Made available through the combined efforts of
Brady Bouchard, Brett Burrett, Cameron Curtis,
Meg O’Connell, & Maximilian Stephens.
Jenny Z is a 63 year old mother of four. She comes into your
clinic one chilly June day complaining of shortness of breath
and difficulty breathing, You request that Jenny undergoes
some pulmonary function tests and a blood test. The following
flow volume loop was obtained:
a. Based on the presenting
symptoms and the flow-volume
loop provided, what disease is
Jenny likely to have? Provide 2
reasons. Ensure that you
describe the mechanism by
which peak expiratory flow (PEF)
and forced vital capacity (FVC)
are reduced.
(2 marks)
Respiratory – Flow-volume – Card 1 of 3
a. Jenny is likely to have asthma.
(0.5 marks)
• decreased PEF
• scooped out shape following PEF
• unaffected inspiration (i.e normal PIF)
(0.5 marks for providing any two of the above reasons or other
reasonable answers)
Respiratory – Flow-volume – Card 1 of 3
b. Based on the flow-volume curve above, superimpose
onto the normal vitalograph below, a curve that Jenny is
highly likely to produce. Be sure to include key points
such as FEV1, FVC and note if there is any change of the
FEV1/FVC ratio.
(1 mark)
Respiratory – Flow-volume – Card 2 of 3
Respiratory – Flow-volume – Card 2 of 3
c. In the table below is the arterial blood gas report which
you ordered.
Parameter
Units
Result
Reference
PaO2
mmHg
50
80-100
PaCO2
mmHg
30
36-44
7.5
7.35-7.45
pH
HCO3-
mM
24
21-28
PAO2 –
PaO2
mmHg
60
<10
With respect to gas exchange in the lungs, what
information can be deduced from:
i. PaCO2 (1 mark)
ii. PAO2 – PaO2 (1 mark)
Respiratory – Flow-volume – Card 3 of 3
c.
i.
ii.
PaCO2 is low (hypocapnia) so Jenny is
hyperventilating.
(1 mark)
Alveolar-arterial oxygen difference is elevated,
suggesting VQ mismatch (perfusion of
underventilated alveoli).
(1 mark)
Respiratory – Flow-volume – Card 3 of 3
Rick J., a 63-year-old male, presents to your
general practise complaining of shortness
of breath.
a) List four (4) other common presenting
symptoms in patients with respiratory
disease.
(2 marks total)
Respiratory – Respiratory Disease
a) Student must mention four of the following (0.5 marks each):
•
•
•
•
•
•
•
•
•
Sputum
Haemoptysis
Dyspnoea
Cough
Wheeze
Chest pain
Fever
Hoarseness
Night sweats
Respiratory – Respiratory Disease
a) James P., 22, presents to emergency. He is hyperventilating and has
signs of central cyanosis. James is diagnosed with an acute asthma
attack and arterial blood gases were taken immediately (patient is on
room air). In light of James's presenting condition interpret the arterial
blood gas report and discuss the cause of each value.
Arterial Gas
Observed:
Reference
Range:
Temp
37
FiO2
0.21
Bar Pressure
758
pH
7.46
7.35 – 7.45
PaCO2
25
35-45
PaO2
65
75-85
HCO3-
16
22-27
PAO2 –
PaO2
55
<10
b) What type of respiratory
failure is James experiencing?
c) Discuss a typical volumetime and flow-volume loop of a
patient who has asthma. You
may include a diagram in your
answer.
Respiratory – Acute Asthma
a)
•
•
•
•
(4 marks total)
James is hypocapnic (0.5 marks)
• Due to hyperventilation resulting in CO2 being blown off.
James is hypoxic (0.5 marks)
Respiratory alkalosis with partial metabolic compensation (2 marks)
• The kidney's are excreting more bicarbonate out of the body to release H+ and
partially compensate the respiratory alkalosis by lowering pH.
• However only partial compensation as the pH has not completely returned to
within normal ranges yet.
There is a large Alveolar arterial oxygen difference (0.5 marks)
• Due to a high amount of physiological shunting (0.5 marks)
b) Type I respiratory failure (1 mark)
c) (2 marks)
Respiratory – Acute Asthma
Melissa is a 16 year old high school student with mild but persistent
asthma. Two months ago, she was admitted into hospital with an
acute asthma attack. Upon discharge, she was prescribed Flixotide
(fluticasone) Accuhaler a steroid puffer to be used twice a day, along
with her usual Ventolin (salbutamol) inhaler to be used when required.
A week ago, she was admitted into hospital with an acute exacerbation
of her asthma. Upon questioning, the intern learns that Melissa has
been using her steroid puffer "only when it flares up but this time it did
not work at all”.
a. Briefly explain the role of glucocorticoids in the treatment of
asthma.
