1.
a.
b.
c.
d.
e.
Pure mitral stenosis:
tends to cause a loud first heart sound
T
produces displacement of the apex beat
F
Produces a diastolic murmur, the duration of which, rather then the
intensity, determines degree of stenosis
T
Is better heard with the diaphragm than
F
the bell of the stethoscope
Is louder on inspiration
F
Mitral stenosis causes a low volume pulse and is commonly linked to Atrial
fibrillation. There may be a palpable S1 as it tends to be quite loud, but
UNDISPLACED “tapping” apex beat. However, the left atrium may be enlarged to
compensate for the defective valve, causing cardiomegaly on CXR. The murmur
starts with the rigid valve opening, causing a “snap”, followed by mid-diastolic, lowpitched murmur, best heard with the bell in left lateral position.
Although on a world-wide basis quite common, Mitral stenosis has become rare in the
developed world as a result of a decline in rheumatic heart disease. In practice, all MS
relates to prior RF. Typical presentation is progressive exertional dyspnea in 40-50
year olds. Other presentations may include A.Fib and thromboembolic disease.
Mitral facies (malar flush) may also be seen.
The severity of MS is established by duration of the diastolic murmur, and the closer
the opening snap is to S2.
The severity of MR is established by the size of the left ventricle.
AS is determined by signs of left ventricular hypertrophy.
Murmurs louder on inspiration tend to be right heart while those louder on expiration
tend to be left heart…
2.
a.
b.
c.
d.
e.
The following may cause sinus tachycardia
Anemia
T
Atropine
T
atrial flutter
F
thyrotoxicosis
T
carotid sinus massage
F
Common causes of sinus tachycardia include
- pain, fever, hypovolemia, hypoxia, anemia, anxiety, beta-agonists
Thyrotoxicosis increased sympathetic drive and thus leads to sinus tachycardia
(and is also linked to A.fib)
Carotid sinus massage causes vagal stimulation, which decreases heart rate
(sinus
BRADYcardia)
Atrial flutter is a circular re-entrant arrhythmia that bypasses the sinus node.
Atropine is a parasympathetic antagonist, acting via acetylcholine receptor
antagonism. It causes sinus tachycardia by blocking the heart-slowing
effects of the parasympathetic nervous system (via vagus nerve).
3.
a.
b.
c.
d.
e.
Signs of aortic regurgitation include
anacrotic pulse
wide pulse pressure
corrigans neck pulsation
durozier’s sign
Austin-flint murmur
T
T
T
T
T
Classic eponymous signs of Aortic insufficiency/regurg include
Corrigan’s pulse: “Water-hammer” pulse (rapid rise and fall/collapsing)
Hill’s sign:
(Popliteal SBP-Brachial SBP)> 60 mm Hg
Duroziez’s sign: Gradual pressure over femoral artery causes systolic and diastolic
bruits
Traube’s sound: double sound heard at femoral artery when compressed distally
deMusset’s sign: head bobbing with each heartbeat
Muller’s sign: systolic pulsations of the uvula
Quinke’s pulses: subungual capillary pulsations
Austin-Flint murmur: diastolic rumble at apex (AI jet interferes with mitral inflow).
Diastolic decrescendo murmur at left upper sternal base, increased by sitting forward,
expiration and handgrip.
4.
a.
b.
c.
d.
e.
A third heart sound may be heard in:
cardiac failure
mitral incompetence
systemic HTN with normal ECG
pure mitral stenosis
contrictive pericarditis
T
T
F
F
T
Heart failure can cause a “gallop rhythm” which is associated with an S3 (third heart
sound). This gallop rhythm is specific for Left heart failure.
It’s easy to remember what causes S3 cause they all appear to cause heart failure
(MR, Constrictive pericarditis, AR etc). HTN doesn’t necessarily cause heart failure
nor would MS.
In mitral regurgitation, the murmur is at the apex, pansystolic and loud. It may NOT
be pansystolic in functional MR. The murmur radiates up the left ventricular outflow
tract. An S3 may be heard due to volume overload.
Systemic HTN is not sufficient to cause an S3, unless associated with abnormality.
Normal ECG and systemic HTN are not by themselves or together associated with S3.
Mitral stenosis does not cause an S3. An opening snap, followed by a middiastolic
murmur, is more characteristic.
Constrictive pericarditis is caused by TB or radiotherapy, and leads to an acute,
chronic or relapsing course. Pericardial fibrosis sufficient to constrict the heart leads
to impaired cardiac filling and decreased cardiac output. Progressive exertional
dyspnea, peripheral edema and ascites can occur. The increase in intravascular
volume cause increased JVP-a pericardial knock also occurs in diastole (loud diastolic
heart sound). Diuretics relieve symptoms and surgery may be needed. S3 is present
(just think it causes heart failure).
5.
a.
b.
c.
d.
e.
Recognized features of acromegaly include
loss of libido
T
reduced fields of vision
T
arterial HTN
T
hydronephrosis
F
enlargement of the tongue
T
Acromegaly usually results from a GH secreting tumor of the pituitary (pituitary
adenoma). Signs and symptoms include:
- increased soft tissue, arthralgias, jaw enlargement (“lantern jaw”)
- carpal tunnel syndrome, headache, macroglossia, hoarseness
- sleep apnea, amenorrhea, impotence, DM, acanthosis, sweating, HTN
- glucose intolerance, cardiomyopathy
Since acromegaly typically results from pituitary adenoma, which can cause visual
field disturbance (classically bitemporal hemianopia), reduced fields of vision may
feature in acromegaly.
6.
a.
b.
c.
d.
e.
Nephrotic syndrome is a well recognized feature of
chronic pyelonephritis
F
renal papillary necrosis
F
thrombosis of renal veins
F
proliferative glomerulonephritis
T
disseminated lupus erythematosis
T
Nephrotic syndrome is the triad of proteinuria (>3g/day), hypoalbuminemia (albumin
<30g/L) and edema. Causes of nephrotic syndrome can be categorized into primary
glomerular disease or Systemic disease.
PRIMARY glomerular diseases causing nephrotic syndrome include:
- focal segmental glomerulosclerosis
- membranous nephropathy: includes
HBV/HCV/syphilis/SLE/RA/Sjogrens/breast,lung,colonCa/
Drugs (gold/penicillamine/ACEi/NSAIDs)
- minimal change disease
- membranoproliferative glomerulonephritis
- glomerulopathy
- IgA nephropathy
- Mesangial proliferative GN
SYSTEMIC diseases include:
- Diabetes mellitus (Kimmelsteil-Wilson lesion in kidney reflects
nodular glomerulosclerosis
large kidneysmicroalbuminurianephrotic range in 10-15
years.
- Amyloidosis/SLE/Cryoglobinemia
Incidentally, nephritic syndrome comprises hematuria and proteinuria. It is usually
associated with hypertension, pulmonary edema, oliguria and rising plasma urea and
creatinine. Nephritic syndrome causes include ANCA vasculitis, anti-GBM disease,
and immune complex disease (both renal-limited and systemic).
ANCA vasculitis includes Churg-Strauss syndrome, Microscopic polyangiitis
and Wegener’s granulomatosis. Anti-GBM disease includes both anti-GBM disease
(limited to linear staining of kidneys ONLY) and Goodpastures (includes linear
staining of renal and pulmonary areas). Immune complex disease can be renal-limited
(post-streptococcal GN, membranoproliferative GN, fibrillary GN, IgA nephropathy)
or systemic (SLE, endocarditis, Henoch-Schonlein purpura, cryoglobinemia).
7.
a.
b.
c.
d.
e.
Excretion urography can be diagnostic in
chronic pyelonephritis
F
acute glomerulonephritis
F
renal artery stenosis
F
polycystic kidney disease
F
nephritic syndrome
F
Excretion urography is a study for defining anatomy and detecting pathology
distorting the collecting system. Abdominal films are taken before and after IV
contrast, which is filtered goes from renal artery to kidney, reaching the glomeruli,
then renal tubules, then collecting ducts, then minor then major calyces, then renal
pelvis, then ureters, then bladder. Xrays are taken (KUB) to radiologically visualize.
Nephritic syndrome is diagnosed by proteinuria and hematuria, both of which can be
diagnostically established my urine sample
Polycystic kidney disease can not be detected by urography, since the cysts are on the
outside of the kidney and not part of the collecting system.
While renal artery stenosis can be detected by excretion urography, it is usually at the
glomeruli that the initial part of the study is considered. Moreover, a renal arteriogram
is considered diagnostic.
The cause of acute glomerulonephritis can not be determined by excretion urogram.
Usually the diagnosis is made by FBC, U+E, LFTs, ESR/CRP, Ig, complement
(C3,C4) and autoantibodies, blood culture, ASOT, and detection of protein or blood in
the urine (for nephrotic or nephritic syndrome) is commonly done. A renal biopsy or
ultrasound may also be needed.
8.
a.
b.
c.
d.
e.
Hemolytic anemia is a feature of
Malaria
T
tropical sprue
F
hookworm disease
F
thalassemia
T
brucellosis
F
Hemolytic anemia is classified into congenital or acquired causes. Congenital
hemolytic anemias are classified into cell wall defects, metabolic defects and
hemoglobin defects.
CONGENITAL
Cell wall defects:
Hereditary spherocytosis, hereditary elliptocytosis
Metabolic defects:
G6PDH or pyruvate kinase deficiency
Hemoglobin defects: Thallessemias and sickle cell disease
ACQUIRED
Drugs
Penicillin, Cephalothin, Ampicillin
Methicillin, Quinine, Quinidine
Autoimmune
Cold or warm antibody mediated
Warm-antibody:
SLE, IBD, CLL, Non-Hodgkins
Cold-antibody:
Mycoplasma pneumoniae, EBV/CMV
Infection
Hep C, EBV
Cardiac:
Prosthetic valve
Hemolytic transfusion reaction
Microangiopathic
TTP, HUS,
Paroxysmal nocturnal hemoglobinuria
rbc GPI-anchored protein that
normally binds (and thus
inactivates) complement
9.
a.
b.
c.
d.
e.
Peripheral neuropathy is a recognized complication of
Diphtheria
T
Leprosy
T
snake bite
?
weil’s disease
F
typhus
F
Typhus is causes by Salmonella typhi and causes headache, dry cough and
constipation. Fever and bradycardia occur and precede a erythematous maculopapular
rash. Splenomegaly, lymphadenopathy and hepatomegaly occur, and complications
may include pneumonia, meningitis, acute cholecystitis, osteomyelitis, intestinal
perforation and hemorrhage.
Peripheral neuropathy is the medical term for damage to nerves of the peripheral
nervous system, which may be caused either by diseases of the nerve or from the sideeffects of systemic illness. Peripheral neuropathies vary in their presentation and
origin, and may affect the nerve or the neuromuscular junction.
Neuropathies can be classified into polyneuropathies or mononeuropathies. Causes of
polyneuropathies can be diabetes, amyloidosis, renal failure, alcohol, vasculitis,
cancer, alcohol. Mononeuropathies can be caused by diabetes, vasculitis, leprosy,
sarcoid, cancer and HIV. Infective causes include leprosy, Lyme disease, HIV and
diphtheria. Agent Orange defoliants used by the US armed forces during the Vietnam
War is also a major cause of peripheral neuropathy.
Mechanical pressure from staying in one position for too long, a tumor, intraneural
hemorrhage, exposing the body to extreme conditions such as radiation, cold
temperatures, or toxic substances (including some chemotherapy drugs such as
vincristine) can also cause peripheral neuropathy.
Many of the diseases of the peripheral nervous system may present similarly to
muscle problems (myopathies), and so it is important to develop approaches for
assessing sensory and motor disturbances in patients so that a physician may make an
accurate diagnosis.
Peripheral neuropathies may either be symmetrical and generalized or focal and
multifocal, which is usually a good indicator of the cause of the peripheral nerve
disease.
Generalized peripheral neuropathy
Generalized peripheral neuropathies are symmetrical, and usually due to various
systematic illnesses and disease processes that affect the peripheral nervous system in
its entirety. They are further subdivided into several categories:
Distal axonopathies are the result of some metabolic or toxic derangement of neurons.
They may be caused by metabolic diseases such as diabetes, renal failure, deficiency
syndromes such as malnutrition and alcoholism, or the effects of toxins or drugs.
Myelinopathies are due to a primary attack on myelin causing an acute failure of
impulse conduction. The most common cause is acute inflammatory demyelinating
polyneuropathy (AIDP; aka Guillain-Barré syndrome), though other causes include
chronic inflammatory demyelinating syndrome (CIDP), genetic metabolic disorders
(e.g., leukodystrophy), or toxins.
Neuronopathies are the result of destruction of peripheral nervous system (PNS)
neurons. They may be caused by motor neurone diseases, sensory neuronopathies
(e.g., Herpes zoster), toxins or autonomic dysfunction. Neurotoxins may cause
neuronopathies, such as the chemotherapy agent vincristine.
Signs and symptoms
Those with diseases or dysfunctions of their peripheral nerves can present with
problems in any of the normal peripheral nerve functions.
In terms of sensory function, there are commonly loss of function (negative)
symptoms, which include numbness, tremor, and gait imbalance.
Gain of function (positive) symptoms include tingling, pain, itching, crawling, and
pins and needles. Pain can become intense enough to require use of opiate drugs (i.e.,
morphine, oxycontin).
Weil’s disease is caused by leptospira interrogans, and is characterized by
hepatosplenomegaly, jaundice, hemolytic anemia, myocarditis and renal failure with
hematuria.
10.
The following associations are correct
a. Early morning waking and depression
b. Morning headache and depression
c. SLE and psychosis
d. Late pregnancy and Down’s syndrome
e. Right sided endocarditis and drug addiction
T
F
T
T
T
Depression causes, classically, early morning waking, poor sleep, and early REM
onset.
Morning headache is not associated with depression. It may related to increased
intracranial pressure,
SLE can cause effects on the:
Brain:
fits/psychosis/anxiety/headaches
Lungs
PE from antiphospholipid syndrome, pulmonary fibrosis
Hands
Arthralgia, Raynauds
Legs
Peripheral neuropathy, Myositis
Skin
Malar rash, livedo reticularis (antiphospholipid antibody)
HTN
End stage renal disease
Fetal loss
Drug addiction classically causes endocarditits of the valves on the right side of the
heart (tricuspid or pulmonary).
The incidence of Down’s syndrome increases as maternal age increases. At age 20,
the risk is 1 in 1500. At age 40, the risk is 1 in 40. Nuchal tranluscency test takes the
sum of the thickness of the fold of skin over the back of the fetal nack and size of
baby, between 11 and 14 weeks. A greater translucency is associated with greater risk
of Down’s syndrome. A high NT is also associated with trisomy 18, trisomy 13 and
Turner’s syndrome.
11. Regarding pernicious anemia:
a. Hypersegmentation of neutrophils is a common finding
b. Glossitis may be seen
c. Platelets are usually normal
d. Low serum B12 levels are diagnostic
e. Histamine-fast achlorhydia is usual
T
T
T
F
T
Pernicious anemia involves autoantibodies against parietal cells, causing lack of acid
and intrinsic factor. The lack of acid causes chronic fundal gastritis, achlorhydia and
hypergastrinemia. The lack of intrinsic factor causes insufficient B12 absorption in
the terminal ileum and thus B12 deficiency, associated with megaloblastic anemia,
peripheral neuropathy in posterior and lateral columns (decrease vibration and
position sense, ataxia), glossitis (red sore tongue), angular stomatitis, mild jaundice.
Leucopenia and thrombocytopenia may be present in severe cases of B12 deficiency.
Megaloblastic anemia is associated with neutrophil hypersegmentation (B12 also
needed in development of wbc), increased LDH and indirect bilirubin. The
macrocytotic anemia develops because the cytoplasm develops faster than the
nucleus, which (as we all remember from histology) is extruded from the rbc during
development. For diagnosis to be made in pernicious anemia, serum autoantibodies
must be present.
12. In rheumatoid arthritis
a. ESR is good index of disease activity
T
b. Renal lesions commonly occur
F
c. Amyloidosis may develop
T
d. Nodules may occur over bony prominences
T
e. Osteoporosis is a common radiological finding adjacent to the affected joint T
Rheumatoid arthritis is a chronic symmetrical polyarthritis of unknown cause. RA
affects 1-3% of population worldwide. Women are affected 3x more commonly than
men. RA is a disease of the synovium, causing infiltration of chronic inflammatory
cells (lymphocytes, plasma cells and macrophages) with secretion of proinflammatory
cytokines. Presentation is with pain, stiffness and swelling in small joints of hands
and feet, marked on waking (early morning stiffness). Ulnar deviation, Boutonniere
deformity and Swan neck deformity are common and swelling in
metacarpophalangeal and proximal interphalangeal joints are common. The DIP joints
are SPARED.
Rheumatoid nodules are present in 20% of cases, usually on the ulnar surface of the
forearm just below the elbow (may be over the bony part of the elbow).
ESR and CRP are raised in proportion to the activity of the inflammatory process.
Serum antibodies are positive in 70% of cases and antinuclear factor in 30%.
Radiology shows joint space narrowing, erosions of margins of joints and porosis of
periarticular bone and cysts.
Extraarticular manifestations of RA include:
Systemic:
Fever, fatigue, weight loss
Eyes:
Sjogrens, scleritis, scleromalacia perforans (eye perforation)
Neurological
Carpal tunnel syndrome, Atlanto-axial subluxation, cord
compression, polyneuropathy, mononeuritis multiplex
Reticuloendothelial Lymphadenopathy, Felty’s (RA, splenomegaly, neutropenia)
Blood
Anemia (chronic disease, hypersplenism, NSAIDs, hemolysis)
Thrombocytosis
Pulmonary
rheumatoid nodules, small airway disease, diffuse fibrosing
alveolitis, Caplans (rheumatoid pneumoconiosis)
Heart
Pericarditis, pericardial effusion
Kidneys
Amyloidosis, analgesic nephropathy
Vasculitis
While renal amyloidosis CAN occur, it tends not to be terribly common.
Osteoporosis is a reduction in bone mass causing thin bone. It includes all bone
components, not just calcium. Increased risk of fracture is common.
13. Gynecomastia may occur with
a. Adrenal tumors
b. Renal tumors
c. Cirrhosis of liver
d. Myxoedema
e. Digitalis treatment
T
F
T
F
T
Gynecomastia is the development of benign breast tissue in the male and is the result
of an increase in the estrogen:androgen ratio. Causes include:
- liver disease
- neonatal (from maternal hormones)
- early puberty/old age
- hypogonadism
- estrogen producing tumors of the testis or adrenal gland
- HCG tumors of the testis or lung
- PRL secreting tumors of the pituitary
-
Hyperthyroidism (not hyPOthyroidism aka myxoedema)
Drugs: spironolactone, digitalis, cyproterone, cimetidine, estrogens,
heroin, cannabis
14. Sacro-iliac involvement is commonly found in the arthropathy of:
a. ankylosing spondylitis
T
b. Reiter’s syndrome
T
c. Gout
F
d. Rheumatoid arthritis
F
e. Ulcerative colitis
T
Seronegative spondyloarthropathies include:
AnkSpon
Reactive
Sex
M>F
M>F
Age
<30
<30
Peripheral joints
40%
>90%
Axial spine (sacroiliitis)
100%
20%
IBD
M=F
any
>90%
30%
Psoriasis
M=F
any
>90%
30%
Extra-articular
Uveitis
Conjunctivitis
Skin
Mucous membrane
Aortic incompetence
Urethritis
Prostatitis
+
+
+
0
0
0
0
+
++
+++
0
0
0
0
+++
0
0
0
+
0
++
++
+++
++
+ (balanitis)
+
++
++
15. Hypokalemia can be associated with
a. Administration of insulin
T
b. Conn’s disease
T
c. Addison’s
F
d. Diarrhea
T
e. Terminal stages renal failure
F
Hypokalemia can be caused by:
Gastrointestinal loss: vomiting or diarrhea
Urinary tract loss:
Diuretic therapy,
mineralicorticoid excess
(Cushing’s, Conn’s, ectopic ACTH tumors, secondary
hyperaldosteronism [RAS, HTN, heart failure] all 
excessive aldosteroneinc Na+/K+ ATPase activity 
increased Na+ absorption+ increased K+ excretion
Poor intake:
Beta stimulation:
renal tubular acidosisinc activity H+/K+ exchanger
 increased H+ reabsorption and increased K+
excretion
eating disorders
Causes increased potassium into cells
Hyperkalemia can be caused by:
Hypoaldosteronism: Addison’s, spironolactone/amiloride, ACE inhibitors
Cell destruction
hemolysis, cytotoxic therapy, rhabdomyolysis
Renal failure
The ECG changes for altered potassium levels are fairly classic
HyPOkalemia:
Increased P wave, short QRS, short ST interval, flat/inverted T
wave, U waves
HyPERkalemia:
Decreased P wave, wide QRS (+sine wave), prolonged ST
interval,
peaked T wave
16. A 75 year old male patient with gross painless hematuria
a. Should have a rectal examination
T
b. May have TB
T
c. Should be reassured if JVP normal
F
d. Should be given Vitamin K
F
e. Is likely to have renal stones
F
Hematuria can be caused by intrarenal or extrarenal causes. Extrarenal causes are
much more common.
EXTRArenal: Nephrolithiasis
neoplasm (prostate/bladder)
infection (urethra/bladder/prostate)
Trauma from foley catheter
INTRArenal Nephrolithiasis or crystalluria
Neoplasm
Infection
Trauma
Vascular (renal infarct, renal vein thrombosis)
Glomerulonephritis
“Blood In Urine Goes To Nephrotic Syndrome” = Blood clot (vascular), Infection,
urine,
Glomerulonephritis, Trauma, Neoplasms, Stones
Rectal examination may confirm the presence of a prostate neoplasm, or texture
consistent with prostatitis.
TB may cause infection of the bladder, prostate or urethra.
JVP being normal means absolutely nothing as far as reassuring this patient.
Vitamin K is given only if the source of the bleeding is related to vitamin K
deficiency.
As noted above, none of these causes relate to vitamin K deficiency
While renal stones do commonly cause hematuria, and men are affected three times
more often than women, the peak age is 30-40. Similar pain presentation in a 75 year
old male should raise suspicion of AAA. Incidentally, renal stones can be composed
of calcium oxalate, urate, cystine, xanthine, calcium phosphate.
17. Fibrosis of the left upper lobe
a. TB is likely cause
b. Trachea is deviated to the right
c. Tactile vocal fremitus increased in the left apex
d. Apex displaced left
e. Hamman’s sign
F
F
F
T
F
Spontaneous pneumomediastinum may be defined as the presence of free air in the
mediastinal structures without an apparent precipitating cause. Pneumomediastinum
was first reported by Laennac[2] in 1819, when he described an entity termed
interlobular emphysema, which consisted of free air in the tissues of the body. In
1927, Gordon[3] described 127 cases of subcutaneous emphysema and dyspnea in
women following childbirth. Spontaneous pneumomediastinum remained a poorly
recognized problem, however, until 1939, when Hamman[4] described a precordial
crunching noise synchronous with the heart beat - Hamman's sign - in seven patients,
and recognized that it was related to free air within the mediastinal compartment.
Disorder
Mediastinal Chest wall
Displacement Movement
Consolidation NONE
decreased
Collapse
I/L
decreased
Pneumothorax C/L (tension) decreased
Pleural effusion C/L
decreased
Percussion
Dull
Dull
Resonant
Stony dull
Breath
Sounds
bronchial
decreased
decreased
absent
Resonance
Fremitus
increased
decreased
decreased
decreased
Pulmonary Fibrosis involves scarring of the lung. Gradually, the air sacs of the lungs
become replaced by fibrotic tissue. When the scar forms, the tissue becomes thicker
causing an irreversible loss of the tissue’s ability to transfer oxygen into the
bloodstream.
Symptoms of pulmonary fibrosis include: Shortness of breath, particularly with
exertion
Chronic dry, hacking cough, Fatigue and weakness, Discomfort in the chest, Loss of
appetite, Rapid weight loss
There are five million people worldwide that are affected by this disease. In the
United States there are over 200,000 patients with Pulmonary Fibrosis. As a
consequence of misdiagnosis the actual numbers may be significantly higher. Of these
more than 40,000 expire annually.
Traditional theories have postulated that it might be an autoimmune disorder, or the
after effects of an infection, viral in nature. There is a growing body of evidence
which points to a genetic predisposition. A mutation in the SP-C protein has been
found to exist in families with a history of Pulmonary Fibrosis. The most current
thinking is that the fibrotic process is a reaction to microscopic injury to the lung.
While the exact cause remains unknown, associations have been made with the
following:
Inhaled environmental and occupational pollutants
Cigarette smoking
Diseases such as Scleroderma, Rheumatoid Arthritis, Lupus and Sarcoidosis
Certain medications
Therapeutic radiation
Current treatments are relatively ineffective. Corticosteroids have been tried, and
recent trials of interferon may be promising. Lung transplant is effective, but all too
often not available.
