duct </div>
What valve regulates the ampulla of Vater?- <b>Sphincter of Oddi</b>
What supplies the gallbladder?<b>Cystic artery</b>- a branch of the <b>right hepatic </b>artery
What is the venous drainage of the gallbladder?<b>Fundus + Body: </b>Hepatic <b>sinusoids</b><div><b>Neck: </b>Cystic veins, which drains into<b> portal vein</b></div>
What is the response to parasympathetic stimulation of the gallbladder?- <b>Contraction of gallbladder</b><div>- <b>Relaxation of sphincter</b> of Oddi- secretion of bile</div>
What is mostly responsible for <b>contraction</b> of the gallbladder and<b> secretion </b>of bile into the cystic duct?Chole cysto kinin (as part of the gustatory response)(CCK)
What consideration should be made in the management of ascites in a paitent with CKD?As reduced kidney function, medical management (spironolactone, furosemide) may only have a limited effect 
Who is at higher risk during liver transplant surgery, patients with alcoholic liver cirrhosis, or cirrhosis 2° to NASH?NASH patients: <div>- Causes of NASH (dyslipidemia, obesity, HTN) also risk factors for CVD --> increased risk of cardiovascular events</div>
Which aminotransferase is specific to the liver?ALT (AST also released in by myocyte destruction e.g. in MI)
Which biomarkers in a liver function test are released by bile canaliculi?ALP & GGT
<span class=cloze>[LFT biomarker]</span> is particularly raised by drugs e.g. alcohol<span class=cloze>GGT</span> is particularly raised by drugs e.g. alcohol<br> GGT is particularly raised by <span class=cloze>[...]</span>GGT is particularly raised by <span class=cloze>drugs e.g. alcohol</span><br> What are tests of synthetic function in the liver?- Prothrombin time/INR<div>- Albumin</div>
What are potential causes of a cholestatic picture of jaundice (↑ALP, ↑GGT)?- Biliary Obstruction<div>- PBC/PSC</div>
How might pancreatic head cancer be seen on ultrasound?<div>Dilation of: </div>- Common bile duct<div>- Pancreatic duct</div>
What are causes of a dramatic increase in serum aminotransferases? (e.g. in the thousands)1. Paracetamol toxicity<div>2. Ischaemic hepatitis (following hypotensive events)</div><div>3. Viral infection of liver</div>
What events confirm liver failure?Development of:<div>- Coagulopathy</div><div>- Encephalopathy</div>
What is the <b>Child-Pugh score</b> used for?Assess prognosis of chronic liver disease (typically cirrhosis) 
How is the Child-Pugh Score calculated?5 clinical measures, scored out of 3:<div><br></div><div>1. Total bilirubin</div><div>2. Serum albumin</div><div>3. Prothrombin time/ INR</div><div>4. Ascites</div><div>5. Encephalopathy</div>
How can Child-Pugh scores be interpreted?"<img src=""paste-f10e531e1a3a4fbe19abb877d654450594eca9a4.jpg"">"
What is the UKELD score used for?Assess severity of chronic liver disease, and determines prognosis and prioritising for receipt of a liver transplant
What clinical findings support alcohol as being the likely cause of cirrhosis?- Gynaecomastia<div>- Spider naevi (telangiectasia)</div><div>- Testicular atrophy</div>
What laboratory findings would confirm chronic hepatitis B infection?- Hepatitis B surface antigen (HBsAg)<div>- IgG antibodies to hepatitis B core protein (IgG anti-HBc)</div>
In cirrhosis, presence of <span class=cloze>[...]</span> suggests primary biliary cholangitisIn cirrhosis, presence of <span class=cloze>antimitochondrial antibodies</span> suggests primary biliary cholangitis<br> In cirrhosis, presence of antimitochondrial antibodies suggests <span class=cloze>[...]</span>In cirrhosis, presence of antimitochondrial antibodies suggests <span class=cloze>primary biliary cholangitis</span><br> What is the finding of primary sclerosing cholangitis on MRCP?"Strictures + Dilations of intrahepatic and extrahepatic bile ducts <div><img src=""a50979796e5172_Afbeelding-10.jpg""><br></div>"
What is an MRCP?"Magnetic Resonance Cholangiopancreatography: non-invasive use of MR to visualise biliary and pancreatic ducts<div><br></div><div><img src=""280px-MRCP_Choledocholithiasis.jpg""><br></div>"
What is an ERCP?Endoscopic retrograde cholangiopancreatography:<div><br></div><div>- Technique using endoscopy and fluoroscopy to diagnose + treat problems of the biliary + pancreatic ducts</div>
How is an ERCP carried out?- Duodenoscope inserted via mouth to reach duodenum, where ampulla of Vater exits<div>- Cannula inserted through ampulla, to inject radiocontrast into the bile ducts </div>
What is a significant risk of ERCP procedures?- Post-ERCP Pancreatitis<div>- Ascending cholangitis (if enteric bacteria are introduced into biliary tree)</div>
What is the management of liver cirrhosis?"Supportive: <div>- Stop injurious drugs</div><div>- Provide nutrition</div><div>- Treat underlying disorders + complications. </div><div><br></div><div>Avoid alcohol + hepatotoxic substances</div><div><br></div><div><font color=""#0000ff"">Liver transplantation indicated for end-stage liver failure</font> in suitable candidates</div>"
What are contradindications of liver transplantation for those with cirrhosis?"- Extrahepatic malignancy<div>- Severe cardiorespiratory disease</div><div>- Systemic sepsis</div><div>- Expected non-compliance with drug therapy</div><div>- Ongoing alcohol consumption (if alcohol-related iver disease)</div><div>- <font color=""#0000ff"">Anorexia (poor physiological reserves)</font></div>"
What are symptoms of acute rejection in liver transplant patients?- Pyrexia<div>- Tender hepatomegaly </div><div><br></div><div>Occurs 5-10days post durgery</div>
What is the prognosis of liver cirrhosis?- 5yr survival is around 50%
What are the different subclassifications of acute liver failure?"<font color=""#0000ff"">Hyperacute</font>: ≤7 days<div><font color=""#0000ff"">Acute</font>= 8-21 days</div><div><font color=""#0000ff"">Subacute</font>= 4-26 weeks</div>"
What is <b>fetor hepaticus?</b>Presence of thiols in the breath- give a sweet, faceal smell (freshly mown hay/pear drops) (describes what?)
Presence of thiols in the breath- give a sweet, faceal smell (freshly mown hay/pear drops) (describes what?)What is <b>fetor hepaticus?</b>
What causes fetor hepaticus?Seen in portal hypertension- portosystemic shunting allows thiols to pass directly into lungs<div><br></div><div>(often associated with acid/base disorders e.g. DKA, or isopropyl alcohol intoxication)</div>
What infections can cause liver failure?- Viral hepatitis (esp Hep B, C and CMV)<div>- Yellow fever</div><div>- Leptospirosis </div>
What toxins can cause liver failure?- Amanita phalloides mushroom<div>- Carbon tetrachloride (in dry cleaning chemicals)</div>
What drugs should be avoided in liver failure?- Drugs which cause constipation (risk of encephalopathy)<br>- Oral hypoglycaemics<div>- Saline-containing IV infusions </div>
What is the grading of hepatic encephalopathy?"<font color=""#0000ff"">I</font>: Altered mood/behaviour; sleep disturbance; dyspraxia; poor arithmetic. No asterixes<div><font color=""#0000ff"">II</font>: Increasing drowsiness, confusion, slurred speech ± asterixes, inapprorpiate behaviour/personality change </div><div><font color=""#0000ff"">III</font>: Incoherent, restless, asterixes, stupor</div><div><font color=""#0000ff"">IV</font>: Coma</div>"
How is your total body water divided?"<font color=""#0000ff"">Extracellular </font>(2/3) and <font color=""#0000ff"">Intracellular </font>(1/3)<div><br></div><div>Extracellular further divided into: <font color=""#0000ff"">Interstitial fluid </font>(2/3), <font color=""#0000ff"">Blood Plasma </font>(1/3), <font color=""#0000ff"">Transcellular fluid</font> (around 1L)</div>"
What are examples of <b>crystalloids</b>?"- <b>Hartmann's </b>(ringer's Lactate)<div>- Saline</div><div>- Glucose</div><div>- Dextrose saline </div>"
What is the purpose of infusing 5% glucose/dextrose?A way of giving free water (as glucose is metabolised)
What is the difference between osmolality and osmolarity?"<font color=""#0000ff"">Osmolality</font>: Number of osmoles in 1<b>Kg</b> of water<div><font color=""#0000ff"">Osmolarity</font>: Number of osmoles in 1<b>L</b> of water</div>"
"Why is Hartmann's frequently preferred to 0.9% saline?""0.9% saline is hypertonic, ↑ acidic and has ↑[Cl<sup>-</sup>]<div><br></div><div>Hartmann's closer to physiological levels of plasma </div>"
In which body distribution does fluid go if infusing saline?Extracellular volume: cell membrane is impermeable to sodium
How is dextrose distributed across the body following an infusion?Hypotonic fluid (as dextrose is metabolised). Distributed equally through all fluid compartments
What fluids would you give to a dehydrated patient?Dehydration- mainly depletion of ICF. <div><br></div><div>Give dextrose</div>
What fluids would you give to a hypovolaemic patient?"Hypovolaemic= Depletion of IV compartment<div><br></div><div>Give isotonic fluids (Hartmann's, Saline), as distributed solely across ECF</div>"
What are colloid fluids?- Contain large particles designed to stay in plasma + maintain plasma oncotic pressure within the intravascular compartment to keep fluid intravascular 
What are <b>disadvantages of colloids</b>?- May cause <b>allergic reactions</b> (to bovine protein)<div>- More <b>expensive</b></div><div><br></div><div>Insufficient evidence to show it performs better than crystalloids </div>
What are risks of blood transfusions?"<font color=""#0000ff"">Acute:</font><div>- Haemolytic reactions </div><div>- Non-haemolytic febrile reactions</div><div>- Allergy to proteins</div><div>- Transfusion related acute lung disease (TRALI- if leukocytes still in blood product)</div><div>- Hypothermia</div><div>- Hyperkalaemia/hypocalcaemia </div><div><br></div><div><font color=""#0000ff"">Late:</font></div><div>- Iron overload (if repeated)<br></div><div>- Immune sensitisation (develop Abs against minor antigens on RBC surface)</div><div>- Transmission of infection</div>"
What is the benefit of cell salvage?- Gives patient their own red cells back, so no risk of immune reaction 
What can cause tertiary hyperparathyroidism?Chronic hyperstimulation of parathyroids, leading to overdrive<div><br></div><div>e.g. in CKD, where renal produdction of vitD is low → 2° hyperparathyroidism which converts to 3° hyperparathyroidism </div>
"A woman presents with a 3-month history of bilateral hip discomfort, as well as general malaise + fatigue. She spends most of her time indoors. An X-ray is shown below. What is the most likely diagnosis?<div><img src=""xrsJbiisdD_-_IJGyTanrhZLDmDzdOp_FP8owOhGEmWCrg_r_YYSSBTMrYT6jHfpc-wfNUMbT_xBUwtO7eEVU26e26PYmKXiX7wM8MhL0jKJIOfA1f5pNNay4uve=w517.png""><br></div>""Bilateral undisplaced subtrochnateric psuedofractures- <b>""Looser's zones"" </b>of the femur. "
What endocrine conditions are risk factors for osteoporosis?- Hyperparathyroidism<div>- Hyperthyroidism</div><div>- Type 1 Diabetes mellitus (not T2DM)</div>
What is atelectasis?Collapse or closure of a lung resulting in reduced/absent gas exchange (commonly occurs post-operatively)
What are common symptoms of atelectasis?- Fast, shallow breathing<div>- Low O<sub>2</sub> saturation</div><div>- Low-grade fever</div><div>- Cough</div>
How should atelectasis be managed?- Optimise pain control<div>- Deep breathing exercises</div><div>- Chest physio</div>
How should a Pulmonary Embolus be treated?Treatment-dose tinzaparin
What is delirium?Condition with acute + fluctuating change in attention, awareness and cognition, often due to an organic cause
"What is the ""sepsis six""?"<b>Give:</b><div>- Oxygen<div>- Empirical Abx</div><div>- IV fluids</div><div><br></div><div><b>Take</b></div><div>- Lactate</div><div>- Blood Cultures (before Abx given)</div><div>- Urine output (catheterisation)</div></div>
What is the Q-SOFA criteria, what is it used for?Predicts sepsis:<div>- RR >22</div><div>- Altered mentation (confusion, GCS<15)<br>- Hypotension (SBP≤100)</div>
How should a suspected PE be confirmed?CT Pulmonary Angiogram 
What are risk factors of post-operative ileus?- Manual handling of bowel during surgery<div>- Electrolyte disturbances</div><div>- Immobility</div><div>- Medications inc. general anaesthesia</div><div>- Infection and sepsis</div><div>- Comorbidities (e.g. heart failure, hypothyroidism, diabetes)</div>
What is <b>ileus?</b>Functional obstruction from decreased bowel motility
What is the management for post-operative ileus?- Electrolyte correction<div>- Mobilisation of patient</div>
What are signs of post-operative peritonitis?Rigid and extremely tender abdomen
What is the appropriate response to post-op peritonitis?Immediate return to theatre for relook laparotomy (to stop abdominal bleeding or anastomotic failure)
How should bowel obstruction be initially managed?"""Drip and suck""<div><br></div><div>- Set up IV fluid drip to treat dehydration</div><div>- Insert nasogastric tube to suck + relieve distention </div>"
What are the most common causes of small bowel obstruction?- Adhesions<div>- Incarcerated hernias </div>
What are the most common causes of large bowel obstructions?- Colorectal cancer<div>- Volvulus</div><div>- Constipation </div>
What are <b>adhesions</b>?Fibrous scar tissue in the abdomen (describes what?)
Fibrous scar tissue in the abdomen (describes what?)What are <b>adhesions</b>?
What is a <b>volvulus?</b>Loop of intestine which twists around itself and its mesentery, causing bowel obstruction (describes what?)
Loop of intestine which twists around itself and its mesentery, causing bowel obstruction (describes what?)What is a <b>volvulus?</b>
What are the signs of a pulmonary embolism?"- <font color=""#0000ff"">Sudden</font> onset dyspnoea<div>- Tachypnoea<br><div>- Cough</div><div>- Pleuritic chest pain</div><div>- Haemoptysis</div></div><div>- Tachycardia</div><div>- Pyrexia</div><div><br></div><div>- Unilateral swollen leg</div>"
Who does Primary Biliary Cholangitis typically affect?Women aged 35-70 (account for 95% of cases)
What is <b>primary biliary cholangitis?</b>Chronic autoimmune granulomatous inflammation in interlobular bile ducts causes cholestasis (describes what disease?)
Chronic autoimmune granulomatous inflammation in interlobular bile ducts causes cholestasis (describes what disease?)What is <b>primary biliary cholangitis?</b>
What other diseases are associated with <b>primary biliary cholangitis?</b>"Other autoimmune disorders:<div>- RA</div><div>- Systemic sclerosis</div><div>- Sjogren's syndrome</div><div>- Autoimmune thyroidits</div><div>- Renal tubular acidosis</div>"
What is the pathophysiology behind primary biliary cholangitis?"Unknown <font color=""#0000ff"">environmental trigger </font>(?pollutants, xenobiotics, non-pathogenic bacteria) + <font color=""#0000ff"">genetic predisposition</font> (e.g. IL12A locus) leads to <font color=""#ff0000"">loss of immune tolerance to self-mitochondrial proteins. </font><div><br></div><div>T-cell mediated attack and destroy bile ducts → <b>cholestasis</b></div><div><br></div><div>Retained <font color=""#0000ff"">toxic materials (e.g. bile acids) cause further damage</font>, <b>esp. to hepatocytes. </b></div>"
What are particular risk factors for Primary Biliary Cholangitis?- +ve FHx<div>- Many UTIs</div><div>- Smoking</div><div>- Past pregnancy,</div><div>- Other autoimmune disease</div><div>- ↑ Use of nail polish/hair dye</div>
How does<b> primary biliary cholangitis</b> typically present?"<font color=""#0000ff"">Many asymptomatic.</font><div><br></div><div><b>Pruritus, fatigue + dry mouth + eyes are initial symptoms</b>, and can precede jaundice by months/years. </div><div><br></div><div>May also have enlarged firm non-tender liver, hyperpigmentation, xanthelasma, jaundice. </div><div><br></div><div>(describes the presentation of what disease?)</div>"
"<font color=""#0000ff"">Many asymptomatic.</font><div><br></div><div><b>Pruritus, fatigue + dry mouth + eyes are initial symptoms</b>, and can precede jaundice by months/years. </div><div><br></div><div>May also have enlarged firm non-tender liver, hyperpigmentation, xanthelasma, jaundice. </div><div><br></div><div>(describes the presentation of what disease?)</div>"How does<b> primary biliary cholangitis</b> typically present?
How are asymptomatic patients with Primary Biliary Cholangitis typically detected?Abnormal LFTs:<div>- ↑ALP & GGT</div><div>- Mildly ↑ AST & ALT</div>
What findings would you expect in the blood of a patient with Primary Biliary Cholangitis?"- ↑ALP ↑GGT<div>- Mildly ↑AST&ALT</div><div><font color=""#0000ff"">- Antimitochondrial Antibodies +ve (in titre of 1:40)</font></div><div>- ↑ Serum IgM</div><div><br></div><div>in late disease:</div><div>- ↑Bilirubin ↓Albumin ↑PT (sign of cirrhosis) </div>"
What investigation should be carried out in a patient with ↑ALP & ↑GGT?Ultrasound: Helps differentiate between extrahepatic cholestasis, or PBC/PSC
How is autoimmune cholangitis diagnosed?In patients who would otherwise be diagnosed with Primary Biliary Cholangitis but <b>negative for Antimitochondrial antibodies</b>
What is the prognosis of Primary Biliary Cholangitis?Typically progresses to terminal stages over 15-20years (though variable). <div><br></div><div>Tend to take 2-7years to develop symptoms. Once develop symptoms, median life expectancy around 10 years </div>
How should Primary Biliary Cholangitis be managed?"<font color=""#0000ff"">Ursodeoxycholic acid</font>: ↓Liver damage, ↑Survival + delays need for transplantation<div><br></div><div><font color=""#0000ff"">For Pruritus</font>: Cholestyramine 4-8g/24h PO; naltrexone and rifampicin may also help</div><div><br></div><div><font color=""#0000ff"">For Diarrhoea</font>: Codeine</div><div><br></div><div><font color=""#0000ff"">Fat-soluble vitamin prophylaxis</font>: Give Vitamins A, D, E and K. </div><div><br></div><div><span style=""color: rgb(0, 0, 255);"">Osteoporosis prevention</span><br></div><div><span style=""color: rgb(0, 0, 255);""><br></span></div><div><span style=""color: rgb(0, 0, 255);"">Liver transplantation if decompensated liver disease</span></div>"
How should Primary Biliary Cholangitis be monitored?- Regular LFTs<div>- Ultrasound + Alpha-fetoprotein twice-yearly if cirrhotic </div>
What are <b>alpha-fetoprotein </b>assays used for?Monitoring of <b>hepatocellular carcinoma</b> (is done through what assays?)
Monitoring of <b>hepatocellular carcinoma</b> (is done through what assays?)What are <b>alpha-fetoprotein </b>assays used for?
What is <b>primary sclerosing cholangitis?</b>Progressive cholestasis with (intra and extra-hepatic) bile duct inflammation and strictures
Who is mostly affected by Primary sclerosing cholangitis?- Men (70%)<div><br></div><div>Mean age at diagnosis is 40y/o</div>
What are the main symptoms of <b>primary sclerosing cholangitis</b>?"Insidious onset, starting with<font color=""#0000ff""> pruritus and fatigue</font><div><br></div><div>If advanced: ascending cholangitis, cirrhosis + hepatic failure </div><div><br></div><div>(describes the symptoms of what disease?)</div>"
"Insidious onset, starting with<font color=""#0000ff""> pruritus and fatigue</font><div><br></div><div>If advanced: ascending cholangitis, cirrhosis + hepatic failure </div><div><br></div><div>(describes the symptoms of what disease?)</div>"What are the main symptoms of <b>primary sclerosing cholangitis</b>?
<span class=cloze>[...]</span> and <span class=cloze>[...]</span> tends to develop in 75% of Primary sclerosing cholangitis patients<span class=cloze>Symptomatic gallstones</span> and <span class=cloze>choledocholithiasis</span> tends to develop in 75% of Primary sclerosing cholangitis patients<br> Does total colectomy in UC affect the risk of developing PSC?No
What are long-term risks of primary sclerosing cholangitis?Increased risks of bile duct, gallbladder, liver and colon cancers 
How do PBC and PSC differ in terms of geography?"<font color=""#0000ff"">PBC</font>: Affects interlobular bile ducts<div><font color=""#0000ff"">PSC</font>: Affects both intra and extra-hepatic bile ducts</div>"
What are associations with Primary Sclerosing Cholangitis?"- Inflammatory Bowel Disease: 5% of UC patients, 1% of Crohn's Patients<div>- Male sex</div><div>- HLA A1, B8, DR3 (often associated with auto-immune)</div><div>- Autoimmune hepatitis</div>"
<span class=cloze>[...]</span> develops in 10-15% of Primary Sclerosing Cholangitis patients<span class=cloze>Cholangiocarcinoma</span> develops in 10-15% of Primary Sclerosing Cholangitis patients<br> Cholangiocarcinoma develops in <span class=cloze>[...]</span> of Primary Sclerosing Cholangitis patientsCholangiocarcinoma develops in <span class=cloze>10-15%</span> of Primary Sclerosing Cholangitis patients<br> What are expected blood test results in PSC?- LFTs: ↑ALP and ↑GGT (rather than aminotransferases)<div>- ↑IgG and IgM levels</div><div>- Abs: Anti-smooth muscle and pANCA </div><div>- Antimitochondrial antibody <b>negative</b>  </div>
What is the 1st choice investigation to diagnose Primary Sclerosing Cholangitis?- MRCP (ERCP 2nd choice: gold-standard, but invasive)
What woule be found on liver biopsy of Primary Sclerosing Cholangitis?- Bile duct proliferation<div>- Periductal fibrosis</div><div>- Inflammation</div><div>- Loss of bile ducts </div>
How is Primary Sclerosing Cholangitis treated?"- Ursodeoxycholic acid for pruritus + improves biochemical markers (but not survival) <div>- Cholestyramine for pruritus</div><div>- Abx for ascending bacterial cholangitis <br><div>- Supportive treatment for cirrhosis/chronic cholestasis</div></div><div><br></div><div><font color=""#0000ff"">- Liver transplant only treatment which improves life expectancy in PSC + offers cure. </font></div>"
What are reasonable indications for liver transplantation of PSC?- Recurrent bacterial cholangitis<div>- Complications of end-stage liver disease (intractable ascities, hepatic encephalopathy, bleeding oesophageal varices)</div>
What can cause secondary sclerosing cholangitis?- Immune deficiencies (congenital in children, acquired in adults as AIDS acholangiopathy) with superimposed infections, or use of drugs
What is <b>haematochezia?</b>Passage of fresh blood through the anus  (describes what?)
Passage of fresh blood through the anus  (describes what?)What is <b>haematochezia?</b>
<span class=cloze>[Biochemistry finding]</span> can indicate an upper GI bleed rather than a lower GI bleed<span class=cloze>High urea levels</span> can indicate an upper GI bleed rather than a lower GI bleed<br> How will autoimmune hepatitis affect the LFTs?Predominantly raised ALT/AST vs ALP
What are the three different types of autoimmune hepatitis and thir antibodies?"<font color=""#0000ff"">Type I</font>: ANA (10%) and anti-Smooth Muscle Antibodies (80%)<div><font color=""#0000ff"">Type II:</font> Anti-liver/kidney microsomal type 1 antibodies (LKM1)<br><font color=""#0000ff"">Type III:</font> Soluble liver-kidney antibodies</div>"
Who do the different types of Auto-immune hepatitis affect?"<font color=""#0000ff"">Type I</font>: Adults and children<div><font color=""#0000ff"">Type II</font>: Children only</div><div><font color=""#0000ff"">Type III</font>: Adults in middle-age</div>"
What is found on liver biopsy of auto-immune hepatitis?- Piecemeal necrosis: Inflammation extending beyond limiting plate<div>- Bridging necrosis</div>
How do people with <b>Plummer-Vinson Syndrome</b> present?Triad of:<div>- Dysphagia</div><div>- Glossitis</div><div>- Iron-deficiency anaemia </div><div><br></div><div>(describes the typical presentation of what?)</div>
Triad of:<div>- Dysphagia</div><div>- Glossitis</div><div>- Iron-deficiency anaemia </div><div><br></div><div>(describes the typical presentation of what?)</div>How do people with <b>Plummer-Vinson Syndrome</b> present?
What is <b>Mallory-Weiss syndrome?</b>"Severe vomiting → painful mucosal lacerations at <font color=""#0000ff"">gastro-oesophageal junction </font>→haematemesis<div><br></div><div>(describes what?)</div>"
"Severe vomiting → painful mucosal lacerations at <font color=""#0000ff"">gastro-oesophageal junction </font>→haematemesis<div><br></div><div>(describes what?)</div>"What is <b>Mallory-Weiss syndrome?</b>
What is <b>Boerhaave syndrome?</b>Spontaneous perforation of oesophagus from ↑intra-oesophageal pressure and ↓intrathoracic pressure (e.g. straining or vomiting) (describes what?)
Spontaneous perforation of oesophagus from ↑intra-oesophageal pressure and ↓intrathoracic pressure (e.g. straining or vomiting) (describes what?)What is <b>Boerhaave syndrome?</b>
What parameters are used to calculate a Modified Glasgow Score for pancreatitis?PANCREAS<div><br></div><div>PaO<sub>2</sub></div><div>Age</div><div>Neutrophilia</div><div>Calcium</div><div>Renal Function</div><div>Enzymes</div><div>Albumin</div><div>Sugar</div>
Describe Hepatitis D virus?ssRNA virus transmitted parenterally<div><br></div><div>Incomplete RNA virus- requires Hepatitis B surface antigen to complete replication and transmission cycle</div>
What is Hepatitis B and D superinfection associated with?↑ Risk of fulminant hepatitis, chronic hepatitis + cirrhosis
How does the oral contraceptive pill cause jaundice?Oestrogens in the pill reduce excretion of bile acids + conjugated bilirubin → Build up and diffusion into bloodstream
How might you differentiate between someone with choledocholithiasis and drug-induced cholestasis (e.g. contraceptive pill)"<div>Both will have very similar LFT picture. </div><div><br></div><font color=""#0000ff"">Choledocholithiasis should come with biliary colic pain</font>"
What is carcinoid syndrome?<div>Carcinoid tumour metastases in liver, which release serotonin into systemic circulation <br></div>
How should symptomatic relief be provided from carcinoid tumours?Octreotide- somatostatin analogue
What are common predisposing features for bowel ischaemia?- Increasing age<div>- Atrial fibrillation</div><div>- Other causes of emboli (endocarditis, malignancy) </div><div>- CVD risk factors (smoking, HTN, diabetes)</div><div>- Cocaine</div>
What are the 3 main different types of bowel ischaemia?- Acute mesenteric ischaemia<div>- Chronic mesenteric ischaemia</div><div>- Ischaemic colitis</div>
Patients with acute mesenteric ischaemia classically have a history of <span class=cloze>[...]</span>Patients with acute mesenteric ischaemia classically have a history of <span class=cloze>atrial fibrillation</span><br> How should bowel ischaemia be imaged?CT
What is <b>ischaemic colitis</b>?Acute but transient compromise in blood flow to large bowel (describes what?)
Acute but transient compromise in blood flow to large bowel (describes what?)What is <b>ischaemic colitis</b>?
Where is ischaemic colitis most likely to occur?"""Watershed areas"" e.g. splenic flexure, which is at borders of area supplied by superior and inferior mesenteric arteries"
How are the bowel ischaemia disorders managed?"<font color=""#0000ff"">Acute mesenteric ischaemia</font>: Urgent surgery <div><font color=""#0000ff"">Ischaemic colitis</font>: Supportive, surgery if conservative measures fail </div>"
Why can certain antibiotics such as neomycin and rifaximin be useful in hepatic encephalopathy?Encephalopathy caused by nitrogenous waste such as ammonia, which are generated + converted by intestinal bacteria. <div><br></div><div>Killing these bacteria reduces generation of these waste products</div>
In the context of gastroenterology, what is meant by anorexia?Lack or loss of appetite for food<div><br></div><div>(different from anorexia nervosa)</div>
What are important distinctions to make in bowel obstruction?- Obstruction in small or large bowel?<div>- Is there an ileus/ mechanical obstruction</div><div>- Is obstructed bowel simple/closed loop/strangulated </div>
What are clinical signs suggesting small bowel vs large obstruction?"<div><font color=""#0000ff"">Small bowel obstruction</font></div>- Vomiting occurs early<div>- Less distention</div><div>- Pain is higher in the abdomen </div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Large bowel obstruction</font></div><div>- Pain tends to be more constant</div><div><br></div><div>(would usually use an AXR to differentiate)</div>"
How do you differentiate between ileus and mechanical obstruction?"<font color=""#0000ff"">Ileus:</font><div>- Absent bowel sounds</div><div>- Pain tends to be less</div>"
What is pseudo-obstruction?Signs and symptoms resembling mechanical GI obstruction but with no obstructing lesion
"What is <b>Ogilvie's syndrome?</b>"Acute colonic pseudo-obstruction (describes what?)
Acute colonic pseudo-obstruction (describes what?)"What is <b>Ogilvie's syndrome?</b>"
What are predisposing factors for Pseudo-obstruction?- Puerperium<div>- Pelvic surgery</div><div>- Trauma</div><div>- Cardio-respiratory and neurological disorders</div>
How is pseudo-obstruction treated?- Neostigmine<div>- Colonoscopic decompression</div><div><br></div><div>Can be useful </div>
What is a <b>simple </b>bowel obstruction?- One obstructing point + no vascular compromise
What is a <b>closed loop bowel obstruction</b>- Obstruction at two points forming loop of grossly distended bowel at risk of perforation 
What is a <b>strangulated </b>bowel obstruction?"Blood supply to the bowel is compromised: sharper, more constant + localised pain with <font color=""#0000ff"">peritonitism</font>"
What is <b>puerperium?</b>"Period of 6 weeks after childbirth during which mother's reproductive organs return to their original non-pregnant condition (describes what?)"
"Period of 6 weeks after childbirth during which mother's reproductive organs return to their original non-pregnant condition (describes what?)"What is <b>puerperium?</b>
What type of bowel obstructions should be operated on?- Strangulation<div>- Large bowel obstruction </div><div><br></div><div>(ileus and small bowel obstruction can initially be conservatively managed)</div>
What is the immediate action for bowel obstruction?"<font color=""#0000ff"">Drip and suck:</font><div><br></div><div>- NG-Tube and IV fluids to rehydrate and correct electrolye imbalance. </div>"
What causes <b>sigmoid volvulus</b>?Bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction (describes what?)
Bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction (describes what?)What causes <b>sigmoid volvulus</b>?
How is sigmoid volvulus treated?"1st line: Sigmoidoscopy w/ Flatus tube insertion (left in situ for 24hrs)<div><br></div><div><br></div><div>Surgery: Laparoscopic Hartmann's procedure/ Laparotomy for sigmoid colectomy <br></div>"
What are potential complications of sigmoid volvulus?<div>- Bowel obstruction</div>- Perforation and fatal peritonitis
Why might a patient with chronic liver disease present with shortness of breath?Hepatic hydrothorax: pleural effusion secondary to cirrhosis<div><br></div><div>In cirrhosis, fluid can be found: in abdomen (ascites), in periphery (ankle oedema) and in pleural cavity (hepatic hydrothorax</div>
What is<b> dyspepsia?</b>Indigestion: Upper abdominal pain, fullness, early satiety, bloating and nausea 
What is the most sensitive radiographic study to detect the presence of <b>free gas</b> in the abdomen?<b>Erect </b>chest X-Ray
"<div>What is seen here?</div><img src=""paste-d7bce1107650eec70492f5058c5faf1a10b99e1a.jpg"">"<b>Pneumoperitoneum</b>- free gas in the abdomen 
"What can cause pneumoperitoneum, seen below?<div><img src=""paste-d7bce1107650eec70492f5058c5faf1a10b99e1a.jpg""><br></div>"- Perforation of abdominal viscus<div>- Insufflation of gas during laparoscopic operation</div>
If a patient is too unwell to be positioned for an erect chest X-Ray, how else can pneumoperitoneum be investigated?Use <b>decubitus </b>positioning:<br>- Patient lies on side, and X-Ray pass from Posterior-Anterior<div><br></div><div>Gas should raise to upper part of abdomen and so be seen on one side of the AXR</div>
What is generally the upper limit of normal diameter of the bowel?Small bowel: 3cm<div>Colon: 6cm</div><div>Caecum: 9cm</div>
"What is seen here?<div><img src=""paste-eb9e47f3a531e6c07c85c42e38014f6aa7db8386.jpg""><br></div>""Central position, <b>valvulae conniventes</b> (<font color=""#0000ff"">cross the full width of bowel</font>)<div><br></div><div><b>Normal small bowel</b></div><div><img src=""paste-9aec73cec686be297da4ae37353060f468d70baa.jpg""><br></div>"
"What is seen here?<div><img src=""paste-4a2193fee0aa8bb093bc46011f9aa52663df21bf.jpg""><br></div>""<b>Haustra</b>- <font color=""#0000ff"">do not completely cross the diameter of the bowel,</font> faeces, and peripheral position in abdomen <div><br></div><div><b>Normal large bowel</b></div>"
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""ee03bb521a084dada6fa6f76da888108-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmpi2_wmsij.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""ee03bb521a084dada6fa6f76da888108-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmpi2_wmsij.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""ee03bb521a084dada6fa6f76da888108-ao-2-Q.svg"" /></div> <div id=""io-original""><img src=""tmpi2_wmsij.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""ee03bb521a084dada6fa6f76da888108-ao-2-A.svg"" /></div> <div id=""io-original""><img src=""tmpi2_wmsij.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""ee03bb521a084dada6fa6f76da888108-ao-3-Q.svg"" /></div> <div id=""io-original""><img src=""tmpi2_wmsij.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""ee03bb521a084dada6fa6f76da888108-ao-3-A.svg"" /></div> <div id=""io-original""><img src=""tmpi2_wmsij.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
"What is seen here?<div><img src=""paste-2868ba2caf3283a1a6c9137f581228901485ea4e.jpg""><br></div>"Psoas edge
"What is seen here?<div><img src=""paste-c7bc369674b10802015c35809aedb45d3919e609.jpg""><br></div>""Kidney: see the contrast between the kidney and the low density retroperitoneal fat<div><img src=""paste-d83868008d77c73a842cbbbaf47d4a2b7f7d7f23.jpg""><br></div><div><br></div>"
What level do the kidneys typically lie?T12-L3, lateral to psoas muscles
The <span class=cloze>[...]</span> kidney is usually lower than the <span class=cloze>[...]</span>The <span class=cloze>right</span> kidney is usually lower than the <span class=cloze>left</span><br> Due to position of the liver
What can be as landmarks for the course of the ureters on an abdominal X-Ray?"Transverse processes of lumbar vertebrae<div><img src=""paste-af52e587b349eee4941082015515fc4a044f7464.jpg""><br></div>"
What landmark can be used for the <b>vesico-ureteric</b> junctions?"Level of ischial spines (ca be use as a landmark for what?)<div><img src=""paste-af52e587b349eee4941082015515fc4a044f7464.jpg""><br></div>"
"Level of ischial spines (ca be use as a landmark for what?)<div><img src=""paste-af52e587b349eee4941082015515fc4a044f7464.jpg""><br></div>"What landmark can be used for the <b>vesico-ureteric</b> junctions?
Can gallstones be seen on an abdominal X-Ray?Only if calcified (only 20% of gallstones are calcified)
What is an appropriate investigation for gallstone disease?Ultrasound
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-2-Q.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-2-A.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-3-Q.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-3-A.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-4-Q.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-4-A.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-5-Q.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""3e1970ef01fb47caa3e25aec8d33ecff-ao-5-A.svg"" /></div> <div id=""io-original""><img src=""tmp2uf5aisy.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
What are <b>phleboliths?</b>Calcified pelvic veins (are what?)
Calcified pelvic veins (are what?)What are <b>phleboliths?</b>
"What is<b> Rigler's sign</b>?""Appearance of gas on both sides of the bowel wall- means both sides can be visible<div><br></div><div><img src=""paste-15aef5170f5d86dbf39d7b6f7f436d9a665af140.jpg""><img src=""paste-14b6db17286221711888638ee4e2a5d0da9a3883.jpg""><br></div>"
"What is seen here?<div><img src=""ajeccm-v1-id1004-g001.gif""><br></div>""Rigler's sign: both sides of the bowel wall are visible- suggests pneumoperitoneum"
"What is seen here?<div><img src=""paste-7ac135434f59fae331ca7833672e460547d19f38.jpg""><br></div>""Normal stomach bubble: Round ""bubble shape"", and thick upper wall shows air is still within the stomach (not under the thin diaphragm)"
"What is seen here?<div><img src=""paste-55cef5cf808e3654d654dc434a4fc1f7c2f740f3.jpg""><br></div>""Chilaiditi's phenomenon: mimics pnuemoperitoneum, but is actually gas within bowel. Can tell, <font color=""#0000ff"">as it has a thick upper wall (due to bowel wall + diaphragm)</font><div><br></div><div>Due to patients with small livers (e.g. in chronic cirrhosis) or flattened diaphragms (due to lung hyperexpansion).</div>"
"What is seen here?<div><img src=""paste-cdfd279dc688c2d74e59f5ceac3684825f9f2c65.jpg""><br></div>""False Rigler's sign- whilst it looks like double wall, it is just two adjacent bowel. <div><br></div><div>No black triangles or sharp angles on oustide of bowel wall</div>"
"What is seen here?<div><img src=""paste-80cf72617b73675a312cc944c69e478bd1654603.jpg""><br></div>""<div>Centrally located + valvulae conniventes seen → Small bowel</div><div><br></div>Multiple dilated loops of gas filled bowel >3cm → bowel obstruction <div><br></div><div>Anastomosis site (seen in red) suggests adhesions post surgery is most likely cause of small bowel obstruction. </div><div><img src=""paste-631faef200663c31b39a58c55ef885d181360c15.jpg""><br></div><div><br></div>"
"What is seen here?<div><img src=""paste-f10f1103edb2a2721834f1ef517221cb31a4939a.jpg""><br></div>"Sentinel loop: single loop of small bowel is dilated. <div><br></div><div>Can occur with intra-abdominal inflammation (e.g. pancreatitis)</div>
"What is seen here?<div><img src=""paste-4ad1aec89f757a0c2a89084d23283a4b01c13519.jpg""><br></div>""Peripheral structure with haustra (incomplete) → large bowel<div><br></div><div>Dilated beyond normal levels (6cm for colon, 9cm for caecum) → obstruction</div><div><br></div><div>Obstruction is not absolute, as small volume of gas has reached the rectum.</div><div><br></div><div><img src=""paste-0e61adf746c1a7ca37db80cc729b5add825a0bb5.jpg""><br></div>"
Which part of the intestines is most prone to volvulus?Sigmoid colon- as it has its own mesentery, and so is more mobile
"What is seen here?<div><img src=""paste-8212c5b74cd198fbb22e18b3d2fbd1cf676de737.jpg""><br></div>""Coffee- bean sign: sigmoid volvulus (proximal large bowel is also dilated, *)<div><br></div><div><div><img src=""paste-9f62264526cfeb0c072e58dc572e9e12dd3adfc5.jpg""><br></div><div><br></div></div>"
"What is seen here?<div><img src=""paste-6b152cc991c453fb946fec42e940931f2db1f989.jpg""><br></div>"Thumbprinting- sign of <b>ulcerative colitis</b>: caused by increased distance between loops of bowel + thick haustral folds. 
"What is seen here?<div><img src=""paste-0e603e5b40eebf64cfc3cc6dfc1f4d0ec60cc68d.jpg""><br></div>""<font color=""#0000ff"">Lead pipe colon- sign of longstanding Ulcerative Colitis</font>: Segment of transverse colon with loss of normal haustral markings"
What is the most appropriate initial investigation to carry out for a 19 y/o female with right iliac fossa pain and fever?Urinary beta-hCG: <b>any female patient of child bearing age should have pregnancy test done</b><div><b><br></b></div><div>- Done to rule out ectopic pregnancy + important to do before exposing patient to radiation from CT scans</div>
What is intussuscpetion?"Intestine folds into section immediately ahead of it (typically in small bowel)<div><img src=""ds00694_-ds00798_-ds00823_im00711_ans7_intussusceptionthu_jpg.jpg""><br></div>"
What are symptoms of intussusception?- Colicky abdominal pain<div>- Vomiting</div><div>- Bloody stool (red-currant jelly)</div>
How is intussusception typically treated?"<font color=""#0000ff"">In children:</font><div>- Enema (creates pressure within the intestine to right the bowel and relieve obstruction)</div><div>- (Surgery if refractory)<br></div><div><br></div><div><font color=""#0000ff"">In adults:</font></div><div>- Surgical removal of part of bowel</div>"
In what patients is intussusception most common?Children (6-18 months), more often males
What is an <b>irreducible </b>hernia?Contents cannot be pushed back into place (refers to what type of hernia?)
Contents cannot be pushed back into place (refers to what type of hernia?)What is an <b>irreducible </b>hernia?
What is an<b> obstructed </b>hernia?Bowel contents cannot pass 
What is a <b>strangulated </b>hernia?Ischaemia occurs- requires urgent surgery (refers to what type of hernia?)
Ischaemia occurs- requires urgent surgery (refers to what type of hernia?)What is a <b>strangulated </b>hernia?
What is an <b>incarcerated </b>hernia?Contents of hernial sac are stuck inside by adhesions (describes what?)
Contents of hernial sac are stuck inside by adhesions (describes what?)What is an <b>incarcerated </b>hernia?
What is a <b>hernia?</b>Protrusion of a viscus or part of a viscus into an abnormal position, through a defect of the walls of its containing cavity
What is the most common type of abdominal hernia?Inguinal hernias
What occurs in a <b>femoral hernia?</b>"Bowel enters the femoral canal, presenting as mass in upper medial thigh/above the inguinal ligament. <div><br></div><div>Points down the leg (unlike inguinal which points to groin)</div><div><img src=""paste-be08d8d5e05961a9adf317c1d778e9b79e665653.jpg""><br></div>"
In what population do femoral hernias occur more in?Women (due to wider bony pelvis), especially in middle age and elderly 
Where does the inguinal ligament run between?ASIS and the pubic tubercle
What is the landmark for the <b>femoral artery?</b><b>Mid-inguinal point</b>: halfway between the ASIS and pubic symphysis (is the landmark for what?)
<b>Mid-inguinal point</b>: halfway between the ASIS and pubic symphysis (is the landmark for what?)What is the landmark for the <b>femoral artery?</b>
What is the landmark for the <b>femoral nerve?</b><b>Midpoint</b> of the inguinal ligament, between the ASIS and the pubic tubercle (is the landmark for what?)
<b>Midpoint</b> of the inguinal ligament, between the ASIS and the pubic tubercle (is the landmark for what?)What is the landmark for the <b>femoral nerve?</b>
From medial to lateral, what are the structures which run <b>under</b> the inguinal ligament? (AVN, canal w lymph)"- Femoral Canal (containing lymphatic vessels, loose connective tissue, and deep lymph node)<div>- Femoral vein</div><div>- Femoral artery</div><div>- Femoral nerve</div><div><img src=""c007_f002.jpg""><br></div><div><br></div>"
What are the borders of the <b>femoral </b>canal?"<div><font color=""#0000ff"">Anteriorly</font>: Inguinal ligament</div><font color=""#0000ff"">Medial</font>: Lacunar ligament (+ pubic bone)<br><font color=""#0000ff"">Lateral</font>: Femoral vein<div><font color=""#0000ff"">Posterior</font>: Pectineal ligament + pectineus</div><div><img src=""Borders-of-the-Femoral-Canal.jpg""><br></div>"
What is <b>herniotomy</b>?Ligation and excision of hernial sac
What is <b>herniorraphy?</b>Repair of hernial defect
Where do paraumbilical hernias typically herniate?<div>Just above or below the umbilicus, through the linea alba- fibrous structure in the middle of the abdomen</div>
What are risk factors of paraumbilical hernias?- Obesity<div>- Ascites</div>
How are paraumbilical hernias surgically repaired?Mayo repair: Repair of the rectus sheath 
Where do epigastric hernias occur?Above the umbilicus, through the linea alba 
How do incisional hernias arise?- Weakness of surgical wounds, from decreased wound healing (as a result of haematoma, seroma, infection etc.)<div>- Increase intra-abdominal pressure (e.g. chronic cough in COPD, constipation, ascites)</div>
How are incisional hernias repaired?- Re-incise the old wound<div>- Reinforce using prosthetic mesh</div><div><br></div><div>(↓recurrence, but ↑infection)</div>
Where do spigelian hernias occur?Occur through linea semilunaris, at lateral edge of rectus sheath (below and lateral to umbilicus)
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"What are <b>Richter's hernias?</b>"Hernias which involve bowel wall only- not whole lumen (describes what?)
Hernias which involve bowel wall only- not whole lumen (describes what?)"What are <b>Richter's hernias?</b>"
"What are <b>Maydl's </b>hernias?""Hernial sac contains two loops of bowel, with another strangulated loop of bowel being intra-abdominal<div><br></div><div><img src=""Schematic-diagram-of-Maydls-hernia-strangulated-intestine-at-apex-of-W.png""><br></div><div>(describes what?)</div>"
"Hernial sac contains two loops of bowel, with another strangulated loop of bowel being intra-abdominal<div><br></div><div><img src=""Schematic-diagram-of-Maydls-hernia-strangulated-intestine-at-apex-of-W.png""><br></div><div>(describes what?)</div>""What are <b>Maydl's </b>hernias?"
"What is <b>Littré's hernia?</b>""Hernial sacs containing strangulated Meckel's diverticulum (describes what?)"
"Hernial sacs containing strangulated Meckel's diverticulum (describes what?)""What is <b>Littré's hernia?</b>"
What are <b>sliding</b> hernias? (not hiatal hernia)Sac contain partially extraperitoneal structure (e.g. caecum, sigmoid colon) and does not completely surround contents (describes what?)
Sac contain partially extraperitoneal structure (e.g. caecum, sigmoid colon) and does not completely surround contents (describes what?)What are <b>sliding</b> hernias? (not hiatal hernia)
What are common paediatric hernias?- Umbilical hernias (3% of live births)<br>- <b>Indirect</b> inguinal hernia (4% of all male births) <br><div>- Gastroschisis</div><div>- Exomphalos</div>
What is <b>gastroschisis?</b>"Protrustion of abdominal contents through defect in anterior abdominal wall to right of umbilicus<div><img src=""Gastroschisis-web.jpg""><br></div><div><br></div><div>(describes what?)</div>"
"Protrustion of abdominal contents through defect in anterior abdominal wall to right of umbilicus<div><img src=""Gastroschisis-web.jpg""><br></div><div><br></div><div>(describes what?)</div>"What is <b>gastroschisis?</b>
What is <b>omphalocoele/exomphalos</b>?"Abdominal contents found outside abdomen, covered in three layer membrane consisting of periteonum, wharton's jelly (gelatinous substance within umbilical cord) and amnion<div><img src=""Omphalocele-drawing.jpg""><br></div><div><br></div><div>(describes what?)</div>"
"Abdominal contents found outside abdomen, covered in three layer membrane consisting of periteonum, wharton's jelly (gelatinous substance within umbilical cord) and amnion<div><img src=""Omphalocele-drawing.jpg""><br></div><div><br></div><div>(describes what?)</div>"What is <b>omphalocoele/exomphalos</b>?
What is more urgent, gastroschisis or omphalocoele?<b>Gastroschisis</b>, as in omphalocoele, bowel is still protected by three layer membrane
What can cause a paediatric umbilical hernia?Defect in transveralis fascia
What predisposes male infants to indirect inguinal hernias?"<b>Patent processus vaginalis</b><div><img src=""Hydrocele_communicating_w.jpg""><br></div>"
What is the difference between an indirect and direct inguinal hernia?"<b><font color=""#0000ff"">Indirect</font>: Push through deep inguinal ring</b> (and if large enough, through superficial inguinal ring too)<div><b><font color=""#0000ff"">Direct</font>: Push directly forward through posterior wall of inguinal canal</b></div><div><img src=""cbb127bd3b7804c5a35deefdef5f345b.jpg""><br></div>"
<span class=cloze>[...]</span> inguinal hernias will be <b>lateral</b> to the inferior epigastric whereas <span class=cloze>[...]</span> inguinal hernias will be medial to the inferior epigastric"<span class=cloze><b>Indirect</b></span> inguinal hernias will be <b>lateral</b> to the inferior epigastric whereas <span class=cloze>direct</span> inguinal hernias will be medial to the inferior epigastric<br> <img src=""paste-9766d24f5011dc637d9b1e7684bf63fae39134c3.jpg"">"
<b>Indirect</b> inguinal hernias will be <span class=cloze>[...]</span> to the inferior epigastric whereas direct inguinal hernias will be <span class=cloze>[...]</span> to the inferior epigastric"<b>Indirect</b> inguinal hernias will be <span class=cloze><b>lateral</b></span> to the inferior epigastric whereas direct inguinal hernias will be <span class=cloze>medial</span> to the inferior epigastric<br> <img src=""paste-9766d24f5011dc637d9b1e7684bf63fae39134c3.jpg"">"
<b>Indirect</b> inguinal hernias will be <b>lateral</b> to the <span class=cloze>[...]</span> whereas direct inguinal hernias will be medial to the <span class=cloze>[...]</span>"<b>Indirect</b> inguinal hernias will be <b>lateral</b> to the <span class=cloze>inferior epigastric</span> whereas direct inguinal hernias will be medial to the <span class=cloze>inferior epigastric</span><br> <img src=""paste-9766d24f5011dc637d9b1e7684bf63fae39134c3.jpg"">"
Where is the <b>deep inguinal ring</b> found?<b>Mid-point of inguinal ligament</b>, 1.5cm above the femoral pulse
Where is the superficial inguinal ring found?"Split in<b> external oblique aponeurosis</b>, <font color=""#0000ff"">superior + medial</font> to pubic tubercle "
What conditions can give erythema nodosum?"Granuloma forming diseases:<div>- TB</div><div>- Crohn's </div><div>- Sarcoidosis</div>"
"What is the aim of management of Crohn's?"Achieve deep remission:<div><br></div><div>- Absence of symptoms </div><div>- Endoscopic healing</div>
What is the most common type of anaemia worldwide?Iron-deficiency anaemia
What is <b>Pica</b>?Eating items that are not typically thought of as food and do not contain significant nutritional value (hair, dirt, paint chips)<div><br></div><div>(Describes what?)</div>
Eating items that are not typically thought of as food and do not contain significant nutritional value (hair, dirt, paint chips)<div><br></div><div>(Describes what?)</div>What is <b>Pica</b>?
"What is seen here?<div><img src=""Esophageal_web.jpg""><br></div>"Oesophageal web
"<div>What is seen here?</div><div><br></div><img src=""angiodysplasia_high.jpg"">"Telangiectasia
"What is seen here?<div><img src=""diverticulosis_high.jpg""><br></div>"Diverticulosis
When is iron given IV to patients in Iron-Deficiency Anaemia? In what form is it given?"If patient cannot tolerate oral tablets (too big, uncomfortable etc.)<div><br></div><div>Typically given as iron dextran</div><div><br></div><div><font color=""#0000ff"">Note: Takes as long as iron in tablet form </font></div>"
Why is ascending colon cancer often asymptomatic (apart from Iron-Deficiency Anaemia)?Ascending colon (left side) lumen has very wide lumen (compared to descending colon), so less likely to have obstructions etc. 
Why is the ascending colon wider than the descending colon?Descending colon has thicker muscular walls to move the more solid stools (as more water has been absorbed)
How should iron tablets be taken?On empty stomach- 30 mins before meal, or 2hrs after<div><br></div><div>(Having with meal can reduce absorption by 60%)</div>
What is<b> intestinal failure</b>? Reduced gut function below minimum necessary for absorption of macronutrients and/or water + electrolytes, such that IV supplementation is required(describes what?)
Reduced gut function below minimum necessary for absorption of macronutrients and/or water + electrolytes, such that IV supplementation is required(describes what?)What is<b> intestinal failure</b>? 
What are causes of intestinal failure?- Anatomical reduction of gut length<div>- Neuromuscular diseases involving the GI tract (dysmotility)</div><div>- Congenital disease involving the intestinal epithelium</div>
What are the different types of intestinal failure?Type I: Acute, self-limiting<div>Type II: Prolonged acute, metabolically unstable patients. IV supplementation over weeks/months</div><div>Type III: Chronic, metabolically stable. IV supplementation over months/years</div>
How should Type 1 Intestinal failure be treated?Type I only acute- supportive therapy until intestinal function returns:<div><br></div><div>- Short-term parenteral fluid + nutrition</div><div>- Recovery techniques: promote early mobilisation + early introduction of oral nutrition</div>
How long is the small intestines usually?4-6m
Where are the fat-soluble vitamins absorbed from?Terminal ileum 
What does the colon typically absorb?Water 
Why are patients with IBD particularly at risk of VTEs?Systemic inflammation increases chances of thrombosis formation
Aside from colorectal cancer, what other cancers does HNPCC predispose to?"<div><font color=""#0000ff"">Females:</font></div>- Endometrial cancer <div><font color=""#0000ff"">Males:</font><br>- Pancreatic cancer</div>"
What are the three types of colon cancer?- Sporadic (95%)<div>- Hereditary Non-polyposis colorectal carcinoma (HNPCC, 5%)</div><div>- Familial adenomatous polyposis (FAP, <1%)</div>
What is the most common cause of inherited colon cancer?Lynch syndrome- HNPCC
What are the most common genes involved in Hereditary Non-polyposing Colorectal Carcinoma?- MSH2 (60%)<div>- MLH1 (30%)</div>
What causes familial adenomatous polyposis?Mutation in TSG called Adenomatous Polyposis Coli Gene (APC), on chromosome 5
In the acute management of UC, if patient is not responding to steroids, what could you try?- Cyclosporin<div>- Infliximab</div><div><br></div><div>(azathioprine takes 6-10 weeks to respond)</div>
Aside from colorectal cancers, patients with FAP are at risk of what?"- Duodenal tumours<div><br></div><div>(in Gardner's syndrome, osteomas of skull + mandible, thyroid carcinoma may also occur)</div>"
If a patient has the gene to cause Familial Adenomatous Polyposis, how should they be managed?Total colectomy, with ileo-anal pouch formation 
"What is <b>Gardner's syndrome?</b>"Variant of FAP with:<div>- Osteomas of skull & mandible</div><div>- Retinal pigmentation</div><div>- Thyroid carcinoma</div><div>- Epidermoid cysts</div><div>On top of usual colorectal polyps + duodenal tumour risk</div>
What cohort of Ulcerative Colitis patients are particularly at risk of developing colorectal cancer?Patients who also have Primary Sclerosing Cholangitis
What is associated with ulcerative colitis?- Ankylosing spondylitis<div>- Anterior uveitis</div><div>- Primary Sclerosing cholangitis</div>
A patient with a biliary colic pain may have a pain which develops into a constant nature. What might this be?Biliary colic --> <b>acute cholecystitis</b>
What is the typical pain felt in renal colic?"Colicky pain which radiates from 'loin to groin' "
If a patient is hypovolaemic, what should they be given?Crystalloids IV- 500mL bolus
How can the cause of ascites be determined?Measuring the SAAG- Serum ascites albumin gradient<div><b><br></b></div><div><b>If SAAG> 11g/L:</b> suggests low albumin/protein in ascites- <b>transudate</b></div><div><br></div><div><b>If SAAG<11g/L:</b> Suggests high albumin/protein in ascites- <b>exudate</b></div>
How is the SAAG calculated?Serum-albumin ascities gradient/gap:<div><br></div><div>Serum Albumin- Albumin level of ascitic fluid </div>
What are the physiological processes underlying <b>ascites</b> in liver cirrhosis?Liver <b>cirrhosis</b> causes release of <b>Nitrous Oxides</b> → Splanchnic arterial <b>vasodilation</b><div><br></div><div><b>Pooling of blood </b>in splanchnic circulation → effective <b>hypovolaemia</b></div><div><br></div><div>Effective hypovolaemia activates:</div><div>- <b>Baroreceptor reflex</b>- SNS activation + extra-splanchnic vasoconstriction</div><div>- ↑<b>RAAS</b></div><div><br></div><div>Which leads to <b>Na<sup>+</sup> retention + water retention </b>→ 3rd pool spacing of water- <b>ascites</b></div>
Why might you see hyponatremia in late-stage ascites?Retain higher amount of water than Na<sup>+</sup> → Dilution of Na<sup>+</sup> ions
In a primary presentation of ascites, what should the ascitic fluid be sent off for?"- Serum-Albumin Ascitic Gap (SAAG)<br><div>- PMN count<br></div><div>- WCC count </div><div>- Cytology (to check for malignancy)'</div>"
In the case of spontaneous bacterial peritonitis, what test should be done at 48hrs?Repeat ascites for PMN and WCC to see if has responded to therapy
What should be given to patients with ascites undergoing paracentesis?Human albumin solution- for every 2L drained- helps maintain oncotic pressure of plasma 
What are contraindications of using a TIPS?<div>- Clinical encephalopathy or abnormal EEG</div><div>- Patients at risk of heart failure (TIPS ↑shunting into systemic circulation ↑ preload which could predispose RHF)</div><div>- Patients with high bilirubin/INR levels (will worsen these, as you are diverting blood away from liver)</div>
Are cachexic or obese patients higher at risk of hepatic encephalopathy?Cachexic:<div><br></div><div>- Muscles can also breakdown ammonia. </div><div>- Patients with decreased muscle mass will have ↓capacity to metabolise ammonia → increased risk of developing encephalopathy</div>
What should patients with ascites be screened for before considering a TIPS?- EEG: assess for clinical encephalopathy<div>- Bilirubin + INR levels: will be worsened by TIPS</div><div>- ECHO/ECG to assess heart </div>
What causes secondary bacterial peritonitis?Perforation of bowel contents into ascitic fluid
Why are patients with chronic alcoholic liver disease expected to be abstinent before a liver transplant?- If abstinent and liver still has capacity to regenerate, expected to recover within 3 months.<div>- Reduces risk patients resume drinking after transplantation </div><div><br></div><div><b>Note no fixed period of abstinence required- patient selection more important- adequate cardiac output essential to preserve a healthy liver</b></div>
"Why does Ulcerative Colitis present with less weight loss than Crohn's?"In UC- most of the absorption will be completed by small bowels anyway 
"When should budenoside be used in Crohn's?"Not as effective as IV hydrocortisone, so only used in those who cannot tolerate glucocorticoids
"What is seen here?<div><img src=""xrb221.jpg""><br></div>"Ulcerative colitis with toxic megacolon
What is toxic megacolon?<div>Widening of the large intestine due to thinning of bowel muscle wall</div><div><br></div><div>Often caused by UC, but can be caused by c.diff</div>
What is usually given as first and second line therapy in hepatic encephalopathy?"<b><font color=""#0000ff"">1st line:</font> Lactulose</b>: acidifies colonic lumen inhibiting ammonia-generating bacteria, and reduces intestinal ammonia load through its action as a cathartic <div><b><font color=""#0000ff"">2nd line:</font> Rifaximin (or neomycin if this fails): </b>Non-systemic antibiotic, kills ammonia-genic bacteria</div>"
What are the most consistent symptoms of <b>irritable bowel syndrome</b>?- Abdominal pain<div>- Bloating</div><div>- Change in bowel habit (either diarrhoea or constipation)</div><div><br></div><div>Unlikely to present with any abnormal blood tests</div><div><br></div><div>(describes what?)</div>
- Abdominal pain<div>- Bloating</div><div>- Change in bowel habit (either diarrhoea or constipation)</div><div><br></div><div>Unlikely to present with any abnormal blood tests</div><div><br></div><div>(describes what?)</div>What are the most consistent symptoms of <b>irritable bowel syndrome</b>?
What is the classical presentation of diverticulitis?- Left lower quadrant pain<div>- Diarrhoea</div><div>- Fever </div>
What causes <b>overflow diarrhoea?</b>Constipated poo is unable to be pushed out, so bowel begins to leak out watery stools around the poo, causing diarrhoea (describes what type?)