(1 mark)
b. Based on your answer in (a) describe how you would explain this
to Melissa to improve her compliance, including an explanation
about the Ventolin inhaler.
(5 marks)
Respiratory – Asthma
a. Glucocorticoids reduce airway inflammation (0.5 marks), and
decrease airway hyper-responsiveness (0.5 marks).
b. The steroid (glucocorticoid) inhaler she was prescribed 2 months
ago is to be used in addition to her ventolin and must be used on a
regular basis - not only when she is experiencing symptoms (0.5
marks). She must use the steroid inhaler on a regular basis as it
may take months to achieve maximal effect (0.5 marks). For
immediate relief of asthma symptoms she should use the ventolin
inhaler (0.5 marks). The steroid inhaler will not have an effect on
her symptoms if only used when she experiences asthma
symptoms beccause it is a long term controller that reduces
inflammation in her lungs (0.5 marks) and reduces the bronchial
spasms that cause asthma attacks over time. Provide written
treatment instructions to improve recall and develop a
management plan (1 marks).
Respiratory – Asthma
An adolescent, Mungo B, with previously diagnosed
asthma comes to your general practice for a routine
check-up and is frustrated by his dependence on
“puffers”.
a. What are the two main aims of asthma therapy
delivered by “puffers”?
(1 mark)
Mungo is on Salbutamol and Fluticasone.
b. What are their mechanisms of action?
(5 marks)
Respiratory – Asthma Therapy
a.
Prevention (0.5 marks) and relief (0.5 marks)
b.
(5 marks total):
Salbutamol is a B2 agonist (0.5 marks), which acts on the beta-2
adrenergic receptors of bronchioles (0.5 marks), causing
bronchodilation (0.5 marks). This is used in circumstances of
bronchoconstriction (0.5 marks), such as an acute asthma attack
(0.5mk) (or excerbation of asthma).
Fluticasone is a corticosteroid (0.5 marks) used for prevention (0.5
marks) of asthmatic attacks. Corticosteroids act to inhibit
inflammation (0.5 marks) by a variety of mechanisms, including
inhibition of COX expression, down-regulation of pro-inflammatory
mediators such as interleukin-(IL)-1, 3, and 5 (or other acceptable
alternate answer) (0.5 marks). Preventive medications must be
taken regularly by people with asthma in order to prevent attacks
(0.5 marks)
Respiratory – Asthma Therapy
Fill in the table below to define and differentiate between Type I and
Type II respiratory failure. Also, list one example of
diseases/conditions that could potentially cause each type of
respiratory failure. (5 marks)
Type 1 Respiratory Failure
Type 2 Respiratory Failure
Definition
(1 mark each)
Blood Gases
• PaO2
• PaCO2
• PAO2 – PaO2
(1 mark each)
Example
(0.5 marks each)
Respiratory – Respiratory Failure
Type 1 Respiratory Failure
Type 2 Respiratory Failure
Hypoxaemia without hypercapnia
Hypercapnia (usually with hypoxaemia)
Typically caused by a
ventilation/perfusion (V/Q) mismatch
Underlying causes:
Blood Gases
•
PaO2
•
PaCO2
•
PAO2 – PaO2
(1 mark each)
•
•
•
•
•
•
Example
(0.5 marks each)
• Cardiogenic/non-cardiogenic
pulmonary oedema
• Parenchymal disease
• Diseases of vasculature and shunts:
right-to-left shunt, pulmonary embolism
• Interstitial lung diseases e.g. Acute
Respiratory Distress Syndrome,
pneumonia, emphysema
Definition
(1 mark each)
Low (< 60 mmHg)
Normal/low (< 45 mmHg)
Increased
• Impaired central nervous system drive to
breathe resulting in reduced respiratory effort
• Impaired strength with failure of
neuromuscular function in respiratory system
• Increased load on respiratory system
Low
High (> 50 mmHg)
Decreased
• CNS effects e.g. Drug overdose,
brainstem injury, hypothyroidism
• Neuromuscular diseases e.g.
myopathy (respiratory muscle
weakness), myasthenia gravis or
Guillain-Barre syndrome (impaired
neuromuscular transmission)
• Reduced lung compliance and chest
wall compliance e.g. pneumothorax,
pleural effusion
• Severe airway disorders e.g. asthma,
chronic obstructive pulmonary disease
(COPD)
Respiratory – Respiratory Failure
A patient presents to your office with shortness of breath, and ongoing
cough, wheeze and chest tightness. She is a 45 year old woman who
has smoked a pack of cigarettes a day for 25 years. Upon
investigation, you notice her lips and fingernails are cyanosed, she
appears slightly confused, is a little bit tachycardic (HR 104) and her
respiratory rate is 24 BPM. While doing your examination, your patient
mentions that her sister is asthmatic, and she had tried using her
Ventolin puffer an hour ago but this did not improve her symptoms.