I could find nothing specific to the clinical examination findings in interstitial
fibrosis…so my answers above are based on the assumption that fibrosis, being
scarring, causes pseudo-contraction of the tissues in the area and thus deviation
ipsilaterally, and bronchial breath sounds…
18. Clinical features of acute hepatitis include
a. Dislike of cigarettes
T
b. Splenomegaly
T
c. Glycosuria
F
d. Anorexia
T
e. Bilirubinemia
T
Hep C affected smokers may find a sudden dislike for cigarettes.
Acute hepatitis causes malaise, anorexia, jaundice, splenomegaly (10% HepA),
arthralgia, and abnormal LFTs. Abnormal LFTs tend to be a predominant
hepatocellular derangement of transaminases (AST/ALT). There is a less marked rise
in bilirubin and alkaline phosphatase.
19. Following statements are correct
a. Carpal tunnel syndrome is commonest in middle aged women
b. Pretibial myxoedema is seen in thyrotoxicosis
c. Cushing’s syndrome in females usually gives rise to amenorrhea
d. Acromegaly may give rise to HTN
e. Calcified ascending aorta on Xray suggests syphilis
T
T
T
T
F
Women are three times more likely than men to develop carpal tunnel syndrome,
perhaps because the carpal tunnel itself may be smaller in women than in men. The
dominant hand is usually affected first and produces the most severe pain. Persons
with diabetes or other metabolic disorders that directly affect the body's nerves and
make them more susceptible to compression are also at high risk. Carpal tunnel
syndrome usually occurs only in adults. The risk of developing carpal tunnel
syndrome is not confined to people in a single industry or job, but is especially
common in those performing assembly line work - manufacturing, sewing, finishing,
cleaning, and meat, poultry, or fish packing. In fact, carpal tunnel syndrome is three
times more common among assemblers than among data-entry personnel. A 2001
study by the Mayo Clinic found heavy computer use (up to 7 hours a day) did not
increase a person's risk of developing carpal tunnel syndrome. Carpal tunnel
syndrome can occur in people of any age, but it most often occurs in people 50 or
older (OK, “middle age” should refer to the middle of average life expectancy, say
about 35-40…Is 50 “middle aged”? My dad is 63 and says he’s “middle aged.” I’m
going with true.)
Pretibial myxoedema is seen in thyrotoxicosis, though hypothyroidism is also known
as myxoedema
Syphilis may affect the aorta, but does so on the descending portion. Thus, when it
causes aortic dissection, it is type 2.
Acromegaly gives rise to lantern jaw, macroglossia, enlargement of soft tissues,
enlargement of feet and hands, hypothyroidism, impotence, hypertension, glucose
intolerance…
Cushing’s disease affects women 4x more often than men. It can cause depression,
psychosis, thinned hair, “moon face” and “buffalo hump,” acne, hirsutism, HTN,
obesity, peptic ulcers, striae, impotence, thin skin and easy bruising, proximal
myopathy.
20. Diuretic therapy
a. May precipitate hepatic encephalopathy
b. may cause secondary gout
c. May cause collapse in elderly patients
d. Should not be prescribed for patients with diabetes mellitus
T
T
T
F
Diuretic therapy includes thiazides, loops and potassium-sparers. Any agent that can
aid in blood pressure decrease can cause collapse, so diuretics can cause collapse.
Diabetics may have blood pressure INCREASE on diuretic therapy. This simply
requires a change in drug, diet, insulin or oral antidiabetic dosage. Diuretics are
commonly prescribed to diabetics
Diuretics (thiazides especially) may cause hyperuricemia and thus gout.
In patients with cirrhosis, dehydration induced by diuretics is a common precipitant of
hepatic encephalopathy (HE), which may respond to volume expansion.
21. Erythema multiforme
a. May have associated oral lesions
b. Is a vasculitic eruption seen in rheumatic fever
c. May be very toxic and require steroid therapy
d. Is frequently seen in amyloidosis
e. May be fatal
T
F
T
F
T
Erythema multiforme (EM) is a hypersensitivity rash of acute onset frequently caused
by infection or drugs. A cell-mediated T cell hypersensitivity response occurs in the
skin, causing epidermal cell death. The cause is often idiopathic, but KNOWN causes
include:
Infection: HSV, EBV, orf, mycoplasma, HIV,
Drugs: Sulphonamides, anticonvulsants
Neoplasms: Carcinoma and lymphoma
CT disease (SLE, polyarteritis nodosa, Wegeners)
Lesions can be erythema multiforme (erythematous, polycyclic with “target lesions.”
Extensive mucosal involvement can occur in a variant calles Stevens-Johnson
syndrome.
The difference between EM minor and EM major is that in EM major, mucosal
surfaces are involved.
Treatment is usually symptomatic; however, some advocate oral steroid therapy in
severe disease (this is controversial). Prophylactic oral acyclovir may be helpful.
Resistant cases sometimes respond to azathioprine.
EM major can (rarely) be fatal.
Amyloidosis is rare and may result from a primary amyloidosis, but is more often
secondary to CT diseases such as RA, MM, Non-Hodgkin’s Lymphoma, IBD).
Rarely, EM can occur with a cause of amyloidosis. Thus I’d say this is false.
22. Acute myocarditis
a. Is usually viral in origin
T
b. May be produced by steroid therapy
F
c. Produces T-wave abnormality on ECG
T
d. May result in ventricular dysrhythmias T
e. Frequently exhibits Bell’s sign
F
Bell, who described CN VII palsy in conjunction with the Ramsay Hunt Syndrome,
noticed that when patients with a dense facial palsy are asked to close their eyes
tightly, the eye on the affected side will roll upwards. This is a positive Bell's sign.
Myocarditis is inflammation of the heart muscle caused by:
Infections:
VIRUSES:
Coxsackie/Mumps/Influenza
BACTERIA Septicemia
Radiation
Autoimmune Rheumatic fever
Toxin
Diphtheria
Tachycardia in acute myocarditis is out of proportion with the severity of the heart
failure. Tachypnea may also be present
A widely inflamed heart shows the classic signs of ventricular dysfunction including
Jugular venous distention, Bibasilar crackles, Ascites, Peripheral edema.
S3 or a summation gallop may be noted with significant biventricular involvement.
Intensity of S1 may be diminished.
Cyanosis may occur.
Hypotension caused by left ventricular dysfunction is uncommon in the acute setting
and indicates a poor prognosis when present.
Murmurs of mitral or tricuspid regurgitation may be present due to ventricular
dilation.
In cases where a dilated cardiomyopathy has developed (chronic myocarditis causes
dilatated cardiomyopathy), signs of peripheral or pulmonary thromboembolism may
be found.
Diffuse inflammation may develop leading to pericardial effusion, without
tamponade, and pericardial and pleural friction rub as the inflammatory process
involves surrounding structures.
Toxic myocarditis has a number of etiologies including both medical agents and
environmental agents. Among the most common drugs that cause hypersensitivity
reactions are penicillin, ampicillin, hydrochlorothiazide, methyldopa, and sulfonamide
drugs. This syndrome is associated with peripheral eosinophilia, fever, and rash in
patients who have biopsy findings of an eosinophilic infiltrate of the myocardium.
Numerous medications (eg, lithium, doxorubicin, cocaine, numerous catecholamines,
acetaminophen) may exert a direct cytotoxic effect on the heart. Zidovudine (AZT)
has been associated with myocarditis.
Environmental toxins include lead, arsenic, and carbon monoxide, Wasp, scorpion,
and spider stings (they don’t just cause pancreatitis holy crap).
Echocardiography in ACUTE Impaired contractile function
CHRONIC dilatation of left ventricle and atrium
Cardiac enzymes:
Elevated for many days or weeks
CRP and ESR raised
Serology for responsible organism (usually viral)
ECG findings include:
a. Sinus tachycardia is the most frequent finding.
b. ST-segment elevation without reciprocal depression, particularly when diffuse, is
helpful in differentiating myocarditis from acute myocardial infarction.
c. Decreased QRS amplitude and transitory Q-wave development is very suggestive
of
myocarditis.
d. As many as 20% of patients will have a conduction delay, including Mobitz I,
Mobitz
II, or complete heart block.
e. Left or right bundle-branch block is observed in approximately 20% of abnormal
ECG
findings and may persist for months.
23. Rheumatoid disease
a. May lead to impotence
b. Usually requires steroid therapy
c. May involve temporomandibular joint
d. Occasionally causes hypersplenism
e. May affect the lungs
T
T
T
T
Rheumatoid arthritis is a systemic autoimmune disorder characterized by chronic,
symmetric and erosive arthritis of synovial joints resulting in disability and handicap.
It is associated with extra-articular and circulating autoantibodies to immunoglobulin
known as rheumatoid factor (RF). Joints involved include:
Metacarpophalangeal joints
85%
Carpus
80%
Knee
80%
Metatarsophalangeal joints
80%
Elbow
70%
Proximal interphalangeal joints
65%
Glenohumeral joint
60%
Angle
40%
C-spine
35%
Temporomandibular joint
25%
Extra-articular manifestations of RA include:
ON EXAMINATION:
Hands splinter hemorage + periungal erythema
Carpal tunnel syndrome
Elbow nodules
Episcleritis, scleritis, kerato-conjunctivitis.
Pericarditis + AV block (nodule in conducting system)
Lungs effusion and pleuritis and alveolitis
Splenomegaly (1% RA get Felty’s = “Felty’s Needs Large Spleen!”
Neutropenia, Lymphadenopathy, Splenomegaly)
Renal disease (drugs or amyloidosis)
Legs: ulcers and distal sensorimotor symmetrical neuropathy.
Popular places for nodules include: elbows, Achilles tendon, hands/feet.
24. Acute nephritis is a recognized feature of:
a. Brucellosis
T
b. Ankylosing spondylitis
T
c. Polyarteritis nodosa
T
d. Polyposis coli
F
e. Bacterial endocarditis
T
Causes of nephritis include postinfectious, renal, and systemic etiologies.
Postinfectious etiologies
The most common cause is postinfectious Streptococcus species (ie, group A, betahemolytic). Other specific agents include viruses and parasites, systemic and renal
disease, visceral abscesses, endocarditis, infected grafts or shunts, and pneumonia.
Bacterial : diplococcal, streptococcal, staphylococcal, mycobacterial, and Salmonella
typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, and
actinobacilli
Viral: CMV, EBV, coxsackievirus, HepB, rubella, rickettsial scrub typhus, and
mumps are accepted as causes only if group A beta-hemolytic strept infection can be
excluded.
Fungal and parasitic: Attributing glomerulonephritis to a parasitic or fungal etiology
requires the exclusion of a streptococcal infection. Identified organisms include
Coccidioides immitis and the parasites: Plasmodium malariae, Plasmodium
falciparum, Schistosoma mansoni, Toxoplasma gondii, filariasis, trichinosis, and
trypanosomes.
Systemic causes
Wegener granulomatosis
Hypersensitivity vasculitis
Cryoglobulinemia
Systemic lupus erythematosus
Polyarteritis nodosa
Henoch-Schönlein purpura
Goodpasture syndrome
While this list does not include Ankylosing spondylitis or IBD (both of which are
included in seronegative arthritides, a pubmed search revealed numerous case reports
of nephritis and seronegative arthritides coexisting in a disproportionately high
amount. Most recently (2004), the journal Rheumatology has published a paper
entitled “Increased incidence of recurrent hematuria in ankylosing spondylitis: a
possible association with IgA nephropathy” in which nephritis is confirmed…
Renal diseases
Any cause of glomerulonephritis can cause acute nephritis.
25. In sarcoidosis
a. Pleural effusions are common
b. Hypocalcemia can occur
c. Liver biopsy is often helpful in diagnosis
d. Spontaneous remission commonly occurs
e. Treatment with steroids or ACTH is mandatory
F
F
T
T
F
Sarcoidosis is a multi-system disease of unknown etiology characterized by presence
of non-caseating granulomas in affected organs. It may relate to dust inhalation and a
significant genetic contribution is suggested with HLA-B8. Genetic linkage is
especially likely if arthritis and erythema nodisum are also present.
Sarcoidosis does NOT result from TB.
Sarcoid is 15x more common in African-Carribeans, and affects women more often
than men.
Pathological lesion is the non-caseating granuloma. A syndrome clinically and
histologically indistinguishable from sarcoidosis is found occasionally in
malignancies. This is an especially important consideration in elderly patients.
Two clinical patterns are typical:
1. ACUTE: Bilateral hilar lymphadenopathy + erythema nodosum + arthralgia.
This is most common and has a good prognosis (80% resolve within a year).
2. CHRONIC: slowly progressing breathlessness caused by pulmonary fibrosis.
This
has a worse prognosis
FBC lymphopenia + thrombocytopenia
ESR raised in active disease
10% have hypercalcemia caused by abnormal Vitamin D metabolism, MORE
COMMON in summer months!
Serum ACE is raised 2/3 cases
The Kveim test involved injecting splenic tissue from someone with sarcoidosis and
subsequent skin collection to establish presence of non-caseating granuloma.
Concerns about infection meant this is no longer done. Instead, a tissue diagnosis by
transbronchial biopsy is preferred, and is positive in 80%. Liver biopsy is diagnostic
in 70% of cases, but liver biopsy is not standardly used (but can be helpful and thus
“true”).
Pleural effusions are relatively uncommon (<5%)
Classification of sarcoidosis:
Grade
Abnormality
0
Normal
1
BHL
2
BHL+ pulmonary infiltrate
3
Pulmonary infiltrate ONLY
% resolution
all
80%
50%
25%
Extrathoracic symptoms are MORE common in cases of sarcoid with a BETTER
prognosis (the more extrathoracic symptoms you have the better prognosis you have).
No treatment is given in good prognosis sarcoid (BHL, erythema nodosum)
If radiological changes persist for 6 months, oral steroids are given. Neurological or
cardiac disease can also be treated by steroids.
Topical steroids for uveitis
Prognosis is worse with age and African-Carribean ancestry. Fewer than 3% of
patients die from sarcoidosis.
26. Tetanus
a. Is caused by an anaerobic spore-forming organism,
which produces tissue destroying enzymes
b. Is commoner in underdeveloped countries
c. Does not cause sequelae in those who recover
d. Confers a high degree of immunity against a second attack
e. May resemble strychnine poisoning
F
T
F
F
T
Strychnine is a strong poison; only a small amount is needed to produce severe effects
in people. Strychnine poisoning can cause extremely serious adverse health effects,
including death. The primary natural source of strychnine is the plant Strychnos nux
vomica. This plant is found in southern Asia (India, Sri Lanka, and East Indies) and
Australia. In the past, strychnine was available in a pill form and was used to treat
many human ailments. Today, strychnine is used primarily as a pesticide, particularly
to kill rats. Uncommonly, strychnine is found mixed with “street” drugs such as LSD,
heroin, and cocaine. Strychnine prevents the proper operation of the chemical that
controls nerve signals to the muscles. The chemical controlling nerve signals works
like the body’s “off switch” for muscles. When this “off switch” does not work
correctly, muscles throughout the body have severe, painful spasms. Even though the
person’s consciousness or thinking are not affected at first (except that the person is
very excitable and in pain), eventually the muscles tire and the person can’t breathe.
Given strychnine’s ability to target muscle contractions and cause severe and painful
spasms, it could quite easily be confused with tetanus.
Tetanus can be neonatal, and the anoxia caused by neonatal tetanus commonly causes
long term sequelae such as cerebral palsy, mental deficit and behavioral disturbance.
Tetanus is a medical term indicating a prolonged contraction of skeletal muscle fibers.
Tetanus is the primary symptom caused by the neurotoxin, tetanospasmin, produced
by the Gram-positive, obligate anaerobic bacterium Clostridium tetani (which does,
incidentally, form spores). Infection usually originates from a contaminated wound,
often a cut or deep puncture wound. Common symptoms are muscle spasms in the
jaw (hence the common name lockjaw), followed by difficulty swallowing and
general muscle stiffness of other parts of the body. The term tetany refers to a state of
muscle tension.
Whether tetanospasmin qualifies as a “tissue-destroying enzyme” is debatable. It is a
neurotoxin but it’s effect is indirect (it doesn’t digest the tissue as implied in the
statement-rather it paralyzes it). Thus I would say this is false, although the rest of the
statement is true. Incidentally, tetanospasmin works by:
1. Taken up by neuromuscular junction
2. Transported to CNS
3. Acts on Renshaw interneurons by preventing GABA and glycine release
4. Since GABA and gylcine are inhibitory neurotransmitters, the inhibition of
inhibitory NTs causes high frequency impulses to muscle cellstetany.
The wound must be cleaned; dead and infected tissue should be removed by surgical
debridement. Metronidazole treatment decreases the amount of bacteria but has no
effect on the bacterial toxin. Penicillin has been used in the past to treat tetanus, but is
no longer the treatment of choice because of a theoretical risk that it increases spasms;
however, if metronidazole is not available penicillin should still be used. Passive
immunization with human anti-tetanospasmin immunoglobulin (or tetanus immune
globulin) is a crucial part of treatment; if specific anti-tetanospasmin immunoglobulin
is not available then human normal immunoglobulin may be given instead. All tetanus
victims should be vaccinated against tetanus or offered a booster vaccine if they have
been previously vaccinated. In the most severe of cases, it may be necessary to
paralyze the patient using a naturally occurring substance, and engage a machine to
continue breathing.
It takes 2-14 days for symptoms to develop after infection. Symptoms peak 17 days
after infection.
Tetanus can be prevented by vaccination. The CDC recommends that adults receive a
booster vaccine every ten years, and standard care in many places is to give the
booster to any patient with a puncture wound who is uncertain of when he or she was
last vaccinated. This booster cannot prevent a potentially fatal case of tetanus from the
current wound as it takes 2 weeks for antibodies to form. For children under the age
of seven, the tetanus vaccine is often administered as a combined vaccine, TDap or
DTaP, which include vaccines against diphtheria and pertussis as well. For adults and
children over seven, the Td vaccine (tetanus and diphtheria) is commonly used.
27. Neoplasms of the esophagus
a. Are usually adenocarcinomas
b. Are commoner in males
c. Are more prevalent in patients with achalasia
d. Usually present with retrosternal pain
e. If resectable, have a good prognosis
T
T
T
F
F
The epidemiology of esophageal carcinoma has changed markedly over the past
several decades in the United States. Until the 1970s, squamous cell carcinoma was
the most common type of esophageal cancer (90-95%). It was located in the thoracic
esophagus and affected mostly African American men who had a long history of
smoking and alcohol consumption. Over the last 2 decades, the incidence of
adenocarcinoma of the distal esophagus and gastroesophageal junction has
progressively increased. Currently, it accounts for more than 50% of all new cases of
esophageal cancer. Unlike squamous cell carcinoma, it affects mostly white men, and
its pathogenesis is linked to gastroesophageal reflux disease (GERD) and the
development of Barrett epithelium
Esophageal carcinoma now represents 1% of all malignant lesions, with a male to
female preponderance of 3:1. The upper, middle and lower 1/3 of esophagus are
affected 20, 30 and 50% of the time. Risk factors include exposure (smoking, alcohol,
nitrosamines, radiation) and anatomical deficits (diverticula/hiatus
hernia/achalasia/GERD/Barret’s). Plummer-Vinson syndrome also increases risk.
The most common presentation is with dysphagia, first for solids then with liquids.
Weight loss and weakness are also common. Hematemesis, anemia,
tracheoesophageal and bronchoesophageal fistulae can also occur. Odynophagia and
then constant pain may occur but are not the most common presentation.
Esophageal cancer is a treatable disease that is rarely curable. The overall 5-year
survival rate in patients amenable to surgery ranges from 5% to 20%. The occasional
patient with very early disease has a better chance of survival. Patients with severe
dysplasia in distal esophageal Barrett's mucosa often have in situ or even invasive
cancer within the dysplastic area. Following resection, these patients usually have an
excellent prognosis. Reading this question is difficult-surgical resection of primary
tumor is linked (above) to a dismal prognosis of 5-20%, while the “resection” of in
situ lesions has “excellent prognosis.” Since it must be assumed that this answer stem
refers to ALL resections done in esophageal cancer, I answer false.
Incidentally (I’m starting to love that word), the staging of esophageal cancer is by
TNM system
T0
Tis
T1
T2
T3
T4
No evidence of tumor
In situ lesion only (usually found in biopsy of Barrett’s esophagus)
Invades submucosa
Invades muscularis propria
Invades adventitia
Invades surrounding structures (eg. Aorta, recurrent laryngeal nerves).
N0
N1
M0
M1
No lymph node involvement
Lymph node involvement
No mets
Mets
28. Complications of Ulcerative colitis include:
a. cirrhosis
T
b. colon cancer
T
c. arthritis
T
d. thyroiditis
F
e. pleural effusion
F
Extra-articular manifestations of IBD (UC and CD) include
Erythema nodosum
Pyoderma gangrenosum
Seronegative arthritides (sacro-iliitis and monoarthritis)
Ankylosing spondylitis (esp. HLA-B27)
Hepatitis, gallstones, renal stones, primary biliary cirrhosis
IT should be noted that ankylosing spondylitis and sacroiliitis occur independently of
disease flares and thus are not good indicators of disease activity.
There is an increased risk of colon cancer in ulcerative colitis and CD (higher risk in
UC).
29. Patients suffering from regional enteritis have a tendency to develop
a. fistulae
T
b. low serum iron
T
c. vitamin B12 insufficiency
T
d. cholelithiasis
T
e. recurrence of disease after surgery
T
Regional enteritis is also known as Crohn’s disease.
Distinguishing Features of CD Versus UC
Features
Crohn Disease
Skip areas
Common
Cobblestone mucosa
Common
Transmural involvement
Common
Rectal sparing
Common
Perianal involvement
Common
Fistulas
Common
Strictures
Common
Granulomas
Common
Ulcerative Colitis
Never
Rare
Occasional
Never
Never
Never
Occasional
Occasional
Vitamin B12 is bound by intrinsic factor (secreted by parietal cells in stomach), and
absorbed in the terminal ileum. Crohn’s disease commonly involves this portion and
thus may limit absorption. Iron absorption may also be affected.
The increased incidence of kidney stones has a curious physiology. Usually fat is
absorbed in the small intestine, but chronic inflammation in Crohn’s decreases fat
absorption. Simultaneously, calcium is usually bound to oxalate, which is poorly
soluble and thus mostly excreted. However, in CD, the malabsorbed fatty acids bind
calcium, so that the oxalate is bound instead to sodium, which is easily absorbed. The
excessive amounts of body oxalate cause them to precipitate in the renal system as
calcium oxalate stones.
30. The following are causes of hypercalcemia:
a. Milk-alkali syndrome
b. Paget’s disease of bone
c. Sarcoidosis
d. Multiple myeloma
e. Rickets
The causes of hypercalcemia include:
Neoplastic
Multiple myeloma, malignancy and metastasis
Bone
Increased osteoclast activity (Paget’s disease)
Increased VitD action
Sarcoidosis (10%), excessive intake (“Vit D
intoxication”)
Endocrine
Addison’s, Phaeochromocytoma, inc T4.
Drugs
Thiazides, Lithium,
Milk-alkali syndrome
Increased dietary Ca++
Increased PTH
Primary or tertiary, ectopic
31. The following drugs are know to give rise to lesions of the eighth cranial nerve
a. chloramphenicol
b. kanamycin
c. cyclophosphamide
d. salicylates
e. streptomycin
The CN VIII is the acoustic (aka vestibulocochlear) nerve. Anything that is ototoxic
can affect this nerve…
Antibiotics
amikacin, streptomycin, neomycin, gentamicin, erythromycin,
Kanamycin, Tobramycin, netilmycin, vancomycin
Aminoglycosides, Vancomycin and the macrolide
erythromycin…
Anti-cancer drugs cisplatin, bleomycin, vincristine
Anti-malarial drugs quinine and chloroquine
Diuretics
acetazolamide, furosemide, bumetanide, ethacrynic acid
Salicylates can cause ringing in the ears (salicylism).
32. Gout
a. Is characterized by deposits of sodium urate in joints and other structures
b. Causes symmetrical arthritis
c. May lead to renal dysfunction
d. May be exacerbated by diuretics
T
F
T
T
e. An acute attack usually responds to allopurinol
F
Gout is the deposition of monosodium urate crystals into joint. The resulting
synovotis may be limited to a single joint (monoarticular) or become more widespread
(polyarticular). Pseudogout is similar except it is calcium pyrophosphate dehydrate
that is deposited. Gout is 6x more common in men and almost never found in premenopausal women.
Disorders that increase uric acid (severe psoriasis, myeloproliferative disorders, rich
diet, alcohol), drugs (thiazides, furosemide, low dose aspirin), renal disease, age,
dehydration may all increase risk of gout.
Therapy to lower uric acid formation includes allopurinol, and probenecid can be used
to increase excretion.
Most presentations of gout are monoarticular. Attacks are agonizing and last 7-10
days. Acute episodes can be triggered by alcohol, exercise, starvation or trauma.
Gouty nephropathy and renal stones are common. Chronic gout requires uric acid
lowering therapy and NSAIDs. Colchicine is used in acute attacks since allopurinol
prolongs acute attacks.
Uric acid levels may be normal in 20% of attacks.
Gout causes punched out cortical erosions, usually away from the joint margin.