Constipated poo is unable to be pushed out, so bowel begins to leak out watery stools around the poo, causing diarrhoea (describes what type?)What causes <b>overflow diarrhoea?</b>
How might someone suffering from overflow diarrhoea present?History of alternating diarrhoea and constipation <div><br></div><div>(Can cause faecal incontinence in the elderly)</div>
What factors indicate severe clostridium difficile infection?<div><span class=cloze>[...]</span><div>Shock</div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div>What factors indicate severe clostridium difficile infection?<div><span class=cloze> ITU admission</span><div>Shock</div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div><br> What factors indicate severe clostridium difficile infection?<div> ITU admission<div><span class=cloze>[...]</span></div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div>What factors indicate severe clostridium difficile infection?<div> ITU admission<div><span class=cloze>Shock</span></div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div><br> What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div><span class=cloze>[...]</span></div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div>What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div><span class=cloze>WCC >15</span></div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div><br> What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div>WCC >15</div><div><span class=cloze>[...]</span><br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div>What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div>WCC >15</div><div><span class=cloze>Acutely rising blood creatinine (>50% increase above baseline)</span><br>Temperature >38.5°</div><div>Evidence of severe colitis</div></div><br> What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br><span class=cloze>[...]</span></div><div>Evidence of severe colitis</div></div>What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br><span class=cloze>Temperature >38.5°</span></div><div>Evidence of severe colitis</div></div><br> What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div><span class=cloze>[...]</span></div></div>What factors indicate severe clostridium difficile infection?<div> ITU admission<div>Shock</div><div>WCC >15</div><div>Acutely rising blood creatinine (>50% increase above baseline)<br>Temperature >38.5°</div><div><span class=cloze>Evidence of severe colitis</span></div></div><br> How should <i>Clostridium difficile </i>infection be treated?"<div><b>First discontinue casuative agent + provide supportive care (fluids etc.) </b></div><div><br></div>Depends on severity:<div><br></div><div><font color=""#0000ff"">Usually</font>: Metronidazole (400mg/8h PO) for 14 days</div><div><br></div><div><font color=""#0000ff"">If severe infection, or treatment resistant</font>: Vancomycin (125mg/6h PO) (+/- metronidazole)</div>"
What is the most common causative organism causing Spontaneous Bacterial Peritonitis?E. coli
How is spontaneous bacterial peritonitis typically treated?IV Cephalosporin (e.g. Cefotaxime)<div><br></div><div>Antibiotic prophylaxis post treatment if fluid protein <15g/L (usually ciprofloxacin, norflaxacin)</div>
When should antibiotic prophylaxis be given to patients with cirrhosis?- Patients w/ Hx of SBP<div>- Patients with fluid protein <15g/L <b>and</b> Child-Pugh at least 9 or hepatorenal syndrome </div>
What is <b>gastritis?</b>Inflammation of gastric mucosa (describes what?)
Inflammation of gastric mucosa (describes what?)What is <b>gastritis?</b>
How can gastritis be classified?"<font color=""#0000ff"">Erosive/non-erosive</font>: Based on severity of mucosal injury<div><font color=""#0000ff"">Acute/chronic</font>: Based on inflammatory cell type </div>"
Where is gastric acid secreted in the stomach?Proximal 2/3 of stomach
What typically stimulates gastrin secretion?"Food: thought/smell or taste of food causes <font color=""#0000ff"">vagal stimulation of gastrin-secreting G cells</font>, located in antrum of stomach"
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9d2f3e663ad54c0fa0f7e40e255c1c25-ao-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmpdgb4_k37.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""9d2f3e663ad54c0fa0f7e40e255c1c25-ao-1-A.svg"" /></div> <div id=""io-original""><img src=""tmpdgb4_k37.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
At what level is the superior opening of the stomach?T11
At what level is the py<b>l</b>oric sphincter?L1
What arteries supply the greater curvature of the stomach?"- <b>Short gastric</b> arteries (arise from the splenic artery)<div>- Right & Left<b> gastro-ometnal</b> arteries</div><div><br></div><div><img src=""Blood-Supply-to-the-Stomach-Arteries-1024x495.jpg""><br></div>"
What supplies the <b>lesser</b> curvature of the stomach?- Left<b> gastric</b> artery (arises directly from coeliac trunk)<div>- Right <b>gastric</b> artery (branch of the common hepatic artery)</div>
Where does the right<b> gastro-omental</b> artery arise from?Terminal branch of the <b>gastroduodenal</b> artery (which arises from the <b>common hepatic </b>artery)
Where does the <b>l</b>eft <b>gastro-omental</b> artery arise from?Sp<b>l</b>enic artery (which arises from the coeliac trunk)
Describe the venous drainage of the stomach?Veins run parallel to the arteries:<div><br></div><div>- Right and Left <b>gastric veins</b> drain into <b>hepatic portal vein</b></div><div>- <b>Short gastric vein,</b> left & right<b> gastro-omental veins</b> drain into <b>superior mesenteric vein</b></div>
What is the function of the pyloric sphincter?Controls <b>exist of chyme </b>from the stomach into first part of duodenum
What are the omenta of the stomach?"Two layers of <b>peritoneum</b> (so 4 membrane layers) which attach to the stomach. <div><img src=""Greater-and-Lesser-Sacs-Greater-and-Lesser-Omenta-and-the-Stomach.jpg""><br></div>"
What does the lesser omentum join?Joins <b>stomach + duodenum</b> to the <b>liver</b>
How is the abdominal cavity divided into the greater and lesser sac?"Greater and lesser omenta divide into two, with <b>stomach</b> lying <b>anterior to the lesser</b> <b>sac.</b> <div><img src=""Greater-and-Lesser-Sacs-Greater-and-Lesser-Omenta-and-the-Stomach.jpg""><br></div><div><br></div>"
How do the greater and lesser sac of the abdomen communicate?<b>Epiploic foramen</b>- hole in the lesser omentum
What provides the innervation to the stomach?"<b>Autonomic nervous system:</b><div><br></div><div><font color=""#0000ff"">Parasympathetic</font>: Anterior + posterior<b> vagal trunks</b>, from vagus nerve</div><div><font color=""#0000ff"">Sympathetic</font>: From <b>T6-T9 </b>spinal cord segments, passing to <b>coeliac plexus</b> via <b>greater splanchnic</b> nerve </div>"
What is the result of vagus action on the stomach?- <b>Increased</b> <b>peristalsis</b><div>- <b>Reduecd somatostain </b>secretion</div><div>- <b>Increased acid secretion</b></div>
What are symptoms of gastritis?- Epigastric <b>pain</b><div>- <b>Vomiting</b></div>
What are risk factors of gastritis?"<div>- <i><b>H. pylori</b></i></div>- Alcohol<div>- <b>NSAIDs</b></div><div><br></div><div>- Reflux/<b>hiatus hernia</b></div><div>- Atrophic gastritis</div><div>- <b>Granulomas </b>(crohn's, sarcoidosis)<br>- CMV</div><div><br></div><div>- <b>Zollinger-Ellison Syndrome </b>(gastrin producing neuroendocrine tumour)</div><div>- Ménétrier's disease (big gastric folds & excessive mucous production)</div>"
What is <b>atrophic gastritis</b>?Chronic inflammation of gastric mucosa, leading to<b> loss of gastric glandular cells</b> and replacement by intestinal + fibrous tissues
What is <b>Zollinger-Ellison syndrome</b>?<b>Gastrinomas</b> form in duodenum or pancreas, which secrete gastrin, causing excessive acid production in stomach (describes what?)
<b>Gastrinomas</b> form in duodenum or pancreas, which secrete gastrin, causing excessive acid production in stomach (describes what?)What is <b>Zollinger-Ellison syndrome</b>?
Where are gastrinomas typically found in Zollinger-Ellison syndrome?Typically found in pancreas (though also found in stomach and duodenum)
20% of Zollinger-Ellison syndrome are associated with <span class=cloze>[...]</span>20% of Zollinger-Ellison syndrome are associated with <span class=cloze>Multiple Endocrine Neoplasia, Type 1</span><br> What are typical symptoms of Zollinger-Ellison syndrome?- Abdominal pain + dyspepsia (from ulcer)<div>- Chronic diarrhoea/steatorrhea (inactivation of pancreatic enzymes + damage to intestinal mucosa)</div>
What investigations could confirm Zollinger-Ellison syndrome?"- <font color=""#0000ff"">↑ Fasting serum gastrin levels</font> (rule out hypochlohydria- reduced acid production e.g. in atrophic gastritis, as also has ↑serum gastrin- <b>pH should be <2)</b><div>- Secretin stimulation test </div><div>- Localise and stage adenoma w/ s<font color=""#0000ff"">omatostatin receptor scintigraphy, endoscopic ultrasound + CT </font></div>"
What is <b>hypochlorhydria?</b>Reduced acid production e.g. in chronic atrophic gastritis<div><br></div><div>(will present with increased serum gastrin- as body attempts to compensate)</div>
How can Zollinger-Ellison be managed?"<div><font color=""#0000ff"">If localised disease:</font> </div><div>- High-dose PPI: e.g. 60mg/day omeprazole (adjust and monitor with measurements of intragastric pH)</div><div>- Surgery (as gastrinomas have malignant potential) w/ lymph node clearance if tumour is >2cm</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If metastatic disease:</font></div><div>- Somatastatin analogue + PPI if predominantly hepatic tumours</div><div>- PPI + Fluorouracil, doxorubicin, streptozocin + therpay for extrahepatic tumours</div>"
How should gastritis be managed?"<font color=""#0000ff"">Lifestyle</font>: ↓Alcohol & Tobacco<div><font color=""#0000ff"">H. pylori eradication</font></div><div><font color=""#0000ff"">Drugs</font>: PPIs, or H<sub>2</sub> antagonists</div><div>Stop drugs, if drug-induced ulcers</div>"
"What is the action of <font color=""#0000ff"">misoprostol</font>?"Prostaglandin analogue- has antisecretory + protective proeprties which promotes healing of gastric + duodenal  ulcers <div><br></div><div>[note potent uterine stimulant, often used in termination of pregnancies] </div><div><br></div><div>(describes what?)</div>
Prostaglandin analogue- has antisecretory + protective proeprties which promotes healing of gastric + duodenal  ulcers <div><br></div><div>[note potent uterine stimulant, often used in termination of pregnancies] </div><div><br></div><div>(describes what?)</div>"What is the action of <font color=""#0000ff"">misoprostol</font>?"
What is functional dyspepsia?<div>- Case where OGD did not reveal cause of dyspepsia</div>- Post-infectious onset of dyspepsia + psychosocial factors 
How should functional dyspepsia be managed?- H. pylori eradication (if +ve result)<div>- PPIs & Pyschotehrapy</div><div>- Low dose amitriptyline may help</div>
What disease is associated with gastroparesis?Diabetes (nearly half of patients, both T1DM and T2DM) have gastroparesis, which can cause diabetic dyspepsia
What are red flag conditions to consider when assessing a patient with epigastric pain suggestive of dyspepsia?"- <font color=""#0000ff"">Coronary Artery Disease</font> (heartburn can be difficult to differentiate from chest pain): Consider ECG, serum troponin etc. <div>- <font color=""#0000ff"">Upper GI malignancy:</font> Typically in individuals >60y/o. Carry out endoscopy (consider barium contrast + abdo CT + abdo USS)</div>"
<span class=cloze>[...]</span> = Osler-Weber-Rendu Syndrome<span class=cloze>Hereditary Haemorrhagic Telangiectasia</span> = Osler-Weber-Rendu Syndrome<br> Hereditary Haemorrhagic Telangiectasia = <span class=cloze>[...]</span>Hereditary Haemorrhagic Telangiectasia = <span class=cloze>Osler-Weber-Rendu Syndrome</span><br> What is <b>Osler-Weber-Rendu syndrome?</b>Rare autosomal dominant condition consisting of:<div>- Telangiectasia of skin & mucous membranes</div><div>- Arteriovenous malformations (pulmonary, hepatic and cerebral)</div>
"What is <b>Dieulafoy's lesion?</b>"Large tortuous arteriole (usually in stomach wall) which erodes and bleeds, causing upper GI bleeding (describes what?)
Large tortuous arteriole (usually in stomach wall) which erodes and bleeds, causing upper GI bleeding (describes what?)"What is <b>Dieulafoy's lesion?</b>"
"What causes dieulafoy's lesions?"Developmental malformations leading to arteriole erosion (as opposed to degenerative changes)
What is <b>haemobilia?</b>Bleeding into the biliary tree (describes what?)
Bleeding into the biliary tree (describes what?)What is <b>haemobilia?</b>
What causes haemobilia?Fistula between splanchnic vessel and biliary system
How does haemobilia present?"Quincke's triad:<div><br></div><div>- Upper abdominal pain</div><div>- Upper GI haemorrhage</div><div>- Jaundice</div><div><br></div><div>(Classical, but only presents in 22% of cases)</div>"
A patient who recently had an abdominal aorta repair reports malaena. What has likely happened?Aorto-enteric fistula formed: connection between aorta + GI tract --> upper GI bleeding
What is the most common congenital abnormality of the small bowel?"Meckel's diverticulum- present in 1-3% of the population<div><br></div><div><img src=""ea533dc4212314b30b20fe9bbbfe3171.png""><br></div>"
"How does a patient typically present with Meckel's diverticulum?"Majority remain asymptomatic but those who are symptomatic present with GI bleeding, (typically in those younger than 2).<div><br></div><div>- Often clinically undistinguishable from appendicits</div>
"What is the gold standard for diagnosis of Meckel's diverticulum?"Technetium-99m pertechnetate scan (adults sometimes given H<sub>2</sub> antagonists to enhance scan):<div><br></div><div>- Pertechnetate preferntially taken up by mucus-secreting cells of ectopic gastric tissue in diverticulum </div><div><br></div><div><br></div>
"What is seen here, taken from histology of the greater curvature of the stomach?<div><img src=""3efe3ZTARJmQ1aoWghW07YnEDBbVCTWz16l1-PuimdQ5Jod3UiUVcU0rl1JFT6r1MczEfuaSkJezh2MPHH9Xu6PCGah--k1Os_CeY3dMNeMkF8egRuPPqnpbyOAg=w500.jpg""><br></div>"<b>Gastric cancer</b>: Signet ring cells, where nucleus pushed to periphery of the cell
Gastric ulcers found on the <span class=cloze>[...]</span> are more commonly benign, whereas ulcers <span class=cloze>[...]</span> are more commonly malignantGastric ulcers found on the <span class=cloze>lesser curvature</span> are more commonly benign, whereas ulcers <span class=cloze>elsewhere</span> are more commonly malignant<br> Gastric ulcers found on the lesser curvature are more commonly <span class=cloze>[...]</span>, whereas ulcers elsewhere are more commonly <span class=cloze>[...]</span>Gastric ulcers found on the lesser curvature are more commonly <span class=cloze>benign</span>, whereas ulcers elsewhere are more commonly <span class=cloze>malignant</span><br> What type of malignancy can <i>H. pylori </i>cause?MALT lymphoma, which can be cured by treating H. pylori infection directly
What other diseases is coeliac disease associated with?- Type 1 Diabetes mellitus<div>- Vitiligo</div><div>- Other autoimmune conditions e.g. autoimmune thyroiditis, dermatitis herpetiformis</div>
"What is seen here?<div><img src=""499-dermatitis-herpetiformis-slide-10-spriinger-high.jpg""><br></div>"Dermatitis herpetiformis (often looks like herpes simplex infection) and is associated with coeliac disease
"What is the typical presentation of coeliac's disease?"- Diarrhoea<div>- Abdominal pain</div><div>- Steattorhoea</div>
"At what ages to patients with Coeliac's disease typically present?"- Young children<div>- 50-60s</div>
"What antibodies are positive in Coeliac's Disease?""- Anti-gliadin<div><font color=""#0000ff"">- Anti-transglutaminase</font></div><div>- Anti-endomyseal</div>"
"If you are doing antibody testing to investigate Coeliac's Disease, what else should you test for?"IgA: IgA deficiency (a common asymptomatic immunodeficiency), will cause false-negative for these antibodies 
"What is the gold standard test to diagnose <b>Coeliac's disease</b>?"- Small bowel biopsy: shows villous atrophy and crypt hyperplasia <div><br></div><div>(describes a finding suggesting what disease?)</div>
- Small bowel biopsy: shows villous atrophy and crypt hyperplasia <div><br></div><div>(describes a finding suggesting what disease?)</div>"What is the gold standard test to diagnose <b>Coeliac's disease</b>?"
"What cancers is Coeliac's disease linked with?""- Non-Hodgkin's lymphoma (enteropathy-associated T-cell lymphoma)"
What patient groups should be given a 2 week wait referral for colorectal cancer?<div>- Positive Faecal Immunochemical Test </div>If >40: With unexplained weight loss + abdominal pain<div>If >50: Unexplained rectal bleeding</div><div>If >60: Iron-deficiency anaemia, or changes in bowel habit</div>
How should cancers in the rectum be surgicall managed?"<font color=""#0000ff"">If in sigmoid colon/proximal 2/3 of rectum:</font> Anterior resection<div><font color=""#0000ff"">If in lower 1/3 of rectum</font>: Removal of sphincter compelx with Abdominoperineal resection</div>"
When is a panprotocolectomy used?- Severe UC<br>- Polyposis syndromes e.g. FAP<div><br></div><div>Only used when risk of leaving colon in situ outweighs risk of operation + morbidity created with permanent ileostomy</div>
What is the difference between a panprotocolectomy and a subtotal colectomy?Subtotal colectomy leaves rectum in situ and aims to join small bowel to rectal stump, so no stoma is required 
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Onset of ulcerative colitis may follow <span class=cloze>[...]</span>Onset of ulcerative colitis may follow <span class=cloze>smoking cessation</span><br> What is <b>diverticular disease</b>?Sac-like protrusions of mucosa through muscular colonic wall, cause intermittent lower abdominal pain +/- bleeding in absence of inflammation or infection (describes what?)
Sac-like protrusions of mucosa through muscular colonic wall, cause intermittent lower abdominal pain +/- bleeding in absence of inflammation or infection (describes what?)What is <b>diverticular disease</b>?
The majority of patients with diverticular disease are <span class=cloze>[...]</span> years oldThe majority of patients with diverticular disease are <span class=cloze>>50</span> years old<br> Where is typically affected in diverticular disease?Caucasian populations: Left side of colon<div>South + South-east asian populations: Right side of colon</div>
What is diverticulitis?When diverticula become inflamed and infected
When is surgery required in divertiulitis?- Diffuse peritonitis/perforation<div>- Elective surgery in recurrent cases</div>
What is the surgical management of diverticulitis?Colectomy
What are the most common causative organisms for infective endocarditis?1. Staphylococcus aureus<div>2. Viridans group of Streptococcus </div><div>3. Streptococcus bovis</div><div>4. Enteroccocci and HACEK organisms</div><div>5. Libman-Sacks syndrome (SLE)</div>
Endocarditis caused by <span class=cloze>[...]</span> is associated with poor dentitionEndocarditis caused by <span class=cloze>Viridans group streptococci</span> is associated with poor dentition<br> Streptococcus viridans asymptomatic commensal usually found in mouth 
Endocarditis caused by Viridans group streptococci is associated with <span class=cloze>[...]</span>Endocarditis caused by Viridans group streptococci is associated with <span class=cloze>poor dentition</span><br> Streptococcus viridans asymptomatic commensal usually found in mouth 
Infective Endocarditis caused by <span class=cloze>[...]</span> is usually associated with IVDUsInfective Endocarditis caused by <span class=cloze>staphylococcus aureus</span> is usually associated with IVDUs<br> As port of entry via broken skin (though is also the most common cause of infective endocarditis)
Infective Endocarditis caused by staphylococcus aureus is usually associated with <span class=cloze>[...]</span>Infective Endocarditis caused by staphylococcus aureus is usually associated with <span class=cloze>IVDUs</span><br> As port of entry via broken skin (though is also the most common cause of infective endocarditis)
Infective Endocarditis caused by <span class=cloze>[...]</span> is usually associated with breaches in the gut- e.g. malignancyInfective Endocarditis caused by <span class=cloze>Streptococcus bovis</span> is usually associated with breaches in the gut- e.g. malignancy<br> Infective Endocarditis caused by Streptococcus bovis is usually associated with <span class=cloze>[...]</span>Infective Endocarditis caused by Streptococcus bovis is usually associated with <span class=cloze>breaches in the gut- e.g. malignancy</span><br> What type of bacteria is <i>Streptococcus bovis</i>Beta haemolytic- lancefield group D streptococcus
How are staphylococci categorised?- Coagulase positive (e.g. staph aureus)<div>- Coagulase negative (Commensal bacteria)</div>
How are streptococci categorised?- Alpha, beta, or gamma haemolytic<div>- Beta further split into Lancefield groups A-E</div>
<span class=cloze>[Bacteria]</span> are most commonly associated with neonatal infections<span class=cloze>Lancefield Group B Streptococci</span> are most commonly associated with neonatal infections<br> B is for Babies
Lancefield Group B Streptococci are most commonly associated with <span class=cloze>[...]</span>Lancefield Group B Streptococci are most commonly associated with <span class=cloze>neonatal infections</span><br> B is for Babies
Onset of <span class=cloze>[...]</span> may follow smoking cessationOnset of <span class=cloze>ulcerative colitis</span> may follow smoking cessation<br> How is acute diarrhoea defined vs chronic?<2 weeks<div><br></div><div>(Chronic is >4 weeks)</div>
What is the most typical cause of acute diarrhoea?Gastroenteritis
What are infectious causes of bloody diarrhoea?- Campylobacter<div>- Shigella</div><div>- Salmonella</div><div>- E. coli</div><div>- Amoebiasis</div>
What are causes of bloody diarrhoea?"- <font color=""#0000ff"">Infectious</font>: Campylobacter, shigella, salmonella, e. coli, amoebiasis<div>- <font color=""#0000ff"">IBD</font>: UC, Crohn's (though more often UC)</div><div>- Coloretal cancer, colonic polyps</div><div>- Pseudomembranous colitis</div><div>- Ischaemic colitis</div>"
What is <b>pseudomembranous colitis</b>?Infection of colon caused by overgrowth of <i>C. difficile </i>(describes what?)
Infection of colon caused by overgrowth of <i>C. difficile </i>(describes what?)What is <b>pseudomembranous colitis</b>?
What typically causes pseudomembranous colitis?Patients whose normal bowel flora has been disrupted by recent antibiotic (usually broad-spectrum) use. 
What patients are particularly at risk of <i>Clostridium difficile-</i> associated disease?- Older pts<div>- Recent Hx of Abx use</div><div>- Comorbid conditions (e.g. IBD, CKD, HIV infection)</div><div>- Prolonged hospitalisation/residence in nursing home</div><div>- Hx of taking acid-suppressing drugs</div><div>- Hx of transplants</div>
What are the most common antibiotics which typically pre-dispose to pseudomembranous colitis?- Ampicillin<div>- Cephalosporins</div><div>- Clindamycin</div><div>- Carbapenems</div><div>- Fluoroquinolones (NB. same as quinolones, only fluoroquinolones available in the UK)</div>
What disease can cause diarrhoea containing mucus?- IBS<div>- Ulcerative Colitis</div><div>- Colorectal Cancer</div><div>- Polyps</div><div><br></div>
What disease can cause frank pus to be found in the diarrhoea?- IBD<div>- Diverticulitis</div><div>- Fistula/abscess</div>
What typically causes explosive diarrhoea?- Cholera<div>- Giardia</div><div>- Yersinia</div><div>- Rotavirus</div>
What characterises steatorrhoea?- ↑Gas<div>- Offensive smell</div><div>- Floating, hard-to-flush stools </div>
What are signs of dehydration?- Dry mucous membranes <div>- ↓ Skin turgor</div><div>- Capillary refill >2s</div><div>- Shock </div>
How might blood tests be useful to investigate diarrhoea?"<font color=""#0000ff"" style="""">FBC</font><b>: </b>↓MCV/Fe deficiency- coeliac/colon cancer; ↑MCV if alcohol abuse or ↓B12 absorption- coeliac, Crohn's; ↑Eosinophils if parasites<div><font color=""#0000ff"">ESR/CRP:</font> ↑ in infection, IBD, cancer</div><div><font color=""#0000ff"">U&E</font>: ↓K<sup>+</sup> in severe diarrhoea & vomiting</div><div><font color=""#0000ff"">TFTs</font>: ↓TSH in thyrotoxicosis</div><div><font color=""#0000ff"">Coeliac serology</font></div>"
How can a stool sample be used to investigate the pancreas?<b>Measure faecal elastase</b>: if ↓ suggests pancreatic insufficiency (chronic pancreatitis or pancreatic cancer)
How can stool samples be useful in investigation of diarrhoea?- MC&S: Bacterial pathogens, Ova cysts, parasites<div>- Stool leukocytes<br><div>- CDT</div><div>- Viral PCR</div><div>- Faecal elastase</div></div>
What type of endoscopy should be used in an acutely unwell patient with diarrhoea?Limited flexible sigmoidoscopy w/ biopsies
Onset of diarrhoea that begin within <span class=cloze>[...]</span> contaminated food suggest Staph aureus or Bacillus cereusOnset of diarrhoea that begin within <span class=cloze>6 hours of ingesting</span> contaminated food suggest Staph aureus or Bacillus cereus<br> Pre-formed toxins 
Onset of diarrhoea that begin within 6 hours of ingesting contaminated food suggest <span class=cloze>[...]</span>Onset of diarrhoea that begin within 6 hours of ingesting contaminated food suggest <span class=cloze>Staph aureus or Bacillus cereus</span><br> Pre-formed toxins 
Diarrhoea due to <span class=cloze>[...]</span> tend to have more frequent stool passageDiarrhoea due to <span class=cloze>infectious causes</span> tend to have more frequent stool passage<br> Diarrhoea due to infectious causes tend to have <span class=cloze>[...]</span>Diarrhoea due to infectious causes tend to have <span class=cloze>more frequent stool passage</span><br> "What is seen here on colonoscopy?<div><img src=""ColitisssPseudoMembranousx4.jpg""><br></div>""<div>Yellow adherent plaques on inflamed non-ulcerated mucosa- <font color=""#0000ff"">Pseudomembrane</font></div><div><b><br></b></div><div><b>Clostridium difficile infection</b></div>"
When is stool culture carried out in patients with diarrhoea?- Immunocompromised pts<div>- Multiple comorbidities</div><div>- Severe inflammatory diarrhoea</div><div>- Pts with underlying IBD (to make distinction between flare + infection)</div><div>- Positive stool leukocyte </div><div>- Food handlers, who need negative stool cultures to return to work </div>
How should acute diarrhoea be managed?"<b>Treat underlying cause</b> and:<div>- <font color=""#0000ff""><b>Rehydration</b></font>: Oral better than IV, but if sustained diarrhoea/vomiting, IV fluids w/ electrolyte replacement may be necesssary</div><div>- <font color=""#0000ff"">Decrease stool frequency</font>: Codeine phosphate 30mg/8hrs PO; or loperamdie 2mg PO after each loose stool (max 16mg) [Avoid in colitis, as this may precipitate toxic megacolon]</div><div>-<font color=""#0000ff""> Avoid Abx</font>, unless cause is infective diarrhoea</div>"
What are the most common causes of diarrhoea?"<div><font color=""#0000ff"">Acute:</font></div>- Gastroenteritis<div>- Traveller's diarrhoea</div><div>- C. difficile</div><div><font color=""#0000ff"">Chronic: </font></div><div>- IBS</div><div>- Colorectal cancer</div><div>- IBD</div><div>- Coeliac</div>"
How is chronic diarrhoea defined?Presence of ≥3 loose stools per day for more than 4 weeks
What is <b>microscopic colitis?</b>Inflammation of the colon which causes persistent watery diarrhoea- appears normal on colonoscopy<div><br></div><div>(describes what?)</div>
Inflammation of the colon which causes persistent watery diarrhoea- appears normal on colonoscopy<div><br></div><div>(describes what?)</div>What is <b>microscopic colitis?</b>
How should micorscopic colitis be diagnosed?Biopsy- Necessary to examine under microscope as will appear normal on colonoscopy
What are non-GI causes of diarrhoea?"- Thyrotoxicosis<div>- Autonomic neuropathy</div><div>- Addison's disease</div><div>- Ischaemic colitis</div><div>- Tropical Sprue</div><div>- Gastrinoma</div><div>- Carcinoid</div><div>- Pellagra</div><div>- VIPoma</div><div>- Amylodisosis</div>"
What is <b>pellagra?</b>Disease caused by low levels of niacin (Vit B3), marked by:<div><br></div><div>- Dementia</div><div>- Diarrhoea</div><div>- Dermatitis</div><div><br></div><div>(describes what?)</div>
Disease caused by low levels of niacin (Vit B3), marked by:<div><br></div><div>- Dementia</div><div>- Diarrhoea</div><div>- Dermatitis</div><div><br></div><div>(describes what?)</div>What is <b>pellagra?</b>
What is a VIPoma?Vasoactive Intestinal Peptide(VIP)-secreting tumour: Non-beta pancreatic islet cell tumour 
How does a VIPoma present?- Watery diarrhoea<div>- Metabolic Acidosis</div><div>- Electrolyte disturbacne: ↓K<sup>+</sup> ↑Ca<sup>2+</sup> ↓Mg<sup>2+</sup> </div><div>- Achlorhydria </div>
What is <b>dysentery?</b>Type of gastroenteritis resulting in diarrhoea with blood (describes what?)
Type of gastroenteritis resulting in diarrhoea with blood (describes what?)What is <b>dysentery?</b>
What are signs of systemic illness in an infective diarrhoea?- Fever >39°C<div>- Dehydration</div><div>- Dysentery for >2 weeks</div>
What are signs of pseudomembranous colitis?- ↑ Temp<div>- Colic</div><div>- Diarrhoea </div><div>- Systemic upset: ↑↑CRP, ↑WCC, ↓Albumin + Colitis </div>
What percentage of adults have asymptomatic carriage of <i>C. diff</i>?2-5%- only problematic when gut ecology is disrupted, leading to rapid proliferation & haemodynamic instability
How should <b>pseudomembranous colitis</b> be diagnosed?- Rapid screening test (or <b>PCR</b>) for <b><i>C. diff</i> protein </b><div>- <b>ELISA </b>for <b><i>C. diff </i>toxins </b></div><div><br></div><div>- <b>AXR</b> to check for<b> toxic megacolon </b></div>
What percentage of patients w/ pseudomembranous colitis will have recurrent disease?25%- relatively comon 
What should be the management of patients with recurrent C. difficile infections?- Fidaxomicin (minimally absorbed oral antibiotic, associated with lower relapse rates)<br>- Faecal transplantation 
What is <b>tropical sprue</b>?Malabsorption disease commonly found in tropical regions, likely due to infectious aetiology (describes what?)
Malabsorption disease commonly found in tropical regions, likely due to infectious aetiology (describes what?)What is <b>tropical sprue</b>?
How does tropical sprue typically present?"<font color=""#0000ff"">Attack of:</font><div>- Acute diarrhoea</div><div>- Fever</div><div>- Malaise</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Patient then settles into chronic phase of: </font></div><div>- Diarrhoea</div><div>- Steatorrhoea</div><div>- Weight loss + Anorexia</div><div>- Malaise </div><div>- Nutritional deficiencies </div>"
"What is seen here, on endoscopy of duodenum?<div><img src=""637-4_default.jpg""><br></div>"<b>Tropical Sprue: </b>Scalloping, mosaic apperance + mucosal grooves
"What is seen here, on endoscopy of duodenum?<div><img src=""637-3_default.jpg""><br></div>"Normal duodenum
What are the changes to the villi in tropical sprue?"Villi become shortened, giving a stubbed pattern<div><img src=""637-5_default.jpg""><br></div>"
How should tropical sprue be managed?"<font color=""#0000ff"">1st line:</font><div>- Folic acid supplementation<br></div><div>- Antibiotics (tetracycline)</div><div>Plus </div><div>- Vitamin B12 supplementation</div>"
What are three aetiological categories of steatorrhoea?"<font color=""#0000ff"">Pancreatic insufficiency</font>: Insufficient lipase & colipase to allow normal lipid hydrolysis <div><font color=""#0000ff"">Bile salt deficiency</font>: Impaired production or secretion</div><div><font color=""#0000ff"">Malabsorption</font>: Small intestinal disease, surgery or medications</div>"
What are the most common causes of gastrointestinal malabsorption in the UK?"- Coeliac disease<div>- Chronic pancreatitis</div><div>- Crohn's disease</div>"
What changes to the small bowel can lead to GI malabsorption?"- Whipple's disease<div>- Radiation enteritis</div><div>- Tropical sprue</div><div>- Small bowel resection</div><div>- Brush border enzyme deficiencies (e.g. lactase insufficiency)</div><div>- Drugs (metformin, neomycin, alcohol)</div><div>- Amyloidosis  </div>"
"What is Whipple's Disease?"Disease featuring GI malabsorption, caused by Tropheryma Whipelii which can also produce systemic disease in defective cell-mediated immunity
"What demographic is affected most commonly by Whipple's disease?"Middle-aged white males 
"What arthralgia is produced by Whipple's disease?"Insidious chronic migratory seronegative arthropathy, affecting mainly peripheral joints
"How does Whipple's disease typically present?"- Insidious arthralgia (migratory, mainly peripheral joints)<div>- GI symptoms: Colicky abdominal pain, weight loss, steatorrhoea → malabsorption</div><div><br></div><div>Can then develop systemic symptoms: chronic cough, fever, sweats, skin hyperpigmentation </div><div><br></div><div>May also develop CNS features (reversible dementia, ophthalmoplegia, facial myoclonus) + hypothalamic syndrome </div>
"How is Whipple's disease diagnosed?"- Jejunal biopsy shows stunted villi. <div>- Deposition of macrophages in lamina propria, containing granules positive for Periodic Acid-Schiff</div><div>- MRI may show CNS involvement </div>
"How is Whipple's disease treated?"ABx which cross BBB:<div>- IV Ceftriaxone (or penicillin + streptomycin) for 2 weeks, then </div><div>- Oral co-trimoxazole for 1 year </div><div><br></div><div>Usually produces rapid improvement in symptoms</div>
What is small intestine bacterial overgrowth?- Excessive bacterial growth in small intestine (unlike colon, small bowel usually has fewer than 10,000 microorganisms per mL)
What are symptoms of small intestinal bacterial overgrowth?- Nausea+ vomiting<div>- Bloating</div><div>- Diarrhoea</div><div>- Malnutrition and malabsorption</div><div>- Weight loss</div>
How is small bacterial overgrowth diagnosed?"<font color=""#0000ff"">Gold Standard</font>: Jejunal aspirate, + verify more than 10<sup>5</sup> bacteria per mL<div><font color=""#0000ff"">Hydrogen breath test</font>: Fast for 12hrs, then drink substrate of glucose/lactulose + measure expired hydrogen + methane concentrations</div>"
Biopsies of small bowel in <span class=cloze>[...]</span> can mimic coeliac disease, with partial villlous atrophyBiopsies of small bowel in <span class=cloze>bacterial overgrowth</span> can mimic coeliac disease, with partial villlous atrophy<br> What is associated with Small Intestinal Bacterial Overgrowth?- IBS (80% of patients with IBS have +ve hydrogen breath test)<div>- Fibromylagia </div><div>- Rosacea</div>
What are risk factors for small intestinal bacterial overgrowth?- Dysmotility (e.g. scleroderma)<div>- Anatomical disturbances in bowel (fistulae, diverticula, blind loops post surgery)</div><div>- Resection of ileo-coecal valve</div><div>- Gastroenteritis-induced alterations to small intestines</div><div>- T1DM</div><div>- Drugs e.g. PPIs</div>
How should small bowel bacterial overgrowth be treated?- Metronidazole 400mg/8h PO<div>- Elemental diet</div><div><br></div><div>- Prokinetic drugs to prevent recurrence if dysmotility is suspected cause</div>
What infections can cause gastrointestinal malabsorption?- Giardiasis<div>- Cryptosporidium</div><div>- Isospora belli</div><div>- Cyclospora cayteanesis</div><div>- Microsporidia<br><div>- Diphyllobothriasis (B<sub>12</sub> malabsorption)</div><div>- Strongyloidiasis </div></div>
What are signs of deficiency in the case of GI malabsorption?- Anaemias (↓Fe, Folate, B12)<div>- Bleeding disorders (↓Vit K)</div><div>- Oedema (↓Protein)</div><div>- Metabolic bone disease (↓vit D)</div><div>- Neurological features (e.g. neuropathy)</div>
How can steatorrhoea be confirmed?Sudan staining of stool for fat globules 
What is a positive finding from hydrogen breath tests?Early ↑exhaled hydrogen  
Patients from which countries (or travelling to) would make you suspect tropical sprue?- Far & Middle <b>East</b><div><b>- Carribean </b></div>
How does bacterial overgrowth cause GI malabsorption?- Results in deconjugation & dehydroxylation of bile salts → limits absorption of fats <div>- Unabsorbed bile salts stimulate water secretion in colon → diarrhoea</div>
How are fats digested and absorbed?- Pancreatic enzymes (lipase & colipase) break down long chain triglycerides → fatty acids & monoglycerides. <div>- These combine with bile acids & phospholipids to form miscelles, which are absorbed by <b>jejunal enterocytes</b></div><div>- Fatty acids then resynthesised into chylomicrons, transported by <b>lymphatic system</b>. </div>
How are carbohydrates digested and absorbed?Pancreatic enzyme amylase, and Brush Border enzymes on microvilli lyse carbohydrates & disacchardies into monosaccharides. 
What is responsible for distention and bloating in GI malabsorption?Unabsorbed carbohydrates are fermented by colonic bacteria into CO<sub>2</sub>, Methane, hydrogen and SCFAs. <div><br></div><div>Gases cause abdominal distention and floating (FAs, cause diarrhoea)</div>
How are proteins digested?"<font color=""#0000ff"">Gastric pepsin</font> initiates digestion of proteins in stomach & stimulates<font color=""#0000ff""> release of CCK,</font> which is critical in secretion of pancreatic enzymes<div><br></div><div><font color=""#0000ff"">Enterokinase </font>(a BBM enzyme), <font color=""#0000ff"">activates trypsinogen into trypsin</font>, which converts pancreatic proteases into active forms. </div><div><br></div><div>Active pancreatic proteases hydrolyse proteins into oligopeptides</div>"
How might Zollinger-Ellison cause GI malabsorption?Increases luminal acidity, which inhibits lipase and fat digestion
What are HLA associations with Coeliac disease?- HLA DQ2 (in 95%)<div>- Rest have DQ8</div>
At what ages does Coeliac disease typically present?- Childhood<div>- 50-60yrs</div>
How can diagnosis of coeliac disease be made?"-<b> Duodenal biopsy (From D2)</b>: Shortening of villi, increased intraepithelial cells + crypt hyperplasia. <font color=""#0000ff"">Not specific</font><div><b>- Serologic markers:</b> Anti-tTG (tissue-transglutamase) and anti-EMA (endomysial antibody). Both are IgAShould be done on a gluten-containing diet </div>"
What are complications of coeliac disease?- Increased risk of malignancy (lymphoma, gastric, oesophageal, colorectal)<div>- Dermatitis herpetiformis</div><div><b>From malabsorption:</b></div><div>- Anaemia<br></div><div>- Osteopenia/osteoporosis</div><div>- Hyposplenism </div><div>- Neuropathies</div>
"How is Coeliac's disease managed?"Treatment:<div>- Lifelong gluten-free diet</div><div><br></div><div>Repeat small-bowel biopsy after 3-6 months of gluten-free diet, to see if abnormalities persist (consider other diagnoses if so). </div><div><br></div><div>If refractory disease (i.e. in gluten withdrawal) corticosteroids may be required</div>
What is <b>Irritable Bowel Syndrome?</b>Mixed group of abdominal symptoms for which no organic cause can be found (describes what?)
Mixed group of abdominal symptoms for which no organic cause can be found (describes what?)What is <b>Irritable Bowel Syndrome?</b>
What are the different likely causes of Irritable Bowel Syndrome?- Intestinal mobility<div>- Enhanced visceral perception (brain-gut axis)<br>- Microbial dysbiosis</div>
What is the prevalence of IBS?10-20%, affecting females 2x more 
Why does enhanced visceral perception lead to IBS?- Hypersensitvity to normal amounts of intraluinal distention & heightened perception of pain in presence of normal quantities of intestinal gas 
When can a diagnosis of IBS be made?Recurrent abdominal pain/discmofort associated with at least 2 of:<div>- Relief by defecation</div><div>- Altered stool form</div><div>- Altered bowel frequency (constipation & diarrhoea may alterante)</div>
What is the nature of symptoms in IBS?Chronic (>6 months), and exacerbated by:<div> - Stress</div><div>- Menstruation</div><div>- Gastroenteritis (post-infectious IBS)</div>
In a patient with symptoms like IBS, when should you think about other diagnoses?- Age >60<div>- History <6 months</div><div>- Anorexia</div><div>- ↑ Weight</div><div>- Waking at night with pain/diarrhoea</div><div>- Mouth ulcers</div><div>- Abnormal CRP, ESR</div>
How can the diagnosis of IBS be made?"Rome criteria: Diagnosis of IBS is made when:<div><br><div>Pt has <b>abdominal pain</b> <font color=""#0000ff"">relieved by defecation</font> or <font color=""#0000ff"">associated with altered bowel frequency</font>, and<b> 2 of the following</b>:</div><div>- Altered stool passage</div><div>- Abdominal bloating (more common in women)</div><div>- Symptoms made worse by eating</div><div>- Passage of mucus</div></div><div><br></div><div>(no tests required)</div>"
How should IBS be managed?"<div><font color=""#0000ff"">First line:</font><br></div><div>- Diet: Reduce fibre intake (esp. insoluble fibre eg bran), regular meals, reduce alcohol and fizzy drinks</div><div>- Symptom control: Antispasmodics for pain, laxatives for constipation, loperamide for diarrhoea</div><div><br></div><div><font color=""#0000ff"">Second line:</font></div><div>- Low-dose TCAs</div><div><br></div><div><font color=""#0000ff"">Others:</font></div><div>- Psychological interventions</div>"
How can constipation be managed in IBS?"<font color=""#0000ff"">Lifestyle</font>: Ensure adequate water & fibre (avoiding insoluble fibre) intake; and promote physical activity.<div><br></div><div><font color=""#0000ff"">Medication</font>: Simple laxatives, but if 2 of these fail, prucalopride, linaclotide or lubiprostone; or self-administered anal irrigation</div>"
How should diarrhoea be managed in IBS?"<font color=""#0000ff"">Lifestyle</font>: Avoid sorbitol sweeteners, alcohol & caffeine. Reduce dieteary fibre content; encourage pts to find their own trigger foods. <div><br></div><div><font color=""#0000ff"">Medication</font>: Try bulking agent + loperamide 2mg after each loose stool</div>"
How should colic/bloating be managed in IBS?"<font color=""#0000ff"">Lifestyle</font>: Low FODMAP diet<div><br></div><div><font color=""#0000ff"">Medical</font>: Oral spasmodics (mebeverine, or hyoscine) Combination probiotics in sufficeint doses may help.</div>"
What does the low FODMAP diet stand for?Diets low in:<div>- Fermentable</div><div>- Oligosaccharides</div><div>- Disaccharides</div><div>- Monosaccharides</div><div>- And </div><div>- Polyols</div>
How can you manage psychological symptoms/visceral hypersensitivity in IBS?"<font color=""#0000ff"">Lifestyle</font>: Education- excluded sinister pathology, and symptoms tend to improve<div><br></div><div><font color=""#0000ff"">Medical</font>: CBT, Hypnosis and Tricyclics (at low dose for visceral pain, not for depression)</div>"
Broadly speaking, what causes constipation?- Pelvis dysfunction<div>- ↑Transit time </div>
What is categorised as constipation?- ≤2 bowel motions/ week<div>- Bowels passed with difficulty, straining, pain </div><div>- Sense of incomplete evacuation </div>
Constipation + <span class=cloze>[...]</span> = Colorectal cancerConstipation + <span class=cloze>rectal bleeding</span> = Colorectal cancer<br> Constipation + rectal bleeding = <span class=cloze>[...]</span>Constipation + rectal bleeding = <span class=cloze>Colorectal cancer</span><br> Constipation + <span class=cloze>[...]</span> = Stricture/GI obstructionConstipation + <span class=cloze>Distention + active bowel sounds</span> = Stricture/GI obstruction<br> Constipation + Distention + active bowel sounds = <span class=cloze>[...]</span>Constipation + Distention + active bowel sounds = <span class=cloze>Stricture/GI obstruction</span><br> Constipation + <span class=cloze>[...]</span> = HypothyroidismConstipation + <span class=cloze>Menorrhagia</span> = Hypothyroidism<br> Constipation + Menorrhagia = <span class=cloze>[...]</span>Constipation + Menorrhagia = <span class=cloze>Hypothyroidism</span><br> What is a <b>rectocele?</b>Front wall of rectum bulges into back wall of vagina (describes what?)
Front wall of rectum bulges into back wall of vagina (describes what?)What is a <b>rectocele?</b>
What is suggestive of a <b>rectocele</b>?Constipated woman digitating rectum or vagina to pass stool (suggests what?)
Constipated woman digitating rectum or vagina to pass stool (suggests what?)What is suggestive of a <b>rectocele</b>?
What lifestyle advice can you give for constipation?- Reassurance (if no red flags)<br><div>- Drinking more</div><div>- Diet/Excercise </div><div>- High-fibre diet (though may cause bloating without helping constipation) </div>
How do bulking agents help constipation?Increase faecal mass, so stimulates peristalsis
When are bulking agents contraindicated in the treatment of constipation?- GI obstruction<div>- Colonic atony</div><div>- Faecal impaction </div>
What are examples of bulking agents?- Bran powder<div>- Isphaghula husk</div><div>- Methylcellulose</div><div>- Sterculia </div><div><br></div><div>These should all be taken with plenty of fluid </div>
When are stimulant laxatives contraindicated in the management of constipation?- Intestinal obstruction<div>- Acute colitis</div><div><br></div><div>(as these increase intestinal motility) </div>
What are examples of stimulant laxatives?- Bisacodyl tablets/suppsoitories<div>- Senna </div><div>- Docusate sodium & dantron (stimulate and softening actions)</div><div>- Glycerol suppositories (rectal stimulant)</div><div>- Sodium picosulfate</div>
When should dantron be used in constipation?Very elderly or terminally ill (shown to cause colon and liver tumours in animals)
How do stimulant laxatives work?Increase intestinal motility 
What are examples of stool softeners?- Arachis oil enemas<div>- Liquid paraffin (only short-term use)</div>
What are side effects of the use of liquid paraffin in the management of constipation?- Anal seepage<div>- Lipoid pneumonia</div><div>- Malabsorption of fat-soluble vitamins </div>
What are the action of osmotic laxatives?- Retain fluid in bowel, making it easier to pass stools 
What is the action of lactulose?Produces osmotic diarrhoea of low faecal pH which discourages growth of ammonia-genic organisms <div><br></div><div>Does cause bloating as a side effect </div>
What are examples of osmotic laxatives?- Lactulose<div>- Macrogol</div><div>- Magensium salts (for rapid bowel evacuation)</div><div>- Phosphate enemas (useful prior to procedures)</div><div><br></div><div>(sodium salts, but these cause sodium and water retention so tend to be avoided)</div>
What is the preferred medical management of constipation?"- Stimulant laxative e.g. senna, <font color=""#0000ff"">with a bulking agent </font>"
What is the action of <b>prucalopride</b>?- 5HT<sub>4</sub> agonist: prokinetic (describes what drug?)
- 5HT<sub>4</sub> agonist: prokinetic (describes what drug?)What is the action of <b>prucalopride</b>?
What is the action of <b>lubiprostone?</b>Chloride-channel activator- increases intestinal fluid secretion (describes what?)
Chloride-channel activator- increases intestinal fluid secretion (describes what?)What is the action of <b>lubiprostone?</b>
What is the action of <b>linaclotide?</b>- Guanylate cyclase-C agonist which increases intestinal fluid secretion and decreases visceral pain (describes what?)<div><br></div><div>(used in constipation) </div>
- Guanylate cyclase-C agonist which increases intestinal fluid secretion and decreases visceral pain (describes what?)<div><br></div><div>(used in constipation) </div>What is the action of <b>linaclotide?</b>
What drugs can you try if conventional medical treatments (bulking agents, stool softeners, stimulant and osmotic laxatives) fail in treating constipation?- Prucalopride<div>- Lubiprostone</div><div>- Linaclotide</div>
What are general causes of constipation?- Poor diet + lack of exercise<div>- Poor fluid intake/dehydration</div><div>- IBS<br>- Old age</div><div>- Post-operative pain</div><div>- Hospital environment (↓ privacy, having to use a bed pan)</div>
What is <b>proctalgia fugax?</b>Severe, episodic pain in regions of rectum and anus, caused by cramping of levator ani muscle (describes what?)
Severe, episodic pain in regions of rectum and anus, caused by cramping of levator ani muscle (describes what?)What is <b>proctalgia fugax?</b>
What are endocrine causes of constipation?- Hypercalcaemia<div>- Hypokalemia</div><div>- Porphyria</div><div>- Lead poisoning<br><div>- Hypothyroidism (though rarely present with constipation) </div></div>
What drugs can cause constipation?- Opiates<div>- Anticholinergics</div><div>- Iron </div><div>- Some antacids (e.g. those with aluminium)<br>- Diuretics e.g. furosemide</div><div>- Calcium channel blockers</div>
What cause <b>scurvy</b>?Deficiency in vitamin C (causes what?)
Deficiency in vitamin C (causes what?)What cause <b>scurvy</b>?
What are risk factors of developing scurvy?- Poor <div>- Pregnant</div><div>- Or on strange diet </div>
What are signs of scurvy?1. Listlessness, anorexia, cachexia<div>2. Gingivitis, loose teeth and halitosis</div><div>3. Bleeding from gum, nose, hair follicles, or into joints, bladder, gut</div><div>4. Muscle weakness/pain</div><div>5. Oedema</div>
What laboratory findings may support a diagnosis of scurvy?- ↓ Ascorbic acid levels in WBCs <div><br></div><div>- Skeletal X-ray changes in childhood scurvy</div>
What radiographic findings are apparent in childhood scurvy?"- Loss of trabeculae- ground-glass appearance<div>- Thinning of cortex</div><div>- Line of calcified, irregular cartilage at metaphysis</div><div><img src=""220px-ASM-30-325-g003.jpg""><br></div>"
How should scurvy be managed?- Dietary education<div>- Ascorbic acid >250mg/24h PO </div>
How long does it take for signs of scurvy to disappear following supplementation?1-2 weeks (though chronic gingivitis may persist longer)
What is <b>beriberi?</b>Deficiency of thiamine- Vitamin B1 (causes what?)
Deficiency of thiamine- Vitamin B1 (causes what?)What is <b>beriberi?</b>
<span class=cloze>[...]</span> = Vitamin B1<span class=cloze>Thiamine</span> = Vitamin B1<br> Thiamine = Vitamin <span class=cloze>[...]</span>Thiamine = Vitamin <span class=cloze>B1</span><br> How does beriberi present?Heart failure with:<div>- General oedema (wet beriberi)<br>- Neuropathy (dry beriberi)</div>
What is <b>Pellagra</b>?Deficiency of Niacin- Vitamin B3 (causes what?)
Deficiency of Niacin- Vitamin B3 (causes what?)What is <b>Pellagra</b>?
How does <b>Pellagra </b>present?"Triad of:<div>- Diarrhoea</div><div>- Dementia</div><div>- Dermatitis (Casal's necklace)</div><div><br></div><div>Can also have neuropathy, depression, insomnia, tremor, rigidity, ataxia, fits. </div><div><br></div><div>(describes presentation of what?)</div>"
"Triad of:<div>- Diarrhoea</div><div>- Dementia</div><div>- Dermatitis (Casal's necklace)</div><div><br></div><div>Can also have neuropathy, depression, insomnia, tremor, rigidity, ataxia, fits. </div><div><br></div><div>(describes presentation of what?)</div>"How does <b>Pellagra </b>present?
"What is seen here?<div><img src=""3N_pZY1Jn5C2ItU7EZMJnydvXk_I_T2Dy854uV19FTk.jpg""><br></div>""Casal's necklace- sign of Pellagra"
Pellagra can occur in <span class=cloze>[...]</span> and <span class=cloze>[...]</span>Pellagra can occur in <span class=cloze>Carcinoid syndrome</span> and <span class=cloze>Anti-TB drugs</span><br> Carcinoid syndrome uses tryptophan for 5-HT production which is important for niacin synthesis
Where is Pellagra endemic?China and Africa 
How is Pellagra managed?- Education<div>- Electrolyte replacemnet</div><div>- Nicotinamide 100mg/4h</div>
What is <b>xerophtalmia?</b>Vitamin A deficiency syndrome- causes blindness (describes what?)
Vitamin A deficiency syndrome- causes blindness (describes what?)What is <b>xerophtalmia?</b>
What occurs in xerophthalmia?"- Conjunctivae become dry + develop oval/triangular spots (Bitot's spots)<div>- Corneas become cloudy and soft</div>"
"What is seen here?<div><img src=""F1.large (2).jpg""><br></div>""Bitot's spots- sign of Xerophthalmia "
Why must you be wary of treating pregnant mothers with xerophthalmia?- Vitamin A is teratogenic
What is <b>Haemasuccus Pancreaticus</b>?- <b>Bleeding from pancreatic duct </b>into GI tract via the ampulla of vater (describes what?)
- <b>Bleeding from pancreatic duct </b>into GI tract via the ampulla of vater (describes what?)What is <b>Haemasuccus Pancreaticus</b>?
What is <b>Gastric antral vascular ectasia?</b>- Dilation of small blood vessels in pyloric antrum, associated with scleroderma, portal HTN, chronic kidney failure, & collagen vascular diseases 
"What is seen here, on endoscopy of the stomach<div><img src=""15-RHE-1501-GAVE-650x450.jpg""><br></div>"Gastric antral vascular ectasia
What are different options for endoscopic management of GI bleeding?"- Injection: Adrenaline or saline<div>- Thermal: Contact or non-contact</div><div>- Mechanical: Clips or bands  </div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Need combination of at least 2 methods</font></div>"
How is injection useful in the endoscopic management of GI bleeding?- Injections of saline or adrenaline around ulcer, in quadrants around. <div>- Provides a tamponade effect</div>
What are the different types of thermal management of GI bleeding?- Contact e.g. diathermy: electricity between two points causing heating- cauterises the vessel<div>- Non-contact: e.g. argon plasma coagulation </div>
What are mechanical methods of endoscopically managing GI bleeding?"- Clips: Remain on vessel for 7-10 days. Ulcer heals, and clips are passed through digestive system. <div><img src=""WJGE-1-7-g004.jpg""><br><div>- Bands: Useful for varices</div><div><img src=""HTB12qqZQpXXXXXZXFXXq6xXFXXXr.jpg""><br></div></div>"
What are newer methods of endocopic management of GI Bleeding?"Topical therapies:<div>- e.g. Haemo-spray (provides temporary heamostasis- particularly useful for heavy bleeding where you can't see the vessel)</div>"
How you differentiate between intra and extra-hepatic cholestasis?"Carry out ultrasound:<div><font color=""#0000ff"">Intra</font>- Normal biliary tree (microscopic changes, so won't be seen on USS)</div><div><font color=""#0000ff"">Extra</font>- Dilation of biliary tree</div>"
What is the difference between extra-hepatic cholestasis and obstructive jaundice?Jaundice is a clinical sign- can have cholestasis without clinical signs. 
What can be used to establish a diagnosis of cholecystitis?Ultrasound: <div>- Gallbladder wall thickening</div><div>- Gallstones</div>
Does cholecystitis cause jaundice?"- Usually not, as will still get bile release directly from common hepatic ducts. <div><br></div><div>Cholecystitis only causes jaundice in Mirizzi's syndrome </div>"
How are pathogenic gallstones treated?ERCP- Remove gallstones 
What are <b>Klatskin tumours?</b>"Tumours located at bifurcation of biliary system<div><img src=""a5097979702b8a_4.jpg""><br></div><div><br></div><div>(describes what?)</div>"
"Tumours located at bifurcation of biliary system<div><img src=""a5097979702b8a_4.jpg""><br></div><div><br></div><div>(describes what?)</div>"What are <b>Klatskin tumours?</b>
What from the Hx might suggest a dysphagia caused by oesophageal cancer?"- Weight loss, anorexia, or vomiting<div>- PMH: May have Barrett's Oesophagus, GORD, excessive smoking/alcohol</div>"
What from the Hx may suggest dysphagia caused by oesophagitis?- Hx of heartburn<div>- Odynophagia, but no weight loss and systemically well</div>
What from the Hx might suggest dysphagia caused by achalasia?- Dysphagia of both liquids and solids from the start<div>- Heartburn</div><div>- Regurgitation of food- may lead to cough, aspiration pneumonia etc. </div>
What is a pharyngeal pouch?"Posteromedial herniation between thyropharyngeus and cricopharyngeus muscles<div><img src=""zenker.gif""><br></div><div><br></div>"
What might be seen on manometry of a patient with systemic sclerosis?<b>Decreased </b>lower oesophageal sphincter pressure (in contrast to Achalasia)
What from the Hx might suggest dysphagia caused by Myasthenia gravis?- Extra-ocular muscle weakness/ ptosis<div>- Dysphagia with liquids as well as solids </div>
What from the Hx might suggest dysphagia caused by globus hystericus?- Hx of anxiety<div>- Intermittent symptoms, relieved by swallowing</div><div>- Usually painless (if pain, investigate other causes)</div>
What is a <b>Schatzki ring?</b>Ring of mucosal tissue causing narrowing of lower oesophagus → dysphagia (describes what?)
Ring of mucosal tissue causing narrowing of lower oesophagus → dysphagia (describes what?)What is a <b>Schatzki ring?</b>
How is a Schatzki ring diagnosed?OGD, or barium swallow 
"What is seen here?<div><img src=""220px-Schatzkiring.jpg""><br></div>"Schatzki Ring
What are oesophageal webs?Thin membranes occuring along the oeosphagus, causing dysphagia 
"What is seen here?<div><img src=""Zervikales_Web.jpg""><br></div>"Oesphageal web
In which condition are oesophageal webs typically observed?Plummer-Vinson syndrome (but also ceoliac disease)
How does a urea breath test work?- Pts consume drink containing 13C enriched urea<div>- Urea broken down by <i>H. pylori </i>urease</div><div>- After 30mins, pt exhales into glass tube. </div><div>- Calculate amount of 13C CO<sub>2</sub></div>
What should be stopped prior to a urea breath test?- Antibacterial - 4 weeks before<br>- Antisecretory (e.g. PPI) - 2 weeks before
How is a rapid urease test (CLO test) carried out?- Biopsy sample mixed with urea and pH indicator<div>- Colour change if H. pylori urease activity </div>
What tests can be used to detect <i>H. pylori?</i>- Urea breath test (gold standard)<div>- Rapid urease test</div><div>- Serum antibody (though remains positive after eradication)</div><div>- Culture of gastric biopsy </div><div>- Histoloigcal evaluation of gastric biopsy</div><div>- Stool antigen</div>
How is pharyngeal pouch managed?Surgical repair, to close defect 
In what patients does pharyngeal pouch typically occur in?- >70y/o<div>- 5x more common in men</div>
"What is seen here?<div><img src=""xrb156.jpg""><br></div>"Pyogenic liver abscess
What are the most common causative organisms in pyogenic liver abscesses?"<font color=""#0000ff"">In children</font>: Staphylococcus aureus<div><font color=""#0000ff"">In adults</font>: E. coli </div>"
How should pyogenic liver abscess be managed?Percutaneous drainage and IV antibiotics: <div>- Amoxicillin, Ciprofloxacin and metronidazole</div><div>- Or if penicillin allergic: ciprofloxacin and clindamycin</div><div><br></div><div>Surgical resection if this is refractory</div>
What is the management of a hydatid cyst?- Surgical resection 
"What is seen here?<div><img src=""TropParasitol_2016_6_2_103_190812_u29.jpg""><br></div>"Hydatid cyst
What cardiac abnormalities are associated with<b> Carcinoid </b>syndrome?- Pulmonary <b>stenosis</b><div>- Tricuspid <b>regurgitation</b></div>
What causes cardiac manifestations in carcinoid tumours?Parenoplastic effects of 5-HT: causes fibrous tissue to form on the right side of heart (tricuspid, pulmonary valve)
"What is <b>Rovsing's sign?</b>"RIF pain on palpation of LIF- sign of appendicits (describes what?)
RIF pain on palpation of LIF- sign of appendicits (describes what?)"What is <b>Rovsing's sign?</b>"
What is the Psoas sign?<div>- Patient lies on left side and doctor extends right hip with knee fully extended. </div><div>- If positive, generates abdominal pain, indicating irritation of illiopsoas + possible appendicitis</div>
What does a positive Psoas sign usually indicate?Iliospsoas irritation and possible appendicitis<div><br></div><div>Usually indicates appendix in the retrocaecal position </div>
"Where is McBurney's point?"Right side of abdomen, 1/3 of distance from ASIS to umbilicus 
If you feel a liver edge which is firm, smooth, tender and pulsatile, what is the likely cause?Hepatomegaly caused by right heart failure
What is the guidelines on alcohol intake?- No more than 14 units a week<div>- Space over at least 3 days. </div><div><br></div><div>Same for men and women</div>
<span class=cloze>[...]</span> = Vitamin B2<span class=cloze>Riboflavin</span> = Vitamin B2<br> Riboflavin = Vitamin <span class=cloze>[...]</span>Riboflavin = Vitamin <span class=cloze>B2</span><br> <span class=cloze>[...]</span> = Vitamin B6<span class=cloze>Pyrodoxine</span> = Vitamin B6<br> Pyrodoxine = Vitamin <span class=cloze>[...]</span>Pyrodoxine = Vitamin <span class=cloze>B6</span><br> Deficiency of Thiamine causes what?"- Beriberi<div>- Wernicke's encephalopathy</div>"
Deficiency of riboflavin causes what?- Angular stomatitis 
What are consequences of deficiency of <b>Pyridoxine</b>?- Polyneuropathy (can be caused by deficiency of what?)
