MED 2 – GENERAL EXAM CONTENT FROM SEM 1 AND 2
HAEM AND RENAL
MCQ
1. You do a blood smear on a patient with colon cancer. Which cell would you expect to see?
A – reticulocytes (I think it’s this – immature RBCs/’reserve’)
B – erythroblasts…
2. What laboratory test is used for checking Warfarin? (Prothrombin time = INR)
3.
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20. Which of the following structures does the posterior aspect of the kidney NOT touch?
A – 12th rib
B – central tendon of the diaphragm (I think it was this one)
C – quadratus lumborum
Question about intravascular haemolysis and what colour the urine will be Hemoglobinuria – presence of RBC’s in blood (red-brown colour)
Hemosiderinuria – kidneys overloaded with haemosiderin –appears in urine
4. Haematotlogy – disease, cells and clotting cascade
5. Renal – disease and function of tubule sections
KFP/Random exam questions
RENAL - Anatomy/general physiology – hormones/reabsorption
- Renal control of BP – what are the mechanisms? Renin-angiotensin, aldoster one, ADH
Kidneys play key role in regulating BP. The mechanism is Renin angiotensin system.
macula densa detct changes in solute content signaling JGand reduced JG stretch stimulate the
relasease of renin. Renin converts angiotensinogen into angiotensin 1. Angiotensin converting
enzyme (ACE) stimulate the conversion into angiotensin 2. Angiotensin 2 causes:
Increase release of vasopressin
Stimulates adrenal release of aldosterone
Both causes increase reabsorption of water in the distal tubule, increasing plasma volumeincrease blood volume- increase blood pressure- homeostasis.
Angiotensin 2 also cause arteriolar vasoconstriction to increase BP.
- Micturition – control of micturtion
Bladder fills with urine until the pressure rises to a critical, threshold level – initiates Micturition
reflex
Micturition is an autonomic spinal cord reflex, but it can be inhibited or facilitated by centres in the
brain
Activation of stretch receptors initates parasympathetic-mediated contractions of the bladders
smooth muscle (detrusor)
Voluntary relaxation of the external sphincter permits the flow of urine thorugh the external meatus
and urethra.
- Autonomic spinal cord reflex. Activation of stretch receptors initiates parasympathetic –
mediated contraction of the bladder smooth muclse.
- Definitely know anatomy of kidney and where stuff is absorbed ect. ie..prox tubules.. you'll
probably get a picture of this
- 2 structures adjacent to the (renal) cortex ?
RHS: liver, colon, duodenum LHS: spleen, tail of pancreas, left colic flexure, stomach, jejunum
- What epithelium is present in the ureter?transitional epithelium-stretch readily,allow distension, peristaltic.
- Bladder mucosal layer cell type?
3 layers:
A mucosa containing transitional epithelium
A thick muscular layer – intermingled smooth muscle fibre- allow thrusting of urine out
A fibrous adventitia (outermost)
- Asked to identify regions on the histological slides, and where they are on the kidney picture.
- What hormone acts on the collecting ducts and distal tubule to retain water?
ADH
- how do the kidneys regulate BP?juxtaglomerular apparatus – detect changes in BP, macula
densa- detct in concentration of solute
- vasa recta – where from?
Long straight vessel that extend deep into medulla paralleling the loop of Henle. Coming from efferent
arteriole which drains the glomeruli.
- sequence of artery to kidney to vein? Aorta- renal artey- segmental artery- interlobar arteryarcuate artery- interlobular artery- afferent arteriole- glomeruslus- efferent arteriole- peritubular
capillaries and vasa recta- cortical radiate vein- interlobulaar vein- arcuate vein- interlobar veinsegmental vein-renal vein
- What area of nephron does aldosterone act on? i.e. DCT/CD
- -Cell types in the nephron? i.e.
PCT – simple cuboidal epithetlium, with microvili to increase surface area
DCT- simple cuboidal/columnar epithelium – some reabsorption occurs
Collecting Ducts, Bowman’s –transitional epithelium
Capsule(visceral podocyte, parietal simple squamous epithelium) etc.
- -Aldosterone effects – Na+, HCO3-, etc.
- Man falls off a motor bike and has head trauma  diabetes insipidus - How does ADH
decreases urine osmolality? - Where is ADH released from? (posterior pituitary) - Briefly
explain how the kidneys allow dilute and concentrated urine to be made
Dilute urine: at the absence of ADH at the distal tubule, basal membrane impermeable to waterreabsorption of water ceased- dilute urine
Concentrated urine – when ADH deposited at the luminal membrane of tubule, making it
permeable to water, reabsorption takes place
- What are principal cells?
Renal Disease
- The effects of end stage renal failure on fluids and electrolytes
Defined as GFR less than 5%, terminal stage of uraemia.
Dehydration- ADH action ceased, unable to reabsorb water
Oedema- high volume of blood plasma,
Hyperkalaemia –Na+ reabsorption ceased, unable to secrete K+ out,
metabolic acidosis – excess H+ are not secreted in urine
Renal regular function are affected. Loss of blood pressure control.
- Acute Renal failure – effect on electrolyte balance, fluid, Calcium, phosphate and bone
(Pathophysiology of how chronic renal failure causes bone disease.)
GFR less than 20-25% kidneys unable to regulate blood volume and solute composition.
Renal failure- complex disturbance of ca and phosphate metabolism. Hyperphosphataemiacause hypocalcaemia. Stimulate osteoclast action to breakdown bone to release Ca2+ and PO43
into the ECF. Bone lysis- bone disease.
- Post-streptococal glomerularnephritis – what are causes? Preventions?
Autoimmune response to GAS infection
in which antigen antibody complexes are deposited in the glomerular capillary walls,
activating the complement system
which leads to an inflammatory response
manifested by cellular proliferation and oedema of the glomerular tuft.
- Urine dipstick: Explain why she would be dehydrated (Ketoacidosis from Diabetes)
- What does it mean when protien/blood/sugar in the urine ect. Reach maximum transport
- What is inflammation of renal pelvis called, and how does it occur?
Pyelonephritis; inflammation of renal pelvis and kidney tissue that has been present for a long time.
Due to bowel organism eg E coli that enter urinary tract.
Nephritic syndrome- due to autoimmune, post streptocoal
- enlarged prostate, what damage might it do to kidneys (pyelonephritis)- back pressure- urine are
redirected back into the ureter, predispose to bacterial onfection- leads to inflammation. Cases
enlarged walls, diverticular formation and traberculation.
- Primary Interstitial Nephritis – what histological aspect is NOT associated with this disease?
HAEMATOLOGY - Anaeamia/Polycythaemia/Thrombocytopaenia
- What are the 3 types of anemia? Normocytic,microcytic, macrocytic
-
Normochromic, normocytic - MCV MCH normal - blood loss, haemolysis, chronic disease
macrocytic,– MCV raised megaloblastic anemias
hypochromic microcytic MCV and MCH low – iron deficiency, Thalessaemia (poikilocytosis
shape)
- Which type of leukeamia mostly occurs in elderly? What is the cause? How does it lead to
anemia?
Chronic lymphocytic leukaemia. Clonal expansion of b lymphocytes. Appear morphologically
normal but are arrested at an early stage of development. Therefore immune suppression.
Overproduction of immature lymphocytes take over bone marrow, less production of red blood
cells.
- Where heamoglobin produced in baby after birth? (Premature baby and erythropoiesis)
- At bone marrow. However extramedullary haematopoiesis takes place if there is increased
demands of rbc
- Haem - picture of cells ect. Not as many as you would expect though
- What is meant by megaloblastic anaemia? Explain the abnormal cellular processes during
erythropoiesis that leads to this form of anaemia?
Anaemia that is classified as having enlarged rbc, usually hypersegmented. Usually due to deficiency of B12
and folate required for rbc DNA- the rate of cytoplasm growth is higher than the nucleus. Enlarged rbc.
- What anemia is it? Large blast cells, B12/folate deficiencies: what happens to EPO when you
don’t have enough vit B. Say why they’re anemic? Not as much Hb carrying capacity?
- polycythaemia, what is it ? why does it occur?
An abnormality caused by an increase in rbc count. True polychthaemia – actual increases in
RBC, relative – dilutional effect- dehydration.
-
What is primary polycythaemia?
Due to actual increase of Hb & Hctdue to unregulated control of erythrocyte production.
What is secondary polycythaemia?
Due to physiologic condition – COPD, high altitude- low O2 stimulates peritubular cells of
kidney to undergo erythropoeisis
- Give an example as to why the erythrocytes are larger than normal and the neutrophils have a
hypersegmented nucleus in VitB12 deficiency
- How Do You Determine The Difference Between Macrocytic and Microcytic?
- Morphology
- Causes of Thrombocytopenia
Thrombocytopaenia- deficiency in platelet causing excessive bleeding. Maybe caused by
increased destruction of platelets, increased splenic sequestaration, dilution. Often develop in
leukaemia bcz immature wbc takes over megakaryocytes in bone marrow, megakaryocytes fail
to develop
- Causes of Microcytic hypochromic Anaemia
Iron deficiency, haemoglobin production abnormality- Thalessaemia, malnutrion, chronic blood
loss
Leukaemia
- Which is the leukaemia that causes shortness of breath and most common
- Polyc
- Know Leukeamias - basically know the main types and what the cells would look like in each
- HRM: Running out of puff may be associated with development of anemia associated with
leukaemia. Which is the most common type of leukaemia in someone of stan’s age? ?CLL (not
CML) (which leukaemia of the elderly? And how does it cause anaemia?)
- How does anaemia develop in this form of leukaemia: bone marrow – lymphocytic takes u
space & then don’t produce RBC
- myeloperoxidase – what leukaemia? (AML)
- changes in haemoglobin from child to adult
General Haem questions
- Describe what the packed cell volume is (not cytoplasm) & why is it elevated?
he hematocrit (Ht or HCT) or packed cell volume (PCV) or erythrocyte volume fraction (EVF) is the
proportion of blood volume that is occupied by red blood cells. It is normally about 48% for men and 38%
for women. It is the percentage of haemotocrit.
- Know definition of full blood count, understand what makes each one go up and down
- 5 of the kidney’s physiological mechanisms to retain sodium and fluid.
- What effect might oestrogen have on thrombosis?
- Life expectancy of neutrophils?
- Splenectomy – What won’t you see?
- Howell Jolly Bodies?
- Three histological changes associated with glomerulonephritis.
Hypercellularization-cellular proliferation leukocytic proliferation, basement membrane thickening,
hyalinization and sclerosis-accumulation of precipitated protein
- Reid – Steinberg Cells?
- what doesn’t thrombin activate? (plasmin)
- Action of aspirin?- antiplatelet agent
- Effect of heparin?- anticoagulant agent
- what is thrombophilia?
- Name cell type responsible for synthesising and secreting vWF?; mucosal cell of endothelial
layer
Haemolytic Disease of the Newborn
- Haemolytic disease of the newborn; Rh+, elevated bilirubin and increased reticulocytes and
anaemia
- Jaundice causes?
Physiology
Excessive blood destruction
Hepatic
- Direct Coomb’s test and Indirect Coombs - Direct Coomb’s – Anti-D on RBC – Indirect
Coomb’s antibodies in serum (cross-matching)
- What is extramedullary heamopoiesis?
- What are the organs where extramedullary heamotopoeisis occurs in the newborn? (?liver &
spleen)
- where erythropoiesis occurs in baby – know the different stages until adulthood
Med 2 KFP mid-semester (2006)
- Given values of MCV, MCHC, etc, and asked to say what type of anaemia they had. What was
the likely cause of the anaemia?
- What are the 3 types of anemia?
- Three histological changes associated with glomerulonephritis. – hypercellularization, increased
membrane thickening, hyalinization
- Basis of post-streptococcal glomerulonephritis – autoimmune
- What is xenotransplantation?
Name 5 issues to overcome before it is used (technical, ethical, psychological, etc)
- What is primary polycythaemia?
- What is secondary polycythaemia?
- List two ways how smoking can contribute to secondary polycythaemia.
- Pathophysiology of how chronic renal failure causes bone disease.
- What will you find in the urine in acute glomerulonephritis?
- Explain the neurophysiological mechanism of micturition