33. CO2 retention is a feature of
a. status asthmaticus
b. coma associated with barbiturate intoxication
c. Acute PE
d. Bronchopneumonia
e. Respiratory muscle involvement in myasthenia gravis
T
T
F
F
T
Asthma triad is asthma+ ASA/NSAID hypersensitivity + nasal polyps. IN any acute
attack of asthma, an ABG and CXR must be done.
Airway obstruction V/Q mismatch  hypoxemia  increased ventilation 
decreasing PaCO2 Inc. pH and fatigue  dec. ventilation  increased PaCO2 and
acidosis. So…as the severity of asthma attack increases, CO2 retention occurs.
Other causes of CO2 retention include defective control of breathing or
hypoventiliation (drug OD, ALS, Myasthenia gravis, Guillain-Barre, kyphoscoliosis)
or structural problems (COPD).
While bronchopneumonia can cause hypoxemia, it rarely causes hypercapnia cause it
causes tachypnea, thus clearing the lungs of CO2.
PE can cause hypoxemia but not hypercapnia.
34. In bronchiectasis
a. Hemoptysis is common
b. Clubbing of fingers is rare
c. CXR commonly confirms the diagnosis
T
F
F
d. Coarse crepitations may be heard over the involved area
e. Surgery is eventually necessary in most patients
T
F
Bronchial wall dilatation, aka bronchiectasis, is often accompanied by super-added
pulmonary infection. Prevalence is about 1:1000, but this is falling because of the
decreases in TB and whooping cough. Bronchiectasis can be localized or generalized.
LOCALIZED: post-severe pneumonia,
distal to obstruction caused by endobronchial (foreign body/tumor) or
extrabronchial (Brocks syndrome=TB hilar lymphadenopathy)
GENERALIZED: CF, Kartagener’s syndrome, immune defects
Immune complex in IBD, RA
Marfan’s, Alpha-1 antitrypsin deficiency, yellow nail syndrome
Presentation usually includes chronic cough and mucopurulent sputum
Other symptoms include:
- unpleasant breath
- Hemoptysis (50%)
- Chronic sinusitis (40%)
- anemia (chronic illness)
or polycythemia (from respiratory
failure)
Cyanosis and other signs or cor pulmonale are present in late stages.
Crackles are present over affected areas, but airways obstruction and wheeze may also
occur. Look for other signs of underlying disorder
(Kartagener’s infertility, sinusitis, dextrocardia)
Amyloidosis may occur in longstanding severe bronchiectasis.
Common findings in bronchiectasis in the clinical exam include: anemia, cyanosis,
increased JVP, coarse crackles over affected area, chronic cough with mucopurulent
sputum, finger clubbing, and cor pulmonale (right heart failure due to lung disease
leg edema and RV heave).
The diagnosis of bronchiectasis can only be confirmed by HRCT (high resolution
CT), which shows the “signet ring” sign (thick-walled bronchus, larger than adjacent
blood vessel. Sputum culture for Pseudomonas should be undertaken.
35. Characteristic features of subacute bacterial endocarditis include
a. Heberden’s nodes
F
b. Proteinuria
T
c. Osler’s nodes
T
d. Thrombocytopenia
T
e. Conjunctival hemorrhages T
Osteoarthritis causes the formation of hard bony enlargements of the small joints of
the fingers. Classic bony enlargement of the small joint at the end of the fingers is
called a Heberden's node, named after a very famous British doctor. The bony
deformity is a result of the bone spurs from the osteoarthritis in that joint. Another
common bony knob (node) occurs at the middle joint of the fingers in many patients
with osteoarthritis and is called a Bouchard's node. Dr. Bouchard was a famous
French doctor who also studied arthritis patients in the late 1800s. The Heberden's and
Bouchard's nodes may not be painful, but they are often associated with limitation of
motion of the joint.
Osler's nodes: These are small (the size of split peas), tender, transient nodules in the
pads of fingers and toes and the palms and soles. They are a highly diagnostic sign of
bacterial infection of the heart (subacute bacterial endocarditis). Named for the
Canadian-born physician Sir William Osler (1849-1919).
Infective endocarditis can cause splinter hemorrhages, Osler’s nodes and clubbing in
the hands. Conjunctival hemorrhages and Roth spots (fundal infarcts). A tachycardia
and collapsing pulse may be found (from Aortic regurg). Murmurs may change with
time. Splenomegaly and hypersplenism can cause thrombocytopenia and anemia to
occur. Abscesses can be found intracranially, intrasplenically…and renal problems
may include glomerulonephritis leading to hematuria or renal failure.
36. Recognized causes of amyloid disease include:
a. Osteoarthritis
F
b. Cirrhosis of the liver
F
c. Osteomyelitis
T
d. TB
T
e. Rheumatic valvular disease F
Amyloids are insoluble fibrous protein aggregations sharing specific structural traits.
The classical, histopathological definition of amyloid is an extracellular,
proteinaceous deposit exhibiting cross-beta structure. Common to most cross-beta
type structures they are generally identified by apple-green birefringence when
stained with congo red and seen under polarized light.
Diseases featuring amyloid
The phenotypes of genetically transmitted amyloid diseases are often inherited in an
autosomal dominant fashion. Sometimes, the difference between aggressive amyloid
diseases and senescent amyloid diseases is due to a mutation that makes the protein
more prone to aggregation. Most commonly seen are point mutations, which affect the
cohesiveness of the protein and promote misfolding; other mutations cause
aggregation-prone pieces of the protein to be cleaved off from the rest of the protein.
In almost all of the organ-specific pathologies, there is significant debate as to
whether the amyloid plaques are the causal agent of the disease or instead a symptom
downstream of a common idiopathic agent. The associated proteins are indicated in
parentheses. Note that amyloidosis by default usually refers to AA amyloidosis, but
any disease which presents amyloid deposition is an amyloidosis. CJD, Alzheimer's
and diabetes are almost never referred to as amyloidoses.
AL amyloidosis (Ig light chains):
MM, Waldenstrom’s, or non-Hodgkins lymphoma
Secondary amyloidosis aka reactive systemic amyloidosis: from serum amyloid A
(SAA)
IBD, RA, TB, osteomyelitis, bronchiectasis. Often presents with hepatosplenomegaly.
(Chronic inflammation or chronic infection )
Familial or Hereditary amyloidosis
COMMON: transthyretin protein mutations
RARE: apolipoprotein A1, gelsolin, fibrinogen, and lysozyme mutations.
Importantly, dialysis can cause amyloidosis. This is because dialysis machines (older
ones) could not filter out large proteins (esp. beta-2 microglobulin), and thus they
precipitate out.
Organ-specific amyloidosis
Diabetes mellitus type 2 (amylin, also known as IAPP)
Alzheimer's disease (Aβ 39-42)
Parkinson's disease (alpha-synuclein)
Huntington's disease (huntingtin)
Transmissible spongiform encephalopathies (prion protein, PrP)
Creutzfeldt-Jakob disease (PrP in cerebrum)
Kuru (diffuse PrP deposits in brain)
Fatal Familial Insomnia (PrP in thalamus)
Bovine spongiform encephalopathy (PrP in cerebrum)
Congophilic angiopathy (Amyloid beta)
Cardiac amyloidosis
congestive heart failure; some instances (PrP or transthyretin in heart)
Inclusion body myositis
Iatrogenic conditions
insulin amyloidosis (injection-administered insulin)
Excessive calcitonin can also form amyloid but no known disease results
37. In CLL:
a. Children are affected more commonly than adults
b. Immune response is enhanced
c. Spleen is characteristically extremely large
d. Sternal marrow biopsy reveals an excess of myelocytes
e. Cyclophosphamide is the drug of choice
F
F
F
T
F
The incidence of CLL increases with advancing age, and males are affected more
commonly than females. CLL is a malignant illness of B-cells whereby cells look
mature but functionally are immature (CLL is the Ben of Cancers! B-cell for Ben,
LOOKS mature but actually quite immature!). Half of CLL patients are diagnosed by
chance, while the others may present with painless palpable lymphadenopathy,
recurrent sepsis (from hypogammaglobinemia), and anemia. Hepatosplenomegaly
may occur but is more common in more advanced disease. By definition, the
lymphocyte count must be >5x109/L in absence of viral infection. Usually Hb and
platelets are normal although thrombocytopenia and anemia may occur. LDH and
alkaline phosphatase may be raised. CLL is a chronic and incurable disease-while it
may be asymptomatic for years, symptoms may prompt the use of chlorambucil
(“ChLorambuciL for CLL”).
CML classically presents in middle age, and benzene and ionizing radiation may be
causally linked. CML is a clonal disorder of a pluripotent stem cell that contains
Philadelphia chromosome (remember the 9:22 translocation, thus producing the BCRABL tyrosine kinase-not targeted pharmacologically by Glevec (Imitanib the
monoclonal antibody), which can also be used in ALL). Splenomegaly is
characteristically extremely large! While hydroxyurea can be used to decrease the cell
counts, eventually an acute phase occurs which is resistant to intensive chemotherapy.
Recently however, Glivec has been shown to improve long-term survival in CML.
Marrow transplantation can be curative in both CML and CLL, but is usually reserved
for younger patients.
38. In pneumonic consolidation the following statements are correct:
a. The percussion note is characteristically stony dull
F
b. Breath sounds are bronchial
T
c. Kerley’s lines are seen on CXR during resolution
T
d. Sputum contains Curschmann’s spirals
F
e. Cavitation suggests staphylococcal aetiology
T
Condition
Percussion Mediastinum Vocal fremitus
Auscultation
Consolidation
Dull
None
increased
Bronchial
breathing
Alveoli filled with fluid
Pleural effusion Stony dull
C/L
decreased
reduced/absent
Fluid in pleural space
Pneumothorax Hyperresonant C/L (tension) decreased
reduced/absent
Air in pleural space
Collapse
Dull
I/L
decreased
reduced/absent
Chest wall movement decreased over area in pleural effusion, pneumothorax, collapse
or consolidation.
Curschmann's spirals are spirally twisted masses of mucus occurring in the sputum in
bronchial asthma.
In chest radiology, Kerley B lines are a sign seen with interstitial pulmonary edema.
Often, they suggest the diagnosis of congestive heart failure, but are also seen in
various non-cardiac conditions such as carcinomatous of the lung. Kerley B lines are
short horizontal lines at the lung periphery. These lines represent interlobular septal
lines, which are usually less than 1 cm in length and parallel to one another at right
angles to the pleura. They are located peripherally in contact with the pleura, but are
generally absent along fissural surface. They may be seen in any zone but are most
frequently observed at the lung bases. In most cases, heart problems are the cause of
pulmonary edema. But fluid can accumulate in your lungs for other reasons, including
lung problems such as pneumonia, exposure to certain toxins and medications, and
exercising or living at high elevations. Thus, pneumonia can cause pulmonary edema
which can cause Kerley B lines. Is this in resolution however? I’ve no clue…I’m
saying true to this…
The differential diagnosis for cavitating lung lesion is “CAVITEY.”
Cancer:
Bronchogenic carcinoma
and Café-au-lait spots as in NFT-1
Autoimmune RA, Takayasu’s arteritis
Vascular
PE
Infective
Parasites:
Alveolar hydatid disease
Fungi:
Pneumocystis carinii, Histoplasmosis
Bacteria:
Staph aureus, TB, Klebsiella
Trauma
Emphysema
Youth (congenital)
39. Characteristic features of aortic incompetence include:
a. Atrial fibrillation
F
b. Heaving apex impulse
T
c. Right ventricular hypertrophy
F
d. BP 145/110
F
e. Diastolic murmur heard in carotid arteries
F
Aortic incompetence is also known as aortic regurgitation. It involves
backflow/leaking of aortic blood back into the left ventricle during diastole.
Collapsing pulse with volume-overloaded left ventricle (hyperdynamic apex
beat);chronic AR causes left ventricular hypertrophy. There is a wide pulse pressure
(145/110 is not wide pulse pressure), and the diastolic BP is a good guide to the
severity of chronic AR (low diastolic BP=severe AR). Atrial fibrillation is not a
common feature, as it would be in mitral stenosis. There is an early diastolic murmur
heard along left sternal edge. A murmur heard in the carotid arteries would raise
suspicion for AS, which typically radiates to the carotids, in systole! Wide pulse
pressure causes:
Corrigan’s sign:
visible carotid pulsations
De Musset’s sign
head bobbing
Quinke’s sign
nail-bed pulsations
Traube’s phenomemon
pistol shot femorals
Austin-Flint murmur
mid-diastolic, low-pitched rumbling heard at the apex,
caused by blood from aorta mixing with entering blood across mitral valve
Duroziez’s murmur
To and fro murmur over femoral artery.
40. Recognized causes of hypokalemia include:
a. Conn’s syndrome
T
b. Diuretic therapy
T
c. purgatives
T
d. metabolic acidosis
F
e. Cushing’s syndrome
T
Hypokalemia can be caused by:
HyPERadrenalism
Conns syndrome, Cushing’s syndrome
Diuretics
Thiazides or loop diuretics
Loss from GIT
Diarrhea or vomiting
Shift into cells
Insulin therapy, beta-agonists (salbutamol), catecholamines
Hyperkalemia can be caused by:
HyPOadrenalism
Addison’s
Renal failure
Drugs
Spironolactone, amiloride, ACE inhibitors
Cell destruction
Chemotherapy, tumor lysis syndrome, rhabdomyolysis
Acidosis
Acidosis (high [H+] in plasma) causes hydrogen to be taken up
by muscle cells out of the blood in an exchange mechanism involving the
transfer of potassium ions into the bloodstream (H+/K+ exchanger). This
abnormally elevates the plasma's concentration of potassium ions.
Hypokalemia
Hyperkalemia
peaking.
↑p wave, ↓PR interval, ↓QRS width, T wave flattening, U wave
“You (“U”) wave cause the potassium has gone”
↓p wave, ↑PR interval, ↑QRS width (sine wave), T wave
41. Hemolytic anemia
a. Excess urobilinogen is present in the urine
b. Itching is a feature
c. Coombs test may be positive
d. Red cell fragility may be increased
e. Feces are pale
T
F
T
T
F
Hemolytic anemia causes the red cell life span to be markedly reduced. Hemolysis
can be categorized into congenital or acquired causes.
Congenital causes:
Membrane
Congenital spherocytosis, congenital elliptocytosis
Enzyme
G6P DH deficiency, pyruvate kinase deficiency
Hemoglobin Thallesemias, sickle cell anemias
Acquired causes:
Infection
EBV/CMV
MAHA
TTP/HUS
Cardiac
Prosthetic valve replacement
Autoimmune Warm antibody:
IgG binds to cells, from:
SLE, IBD, CLL, Non-Hodgkins lymphoma
Coombs test positive (detects antibody and
complement on rbc surface)
Cold antibody:
Ig M binds to cells, from:
Infection: CMV, EBV, mycoplasma
pneumoniae.
Cold hemagluttinin disease: acrocyanosis and
Coombs test positive for complement but
NOT antibody, as IgM falls off in vitro.
Paroxysmal nocturnal hemoglobinuria (defective GPI-anchored proteinusually
binds complement preventing breakdown-when
defective, complement binds and causes
hemolysis)
Hemolysis is considered a cause of pre-hepatic jaundice as the outflow of excessive
hemoglobin metabolites causes hyperbilirubinemia and thus jaundice. Clinical
findings:
Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut
flora has not developed).
Serum: increased unconjugated bilirubin.
Stools become darker (deep brown)
Hepatic jaundice:
Urine: bilirubin present, Urobilirubin > 2 units but variable (Except in children)
Post-hepatic jaundice:
The presence of pale stools and dark urine suggests an obstructive or post-hepatic
cause as normal faeces get their colour from bile pigments. Patients sometimes also
complain of itching.
42. Right homonymous hemianopia found in
a. Retinal detachment
F
b. Pituitary neoplasms
F
c. Optic nerve glioma
T
d. Left cerebral infarct
T
e. Right occipital tumour
F
In homonymous hemianopia - literally, a loss of vision on the same side in both eyes the field loss is usually the result of a lesion in the optic radiation or tract on one
side. The visual defect is dependent on the site of the lesion:
right-hand sided lesions lead to left temporal and right nasal field loss
left-hand sided lesions lead to right temporal and left nasal field loss
Macular vision is usually lost in lesions arising in the optic tract; it is usually spared
in lesions arising in the more posterior optic radiation.
Causes of homonymous hemianopia include vascular disease, head injury or cerebral
tumours.
43. The findings of weakness, spasticity, and impairment of sensations are compatible
with:
a. Polymyositis
b. Spinal cord compression
???
44. Manifestations of ankylosing spondylitis include
a. Aortic incompetence
T
b. Proteinuria
T
c. Blood uric acid level of 9mg/100mL
F
d. Narrowing of sacroiliac joint space
T
e. Punched out lesions in vertebral bodies F
Aortic incompetence is seen in Ank Spon and Reiter’s, but not in IBD or Psoriatic
arthritides, when considering seronegative arthritides. Since ankylosing spondylitis is
chronic inflammation, and chronic inflammation can cause amyloidosis which can
cause proteinuria, proteinuria may be a manifestation of Ank Spon. Also, IgA
nephropathy is more common in Ank Spon than the non-Ank Spon population.
The term “Punched out lesions” is reserved for gout and multiple myeloma only.
45. In rheumatoid arthritis
a. There is an association with HLA-B27
b. Bony erosions occurring early in the disease imply an adverse prognosis
c. Gold therapy may cause fatal pancytopenia
d. Carpel tunnel syndrome may be a complication
e. Rheumatoid factor is usually negative if subcutaneous nodules are present
F
T
T
T
F
Rheumatoid arthritis is a chronic inflammatory disease affecting synovial joints. It
commonly affects proximal interphalangeal, metacarpophalangeal,
metatarsophalangeal, elbow, knees, ankles, hips, wrist, TMJ, glenohumeral and cspine. It is linked to HLA-DR4.
Poor prognosis factors in RA include:
- generalized polyarthritis (>20 joints involved)
- High ESR and CRP despite therapy
- Extra-articular features (also a sign of disease in IBD, except
sacroiliitis)
- RF positive
- Erosions on plain radiograph within 2 years onset
- HLA-DR4
Extra-articular features include:
Spinter hemorrhages, elbow nodules, carpal tunnel disorder, Felty’s (“Need Large
Spleen!” = neutropenia, lymphadenopathy, splenomegaly), vasculitic ulcers, eyes
(scleritis, episcleritis, keratoconjunctivitis), pericarditis, AV block (nodule in
conducting system), alveolitis, pleuritis and effusion, renal disease (amyloidosis or
secondary to NSAIDs, penicillamine).
Common side effects to commonly prescribed medications in RA include:
NSAIDs
GI ulceration and hemorrhage, renal impairment, fluid retention
DMARDs
Methotrexate myelosuppresion, hepatotoxicity, pneumonitis,
Alopecia, diarrhea/nausea/mucositis
Sulfasalazine Rash, myelosuppression, hepatotoxicity,
dizziness
Gold IM myelosuppression, rash, proteinuria, stomatitis
Azathioprine myelosuppression, hepatotoxicity
Anti-TNFalpha
Reactivation of TB, increased infection risk, lupus like reaction
46. Red cells may be found in the urine of patients with:
a. Acute pyelonephritis
T
b. Post streptococcal acute glomerulonephritis
T
c. Acute tubular necrosis
T
d. Subacute bacterial endocarditis
T
e. prerenal uremia
F
Hematuria can be caused by pathology at any site in the urinary tract, including renal,
ureteric, bladder and urethra
Renal:
- pyelonephritis
Ureter:
- stone
- renal calculi
- carcinoma
- trauma
- renal cysts including PCKD Bladder:
- cystitis
- renal carcinoma
- trauma
- glomerulonephritis
- stone
- papillary necrosis
- carcinoma
- TB
- AV malformation
Urethra:
- Prostate Ca
- stone/trauma
- BPH
Glomerulonephritis red cell casts, dysmorphic red cells, abnormal renal function
and
Proteinuria
Structural lesions pain and hematuria terminal or initial!
Glomerulonephritis can be caused by infective endocarditis.
47. Postural hypotension occurs in
a. Hemolytic anemia
T
b. Addison’s disease
T
c. Autonomic neuropathy
T
d. Salt depletion
T
e. Hypercalcemia
F
Orthostatic hypotension (also known as postural hypotension and, colloquially, as
head rush) is a sudden fall in blood pressure, typically greater than 20/10 mm Hg, that
occurs when a person assumes a standing position.
Symptoms, which generally occur after sudden standing, include dizziness,
lightheadedness, headache, blurred or dimmed vision (possibly to the point of
momentary blindness), and syncope (temporary loss of consciousness).
Causes
Orthostatic hypotension is substantially more common in tall patients.
It may be caused by: - hypovolemia
- dehydration
- prolonged bed rest
- anemia
- drugs (diuretics, beta-blockers, calcium channel blockers,
vasodilators, ACE inhibitors, tricyclics, antipsychotics,
Parkinson’s drugs)
- autonomic neuropathy (esp. diabetes)
- Addison’s
- atherosclerosis
- Shy-dragar syndrome (causes damage to autonomic nervous
system)
Salt depletion can be accompanied by hypovolemia and thus postural hypotension.
48. AIDS:
a. Occurs exclusively in homosexuals
b. Is uniformly fatal in less than two years
c. Is commonly complicated by pneumocystis carini pneumonia
d. The latent period after exposure is short, usually less than two months
e. Responds to treatment with interferon
F
F
T
F
F
AIDS develops from HIV, and is contracted by sharing of bodily fluids (blood and
semen especially). Transmission occurs by homosexual/heterosexual intercourse, IV
drug use, blood product transfusion and maternal-child transmission.
Once transmitted, HIV enters lymphoid tissue where it infects CD4-T lymphocytes
and monocyte/macrophages. The virus enters the cells by binding to the CD4 or
chemokine receptors, then replicates itself into host DNA. Progressive loss of CD4+
cells and a number of other mechanisms cause immune function impairment.
Clinical patterns:
Primary HIV infection:
Asymptomatic HIV:
Symptomatic HIV:
acute clinical syndrome when viral replication occurs.
Includes: fever, malaise, maculopapular rash.
During this phase, seroconversion occurs
MOST patients have prolonged asymptomatic period
(median 10 years without treatment) before clinical
features develop.
As HIV infection progresses, symptoms occur
(weight loss, diarrhea and fever)
Opportunistic infections include:
CD4 count
Infection
.
>500
200-500
50-200
<100
Rare
Herpes zoster, oral candidiasis, TB
Pneumocystic carinii pneumonia,
Mucocutaneous herpes
CMV, toxoplasmosis, Cryptococcus,
MAC (mycobacterium avium
intercellulare)
PML (progressive multifocal
leukoencephalopathy)
It should be mentioned that the incidence of Kaposis sarcoma and NonHodgkin’s
lymphoma is also significantly increased in AIDS.
PML= progressive multifocal leukoencephalopathy =uncommon
demyelinating disease caused by polyoma JC virus. Diagnosis is by imaging (white
matter lesions) and PCR of CSF for polyoma JC virus. Treatment is with HAART.
Treatment in HIV is with a number of drugs in combination (HAART=highly active
antiretroviral therapy), which has led to a significant decrease in mortality and delay
in progression to AIDS. Classes of drugs exist including:
- nucleoside RT inhibitors
ddI=didanosine
AZT=azidothymidine aka Zidovudine
3TC=lamivudine
- non-nucleoside RT inhibitors
nevirapine, efavirenz
- protease inhibitors
ritonavir, indinavir, nelfinavir,
HAART= 2 nucleoside RT inhibitors + either non-nucleoside RT inhibitor
Or 1 or 2 protease inhibitors
49. Hookworm disease
a. Causes iron deficiency anemia
T
b. Causes megaloblastic anemia
F
c. Causes liver abscess
F
d. Is treated with penicillin
F
e. Is common in Africa
T
Human hookworm infection is a common soil-transmitted helminth infection that is
caused by the nematode parasites, Necator americanus and Ancylostoma duodenale.
Worldwide, hookworm infects an estimated 740 million people, most of whom are
asymptomatic. Despite this lack of symptoms, hookworm substantially contributes to
the incidence of anemia and malnutrition in developing nations. The greatest number
of cases occurs in the rural tropical and subtropical areas of China and sub-Saharan
Africa, followed in number by India, South Asia, and Latin America.
The life cycle of hookworms begins with the passing of hookworm eggs in human
feces and their deposition into the soil. Larval growth is most proliferative in
favorable soil that is sandy and moist, with an optimal temperature of 20-30°C. Under
these conditions, the larvae hatch in 1 or 2 days to become rhabditiform larvae, also
known as L1. The rhabditiform larvae feed on the feces and undergo 2 successive
molts, such that, after 5-10 days, they become infective filariform larvae, or L3. These
L3 go through developmental arrest and can survive in damp soil for as long as 2
years. However, they quickly become desiccated if exposed to direct sunlight, drying,
or salt water. L3 live in the top 2.5 cm of soil and move vertically toward moisture
and oxygen. Infection of the human host is established when filariform larvae
penetrate the skin, typically on the hands or feet. This penetration may cause a local
pruritic dermatitis, also known as ground itch. The larvae migrate through the dermis,
entering the bloodstream and moving to the lungs within 10 days. Once in the lungs,
the hookworms penetrate the alveoli and are carried to the glottis by means of the
ciliary action of the respiratory tract. During pulmonary migration, the host may
develop a mild reactive cough, sore throat, and fever that resolve after the worm
migrates into the intestines. At the glottis, the larvae are swallowed and carried to
their final destination, the small intestine. During this part of the migration, the larvae
undergo 2 further molts, developing a buccal capsule and attaining their adult form.