- Polyneuropathy (can be caused by deficiency of what?)What are consequences of deficiency of <b>Pyridoxine</b>?
What are consequences of B12 deficiency?- Macrocytic anaemia<div>- Neuropathy</div><div>- Glossitis </div>
What vitamins are absorbed from the <b>proximal ileum?</b>Vitamin C (is absorbed from where?)
Vitamin C (is absorbed from where?)What vitamins are absorbed from the <b>proximal ileum?</b>
"Deficiency in <span class=cloze>[...]</span> causes Menkes' kinky hair syndrome""Deficiency in <span class=cloze>copper</span> causes Menkes' kinky hair syndrome<br> "
Deficiency in copper causes <span class=cloze>[...]</span>"Deficiency in copper causes <span class=cloze>Menkes' kinky hair syndrome</span><br> "
Deficiency in <span class=cloze>[...]</span> causes dental cariesDeficiency in <span class=cloze>Fluoride</span> causes dental caries<br> Deficiency in Fluoride causes <span class=cloze>[...]</span>Deficiency in Fluoride causes <span class=cloze>dental caries</span><br> Deficiency in <span class=cloze>[...]</span> causes goitre; cretinismDeficiency in <span class=cloze>iodide</span> causes goitre; cretinism<br> Deficiency in iodide causes <span class=cloze>[...]</span>Deficiency in iodide causes <span class=cloze>goitre; cretinism</span><br> Deficiency in <span class=cloze>[...]</span> causes osteopororis, anorexia, weaknessDeficiency in <span class=cloze>phosphate</span> causes osteopororis, anorexia, weakness<br> Deficiency in phosphate causes <span class=cloze>[...]</span>Deficiency in phosphate causes <span class=cloze>osteopororis, anorexia, weakness</span><br> Deficiencies in selenium causes <span class=cloze>[...]</span>Deficiencies in selenium causes <span class=cloze>cardiomyopathy</span><br> Deficiencies in <span class=cloze>[...]</span> causes cardiomyopathyDeficiencies in <span class=cloze>selenium</span> causes cardiomyopathy<br> Deficiencies in Zinc causes <span class=cloze>[...]</span>Deficiencies in Zinc causes <span class=cloze> poor wound healing</span><br> Deficiencies in <span class=cloze>[...]</span> causes  poor wound healingDeficiencies in <span class=cloze>Zinc</span> causes  poor wound healing<br> <span class=cloze>[...]</span> causes zinc deficiency <span class=cloze>Acrodermatitis enteropathica</span> causes zinc deficiency <br> Acrodermatitis enteropathica causes <span class=cloze>[...]</span> deficiency Acrodermatitis enteropathica causes <span class=cloze>zinc</span> deficiency <br> What characterises <b>acrodermatitis enteropathica</b>?- Periorificial dermatitis<div>- Alopecia</div><div>- Diarrhoea</div><div><br></div><div>(is the classic presentation of what?)</div>
"What is seen here?<div><img src=""smith_erythemaabigne_f1.jpg""><br></div>"Mottled dusky greyness- skin reaction caused by chronic exposure to IR radiation in form of heat (e.g. constant use of hot water bottles)
What is chronic pancreatitis?Persistent inflammation of the pancreas, resulting in permanent strucutral damage w/ fibrosis & ductal strictures, followed by a decline in exocrine and endocrine function 
What are the most common causes of chronic pancreatitis?- Heavy alcohol consumption<div>- Smoking</div><div>- Autoimmune </div><div><br></div>
What are rare causes of chronic pancreatitis?<div>- Familial</div><div>- Cystic fibrosis</div><div>- Haemochromatosis (excessive iron absorption)</div><div>- Pancreatic duct obstruction</div><div>- Congenital (pancrea divisum)<br></div><div>- Tropical pancreatitis (typically in India, INdonesia, Nigeria)</div>
What are symptoms of chronic pancreatitis?- Epigastric pain which radiates to back<div>- Bloating</div><div>- Steatorrhoea</div><div>- ↓ Weight</div><div>- Labile diabetes (hard-to-control)</div><div><br></div><div>Symptoms relapse and worsen</div>
Why are amylase/lipase levels unhelpful in the diagnosis of chronic pancreatitis?Will frequently be normal, due to significant loss of pancreatic function
How should chronic pancreatitis be investigated?"<font color=""#0000ff"">Abdominal CT + Ultrasound:</font> Pancreatic calcifications<div><font color=""#0000ff"">MRCP</font>: Investigates ductal abnormalities</div><div><font color=""#0000ff"">AXR</font>: Not as good as CT, but may show speckled calcification </div><div><font color=""#0000ff"">Faecal elastase</font></div>"
How should chronic pancreatitis be managed?"<div><font color=""#0000ff"">Lifestyle: </font>Smoking cessation, alcohol abstinence. Low fat diet to ↓secretion of pancreatic enzymes</div><div><br></div><div><font color=""#0000ff"">Drugs: </font></div><div>- Analgesia (consider coeliac-plexus block for brief relief), </div><div>- Lipase (suppresses release of CCK from duodenum, which reduces secretion of pancreatic enzymes)</div><div>- Fat-soluble vitamins</div><div>- Insulin for management of diabetes</div><div><br></div><div><font color=""#0000ff"">Surgery</font>: Used in unremitting pain, only in those who are alcohol abstinent</div><div>- Pancreatectomy</div><div>- Pancreaticojejunostomy</div>"
When is surgery indicated to treat chronic pancreatitis?"<font color=""#0000ff"">Pts with unremitting pain who: </font><div>- Have stopped alcohol use</div><div>- Can manage diabetes (which may be intensified by pancreatic resection)</div>"
What is a pancreaticojejunostomy, and when is it used?"Side to side anastomosis of pancreatic duct and jejunum,<font color=""#0000ff""> used to treat chronic pancreatitis with pancreactic duct obstruction (dilated >6mm)</font><div><br></div><div><img src=""464_2016_5294_Fig3_HTML.gif""><br></div>"
What are complications of chronic pancreatitis?- Malabsorption: steatorrhoea, weight loss and loss of fat-soluble viatmins<div>- Diabetes</div><div>- Psuedocyst </div><div>- Billiary obstruction </div><div>- Splenic vein thrombosis (which can cause gastric varices)</div><div>- Local arterial aneurysm</div><div><br></div><div>Increased risk of pancreatic adenocarcinomas </div>
Discuss the epidemiology of pancreatic cancer?3% of all malignancies, around 9000 deaths a year in the UK. <div><br></div><div>Incidence rising </div>
What are risk factors of pancreatic cancers?- Smoking (1 in 4attributed to smoking)<div>- Alcohol</div><div>- Carcinogens</div><div>- Genetics (e.g. Lynch syndrome, BRCA1/2, FHx of pancreatic cancer)</div><div><br></div><div>- Diabetes Mellitus</div><div>- Chronic pancreatitis</div><div>- Adiposity</div><div><br></div><div>Possibly high-fat and red/processed meat diet </div>
What type of carcinoma is typically in pancreatic cancer?Ductal adenocarcinomas (metastasise early, present late)
Where do the pancreatic tumours arise?- 60% in pancreatic head<div>- 25% in body</div><div>- 15% in tail </div>
What is an ampullary tumour?Malignant tumour in the ampulla of vater
What tumours can arise from pancreatic islet cells?- Insulinoma<div>- Gastrinoma</div><div>- Glucagonomas</div><div>- Somatostatinomas</div><div>- VIPomas </div>
Which pancreatic carcinomas have better prognoses?- Ampullary tumour<div>- Tumours in pancreatic islet cells </div>
95% of pancreatic islet cells in pancreatic carcinomas have mutations in <span class=cloze>[...]</span> gene95% of pancreatic islet cells in pancreatic carcinomas have mutations in <span class=cloze>KRAS2</span> gene<br> What are common features of pancreatic carcinomas?- Painless obstructive jaundice (if in head)<div>- Epigastric pain (75% of tumours in head and tail), which radiates to back, and relieved by sitting forward </div><div>- Weight loss</div><div>- Diabetes</div><div>- Acute pancreatitis </div>
What is <b>thrombophlebitis migrans</b>?Clot which moves around the body- will cause swollen vein, and then move 
What are rarer features of pancreatic carcinomas?- Thrombophlebitis migrans<div>- ↑Ca<sup>2+</sup></div><div>- Marantic endocarditis</div><div>- Portal hypertension</div><div>- Nephrosis (through renal vein metastasis)</div>
What are signs of pancreatic carcinoma?- Jaundice & palpable gallbladder<div>- Epigastric mass</div><div>- Hepatomegaly</div><div>- Splenomegaly</div><div>- Lymphadenopathy</div><div>- Ascites</div>
What marker is useful in assessing prognosis of <b>pancreatic carcinomas?</b>CA19-9 (is a useful marker in what?)
CA19-9 (is a useful marker in what?)What marker is useful in assessing prognosis of <b>pancreatic carcinomas?</b>
How should a diagnosis of pancreatic carcinoma be made?"<font color=""#0000ff"">Bloods</font>: Cholestatic jaundice, and CA19-9<div><font color=""#0000ff"">Imaging:</font></div><div>- US/CT can show pancreatic mass + dilated biliary tree + hepatic metastases. Can guide biopsy and help stating</div><div>- ERCP/MRCP: Localise site of biliary obstruction</div><div>- EUS</div>"
What is the prognosis of pancreatic carcinomas?"Very poor, as early metastasis and late presentation:<div>- Mean survival <6 months</div><div>- 5 yr survival: 3% (after Whipple's procedure, 5-14%)</div>"
What are positive prognostic markers for pancreatic carcinomas?- Tumour <3cm<div>- No nodes involved</div><div>- -ve resection margins at surgery</div><div>- Ampullary or islet cell tumours</div>
What proportion of pancreatic cancers are able to be surgically removed?<20%: most are considered surgically unresectable, because of metastases or invasion of major blood vessels
What is the treatment of pancreatic cancers?"<div><font color=""#0000ff"">Surgical management:</font> </div><div>- Whipple's procedure- pancreaticoduodenectomy</div><div>- Post-op chemotherapy (delays disease progression) </div><div><font color=""#0000ff"">Palliation of jaundice:</font></div><div>- Endoscopic/percutaneous stent insertion</div><div><font color=""#0000ff"">Pain: </font></div><div>- Opiates</div><div>- Radiotherapy</div><div>- Coeliac plexus infiltration of anaesthesia</div>"
How might you differentiate between oropharyngeal dysphagia and oesophageal dysphagia?"<font color=""#0000ff"">Oropharyngeal</font>: <div>- Unable to initate a swallow, and may have repeated attempts.</div><div>- Cough, choking </div><div><br></div><div><font color=""#0000ff"">Oesophageal</font>:</div><div>- May localise symptoms to lower sternum, or epigastric region</div><div>- Can be relieved by repeated swallowing, raising arms over the head, using Valsalva manouevre </div>"
What is Globus?Feeling of lump or tightness in throat, unrelated to swallowing <div><br></div><div>(Swallowing or drinking may give temporary relief)</div>
A <span class=cloze>[...]</span> tinge to the skin is associated with pernicious anaemiaA <span class=cloze>lemon</span> tinge to the skin is associated with pernicious anaemia<br> A lemon tinge to the skin is associated with <span class=cloze>[...]</span>A lemon tinge to the skin is associated with <span class=cloze>pernicious anaemia</span><br> What causes a light yellow tinge in pernicious anaemia?- Pallor (due to anaemia)<br>- Mild jaundice (caused by haemolysis)
"What is <b>Killian's dehiscence?</b>"Triangular area in wall of pharynx between thyropharyngeus and cricopharyngeus muscles<div><br></div><div>Area through which pharyngeal pouch forms </div><div><br></div><div>(describes what?)</div>
Triangular area in wall of pharynx between thyropharyngeus and cricopharyngeus muscles<div><br></div><div>Area through which pharyngeal pouch forms </div><div><br></div><div>(describes what?)</div>"What is <b>Killian's dehiscence?</b>"
What is the first-line investigation for acute mesenteric ischaemia?"ABG/VBG for <font color=""#0000ff"">serum lactate</font>- will be raised"
What causes a raised lactate in acute mesenteric ischaemia?- Lack of blood supply- anaerobic metabolism<div>- Lactate production from ischaemic bowel </div>
How should haemochromatosis be managed?"<font color=""#0000ff"">1st line: </font><b>Venesection </b>(aim for transferrin sats< 50%; and serum ferritin <50ug)<div><font color=""#0000ff"">2nd line:</font> If not tolerated (e.g. if patient very anaemic) <b>Iron chelation</b> (desferrioxamine SC)<br></div><div><br></div><div><b>Others</b>:</div><div>- Lifestyle modification: Eat less iron-containing foods, avoid iron supplements</div><div>- Give HAV and HBV vaccination</div>"
What causes haemochromatosis?Autosomal recessive disorder of iron absorption & metabolism → iron accumulation. <div><br></div><div>Inheritance of mutations in HFE gene on both copies of chromosome 6</div>
What is the most useful marker to screen for Haemochromatosis?- Transferrin saturation 
What are diagnostic tests for Haemochromatosis?"- Molecular genetic testing for C282Y and H63D mutations<div>- Liver biopsy: Perl's stain </div>"
What anti-emetics should be avoided in bowel obstruction?Metoclopramide and domperidone- these are pro-kinetics, which would increase the risk of perforation 
Patients with <span class=cloze>[...]</span> should be screened for coeliac disease on diagnosisPatients with <span class=cloze>T1DM & Autoimmune thyroiditis</span> should be screened for coeliac disease on diagnosis<br> Patients with T1DM & Autoimmune thyroiditis should be screened for <span class=cloze>[...]</span> on diagnosisPatients with T1DM & Autoimmune thyroiditis should be screened for <span class=cloze>coeliac disease</span> on diagnosis<br> What is the most common cause of liver disease in the developed world?Non-alcoholic fatty liver disease 
What diseases fall within Non-alcoholic fatty liver disease?- Steatosis: Fat in liver<div>- Steatohepatitis, NASH<br>- Fibrosis and liver cirrhosis</div>
What is thought to be the key mechanism causing steatosis in Non-alcoholic fatty liver disease?Insulin resistance (NAFLD is hepatic manifestation of metabolic syndrome)
On an incidental finding of NAFLD on ultrasound, what further testing should be done?Enhanced Liver Fibrosis (ELF) Blood test:<div>- Hyaluronic acid</div><div>- Procollagen III</div><div>- Tissue inhibitor of metalloproteinase. </div><div><br></div><div>Assesses advanced fibrosis</div>
What is the classic presentation of chronic mesenteric ischaemia?Triad of:<div>- Severe, colicky, post-prandial abdominal pain</div><div>- Weight loss</div><div>- Abdominal bruit </div>
What is the most common cause of chronic mesenteric ischaemia?Atherosclerotic disease in arteries supplying GI Tract (so can hear abdominal bruits)
What are the two types of hepatorenal syndrome?"<font color=""#0000ff"">Type 1:</font><div>- Rapidly progressive</div><div>- Doubling of serum creatnine</div><div>- Very poor prognosis</div><div><br></div><div><font color=""#0000ff"">Type 2: </font></div><div>- Slowly progressive </div><div>- Poor prognosis, but patients may live for longer</div>"
How should hepatorenal syndrome be managed?- Vasopressin analogues (e.g. terlipressin): Cause vasoconstriction of splanchnic circulation<br><div>- Volume expansion with albumin</div><div>- TIPS</div>
What is the classic patient who has biliary colic?Fat, fair female in their forties
What are common symptoms of viral hepatitis?- Nausea & vomiting, anorexia<div>- Myalgia</div><div>- Lethargy</div><div>- RUQ pain </div><div><br></div><div>May have had recent foreign travel or IV drug use </div>
What causes congestive hepatomegaly?- Congestive heart failure causes backlog of blood → hepatomegaly. <div>- Stretches the liver, causing pain</div>
How does ascending cholangitis and acute cholecystitis present differently?"Cholangitis will present with jaundice (as obstruction of common bile ducts)<div>Cholecystitis will usually present without jaundice (unless Mirizzi's)</div>"
What is gallstone ileus?Small bowel obstruction secondary to impacted gallstone (mechanical obstruction, despite the name)
What causes a gallstone ileus?Formation of fistula between gangrenous gallbladder and duodenum
What signs may be seen in cholangiocarcinoma?"<font color=""#0000ff"">Courvoisier sign</font>: Palpable mass in RUQ<div><font color=""#0000ff"">Sister Mary Joseph nodes</font>: Periumbilical lymphadenopathy</div><div><font color=""#0000ff"">Virchow's node</font></div>"
"What is seen here?<div><img src=""Bilateral-Grey-Turners-sign-Fig-3-Contrast-enhanced-CT-of-the-abdomen-showing-a-huge.png""><br></div>""Grey-Turner's sign: sign of retroperitoneal bleed "
What is the classic presentation of acute fatty liver of pregnancy?Abdominal pain and pruritus, followed by jaundice
What are classic symptoms of carcinoid syndrome?- Flushing<div>- Diarrhoea</div><div>- Bronchospasm</div><div>- Hypotension</div><div>- Weight loss </div>
How should carcinoid tumours be investigated?- Measure urinary 5-HIAA (5-HT metabolite, so will be ↑)<div>- Plasma chromogranin A (reflects tumour mass)</div><div>- CXR & chest/pelvis MRI/CT can help locate primary tumours </div><div><br></div><div>- Octreoscans and PET may also have a role</div>
How should carcinoid heart disease be investigated?- Echocardiography<div>- BNP</div>
Where are common sites of carcinoid tumours?- Appendix (45%)<div>- Ileum (30%)</div><div>- Rectum (20%)</div>
What are carcinoid tumours?Neuroendocrine tumour: Tumours of enterochromaffin cell origin, capable of producing 5-HT
Carcinoid syndrome occurs in <span class=cloze>[...]</span> of carcinoid tumoursCarcinoid syndrome occurs in <span class=cloze>5%</span> of carcinoid tumours<br> Carcinoid syndrome= carcinoid tumour which produces excessive hormones
What is a carcinoid crisis?When tumour outgrows its blood supply, or handled too much in surgery, mediators flood out, causing:<br><div>- Life-threatening vasodilation and hypotension</div><div>- Tachycardia</div><div>- Bronchoconstriction</div><div>- Hyperglycaemia</div>
How should a carcinoid crisis be treated?- High-dose octreotide<div>- Supportive measures</div><div>- Careful management of fluid balance (central line required)</div>
How should carcinoid syndrome be treated?- Octreotide: somatostatin analogue, blocks release of tumour mediators & counters peripheral effects (lanreotide a long-acting alternative)<div>- Loperamide for diarrhoea </div>
How should carcinoid tumours be managed?Surgical resection (w/ octreotide cover, to prevent carcinoid crisis)
What test is appropriate for post-eradication therapy testing of H. Pylori?Urea breath test
"When is an intervention required in Barrett's oesophagus?"Dysplasia on biopsy- requires endoscopic mucosal therapy
"What is seen here?<div><img src=""pdd121.jpg""><br></div>""Barrett's oesophagus"
What are early signs of haemochromatosis?- Fatigue<div>- Erectile dysfunction</div><div>- Arthralgia</div>
"What is seen here, from barium enema?<div><img src=""xrb055.jpg""><br></div>"Diverticulosis: outpouchings of mucosa <b>away </b>from lumen<div><br></div><div>(Polyps are outpouchings of mucosa <b>into </b>lumen)</div>
What tool should be used to screen for malnutrition?Malnutrition Universal Screen Tool (MUST) score
What factors are thought to cause acute pancreatitis?"<font color=""#0000ff"">Mechanical blockage:</font> ↑ ductal presssure + stasis of pancreatic enzymes and autodigestion<div><font color=""#0000ff"">Dysfunctional Ca<sup>2+</sup> signalling:</font> Lead to mitochondrial dysfunction. Reduced ATP and acinar necrosis</div><div><font color=""#0000ff"">Premature trypsin activation:</font> Leads to pancreatic autodigestion and recruitment of inflammatory cells at site of acinar damage</div><div><font color=""#0000ff"">Reduced bicarbonate secretion:</font> Intraductal stasis and premature activation of enzymes</div>"
What can cause cholecystitis?- Gallstones (90%)<div>- Acalculous cholecystitis (10%, associated with ↑ morbidity and mortality)</div>
What is the management of cholecystitis?- IV Abx<div>- Patient NBM + Parenteral fluid</div><div>- Analgesia</div><div>-<b> Laparoscopic cholecystectyomy within 1 week</b></div>
"Where is <b>Sister Mary Joseph's </b>node found?"<b>Umbilicus</b>
"What is a Whipple's procedure?""Surgical opertaion to remove head of pancreas, duodenum, proximal jejunum, gallbladder and part of stomach (as share blood supply with head of pancreas)<div><br></div><div><img src=""paste-4e7e6d034c32b2c390933e1a5985c1855141bc9c.jpg""><br></div>"
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What are the phases of acute viral hepatitis?"<font color=""#0000ff"">Incubation period: </font>Virus multiples & spread without causing symptoms<div><font color=""#0000ff"">Prodromal phase:</font> Non-specific symptoms e.g. anorexia, malaise, nausea & vomiting</div><div><font color=""#0000ff"">Icteric Phase</font>: Urine darkens, followed by jaundice. Systemic symptoms often regress, but jaundice worsens. </div><div><font color=""#0000ff"">Recovery phase:</font> Jaundice fades </div>"
What symptoms typically occur in the prodromal phase of acute viral hepatitis?- Profound anorexia<div>- Malaise</div><div>- Nausea and vomiting</div><div>- Newly developed distaste for cigarettes (in smokers) </div><div>- Fever</div><div>- RUQ abdominal pain </div><div><br></div><div>(Urticaria and arthralgia, particularly in HBV) </div>
What changes happen to the liver in acute viral hepatitis?Usually enlarged & tender, but liver edge remains soft & smooth 
What is <b>anicteric hepatitis</b>?Hepatitis without jaundice- manifests as minor flu-like illness
In what viral infections is anicteric hepatitis a more common presentation than icteric hepatitis?- HCV infection<div>- Children with HAV infection </div>
What is <b>recrudescent hepatitis?</b>- Recurrent manifestations (re-activations) during recovery phase of acute viral hepatitis 
How do ALT/AST values change in acute viral hepatitis?"Levels increase early in prodromal phase and<font color=""#0000ff""> peak before jaundice is maximal, </font>and fall slowly during recovery phase"
What serology is done to confirm acute hepatitis B infection?- Hepatitis B Surface antigen (HBsAg)<div>- IgM antibody to hepatitis B core (IgM anti-HBc)<br><div><div><br></div></div></div>
What serology is done to confirm acute Hepatitis A viral infection?- IgM antibody to HAV (IgM anti-HAV)
What serology studies are done to screen for hepatitis viruses A-C?- IgM anti-HAV<br>- HBsAg<div>- IgM anti-HBc</div><div>- Anti-HCV</div><div>- HCV-RNA PCR</div>
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" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""bfb0d73399c645d593d86f0c70503eb9-ao-3-Q.svg"" /></div> <div id=""io-original""><img src=""tmpzm56a_o2.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""bfb0d73399c645d593d86f0c70503eb9-ao-3-A.svg"" /></div> <div id=""io-original""><img src=""tmpzm56a_o2.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""bfb0d73399c645d593d86f0c70503eb9-ao-4-Q.svg"" /></div> <div id=""io-original""><img src=""tmpzm56a_o2.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""bfb0d73399c645d593d86f0c70503eb9-ao-4-A.svg"" /></div> <div id=""io-original""><img src=""tmpzm56a_o2.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
If serology detects HBsAg, what additional testing should be done?- Hepatitis B e antigen (HBeAg) <div>- Antibody to Hepatitis B e antigen (Anti-HBe)</div><div><br></div><div>Helps determine prognosis and guide antiviral therapy </div>
When should Hepatitis D infection be considered?If serologically confirmed HBV infection is severe
What is the relevance of testing HBsAg and anti-HBs?- Appears during incubation period, 1-6 weeks before clinical illness develops. <div>- Disappears during convalescence. </div><div><br></div><div>- Anti-HBs appears weeks/months later & usually persists for life</div>
What happens to patients with persistent HBsAg and who do not develop antibodies?Pts become asymptomatic carriers of virus, or develop chronic hepatitis 
<span class=cloze>[...]</span> of patients with Hepatitis B become asymptomatic carriers or develop chronic hepatitis<span class=cloze>5-10%</span> of patients with Hepatitis B become asymptomatic carriers or develop chronic hepatitis<br> As they have persistent HBsAg, and do not develop antibody 
5-10% of patients with Hepatitis B become <span class=cloze>[...]</span>5-10% of patients with Hepatitis B become <span class=cloze>asymptomatic carriers or develop chronic hepatitis</span><br> As they have persistent HBsAg, and do not develop antibody 
Where is HBcAg detected?Viral core- detected in infected liver cells, but not in serum (except through special techniques)
When do antibodies to HBcAg appear?Appears at onset of clinical illness (but gradually diminish over time) 
Presence of <span class=cloze>[...]</span> indicate recovery from previous HBV infectionPresence of <span class=cloze>anti-HBs and anti-HBc</span> indicate recovery from previous HBV infection<br> Presence of anti-HBs and anti-HBc indicate <span class=cloze>[...]</span>Presence of anti-HBs and anti-HBc indicate <span class=cloze>recovery from previous HBV infection</span><br> Chronic HBsAg carriers may have what antibodies?IgG Anti-HBc and Anti-HBe (not anti-HBs)
A serology screen of a patient with suspected acute viral hepatitis reveals only IgM anti-HBc. What does this suggest?- IgM suggests acute HBV infection<div>- No HBsAg as decreases during convalescence, and no anti-HBs, as too early for antibodies to HBsAg to develop </div>
What do positive HBeAg and anti-HBe suggest?"HBeAg only present in HBsAg positive serum, and suggests <font color=""#0000ff"">more active viral replication & greater infectivity</font><div><font color=""#0000ff""><br></font></div><div>Anti-HBe suggests lower infectivity. </div>"
Chronic liver disease develops more often among patients with <span class=cloze>[HBeAg/Anti-HBe]</span> and less often in <span class=cloze>[HBeAg/Anti-HBe]</span>Chronic liver disease develops more often among patients with <span class=cloze>HBeAg</span> and less often in <span class=cloze>Anti-HBe</span><br> Chronic liver disease develops <span class=cloze>[...]</span> often among patients with HBeAg and <span class=cloze>[...]</span> often in Anti-HBeChronic liver disease develops <span class=cloze>more</span> often among patients with HBeAg and <span class=cloze>less</span> often in Anti-HBe<br> Why is intussusception more common in 6-18 months? "6 month year old starts to take in more pathogens (start moving around and chewing things)<div><br></div><div>↑ in lymphocytes --> ↑ size of peyer's patches, which can trigger intussusception</div>"
"What is <b>Wilson's disease?</b>"Autosomal recessive disorder characterised by excessive copper deposition in tissues (describes what?)
Autosomal recessive disorder characterised by excessive copper deposition in tissues (describes what?)"What is <b>Wilson's disease?</b>"
"What gene defect causes <b>Wilson's disease?</b>"ATP7B on chromosome 13 (mutations cause what disease?)
ATP7B on chromosome 13 (mutations cause what disease?)"What gene defect causes <b>Wilson's disease?</b>"
"How do people typically present with Wilson's disease?""Onset usually between 10-25y/o: <div><br></div><div><font color=""#0000ff"">Children</font>: Liver disease (Hepatitis, cirrhosis, fulminant liver failure)</div><div><font color=""#0000ff"">Young adults</font>: Neurological disease (Tremor, dysarthria, dysphagia, dyskinesias, dystonias, Dementia, Parkinsonism, ataxia)</div>"
"How can <b>Wilson's disease </b>be diagnosed?""<div><font color=""#0000ff"">Slit lamp exam</font>- Kayser-Fleischer rings</div><div><font color=""#0000ff"">Copper tests</font>:</div>- ↓ Serum caeruloplasmin (as deposited in tissues)<div>- ↑ 24hr urinary copper excretion</div><div><font color=""#0000ff"">Liver biopsy</font>: ↑Hepatic copper, hepatitis, cirhrosis</div><div><font color=""#0000ff"">Molecular genetic testing</font></div><div><font color=""#0000ff"">MRI: </font>Degeneration in basal ganglia, fronto-temporal, cerebellar and brainstem</div>"
"What is the first-line treatment for Wilson's disease?"Zinc maintenace therapy <div><br></div><div>(Penicillamine mentioned commonly in Passmed, but can worsen neurological symptoms and is third line)</div>
What conditions typically cause acute abdominal pain in the <b>Right upper quadrant?</b> - Biliary Colic<div>- Acute cholecystitis</div><div>- Ascending cholangitis </div>
How can you differentiate between biliary colic and acute cholecystitis?"- Biliary colic will have no fever & normal inflammatory markers <div>- Acute cholecystitis pain will tend to be more constant, and will have murphy's sign </div>"
How is pain felt in <b>acute pancreatitis?</b>Epigastric pain, sometimes radiating to back. Often relieved by leaning forwards<div><br></div><div>(describes pain felt in what acute abdominal pain?)</div>
Epigastric pain, sometimes radiating to back. Often relieved by leaning forwards<div><br></div><div>(describes pain felt in what acute abdominal pain?)</div>How is pain felt in <b>acute pancreatitis?</b>
What are the causes of acute pancreatitis?I GET SMASHED<div><br></div><div>Idiopathic</div><div><br></div><div>Gallstones</div><div>Ethanol (alcohol)<br></div><div>Trauma</div><div><br></div><div>Steroids</div><div>Mumps/malignancy</div><div>Autoimmune</div><div>Scorpion sting (Tityus trinitatis in Trinidad)</div><div>Hypercalcaemia/hyperparathyroidism/hypertriglyceridaemia/hypothermia</div><div>ERCP</div><div>Drugs </div>
What can typically cause acute abdominal pain in the <b>epigastric region?</b>- Pancreatitis<div>- Peptic ulcers</div><div>- Gastritis</div><div>(Gastric cancers, if acute bleeding or perforation)</div><div><br></div><div>(cause acute abdominal pain in which area?)</div>
- Pancreatitis<div>- Peptic ulcers</div><div>- Gastritis</div><div>(Gastric cancers, if acute bleeding or perforation)</div><div><br></div><div>(cause acute abdominal pain in which area?)</div>What can typically cause acute abdominal pain in the <b>epigastric region?</b>
Where is pain felt typically in appendicitis?Initially in umbilical area (referred, as midgut organ), then localises to right iliac fossa (following inflammation of surrounding peritoneum)
What are features of appendicitis?"- Anorexia<div>- Tachycardia</div><div>- Low-grade pyrexia</div><div>- Periumbilical pain --> Tenderness in RIF</div><div><br></div><div>Rovsing's sign</div>"
Where is pain felt in acute diverticulitis?Left lower quadrant
How does acute diverticulitis typically present?- Colicky pain in LLQ<div>- Diarrhoea, sometimes bloody</div><div>- Fever, ↑ inflammatory markers + white cells</div><div>- Localised or generalized peritonitis </div>
Where does pain typically present in small bowel obstruction?Umbilical area- as midgut organ, pain referred to around here
What are features of intestinal obstruction?"- Hx of malignancy, or previous operations<div>- Vomiting, absolute constipation (vomiting relieves the pain)</div><div>- ""tinkling"" bowel sounds</div>"
How does renal colic typically present?- Severe intermittent pain, radiating from loin to groin. <div>- Haematuria</div><div>- Pts are characteristically restless </div>
What are common features of acute pyelonephritis?- Fevers and rigors<div>- Vomiting </div>
How does ectopic pregnancy typically present?- Right/left iliac fossa pain<div>- Amenorrhoea for past 6-9 weeks</div><div>- Vaginal bleeding may be present</div>
Where is pain felt in a ruptured abdominal aortic aneurysm?Central abdominal pain, radiating to back 
What additional considerations should be made if a patient develops <i>C. diff </i>infection?Should be isolated for at least 48 hours
"Oesophageal <span class=cloze>[...]</span> is associated with GORD/Barrett's""Oesophageal <span class=cloze>adenocarcinoma</span> is associated with GORD/Barrett's<br> "
Oesophageal adenocarcinoma is associated with <span class=cloze>[...]</span>"Oesophageal adenocarcinoma is associated with <span class=cloze>GORD/Barrett's</span><br> "
On top of ordinary management of Coeliac disease, what else should be offerred?Yearly pneumococcal vaccine (also consider influenza vaccine), as pts often have hyposplenism
"What causative organism typically causes <b>watery traveller's diarrhoea w/ stomach cramps and nausea?</b>"Enterotoxigenic <i>E. coli</i> (typically causes what type of diarrhoea?)
Enterotoxigenic <i>E. coli</i> (typically causes what type of diarrhoea?)"What causative organism typically causes <b>watery traveller's diarrhoea w/ stomach cramps and nausea?</b>"
What is <b>melanosis coli</b>?Disorder of pigmentation of bowel wall, associated with laxative abuse (describes what?)
Disorder of pigmentation of bowel wall, associated with laxative abuse (describes what?)What is <b>melanosis coli</b>?
What is found on histology of <b>melanosis coli?</b>Pigment-laden macrophages (is found on histology of what condition?)
Pigment-laden macrophages (is found on histology of what condition?)What is found on histology of <b>melanosis coli?</b>
"What is seen here?<div><img src=""LargeBowel_MelanosisColi_Clinical_resized.jpg""><br></div>"Melanosis coli
How can sickle cell disease cause biliary colic?-Causes haemolysis, which causes pigment stones
In what patients do pigment stones form?- Asian populations<div>- Haemolysis (e.g. sickle cell disease)</div>
What is the classic presentation of haemochromatosis?Triad of:<br>- Diabetes<div>- Bronze skin</div><div>- Hepatomegaly</div>
What are the classic hallmarks of autoimmune hepatitis?- Young female<div>- Signs of liver disease</div><div>- Amenorrhoea </div>
"What is seen here, on OGD?<div><img src=""QOSruvrqqHRQsuZq5qsJUKI1Y1EnJ20357KU5CrSGqtz5eVDZFeVvJ56gY4iXPTjyuE1fizJt4vhTwB9mPugzOM5iuGtcuVBxL-p9pEpQx6A_smw4nkMqF6MI71C=w600.jpg""><br></div>"Oesophageal varices
What is the appropriate management for oesophageal varices which are not bleeding?- Beta blockers: reduce risk of bleeding by around 50% <div>- Consider endoscopic variceal ligation </div>
How can the severity of acute pancreatitis be assessed? Glasgow criteria- if patient scores ≥ 3, severe pancreatitis likely 
What makes up the Glasgow Criteria?<div><br></div><div>P<span class=cloze>[...]</span></div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>P<span class=cloze>aO<sub>2</sub> <8kPa</span></div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>A<span class=cloze>[...]</span></div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>A<span class=cloze>ge >55</span></div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>N<span class=cloze>[...]</span></div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>N<span class=cloze>eutrophils: WCC >15</span></div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>C<span class=cloze>[...]</span></div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>C<span class=cloze>alcium <2mmol</span></div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>R<span class=cloze>[...]</span></div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>R<span class=cloze>enal function: Urea >16</span></div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>E<span class=cloze>[...]</span></div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>E<span class=cloze>nzymes LDH >600, AST > 200</span></div><div>Albumin <32g/L </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>A<span class=cloze>[...]</span> </div><div>Sugar >10mmol/L</div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>A<span class=cloze>lbumin <32g/L</span> </div><div>Sugar >10mmol/L</div><br> What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>S<span class=cloze>[...]</span></div>What makes up the Glasgow Criteria?<div><br></div><div>PaO<sub>2</sub> <8kPa</div><div>Age >55</div><div>Neutrophils: WCC >15</div><div>Calcium <2mmol</div><div>Renal function: Urea >16</div><div>Enzymes LDH >600, AST > 200</div><div>Albumin <32g/L </div><div>S<span class=cloze>ugar >10mmol/L</span></div><br> What are the parameters which make up the Glasgow Criteria?PaO<sub>2</sub><div>Age > 55</div><div>Neutrophils: WCC</div><div>Calcium</div><div>Renal function: Urea</div><div>Enzymes: LDH, AST</div><div>Albumin</div><div>Sugar</div>
How are spider naevi typically distributed?Follow distribution of superior vena cava
What causes spider naevi?Increased oestrogen, from chronic liver disease 
What is a defunctioning stoma?A temporary stoma- created to allow more distal part of bowel to heal after surgery
What is a <b>loop </b>stoma?"One side of bowel wall is divided and two open parts are brought to surface<div><img src=""End-loop-or-defunctioned-loop-colostomy-from-Prasad-et-al-9-A-The-entire-divided.png""><br></div><div><br></div><div>(describes what?)</div>"
"One side of bowel wall is divided and two open parts are brought to surface<div><img src=""End-loop-or-defunctioned-loop-colostomy-from-Prasad-et-al-9-A-The-entire-divided.png""><br></div><div><br></div><div>(describes what?)</div>"What is a <b>loop </b>stoma?
Which stomas are typically raised and why?Ileostomies: raised to prevent active enzymes from irritating the skin 
Coeliac disease is associated with what deficiencies?- Iron<div>- Folate</div><div>- Vitamin B12</div>
"What is frequently an early manifestation of Wilson's disease?"- Psychiatric problems 
When should PPIs be prescribed in an acute GI bleed?<b>After </b>endoscopy, as they may mask site of bleeding
What is the most common cause of hepatocellular <b>caricnoma </b>in Europe?Hepatitis<b> C</b>
"<div>What is <b>1</b>?</div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg"">""Kocher's incision (is what number?)<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"
"What is 2?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"Midline incision 
"What is 3?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>""Grid-iron incision/McBurney incision (is what number?)<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"
"What is 5?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>""Lanz incision (is what number?)<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"
"Lanz incision (is what number?)<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>""What is 5?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"
"What is 6?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"Paramedian incision
"What is 7?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"Transverse incision 
"What is 9?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>""Pfannestiel incision (is what number?)<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"
"Pfannestiel incision (is what number?)<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>""What is 9?<div><img src=""paste-51c664ea4757b947f04d9b1bb303b8c4161200bc.jpg""><br></div>"
"<b>Pfannenstiel's </b>incision is typically used for what procedures?"- Caesarian section<div>- Abdominal hysterectomy</div><div><br></div><div>(Require what incision?)</div>
- Caesarian section<div>- Abdominal hysterectomy</div><div><br></div><div>(Require what incision?)</div>"<b>Pfannenstiel's </b>incision is typically used for what procedures?"
"What is <b>Kocher's incision</b> required for?"- Open cholecystectomy<div>- Operations on liver, gallbladder and biliary tract </div><div><br></div><div>(require what incision?)</div>
- Open cholecystectomy<div>- Operations on liver, gallbladder and biliary tract </div><div><br></div><div>(require what incision?)</div>"What is <b>Kocher's incision</b> required for?"
What is the <b>rooftop incision</b>?"- Continued Kocher's incision across LUQ, provides access to pancreas and biliary tree "
What incisions can be used for appendectomy?- Gridiron incision<div>- Lanz incision (more cosmetically subtle)</div>
"What is seen here, on a barium study? <div><img src=""xrb171.jpg""><br></div>""Long segment of narrowed terminal ileum- 'string-like configuration'- <b>Kantor's string sign</b>. <font color=""#0000ff"">Sign of Crohn's disease</font>"
Which class of antibiotics are the leading cause of <i>Clostridium difficile </i>infections?2nd and 3rd generation cephalosporins 
How is <i>C. diff</i> infection diagnosed?Detected <i>Clostridium difficile </i>toxin (CDT) in stool 
What does <i>C. diff</i> antigen positivity indicate?Shows previous exposure to bacteria, not necessarily current infection
Patients who experience intermittent dysphagia and odynophagia following systemic antibiotics should be investigated for what?Oesophageal candidiasis
What blood marker is used to assess <b>ovarian cancer?</b>CA 125 (is used as a marker for what?)
CA 125 (is used as a marker for what?)What blood marker is used to assess <b>ovarian cancer?</b>
What should be the initial investigation for suspected Budd-Chiari syndrome?USS with Doppler Flow studies
What is the recommended treatment for severe alcoholic heaptitis?Corticosteroids <div><br></div>
Aside from usual blood tests, what test can help differentiate between IBS and IBD in primary care?- Faecal calprotectin
What is the best non-invasive way to assess liver cirrhosis?Transient elastography/fibroscan- USS and low-frequency elastic waves
<span class=cloze>[...]</span> is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease<span class=cloze>Thrombocytopenia</span> is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease<br> Thrombocytopenia is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in <span class=cloze>[...]</span>Thrombocytopenia is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in <span class=cloze>those with chronic liver disease</span><br> "What is the <b>King's College Hospital Criteria </b>used for?""- Determines if poor prognosis in <font color=""#0000ff"">acute liver failure (</font>+therefore prompt consideration for transplantation)"
"What factors make up the King's College Hospital Criteria in paracetamol-induced liver failure?"- Arterial pH <7.3 24h after ingestion<div>- Or all of: PT>100s (INR>6.5), Creatinine >300μmol/L, Grade III or IV encephalopathy</div>
"What are the King's College Hospital Criteria in Non-paracetamol liver failure?"- PT >100s<div>- Or 3 out of the following 5:</div><div><br></div><div>1. Drug-induced liver failure</div><div>2. Age <10, or >40</div><div>3. >1wk from1st jaundice to encephalopathy</div><div>4. PT>50s</div><div>5. Bilirubin ≥300μmol/L</div>
What is the median survival for Hepatorenal syndrome type 1 and 2?"<font color=""#0000ff"">Type 1</font>: 2 weeks<div><font color=""#0000ff"">Type 2</font>: 6 months</div>"
What are the different types of liver transplants?- Cadaveric (heart beating or non-heart beating)<br>- Live donors (right lobe)
What parameters is used to calculate the UKELD?- Serum Na<sup>+</sup><div>- Creatinine</div><div>- Bilirubin</div><div>- INR</div>
How is Hepatitis A virus typically spread?Faecal-oral or in shellfish 
Hepatitis <span class=cloze>[...]</span> is endemic in Africa and South AmericaHepatitis <span class=cloze>A</span> is endemic in Africa and South America<br> Hepatitis A is endemic in <span class=cloze>[...]</span>Hepatitis A is endemic in <span class=cloze>Africa and South America</span><br> What is the incubation period of Hepatitis A virus?2-6 weeks
At what point can IgM anti-HAV be detected?Day 25 of infection (AST/ALT rise 22-40days after exposure)
How should Hepatitis A infection be managed?- Supportive: fluids etc. <div>- Avoid alcohol. </div><div><br></div><div>- Interferon Alpha rarely, if fulminant hepatitis</div>
How is Hepatitis A vaccinated for?- Immunisation with inactivated viral protein, IM<div>- 1 dose gives immunity for 1 year, 20 years if further booster given at 6-12 months</div>
What is the prognosis of Hepatitis A?- Usually self-limiting + no chronicity<div>- Fulminant hepatitis is rare</div>
What type of virus is Hepatitis A?Single stranded picornavirus
When does faecal shedding of Hepatitis A occur?Occurs before symptoms develop and usually ceases a few days after symptoms begin: infectivity ceased when hepatitis becomes clinically evident
What type of virus is Hepatitis B Virus?DNA Hepadnavirus
How is Hepatitis B virus spread?- Blood products<div>- IV drug users</div><div>- Sexual, direct contact</div><div>- Vertical transmission</div>
Hepatitis <span class=cloze>[...]</span> is endemic in Far East, Africa, Mediterranean Hepatitis <span class=cloze>B</span> is endemic in Far East, Africa, Mediterranean <br> Hepatitis B is endemic in <span class=cloze>[...]</span>Hepatitis B is endemic in <span class=cloze>Far East, Africa, Mediterranean </span><br> What is the incubation period of Hepatitis B virus?1-6 months 
What increases the risk of developing chronic infection in Hepatitis B infection?Younger the age when acute infection occurs, higher the risk:<div><br></div><div>- 90% for infants</div><div>- 25-50% for 1-5y/o</div><div>- 5% for adults </div>
When does HBeAg typically persist?1.5-3 months after acute illness 
<span class=cloze>[...]</span> defines carrier status in Hepatitis B infection <span class=cloze>HbsAg persisting for >6months</span> defines carrier status in Hepatitis B infection <br> HbsAg persisting for >6months defines <span class=cloze>[...]</span> in Hepatitis B infection HbsAg persisting for >6months defines <span class=cloze>carrier status</span> in Hepatitis B infection <br> What are complications of Hepatitis B infection?"- Fulminant hepatitis<div>- Cirrhosis</div><div>- HCC</div><div>- Cholangiocarcinoma</div><div><br></div><div><font color=""#0000ff"">Associated:</font></div><div>- Cryoglobulinaemia</div><div>- Membranous nephropathy</div><div>- Polyarteritis Nodosa</div>"
How should Hepatitis B infection be managed?"- Avoid alcohol<div>- Immunise sexual contacts</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If fulminant hepatitis:</font></div><div>- Oral nucleoside/nucleotide analaogues</div><div>- Pegulated interferon alpha-2a</div><div><br></div><div><b>Note: No treatments help acute viral hepatitis- can only treat fulminant or chronic</b></div>"
What drugs are used to treat fulminant hepatitis B infection?- Entecavir<div>- Tenofovir (preferred in pregnancy)</div><div><br></div><div>- Peginterferon alfa 2a (if elevated Hepatitis D virus RNA and ALT levels)</div>
What type of virus is Hepatitis C virus?RNA flavivirus 
How is Hepatitis C spread?- Blood (transfusion, IV drug abuse, sexual contact)
What is the typical outcomes of Hepatitis C infection?- 85% develop silent chronic infection (1/4 of these develop cirrhosis in 20 years, then 4% of these get HCC)
What are risk factors for progression of Hepatitis C virus?- Male<div>- Older</div><div>- Higher viral load</div><div>- Use of alcohol</div><div>- HIV</div><div>- HBV</div>
Hepatitis C infection sometimes occurs simultaneously with which disorders?- Essential mixed cryoglobulinaemia<div>- Porphyria cutanea tarda</div><div>- Glomerulonephritis</div>
How should Hepatitis C virus be managed?- Stop alcohol<div>- Supportive care</div><div><br></div><div>Only provide antiviral drugs if patients fail to spontaneously clear HCV within 6 months </div>
What drugs can be used to treat chronic Hepatitis C infection?- Ledipasvir + Sofosbuvir: inhibitors of non-structural viral proteins<div>- Ribavirin- nucleoside analogue (useful in genotypes 2/3)<br></div>
<span class=cloze>[...]</span> of HBV carriers have HDV co-infection<span class=cloze>5%</span> of HBV carriers have HDV co-infection<br> Where is Hepatitis E common?Indochina 
Is Hepatitis A or E more common in the UK?Hepatitis E
What disease is associated with microscopic colitis?Coeliac disease- increases risk of lymphocytic colitis 
How is giardiasis diagnosed?Detection of cysts or trophozoites in stool sample 
What are key diagnostic features of giardiasis?- Chronic Diarrhoea: watery with no mucus, pus or blood. <div>- Frequent belching (often has a sulphuric smell)</div>
How can giardiasis be treated?"<div><font color=""#0000ff"">1st line:</font></div>- Nitroimidazoles: Metronidazole, Tinidazole <div><font color=""#0000ff"">2nd line:</font></div><div>- Nitazoxanide or albendazole if pt intolerant to nitroimidazoles</div>"
What is a common cause of<b> infectious chronic </b>diarrhoea?<b>Giardiasis</b>
If <i>C. diff </i>infection has failed to be treated with a 14 day course of metronidazole, what should happen next?Switch to Oral vancomycin 
When should a patient suffering from <i>C. diff</i> infection be switched from metronidazole to oral vancomycin and IV metronidazole?If infection fails to respond to metronidazole and <b>if life-threatening infection</b>
"What is seen here on barium enema?<div><img src=""650664_s-227x300.jpg""><br></div>"Normal bowels- no pathology
"What is seen here, on barium enema?<div><img src=""xrb170.jpg""><br></div>"Ulcerative Colitis- loss of haustra markings continuously 
"What is the management of Gilbert's syndrome?"Reassurance- benign condition causing mild rise in bilirubin, so no treatment required
<span class=cloze>[...]</span> seen on an ERCP is suggestive of Primary Sclerosing Cholangitis"<span class=cloze>Beaded strictures</span> seen on an ERCP is suggestive of Primary Sclerosing Cholangitis<br> <img src=""Primary-sclerosing-cholangitis-PSC-ERCP-shows-stenosis-and-beaded-appearance.png"">"
Beaded strictures seen on an ERCP is suggestive of <span class=cloze>[...]</span>"Beaded strictures seen on an ERCP is suggestive of <span class=cloze>Primary Sclerosing Cholangitis</span><br> <img src=""Primary-sclerosing-cholangitis-PSC-ERCP-shows-stenosis-and-beaded-appearance.png"">"
What is important to establish when being bleeped about a patient in an acute situation?- Age of patient<div>- Reason for current admission/ how long have they been in for</div><div>- What the current problem is</div><div>- Level of consciousness</div><div>- Obs </div>
What are signs of complete airway obstruction?"- See-saw breathing<div>- No ""misting"" of face mask</div><div>- No breath sounds</div><div>- Unable to feel air movement from mouth</div>"
What are signs of partial airway obstruction?"- Increased work of breathing<div>- ""noisy breathing""- gurgling, snoring, stridor</div><div>- Some air movement can be felt</div>"
If there are issues with the patients airways, what can you do?-- Suction/ removal of obstruction<div>- Airway manouvres</div><div>- 100% Oxygen</div><div>- Call for help</div>
"What should you consider in the ""D"" of ABCDE"Disability:<div><br></div><div>- GCS/AVPU</div><div>- Pupils (equal and reactive?)</div><div>- Blood glucose</div><div>- Drugs </div>
What does SBAR stand for?Situation<div>Background</div><div>Assessment</div><div>Recommendations </div>
What is different about critical care?- ↑ number of staff: 1:1 nursing<div>- Special equipment to monitor or replace failing organ function (ventilators, haemofiltration, CO monitors, etc.)</div><div>- Some drugs can only safely be given on ITU e.g. inotropes</div>
What is meant by level 0 care?Requires hospitalisation:<div>- IV therapy</div><div>- Obs <4hrs</div>
What is meant by Level 1 care?- Recently discharged from higher levels of care<div>- Needs additional monitoring/clinical interventions, inputs or advice</div><div>- Requiring CCU outreach </div>
What is meant by Level 3 care?- Advanced respiratory support <div>- Minimum of 2 organs supported </div>
What is chromogranin A?Unspecific biomarker for Neuro-endocrine tumours 
How is the risk of post-ERCP pancreatitis reduced?Diclofenac suppository
- Periorificial dermatitis<div>- Alopecia</div><div>- Diarrhoea</div><div><br></div><div>(is the classic presentation of what?)</div>What characterises <b>acrodermatitis enteropathica</b>?
Hepatitis <span class=cloze>[...]</span> has a particularly high mortality in pr<b>e</b>gnant patientsHepatitis <span class=cloze><b>E</b></span> has a particularly high mortality in pr<b>e</b>gnant patients<br> 15-25%
Hepatitis <b>E</b> has a particularly high mortality in <span class=cloze>[...]</span> patientsHepatitis <b>E</b> has a particularly high mortality in <span class=cloze>pr<b>e</b>gnant</span> patients<br> 15-25%
What are <b>granulomas?</b>Collection of <b>activated macrophages </b>
"What is the surgical management of Crohn's disease? (RDS)""- <b>Resection</b><div><b>- Diversion</b></div><div>- <b>Stricturo plasty</b>: widens bowel without losing any bowel. </div><div><br></div><div><img src=""Stricturoplasty-Rework.png""><br></div>"
What are the different surgical options to manage ulcerative colitis?"<div>- <b>Procto colectomy</b> (only L intestine & rectum removed) with <b>terminal ileostomy</b></div><div><img src=""paste-06a930db483e257b27bfdede3a74c6f40ae8c7e3.jpg""><br></div><div>- <b>Total colectomy</b> and <b>ileorectal anastomosis</b></div><div><img src=""59d6915255853481d30c155e70184bf1.jpg""><br></div>- <b>Proctocolectomy</b> with construction of <b>Ileoanal pouch</b> (construction of reservoir from healthy ileum to reduce stool frequency)<div><img src=""ac75bfb70b42a822662bfb3b07b04d3d.jpg""><br></div>"
What is diverticulosis?Presence of one or more diverticula
What is the management of <b>uncomplicated </b>diverticular disease?- <b>Avoid insoluble fibre </b><div>- <b>Anti spasmodic drugs</b> (mebeverine/peppermint oil) (hyoscine butylbromide, atropine sulfate etc)</div>
Where in the body is diverticulosis most common?<b>Sigmoid</b> colon- in 95%<div><br></div><div>(can be found in the right colon, esp. in Asian pts)</div>
What is the lining of the anus?Lower 1/3: <b>Squamous</b> epithelium<div>Upper 2/3: <b>Columnar </b>epithelium </div><div><br></div><div>Separated by <b>pectinate line</b></div>
What controls the sphincters of the anus?"<font color=""#0000ff"">Internal</font>: <b>Autonomic </b>control, as continuation of circular smooth muscle<div><font color=""#0000ff"">External</font>: Striated muscle- <b>voluntary</b> control via <b>Pudendal </b>(S2-S4)</div>"
What causes anal fissures?Longitudinal anodermal split:<div>- Caused by <b>mechanical trauma </b>and hypertonicity of the external anal sphincter</div>
How should an anal abscess be managed?- <b>Drain</b> abscess (must exclude proctitis first)<div>- <b>Pack </b>wound</div><div>- Heal by <b>secondary intention </b>(closes naturally)</div>
In which patients is rectal prolapse more common in?<b>Elderly multiparous females</b>
What occurs in rectal prolapse?"Intussussception of rectum:<div><img src=""rectal-prolapse-8col.jpg""><br></div><div><br></div>"
What are haemorrhoids?<b>Vascular-rich connective tissue</b> within anal cushions, causing <b>hypertrophy </b>
What causes anal warts?<b>HPV</b> types 6, 11, 16 and 18 
What is the long-term risk of anal warts?- Anal intra-epithelial <b>neoplasia</b><div>- Squamous cell <b>carcinoma</b> of the anus </div>
What <b>non-invasive</b> methods can be used to test for <i><b>H. pylori?</b></i>- <b>Urea</b> <b>breath test</b><div>- Stool <b>antigen</b> testing (more preferred, as widely available and more acceptable to patient)</div>
What can a raised amylase suggest?"- <b>Pancreatitis</b><br><div>- <b>Appendicitis<br></b>- <b>Cholecystits</b><b><br></b></div><div>- <b>Mumps <br><br>PACManylase</b></div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff""><b>Lipase is more specific to pancreatitis</b></font></div>"
What are the most common triggers of acute pancreatitis?- Gallstones (40%)<div>- Alcohol (30%)</div>
How can alcohol intake cause acute pancreatitis?"Pancreatic <font color=""#0000ff"">acinar </font>cells metabolise alcohol into toxic metabolites→ predisposes cells to autodigestive injury "
What mediates the pathogenesis of acute pancreatitis?- Intra-acinar activation of pancreatic enzymes → autodigestive injury <div><br></div><div>Damaged tissue activates complement + inflammatory cascade → oedema + hypovolaemia. </div><div><br></div><div>Activated enzymes & cytokines which enter peritoneum can cause chemical burn + third-spacing of fluid, those that enter systemic circulation causes systemic inflammatory response- ARDS & acute kidney injury </div>
What proportion of acute pancreatitis cases are mild?80%- remaining 20% develop into severe complicated and life-threatening disease
What are early complications of acute pancreatitis?- Shock<div>- ARDS</div><div>- Renal failure</div><div>- Disseminated Intravascular Coagulation</div><div>- Sepsis</div><div>- ↓Ca<sup>2+</sup></div><div>- ↑ Glucose (transient; 5% need insulin)</div>
What are symptoms of acute pancreatitis?- Gradual or sudden severe epigastric or central abdominal pain (radiates to back, may be relieved by sitting forwards)<div>- Vomiting </div>
What are late (>1 week) complications of acute pancreatitis?- Pancreatic necrosis & pseudocyst<div>- Abscesses</div><div>- Bleeding (from elastase erosion of blood vessels)</div><div>- Thrombosis</div><div>- Fistulae (though they normally close spontaneously) </div><div>- Recurrent oedematous pancreatitis</div>
What forms pancreatic pseudocysts?"Collections of enzyme-rich pancreatic fluid within the <font color=""#0000ff"">lesser sac of the abdomen</font> "
"What is seen here?<div><img src=""Pancreaticpseudocyst.png""><br></div>"Pancreatic pseudocyst: collection of enzyme-rich pancreatic fluid in the lesser sac 
How do pancreatic pseudocysts present?- Fever<div>- Mass </div><div>- Persistent ↑ Amylase/LFTs</div><div><br></div><div>1/3 spontaneously resolve, the rest need draining </div>
What is a further complication of pancreatic necrosis?Infection: pseudocysts can be infected by gut bacteria → high morbidity and mortality
Where do thromboses typically form in acute pancreatitis?- Splenic/gastroduodenal arteries<div>- Colic branches of the SMA</div><div><br></div><div>Can cause bowel necrosis </div>
Why is serum lipase a better marker than amylase for acute pancreatitis?- More specific to pancreatitis<div>- More sensitive: rises earlier, and falls later </div>
What can be seen on AXR of acute pancreatitis?- Loss of psoas shadow (due to ↑ retroperitoneal fluid)<div>- Sentinel loop of bowel </div>
Why might scleral icterus be seen in acute pancreatitis?Obstruction of bile duct by:<div>- Gallstone or Inflammation swelling of pancreatic head</div>
What is the imaging study of choice to investigate pancreatitis?- CT w/ IV contrast 
What is the value of a repeat CT 72hrs after onset of acute pancreatitis?Identifies complications e.g. necrosis fluid collection of pseudocysts. <div><br></div><div>(necrotic tissue will not enhance after IV contrast, but may only appear 48-72hrs after onset)</div>
"What is seen here?<div><img src=""0100-3984-rb-47-03-0165-gf04-en.jpg""><br></div>"Pancreatic necrosis: does not take up contrast so remains black 
When should abdominal USS be used in acute pancreatitis?If gallstone pancreatitis is suspected + ↑ AST
What defines SIRS? Systemic inflammatory response syndrome:<div><br></div><div>- Temperature >38.3°C or <36°C</div><div>- HR > 90 bpm</div><div>- RR > 20</div><div>- WCC > 12 x 10<sup>9</sup>/L, or <4 x 10<sup>9</sup>/L </div>
What is the pathophysiology of ARDS 2° to pancreatitis?- Release of inflammatory mediators causes ↑ capillary permeability → pulmonary oedema. <div>- Often accompanied by multi-organ syndrome </div>
How should the modified Glasgow criteria be interpreted?"3 or more positive factors detected within 48h of onset suggests severe pancreatits + <font color=""#0000ff"">should prompt transfer to ITU</font>"
What is the management of acute pancreatitis (uncomplicated)?"-<font color=""#0000ff""> Fluid resuscitation</font>: lots of crystalloid, to counter third-spacing <div>- <font color=""#0000ff"">Analgesia</font>: Pethidine or morphine (morphine better analgesic, but can cause sphincter of oddi to contract more)</div><div>-<font color=""#0000ff""> Nutritional support</font>: NBM, consider NJ feeding to decrease pancreatic stimulatiom. </div><div><br></div><div>- ERCP for gallstone removal may be needed if progressive jaundice</div><div>- Monitor vitals, urine output</div><div>- Repeat imaging to monitor progress</div>"
Why is enteral feeding preferred to parenteral feeding in pancreatitis?- Helps maintain intestinal mucosal barrier<div>- Prevents intestinal atrophy which can occur with prolonged bowel rest</div><div>- Avoids risk fo infection of IV catheter</div><div>- Less expensive</div>
Why is intestinal atrophy concerning in acute pancreatitis?Promotes translocation of bacteria which can seed pancreatic necrosis
Why is a nasojejunal tube preferred in enteric feeding in acute pancreatitis?Helps decrease pancreatic stimulation + prevents further release of enzymes causing autodigestion 
"What is Ranson's criteria used for?""Assesses severity of acute alcohol-induced pancreatitis (<font color=""#0000ff"">and can only be fully applied after 48h)</font>"
When is the modified <b>Glasgow Criteria</b> used?"Predicts<b> severity</b> of<b> acute pancreatitis</b> caused by<font color=""#0000ff""> gallstones and alcohol</font>"
What is meant by<b> diverticular disease</b>?Diverticula are <b>symptomatic</b> (describes what?)
Diverticula are <b>symptomatic</b> (describes what?)What is meant by<b> diverticular disease</b>?