- 5 of the kidney’s physiological mechanisms to retain sodium and fluid.
- What effect might oestrogen have on thrombosis?
- What kind of injuries would a patient with a severe spinal injury at the level of the 1 st L, what
impact would this have had a normal bladder emptying?
- Pt w severe spinal injury at the level of C8. Know level vaqus nerve comes off, then look at
sympathetic, parasympathetic.
[KFP - END OF YEAR 2006]
- What diseases could possibly have causes end-stage renal failure
Diabetes – damage of microcirculation in kidneys.
Chronic hypertension – damage to glomerulus.
Post-Streptococcal glomerulonephritis.
- How does renal failure causes bone problems
Unable to excrete phosphate
- Why would get anaemia
Erythropoietin secretion  not happening!!! Due to renal failure.
- What happens to glomerulus due to hypertension
Damage to filtration membrane.
- Two hormones responsible for water retention (ADH and aldosterone?) – how they work.
How would make peripheral oedema worse?
ADH stimulates insertion of aquaporins into DCT/collecting duct.
ADH stimulates sodium reabsorption DCT.
Increased fluid = increased hydrostatic pressure.
- What hormone is antagonist to this? How would that improve condition?
Atrial natriuretic peptide.
Less fluid retention.
- What types of leukaemia are common in a 65 year old
Chronic Lymphoblastic leukaemia.
- Why get anaemia with leukaemia
Due to infiltration of the bone marrow by malignant blast cells.
- Joyce Bence proteins
A Bence Jones protein is a monoclonal globulin protein found in the blood or urine. In Multiple
myeloma, excessive production of immunoglobulins cause infiltration of proteins on kidney tubule
- Anaemia
[KFP – 2005]
Explain micturition (sympathetic and parasympathetic control)
Why would man get vesicoureteral reflux- chronic reflux of urine up the ureter and into the
kidney during micturition.
Extreme action of the sympathetic system would prevent the relaxation of the sphincters and the
contraction of detrusor muscle this would prevent normal micturition from occurring.
Case 11: Man falls off a motor bike and has head injury= diabetes insipidus.
How does ADH increase urine osmolarity.
Where is ADH released from.
Briefly explain how the kidneys allow dilute and concentrated urine to be formed.
Multiple Myeloma causes kidney disease. How does this occur?
Bence-Jones proteins.
What is extramedullary hematopoiesis ?
Where does it occur in newborn?
Liver and spleen.
Leukaemia- why myeloma causes proteinuria
MSAT – end of year 2006
Station 4 – Kidney diagram and histology. Label areas; what epithelium lines the ureter;
inflammation of kidney and how does bacteria reach kidney; what hormone controls water
absorption and where is it produced;
Station 13 – Anaemia. What type of anaemia (increased mean cell red volume and decreased haem
concentration); what vitamin def. causes this; what gastric abnormality causes this vitamin
deficiency; what happens during cell proliferation to make abnormal cells; why is patient jaundiced
(excessive haemolysis?);
MSAT – 2005
1.
Anaemia histology – what morphological classification? What deficiency? Why low platelet
and leukocytes?
2.
Renal anatomy and histology – histology of cortex and medulla. How does pyelonephritis
occur? Label the renal pelvis. What is the epithelium of ureter?
[RANDOM other MSAT MATERIAL]
1. Histology of the kidney and had to identify
2. Had to say why erythrocytes present in the histo.
3. Identify externally which parts were which for the kidney
4. Name which artery came in and out
5. Needed to know histology for loop of henle
HRM – Picture of kidney and two histological slides of kidney.
-4 labelled parts of the kidney
-2 structures adjacent to the cortex
-What epithelium is present in the ureter?
-What is inflammation of renal pelvis called, and how does it occur?
-Asked to identify regions on the histological slides, and where they are on the kidney picture.
-What hormone acts on the collecting ducts and distal tubule to retain water?
Urine dipstick: Explain why she would be dehydrated
Acid- base disturbance & rapid respiration rate, explain what it does (CO2)
3 Reasons why she is dehydrated?
Dipstick Test
Interpret results – High Glucose, ? trace of protein
Explain Diabetes
Metabolic Acidosis
Compensatory cause – Increased pulse pressure. ? Why was this. Increased HR to blow off CO2.
HRM – Given basic blood count values (MCV, MCH), plus a list of symptoms (swollen tongue,
grayish areas around mouth, slight jaundice).
-What gastrointestinal problem is causing this anaemia? Lack of intrinsic factor- pernicious
anaemia. Destruction of the parietal cells in the gastric glands. Lack of intrinsic factor. Vit B 12 NO
LONGER REABSORBED.
-How would you classify this anaemia and why? (macrocytic, etc) DUE TO the size of the cells
-Judging by her blood count, what are the physiological processes happening to her?
-What is causing her jaundice?
-Why is the platelet and white blood cell count low?
4 slides and had to describe the type of Leukaemia
? Acute Myeloid Leukaemia or Chronic Myeloid Leukaemia
Why does patient have small red hemorrhages on the body – petechia
Thrombocytopenia
Packed Cell volume and the reason for this
What is the other the form of Leukaemia that is similar in patients of this age
Leukaemia
Shown histology slides a-e of individual cells. Stem says pt is old, has anaemia, staining picks up
granules (must be myeloma/granules). Asks what other stain you could use on this slide:
myeloperoxidase will pick up myeloma/granules
Describe what the packed cell volume is (not cytoplasm) & why is it elevated?
Definition: Full blood count
In polycythaemia
Anaemia histology slide
– what morphological classification?
What deficiency?
Why low platelet and WBC/leukocytes?
Explain what could cause this anaemia?
Explain why this patient may be jaundiced? – megaloblastic anaemia…
Renal anatomy and histology – histology of cortex and medulla.
How does pyelonephritis occur?
Label the renal pelvis.
What is the epithelium of ureter?
Renal histology in tubules and pressures arterioloes
60 year old man – presents with weight loss, pain, fatigue.
White Cell Count - elevated
Blood smear – know if it the cells are blasts or more mature (“cytes) then acute or chronic. Just
know the erythropoetic differentiation.
Know anemias: haemolytic, etc..,
haem examples:
Looking at slides and distinguishing between microcytic and macrocytic anaemia. Determining
which anaemia it is using information from the image plus history given.
Performing a basic blood analysis to find phenotype (ie Ab-) - remember the activity we did in the
laboratory
Looking down a microscope and distinguishing between cells (ie neutrophil, lymphcyte, monocyte)
Conducting a Blood Count
Looking at a slide and recognising certain cells/abnormal cells
RESPIRATORY
- A patient has moderate-severe emphysema and you perform a lung spirometry on them.
What would be their values for FEV1, FVC, TLC & RV?
- A – FEV1: 4.5L/5L FVC: ?
TLC: 6/7 L RV: 1.2/1.5/2L
Gas Exchange/General lung anatomy+histology
- Surfactant and what’s the effect of lack of surfactant
- Respiratory membrane
- Old fellow slowing down a bit, runs out of puff after carrying the groceries up the stairs at
home. Has to do more around house with wife’s osteoarthritis is slowly getting worse, but
doesn’t mind. 39:40 Stans breathlessness may be due to changes is respiratory function. Outline
no more than 3 factors that outline efficient gas exchange (RM, HRM)
- What factors affect the gas exchange in the lung?
- 3 factors that affect normal gas exchange
- How is patency of airway maintained?
- what is meant by compliance of lungs?
- what is the thickness of the resp. membrane?
- muscles in forced expiration? (abs)
- section of lung with highest percentage of muscle?
- reason for reduced surfactant production in premature birth?
- Type 2 alveolar cells function?
- muscles involved in blowing up a balloon?
- What factors affect the gas exchange in the lung?
- Stages of development of the fetus – last two
- when are the lungs fully functional? (2 wk after birth)
Asthma
- Three factors that can lead to airway hypersensitivity and bronchoconstriction
- How do corticosteroids and bronchodilators work in treating asthma?
 Inhaled corticosteroids
 Short-acting beta2 agonists
- Hypersensitivity and asthma
asthma – how type1 sensitivity works – why give reliever (bronchodilator) and controller
(corticosteroids)
- initial phase of atopic asthma?
Acidosis/Alkalosis
- Respiratory acidosis and metabolic compensations and stuff
- Acidosis and alkalosis –Patient has diarrhea and vomiting – metabolic acidosis, repiratory
compensatory mechanism
- Acid base question
- Acid- base disturbance & rapid respiration rate, explain what it does
- Why can diabetes cause acidosis?
- acid/base – with regard to diabetes mellitus – leads to acidosis and how does resp. compensate?
- three things that effect the diffusion of gas?
- Blood pH of 7.05 and pCO2 of 24, and asked what type of acid-base disturbance the patient had.
- respiratory acidosis due to high CO2 and low bicarbonate
Smoking and Lungs  COPD
- Polycythamia in smoking and why?
- Smoker & expected changes
- Chronic bronchitis – what are the changes?
- Chronic bronchitis and how it causes right sided heart failure
- Lung function test results fev1/pev 60% compared to 2 main types of COPD
- How does smoking effect the lungs?
 Irritant. Submucosal gland hypertrophies, increase in goblet cell numbers, infiltration
of white blood cells and fibrosis occurs.
 Smoking also impairs the mucociliary clearance through damaging the mucociliary
apparatus (loss of cilia). Increased risk & morbidity from respiratory tract infections.
Smokers cough may compensate to help clear mucous from airways.
- chronic bronchitis – how aggravated by smoking – affect of resp function
- How does COPD (chronic obstructive pulmonary disase) lead to pulmonary hypertension?
- emphysema definition?
- alpha1-antitrypsin deficiency related to what disease?
Spirometry
- Know the graph of lung volumes!!!!!
- FEV1/FVC 60%: obstructive airway
- FEV/FVC questions in regards to obstruction
- functional residual volume?
- vital capacity is what?
- Tidal Volumes – 500ml
- What does FEV1/FVC indicate? Three ways that smoking can cause emphysema?
- effect of EPP in obstructive lung disease?
- FVC Test Manoeuvre
Pneumothorax
- Pulmonary odema and pulmonary hypertension
- Pneumothorax – how it affects the lung?
- Physiological changes that occur due to the elevated air pressure 1538… & consequences to
lung function, morphological changes 1547 to the … & response to …1550 due to elevated
blood pressure
- pneumothroax
- What happens to ventilation in a pneumothorax?
Regulation of respiration
- what is the normal mechanism why fluid is cleared from lungs ie why you don’t get oedema
- Role of pleural membranes and pleural cavity in ventilation.
- What role H+ ions play in regulating ventilation? What role CO2 plays in regulating
ventilation?
- Pneumotaxic centre located?
- H+ does not cross the BBB – so does not affect central control of respiration
- Sleep Apnoea - BMI determination (~40.1=obese) - Explain airway obstruction and tiredness in
sleep apneoa - What are two affects of sympathetic nervous system activation? - How does the
hypothalamus act in response to stimuli to activate the sympathetic nervous system? - What
other assessments are recommended for middle aged adults? (adult health check; blood
lipids/blood sugar levels/blood pressure)
- Nitrogen narcosis, red rash & SOB. Nitrogen comes out as a gas in the blood stream, expansion
of gas in joints that causes pain, forms bubbles not clots – rash is little haemhorrages. Reduced
consciousness level.
[KFP mid-semester (2006)]
- What does FEV1/FVC indicate?
- Three ways that smoking can cause emphysema?
- Role of pleural membranes and pleural cavity in ventilation
- What happens to ventilation in a pneumothorax?
- How does COPD (chronic obstructive pulmonary disase) lead to pulmonary hypertension?
- Blood pH of 7.05 and pCO2 of 24, and asked what type of acid-base disturbance the patient had.
- What role H+ ions play in regulating ventilation
- What role CO2 plays in regulating ventilation.
[KFP end of year 2006]
- Apart from surfactant what are two other aspect of respiratory development that occur late in
gestation
- Role of inflammation in asthma hypersensitivity
- Pneumothorax and how affected by flying
[KFP – 2005]
5.Sleep Apnoea: Stop breathing whilst sleeping
Diagnosis criteria