Using this buccal capsule, the worms attach themselves to the mucosal layer of the
proximal small intestine, including the lower part of the duodenum, jejunum, and
proximal ileum. In 3-5 weeks, the adults become sexually mature, and the female
worms begin to produce eggs that appear in the person's feces.
Intestinal blood loss secondary to infection is the major clinical manifestation of
hookworm infection. In fact, hookworm disease historically refers to the clinically
significant hypochromic, microcytic anemia and the depletion of iron stores resulting
from chronic intestinal blood loss secondary to hookworm infection. Attaching to the
mucosal layer and using their mouth parts, hookworms rupture the arterioles and
venules along the luminal surface of the intestine. The worms ingested and digested
some of the blood from the injured mucosa by means of a multienzyme cascade of
metallohemoglobinases. Inhibited host coagulation due to a series of anticoagulants
directed against factor Xa and the factor VIIa–tissue factor complex, as well as again
platelet aggregation, further exacerbate blood loss.
Diagnosis is made by finding eggs in the feces. Treatment is with anti-helminths
(Albendazole, mebendazole)
50. The following are frequently seen in systemic sclerosis (scleroderma)
a. Raynaud’s phenomenon T
b. Ulcers on fingers
T
c. Dysphagia
T
d. Peripheral neuritis
F
e. Hemiplegia
F
Ulcers may be seen on the fingers due to digital ischemia.
Systemic sclerosis is also known as scleroderma, and is classified into systemic or
localized types:
SYSTEMIC: - systemic sclerosis with diffuse cutaneous disease
- systemic sclerosis with limited cutaneous disease (CREST)
- systemic sclerosis without scleroderma (no cutaneous involvement)
LOCALIZED: morphea (plaques of fibrotic skin)
- linear (fibrotic bands)
- “en coup de saber” = linear scleroderma of one side of scalp and
forehead.
Pulmonary fibrosis and pulmonary HTN,
Amenorrhea and infertility
Thyroid fibrosis + hypothyroidism
Myocardial fibrosis, pericarditis, restrictive cardiomyopathy
GERD, Biliary cirrhosis,
classic facies (purse-string mouth and mouse-like facies)
Renal crisis (RPGN, MAHA)
CREST= Calcinosis+Raynauds+Esophageal
dysmotility+Sclerodactyly+Telangiectasias
51. Abdominal pain relieved by defecation and associated with loose bowel motions
is a feature of:
a. Irritable bowel syndrome T
b. Anorexia nervosa
T
c. Peptic ulcer of stomach
F
d. Gall stones
F
e. Crohn’s disease of colon
F
IBS is a primarily functional bowel disorder characterized by abdominal pain that is
relieved by defecation, alternating loose stool and hard stool, mucus in the stool, and a
frequent sensation of incomplete evacuation. Serotonin is implicated in the
pathophysiology of IBS, as it modulates visceral sensation within the central nervous
system. A serotonin4-receptor agonist, tegaserod, has demonstrated efficacy in the
treatment of constipation-dominant IBS.
As stated previously, extra-GI conditions associated with IBS are numerous. In a
review of the published literature on IBS since 1966, Whitehead, Palsson, and Jones
(2002) noted that non-GI, nonpsychiatric disorders with the best-documented
association with IBS included fibromyalgia (49% have IBS), chronic fatigue
syndrome (51%), temporomandibular joint disorder (64%), and chronic pelvic pain
(50%). Similar to IBS, the female predominance in these conditions is well
documented. It is certin, however, that “abdominal pain relieved by defecation” is a
classic expression of functional bowel syndrome, and thus underlying pathology (gall
stones, ulcer, IBD) must be excluded.
The Rome criteria, rather than the Manning criteria, were applied to identify IBS
subjects. IBS was defined as abdominal pain that kept recurring over a period of more
than three months in the prior year, in combination with: (1) one or more of the
following symptoms: (i) abdominal pain relieved by defecation, often (more than 25%
of the time); (ii) more frequent and/or less frequent bowel movements with pain,
often; or (iii) looser and/or harder stools with pain, often; and (2) two or more of the
following: (i) more than three bowel movements a day, often and/or less than three
bowel movements a week, often; (ii) stools very lumpy or hard, often and/or stools
very loose or watery, often; (iii) incomplete rectal evacuation, often and/or urgency,
often and/or straining, often; (iv) abdominal bloating or distension, often; or (v)
mucus in stools.
Eating disorders and a history of eating disorders are significantly (5-15x) more
common in functional bowel diseases than in either the population at large, or nonfunctional bowel diseases. Thus, I would say this is true.
52. The following have hematuria
a. Steroid sensitive but recurrent minimal change GN
b. IgA nephropathy
c. Nephropathy associated with diabetes
d. Infective endocarditis
e. Acute papillary necrosis
F
T
T
T
T
See question 46
53. A 50 year old woman is thought likely to have osteoporosis
a. A history of alcoholism would suppose the diagnosis
b. A history of thyrotoxicosis would support the diagnosis
c. A-P and lateral xrays of spine are sensitive
indicator of disease progression
d. Bone loss is mainly cortical, not trabecular
T
T
F
F
e. Vitamin D replacement is mandatory
F
Trabecular bone is the thin bars of bone tissue in spongy bone
Cortical bone is the outer part of the bone.
Osteoporosis is quantitative decrease in bone matrix components of bone.
Osteoporosis may be primary or secondary. Osteoporosis is common in elderly
women, especially with late menarche, early menopause, long history of
oligomenorrhea. Other risk factors include alcohol, smoking, sedentary lifestyle,
family history and lean body type.
Secondary osteoporosis occurs in:
Endocrine:
Cushing’s, thyrotoxicosis, hyperparathyroidism, hypogonadism
Rheumatological disease:
any inflammatory arthropathy.
Gastrointestinal:
malabsorption, cirrhosis
Drugs:
Corticosteroids, heparin, warfarrin, phenytoin
Neoplasia
Osteoporosis causes low impact fractures and thoracic vertebral fractures loss of
height, exaggerated dorsal kyphosis and pain.
While plain radiographs can be used to establish fractures, it is DEXA (dual emission
X-ray absorptiometry) used to measure bone density, to quantify disease progression
from normal to osteopenia (mild moderate bone loss) to osteoporosis (severe bone
loss).
54. Characteristic features of sarcoidosis include:
a. fatigue
T
b. hypocalcemia
F
c. erythema marginatum
F
d. positive mantoux test
F
e. Uric acid stones
F
Sarcoidosis is a multi-system disease characterized by non-caseating granulomas.
Association with HLA-B8 has been demonstrated, especially with erythema nodosum
and arthalgia. Two classic presentations exist:
ACUTE:
erythema nodosum, arthralgia, BHL
CHRONIC: Slowly progressive dyspnea as a result of progressive pulmonary
fibrosis
There is no relationship with TB and sarcoidosis. Mantoux test is for TB, not for
sarcoidosis.
Erythema marginatum is described as the presence of pink rings on the trunk and
inner surfaces of the arms and legs which come and go for as long as several months.
The rings are barely raised and are pruritic. The face is generally spared. It occurs in
less than 5% of patients with rheumatic fever (5% from emedicine.com, 50% if you
take it from Medicine at a Glance), but is considered a major Jones criterion when it
does occur. It is an early feature of rheumatic fever and may be associated with mild
carditis (inflammation of heart muscle).
10% get hypercalcemia.
55. With regards to acute stroke, the following statements are true
a. cerebral ischemia is readily differentiated from
F
cerebral hemorrhage from clinical signs
b. early CT scanning always demonstrates the lesion
F
c. Infarction of the cerebral cortex is
T
commonly associated with dysphagia
d. cerebellar hemorrhage often requires surgical intervention
T
e. patients with A.fib should be anticoagulated immediately
F
The mechanism of stroke (infarct or bleed) must be demonstrated by CT or MRI. If
infarct, the origin or the thrombus should be worked out by carotid ultrasound or
transesophageal echo (aortic arch). If hemorrhage, angiography to exclude an
aneurysm and sugery/intervention may be needed.
INFARCTS: 1. keep BP low (don’t decrease acutely- this can cause watershed
infarcts).
2. give aspirin and other antiplatelet agents.
3. thrombolysis may be indicated if given within 3 hours of symptom onset.
HEMORRAGE: 1. Lower BP (rapidly if needed.)
2. If in posterior fossa, neurosurgical intervention is required to prevent
coning. If intracerebral with mass effect, evacuation may be
needed.
The assessment and management in stroke: Imagine a Scottish lady from Glasgow
with large DDDD breasts. With regards to Glasgow scale, remember how lovely
Glasgow is, so lovely we Must Vacate Edinburgh!
Glasgow coma scale: Assess best motor response, best verbal response, best eye
response
Must
Motor (6)
6
Obeys commands
5
localizes to pain
4
withdraws
3
Flexes from pain
2
extends from pain
1
No limb movement
Vacate
Verbal (5):
Edinburgh
Eyes (4)
D
Dysphagia:
D
DVT
5
4
3
2
1
Oriented
Disoriented speech
Incoherent words
Non-sensicle vocalizations
No speech
4
Spontaneous eye opening
3
Eyes open on command
2
Eyes open to pain
1
No eye opening
assess swallowing. If aspiration risk high, NG tube short term
and PEG tube long term
prevent DVT using low-dose heparin
(unless BLEED in which case avoid)
D
D
Disability
Depression
Assess rehabilitation needs on basis of disability
50-75% of patients get depression and antidepressants may help
Clinical signs do not readily distinguish between bleeds and ischemia. Moreover, a
CT scan may not always show a bleed immediately, and early ischemia may be
difficult to see. Moreover, a patient with A.Fib may still get a bleed, in which case
anticoagulation may be contraindicated.
56. With regards to hemochromatosis, the following statements are true
a. It is an autosomal recessive condition
b. Patients may present with glycosuria
c. The condition may be complicated by hepatoma development
d. Therapy usually involves desferrioxamine
e. A genetic screen is available to aid diagnosis
T
T
T
F
T
Hemochromatosis is the abnormal accumulation of iron in parenchymal organs,
leading to organ toxicity. It is the most common inherited liver disease in whites and
the most common autosomal recessive genetic disorder.
Hereditary hemochromatosis is an adult-onset disorder characterized by
inappropriately high iron absorption resulting in progressive iron overload. The
organs involved are the liver, heart, pancreas, pituitary, joints, and skin.
In hereditary hemochromatosis, dysregulation of intestinal iron absorption occurs,
wherein iron continues to be efficiently absorbed even in the face of substantial
elevation of body iron stores.
The gene responsible for the disease is called HFE and is located on chromosome 6. It
is mutated in the vast majority of individuals with hereditary hemochromatosis. HFE
interacts with the transferrin receptor and causes a clear decrease in the affinity with
which the receptor binds transferrin. This interaction also may modulate cellular iron
uptake and decrease ferritin levels. When a mutant or nonfunctional variant of the
HFE gene is present, ferritin levels are not under influence of a normal and functional
HFE gene, which leads to enhanced accumulation of iron in peripheral tissues. Firstdegree relatives can be screened for hemachromatosis using genetic mutation analysis
(HFE mutation analysis).
Findings suggestive of increased iron transport at the basolateral membrane of
enterocytes in hemochromatosis have emerged from numerous studies of HFE-related
hemochromatosis in humans and in mice.
Hepcidin, a human antimicrobial peptide synthesized in the liver, plays a key role in
the down-regulation of iron release by enterocytes and macrophages. The absence of
this new peptide is associated with severe early-onset iron-loading phenotype. It is
also inappropriately low in adult-onset HFE-related disease.
Excess iron is hazardous because it produces free radical formation. The presence of
free iron in biological systems can lead to the rapid formation of damaging reactive
oxygen metabolites such as the hydroxyl radical and the superoxide radical. These can
produce DNA cleavage, impaired protein synthesis, and impairment of cell integrity
and cell proliferation, leading to cell injury and fibrosis.
Symptoms usually begin between age 30 years and age 50 years, but they may occur
much earlier. Clinical manifestations include the following:
Liver disease (cirrhosis and later, hepatoma/hepatocellular carcinoma)
Skin pigmentation
Diabetes mellitus (can of course cause glycosuria…)
Arthropathy
Impotence in males and amenorrhea in females
Cardiac enlargement, with or without heart failure or conduction defects
Dilated cardiomyopathy
Hypothyroidism
Cirrhosis: This is one of the most common disease manifestations of the tissue
damage caused by hemochromatosis, and it may progress to liver cancer years later
(risk >200-fold). It also is the most common cause of death in patients with
hereditary hemochromatosis.
Reversibility with iron removal has been reported even with development of varices,
but this is more likely early in the course of liver disease.
Iron removal is typically performed with blood letting (venesection 500 g whole
blood weekly until excess iron stores removed, then every 3 months after). If this is
insufficient (rarely), iron-chelators such as desferrioxamine may be used.
All patients with cirrhosis should undergo diagnostic endoscopy to document the
presence of varices and to determine their risk of variceal hemorrhage. Patients at risk
for variceal hemorrhage should be considered for primary prophylaxis with
propranolol or nadolol.
Most patients are asymptomatic (75%) and are diagnosed when elevated serum iron
levels are noted on a routine a chemistry screening panel or when screening is
performed because a relative is diagnosed with hemochromatosis.
57. The following are causes of secondary hyperlipidemia
a. Loop diuretics
F
b. Chronic renal failure
T
c. Hypothyroidism
T
d. High alcohol intake
T
e. Obstructive jaundice
T
Secondary causes contribute to most cases of dyslipidemia in adults. The most
important secondary cause in developed countries is a sedentary lifestyle with
excessive dietary intake of saturated fat, cholesterol, and trans fatty acids (TFAs).
TFAs are polyunsaturated fatty acids to which hydrogen atoms have been added; they
are commonly used in many processed foods and are as atherogenic as saturated fat.
Other common secondary causes include diabetes mellitus, alcohol overuse, chronic
renal insufficiency and/or failure, hypothyroidism, primary biliary cirrhosis and other
cholestatic liver diseases, and drugs, such as thiazides, β-blockers, retinoids, highly
active antiretroviral agents, estrogen and progestins, and glucocorticoids. While
thiazide diuretics classically cause hyperlipidemia, loop diuretics can cause a
temporary increase in plasma cholesterol and triglyceride concentrations. Since this is
temporary only, I’d say false for a.
58. With regards to Atrial fibrillation
a. Commonly occurs in patients with a structurally normal heart
b. May be precipitated by alcohol excess
c. tends to be asymptomatic in patients with
hypertrophic cardiomyopathy
d. On careful auscultation, a fourth heart sound can be heard
e. a-waves are often visible in JVP
T
T
F
F
F
The typical JVP appears like:
Since the a wave refers to the atrial systole, there is no a wave in A.Fib.
Risk factors for atrial fibrillation include age, male sex, long-standing hypertension,
valvular heart disease, left ventricular hypertrophy, coronary artery disease (with or
without depressed left ventricular function), diabetes mellitus, smoking, and any form
of carditis.
Heart sounds S1 and S2 are still present but irregularly irregular.
Causes of atrial fibrillation can be divided into cardiovascular versus
noncardiovascular causes.
cardiovascular causes:
HTN, IHD, CHF, carditis, cardiomyopathy
Infiltrative heart disease of any type
Sick sinus syndrome
Noncardiovascular causes:
Hyperthyroidism
Low levels of potassium, magnesium, or calcium
Pheochromocytoma
Sympathomimetic drugs, alcohol, electrocution
Noncardiovascular respiratory causes:
Pulmonary embolism
Pneumonia
Lung cancer
Hypothermia
59. In primary hyperparathyroidism
a. Most patients present with urinary tract calculi
b. Serum calcium is always higher than normal
c. PTH is usually within normal limits
d. Chloride:phosphate ratio is elevated
F
F
F
T
The chloride/phosphate (Cl:PO[4]) ratio is known to help distinguish between the
hypercalcemia of primary hyperparathyroidism (HPT) and hypercalcemia from other
causes. In the absence of renal failure, the chloride phosphate ratio is elevated in
primary hyperparathyroidism but not other causes of hypercalcemia.
Primary hyperparathyroidism is usually (90%) caused by a parathyroid adenoma. This
may or may not be in conjunction with MEN-1 syndrome (parathyroid hyperplasia+
pituitary adenoma+ pancreatic polypeptide tumors)
Incidentally: MEN2a Thyroid medullary Ca, parathyroid hyperplasia,
phaeochromocytoma (70% bilateral)
MEN2b MEN2A+ Mucosal neuromas+ Marfanoid body habitus.
KNOWN defect=Chr.10 oncogene Ret
Primary hyperparathyroidism has a female to male preponderance of 2:1. It is the
most common cause of hypercalcemia, although 50% are asymptomatic and only
discovered because of incidental investigations. Mild or normal calcium levels may be
present. Definitive treatment is surgical resection. Postoperative hypocalcemia is
usually transient and treatable with calcium supplements and vitamin D.
60. Which of the following suggests that a thyroid swelling is malignant
a. Thyrotoxicosis
F
b. Hoarseness
T
c. Palpable lymph glands
T
d. Increased uptake of iodine F
Thyrotoxicosis can be caused by Hashimotos thyroiditis (transient hyperthyroidism
before becoming hypothyroid), Graves disease (most common cause), toxic
multinodular goiter, or toxic adenoma. Thus thyrotoxicosis does not imply
malignancy.
Hoarseness and thyroid swelling implies the swelling has invaded either the recurrent
laryngeal nerve, or the larynx/vocal cords. This implies malignancy.
Palpable lymph nodes may be present in infection, chronic inflammatory conditions
(RA, etc) or neoplasms, but in the setting of a thyroid swelling, palpable
lymphadenopathy would be suggestive of malignancy.
Thyroid uptake scan, when increased, may suggest Graves, toxic adenoma or
multinodular goiter, thus no suggestion is established.
61. The following are recognized complications of Crohns disease
a. Iritis
T
b. Ascending cholangitis
F
c. Sclerosing cholangitis
T
d. Erythema nodosum
T
PBC (primary biliary cirrhosis) is associated with celiac, rheumatoid disease and
autoimmune thyroid disease. This is easy to remember cause PBC has a
female:male ratio of 9:1, and is similar to thyroiditis and rheumatoid disease in
its female preponderance.
PSC (primary sclerosing cholangitis) is associated with IBD.
This is easy to remember cause IBD includes two pathologies (UC and CD),
as
does PSC, which includes intrahepatic and extrahepatic duct disease.
The extraintestinal manifestations of Crohn’s disease include:
Uveitis and iritis
Ankylosing spondylitis
Sacroiliitis
Anemia (iron and B12 deficiency, and chronic)
Hepatitis
Mouth ulcers
Gallstones
Fistulas (enterocolic/enterovesical, etc.)
PBC
Monoarthritis
Pyoderma gangrenosum
Erythema nodosum
62. Pancreatic pseudocysts
a. Are developmental in origin
b. Usually arise in the lesser peritoneal sac
c. May be effectively treated by internal drainage
d. Occur following pancreatic abscess
F
F
F
Single or multiple fluid collections that look like cysts on pancreatic imaging are
often observed during acute pancreatitis. Because of increasing sensitivity of imaging
modalities and improvements in technology providing enhanced therapeutic abilities,
the questions of when and whether drainage should be performed and what modality
should be used to drain the cysts are often asked. Strictly defining the type of fluid
collection is very important when reviewing pancreatic fluid collections. The
therapeutic approach is different depending on the type of collection.
Pseudocysts are best defined as a localized fluid collection that is rich in amylase and
other pancreatic enzymes, that has a nonepithelialized wall consisting of fibrous and
granulation tissue, and that usually appears several weeks after the onset of
pancreatitis.
These characteristics contrast with those of acute fluid collections, which are more
evanescent and are serosanguinous inflammatory reactions to acute pancreatitis.
These collections are noted in moderate-to-severe pancreatitis. Acute fluid collections
usually have an irregular shape and lack a well-defined wall. In general, they resolve
in about 65% of cases.
Pathophysiology: Pancreatic pseudocysts can be single or multiple. Multiple cysts
are more frequently observed in patients with alcoholism, and they can be multiple in
about 15% of cases. Size varies from 2-30 cm. About one third of pseudocysts
manifest in the head of the gland, and two thirds appear in the tail. The fluid in
pseudocysts has been well characterized as clear or watery, or it can be
xanthochromic. The fluid in pseudocysts usually contains very high amounts of
amylase, lipase, and trypsin, though the amylase level may decrease over time.
The pathogenesis of pseudocysts seems to stem from disruptions of the pancreatic
duct due to pancreatitis and extravasation of enzymatic material. Two thirds of
patients with pseudocysts have demonstrable connections to the pancreatic duct. In
the other third, an inflammatory reaction is supposed to have sealed the connection so
that it is not demonstrable. The cause of pseudocysts parallels the cause of acute
pancreatitis; 75-85% of cases are caused by alcohol or gallstone disease–related
pancreatitis. In children, pseudocysts and trauma are frequently associated.
Sex: The male predominance in the incidence of pseudocysts mirrors the male
predominance in the incidence of pancreatitis.
Age: Pseudocysts may occur after pancreatitis in any age group. In children,
pseudocysts are most likely observed after abdominal trauma. In elderly persons, take
care not to confuse cystic neoplasms with pseudocysts.
Treatment:
Most pseudocysts resolve without interference and only require supportive care.
Several studies have indicated that the size of the cyst and the length of time the cyst
has been present are poor predictors of complications. In general, larger cysts are
more likely to become symptomatic or cause complications. However, some patients
with larger collections do well; therefore, size of the pseudocyst alone is not an
indication for drainage.
Prognosis:
Most pseudocysts resolve without interference, and patients do well without
intervention.
Outcome is much worse for patients who develop complications or who have the cyst
drained. The presence of pancreatic necrosis is a poor prognostic sign.
The failure rate for drainage procedures is about 10%, the recurrence rate is about
15%, and the complication rate is 15-20%.
Indications for drainage include the following:
Complications
Symptoms
Concern about possible malignancy
Drainage can be carried out by catheter drainage, ERCP, or surgical drainage.
Lab Studies:
CEA
CEA-125
Fluid viscosity
Amylase
Pseudocyst fluid
Low
Low
Low
High
Neoplasm sample
Elevated
Elevated
Elevated
Low
Imaging Studies:
CT scan is the imaging criterion standard for pancreatic pseudocysts. It has a
sensitivity of 90-100% and is not operator dependent.
The usual finding on CT scan is a large cyst cavity in and around the pancreas.
Multiple cysts may be present.
63. Acute protrusion of L4/L5 or L5/S1 intervertebral disc
a. Is usually associated with lumbar scoliosis
b. Causes reduction in straight leg raising
c. Commonly causes loss of knee tendon reflex
d. May be associated with sensory change
at the lateral border of the foot
F
T
T
T
A spinal disc herniation is a pathological condition in which a tear in the outer,
fibrous ring (annulus fibrosus) of an intervertebral disc allows the soft, central portion
(nucleus pulposus) to be extruded (herniated) to the outside of the disc. It is normally
a further development of a previously existing disc protrusion, a condition in which
the outermost layers of the annulus fibrosus are still intact, but can bulge when the
disc is under pressure.
Disc herniation can occur in any disc in the spine, but the two most common forms
are the cervical disc herniation and the lumbar disc herniation. The latter is the most
common, causing lower back pain (lumbago) and often leg pain as well, in which case
it is commonly referred to as sciatica.
Lumbar disc herniation occurs 15 times more often than cervical (neck) disc
herniation, and it is one of the most common causes of lower back pain. The cervical
discs are affected 8% of the time and the upper-to-mid-back (thoracic) discs only 1 2% of the time.
The upper two cervical intervertebral spaces, the sacrum, and the coccyx have no
intervertebral discs and are thus exempt from herniated discs.
The classic presentation of a HNP (herniated nuclear palposus) includes the complaint
of sciatica (an intractable radiating pain), with associated objective neurological
findings of weakness, reflex change, or dermatomal numbness.
Causes of a disc herniation can include general wear and tear on the disc over time,
repetitive movements, stress on the disc that occurs while twisting and lifting, or other
injuries. The discs cushion the spine from compressive forces, but are weak to
pressure applied during rotational movements. That is why a person who bends to one
side, at a bad angle, to pick up a piece of paper may more likely herniate a spinal disc
than a person falling from a ladder and landing on his or her back.
Pain that radiates from your lower (lumbar) spine to your buttock and down the back
of your leg is the hallmark of sciatica. You may feel the discomfort almost anywhere
along the nerve pathway, but it's especially likely to follow a path from your low back
to your buttock and the back of your thigh and calf.