1. What is the most likely diagnosis (1 mark)? Explain the major
pathophysiological effects of this condition (2 marks)
2. Explain what PaO2 and PaCO2 you would expect to see when you
take her blood gas levels? (0.5 marks) Is this due to an increase or
decrease in ventilation? (1.5 marks)
3. How do the flow volume loop on spirometry testing differ between
obstructive and restrictive airway disease? (3 marks)
Respiratory – Respiratory Pathology
1. Chronic Obstructive Pulmonary Disease (COPD) (1 mark)
COPD is an irreversible condition causing early small airway closure
increased compliance, and airway narrowing (1 mark).
It leads to reduced surface area for gas exchange due to airway
collapse/compression (1 mark).
2. Low PaO2 and Low PaCO2 (0.5 mark). Patient is hyperventilating,
blowing off carbon dioxide but not allowing adequate oxygen
uptake- which results in a V/Q mismatch (1.5 marks).
3. (3 marks):
Obstructive
Restrictive
FEV1
Decreased
Decreased/normal
FVC
Decreased/normal
Decreased
FEV1/FVC
Decreased
Normal/increased
Respiratory – Respiratory Pathology
1
a. Rationalise why a distal lesion (e.g. at the wrist)
of the ulnar nerve might give a “claw-like”
appearance, while a more proximal lesion (e.g.
at the elbow) may give a less “claw-like”
appearance.
(5 Marks)
b. Explain what sort of appearance the hand/wrist
might take on if the radial nerve had a distal
lesion.
(3 Marks)
MSK – Ulnar Claw
1.
a.
• Distal lesion = finger flexors/extensors acting
without medial two lumbricals
• Medial two lumbricals have ulnar nerve
innervation
• Action of lumbricals is to extend IP joints but flex
MCP joints.
• Proximal lesion = also lose medial Flex. Dig. Prof.
• Extension predominates and extends fingers (less
“claw-like”)
1.
b.
• Appearance is wrist drop
• Because radial nerve supplies all wrist extensors
• Without extensors, gravity+flexors flex the wrist
MSK – Ulnar Claw
1.
a. Laceration causes parasthesia over central
proximal palm between thenar/hypothenar – what
nerve was lesioned?
(1 Mark)
b. Upper limb injury involving
alcohol/violence/lacerations. Other than fractures,
what else should you see in X-ray?
(0.5 Marks)
c. Wrist injury with lacerations. You suture
lacerations without physical exam. What have
you neglected?
(1 Mark)
d. Why is this important? Likely Sequalae?
e. Describe 1 difficulty arising from assessing
drunken patient in terms of wrist
injury/parasthesia/history?
MSK – Wrist Injury
1.
a. Palmar cutaneous branch of the median nerve
b. Foreign bodies/objects
c. Checking anatomical snuffbox for occult
scaphoid fracture
d. Commonly fractured, often invisible on x-ray, if
missed, may lead to avascular necrosis of the
scaphoid, resulting in pain and permanent
disability of hand. As the blood supply is mostly
distal, a fracture will disrupt supply to the
proximal end -> necrosis
e. Consciousness/Pain/Range of Motion/Parasthesia
MSK – Wrist Injury
Leah is a 75 year old woman who has fallen and
broken her hip. She is diagnosed as having
osteoporosis and requires a complete hip
replacement.
1.
a. Based on her age/sex describe most likely
mechanisms behind the osteoporosis (4 Marks)
b. List 4 modifiable risk factors for osteoporosis (2
Marks)
MSK – Osteoporosis
1.
a. Gender: after menopause,  oestrogen in
IL-6, IL-1 and TNF-α and  RANKL:OPG ratio osteoclast maturation bone resorption
Age:  age -  osteoblastic replicative and
biosynthetic potential. Growth factors stored in
bone which are normally release by osteoclastic
digestion no longer activate osteoblasts. Skeleton
is populated by osteoblasts which diminished
capacity to make bone.
b. Excessive alcohol, smoking, calcium/vitamin D
deficient diet, lack of exercise/sedentary lifestyle,
poorly controlled diabetes mellitus, having small
thin stature.
MSK – Osteoporosis
1.
a. Hyperparathyroidism is a consequence of renal
osteodystropy. What bone cells do parathyroid
hormone (PTH) stimulate, and what effects does
this hormone have in the body with respect to
bone homeostasis?
(3 marks)
b. What effect does renal failure have on vitamin D
levels? List two (2) consequences of this effect.
(2 Marks)
c. List two (2) classes of drugs and their mechanisms
of action that are used to treat the reduced bone
density resulting from osteoporosis.