BMI=(Weight in kg)/(height in kg2)

Airway Obstruction in Sleep Aponea (central vs obstructive)
Case 6: Atopic Asthma
Describe how reaction occurs due to an allergen.
Type 1 Hypersensitivity Reaction (late phase, epithelial cells, role of eosinophils)
Case 9: Fit Young man whom runs marathons wants to go diving, but gets sudden onset of acute
asthma. He wants you to overlook his asthma and let him go SCUBA diving.
Explain why not breathing out during surfacing during diving is dangerous. [think nitrogen narcosis
AND ALSO lung volume expanding as pressure reduces as surfacing – can get lung exploiding
perhaps]

Explain why the pleural cavity and pleural viscera are important in breathing.
 Parasympathic of airway= Bronchoconstriction
MSAT – 2006
Station 9 – Trachea histology. Be able to label diagram; how cartilage rings assist during normal
ventilation; what epithelium lines trachea;
Station 16 – Basic Life Support Station – name apparatuses; which cannot be used on someone
with an intact gag reflex and why; head tilt and jaw thrust – which one cannot be used on someone
with suspected spinal injuries; EAR and required rate; CPR; carotid pulse and how long should take
pulse for and why
Station 2 – Communication – Spirometry. Be able to perform FVC, explain test, interpret and
explain results
MSAT – 2005
- Communication station: Asking a teenager to do spirometry test and explain the result. Explain
what FCV, FEV1, and FEV1/FVC% means
- Paranasal sinuses, its opening and where it drains. Movement of ribs during forced inspiration
(pump handle and bucket handle). Where to place the stethoscope to listen to each lobe of the lung?
- Basic life support – know CPR and EAR. Names of the apparatus used eg ventilator, artificial
airway. Know head tilt and jaw thrust and which one is used when there is spinal injury. Why not to
use artificial airway when someone has gag reflex?
[RANDOM OTHER MSAT MATERIAL]
RM – Given histological picture of the trachea
-identify what the slide is looking at
-what type of epithelium is present
-label three parts of the slide
-why cartilage is needed in the trachea – due to ventilation pressures
-something about how ventilation works
Question 4. Lung Xray and Spirometry printout
1. Identify what the areas were that were indicated with an arrow
2. What needs to happen with breathing when taken an AP Xray
3. Spirometry – had to identify expiratory reserve volume, functional vital capacity, residual
volume, vital capacity
Spirometry
45years - Female lady coming in for health check – smoker for 20 year, need to try and get her to
stop.
Explain why need to do the test
How to perform the test – did not have to actually do it.
Interpretation of FEV1/FVC
Results showed 70% - Mild Obstruction
Explain possible causes – emphysema, chronic bronchitis, asthma
Other systems that can be affected by smoking
Techniques for giving up smoking
MSAT Question
Billy, 42 years of age, comes into see his GP. He complains of waking up in the morning and
having to cough for a good 10 minutes to bring up flem from his lungs. On enquiry it is found that
he
has
been
smoking
a
pack
a
day
for
the
last
20
years.
Perform
a
spirometry
test
on
Billy
Interpret
the
results
and
explain
this
to
him
- Give him possible recommendations
 Why this test is performed and what the results will show
 Step-by-step process on how to perform the test
 Demonstrate how to perform the test for the patient
Bob’s FEV/FVC is 55%. What does this mean?
Bob enquires about the impact of smoking on his body. Explain the physiological impacts of
smoking.
RM – Patient who wants to start diving needs a medical exam to test FEV1/FVC. Need to ask
about self and family respiratory history, and complete a spirometry test. Then explain to patient
what the results mean.
How to Perform FVC:
 Breathe normally several times
 Execute a maximal inspiration
 Execute a maximal forced expiration
 Breathe normally
Tips for performing with a patient:

initially, give basic explain what the test measures: ‘… basically measures how well the lungs
are functioning and gives an indication if there is anything that may be wrong…’ (doesn’t hurt)
 go on to explain how the test is performed, give a demonstration with the mouthpiece
ensure the patient is sitting upright, not hunched forward
Given three pictures and asked to identify them – oropharyngeal airway, mouth mask and
bag-valve mask. Which one is not used on a patient with intact gag reflex and why?
-Two procedures as pictures and had to identify what they were – jaw thrust and chin lift/head tilt.
Which one is used in a patient with potential spinal injury?
-Identified more procedures from pictures – EAR, CPR.
-What is the rate of breathing in EAR? 30 compressions: 2 breaths in 15 sec
-What is the name for starting CPR in hospitals? ?code Blue??
Patient had been diving and ascending too quickly
Was SOB and had aching joint ? cause
Explain Narcosis and the effects on the body
Patient had the Bends
Explain what the bends is
Define the purpose of a Decompression Chamber – brings them back to pressure at sea level,
decreases the nitrogen in the fat and joints and can then recover fully
Paranasal sinuses, its opening and where it drains.
Movement of ribs during forced inspiration (pump handle and bucket handle).
Where to place the stethoscope to listen to each lobe of the lung?
RRITH
MCQ
- What is the reason for a higher neonatal mortality rate in other remote areas? (given a graph
based on ARIA locations)
o A – increasing distance from services & increasing % Aboriginal
o B – decreased obstetric care & increasing % Aboriginal
o C – lower socioeconomic status & increasing % Aboriginal
- What is a common feature of a rural town?
o A – a number of services
o B – reliant upon one industry
o C-?
o D – all of the above
- You arrive at the scene of an accident to find the following people. Who do you treat first?
o A – Maria had a head trauma and is deeply unconscious
o B – Pete has a chest injury and is complaining loudly
o C – Sid has a bleeding head wound and airway obstruction
- What combines mortality and quality of life? (extended matching question; QALY not an
option, but ‘disability adjusted life years’ was an option)
- RRith – characteristic of rural setting
[Random KFP questions]
Rural health (in general)
- S.A. - RRith. Pretty much every patient was from rural or aboriginal ect. Had to list off things
like "What are the difficulties of this patient getting to the doctor??" Then would have to list 3
things ect. You might have to construct ways to implement a strategy in a rural town ect. .
- Why does a maternity unit in a rural area close?
- Why do doctors leave rural practice
- Briefly state 4 different factors that make it difficult for hospitals to remain open and maintain
services in rural towns?
- How can a rural home and lifestyle affect smoking?
- 3 common reasons why a rural health service might have to close down.
- Motor vehicle accidents – 4 reasons why it is worse in a rural setting than city.
- 4 reasons why you should be concerned about a particular patient in a case – he was reticent,
had haemodialysis, in rural town, etc
- Ethical questions eg a principal asks u abt a teacher and what you should tell the principal?
- 4 ways a health clinic can give a community with a few diabetes cases support without bringing
in extra staff.
- rural economy decreasing?
- Shortage of doctors in rural area – Why? Strategies?
- Causes of higher death rates and cancer in rural Australia
- Bloke didn’t follow up with treatment for high blood pressure and explain what long term
consequences would be?
- Men and health – ie functional view, stoicism
- 3 common reasons why a rural health service might have to close down?
(Emergency stuff)
- DRABCDE: know emergency treatment ALSO 2003 we had a list of patients and we had to
triage them
- During a crash scene, after danger and response, what do you do – need to know First Aid
measures.
- How to treat an injury;
- How to treat a snake bite;
- If aero medical evacuation is used, which patient will be adversely affected
- Emergency medicine (RRITH) - Extended MCQ q on this. If a patient is hurt would you use
helicopter, ambo ect.
- What to do in anaphylactic shock? (adrenaline – IV fluids – O2)
- DRABC – emergency scenarios
- How to treat a snake bite;
- What are the three common affects of Australian snake venoms (nephrotoxic, myotoxic and
haemotoxic)
Epidemiology/calculations
- QALY – explain this in lay term
- Qaly question and how you would explain that to some one – had costs for different procedure
ie. $17000 renal transplant, $35000 for dialysis
- QALYs with regard to kidney treatment
- peritoneal vs haemodialysis – cost-effective analysis
- look at some graphs – birth rates, death rates
- Know all the RRITH stuff maggie did about rates and ratios ect.
Indigenous Health
- Def of primary prevention AND secondary prevention
- Secondary prevention activities the clinic needs to undertake to reduce the risk of rheumatic
heart disease in aboriginal people who have previously had rheumatic fever (3 marks)
- What 7 activities does the clinic need to undertake to reduce the risk of rheumatic heart disease
in people who have previously had rheumatic fever?
- Post-streptococal glomerularnephritis – what are causes? Preventions?
- Explain rheumatic fever to a science teacher in an aboriginal community
- Explain why valve replacements for rural indigenous people is so common (social aspects of
developing rheumatic fever
- Medical student asks you why you give antibiotics for a relatively minor sore throat, even
though current medical aim is to reduce antibiotic use.
- 7 things the clinic can do to prevent the reoccurrence of rheumatic heart disease in patients who
used to have it.
- Greatest risk factor causing ESRD? (Glomerular nephritis - you had to relate it to indigenous
communities; know aetiology and pathology)
- why aboriginals do not get renal transplant?
- How is it children could have been legally removed from families under ‘the act’ as pop was? 2
marks
- What are 4 reasons why aboriginal men don’t get transplants
- Had a aboriginal guy who was an elder and you were going to the community and had to ask
him about the community and how you could fit in ect
- Why indigenous less likely to get kidney transplant?
- Why were Aboriginal children taken away from their families in the time of the stolen
generation?
- Diabetes primary reason for ESRD, what is the second most common? (glomerulonephritis)
- Case about an Aboriginal family, whose father was part of the stolen generation, and a daughter
has a sore throat, for which you prescribe antibiotics.
Tropical Medicine
- which is not vector borne? (melioidosis)
- which is the fatal malaria?
- some stuff about vectors and reserve species
- most common cause of HIV spread in the world?
- How do u protect yourself from getting vomiting and diarrhea in South-east Asia?
[KFP – End of Year – 2006]
 5 reasons why obstetric services in rural areas closing down? 4 strategies to reopen them?

Aboriginal mother and son go to city for treatment – what are 4 social and cultural issues they
will have to deal with

What is the act by which an aboriginal family were taken from their homes?

What type of communicable disease is most likely to cause this anaemia? What conditions make
this disease optimal (bad sanitation, water, food, lots of people living in the same house etc)

After DRABC what should be next treatment to motorcycle accident patient
[KFP – 2005]
3. Snake Bite- What are the 3 common affects of Australian snake venoms

What other assessments are recommended for middle aged adults?
*Adult health check
*Blood lipid levels
*Blood sugar levels
*Blood pressure

What are some of the reasons why more aged care accommodation wouldn’t be made in a town
ARIA 7by the seaside

Why is cancer rate so high in rural areas.
Case 13: Adult Aboriginal requiring heart valve operation due to untreated rheumatic fever as child.
 Act that allowed taking aboriginal children from parents.

Explain rheumatic fever to a science teacher in an aboriginal community.

Why so common in aboriginal communities?