The pain can vary widely, from a mild ache to a sharp, burning sensation or
excruciating discomfort. Sometimes it may feel like a jolt or electric shock. Sciatic
pain often starts gradually and intensifies over time. It may be worse when you cough
or sneeze, and prolonged sitting or walking can also aggravate symptoms. Usually
only one lower extremity is affected.
In addition to pain, you may also experience:
Numbness or muscle weakness along the nerve pathway in your leg or foot. In some
cases, you may have pain in one part of your leg and numbness in another.
Tingling or a pins-and-needles feeling, most commonly in your toes or part of your
foot.
A loss of bladder or bowel control. This is a sign of cauda equina syndrome, a rare but
serious condition that requires emergency care.
64. The following are features of Horner’s syndrome
a. Unilateral enophthalmos
b. Atrophy of the hand muscles
c. Miosis
d. Loss of sweating on one side of face
T
F
T
T
Horner’s syndrome is a disruption in the cervical sympathetic chain, and can be
caused by:
Thyroid carcinoma
Syringomyelia
Apical lung Ca
Cervical rib
Aortic aneurysm
MS/glioma in posterolateral brain stem
Trauma
Carotid dissection
Signs found in all patients, regardless of the level of interruption include mild-tomoderate ptosis owing to denervation of the sympathetically controlled Müller
muscle, slight elevation of the lower lid (upside-down ptosis) due to denervation of
the lower lid muscle analogous to Müller muscle in the upper lid, and miosis and
dilation lag, where pupillary dilation after psychosensory stimuli is slower in the
affected pupil than the unaffected pupil.
Depending on the level of the lesion, impaired flushing and sweating may be found
ipsilaterally.
65. Diagnosis of insulinoma is suggested by the following
a. Fasting hypoglycemia
b. Hypoglycemia relieved by meals
c. Hypoglycemia coming 1-2 hours after meals
d. Hepatic disease in an alcoholic
T
T
T
F
e. Hypoglycemia with very low plasma insulin
F
Insulinomas are the most common cause of hypoglycemia resulting from endogenous
hyperinsulinism.
Pathophysiology: An insulinoma is a neuroendocrine tumor deriving mainly from
pancreatic islet cells that produce excessive amounts of insulin. About 90% of
insulinomas are benign. In healthy individuals, insulin and C-peptide are secreted in
equimolar quantities because they derive from the same inactive precursor, proinsulin.
Normally, less than 20% of proinsulin is released directly into the circulation.
Some insulinomas secrete additional hormones, such as gastrin, 5-hydroxyindolic
acid, adrenocorticotropic hormone (ACTH), glucagon, human chorionic
gonadotropin, and somatostatin. The tumor may secrete insulin in short bursts,
causing wide fluctuations in blood levels.
Approximately 10% of insulinomas are malignant (metastases are present), and 10%
are multiple, particularly in patients with multiple endocrine neoplasia type 1 (MEN
1). Of patients with multiple insulinomas, 50% have MEN 1. Insulinomas are
associated with MEN 1 in 5% of patients. On the other hand, 21% of patients with
MEN 1 develop insulinomas.
About 85% of patients present with symptoms of hypoglycemia with diplopia, blurred
vision, palpitations, or weakness.Other symptoms include confusion, abnormal
behavior, unconsciousness, or amnesia. About 12% of patients have grand mal
seizures.
Adrenergic symptoms (hypoglycemia causes adrenalin release) include weakness,
sweating, tachycardia, palpitations, and hunger. Symptoms may be present from 1
week to as long as several decades prior to the diagnosis (1 mo to 30 y, median 24
mo, as found in a large series of 59 patients). Hypoglycemia usually occurs several
hours after a meal.
In severe cases, symptoms may develop in the postprandial period. Symptoms can be
aggravated by exercise, alcohol, hypocaloric diet, and treatment with sulfonylureas.
Weight gain occurs in 20-40% of patients.
66. The following are true of ankylosing spondylitis
a. It is commonest in females over 40
F
b. Can be associated with arthritis of the hip joint F
c. It may present with sciatica
T
Ankylosing spondylitis is a chronic inflammation of the spine that may gradually
result in a fusion of vertebrae. Symptoms include a slow development of back
discomfort, with pain lasting for more than three months. The back is usually stiff in
the morning; pain improves with exercise. In severe cases, the patient must
continually stoop over. It can be quite mild, however, and it rarely affects a person's
ability to work. It occurs mostly in young Caucasians in their mid-twenties. The
disease is more common in men, but about 30% of the cases are in women.
Researchers believe that in most cases it is hereditary. About 20% of people with
inflammatory bowel disease and about 20% of people with psoriasis develop a form
of ankylosing spondylitis. There are few effective treatments for this potentially
disabling disease, although etanercept (Enbrel) and infliximab (Remicade), antiinflammatory agents known as TNF-blockers, are proving to be beneficial.
67. A 70 year old lady presented with a cough. She is also anorexic of late. The
following should be performed immediately?
a. ESR
T
b. CXR
T
c. Psychiatric evaluation
F
d. Sedate her, send her home and review in a week F
e. Examine sputum for AFB
T
ESR: This presentation may be consistent with an infection or inflammatory
process, both of which would raise ESR. This would gage recovery as well.
CXR: May have TB or other chest infection.
Psychiatric evaluation: anorexia may be psychiatric, but cough suggest organic cause.
Sedation, send home and review later: Obviously this woman needs to be
investigated.
Examine sputum for AFB: Acid-fast bacilli may be found in TB, so do it.
68. Subdural hematoma is suggested by the following:
a. Change of personality
T
b. Brain spinal tap
F
c. History of trauma
T
d. Central scotoma
F
Subdural hematoma is usually a venous bleed in brain shrinkage (old age, dementia,
chronic alcoholism). Blood oozes into subdural space. Space-occupying lesions result.
There may be a history of trauma. Focal neurological deficit, decreased mobility,
decreased mental agility (if in frontal area, personality change may occur). CT scan is
diagnostic. Brain spinal tap (I assume they mean lumbar puncture) is diagnostic in
subarachnoid hemorrhage, not subdural. Evacuation should be considered.
Central scotoma is an area of depressed vision that corresponds with the point of
fixation and interferes with central vision. It suggests a lesion between the optic nerve
head and the chiasm. Possible causes include:
multiple sclerosis - which may cause unilateral or asymmetrical bilateral scotoma
methyl alcohol - which may cause symmetrical bilateral scotoma
nutritional causes - which may be due to, e.g. alcohol or tobacco amblyopia, B12
deficiency
vascular lesions – hemorrhage (into macula) may cause unilateral scotoma; this is not
subdural however
gliomas of the optic nerve - this may cause unilateral scotoma
simple glaucoma - which may initially cause an off-centre scotoma
69. The following investigations are indicated in a patient with bilateral hilar
lymphadenopathy.
a. Mantoux test
T
b. Kveim test
T
c. Serum calcium
T
d. CT scan
T
e. Lung biopsy
T
Bilateral hilar lymphadenopathy is classically associated with sarcoidosis, which can
cause hypercalcemia and a positive Kveim test (splenic extract from sarcoid patient A
injected into patient B suspected of having sarcoidosis. The reaction is biopsied and
histologically examined for presence of non-caseating granuloma). This test is no
longer done, however, because of concerns over infection. Instead, a lung biopsy can
be 90% sensitive or a liver biopsy 70% sensitive for the pathognomonic lesion of
sarcoidosis.
Alternative causes of bilateral hilar lymphadenopathy include TB, for which a
Mantoux test can be performed, and neoplasm, for which a CT would be indicated.
70. Complications of Diabetes mellitus include
a. LOAD
?
b. Liver cysts
F
c. Proteinuria
T
d. Raynaud’s phenomenon
F
e. Neovascularization of the retina
T
Diabetic complications can be categorized into microvascular or macrovascular:
Microvascular typically affects nerves, eyes, kidneys (neuropathy, retinopathy,
nephropathy). Macrovascular affects the large arteries (atherosclerosis increasing
MI/stroke). Neuropathy includes autonomic, sensory or motor neuropathy.
Retinopathy is divided into background (dot-blot hemorrages, exudates ),
preproliferative (cotton wool spots + venous beading + IRMAs), and proliferative
(neovascularization) diabetic retinopathy. Maculopathy risk is also increased in
diabetes. Nephropathy includes basement membrane thickening to KimmelsteinWilson lesion (glomerulosclerosis). Nephrotic and nephritic syndrome may result.
Raynaud’s phenomenon is episodic, painful, digital ischemia in response to cold or
emotional stimuli, causing a classical color change from white to blue to red (“With
Boys Rarely” as it affects mostly women!). Causes include:
Idiopathic
Affects young women mostly
Secondary
Cervical rib
Vibrating tools
Vasculitis
CT disease (SLE, RA, dermatmyositis)
Cryoglobinemia
Cold agglutinins
Hyperviscosity
Drugs (beta-blockers, cytotoxics)
71. An alcoholic presents with hepatosplenomegaly and hematemesis
a. The bleeding can be assume to be esophageal varices
F
b. Vitamin K will reverse all clotting defects
F
c. The presence of blood in the GIT may be harmful
T
d. Lactulose, magnesium sulphate and
F
neomycin may all be useful
e. The features of encephalopathy include
T
altered consciousness
The combination of lactulose (osmotic diuretic), magnesium sulphate (osmotic
diuretic), neomycin (counteracts constipation)-this is seen and used in IBS (irritable
bowel syndrome).
Encephalopathy literally means disease of the brain. It refers to the central nervous
system, or parts of it. Pathologists are more likely to use this term. Descriptions of the
living usually refer to dementia. Medical Imaging has made physiopathology more
practical on the living, however. Encephalopathy alters brain function and/or
structure. It may be caused by an infectious agent (bacteria, virus, or prion), metabolic
or mitochondrial dysfunction, brain tumor or increased intracranial pressure,
prolonged exposure to toxic elements (including solvents, drugs, radiation, paints,
industrial chemicals, and certain metals), chronic progressive trauma, poor nutrition,
or lack of oxygen or blood flow to the brain. It is also known that concomitant use of
lithium with other neuroleptics may, in rare cases, cause encephalopathy. The
hallmark of encephalopathy is an altered mental state. Depending on the type and
severity of encephalopathy, common neurological symptoms are progressive loss of
memory and cognitive ability, subtle personality changes, inability to concentrate,
lethargy, and progressive loss of consciousness. Other neurological symptoms may
include myoclonus (involuntary twitching of a muscle or group of muscles),
nystagmus (rapid, involuntary eye movement), tremor, muscle atrophy and weakness,
dementia, seizures, and loss of ability to swallow or speak.
Hematemesis is the vomiting of fresh red blood. The source is generally the upper
gastrointestinal tract. Patients can easily confuse it with hemoptysis (coughing up
blood), although the former is more common.
CAUSES:
Vomiting of ingested blood after hemorrhage in the oral cavity, nose or throat
Mallory-Weiss syndrome (esophageal tear)
Esophageal varices
Peptic ulcer
Gastritis
Gastric varices
Dieulafoy's lesion:
Dieulafoy's lesion is an uncommon cause of gastric bleeding
thought to cause less then 5% of all gastro-intestinal bleeds in adults. It was
named after French surgeon Paul Georges Dieulafoy who described this
condition in his paper "Exulceratio simplex: Leçons 1-3" in 1898. Dieulafoy's
Lesions bleed into the gastro-intestinal tract from an arteriole protruding
through a minute defect in the mucosa. 95% of Dieulafoy's lesions occur in the
upper part of the stomach, within 6cm of the gastro-oesophageal junction,
however they can occur anywhere in the GI tract. Interestingly and in contrast
to peptic ulcer disease, a history of alcohol abuse or NSAID use is usually
absent in Dieulafoy's.
In a "hemodynamically significant" case of hematemesis, that is hypovolemic shock,
resuscitation is an immediate priority to prevent cardiac arrest. Fluids and/or blood is
administered, preferably by central venous catheter, and the patient is prepared for
emergency endoscopy, which is typically done in theatres. Surgical opinion is usually
sought in case the source of bleeding cannot be identified endoscopically, and
laparotomy is necessary.
72. Polycystic kidney
a. Is transmitted autosomal dominant
b. Often presents in childhood
c. Causes hypertension
d. Is associated with cystic liver disease
F
F
T
T
PKD is transmitted autosomal dominant OR autosomal recessive, thus a is false.
PKD can present in childhood if autosomal recessive. This is rare compared to
autosomal dominant variant.
Polycystic kidney disease (PKD) is a progressive, genetic disorder of the kidneys. It
occurs in humans and other organisms. PKD is characterised by the presence of
multiple cysts (polycystic) in both kidneys. The disease can also damage the liver,
pancreas and rarely the heart and brain. The two major forms of polycystic kidney
disease are distinguished by their patterns of inheritance.
Autosomal dominant polycystic kidney disease (ADPKD) is generally a late onset
disorder characterized by progressive cyst development and bilaterally enlarged
kidneys with multiple cysts. Kidney manifestations in this disorder include renal
function abnormalities, hypertension, renal pain, and renal insufficiency.
Approximately 50% of patients with ADPKD have end-stage renal disease (ESRD)
by age 60 years. ADPKD is, however, a systemic disease with cysts in other organs
such as the liver (which may lead to cirrhosis), seminal vesicles, pancreas, and
arachnoid mater and non-cystic abnormalities such as intracranial aneurysms and
dolichoectasias, dilatation of the aortic root and dissection of the thoracic aorta, mitral
valve prolapse, and abdominal wall hernias.
Initial symptoms are hypertension, fatigue and mild to severe back or flank pain and
urinary tract infections. The disease often leads to chronic renal failure and may result
in total loss of kidney function, known as end stage renal disease (ESRD) which
requires some form of renal replacement therapy (e.g. dialysis).
Autosomal recessive polycystic kidney disease (ARPKD) is much rarer than ADPKD
and is often lethal. The signs and symptoms of the condition are usually apparent at
birth or in early infancy.
85% of Polycystic kidney disease is autosomal dominant and thus “adult-onset” while
15% is autosomal recessive and presents at birth or early infancy.
73. Extraintestinal manifestations of IBD:
a. Sacroiliitis
T
b. Erythema nodosum
T
c. Syndenhams’s Chorea
F
d. Pyoderma gangrenosum T
e. Entrapment neuropathy. F
IBD extraintestinal manifestations include:
Clubbing
Anemia (B12 deficiency/iron deficiency/chronic disease)
Arthralgia (seronegative, includes sacroiliitis)
PSC (esp. UC)
CRC likelihood increased
Erythema nodosum and pyoderma gangrenosum
74. An 80 year old female presented in an acute confusional state with very
aggressive behavior. Immediate steps in her management include:
a. Acute psychiatric admission
F
b. Review for drug therapy if any
T
c. Physical examination to exclude
T
focus of infection
d. Start broad spectrum antibiotic
F
e. Isolate and review in a week
F
IMMEDIATE steps include: History and exam, including collateral history. Vitals.
Review drugs.
Medications should not be started until the aetiology is established.
Confusion (encephalopathy) is defined as the inability to maintain a coherent stream
of thought or action. The hallmark of acute confusional states is impairment in
attention and/or arousal or acute changes in perception or other higher order
behaviors. Delirium is a more specific syndrome, defined as an impairment of
attention or arousal. The usage of the two terms overlaps considerably.
Causes: Potential causes of acute confusional states are numerous. A good clinician is
thorough and systematic in the evaluation.
Intoxication
Intoxicants can include prescription and over-the-counter medications, as well as
alcohol and illegal drugs. Although these causes often are suspected in the emergency
department (ED), they may be unsuspected in other settings (eg, postoperative
delirium tremens in closet alcoholics). Prescription medicines may be used
inappropriately. Prednisone, dexamethasone, and other steroids can cause paradoxical
confusion, as can a host of other medications.
Focal brain lesions
Focal brain lesions occasionally can cause acute confusion. Subdural hematomas,
strokes, and mass lesions may be found on CT scan and MRI. Contrast scans are more
sensitive for the above. If the confusion is due to increased intracranial pressure, as in
a subdural hematoma, arousal may be most affected and the patient may be sleepy. If
due to a stroke, the "confusion" is likely to be misdiagnosed aphasia, or vice-versa,
unless a huge lesion is present, in which case associated hemiparesis makes the
diagnosis obvious.
Uncommonly, strokes can present as confusional states with highly select lesion loci.
Brain tumors often develop slowly, allowing the brain to compensate; therefore, they
are somewhat less likely to present as acute confusional states.
Occasionally, focal lesions can result in confusion. Patients develop an agitated
confusion with head lesions affecting the caudate, thalamus, or basal forebrain.
Patients may appear agitated with lesions of the Wernicke area or of the mirror-image
homologous area of the right hemisphere.
Infections
Urinary tract infections and pneumonias are common infections that cause confusion
in debilitated, nursing home, and other elderly patients. If these common infections
are not present, patients should be checked for other common metabolic
abnormalities, including abnormalities of glucose, sodium, BUN, calcium,
magnesium, and phosphorus.
The blood oxygen should be checked and the anion gap measured. Once these are sent
for investigation, other common conditions should be sought, including cobalamin
deficiency, thyroid disease, vasculitis, and latent syphilis. Ammonia should be
checked, especially if asterixis is present.
Neurologic diseases
Specific neurologic diseases besides stroke, tumor, and subdural hematoma need to be
considered. Paramount among these are neurologic infections, especially those that
are treatable. Young patients presenting with high fever and confusion should be
evaluated for herpes virus and treated presumptively until the condition is ruled out.
West Nile virus can present with fever.
Epilepsy
Epilepsy can present as confusion. Patients may have nonconvulsive status
epilepticus, a condition that can be easily diagnosed and treated. Two types may
occur—absence status may occur in patients who may or may not have had prior
absence seizures, and complex partial status epilepticus may occur in patients with or
without a history of complex partial seizures. The 2 types are differentiated by EEG.
In absence epilepsy, spike-and-wave discharges are seen at a rate of 3 per second. In
complex partial status (the more common type), a focal discharging pattern may be
seen.
Vascular dememtia, given it’s stepwise progression, may also appear like acute
confusional state in some settings.
75. Multiple blood transfusions increase the risk of
a. Malaria
T
b. Hepatitis A
F
c. Non-A Non-B Hepatitis T
d. Chicken pox pneumonia ??
e. AIDS
T
I would think multiple blood transfusions would DECREASE the risk of chicken pox
pneumonia, since there would be antibodies versus varicella zoster virus in the
transfusion…I don’t know this one though
Blood donation centers in different countries may have different guidelines about who
can serve as a blood donor. Common contraindications to being a blood donor
include:
previous malaria or hepatitis
a history of intravenous drug abuse
donors who have received human-derived pituitary hormones
donors with high-risk sexual behaviour (variably defined)
donors who have previously been transfused (12-month min. deferral)
As of mid-2005, all donated blood in the United States is screened for the following
infectious agents:
HIV-1 and HIV-2
Human T-lymphotropic virus (HTLV-1 and HTLV-2)
Hepatitis B or C virus
West Nile virus
Treponema pallidum (the causative agent of syphilis)
76. The following attack both skin and mucosal surfaces
a. Erythema multiforme
T
b. Lichen planus
T
c. Granuloma annulare
F
d. Discoid lupus
F
e. Herpes simplex
T
Erythema multiforme is a hypersensitivity rash of acute onset caused by infection or
drugs. T-cell lymphocyte mediated response is seen on skin. Causes include:
Idiopathic (50%)
HSV, HIV, EBV, CMV, orf infection
CT disease (SLE, polyarteritis nodosa)
Wegener’s granulomatosis
Drugs (anticonvulsants, sulphonamides)
Target lesions occur symmetrically on limbs, palms and soles, and mucosal
involvement occurs in “EM major” aka Stevens-Johnson syndrome.
Lichen planus is a pruritic inflammatory dermatosis commonly associated with
mucosal involvement, nail dystrophy and less commonly, scarring alopecia. White
lacy pattern on the lesion surface may be present, and is known as “Wickham’s
striae.” A T-cell mediated mechanism is postulated. Small purple, flat-topped,
intensely pruritic papules seen on wrist flexors, lower legs especially. Mucosal
involvement is common, with mouth, esophagus and anogenital region commonly
affected.
Granuloma annulare is a dermatosis of young adults and children, characterized by
clusters of small dermal papules forming rings, commonly found on dorsum of hands
and feet. Diffuse forms may be associated with diabetes mellitus. Mucosal
involvement generally does not occur.
Discoid lupus erythematosus (DLE) is a chronic, scarring, atrophy producing,
photosensitive dermatosis. DLE may occur in patients with systemic lupus
erythematosus (SLE), and some patients (<5%) with DLE progress to SLE. Some
patients also have the lesions of subacute cutaneous lupus erythematosus (SCLE), and
some may have a malar rash. DLE lesions frequently are characteristic. The primary
lesion is an erythematous papule or plaque with slight-to-moderate scaling. As the
lesion progresses, the scale may thicken and become adherent, and pigmentary
changes may develop, with hypopigmentation in the central or inactive area and
hyperpigmentation at the active border. Several unusual variants of chronic Cutaneous
Lupus Erythematous, other than DLE, have been reported; in one of which mucosal
surfaces may be affected by lesions that appear identical to DLE of the skin or by
lesions that may simulate lichen planus. However, DLE does not involve mucosal
surfaces on its own.
Herpes simplex can affect the genitals (HSV-2 usually) or gingivostomatis with
mouth ulcers (HSV-1 usually). Mucosal surfaces commonly involved in oral area.
77. Causes of gynecomastia include
a. Puberty
b. Klinefelters syndrome
c. Spironolactone therapy
d. Untreated essential hypertension
e. decreased thyroid function
T
T
T
F
F
Gynecomastia occurs when excessive estrogens, prolactin or HCG are produced, as
can occur in:
Liver disease
Tumors of:
adrenal gland, testicle, lung
Breast carcinoma, prolactinoma
Neonatal, Puberty and old age
Hyperthyroidism
Drugs:
spironolactone, phenytoin, digoxin, cannabis, opiates, gonadotrophins
Genetic
Klinefelters
78. The following are features of LVF
a. Basal creps
T
b. Gallop rhythm
T
c. Pulsus alternans
T
d. Peripheral edema
F
e. Elevated pulsatile JVP
F
The features of right heart failure include:
Increased JVP
Hepatomegaly
Ascites
Ankle edema
Features of left heart failure include
Pulsus alternans (alternating large and small amplitude beats noted in pulse)
Bibasal crepitations
Cyanosis
Pink frothy sputum
Orthopnea
Third heart sound (“gallop rhythm”)
79. A 23 year old man with 6/12 history of treatment of frequent bowel motions with
release of blood and mucus PR.
a. A perianal fistula would suggest Crohns
T
b. A barium enema may aid diagnosis
T
c. You would expect anemia and low serum iron
T
d. A barium follow through may be needed
T
e. An infective cause would be likely
F
80. A 60 year old man presents with bilateral ptosis. Diplopia is worse in the
evenings. Pupils are equal and reactive to light and accommodation. Bedrest
improved ocular movements. The most likely diagnosis is:
a. Myasthenia gravis
b. Ocular myopathy
c. Myotonic dystrophy
d. Endocrine exopthalmic exopthalmoplegia
e. Midbrain vascular lesion
81. The following murmurs are correctly associated:
a. Mitral stenosis: mid diastolic murmur
b. Pulmonary stenosis: pansystolic murmur
c. Mitral regurgitation: pansystolic murmur
d. Aortic stenosis: ejection murmur
e. Aortic regurgitation: pan-diastolic murmur
82. The following are suggestive of carcinoma in a patient with hoarseness:
a. Unilateral recurrent laryngeal nerve palsy
b. Myxedematous thickening of the vocal cord
c. Cervical lymphadenopathy
d. Single nodule in the thyroid gland
e. Sudden enlargement of???