(2 marks)
MSK – Renal Osteodystrophy
1.
a. PTH is detected by osteoblasts. Osteoblasts then
 RANLK:OPG ratio which increases osteoclast
maturation/activity.  osteoclast activity  bone
resorption  serum Ca2+  bone density
b. Renal failure  activated vitamin D. Secondary
hyperparathyroidism, hypocalcaemia,
hyperphosphataemia (due to the kidney failure,
not PTH)
c.
• Bisphosphonates: apoptose osteoclasts
• Oestrogen replacement (HRT): decreases osteoclastic activity indirectly
through osteoblasts or directly by  chemical mediators like IL-6
• Selective oestrogen receptor modulators: e.g. raloxifene (same as above)
• Calcitriol/Vit. D: increased absorption of calcium and phsophates in gut
and kidney
• Calcitonin: inhibits osteoclasts
• Intermittent rPTH (Teriparatide): activates osteoblasts>osteoclasts
• Strontium ranelate:  bone formation via  osteoblasts and  OPG which
 osteoclasts
MSK – Renal Osteodystrophy
1. What type of joint is the hip joint? Provide
both general and specific classification
(2 Marks)
2. What are the major anatomical features
contributing to the stability of the hip joint?
(3 Marks)
3. List the normal movements of the hip joint
(3 Marks)
4. What important anatomical structures
related to hip joint might be damaged by
dislocation? List 4
(2 Marks)
5. List 4 other signs or symptoms that are
associated with dislocation of hip joint
(2 Marks)
MSK – Hip Dislocation
1. Ball and socket, synovial joint
2. Surrounding musculature, shape of
acetabulum/head of femur, fibrous capsule
3. Flexion, extension, adduction, abduction,
internal/medial rotation, external/lateral
rotation
4. Ligament of head of femur, bony rim of
acetabulum, fibrous capsule, sciatic nerve,
circumflex arteries
5. Pain, pain exacerbated by movement,
parasthesia, deformity, swelling, loss of
function, altered gait, positive
trendelenburg sign
MSK – Hip Dislocation
1.
a. Name the rotator cuff muscles.
(2 Marks)
b. Describe one clinical test to assess the function or
integrity of the glenohumeral joint, with reason for
test.
(2 Marks)
c. What type of joint is the glenohumeral jont?
(1 Mark)
MSK – Shoulder Injury
1a) Supraspinatus, infraspinatus, teres minor,
subscapularis
1b)
•Apley’s scratch: patient instructed to scratch opposite shoulder
anteriorly (adduction), behind neck (external rotation,
adduction), behind back (internal rotation, adduction)
•Hawkin’s Kennedy: flex arm and forearm 90° then internally
rotate. Tests impingement of local structures e.g. nerve
•Apprehension: arm abducted to 90° and externally rotated.
Joint pushed anteriorly. Tests impending dislocation
•Empty can/rotator cuff: abduct to 90° externally rotated-test
abduction power. Repeat at 30° internally rotated. Tests
supraspinatus tear.
•Winged scapula: patient pushes with both hands arms length
against wall. Tests serratus anterior.
1c) Ball and socket, synovial joint
MSK – Shoulder Injury
1a) What are the three phases of endometrial growth
in the monthly female sexual cycle? (1.5 Marks)
1b) What two anterior pituitary sex hormones are
secreted during the female sexual cycle and how are
they involved with ovulation? (2 Marks)
Reproductive – Menstrual Cycle
1a)
•Menstrual
•Proliferative
•Secretory
1b)
Follicle-stimulating hormone (FSH): Increased FSH
levels stimulate several primordial follicles to develop
into primary follicles and then into secondary
follicles.
Luteinising Hormone (LH): Increased LH levels cause
a rupture of the mature Graafian follicle and expulsion
of a secondary oocyte.