Barker hypothesis
MSAT – end of year 2006
Station 7 – Communication – aboriginal; explain blood sugar and blood pressure tests – why have
them, what they involve, ask if patient wants tests done
Station 18 – RRITH Station. Know CI stuff; relative risk; putting data into 2x2 table; why stroke
more prevalent in rural and remote areas
MSAT – 2005
- Communication station: An elderly guy talking how Aboriginal get all the health benefit and
welfare, how aboriginal drink a lot (you have to go against his view but also be compassionate).
- Epidemiology: read a case on a country town. calculate incident rate, risks factor of CVD
[RANDOM EXTRA MSAT MATERIAL]
RRITH Aboriginal Health Check (RRITH)
Aboriginal patient comes into clinic - needs blood sugar and pressure levels tested. Identical to
Communication Skills workshop.
Screening test for sugars and impact on cardiovascular
Had to Explain Sugar and the effects on the body
Impact that high sugar can have on Cardiovascular Dx
 Build Rapport
 Explain why doing the test
 Previous Family History
 The importance of early screening
 What you are testing
 Fasting Blood Glucose – coming back the next day
Aboriginal patient comes into clinic - needs blood sugar and pressure levels tested. Identical to
Communication Skills workshop.
Mention to assessor; “I would wash hands on entering & exiting”
Introduce self to pt
Ask them what pt prefers to be called (may have kummanarra)
Mention you’re new to the area
Ask about where they grew up, where family is, where currently living – in/out town. FIND
COMMON GROUND & USE APPROPRIATE SELF DISCLOSURE TO PUT PT AT EASE
Ask if they know why they have been asked to come in today…
Explain importance of health check when not sick
POSSIBLY MAY GET PHONE CALL: child has asthma attack on rural property, older
sibling calls, mum & dad out working somewhere else today
Give bronchodilator
Does pt use any regular medicines, did he take them today? Resp. rate (can you tell me how quickly
he’s breathing? Child 16-20, adult 12-20), colour: pink/blue, look distressed? can the pt talk or
drink water? (how severe is this?) level of consciousness – wait on the phone, how did child
respond to the 5 puffs + steroid puffer
May give large dose of steroid
Use of preventer medicines?
Adrenaline auto-injector – into the thigh if unconscious (antero-lateral)
If medi-vacced out – add positive airway O2
RRITH – Given table of relative risk for stroke amongst diabetics, rural people, Aboriginals
and males.
-What does CI mean and describe it
-How would you explain the relative risk of diabetes (stats from table provided) to a layperson?
EXTRA:
Q: Calculate the prevalence of CVA in the community
To work out prevalence of CVA in the community: (no of new disease cases/population at risk of
disease)
Prevalence = no of obese people with CVAs =200 = 0.02 or 20% of people w CVAs were obese
All CVAs in 1 year
10 000
Q: What is the incidence of CVA in those that were obese & those that were not?
To work out INCIDENCE of CVA in the community:
Incidence = all new cases of CVA in obese people = 200 = 0.04 40% of people w CVAs were
obese
All CVAs in obese people
4 700
Incidence = all new cases of CVA in non-obese people =250
were
All CVAs in non-obese people
10 000
= 0.025 25% of people w CVAs
non-obese
Age standardisation: removes the effect of different age structures so rates in different populations
can be reasonably compared (compare apples to apples)
CDR Crude Death Rate: incidence measure
No of deaths =
22 849
= 0.00650 or 650 deaths/100 000 population
Total population
3 511 544
Discuss Atherosclerosis plaque/histology (name what histology pictures were, e.g. fatty streak
formation, plaque, complicated plaque + explain pathogenesis of these) + process of thrombus
formation. How clotting cascade causes thrombus.
Communication station: Asking a teenager to do spirometry test and explain the result. Explain
what FCV, FEV1, and FEV1/FVC% means.
CARDIO
MCQ?? maybe
Heart failure/CVD disease risk factors/congenital heart diseases
Heart failure
- 4 causes of heart failure.
Congestive heart failure, heart muscle weakness- due to loss of myocytes, heart valve stenosis
or incompetence, whole body circulatory failure, myocardial infarction, cardiac arrest (from
stroke, drowning)
- Forward failure and backward failure
- Failure of the left side of the heart to pump adequate cardiac output to th systemic circulation
due to increased peripheral vascular resistance. As heart tries harder to pump blood, heart
pressure in the left side rises, causing pooling of blood, fluid transmitted to the pulmonary
circulation causing shortness of breath and pulmonary oedema.
- Backward failure due to failure of the capacitance vessel to transmit blood back into the right
side of the heart due to increased right sided heart pressure from increased pulmonary pressure.
Causes liver and kidney failure.
- Cause of distended neck veins?
Distended neck vein is due to congestive heart failure. Failure of the right side of the heart. Backward heart
failure. Veins from the right side of heart unable to deliver blood back into the right side of the heart due to
increased pressure in the right side, may be due to increased pulmonary circulatory failure. Prolonged right
sided heart failure may also lead to right sided heart failure which ultimately causes distended neck veins.
- What is congestive heart failure?
Congestive heart failure is abnormalities of the heart in which the heart fails to pump blood at a
rate commensurate to the body’s need. Congestion is defined as the abnormal accumulation of
fluid periphery as oedema in the lung. This can result from narrowed arteries that supply blood to
the heart muscle.
- Difference between stenosis and regurgitation (regarding heart valves)?
Stenosis is blockage of the valve, regurgitation is backward flow of blood
Myocardial Infaction
- Myocardial infarction – def’n & pathology
MI is an irreversible myocytes damage due to prolonged myocardial ischaemia. The cells
affected are deprived of oxygen, leading to cell death due to blocked blood flow.
- Reversible vs irreversible cells damage – sign of transmistion
- Reversible damage when there is no loading of intracellular Ca. Blockade of blood flow reduce
flow of O2 which reduces ATP , increase in ADP, pi. Also disturbed metabolite concentration.
After brief imbalance in metabolite concentration, return back to normal condition. No
permanent damage.
- Irreversible cell damage when there is reduced ATP, ATP function reduces from 50% to 10%.
Haemorrhage, wavy fibres take place. Coagulation necrosis causes formation of small dots of
neutrophils. Total coagulative necrosis, neutrophils more visible btw ECM, dead cells
reabsorbed, neutrophils die off, replaced by fibrous tissue. Vascular remodeling then takes
place, early deposition of collagen. Complete formation of fibrous and scar tissue, more
collagen appeared.
- Regional infarction areas- LAD vs RCA vs PIV
LAD affects left ventricular region of the heart.
RCA affect right atrium and some area of right ventricle.
-
Dx MI – 3 criteria
Persistent changes in ECG tracings
Fluctuations of cardiac serum markers (creatinine kinase & troponin)
History of angina-type chest pain
- Cardiac damage markers – 3 chemical markers, when they peak, 3types of troponins
CKMB peaks at 18 hours,
Troponin I level peaks at 3-12hrs
Toponin I TROPONIN t
- Therapeutics for MI
Antiplatelet, beta blockers, nitrates, ca channel blockers
- Causes of death from MI - ↓CO, ↑venous blood fibrillation infarct repair
- What is endocarditis?
Inflammation of the endocardial layer (deepest layer of the heart wall, consist of endothelial cells)
Congenital Heart defects
- Patent Ductus Arteriosus – what effect on the child?
- PDA is when there is incomplete closure of ductus arterious after a baby was borned. Ductus
arteriosus is the vessel that connects pulmonary artery to descending aorta. This causes mixture
of oxygenated and deoxygenated of blood in the aorta, sending less o2 saturated blood to the
systemic circulation.
- Kid with Ventricular septal defect- implications in cardiovascular function
Ventrucular septal defect is the presence of whole in the ventricular septum. Causing shift of blood flow
from higher pressure region of left ventricles to the right ventrivcle. Over time, the shift of blood change
from the right V to LV due to increased pressure in the pulmonary circulatory. (Eismenger syndrome)
Heart failure + risk factors for CVD
- lots of RV and LV hypertrophy and links to oedema
- How the changes in plasma hydrostatic and colloid osmotic pressure lead to oedema?
Increased plasma hydrostatic pressure pushes fluid via osmosis out of cell into the interstitial
space.
Smoking
- What are 3 ways smoking affects the heart?
o Increases BP
o Increases coagulation
o Decreases HDL, good cholesterol that fights LDLs which form atherosclerotic
plaques
- Major factor to decrease CVD? (stop smoking)
- How smoking causes heart problems, list three
- Know your risk factors for cardio. Also know your heart failure pretty well, and MI's. Three
compensatory mechanisms in heart failure, frank starling curve ect.
Frank straling mechanism – increase preload. Try to match CO by increasing venous return.
Hypertrophy of the heart- heart becomes larger and rounder, become weaker, not
stronger.Pressure OVERLOAD (concentric hypertrophy). Volume overload due to eccentric
hypertrophy
Neurohormonal regulation- noradrenaline, rennin angiotensin, atrial natriupeptide
- AS and vasoconstriction .. why?
AS- endothelial injury, immediate effects - vasocnstriction
- Lots of questions on diabetes and its effects
Ageing heart
– how can pulm. Oedema occur from HTN? How does this lead to right side HF? How can right
sided HF occur from CB?
- Ageing of Heart – changes in ageing heart
At rest- same CO as young by reducing HR- allow more filling time, more blood volume in the
right ventricle, increase SV, same CO
During exerciseYoung heart – increase contrsctility, old heart dilate more to compensate the need og blood flow
to the body. Overall HR increase, but not as high as young heart.
Changes- decerase myocytes no , decrease metabolite concentration- sarcoplasmic reticulum
concentration of Ca reduced - decrease contractility, increase calcification of the heart- heart
becomes stiffer and reduced compliance, decrease B adrenergic sensitivity hence reduce
sympathetic action
Blood pressure
Why is high blood pressure a risk factor for ischemic heart disease development?
High BP – higher concentration of LDL, blood particles more likely to aggregate endothelial layer,
increased risk factor of injury to endothelial layers. Damage to endothelial layer causes increased
permeability of endothelial cells allowing monocytes to enter intima layer. Atherosclerosis takes
place; production of fatty acid streak, lipid plaque and complicated plaque. Rupture of complicated
plaque causes thrombus, causing reduced blood flow- ischaemia.
ECGs
- Calculate heart rate from an ECG trace. ECG has very large R waves – what are they
called?premature ventricular complex
- Prolonged PR segment means conduction wave going through which conduction pathway?
- Changes in ECG tracings - MI – how this changes over time
Had an Ecg and had to state why the QRS way tall and wide
- ECG - had to say what was wrong
- ECG trace
- early after-depolarisation?
- Person with suprventricular tachychardia – asked to explain the re-entry mechanism
- ectopic beat – what is it? Why does it occur?
Coronary/Peripheral vessels
- blockage in marginal branch effects where? (RV)
- which parts of heart supplied by LCA, RCA and circumflex? Left ventricle, right ventricle,
posterior left atrium and ventricle
- What name is given to the junction of two arteries? (anastomoses)
- What blood vessel controls blood flow into capillaries? (arterioles)
- cephalic trunk of abdominal aorta supplies which organ?
- What connects to the common hepatic artery? (extended matching question)
A – abdominal aorta
- What is the order of the branches from the abdominal aorta from ascending to descending?
- A – celiac trunk, superior mesenteric, renal artery, inferior mesenteric
- B – celiac trunk, renal artery, superior mesenteric, inferior mesenteric
- Which artery does the middle suprarenal artery branch off?
o A – inferior phrenic (no – this gives the superior suprarenal artery)
o B – abdominal aorta (I think so)
o C – renal artery (I’d assume this gives the inferior suprarenal artery?)
- MCQ: arteries in order from the abdominal aorta
Heart Anatomy (including histology), Auscultation points/heart sounds
- heart pericardium layers?
The pericardial connective tissues consist of three layers.
The serous pericardium provides lubrication for the heart. It has 2 layers.
Parietal and visceral which are continuous with each other .
the visceral layer lie in direct contact with the heart itself.
The parietal layer is on the outside.
The fibrous pericardial layer is attached to the outer surface (parietal) of the serous pericardium. It
is a much thicker connective tissue which helps to anchor and stabilise the position of the heart.
- heart muscle?
- Heart muscle consists of three layers.
- The outermost part is the epicardial layer which is also known as the visceral layer of the serous
pericardium. The second outermost layer is the myocardium which consists of heart muscles,
responsible for the contraction of the heart. The innermost layer is the endocardial layer which
is made up o f endothelial cells
- Intercalated Discs – purpose?
- More effective transfer of signal.
- Desmosome – prevent tearing
- Gap junction- transfer of signal
- effects of vasodilators on BP?
Vasodilators reduces BP by reducing the vessel diameter.
- Know how to take blood pressure, take the pulses at all the different points, also know where to
locate all the heart sounds - we had to mark them on a diagram (4).
- Where is Intracellular Calcium stored? (SR)
-
-
what are the heart sounds? The four heart sounds are the
mitral sound – mid clavicular or anterior axillary 5th ICS
tricuspid sound – right sterna border, 5th ICS
aortic sound- right sterna border, 2nd ICS
pulomonic – left sterna border, 2nd IC
Regulation of Blood pressure + heart rate/Reflexes/Cardiac cycle/Preload, afterload
- what effect does PNS supplying heart –
- contractility and HR?
- PNS only innervates the AV nodes and SA nodes. Hence PNS causes affects on the heart rate
and rhythm.Firing of these nodes.
- what does not increase BP? (adenosine, NO)
vasodilators- NO, prostaglandins, adenosine. B blockers- reduce sympathetic effects
- what does blood viscosity affect?
- Increase peripheral BP blood pressure- increase afterload, increasing ESV reducing SV.
Reduced SV reduces CO. Increase BP detected by baroreceptors- aortic and carotid bodies
detect changes; causes compesnsatory effect to reduce BP by increasing heart contractility and
and vasodilation to match CO that commensurate with the body’s needs.
- (venous return and heart rate)
- Preload and Afterload Definitions?
Preload- degree of stretching during ventricular diastole (directly proportional to EDV). It
affects the ability of muscles to produce tension. According to Frank Starling Law, increase in
EDV causes increase in SV.
AfterloadAmount of tension the contracting ventricle must produce to force open semilunar valve and eject
blood. Increasing afterload causes increase in ESV causes reduced SV.
- Cardiac cycle
- Question on BP
- Has does exercise increase heart rate
Increased sympathetic drive; Beta1 adrenergic receptor in the heart muscle respond to acetylcholine to
increase heart rate and contractility
- Why does blood pressure increase during exercise?
- Exercise- need to meet body’s need  has to increase tissue perfusion pressure to ensure exercising
muscle receive adequate supply of O2
- how baroreceptor reflex works
- What does ejection fraction mean? What is a normal ejection fraction value? How is it
calculated?
Total amount of blood that is actually ejected from heart from the initial amount of blood present during
end diastole . Normal > 67% SV/EDV. It is an important measurement to access heart f(x) and
disease.
[KFP - mid-semester (2006)]
- Cause of distended neck veins?
- Elderly patient – how does the heart change with age in regard to:
- Why does blood pressure increase during exercise?
- 4 causes of heart failure.
- What is endocarditis?
- What is congestive heart failure?
- Calculate heart rate from an ECG trace.
- ECG has very large R waves – what are they called?
- What does ejection fraction mean?
- What is a normal ejection fraction value?
- How is it calculated?
- Two immediate, and two delayed effects that pulmonary hypertension has on the heart.
(possibly wrong look up later)
Difference between stenosis and regurgitation (regarding heart valves).
[KFP – 2006]
 Ventral septal defect – what is it? Will child be cyanotic?