83. In Cor pulmonale
a. Digoxin in the best treatment
b. Diuretics are indicated
c. The 5 year survival rate exceeds 75%
d. Hypoxia causes reduced pulmonary vascular resistance
e. Home oxygen has little or no place in the treatment
84. Heberdens nodes:
a. Occur at the base of the terminal phalanges
b. Occur in subacute bacterial endocarditis
c. Are commoner in fat people than in thin people
85. A teacher, asthmatic, with a 2month history of epigastric pain. Barium meal is
negative. She is currently taking theophylline and a B12 stimulant. No other
medications. Three days later she is complaining of nausea. What is the single most
appropriate action to take?
a. Repeat barium meal
b. Measure theophylline levels
c. Gastric acid stimulation test
d. Gastroscopy
e. FOB
86. Cerebellar ataxia may be caused by:
a. Folate deficiency
b. Thiamine
c. Phenytoin
d. Alcohol
e. Carbamazepine
87. A young man presents with rigors, dysuria and pyrexia. What do you do?
a. MSU, differential wcc, blood culture
b. IVP before starting treatment
c. Do not treat with antibiotics before getting cultures
d. Oral penicillin is the first line treatment
88. Mitral valve prolapse:
a. Is found in 5-10% of the population
b. Presents with a mid-late systolic cluck and late systolic murmur
c. Presents with chest pain and palpitations
d. Patients should receive antibiotic prophylaxis
e. Patients have a higer incidence of endocarditis
89. The following statements are correct:
a. Amiodarone causes corneal microdeposits and pulmonary fibrosis
b. Amiodarone causes a peripheral neuropathy
c. Adenosine is contraindicated in complete heart block
d. Aortic incompetence is best heard with the patients sitting forward and on
inspiration
e. A collapsing pulse is a feature of aortic incompetence
Common drugs used in arrythmias include:
Arrythmia
Drug
Contraindications and Side effects
Supraventricular
Slow AV node
tachycardia
IV adenosine
ConInd:
2nd/3rd degree heart block
sick sinus syndrome
Caution:
SidEff:
Asthma (bronchospasm)
“ABCDEF”
Adenosine
Bronchospasm
Chest pain
Dyspnea
ECGtransient rhythm
Disturbance
Flacial flushing
Nausea
B-blockers Esmolol ConInd:
SidEff:
Asthma
Marked bradycardia
2nd/3rd degree heart block
Metabolic acidosis
Uncontrolled heart failure
Phaeochromocytoma
(without alphablockade)
Bradycardia
Heart failure
Bronchospasm
Peripheral
vasoconstriction
Verapamil
ConInd
GI/sleep disturbance
Sexual dysfunction
Exacerbation of psoriasis
Renal failure
Hypotension
2nd/3rd degree heart block
Cardiogenic shock
Hx heart failure or LV
Dysfunction
A.Fib/A Flutter with
WPW
SidEff:
Syndrome
Constipation
N+V/headache
Allergic reactions
(urticaria/StevensJohnson
)
Increased PRL secretion
Fleicainide
Atrial Fibrillation
Rate Control
Digoxin
Beta-blockers
Ca channel blockers
Rhythm control
Amiodarone
Flecainide
Sotalol
Anticoagulation
INR 2.5-3 Warfarrin
Ventricular
tachycardia
Hemodynamically stable VT
IV lidocaine
Amiodarone
Pulseless VT or Polymorphic VT
DC cardioversion
90. During cardio-pulmonary resuscitation
a. External cardiac massage must be discontinued during inflation of the lungs
b. Intubation should be attempted immediately
c. PEA should be treated with IV adrenaline
d. 50 mL of 8.4% sodium bicarbonate should be given as soon as central access is
established
e. Ventricular fibrillation associated with hypotension is best treated with IV
Lignocaine
132. Clubbing is associated with which of the
following
a. severe asthma F
b. chronic bronchitis F
c. bronchiectasis T
d. cirrhosis T
e. pulmonary fibrosis T
The causes of clubbing can be divided into the following categories:
Cardiac:
Infective Endocarditis
Cyanotic Congenital Heart Disease
Atrial Myxoma
Respiratory:
Bronchial Carcinoma
Chronic Suppurative Lung Diseases (e.g. Bronchiectasis, Lung Abscess, Empyema)
Pulmonary Fibrosis
Cystic Fibrosis
Pleural Mesothelioma
Asbestosis
Gastrointestinal:
Liver Cirrhosis
Inflammatory Bowel Disease
Coeliac Disease
Miscellaneuous:
Thyrotoxicosis
Familial
Pregnancy
Neurogenic Diaphragmatic Tumours
133. Radioiodine treatment for hyperthyroidism
a. can be given in an outpatient clinic T
b. is the treatment of first choice in the elderly F
c. The results of this treatment can be seen in 2-3
Weeks F
d. Is absolutely contraindicated in women who are
Lactating T
e. Is absolutely contraindicated in women planning a
future pregnancy F (T if conception planned for up to 4 months post-treatment)
Radioiodine therapy for hyperthyroid patients is almost always done on an outpatient
basis, because the dose required is relatively small compared with the doses typically
used for treatment of thyroid cancer. If a patient has received a higher radioiodine
dose for treatment of thyroid cancer, he/she may need to be admitted to hospital for
several days depending on the amount of radioiodine administered, their living
environment, state of residence, or local practice patterns.
Radioiodine treatment is the treatment of choice in elderly people in the United
States. However in the UK and Ireland, antithyroid drugs such as carbimazole or
propylthiouracil in combination therapy with a beta-blocker e.g. propanolol is still
the first treatment of choice. However radioiodine being used more widely in Ireland
and the UK than previously, particularly in hyperthyroid patients who are not
pregnant or lactating. Thus this treatment is considered more in the elderly
population, particularly in those who also have thyroid-related heart disease e.g.
atrial fibrillation, high-output cardiac failure.
The results of radioiodine therapy for hyperthyroidism usually take 2-3 months to
develop i.e. to revert back to euthyroidism.
Radioiodine treatment is absolutely contraindicated in women who are lactating
because there is a risk of the radioiodine being absorbed by the infant’s thyroid gland
too, causing it to be irradiated and the child to become hypothyroid.
Radioactive iodine is absolutely contraindicated during pregnancy, or if the patient is
planning to get pregnant within 4 months after treatment, because from the third
month of pregnancy the thyroid gland of the foetus absorbs iodine and therefore the
baby’s thyroid would become irradiated too. As a result, the baby would not have a
functioning thyroid gland. It is also important not to come into close contact with
babies, children or women of childbearing years for approximately 2-3 weeks for the
same reasons. The above guidelines apply to both male and female patients. However
the radioiodine is completely excreted from the body 4 months post-treatment, so
conception after 4 months is not harmful to the foetus. Finally radioiodine therapy
has not been found to alter patient’s fertility or the viability of future pregnancies in
any way.
134. Collapsing pulse is associated with:
a. aortic stenosis F
b patent ductus arteriosus T
c. fever T
d. anaemia T
e. aortic regurgitation T
A collapsing pulse is defined as a pulse with a fast upstroke and fast down stroke.
Causes of a collapsing pulse include aortic regurgitation, patent ductus arteriosus,
and hyperdynamic circulations e.g. thyrotoxicosis, pyrexia/fever, anaemia and AV
fistulae.
135. Features of an innocent murmur are
a. diastolic rhythm F
b. loud S1 F
c. Normal S2 in expiration T
d. Radiation throughout precordium F
e. PR interval 0.12-0.2 seconds T
Characteristics of innocent murmurs include the following:
1. Systolic murmur, which is neither diastolic or pan systolic, except for the
continuous murmur of a venous hum, which is reduced on lying down.
2. No other abnormality detected (no cardiac enlargement)
3. No thrills or added sound
4. Intensity of murmur often varies with a change in posture
5. No radiation of murmur heard on auscultation
136. Features of a pleural effusion
a. bronchial breaths T
b. increased vocal fremitus F
c. Increased vocal resonance F
d. Dullness on percussion T
e. Crackles F
A pleural effusion is fluid in the pleural space. Features of pleural effusion on clinical
examination include the following:
1. Decreased chest expansion on affected side
2. Stony dull percussion note
3. Diminished breath sounds occur on the affected side.
4. Tactile vocal fremitus and vocal resonance are decreased (inconstant and
unreliable)
5. Above the effusion where the lung is compressed, there may be bronchial breathing
and megaphone (bleating vocal resonance).
6. With large pleural effusions, there may be tracheal deviation away from the
effusion.
137. Thrombocytosis is a feature of
a. Post operatively T
b. Post-splenectomy T
c. Malignancy T
d. SLE T
e. After blood transfusion F
Thrombocytosis occurs when the platelet count exceeds 450,000 per cubic mm
although numbers may exceed 1,000,000 per cubic mm without symptoms.
Thrombosis and paradoxically, haemorrhage are the main symptoms but their
occurrence is as much dependent on qualitative defects in the platelets as much as
their number. Two types of thrombocytosis are recognised: reactive thrombocytosisfor which the term thrombocytosis is reserved and essential thrombocythaemia- an
essential or autonomous thrombocytosis. Reactive thrombocytosis (RT) refers to
thrombocytosis in the absence of a chronic myeloproliferative or myelodysplastic
disorder, in patients who have a medical or surgical condition likely to be associated
with an increased platelet count, and in whom the platelet count normalizes, or is
expected to normalize, after resolution of this condition.
Reactive thrombocytosis is commonly associated with:
inflammation
bacterial infection
trauma
bleeding
malignancy
iron deficiency
following splenectomy
following recent surgery
Counts may exceed 1,000,000 per cm^3. The platelets are functionally normal. Very
severe iron deficiency may cause thrombocytopenia rather than thrombocytosis.
138. Crackles can be a sign of:
a. Cryptogenic fibrosing alveolitis T
b. Extrinsic allergic alveolitis T
c. Sarcoidosis T
d. Pulmonary fibrosis T
e. TB T
Crackles are caused by the re-opening , during inspiration, of the small airways,
which have become occluded during expiration. They may be fine and high pitched if
coming from distal air spaces (e.g. pulmonary oedema, fibrosing alveolitis) or coarse
and low pitched if they originate more proximally (e.g. bronchiectasis).Extrinsic
allergic alveolitis and pulmonary fibrosis are also known to cause crackles to be
heard on auscultation. Although 80% of patients with acidosis have lung involvement,
they usually have no respiratory signs. In severe disease however, there may be signs
of pulmonary fibrosis, and so crackles heard. In the case of TB, usually no abnormal
chest signs are found, and clues to the diagnosis lie in the classical history of cough,
haemoptysis, weight loss, night sweats and malaise. However TB, particularly
primary TB, results in consolidation, and crackles can be appreciated on auscultation
of some patients.
139. The following are true about hypertension
a. Thiazide diuretics are treatment of choice in
Elderly T
b. There is more of a chance of finding a cause for
the more severe malignant form than from the more
common benign form T
c. Headache and dizziness are signs/symptoms of mild
or moderate hypertension F
d. Systolic hypertension alone requires no treatment F
Essential/benign hypertension (primary, cause unknown) represents 95% of cases and
is usually asymptomatic. Secondary hypertension represents the remaining 5% of
hypertensive patients. Malignant/secondary hypertension refers to severe
hypertension (e.g. >200/>130 mm Hg )in conjunction with bilateral retinal
haemorrhages and exudates, and papilloedema may or may not be present. Symptoms
such as headache +/- visual disturbance are common, and malignant hypertension
alone requires urgent treatment and thorough investigation of underlying cause such
as renal disease, endocrine disease, forestation of aorta, pregnancy etc.
Evidence from three major studies indicates, beyond doubt, that benefits of treating
elderly patients with systolic hypertension are even greater than treating moderate
hypertension in middle-aged patients. Systolic blood pressure is the most important
determinant of cardiovascular risk in the over 50s.Thiazide diuretics are considered
the first-line treatment of choice for hypertension in the elderly, being both
therapeutically and cost-effective.
140. A woman presents with a facial rash of four weeks
a. History is compatible with a diagnosis of acne
Rosacea T
b. Psoriasis could be a cause F
c. Oral steroids trial is advised F
d. H2 blockers could be a cause of the rash T
e. Photosensitive rash is a possible diagnosis T
Acne rosacea refers to a chronic relapsing and remitting facial disorder of unknown
aetiology, where chronic flushing triggered by alcohol, spicy foods etc. often precedes
the development of fixed erythematic (chin, nose, cheeks, forehead), telangiectasia,
papules and pustules.
Psoriasis is usually characterised by symmetrical well-defined red plaques with
silvery scale, on the extensor surface of the elbows, knees, scalp and sacrum. The
flexures are frequently also involved, but lesions are not scaly here. The face is not
affected in psoriasis.
Oral steroid treatment is not without its complications, and is not indicated here.
Topical steroids can be used for treatment of inflammatory skin conditions (other
than those arising from infection), in particular eczema, contact dermatitis and insect
stings. However they are of no value in the treatment of urticaria and are contraindicated in the case of rosacea. They are also not recommended for acne vulgaris.
H2-blockers can cause erythema multiforme and toxic epidermal necrolysis, the latter
causing widespread erythema.
Photosensitive rash or rash that is triggered by exposure to light, such as the
characteristic malar rash of SLE, is a possible diagnosis.
141. A 45 year old man, non smoker, presents to
casualty with chest pain of 3 hours, no history of
hypertension
a. IV analgesics are indicated T
b. PO aspirin advised T
c. IV thrombolytic therapy is not contraindicated T
d. Monitoring of BP and ECG is necessary T
e. Patient is allowed home to return in 24 hours for
ECG F
Have to manage this man’s complaint of chest pain for 3 hours as an myocardial
infarct until proven otherwise.
Contraindications to Thrombolytics:
Absolute Contraindications to Fibrinolytic Therapy
Active internal bleeding
CNS neoplasm, AV malformation, or aneurysm.
CNS procedure or CVA within two months.
Severe uncontrolled hypertension (over 200/130 or complicated by retinovascular
disease or encephalopathy)
Known bleeding diathesis
MI due to aortic dissection
Allergy to either streptokinase or anistreplase, if streptokinase or anistreplase will be
used
Relative Contraindications to thrombolytic therapy
Age over 75
Cerebrovascular disease
Pregnancy or early postpartum
Recent major surgery (less than 10 days), noncompressable vessel puncture, or organ
biopsy
Recent trauma, including CPR of over 2 minutes duration
Recent GI bleeding or active ulcer disease (less than 10 days)
Acute pericarditis or subacute bacterial endocarditis
Septic thrombophlebitis
High likelihood of left heart thrombus (eg. mitral stenosis with atrial fibrillation)
Known coagulation defects, including anticoagulant therapy
Significant liver dysfunction
Conditions associated with bleeding risks, such as diabetic retinopathy.
Menstruation
Terminal cancer or other end-stage disease
Recent streptococcal infection, if streptokinase or anistreplase will be used
142. Anemia of chronic disorders is associated with
a. Low ESR F
b Reduced serum iron T
c. Reduced utilization of iron T
d. No response to oral iron T
e. Reduced serum transferring F
Anaemia of chronic disorders is associated with many diseases e.g. infection, collagen
vascular disease, rheumatoid arthritis, malignancy, renal failure.
Investigations reveal the following:
Mild normocytic anaemia (e.g. Hb <8 g/dl)
Decreased Total Iron Binding Capacity
Decreased serum iron
Normal or increased serum ferritin
Serum soluble transferrin receptor level is normal
ESR is often raised as a result of an often underlying inflammatory process.
Management is largely treatment of the underlying cause. The anaemia of renal
failure is partly due to erythropoietin deficiency and recombinant erythropoietin is
effective in raising the haemoglobin level. It is also effective in raising Hb and
improving quality of life in those with malignant disease. IV iron can be given with
erythropoietin safely in patients with anaemia of chronic disease with some benefit.
However oral iron causes many disagreeable side-effects such as nausea and
constipation which reduce patient compliance, is associated with drug-drug
interactions and has limited efficacy in anaemia of chronic disorders. Randomised
controlled trials of treatment of anaemia chronic disease, have shown no added
efficacy in using oral iron with recombinant erythropoietin in patients, compared with
recombinant erythropoietin alone.
143. Low serum potassium could be from:
a. Diuretic therapy T
b. Digoxin therapy F
c. Addison’s disease F
d. Phaeochromocytoma F
e. Acute renal failure T (in recovery phase of acute tubular necrosis, where low
serum potassium can occur).
Causes of Hypokalaemia:
Diuretics (common cause)
Vomiting and diarrhoea
Pyloric stenosis
Villous adenoma rectum
Intestinal fistulae
Cushings Syndrome/glucocorticoids/ACTH
Conn’s Syndrome
Alkalosis
Purgative and liquorice abuse
Renal tubular failure
Digoxin toxicity does not cause hypokalemia, but hypokalemia can worsen digoxin
toxicity.Hyperkalemia is the usual electrolyte abnormality precipitated by digoxin
toxicity, primarily in the acute setting. Hyperkalemia may be associated with acute
renal failure that subsequently precipitates digoxin toxicity. Chronic digoxin toxicity
does not usually cause hyperkalemia.
144. A 64 year old smoker presents with left pleuritic
chest pain, cough and hemoptysis. On examination,
clubbing was noticed. A reasonable differential
diagnosis would include
a. Pulmonary TB T
b. Mycoplasma pneumonia F
c. Cancer of bronchus T
d. CFA ?
e. Left Upper Lobe Strep pneumonia F
Pleuritic chest pain (pain exacerbated by inspiration) implies inflammation of the
pleura secondary to pulmonary infection, inflammation or infarction. Cough and
haemoptysis broaden the differential diagnosis to include Tuberculosis, Pulmonary
Infarction secondary to Embolism, Bronchial Carcinoma and Left-sided CommunityAcquired Pneumonia. The addition of finger clubbing however makes Bronchial
Carcinoma, Chronic Suppurative Lung Diseases such as lung abscess, empyema and
bronchiectasis more likely, and helps to largely rule out acute mycoplasma pneumonia
and left upper lobe strep pneumonia. As pulmonary TB may sometimes cause finger
clubbing and the history is certainly suggestive of possible pulmonary TB,it is still a
reasonable differential here.
145. Tests on the above man should include
a. Sputum for regular cytology and serology T
b. Sputum for PCP and H+E F
c. MRI thorax F
d. Mantoux test T
e. Videooptic bronchoscopy T
146. A 45 year old man presents with a 10 year history
of tremor which is worse on picking up a glass. The
patient says his father and sister also had the tremor
a. Tremor decreases during sleep T
b. Propranolol is drug of choice T
c. Diagnosis is likely to be familial parkinsonism F
d. Amantadine is next drug of choice F
e. Tremor is thought to be a disorder of the red
Nucleus F
Familial tremor is a neurologic disorder that tends to run in families, which results in
shaking/tremor that gets worse during movement or activity. Tremors can affect
people at any age, but they are most common in older people. Familial tremors affect
more than one person in a family and is usually a dominant trait, which means about
50% of a patient‘s children will also have the tremor. Over time, the tremors may
affect the hands, arms, head, voice box, eyelids, or other muscles. The tremors rarely
involve the legs or feet. In children, these tremors are usually limited to the hands and
rarely require treatment. Tremors may not affect both sides of the body equally. The
exact pathophysiology is unknown. Familial tremor worsens with voluntary
movement and emotional stress, disappears during sleep and may improve with
alcohol consumption.
Treatment may not be necessary unless the familial tremor interferes with your ability
to perform daily activities. How well medicine works depends on the individual
patient. Medications that may reduce tremors include propranolol, mysoline and other
anticonvulsants, and mild tranquilizers. If the above are ineffective diamox,neptazane
(methazolamide), clonidine, amantadine, clonazepam, neurontin and clozapine have
been suggested as other options. If tremors are severe and do not go away with
medicine, surgery to implant a deep brain stimulator (DBS) in the brain may be an
option.
Caffeine and other stimulants should be avoided because they can make tremors
worse.
Alcoholic beverages in small quantities may decrease the tremor, but drinking should
be carefully monitored to avoid alcohol abuse and alcohol dependence, especially if
there is a family history of alcohol problems. How alcohol decreases an essential
tremor is unknown.
147. A 40 year old man presents to casualty in a
confused state
a. Alcohol may be a cause T
b. Confabulation is a feature of Korsakoff’s
Syndrome T
c. Ophthalmaplegia and ataxia are indications for
Pyridoxine F
d. Foeter and liver flap indicate hepatic
Encephalopathy T
e. Chlordiazepoxide is used for treatment of DTs T
Pyridoxine is Vitamin B6, and is not used to prevent and treat Wernicke’s
Encephalopathy triad of symptoms: ophthalmoplegia, ataxia and confusion, rather
Vitamin B1/thiamine. The severe deficiency states Wernicke's encephalopathy and
Korsakoff's psychosis, especially as seen in chronic alcoholism, are best treated
initially by the parenteral administration of B vitamins (Pabrinex®), followed by oral
administration of thiamine in the longer term. Anaphylaxis has been reported with
parenteral B vitamins (see CSM advice, below).
148. In a patient who has pulsus alternans
a. The pulse is irregular F
b. Digitalis intoxication is the most likely cause F
c. The pulse waves are unequal in size T
d. It is most easily observed when taking BP F
e. Pulse rate varies with respiration F
Pulsus alternant refers to regular rhythm with alternating strong and weak beats. It
suggests left ventricular failure for the most part, but also can be caused by
cardiomyopathy and aortic stenosis. It is most easily detected on examination of
peripheral pulses.
149. Pericardial rub is a recognized feature of:
a. Hypertensive cardiac failure F
b. Extrarenal uraemia T
c. Terminal uraemia T
d. Minority of cases of MI T
e. Atrial flutter F
Pericardial friction rub occurs in inflammation of the pericardium which may be
primary or secondary to systemic disease. Causes include:
Viruses (Coxsackie’s, influenza, Epstein-Barr, mumps, vermicelli, HIV)
Bacteria (pneumonia, rheumatic fever, TB)
Fungi
Myocardial infarct
Dressler’s Syndrome
Uraemia
Rheumatoid Arthritis
SLE
Myxoedema
Trauma
Surgery
Malignancy
Radiotherapy
Drugs e.g. procainamide, hydralazine.
150. In active pulmonary TB:
a. Physical signs are always present on careful
examination of the chest F
b. Clubbing is common F
c. In most cases ESR is raised T
d. Radiological changes are commonest in the apex of
the lung T
e. Pneumothorax occurs in about 10% of cases F
Active pulmonary TB may be silent or present with cough, sputum, malaise, weight
loss, night-sweats, pleurisy, haemoptysis, pleural effusion, or superimposed
pulmonary infection. Clubbing may occur in TB, but is uncommon. As TB is a
chronic infective process, the ESR in most cases should be raised. Pneumothorax
occurs in about 2-3% of cases pf active pulmonary TB.
151. Mitral stenosis
a. Is more likely to develop SBE than incompetence F
b. Always give antibiotic prophylaxis T
c. Systolic murmur F
d. Give anticoagulation T
e. Presents with sudden death F
Mitral stenosis nearly always due to rheumatic heart disease, but rarely may be
congenital.
History: Many patients are asymptomatic. Some patients may develop symptoms
during physiologic stress such as infection, exercise, fever, or pregnancy.
Exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea (symptoms of left
heart failure) are most common. Dyspnea may be accompanied by cough and
wheezing. Acute pulmonary oedema may occur precipitated by exertion, pregnancy or
onset of AF.
Chest pain due to right ventricular ischemia, concomitant coronary atherosclerosis,
or a coronary embolism may be present.
Hemoptysis from pulmonary venous hypertension results in rupture of anastomosis
between bronchial veins.
Recurrent bronchitis
In later stages, symptoms of RV failure.
Patients may present with complications of mitral stenosis.
New-onset atrial fibrillation
Systemic embolism
Infective endocarditis (more common with incompetence)
Physical: Look for findings not only intrinsic to valvular deformity but also
hemodynamic disturbance from the stenotic valve and its complications.
Cardiac examination of stenotic mitral valve (best at the apex with the patient in the
left lateral recumbent position)
Palpable diastolic thrill
An accentuated S1, followed by S2, and an opening snap (OS)
Characteristic diastolic low-pitched, rumbling murmur
The duration, and not intensity, of the murmur is a guide to the severity of mitral
valve narrowing. However, murmur may diminish in intensity as the stenosis
increases.
Pulmonary crackles
Signs of right heart strain/failure in later stages.
Other findings
A pansystolic murmur of mitral regurgitation may accompany the valvular deformity
of mitral stenosis.
“Mitral facies” characterized by pinkish purple patches on the cheeks may be
present.
Managemant: If in AF -digoxin +/- beta-blocker + warfarin.
Diuretics decrease preload and pulmonary venous congestion.
Balloon valvuloplasty, open mitral valvotomy or valve replacement if this fails to
control symptoms.
SBE/IE prophylaxis for dental or surgical procedures. Oral penicillin as prophylaxis
against recurrent fever if < 30 years old.
152. A 35 year old Indian vegetarian presents with
difficulty getting out of a chair and parasthesia;
useful tests include
a. Calcium
b. Alkaline phosphatase
c. ACTH
d. bilirubin
e T4
a. T. Hypocalcaemia could account for the paraesthesia and proximal myopathy
b. T. alk phos will be increased in osteomalacia, which is a cause of hypocalcaemia
c. T. Cushings is a cause of proximal myopathy
d. F
e. T. thyrotoxicosis is a cause of proximal myopathy
a. and b.
Difficulty getting out of a chair=proximal myopathy. In osteomalacia there is low
calcium which could account for the proximal myopathy and paraesthesia. In
osteomalacia there is a normal amount of bone but its mineral content is low. It occurs
due to lack of vitamin D:
1. Vitamin D deficiency due to malabsorption, poor diet, lack of sunlight
2.Renal Failure-failure of hydroxylation of vitamin D
3.Liver Disease: reduced production of 25-OH Vitamin D
4. Drugs e.g. anticonvulsants as they induce liver enzymes leading to increased
Vitamin D breakdown.
5. Vitamin D resistance: a number of rare inherited defects in vitamin D receptors
Vitamin D increases calcium and phosphate levels. In osteomalacia therefore you get:
Decreased PO4, decreased Ca and increased alk phosphate
b. Cushings can cause proximal myopathy. I would say true for this although
ACTH levels would certainly not be the first line investigation in Cushings.
However, 90% of cushings is ACTH dependent. The majority of these are from a
pituitary adenoma. Dexamethasone suppression tests would be used to confirm the
diagnosis of cushings and ACTH levels can then be used to help localize the cause of
the cushings.