Reproductive – Menstrual Cycle
1a) Interpret each element of the following karyotype:
46,XY, der(14;21)(q10;q10)mat,+21 (2 Marks)
1b) The above karyotype is an example of
Robertsonian translocation. Name and briefly explain
the other two mechanisms by which Down syndrome
can occur. (2 Marks)
1c) List five (5) signs of Down syndrome that you may
see on general observation. (2.5 Marks)
1d) List one (1) psycho-social implication of Down
syndrome for the i) Child ii) Teenager iii) Adult (1.5
Marks)
Reproductive – Down Syndrome – Card 1 of 2
1a)
46: Normal no. of chromosomes/46 chromosomes
XY: Male
der(14;21)(q10;q10)mat: Breakage and reunion have
occurred at band 14q10 and band 21q10 in the
centromeric regions of maternal chromosomes 14
and 21
+21: gain of chromosome 21/trisomy 21/extra copy of
21
1b)
1. Meiotic non-disjunction: Failure of separation of
chromosome 21 during meiosis results in one
gamete having two copies of chromosome 21
which after fertilisation results in a zygote with
trisomy 21
2. Mosaic: Mitotic nondisjunction of chromosome 21
in an early stage of embryogenesis
Reproductive – Down Syndrome – Card 1 of 2
Down syndrome cont’d on back
Reproductive – Down Syndrome – Card 2 of 2
1c) simian crease (single palmar crease), flat facial
profile, epicanthic folds, oblique eye fissures,
macroglossia, large gap between 1st and 2nd toes,
microgenia, Brushfield spots, small ears
1d) i) slow cognitive development/difficulties learning
speech ii) social gap from peers, self discovery,
social isolation iii) independent living, employment,
death of carers/parents
Reproductive – Down Syndrome – Card 2 of 2
1a) List five (5) signs or symptoms of pregnancy
which you would observe during a general inspection
(2.5 Marks)
1b) Which hormone is tested for in the home
pregnancy test? Further include the specific site of
production for this hormone and its key physiological
role (2 Marks)
1c) Outline three psychosocial issues of teen
pregnancy (1.5 Marks)
Reproductive – Pregnancy
1a)
Amenorrhoea, nausea/vomitting, breast tenderness,
urinary frequency/urgency, breast changes, softening
of cervix (Hegar’s sign), uterine enlargement,
increased vaginal discharge, blue colouration of
cervix/vagina (Chadwick’s sign)
1b) β-human chorionic gonadotrophin: it is produced
by the syncytiotrophoblasts of the placenta. Its role is
to maintain the corpus luteum during pregnancy (LhhCG receptor)
1c) Increased incidence of alcohol/drug use during
pregnancy, truancy from school and corresponding
decrease in grades, increased risk of
depression/anxiety, less concordance and antenatal
care leading to poor outcomes
Reproductive – Pregnancy
1a) A couple been trying to conceive for the last 6
months without success. Can they be defined as
clinically infertile? Explain your answer. (2 Marks)
1b) List two categories of male causes of infertility.
Give an example for each (2 Marks)
1c) Endometriosis is one cause of female infertility.
List two other categories of female infertility. Give an
example for each (2 Marks)
1d) List one initial investigation for each partner
which could be used to determine couple’s cause of
infertility (1 Mark)
Reproductive – Fertility
1a) No, couple cannot be defined as infertile. Infertility
is defined as 12 months of unsuccessful regular
unprotected sexual intercourse.
1b) Reduced or abnormal sperm count (from
Klienfelter’s), ductus deferens obstruction (from
scarring from infection)
1c) Ovulatory disorder (extreme mental or physical
stress  hypothalamus), tubal disease (from damage
from previous ectopic pregnancy)
1d) Male: semen analysis
Female: mid-luteal progesterone or basal body temp.
chart
Reproductive – Fertility
1a) Describe 1 function of:
Testes:
Epididymis:
Seminal vesicle:
Prostate gland:
Bulbourethral gland:
Reproductive – Male Reproductive System
1a)
Testes: produce sperm/secrete testosterone
Epididymis: matures sperm/stores sperm
Seminal vesicle: supply fructose to sperm/secrete
prostaglandins/provide precursors for semen clotting
Prostate gland: secrete alkaline fluid to neutralise
vaginal acid/trigger clotting of semen via factors
Bulbourethral gland: secretes lubricating mucus
Reproductive – Male Reproductive System
Neil Legstrong, a 58 year old male comes into Emergency with a mild but constant
crushing chest pain experienced over the last 4 hours. He also feels short of breath
and it seems the neural Impending Doom sensor has also been activated. With a
history of stressful travel and a gradual reduction in physical conditioning following
retirement, a Myocardial Infarct (MI) is strongly suspected.
1.
2.
3.
List three (3) physiological signs or symptoms of an MI (1.5 marks)
You order a serum serology test. What are two (2) biochemical markers you
would request if you suspect an MI? Describe the limitations of each with
respect to time. (3 marks)
In the emergency room, your intern prescribes five (5) drugs for the patient.
You raise an eyebrow (up and slightly to the side for maximal ‘constructively
critical but not derogatory’ effect), and tell your intern not to prescribe
verapamil.
•
•
•
•
•
GTN (glyceryl tri-nitrite)
Aspirin
Morphine
Atenolol
Verapamil
a) Describe a fairly detailed mechanism of action for GTN and aspirin, and justify
their use in the acute management of myocardial infarction (4 marks)
b) Explain, with reference to their mechanisms of action, why it is dangerous to
prescribe β-blockers with Ca2+ channel blockers? (2 marks)
Cardiovascular – MI – Card 1 of 2
1. (1.5 marks)
Any 3 of the following:
• SOB (dyspnoea)
• Sudden Death
• Syncope or near-syncope
• Low-grade fever
• Extra heart sounds (particularly
3rd)
• Sweating (diaphoresis)
• Cold, grey periphery (peripheral
vasoconstriction)
• Impairment of cognitive function
• Irregular heart beat
• Dysrhythmias
• Restless patient
• Increased respiratory rate
• Change in blood pressure (may
be elevated OR lowered)
2. (3 marks - any 2 of the below; 1⁄2 mark for each
biochemical marker and another 1 mark for the
description of time limitations.)