What causes diverticula to form?<b>High intraluminal pressures</b> force <b>mucosa</b> to <b>herniate</b> through <b>muscle layers</b> of gut 
What is a diverticulum?"Sac-like <b>mucosal pouch</b> which protrudes through bowel wall, <b>away from lumen</b><div><img src=""diverticulitis_s1.jpg""><b><br></b></div>"
What is the difference between true and pseudo-diverticula?"<font color=""#0000ff"">True diverticula</font>: Contain <b>all layers of GI wall</b> e.g. Meckel's diverticula<div><br><div><font color=""#0000ff"">Pseudo-diverticula</font>: Mucosal/submucosal protrusions through muscular wall of bowel e.g colonic diverticula</div></div><div><img src=""paste-664cadc5d00c64e30d9685735ae36009bb46b61f.jpg""><br></div><div><br></div>"
What proportion of patients with colonic diverticulosis present with symptoms?<b>20%</b> (when inflammatory or haemorrhagic complications develop)<div><br></div><div>80% remain asymptomatic or only have non-specific GI symptoms</div>
How does a pt with symptomatic uncomplicated diverticular disease (SUDD) present?"Non-specific GI symptoms:<br>- Abdo pain,<div>- Bloating</div><div>- Constipation/ Diarrhoea</div><div>- Passage of mucus from rectum</div><div><br></div><div><font color=""#0000ff"">There is debate whether this is actually a condition, or just coincidental diverticular in IBS</font></div>"
What are complications of diverticular disease?- Diverticul<b>itis</b><div>- Diverticular<b> bleeding</b></div><div>- <b>Fistulae</b></div><div>- <b>Abscesses</b></div><div>- Post-infective <b>strictures</b></div>
Diverticular bleeding occurs in <span class=cloze>[...]</span> of pts with diverticulosisDiverticular bleeding occurs in <span class=cloze>10-15%</span> of pts with diverticulosis<br> What is <b>segmental colitis associated with diverticular disease?</b>Manifestations of colitis (haematochezia, abdominal pain, diarrhoea) which develop in 1% of pts with diverticulosis
What is the most common cause of brisk lower GI bleeding in adults?<b>Diverticular bleeding</b>
What can cause diverticular bleeding?- Local <b>trauma</b> from <b>impacted faeces</b> in diverticulum, eroding adjacent vessel<div>- <b>Enlargement</b> of diverticulum, which <b>stretches</b> + tears the vessel </div>
What increases the risk of developing complications in diverticulosis?- Smoking<div>- Obesity</div><div>- Use of<b> NSAIDs</b></div>
What imaging modality is best to investigate <b>acute diverticulitis</b>?<b>CT</b> abdomen- can identify extent of disease and any complications <div><br></div><div>(colonoscopy carries increased risk of perforation in acute diverticulitis)</div>
How are most diverticula discovered?<b>Incidental</b> finding on colonoscopy (as asymptomatic most of the time)
When should lower GI bleeding due to diverticulosis be suspected?<b>Painless rectal bleeding</b>, particularly in an elderly patient or patient with history of diverticular disease
How should diverticular bleeding be managed?75% stop spontaneously- so <b>supportive therapies</b> e.g. blood transfusions/ fluids.<div><br></div><div>Endoscopic options to control bleeding if unresolved </div><div><br></div><div><b>Surgery</b> (removal of affected bowel, or subtotal colectomy if not identified) if uncontrollable massive bleeding</div>
What are causes of rectal bleeding?- <b>Diverticulitis</b><div>- <b>Colorectal cancer</b></div><div>- <b>Haemorrhoids</b></div><div>- <b>IBD</b></div><div>- Perianal disease</div><div>- Angiodysplasia </div><div><br></div><div>Rarer: Trauma, ischaemic colitis, radiation proctitis or aorto-enteric fistula </div>
How should acute <b>rectal bleeding</b> be managed?- ABCDE assessment and resuscitation<div>- <b>Blood</b> tests: FBC, U&E, LFT, Clotting, Amylase, CRP, Group and save</div><div>- <b>Imaging</b>: <b>AXR,</b> or Erect CXR if suspect perforation (gas more visible on Xray)</div><div>- <b>Fluid </b>management: 2 widebore cannulae, crystalloids and blood transfusions if necessary. Catheterise if appropriate</div><div>- <b>Clotting</b>: Withold and r<b>everse anticoagulation</b> and antiplatelet agents</div><div>- <b>Keep bedbound</b>: could cause pt to collapse</div><div>- <b>Stool chart</b> to monitor volume and frequency of motons</div><div>- Diet: <b>clear fluids</b></div><div>- Interventions: if not settling with sconservative management</div><div>- <b>Surgery</b></div>
What interventions could be used for <b>acute rectal bleeding?</b>"<div>- <font color=""#0000ff"">Colonoscopy</font>: for endoscopic haemostasis<br></div>- <font color=""#0000ff"">Angiography </font>(to identify location) and <font color=""#0000ff"">embolisation</font>- done with interventional radiology (only if colonoscopy unssuccessful and ongoing massive bleeding)<div><br></div>"
What are symptoms of diverticular disease?- Altered <b>bowel habit</b><div>- Left-sided<b> colicky pain</b> <b>relieved by defecation</b></div><div>- <b>Nausea</b></div><div>- <b>Flatulence </b></div>
How should diverticular disease be managed?"- <b>Antispasmodics</b><div>- <b>Increase fibre</b> intake</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If severe, and conservative management fails:</font><br></div><div>- Occasionally <b>surgical resection</b></div>"
How should <b>mild </b>diverticulitis be managed?Treated at home:<div>- Rest and<b> liquid diet</b></div><div>- Oral <b>antibiotics </b></div><div>- <b>Paracetamol </b></div>
When should people with diverticulitis be admitted?- More <b>severe pain</b>, fever<div>- <b>Cannot tolerate fluids </b>and pain</div>
Which patient group should you be particularly worried about if presenting with diverticulitis?<b>Immunocompromised </b>patients- often have few symptoms and present late 
What are possible complications of diverticulitis?<b>- Abscess</b><div><b>- Fistula</b></div><div><b>- Obstruction</b></div><div><b>- Perforation </b></div>
How should <b>abscesses</b> in colonic diverticulitis be treated?Percutaneous <b>CT-guided drainage </b>
How is the degree of diverticulitis graded?Stage 1: Pericolic or mesenteric abscess<div>Stage 2: Walled off or pelvic abscess</div><div>Stage 3: Generalised purulent (pus) peritonitis</div><div>Stage 4: Generalised faecal peritonitis</div><div><br></div><div>(Stage 3 and 4 require surgery, stage 2 may resolve without). </div>
What are indications for elective surgery of diverticulitis?- <b>Stenosis</b><div>- <b>Fistulae</b></div><div>- <b>Recurrent bleeding </b></div>
In cases of suspected abscesses, if there is no localising signs, where should be suspected?Under diaphragm:<div><br></div><div>Urgent USS for Subphrenic abscess</div>
How does cyclical vomiting syndrome present?- Severe nausea and sudden vomiting lasting hours-days<div>- Prodromal intense sweating and nausea</div><div>- Well in between episodes</div><div><br></div><div>- Often associtaed with migraines (particularly in children)</div>
Who is mostly affected by cyclical vomiting syndrome?- Children<div>- Females > Males </div>
How should cyclical vomiting syndrome be diagnosed?Clinical diagnosis:<div><br></div><div>- Urinary Beta-HCG to rule out pregnancy</div><div>- Routine blood tests to exclude other conditions</div>
How should cyclical vomiting syndrome be managed?- Avoidance of triggers<div>- Prophylactic treatments: <b>Amitriptyline</b>, <b>propranolol,</b> <b>topiramate (antiepileptic)</b></div><div>- In acute episodes: <b>ondansetron</b> (5HT3 antagonist), <b>prochloperazine</b> (D2 antagonist), triptans</div>
What is an important consideration when testing coeliac disease in patients?If patient is following gluten-free biopsy, serological tests and jejunal biopsy may be negative:<div><br></div><div>- Encourage pt to eat gluten in more than one meal every day for at least 6 weeks before further testing</div>
What is found on colonoscopy and biopsy of <b>Peutz-Jeghers</b> syndrome?Hamar tomatous <b>polyps</b>
A patient with a Hx of COPD, with DH of <b>salbutamol</b> and <b>beclomethasone </b>inhalers presents with<b> pain on swallowing</b>. What is the most likely cause?Oesophageal <b>candidiasis </b>(complication of <b>inhaled steroid</b> therapy)
How does bleeding occur in peptic ulcer disease?<b>Base of ulcer erodes into vessel </b>
<span class=cloze>[...]</span> ulcers classically cause bleeding through erosion of the gastroduodenal artery<span class=cloze>Posterior duodenal</span> ulcers classically cause bleeding through erosion of the gastroduodenal artery<br> Posterior duodenal ulcers classically cause bleeding through erosion of the <span class=cloze>[...]</span>Posterior duodenal ulcers classically cause bleeding through erosion of the <span class=cloze>gastroduodenal artery</span><br> What is <b>xerostomia?</b><b>Dry mouth</b> due to decreased saliva (describes what?)
<b>Dry mouth</b> due to decreased saliva (describes what?)What is <b>xerostomia?</b>
What is the best first-line management for NAFLD?Weight loss
A patient on long-term PPI therapy complains of muscle aches and weakness. What is responsible?PPI can cause <b>hypo magnesaemia</b>, which can cause muscle weakness and aches
Unintentional weight loss greater than <span class=cloze>[...]</span> within the last <span class=cloze>[...]</span> is diagnostic of malnutritionUnintentional weight loss greater than <span class=cloze>10%</span> within the last <span class=cloze>3-6 months</span> is diagnostic of malnutrition<br> What are the three possible criteria for a diagnosis of malnutrition?- BMI < 18.5<div>- BMI <20 and unintentional weight loss greater than 5% within last 3-6 months</div><div>- Unintentional weight loss greater than 10% within the last 3-6 months </div>
How should malnutrition be managed?"- Dietician support (if pt is high-risk)<div>- ""Food-first"" approach instead of just prescribing oral nutritional supplements (ONS- e.g. Ensure)</div><div>- ONS should be taken between meals, rather than instead of meals </div>"
Which cause of cirrhosis is <b>not </b>associated with increased risk of hepatocellular carcinoma?"- Wilson's disease (excess copper)"
What percentage of alcoholics will have a clinically normal liver?50%
What can cause fatty liver?- Alcohol<div>- Obesity</div><div>- Diabetes mellitus</div><div>- Amiodarone (antiarrythmic)</div>
What is seen on biopsy of <b>alcoholic</b> hepatitis?"- <b>Mallory </b>Bodies: Inclusion found in cytoplasm of hepatocytes (twisted rope appearance)<div><img src=""paste-ee922029629c2f7c84dd5a62c6bed654bae9fc35.jpg""><br><div>- <b>Neutrophil infiltrate</b> </div><div><br></div><div>Indistinguishable from NASH<br></div></div>"
What percentage of<b> alcoholic hepatitis</b> progresses to <b>cirrhosis</b>?80%
How can the CNS be affected by alcoholism?"- Self neglect<div>- ↓ Memory/cognition (may be reversed by high-potency vitamins IM)</div><div>- <b>Cortical atrophy</b></div><div>- Retrobulbar neuropathy</div><div>- <b>Fits</b></div><div>- <b>Falls</b></div><div>- Wide-based <b>gait</b></div><div>- Neuropathy</div><div>- Confabulation/ <b>Korsakoff's + Wernicke's</b> encephalopathy</div>"
How can the gut be affected by alcoholism?- Obesity<div>- Diarrhoea and vomiting</div><div>- Gastric erosions</div><div>- Peptic ulcers</div><div>- Varices</div><div>- Pancreatitis (both acute and chronic)</div><div>- Cancer</div><div>- Oesophageal rupture </div>
How can the heart be affected by alcoholism?- Arrhythmias<div>- ↑BP<br>- Cardiomyopathy</div><div>- Sudden death in binge drinkers</div>
How can the reproductive system be affected by alcoholism?- Testicular atrophy<div>- ↓Testosterone/progesterone</div><div>- ↑Oestrogen</div><div>- Foetal alcohol syndrome</div>
How does foetal alcohol syndrome present?- ↓IQ<div>- Short palpebral fissure</div><div>- Absent philtrum</div><div>- Small eyes</div>
When does alcohol withdrawal begin?10-72hrs after last drink 
What are signs of alcohol withdrawal?- <b>↑Pulse</b><div><b>- ↓BP</b></div><div><b>- Tremor</b></div><div><b>- Confusion</b></div><div>- Fits</div><div>- Hallucinations </div>
How should alcohol withdrawal be managed?- Chlordiazepoxide (BDZ)<div>- Monitor and <b>manage BP </b></div>
What is the mechanism of action of<b> acamprosate</b> in alcoholism?Acts as a <b>NMDA antagonist </b>and a <b>positive allosteric modulator of GABA receptors</b>:<div><br></div><div>Helps with withdrawal symptoms: reduces:</div><div>- Anxiety</div><div>- Insomnia</div><div>- Craving </div>
What are contraindications of acamprosate (reduces alcohol cravings)?- <b>Pregnancy</b><div>- Severe <b>liver failure </b>(cant break down drug)</div><div>- <b>Creatinine</b> >120μmol/L</div>
When should acamprosate be given in alcoholics?<b>After acute withdrawal </b>is complete- should be continued for a year. <div><br></div><div>Helps reduce withdrawal symptoms </div>
What is the action of <b>disulfiram</b>?- Inhibits acetaldehyde dehydrogenase → causes acetaldehyde build-up → causes <b>unpleasant effects to any alcohol ingestion</b>:<div><br></div><div>- Flushing</div><div>- Throbbing headache</div><div>- Palpitations </div>
What questions make up the CAGE questionnaire?"1. Have you ever felt you ought to <b><font color=""#0000ff"">c</font></b>ut down on your drinking?<div>2. have people <b><font color=""#0000ff"">a</font></b>nnoyed you by criticising your drinking?</div><div>3. Ever felt <b><font color=""#0000ff"">g</font></b>uilty about your drinking?</div><div>4. Ever had an<font color=""#0000ff""> <b>e</b></font>ye opener in the morning?</div>"
How should the CAGE questionnaire be interpreted?Answering yes to ≥ 2 questions may be exhibiting dependency
What changes in blood would you expect from an alcoholic?- ↑GGT, ↑ALT<div>- ↑MCV</div><div>- AST:ALT>2</div><div>- ↓ Urea</div><div>- ↓ Platelets</div>
What are symptoms of alcoholic hepatitis?- Fatigue<div>- Fever</div><div>- RUQ pain</div><div>- Tender <b>hepatomegaly</b> (sometimes with<b> bruit</b>) <br></div><div>- <b>Jaundice</b>, encephalopathy, <b>coagulopathy</b></div>
How should alcoholic hepatitis be managed?"- Usually admit: urinary catheter and CVP monitoring may be needed<div>- Screen for infections (ascitic fluid tap if necessary)</div><div>- Stop alcohol consumptions (if chlordiazepoxide PO not tolerated, try lorazepam IM)</div><div>- Vitamins: Vit K, Thiamine</div><div>- Optimise nutrition: <b>avoid low-protein diets</b></div><div>- <font color=""#0000ff"">Corticosteroids in severe disease</font></div>"
What is the prognosis of alcoholic hepatitis?- Mild cases have very little affect on mortality<div>- Severe cases 40% 1yr mortality </div>
How can autoimmune hepatitis present?- Acute hepatitis & signs of autoimmune disease (fever, malaise, urticaria, polyarthritis etc.) [40%]<div> </div><div>- Remainder present with gradual jaundice or are asymptomatic</div><div><br></div><div><b>Amenorrhoea </b>is common </div>
Autoimmune hepatitis tends to attenuate during <span class=cloze>[...]</span>Autoimmune hepatitis tends to attenuate during <span class=cloze>pregnancy</span><br> What <b>class </b>of antibodies are prevalent in autoimmune hepatitis?IgG: hypergammaglobulinaemia 
What is the prognosis of the different subtypes of autoimmune hepatitis?"<font color=""#0000ff"">Type I:</font> Good response to immunosuppression in 80%<div><font color=""#0000ff"">Type II:</font> More commonly progreses to cirrhosis and less treatable</div><div>Type III behaves as type I</div>"
How should autoimmune hepatitis be managed?- <b>Prednisolone</b>/corticosteroids: 30mg/d PO for 1 month, then wean to maintenance dose of 5-10mg. (frequent relapse when stopped)<div>- <b>Azathioprine</b> can be used to maintain remission </div>
What conditions are associated with autoimmune hepatitis?- <b>Pernicious anaemia </b>(Immune system attacks cells that produce instrinsic factor, so VitB12 cant be absorbed)<br>- Autoimmune <b>haemolysis</b><div>- Ulcerative <b>colitis</b></div><div>- <b>Diabetes</b> mellitus</div><div>- Glomerulo<b>nephritis</b></div><div>- PSC</div><div>- Autoimmune <b>thyroiditis</b></div>
What is the prevalence of NAFLD?<b>20%</b> in Western industrialised countries 
How is Non-alcoholic fatty liver disease defined?<b>Steatosis</b> (↑Fat) in hepatocytes <b>visualised</b> (e.g. on USS) that cannot be attributed to other causes 
When does NAFLD become NASH (non alcool related steato hepatitis?If <b>inflammation </b>is also present- ↑LFT (usually ↑ALT)
What is the action of ursodeoxycholic acid in the treatment of PBC?- Increases rate of bile flow from hepatocytes → combats cholestasis<div>- Inhibits production of bile acids</div><div>- Inhibits apoptosis and mildly inhibits immune response in liver. </div>
"What is this?<div><img src=""51uz+WRPd0L._SL1500_.jpg""><br></div>"Yankauer sucker- useful to clear secretions which might otherwise block the airway
"What is seen here?<div><img src=""comfortgel-blue-full-face-cpap-mask_600x600.jpg""><br></div>"CPAP: continuous positive airway <b>pressure </b>
What is the action of a CPAP mask?Applies mild air on continuous basis to keep <b>airways </b>continuous <b>open</b>
"What is seen here?<div><img src=""lma-unique.jpg""><br></div>"Laryngeal Mask Airway
When is the use of an LMA contraindicated?↑Risk of aspiration 
At what level of oxygen saturation should you be worried? ≤<b>94%</b>
Why does hypotension occur as a result of induction of anaesthesia?"Propofol is a <font color=""#0000ff"">negative inotrope</font> <b>and </b><font color=""#0000ff"">vasodilator</font>"
What is the importance of muscle relaxants in induction of anaesthesia?- Important to relax muscles of <b>vocal cord</b>, so <b>can intubate</b>.<div>- Will relax muscles of <b>abdomen</b> and diaphragm, to aid operation. </div>
Give some examples of neuromuscular blocking drugs?"<font color=""#0000ff"">Non-depolarising:</font><div>- Vecuronium</div><div>- Rocuronium</div><div>- Pancuronium</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Depolarising:</font></div><div>- Suxamethonium</div>"
How can neuromuscular blockers be reversed?"Use of anticholinesterases e.g. <font color=""#0000ff"">neostigmine</font>. <div><br></div><div>Note anticholinesterases reverse <b>non-depolarising</b> blockers e.g. pancuronium, but <b>prolong action of depolarising </b>e.g. suxamethonium</div>"
What are risk factors for Post-operative nausea and vomiting?- Pain/anxiety<div>- Younger age</div><div>- Females</div><div>- Use of opioids</div><div>- Hx of post-operative nausea</div><div>- Dehydration </div><div>- Type of surgery (esp. breast, bowel, uterus, middle ear)</div>
What is a good approach to treating Post-operative nausea and vomiting?"1. <font color=""#0000ff"">Cyclizine</font><div>2. <span style=""color: rgb(0, 0, 255);"">5HT</span><sub style=""color: rgb(0, 0, 255);"">3</sub><span style=""color: rgb(0, 0, 255);""> antagonist (ondansetron</span>) if no response to cyclizine in 30 mins</div><div>3. <font color=""#0000ff"">Dopamine antagonist (metoclopramide, prochloperazine)</font> if no response to 5HT<sub>3</sub> antagonist within 30 minutes </div>"
In what patients are thromboembolic stockings <b>contraindicated</b>?- Hx of <b>peripheral </b>vascular disease<div><br></div><div>(Could occlude the vessels, and cause tissue ischaemia and necrosis)</div>
What is the approach with the systemic analgesic ladder in post-operative pain?<b>Strong analgesic drugs required in early stages</b>, and stopped first, leaving less strong analgesics. <div><br></div><div>Because post-operative pain usually starts bad and improves</div>
How does a PCA work?<b>Patient Controlled Analgesia</b>:<div><br></div><div>- Patient can give themselves dose of morphine, when they want. </div><div>- Timer set, so patient c<b>annot continually give </b>themselves morphine</div>
What is a consideration with regard to pain management of a patient with a PCA?<b>Do not prescribe further opioids</b>, can cause serious <b>respiratory depression</b>
Why are some people not affected by codeine?Codeine metabolised to morphine in liver:<div><br></div><div><b>25% of population lack the enzyme which metabolises codeine</b>, so it is ineffective in these people </div>
What is the <b>haematocrit?</b><b>Ratio</b> of <b>volume of RBCs</b> to total <b>volume of blood</b> (refers to what?)
<b>Ratio</b> of <b>volume of RBCs</b> to total <b>volume of blood</b> (refers to what?)What is the <b>haematocrit?</b>
What is the typical haematocrit of a patient?<b>40-45% </b>
How should preoperative anaemia be managed before a surgery?Optimised w/ Red Cells prior to elective surgery- aim to have Hb > 100g/L before surgery
How long does it typically take for a full cross-match?1hr 
What is the effect of the <b>stress response to surgery </b>on electrolytes?- Na<sup>+</sup> and water retention<div>- K<sup>+</sup> loss </div><div><br></div><div>(therefore sometimes necessary to give extra potassium in IV regimen)</div>
"What is the effect of many blood transfusions on a patient's K<sup>+</sup>, Ca<sup>2+</sup>, and body temperature?""<font color=""#0000ff"">↑K<sup>+</sup></font> : As haemolysis will occur (when taken out of fridge), releasing intracellular K<sup>+</sup><div><font color=""#0000ff"">↓Ca<sup>2+</sup></font>: As RBCs are stored with citrate, which reduces Ca<sup>2+</sup> levels</div><div><font color=""#0000ff"">Hypothermia</font>: As RBCs are stored in the fridge</div><div><br></div><div>(note can still become hyperthermic with blood transfusion, with transfusion reactions)</div>"
What are the four principles of prescribing IV fluids on the ward according to NICE guidelines?- Assessment<div>- Resuscitation</div><div>- Routine Maintenance</div><div>- Replacement redistribution </div><div><br></div><div><b>Then reassessment</b></div>
If fluid resuscitation is required, how is it given?500mL crystalloid IV (consider 250mL in some patients e.g. heart failure) over less than 15 minutes
What is required in fluids for routine maintenance in one day?- 25-30mL/kg of water<div>- 1 mmol/kg of Na<sup>+</sup>, K<sup>+</sup>, Cl<sup>-</sup></div><div>- 50-100g of glucose(regardless of weight)</div>
In which patients should you consider prescribing less fluid for routine maintenance than normally recommended?- Older/frail<div>- Renal impairment</div><div>- Cardiac failure</div><div>- Malnourished</div>
What is hypovolaemic shock?Inadequate tissue perfusion due to loss of intravascular blood volume 
What are signs of early hypovolaemic shock (<15% loss of blood volume)- Tachycardia<div>- Tachypnoea</div><div>- Anxiety</div><div> </div><div>No loss in blood pressure, as cardiac output maintained by baroreceptor refelx etc</div>
What are signs of an acute loss of 15-30% blood volume?Beginnign to decompensate- CO begins to fall:<div>- Cool, poorly perfused periphery</div><div>- Delayed capillary reflex (due to peripheral vasoconstriction from ↑SNS)</div><div>- Sweating (from ↑catecholamines)</div><div>- Altered conscious level (decreased perfusion to brain)</div><div>- Reduced urine output </div><div>- MAP may be maintained but decrease in pulse pressure </div>
What are signs of an acute loss of >40% of blood volume?- Almost no urine output<div>- BP plummets</div><div>- Conscious levels falls </div><div>- Patient appears deathly pale and sweaty</div><div>- Peripheral pulses may be difficult to feel, central pressures are rapid and weak</div>
What are the ASA gradings?"<font color=""#0000ff"">ASA I</font>: Normal, healthy patient. Non smoker<div><font color=""#0000ff"">ASA II:</font> Mild systemic disease</div><div><font color=""#0000ff"">ASA III</font>: Severe systemic disease</div><div><font color=""#0000ff"">ASA IV</font>: Severe systemic disease that is a constant threat to life</div><div><font color=""#0000ff"">ASA V</font>: Patient close to death who is not expected to survive without surgery</div><div><font color=""#0000ff"">ASA VI</font>: Declared brain-dead patient who is donating organs. </div>"
Patients with GORD being considered for fundoplication surgery require what investigations?- Oesophageal pH<div>- Manometry studies</div>
What should be assessed before starting a patient on azathioprine or mercaptupurine therapy?"<font color=""#0000ff"">Thiopurine methyltransferase activity</font>: pts lacking this may be unable to metabolise these drugs and can experience greater side effects"
"What is a <b>Hartmann's procedure?</b>""Resection of recto-sigmoid colon, <font color=""#0000ff"">with formation of permanent end colostomy</font> and closure of rectal stump. <div><br></div><div><img src=""Hartmanns-Procedure.jpg""><br></div>"
Which TB medication can cause peripheral neuropathy, and how is this prevented?"Isoniazid- causes peripheral neuropathy through Vit B6 deficiency, so <font color=""#0000ff"">give Pyridoxine (B6) supplementation</font>"
When should oral thiopurines (azathioprine, mercaptopurine) be given in ulcerative colitis?If pt has severe relapse, or ≥2 exacerbations in the last year<div><br></div><div>(Takes around 6-10 weeks to take an effect, so not used to achieve acute remission)</div>
"How is Barrett's Oesophagus managed?"- High-dose <b>PPI</b><div>- <b>Endoscopic surveillance</b> with biopsies- every 2-3 years </div>
At what level does the inferior mesenteric artery branch off the aorta?L3
At what level does the superior mesenteric artery branch off the aorta?L1
At what level does the coeliac<b> t</b>runk branch off the aorta?T12
<span class=cloze>[...]</span> increases the risk of developing oesophageal adenocarcinoma "<span class=cloze>Barrett's oesophagus</span> increases the risk of developing oesophageal adenocarcinoma <br> "
"Barrett's oesophagus increases the risk of developing oesophageal <span class=cloze>[...]</span> ""Barrett's oesophagus increases the risk of developing oesophageal <span class=cloze>adenocarcinoma</span> <br> "
<span class=cloze>[Condition]</span> increases the risk of developing squamous cell carcinoma of the oesophagus<span class=cloze>Achalasia</span> increases the risk of developing squamous cell carcinoma of the oesophagus<br> achalasia = difficulty swallowing
Achalasia increases the risk of developing <span class=cloze>[...]</span> of the oesophagusAchalasia increases the risk of developing <span class=cloze>squamous cell carcinoma</span> of the oesophagus<br> achalasia = difficulty swallowing
How does <b>Budd-Chiari</b> syndrome typically present?Triad of:<div><br></div><div>- Sudden onset abdominal <b>pain</b></div><div>- <b>Ascites</b></div><div>- Tender <b>hepatomegaly</b></div>
In what causes of dysphagia is upper GI <b>endoscopy contraindicated</b>?- <b>Pharyngeal pouch</b>: can cause iatrogenic perforation<div><br></div><div>- If pt is at high risk of <b>aspiration pneumonia </b></div>
What is a common side effect of metoclopramide?Extrapyramidal side effects: acute dystonia. <div><br></div><div>- Most commonly results in oculogyric crises (eyes locked in a position)</div><div><br></div><div>More common in young people</div>
What medications should be <b>stopped</b> in <i>C. diff </i>infections?<b>Anti-motility </b>and<b> anti-peristaltic</b> medications e.g. opioids, or metoclopramide
How does Boerhaave syndrome typically present?"Traid of:<div>- Vomiting</div><div>- Thoracic pain</div><div>- Subcutaneous emphysema (presents as crepitus, 'like feeling rice krispies')</div>"
In what patients does Boerhaave syndrome typically present?Middle aged men, w/ background of alcohol abuse
What is the best method of assessing <b>mural invasion</b> of an oesophageal/gastric cancer?<b>Endoscopic ultrasound</b>
What are <b>duodenoscopes</b> and what are they used for?"Specialised endoscopies used <b>for ERCP</b>: <font color=""#0000ff"">side-viewing </font>rather than forward viewing"
Which carbohydrate foods are gluten-free?- Rice<div>- Potato</div><div>- Corn (maize)</div>
At what age does <b>haemochromatosis</b> typically present in women?"<b>10+ years post menopause</b>: mensses reduce iron load (think 'natural venesection'!)"
<span class=cloze>[Result from investigation]</span> is present in 80-90% of pts with <b>appendicitis</b><span class=cloze><b>Neutrophil</b> predominant<b> leukocytosis</b></span> is present in 80-90% of pts with <b>appendicitis</b><br> <b>Neutrophil</b> predominant<b> leukocytosis</b> is present in 80-90% of pts with <span class=cloze>[cause of acute abdomen]</span><b>Neutrophil</b> predominant<b> leukocytosis</b> is present in 80-90% of pts with <span class=cloze><b>appendicitis</b></span><br> What are the metabolic consequences of <b>refeeding syndrome</b>?- <b>Hypo</b> phosphataemia<div>- Hypo kalaemia</div><div>- Hypo magnesaemia </div><div>- Abnormal fluid balance </div>
What is refeeding syndrome?Metabolic abnormalities which occur when feeding a person following period of starvation 
What is responsible for causing the metabolic consequences of refeeding syndrome?Extended period of catabolism ends abruptly with switching to carbohydrate metabolism:<div><br></div><div>- <b>Spike in insulin causes cellular uptake of phosphate</b>, developing a hypophophataemic state</div>
What are high risk factors of developing refeeding syndrome?- BMI < 16kg/m<sup>2</sup><div>- Unintentional weight loss >15% over 3-6 months</div><div>- Little nutritional intake > 10 days</div><div>- Hypokalaemia, hypophosphataemia, hypomagnesaemia prior to feeding </div>
What are the foregut structures?<div>- Oesophagus</div>- Stomach<div>- Duodenum (up to ampulla of vater)</div><div>- Liver + Gallbladder</div><div>- Pancreas</div><div>- Spleen</div><div><br></div><div>(Lower respiratory tract)</div>
What are the midgut structures?"<div></div><div>-<font color=""#0000ff""> Small bowel</font>: Distal half of duodenum, jejunum, ileum, caecum </div><div>- Appendix</div><div>- <font color=""#0000ff"">Large bowel</font>: Ascending colon, <b>proximal 2/3 of transverse colon</b></div>"
What forms the <b>hind</b>gut?- <b>Distal 1/3 of transverse colon</b><div>- Splenic flexure</div><div>- Descending colon</div><div>- Sigmoid colon</div><div>- Rectum</div>
Where does <b>visceral pain </b>tend to refer to from the foregut, midgut and hindgut?"<font color=""#0000ff"">Foregut</font>: <b>Epigastric </b><div><font color=""#0000ff"">Midgut</font>: <b>Umbilical area</b></div><div><font color=""#0000ff"">Hindgut</font>: <b>Suprapubic area</b></div>"
What is the arterial supply to the<b> hind</b>gut structures?<b>Inferior </b>mesenteric artery 
What provides the arterial supply to the <b>mid</b>gut?<b>Superior</b> mesenteric artery
What is <b>visceral </b>pain?Innervated by <b>autonomic</b> nerve fibres, respond to <b>distention</b> and muscular <b>contraction</b>
What is peritonitis?Inflammation of the peritoneal cavity 
What causes peritonitis?"- <font color=""#0000ff"">Perforation of GI Tract</font>: causes chemical inflammation followed by infection from intestinal organisms<div>- <font color=""#0000ff"">Inflammation </font>(e.g. appendicitis, diverticulitis)</div><div>-<font color=""#0000ff""> Intraperitoneal blood</font> (e.g. from ruptured aneurysm, trauma, ectopic pregnancy)</div><div>- <font color=""#0000ff"">Barium </font>(so avoid barium swallow in suspected perforation)</div>"
Where will pain typically be felt in a<b> perforated duodenal ulcer</b>?Right upper quadrant  (makes sense)
A presentation of <b>acute abdominal pain </b>with pain out of proportion to physical findings suggests what?<b>Mesenteric ischaemia </b>
What is <b>mittel schmerz?</b>Ovulation pain: lower abodminal/pelvic pain which occurs roughly halfway through the menstruation cycle<div><br></div><div>(describes what?)</div>
Ovulation pain: lower abodminal/pelvic pain which occurs roughly halfway through the menstruation cycle<div><br></div><div>(describes what?)</div>What is <b>mittel schmerz?</b>
Describe the pain often felt in Mittelschmerz?- <b>Sudden</b> pain<div>- Usually <b>subsides </b>within hours</div><div>- One-sided (the side which produced the ovary)</div>
Acute abdominal pain which<b> radiates</b> to the <b>left shoulder region</b> suggests what?- Ruptured <b>spleen</b><div>-<b> Pancreatitis</b></div>
What are characteristic features of peritonitis?"- Patients often <font color=""#0000ff"">lay completely still</font>, not move their abdomen and look unwell<div>- <font color=""#0000ff"">Tachycardia</font> (plus potential <font color=""#0000ff"">hypotension</font>)</div><div>- Rigid abdomen with percussion tenderness</div><div>- Involuntary <b>guarding</b></div><div>- Reduced/absent bowel sounds (= paralytic ileus)</div>"
What is the most common cause of <b>acute </b>abdominal pain?<b>Appendicitis </b>
A sudden onset of abdominal pain suggests what causes?- Perforation (e.g. of duodenal ulcer)<div>- Rupture (e.g. of ectopic pregnancy)<br></div><div>- Acute pancreatitis<br>- Torsion (e.g. of ovarian cyst)<br></div><div>- Infarction</div>
What does back pain in an acute abdomen suggest?- <b>Pancreatitis</b><div>- Rupture of an <b>aortic aneurysm</b></div><div>-<b> Renal</b> tract disease </div>
What is the pathophysiology underlying <b>acute porphyrias?</b><b>Deficiency of enzymes </b>involved in <b>haem synthesis</b>, causing accumulation of haem precursors (leads to what disease?)
<b>Deficiency of enzymes </b>involved in <b>haem synthesis</b>, causing accumulation of haem precursors (leads to what disease?)What is the pathophysiology underlying <b>acute porphyrias?</b>
What are common symptoms of an acute porphyric attack?"- <font color=""#0000ff"">Abdominal pain</font>: excruciating disproportionate to abdominal tenderness<div>- <font color=""#0000ff"">Vomiting</font></div><div>- Nervous system also involved:<font color=""#0000ff""> motor neuropathy and muscle weakness</font></div><div>- <font color=""#0000ff"">Tachycardia</font></div><div><font color=""#0000ff"">- Dark red urine</font></div><div><br></div><div>No inflammation, so abdomen is not tender & normal temperature and WCC. </div>"
What precipitates acute porphyric attacks?"<font color=""#0000ff"">- Hormonal changes in women</font><div>- Drugs</div><div>- Low-calorie, low-carbohydrate diets</div><div>- Alcohol</div><div>- Infections</div><div>- Surgery</div><div>- Emotional stress</div>"
How should an suspected acute porphyric attack be investigated?"- Urine: Screen for <font color=""#0000ff"">porphobilinogen</font><div>- <font color=""#0000ff"">Quantitative ALA and PBG</font> (porphyrin precursors) measurements from urine</div><div>-<font color=""#00aa00""> PBG deaminase activity</font> in erythrocytes (to confirm <font color=""#00aa00"">acute intermittent porphyria</font>)</div>"
What causes <b>porphyria cutanea tarda?</b>Inherited deficiency in activity of hepatic uroporphyrinogen decarboxylase- enzyme in haem biosynthetic pathway (causes what disease?)
Inherited deficiency in activity of hepatic uroporphyrinogen decarboxylase- enzyme in haem biosynthetic pathway (causes what disease?)What causes <b>porphyria cutanea tarda?</b>
What are the different types of porpyria cutanea tarda?"<font color=""#0000ff"">Type 1: Acquired/sporadic</font>- decarboxylase deficiency just in liver- usually manifests in middle age or later<div><font color=""#0000ff"">Type 2: Hereditary</font>- decarboxylase deficiency in all cells (inc. RBCs). May develop earlier than type 1. </div><div>(Type 3: Hereditary but no defect in UROD gene- accounts for <1% of PCT cases)</div>"
How do patients with porphyria cutanea tarda typically present?- Blistering & crusted skin lesions on sun-exposed areas of body<div>- Bullae </div><div>- Facial hypertrichosis</div><div>- Dark red urine</div>
How can porphyria cutanea tarda be differentiated from acute porphyrias with cutaneous symptoms?- ↑ Urinary uroporphyrin & hpatocarboxyl porphyrin<div>- ↑ Faecal isocoproporphyrin</div><div><br></div><div>Suggests PCT </div><div><br></div><div>Normal urine levels of PBG </div>
What are risk factors of porphyria cutanea tarda? - Hepatitis C infection<div>- Smoking</div><div>- Alcohol use</div><div>- ↑ Ferritin</div><div>- Being middle aged, white men</div>
How is porphyria cutanea tarda treated?"- <font color=""#0000ff"">Venesection</font>: reduces body iron stores<div>-<font color=""#0000ff""> Low-dose chloroquine/hydroxychloroquine</font>: Increases porphyrin excretion from liver. </div>"
What is the classic presentation of Familial Mediterranean Fever?- Fever up to 40°C<div>- Peritonitis</div><div>- Abdominal pain: starts in one quadrant and spreads to whole abdomen</div><div><br></div>
How is Familial Mediterranean Fever diagnosed?"- Clinical evaluation: Fever, Peritonitis<div>- <font color=""#0000ff"">Genetic testing</font>: MEFV gene </div>"
What is the most common complication of Familial Mediterranean Fever?- Renal amyloidosis → renal failure 
How is Familial Mediterranean Fever managed?"- <font color=""#0000ff"">Prophylactic colchicene</font>: Provides complete remission/distinct improvement in around 85% of patients <div><br></div><div>- <font color=""#0000ff"">Anakinra </font>(IL1-R antagonist) for nonresponders</div>"
What causes appendicitis?<b>Obstruction of appendiceal lumen</b> (either by lymphoid hyperplasia, faecalith, foreign body etc.)<div><br></div>
What is the gold standard investigation to confirm <b>appendicitis</b>?"- <b>CT</b>: Shows wall thickening, wall enhancement and inflammatory changes (must confirm not pregnant first, and not done regularly in the UK)<div><br></div><div><img src=""290-2_default.jpg""><br></div>"
When is an abdominal ultrasound indicated for diagnosis of appendicitis?- <b>Atypical presentations</b> of appendicitis<div>- May be preferred in <b>children</b> to limit radiation exposure</div>
How is appendicitis diagnosed on ultrasound?"- <b>Aperistaltic non-compressible</b> structure with outer diameter >6mm<div><img src=""a937ef488529721ddb9dcfac800507_big_gallery.jpg""><br></div>"
What are differential diagnoses for appendicitis?"- Non-specific <b>mesenteric lymphadenopathy</b><div>- Acute <b>terminal ileitis</b> (Crohn's, or Yersinia infection)(appendix fine but adjacent ileum not)</div><div>-<b> Inflamed Meckel's </b>diverticulum</div><div><br></div>"
How is appendicitis managed?"<font color=""#0000ff"">If uncomplicated presentation</font>: <b>NBM, IV fluids</b>, immediate <b>appendectomy</b> through laparoscopic surgeyr<div><font color=""#0000ff"">If gangrene, or abscess</font>: NBM, IV Fluids +<b> IV antibiotics</b> (+<b>drainage</b>), until patient is afebrile and abscess resolved, then delayed appendectomy: interval appendectomy</div>"
What is acute <b>salpingitis?</b>Infection of the <b>fallopian tubes</b> (is describes as what?)
Infection of the <b>fallopian tubes</b> (is describes as what?)What is acute <b>salpingitis?</b>
What are gynaecological causes of an acute abdomen?- <b>Ruptured ectopic</b> pregnancy<div>- <b>Torsion</b>/rupture of ovarian cyst</div><div>- Mittelschmerz (period pain)</div><div>- Acute<b> salpingitis </b></div>
How do patients with acute salpingitis present?- <b>Bilateral </b>low abdominal pain<div>- Fever</div><div>- Vaginal<b> discharge</b></div><div><br></div><div>(associated with STIs) </div>
What occurs in<b> Fitz-Hugh-Curtis </b>syndrome?-<b> Pelvic inflammatory disease</b> where <b>chlamydia or Gonorrhoea </b>travel up <b>right paracolic gutter</b>, to cause perihepatitis<div><br></div><div>(describes what?)</div>
-<b> Pelvic inflammatory disease</b> where <b>chlamydia or Gonorrhoea </b>travel up <b>right paracolic gutter</b>, to cause perihepatitis<div><br></div><div>(describes what?)</div>What occurs in<b> Fitz-Hugh-Curtis </b>syndrome?
How is peritonitis managed?<b>Resuscitation and re-establishment of good urinary output</b> (<b>NG tube, IV fluids, Abx</b>), then surgery to:<div><br></div><div>- <b>Peritoneal lavage</b> of abdominal cavity</div><div>- <b>Treatment of underlying condition </b></div>
What is the most common chemical composition of <b>renal</b> calculi?<b>Calcium</b> calculi (usually calcium oxalate)
What are the symptoms of and signs of urinary calculi obstruction?"-<font color=""#0000ff""> Renal colic pain</font>: Excruciating and intermittent, lasts 20-60 mins. <div>- <font color=""#0000ff"">Nausea and vomiting</font></div><div>- Patients often in obvious extreme discomfort: often <font color=""#0000ff"">unable to lie still,</font> will pace, writhe and shift position </div>"
What are the three most common areas which urinary calculi may lodge?"- Ureteropelvic junction<div>- Distal ureter (at level of iliac vessels)</div><div>- Vesicoureteric junction</div><div><br></div><div><img src=""39586tn.jpg""><br></div>"
How can symptoms of urinary calculi obstruction differentiate between areas of obstruction?"Pain in flank/kidney area, which<font color=""#0000ff""> radiates across abdomen</font>: <b>Upper</b> ureteral/renal pelvic obstruction<div><br></div><div>Pain which <font color=""#0000ff"">radiates along course of ureter</font>: <b>Lower </b>ureteral obstruction</div><div><br></div><div><font color=""#0000ff"">Suprapubic pain, with urinary urgency and ↑ frequency</font>: <b>Distal </b>ureteral, vesicouterteric, bladder calculus</div>"
How is nephro lithiasis investigated? (kidney & ureter stones)- Urinalysis: haematuria, calculus (possible pyuria if infection)(WBC in piss)<div>- <b>Non-contrast</b> helical <b>CT</b></div>
How is <b>eosinophilic</b> oesophagitis managed?Topical <b>corticosteroids</b>: ingested <b>fluticasone </b>
Blood mixed in the stool suggests what?Bleeding from colon 
Fresh blood which coats the stool/seen on tissue is caused by what?Bleeding at or above level of anus: haemorrhoids or anal fissure 
How should patients on warfarin be managed for an acute upper GI bleed?<b>Prothrombin complex concentrate</b>:<div><br></div><div>- Factors II, VII, IX and X </div>
How does a <b>candida</b> infection in the mouth present as?- <b>White patches</b> which can be scraped off<div>- Mucosal <b>erythema</b></div><div>- Discomfort</div>
If triple therapy of <b>omeprazole</b>, <b>amoxicillin</b> and <b>clarithromycin</b> fails to eradicate <i>H. pylori</i> the first time, what is the next step?Repeat treatment with <b>metronidazole </b>instead of clarithromycin:<div><br></div><div>Omeprazole, amoxicillin and metronidazole for 7 days</div>
"According to <b>Truelove</b> and Witt's criteria, what makes an exacerbation of UC <b>severe?</b>"- <b>Copious blood </b>in stools or<b> ≥6 bowel movements a day</b> and one of:<div><br></div><div>- Temperature >37.8°</div><div>- Pulse > 90bpm</div><div>- Anaemia (Hb below 75% normal for sex)</div><div>- ESR >30</div>
In an adult, how long does it take for upper and lower limb fractures to heal?Upper: 6 weeks<div>Lower: 12 weeks </div><div><br></div><div>(Half in children)</div>
At what age would you consider giving cannulated screws instead of THRs for Garden Classification III/IV?Very young- <35y/o (as hip replacements would wear out)
How should scaphoid fractures be managed?"<div>Cast and repeat X-Ray in 10 days (as scaphoid fractures are often not visible immediately)<font color=""#0000ff""><br></font></div><div><font color=""#0000ff""><br></font></div><font color=""#0000ff"">Visible # on X-ray</font>: Cast for 6/52<div><font color=""#0000ff"">If no visible # on X-ray</font>: Cast for 2/52 and re-scan in # Clinic</div>"
How is compartment syndrome diagnosed?- Clinical diagnosis<div>(Pressure measurements can be used, >20mmHg abnormal)</div>
What is the management of acute compartment syndrome?- Rehydration (due to myoglobinuria build up) <div>- Fasciotomy </div>
How is carpal tunnel syndrome managed?"<font color=""#0000ff"">Conservative</font>: Wrist splinting at night<div><br></div><div><font color=""#0000ff"">Medical</font>: Corticosteroid injections</div><div><br></div><div><font color=""#0000ff"">Surgical</font>: Decompression by division of flexor retinaculum </div>"
What are symptoms of sciatic nerve damage?- Foot drop<div>- Widespread sensory loss below knee </div>
"Anti-smith's antibody is important in what rheumatological condition?"SLE: Most specific antibody, also a marker for poor prognosis
How is scleroderma managed?- Mycophenolate mofetil (DMARD)<div>- Iloprost infusions</div>
What is seen on biopsy of myositis/dermatomyositis?- Endomysial mononuclear cells<div>- Myonecrosis</div>
How should polyarteritis nodosa be managed if the pt also have Hepatitis B?Plasma exchange, on top of prednisolone/DMARD
"What is Kawasaki's disease?"Medium-vessel vasculitis, typically in children under the age of 5
What is <b>achlorhydria?</b>Absence of hydrochloric acid in gastric secretions (is described by what term?)
Absence of hydrochloric acid in gastric secretions (is described by what term?)What is <b>achlorhydria?</b>
What mutations cause <b>Familial Adenomatous Polyposis </b>syndrome?<b>Adenomatous Polyposis Coli</b> (APC) Gene
"How does <b>Garner's </b>variant of <b>Familial Adenomatous Polyposis</b> present?"<div>- <b>Supernumerary Teeth</b></div><div>- <b>Lipomas and osteomas</b></div><div>- <b>Epidermoid cysts  </b></div>
What is the most definitive test for a pharyngeal pouch?Barium Swallow <div><br></div><div>(endoscopy has a risk of iatrogenic perforation)</div>
What is the most common cause of MALT lymphoma in the upper GI tract?- <i>H. pylori </i>infection<div><br></div><div>(Low-grade tumours can be successfully treated with <i>H. pylori </i>eradication)</div>
When are antibiotics advised in gastroenteritis?If patient is:<div><br></div><div>- Systematically unwell</div><div>- Immunosuppressed</div><div>- Elderly</div>
How is gastroenteritis typically managed?<b>Conservative</b>: Fluid replacement or oral rehydration<div><br></div><div>Anti-emetics may be used if severe</div><div><br></div><div>Only give antibiotics if systemically unwell/severe disease, immunocompromised or elderly</div>
What causes of gastroenteritis are treated with <b>ciprofloxacin?</b>- Salmonella<div>- Shigella</div><div><br></div><div>(Gastroenteritis are treated with what antibiotic?)</div>
- Salmonella<div>- Shigella</div><div><br></div><div>(Gastroenteritis are treated with what antibiotic?)</div>What causes of gastroenteritis are treated with <b>ciprofloxacin?</b>
What causes of gastroenteritis are treated with macrolides e.g. <b>clarithromycin</b>?Campylobacter<div><br></div><div>(caused Gastroenteritis is treated with what antibiotic?)</div>
Campylobacter<div><br></div><div>(caused Gastroenteritis is treated with what antibiotic?)</div>What causes of gastroenteritis are treated with macrolides e.g. <b>clarithromycin</b>?
Gastroenteritis caused by which bacteria is treated with <b>tetracycline?</b>Cholera<div><br></div><div>(caused gastroenteritis is treated with what antibiotic?)</div>
Cholera<div><br></div><div>(caused gastroenteritis is treated with what antibiotic?)</div>Gastroenteritis caused by which bacteria is treated with <b>tetracycline?</b>
"What is responsible for symptoms in Wilson's Disease?"Copper deposition in liver and CNS (e.g. basal ganglia)
"What is the pathophysiology of Wilson's Disease?"<div>Copper accumulates in liver and rest of body due to: </div><div><br></div><div>- Copper excretion into bile <b>impaired</b> </div>- Copper incorporation into caeruloplasmin in hepatocytes <b>impaired</b>
"How can Wilson's Disease affect the mood?"- Depression/mania<div>- Labile emotions</div><div>- Change in libido (both ↑ and ↓)</div><div>- Personality change </div>
"How can Wilson's disease affect cognition?"- ↓ Memory<div>- ↓ IQ</div><div>- Slow to solve problems</div><div>- Delusions</div><div>- Mutism</div>
"What are signs of Wilson's disease?"<div>- Motor deficits: Tremors, dystonia, dysarthria</div><div>- Kayser-Fleischer rings<br></div><div>- Blue lunulae (nails)</div><div>- Grey skin </div><div>- Haematuria</div><div>- Amenorrhoea</div><div>- Repeated miscarriages</div>
"How is Wilson's disease managed?""<b><font color=""#0000ff"">Dietary restriction</font> </b><div>- Avoid foods with high copper content (liver, chocolate, nuts, mushrooms, legumes [peas, lentils, chickpeas] and shellfish)</div><div><b><font color=""#0000ff"">Drugs:</font></b></div><div>1st line: Zinc maintenance therapy<br></div><div>2nd line: Trientine maintenance therapy</div><div>3rd line: Penicillamine</div><div><font color=""#0000ff"">Liver transplantation</font> if severe</div><div><br></div><div><font color=""#0000ff"">Screen siblings</font></div>"
"What is the inheritance pattern of Wilson's disease?"Autosomal recessive 
What are side effects of pencillamine?- Nausea<div>- Rash</div><div>- ↓WCC, ↓Hb, ↓ Platelets</div><div>- Haematuria</div><div>- Nephrosis</div><div>- SLE</div>
What are the most common type of liver tumours?90% are metastases, from breast, bronchus or GI Tract 
What are the most common origins of secondary liver tumours in men?- Stomach<div>- Lung</div><div>- Colon </div>
What are the most common origins of secondary liver tumours in women?- Breast<div>- Colon</div><div>- Stomach</div><div>- Uterus</div>
What are symptoms of liver tumours?- Fever<div>- Malaise</div><div>- Anorexia</div><div>- ↓ Weight </div><div>- RUQ pain (due to stretching of liver capsule)</div><div><br></div><div><br></div><div>(Jaundice is late, except in cholangiocarcinoma)</div>
What does a hepatic bruit indicate?- Primary/metastatic cancer<div>- Alcoholic hepatitis</div>
What is the prognosis of liver metastases?Often <6 months
How is liver metastases managed?Depends on type and extent of primary tumour, but as liver mets signifies advanced disease, most management is palliative
What is the most common type of primary liver cancers?Hepatocellular carcinoma 
Globally, where are hepatocellular carcinomas most common?China and Africa- represent 40% of cancers (vs 2% in UK)
What is the management of hepatocellular carcinomas?"- <font color=""#0000ff"">Resecting solitary tumours <3cm:</font> ↑3 year survival from 13-59%, but around half have recurrence. <div>- <font color=""#0000ff"">Liver transplant: </font>5 year survival of 70% </div><div>- Percutaneous ablation, tumour embolisation and sorafenib are options</div>"
What are causes of cholangiocarcinoma?"- Flukes (<i>Clonorchis</i>)<div>- Primary Sclerosing Cholangitis</div><div>- Biliary cysts</div><div>- Caroli's disease </div><div>- HBV, HCV</div><div>- DM</div><div>- N-nitroso toxins</div>"
"What is <b>Caroli's disease?</b>"Multiple segmental cystic/saccular dilations of intrahepatic bile ducts with congenital hepatic fibrosis<div><br></div><div>(describes what?)</div>
Multiple segmental cystic/saccular dilations of intrahepatic bile ducts with congenital hepatic fibrosis<div><br></div><div>(describes what?)</div>"What is <b>Caroli's disease?</b>"
"How does Caroli's disease present?"Often presents in 20 year olds, with portal HTN, and recurrent cholangitis/cholelithiasis
What is the prognosis of cholangiocarcinoma?Around 5 months 
How is cholangiocarcinoma managed?- Surgery: But 70% inoperable at presentation, and 76% remission<div>- Stenting of obstructed extrahepatic biliary tree may improve QOL</div><div><br></div><div>- Liver transplantation rarely possible </div>
What are the most common benign tumours that are found in the liver?- Haemangiomas 
What causes liver adenomas?- Anabolic steroids<div>- Oral contraceptive pill</div><div>- Pregnancy </div>
How is Hepatitis B vaccine given?IM injections: 3 times, at 0, 1 and 6 month intervals. 
How is Hepatitis B typically transmitted?Parenterally, typically by contaminated blood or blood products (and in vertical transmission)
What is the risk of an infected mother passing Hepatitis B to her child (without intervention)?70-90%
How is risk of vertical transmission of Hepatitis B reduced?Neonate treated with:<div>- Hepatitis B immunoglobulin</div><div>- Vaccination after delivery  </div>
In which ancestries is Hereditary Haemochromatosis more common in?- Northern European, esp. Celtics
What is the most common genetic mutation responsible for hereditary haemochromatosis?C282Y (60-90% of HH)
What consideration must be made with a diabetic patient with Hereditary Haemochromatosis?Monitoring with HbA1c may be falsely low, as venesection may decrease time available for Hb glycosylation 
What provides most of the iron used in erythropoiesis?Macrophage recycling of haem iron following phagocystosis of old RBCs<div><br></div><div>(intestinal iron absorption is only 1-2mg/day and compensates for daily iron losses)</div>
Where is iron mostly absorbed, and in what form?Mostly in duodenum and jejunum, as Fe<sup>2+</sup>
How does α<sub>1</sub>-antitrypsin deficiency typically present in adults and children?Children: Liver disease (cirrhosis, HCC)<div>Adults: Lungs (Emphysema)</div>
What is the action of α<sub>1</sub>-antitrypsin?Serine protease inhibitor, which controls inflammatory cascades in the liver, and protects against tissue damage from neutrophil elastase in the lung 
Describe the genotypes of α<sub>1</sub>-antitrypsin deficiency?Typed by mobility on electrophoresis, M- medium (normal) S- slow Z- very slow. <div><br></div><div>P<sub>i</sub> MM is normal homozygous</div><div><br></div><div>P<sub>i</sub>ZZ is high risk homozygous</div><div><br></div><div>P<sub>i</sub>MZ or P<sub>i</sub>SZ are heterozygotes (and at low risk of developing the disease)</div>
What is the typical presentation of a patient with α<sub>1</sub>-antitrypsin deficiency?- Dyspnoea (from emphysema)<br><div>- Cirrhosis</div><div>- Cholestatic jaundice </div>
What is found on liver biopsy of α<sub>1</sub>-antitrypsin deficiency?- Periodic acid Schiff +ve<div>- Diastase-resistant globules </div>
How can a diagnosis of α<sub>1</sub>-antitrypsin deficiency be made?- Serum α<sub>1</sub>-antitrypsin levels<div>- Genotyping </div><div>-  CXR</div><div>- Spirometry <br>- Liver Biospy: Periodic Acid Schiff +ve; diastase-resistant glovules</div><div><br></div><div><br></div>
What is the prognosis of α<sub>1</sub>-antitrypsin deficiency?- Some pts have life-threatening symptoms in childhood<div>- Others remain asymptomatic and healthy into old age </div>
What worsens prognosis of α<sub>1</sub>-antitrypsin deficiency?- Male<div>- Smoker</div><div>- Obese </div>
What is the most common cause of death in α<sub>1</sub>-antitrypsin deficiency?Emphysema 
What are <b>anti-endomysial</b> antibodies in <b>Coeliac </b>disease?- <b>Anti-tissue transglutaminase </b>specific to the endomysial layer
"What is the best imaging modality (colonoscopy aside) for Crohn's disease?"<b>MRI- abdo pelvis</b>:<div><br></div><div>- Helps localise disease and <b>diagnose fistulae, abscesses, and other extra-mural complications</b></div><div>- Superior to CT scanning, and has high diagnostic accuracy for small bowel disease </div>
"What is seen here?<div><img src=""S_0619__Hemorrhoid_C0197929.2e16d0ba.fill-320x213.jpg""><br></div>"Haemorrhoids
What is an <b>omental patch?</b>Surgical technique to <b>close duodenal perforation</b>:<div>- Piece of <b>omentum used to cover perforation</b></div>
What is <b>arthritis mutilans?</b>Severe form of psoriatic arthritis or RA, characterised by resorption of bones and consequent collapse of soft tissue (describes what?)
Severe form of psoriatic arthritis or RA, characterised by resorption of bones and consequent collapse of soft tissue (describes what?)What is <b>arthritis mutilans?</b>
"What is seen here?<div><img src=""paste-0c890908e575f5e605688acf0c3a9df3d5edd8a5.jpg""><br></div>"Arthritis mutilans- seen in psoriatic arthritis or chronic RA
What corticosteroid are used in intra-articular corticosteroid injections?- Methylprednisolone<div>- Traimcinolone</div>
What rheumatological conditions present with raised ESR, but normal CRP?"- SLE<div>- Sjogren's (will always have high ESR, even if treated)</div>"
How should displaced intertrochanteric fractures be managed?Extracapsular fracture (but not subtrochanteric)- DHS
Which bones are at high risk of avascular necrosis following fracture?- Femoral head<div>- Proximal humerus</div><div>- Scaphoid</div><div>- Talus</div>
"Ask pt to kneel on chair with feet hanging off the edge, then squeeze calves. <div><br></div><div>+ve result: Foot will not move- achilles tendon rupture</div><div>-ve result: Foot will plantarflex</div><div><br></div><div><img src=""tenor.gif""><br></div><div>(+ve result shown here)</div><div><br></div><div>(describes what test?)</div>""How is <b>Thompson's test </b>carried out?"
What radiographic view is particularly good for slipped capital femoral epiphysis?Frog-legged lateral views 
What are prophylactic antibiotics for in surgery?- Reduce risk of wound infection 
When should prophylactic antibiotics be given in surgery?IV prophylaxis 30mins prior to surgery; (metronidazole PR given 2h before).<div><br></div><div>Maximises skin concentration at time of surgery </div>
How are surgical procedures classified with regard to wound infection risk?"<font color=""#0000ff"">Clean</font>: Incising uninfected skin without opening a viscus<div><font color=""#0000ff"">Clean-contaminated</font>: Intra-operative breach of a viscus (but not colon)</div><div><font color=""#0000ff"">Contaminated</font>: Breach of a viscus & spillage or opening of colon</div><div><font color=""#0000ff"">Dirty</font>: Site already contaminated with pus or faeces, or from exogenous contagion</div>"
What is the infection risk of clean, clean-contaminated, contaminated and dirty surgical procedures?"<font color=""#0000ff"">Clean</font>: <2%<div><font color=""#0000ff"">Clean-contaminated</font>: 8-10%</div><div><font color=""#0000ff"">Contaminated</font>: 12-20%</div><div><font color=""#0000ff"">Dirty</font>: 25%</div>"
What is <b>malignant hyperpyrexia?</b>Severe response to volatile agents in general anaesthesia causing muscle rigidity, high fever, and tachycardia. <div><br></div><div>(describes what?)</div>
Severe response to volatile agents in general anaesthesia causing muscle rigidity, high fever, and tachycardia. <div><br></div><div>(describes what?)</div>What is <b>malignant hyperpyrexia?</b>
What are complications of malignant hyperpyrexia?- Hypoxaemia<div>- Hypercarbia</div><div>- Hyperkalaemia</div><div>- Metabolic acidosis </div><div>- Arrhythmias </div>
Who can get malignant hyperpyrexia?Susceptible individuals arise from genetic mutations, inherited in autosomal dominant fashion 
How is malignant hyperpyrexia managed>- Prompt treatment with dantrolene (skeletal muscle relaxant)<div>- Active cooling</div><div>- ITU care </div>
What are signs of a deep vein thrombosis?- Calf warmth/tenderness/swelling/erythema<div>- Mild fever</div><div>- Pitting oedema </div>
What is a raised D-dimer suggestive of?- DVT<br>- Infection<div>- Pregnancy</div><div>- Malignancy</div><div><br></div><div>Also normal post-op</div>
How should Wells score (for DVT) be calculated?"<font color=""#0000ff"">1 point for each of:</font><div><b>C3P(3)O and R2D2</b></div><div>Cancer</div><div>Collateral superficial veins visible</div><div>Calf swelling >3cm (comapred to asymptomatic leg)</div><div>Pitting oedema</div><div>Previous DVT</div><div>Paralysis/paresis or recent plaster immobilisation </div><div>Oedema of the whole leg</div><div><br></div><div>Recent surgery </div><div>Recent immobilisation</div><div><br></div><div>If alternative diagnosis as likely -2 points (D2)</div>"
How is Wells score for DVT interpreted and acted upon?"<font color=""#0000ff"">≤1: DVT unlikely</font>.<b> Perform D-dimer</b>. If negative, DVT excluded, <u>if positive, proceed to USS</u>. <font color=""#ffaa00"">If D-dimer positive and USS negative, repeat USS in 1 week</font><div><br></div><div><font color=""#0000ff"">≥2: DVT likely</font>.<b> Do D-dimer and USS.</b> If both negative, DVT excluded, if USS positive, treat as DVT. <font color=""#ffaa00"">If D-dimer positive, and USS negative, repeat USS in 1 week. </font></div><div><font color=""#ffaa00""><br></font></div><div><img src=""paste-5f8b1109bd902b65324c67afff66360d70c92c5b.jpg""><font color=""#ffaa00""><br></font></div>"
What is the action of <b>fondaparinux?</b>Activates antithrombin III → inhibits Factor Xa Used to reduce risk of DVT (performs better than LMWH without ↑ risk of bleeding)
How can Deep Vein Thrombosis be prevented in surgery?- Stop oral contraceptive pill 4 weeks pre-op<div>- Mobilise early</div><div>- LMWH (e.g. heparin)</div><div>- Fondapirinux (Anti Factor Xa)</div><div>- Thromboembolic Deterrent (TED) Stockings/ Intermittent pneumatic compression devices</div><div><br></div>
When is unfratctionated heparin used over LMWH?- Renal failure<div>- If ↑ risk of bleeding</div>
What are common causes of asymmetric leg swelling?"- DVT<br>- Soft-tissue trauma<div>- Cellulitis</div><div>- Obstruction of pelvic pain/lymphatic vessel in pelvis</div><div>- Ruptured Baker's cyst  </div>"
How should deep vein thrombosis be treated?"<font color=""#0000ff"">Anticoagulation:</font> <div>- LMWH e.g. enoxaparin</div><div>- Fondapirinux</div><div>- Warfarin (but give LMWH to bridge first 5-7 days)</div><div>- DOACs e.g. Dabigatran, apixaban, rivoraxaban</div><div><br></div><div>- <font color=""#0000ff"">Inferior vena caval filters</font> if contraindications to anticoagulant or in active bleeding. </div><div><br></div><div>- <font color=""#0000ff"">Thrombolytic drugs </font>effective, but cause ↑ risk of bleeding. Only used in highly selected patients with no risk factors for bleeding</div>"
What is the purpose of Inferior Vena Cava filters?- Prevent clot passing into pulmonary artery- reduces risk of PE.  