153. A student tested Mantoux positive after contact
with TB; CXR normal and there were no signs but sputum
was not available for testing
a. Discharge her saying she will never get TB
b. Discharge her saying come back only if pregnant
c. Tell her to miss college for 3 months
d. Three month prophylaxis with rifampicin and
streptomycin
e. Six month prophylaxis with rifampicin and
streptomycin
a. F
b. F
c. F
d. F
e. F
According to Kumar and Clark, in adults who have contact with TB even if they are
mantoux test positive they do not require any treatment if CXR is negative. In
children however, positive tuberculin test is taken as evidence of infection and
treatment is started.
154. A 40 year old male who worked in Saudi, presented
with dyspnea, slight wheeze. He had a history of
smoking and alpha-1 anti-trypsin deficiency. The
likely findings are:
a. Enlarged lung fields on CXR
b. Diagnosis of asthma
c. Diagnosis of emphysema
d. Reduced FEV1/FVC
e. Improvement with bronchodilators
a. T. the lung fields are hyperinflated in emphysema
b. F.
c. T.
d. T. This is characteristic of an obstructive pattern
e. F. I would say F here. Some patients with COPD have a bronchodilator response
but this relates to reversible airways obstruction. This is unlikely if emphysema is
predominating the picture as the obstruction here is due to enlargement of airsapces
with destruction of the alveolar walls.
This man most likely has emphysema as alpha 1 antitrypsin deficiency and smoking
are the big risk factors. The symptoms of cough and wheeze also fit with this
diagnosis. There would be an obstructive pattern with decreased FEV1/FVC ratio.
155. Gout:
a. Commoner in females than males
b. Treat an acute attack with allopurinol
c. Initial attacks are commonly a polyarthritis
d. May occur with a normal serum uric acid
e. Tophi are an early feature of disease
a. F = M:F ratio is 5:1.In fact, gout is rare in prememopausal women.
b. F = allopurinol is a xanthine oxidase inhibitor which is used as a preventative agent
for people who suffer recurrent attacks of gout or who have risk factors e.g. those on
chemotherapy. However, allopurinl MUST NEVER be used in the acute attack as it
can worsen symptoms
c. F= the most common initial presentation is a monarthritis, classically of the first
metartarsal
d. T = serum uric acid levels are not that useful in the diagnosis of gout as the
condition can occur with normal serum uric acid levels.
e. F = tophi deposits are found in the peripheries, e.g. pinna, ear, only after repeated
attacks of gout
Gout occurs due to the deposition of monosodium urate crystals in joints which leads
to synovitis and results in an acutely swollen, red, tender joint which is exquisitely
painful. Attacks may be precipitated by trauma, surgery, infection, starvation or
diuretics. Secondary causes include polycythaemia, leukemia, chemotherapy, renal
failure and long-term alcohol excess.
Treatment for the acute attack includes NSAIDS or colchicine if NSAID intolerant.
Allopurionol is used as a prophylactic agent
156. These conditions cause a polymorphonuclear
leucocytosis
a. Acute blood loss
b. Malignant infiltration of the bone marrow
c. Acute brucellosis
d. Chronic pyelonephritis
e. Acute pyelonephritis
a. T. can be caused by any trauma, sugery, burns or haemorrhage.
b. F. this is a cause of pancytopenia.
c. F. pancytopenia occurs in brucellosis.
d. T. can be caused by any inflammation.
e. T. can be caused by any bacterial infection.
157. The following statements are correct
a. Hip joint disease may present as pain in the knee
b. A normal joint contains as little synovial fluid
that the clinical demonstration of fluid in a joint
always implies an abnormality
c. Joint disease alone is seldom a cause of gross
muscle wasting
d. A positive &#8220;patellar tap&#8221; test is a
sign of patello-femoral arthritis
e. Carpal tunnel syndrome typically remits during
pregnancy
a. T
b. ?
c. F. Disuse atrophy can cause extensive muscle wasting.
d. T. The patellar tap: The suprapatella pouch is compressed with one hand whilst the
other hand pushes the patella sharply backwards; with a positive test the patella can be
felt striking the femur and bouncing off again. If positive it is a sign of an effusion.
An effusion can occur in patello femoral arthritis. Other causes of an effusion would
include trauma and haemarthrosis.
e. F. Carpal tunnel often occurs for the first time in pregnancy
158. Characteristics of typhoid fever include:
a. Incubation period of 4 weeks
b. Polymorph leucocytosis in the early stages of the
illness
c. Macular rash on the trunk
d. Profuse watery diarrhea in the first week of fever
e. Resolution of the fever within 3-4 days of
starting chloramphenicol in appropriate dosage
a. F. The incubation period is 10 to 20 days
b. F. Leucopenia occurs
c. T. A maculopapular rash, so called “rose spots” occurs in 40% of cases. However
this is usually scanty and difficult to see.
d. F. Presentation is usually with malaise, headache, high fever and abdominal pain.
Diarrhoea is more common after the first week.
e. F. the temperature may stay elevated for several days after starting antibiotics, and
this is not a sign of treatment failure.
159. The following drugs may aggravate or cause GI
ulceration
a. Paracetamol
b. Codeine phosphate
c. Ibuprofen
d. Indomethacin
e. Enteric-coated potassium chloride
a. F. Side effects are rare but include rashes and blood disorders. Liver failure can
occur following overdose
b. F. This is a opioid analgesic, of which the common side effects are nausea and
vomiting, constipation and drowsiness. Larger doses can cause respiratory depression
and hypotension. No mention of GI ulceration
c. T. This is an NSAID, thus GI ulceration is a possible side effect. are
d. T. This is also an NSAID
e. T. KCL can cause cause oesophageal and small bowel ulceration. The other main
side-effect is nausea and vomiting. KCL is oral potassium which is used to treat
potassium depletion, most often in patients taking digoxin or other antiarrythmics, in
patients with secondary hyperakldosteronsim, and patients with excessive loss of K in
the stool i.e. severe diarrhoea with intestinal malabsorption
160. Impaired elimination of the following drugs
occurs in advanced renal failure and will necessitate
dosage reduction when they are used in this situation
a. Chlorpropamide
b. Warfarrin
c. Streptomycin
d. Morphine
e. Benzylpenicillin
a. T. This is a long-acting sulphonylurea. Sulphonylureas should be avoided where
possible in severe renal and hepatic failure, as reduced elimination of the drug will
increase the risk of hypoglycaemia, especially in elderly patients.
b. T. Caution is advised when prescribing warfarin to anyone with renal or hepataic
failure
c. T. This is an aminoglycoside. Excretion is principally via the kidney thus
accumulation occurs in renal impairment. Aminoglycosides are also ototoxic
d. T. Dose should be reduced or avoided in renal impairment.
e. T. Caution in renal impaiment.
161. Harmful results are not infrequent when working
with
a. Asbestos
b. Emulsion paint
c. Beryllium
d. Coarse sand
e. Cotton dust
a. T. Can cause asbestosis (lung fibrosis) or malignant mesothelioma (90% of
malignant mesotheliomas are associated with asbestos exposure, which may have
been up to 45yrs previously i.e. long latent period. It is a highly aggressive tumour
with prognosis less than 2 years at diagnosis.)
b. F.
c. T. Berylliosis can cause an cute pneumonitis or chronic pulmonary fibrosis.
However, stirct control of leverls in th workplace have made the disease a rarity.
d. T. This can cause extrinsic allergic alveolitis.
e. T. This can cause extrinsic allergic alveolitis
162. Low fibre diet is at present commonly believed to
be a major factor in the causation of
a. Diverticular disease of the colon
b. Crohn&#8217;s disease
c. Varicose veins
d. Colon cancer
e. Esophageal cancer
a. T
b. F
c. F
d. T
e. F
163. Hypernatremia is an expected finding in the
following disorders
a. Acute renal failure caused by abruption placentae
b. Dehydration complicating renal tubular acidosis
c. Dehydration in an elderly confused man being
treated with chlorpromazine
d. Non-ketotic hyperglycemic coma
e. Dehydration complicating diuretic therapy
a. T. if Sheehans syndrome (pituitary infarction) occurs this can cause pituitary
diabetes insipidus, which is cause of hypernatramia
b. T. Renal tubular acidosis is a cause of nephrogenic diabetes insipidus
c. F.
d. T. Osmotic diuresis can cause hypernatraemia, for example due to HONK.
e. F. Diuretic therapy causes hyponatraemia
The causes of hypernatraemia are:
impaired thirst or conscious state.
pituitary diabetes insipidus i.e. failure of ADH secretion
nephrogenic diabetes insipidus i.e. failure of response to ADH
osmotic diurese
excessive loss of water through the skin or lungs
excessive administration of Na may contribute
164. The following are characteristic hematological
findings in the named systemic disorders
a. Leucopenia in active SLE
b. Leucopenia in active PAN
c. Lymphocytosis in acute leptospirosis
d. Lymphopenia in acute sarcoidosis
e. Lymphpenia in HIV infection
a. T. Leucopenia, lymphopenia and thrombocytopenia may occur.
b. F. PAN is a necrotizing vasculitis that causes aneurysms of medium-sized arteries.
It is a multisystem condition that can affect many organs. Hamatological
abnormalities include: increased WCC, eosinophilia in 30%, anaemia, increased ESR
and increased CRP.
c. F. Leucocytosis characteristically occurs.
d. T. Sarcoidosis is a multisystem granulomatous disorder of unknown aetiology.
Haematological investigations may show: lymphopenia, increased ESR, increased
serum ACE and increased Igs.
e. T. Laboratory abnormalities include lymphopenia with atypical reactive
lymphocytes, thrombocytopenia and raised liver enzymes.
165. Hypophosphatemia is associated with
a. Osteomalacia due to celiac disease
b. Parathyroid adenoma-associated hypercalcemia
c. Rickets due to progressive chronic renal failure
d. Osteoporosis associated with exogenous steroid
therapy
e. Sarcoidosis associated hypercalcemia
a. T. Osteomalacia can occur as a result of malabsorption of Vitamin due to Coeliac
diaease. Lack of Vitamin D results in hypophosphataemia and hypocalcaeimia with
an increased alk phos.
b. T. parathyroid adenoma accounts for 80% of cases of hyperparathyroidism. PTH
increases Ca and decreases PO4 reabsorption in the kidney; increases osteoclastic
activity and increases Vitamin D production. The overall net effect is to increase
serum Ca. Findings include increased Ca and decreased Po4
c. F. Although the lack of vitamin will result in decrased PO4 absorption in the gut the
CRF will result in PO4 retention, therefore hypophosphataemia is unlikely.
d. F. Serum Po4, Ca and alk phos are all normal in osteoporosis.
e. F. Sarcoidosis associated hypercalcaemia is due to increased vitamin D action.
Vitamin D acts to increase the reabsorption of both Ca and Po4 therefore
hypophosphataemia will not occur in this instance.
166. The following are frequently found in association
a. Chronic ulcerative colitis and membranous
glomerulonephritis
b. Acute-on-chronic renal failure and prolonged
bleeding time
c. Pericarditis and sarcoidosis
d. Spironolactone treatment and gynecomastia
e. Thrombocytopenia with renal failure caused by the
HUS
a. T?. Associations include SLE, bowel malignancy, bronchus malignancy,
penicillamine therapy and hepatitis B. Since chronic UC predisposes to bowel ca this
could be an association, but maybe this is a long shot. Make up your own minds
b. F
c. F. Cardiac involvement is rare and includes ventricular dysrhythmias, conduction
defects and cardiomyopathy. No mention of pericarditis
d. T. Spironolactone is a cause of gynaecomastia. Other drug causes include
oestrogens, anti-androgens and digoxin.
e. T. HUS is characterized by: ARF, thrombocytopenia and micrangiopathic
hemolytic anaemia.
167. The following may be of value in the treatment of
hirsutism
a. Regular waxing
b. Cyproterone acetate
c. Minoxidil
d. Spirolactone
e. Low dose dexamethasone at night
a. T
b. T. This is an anti-androgen and progestogen.
c. F. This is for the treatment of alopecia
d. F
e. F. Hirsutism can occur as a side effect of corticosteroids
166. Regarding hypoglycemia
a. When insulinoma is suspected this is best diagnosed
by a glucose tolerance test
b. It is not a clinical problem in diabetic patients
if they have diminished awareness of their symptoms
c. May be precipitated in insulin-dependent patients
by unaccustomed exercise
d. Does not occur in diabetic patients treated with
oral hypoglycemics
e. Is rarely a cause of death in insulin-dependent
diabetics
F. A suppressive test must be administered to diagnose insulinoma. IV insulin is given
and C-peptide levels are measured. Normally exogenous insulin suppresses C-peptide
but this does not occur in insulinoma.
F. Hypoglycamia is much more dangerous in patients who have hypoglycaemic
unawareness. Normally patients will experience “warning symptoms”, such as
sweating, tremor, hunger, which will allow them to ingest some glucose before
symptoms progress. If a patient has hypoglycaemic unawareness they will not have
any symptoms and may progress to coma very quickly.
T. The following can precipitate hypoglycaemia in an insulin dependent diabetic:
exercise, alcohol, excess insulin.
F. Oral hypoglycamics can cause hypoglyaemia, in particular sulphonylureas.
?F. Id say false here as hypoglycaemia is the commenest endocrine emergency,
however I don’t know if many people actually die from it.
167. In the jaundiced patient
a. A palpable gallbladder suggests gallstones
b. Pruritus suggests obstructive jaundice
c. With hemolytic anemia, the urine is of normal color
but contains urobilinogen
d. Carcinoma of the head of the pancreas typically
causes &#8220;boring&#8221; back pain
e. Xanthelasmata are usually found in jaundiced
patients with chronic active hepatitis
a. F. Courvoisier’s law states that a palpable gallbladder in the presence of jaundice is
unlikely to be due to gallstones as gallstones cause fibrosis of the gallbladder, which
results in a small gallbladder. Carcinoma of head of pancreas is a more likely cause.
b. T. Pruritus is due to the deposition of bile salts in the soft tissues.
c. T
d.?T. I would say T for this. Carcinoma of the head of the pancreas typically causes
painless jaundice but carcinoma of the body and tail of the pancreas typically causes
epigastric pain that radiates to the back and may be relieved by sitting forward.
e. ?
168. In a patient with a pleural effusion
a. Bronchial breathing may be heard above the effusion
b. Protein content of 40g/L suggests heart failure may
be the cause
c. Pleural effusion may occur in the patient with an
ovarian tumor
d. Atypical pneumonia is a classical cause of a
pleural effusion
e. Acute pancreatitis may cause a left-sided pleural
effusion and ascites
a. T. This is a common finding, due to compression of the lung above the effusion.
b. F. A protein content greater than 40g/L suugest an exudate, while CCF is a
common cause of a transudate. The causes of an exudate include: malignancy,
pneumonia, TB, pulmonary infarction, RA, SLE. The causes of a transudate are: CCF,
constrictive pericarditis, cirrhosis, nephrotic syndrome, malabsorption,
hypothyroidism and Meigs syndrome.
c. T. Meigs syndrome is the association of a right pleural effusion (transudate) and an
ovarian fibroma
d. ?. Any pneumonia can cause a pleural effusion but I don’t know if is classical for
atypical. Atypical pneumonias tend to have more vague symptoms and signs in
general so maybe its false. I don’t know
e. ? Acute pancreatitis may cause a pleural effucion but I don’t know of its left sided
169. In the patient with mitral stenosis
a. History of rheumatic fever almost always obtained
b. Loud first heart sound and opening snap suggests
the valve is calcified
c. A &#8220;p&#8221; mitrale may be seen on ECG
d. Bacterial endocarditis is an uncommon complication
of mitral stenosis
f. Mitral stenosis may cause hoarseness
T. Rheumatic fever is commonest cause. Other causes include congenital,
mucopolysaccharidoses, endocardial fibroelastosis, malignant carcinoid.
F. These findings are found in mitral stenosis but opening snap suggests a pliable
valve, not calcified.
T. P-mitrale may be seen on ECG if in sinus rhythm
T. Infective endocarditis can occur but it is a rare complication
T. This can occur as a complication of mitral
stenosis due to pressure on
recurrant laryngeal nerve from an enlarged left atrium.
170. A 65 year old man is found to have hypercalcemia
a. Diarrhoea and itching would be expected symptoms
b. Serum electrophoresis would be a relevant investigation
c. Fluid restriction is the first line of treatment
d. Thiazide diuretics may be a cause
e. If he has a lung tumour, it is likely to be a squamous cell carcinoma
F
T
F
T
T
a) F For the symptoms of hypercalcaemia remember ‘bones, stones, groans and
psychic moans’.
General Features:- tiredness, weakness, dehydration, depression, weight loss,
abdominal pain, vomiting
Renal Features:- Renal colic from renal stones, polyuria, haematuria, and
hypertension
Bones:- bone pain ( bone cysts and ‘bone tumours’)
Corneal calcification
Cardiac arrest ( prolonged Q-T interval)
b) T Serum electrophoresis to exclude multiple myeloma, a neoplastic proliferation of
plasma cell which produces a monoclonal immunoglobulin band on serum or urine
electrophoresis.
Causes of Hypercalaemia are as follows
The commonest causes are Primary Hyperparathyroidism and Malignancies
Excessive Parathormone (PTH) secretion
Primary Hyperparathyroidism
Adenoma
Hyperplasia or Carcinoma
Tertiary Hyperparathyroidism
Ectopic PTH secretion
Malignant Disease
Myeloma
Secondary deposits in bone
Production of osteoclastic factors by tumours
PTH- related protein secretion
Excess action of Vitamin D
Iatrogenic or self administered
Granulomatous disease e.g. Sarcoidosis, TB
Lymphoma
Excessive calcium intake
‘milk alkali’ syndrome
Drugs
Thiazide diuretics
Vitamin D analogous
Lithium
c) F Patients with hypercalcaemia are dehydrated so fluid restriction would be a
crime against humanity. Normal calcium is 2.12 – 2.65 mmol/l . While investigation
of the cause is under way , immediate treatment is mandatory if the patient is
seriously ill or if the serum Ca2+ is above 3.5 mmol/l
1.Rehydrate with IV 0.9% saline e.g. 4-6 L I 24 hours as needed. Correct
Hypokalaemia and hypomagnesaemia. Monitor Urea and electrolytes.
2. Intravenous bisphospanate, Pamidronate. It inhibits osteoclast activity and so bone
resorbption.
3. Prednisolone is effective in some instances e.g. myeloma, sarcoidosis and vitamin
D excess) but in most cases is ineffective
d) T, thiazides lead to increased resorption of Ca2+ in the Kidneys
e) T, True ‘ectopic PTH secretion’ by the squamous cell tumour of the lung is very
rare and is mostly associated with raised levels of PTH related peptide.
---------------------------------------------------------------------------------------------------------------171. In Irritable Bowel Syndrome
a. Nocturnal diarrhoea is typical
b. Daily stool weight is normal
c. Symptoms typically develop in late middle life
d. Rectal biopsy is diagnostic
e. Carcinoma of the colon is a late complication
F
T
F
F
F
171. In Irritable Bowel Syndrome
a). Nocturnal diarrhoea is typical F
More associated with diabetic autonomic neuropathy. Irritable bowel syndrome is a
heterogeneous group of disorders for which no cause can be found and may be due to
disorders of intestinal motility.
Diagnostic Criteria (Rome II)
In the preceding 12 months there should be at least 12 consecutive weeks of
abdominal discomfort or pain that has two or three of the following features
1. relieved with defecation
2. onset associated with a change in frequency of stool
3. onset associated with a change in form of stool
The following symptoms cumulatively support the diagnosis of IBS
1. Abnormal stool frequency (more than 3 a day or less than 3 a week)
2. Abnormal stool form (hard or loose)
3. Abnormal stool passage (straining , urgency or tenesmus)
4. Passage of mucus
5. Bloating or feeling of abdominal distension
These symptoms are used to classify patients into diarrhoea or constipation
predominant forms of IBS. A third group in which diarrhoea and constipation
alternate also exists. Are ye bored stiff now?
b). Daily stool weight is normal T
1ST step is to exclude organic disease so
Look for markers of organic disease, age greater than forty, weight loss, rectal
bleeding, waking at night with pain and diarrhoea.
Based on clinical judgment ( what isn’t?)
If young , with classic history, FBC, ESR,LFT, Coeliac serology and urinalysis,
maybe sigmoidoscopy with rectal biopsy
If patient greater than 45 years or has markers of organic disease do colonoscopy.
If diarrhoea prominent do LFT, stool culture, B12/ Folate, Coeliac serology, TSH,
referral for barium follow through , rectal biopsy
c). Symptoms typically develop in late middle life F
Patients are usually 20-40 yrs old and females more than males
d). Rectal biopsy is diagnostic F
rectal biopsy may be done to rule out a possible cause but there is no pathology (
discovered as yet)
e). Carcinoma of the colon is a late complication F
Has no late complications
Treatment
Refer to dietician, Ispaghula husk for constipation, Loperamide for diarrhoea,
Mebeverine and dicloverine (antispasmodics for colic and bloating), sometimes
cognitive behavioural therapy, antidepressants.
--------------------------------------------------------------------------------------------------------------------------172. A 25 year old female is found to have microscopic hematuria on routine
insurance exam. The following statements are correct:
a. The finding is compatible with IgA nephropathy
T
b. The finding is consistent with Alport&#8217;s nephropathy
T
c. The finding is compatible with a residuum from an episode of minimal change
nephrosis eight months previously
F
d. The finding is compatible with a residuum from an episode of post-streptococcal
nephritis eight months previously
F
e. If the patients has insulin-dependent diabetes mellitus of 12 years standing, the
finding is likely to indicate the early phase of diabetic nephropathy
F
172. A 25 year old female is found to have microscopic hematuria on routine
insurance exam. The following statements are correct:
a). The finding is compatible with IgA nephropathy T
However IgA would be more likely in children and young females. It is the
commonest glomerulonephritis in the west – causing episodic haematuria that may
coincide wit viral infections. IgA is deposited in glomeruli. Heavy proteinuria and
hypertension indicate a poor prognosis. Tx Steroids, ACE inhibitors, dietary fish oil,
tonsillectomy and renal transplantation
b). The finding is consistent with Alport&#8217;s nephropathy T
Alport’s syndrome is a rare condition characterised by a hereditary nephritis with
haematuria, proteinuria, progressive renal failure and sensorineural deafness. Also
associated lenticonus ( bulging of eye lens) seen in some. Inheritance can be Xlinked dominant, autosomal dominant or rarely autosomal recessive. Tx control Blood
Pressure, supportive management of renal failure, dialysis, transplantation.
c). The finding is compatible with a residuum from an episode of minimal change
nephrosis eight months previously F
Get proteinuria in minimal change disease, not haematuria, it can relapse however.
d). The finding is compatible with a residuum from an episode of post-streptococcal
nephritis eight months previously F
A small number of adults develop hypertension and / or renal impairment later in life
after post – streptococcal nephritis. Therefore an annual blood pressure check and
estimate of serum creatinine, is a reasonable precaution, even after apparent complete
recovery.
e). If the patients has insulin-dependent diabetes mellitus of 12 years standing, the
finding is likely to indicate the early phase of diabetic nephropathy F
Type 1 DM nephropathy occurs 10-15yrs post diagnosis and is characterized by
proteinuria, NOT Haematuria, (albumin excretion >300 mg/d), fall in GFR, and raise
BP. Renal failure occurs 15-30 years post diagnosis.
--------------------------------------------------------------------------------------------------------------------------173. Erythema nodosum may be associated with:
a. OCP
b. Streptococcal sore throat
c. Sarcoidosis
d. Pemphigus
e. Diabetes Mellitus
T
T
T
F
F
173. Erythema nodosum may be associated with:
a). OCP T
b). Streptococcal sore throat T
c). Sarcoidosis T
d). Pemphigus F
e). Diabetes Mellitus F
Erythema Nodosum is a cutaenous sign of systemic disease. It presents as painful
dusky blue-red nodules, commonly over the shins which fade over 2-3 weeks.
Common in young adults esp. females. The inflammation involves the dermis and the
subcutaneous layer.
Causes of erythema nodosum
Streptococcal infection
Drugs (sulphonamides, oral contraceptive)
Sarcoidosis
Idiopathic
Yersinia infection
Fungal Infection (histoplasmosis, blastomycosis)
Tuberculosis
Leprosy
Inflammatory Bowel Disease
Chlamydia Infection
Treated with NSAID’s light compression bandages and bed rest. Treat underlying
cause. In persistent cases try dapsone, colchicines and perdnisolone.
------------------------------------------------------------------------------------------------------174. The following are true in rheumatoid disease:
a. Rheumatoid nodules are tender
F
b. Proximal interphalangeal joints are commonly affected
T
c. Presence of swan-neck deformities is a good guide to current disease activity F
d. Rheumatoid nodules are usually located on the dorsum of the hand
F
e.Charcot’s joints are a complication
F
174. The following are true in rheumatoid disease:
a). Rheumatoid nodules are tender F
Rheumatoid nodules are non-tender. They indicate disease activity. They are
granulomata with a central zone of fibrinoid necrosis, with surrounding macrophages
and fibroblasts.