• Myoglobin (Mb)
•
•
•
•
Creatine kinase-MB isoenzyme (CK-MB)
•
•
•
•
Detected in serum 4-8 hours after onset of AMI
Peaks 12-30 hours after onset of AMI
Normal 3 days after onset of AMI
Cardiac Troponin T (cTnT)
•
•
•
•
Detected in serum 3-12 hours after onset of
AMI
Peaks at 12-18 hours after onset of AMI
Normal for 2-3 days after onset of AMI
Total Creatine kinase (CK)
•
•
•
•
Detected in serum 1-4 hours after onset of AMI
Peaks at 6-7 hours after onset of AMI
Normal 24 hours after onset of AMI
Detected in serum 4-12 hours after onset of
AMI
Peaks at 12-48 hours after onset of AMI
Present for 5-15 days after an AMI
Cardiac Troponin I (cTnI)
•
•
•
Detected in serum 4-12 hours after onset of
AMI
Peaks at 12-48 hours after onset of AMI
Present for 4-7 days after an AMI
Cardiovascular – MI – Card 1 of 2
Answer to Question 3 on reverse.
Cardiovascular – MI – Card 2 of 2
3. a. (4 marks)
• Glyceryl trinitrate (GTN): GTN is a peripheral vasodilator (1/2 mark) that is metabolised to
provide an exogenous source of nitric oxide (NO) (1/2 mk). NO stimulates increased
production of cGMP, leading to relaxation of vascular smooth muscle (1/2 mk). This
reduces venous return and preload to the heart, reducing myocardial oxygen requirement
(1/2 mk).
• Aspirin: Low dose aspirin inhibits the cyclo-oxygenase enzyme (1/2 mk) and therefore
irreversibly inhibits thromboxane A2 synthesis in platelets (1/2 mk) and prostacyclin
synthesis in endothelium (1/2 mark), hence decreasing platelet aggregation and
decreasing the risk of myocardial infarction (1/2 mk).
b. (1 mark)
1⁄2 mark for mentioning AV node block
1.5 marks for mentioning why:
- β-blockers reduce myocardial workload by preventing the noradrenaline- induced increases
in force and rate of contraction, and common adverse effects include bradycardia and AV
block.
- Calcium channel blockers block voltage-operated L-type Ca2+ channels, which decreases
Ca2+ entry into the AV node, slowing AV node conduction, which decreases heart rate and
the force of contraction.
- When used together, the cumulative effects of calcium entry blockers and β- adrenoceptor
antagonists can cause complete AV block, so this combination must be used with caution.
Adverse effects include bradycardia, AV block, hypotension, peripheral oedema, headaches
and nausea.
Cardiovascular – MI – Card 2 of 2
Joseph P. presents to you, a GP in Brisbane city, for a general
check-up. Joseph has never been to your practice before. His
history reveals that he is a 52-year-old lawyer with no significant
medical history. He has smoked approximately 1 pack per day since
he was 19, and drinks 2-3 beers on weekends only. He describes his
diet as “poor”, with high levels of fast food such as burgers and hot
chips, and he does not exercise regularly. Upon examination, his
weight is 110kg and his height is 178cm. His blood pressure is
148/96. Fundoscopy reveals no changes.
(a) Calculate Joseph’s BMI. (1 mark)
(b) List three risk factors for cardiovascular disease relevant to this
patient. (1.5 marks)
Hypertension is often related to the development of atherosclerosis.
(c) Briefly outline the process of atheroma formation. (5 marks)
(d) Explain how atherosclerosis may result in hypertension. (1 mark)
Cardiovascular – Atherosclerosis
(a) BMI = weight (kg) / height2 (m) = 34.7
(b) Obesity, hypertension, hypercholesterolemia, smoking, stress (work), sex
(male), physical inactivity (0.5 marks each up to 1.5 marks total)
(c) Step 1: Chronic endothelial injury (eg. Hyperlipidemia, hypertension, smoking,
toxins, hemodynamic factors, immune reactions, viruses)
Step 2: Endothelial dysfunction (eg. Increased permeability, leukocyte adhesion,
monocyte adhesion and emigration)
Step 3: Smooth muscle emigration from media to intima, macrophage activation
Step 4: Fatty streak (Macrophages and smooth muscle cells engulf lipids = foam
cells)
Step 5: Smooth muscle proliferation, collagen/ECM deposition, extracellular lipid (1
mark for each step)
(d) BP= CO x TPR
Atherosclerosis increases vascular wall thickness, resulting in a decreased lumen.