What are disadvantages of IVC filters in the management of DVT?<div>- IVC filter can dislodge or become obstructed by clot</div>- Venous collaterals can develop, providing pathway for emboli to circumvent filter and cause PE
What is postphlebitic syndrome?Symptomatic chronic venous insufficiency following DVT. <div><br></div><div>(describes what?)</div>
Symptomatic chronic venous insufficiency following DVT. <div><br></div><div>(describes what?)</div>What is postphlebitic syndrome?
What percentage of people with DVT can develop post-phlebitic change?10-30%
What symptoms of post-phlebitic syndrome?- Pain<div>- Swelling</div><div>- Skin changes (ulcers)</div>
How should post-phlebitic syndrome/chronic venous insufficiency be managed?"- <font color=""#0000ff"">Elevation</font>: Above level of right atrium<div>- <font color=""#0000ff"">Compression</font>: Graduated compression stockings </div><div>- <font color=""#0000ff"">Topical wound care</font></div><div><br></div><div><br></div><div>Drugs have no role in routine treatment of chronic venous insufficiency</div>"
Where does oedema typically appear in the bed-bound?Sacral oedema- as gravity distributes it to here from the legs
What are causes of bilateral oedema?- Right heart failure (leading to ↑ venous pressure)<div>- ↓ Albumin (e.g. in renal or liver failure)</div><div>- Venous insufficiency</div><div>- Vasodilators (nifedipine, amlodipine)</div><div>- Pelvic mass</div><div>- Pregnancy (pre-eclampsia) </div>
What is the risk of developing a DVT on a long-distance flight in the general population, and in high-risk groups?General population:1 in 10,000-40,000<div>In high-risk groups: 4-6% </div>
How can individuals reduce their risk of developing a DVT on a long-distance flight?- Leg exercises<div>- Increased water intake</div><div>- Refraining from alcohol or caffeine during journey</div>
What is a <b>stoma?</b>A connection between a hollow organ and the outside world
What is an <b>end stoma?</b>"Bowel divided and <font color=""#0000ff"">proximal end brought out as stoma</font>. Distal end may be <font color=""#00aa00"">resected, closed and left in the abdomen, or exteriorized</font><div><br></div><div>(describes what?)</div>"
"Bowel divided and <font color=""#0000ff"">proximal end brought out as stoma</font>. Distal end may be <font color=""#00aa00"">resected, closed and left in the abdomen, or exteriorized</font><div><br></div><div>(describes what?)</div>"What is an <b>end stoma?</b>
What occurs in an <b>abdominoperineal resection?</b>Anus, rectum and sigmoid colon are removed (describes what operation?)
Anus, rectum and sigmoid colon are removed (describes what operation?)What occurs in an <b>abdominoperineal resection?</b>
In a loop colostomy, what does each stoma pass?"<font color=""#0000ff"">Proximal end</font>: Stool<div><font color=""#0000ff"">Distal end</font>: Mucus</div>"
What happens in a Paul-Mikulicz procedure?"Double-barrelled colostomy: colon divided completely to excise a section. <div><br></div><div>Each end exteriorized as two separate stomas. </div><div><br></div><div><img src=""https://history.amedd.army.mil/booksdocs/wwii/surgeryinwwii/chapter30figure41.jpg""><br></div>"
What is the output of a colostomy?Ideally should pass 1-2 <b>formed </b>motions a day, into plastic pouch. <div><br></div><div>(Some can be managed with irrigation, thus avoiding a pouch)</div>
What occurs in a low anterior resection?"All or part of rectum is excised and proximal colon anatomosed to top of anal canal<div><img src=""Rectal-surgery-anterior-resection-labelled_tcm9-45911.jpg""><br></div>"
What is a cystectomy?Surgical operation to remove the bladder or to remove an abnormal cyst
How is a urostomy formed following cystectomy?"Ureters are connected to an ileal conduit, which is brought to a urostomy<div><img src=""bladder_surgery_ileal_conduit-fig_2.png""><br><div><br></div></div>"
What should be avoided when choosing a stoma site?- Bony prominences (e.g. ASIS)<div>- Umbilicus</div><div>- Old wounds/scars (avoid adhesions)<br>- Skin folds and creases</div><div>- The waistline</div><div><br></div>
What is a <b>laparotomy?</b>Surgical procedure involving a large incision through abdominal wall to gain access into abdominal cavity (describes what?)
Surgical procedure involving a large incision through abdominal wall to gain access into abdominal cavity (describes what?)What is a <b>laparotomy?</b>
What is <b>laparoscopy?</b>Keyhole surgery- operation performed using small incisions and a fibre optic cable system 
What are signs of malnutrition on examination?- Skin hanging off muscles<div>- No fat between fold of skin</div><div>- Hair rough and wiry</div><div>- Pressure sores</div><div>- Sores at corner of mouth </div>
How are nasogastric and nasojejunal tubes placed?"<font color=""#0000ff"">Nasogastric</font>: typically manually inserted without guidance<br><div><font color=""#0000ff"">Nasojejunal</font>: Require endoscopic placement</div>"
When are nasojejunal tubes required for feeding?- Gastric outlet obstruction<div>- Delayed gastric emptying</div><div>- Post-gastrectomy</div><div>- Pancreatitis </div>
What is the difference between polymeric and elemental nutrition?"<font color=""#0000ff"">Polymeric</font>: Consists of undigested proteins, starches and long-chain fatty acids<div><font color=""#0000ff"">Elemental</font>: Individual amino acids, oligo and monosaccharides- requiring minimal digestion </div>"
How should the positioning of a nasogastric and nasojejunal tube be checked?"<font color=""#0000ff"">Nasogastric</font>: Aspirate contents and check pH- should be ≤ 5.5. If this fails, CXR.<div><font color=""#0000ff"">Nasojejunal</font>: Abdominal X-Ray</div>"
What size nasogastric tubes should be used for what purpose?"<font color=""#0000ff"">Large bore (16F):</font> Good for drainage but can be uncomfrotable<div><font color=""#0000ff"">Small bore (10F):</font> More comfortable for feeding,, but difficult to aspirate and poor for drainage</div>"
"What is <b>Hesselbach's triangle?</b>""<div>Inguinal triangle, marked by the lateral border of <b>rectus abdominis</b>, <b>inferior epigastric vessels </b>and the <b>inguinal ligament</b>. </div><div><br></div><div><font color=""#0000ff"">Area of potential weakness through which direct inguinal hernias often occur</font></div><div><br></div><div><img src=""Inguinal-Hesselbachs-Triangle.png""><br></div>"
What are risk factors for inguinal hernias?- Being <b>male</b> (8:1)<div>- Chronic <b>cough</b></div><div>- <b>Constipation</b></div><div>- Urinary obstruction</div><div>- Heavy <b>lifting</b></div><div>- Ascites</div><div>- Past-abdominal <b>surgery  </b></div>
Clinically, how should you distinguish between an indirect and direct inguinal hernia?- <b>Reduce</b> hernia, and occlude the deep ring with two fingers. <div>- Ask pt to cough or stand. If hernia <b>restrained</b>, it is <b>indirect</b>. If not, it is direct </div>
What proportion of inguinal hernias are direct?20%, remaining <b>80% are indirect </b>
<span class=cloze>[...]</span> hernias are more frequent in females and can frequently strangulate<span class=cloze>Femoral</span> hernias are more frequent in females and can frequently strangulate<br> Femoral hernias are more frequent in <span class=cloze>[...]</span> and can frequently strangulateFemoral hernias are more frequent in <span class=cloze>females</span> and can frequently strangulate<br> Femoral hernias are more frequent in females and can frequently <span class=cloze>[...]</span>Femoral hernias are more frequent in females and can frequently <span class=cloze>strangulate</span><br> How should inguinal hernias be repaired?"Both indirect and direct inguinal hernias repaired the same way:<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff""><b>Mesh repairs (requires laparotomy)</b>:</font><div>- Polypropylene mesh <b>reinforces posterior wall</b>- reduces recurrence rate</div></div><div><font color=""#0000ff"">Laparoscopic repair</font></div>"
When is naso-gastric feeding contra-indicated?Head-injury/basal skull fracture: risks associated with tube insertion
What is a feeding jejunostomy?"Surgically sited feeding tube- used for long-term feeding + has low risk of aspiration<div><img src=""Difference-Between-G-tube-and-J-tube1.png""><br></div>"
What are the risks of a <b>feeding jejunostomy?</b>Tube displacement and peritubal leakage following insertion (which can cause peritonitis)
"What is this?<div><img src=""Percutaneous_endoscopic_gastrostomy-tube.jpg""><br></div>"A PEG tube- Percutaneous Endoscopic Gastrostomy tube, used for nutrition 
How should total parenteral nutrition be given?Given through a central vein- strongly phlebitic 
What is the feeding option for a man who has jsut undergone a oesophagectomy for carcinoma?Feeding jejunostomy: surgically sited feeding tube, good for long-term feeding<div><br></div><div>(Not PEG, as no oesophagus to pass endoscope and stomach lifted up in chest, so dangerous trying to insert.)</div>
What muscle relaxant is favoured for rapid sequence intubation?Suxamethonium- short-acting muscle relaxant with rapid onset of action 
Which anaesthetic agent has inherent anti-emetic properties?Propofol
What can be used to reverse the action of midazolam?Flumazenil: antagonises effects of benzodiazepine by competition at GABA sites
What considerations should be made for the oral contraceptive pill pre-op?Stop 4-6 weeks prior; re-start 2 weeks after surgery (if mobile)<div><br></div><div>(As increased risk of VTE)</div>
Where is intraosseous access most commonly obtained?Proximal tibia 
When is intraosseous access indicated in adults?When vascular access is difficult to obtain in an emergency setting )e.g. 2 failed attempts at a peripheral intravenous line)
What are clinical features of haemorrhoids?- Painless rectal bleeding<div>- Pruritus</div><div>- Pain (not significant unless piles are thrombosed)</div><div>- Soiling (only in 3rd/4th degree piles)</div>
Where are the anal cushions found in the anal canal?"- Left lateral (3 o'clock)<div>- Right posterior (7 o'clock)</div><div>- Right anterior (11 o'clock)</div><div><br></div><div><img src=""Usual-position-of-haemorrhoids-when-patient-is-in-supine-position-with-legs-in-stirrups.png""><br></div><div><br></div>"
What are the different types of haemorrhoids?"<font color=""#0000ff"">External</font>: Originate below the dentate line<div><font color=""#0000ff"">Internal</font>: Originate above the dentate line </div>"
What type of haemorrhoids are more likely to be painful?<b>External haemorrhoids</b>- more prone to thrombosis, hence may be painful
How are internal haemorrhoids graded?"<font color=""#0000ff"">Grade I:</font> Do not prolapse out of the anal canal<div><font color=""#0000ff"">Grade II:</font> Prolapse on defecation but reduce spontaneously</div><div><font color=""#0000ff"">Grade III:</font> Can be manually reduced</div><div><font color=""#0000ff"">Grade IV:</font> Cannot be reduced</div>"
What non-operative treatments may be provided for haemorrhoids?"<font color=""#0000ff"">- Rubber band ligation (best)</font><div>- Injection sclerotherapy<br></div><div>- Infra-red coagulation (coagulates vessels and tethers mucosa to subcutaneous tissue)</div><div>- Bipolar diathermy and direct current electrotherapy</div>"
Where is fissure in ano typically located?"<b>Midline</b>: posterior (6 o'clock) and anterior (12 o'clock) position,<font color=""#0000ff""> distal to dentate line. </font>"
What is the relevance of the position of an anal fissure?"<font color=""#0000ff"">Midline posterior</font>: Usually related to passage of hard stool<div><font color=""#0000ff"">Midline anterior (or if multiple fissures)</font>: Suggestive of underlying organic disease- <b>merit endoscopy</b></div>"
"Broadly speaking, outline the Dukes' classification of colorectal cancer?""Dukes' A: Tumour confined to mucosa<div>Dukes' B: Tumour invading bowel wall</div><div>Dukes' C: Lymph node metastases</div><div>Dukes' D: Distant metastases</div>"
"What are the 5-year survival of each Dukes' score?""Dukes' A: 95%<div>Dukes' B: 80%</div><div>Dukes' C: 65%</div><div>Dukes' D: 5% (20% if resectable)</div>"
What is the main advantage of epidural analgesia in the context of colorectal surgery?Decreased time before return of normal bowel function vs other analgesic methods
Why does colonic bleeding rarely present as malaena?Blood in the colon has powerful laxative effect- so not reatined long enough for transformation to occur 
What is <b>angiodysplasia?</b>Small vascular malformation of gut, causing GI bleeding and anaemia
Where is most commonly affected in angiodysplasia?Right side fo the colon (ascending colon) 
How does <b>angiodysplasia </b>present?- GI bleeding<div>- Often have no other symptoms</div>
Should colonoscopy be given in acute lower GI bleeds?No- first line management is usually supportive. <div><br></div><div>Give colonoscopy in the elective setting, and an angiogram if pt acutely unstable despite supportive measures</div>
What are characteristic features of a perianal abscess?- Diabetic<div>- Severe pain around the anus, worse on sitting</div><div>- Unable to defecate</div><div>- Spiking temperatures</div><div>- Pus-like discharge from anus</div>
Which patients do perianal abscesses most commonly affet?- Men (2:1)<br>- Around 40 years<div>- Diabetics </div>
Which causative organisms are generally responsible for peri-anal abscesses?"-<font color=""#0000ff""> </font><i><font color=""#0000ff"">E. coli</font> </i>(gut flora)<div>- Can be caused by <i><font color=""#0000ff"">Staph. aureus </font></i>if originated from infection of skin, rather than digestive tract</div>"
What is the gold-standard investigation for anorectal abscesses?MRI
Which IBD is most likely to cause anorectal abscesses?"Crohn's "
What conditions are associated with anorectal abcesses?- IBD<div>- Diabetes mellitus</div><div>- Malignancy (due to risk of bowel perforation)</div>
When are antibiotics required in anorectal abscesses?- If systemic upset secondary to abscess<div>- Immunocompromised</div><div>- Elderly</div>
Specifically, what is a <b>perianal abscess?</b>Abscess of subcutaneous tissue around the anus
"What are ""medical"" causes of acute abdominal pain?"- MI<div>- DKA<br>- Pneumonia</div><div>- Acute intermittent porphyria</div><div>- Lead poisoning</div>
What differentiate an acute and chronic anal fissure?"<font color=""#0000ff"">Acute</font>: <6 weeks<div><font color=""#0000ff"">Chronic</font>: >6 weeks</div>"
How should an acute anal fissure be managed?- Dietary advice: High-fibre diet with high fluid intake<div>- Bulking laxatives (if not tolerated, try lactulose)<br>- Topical lubricants (vaseline) prior to defecation</div><div>- Topical anaesthetics</div><div>- Analgesia</div><div><br></div><div><br></div><div>NB: Topical steroids do not provide significant relief</div>
How should a chronic anal fissure be managed?Management for acute anal fissure plus:<div>- Topical GTN (first-line)</div><div>- If topical GTN ineffective after 8 weeks, then referral for botulinum toxin or topical diltiazem. </div><div><br></div><div>If all else fails, surgical:</div><div>- Lateral partial internal sphincterotomy</div>
What are the nutritional requirements of parenteral nutrition?<div>In 2-3L: </div>- 2000kCal (50% from fat, 50% from carbohydrate)<div>- 10-14g nitrogen</div>
What are complications from Total Parenteral Nutrition?"- <font color=""#0000ff"">Sepsis</font>: Staph epidermidis, staph aureus, candida, pseudomonas, infective endocarditis<div>- <font color=""#0000ff"">Thrombosis</font>: Central vein thrombosis, resulting in PE, or superior vena caval obstruction</div><div>- <font color=""#0000ff"">Metabolic imbalance</font>: Electrolyte abnormalances, deranged plasma glucose, hyperlipidaemia</div><div>- <font color=""#0000ff"">Mechanical</font>: Penumothorax, embolism of IV line</div>"
What is mainly responsible for the features of refeeding syndrome?Hypophosphataemic state (due to ↑cellular phoshate uptake following insulin uptake and previous hypophophataemia from catabolic state)<div><br></div>
What are the features of refeeding syndrome?<div>- Arrhythmias --> cardiogenic shock</div><div>- Abnormal fluid balance</div><div>- Rhabdomyolysis</div><div>- Respiratory insuffiency</div><div>- Seizures</div><div>- Death</div><div><br></div><br>
How can refeeding syndrome be prevented?- Give high dose pabrinex (Vitamins B1, B2, B6, B12+ Vit C) during re-feeding window<div>- Identify high-risk patients and give 50% of metabolic requirements</div>
How is refeeding syndrome treated?<div>- <b>IV phosphate infusion</b> (phosphate polyfusor)</div>- Treat complications
In which group of diabetes patients is the need to put first on the list less important?Diet-controlled diabetics: patients should be treated as if not diabetic 
What are considerations for patients with obstructive jaundice to undergo elective operations?- ↑ Risk of bleeding, peri-operative infection and renal failure<div>- Consider prior ERCP to relieve the obstruction before surgery</div>
What is the worry of patients taking steroids having operations?Steroids are suppressing the Hypothalamic-Pituitary-Adrenal axis, so may be unable to mount an appropriate adrenal response to meet stress of surgery. <div><br></div><div>Extra corticosteroid cover may be required</div>
What are causes of a <b>smooth</b> hepatomegaly?- <b>Hepatitis</b><div>- <b>Congestive</b> hepatomegaly</div><div>- Sarcoidosis (granulomas)</div><div>- Early alcoholic cirrhosis </div><div>- <b>Tricuspid incompetence</b> (will also have a pulsatile liver)</div>
What causes <b>craggy hepatomegaly</b>?- <b>Secondary liver tumours</b><div>- Primary <b>hepatoma </b></div>
At what age is acute appendicitis most common?10-20 years 
What are additional signs of appendicitis?"- <font color=""#0000ff"">Rovsing's sign</font>: Pain on RIF when LIF is pressed<div>- <font color=""#0000ff"">Psoas sign</font>: Pain on extending hip if retrocaecal appendix</div><div>- <font color=""#0000ff"">Cope's sign</font>: Pain on flexion and internal rotation of right hip if appendix in close relation to obtruator internus</div>"
What investigations can be used to investigate appendicitis?"<font color=""#0000ff"">Bloods</font>: <b>Neutrophil </b>predominant leukocytosis, elevated<b> CRP</b><div><font color=""#0000ff"">Ultrasound</font>: Useful, but appendix not always visualised</div><div><font color=""#0000ff"">CT</font>: Gold standard, but rarely done in the UK</div>"
When is laparoscopic appendectomy not recommended?Cases of suspected gangrenous perforation: ↑ rate of abscess formation 
What increases the risk of perforation in appendicitis?- In young children (as diagnosis more often delayed)<div>- If faecolith present </div>
What causes an appendix mass?Inflamed appendix becomes covered with omentum 
What are predisposing factors for colorectal cancer?- Neoplastic polyps <div>- IBD<br>- Genetic predisposition (FAP and HNPCC)</div><div>- Diet (low-fibre, ↑ red & processed meat)</div><div>- ↑ Alcohol + smoking</div><div>- Previous cancer </div>
What can be given to reduce incidence and mortality of colorectal cancer?- Aspirin (though not currently recommended, due to GI side effects)
How do left-sided colorectal cancers present?- Bleeding/mucus PR<br>- Altered bowel habit/ obstruction (25%)<div>- Tenesmus</div><div>- Mass PR (60%)</div>
How does right-sided colorectal cancer present?- Weight loss<div>- ↓Hb</div><div>- Abdominal pain</div><div><br></div><div>(Obstruction less likely, as lumen is wider)</div>
What tests can be used to investigate colorectal cancer?- FBC (look for micorcytic anaemia from blood loss → IDA)<br><div>- FOBT/FIT</div><div>- Sigmoidoscopy/Colonoscopy </div><div>- CEA used as prognostic marker to monitor disease and effectiveness of treatment </div>
In TNM staging of colorectal staging, how is the Tumour assessed?T1: Invading submucosa<div>T2: Invading muscularis propria</div><div>T3: Invading subserosa and beyond (but not other organs)</div><div>T4: Invasion of adjacent structures </div>
In TNM staging of colorectal cancers, how are Nodes assessed?N0: No node spread<div>N1: Metastases in 1-3 regional nodes</div><div>N2: Metastases in >3 regional nodes </div>
What is the management of colorectal carcinomas?"- <b><font color=""#0000ff"">Surgery</font></b>: aims to cure<div>- <font color=""#0000ff"">Chemotherapy</font>: Adjuvant chemotherapy for stage 3 disease (if lymph node involvement) reduces disease recurrence and mortality. Less benefits for stage 2 disease. </div><div>- <font color=""#0000ff"">Radiotherapy</font>: Typically used in palliation (but can occasionally be used pre-op in rectal cancer to allow resection) </div><div>- <font color=""#0000ff"">Biological therapies</font>: used in combination with chemotherapy in advanced disease. </div>"
What is the typical chemotherapy regime for colorectal cancer?FOLFOX:<div><br></div><div>- Folinic acid</div><div>- Fluorouracil<br></div><div>- Oxaliplatin </div>
What biologics can be used in colorectal cancer?- Bevacizumab (anti VEG-F)<div>- Cetuximab/ panitumumab (anti-EGFR) in KRAS wild-type metastatic colorectal cancer </div>
What are risk factors for oesophageal carcinoma?"- Diet<div>- Alcohol excess</div><div>- Smoking</div><div>- Achalsia</div><div>- Reflux oesophagitis </div><div>- Barrett's oesophagus</div><div>- Obesity</div><div>- Plummer-Vinson syndrome </div>"
Where are squamous cell and adenocarcinomas typically found in the oesophagus?"<font color=""#0000ff"">Squamous cell</font>: Proximal<div><font color=""#0000ff"">Adenocarcinomas</font>: Distal</div>"
Where are oesophageal carcinomas distributed?Upper: 20%<div>Middle: 50%</div><div>Lower: 30%</div>
How do oesophageal carcinomas typically present?- Dysphagia: Progressive<div>- Weight loss</div><div>- Restrosternal chest pain </div><div><br></div><div>If from upper third of oesophagus:<br>- Hoarseness</div><div>- Cough </div><div><br></div>
How are oesophageal carcinomas managed?"- <font color=""#0000ff"">Radical curative oesophagectomy</font>: If localised T1/T2 disease<div>- <font color=""#0000ff"">Chemotherapy</font>: Cisplatin & fluorouracil</div><div>- <font color=""#0000ff"">Radiotherapy:</font> Often used in combination with chemotherapy</div><div><br></div><div>Palliation: aims to restore swallowing with chemo/radio, stenting and laser use </div>"
What is a pilonidal sinus?"Small hole or tunnel in skin, caused by hair debris creating sinuses in skin<div><br></div><div><img src=""C0063997.2e16d0ba.fill-320x213.jpg""><br></div>"
Where are pilonidal sinuses most commonly found?"Natal cleft (above the buttocks), typically in male patients after puberty<div><br></div><div><img src=""IMD_pilonidal_sinus_EN.jpg""><br></div>"
When and how do patients typically present with pilonidal sinuses?- Acute inflammation occurs, leading to abscess in pilonidal sinus. <div>- Causes cycles of asymptomatic & periods of pain, and discharge from teh sinus </div>
Who is most commonly affected by pilonidal sinus disease?- Caucasian males<div>- Coarse dark body hair</div><div>- Often in those who sit for prolonged periods </div><div><br></div><div>(typically does not occur after 45 years of age)</div>
How are pilonidal sinuses managed?"<b>Conservative</b>: <div>- Shave affected region and pluck sinus free of any embedded hair</div><div>- Drainage of abscesses (w/ washout), and Abx in septic episodes</div><div><br></div><div><b>Surgical</b>- removal of the pilonidal sinus tract by:</div><div>- <font color=""#0000ff"">Bascom </font>procedure: Excising tract and laying open wound</div><div>- <font color=""#0000ff"">Karydakis </font>procedure: Excising tract, followed by primary closure of the wound</div><div><br></div><div><b>Cannot operate on acute infection- will result in failure</b></div>"
When can pilonidal sinuses be operated on?<b>If chronic disease</b>- cannot operate acutely, as abscess/sepsis will result in failure of procedure. 
What structure is implicated in the development of a pilonidal sinus?Hair follicle
How can a pilonidal sinus be differentiated from an anal fistula?- Sinus does not open into anal canal
What is the most common cause of an anal fissure?Tear in mucosa due to trauma from defecation of hard stool 
What are the major risk factors for anal fissures?- Constipation<div>- Dehydration</div><div>- IBD</div><div>- Chronic diarrhoea</div><div><br></div><div>(↑ inflammation or trauma to the anal canal)</div>
How does a patient with an anal fissure present?"- <font color=""#0000ff"">Pain</font>: Intense pain post-defecation (can last several hours); out of proportion to size of fissure. <div>- <font color=""#0000ff"">Bleeding</font>: Bright red on wiping</div><div>- <font color=""#0000ff"">Itching</font></div>"
What surgical therapy can be offered for chronic anal fissures?"-<font color=""#0000ff""> Botox injections:</font> given into internal anal sphincter, to relax & promote healing<div>-<font color=""#0000ff""> Lateral sphincterotomy:</font> dividing internal anal sphicnter muscle. </div>"
What is an <b>anal fissure?</b>Tear in mucosal lining of the anal canal (describes what?)
Tear in mucosal lining of the anal canal (describes what?)What is an <b>anal fissure?</b>
What is an <b>anal fistula</b>?Abnormal connection between anal canal and perianal skin (describes what?)
Abnormal connection between anal canal and perianal skin (describes what?)What is an <b>anal fistula</b>?
What is the most common cause of a perianal fistula?Arise from anorectal abscesses (90%)
What are potential causes of a perianal fistula?- Perianal abscess (90%)<div>- IBD</div><div>- Systemic disease (TB, DM, HIV)<br>- Hx of trauma to anal region</div><div>- Previous radiation therapy to anal region </div>
How does a patient with anal fistulae typically present?- Recurrent perianal abscesses<div>- Intermittent/continuous discharge onto perineum (mucus, blood, pus, faeces)</div>
"What is seen here?<div><img src=""paste-9ca8b4c23dfb6380032060b7c8998c598ccefaf9.jpg""><br></div>"Anal fistula: abnormal connection of anal canal to perianal skin
How can suspected anal fistulae be investigated?"- <font color=""#0000ff"">Proctoscopy</font>: visualise opening of tract in anal canal<div><img src=""proctoscope-instrument-250x250.jpg""><br></div><div>- <font color=""#0000ff"">MRI</font>: For complex fistula</div><div><br></div><div> </div>"
How is an anal fistula managed?"If asymptomatic: Conservative approach acceptable. <div><br></div><div>Surgery: 2 different options</div><div>- <font color=""#0000ff"">Fistulotomy</font>: Probe passed along tract to lay it open gradually, allowing it to heal by secondary intention</div><div>- <font color=""#0000ff"">Placement of seton</font>: Promotes opening of perianal skin near the tract, preventing abscess formation</div>"
What causes anorectal abscesses?Plugging of anal ducts → fluid stasis → Infection 
What is the function of the anal ducts/glands?Secrete mucous into anal canal, helping to ease passage of faecal matter 
What are common causative organisms of anorectal abscesses?- E. coli<div>- Bacteroides</div><div>- Enterococcus</div>
<span class=cloze>[...]</span> = Anal sepsis<span class=cloze>Anorectal abscess</span> = Anal sepsis<br> Anorectal abscess = <span class=cloze>[...]</span>Anorectal abscess = <span class=cloze>Anal sepsis</span><br> Where are the anal glands located?"Intersphincteric space<div><img src=""anal-ducts.jpg""><br></div>"
Where is the most common site of anorectal abscess formation?Peri-anal area
How does a patient with an anorectal abscess present?- Pain in perianal region, exacerbated when sat down<div>- Localised swelling</div><div>- Itching</div><div>- Discharge</div><div>- Systemic features: Fever, rigors, general malaise, sepsis</div>
How should anorectal abscesses be managed?"<div>- Analgesia</div><div>- Incision and drainage (performed under general anaesthetic)</div><div><br></div><div><font color=""#0000ff"">- Once drained, carry out proctoscopy to check for fistula-in-ano, so seton insertion can be given if necessary. </font></div><div><font color=""#0000ff""><br></font></div><div>(Abx only if elderly/immunocompromised/systemic features etc)</div>"
What are the main risk factors for haemorrhoids?- Excessive straining (from chronic constipation)<div>- Increasing age</div><div>- Raised intra-abdominal perssure (pregnancy, chronic cough, ascites)</div>
How should haemorrhoids be managed?"<b><font color=""#0000ff"">Most can be managed conservatively:</font></b><div>- ↑ Daily fibre and fluid intake (avoid constipation)<br></div><div><br></div><div><font color=""#0000ff"">Medical</font>: </div><div>- Laxatives</div><div>- Topical analgesia (lignocaine gel)</div><div><br></div><div><font color=""#0000ff"">Outpatient services:</font></div><div>- Rubber-band ligation</div><div><br></div><div><font color=""#0000ff"">Surgery</font>:</div><div>- Haemorrhoidectomy (only given to 5%, when all else fails)</div>"
When is rubber-band ligation indicated for haemorrhoids, and how does it work?"Given to <font color=""#0000ff"">symptomatic II and III degree haemorrhoids:</font><div>- Haemorrhoid drawn into end of suction gun, and rubber band placed over neck of haemorrhoid</div><div><img src=""Rubber-band-Ligation-of-Haemorrhoids.jpg""><br></div>"
Where do <b>femoral </b>hernias typically appear?Below and lateral to pubic tubercle (is the common location of which hernia?)
Below and lateral to pubic tubercle (is the common location of which hernia?)Where do <b>femoral </b>hernias typically appear?
Where do <b>inguinal </b>hernias appear?Above and medial to pubic tubercle (is the common location of which hernia?)
Above and medial to pubic tubercle (is the common location of which hernia?)Where do <b>inguinal </b>hernias appear?
Which type of hernia has a high risk of obstruction and strangulation?Femoral hernias
In what patients are epigastric hernias most common?Men aged 20-30y/o
Obturator hernias typically present with <span class=cloze>[...]</span>Obturator hernias typically present with <span class=cloze>bowel obstruction</span><br> "How can Richter's hernia present?"Strangulation without symptoms of obstruction (as anti-mesenteric border of bowel herniates through, but contents do not)
Which infantile hernias should be immediately surgically repaired?-<b> Congenital inguinal hernias</b> (risk of incarceration)<div><br></div><div><br></div><div>Infantile umbilical hernias tend to resolve without intervention before 4-5yrs</div>
What is the distribution of congenital inguinal hernias?- 60% right-sided<div>- 10% are bilateral </div>
What does a hyperechoic lesion in the liver on USS represent?"Cancer:<div>- Hepatocellular carcinoma</div><div>- Haemangioma</div><div><br></div><div>Can be differentiated by <font color=""#0000ff"">AFP</font> (HCC ↑, normal in haemangioma)</div>"
In what patients do liver cell adenomas develop?- Women in 3rd-5th decade<div>- Linked to use of oral contraceptive pill</div>
How do <b>liver cell adenomas </b>appear on USS?- Mixed echoity, and heterogenous texture<div>- Sharply demarcated from normal liver </div><div><br></div><div>(describes the appearance on Liver USS of what lesion?)</div>
- Mixed echoity, and heterogenous texture<div>- Sharply demarcated from normal liver </div><div><br></div><div>(describes the appearance on Liver USS of what lesion?)</div>How do <b>liver cell adenomas </b>appear on USS?
What is seen on liver USS of <b>liver abscesses?</b>- Fluid-filled cavity<div>- Hyperechoic walls (if chronic abscess)</div>
What is the most common extra-intestinal manifestation of amoebiasis?- Liver abscess
Where do amoebic abscesses typically occur in the liver?- Right lobe (75-90%)
How does a patient with an amoebic abscess in the liver present?- Fever<div>- RUQ pain</div>
What is seen on Liver USS of an <b>amoebic abscess</b>?- Fluid filled structure with poorly defined boundaries<div><br></div><div>(describes the Liver USS finding of what?)</div>
- Fluid filled structure with poorly defined boundaries<div><br></div><div>(describes the Liver USS finding of what?)</div>What is seen on Liver USS of an <b>amoebic abscess</b>?
How is amoebic abscesses in the liver treated?Metronidazole- produces a marked clinical response
Aspiration of a liver amoebic abscess will yield what?"Sterile yellow-brown odourless fluid with consistence of ""anchovy paste"""
<span class=cloze>[...]</span> are seen in the liver in Echinococcus infection<span class=cloze>Hydatid cysts</span> are seen in the liver in Echinococcus infection<br> Hydatid cysts are seen in the liver in <span class=cloze>[...]</span> infectionHydatid cysts are seen in the liver in <span class=cloze>Echinococcus</span> infection<br> How are hydatid cysts managed?"- Sterilisation of cyst with mebendazole, <b>then </b>surgical resection<div><br></div><div><font color=""#0000ff"">Percutaneous aspiration contraindicated</font>.</div>"
What investigations may confirm hydatid cysts?- Abnomral LFTs and eosinophilia<div>- USS: Septa and hydatid sand or duaghter cysts</div><div>- Stool sample</div>
In what patients does polycystic liver disease present?Usually in association with autosomal dominant polycystic kidney disease
What produces symptoms in polycystic liver disease?Stretch on liver capsule- causes visceral pain 
What is seen on Liver USS of <b>cystadenoma?</b>- Large anechoic, fluid-filled area with irregular margins<div><br></div><div>(describes the Liver USS finding of what lesion)</div>
What are <b>cystadenomas</b>?Rare cystic tumours derived from biliary epithelium with malignant potential (decribes what?)
Rare cystic tumours derived from biliary epithelium with malignant potential (decribes what?)What are <b>cystadenomas</b>?
How are cystadenomas managed?Surgical resection in all cases
How does the positioning of duodenal ulcers affect complications?"<font color=""#0000ff"">Anterior</font>: Perforate → peritonitis<div><font color=""#0000ff"">Posterior</font>: Erode gastroduodenal artery → Upper GI bleed</div>"
What conditions are associated with sigmoid volvulus?"- Chagas disease<div>- Neurological conditions e.g. Parkinson's, Duchenne's</div><div>- Psychiatric conditions e.g. schizophrenia</div><div>- Elderly, constipated and confused pts</div>"
What can be used to treat local anaesthetic toxicity?IV 20% lipid infusion<div><br></div><div>(Lipid infusion creates lipid phase which extracts hydrophobic molecules of LA, reducing serum LA concentration)</div>
What is given to reverse overdose of <b>heparin?</b>IV protamine sulfate (is given in overdose of what?)
IV protamine sulfate (is given in overdose of what?)What is given to reverse overdose of <b>heparin?</b>
What should be used for access in paediatrics in acute management (not long-term)?Intraosseous access 
What are exmplaes of tunneled lines?- Groshong<div>- Hickman lines</div>
What are tunneled lines used for?- Given for patients with long-term therapeutic requirements (esp. popular in paediatric practice)
How are tunneled lines inserted?"Inserted using USS guidance into internal jugular vein, then tunneled under skin. <div><br></div><div><img src=""hqdefault (2).jpg""><br></div>"
What are PICC lines?Peripherally Inserted Central Catheter:<div><br></div><div>- Establishment of central venous access through insertion in peripheral veins: reduces complications relating to device insertion</div>
What investigation is preferred to check for anastomosis leakage? (bowel anastamosis not arterial)Gastrografin<b> enema</b> (barium enema more toxic if leaks)
What can cause malignant hyperthermia?- Volatile inhalational anaesthetic agents<div>- Suxamethonium</div>
What is the appropriate safety-netting for a patient sent home w/ Abx for a mild diverticulitis?Go to emergency department if does not improve within 72 hours (admission for IV ceftriaxone and metronidazole)
What are the main stages of wound healing, and when do they typically occur?- Haemostasis (Minutes to hours following injury)<div>- Inflammation (Days 1-5)</div><div>- Regeneration (Days 7-56)</div><div>- Remodelling (6 weeks- 1 year)</div>
What happens in the inflammation stage of wound healing?- Neutrophils migrate into wound <div>- Growth factors released, inc. FGF and VEGF</div><div>- Fibroblasts replicate within adjacent matrix and migrate into wound</div><div>- Macrophages and fibroblasts couple matrix regeneration and clot substitution</div>
What process of wound healing is impaired in diabetes?- Neutrophil migration into wound, in inflammation stage
What happens in regeneration stage of wound healing?- Platelet Derived Growth Factor and transformation growth factors stimulate fibroblasts and epithelial cells<div>- Fibroblasts produce collagen network</div><div>- Angiogenesis occurs- wound resembles granulation tissue</div>
What occurs in the remodeling phase of wound healing?- Fibroblasts → myofibroblasts: cause wound contraction<div>- Collagen fibres remodeled</div><div>- Microvessels regress, leaving pale scar</div>
What is a <b>hypertrophic scar?</b>Excessive collagen within a scar, but remains within confines of original injury (is what?)
Excessive collagen within a scar, but remains within confines of original injury (is what?)What is a <b>hypertrophic scar?</b>
"What is seen here?<div><img src=""paste-082fb97869acdacfa41fd558a1ffdcd04069b592.jpg""><br></div>"Hypertrophic scar: Excessive collagen deposition, but contained within the boundaries of the wound 
What is a <b>keloid scar</b>?Excessive amounts of collagen within scar, but passes boundaries of original injury (describes what?)
Excessive amounts of collagen within scar, but passes boundaries of original injury (describes what?)What is a <b>keloid scar</b>?
"What is seen here?<div><img src=""VID319_230119_Keloid_01_3P2A5321.2e16d0ba.fill-920x613.jpg""><br></div>"<b>Keloid scar</b>: excessive collagen within scar, but extends byeond confines of original wound
What are the difference between keloid and hypertrophic scars?- Hypertrophic scars remain confined within boundaries of the original wound<div>- On histology, hypertrophic scars contain nodules </div>
What drugs impair wound healing?- NSAIDs<div>- Steroids</div><div>- Immunosuppressive agents</div><div>- Anti-neoplastic drugs</div><div><br></div><div>(Anything which reduces inflammation or replication of specific cells)</div>
"Where are Meckel's diverticulum typically found? "2 feet proximal to ileocaecal valve  
"How can a Meckel's diverticulum cause upper GI bleeding?""- Meckel's diverticulitum can be lined by ectopic gastric mucosal tissue- may secrete acid, which causes ulceration and bleeding"
What are the main types of rectal prolapse?"<b>Type 1:</b> Rectal <font color=""#0000ff"">mucosa </font>protrudes out of anus<div><b>Type 2: </b>Rectal <font color=""#0000ff"">wall </font>protrudes out of anus.</div>"
What are risk factors for rectal prolapse?- Age<div>- Female gender</div><div>- Multiple deliveries</div><div>- Straining</div><div>- Anorexia</div><div>- Previous traumatic vaginal delivery</div>
How do patients with rectal prolapse typically present?- Rectal mucous discharge<div>- Faecal incontinence</div><div>- Per rectum bleeding</div><div>- Visible ulceration</div><div><br></div>
How might full thickness rectal prolapses initially present?As they begin internally, present with:<br><div>- Sensation of Rectal fullness</div><div>- Tenesmus</div><div>- Repeated defecation </div>
If a rectal prolapse is not visible in a suspected patient, how can you identify it?Ask patient to strain
How can rectal prolapse be conservatively managed?- ↑ Dietary fibre and fluid intake<div><br></div><div><br></div><div>(Banding of minor mucosal prolapses in clinic possible)</div>
When is conservative management favoured in rectal prolapse?- Pt unfit for surgery<div>- Minimal symptoms</div><div>- Children (most prolapses in children resolve spontaneously)</div>
What is the most effective management for rectal prolapse?Surgical repair (only definitive management)<div><br></div><div>(Abdominal and perineal approach: perineal approach preferred in older patients as generally safer)</div>
What condition does rectal prolapse most commonly co-exist with?"<b>Haemorrhoids</b>: type 1<font color=""#0000ff""> prolapses associated with loosening and stretching of connective tissue joining mucosa and wall-</font> which is the case in haemorrhoids"
What is the management of pruritus ani?"<font color=""#0000ff"">Conservative</font>:<div>- Improve perianal hygiene</div><div>- Avoid scratching</div><div>- Avoid foods which loosen stools</div><div><br></div><div><font color=""#0000ff"">Medical</font>:</div><div>- Mild topical corticosteroids if perianal inflammation</div><div>- Oral antihistamine for nocturnal stitch</div>"
Why is fissure-in-ano commonly a chronic problem?Spasm may constrict inferior rectal artery → ischaemia → impairs healing 
"What is <b>Goodsall's rule?</b>""Determines path of fistula track in anal fistula:<div><br></div><div>- If anterior, fistula track is in a straight line</div><div>- If posterior, interior opening always in 6 o'clock position, taking tortuous course</div><div><br></div><div><img src=""paste-5e250ed2392a58aac2db19c4c26f3dfced9c5e6e.jpg""><br></div>"
What is a perianal haematoma?"Thrombosed external pile <div><img src=""paste-679e8799dbf00892eb203d484fb34c3515508c17.jpg""><br></div>"
What is the most common type of rectal prolapse?Type 2: complete prolapse
What typically causes a rectal prolapse?- Lax sphincter<div>- Prolonged straining</div><div>- Chronic neurological/psychological disorders </div>
What are the surgical options to repair a rectal prolapse?"<b>Abdominal approach</b><div>- Fix rectum to sacrum + mesh insertion +/- rectosigmoidectomy</div><div><br></div><div><b>Perineal approach: </b></div><div>- Delorme's procedure (resect close to dentate line, and suture mucosal boundaries)</div><div>- Anal encirclement with a Thiersch wire </div>"
How are <b>perianal warts </b>managed?- Podophyllotoxin<div>- Imiquimod</div><div>- Cryotherapy/surgical excision </div><div><br></div><div>(if 2° to syphilis, Rx is penicillin)</div>
How does proctalgia fugax present- Intense, brief, stabbing/crampy rectal pain<div>- Often worse at night</div>
"What are these?<div><img src=""skin-tags-on-the-anus.jpg""><br></div>"<b>Skin tags</b>- Excessive skin growths
What type of cancer represents the majority of <b>anal cancers?</b>Squamous cell (85%)
What are risk factors for anal cancer?- Anoreceptive intercourse<div>- HPV (HPV 16 associated with worse prognosis)</div><div>- HIV </div>
Where do anal cancers spread to?"<font color=""#0000ff"">Above dentate line</font>: Pelvic lymph nodes<div><font color=""#0000ff"">Below dentate line</font>: Inguinal nodes</div>"
How does anal cancer typically present?- Bleeding<div>- Pain</div><div>- Bowel habit chnage</div><div>- Pruritus ani</div><div>- Masses</div><div>- Stricture </div>
How is anal cancer typically managed?"- <font color=""#0000ff"">Chemoirradiation: Radiotherapy + fluorouracil + mitomycin/cisplatin (generally preferred)</font><div>- Excisition and colostomy</div>"
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How does injection sclerothearpy work in the management of haemorrhoids, and which grade haemorrhoids is it indicated for?- Sclerosants injected into pile above the dentate line- induces fibrotic reaction<div>- Used for 1st/2nd degree haemorrhoids</div>
What blood vessels supply the mucosal cushions in haemorrhoids?"External: External rectal plexus<div>Internal: Internal rectal plexus </div><div><img src=""paste-590274a635ec59fa6f9dce3002404e4649de0dd8.jpg""><br></div>"
What are cholesterol stones like?"- Large, often solitary<div><img src=""paste-b2ead9ed632568f45ed0c5facee9a484260b0c2e.jpg""><br></div>"
What are risk factors for Cholesterol stones?- Female<div>- Age</div><div>- Obesity </div>
What percentage of those with gallstones are asymptomatic?90%
What are symptoms of chronic cholecystitis?- Vague abdominal discomfort<div>- Distension</div><div>- Nausea</div><div>- Flatulence</div><div>- Fat intolerance </div>
Is it better to carry out an early or delayed cholecystectomy for acute cholecystitis/biliary colic?"<font color=""#0000ff"">Early laparoscopic cholecystectomy</font>: decreases duration of hospital admission, but does not increase mortality or complications"
What are the main different types of calculi that can cause nephrolithiasis?- Calcium oxalate (75%)<div>- Magnesium ammonium phosphate (15%)</div><div>- Urate</div><div>- Hydroxyapatite</div><div><br></div>
What is <b>pyuria?</b>Presence of pus/WBCs in urine (describes what?)
Presence of pus/WBCs in urine (describes what?)What is <b>pyuria?</b>
How does nephrolithiasis present?- Pain: loin to groin; often cannot lie still<div>- Infection </div><div>- Haematuria</div><div>- Proteinuria</div><div>- Sterile pyuria</div><div>- Anuria</div>
What is the initial management for nephrolithiasis?<div>- Analgesia (e.g. NSAIDs)</div><div>- IV fluids </div><div>- Antibiotics if infection</div><div><br></div>
Which cases of nephrolithiasis should be conservatively managed?If stones <5mm and in lower ureter:<div>- 90-95% pass spontaneously, simply ↑ fluid intake. </div>
When should medical expulsive therapy be required for nephrolithiasis?If stones >5mm, or pain nor resolving 
What should be given for medical expulsive therapy of urinary tract calculi?"- Nifedipine<div><font color=""#0000ff"">or</font><br><div>- α-blockers (tamsulosin)</div></div><div><br></div><div>Most pass within 48h</div>"
If pharmacological management of nephrolithiasis fails, would could then be tried?"- <b>Extracorporeal shockwave lithotrispy</b>: USS breaks down kidney stones into small crystals<div>- <b>Ureteroscopy using a basket:</b> fishes out stone</div><div><br></div><div><font color=""#0000ff"">If this fails, surgery:</font></div><div>- Percutaneous nephrolithotomy</div>"
When might an urgent surgical intervention be required for nephrolithiasis?- Presence of infection <b>and </b>obstruction <div>- Urosepsis</div><div>- Intractable pain/vomiting</div><div>- Impeding AKI</div><div>- Obstruction in solitary kidney</div><div>- Bilateral obstructive stones </div>
What is the most common cancer type in the stomach?Adenocarcinomas (90%)
What are risk factors for stomach carcinomas?- Pernicious anaemia<div>- Blood group A</div><div>- <i>H. pylori</i></div><div>- Atrophic gastritis</div><div>- Adenomatous polyps</div><div>- Smoking, diet</div><div>- Nitrosamine exposure</div>
What aspects of diet increases the risk of gastric carcinomas?- High nitrate<div>- High salt</div><div>- Pickled foods</div><div>- Low vitamin C </div>
What are signs of a stomach carcinoma suggesting <b>incurable disease?</b>"- Epigastric mass<div>- Hepatomegaly</div><div>- Jaundice</div><div>- Ascites </div><div>- Large Virchow's node</div><div>- Acanthosis nigricans </div>"
"What is <b>Troisier's sign?</b>""Enlarged Virchow's node (describes what?)"
"Enlarged Virchow's node (describes what?)""What is <b>Troisier's sign?</b>"
What are <b>Krukenberg tumours?</b>Malignancy in the ovaries, which typically metastasise from the GI Tract (Gastric adenocarcinomas most common source) 
What is the prognosis of gastric adenocarcinomas?5 yr survival < 10%, but 20% for patients who undergo radical surgery 
What is the management of gastric cancers?"<div><b>Resection:</b></div><font color=""#0000ff"">If 'early':</font> <b>Endoscopic mucosal resection</b><div><br></div><div><font color=""#0000ff"">If advanced tumour distally: </font>Partial <b>gastrectomy</b></div><div><font color=""#0000ff"">If advanced tumour proximally: </font>Total gastrectomy may be needed</div><div><br></div><div><b>Combination chemotherapy</b></div><div>- Epirubicin, cisplatin and fluorouracil ↑ survival in advanced disease. Also useful peri-op. </div><div><br></div><div><b>Some targted therapies e.g. trastuzumab if HER2 pos</b></div>"
How does <b>acute mesenteric ischaemia </b>classically present?- <b>Acute severe abdominal pain</b>: Tends to be constant, central or around RIF. Out of proportion with clinical signs<div>- No/<b>minimal abdominal signs</b></div><div>- Rapid <b>hypovolaemia </b>→ shock </div>
What investigations could be used to investigate acute mesenteric ischaemia?"- <b>FBC: ↑Hb </b>(due to plasma loss), <b>↑WCC</b><div>- <b>↑ Amylase</b><br></div><div>- <b>↑Lactate</b>, causing persistent metabolic acidosis</div><div><br></div><div>- AXR:<b> 'Gasless' abdomen</b></div><div>- <b>CT/MR:</b> may show some evidence of ischaemia. CT/MR Angiography may be useful</div>"
What are the main complications arising from acute mesenteric ischaemia?- Septic <b>peritonitis</b><div>- SIRS → <b>multi-organ failure</b>, due to bacterial translocation across ischaemic gut wall </div>
How is acute mesenteric ischaemia managed?- Resucitation with IV fluid, Abx<div>- LMWH/heparin</div><div>- <b>Surgery: </b>Remove dead bowel. Attempt revascularisation (often needs a 2nd laparotomy)</div>
How should chronic mesenteric ischaemia be managed?Surgery should be considered (risk of acute infarction): <div>- Percutaneous transluminal angioplasty and stent insertion </div>
What is a Billroth I operation?"Partial gastrectomy with simple gastroduodenal reanastomosis<div><img src=""operation_Billroth.jpg""><br></div>"
What is a Billroth II operation?"- Partial gastrectomy with gastrojejunal anastomosis (through longitudinal incision). <div>- Duodenal stump oversewn to leave blind loop.</div><div><br></div><div><img src=""operation_Billroth.jpg""><br></div>"
What is a Roux-en-Y reconstruction?"Following total/subtotal gastrectomy:<div>- Proximal duodenal stump is oversewn</div><div>- Proximal jejunum divided from distal duodenum and connects with oesophagus(if total)/stomach (if subtotal)</div><div>- Distal duodenum connected to distal jejunum </div><div><img src=""paste-9d80114836a58c1e4b14b8601160bea666c94684.jpg""><br></div>"
What are physical complications of gastrectomy?- Abdominal fullness: early satiety<div>- Afferent loop syndrome </div><div>- Diarrhoea</div><div>- Gastric tumour</div><div>- ↑Amylase: may indicate afferent loop obstruction (e.g. following Billroth II surgery)</div>
What is afferent loop syndrome?"Post-gastrectomy (e.g. Billroth II), afferent loop may fill with bile after a meal.<div><br></div><div>Causes Upper abdominal pain and billous vomiting</div><div><br></div><div><img src=""11642""><br></div>"
What are metabolic complications of gastric surgery?<div>- Dumping syndrome</div><div>- Weight loss (due to poor calorie intake)<br>- Bacterial overgrowth </div><div>- Anaemia (due to lack of iron, hypochlorhydria, and stomach resection)</div><div>- Osteomalacia</div>
What is dumping syndrome?"<div>Absent/insufficiently functioning pyloric sphincter causes food with high osmotic potential (e.g. sugar)to enter duodenum too quickly.</div><div><font color=""#0000ff"">Associated with complications following gastric/oesophageal surgery</font></div>"
What are the two forms of dumping syndrome?"<font color=""#0000ff"">Early</font>: 10-30mins after a meal. Rapid movement of fluid into intestine due to hypertonic contents → osmotic diarrhoea + cramping from small bowel distention<div><br></div><div><font color=""#0000ff"">Late</font>: 2-3hrs after meal. Excessive sugar into intestine causes pancreas to raise insulin level, causing rebound hypoglycaemia </div>"
How is dumping syndrome managed?Will naturally improve with time post surgery, but: <div>- Conservative: Eat less sugar, and more guam gum and pectin (slows glucose absorption)</div><div>- Octreotide may help slow gastric emptying + inhibit relase of insulin </div>
What are complications of laparoscopic fundoplication?- Dysphagia (if wrap is too tight)<div>- Gas-bloat syndrome (inability to belch/vomit)</div><div>- New-onset diarrhoea </div>
What is the NICE guidelines for post-operative wound cleansing?<b>Up to 48hrs</b> after surgery: <b>Sterile saline</b><div>After 48hrs: Can shower safely</div>
What is a complication of long-term mechanical ventilation, which can present as abdominal distension associated with ventilation?"<b>Tracheo-oesopahgeal fistula formation</b>: <font color=""#0000ff"">pressure from</font> <font color=""#0000ff"">endotracheal tube can cause ischaemic necrosis,</font> involving anterior wall of oesophagus.<div><br></div><div>Increases risk of ventilator-assocaited penumonias and aspiration pneumonias. </div>"
What neuromuscular blocker is contraindicated in the use of burn injuries?Suxamethonium- increases the risk of hyperkalemia
How do you decide what anticoagulant to use in anti-phospholipid syndrome?"<font color=""#0000ff"">First line</font>: Low-dose aspirin<div><br></div><div><font color=""#0000ff"">If recurrent thromboses</font>: Warfarin, aiming for INR of 3.5</div><div><br></div><div><b>NOACs are not helpful</b></div>"
What are characteristic features of polyarteritis nodosa?"- Cutaneous nodules and ulcers (palpable purpuric rash)<div>- Testicular pain</div><div>- Livedo reticularis</div><div>- Peripheral neuropathy</div><div>(pancreatitis)</div><div><img src=""3-s2.0-B9780323091381001625-f162-006-9780323091381.jpg""><br></div>"
How does <b>osteochondritis dissecans </b>present?- Swelling after exercise<div>- Joint locking</div><div>- Decreased range of movement </div>
What causes osteochondritis<b> dissecans</b>?Blood supply of bone interrupted → <b>bone and cartilage detaches </b>from area and moves in joint space 
Who and where does osteochondritis dissecans typically affect?Typically in young adults, at:<div>- Knee</div><div>- Elbow</div><div>- Ankle </div>
How is ostechondritis dissecans managed?- Conservatively: Rest, and bone will heal. <div><br></div><div>- In adult cases, arthroscopy may be used to reduce number of frgaments in joint</div>
What are symptoms of Eosinophilic granulomatosis with polyangiitis?- Late-onset asthma<div>- Sx of nasal obstruction, bilateral nasal polyps</div><div>- Eosinophilia</div><div>- Rapidly progressive glomerulonephritis</div><div>- Palpable purpura</div><div>- GI bleeding</div>
What drug is associated with Eosinophilic granulomatosis with polyangitis?Montelukast 
What is the Pathergy reaction test?"Test for Behcet's disease:<div>- Papule forms from a needle prick</div><div><br></div><div><img src=""pathergytest.gif""><br></div>"
In what fistulae are drainage setons and fistulotomies used?"<font color=""#0000ff"">Drainage setons:</font> High trans-sphincteric fistulae<div><font color=""#0000ff"">Fistulotomy</font>: Low fistulae</div>"
How should mechanical back pain be managed, if red flags are excluded?- Gentle exercise & physiotherapy (to prevent stiffness)<div>- Analgesia (to allow movement)</div><div><br></div><div>Bed rest not recommended, as can lead to stiffness which causes further pain → viscious cycle </div>
"Where does Charcot's arthropathy most commonly affect?"- Tarsometatarsal joints 
"What is seen here?<div><img src=""642d95f1b8bd91a1e0b1706706e714_jumbo.jpg""><br></div>"Lipohaemarthrosis: escape of fat and blood from bone marrow into joint.<div><br></div><div>Associated with haemophilia and fractures</div>
What is the most sensitive test for investigating hiatus hernia?- Barium swallow
What is the most likely finding on a blood gas of someone with recurrent vomiting?Hypokalaemic hypochloraemic metabolic alkalosis
Which DMARD is contraindicated in Psoriatic Arthritis?Hydroxychloroquine- inconsistent and can worsen skin lesions
What is <b>Complex regional pain syndrome?</b>Disorder giving severe and debilitating pain in the absence of nerve injury<div><br></div><div>(describes what?) </div>
Disorder giving severe and debilitating pain in the absence of nerve injury<div><br></div><div>(describes what?) </div>What is <b>Complex regional pain syndrome?</b>
<span class=cloze>[...]</span> = Complex Regional Pain Syndrome"<span class=cloze>Sudek's atrophy</span> = Complex Regional Pain Syndrome<br> "
"Sudek's atrophy = <span class=cloze>[...]</span>""Sudek's atrophy = <span class=cloze>Complex Regional Pain Syndrome</span><br> "
What are the features of Complex Regional Pain Syndrome?- Pain<div>- Abnormal Blood flow</div><div>- Trophic changes to the skin</div><div>- Sensory disturbance</div><div>- Autonomic features </div>
"What can cause Sudek's atrophy?"(Complex regional pain syndrome)<br>- Orthopaedic operations<div>- Fractures</div><div>- Herpes Zoster</div><div><br></div><div>Presents weeks-months after initial insult</div>
"What is seen here?<div><img src=""8fcdb4dea6709b69ef91f390f6e09f_jumbo.jpeg""><br></div>""<b>Hiatus hernia:</b> protrusion of stomach (with Gastro-oesophageal junction) beyond diaphragmatic constriction<div><br></div><div><img src=""paste-9f8afad08bae95b207279823084d680efe6b36d5.jpg""><br></div>"
Vitamin <span class=cloze>[...]</span> = FolateVitamin <span class=cloze>B9</span> = Folate<br> Vitamin B9 = <span class=cloze>[...]</span>Vitamin B9 = <span class=cloze>Folate</span><br> Vitamin <span class=cloze>[...]</span>= CobalaminVitamin <span class=cloze>B12</span>= Cobalamin<br> Vitamin B12= <span class=cloze>[...]</span>Vitamin B12= <span class=cloze>Cobalamin</span><br> What are the metabolic (hyper/hypo_____) causes of acute pancreatitis?- Hypercalcaemia<div>- Hyperparathyroidism</div><div>- Hyperlipidemia</div><div>- Hypothermia</div>
What is a FIT test?Faecal Immunochemical Test. <div><br></div><div>Tests for blood in stools- similar but more sensitive than Faecal Occult Blood Test</div>
"What is seen here?<div><img src=""paste-e35e318f2493b5f406d1fc784f7b99890748b0e2.jpg""><br></div>"Varus deformity
"What is seen here?<div><img src=""99803555-valgus-deformity-of-legs.jpg""><br></div>"Valgus deformity
At what point after a fracture does a callous begin to form?3 weeks
When carrying out a hip examination, what questions should you ask the patient before starting?- Are you in any pain?<div>- Are you comfortable for me to proceed?</div><div><b>- Have you had a previous hip replacement? </b>(Important, as if so, ensure internal rotation, adduction and flexion <90°, to reduce risk of dislocation)</div>
What should you be palpating for on a hip examination?- Feel for tenderness/warmth (suggestive of inflammation/infection)<div>- Palpate greater trochanter for tenderness (trochnateric bursitis)</div>
How can you assess leg length?"<font color=""#0000ff"">Apparent leg length</font>: Umbilicus (xiphysternum) to the tip of medial malleolus<div><font color=""#0000ff"">True leg length</font>: ASIS to tip of medial malleolus</div>"
"How should Thomas' test be carried out?""- Place hand under pt's spine<div>- Passively flex unaffected leg as far as possible. (Hand should detect lumbar lordosis has now flattened)</div><div>- Contralateral leg should be flat on bed</div><div><br></div><div>Test is positive if contralateral leg raises off bed, indcating loss of extension in hip → fixed flexion deformity</div><div><br></div><div><img src=""giphy (5).gif""><br></div>"
What ages are offered the faecal immunochemical test, and with what frequency?Given to ages 60-74, and repeated every 2 years 
What are the advantages of the FIT test over the FOBT test?- Specifically detects human haemoglobin (rather than haemoglobin from dietary meat)<div>- Only one faecal sample is needed, rather than 2-3 conventional FOBT</div>
If patients have a positive FIT test, what proportion of these are found to have cancer?<div>- 10% have cancer</div><div>- 40% have polyps, which may be removed due to premalignant potential </div>- 50% have normal exam
What instructions should you give a pt who is to carry out a FIT test?Stool cannot touch the water:<div>- Either poo into a container or line the toilet bowl with cling film. </div><div><br></div><div>Do not need to send the whole stool- just use the provided sticks, making sure all ridges are covered. </div>
How long does it approximately take for a colonoscopy/flexible sigmoidoscopy?Flexi sig= 15 mins<div>Colonoscopy= 30 mins</div><div><br></div><div>But can take longer if removing polyps etc. </div>
How wide is the colonoscope?Around 1cm in diabeter 
What is a very frequent cause of discomfort for colonoscopies?Gas is pumped up into bowel
What is <b>Osgood-Schlatter </b>disease?Osteochondrosis of the tibial tuberosity- causing painful inflammation <div><br></div><div>(describes what?)</div>
Osteochondrosis of the tibial tuberosity- causing painful inflammation <div><br></div><div>(describes what?)</div>What is <b>Osgood-Schlatter </b>disease?