Tachycardia and fibrillation

Why does blood pressure increase during exercise

Why does athlete have lower BP and HR

What mechanism is responsible for 75% of tachycardias and fibrillations? Explain mechanism
and how it results in additional beats (re-entry)
Why does myocardial ischaemia cause severe chest pain?


[KFP – 2005]
How does the response of the heart of a 20yr old and an 80yr old differ in response to exercise.

In aged heart what happens to HR and systolic pressure
Why is there increased blood pressure in response to exercise.

A fit athletic young man has a resting pulse of 50bpm and a BP of 110/60. Explain why this is
different from average person.
MSAT – end of year 2006
Station 10 – ECG and story of patient presenting to ED with chest pains (history – smoker,
overweight, doesn’t exercise, high BP). Calculate heart rate; from ecg and lab results determine
what was wrong with patient (angina?); how social history predisposes her to this condition; what
advice to give to daughter who thinks mother shouldn’t live alone
Station 17 – ECG – Calculate heart rate and certain segments and intervals; determine if the
patient was tachycardic; effects on CO in mild, moderate and severe tachycardia; draw or describe
ventricular tachycardia and ventricular fibrillation
Calculation of HR=
Beats per sec= No. of small squares x 0.04
MSAT – 2005
- Atherosclerosis histology + process of thrombus formation. How clotting cascade causes
thrombus.
- ECG – calculate segments and HR. Effect of mild, moderate and severe tachycardia on CO.
Describe or draw ventricular tachycardia and ventricular fribillation.
[RANDOM MSAT MATERIAL]
Question 2. ECG
1. Had to work out the rate and show workings
2. Had to explain why the ECG was 125 and pulse was 110
3. What do the y axis and x axis mean on the ECG
4. Has does the heart rate in the case alter CO
5. Explain difference between heart rate and pulse ie. electrical to reverberation
CVM – 51 year old widowed female, accompanied by her daughter, enters the ER because of chest
pain and pain down her left arm. Pain was accompanied by nausea and dizziness. Regular smoker,
doesn’t exercise and has a BP of 137/85. 12 hours after GTN was given, pain subsided. Hb of 12
g/dL, normal CK, electrolytes normal.
Calculate heart rate – does she have tachycardia and why/why not?
-What do you think is the cause of the problem?
-How could her problem have been exacerbated or started by her history (4 point question, so talk
about the detrimental effects of smoking, high BP, lack of exercise, etc).
-She is being sent home, but she and her daughter are afraid about what might happen to her if
something like this happens again. What would you say to reassure them?
Angina
 Look at blood test and ECG and say why isn’t an MI when has similar symptoms
 She’s a smoker, overweight, has high blood pressure and does no exercise – how do these
factors increase her risk
 Daughter and mother (who had angina) discuss the daughter moving back in with the mother –
how would you counsel them?
CVM – Given ECG trace
-Calculate P-R interval, S-T segment, heart rate, and T-P interval, showing full working.
-If the patient is a normal, healthy 29-yo male, what could be causing his atrial tachycardia?
-What are the effects of mild, moderate and severe tachycardia on cardiac output?
-Draw or describe the ECG for ventricular tachycardia
-Draw or describe the ECG for ventricular fibrillation.
Interpret ECG traces
1. Sinus Rhythm with 2 ventricular ectopics – any cardiac compromise -no
2. Second Degree AV block – Mobitz I – Wenckebach - ? cardiac compromise
3. Atrial Fibrillation – slow ventricular rate
a. Patient 65years – effect of AF – no real effect
b. Patient 25years athlete - ? effect – yes, cannot operative at low levels
ECG (CVM)
Asked to calculate the MAP
3 ECG strips (2nd degree heart block 4:3, ?bradycardic conduction block, Atrial fibrillation)
provided and same 3 questions for each (worth 5 marks each)
1. What diagnosis would you give this person?
2. What would it mean in terms of C.O?
3. What would be the implication of this for an old man – 60 y/o and a young athlete – 29 y/o?
CVM – Given ECG trace
-Calculate P-R interval, S-T segment, heart rate, and T-P interval, showing full working. ???
-If the patient is a normal, healthy 29-yo male, what could be causing his atrial tachycardia? ???
-What are the effects of mild, moderate and severe tachycardia on cardiac output?
-Draw or describe the ECG for ventricular tachycardia
-Draw or describe the ECG for ventricular fibrillation.
ECG – calculate segments (P-R, P-T INTERVAL) and HR.
Effect of mild, moderate and severe tachycardia on CO.
Describe or draw ventricular tachycardia and ventricular fribillation.
CVM: ECG – arrythmias
Cardiovascular Exam
Measure radial pulse and explain what you are feeling – vibration against the artery wall
Then auscultation points on the mannequin
Find brachial pulse and do a BP
Explain systolic and diastolic pressure
Calculate the mean arterial pressure and explain what this.
Pulses (CLINICAL)
Name the 4 points for chest auscultation & location on manikin
What are the 1st & 2nd heart sounds
Question 5. Live Station
1. Had to take a pulse, carotid, blood pressure and dorsalis pedis
2. Had to mark on a diagram 4 heart sound points – aortic, pulmonic, tricuspid and mitral
3. Had to build the trust of the patient
NEUROSCIENCE
[KPF 2006]
 Three brain regions involved in pleasure and reward and which region is involved with
cognitive recognition of emotion
Ventral Tegmentum
Nucleus Accumbens
Prefrontal cortex – conscious recognition.

Pain gate mechanism- the anatomical gate is at the substantia G which has groups of
inhibitory and excitatory neurons to nociceptive transmission to the brain. Descending
pathway (mainly from PAG) and mechanoreceptors (A Beta) send excitatory signals to SG
to further inhibit nociceptive signalling. Nociceptive afferents (A delta & Cfibres) inhibit
the inhibitory signals of SG to nociceptive signalling, which potentiate nociceptive
signalling to the brain.

Neuropathic pain
Pain that occurs as a result of unknown stimulants. And unrelated to any peripheral tissue
injury. May be due to the activation of Na channel which causes depolarization and activates
pain signal. Mostly occur in Shingles, diabetic neuropathy, stroke

Which cranial nerve is responsible for information from carotid body? What type of
information is this?
From cranial nerve IX- glossopharyngeal. It is a GVA

How fracture to right femur and right clavicle travels to the brain
Paleospinothalamic – C fibres (deep fibres).
Decussates at level of spinal cord.
[KFP 2005]
 Outline how the lady sees the snake. Mention visual pathways throught the brain and emotional
processing stages.
Photoreceptors-> ganglion cells exit via optic disc and form olfactory nerve which travels to the
optic chiasm. Some of the fibres decussate here, some not, leave optic chiasm as optic tract,
travels through hypothalamus, to the lateral geniculate of the thalamus. Crude perception occurs
here- orientation and dark-light aspect of the object, travel via corona radiate to the primary
virsual cortex at the occipital lobe- sent to prefrontal area for interpretation of what and where.
Some signals are sent to amygdale and limbic system- to sense that signal is sent as danger.
The emotional processing of the brain begins at the thalamus. The short route – where the thalamus
sends impulses to the amygdala, where there is a quick response to signify that there “might” be a
snake that has just bitten me and I have to respond to this stimuli by removing my self from the
situation.
A few seconds later, the amygdala receives confirmation that this signal was correct via the long
route – where the thalamus sends impulses to the sensory cortex where it sends the impulses to the
hippocampus (STM and declarative memory – know what to do) which then returns to the
amygdala so that you can respond appropriately.

Jenny has been bitten by the snake but is not feeling any pain. How is this occuring.
Pain Perception depends on *Level of noxious signal; *Other sensory inputs; *Behavioural
Context.
Pain perception is the net interpretation of the brain decision that is influenced by the status of
the body, memory and emotion. Cultural factor also plays a role.



2 Effects of Sympathetic nervous system (bronchodilation, increases blood glucose, increases
CV activity)
Increase HR, increase blood plow- vasodilation of blood vessel and bronchodilation- prepatory
mechanism to anticipate change in homeostatis of body during fight and flight.
How does the hypothalamus act in response to stimuli to activate the sympathetic nervous
system?
Lateral and posterior areas of the hypothalamus are stimulated resulting in the activation of the
division of ANS.
Case 8: Overdose and suicide attempt
Stimulation of the Sympathetic Nervous System
Ecstasy: Passive Release of NA
Cocaine and Tricyclic Antidepressants: Interfere with uptake of NA, potentiate the affects
Monoamine inhibitors: Prevent breakdown.
Special senses (random)
 Effect of Vitamin A deficiency on ‘night vision’ vitamin A responsible for retina formation.
Retina is made from vit a. Night vision- rods are responsible. Lack of retina reduces the degree
of sensitivity of the retina.

How to rods respond to light. Through bleaching. At dark, retina are in bent form- 11-cis
retinal. When photons strike, bleaching occurs; the opsin are dissociated from retinal, changing
11 –cis retinal into all trans retinal.
Case 11: Man falls off a motor bike and has head injury
 A man can recall facts, but does not remember where he learnt them. What type of amnesia?
Retrograde episodic amnesia.
 What are the main factors that regulate cerebral blood flow?
Co2, O2, H+.

How can increased cranial pressure lead to reduced cranial blood flow?
Increased IC pressure causes displacement of brain tissue, squashing the blood vessel, blood
vessel are constricted at the brain area, reducing blood flow.

Brain Regions involved in Long Term Potential
Many different areas. Generally from cortical somatosensory to hippocampus & amygdale to
dienchepalon- prefrontal cortex to the basal forebrain. .
What controls the perfusion of blood to the brain. Autoregulation, not affected by systemic BP
OTHER RANDOM STUFF
 How cholingeric NT is formed. Acetyl CoA + Choline using enzyme ChAT
 Distinguish between nociception and pain
Pain is the net interpretation and decision made by the brain based on the status of the body,
memory and emotion about the pain signal that is received.
Nociception is the pain signal that is sent via spinothalamic/ spinoreticular pathway to alert the brai
n that an injury has occurred. It can be continuous whereas pain can be on and off depending on the
person’s individual perception.
 NTs associated with pain
Substance P (dull) Glutamate (sharp), enkephalins, noradrenaline

Of the caudate and the putamen which has the most motor activity.
Cuadate- automatic checking behavior , Putamen- auntomatic motor control. Putamen involved
in basal ganglia loop that is responsible for initiation of a willed movement. So putamen.
Putamen responsible in basal ganglia loop in initiation of a willed movement.