This then increases the peripheral resistance(1/2) . This causes an increased
afterload, resulting in an increased force of contraction required by the heart (1/2).
Cardiovascular – Atherosclerosis
A male patient David H, aged 69 years, presents to the local ED at 10pm with severe dyspnoea
and an unproductive cough. Mr H reports that his difficult breathing began this morning when
he awoke and has steadily worsened through the day. He also reports that he becomes
quickly exhausted upon exertion. Mr H has a 6 year history of hypertension and suffered a MI
4 months ago.
His vital signs are P 106, BP 145/98, RR 32, t 36.9, and his O2 sats are 89%. Mr H is pale,
sweaty and trembling, physical examination reveals a palpable left ventricular heave and
audible crackles at the lung bases and a S3 heart sound.
1a: What is your provisional diagnosis (1 mark). List two signs you would expect to see on Mr
H’s chest X-ray (1 mark)
1b: List two ways in which this condition has resulted in Mr H’s dyspnoea? (2 marks)
1c: Initially Mr H is administered 40 mg of furosemide (a loop diuretic) and 6.25mg of captopril
(an ACE inhibitor). Explain how furosemide and captopril assist to reduce the workload on the
heart (2 marks)
1d: Prognosis for patients with this condition is extremely poor, and 5-year survival rates are
lower than for most forms of cancer. In addition, once symptoms have reached an advanced
stage, quality of life is often severely compromised and therapeutic options are limited.
Identify one ethical issue with regards to treating Mr H given this prognosis and explain
briefly how it relates to the scenario? (2 marks)
Cardiovascular – Dyspnoea
1a: (2 marks)
Left-sided heart failure (1 mark)
Kerley B lines, cardiomegaly, reticulonodular patterns- lung bases (any 2 for 1 mark)
1b: (2 marks, 1 for each answer)
1) Impaired the ability of the heart to function as a pump to support a physiological circulation
resulting in hypoxia and hypercapnia (insufficient cardiac output).
2) Impaired diffusion of respiratory gases between the alveoli and pulmonary capillaries due
to fluid accumulation in the lungs (pulmonary oedema).
1c: (2 marks, 1 for each answer)
1) A diuretic will reduce extracellular fluid volume and ventricular filling pressure (or
"preload"). Because patients with heart failure often operate on a "plateau" phase of the
Starling curve preload reduction can occur without concomitant reduction in cardiac output.
2) Angiotensin II is a potent arterial vasoconstrictor and an important mediator of Na+ and
water retention through its effects on glomerular filtration pressure and aldosterone
secretion. Consequently, the antagonism of Angiotensin II reduces vasoconstriction and fluid
retention reducing preload and afterload on the heart.
1d: (2 marks)
1) Respecting patient autonomy(1 mark). It is incumbent upon the physician to discuss the
patient's wishes regarding the intensity of treatment and end-of-life care at a time when the
patient is still capable of understanding the issues and making informed choices (1 mark).
OR
2) Discussion of end of life issues (1 mark) . As the patient approaches the terminal stages of
disease, there should be discussions with the patient and family regarding where the patient
would like to spend his or her final days. (1 mark)
Cardiovascular – Dyspnoea
Please complete the tables below; outline where all of these leads will be attached on the body and what
these leads are intended to measure: (4 marks)
Lead
Negative
Electrode
Positive
Electrode
Rationale
for use
1
Right arm
Left arm
Measures
cardiac
activity
along the
frontal
plane.
2
Left leg
3
Left leg
Lead
Electrode Location
V1
4th intercostal space
at the right sternal
border
V2
V3
Midway between V2
and V4
V4
aVF
L1 leads
aVL
L2 leads
aVR
L3 leads
Rationale for
use
Left leg
V5
5th intercostal space
in the anterior axillary
line
V6
5th intercostal space
in the mid-axillary line
Measures
cardiac
electrical
activity
through the
chest wall’s
depth
Cardiovascular – ECG Leads
Please complete the tables below; outline where all of these leads will be attached on the body and what
these leads are intended to measure: (4 marks)
Lead
Negative
Electrode
Positive
Electrode
Rationale
for use
1
Right arm
Left arm
2
Right arm
Left leg
Measures
cardiac
activity
along the
frontal
plane.