Who does Osgood-Schlatter commonly affect?Boys between 10-15y/o<div><br></div><div>(becoming more common in girls, as more are involved in sports)</div>
What is thought to cause Osgood-Schlatter disease?"Trauma from excessive traction by patellar tendon on immature epiphyseal insertion → microavulsion fractures<div><br></div><div><img src=""osgoodSchlatter-415x233-rd6-enIL.png""><br></div>"
Pain and swelling in a young boy, over the area of the tibial tubercle, accompanied by redness and warmth is indicative of what?Osgood-Schlatter Disease
How is Osgood Schlatter disease managed?"- Analgesics<div>- Resolution usually spontaneous within weeks/months</div><div><br></div><div>Avoid excessive exercise (esp. deep knee bending). <span style=""color: rgb(0, 0, 255);"">Complete avoidance of sports unnecessary</span></div>"
What is <b>osteochondrosis?</b>Self-limiting developmental derangement of normal bone growth, usually involving centres of ossification in the epiphysis<div><br></div><div>(describes what?)</div>
Self-limiting developmental derangement of normal bone growth, usually involving centres of ossification in the epiphysis<div><br></div><div>(describes what?)</div>What is <b>osteochondrosis?</b>
What is <b>Legg-Calv­é- Perthes </b>disease?Osteochondrosis involving idopathic aseptic necrosis of femoral capital epiphysis<div><br></div><div>(describes what?)</div>
Osteochondrosis involving idopathic aseptic necrosis of femoral capital epiphysis<div><br></div><div>(describes what?)</div>What is <b>Legg-Calv­é- Perthes </b>disease?
Who does Legg-Calvé-Perthes disease most commonly effect?5-10 y/o boys 
A 16y/o male with a history of Cystic fibrosis presents with a Hx of diarrhoea and recurrent abdominal pain. <div><br></div><div>What is the most appropriate treatment?</div><b>Creon (pancreatic lipase replacement)</b><div><br></div><div>Pt has developed pancreatic insufficiency 2° to CF. </div>
What is <b>Creon</b>?Pancreatic Lipase Replacement therapy (is known as what?)
Pancreatic Lipase Replacement therapy (is known as what?)What is <b>Creon</b>?
What is the most common primary bone malignancy?Osteosarcoma
Who and where does osteosarcoma most commonly affect?Adolescent males:<div><br></div><div>- Usually around knee</div><div>- Or in other long bones (particularly metaphyseal-diaphyseal area)</div>
What are X-ray features of osteosarcoma?"- Periosteal reaction<div>- Codman's triangle (elevation of periosteum from surface of bone)</div><div>- Sunburst appearance (formation of new bone, in sunburst pattern)</div><div><img src=""ee51a8f55e74401e935211c31e554542.aspx""><br></div>"
"Where do Ewing's Sarcoma present?""Occurs in adolescents:<div>- Enlarging mass along long bone diaphysis</div><div><br></div><div><img src=""y5rdhdhdj.jpg""><br></div>"
"What are X-ray changes seen in Ewing's sarcoma?""Onion skin periosteal reaction:<div><img src=""A-Multilamellar-periosteal-reaction-white-arrow-with-an-onion-skin-pattern.png""><br></div>"
What are the common primary bone malignancies, and who do they commonly affect?"- Osteosarcoma (most common): Adolescent males <div>- Ewing's sarcoma: Adolescents</div><div>- Chondrosarcoma: Older patients, >40</div>"
How does chondrosarcoma present?Pain and a lump- often arising from prev. chondromas which have become malignant. 
What is the X-ray finding of a chondrosarcoma?"Lytic lesion with 'fluffy popcorn calcification'<div> </div><div><img src=""9370dc78b36b32ea0376e9aa27f0ae_gallery.jpeg""><br></div>"
Where do chondrosarcomas tend to develop?- Flat bones (pelvis, scapula)<div>- But can develop in any bone and can implant in surrounding soft tissues</div>
"How is Ewing's sarcoma treated?"Combinations of surgery, chemotherapy and radiation therapy <div><br></div><div>(>60% w/ localised Ewing sarcoma can be cured)</div>
How is osteosarcoma treated?- Chemotherapy<div>- Surgery <br></div>
How are chondrosarcomas treated?"<font color=""#0000ff"">Low-grade</font>: Treated intralesionally w/ adjuvant<div><font color=""#0000ff"">High-grade</font>: Surgical resection (amputation may be necessary, if maintenance of function is impossible)</div>"
"What is <b>Jaccoud's arthropathy</b>?"Occurs in association with SLE, and presents with rheumatoid-like hands <b>which are reducible in extension </b><div><b><br></b></div><div>(describes what?)</div>
Occurs in association with SLE, and presents with rheumatoid-like hands <b>which are reducible in extension </b><div><b><br></b></div><div>(describes what?)</div>"What is <b>Jaccoud's arthropathy</b>?"
" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""dbc0e626d0934cd0900408fcc0e527e2-oa-1-Q.svg"" /></div> <div id=""io-original""><img src=""tmp1qm8if5a.png"" /></div> </div> <div id=""io-footer""></div> <script> // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "" <div id=""io-header""></div> <div id=""io-wrapper""> <div id=""io-overlay""><img src=""dbc0e626d0934cd0900408fcc0e527e2-oa-1-A.svg"" /></div> <div id=""io-original""><img src=""tmp1qm8if5a.png"" /></div> </div> <button id=""io-revl-btn"" onclick=""toggle();"">Toggle Masks</button> <div id=""io-extra-wrapper""> <div id=""io-extra""> </div> </div> <script> // Toggle answer mask on clicking the image var toggle = function() { var amask = document.getElementById('io-overlay'); if (amask.style.display === 'block' || amask.style.display === '') amask.style.display = 'none'; else amask.style.display = 'block' } // Prevent original image from loading before mask aFade = 50, qFade = 0; var mask = document.querySelector('#io-overlay>img'); function loaded() { var original = document.querySelector('#io-original'); original.style.visibility = ""visible""; } if (mask === null || mask.complete) { loaded(); } else { mask.addEventListener('load', loaded); } </script> "
How should colorectal cancer be screened for in Ulcerative Colitis?Colonoscopy (usually give CEA for general poplation but because increased risk in this cohort, give colonoscopy)
Why is there amenorrhoea in auto-immune hepatitis?Liver involved in sex hormone production <div><br></div><div>(can also be found in late stage cirrhosis)</div>
What drug is useful in Crigler-Najjar?Phenobarbital (though only in Type 2 where there is partial expression). <div><br></div><div>Acts as a P450 inducer, to increase UDP glucoronyltransferase activity</div>
"What is seen here?<div><img src=""60669tn.jpg""><br></div>"Xanthelesma- suggests hypercholesterolaemia
In what locations can gallstones occur?- Gallbladder<div>- Gallbladder neck- causing biliary colic + cholecystitis</div><div>- Common Bile Duct- Choledocholithiasis + Ascending cholangitis</div><div>- Joining of pancreatic and CBD- causing pancreatitis</div><div>- Small bowel- causing gallstone ileus</div>
What are the two autoimmune causes of pancreatitis?- Polyarteritis nodosa<div>- IGG4 disease</div>
What are drugs that can cause acute pancreatitis?FAT SHEEP<div><br></div><div>Furosemide</div><div>Azathioprine/Asparaginase</div><div>Thiazides/tetracycline</div><div>Statins/sulphonamides/sodium valproate</div><div>Hydrochlorothiazide</div><div>Estrogens</div><div>Ethanol</div><div>Protease inhibitors and NRTIs</div>
Which disease is commonly associated with<b> Ankylosing spondylitis</b>?<b>Ulcerative Colitis</b>- as both are increased in HLA-B27<div><br></div><div>(having UC and Ank spond indication to start <b>anti-TNF therapy</b> as this would be helpful for both)</div>
What are endocrine causes of an abdominal pain?"- Diabetic Ketoacidosis<div>- Adrenal insufficiency (in Addison's)</div>"
What drugs can cause gastric ulcers?- SSRIs<div>- NSAIDs </div><div>- Steroids</div>
What should be considered in a 40+y/o woman presenting with bloating, abdominal pain relieved by defecation?Ovarian cancer- rare for IBS to appear above 40s<div><br></div><div>IBS in a middle aged woman- think ovarian cancer</div>
What skin signs are more associated with each type of IBD?"<font color=""#0000ff"">Crohn's</font>: Erythema nodosum<div><font color=""#0000ff"">UC</font>: Pyoderma gangrenosum </div>"
Urinary retention alongside abdominal pain could suggest what?- Urinary obsturction e.g. BPH, or prostate cancer- causing bladder distension → visceral abdominal pain 
Abdominal pain <span class=cloze>[...]</span> by periods suggests endometriosisAbdominal pain <span class=cloze>worsened</span> by periods suggests endometriosis<br> Abdominal pain worsened by periods suggests <span class=cloze>[...]</span>Abdominal pain worsened by periods suggests <span class=cloze>endometriosis</span><br> Polymyalgia rheumatica presents with <span class=cloze>[ inflammatory/mechanical]</span> stiffnessPolymyalgia rheumatica presents with <span class=cloze>morning- inflammatory type</span> stiffness<br> What is often the first joint to be affected in osteoarthritis? Hip
What is <b>pannus?</b>Abnormal layer of tissue growth in joint surfaces or over cornea<div><br></div><div>(describes what?)</div>
Abnormal layer of tissue growth in joint surfaces or over cornea<div><br></div><div>(describes what?)</div>What is <b>pannus?</b>
Pannus formation is associated with <span class=cloze>[...]</span>Pannus formation is associated with <span class=cloze>Rheumatoid Arthritis</span><br> What interleukins are responsible for causing a red, hot, swollen joint?IL-1, IL-6 
What is the trigger for gout?"Not just high uric acid levels- rapid change in uric acid levels (as provides concentration gradient for uric acid to move into synovial fluid).<div><br></div><div>Hence why starting on <font color=""#0000ff"">allopurinol may exacerbate or induce an acute attack </font></div>"
All seronegative spondyloarthropathies are responsive to <span class=cloze>[...]</span>All seronegative spondyloarthropathies are responsive to <span class=cloze>NSAIDs</span><br> In ankylosing spondylitis what should be considered with managing the spine?"Often have kyphotic cervical spine- do not attempt to immobilise or 'correct' as can cause cervical vertebral fracture "
"What is seen here?<div><img src=""27915tn.jpg""><br></div>"Discoid rash: Coin/disc shaped rash 
<span class=cloze>[...]</span> involves inflammation of endomysium whereas <span class=cloze>[...]</span> involves inflammation of the perimysium<br><span class=cloze>Polymyositis</span> involves inflammation of endomysium whereas <span class=cloze>dermatomyositis</span> involves inflammation of the perimysium<br><br> If endomysium, contained. <div>If perimysium, can access the skin </div>
Polymyositis involves inflammation of <span class=cloze>[...]</span> whereas dermatomyositis involves inflammation of the <span class=cloze>[...]</span><br>Polymyositis involves inflammation of <span class=cloze>endomysium</span> whereas dermatomyositis involves inflammation of the <span class=cloze>perimysium</span><br><br> If endomysium, contained. <div>If perimysium, can access the skin </div>
<span class=cloze>[Antibody]</span> is more associated with polymyositis whereas <span class=cloze>[Antibody]</span> is more associated with dermatomyositis<br><span class=cloze>Jo-1</span> is more associated with polymyositis whereas <span class=cloze>Mi-2</span> is more associated with dermatomyositis<br><br> Jo-1 is more associated with <span class=cloze>[...]</span> whereas Mi-2 is more associated with <span class=cloze>[...]</span><br>Jo-1 is more associated with <span class=cloze>polymyositis</span> whereas Mi-2 is more associated with <span class=cloze>dermatomyositis</span><br><br> Which specific ANCA antibody is associated with <b>microscopic polyangiitis (+eosinophilic granulomatosis with polyangiitis)?</b>MPO-ANCA<div><br></div><div>(is associated with which vasculitis?)</div>
Which specific ANCA antibody is associated with <b>granulomatosis with polyangiitis</b>?ANCA-PR3
<span class=cloze>[...]</span> = Pharyngeal pouch"<span class=cloze>Zenker's diverticulum</span> = Pharyngeal pouch<br> "
"Zenker's diverticulum = <span class=cloze>[...]</span>""Zenker's diverticulum = <span class=cloze>Pharyngeal pouch</span><br> "
What is a peptic ulcer?Defect in mucosa which penetrate the muscularis mucosa
ALT/AST >3000s suggests what cause?- Toxic/ischaemic hepatic injury <div><br></div><div>(acute viral hepatitis will cause ALT/AST in the 1000s, but not quite as high as toxic/ischaemic injury)</div>
What should be given to treat H pylori in penicillin allergic patients?Still triple therapy, but metronidazole for amoxicillin:<div>- PPI, Metro + Clarithromycin </div>
Albumin is <span class=cloze>[...]</span> in acute illness Albumin is <span class=cloze>decreased</span> in acute illness <br> Only if albumin AND CRP is low, consider malnutrition
What are Genetic hepatopathies?"- Wilson's Disease<div>- Haemochromatosis</div><div>- Alpha-1-antitrypsin deficiency</div>"
Aside from the Hepatitis viruses- what other viruses can cause Viral Hepatitis?- CMV, EBV<div>- Yellow Fever </div><div><br></div>
The most important test to do in a woman with acute abdominal pain is a <span class=cloze>[...]</span>The most important test to do in a woman with acute abdominal pain is a <span class=cloze>urinary bHCG</span><br> Obviously less relevant if passed the menopause- but always be aware!
What are risk factors for diverticular disease?- Increased age<div>- Western (low fibre) diet</div><div>- Obesity</div>
What is the management of biliary colic?"-<font color=""#0000ff""> Conservative management </font>(paracetamol/NSAIDs/opiate analgesia)<div>- <font color=""#0000ff"">Lifestyle factors</font> to help control sx: low fat diet, weight loss, more exercise<br><div>- <font color=""#0000ff"">Elective cholecystectomy</font> (within 6 weeks of first presentation- as high chance of sx recurrence/development of complications)</div></div>"
How should simple hernias be managed (i.e. no strangulation etc)?"- Lifestyle changes<div>- Analgesia </div><div>- Hernia truss (see below)</div><div><br></div><div><img src=""61J95aFOzCL._SX355_.jpg""><br></div>"
What is <b>hypoxaemia?</b>Low PaO<sub>2</sub> in blood <div><br></div><div>(describes what?)</div>
Low PaO<sub>2</sub> in blood <div><br></div><div>(describes what?)</div>What is <b>hypoxaemia?</b>
How can Mean Arterial Pressure be calculated from blood pressure?1/3 Systolic pressure + 2/3 Diastolic pressure<div><br></div><div>(As 2/3 of your cardiac cycle is in diastole)</div>
What is the purpose of pre-oxygenation before induction of anaesthesia?"Fill the pt's lung's with 100% oxygen- washes out Nitrogen in and leaves 100% in FRC (rather than 21%)<div><br></div><div>Gives more time of apnoea before patient desaturates </div>"
Which volatile general anaesthetic agent is preferred for those who are obese?Desflurane<div><br></div><div>(as lowest absorption into fat, meaning quicker recovery from anaesthesia- but very expensive and side effects of hepatitis)</div>
What is the action of <b>sugammadex?</b>Selective Relaxant Binding Agent:<div><br></div><div>- Engulfs competitive neuromuscular blockers (rocuronium, vecuronium) and prevents them inhibiting neuromuscular junctions </div>
<span class=cloze>[...]</span>pharyngeal airways are generally preferred in semi/conscious patients<br><span class=cloze>Naso</span>pharyngeal airways are generally preferred in semi/conscious patients<br><br> Oropharyngeal airways can induce gag reflex 
What is a bougie used for?Used to help intubate difficult airways:<div>- Slim flexible instrument which goes in first, and endotracheal tube can be railroaded over the top</div>
What is the purpose of a tracheostomy in anaesthetics?Bypasses upper airway, allowing pt to be ventilated via front of neck<div><br></div><div>(in ICU, can be done to assist weaning of pt- can take ETT out of tracheostomy and put on a trache mask- when pt is breathing by themselves through the tracheostomy)</div>
What is the action of <b>flumazenil?</b>Benzodiazepine antagonist<div><br></div><div>Can be used to reverse benzodiazepines e.g. midazolam</div>
What is the most likely first sign of an anaphylactic reaction?"Hypotension<div><br></div><div>(Because of sigmoid curve- PaO<sub>2</sub> needs to fall a lot before being reflected on saturation)</div><div><img src=""oxydiscrv.gif""><br></div>"
What is the effect of pH on serum potassium levels?Acidosis --> Movement of K<sup>+</sup><sub> </sub> out of cells (hyperkalemia)<div>Alkalosis --> Movement of K<sup>+</sup> into cells (hypokalemia)</div>
What makes up a fracture callus?<div>Healing phase of bone healing:<br><br></div>Hyaline cartilage (from chondroblasts) + woven bone (osteoblasts)
What is the difference between a soft and hard callus?Soft callus: Mostly composed of hyaline cartilage<div>Hard callus: Mostly composed of woven bone </div>
What is the difference between open and closed reduction?"<font color=""#0000ff"">Closed reduction</font>: Reduce fracture without surgery + opening of skin (often done in A&E)<div><font color=""#0000ff"">Open reduction:</font> Operation required to reduce the fracture</div>"
When is open reduction used?- Failed conservative management<div>- Accurate reduction required</div><div>- Intra-articular fractures</div><div>- Open fractures </div>
When is external fixation used?- Open #s<div>- Excessive swelling</div><div>- Tissue loss & burns</div><div><br></div><div>(when difficult to close a surgical wound/not enough soft tissue)</div>
What is the benefit of internal fixation over external fixation?Internal fixation aids early mobilisation
What are fat embolisms associated with?Fractures of long bones (classically with fracture of femurs)
What are early complications of fractures?- Compartment syndrome<div>- Fat embolism</div><div>- Infection </div>
What are late complications of fractures?- Mal-union<div>- Avascular necrosis (in specific bones)</div><div>- Growth plate disturbance (if paediatric fractures)</div>
How can ankle fractures be classified with the WEBER classification?<div><br></div>"<font color=""#0000ff"">Weber A: </font><div>- Fracture inferior to syndesmosis</div><div><br></div><div><font color=""#0000ff"">Weber B:</font></div><div>- Fracture at level of syndesmosis</div><div><br></div><div><font color=""#0000ff"">Weber C: </font></div><div>- Above level of syndesmosis, unstable</div><div><br></div><div><img src=""Danis-Weber-ankle-fx-1024x577.jpg""><br></div>"
What is the syndesmosis?"Ligament connecting the tibia and fibula<div><br></div><div><img src=""Anatomical-illustration-of-the-tibiofibular-syndesmosis.png""><br></div>"
Which Weber ankle fractures are more likely to require Open reductions?Weber C: Fracture above syndesmophyte & unstable. <div><br></div>
What are the symptoms of varicose veins?"Usually <font color=""#0000ff"">asymptomatic</font>. <div><br></div><div>If present:</div><div>- Initially <font color=""#0000ff"">cosmetic issues </font>(discolouration of skin, unsightly visible veins)</div><div>- If severe, <font color=""#0000ff"">pain, aching, or itching</font> (often worse on standing/at end of day)</div><div><div><br></div></div>"
What drugs can cause hyperkalaemia?- ACEi/ARBs<div>- Spironolactone</div><div>- Heparin + LMWHs</div><div>- Cyclosporin</div>
What should an appropriate field of view be for an AXR?Diaphragm to pelvis 
What is found within the carpal tunnel?9 tendons and 1 nerve:<div>- 4 tendons of flexor digitorum superficialis</div><div>- 4 tendons of flexor digitorum profondus</div><div>- Tendon of flexor pollicis longus</div><div>- Median nerve </div>
What blood tests can be useful to probe bone disease?- ALP <div>- Ca<sup>2+ </sup>and Phosphate</div><div>- PTH</div>
"What is seen here?<div><img src=""images (3).jpg""><br></div>"Lytic lesions (one on right is raindrop skull)
"What is seen here?<div><img src=""290px-Untreated_Carpal_Tunnel_Syndrome.JPG""><br></div>"Wasting of the thenar eminences- due to carpal tunnel syndrome 
What muscles are supplied by the median nerve?LOAF:<div>- Lateral 2 lumbricals</div><div>- Opponens pollicis</div><div>- Abductor pollicis brevis (only one which is always supplied by the median!)</div><div>- Flexor pollicis</div>
"Why can someone with Paget's disease present with pulmonary oedema?"High-output cardiac failure:<div><br></div><div>- Increased bone activity requires increased energy --> increased cardiac output</div><div>- Causes heart failure secondary to high-output </div>
"What are causes of osteomalacia/Rickett's?""<font color=""#0000ff"">- Vitamin D deficiency (most common)</font><div><br></div><div>- Vit D resistance</div><div>- Hypocalcaemia</div><div>- Phosphate leak from kidney</div>"
What are causes of carpal tunnel syndrome?MEDIAN TRAP:<div><br></div><div>Myxoedema</div><div>Edema premenstrually</div><div>Diabetes</div><div>Idiopathic</div><div>Acromegaly</div><div>Neoplasm</div><div>Trauma</div><div>Rheumatoid Arthritis</div><div>Amyloidosis</div><div>Pregnancy</div>
What are signs of a Basal skull fracture?- Racoon eyes<div>- Battle sign</div><div>- Leakage of CSF (from ears/nose)</div>
"What is seen here?<div><img src=""642x361_Battle-Sign_Pictures-SLIDE_1.jpg""><br></div>"Battle sign- bruising around the mastoid 
What features suggest Churg-Strauss syndrome versus other vasculitides?- Asthma<div>- Eosinophilia (>10%)</div><div>- Paranasal sinusitis</div><div>- Pulmonary infiltrates</div><div>- Mononeuritis multiplex/polyneuropathy </div><div>- Histology: Vasculitis with extravascular eosinophils</div>
What are causes of dual positivity of ANCA (c-ANCA and p-ANCA)?Often false positive result:<br>- Subacute bacterial endocarditis (+ other chronic infections)<br><div>- Haematological malignancy</div><div>- IBD</div><div>- Drug-induced vasculitis </div>
"How will Pott's Disease present compared to staphylococcal osteomyelitis in the spine?""Pott's disease= Osteomyelitis in spine caused by TB. <div><br></div><div>Will present with more chronic picture, slower progression of symptoms </div>"
What drugs are known to cause oesophagitis?- NSAIDs<div>- Antibiotics (tetracyclines)<br>- Quinidine</div><div>- Bisphosphonates</div><div>- Steroids</div><div>- Potassium e.g. Sando-K</div>
To minimise the risk of oesophagitis, what advice should be given to patients taking drugs that carry this risk (e.g. tetracyclines, potassium, quinidine, bisphosphonates)Take with large glass of water, whilst in upright position. Take medication with food
What are side effects of ACE-i?- <b>Dry cough </b>(switch to ARB if so)<br>- Urticaria (<b>hives</b>)
"What is seen here?<div><img src=""heliotrope-rash.jpg""><br></div>"Heliotrope rash- associated with dermatomyositis
"What is seen here, in a pt complaining of muscle pain?<div><img src=""dm-shawl-skinrash-back.jpg""><br></div>"Shawl sign - suggestive of dermatomyositis
How can gallstone ileus be diagnosed?"Requires radiographic studies:<div><b>Rigler's triad</b> of:</div><div>- Pneumobilia (air within the biliary tree)</div><div>- Evidence of small bowel obstruction (>3cm wide)</div><div>- Radiopaque gallstone on abdominal radiograph </div>"
Why is the AST:ALT ratio >2 in alcoholic liver disease?In alcoholics, <b>dietary deficiency</b> of pyridoxine (<b>vit B6</b>) --> ↓ALT. <div><br></div><div>Has more of an effect on ALT than AST</div>
How can the pathophysiology of diarrhoea be divided?- Osmotic<div>- Secretory</div><div>- Inflammatory/infectious</div><div><br></div><div>(Rarely, deranged motility)</div><div><br></div>
Why is mannitol no longer used as bowel prep in colonoscopy/surgery?Mannitol can be metabolised by colonic flora, producing methane &hydrogen<div><br></div><div>(both uncomfortable, and inflammable!)</div>
What causes secretory diarrhoea?<div>When water secreted in small intestine > water reabsorbed in the intestine</div><div><br></div>- Excessive secretion: Cholera toxin, <i>e. coli</i><div><div>- Impaired reabsorption: anything that causes villous destruction or damage to intestinal </div></div>
How does cholera toxin cause a secretory diarrhoea?Cholera toxin keeps chloride channels open, causing chloride ions to enter the lumen of the intestines. <div><br></div><div>Water follows → secretory diarrhoea </div>
How do inflammatory bowel diseases cause diarrhoea?Secretory diarrhoea:<br>- Inflammation across intestinal mucosa → damages villi →less reabsorption of water
When should you consider small intestine bacterial overgrowth?Coeliac symptoms in a patient >40y/o
A <span class=cloze>[...]</span> is used to diagnose lactose intoleranceA <span class=cloze>hydrogen breath test</span> is used to diagnose lactose intolerance<br> SIBO measures hydrogen after giving carbohydrates (lactulose) as opposed to lactose
A hydrogen breath test is used to diagnose <span class=cloze>[...]</span>A hydrogen breath test is used to diagnose <span class=cloze>lactose intolerance</span><br> SIBO measures hydrogen after giving carbohydrates (lactulose) as opposed to lactose
What are the consequences of taking trimethoprim and methotrexate?- Bone marrow suppression → pancytopenia<div>- Mucositis (typically in oral mucosa)</div><div>- Nephrotoxicity </div>
Which patients should receive a cervical spine X-ray before surgery?- Rheumatoid arthritis<div>- Ankylosing spondylitis</div><div>- Down Syndrome</div><div><br></div><div>All have risk of atlantoaxial subluxation- could cause cervical spine fracture when trying to secure airway</div>
What drugs are associated with precipitating gout?- Thiazide and loop diuretics<div>- Cytotoxics</div><div>- Alcohol</div><div>- Cyclosporin</div><div>- Pyrazinamide</div><div>- Beta blockers</div><div>- Penicillins</div>
What is the action of <b>febuxostat?</b>Xanthine oxidase inhibitor- used to reduce urate levels (2nd line if allopurinol is not well tolerated)
What anti-TB drugs can cause drug-induced SLE?Isoniazid
<span class=cloze>[...]</span> is associated with Eosinophillic Granulomatosis with Polyangitis<br><span class=cloze>Late onset asthma</span> is associated with Eosinophillic Granulomatosis with Polyangitis<br><br> Late onset asthma is associated with <span class=cloze>[Rheum condition]</span><br>Late onset asthma is associated with <span class=cloze>Eosinophillic Granulomatosis with Polyangitis</span><br><br> How long should fractures in the upper and lower limb be casted for?Upper: 6 weeks<div>Lower: 12 weeks </div>
Damage to what nerve is at risk in a Colles fracture?Median nerve 
Bakers cysts can press on and cause a lesion in what nerve?Common peroneal nerve- leads to foot drop
What antibodies are found in dermatomyositis/polymyositis?- ANA (though not specific)<div>- Antisynthetase antibodies, including Jo-1, Mi-2 and SRP</div>
How can limited and diffuse cutaneous systemic sclerosis be differentiated?"<font color=""#0000ff"">Limited</font>: Typically affects face and distal limbs<div><font color=""#0000ff"">Diffuse</font>: Typically affects trunk and proximal limbs predominately</div>"
What is the most common cause of death in diffuse cutaneous systemic sclerosis?Respiratory involvement (seen in 80%):<div>- Interstitial lung disease</div><div>- Pulmonary arterial hypertension </div>
What are features of CREST syndrome?"Calcinosis<div>Raynaud's phenomenon</div><div>Esophageal dysmotility</div><div>Sclerodactyly</div><div>Telangiectasia </div>"
What is CREST syndrome?Subtype of limited cutaneous systemic sclerosis 
What muscles are supplied by the anterior interosseous branch of the median nerve?<div>Supplies deep muscles:</div><div><br></div>- Flexor polllicis longus<div>- Radial 1/2 of flexor digitorum profundus</div><div>- Pronator quadratus </div>
"A patient unable to do the 'OK' sign has what nerve affected?""Anterior interosseous nerve (of median nerve)<div><img src=""card-27909211-front.jpg""><br></div>"
A patient who cannot cross their fingers has what nerve damaged?Ulnar nerve (as interosseous muscles will not allow adduction of fingers)<div><br></div>
What hand movement can be used to test an ulnar nerve lesion?- Cannot Cross fingers <div>- Cannot spread fingers horizontally (abduct)</div>
What hand movement can be used to test an anterior interosseous nerve lesion?OK sign 
What hand movements can test a radial nerve injury?- Wrist and finger extension<div>- Cannot move wrist towards thumb laterally</div>
If a person uses crutches that are not adjusted correctly, what nerve is frequently affected?Radial nerve: can cause paralysis of muscles supplied by the radial nerve
What is <b>Saturday night palsy?</b>Falling asleep with arm hanging over the arm-rest of a chair can compress the radial nerve, causing paralysis (e.g. wrist drop)
What muscles are supplied by the radial nerve?- Brachioradialis<div>- Extensor muscles</div><div>- Supinator</div><div>- Triceps </div>
How can L5 radiculopathy be differentiated with damage to the common peroneal nerve?"Both present with weakness of foot dorsiflexors & toe extensors<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">L5 radiculopathy</font>: Weakness in inversion and eversion</div><div><font color=""#0000ff"">Common peroneal nerve neuropathy</font>: Weakness in eversion</div>"
Why is spironolactone first-line medical therapy for ascites?Ascites primarily caused by overactivation of RAAS (after splanchnic pooling). <div><br></div><div>Spironolactone an aldosterone antagonist</div>
Why is terlipressin usedful in hepatorenal syndrome?- Causes splanchnic vasoconstriction (counteracts splanchnic vasodilation in hepatorenal syndrome)
"Who does Takayasu's arteritis commonly affect?"- Females<div>- Asian people </div>
"What condition is Takayasu's arteritis commonly associated with?"Renal artery stenosis 
"How is Takayasu's arteritis managed?"Steroids
Outline the medical management of osteoporosis?"<font color=""#0000ff"">First line</font>: Alendronate (unless GFR <35)<div><font color=""#0000ff"">Second line:</font> Risedronate/etidronate (IV bisphosphonate)</div><div><font color=""#0000ff"">Third line</font>: Denosumab</div><div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Consider: </font>HRT, raloxifene </div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If tried all other management</font>: Strontium ranelate</div><div><br></div></div>"
Who does polyarteritis nodosum most commonly affect?- Men<div>- 40-50s</div>
What drugs cause drug-induced Lupus?CHIMP:<div>- Carbamazepine +<sub> </sub>chlorpromazine</div><div>- Hydralazine</div><div>- Inflixmiab + isoniazid</div><div>- Minocycline + minoxidil</div><div>- Pyrazinamide + Procainamide + Penicillamine </div>
Typically drug-induced lupus is only localised to the mucosa. Which drug can cause drug-induced lupus with renal impairment?Infliximab
On an ascitic tap, what level of neutrophils is diagnostic of Spontaneous Bacterial Peritonitis?250cells/ul
What is a good screening test for early hepatic encephalopathy (if not demonstrating asterixes)?Check for dyspraxia- ask them to draw a 5 pointed star. <div><br></div><div>(Also ask about fatigue or confusion)</div>
"When does metronidazole have a role in Crohn's disease?""If perianal Crohn's disease "
In the diagnosis of IBS, what investigations are recommended by NICE to exclude organic differentials?<div>- FBC and ESR/CRP </div><div>- Coeliac serology </div><div>- Faecal calprotectin (if raised suggests IBD)<br></div>
How can ascites be determined as an exudate or transudate?"Ascitic tap + measure the SAAG.<div><br></div><div><font color=""#0000ff"">SAAG <b>>11g/L</b></font>: Low protein --> Transudate</div><div><font color=""#0000ff"">SAAG<b><11g/L</b></font>: High protein --> Exudate</div>"
What are causes of ascites with a high SAAG?High SAAG → Low protein → Transudate:<div><br></div><div>- Heart failure</div><div>- Liver failure</div><div>- Kidney failure</div><div>- Budd-Chiari Syndrome/Portal Vein Thrombosis</div>
What are causes of ascites with a low SAAG?Low SAAG → High protein → Exudate:<div><br></div><div>- Malignancy</div><div>- Infection</div><div>- Pancreatitis </div><div>- Nephrotic syndrome</div><div><br></div><div>(think of things that cause increased proteins in the ascites- cancer cells producing lots of proteins, inflammatory markers in infection& pancreatitis. Nephrotic has low SAAG as serum albumin is low to begin with)</div>
"What is found on colonoscopy in <b>Crohn's disease</b>?"<div>- Deep ulcers</div>- Intermittent inflammation- skip lesions<div>- Cobblestone mucosa (due to ulceration and mural oedema)</div><div><br></div><div>(describes the findings on colonscopy of which IBD?)</div>
What is seen on colonoscopy of Ulcerative Colitis?<div>- Erythematous mucosa<br></div><div>- Pseudopolyps (scar tissues which develops but does not have malignant potential)</div><div><br></div><div>(describes the colonoscopic findings of which IBD?)</div>
What is found on biopsy in <b>Ulcerative Colitis</b>?- Loss of goblet cells<div>- Crypt abscesses</div><div>- Inflammatory cells (predom lymphocytes)</div><div><br></div><div>(describes the biopsy findings in which IBD?)<br></div>
"What is found on biopsy in <b>Crohn's disease</b>?"- Increased goblet cells<div>- Granulomas </div><div><br></div><div>(describes the biopsy findings in which IBD?)<br></div>
- Loss of goblet cells<div>- Crypt abscesses</div><div>- Inflammatory cells (predom lymphocytes)</div><div><br></div><div>(describes the biopsy findings in which IBD?)<br></div>What is found on biopsy in <b>Ulcerative Colitis</b>?
- Increased goblet cells<div>- Granulomas </div><div><br></div><div>(describes the biopsy findings in which IBD?)<br></div>"What is found on biopsy in <b>Crohn's disease</b>?"
<div>- Erythematous mucosa<br></div><div>- Pseudopolyps (scar tissues which develops but does not have malignant potential)</div><div><br></div><div>(describes the colonoscopic findings of which IBD?)</div>What is seen on colonoscopy of Ulcerative Colitis?
What is found on barium studies in <b>Ulcerative Colitis</b>?"<div>- Loss of haustral markings<br></div><div>- Superficial ulceration</div><div>- In long standing disease- colon is narrowed and short- drainpipe colon</div><div><br></div><div><img src=""paste-86f0d6d31cadad27fb1af12f635962584835371a.jpg""><br></div><div><br></div><div>(describes the barium study findings of which IBD?)</div>"
"<div>- Loss of haustral markings<br></div><div>- Superficial ulceration</div><div>- In long standing disease- colon is narrowed and short- drainpipe colon</div><div><br></div><div><img src=""paste-86f0d6d31cadad27fb1af12f635962584835371a.jpg""><br></div><div><br></div><div>(describes the barium study findings of which IBD?)</div>"What is found on barium studies in <b>Ulcerative Colitis</b>?
<div>- Deep ulcers</div>- Intermittent inflammation- skip lesions<div>- Cobblestone mucosa (due to ulceration and mural oedema)</div><div><br></div><div>(describes the findings on colonscopy of which IBD?)</div>"What is found on colonoscopy in <b>Crohn's disease</b>?"
"What is found on barium studies in <b>Crohn's disease?</b>""<div>- Rose-thorn ulcers (due to transmural inflammation)<br></div><div><div>- Strictures: ""Kantor's string sign"" - particularly at terminal ileum</div><div>- Proximal Bowel dilation</div><div>- Fistulae</div><div><br></div><div><img src=""bYy91CfP6aW1xVnE2L4JF9ox1vvmxGK20o6KtYaRxcU2z2SQ1BdxRl6Um98OLGJcdCiteJZ52eiFuQ4K8A5h-RaOzXim3VxqLOJM6yfGL-6UIHGv1hH-MTRBTT-epQ.jpg""><br></div><div><br></div></div>"
Why is terlipressin used in variceal bleeds?Not used for its ADH actions, more for its potent vasoconstrictor actions:<div>- Decreases volume of blood going to varices</div><div>- Helps maintain blood pressure </div>
Why is terlipressin used in hepatorenal syndrome?Causes vasoconstriction of splanchnic circulation → less pooling of blood in splanchnic circulation and more flow to kidneys 
What is meant by the term <b>splanchnic circulation?</b>All blood flow originated from the coeliac, superior mesenteric and inferior mesenteric arteries <div><br></div><div>(thus distributed to the abdominal viscera)</div>
How can the Rockall Score be interpreted pre-endoscopy?"<font color=""#0000ff"">If score of >0</font>: Have inpatient OGD<div><font color=""#0000ff"">If score of 0</font>: Can have urgent outpatient OGD</div>"
What is a <b>periosteal reaction?</b>Formation of new bone in response to injury or other stimuli 
"What can cause 'onion skin' periosteal reactions?"<div>- Osteosarcoma</div><div>- Ewing sarcoma</div><div>- Hypertrophic osteoarthropathy</div>
When should you get an X-Ray for an ankle?Ottawa Rules:<div>If pain in the malleolar zone and:</div><div>- Bony tenderness on lateral malleolar zone</div><div>- Bony tenderness on medial malleolar zone</div><div>- Inability to weight bear across 4 steps</div>
What is one of the earliest signs of OA of the hip?Reduced internal rotation 
"How would you grade this hip fracture according to the Garden Classification?<div><img src=""cTgs-4Ixcf5scXSAHm8EItf2Ibcz77QzHO4F01EsxwCjAsPHl93ip4MoXJIPKy41sUjQ8tWdHJT9w4mQ327VIip6dSu6Mig.jpg""><br></div>"Garden I: Incomplete fracture, no displacement
"How would you grade this hip fracture according to the Garden classification?<div><img src=""article-g01_400_300.jpg""><br></div>"Garden II: Complete fracture, no displacement 
"How would you grade this hip fracture according to the Garden Classification?<div><img src=""78c4bf7dbb89861ce7fcb3a77c1c85_big_gallery.jpg""><br></div>"Garden III: Complete fracture, partially displaced
"What is the grade of this hip fracture, according to the Garden classification?<div><img src=""581245c10c78faebb101ea798b6508_big_gallery.jpg""><br></div>"Garden IV: complete fracture, complete displacement
How quick is an urgent referral to Rheumatology and when is it required for Rheumatoid Arthritis?<div>Appt within 3 days:</div><div><br></div><div>In RA:</div>- If >3 months from symptom onset<div>- If >1 joint or small joints in hands; urgent referral required </div>
What DMARD is effective in <b>palindromic rheumatoid arthritis</b>?Hydroxychloroquine<div><br></div><div>(is indicated 1st line in RA, in what case?)</div>
Hydroxychloroquine<div><br></div><div>(is indicated 1st line in RA, in what case?)</div>What DMARD is effective in <b>palindromic rheumatoid arthritis</b>?
What features would make you think of an acute tendon rupture, rather than a tendonitis?- <b>Sudden </b>inability to move <div>- Pain & weakness<b> following trauma</b></div>
What is an appropriate resposne to a suspected acute tendon rupture?Urgent referral to secondary care 
Tears in the rotator cuff most commonly affect which tendon?Supraspinatus tendon 
What investigations should be done for ?tendon rupture?"<font color=""#0000ff"">1st line</font>: Shoulder US<div><font color=""#0000ff"">2nd line</font>: MRI</div>"
What is first-line therapy for rheumatoid arthritis?- DMARD monotherapy +/- short course of bridging prednisolone <div><br></div>
How should you monitor response to RA treatment?- CRP <div>- Disease activity score e.g. DAS28</div>
How are flares of Rheumatoid Arthritis typically managed?- Methylprednisolone IM or PO<div><br></div><div><b>(not IV)</b></div>
When biologics are used in RA, what are they given with?Used in combination with methotrexate 
An 83y/o F presents to A&E after a fall onto an outstretched hand. Her upper arm is painful, swollen with global loss of range of movement. <div><br></div><div>What nerve function should you test?</div>Likely a proximal humeral fracture, damaging axillary nerve. <div><br></div><div>Check sensation over regimental badge area</div>
If a Lisfranc injury is suspected, what should be done?"Weight bearing X-Ray, with AP and oblique views: metatarsals need to line up with the navicular/cuneiform/cuboid. <div><img src=""paste-5ae8bce7d3cc5b41bc051ef804645196797a50c1.jpg""></div><div><br></div><div>Can see the 5th metatarsal is hanging over (>3mm)- as ligaments are damaged </div><div><div><br></div></div>"
What are causes of an isolated rise in bilirubin, with normal LFTs (ALT and ALP normal)?"Pre-hepatic cause of jaundice:<div><br></div><div>- Gilbert's syndrome </div><div>- Haemolysis </div>"
Jaundice:<div><br></div><div><span class=cloze>[...]</span> urine and <span class=cloze>[...]</span> stools = Pre-hepatic cause</div>Jaundice:<div><br></div><div><span class=cloze>Normal</span> urine and <span class=cloze>normal</span> stools = Pre-hepatic cause</div><br> As pre-hepatic cause of jaundice is ↑↑unconjugated bilirubin (water insoluble) and not passed in urine; and normal liver function so still conjugating bilirubin and releasing bile, meaning normal coloured stools 
Jaundice:<div><br></div><div>Normal urine and normal stools = <span class=cloze>[...]</span> cause</div>Jaundice:<div><br></div><div>Normal urine and normal stools = <span class=cloze>Pre-hepatic</span> cause</div><br> As pre-hepatic cause of jaundice is ↑↑unconjugated bilirubin (water insoluble) and not passed in urine; and normal liver function so still conjugating bilirubin and releasing bile, meaning normal coloured stools 
Jaundice:<div><br></div><div><span class=cloze>[...]</span> urine and <span class=cloze>[...]</span> stools suggests Intra-hepatic jaundice<br></div>Jaundice:<div><br></div><div><span class=cloze>Dark</span> urine and <span class=cloze>normal</span> stools suggests Intra-hepatic jaundice<br></div><br> As hepatic jaundice is mixed picture of ↑unconjugated bilirubin and ↑conjugated bilirubin (less functioning hepatocytes, so ↑unconjugated, but death of hepatocyte means ↑conjugated bilirubin). <div><br></div><div>↑Conjugated bilirubin in bloodstream --> Dark urine</div><div>But still some release of bile into digestive tract --> normal stools (May be slightly pale)</div>
Jaundice:<div><br></div><div>Dark urine and normal stools suggests <span class=cloze>[...]</span> jaundice<br></div>Jaundice:<div><br></div><div>Dark urine and normal stools suggests <span class=cloze>Intra-hepatic</span> jaundice<br></div><br> As hepatic jaundice is mixed picture of ↑unconjugated bilirubin and ↑conjugated bilirubin (less functioning hepatocytes, so ↑unconjugated, but death of hepatocyte means ↑conjugated bilirubin). <div><br></div><div>↑Conjugated bilirubin in bloodstream --> Dark urine</div><div>But still some release of bile into digestive tract --> normal stools (May be slightly pale)</div>
Jaundice:<div><br></div><div><span class=cloze>[...]</span> urine and <span class=cloze>[...]</span> stools suggests Post-hepatic jaundice<br></div>Jaundice:<div><br></div><div><span class=cloze>Dark</span> urine and <span class=cloze>pale</span> stools suggests Post-hepatic jaundice<br></div><br> Post-hepatic suggests obstruction- preventing bile secretion into digestive tract (and causing backlog, so conjugated bilirubin absorbed in bloodstream)<div><br></div><div>Conjugated bilirubin in bloodstream --> Dark urine</div><div>No release of bile into digestive tract --> Pale stools</div>
Jaundice:<div><br></div><div>Dark urine and pale stools suggests <span class=cloze>[...]</span> jaundice<br></div>Jaundice:<div><br></div><div>Dark urine and pale stools suggests <span class=cloze>Post-hepatic</span> jaundice<br></div><br> Post-hepatic suggests obstruction- preventing bile secretion into digestive tract (and causing backlog, so conjugated bilirubin absorbed in bloodstream)<div><br></div><div>Conjugated bilirubin in bloodstream --> Dark urine</div><div>No release of bile into digestive tract --> Pale stools</div>
Aside from hepatitic pathology, what else can cause a raised AST?Found in heart, muscle, kidney and brain. <div><br></div><div>- MI, muscle injury and CCF can all cause raised AST</div>
How is the AST:ALT ratio useful in viral hepatitis?ALT is usually greater than AST unless cirrhosis is present<div><br></div><div>If AST:ALT >1 in a pt with viral hepatitis, suggests cirrhosis</div>
What drugs can cause an isolated rise in GGT?- Alcohol<div>- Phenytoin</div><div>- Warfarin</div><div>- Rifampicin </div>
What are useful blood tests to assess patients with chronic liver conditions?"Tests of synthetic function: Albumin, platelets and INR<div><br></div><div>As in chronic hepatitis/ liver cirrhosis, aminotransferases may be in normal normal range </div><div><br></div><div><img src=""28FF2.jpg""><br></div>"
If a patient has stopped warfarin 5 days before elective surgery, but INR is ≥1.5 the day before surgery what should be done?Give phytomenadione (Vitamin K1)
What are causes of avascular necrosis?- Corticosteroid therapy<div>- Sickle cell disease</div><div>- Connective tissue diseases</div><div>- Fracture disrupting blood supply to the bone </div>
What can be given as prophylaxis to prevent hepatic encephalopathy from developing?- Lactulose<div>- Rifaximin </div><div><br></div><div>(same medication as used to treat)</div>
On top of medication, what general advice should you give ot a patient with Anti-phospholipid syndrome?"<font color=""#0000ff"">Reduce risk factors for thromboembolism:</font><div>- Venous: Avoid COCP, hormone replacement therapy and long periods of immobility</div><div>- Arterial: Control cardiovascular risk factors (e.g. smoking, blood pressure, cholesterol, blood glucose)</div>"
If a women is discovered to have Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin and anti-beta2-glycoprotein I) incidentally, what is the most appropriate management?If incidental, no need to start anticoagulation. <div><div>Manage risk factors (stop smoking, avoid oestrogen use and immovility)</div></div><div><br></div><div>Only start anticoagulation if thrombosis</div>
How should antiphospholipid syndrome be managed in a pregnant woman?Aspirin + unfractionated/low weight molecular heparin <div><br></div><div>(warfarin is teratogenic)</div>
What scars might be identified in a patient with a prev/ open appendectomy?"- Lanz (horizontal scar at McBurney's point)(1/3 of way from ASIS to navel)<div>- Gridiron/McBurney's (scar parallel to inguinal ligament, present at McBurney's point)</div><div><br></div><div><img src=""Abdominal-incision-types.jpg""><br></div>"
How is ascending cholangitis managed?- IV antibiotics (broad-spectrum)<div>- ERCP after 24-48hrs to relieve obstruction</div>
What causative agent is most commonly responsible for ascending cholangitis?<i>E. coli</i>
How does ascending cholangitis present?"Charcot's triad of:<div>- Fever</div><div>- RUQ pain</div><div>- Jaundice</div><div><br></div><div>Often also features:<br></div><div>- Hypotension </div><div>- Confusion </div>"
What is the best diagnostic investigation for ascending cholangitis?MCRP:<div><br></div><div>- US abdomen may initially detect bile duct dilation, but not good at picking up stones in mid/distal biliary duct </div><div>- CT may show good anatomical detail, but poor at viewing radiolucent cholesterol stones, which are most common </div>
What are the most common type of gallstone?Cholesterol stones (in 90%)<div>- Associated with females, increasing age and obesity</div><div><br></div><div>(pigment stones associated with haemolysis, stasis and infection)</div>
Lillian is about to start methotrexate for her Rheumatoid Arthritis. How often should she take it, and what else should she be given?"Should also give folic acid (as methotrexate is an anti-folate)<div><br></div><div>Both should be given once a week (methotrexate powerful cytotoxic so only given once weekly)</div><div><br></div><div>Folic acid should not be given on same day as methotrexate.</div><div><br></div><div>'Methotrexate Monday, Folate friday'</div>"
For which inguinal hernias is watchful waiting and safety netting appropriate?Only if patient is not medically fit for surgery:<div><br></div><div>- Even if small and asymptomatic, consensus is to treat medically fit pts, as most pts will eventually become symptomatic. </div><div><br></div><div>Inguinal hernias <b>do not resolve spontaneously</b></div>
For which inguinal hernias is a <b>Truss support belt </b>appropriate?Inguinal hernia in pts w/ very high surgical risk and low life expextancy<div><br></div><div>(symptomatic hernias should be surgically managed)</div>
With inguinal hernias, when should you perform a mesh or non-mesh repair?"<font color=""#0000ff"">Mesh</font>: Generally preferred (as lower risk of recurrence)<div><font color=""#0000ff"">Non-mesh</font>: If <b>irreducible</b> or <b>strangulated </b>hernia, or bowel obstruction (as higher risk of infection)</div>"
<span class=cloze>[...]</span> inguinal hernias tend to occur in young male patients whereas <span class=cloze>[...]</span> inguinal hernias tend to occur in elderly male patients<br><span class=cloze>Indirect</span> inguinal hernias tend to occur in young male patients whereas <span class=cloze>direct</span> inguinal hernias tend to occur in elderly male patients<br><br> Indirect inguinal hernias tend to occur in <span class=cloze>[...]</span> patients whereas direct inguinal hernias tend to occur in <span class=cloze>[...]</span> patients<br>Indirect inguinal hernias tend to occur in <span class=cloze>young male</span> patients whereas direct inguinal hernias tend to occur in <span class=cloze>elderly male</span> patients<br><br> "What are the boundaries of Hesselbach's Triangle?""<font color=""#0000ff"">Medial</font>: Rectus abdominis<div><font color=""#0000ff"">Lateral</font>: Inferior epigastric vessels</div><div><font color=""#0000ff"">Inferior</font>: Inguinal ligament</div><div><br></div><div><img src=""Inguinal-Hesselbachs-Triangle.png""><br></div>"
"How do inguinal hernias relate to Hesselbach's triangle?""<font color=""#0000ff"">Direct</font>: Occur within Hesselbach's triangle<div><font color=""#0000ff"">Indirect</font>: Occur outside</div><div><br></div><div><img src=""hesselbachs-triangle-boundaries.png""><br></div>"
Which inguinal hernias are more likely to strangulate?<b>Indirect</b> inguinal hernias
What mutation is responsible for malignant hyperthermia?Autosomal dominant mutation in ryanodine receptor 1
What is the most likely artery to be affected in GCA?Temporal Artery 
What is the definitive investigation in the diagnosis of oesophageal spasm?"<b>Barium swallow:</b> may show a corkscrew oesophagus<div><br></div><div><img src=""Radiology_0012_Nevit.jpg""><br></div><div><br></div>"
What is the management of angiodysplasia?"<font color=""#0000ff"">1st line</font>: Interventional endoscopy (cautery or argon plasma coagulation)<div><font color=""#0000ff"">2nd line</font>: Angiography with embolisation</div>"
A <span class=cloze>[clinical finding]</span> suggests peritonitis A <span class=cloze>rigid abdomen with rebound tenderness</span> suggests peritonitis <br> Giant cell arteritis is associated with aortic <span class=cloze>[...]</span>Giant cell arteritis is associated with aortic <span class=cloze>aneurysm</span><br> Arthritis in the hands:<div><br></div><div><span class=cloze>[...]</span> joint involvement suggests rheumatoid arthritis, whereas <span class=cloze>[...]</span> joint involvement suggests osteoarthritis</div>Arthritis in the hands:<div><br></div><div><span class=cloze>MCP</span> joint involvement suggests rheumatoid arthritis, whereas <span class=cloze>DIP</span> joint involvement suggests osteoarthritis</div><br> Both can affect the PIP and wrist joints, but RA very rarely affects the DIP and vice versa
Arthritis in the hands:<div><br></div><div>MCP joint involvement suggests <span class=cloze>[...]</span>, whereas DIP joint involvement suggests <span class=cloze>[...]</span></div>Arthritis in the hands:<div><br></div><div>MCP joint involvement suggests <span class=cloze>rheumatoid arthritis</span>, whereas DIP joint involvement suggests <span class=cloze>osteoarthritis</span></div><br> Both can affect the PIP and wrist joints, but RA very rarely affects the DIP and vice versa
When can you start biologic therapy first line in a pt with Ankylosing spondylitis?If pt has co-existing IBD:<div><br></div><div>- Often co-incide, and biologic therapy can help both diseases</div>
How should Garden I and II fractures be managed?As risk of AVN is low --> cannulated hip screw
When might a cannulated hip screw be used in a patient with a Garden III/IV fracture?In patients <35y/o:<div><br></div><div>- Even though risk of AVN, if doing a hip replacement, the joint will wear out and require a second operation at some point </div><div><br></div><div>Cannulated hip screw to try and prevent multiple operations</div>
What skin complication is most common in ulcerative colitis?"Erythema nodosum:<div><br></div><div>- Pyoderma gangrenosum more closely associated with UC than Crohn's but still very rare occurrence- erythema nodosum more prevalent</div>"
"What is <b>Marjolin's ulcer</b>?"An aggressive ulcerating squamous cell carcinoma which presents in an area of chornically inflamed/scarred skin <div><br></div><div>(describes what?)</div>
An aggressive ulcerating squamous cell carcinoma which presents in an area of chornically inflamed/scarred skin <div><br></div><div>(describes what?)</div>"What is <b>Marjolin's ulcer</b>?"
"What is seen here?<div><img src=""1200px-Marjolin_ulcer.JPG""><br></div>""Marjolin's ulcer- an SCC which develops from an old wound/ulcer"
"What are causes of the following sign?<div><img src=""280x190_acanthosis_nigricans_other.jpg""><br></div>""Acanthosis nigricans:<div>- Obesity</div><div>- T2DM </div><div>- Endocrine issues: acromegaly, PCOS, Cushing's Disease</div><div>- Malignancy: typically GI adenocarcinomas, and genitourinary cancers</div>"
What is a <b>giant cell</b>?"Union of several distinct cells (often macrophages), giving the appearance of a large multinucleate cell<div><br></div><div><img src=""1200px-Giant_cells1.jpg""><br><div><br></div></div>"
"What is seen here, on biopsy of the temporal artery?<div><img src=""rsztemporalarteritisss3y13_1233144-640x393.jpg""><br></div>"- Narrowed lumen<div>- Multinucleate giant cells</div><div><br></div><div>Suggestive of temporal arteritis</div>
"What is seen here, on temporal artery biopsy?<div><img src=""800wm (2).jpg""><br></div>"Wide lumen, normal mononuclear cells (no giant cells)<div><br></div><div>Normal temporal artery</div><div><br></div><div>(Note this does not rule out GCA, as skip lesions present in 15%)</div>
At what CD4 count are HIV patients vulnerable to developing cryptosporidiosis?CD4 <200:<div><br></div><div>(Pts with CD4 of 200-500 may develop, but disease usually self-limiting and similar to that in immunocompetent hosts)</div>
How will a bleeding in a ruptured ectopic pregnancy manifest?- May present with some per vaginal bleeding<div>- Most bleeding into retroperitoneal space → presents with more abdominal pain than bleeding </div>
Why does fresh red blood passed through the rectum not necessarily indicate a lower GI bleed?If bleeding in an upper GI bleed is brisk, may not have time to for Hb to be digested and so may not present as malaena<div><br></div><div>Important to check urea levels to ascertain whether upper or lower GI bleed</div>
In a patient with a variceal bleed, what should be checked and done before giving IV terlipressin?- Ask pt if they have chest pain, and do an ECG to rule out MI<div>- Make sure pt is haemodynamically resuscitated </div>
What clinical sign/obs is the most sensitive for hypovolaemia?Lying and Standing BP:<div>- Younger pts very good at compensating for hypovolaemia with vasoconstriction, but may experience postural hypotension </div>
Explain what happens to LFTs in a patient with a cardiac arrest?ALT/AST dramatically raised, in the thousands:<div>- Cardiac arrest causes decreased blood supply to the liver --> ischaemic hepatitis </div>
What caustive agents typically cause <b>cellulitis?</b><b>- </b><i><b>Strep</b>tococcus <b>pyogenes</b></i><div><i>- <b>Staph</b>ylococcus <b>aureus</b></i></div><div><i><br></i></div><div>(can be differentiated by testing for<b> Anti-streptolysin </b>O or<b> Anti-DNAse</b> B → strep pyogenes markers)</div>
When should IV antibiotics be considered in the treatment of cellulitis?"- <font color=""#0000ff"">Eron Class III/IV</font> (III= sig systemic upset, unstable co-morbidites, or limb-threatening condition due to vasc compromise; IV= sepsis or nec fasc)<div>-<font color=""#0000ff""> Severe or rapidly deteriorating </font>cellulitis (e.g. extensive areas of skin)</div><div>- <font color=""#0000ff"">Very young (<1y/o) or frail</font></div><div>- <font color=""#0000ff"">Immunocompromised</font></div><div>- <font color=""#0000ff"">Facial </font>celluitis/<font color=""#0000ff"">periorbital </font>cellulitis</div><div>- Significant <font color=""#0000ff"">lymphoedema</font></div>"
In severe cellulitis, what anitbiotics should be offerred?IV antibiotics:<br>- Co-amoxiclav<div>- Cefuroxime</div><div>- Clindamycin</div><div>- Ceftriaxone</div>
What is the basis of <b>all </b>fracture management?"<font color=""#0000ff"">Reduce</font>: Return to correct position<div><font color=""#0000ff"">Fix</font>: Keep in correct position</div><div><font color=""#0000ff"">Rehabilitate</font>: Encourage movement of joint and regain normal function</div>"
In Orthopaedics, how can fractures be reduced?"<font color=""#0000ff"">Open reduction</font>: Requires 'opening' of skin: surgeon makes an incision to visualise joint and reduce. <div><br></div><div><font color=""#0000ff"">Closed reduction</font>: Re-aligning without cutting open skin. Can be done in ED</div>"
In orthopaedics, how can fixation be achieved?"<font color=""#0000ff"">Internal fixation</font>: Components positioned within the patient's body e.g. plates, screws<div><font color=""#0000ff"">External fixation</font>: Components placed outside patient's body e.g. plaster, external fixators</div>"
- Fixed flexion<div>- Fusiform swelling</div><div>- Tenderness</div><div>- Pain on passive extension</div><div><br></div><div>(suggest what?)</div>"What are the signs of <b>flexor tendon sheath infection</b> (Kanavel's signs)?"