Types of memory disorders (EG: difficulty creating memories and/or accessing memories)

Types of AMNESIA- retrograde, amnesia, episodic

KORSAKOFF SYNDROME (alcoholics) type of deficiency, destruction of ?, type of memory
loss?.
Due to thiamine deficiency- malnutrition(rare in Oz) or alcolosim. Thiamine deficiency causes
degeneration of mammillary bodies which is anatomically in close position with the
hippocampus- therefore responsible in short term memory formation. Memory loss anterogradeunable to form new information. Some degree of retrograde as mammillary bodies also
responsible in LTM pathway. Afferent & efferent fibres are both affected.

Pain Pathway – carried in? ascending pathway- apinpthalamic and spinoreticualr. decussates
where? At the spinal cord
Pain gate mechanism



Sensory and Motor Pathways.
Sensory – pathways- , decussation, types of information carried.
Spinothalamic- decussates at the spinal cord before ascending- carry non specific signals- pain,
temperature, some touch
Dorsal medial lemnisical pathway- 1st order neuron synapse at the spinal cord ascend without
decussating, decussates at the medulla- fasciculus cuneatus, fasciculus gracilis- specific pain- 2
point touch, vibration, discriminative touch, consiouc proprioception
Spinocerebellar- ipsilateral- subconscious proprioception

Motor (ventromedial and lateral. General type of information, decussation location):
Lateral- corticospinal (voluntary motor control) & rubrospinal (fine motor control – eg writing)
Ventromedial:
Tectospinal- visual reflex
Vestibular- head balance
Reticulospinal- antigravity, posture, balance

Why is pain a subjective experience: depends on status of body,memory and emotion, depends
on support network available.
ALZHEIMER’S DISEASE (lose ability to?, types of emotional disturbances, progression?)
Diagnosis: - No real tests available. Made through ruling out other causes of dementia by CT and
blood tests.
History including mental status examination and course of illness.
DEFINITIVE DIAGNOSIS UPON AUTOPSY (neurofibrillary tangle, amyloid plagues)
MSAT – end of year 2006
Station 3 – Communication – Pain. Explain to patient productive vs non-productive pain; phantom
limb pain; allodynea; how mood and motivation affects pain perception
Station 14 – Sympathetic and parasympathetic divisions and affects if spinal cord damaged at
certain points (pic similar to those on 536 and 538 in Marieb)
MSAT – 2005
- Basal ganglia motor loop (Bear 480) – Label parts of the loop. Mechanism of Parkinson Disease in
relation to neurotransmitters. Why if u take dopamine tablet doesn’t help? What can u do instead?
Degeneration of subtantia niagra that is the dopamine-producing area of the brain. Deficits of
dopamine affect dopamine diffuse modulatory system ; the basal ganglia. Basal ganglia responsible
for the voluntary motor control, defects in basal ganglia cause rigidity & difficulty initaiating and
stopping a movement. Use L Dopa because dopamine cannot bypass BBB. However have to use
dopa decarboxylase inhibitor as well to prevent it from being converted to dopamine before
reaching the brain.
- Cerebral arteries + MRI scan of the brain – Right motor and sensory paralysis. Which part of the
brain is damaged. And which cerebral artery is blocked. Which descending spinal tract could be
damaged?
HUMAN DEVELOPMENT AND BEHAVIOUR
[KFP 2006]
 Types of anxiety disorders
Post Traumatic Stress Disorder, Generalized Phobia, Obsessive Complusive Disorder

How cancer develops referring to NK cells and T lymphocytes
NK cells activity reduces, T lymphocytes increased

At 2 ½ years at what stage of Paiget’s cognitive development would child be at
Preoperational stage
Development of motor and sensory control, egocentricsm.
Not yet master conversational rules. Perceptual bound and centralization

What are the highlights of development in infancy stage
Perceptual development
From birth: indicate taste preference by facial expressions and selective eating behaviour
Hours after birth: respond to light and sound stimuli
10 days: respond to mother’s smell
4 months: Develop full visual accommodation
6 months: mastery of 3D, not cross over a visual cliff
12months: preference for natural face arrangements

Ulratarianism – three characteristics of it?
Provide the maximum no. Of happiness to the greatest no. Of people
Focus on the result, not the actual outcome
Morality should minimise harm to peoples and maximise group welfare
Promote individual freedom but not necessarily self interest

What community agencies (3) can send patient to for psychological help?
Beyond Blue
Townsville Mental Health Community
Lighten Up Programme by Queensland Health

What are two areas that would impact on a child diagnosed with a chronic condition
[KFP 2005]
4. Piaget/ Eriksons/ HBD
 What stages are various people at?

Erikson’s: Psychosocial Development.
0-1: Trust vs mistrust
1-3: Autonomy vs Shame
3-6/7: Initiative vs Guilt
7-11: Industry vs inferiority
Adolescence: Identity vs Role Confusion
Young adulthood: Intimacy vs Isolation
Adulthood: Generation vs Stagnat
Older Adulthood: Integrity vs Despair

Piaget: Cognitive Development
0-2:Sensorymotor
2-6/7:Pre-operational
7-11/12:Concrete Operational
11 and abobe:Formal Operational

Motor Development
2 months: lifts head up
2.5: rolls over
3:sits propped up
6: sits without support
6.5: stand holding on
9: walks holding on
10: stand momentarily
11: walk without support
14: walk backwards
20: can kick ball

Communication Skills  brief from language week – *stages*
6months to 12 months:babbling, involve in turn taking games, 3-50 words, express wants from
gestures
12 to 24 months: 50-300 words 2 words utterences, asking questions and request info, answer
questions
2-3years: mastery early speech sounds- m, t, b, w, understand who what where queatiins, use language
in pretend play
3-5years:master middle speech sounds- ng, f, use language to report events, 2000 words of expressive
language
6-11yrs: master late speech- l, r, sh, sz
12-18yrs:use language for social purpose

Personality Disorders (and components?)
CLUSTER A= ODD – paranoid, schizoid, schizotypal
CLUSTER B= DRAMATIC – antisocial, histrionic, borderline, narcissistic
CLUSTER C=ANXIOUS- avoidant, dependent, obsessive compulsive
Case 8: Overdose and suicide attempt  coping strategies/Kubler ross stages of grief/primary
emotions/homosexuality
Stimulation of the Sympathetic Nervous System
Ecstasy: Passive Release of NA
Cocaine and Tricyclic Antidepressants: Interfere with uptake of NA, potentiate the affects
Monoamine inhibitors: Prevent breakdown.

Which this man leaves hospital which organization could he be referred to?

Adaptive and Maladaptive Coping Strategies
Psychological: Personality structure and defences.
ADAPTIVE (eg: humour, suppression, sub limitation, altruism)
MALADATIVE (projection/repression/denial)

What are the Kubler Ross Stages of Grief
Shock, despair, loneliness, guilt, anger, bargaining, acceptance

Name the 6 primary emotions
Happy, sad, fear, anger, surprise, disgust

Reasons why homosexual individuals commit suicide
Discrimination, stigma, kept in secrecy. Not disclosing increase risk of psychological problem.

Is gay born or made?
Born, but may influenced from stages of life
Case 10: Aid organization in Africa  Definition of stress, physiological response to stress,
management.
 Definition of Stress:[force for change, disequilibrium and strain.

Physiological responses of stress [hdb]:
Inrease risk of infection
Chest pain
Nausea
Rapid heart rate
Breathlessness
Fight flight responses

Management of Stress:
Problem solving – identify problem, list out available solving methods with pros and cons, decision, try and
evaluate
Time management- prioritization, schedule and execution
Behavior modification- recognize problematic behavior, make amendments
Cognitive Behavioural Therapy
Relaxation- simple muscle relaxation to reduce physiological symptoms of stree
Case 12: Rural Property Owner and Cancer (NK cells, psychoneuroimmunology)
 What is link between NK and cytokines and the development of cancer?
NK cells: are involved in the surveillance and destruction of tumour cells and virally infected cells.
Stressful life events and loneliness has decreases NK cell activity. Therefore more tumour cells not
eradicated.

What are some of the negative/positive psychosocial affects of being diagnosed with cancer.
Positive: appreciate life more, freed from responsibility, attention, more motivated to make the most
out of time left.
Negative: chronic illness slowly debilitating, not be able to achieve all goals, depression, isolation

Pro-inflammatory cytokine associated with gastric ulcers- IL-1
Case 14: Emilino the bull-rider from Guatemala hurts chest during tournament (Cultural
sensitivity)
What are attributes of a culturally sensitive doctor?
Able to accommodate the differences in culr=tures btw patient and doctor
Allows for culturally sensitive atmosphere and healthy effective communication
Shared understanding of each other’s behavioral expectations
Consequences of domestic violence (in childhood and adulthood)
 Consequences of domestic violence (failures of family in what areas?).
In adult- physical injury, pregnancy complication, increased emotional disturbance
Child- anxiety, bedwetting, self harm, conduct problems, violence to others, poor school
performance

Consequences in childhood:
Attachment problems
Aggression
Self Harm
Educational failure

Consequences in adulthood Adulthood:
Personality disorder
Increase vulnerability to mental disorder
Alcohol & drug abuse
Criminality
Ethics
Explain Utilitarianism:
Panic attacks
What other disorders have similar symptoms to panic disorder?
MI, gastrointestinal disorder
MSAT – end of year 2006
Station 5 – Communication – genogram
Station 8 – Communication – young woman presented with panic attack – need to explain what a
panic attack is; why get symptoms; draw panic cycle; advice on how to prevent future panic attacks
MSAT – 2005
-- Communication station: A mother is depressed while her son is having trouble sleeping,
bedwetting, doesn’t want to go to school. (Link to Kubler-Ross)
-- Communication station: A high school student is stressed due to exam and isn’t sleeping well.
Give advice and refer to program. ( Need to give advice about dealing with and managing the
stress)
ENDOCRINOLOGY
[KFP 2006]
Child in coma because of one of two most common causes of coma in diabetes patients – in
hypothermic, tachycardic and breath sweet smelling.
 Comment if blood glucose, blood ketones and pH would be increased, decreased or normal
and why.
Hypothermic, tachycardic and sweet swelling indicates that the child has diabetic
ketoacidosis- hyperglycaemic coma. Her blood glucose is expected to be high due to
reduced uptake of glucose into muscle and adipose tissue (dur to lack of insulin), the whole
body system is glucose deprived, counterregulatory hormones dominate (GH, glucagon,
cortisol). Glucagon shift from carbohydrate metabolism to fat metabolism causeing the
release of free fatty acid to compensate energy needs, excessive f acid and acetyl coA, that
is converted into ketone, ketone is used for energy, blood pH would decrease because of
high level of acidic fatty acid.
Glucagon- stimulates glycogenolysis & lipolysis- increases fatty acids
Cortisol- stimulates gluconeogenesis and lipolysis.
Hyperglycaemic coma.
Blood glucose, blood ketones increased.
pH decreased.
Unable to uptake glucose from blood into major tissue reservoirs due to lack of insulin.
Glucagon and counter regulatory hormones dominate – promoting lipolysis, glycogenolysis,
gluconeogenesis, ketone body production (from FFA by liver).
pH decreased – due to large production of ketone bodies – acidic.