Poor Prognostic factors
1. Systemic features- weight loss, extra-articular manifestations
2. Slow onset
3. Rheumatoid nodules
4. Presence of Rheumatoid Factor
5. Early bone erosions
6. Persistent activity of the Disease for over 12 months
b). Proximal interphalangeal joints are commonly affected T
The diagnosis of Rheumatoid arthritis is typically made when 4 of 7 qualifying
criteria established by the American Rheumatism Association are met. These
qualifying criteria are as follows:
Morning stiffness lasting longer than 1 hour before improvement
Arthritis involving 3 or more joints
Arthritis of the hand, particularly involvement of the proximal interphalangeal (PIP)
joints, metacarpophalangeal (MCP) joints, or wrist joints
Bilateral involvement of joint areas (i.e., both wrists, symmetric PIP and MCP joints)
Positive serum rheumatoid factor (RF)
Rheumatoid nodules
Radiographic evidence of RA
c). Presence of swan-neck deformities is a good guide to current disease activity F
Swan neck deformities are a good guide to the chronicity i.e. how long a person has
had rheumatoid arthritis.
d). Rheumatoid nodules are usually located on the dorsum of the hand F
Rheumatoid nodules are generally found around the elbow. However they can also be
found on the flexor and extensor tendons of the hand, sacrum, Achilles tendon, sclera,
lungs and myocardium.
e). Charcots joints are a complication F
Charcots joints are joints damaged by trauma as a result of the loss of protective pain
perception. Seen in Syphilis (knees and ankles), diabetes mellitus (joints of tarsus),
Syringomyelia (shoulder) and Leprosy
------------------------------------------------------------------------------------------------------175. Mark the following True or False
a. In Iron deficiency anaemia, mean corpuscular volume is frequently 65-75 Fl
b. Poor dietary B12 is the main cause of pernicious anaemia
c. Celiac disease frequently causes folic acid deficiency
d. Normal isotope bone scan is typical of multiple myeloma
e. Haemolytic anaemia causes increased conjugated bilirubinemia
T
F
T
T
F
175. Mark the following True or False
a). In Iron deficiency anaemia, mean corpuscular volume is frequently 65-75 Fl T
Normal mean cell volume (MCV) is 76-96 FL, iron deficiency anaemia causes
microcytosis i.e. low MCV
b). Poor dietary B12 is the main cause of pernicious anaemia F
Pernicious anaemia is due to malabsorption of B12 resulting from atrophic gastritis
and lack of gastric intrinsic factor.
c). Celiac disease frequently causes folic acid deficiency T
Due to malabsorption
d). Normal isotope bone scan is typical of multiple myeloma T
Isotope scans have a low sensitivity for Multiple Myeloma, so most scans would look
normal as the osteoblastic response to bone destruction is diminished. Remember that
all patients that have Multiple Myeloma need skeletal survey with X-rays.
99m
Technetium methoxyisobutylisonitrile (99mTc-MIBI) has been shown to be superior
to plain film radiography and skeletal scintigraphy in detecting bone and bone marrow
involvement.
e). Haemolytic anaemia causes increased conjugated bilirubinemia F
Haemolytic anaemia causes an unconjugated Bilirubinemia as the red blood cells are
haemolysed outside the liver, where bilirubin is conjugated
------------------------------------------------------------------------------------------------------176. The following are recognized associations
a. Hypothyroidism: pretibial myxoedema
b. thyrotoxicosis: Proximal myopathy
c. Cushing’s disease: hypoglycaemia
d. Addison’s disease: hypertension
e. Acromegaly: Homonymous hemianopia
F
T
F
F
F
176. The following are recognized associations
a). Hypothyroidism: pretibial myxoedema F
Pretibial ‘myxodema’ (oedematous swellings above the lateral malleollus) is seen in
HYPERTHYROIDISM
b). thyrotoxicosis: Proximal myopathy T
Causes of Myopathy
Hereditary Muscular Dystrophy
Congenital Myopathies
Acquired Myopathies (PACE PODS)
Polymyositis or dermatomyosistis
Alcohol, AIDS
Carcinoma
Endocrine e.g. hyperthyroidism, hypothyroidism, Cushing’s syndrome, acromegaly,
hypopituitarism
Periodic paralysis (hyperkalaemic, hypokalaemic or Normokalaemic)
Osteomalacia
Drugs – e.g. clofibrate, chloroquine, steroids, Zidovudine
Sarcoidosis
c). Cushing’s disease: hypoglycaemia F
Glucocorticoids which are over secreted in Cushing’ disease, are diabetogenic. Hence
they cause a hyper glycaemia
d). Addison’s disease: hypertension F
Addison’s Disease (adrenal insufficiency) causes postural hypotension
e). Acromegaly: Homonymous hemianopia F
Associated with bitemporal hemianopia due to a growth hormone secreting tumour
compressing the optic chiasma
------------------------------------------------------------------------------------------------------177. The following disorders and findings on examination is correctly paired:
a. Pulmonary fibrosis: fine end inspiratory crepitations
b. Emphysema: increased intensity of breath sounds
c. Pleural effusion: reduced tactile and vocal fremitus
d. Right upper lobe collapse: trachea deviated to right
e. Left apical lung tumour: Left Horner’s syndrome
T
F
T
T
T
177. The following disorders and findings on examinations are correctly paired:
a). Pulmonary fibrosis: fine end inspiratory crepitations T
Fine (Velcro- like) late inspiratory or pan-inspiratory crackles heard over the affected
lobes
b). Emphysema: increased intensity of breath sounds F
Breath sounds are decreased
c). Pleural effusion: reduced tactile and vocal fremitus T
Tactile and vocal fremitus are reduced. They are increased over consolidated lung.
d). Right upper lobe collapse: trachea deviated to right T
In collapse the trachea is deviated to the same side. Trachea is displaced to the
opposite side in massive pleural effusion and pneumothorax
e). Left apical lung tumour: Left Horner’s syndrome T
------------------------------------------------------------------------------------------------------178. True or false:
a. In pulmonary TB, the presence of acid fast bacilli on a sputum smear indicated
infectivity
b. Treatment of TB is with combination chemotherapy for a 2 month period
c. Mycoplasma pneumoniae is a common cause of community acquired pneumonia
d. In meningococcal meningitis, gram+ diplococcic are seen in CSF
e. IN Meningococcal meningitis, CSF neutrophilia is seen
T
F
T
F
T
178. True or false:
a). In pulmonary TB, the presence of acid fast bacilli on a sputum smear indicated
infectivity T
Patients whose bronchial washings (Bronchoalevolar lavage) are smear positive
should be managed as if non-infectious unless (1) the sputum is also smear positive or
becomes so after bronchoscopy, (2) they are on a ward with immunocompromised
patients, or (3) they are known or suspected of having MDR-TB (Multi-drug resistant
T.B.)
b). Treatment of TB is with combination chemotherapy for a 2 month period F
Initial chemotherapy for 2 months Rifampicin, Isoniazid, Pyrazinamide and
ethambutol or streptomycin. Continue for another 4 months with Rifampicin and
Isoniazid. Remember to give pyridoxine throughout treatment as Isoniazid causes
pyridoxine deficit.
c). Mycoplasma pneumoniae is a common cause of community acquired pneumonia
True
Streptococcus pneumoniae is the commonest cause of community acquired
pneumoniae, followed by Haemophilus influenzae and Mycoplasma pnuemoniae.
d). In meningococcal meningitis, gram+ diplococcic are seen in CSF F
Nesseria Meningitis, Alias meningococcus, is a gram negative diplococcic (kisses
and hugs from Prof Prentice)
e). IN Meningococcal meningitis, CSF neutrophilia is seen T
Meningococcus is a bacterium, Neutrophils eat bacteria. Also CSF is turbid/ purulent
in appearance, with high protein and low glucose (bacteria have a sweet tooth too!)
------------------------------------------------------------------------------------------------------179. The following skin manifestations and systemic diseases are correctly paired
a. Neurofibromatosis: Café-au-lait patches
b. Diabetes Mellitus: Livedo Reticularis
c. Chronic liver disease: Spider naevi
d. Erythema nodosum: IBD
e. Polyarteritis nodosa: telangiectasia
T
F
T
T
F
179. The following skin manifestations and systemic diseases are correctly paired
a). Neurofibromatosis: Café-au-lait patches T
Café –au- lait patches are brown macules seen in Neurofibromatosis type 1 and 2 .
Also seen in tuberous sclerosis, ataxia telangiectasia, Faconi’s Anaemia, Multiple
endocrine neoplasia type 1, McCune-Albright syndrome.
b). Diabetes Mellitus: Livedo Reticularis F
Stasis in skin venules e.g. induced by cold, causes immune complex deposition and
pink-blue mottling. If this becomes irreversible , it is called Livedo reticularis.
Generally seen in Vasculitis like Polyarteritis nodosa.
Skin Signs in Diabetes are
Cutaneous infections
Neuropathic ulcers
Necrobiosis lipoidica diabeticorium
Diabetic Dermopathy (small brown scar like lesions seen on the skin)
Diabetic Bullae ~( uncommon blistering disorder of hands and feet)
Xanthomas
Acanthosis Nigrican’s
Lipoatropy
Cheiroarthropathy (scleroderma- like thickening of the skin)
c). Chronic liver disease: Spider naevi T
d). Erythema nodosum: IBD T
e). Polyarteritis nodosa: telangiectasia F
Poly arteritis Nodosa is a necrotising vasculitis that causes aneurysms of mediumsized vessels. Skin signs are utricaria, purpura, infarcts, livedo reticularis, nodules.
--------------------------------------------------------------------------------------------------------------180. The following conditions are correctly paired with an accurate description of
typical symptoms:
a. MI: central anterior chest tightness
T
b. Unstable angina: central anterior chest tightness
T
c. Pericarditis: pain exacerbated by sitting forward
F
d. Psoriasis: itch
T
e. Subarachnoid haemorrhage: frontal headache
F
180. The following conditions are correctly paired with an accurate description of
typical symptoms:
a). MI: central anterior chest tightness T
b). Unstable angina: central anterior chest tightness T
c). Pericarditis: pain exacerbated by sitting forward F
Inflammation of the Pericardium. Central Chest pain worse on inspiration or lying flat
+- relief by sitting forward. A pericardial friction rub may be heard. ECG classically
shows concave (saddle shaped) ST segment elevation. Causes Viruses ( Epstein Barr,
mumps, coxsackie), MI, Uraemia, Rheumatoid Arthritis, SLE, Hypothyroidism,
Radiotherapy .Treat cause and give analgesia e.g. ibuprofen.
d). Psoriasis: itch T
Classically it is said that psoriasis is not itchy, a significant number of patients
complain of severe itching, while most complain of itch some of the time.
e). Subarachnoid haemorrhage: frontal headache F
Sudden devastating headache which tends to be occipital;
--------------------------------------------------------------------------------------------------------------------------181. The following occupations are correctly paired with a recognized occupational
hazard
a. Asbestos insulation: pleural mesothelioma
T
b. Pottery worker: silicosis
T
c. Animal laboratory worker: asthma
T
d. Pneumatic drill operator: Raynaud&#8217;s phenomenon
T
e. Deep sea diver: bony infarction
T
181. The following occupations are correctly paired with a recognized occupational
hazard
a). Asbestos insulation: pleural mesothelioma T
Can be caused by light exposure to asbestos (interval of 20-40 years from exposure to
disease) Presents with pleuritic pain, increasing dyspnoea and pleural effusions.
Median survival is 2 years.
b). Pottery worker: silicosis T
Silicosis is uncommon though it can still be encountered in stone masons, sand
blasters, pottery and ceramic workers . It is caused by inhalation of silica (silicon
dioxide), which is highly fibrogenic.
c). Animal laboratory worker: asthma T
Can be triggered by animal fur
Non – IgE related
Isocyanates - varnishes, spray painting
Colophony fumes – soldering/ welders, electronics industry
IgE related
Allergens from animals, insects and antibiotics-
Laboratories
Allergens from flour and grain- Farmers, millers, grain workers
Latex- Health care workers
Complex salts of platinum- Metal refining
d). Pneumatic drill operator: Raynaud&#8217;s phenomenon T
Consists of episodic digital ischemia, precipitated by cold or emotion. Fingers ache
and change colour pale to blue to red. It may be idiopathic and called Raynaud’s
disease. It may have an underlying cause Raynaud’s phenomenon.
Reflex- Raynaud’s disease, Vibrating machinery injury, cervical spondylosis
Connective tissue disease – Scleroderma, SLE, Polyarteritis nodosa, Rheumatoid
arthritis, polymyositis
Arterial Disease- Embolism or thrombosis, trauma, Buerger’s disease
Haematological – Polycthaemia, leukaemia, Dysproteinaemia, cold agglutinin disease
Poison’s- drugs like beta – blockers, ergotamine, Vinyl chloride
e). Deep sea diver: bony infarction T
Decompression sickness ‘the bends’ occurs in divers on too rapid ascent to the surface
and is caused by release of bubbles of inert gases ( nitrogen and helium).Bends can be
mild with skin irritation, mottling or joint pain only. Bends can be more serious with
cortical blindness, hemi paresis or cord lesions. Treatment is with oxygen in a
pressure chamber. A long term problem is aseptic necrosis ( e.g. of the hip) due to
nitrogen bubbles causing infarction of nutrient arteries of bone.
---------------------------------------------------------------------------------------------------------------182. The following nail findings are correctly paired with underlying disease states:
a. Spoon shaped nails: B12 deficiency
F
b. Leuconychia: chronic liver disease
T
c. Splinter haemorrhages: infective endocarditis
T
d. Nail pitting: Steven-Johnson syndrome
F
e. Finger clubbing: chronic liver disease
T
182. The following nail findings are correctly paired with underlying disease states:
a). Spoon shaped nails: B12 deficiency F
Koilonychia is associated with iron deficiency anaemia, fungal infection and
Raynaud’s phenomenon
b). Leuconychia: chronic liver disease T
Leuconychia is caused by hypoalbunaemia which can be due to chronic liver disease
c). Splinter haemorrhages: infective endocarditis T
Splinter Haemorrhages are caused by nail bed infarcts due to immune complex
deposition
d). Nail pitting: Steven-Johnson syndrome F
Steven Johnson syndrome is a severe form of Erythema Multiforme, with mucosal
involvement, blisters , high fever, Anterior uveitis, pneumonia, renal failure and
polyarthritis. Triggers are Herpes Simplex (the commonest), other viruses – orf,
hepatitis, mumps, radiotherapy, cancers, connective tissue diseases, drugs like
sulphonamides. Close attention to fluid balance and nutrition. Role of steroids
controversial as morbidity from steroids may outweigh that of the disease.
e). Finger clubbing: chronic liver disease T
---------------------------------------------------------------------------------------------------------------183. The following are recognized complications of diabetes mellitus:
a. Impotence
T
b. Postural hypotension
T
c. Charcot&#8217;s joint
T
d. 3rd nerve palsy
T
e. Pneumothorax
F
183. The following are recognized complications of diabetes mellitus:
a). Impotence T
Impotence is common. Part of the autonomic neuropathy of diabetes. Impotence has
many causes including anxiety, depression, alcohol excess, drugs, hypothyroidism.
After appropriate history and examination blood is taken for LH, FSH, testosterone,
prolactin and thyroid function. Sympathetic counselling of both partners, try
Phosphodiesterase type -5 inhibitors ( sildenafil, tadafil, vardenafil)
b). Postural hypotension T
Due to autonomic neuropathy, loss of sympathetic tone to peripheral arterioles
.
c). Charcot&#8217;s joint T Develops in the ankle
d). 3rd nerve palsy T
Isolated palsies of nerves to the external eye muscles, especially the third and sixth
nerves, are more common in diabetics. In diabetic third nerve palsies the pupil
reflexes are intact as the pupillomotor fibres are spared.
e). Pneumothorax F
Spontaneous Pnuemothorax in young men.
Other causes asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic
fibrosis, lung fibrosis, sarcoidosis, connective tissue disorders, trauma, iatrogenic.
-----------------------------------------------------------------------------------------------------184. Subacute bacterial endocarditis can manifest itself as:
a. Cerebrovascular accident
b. Anaemia
c. Hematuria
d. Hypertension
e. Vasculitis
T
T
T
F
T
84. Subacute bacterial endocarditis can manifest itself as:
a). Cerebrovascular accident T
Emboli from infected valves can cause infarction in the brain. Can lead to formation
of cerebral abscess.
b). Anaemia T
Anaemia of chronic disease. There is decreased release of iron from the bone marrow
to developing erythroblasts, an inadequate erythropoietin response to anaemia and
decreased red cell survival. The serum iron and The Total Iron Binding Capacity are
low, while the serum ferritin is normal or raised because of the inflammatory process.
Patients do not respond to iron therapy and treatment in general is of the infective
endocarditis.
c). Hematuria T
Caused by immune complex deposition due a vasculitis. Glomerulonephritis and renal
failure may occur.
d). Hypertension F
e). Vasculitis T see above
------------------------------------------------------------------------------------------------------185. In TB meningitis
a. There is usually a high polymorph cell count in CSF
b. Blood glucose is usually low
c. CSF protein is usually low
d. Presentation can be with inappropriate ADH secretion (SiADH)
e. Cranial nerve palsies may occur
185. In TB meningitis
a). There is usually a high polymorph cell count in CSF F
Generally tends to be mononuclear
b). Blood glucose is usually low T
F
T
F
T
T
c). CSF protein is usually low F tends to be high
d). Presentation can be with inappropriate ADH secretion (SiADH) T
Meningitis (which can be due to T.B. ) and pulmonary T.B. can cause SiADH.
Cause of hyponatremia. Diagnosis of SiADH requires
1. Concentrated urine (sodium > 20 mmol/l & osmolality >500 mosmol/kg)
2. Hyponatraemia (< 125 mmol/l)
3. Low plasma osmolality (< 260 mmol/kg)
4. Normal fluid volume
5. No adrenal, thyroid, pituitary, renal insufficiency or diuretic use
Other Causes of SiADH are
Central Nervous system – stroke, subarachnoid haemorrhage, head trauma, brain
tumour
Pulmonary – neoplasms, tuberculosis, pneumonia
Malignancies – small cell lung cancer, pancreas, lymphoma
Drugs – Antidepressants, Neuroleptics, carbamazepine
e). Cranial nerve palsies may occur T
Can lead to cranial nerve palsies
------------------------------------------------------------------------------------------------------186. Vasculitis lesions can be found in:
a. Polyarteritis nodosa
b. Drug reactions
c. Hypertension
d. Rheumatoid arthritis
e. Hepatitis A
186. Vasculitis lesions can be found in:
a). Polyarteritis nodosa T
b). Drug reactions T
Sulphonamides, penicillins, Thiazides
c). Hypertension F
Many of the conditions associated with a vasculitis can lead to hypertension.
d). Rheumatoid arthritis T
e). Hepatitis A F
T
T
F
T
F
Hepatitis B and C infection is common in Cutaneous Leucocytoclastic vasculitis and
may be an aetiological agent
Vasculitis is a term applied to an inflammatory disorder of blood vessels which
causes endothelial damage. The clinical manifestations are due to ischaemic necrosis.
The Vasculides are systemic diseases which affect the skin, musculoskeletal, renal
and gastro intestinal systems. Classification of Systemic Vasculitis is usually based on
the type of artery affected
Types of Systemic Vasculitis
Large (aorta and major tributaries)
Giant cell arteritis
Takayasu’s arteritis
Medium ( medium and small sized arteries and arterioles)
Classical polyarteritis nodosum
Kawasaki’s Disease
Small (small arteries, arterioles, venules and capillaries)
Microscopic polyangitis (ANCA antinuetrophilic cytoplasmic antibody)
Wegner’s granulomatosis (ANCA)
Churg-Strauss syndrome (ANCA)
Henoch-Schonlein purpura
Cutaneous leucocytoclastic vasculitis
Essential cryoglobulinaemia
Other conditions associated with vasculities
Infective- syphilis, Hepatitis B and C, T.B., group A streptococci
Non Infective- Rheumatoid arthritis, SLE, Scleroderma, Polymyositis,
Dermatomyositis, Bechet’s, Paraneoplastic syndromes, Inflammatory bowel disease ,
drugs mentioned above
-----------------------------------------------------------------------------------------------------------187. Mycoplasma pneumoniae
a. Occurs in young adults
b. Can have CNS manifestations
c. Can be accompanied by skin rash
d. Responds to treatment with penicillin
e. Can show a significant titre of cold agglutinins
T
T
T
F
T
187. Mycoplasma pneumoniae
a). Occurs in young adults T
Mycoplasma Pneumonia is a relatively common cause of pneumonia and occurs in
epidemics in cycles of 3-4 years. It most often occurs in patients in teenagers and
twenty. (from Prof Prentice with love, Mycoplasmas are similar to bacteria but lack
certain structure like cell walls. They bind to the surface of epithelial cells and cause
atypical pneumonia).
Presents with headache, malaise, myalgia, arthralgia which is then followed by chest
symptoms like cough. There may not be any physical signs. Chest X-ray only one
lobe is usually involved with patchy consolidation. There may be no correlation
between x-ray appearance and the clinical status of the patient i.e. the x-ray may look
horrible but the patient is well
b). Can have CNS manifestations T
Check out the complications below
c). Can be accompanied by skin rash T
Complications include skin rash (Erythema Muliforme and Steven-Johnson
syndrome), meningioencephalitis or myelits, Gullian- Barre syndrome, myocarditis
and pericarditis, gastro intestinal symptoms like vomiting and diarrhoea.
d). Responds to treatment with penicillin F
Treated with erythromycin/ clarithromycin (macrolides) or Tetracycline
e). Can show a significant titre of cold agglutinins T
Cold agglutins are present in 50% which can cause an autoimmune haemolytic
anaemia. White cell count is not raised. Diagnosed with antibodies to mycoplasma.
-------------------------------------------------------------------------------------------------188. In a patient with harsh ejection systolic murmur at the precordial base, the
following might indicate aortic stenosis
a. History of syncope
T
b. Large volume pulse
F
c. ECG showing left ventricular hypertrophy and strain
T
d. Doppler echocardiography showing a large pressure gradient
across the aortic valve
T
e. A mid-systolic click at left sternal edge
T
188. In a patient with harsh ejection systolic murmur at the precordial base, the
following might indicate aortic stenosis
a). History of syncope T
May also have angina, dyspnoea, systemic emboli from infective endocarditis,
congestive cardiac failure and sudden death
b). Large volume pulse F
Small volume pulse as the blood finds it difficult to get out of the heart, with narrow
pulse pressure
c). ECG showing left ventricular hypertrophy and strain T
Can also show P- mitrale (bifid p-wave indicates left atrial hypertrophy), left anterior
hemiblock, poor R wave progression, left bundle branch block or complete block
d). Doppler echocardiography showing a large pressure
gradient across the aortic valve T
Valve gradient greater than > 50 mmhg indicates severe stenosis
e. A mid-systolic click at left sternal edge T
Ejection mid-systolic murmur heard at left sternal area, aortic area and radiates to the
carotids. In congenital aortic stenosis where the valve cusps remain mobile and come
to an abrupt halt, an ejection click may precede (come before the murmur). This click
is absent if the valve is calcified.
------------------------------------------------------------------------------------------------------189. Regarding hypercholesterolemia
a. Fasting sample is necessary for screening
b. May be due to a decrease in LDL receptors
c. Total cholesterol and LDL cholesterol are usually closely associated
d. Increased HDL cholesterol is associated with an increased risk of cardiovascular
disease.
e. Reduction of total cholesterol has been shown to significantly reduce
cardiovascular risk.
F
T
T
F
T
189. Regarding hypercholesterolemia
a). Fasting sample is necessary for screening F
Serum cholesterol concentration does not change significantly after a meal and as a
screening test a random blood sample is sufficient. It total cholesterol concentration is
raised, HDL cholesterol, triglyceride, and LDL cholesterol concentrations should be
quantified on a fasting sample. If a test for hypertriglyceridaemia is needed, a fasting
blood sample is mandatory.
b). May be due to a decrease in LDL receptors T
On all the cells of the body and mainly in the liver there is a low density lipoprotein
receptor that collects LDL (low-density lipoprotein) cholesterol from the
bloodstream.
People with Familial Hypercholesterolemia have a defect in the gene of this LDLcholesterol receptor which causes an accumulation of LDL-cholesterol in the blood
and ultimately in the arterial vessel wall. There are more than 300 different gene
defects that lead to FH.
c). Total cholesterol and LDL cholesterol are usually closely associated T
Population studies have repeatedly shown a strong association between both total and
LDL Cholesterol concentration and coronary heart risk.
d). Increased HDL cholesterol is associated with an increased risk of cardiovascular
disease. F
High Density Lipoprotein protects against cardiovascular disease
e). Reduction of total cholesterol has been shown to significantly reduce
cardiovascular risk. T
National Cholesterol Education Program guidelines suggest that drug therapy should
be used if there is inadequate response to diet therapy and the individual has a low
density lipoprotein concentration above 4.1 mmol/l (corresponding roughly to a total
cholesterol concentration over 6.2 mmol/l) together with existing coronary heart
disease or two other coronary heart disease risk factors.
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