What is an early symptom of carpal tunnel syndrome?Paraesthesia in radial 3.5 fingers (median nerve distribution):<div>- Tend to drop items, not due to weakness, but due to loss of sensory feedback. </div><div><br></div><div>May manifest as difficulty putting in buttons, sewing etc. </div><div><br></div><div>Progresses to paralysis and weakness</div>
What is the best diagnostic investigation for Carpal Tunnel Syndrome?Nerve conduction studies:<br>- Affects both motor and sensory nerves: shows prolongation of the AP
What causes trigger finger?"Nodule on swollen tendon come out of flexor sheath and traps the finger in flexion<div><br></div><div>(as tendon stuck and cannot pass through the 'pulley')<br><div><br></div><div><img src=""paste-8a50516fe6ec5a2c383563ae275b406a82034803.jpg""><br></div></div>"
What fingers tend to be affected in trigger finger?- Thumb, middle or ring finger
"What is <b>Hueston's tabletop test, </b>and what is it used for?""Assess Dupuytren's contracture: if pt cannot place hand flat on table, positive sign. <div><br></div><div>Indicates need for surgery</div>"
"What are the stages of development of Dupuytren's contracture?""1. Nodules may appear in palm<div>2. Rope-like cords form</div><div>3. Flexion of 4th and pinky fingers</div><div><br></div><div><img src=""paste-84208e350f3c4af80ae6209947b1051632cb215c.jpg""><br></div>"
"What is the most established risk factor for Dupuytren's contracture?"Genetics: 60-70% of pts have a positive family Hx 
"How can Dupuytren's contracture be treated?"Only treat if table-top test is positive:<div>- Injecting collagenases (to degrade collagen and reduce contraction) - specialist</div><div>- Splinting and steroid injections</div><div>- Fasciectomy</div><div><br></div><div>Give allopurinol to reduce re-occurence rate </div>
What are <b>ganglions?</b>"'Cyst' arising from joint or tendon sheath, most commonly seen on back of wrist<div><img src=""ganglioncyst.jpg""><br></div>"
What are associations with ganglion cysts?- 3x more common in women<div>- Gymnastics is a risk factor </div>
What should be done in the diagnosis of a ganglion cyst?"- Clinical examination: pliable, should transilluminate<div>- X-Ray: AP and lateral veiws, to exclude more serious underlying pathology</div><div><br></div><div><img src=""31907tn.jpg""><br></div>"
How should ganglion cysts be managed?"- Reassurance- many resolve on their own <div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If symptomatic</font>: USS guided aspiration (but try to avoid as high recurrence rate)</div><div><br></div><div>Surgical treatment via arthroscopic method may have lower recurrence </div>"
"How is de Quervain's tenosynovitis managed?""<font color=""#0000ff"">First line</font>- Conservative: RICE and NSAIDs<div><font color=""#0000ff"">Second line</font>- Steroid injection</div><div><br></div><div>If still not under control, surgically split tendon sheaths </div>"
What is <b>mallet finger?</b>"Injury of extensor tendon at DIP- unable to extend finger tip without manually pushing it<div><img src=""300px-Mallet_Finger_Injury.jpg""><br></div><div><br></div><div>(describes what/)</div>"
"Injury of extensor tendon at DIP- unable to extend finger tip without manually pushing it<div><img src=""300px-Mallet_Finger_Injury.jpg""><br></div><div><br></div><div>(describes what/)</div>"What is <b>mallet finger?</b>
What type of injury causes mallet finger?"Over bending of finger tip (e.g. if ball hits an outstretched finger)<div><img src=""images (5).jpg""><br></div>"
How should mallet finger be managed?"<font color=""#0000ff"">1st line</font>: Splint finger straight for 8 weeks<div><font color=""#0000ff"">2nd line</font>: Surgery (acts to immobilise DIP, to keep it straight)</div><div><br></div><div>Failure to treat causes swan-neck's deformity</div>"
"What is the management of a colles' fracture?""<div>Check for nerve damage (median nerve most likely affected)<font color=""#0000ff""><br></font></div><font color=""#0000ff""><div><font color=""#0000ff""><br></font></div>Reduce</font>: Closed reduction- manipulate under local anaesthetic<div><font color=""#0000ff"">Fix</font>: Plaster of Paris for at least 6 weeks. Fix in palmar flexion</div><div><font color=""#0000ff"">Rehabilitate</font>: Physio</div><div><br></div><div>Surgery indicated if:</div><div>- Comminuted fracture</div><div>- Dorsal tilt >20°<br></div><div>- Intraarticular displacement >1mm</div><div>- Loss of radial height >2mm</div>"
What is the most sensitive investigation for a scaphoid fracture?MRI- though not commonly done
"What is a <b>boxer's fracture?</b>"Fracture at the neck of the 5th metacarpal <div><br></div><div>(describes what?)</div>
Fracture at the neck of the 5th metacarpal <div><br></div><div>(describes what?)</div>"What is a <b>boxer's fracture?</b>"
"What is seen here?<div><img src=""1212Con_PCBoxer_AB.jpg""><br></div>""Fracture across neck of 5th metacarpal- <b>Boxer's fracture</b>"
"What is seen here?<div><img src=""5801f5a44ae41a6207a48d285bcf3f_gallery.jpeg""><br></div>""Barton's fracture: Intra-articular dislocation of distal radius, with dislocation of radiocarpal joint<div><br></div><div>(Ba<b>r</b>ton's not Bennett's, as <b>R</b> for radius)</div>"
"What fracture is seen here?<div><img src=""cow701_moved.jpg""><br></div>""<b>Bennett's fracture</b>: Fracture of 1st metacarpal, extending into CMC joint<div><br></div>"
"What is a <b>Chauffeur's fracture?</b>"Fracture of the radial styloid process, caused by compression from the scaphoid bone of the hand<div><br></div><div>(describes what/)</div>
Fracture of the radial styloid process, caused by compression from the scaphoid bone of the hand<div><br></div><div>(describes what/)</div>"What is a <b>Chauffeur's fracture?</b>"
"What is seen here?<div><img src=""300px-Displaced_distal_radius_fracture.jpg""><br></div>""Chaffeur's fracture: fracture of radial styloid process"
What muscles mediate flexion of the elbow joint?"- Biceps<div>- Brachialis</div><div>- Brachioradialis </div><div><br></div><div><img src=""Bodyman-Biceps-Brachii-Barchialis-Corico-Brachialis.jpg""><br></div>"
The radial collateral ligament extends from the <span class=cloze>[...]</span> to the <span class=cloze>[...]</span>The radial collateral ligament extends from the <span class=cloze>lateral epicondyle</span> to the <span class=cloze>annular ligament of radius</span><br> The <span class=cloze>[...]</span> collateral ligament extends from the lateral epicondyle to the annular ligament of radiusThe <span class=cloze>radial</span> collateral ligament extends from the lateral epicondyle to the annular ligament of radius<br> The ulnar collateral ligament extends from the <span class=cloze>[...]</span> to the <span class=cloze>[...]</span>The ulnar collateral ligament extends from the <span class=cloze>medial epicondyle</span> to the <span class=cloze>coronoid process and olecranon of ulna</span><br> The <span class=cloze>[...]</span> collateral ligament extends from the medial epicondyle to the coronoid process and olecranon of ulnaThe <span class=cloze>ulnar</span> collateral ligament extends from the medial epicondyle to the coronoid process and olecranon of ulna<br> Who is typically affected by olecranon bursitis?- Middle-aged males<div>- Students (all that studying!)</div>
"A man presents with the following sign. This is aspirated, and fluid sent off for further analysis. What further management might be necessary?<div><img src=""1200px-Bursitis_Elbow_WC (1).JPG""><br></div>""Olecranon bursitis- fluid sent for MC&S and microsopy for crystals:<div><br></div><div>-<font color=""#0000ff""> If abscess formation</font>: Drain completely and IV Abx</div><div>- <span style=""color: rgb(0, 0, 255);"">If gout</span>: treat with NSAIDs</div><div>-<font color=""#0000ff""> If normal</font>: conservative- RICE + NSAIDs</div>"
How might severe olecranon bursitis be managed?- Hydrocortisone injection (relieves inflammation and prevents further accumulation of fluid)<div><br></div><div>If causing pain, or continual recurrence after drainage: Surgery to remove buras from elbow</div>
"What symptoms may accompany pain in golfer's elbow?"Medial epicondylitis:<div>- Ulnar nerve involvement: tingling in 4th and 5th finger </div>
The <span class=cloze>[...]</span> epicondyle is a common extensor origin whereas the <span class=cloze>[...]</span> epicondyle is a common flexor origin for muscles"The <span class=cloze>lateral</span> epicondyle is a common extensor origin whereas the <span class=cloze>medial</span> epicondyle is a common flexor origin for muscles<br> <img src=""epicondylitis.jpg"">"
The lateral epicondyle is a common <span class=cloze>[...]</span> origin whereas the medial epicondyle is a common <span class=cloze>[...]</span> origin for muscles"The lateral epicondyle is a common <span class=cloze>extensor</span> origin whereas the medial epicondyle is a common <span class=cloze>flexor</span> origin for muscles<br> <img src=""epicondylitis.jpg"">"
"What worsens pain in golfer's elbow?"Medial epicondylitis- medial epicondyle source of flexor muscles:<br>- Wrist flexion and pronation
What movements worsens pain in tennis elbow?Lateral epicondylitis: lateral epicondyle common extensor source:<div>- Pain on resisted wrist extension or supination (w/ elbow extended)</div>
How long can episodes of lateral epicondylitis last?6months- 2 years <div><br></div><div>(tend to have acute pain for 6-12 weeks)</div>
How should lateral/medial epicondylitis be managed?- Avoid weights, Rest joint<div>- NSAIDs + Steroid injections</div><div>- Physio (most effective non-surgical management)</div><div><br></div><div>Surgery: Arthroscopic release of flexor/extensor origins </div>
When is surgery indicated in osteoarthritis of the elbow?- Not responding to conservative measures (physio, analgesia)<div>- Signs of joint locking </div><div><br></div><div>(note total elbow replacement is very effective for RA, but less so in OA)</div>
How does cubital tunnel syndrome present?- Tingling in 4th/5th finger → develops into numbness<div>- May be worse when elbow is resting on firm surface, or flexed for extended periods (compresses ulnar nerve more)</div><div><br></div>
How is cubital tunnel syndrome managed?"Surgical decompression<div><img src=""pmuscsk20140312v0004.jpg""><br></div>"
Lesion of the radial nerve at the wrist causes what sign?Finger drop
Lesion of the radial nerve due to humeral mid-shaft fracture causes what?- Wrist drop and loss of sensation on posterior element of forearm
Lesion of the radial nerve at the axilla (e.g. in saturday night palsy) causes what sign?- Cannot extend arm or wrist<div>- Loss of sensation along posterior side of arm </div>
What nerve should be checked in an elbow dislocation?Ulnar nerve- as often coronoid process fracture (and ulnar passes behind elbow joint)
In which direction does elbow dislocation occur most frequently?"Posterior:<div><img src=""f4cb459274ce88e8169d3baf9334dd_jumbo.jpeg""><br></div><div>(Posterior of ulnar relative to humerus)</div>"
Where is the radial head?Proximal end of radius, near the elbow joint 
What causes a radial head/neck fracture and how does it present?Fall on outstretched hand<div><br></div><div>Sharp pain on lateral side of elbow at extremes of rotation </div>
What is the most common elbow fracture in children?"Supracondylar humeral fractures<div><img src=""Wr4unTQ8V64MF2TWAWxmrUn-htqvfvL2PJF9XFjBtKYF_oxyL0CyFfeMGz46RMAgWqkvyk7Bv-YJyzUFem9xjwm_pGPhlxB-HWkI8vBXriwIZnJIkU_oaWU1YQGKgksovbRc.jpg""><br></div>"
What should be checked in pts with a supracondylar humeral fracture?- Radial pulse- fracture may damage the brachial artery <div>- All nerves: ulnar (index abduction), median (thumb abduction), radial (wrist extension)</div>
In appendicitis, what imaging must be done before an appendectomy?No imaging necessary- ↑inflammatory markers with compatible history and examination findings enough to justify appendicetomy 
In a case of suspected appendicitis, what differentials should be excluded?"-<font color=""#0000ff""> Ectopic pregnancy</font>: Pregnancy test <div>- <font color=""#0000ff"">UTI/Renal colic</font>: Urine dipstick</div><div>- <font color=""#0000ff"">Mesenteric adenitis</font>: Hx post URTI, and lympahdenopathy</div>"
If a patient with suspected appendicitis is due for appendectomy, what should be done beforehand?Administration of prophylactic IV antibiotics- reduces wound infection rates 
What is the most common position of the appendix?Retrocaecal position
What is an <b>interval appendectomy?</b>"Carried out if gangrenous appendix:<div><font color=""#0000ff"">1st procedure</font>: To drain pus and fluid in peritoneum. Give broad spectrum Abx </div><div><font color=""#0000ff"">2nd procedure</font>: Done 8-12 weeks later, to remove appendix </div>"
What method of appendectomy is the treatment of choice of appendicitis?Laparoscopic:<div><br></div><div>- Default, unless gangrenous or perforated appendix- smaller incision and so shorter admission</div>
When should a patient with haemorrhoids be referred to the general surgeons?If haemorrhoids are acutely thrombosed (<72hrs) (as these can be surgically removed within 72hrs window)
How is proctalgia fugax managed?- Reassure<div>- Topical treatment with diltiazem/salbutamol or topical nitroglycerine </div>
A man who has been referred on a 2 week wait for gastro has a colonoscopy. Biopsy revelas hamartamous polyps. <div><br>What is the likely cause?</div>"Hamartamous polyp= genetic cause of tumour<div><br></div><div>Peutz-Jegher's syndrome or Cowden Syndrome</div>"
What is <b>Cowden syndrome?</b>Multiple hamartoma syndrome: rare autosomal dominant condition with increased risk of cancers at all sites
What mutation is associated with <b>Cowden syndrome?</b>PTEN mutations (are associated with which genetic condition that increases the risk of cancer?)
PTEN mutations (are associated with which genetic condition that increases the risk of cancer?)What mutation is associated with <b>Cowden syndrome?</b>
What are the screening tests for colorectal cancer?- <b>FIT test</b>: every 2 years to those 60-74y/o (Pts >74 may request screening)<div>-<b> Flexible sigmoidoscopy:</b> Offered to people who are 55 (but can self-refer up to age of 60 if routine offer had not been taken up)</div>
What test should be done in a patient >50 presenting with occasional diarrhoea and abdominal discomfort which she says is relieved by defecation?IBS symptoms- in >50 → ?ovarian cancer. <div><br></div><div><b>CA-125</b></div><div><b><br></b></div><div>(If positive, urgent 2 week wait for USS Abdo pelvis)</div>
What is the first-line treatment for a mild-moderate flare of ulcerative colitis?Topical mesalazine
"What is the 'double duct' sign?"Dilation of both the common bile duct and pancreatic duct- associated with pancreatitis caused by gallstones
What are indicators that a flare of ulcerative colitis is severe?- >6 bloody stools per day & features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
A patient is diagnosed with UC causing proctitis. How should remission be achieved?Proctitis= localised to rectum:<div><b>1st line</b>: Topical (rectal) mesalazine</div><div><br></div><div>If remission not achieved within 4 weeks, add oral mesalazine, </div><div>If still not acheived, add topical or oral coritcosteroid</div><div><br></div>
A patient is diagnosed with left-sided UC. How should remission be achieved?1st line: Topical mesalazine. <div><br></div><div>If remission not achieved within 4 weeks, add high-dose oral mesalazine OR switch to high-dose oral mesalazine + topical corticosteroid</div><div><br></div><div>If remission still not achieved, stop topical treatment and offer oral mesalazine + oral corticosteroid</div>
A patient is diagnosed with extensive UC. How should remission be achieved?Affecting both left and right side:<div><br></div><div>First line: Topical Mesalazine + High-dose oral mesalazine</div><div><br></div><div>If remission not achieved within 4 weeks: Stop topical treatments, and offer high-dose oral mesalazine + oral corticosteroid</div>
What medications should be given to maintain UC remission?"<font color=""#0000ff"">If proctitis/proctosigmoiditis:</font><div>- Rectal mesalazine OR</div><div>- Oral mesalazine + rectal mesalazine OR<br>- Oral mesalazine (not as effective)</div><div><br></div><div><font color=""#0000ff"">If left-sided/extensive UC:</font></div><div>- Low maintenance dose of oral mesalazine</div>"
"Why are patients with Crohn's disease at higher risk of developing gallstones?""Crohn's often impairs absorption in the terminal ileum (where bile salts are absorbed)<div><br></div><div>Impaired absorption = higher risk of developing gallstones</div>"
What is the difference between an <b>abdominoperineal resection and an anterior resection?</b>"<font color=""#0000ff"">Anterior resection:</font> Removal of the rectum (but does not have removal of anus, and so does not require a stoma)<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Abdominoperineal resection</font>: Removal of anus, rectum and part of descending colon. Requires permanent colostomy</div>"
"What is seen here?<div><img src=""xrb149b.jpg""><br></div>"Subcutaneous emphysema:<div>- Air is outlining the pectoralis major muscle, causing ginkgko leaf sign</div>
What are signs of gastric volvulus?Triad of:<div>- Vomiting & retching </div><div>- Epigastric Pain </div><div>- Failed attempt to pass an NG tube </div>
What are the most common tissue types in colorectal and anal cancers?"<font color=""#0000ff"">Colorectal</font>: Adenocarcinoma<div><font color=""#0000ff"">Anal</font>: Squamous cell carcinoma</div>"
Rectal bleeding alongside nocturnal incontinence and diarrhoea is suggestive of what?"Inflammatory bowel disease e.g. ulcerative colitis or crohn's disease<div><br></div><div>(Nocturnal incontinence suggests IBD over colorectal cancer)</div>"
What are the histological appearances of solitary rectal ulcers?Extensive collagenous deposits- termed <b>fibromuscular obliteration</b>
Patients presenting with rectal bleeding require what investigations?- PR exam<div>- Proctosigmoidoscopy</div><div><br></div><div>As a minimal baseline </div>
When is colonoscopy preferred over proctosigmoidoscopy in patients presenting with PR bleeding?- Altered bowel habit (suspicion of colorectal cancer)<div>- ?Inflammatory Bowel Disease</div><div><br></div><div>(important to image the whole colon) </div>
When might you avoid doing an immediate proctosigmoidoscopy in a patient with PR bleeding?If young pt with external stigmata & comparable hx of fissure. <div><br></div><div>Treat medically first, and defer internal examination until healed. </div><div><br></div><div>If fissure fails to heal, important to carry out internal examination to exclude internal disease</div>
What investigations are necessary for patients who are discovered to have a mass in the rectum?"-<font color=""#0000ff""> MRI rectum</font>: to identify resection margin compromise and identify mesorectal nodal disease<div>- <font color=""#0000ff"">CT abdo pelvis</font>: to stage for more distant disease</div>"
When is surgery indicated in anal fissures, and what is done?If botulinum toxin treatment fails to help:<div>- Carry out lateral internal sphincterotomy </div>
If conservative and interventional methods fail to manage haemorrhoids, what surgical options can be considered?If external haemorrhoid: Excision (open) haemorrhoidectomy<div><br></div><div>Modern options:<br>- Stapled haemorrhoidectomy</div><div>- HALO procedure (Haemorrhoid Artery Ligation Operation- reduces flow of blood to haemorrhoids)</div>
What might be found on laparoscopy of a patient with <b>Fitz Hugh Curtis syndrome?</b>Pelvic inflammatory disease causing peri-hepatitis:<div>- Fine peri-hepatic adhesions between the liver and abdominal wall</div><div><br></div>
"What is seen here, on laparoscopy?<div><img src=""Perihepatic_adhesions_2.jpg""><br></div>"Fine peri-hepatic adhesions between liver and abdominal wall: <b>Fitz Hugh Curtis syndome</b><div><b><br></b></div><div>(Chlamydia travels up right paracolic gutter and causes peri-hepatitis)</div>
Presence of fever alongside severe ano-rectal pain suggests what?Anorectal abscess<div><br></div><div>(anal fissures do not cause fever)</div>
Why is topical GTN helpful in anal fissures?Expands blood vessels around the anus, increasing blood supply to fissure and helping it heal faster.<div><br></div><div>Can also reduce pressure in anal canal which should ease the pain</div>
What is <b>pneumaturia</b>, and what is a frequent cause?Passage of gas mixed in with urine- often due to fistula forming between the bowel and bladder (common in diverticular disease)
What are indications for surgery in upper GI bleeds?- Pts >60y/o<div>- Continued bleeding despite endoscopic intervention</div><div>- Recurrent bleeding</div><div>- Known cardiovascular disease w/ poor response to hypotension</div>
If surgical management is required to control upper GI bleeds caused by duodenal/gastric ulcers, what is done?"<font color=""#0000ff"">Duodenal</font>: Laparotomy, duodenotomy and under-running of ulcer<div><br></div><div><font color=""#0000ff"">Gastric</font>: Under-running of bleeding site. Partial or total gastrectomy may be required</div>"
How should Mallory-Weiss tears be managed?Treat as acute upper GI bleed- resuscitate.<div><div><br></div><div>Mallory Weiss tears typically resolve spontaneously. If stable, no need for endoscopy. </div></div>
What is the difference between Mallory-Weiss tears and Boerhaave syndrome?Mallory-Weiss syndrome is from tear in mucosa<div><br></div><div>Boerhaave syndrome is a full-thickness rupture of the oesophagus </div>
What is the distinction between oesophageal rupture and Boerhaave syndrome?Oesophageal rupture most commonly iatrogenic (56%- from endoscopy or paraoesophageal surgery)<div><br></div><div>Boerhaave syndrome is reserved to the 10% of oesophageal rupture that are caused by vomiting</div>
How should the Rockall score be interpreted?Scores of ≤3 are associated with rebleeding rate of 4% - very low risk of mortality, and suitable for early discharge
What is a key fitness measure to assess whether a patient is cardiovascularly fit for surgery?Is the pt able to walk up 1 flight of stairs without experiencing any SOB/symptoms?
How should a patient with Atrial fibrillation be optimised before elective surgery?Rate control: <100bpm
What is the single most worrying cardiovascular co-morbidity for a patient undergoing elective surgery?Cardiac Failure: limits ability of heart to respond under stress during anaesthesia/surgery<div><br></div><div>(More dangerous than IHD)</div>
Which anti-hypertensive medication should be stopped before surgery?ACE-i or ARBs<div><br></div><div>Associated with <b>severe hypotension </b>after induction of anaesthesia </div>
When is a CXR indicated in the pre-operative assessment of a patient?- If clinical indication (dyspnoea,cough)<div>- If pt is having thoracic surgery </div>
When is a FBC indicated for a patient pre-operatively?- Pts whose surgery presents a risk of substantial blood loss<div>- Pts with Anaemia-like symptoms (fatigue)</div>
Why is starving for 6 hrs important before an operation?General anaesthesia suppresses the cough and gag reflex + reduces competence of lower oesophageal sphincter → risk of aspiration<div><br></div><div>Do not want pts to have any contents in stomach</div>
"In a desaturating patient, how do you decide whether to just give them oxygen, or help them ventilate with a bag valve mask/laerdal mask?<div><img src=""AFWMVNCV.jpg""><br></div>""Assess pt's own respiratory drive:<div><br></div><div><font color=""#0000ff"">If pt has evidence of drive w/ adequate respiration rate >8:</font> Give 15L NRBM</div><div><font color=""#0000ff"">If pt has no respiratory drive:</font> Ventilate with Bag valve mask</div>"
How does an LMA work?"Sits on top of larynx, and slides over epiglottis to close off oesophagus and reduce risk of aspiration<div><img src=""209926_1_En_11_Fig7_HTML.gif""><br></div>"
How can you tell the difference between a patient with a low bp due to hypovolaemia and one due to sepsis?Hypovolaemia will have cool peripheries<div>Sepsis (due to vasodilation) will have warm peripheries</div>
What are risk factors which increase the risk of post-operative nausea and vomiting?- Pain/anxiety<div>- Younger age</div><div>- Females</div><div>- Type of surgery (breast/bowel/uterus/middle ear) </div><div>- Use of opioid drugs</div><div>- Hx of prev. post-operative nausea</div><div>- Dehydration </div>
What antibodies are found in Primary Sclerosing Cholangitis?"<font color=""#0000ff"">- pANCA (in 80%)</font><div>- Antinuclear and Anti-smooth muscle antibodies (often found in those who have PSC/AIH overlap)</div>"
What is often used to keep patients warm in theatre?- Bair hugger<div>- Warming of IV fluids </div>
With regards to the WHO pain ladder, what drugs are <b>simple analgesia?</b>Paracetamol<div><br></div><div>(fits under what category of analgesia in the WHO Pain ladder?)</div>
Paracetamol<div><br></div><div>(fits under what category of analgesia in the WHO Pain ladder?)</div>With regards to the WHO pain ladder, what drugs are <b>simple analgesia?</b>
What are examples of <b>weak opioids</b> under the WHO pain ladder?- Codeine<div>- Tramadol </div><div><br></div><div>(are examples of what type of analgesia in the WHO pain ladder/)</div>
- Codeine<div>- Tramadol </div><div><br></div><div>(are examples of what type of analgesia in the WHO pain ladder/)</div>What are examples of <b>weak opioids</b> under the WHO pain ladder?
What are examples of <b>strong opioids </b>in the WHO pain ladder?- Morphine<div>- Diamoprhine</div><div>- Fentanyl</div><div>- Oxycodone</div><div><br></div><div>(are what type of analgesia in the WHO pain ladder?)</div>
- Morphine<div>- Diamoprhine</div><div>- Fentanyl</div><div>- Oxycodone</div><div><br></div><div>(are what type of analgesia in the WHO pain ladder?)</div>What are examples of <b>strong opioids </b>in the WHO pain ladder?
What is <b>co-codamol?</b>Combination of paracetamol and codeine
Although the normal threshold for RBC transfusion is 70g/L, which patient groups should be transfused at 80g/L?If pts cannot compensate with lower Hb due to:<div>- Beta blockade</div><div>- Significant underlying cardiorespiratory disease (heart failure)</div><div>- Significant peripheral vascular disease </div>
Which electrolyte is often decreased post-surgery?Potassium:<div>- Stress response to surgery increases Na<sup>+</sup><sub> </sub>and water retention (at expense of K<sup>+</sup>)</div>
How should you choose the appropriate size of a nasopharyngeal airway for a patient?"Soft to soft:<br>- Tragus of ear to lateral edge of nostril<div><img src=""smtFJjpo54FmzYqQkSoE3WUlBBU-L0qar1Dp35fG1q5Z99h2nGDpaQFNohBZ-CbIDq0FpUTDaM3pDyYtK8VctM1-mt3MBIJeVLtv56IXpAM41rVg4srUkP_UbP_o6SkzY_SR.jpg""><br></div>"
How should you choose the appropriate size of oropharyngeal airway for a patient?"Hard to hard:<div>- Midpoint of incisors to angle fo mandible</div><div><br></div><div><img src=""paste-04d0041726c281f6ac7b89126e05aee1b28ca395.jpg""><br></div>"
If a patient is hypovolaemic, what is their ABG likely to show?Metabolic acidosis:<div><br></div><div>- Due to inadequate tissue perfusion → increased anaerobic respiration → increased lactate </div>
According to the WHO safety checklist, what are the Three Phases of the operation?"<font color=""#0000ff"">Sign in</font>: Before induction of anaesthesia<div><font color=""#0000ff"">Time out</font>: Before incision of skin</div><div><font color=""#0000ff"">Sign out</font>: Before pt leaves theatre</div>"
When should clopidogrel be stopped before an operation?7 days before 
When should warfarin be stopped before an operation?5 days before, aim for INR <1.5; bridge with LMWH (but stop LMWH day before operation)
When should ACEi/ARBs be stopped before an operation?Day before surgery
What changes should you make to diabetes medication before an operation?"<font color=""#0000ff"">Insulin</font>: Continue long-acting, hold short-acting on day of surgery<div><font color=""#0000ff"">Sulphonylureas</font>: Held on day of surgery (risk of hypos)</div><div><font color=""#0000ff"">Metformin</font>: Continue if short procedure, stop if expecting NBM for >48hrs</div>"
If a patient is taking regular PO prednisolone e.g. for GCA, what should be done to their medication pre-op?Switch to IV hydrocortisone<div><br></div><div>Switch back when not NBM</div>
What are examples of hypnotic drugs?"<font color=""#0000ff"">Inhaled</font>:<br>- Isoflurane<div>- Desflurane</div><div><br></div><div><font color=""#0000ff"">IV</font>: </div><div>- Propofol</div><div>- Thiopentone</div>"
What are examples of analgesic drugs (for anaesthesia)?- Fentanyl<div>- Ketamine</div><div>- Morphine </div>
What are examples of muscle relaxant drugs for anaesthesia?"<font color=""#0000ff"">Non-depolarising: </font><div>- Rocuronium</div><div>- Vecuronium</div><div>- Pancuronium</div><div><br></div><div><font color=""#0000ff"">Depolarising:</font><br>- Suxamethonium</div>"
When is thiopentone used in for induction of anaesthesia?"Has an active metabolite so not widely used. <div><br></div><div>Rapid onset- so <font color=""#0000ff"">useful for Rapid Sequence Induction </font>(but causes dramatic hypotension, so do not use if low bp)</div>"
What is <b>Rapid sequence induction?</b>Method of inducing anaesthesia in patient who are at risk of aspiration/emergencies (intubation without face mask ventilation)
What are side effects of depolarising muscle relaxants?- Malignant hyperthermia<div>- Hyperkalaemia</div><div>- Fasciculations </div>
What is the first-line drug given to manage post-op nausea and vomiting?Cyclizine 
What is the gold-standard analgesia for patient suffering pain post thoracoabdominal surgery?Epidural <div><br></div><div>(allows early return of bowel movements too)</div>
A patient who complains of coughing mid-swallow suggests what cause of dysphagia?"Motility issue e.g. bulbar palsy, achalasia <div><br></div><div>(note coughing associated w/ other causes of dysphagia e.g. oesophageal carcinoma, but this isn't directly related to the act of eating- more of a constant cough)</div>"
Worsening odynophagia in a patient with a background of reflux disease suggests what cause?Suggests oesophageal carcinoma (note <b>worsening</b>, so less likely to be oesophagitis)
A patient presenting with upper GI Bleeding and a tender epigastrium with DHx of corticosteroids should raise suspicion of what aetiology?Long-term steroids → ulcers <div><br></div><div>Perforated ulcer</div>
What medication can be given to a patient experiencing acid reflux, who is due for an endoscopy in the next 2 weeks?Avoid PPIs and H<sub>2</sub> receptor antagonists- as can mask the pathology. <div><br></div><div><b>Offer antacids</b>- provide symptomatic relief, but will not affect endoscopy result </div>
"How can Gilbert's syndrome be differentiated clinically from Rotor's syndrome?""Gilbert causes unconjugated hyperbilirubinaemia, whereas Rotor's causes conjugated hyperbilirubinaemia --> dark urine. "
If a 23 year old woman presents with an otherwise asymptomatic bilirubinaemia, what is the likely cause?"Gilbert's syndrome<div><br></div><div>(Crigler-Najjar also causes an unconjugated hyperbilirubinaemia but more severe and presents in neonates requiring liver transplant)</div>"
A 28y/o woman has been admitted with abdominal pain and profuse vomiting and diarrhoea. She is being treated with a number of different drugs for a presumed gastroenteritis<div><br></div><div>She has been seen to have her eyes rolled back and unable to prevent protrusion of her tongue. </div><div><br></div><div>What drug is likely responsible?</div>Metoclopramide- an anti-emetic, but also can cause <b>oculogyric crises</b> (a type of dystonic reaction)<div><br></div><div>esp. common in younger patients </div>
What causes formation of <b>diverticuli?</b>High intraluminal pressures (perhaps due to lack of dietary fibre) force mucosa to herniate through muscle layers of gut at weak points
What fistulae can form in diverticular disease?- Enterocolic<div>- Colovaginal</div><div>- Colovesical </div><div><br></div><div>(should be treated with surgery- resect the area of colon that has formed the fistula)</div>
How does a <b>colovesical fistula </b>present?Pneumaturia ± intractable UTIs, typically in a patient with Hx of diverticular disease <div><br></div><div>(describes what?)</div>
Pneumaturia ± intractable UTIs, typically in a patient with Hx of diverticular disease <div><br></div><div>(describes what?)</div>How does a <b>colovesical fistula </b>present?
If a patient with diverticular disease presents with a swinging fever and leucocytosis, but no localising signs, what should be considered?Swinging fever + leucocytosis suggests abscess formation. <div><br></div><div>If no localising signs, consider abscess under the diaphragm </div>
How can actue diverticulitis be graded?"Hinchey severity classification:<div><font color=""#0000ff"">I</font>: Para-colic abscess</div><div><font color=""#0000ff"">II</font>: Pelvic abscess or walled off</div><div><font color=""#0000ff"">III</font>: Generalised purulent peritonitis</div><div><font color=""#0000ff"">IV</font>: Generalised faecal peritonitis (presence of faeces in peritoneal cavity)</div><div><br></div><div>(Surgery required for III and IV; I-II can be drained and may resolve without surgery)</div><div><br></div>"
Which type of Inflammatory Bowel Disease is more associated with strictures, fistulae and adhesions?"Crohn's disease- as inflammation affects all layers of the bowel, rather than just the mucosa (in UC)"
"Acute/sub acute arthritis in association with: <div>- Inflammatory Bowel Disease</div><div>- GI Bypass</div><div>- Coeliac</div><div>- Whipple's Disease</div><div><br></div><div>(describes what?)</div>"What is enteric arthropathy?
What is the most common extra-intestinal feature in Inflammatory Bowel Diseases?"Enteropathic arthritis- most common feature in both Crohn's and UC"
What features of inflammatory bowel disease can affect the eyes?"<font color=""#0000ff"">Episcleritis</font>: More common in Crohn's<div><font color=""#0000ff"">Uveitis</font>: More common in UC</div>"
What extra-intestinal features of inflammatory bowel disease are related to disease activity?- Arthritis: Pauciarticular, asymmetric<div>- Erythema nodosum</div><div>- Episcleritis</div><div>- Osteoporosis</div>
What extra-intestinal features of inflammatory bowel disease are unrelated to disease activity?- Arthritis: Polyarticlar, symmetric<div>- Uveitis</div><div>- Pyoderma gangrenosum</div><div>- Clubbing</div><div>- Primary sclerosing cholangitis</div>
"What drug might be used to induce remission in Crohn's disease refractory to steroids + mesalazine?""Infliximab (also useful in fistulising Crohn's)<div><br></div><div>(Azathioprine/mercaptuopurine could also be tried as add-on therapy)</div>"
"In a child with Crohn's disease, what might you consider as an alternative to steroids to induce remission (if you are worried about the effect of steroids)?"Enteral feeding with an elemental diet <div><br></div><div>(can also be done alongside other treatment, but may be possible to induce remission with this alone)</div>
"What drug is used to induce remission in peri-anal Crohn's?"Metronidazole
"What is the most common surgical internvention required in Crohn's?""Ileocaecal resection (as most common disease pattern in Crohn's is stricturing terminal ileal disease)"
"A patient has come in with diarrhoea and weight loss and is subsequently diagnosed with Crohn's disease. This is now in remission due to a course of steroids. <div><br></div><div>What is the most important next step before starting him on his drug regimen to maintain remission?</div>"<b>Assess Thiopurine Methyltransferase (TMPT) activity:</b><div>- 1st line drug for maintenance is Azathioprine/Mercaptopurine</div><div><br></div><div>(broken down by TPMT, which is deficient in 1/300. Will cause azathioprine/mercaptopurine toxicity if given in these individuals) </div>
What is the first-line investigation for a patient with suspected haemoperitoneum?FAST scan: Focused assessment with sonography for Trauma<div><br></div><div>(can detect presence of fluid in the abdomen and thorax)</div><div><br></div><div>or CT- depends on which is immediately avaiilable</div>
"How is Boerhaave's syndrome diagnosed?""<font color=""#0000ff"">CT</font>: Shows mediastinal air, pleural effusion or mediastinal widening<div><font color=""#0000ff"">Contrast studies</font>: Ingestion of water-soluble contrast agent- will show leakage</div><div><br></div><div><img src=""paste-4dfcdfa21d3bcac75aec63e3957f63bad6b772e1.jpg""><br></div>"
How does oesophageal rupture typically present?- Chest and abdominal pain (often left-sided)<div>- Hx of vomiting</div><div>- Haematemesis</div><div>- Shock</div><div><br></div><div>- Subcutaneous emphysema may be palpable </div>
How is oesophageal rupture managed?"<div>IV broad-spectrum antibiotics and surgery (typically create a controlled fistula)<br></div><div>(Delay of surgery beyond 24hrs associated with fulminant mediastinitis- usually fatal)</div><div><img src=""211917""><br></div><div><br></div><div><br></div>"
A <span class=cloze>[...]</span> seen on barium swallow is associated with diffuse oesophageal spasmA <span class=cloze>nutcracker oesophagus</span> seen on barium swallow is associated with diffuse oesophageal spasm<br> A nutcracker oesophagus seen on barium swallow is associated with <span class=cloze>[...]</span>A nutcracker oesophagus seen on barium swallow is associated with <span class=cloze>diffuse oesophageal spasm</span><br> For which tumours should you do an anterior and abdominoperineal resection?"<font color=""#0000ff"">Tumour in distal 1/3 of rectum:</font> Abdominoperineal resection. Remove anus, rectum and section of sigmoid colon<div><font color=""#0000ff"">Tumour in proximal 2/3 of rectum</font>: Anterior resection. Removes area of malignancy in rectum and part of colon</div><div><br></div><div><img src=""management-of-rectal-cancer-32-638.jpg""><br></div>"
What monitoring should be done for methotrexate?FBC, LFTs and U&Es<div><br></div><div>Weekly until therapy stabilised; then monitor every 2-3 months</div>
What monitoring should be done for patients on azathioprine?FBC, LFT<div><br></div><div>(As risk of cytopenia and deranged liver function)</div>
For which joints are topical NSAIDs used in osteoarthritis?- Knee<div>- Hand</div>
What is the first-line analgesic for Osteoarthritis?- Paracetamol<div>- Topical NSAID (if knee or hand)</div>
"What is the pathophysiology behind idiopathic Raynaud's disease?"Hyperactive sympathetic system, causing vasoconstriction (in cold weather or stress)
"What is seen here?<div><img src=""paste-7092d0f4fd5bafbbfc72625ad2cfa3bc6254c5a7.jpg""><br></div>"Base of the thumb is squared- feature of osteoarthritis affecting the carpometacarpal joint 
How should ankle fractures be managed?"- Reduce ASAP- removes pressure on skin and neruovascular strcutures<div><br></div><div>If unstable fractures/high velocity/proximal injuries:<br>- <font color=""#0000ff"">Younger pts</font>: Surgical repair, with compression plate</div><div>- <font color=""#0000ff"">Older pts</font>: Conservative management (even if unstable) as thin bone does not hold metalwork well</div><div><br></div><div>Otherwise, conservative management w/ controlled ankle motion boot </div>"
If a patient with an ankle fracture presents with an absent dorsalis pedis pulse, what is the most appropriate initla management?<b>Reduce fracture</b>: bone displacement may be compressing the artery, so reduction can fix this issue<div><br></div><div>If pulse remains absent after reduction, call vascular surgeon</div>
How does an <b>iliopsoas abscess </b>present?- Fever (swinging)<div>- Back pain</div><div>- <u>Pain on extension of hip </u></div>
What type of injury is likely responsible for a <b>meniscal tear</b>?Twisting around flexed knee<div><br></div><div>(will damage what structure in the knee?)</div>
Twisting around flexed knee<div><br></div><div>(will damage what structure in the knee?)</div>What type of injury is likely responsible for a <b>meniscal tear</b>?
Back pain relieved by sitting down or leaning forward suggests <span class=cloze>[...]</span>Back pain relieved by sitting down or leaning forward suggests <span class=cloze>spinal stenosis</span><br> Back pain relieved by <span class=cloze>[...]</span> or <span class=cloze>[...]</span> suggests spinal stenosisBack pain relieved by <span class=cloze>sitting down</span> or <span class=cloze>leaning forward</span> suggests spinal stenosis<br> What is seen on joint aspirate of rheumatoid arthritis?<div>- Cloudy yellow appearance (which is normal)</div>- High WBC, predominantly neutrophils<div>- No Crystals</div><div><br></div><div>(Appears similar to septic arthritic, but different presentation [and septic arthritis will have turbid grey colour])</div>
What would you expect of Calcium, phosphate, PTH and ALP levels in osteogenesis imperfecta?All normal- issue with the bones is due to disorder in collagen, but normal calcium homeostasis
When should sciatica be referred to neurosurgery?After 4-6 weeks of conservative treatment (analgesia and physiotherapy) has failed
Systemic sepsis with changing lower limb neurology suggests <span class=cloze>[...]</span>Systemic sepsis with changing lower limb neurology suggests <span class=cloze>epidural abscess</span><br> Pressing on cauda equina
What is the recommended management of an undisplaced intracapsular fracture?"<font color=""#0000ff"">If no co-morbidities</font>: Internal fixation w/ cannulated hip screws (esp. if young)<div><font color=""#0000ff"">If major illness/advanced organ specific disease</font>: Hemiarthroplasty</div>"
What is the appropriate management for a displaced intracapsular fracture?"<font color=""#0000ff"">If no co-morbidities:</font><div>- Usually total hip arthoplasty (always in >70s)</div><div>- Consider internal fixation if possible in <70s</div><div><br></div><div><font color=""#0000ff"">If major co-morbidities/immobile:</font></div><div>- Hemiarthroplasty</div>"
Which extracapsular fractures usually require intramedullary nails?- Reverse oblique<div>- Transverse</div><div>- Sub-trochanteric<br></div><div><br></div><div>(Otherwise, use DHS)</div>
Why is pain in spinal stenosis worsened when walking?Walking ↑metabolic demands of compressed nerve roots, which have become ischaemic due to spinal stenosis<div><br></div><div><b>Neurogenic claudication</b></div>
Where is pain felt in iliotibial band syndrome?"2-3cm above the lateral knee joint, near the lateral epicondyle of the femur <div><br></div><div><img src=""j38tHf9bItTNNlqd4CEkzWHqGJUb8UryILJ4ZQjYfJTEITh2C6mIb1nh-Ym6YRqyNhvdUPv42t0GT0TrSQGKyrrQSDwIVKR_5ZR4SzctJV71njaFhR1vvbcncw""><br></div>"
Where is pain felt in Osgood-Schlatter disease?- Tibial tubercle 
Where is the pain felt in trochanteric bursitis?- Lateral hip/thigh pain<div>- Tenderness on palpation of the greater trochanter </div><div><br></div><div>(due to repeated movement of the iliotibial band)</div>
How can you differentiate between iliotibial band syndrome and greater trochanteric pain syndrome?IT band syndrome typically associated with running<div><br></div><div>Greater trochanteric pain syndrome usually seen in women aged 50-70years; and has tenderness on palpation of the greater trochanter</div>
What is the gold standard investigation for psoas abscess?CT (alongside bloods and blood/abscess cultures to confirm infection)
How should psoas abscess be managed?- Percutaneous drainage<div>- Administration of IV antibiotics </div>
"What makes up the <b>Simmond's triad?</b>"- Palpation of tendon<div>- Angle of declination at rest</div><div>- Calf squeeze test (Thompson test)</div>
What are risk factors for achilles tendon rupture?- Fluoroquinolone use (e.g. ciprofloxacin)<div>- Hypercholesterolaemia (predisposes to tendon xanthomata)</div>
What is the management of achilles tendinitis?"- Simple analgesia<div>- Reduction in precipitating activities</div><div>- Calf muscle eccentric exercises</div><div><br></div><div><img src=""paste-0f0a26d1f345eafd015b91a874148f0801226f98.jpg""><br></div>"
How does achilles tendinitis present?- Gradual onset posterior heel pain, worse following activity<div>- May have morning pain and stiffness</div>
When should achilles tendon rupture be suspected?"- Audible 'pop' in ankle following sport<div>- Sudden onset significant pain in calf/ankle</div><div>- Inabilility to walk or continue the sport </div>"
What tests should be done before referring suspected Achilles tendon rupture to orthopaedics?"Whilst USS is initial imaging modality of choice, if not available then do not delay referral <div><br></div><div>Simmond's triad (clinical examination) sufficient to make referral</div>"
What injury is responsible for 5th metatarsal fractures?Inversion of foot and ankle
What drugs can be used to maintain remission of IBD in pregnancy?- Mesalazine<div>- Azathioprine/mercaptopurine </div><div><br></div><div>(Inflixmiab not recommended in pregnancy)</div>
Which NSAID is not recommended in gout?Aspirin
What drugs can be used to treat gout?1. NSAIDs (but not aspirin)<div>2. Colchicene (if cannot tolerate NSAIDs/ low eGFR)</div><div>3. Steroids</div>
What is the first-line investigation for a suspected osteoporotic spine fracture?<b>X-ray Spine </b>(If X-ray reveals compression fracture, then CT spine may be indicated)
What muscles are involved in abduction of the arm?"<font color=""#0000ff"">Supraspinatus</font>: first 20° of shoulder abduction<div><font color=""#0000ff"">Deltoid</font>: Does the remaining abduction</div>"
<span class=cloze>[...]</span>= Laryngeal-mask airway<br>"<span class=cloze>I-gel</span>= Laryngeal-mask airway<br><br> <img src=""I-Gel.jpg"">"
I-gel= <span class=cloze>[...]</span><br>"I-gel= <span class=cloze>Laryngeal-mask airway</span><br><br> <img src=""I-Gel.jpg"">"
Why should you avoid putting an oropharyngeal airway in someone who is conscious?If conscious, preserved airway reflexes. <div><br></div><div>May cause gag reflex → vomiting → aspiration </div>
A positive painful arc test suggests what?Impingement of supraspinatus tendon
In a patient with ascending cholangitis, what might be seen on abdominal ultrasound?Dilated common bile duct (as gallstone is lodged there- causing dilation of the duct)
What is <b>hallux valgus?</b>"Bunions- deformity of big toe where toe tilts towards the smaller toes, and metatarsal tilts medially<div><img src=""paste-2c16ae720b03f73a8b042297219edd8027c2070e.jpg""><br></div>"
What is a common complication of bunions?- Secondary osteoarthritis<div>- Callouses on top of toe</div><div>- Painful bunions on medial surface ot MTP </div><div>- Clawing of toe </div>
How should hallux valgus be managed?"<font color=""#0000ff"">Conservative:</font><div>- Education on appropriate footwear and foot exercises</div><div><br></div><div><font color=""#0000ff"">If painful bunions which inhibit lifestyle and footwear choices:</font></div><div>- Consider srugery (bunionectomy, or osteotomy)</div>"
What are associations with bunions?- Genetics<div>- Females</div><div>- High BMI</div><div>- Inappropriate footwear</div><div>- Rhumeatoid Arthritis</div>
How is achilles tendon rupture managed?"<font color=""#0000ff"">Conservative:</font><div>- Splint in equinus position and no weight bearing for up to 2 months</div><div><br></div><div><font color=""#0000ff"">Surgical repair:</font></div><div>- Do in the young and athletic (better potential for healing)</div>"
Which patients are unlikely to receive surgery for an achilles tendon rupture?- Smokers<div>- Diabetes mellitus</div><div>- >50y/o</div><div><br></div><div>(as healing is worse in these populations- less potential for recovery even with surgery)</div>
How long should you keep lower limb fracture in a cast for in a man with diabetes?Lower limb- 12 weeks. Diabetes, takes double the healing time:<div><br></div><div>24<b> </b>weeks</div>
In fracture management, how long does it takes bones to heal? What influences this?"6/52 in upper limb, 12/52 in lower limb.<div><br></div><div>In children: takes half the time</div><div><br></div><div><font color=""#0000ff"">Double healing time if:</font></div><div>- Smoking</div><div>- Steroids/NSAID uses</div><div>- Diabetes</div><div>- <b>Open fractures</b></div>"
What is <b>spondylosis?</b>Degeneration of the vertebral column (typically from osteoarthritis)<div><br></div><div>(describes what?)</div>
Degeneration of the vertebral column (typically from osteoarthritis)<div><br></div><div>(describes what?)</div>What is <b>spondylosis?</b>
What causes symptoms in spondylosis?Narrowing between two adjacent vertebrae causes compression of nerve root<div><br></div><div>Compression of nerve root can cause radiculopathy (sensory & motor disturbances)</div><div><br></div><div>If in cervical spine, can cause narrowing of spinal canal, causing compression of the whole spinal cord --> global weakness, gait dysfunction, loss of balance and loss of bladder/bowel control </div>
What are risk factors for degenerative cervical spinal disease?- >40y/o<div>- FHx</div><div>- Hx of trauma or cervical surgery</div><div>- Prev. whiplash injury  </div>
How should degenerative cervical spine disease be investigated?Cervical spine MRI (if >4-6 weeks pain or neuro signs on examination)
What are complications of cervical spondylosis?- Radiculopathy (if compressing nerve root)<div>- Myelopathy (if narrowing of spinal canal, and causing compression of spinal cord)</div>
How does cervical myelopathy present?Narrowing of spinal cord at cervical level:<div>- LMN signs of upper limb: weakness, clumsiness, atrophy, hyporeflexia</div><div>- UMN signs of lower limb: Weakness, clumsiness, hyperreflexia</div><div>- Sensory deficits</div><div>- Bowel/bladder symptoms and sexual dysfunction</div>
How is radiculopathy managed?- NSAIDs<div>- Consider neuropathic agents (gabapentin/pregabalin) </div><div>- Physio</div><div><br></div><div>Surgery if persistent pain despite 6-12 weeks of conservative management </div>
"What is seen here?<div><img src=""paste-142e27a347c75ec79ec092edf0d9e7dd55b0f5e1.jpg""><br></div>"Gout:<div>- Rat bite erosions: punched out erosions with sclerotic and overhanging margins </div>
What test should be done before starting a patient on bisphosphonates?DEXA scan- NICE guidelines suggest DEXA should be done before <b>any </b>treatment that affects bone density 
What is the investigation of choice to confirm cauda equina syndrome?MRI of the whole spine 
When might dexamethasone have a role in spinal cord compression, or cauda equina syndrome?If due to cancer- dexamethasone can reduce the swelling and provide temporary improvement of symptoms before surgery
A child with a history of retinoblastoma presenting with bone pain is likely due to which bone malignancy?Osteosarcoma 
Which bone cancer presents with<b> sclerotic destruction </b>seen on x-ray<b>?</b>Osteosarcoma
What is the antibiotic of choice for a sickle cell patient with osteomyelitis?Most likely causative organism is salmonella → ciprofloxacin 
What is the standard antibiotic regimen for osteomyelitis?Usually caused by staph aureus:<div>- Flucloxacillin for 6 weeks (Give IV for 2-4 weeks, then followed by Oral Abx to finish the 6 weeks)</div><div><br></div><div>(If pen allergic, give clindamycin)</div>
What is the classification system for <b>open fractures</b>?Gustillo-Anderson <div><br></div><div>(is the classification system for what?)</div>
Gustillo-Anderson <div><br></div><div>(is the classification system for what?)</div>What is the classification system for <b>open fractures</b>?
How is the Gustilo-Anderson Classification graded?I= <1cm wound which is clean <div>II= ≥2cm wound which is relatively clean</div><div>III= Segmental fracture, or open fracture with extensive soft tissue injury</div><div><br></div><div>A= Adequate soft tissue</div><div>B= Bad soft tissue</div><div>C= Circulation issues</div>
What pathological processes occur in osteochondrosis?- Interruption of blood supply to epiphysis<div>- Bone and cartilage necrosis</div><div>- Revascularisation and regrowth of bone </div>
What is <b>Klenbock disease?</b>Osteochondrosis affecting the lunate bone <div><br></div><div>(describes what?)</div>
Osteochondrosis affecting the lunate bone <div><br></div><div>(describes what?)</div>What is <b>Klenbock disease?</b>
What is <b>Panners disease?</b>Osteochondrosis causing AVN of the ossific nucleus of the capitellum (of humerus)<div><br></div><div>(describes what)</div>
Osteochondrosis causing AVN of the ossific nucleus of the capitellum (of humerus)<div><br></div><div>(describes what)</div>What is <b>Panners disease?</b>
"What is <b>Kohler's disease?</b>"Osteochondrosis affecting the navicular bone<div><br></div><div>(describes what?)</div>
Osteochondrosis affecting the navicular bone<div><br></div><div>(describes what?)</div>"What is <b>Kohler's disease?</b>"
"What is <b>Freiberg's disease?</b>"Osteochondrosis of the metatarsals <div><br></div><div>(describes what?)</div>
Osteochondrosis of the metatarsals <div><br></div><div>(describes what?)</div>"What is <b>Freiberg's disease?</b>"
What tests are done to establish a diagnosis of Hepatitis C?"<font color=""#0000ff"">First line</font>: Anti-HCV antibodies<div><br></div><div>If Anti-HCV antibody positive, then do HCV RNA- to see if chronic infection (rather than immunity to cleared infection)</div><div><br></div><div>Do HCV-RNA first-line in immunocompromised</div>"
What investigation should be done in a child with confirmed Kawasaki disease?"- <font color=""#0000ff"">Echocardiogram</font>: Should be done to assess coronary artery aneurysms (a common and severe complication) "
"What is seen in this gallbladder?<div><img src=""paste-5e2ca00d89dce10c96e88224ab8c9f750a837398.jpg""><br></div>"Diffuse Cholesterolosis- change in gallbladder wall due to excess cholesterol
A breast lump with no tethering, pain or discharge in a young woman taking the oral contraceptive pill suggests <span class=cloze>[...]</span>A breast lump with no tethering, pain or discharge in a young woman taking the oral contraceptive pill suggests <span class=cloze>fibroadenoma</span><br> Benign breast tumour- typically in younger premenopausal women, and shrinks after menopause 
"Which drug used in the management of Crohn's disease can cause peripheral neuropathies?"<b>Metronidazole</b>
How do you decide whether an operation requires antibiotic prophylaxis?Use antibiotics in any:<div>- Clean operations involving prosthetics (heart valves, or joints)</div><div>- Clean-contaminated operation<br>- Contaminated operation</div><div><br></div>
"What is seen here?<div><img src=""barretts-oesophagus.jpg""><br></div>""Change from squamous to columnar epithelium- <b>Barrett's oesophagus</b><div><img src=""1-s2.0-S1357303919300453-gr1.jpg""><b><br></b></div><div><b><br></b></div>"
Which opioid is safer to use in patients with moderate to end-stage renal failure?Oxycodone (as mostly metabolised in the liver)<div><br></div><div>Remifentanyl or fentanyl also work well</div>
Which DMARD can cause severe adverse effects in patients with G6PD deficiency?Sulphasalazine:<div><br></div><div>Sulph- drugs can trigger haemolysis (sulphonamides, sulphasalazine, sulphonylureas)</div>
Where in the GI tract is Vitamin B12 absorbed?"Terminal ileum<div><img src=""paste-d398f49e46722f67581ae34b0653a4b3f6b048b9.jpg""><br></div><div><br></div>"
Where in the GI Tract is iron typically absorbed?"Duodenum<div><img src=""paste-d398f49e46722f67581ae34b0653a4b3f6b048b9.jpg""><br></div>"
Where in the GI tract is folate typically absorbed?"Jejunum<div><img src=""paste-d398f49e46722f67581ae34b0653a4b3f6b048b9.jpg""><br></div>"
What complications of haemochromatosis are reversible?- Cardiomyopathy<div>- Skin pigmentation</div>
<span class=cloze>[...]</span> fracture= Chauffeur fracture<br><span class=cloze>Hutchinson</span> fracture= Chauffeur fracture<br><br> Hutchinson fracture= <span class=cloze>[...]</span> fracture<br>Hutchinson fracture= <span class=cloze>Chauffeur</span> fracture<br><br> Where do <b>march </b>fractures frequently occur?Distal 1/3 of <b>m</b>etat<b>ar</b>sals- commonly in 2nd and 3rd metatarsal
What is a <b>march fracture?</b>Fracture in <b>m</b>etat<b>ar</b>sals due to recurrent stress- common in soldiers, but also those who walk/stand a lot
How is a march fracture managed?- Reduce movements for <b>6</b>-12 weeks
What is a <b>stress fracture?</b>Fracture of the bone caused by repeated stress over time 
What is the gold-standard investigation for <b>pancreatic cancer</b>?<b>Endoscopic ultrasound</b> (not CT)<div><br></div><div>- EUS allows staging of the cancer </div>
What investigations are done for <b>acute cholecystitis?</b><b>1st line: Abdominal USS</b><div><br></div><div>If diagnosis remains unclear, cholescintigraphy (HIDA scan) may be used </div>
What is the <b>Parkland formula</b> used for?Calculate the amount of fluid required for fluid resuscitation in patients with burns
What is the Parkland formula?Total fluid requirement in 24hrs (mL)= <div><br></div><div>4 x (total burn surface area [%]) x (body weight [kg])</div><div><br></div><div>With 50% given in first 8hrs, and remaining given in the next 16hrs</div>
"What is seen here?<div><img src=""S_0917_Hidradenitis_suppurativa_C0254591.width-320.jpg""><br></div>"Hidradenitis suppurativa- skin condition causing abscesses near hair follicles with sweat glands 
What is the definitive treatment of hidradenitis suppurativa?Wide local excision
What is the investigation of choice for suspected ischaemia to the<b> lower GI tract </b>(acute mesenteric ischaemia, chronic mesenteric ischaemia, ischaemic colitis)?<b>CT w/ contrast/</b> CT angiogram
What are the most sensitive and specific antibodies for coeliac disease?"<font color=""#0000ff"">Most sensitive</font>: anti tissue <b>transglutaminase</b><div><font color=""#0000ff"">Most specific</font>: <b>Anti-endomysial </b></div>"
A patient with ulcerative colitis has complains of lethargy over the last month. He normally passes a small amount of blood with his motions, which has not changed. <div><br></div><div>Hb 106; MCV 75; Ferritin 10</div><div><br></div><div>What is the most appropriate next step?</div>Iron deficiency anaemia: <b>urgent 2 week wait</b><div><b><br></b></div><div>UC increases the risk of bowel cancer</div>
According to the Rockall Score, which co-morbidites are associated with the worst prognosis? How is it scored?"<font color=""#0000ff"">3 points:</font><div>- Metastases</div><div><br></div><div><font color=""#0000ff"">2 pts:</font><br></div><div>- Renal failure</div><div>- Liver failure</div><div><br></div><div><font color=""#0000ff"">1pt:</font></div><div>- Heart failure</div><div>- Ischaemic heart disease</div>"
What conditions can cause toxic megacolon?- Ulcerative colitis<div>- <i>C difficile </i>infection</div>
How is <i>C difficile </i>infection established?Positive <i>C difficile </i>toxin in stool<div><br></div><div>(<i>C. diff </i>antigen positivity indicates exposure to the bacteria, not necessarily infection)</div>
A patient is admitted to receive IV antibiotics for a cellulitis. <div><br></div><div>She is incidentally found to be <i>C difficile</i> antigen positive. </div><div><br></div><div>What is the most appropriate response?</div>Antigen positivity does not indicate infection- only exposure to bacteria. <b>Do not need to treat. </b><div><b><br></b></div><div>Would probably want to avoid giving broad spectrum Abx for the cellulitis, but Flucloxacillin should be fine. </div><div><br></div><div>(<i>C. diff </i>infection typically only develops when broad spectrum Abx kill normal flora and allow <i>c diff </i>overgrowth. If antigen present, does not necessarily mean infection)</div>
What is the purpose of <b>rapid sequence induction?</b>In emergency intubations, when patient has not been NBM, important to intubate quickly to avoid aspiration 
How should thrombosed external haemorrhoids be managed?"<font color=""#0000ff"">If present within 72hrs:</font><br>- Referral to surgeons for excision<div><br></div><div><font color=""#0000ff"">If >72hrs:</font></div><div>- Stool softeners</div><div>- Ice packs</div><div>- Analgesia </div><div><br></div><div>Symptoms usually settle within 10 days</div>"
What is the most common cause of viral gastroenteritis?Norovirus
How does mesenteric adenitis present?Mimics appendicitis, typically occurs in younger children:<div>- Abdo pain, low grade fever</div><div>- Typically follows upper respiratory tract infection </div><div>- Children often present quite well, with no change in appetite </div>
How is a diagnosis of mesenteric adenitis made?Diagnosis of exclusion- <b>must rule out appendicitis</b><div><b><br></b></div><div>- US abdomen will show normal appendix, and enlarged mesenteric lymph nodes </div><div><br></div>
How is mesenteric adenitis managed?Reassure and safety net- mesenteric adenitis will resolve spontaneously
"What is seen here?<div><img src=""4067-Uveitis-642x361-anterior_uveitis_slide1.jpg""><br></div>"Anterior uveitis- inflammation of the middle layer of the eye (containing iris and ciliary body)
"What is seen here?<div><img src=""Episcleritiseye.jpg""><br></div>"Episcleritis- inflammation on the outermost layer of theeye 
Pseudomembranous white slough coating of the tongue with underlying erythema describes what?"Candida<div><br></div><div><img src=""CandidaUpdate_Header.jpg""><br></div>"
"What is seen here? How should it be managed?<div><img src=""paste-c4226bfbcca37b0715dc84ae7ec6336ac62d2056.jpg""><br></div>"Subconjunctival haemorrhages:<div><br></div><div>Typically resolve spontaneously in 2 weeks- reassure and safety net if no other presenting symptoms </div>
"What is a common CNS manifestation of <b>Whipple's disease?</b>"Oculomasticatory Myorhythmia: <div>- Eyes move side to side in pendualr motion</div><div>- Jaw clenches and relaxes in cycles</div><div><br></div><div>(describes a common manifestation in what infection?)</div>
Oculomasticatory Myorhythmia: <div>- Eyes move side to side in pendualr motion</div><div>- Jaw clenches and relaxes in cycles</div><div><br></div><div>(describes a common manifestation in what infection?)</div>"What is a common CNS manifestation of <b>Whipple's disease?</b>"
What is <b>Mikulicz syndrome?</b>"Variant of Sjogren's syndrome which also present with narrowing of the palpebral fissures (due to enlargement of the lacrimal glands)<div><br></div><div>(describes what?)</div>"
"Variant of Sjogren's syndrome which also present with narrowing of the palpebral fissures (due to enlargement of the lacrimal glands)<div><br></div><div>(describes what?)</div>"What is <b>Mikulicz syndrome?</b>
"What is <b>Reynold's pentad?</b>""Manifestation of ascending cholangitis:<div>- Charcot's triad (Fever, RUQ, Jaundice) + Confusion + Hypotension </div><div><br></div><div>(describes what?)</div>"
"Manifestation of ascending cholangitis:<div>- Charcot's triad (Fever, RUQ, Jaundice) + Confusion + Hypotension </div><div><br></div><div>(describes what?)</div>""What is <b>Reynold's pentad?</b>"
What is the oncological marker used for <b>testicular cancers</b>?β-HCG<div><br></div><div>(can be used as a cancer marker for which cancers?)</div>
β-HCG<div><br></div><div>(can be used as a cancer marker for which cancers?)</div>What is the oncological marker used for <b>testicular cancers</b>?