What hormone would be given and what two separate actions would improve condition.
Insulin causes increase uptake of glucose by liver, skeletal muscle and adipose tissue.
Promote glycolysis and glcogenesis in the muscle. Insulin also inhibits the action of
gluconeogenesis in the liver, reduce uptake of a. Acid, reduce protein catabolism.
Glycogenolysis also inhibited to prevent the release of free f acid into the blood.
Insulin – increased uptake of glucose into muscle and fat (GLUT 4 dependent), promotes
glycolysis.
Inhibits glycogenolysis, helps to inhibit gluconeogenesis (at muscle and liver).

Name two of the counter regulatory hormones and their actions that would go against
insulin.
Cortisol- increase gluconeogenesis, - causing release of a. Acid from protein catabolism.
Also stimulates lipolysis and prvent glucose deposition into adipose tissue, activates
lipolysis- increase TGA and free fatty acids.
Glucagon- stimulates gluconeogenesis, glycogenolysis
Counter regulatory hormones – growth hormone, cortisol, adrenaline, glucagon.
Growth hormone
Inhibits uptake of glucose into muscle and adipose tissue.
Promotes lipolysis in adipose tissue.
Cortisol
Increases gluconeogenesis
Liver
Increases glycogen synthesis
Decreases protein synthesis
Skeletal
muscle
Adipose
tissue
Increases protein degradation
Decreases glucose uptake
Decreases glucose uptake
Increases lipid mobilisation
[KFP 2005]
10yr old girl with suspected type 1 Diabetes
 Explain the insulin-antagonistic (anti-insulin) effects of 2 of either adrenaline/Cortisol/GH
Anti insulin effects in GH causes lipolysis- increase b/down of adipose tissue and release
free fatty acid into blood. It also promotes carbohydrate metabolism which increase blood
glucose conc.
Cortisol- stimulate gluconeogenesis (increase release of a. acid and protein catabolism
form tissue)& lipolysis (increase release of a acids into blood).
Adrenaline – stimulates release of blood glucose & a. acid

The girl thinks that diabetes is due to her having low glucose levels; explain this
conundrum.
She has high level of glucose bcz of the lack of insulin that is due to autoimmune. Her body
is unable to take glucose due to absence of insulin, hence cells become glucose deprived,
causing her to increase glucose uptake albeit her raising blood glucose.
Body not getting enough glucose due to lack of insulin – unable to uptake glucose.

How does insulin affect the liver to decrease/increase blood glucose levels?
During fed state, insulin function to reduce blood sugar level by increasing glucose uptake from
the blood causing accumulation of glucose in the liver, promoting glycogenesis. When there is
very high glucose after the conversion of glucose into glycogen, glucose converted into
glycerolphosphate and converted into triglycerides, lipogenesis takes place.
Acts to decrease blood glucose levels.
Increases glucose uptake at muscle and adipose tissue, promotes glycogenesis, promotes
lipogenesis.

Explain in 3 lines why this girl has high BSL and glucose in her urine.
High BSL- body unable to uptake glucose- activation of counterregulatory hormones that
cause hyperglycaemic effects.
High blood glucose causes renal tubule uptake of glucose exceed the transport maximum
(transport proteins have been saturated), Concentration of glucose in filtrate is very hightubules unable to reabsorb rapidly enough.
High BSL – body unable to uptake glucose – activation of hyperglycemic hormones – counter
regulatory hormones.
Glucose in urine – kidneys reached transport maximum for glucose. All transporters are
saturated – excess glucose excreted.

How does glucagon affect the liver to increase blood glucose levels?
Stimulates gluconeogenesis to produce glucose, cause glucose sparing effects- use of amino
acids and ketones from ketogenesis for energy.inhibit the action of insulin
Growth Hormone
 What are the physiological ways to test growth hormone levels.
Test after Deep Sleep= as REM sleep is a stimulator of GH
Test 2-4 hrs after eating
Test during a physiological/ emotion stress.
Most definitive test: Give Insulin- the hyoglycaemia should stimulate GH levels to increase.
After exercise, during fasting- starvation stimulates release of GH

3 Hormones that control a person’s height.
Insulin-like growth factor (IGF-1 and IGF-2) via Growth Hormone (pubertal phase)
Thyroid hormone
Insulin (during prenatal stage)
Sex hormones (pubertal phase)

What is the birth weight of a baby with growth hormone deficiency?
Normal at birth due to insulin dominating during prenatal stage.

Growth hormone – basic body remodeling - eg: increasing lean muscle mass, decreases
fat/glycogen storage
Case 7 Hypothroidism
 What are 3 other signs of hypothyroidism not including feel cold, difficulty losing weight
and tiredness (including: cardiovascular, haematogical, musculoskeletal, neurological)
Cardiovascular- reduce CO SV HR
Haem- decrease metabolic rate- decrease O2- decrease EPO production reduced cell mass,
normocytic low anaemia
Msk- muscle weakness
Neuro- CNS depression
Cardiovascular:
Reduced SV,HR,CO
Hematological
Reduced Red cell mass: normocytic, normochromic anaemia (decreased metabolic rate and decrease
O2= Decreased EPO production)
Musculoskeletal
Muscle aching and stiffness, slow movement and slow tendon jerk reflexes (decreased rate of muscle
contraction and relaxation)\
Neurological
Confusion, slow speech and thinking, memory loss, headache (Decreased cerebral blood flow= cerebral
hyoxia)

Explain thyroid Hormone Synthesis
Thyroglobulin production and secretion in RER, sent to colloid follicle. Iodide trapping at
the basal follicular cell, btw border of follicular cells and colloid cell, oxidation of iodideremoval of electron, forming iodine. Organification of iodine. Iodine binds to tyrosine. 1
iodine bind to tyrosine forms MIT. 2 iodine bind ti tyrosine- DIT. Coupling of tyroiidoine.
Forming T3 and T4. Thyroglobulin containing tyrosine and T3 T4 and lysozymes are
packaged and endocytosised into follicular cells. Vesicles move near the folliculkar basal
membrane. Lysozyme digest cleave off T3 and T4 from thyroglobulin, release T3 and T4
into bloodstream.
Iodide trapping – influenced by TSH.
Tyrosine AA enter follicular cells and form thyroglobulin. Thyroglobulin (precursor for Thyroid hormones) into
a protein-containing material called colloid which fills follicle. Iodide is active taken up into follicular cells by
iodide trap. Iodide diffuses down concentration gradient into lumen of follicle where is ionized to form iodine.
Iodine undergoes a coupling reaction with throglobulin and in transported by endocytosis back into the
follicular cell. Lysozymes then digest the vesicle and cleave of T3 (tri-iodothyronine) and T4 (thyroxine) which
are released into interstitial fluid.
Cortisol/stress

Control of Cortisol Release
Hypothalamic release of Cortisol Releasing hormone stimulate anterior pituitary to
release ACTH which acts on cortices of adrenal gland. Physiologuc stress stimulates
release of cortisol. Cortisol inhibits the release of ACTH and CRH.

Explain stages of General Adaptation Syndrome [FROM ENDO] (Alarm response,
Adaptation/resistance; exhaustion)
Stage 1: Alarm Resonse
Immediate reaction to stressor
Fight/Flight response = ready for physical activity= Sympathetic Nervous System causes medulla of adrenal
gland to release catecholmines into blood stream.
Stage 2: Adaptation /Resistance.
Adaptation to stressor
Changes take place to reduce effect of stressor (ie. Starvation= don’t feel hungry)
Hypothalamic CRH release= stimulates pituitary to release ACTH= adrenal cortex releases cortisol.
Cortisol is an immunosuppressive= Risk of getting sick
Stage 3: Exhaustion
Continuous stress causes the breakdown of compensatory mechanisms and homeostasis. Immune system
weak= risk of getting disease.
[random] A deficiency in aromatase results in descreased estrogen (converts testosterone to
estrogen)
MSAT – end of year 2006
Station 11 – Thyroid hormone synthesis. Step one involves synthesis of what glocoprotein
(thyroglobulin); step two involves pumping of what (iodide) into cell; how are hormones released
from cells; interaction between two hormones and thyroid hormone actions; Grave’s disease – what
would ask patient to determine if had this disease, and what would their appearance be (Pic p. 621
Marieb)
Hyperthyroidism- due to autoimmune disease affecting thyroid gland causing excessive secretion of
Thyroid hormones. Exopthalmos- protrusion of eyeball if the tissue behind eyeball becomes
edematous. Symptoms include increase nervousness, heat intolerance, rapid heartbeat, polyphagia
but decreased weight.
Station 15 – Hypothalamo-pituitary axis; label diagram; name blood vessels connecting
hypothalamus to pituitary and connecting anterior and posterior pituitary; what is the benefit of
connecting anterior and posterior pituitary?
MSAT – 2005
Growth hormone + Growth charts (Need to draw - height vs age graph, & growth velocity vs age
graph). Explain the graphs drawn and possible causes.