What are risk factors for biliary colic?"- 5Fs: Fat, fertile, forty, fair female<div>- Diabetes mellitus</div><div>- Crohn's disease</div><div>- Rapid weight loss e.g. weight reduction surgery</div><div>- Drugs: Fibrates, COCP</div>"
What drugs are typically given for Rapid-Sequence Induction?- Thiopentone (though do not give if low bp- causes dramatic hypotension)<div>- Suxamethonium</div>
What is the normal range for Mean Arterial Pressure?70-100<div><br></div><div>(Anything below 70 suggests shock)</div>
"What initial test should you do in a patient with suspected Gilbert's syndrome?"Conjugated/unconjugated bilirubin levels 
How does CO<sub>2</sub> pneumoperitoneum present?Iritation of the diaphragm --> pain which can radiate towards the shoulder 
Which operations tend to have an increased risk of PE?Orthopaedic surgeries- as pt is usually immobile before the surgery too. <div><br></div><div>If elective surgeries, patients are usually fit and well, so ↓risk of PE </div>
When intubating, what device can be used to assess correct placement?End-tidal CO<sub>2</sub> Capnograph: measure CO<sub>2</sub> levels <div><br></div>
"You observe an intubation of patient for an elective surgery. The CO<sub>2</sub> capnograph readings are shown below. What has likely happened?<div><img src=""paste-77cd31d0d7450048d95287d4d3bba1eab9f0029a.jpg""><br></div>"Oesophageal intubation- decreasing CO<sub>2</sub> levels suggest endotracheal tube is not in the trachea, but incorrectly placed in the oesophagus 
What is the most common cause of small bowel obstruction in a patient who has had no PMHx or surgery?Spontaneous adhesions (can occur with age- so if no Surgical Hx, do not rule out!)
A patient who has recently received PCI for an MI is due for an elective hernia repair. What is the appropriate response?Cancel elective operation- <div><br></div><div>Pts with drug-eluting stents (and most stents) should have operations delayed until at least 6months after stent insertion </div><div><br></div><div>Pts with bare metal stents should have for at least 2 months</div>
Should doctors continue/withold NSAIDs before an operation?Stop 7 days before operation (like with aspirin & anti-platelets)<div><br></div><div>Reduces the risk of excessive bleeding </div>
What criteria must be met for a pt to qualify for bariatric surgery?<div><b>All following criteria must be met:</b></div><div><br></div>1. BMI ≥ 40 (or ≥35 if c-morbidities would improve with ↓weight)<div>2. Failure of non-surgical management to achieve and maintain clinically beneficial weight loss for 6 months</div><div>3. Fitness for surgery & anaesthesia</div><div>4. Receive intensive management in tier 3 service (guidance on diet, activity nad psychosocial conerns)</div><div>5. Pt must be well informed and motivated</div>
When should bariatric surgery be considered first-line management of obesity?- BMI ≥50<div>- Newly diagnosed T2DM with BMI≥30</div>
What are the Billroth procedures used for?Used for partial gastrectomy in gastric cancers<div><br></div><div>(Not for bariatric surgery)</div>
What are the different methods of bariatric surgery?- Laparoscopic adjustable gastric banding<div>- Sleeve gastrectomy</div><div>- Roux-en-Y Gastric bypass</div>
How does gastric banding work?"Adjustible silicon band placed around top of stomach, creating a smaller pre-stomach pouch. <div><br></div><div>This will be filled earlier and send satiation signals (GLP-1) earlier, reducing appetite</div><div><br></div><div><img src=""0axzB4zFp_YRqcvi5ner5nxsCNbKFpGHDFLAf21CFzohwZF9F1zwiIsRrUz9Ke-d5Vp8CAQj-AEtn11oE6-T0YWdk8zbGRDm7XrWcGinW_ZmwE4belAFKXM.jpg""><br></div>"
What is done in a sleeve gastrectomy?"Division of stomach vertically, reducing it in size by around 75%. Pyloric valve left intact, so function unchanged. <div><br></div><div>Leaves smaller stomach, so earlier satiety signals and reduced appetite</div><div><br></div><div><img src=""paste-b97c83832bd501e98929b13999aebb45901bdb4c.jpg""><br></div>"
What is done in a Roux-en-Y gastric bypass?"Portion of jejunum attached to small stomach pouch, allowing food to bypass stomach, duodenum and proximal jejunum. <div><br></div><div>Means less nutrients are absorbed → lower calories ingested (but also causes malnutrition)</div><div><br></div><div><img src=""paste-a50695a9f400a8c0090dccfa5f86391bb9cd2f34.jpg""><br></div>"
Which method of bariatric surgery has the biggest effect on weight loss? Which has the most severe side effects?Roux-en-Y bypass (for both):<div><br></div><div>- Mean 5 year weight loss is 62.8%</div><div>- Because bypassing most of stomach and duodenum, malnutrition and malabsorption</div>
When should patients be 2WWed for pancreatic cancer?- If >40y/o and have jaundice 
When should pts be 2WWed for anal cancer?- Unexplained anal mass<div>- Unexplained anal ulceration </div>
What is the recommend VTE prophylaxis for pts undergoing elective hip replacements?- TED stockings<div>- LMWH started 6hrs after surgery (for 10 days and then 28 days of aspirin; or 28days of LMWH and TED)</div>
What occurs in suxamethonium apnoea?- Lack of acetylcholinesterase to break down suxamethonium --> prolonged paralysis<div>- Pts make no respiratory effort after being extubated and required intubation and ventilation until effects where off</div>
What is the definitive investigation of bowel obstruction?<b>CT abdo</b>: will show the site where obstruction begins, and can detect cause<div><br></div><div>(AXR first-line but not definitive)</div>
Which bone tumours present as a radiolucent lesion?"Giant cell tumour- 'soap bubble' appearance<div><br></div><div><img src=""a00080f04.jpg""><br></div>"
What is the VTE prophylaxis for an elective knee operation?- Aspirin for 14 days<div>or</div><div>- LMWH for 14 days + TED stockings</div><div>or </div><div>- Rivoraban for 14 days</div>
What is the VTE prophylaxis for pts with fractures of the pelvis, hip or proximal femur?VTE prophylaxis for a month, using LMWH (6-12hrs after surgery) or fondaparinux 
In the conservative management of haemorrhoids, which is the most important component in terms of resolution?Fibre supplementation<div><br></div><div>(shown to be as effective as injection sclerotherapy in some studies)</div>
What is the consideration for anaesthesia in Myasthenia Gravis pts?Pts are very sensitive to Non-depolarising agents (rocuronium); and resistant to depolarising agents (suxamethonium)<div><br></div><div>- Avoid using neuromusclar blocking agents if possible, but if used, reverse with sugammadex rather than neostigmine </div>
"What is <b>Boas' sign?</b>"Hyperaesthesia beneath right scapula in acute cholecystitis (due to referred pain)<div><br></div><div>(is described by which eponymous sign?)</div>
Hyperaesthesia beneath right scapula in acute cholecystitis (due to referred pain)<div><br></div><div>(is described by which eponymous sign?)</div>"What is <b>Boas' sign?</b>"
What induction agent is useful in haemodynamically unstable patients?Ketamine- does not drop blood pressure 
How should infected surgical wounds be managed?"<font color=""#0000ff"">If mild (erythema, no fever):</font><div>- Analgesia</div><div>- Reuglar wound dressing</div><div>- Oral Abx</div><div><br></div><div><font color=""#0000ff"">If severe (discharge, fever, evidence of abscess):</font></div><div>- Wound swabs</div><div>- Removal of sutures, washout wound, <b>leave wound to heal by 2° intention</b></div><div>- IV Abx</div>"
What is the most accurate test for Zollinger-Ellison syndrome?Secretin stimulation test <div><br></div><div>(most accurate imaging is somatostatin receptor scintigraphy)</div>
What is the antibiotic regimen for a pt undergoing laparoscopic appendectomy?IV antibiotics for 24hrs:<div><br></div><div>1 dose before surgery, 2 doses every 8hrs post surgery</div>
What is the most appropriate investigation for a pt presenting with a non-tender lump in the RUQ and with scleral icterus?Suspect pancreatic cancer:<br>- USS Abdomen <div><br></div><div>(CA-19-9 associated, but non-specific; use it as a response to treatmnet rather than a diagnostic marker)</div>
<span class=cloze>[...]</span> tend to present with painless PR bleeding whereas <span class=cloze>[...]</span> tend to present with painful PR bleeding<br><span class=cloze>Haemorrhoids</span> tend to present with painless PR bleeding whereas <span class=cloze>anal fissures</span> tend to present with painful PR bleeding<br><br> Haemorrhoids only painful when thrombosed
Haemorrhoids tend to present with <span class=cloze>[...]</span> PR bleeding whereas anal fissures tend to present with <span class=cloze>[...]</span> PR bleeding<br>Haemorrhoids tend to present with <span class=cloze>painless</span> PR bleeding whereas anal fissures tend to present with <span class=cloze>painful</span> PR bleeding<br><br> Haemorrhoids only painful when thrombosed
Which area in the GI tract is most commonly affected in colorectal cancers?Rectum (50%)
What drug can worsen psoriatic lesions?Beta-blockers
What tests should be done before starting a patient on long-term steroids (e.g. for PMR)?- Random blood glucose<div>- HbA1C</div><div>- DEXA scan</div><div><br></div><div>(note with GCA, this is an emergency, so will not be able to do a full work-up before starting treatment)</div>
What is used to treat dermatitis herpetiformis (typically seen in ceoliac disease)?- Gluten free diet<div>- Dapsone </div>
"Ulcers can appear in both Crohn's disease and Reactive arthritis. How might you differentiate between them?""<b>Crohn's disease</b>: typically painful ulcers<div><b>Reactive arthritis</b>: Less common feature, but if present usually painless</div>"
A patient having undergone two courses of <i>H pylori </i>eradication therapy is found to have a positive urea breath test. <div><br></div><div>What is the most appropriate management?</div>Refer to gastroenterologist- if 2 courses of H pylori eradication unsuccessful
When should patients be 2WW referred for an upper OGD?"<font color=""#0000ff"">At any age:</font><br>- Dysphagia<div><br></div><div><font color=""#0000ff"">55y/o presenting with weight loss AND:</font></div><div>- Upper abdo pain, or reflux, or dyspepsia</div><div>- Upper abdominal mass consistent with stomach cancer</div><div><br></div><div>(note ALARMS symptoms no longer used)</div>"
When should patients receive a non-urgent (within 6 weeks) OGD?"<font color=""#0000ff"">At any age:</font><br>- Haematemesis<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Aged 55 and over with:</font></div><div>- Treatment resistant dyspepsia</div><div>- Upper abdo pain and low Hb</div><div>- Raised platelet count AND one of [Nausea, vomiting, reflux, weight loss, dyspepsia, epigastric pain]</div><div>- Nausea/vomiting AND one of [Weight loss, reflux, dyspepsia, epigastric pain] </div>"
What is <b>ankylosis?</b>Fusion of bones, causing stiffening and immobility of a joint <div><br></div><div>(describes what?)</div>
Fusion of bones, causing stiffening and immobility of a joint <div><br></div><div>(describes what?)</div>What is <b>ankylosis?</b>
"How does Buerger's disease present?"Presents as acutely ischaemic limb, without background of peripheral claudication 
What tests should be done in a woman with suspected ovarian cancer in GP?"<div><font color=""#0000ff"">Usually:</font></div><div>- CA 125, if raised order USS Abdo Pelvis</div><div><br></div><div><font color=""#0000ff"">If presenting with ascites or abdominal mass:</font><br>- Refer urgently to 2° care, for USS Pelvis </div>"
How should wound dehisence be managed?Apply sterile wet guaze, and suture in theatre<div><br></div><div>(Wet gauze protects abdo content, and suturing should be done in sterile environment)</div>
What tests should be done in the investigation of Coeliac Disease?"<font color=""#0000ff"">First line:</font><br>- IgA TTG and IgA levels<div><br></div><div><font color=""#0000ff"">If found to be IgA deficient:</font></div><div>- IgG TTG levels (or IgG DGP)</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">True negative serology</font>= Do not have coeliac disease (but may develop)</div><div><font color=""#0000ff"">Positive serology</font>= Refer to gastroenterology for endoscopy and intestinal biopsy to confirm</div>"
What is a common side effect following treatment of giardiasis?Lactose intolerance- up to 6 weeks following treatment. <div><br></div><div>Advise to avoid milk-containing products</div>
What are the different options in the non pharmacological management of achalasia? Which is preferred in which scenario?"<font color=""#0000ff"">Heller's cardiomyotomy:</font><div>- If fit for surgery </div><div><br></div><div><font color=""#0000ff"">Endoscopic balloon dilatation:</font></div><div>- Older, unfit patients </div>"
What is <b>osteomyelitis?</b>Infection of the bone 
What is a typical finding of osteomyelitis on X-ray?- Periosteal reaction<div>- Focal cortical loss</div><div>- Regional osteopenia</div>
What are risk factors for gastric adenocarcinomas?- Smoking<div>- Pernicious anaemia</div><div>- <i>H. pylori </i>infection</div><div>- High alcohol intake</div><div>- Blood group A </div><div>- Dietary nitrosamines (found in smoked foods)</div>
How is <b>lupus nephritis </b>managed?- Corticosteroids<div>- Cyclophosphamide (tacrolimus or mycophenalate are alternatives)</div>
How should peptic ulcer disease be managed?"If <i>H. pylori</i> <b>positive</b>: Triple therapy w/ amoxicillin, clarithromycin and omeprazole<div><br></div><div>If <i>H. pylori </i><b>negative</b>: 4-8 weeks of full dose PPI treatment + lifestyle advice</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">Should have repeat endoscopy 6-8 weeks after start of treatment to ensure ulcer healing + rule out malignancy</font></div>"
How does <b>Familial Mediterranean Fever present?</b>- Fever<div>- Painful serositis (pain in abdomen [peritoneum] chest [pleura])</div><div>- Erysipelas-like rash</div>
How should changes in DAS scores be interpreted (in response to therapy)?"Change of :<div><br></div><div><font color=""#0000ff""><0.7</font>: No response to current therapy</div><div><font color=""#0000ff"">0.7-1.2</font>: Moderate reponse </div><div><font color=""#0000ff"">>1.2:</font> Good response to therapy</div><div><br></div>"
What should you advise SLE pts to try and avoid to reduce the risk of flare-ups?- Sunlight<div>- Oral contraceptive pill</div><div>- Infections</div><div>- Stress</div>
How does <b>cerebral lupus </b>present?- Seizures<div>- Psychosis</div><div>- Severe unremitting headaches</div>
How should cerebral lupus be managed?- High dose steroids<div>- Immunosuppression (cyclophosphamide)</div>
When is an oral bisphosphonate contraindicated?"- Abnormalities of oesophagus (e.g. varices, Barrett's etc)<div>- Factors which delay emptying (e.g. stricture/achalasia)</div><div>- Hypocalcaemia</div>"
What antibiotic is given for osteomyelitis in penicillin allergic patients?Clindamycin
"What is seen here?<div><img src=""521326050b39fa4105321d841c4489_jumbo.jpg""><br></div>""Prostate cancer metastases- causing sclerotic bone metastases<div><br></div><div>(Could also be Paget's disease but this is less common)</div>"
Aside from a neurological examination, what bedside investigation can be done in a patient with suspected cauda equina syndrome?PR- in cauda equina, may find poor anal tone
What is the most common type of ankle fracture?Weber B- at level of syndesmosis 
A positive finding on <span class=cloze>[...]</span> suggests damage to the ACL"A positive finding on <span class=cloze>Lachman's test</span> suggests damage to the ACL<br> Lachman test more accurate diagnostically than anterior drawer test- as positioning of knee prevents quadriceps from acting and giving a false negative <div><br></div><div><img src=""JFP06703130_f2.JPG""><br></div>"
"A positive finding on Lachman's test suggests damage to the <span class=cloze>[...]</span>""A positive finding on Lachman's test suggests damage to the <span class=cloze>ACL</span><br> Lachman test more accurate diagnostically than anterior drawer test- as positioning of knee prevents quadriceps from acting and giving a false negative <div><br></div><div><img src=""JFP06703130_f2.JPG""><br></div>"
What ligament is typically damaged in an inversion injury of the ankle?Anterior tibiofibular ligament
How should Perthes disease be managed?"<div>- Casts, braces to keep femoral head within acetabulum</div><div><br></div><font color=""#0000ff"">If younger child:</font><br>- Physio and observation<div><br></div><div><font color=""#0000ff"">If older child:</font><br>- Surgery- osteotomy to keep femoral head snug within the acetabulum</div>"
What investigation can be done to confirm colovesical fistulas?Cytoscopy/ cystography
Rheumatological conditions:<div><br></div><div><span class=cloze>[...]</span> presents as muscle pain with no weakness whereas <span class=cloze>[...]</span> presents as muscle pain and weakness<br></div>Rheumatological conditions:<div><br></div><div><span class=cloze>Polymyalgia rheumatica</span> presents as muscle pain with no weakness whereas <span class=cloze>Polymyositis</span> presents as muscle pain and weakness<br></div><br> Rheumatological conditions:<div><br></div><div>Polymyalgia rheumatica presents as <span class=cloze>[...]</span> whereas Polymyositis presents as <span class=cloze>[...]</span><br></div>Rheumatological conditions:<div><br></div><div>Polymyalgia rheumatica presents as <span class=cloze>muscle pain with no weakness</span> whereas Polymyositis presents as <span class=cloze>muscle pain and weakness</span><br></div><br> What can frequently cause painless rectal bleeding in children? What test would confirm it?"Meckel's diverticulum <div><br></div><div>99 Technetium scan </div>"
"In a patient with Crohn's if there is suspected small bowel involvement, what investigation should be done?"MRI small bowel <div><br></div><div>(OGD will not reach small bowel, so MRI is necessary)</div>
What are risk factors for gallbladder carcinoma?- Smoking<div>- Obesity</div><div>- PSC</div><div>- UC (due to association with PSC)<br>- Oestrogens </div>
What is the best investigation for a suspected gallbladder carcinoma?ERCP- allows visualisation of mass and can obtain biopsies
What molecule is responsible for paracetamol toxicity?N-acetyl-p-benzo-quinone (NAPQI)
A 67 year old man complains of pins and needles in his toe. His only past medical history is a gastrectomy 3 years ago. <div><br></div><div>What is the definitive management of this?</div>IM hydroxycobalamin (B12 deficiency following gastrectomy)
What is the most common eye symptom in Rheumatoid Arthritis?"<b>Kerato conjunctivitis sicca</b><div><br></div><div><b>Dryness</b> of conjunctiva and cornea- leaving it inflamed </div><div><br></div><div><img src=""paste-8ef8beeafd462b7d472ff5e0fe9190efc443860a.jpg""><br></div>"
If you are converting a patient on 20mg of prednisolone OD to IV hydrocortisone before an operation, how much should you givePrednisolone = 4 x Hydrocortisone<div><br></div><div>Need 80mg Hydrocortisone across the day (20mg IV QDS)</div>
If you are converting someone on 10mg morphine onto diamorphine, how much should you give?Morphine = 3 X diamorphine<div><br></div><div>30mg diamorphine </div>
Which coagulation factors are low in liver failure?II, VII, IX and X (2,7,9,10)(same as targeted by warfarin)<div><br></div><div>(weirdly factor VIII is increased in liver failure)<br></div>
Where should intramuscular injections be placed in the gluteal muscle?Superolateral quadrant (upper and outer)
Which electrolyte abnormality is common in a patient with a high output from their stoma?Hypokalaemia 
Which IBD is more associated with abscess formation?"Crohn's disease "
What is required for diagnosis of <b>auto-immune hepatitis?</b>Liver biopsy: will show<b> interface hepatitis </b>(aka piecemeal necrosis)
"A liver biopsy demonstrating hepatocytes containing Mallory's hyaline suggests what cause of cirrhosis?"Alcoholic (Mallory body)
How is auto-immune hepatitis managed?"<font color=""#0000ff"">If non-severe</font>: Corticosteroids<div><br></div><div><font color=""#0000ff"">If severe, or not responding</font>: Corticosteroids + immunosuppressant (azathioprine, mercaptopurine)</div><div><br></div><div><font color=""#0000ff"">If decompensated liver disease</font>: transplantation</div>"
What are the three stages of liver damage in alcoholic liver disease?1. Steatosis (fatty liver)<div>2. Alcoholic hepatitis (inflammation and necrosis)</div><div>3. Alcoholic cirrhosis (irreversible structural damage)</div>
What is the first-line diagnostic test for Hepatitis A?HAV IgM<div><br></div><div>(Unlike in Hep B, where you look for HBsAg in a full profile, with all other viral hepatitis (Hep A, C, D and E) you look for IgM against the virus)</div>
If USS of a pt with jaundice reveals mechanical obstruction, what imaging should be ordered to confirm?"<font color=""#0000ff"">If suspected gallstones:</font><div>- MRCP (will not show up well on CT)</div><div><br></div><div><span style=""color: rgb(0, 0, 255);"">If suspected biliary/pancreatic malignancy:</span><br></div><div>- CT</div><div>(though gold-standard for these would be ERCP/EUS respectively)</div>"
How should haemochromatosis be managed if the pt is asymptomatic (i.e. C282Y positive, but not displaying symptoms)?- Observation- 3 yearly follow up<div>- Lifestyle modifications: Avoid iron or iron-containing supplements. Avoid Vit C (as can increase absorption of iron). </div><div>- Hep and Hep B vaccination</div>
What causes increased iron levels in haemochromatosis?Genetic mutation (C282Y, H63D) → decreased <b>hepcidin </b>expression<div><br></div><div>Hepcidin usually acts to decrease iron absorption → in haemochromatosis, excessive duodenal absorption of iron </div>
When should NAC be given in paracetamol overdose <b>without measuring paracetamol levels at 4hrs?</b>- If staggered overdose (taken across >1hr)<div>- If doubt over time of paracetamol ingestion</div><div><br></div><div>You would start them immediately, and then measure paracetamol level at 4hrs (could then consider stopping the infusion)</div>
When should a pt with paracetamol toxicity be treated with liver transplant?"King's College Criteria- if after 24hr:<div>- Arterial pH <7.3</div><div><br></div><div>OR</div><div><br></div><div>- Grade III/IV encephalopathy; INR >6.5 (PT>100secs); Creatinine >300</div>"
<span class=cloze>[...]</span> seen on liver biopsy suggest Hepatitis B infection<span class=cloze>Ground-glass changes</span> seen on liver biopsy suggest Hepatitis B infection<br> Ground-glass changes seen on liver biopsy suggest <span class=cloze>[...]</span>Ground-glass changes seen on liver biopsy suggest <span class=cloze>Hepatitis B infection</span><br> <span class=cloze>[...]</span> seen on liver biopsy suggest Primary Biliary Cholangitis<span class=cloze>Granulomas</span> seen on liver biopsy suggest Primary Biliary Cholangitis<br> Granulomas seen on liver biopsy suggest <span class=cloze>[...]</span>Granulomas seen on liver biopsy suggest <span class=cloze>Primary Biliary Cholangitis</span><br> <span class=cloze>[...]</span> seen on liver biopsy suggest Primary Sclerosing Cholangitis<span class=cloze>Fibro-obliterative scarring of biliary tree</span> seen on liver biopsy suggest Primary Sclerosing Cholangitis<br> Fibro-obliterative scarring of biliary tree seen on liver biopsy suggest <span class=cloze>[...]</span>Fibro-obliterative scarring of biliary tree seen on liver biopsy suggest <span class=cloze>Primary Sclerosing Cholangitis</span><br> <span class=cloze>[...]</span> seen on liver biopsy suggest Drug-induced liver failure<span class=cloze>Eosinophilic deposits</span> seen on liver biopsy suggest Drug-induced liver failure<br> Eosinophilic deposits seen on liver biopsy suggest <span class=cloze>[...]</span>Eosinophilic deposits seen on liver biopsy suggest <span class=cloze>Drug-induced liver failure</span><br> "<span class=cloze>[...]</span> seen on liver biopsy suggest Cirrhosis (typically alcoholic, but also in PBC, HCC, Wilson's)""<span class=cloze>Eosinophilic twisted rope inclusion</span> seen on liver biopsy suggest Cirrhosis (typically alcoholic, but also in PBC, HCC, Wilson's)<br> Mallory body "
Eosinophilic twisted rope inclusion seen on liver biopsy suggest <span class=cloze>[...]</span>"Eosinophilic twisted rope inclusion seen on liver biopsy suggest <span class=cloze>Cirrhosis (typically alcoholic, but also in PBC, HCC, Wilson's)</span><br> Mallory body "
<span class=cloze>[...]</span> seen on liver biopsy suggest viral hepatitis<span class=cloze>Councilman body</span> seen on liver biopsy suggest viral hepatitis<br> Eosinophilic globule in cytoplasm of hepatocyte undergoing apoptosis
Councilman body seen on liver biopsy suggest <span class=cloze>[...]</span>Councilman body seen on liver biopsy suggest <span class=cloze>viral hepatitis</span><br> Eosinophilic globule in cytoplasm of hepatocyte undergoing apoptosis
<span class=cloze>[...]</span> seen on liver biopsy suggest hepatocyte enlargement in cholestasis<span class=cloze>Feathery degeneration</span> seen on liver biopsy suggest hepatocyte enlargement in cholestasis<br> Feathery degeneration seen on liver biopsy suggest <span class=cloze>[...]</span>Feathery degeneration seen on liver biopsy suggest <span class=cloze>hepatocyte enlargement in cholestasis</span><br> What investigations can be done for GORD?"First- try lifestyle changes, antacids and PPI in primary care. If dyspepsia not resolved:<div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">1st line</font>: OGD (can diagnose but not exclude)</div><div><font color=""#0000ff"">2nd line</font>: If OGD inconclusive but still clinical suspicion: <b>oesophageal manometry</b> (gold standard)</div>"
"How should Barrett's Oesophagus be managed if dysplasia is seen on endoscopic assessment?"<b>Low-grade dysplasia:</b><div>- Repeat in 6 months. If confirmed, treat.</div><div><br></div><div><b>High-grade dysplasia or cancer:</b><br>- Offer treatment</div><div><b><br></b></div><div><b>Treatment options:</b></div><div>- Endoscopic resection</div><div>- Radiofrequency ablation</div>
How is colorectal cancer managed according to the Dukes staging?"<font color=""#0000ff"">If A-C:</font><div>- Surgical resection +/- post-op chemo (particularly if lymph nodes are involved)</div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If D (metastasis):</font></div><div>- Surgical resection but, neoadjuvant chemo may be used. </div>"
How is GORD managed?"<font color=""#0000ff"">If OGD not been done- treat as dyspepsia:</font><div>1. Review medications for possible causes of dyspepsia</div><div>2. Lifestyle advice</div><div>3. Trial of full-dose PPI for one month OR test and treat for <i>H. pylori</i></div><div><font color=""#0000ff""><br></font></div><div><font color=""#0000ff"">If endoscopy reveals oesophagitis:</font></div><div>- Full dose PPI for 1-2 months</div><div>- If response, low dose PPI PRN; if no response, double-dose PPI for 1 month</div><div><br></div><div><font color=""#0000ff"">If endoscopy does not reveal oesophagitis/reflux disease</font></div><div>- Full dose PPI for 1 month</div><div>- If response, low dose PPI PRN; if no response try H<sub>2</sub> antagonist or prokinetic for one month</div><div><br></div><div><br></div>"
What is the first-line test for <i>H. pylori</i> infection?- Urea breath test<div>- H pylori stool test </div>
Which type of oesophageal cancer is most common?"<font color=""#0000ff"">Adenocarcinoma in developed countries</font><div><br></div><div>Squamous cell in developing countries</div>"
Where do colorectal cancers most commonly metastasise to?Liver <div><br></div><div>(due to portal circulation from the GI tract)</div>
How should anterior uveitis be managed?- Urgent review by opthalmology<div>- Cycloplegics (dilates pupil to relieve pain and photophobia) e.g. atropine </div><div>- Steroid eye drops</div>
How cna you tell if a stoma is temporary or permanent?Temporary stomas will have two lumen at the surface (as you aim to anastomose these lumen together afterwards)
A spouted loop suggests an <span class=cloze>[...]</span>stomy A spouted loop suggests an <span class=cloze>ileo</span>stomy <br> As contents of ileum can irritate skin, must be spouted off the surface of the skin) 
What monitoring should be done in patients with cirrhosis (or chronic HBV/HCV infection)?Every 6 months:<br>- AFP <div>- Abdo USS</div><div><br></div><div>(to assess for Hepatocellular carcinoma)</div>
What anti-emetic is indicated in bowel obstruction?Cyclizine<div><br></div><div>(not metoclopramide as this is a pro-kinetic → increased risk of bowel rupture)</div>
"A pt due for an elective hip replacement is discovered undergoes a routine ECG in his pre-op assessment. <div><br>What is the most appropriate action?</div><div><br></div><div><img src=""ECG-Strip-3rd-degree-AV-Block-Complete-heart-block-CHB.jpg""><br></div>"3rd degree heart block. <div><br></div><div>Cancel operation- and refer pt for pacing </div>
Blood pressure should be below <span class=cloze>[...]</span> for elective operations Blood pressure should be below <span class=cloze>180/110</span> for elective operations <br> If too high, cancel operation and optimise antihypertensive medication 
If a new dysrhythmia is discovered from pre-operative screening, what should be done?If elective operation:<div>- Delay surgery</div><div>- Fully investigate arrhythmia. </div><div><br></div><div>If AF: If well rate-controlled, accetpable</div><div>Other arrhythmias need careful consideration</div>
Which method of airway maintenance prevents aspiration of gastric contents?Endotracheal tube<div><br></div><div>(LMA does not definitively prevent aspiration)</div>
When can opioids be prescribed IV?- Highly monitored environment (ITU, recovery)<div>- Via PCA</div>
What is the shortest amount of time that should be given between paracetamol doses?4hrs
What <b>one </b>thing must be done before EVERY operation"Conduct the WHO checklist sign in<div><br></div><div>(Consent not needed if emergency treatment, as is checking pt's name DOB etc- which is covered by WHO Checklist anyway)</div>"
If starting a pt on allopurinol, how long after the acute attack of gout should you start?2 weeks after acute attack
What symptoms are associated with solitary rectal ulcer syndrome?- Chronic constipation <div>- Straining </div>
How can solitary rectal ulcer syndrome be differentiated from colorectal malignancies?Biopsy: fibromuscular obliteration seen in rectal ulcers
A man undergoes surgery to remove a colonic tumour. The surgeon resects the tumour entirely and forms an anastomosis, but wants to protect it. <div><br></div><div>What is the most appropriate stoma to create which will allow this, whilst being easiest to reverse in the future?</div>Loop <b>ileostomy</b><div><b><br></b></div><div>(do the small bowel, as it is easier to mobilise and heals better; ileostomy will divert bowel contents away from entire colon)</div><div><br></div><div>[loop colostomies very rarely done]</div>
What is the surgical management of fulminant UC (e.g. toxic megacolon)?Sub total colectomy <div><br></div><div>(leave rectum in situ, as resection of rectum in acutely unwell pts has high risk of complications)</div>
What is a <b>proctectomy?</b>"Removal of whole rectum <div><img src=""Proctectomy-and-abdominal-perineal-resection-C-2005-Terese-Winslow-US-Govt-has.png""><br></div>"
"How should severe rectal Crohn's be surgically managed?"Proctectomy 
What surgical management should be given to a patient with UC where medical management is unsuccessful?Panproctocolectomy (+/- ileoanal pouch)
What can predispose patients to ureteric stones?Dehydration (e.g. Hx of vomiting and diarrhoea)
"What is seen here on liver biopsy?<div><img src=""1200px-Ground_glass_hepatocytes_high_mag_cropped_2.jpg""><br></div>"Ground glass changes to cytoplasm of hepatocytes --> <b>hepatitis B infection </b>
What is normal PSA levels?"<font color=""#0000ff"">50-59y/o</font>: 3.0<div><font color=""#0000ff"">60-69y/o</font>: 4.0</div><div><font color=""#0000ff"">>70y/o</font>: 5.0</div><div><br></div><div>(Age -20, then divide by 10)</div>"
What can raise PSA levels?- Prostate cancer<div>- BPH </div><div>- Prostatis & UTI (delay PSA measuremnet until 1 month after)</div><div>- Ejaculation + vigorous exercise (not in previous 48hrs of measuring)</div><div>- Urinary retention</div><div>- Instrumentation of urinary tract</div>
<span class=cloze>[...]</span> resection is done on rectal tumours <8cm from the anal canal<br><span class=cloze>Abdominoperineal</span> resection is done on rectal tumours <8cm from the anal canal<br><br> Abdominoperineal resection is done on rectal tumours <span class=cloze>[...]</span> from the anal canal<br>Abdominoperineal resection is done on rectal tumours <span class=cloze><8cm</span> from the anal canal<br><br> How can you differentiate between the common eye complications in Rheumatoid arthritis by symptoms?"<font color=""#0000ff""><b>Kerato</b>conjunctivitis sicca</font>: Dry, <b>gritty</b><div><font color=""#0000ff"">Scleritis</font>: Painful</div><div><font color=""#0000ff""><b>Epi</b>scleritis</font>: <b>Not</b> painful</div>"
What is a <b>compound fracture?</b>Same as an <b>open</b> fracture- fracture where there is an open wound or break in skin near site of broken bone 
Yankauer sucker- useful to clear secretions which might otherwise block the airway"What is this?<div><img src=""51uz+WRPd0L._SL1500_.jpg""><br></div>"
<u>Liver function tests</u><br><br>-LFTs help distinguish between hepatocellular injury (hepatic injury) and cholestasis (post hepatic obstructive jaundice)<br>-ALT alanine transaminase<br>-AST aspartate transaminase<br>-ALP alkaline phosphatase<br>-GGT gamma glutamyl transferase<br><br>-ALT, AST, ALP, GGT help differentiate hepatocellular damage & cholestasis<br>-Bilirubin, albumin, PT (prothromin time) are used to assess the livers synthetic function<br><br>-<b>ALT</b> has high conc in hepatocytes & enters blood in <b>hepatocellular injury</b><br>-<b>ALP </b>has high conc in liver, bile duct, bone. ALP is often raised in liver pathology idue to increased synthesis in <b>response to cholestasis</b><br><br>-10 fold increase in <b>ALT </b>suggests <b>hepatocellular injury</b><br>-3 fold increase in<b> AST</b> suggests <b>cholestasis </b><br>-Raised <b>GGT </b>can suggest <b>biliary epithelial damage</b> & <b>bile flow obstruction </b>(also raised in response to alcohol & antiepileptic phenytoin)<br><br>-<b>High GGT w high ALP </b>suggests cholestasis BUT high ALP alone suggests non hepatobiliary pathology (because ALP also made in bone)<br>-Raised ALP could also suggest VitD deficiency, bone fractures, bony metastases<br><br>-If patient is jaundiced but ALT & ALP are normal, bilirubin increase could be due to haemolysis (pre hepatic)<br><br>Liver function<br>-<b>conjugation & elimination</b> of bilirubin<br>-<b>albumin </b>synthesis<br>-<b>clotting factor</b> synthesis<br>-<b>gluconeogenesis</b><br><br>Liver function investigations<br>-serum bilirubin<br>-serum albumin<br>-PT<br>-ALT/AST ratio<br>-Serum blood glucose<br><br>-conjugated bilirubin passes into urine as urobilinogen & causes dark urine<br>-unconjugated bilirubin does not affect urine, but body will turn yellow<br>-If bile and pancreatic lipases are unable to reach the bowel because of a blockage (e.g. in obstructive post-hepatic pathology), fat is not able to be absorbed, resulting in stools appearing pale, bulky and more difficult to flush<br><br><ul> <li>Normal urine + normal stools = pre-hepatic cause (lots of unconjugated bilirubin)</li> <li>Dark urine + normal stools = hepatic cause (lots of conjugated bilirubin)</li> <li>Dark urine + pale stools = post-hepatic cause (lots of conjugated bilirubin that cant enter duodenum)</li></ul><ul> <li>Causes of unconjugated hyperbilirubinemia include: </li><ul> <li>Haemolysis (e.g. haemolytic anaemia)</li> <li>Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)</li> <li>Impaired conjugation (e.g. Gilbert’s syndrome)</li> </ul><li>Causes of conjugated hyperbilirubinemia include: </li><ul> <li>Hepatocellular injury</li> <li>Cholestasis</li> </ul> </ul>-albumin is synthesised in the liver & helps bind water, cations, fatty acids & bilirubin<br>-albumin plays key role in regulating oncotic pressure<br>-albumin can fall due to liver disease, inflammation or nephrotic syndrome<br><br>-Increased PT can indicate liver disease (in absence of anticoagulant medication or vitamin K deficiency)<br><br>-ALT > AST suggests chronic liver disease (lots of heoatocellular injury)<br>-AST > AST suggests cirrhosis & acute alcoholic hepatitis<br><br>Acute hepatocellular injury is caused by:<br>-paracetamol overdose<br>-infection (hep A & B)<br>-Liver ischaemia<br><br>Chronic hepatocellular injury is caused by:<br>-alcohol  -chronic infection -biliary cirrhosis (or less commonly alpha1 antitrypsin deficiency, wilsons disease, haemochromatosis)<br><br>Liver screen<br><ul> <li>LFTs</li> <li>Coagulation screen</li> <li>Hepatitis serology (A/B/C)</li> <li>Epstein-Barr Virus (EBV)</li> <li>Cytomegalovirus (CMV)</li> <li>Anti-mitochondrial antibody (AMA)</li> <li>Anti-smooth muscle antibody (ASMA)</li> <li>Anti-liver/kidney microsomal antibodies (Anti-LKM)</li> <li>Anti-nuclear antibody (ANA)</li> <li>p-ANCA</li> <li>Immunoglobulins <em>–</em> IgM/IgG</li> <li>Alpha-1 Antitrypsin (to rule out alpha-1 antitrypsin deficiency)</li> <li>Serum Copper (to rule out Wilson’s disease)</li> <li>Ceruloplasmin (to rule out Wilson’s disease)</li> <li>Ferritin (to rule out haemochromatosis)</li></ul>(IgM suggests current infection, IgG suggests past  infection)
"Hepatitis<br>-alcoholic hepatitis<br>-non alcoholic fatty liver disease<br>-viral hepatitis<br>-autoimmune hepatitis<br>-drug induced hepatitis<br><br>sx<br>-abdo pain -fatigue -pruritis (itching) -nausea/vomiting -jaundice -fever (viral)<br><br>-typically hepatitis will have high transaminases (ALT/AST) w proportionally less ALP<br><br>viral hepatitis<br>-virus infects hepatocytes<br>-CD8 T cells mediate cytotixic killing of infected hepatocytes<br>-Hepatocytes undergo apoptosis (Councilman bodies) in the portal tracts and lobules of the liver.<br>-This cytotoxic killing of hepatocytes is the main mechanism behind inflammation of the liver<br>-as more and more damage is done to the liver, the amount of transaminases in their blood will increase<br>-ALT will be greater than AST in viral hepatitis<br>-elevated levels of atypical lymphocytes are common to see with <a href=""https://www.osmosis.org/learn/Hepatitis:_Nursing"">viral hepatitis</a><br>-Patients often also end up developing <a href=""https://www.osmosis.org/learn/Jaundice"">jaundice</a>, with a mix of both <a href=""https://www.osmosis.org/learn/Jaundice:_Nursing"">conjugated bilirubin</a> and <a href=""https://www.osmosis.org/learn/Jaundice:_Nursing"">unconjugated bilirubin</a>.<br><br><ul> <li><a href=""https://www.osmosis.org/learn/Jaundice:_Nursing"">conjugated bilirubin</a> leaks out when bile ductules are damaged or destroyed when the <a href=""https://www.osmosis.org/learn/Liver_anatomy_and_physiology"">hepatocytes</a> die, which make up some of its lining!</li> <li>Also, since these <a href=""https://www.osmosis.org/learn/Liver_anatomy_and_physiology"">hepatocytes</a> are dying, you start to lose the ability to conjugate <a href=""https://www.osmosis.org/learn/Jaundice:_Nursing"">bilirubin</a> and make it water soluble, and so you also end up with unconjugated bilirubin as well.</li></ul><ul> <li>If the virus sticks around for more than 6 months, <a href=""https://www.osmosis.org/learn/Hepatitis:_Nursing"">viral hepatitis</a> goes from being called acute to being called <a href=""https://www.osmosis.org/learn/Hepatitis"">chronic hepatitis</a>.</li> <li>At this point, inflammation mostly happens in the <a href=""https://www.osmosis.org/learn/Anatomy_of_the_abdominal_viscera:_Blood_supply_of_the_foregut,_midgut_and_hindgut"">portal</a> tract</li></ul><br><ul> <li>When things progress to <a href=""https://www.osmosis.org/learn/Cirrhosis"">cirrhosis</a>, there may also be increased urobilinogen in the urine.</li> <li>Normally, urobilinogen is made by <a href=""https://www.osmosis.org/answers/lazy-bowel-syndrome"">intestinal</a> microbes that convert the <a href=""https://www.osmosis.org/learn/Jaundice:_Nursing"">bilirubin</a> in bile to urobilinogen.</li> <li>And usually, most of the urobilinogen is reabsorbed from the <a href=""https://www.osmosis.org/answers/lazy-bowel-syndrome"">intestine</a> and goes back to the liver, where it’s converted back to <a href=""https://www.osmosis.org/learn/Jaundice:_Nursing"">bilirubin</a>.</li> <li>However, with <a href=""https://www.osmosis.org/learn/Cirrhosis"">cirrhosis</a>, <a href=""https://www.osmosis.org/learn/Liver_anatomy_and_physiology"">liver cells</a> aren’t working properly anymore, so there’s a lot of <a href=""https://www.osmosis.org/learn/Cirrhosis"">liver fibrosis</a>, so <a href=""https://www.osmosis.org/learn/Liver_anatomy_and_physiology"">hepatocytes</a> can’t process the urobilinogen, which is redirected to the kidneys and excreted, so you end up with more urobilinogen in your urine.</li></ul><br>Hep A<br>-RNA -acute -faecal oral -nausea, vomit, jaundice, RUQ pain<br>-can cause cholestasis<br>-Deranged LFTs & IgM<br>-manage w basic analgesia<br>-prevent w vaccine<br>-notify<br><br>Hep B<br>-DNA -Blood/bodilyfluids transmission<br>-fever, jaundice, ALT/AST high<br>-HBsAg (surface antigen) present in active infection<br>-HBsAb (surface antibody) present in vaccinated people<br>-HBcAg (core antigen) present in active infection (but NOT in blood)<br>-HBeAg (E antigen) implies high infectivity (Results from breakdown of core antigen from infected liver cells)<br>-Hep B can cause liver failure, hepatocellular carcinoma, glomerulonephritis etc<br><br>Hep B management<br>-Notify<br>-stop smoking/alcohol<br>-Test for complications (fibroscan for cirrhosis & ultrasound for hepatocellular carcinoma)<br>-give antiviral meds (interferon-alpha)(tenofovir)<br>-liver transplant<br>-vaccinate -screen pregnant women<br><br>Hep C<br>-RNA -spread via blood?<br>-joint pain<br>-Test w hepC IgG<br>-Hep C RNA testing used to confirm diagnosis, calculate viral load and assess for the individual genotype <br>-similar management to hepB (except no vaccine)<br>-3/4 cases become chronic<br><br>Hep D<br>-co infection w hepB<br>-RNA -an only survive in patients who also have a hepatitis B infection<br>-It attaches itself to the HBsAg (hepatits B surface antigen) to survive and cannot survive without this protein<br>-epatitis D therefore increases the complications and disease severity of hepatitis B<br>-Dx w reverse PCR of hepatitis D RNA<br><br>Hep E<br>-RNA -mild illness -faecal oral<br><br><u>Autoimmune hepatitis</u><br>-young females<br>-could be associated with a genetic predisposition and triggered by environmental factors such as a viral infection that causes a T cell-mediated response against the liver cells<br>-associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3<br><br>-"
"<b><div><span style=""font-weight: 400; text-decoration-line: underline;"">Liver</span></div><br><div><span style=""font-weight: 400;"">-alcoholic liver disease covers alcoholic fatty liver disease, alcoholic hepatitis, cirrhosis</span></div><div><span style=""font-weight: 400;"">-Drinking alcohol leads to a build up of fat in the liver </span></div><div><span style=""font-weight: 400;"">-If drinking stops then this process reverses in 2 weeks</span></div><div><span style=""font-weight: 400;"">-Alcohol also causes inflammation in the liver </span></div><div><span style=""font-weight: 400;"">-Cirrhosis is irreversible because liver made of scar tissue</span></div><div><span style=""font-weight: 400;"">-CAGE questions screen for harmful alcohol use (Cut down? Annoyed? Guilty? Eye opener?</span></div><div><span style=""font-weight: 400;"">-Alcohol can also cause hepatocellular carcinoma, dependence, wernicke korsakoff syndrome, pancreatitis, alcoholic cardiomyopathy </span></div><br><div><span style=""font-weight: 400; text-decoration-line: underline;"">Signs of liver disease</span></div><div><span style=""font-weight: 400;"">-jaundice -hepatomegaly -spider naevi -gynaecomastia -palmar erythema -ascites -bruising -caput medusae -asterixis<br><br></span><b><div><span style=""font-weight: 400; text-decoration-line: underline;"">Hepatology</span></div><br><div><span style=""font-weight: 400;"">-High AST and ALT indicate hepatocellular injury </span></div><div><span style=""font-weight: 400;"">(High AST suggests alcoholic liver disease)</span></div><br><div><span style=""font-weight: 400;"">-ALP is derived from biliary epithelial cells and bones (so raised ALP levels can indicate cholestasis or bone disease)</span></div><div><span style=""font-weight: 400;"">-GGT is found in hepatocytes and biliary epithelial cells </span></div><div><span style=""font-weight: 400;"">(And is a very sensitive marker of liver damage and cholestasis)</span></div><div><span style=""font-weight: 400;"">-(High ALP w normal GGT suggests bone disease, high ALP w higher GGT suggests cholestasis)</span></div><br></b></div></b>"
Liver <b>cirrhosis</b> causes release of <b>Nitrous Oxides</b> → Splanchnic arterial <b>vasodilation</b><div><br></div><div><b>Pooling of blood </b>in splanchnic circulation → effective <b>hypovolaemia</b></div><div><br></div><div>Effective hypovolaemia activates:</div><div>- <b>Baroreceptor reflex</b>- SNS activation + extra-splanchnic vasoconstriction</div><div>- ↑<b>RAAS</b></div><div><br></div><div>Which leads to <b>Na<sup>+</sup> retention + water retention </b>→ 3rd pool spacing of water- <b>ascites</b></div>What are the physiological processes underlying <b>ascites</b> in liver cirrhosis?
- Rapid screening test (or <b>PCR</b>) for <b><i>C. diff</i> protein </b><div>- <b>ELISA </b>for <b><i>C. diff </i>toxins </b></div><div><br></div><div>- <b>AXR</b> to check for<b> toxic megacolon </b></div>How should <b>pseudomembranous colitis</b> be diagnosed?
- Pulmonary <b>stenosis</b><div>- Tricuspid <b>regurgitation</b></div>What cardiac abnormalities are associated with<b> Carcinoid </b>syndrome?
<b>Umbilicus</b>"Where is <b>Sister Mary Joseph's </b>node found?"
Hepatitis<b> C</b>What is the most common cause of hepatocellular <b>caricnoma </b>in Europe?
<b>Giardiasis</b>What is a common cause of<b> infectious chronic </b>diarrhoea?
- Avoidance of triggers<div>- Prophylactic treatments: <b>Amitriptyline</b>, <b>propranolol,</b> <b>topiramate (antiepileptic)</b></div><div>- In acute episodes: <b>ondansetron</b> (5HT3 antagonist), <b>prochloperazine</b> (D2 antagonist), triptans</div>How should cyclical vomiting syndrome be managed?
Oesophageal <b>candidiasis </b>(complication of <b>inhaled steroid</b> therapy)A patient with a Hx of COPD, with DH of <b>salbutamol</b> and <b>beclomethasone </b>inhalers presents with<b> pain on swallowing</b>. What is the most likely cause?
- ↑GGT, ↑ALT<div>- ↑MCV</div><div>- AST:ALT>2</div><div>- ↓ Urea</div><div>- ↓ Platelets</div>What changes in blood would you expect from an alcoholic?
"<div>The front of this card is blank.<br><a href='https://anki.tenderapp.com/kb/card-appearance/the-front-of-this-card-is-blank'>More information</a></div>""<div>The front of this card is blank.<br><a href='https://anki.tenderapp.com/kb/card-appearance/the-front-of-this-card-is-blank'>More information</a></div>"
"<font color=""#0000ff"">Thiopurine methyltransferase activity</font>: pts lacking this may be unable to metabolise these drugs and can experience greater side effects"What should be assessed before starting a patient on azathioprine or mercaptupurine therapy?
Triad of:<div><br></div><div>- Sudden onset abdominal <b>pain</b></div><div>- <b>Ascites</b></div><div>- Tender <b>hepatomegaly</b></div>How does <b>Budd-Chiari</b> syndrome typically present?
<b><u>Liver biopsy</u></b><br><br><b>Percutaneous Liver biopsy</b><br>-remove small piece of liver to examine under microscope<br>-blood tests to check clotting before procedure<br>-local anaesthetic injected between ribs ()<br>-US or CT used to guide needle into iver to extract the tissue sample<br><br>(can also do <b>laparoscopic liver biopsy</b>) <br>(or transvenous liver biopsy if patient has problems w clotting or asictes)<br>(<b>transvenous liver biopsy</b> involves making incision in jugular vein, inserting hollow tube & contrast dye, visualising on x ray, guiding needle through tube to visualise liver)
"Ascitic drain (theraputic paracentesis)<br>-Ascitic fluid drained from abdomen (can be used as sample for analysis)<br>-<span style=""color: rgb(17, 24, 39);"">When draining ascitic fluid, patients should be administered</span><strong> 100ml</strong><span style=""color: rgb(17, 24, 39);""> of </span><strong>human albumin solution 20%</strong><span style=""color: rgb(17, 24, 39);""> (HAS) for every</span><strong> 2-3 litres</strong><span style=""color: rgb(17, 24, 39);""> of ascitic fluid drained.<br><br>-complications include bowel perforation or kidney injury secondary to fluid depletion<br><br><u>Before procedure</u><br>-confirm ascites (w shifting dullness test)<br>-find optimal location for drain w percussion (dullest place) or use US if available<br>-avoid inserting too high to avoid perforating liver/spleen<br>-avoid inferior epigastric artery (runs in rectus sheath 4-8cm from midline)<br><br><u>Procedure</u><br>-<b>clean</b> insertion site w chlorhexidine (antiseptic)<br>-prepare/administer <b>lidocaine </b>subcutaneously using orange needle<br>-<b>aspirate</b> to ensure youre not in a blood vessel<br>-<b>replace orange needle w green needle</b><br>-administer <b>lidocaine deeper</b> into tissue, <b>aspirating </b>until you get a <b>flashback</b> of ascitic fluid<br>-make small<b> incision</b> in patients skin at </span><strong>intended drain insertion site</strong><span style=""color: rgb(17, 24, 39);""> (to make the insertion easier).<br>-Insert needle into a <b>bonanno catheter</b>, remove plastic sheath, attach </span><strong>20ml syringe</strong><span style=""color: rgb(17, 24, 39);""> to end of needle.<br>-insert needle into previously identified location<br>-<b>advance needle</b> slowly, aspirating as you advance<br>-</span><span style=""color: rgb(17, 24, 39);"">Once you aspirate ascitic fluid, insert needle </span><strong>half a centimetre more</strong><span style=""color: rgb(17, 24, 39);"">.<br><b>-</b></span><span style=""color: rgb(17, 24, 39);""><b>Aspirate </b></span><strong>20ml</strong><span style=""color: rgb(17, 24, 39);""> of ascitic fluid.<br>-Start to pull back needle </span><span style=""color: rgb(17, 24, 39);"">whilst </span><strong>simultaneously advancing Bonanno catheter<br>-advance </strong><strong>Bonanno catheter</strong><span style=""color: rgb(17, 24, 39);""> until it is at the hilt.<br>-<b>remove needle<br>-secure catheter</b> w 2 cannula dressings<br>-attach </span><span style=""color: rgb(17, 24, 39);"">Bonanno catheter to </span><strong>catheter bag</strong><span style=""color: rgb(17, 24, 39);""> (it should not be placed on the floor due to infection risk and trip hazard).<br>-</span><span style=""color: rgb(17, 24, 39);"">Leave on </span><strong>free drainage</strong><span style=""color: rgb(17, 24, 39);""> for a </span><strong>maximum</strong><span style=""color: rgb(17, 24, 39);""> of </span><strong>six hours</strong><span style=""color: rgb(17, 24, 39);"">.<br>-Ask ward staff to remove drain after 6 hours & document total vol of ascitic fluid removed </span>"
<u>Arterial blood gas</u><br>-ABG involves using neele & syringe to directly sample blood from an artery<br><br>Equipment<br><ul><li>Gloves</li><li>Apron</li><li><b>Pre-heparinised arterial blood gas syringe </b>and <b>bung </b>or cap</li><li>ABG <b>needle</b> (23 G)</li><li>Alcohol wipe (70% isopropyl)</li><li>Gauze or cotton wool</li><li>Tape</li><li><b>Lidocaine</b> 1% (1 mL)</li><li><b>Subcutaneous needle </b>(25-27 G)</li><li>Small<b> syringe </b>for lidocaine (1-2 ml)</li><li>Sharps container</li></ul>Contraindications<br>-PVD in limb, cellulitis around site, arteriovenous fistula (absolute)<br>-impaired coagulation, liver disease, low platelets (relative)<br><br><b><u>Before procedure</u></b><br>-WIPERQQ<br>-check for contraindications<br>-modified <b>allens tests</b> (clench fist, apply pressure over radial and ulnar arteries, open hand, remove finger from ulnar artery, normal colour should return in 5-15 seconds)<br>-record body temp & whether patient is recieving O2 therapy<br><br><b><u>procedure</u></b><br>Palpation<br>-assess course of radial artery<br>-palpate radial artery over wrist of non dominant hand to identify ideal puncture site<br>-use fingertips to map out course of radial artery & identify distal site when artery is most pulsatile<br>-clean site w alcohol wipe for 30s<br><br>local anaesthetic<br>-prepare & administer subcutaneous lidociane over planned puncture site <br>-aspirate to ensure youre not in a blood vessel<br>-wait 60s<br><br>arterial puncture<br>-remove protective cover from ABG needle & flush through heparin from syringe<br>-hold wrist extended by 20-30 degrees<br>-palpate radial artery w non dominant index finger 1cm proximal from planned puncture site<br>-holding ABG syringe like a dart, insert needle at 30-45 degrees<br>-advance needle slowly until you feel reduction is resistance & see flashback into ABG syringe<br>-ABG syringe should self fill in pulsatile manner<br>-remove needle & apply immediate firm pressure w gauze<br>-Engage needle safety device (clip that covers needle)<br>-remove ABG needle from syringe & discard in sharps bin<br>-carefully expel any air from sample if present, place cap on ABG syringe & gently invert<br>-Attach sticker w patients details<br>-Continue to apply pressure for 3-5 minutes
<b>Anti-motility </b>and<b> anti-peristaltic</b> medications e.g. opioids, or metoclopramideWhat medications should be <b>stopped</b> in <i>C. diff </i>infections?
- <b>Hypo</b> phosphataemia<div>- Hypo kalaemia</div><div>- Hypo magnesaemia </div><div>- Abnormal fluid balance </div>What are the metabolic consequences of <b>refeeding syndrome</b>?
"<font color=""#0000ff"">Foregut</font>: <b>Epigastric </b><div><font color=""#0000ff"">Midgut</font>: <b>Umbilical area</b></div><div><font color=""#0000ff"">Hindgut</font>: <b>Suprapubic area</b></div>"Where does <b>visceral pain </b>tend to refer to from the foregut, midgut and hindgut?
- Perforation (e.g. of duodenal ulcer)<div>- Rupture (e.g. of ectopic pregnancy)<br></div><div>- Acute pancreatitis<br>- Torsion (e.g. of ovarian cyst)<br></div><div>- Infarction</div>A sudden onset of abdominal pain suggests what causes?
"<div></div><div>-<font color=""#0000ff""> Small bowel</font>: Distal half of duodenum, jejunum, ileum, caecum </div><div>- Appendix</div><div>- <font color=""#0000ff"">Large bowel</font>: Ascending colon, <b>proximal 2/3 of transverse colon</b></div>"What are the midgut structures?
"<div>The front of this card is blank.<br><a href='https://anki.tenderapp.com/kb/card-appearance/the-front-of-this-card-is-blank'>More information</a></div>""<div>The front of this card is blank.<br><a href='https://anki.tenderapp.com/kb/card-appearance/the-front-of-this-card-is-blank'>More information</a></div>"
Terminal branch of the <b>gastroduodenal</b> artery (which arises from the <b>common hepatic </b>artery)Where does the right<b> gastro-omental</b> artery arise from?
"<b>Autonomic nervous system:</b><div><br></div><div><font color=""#0000ff"">Parasympathetic</font>: Anterior + posterior<b> vagal trunks</b>, from vagus nerve</div><div><font color=""#0000ff"">Sympathetic</font>: From <b>T6-T9 </b>spinal cord segments, passing to <b>coeliac plexus</b> via <b>greater splanchnic</b> nerve </div>"What provides the innervation to the stomach?
"<b>Subphrenic</b>: Between diaphragm and anterior/superior aspects of liver. <div><b>Subhepatic</b>: Peritoneal space between inferior surface of liver and transverse colon</div><div><b>Morison's pouch</b>: Potential space between visceral surface of liver and right kidney</div>"Where are the hepatic recesses found?
"- Macular<b> rash </b>(shawl sign +ve if over back and shoulders)<div>- Heliotrope <b>rash on eyelids</b>, often with oedema</div><div>- Nailfold erythema (dilates capillary loops)</div><div>- Gottron's papules</div>"What additional signs might you see in<b> dermato</b>myositis (as opposed to myositis)?
Beta-blockersWhat drug can worsen psoriatic lesions?
"<font color=""#0000ff"">Motor</font>: Serratus anteri<b>or</b><div><font color=""#0000ff"">Sensory</font>: None</div><div><font color=""#0000ff"">Nerve roots</font>: C5-C7</div>"What are the motor + sensory functions and nerve roots of the long <b>thor</b>acic nerve?
"<font color=""#0000ff"">Motor</font>: LOAF muscles (thumb etc), <b>flexors</b> of the wrist + <b>pronator teres</b><div><font color=""#0000ff"">Sensory</font>: Palmar aspect of lateral 3.5 fingers (+ nail beds)</div><div><font color=""#0000ff"">Nerve roots</font>: <b>C6, C8, T1</b></div>"What is the motor + sensory functions of the <b>median</b> nerve, and its nerve roots?
"<font color=""#0000ff"">Motor</font>: <b>Hip extension</b> and lateral rotatin<div><font color=""#0000ff"">Sensory</font>: None</div><div><font color=""#0000ff"">Nerve roots</font>: Sacral plexus: <b>L5-S2.</b> </div><div><br></div><div><br></div>"What is the motor + sensory functions + nerve root supply of the inferior gluteal nerve?
- <b>Chole calciferol</b> formed in <b>skin </b>on exposure to UV radiation. <div>- Cholecalciferol, and <b>ergo calciferol</b> (from food) are converted into 2,5 hydroxyvitamin D<b> (calcidiol) </b>in liver and stored</div><div>- Calcidol then hydroxylated in kidney to form 1,25 dihydroxyvitamin D (calcitriol)</div>Describe how active vitamin D is produced?
Distal 1/3 of <b>m</b>etat<b>ar</b>sals- commonly in 2nd and 3rd metatarsalWhere do <b>march </b>fractures frequently occur?
<b>Oslers nodes</b>- indicative of<b> infective endocarditis</b>"If these are painful to touch, what are they?<div><img src=""What-is-Osler-Nodes-300x202.jpeg""><br></div>"
IV antibiotics:<br>- Co-amoxiclav<div>- Cefuroxime</div><div>- Clindamycin</div><div>- Ceftriaxone</div>In severe cellulitis, what anitbiotics should be offerred?
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