3
Left arm
Left leg
aVF
L1 leads
Left leg
aVL
L2 leads
Left arm
aVR
L3 leads
Right arm
Measures
cardiac
electrical
activity
along the
frontal
plane
Lead
Electrode Location
Rationale for
use
V1
4th intercostal space
at the right sternal
border
V2
4th intercostal
space at the left
sternal border
V3
Midway between V2
and V4
Measures
cardiac
electrical
activity
along a
horizontal
plane across
the chest
V4
5th intercostal
space in
midclavicular line
V5
5th intercostal space
in the anterior axillary
line
V6
5th intercostal space
in the mid-axillary line
Measures
cardiac
electrical
activity
through the
chest wall’s
depth
Cardiovascular – ECG Leads
a) Different parts of an ECG trace can be correlated to specific cardiac events. In
the following illustrative ECG trace, define the cardiac event(s) that are/is
happening at each specified time: (4.5 marks)
P wave:
PR Segment:
QRS Complex:
ST Segment:
T Wave:
TP Interval:
b) As well as being able to display normal cardiac events, an ECG trace can also
depict when events go wrong in the heart. The following illustrative ECG trace is
indicative of a specific abnormality in heart rhythm. Give the general name of the
heart condition and briefly describe the reason(s) for your choice and why:
Cardiovascular – ECG Trace
a) TOTAL out of 4.5 Marks
P wave: Atrial depolarisation (0.5 marks)
PR Segment: AV node/nodal delay (0.5 Marks).Time taken for electrical impulse to
travel from sinus node through AV node. i.e. AV node function.
QRS Complex: Ventricular/ventricles depolarisation (0.5 Marks), Atria repolarisation
(0.5 Marks)
ST Segment: Ventricles contracting (0.5 Marks) and emptying (0.5 Marks) T Wave:
Ventricular/ventricles repolarisation (0.5 Marks) TP Interval: Ventricles relaxing (0.5
Marks) and filling (0.5 Marks)
b) TOTAL out of 2.5 Marks
Condition: Heart Block (include any mention e.g. ‘Complete Heart Block’) (0.5
Marks) e.g. 3rd degree (AV) heart block.
Reasoning: The atria still beat regularly, but the ventricles occasionally fail to be
stimulated and thus do not conduct following atrial contraction. (0.5 Marks) The SA
Node via a ventricular focus continues to govern atrial depolarisation, but the
ventricles generate their own impulses at a rate much slower than that of the atria.
(0.5 Marks) On the ECG, the P waves exhibit a normal rhythm. (0.5 Marks) The QRS
and T waves also occur regularly but much slowly than the P waves and are
completely independent of P wave rhythm. (0.5 Marks)
Cardiovascular – ECG Trace
Mr. X was brought in by ambulance from the Valley in Brisbane on a
Saturday night after getting into an argument which escalated to physical
violence. Mr. X received a deep laceration to his left thigh which ruptured
his femoral artery.
a) Name 3 endogenous hormones that would actively compensate for
Mr.X’s blood loss.
b) Briefly describe one function of how each of these hormones would work
in
compensating for Mr. X’s condition.
c) Mrs. X, who is also a nurse, arrives at the Emergency Department and
demands to know why her husband is not receiving Colloids. What would
your explanation be?
PBL 1 – Blood on the Road – Femoral Artery
a) 0.5 marks for each answer, only need three answers.
1. Angiotensin II
2. Vasopressin (ADH)
3. Noradrenaline
4. Adrenaline
5. Aldosterone
b) One mark for each function mentioned for each hormone, only need one function for each
hormone
1. Angiotensin II constricts peripheral arteries and decreases output of water and salt from
the kidneys
• stimulates the release of aldosterone from the adrenal cortex
• stimulates the release of ADH from the posterior pituitary
2. Vasopressin (ADH) constricts peripheral arteries and veins and greatly increases water
retention by the kidneys
3. Noradrenaline/Adrenaline – increases peripheral vascular tone and inotropic effects and
rate of contractility on the heart
4. Aldosterone – retains Na+ and therefore water in the kidneys to increase overall vascular
tone
c) 0.5 marks for each answer (only need 3)
1. no evidence of improved outcome over using crystalloid solutions
2. 2. cost
3. 3. increase risk of oedema
4. 4. increase risk of anaphylaxis
PBL 1 – Blood on the Road – Femoral Artery
a) What is the physiological definition of shock? (1 mark)
b) Briefly list and define the stages of shock. (2 marks)
PBL 1 – Blood on the Road – Shock – Card 1 of 3
a) Shock is defined as a failure to meet the metabolic demands of cells
and tissues [0.5] and the consequences that ensue. A central
component of shock is decreased tissue perfusion [0.5] - multisystem
organ hypoperfusion is apparent. Arterial pressure is usually (though
not always) reduced in shock.
b)Stage
Class
Amount of
blood loss
Characteristics
Non-progressive /
compensated
I
<15%
No significant changes in hemodynamic parameters
Compensations cause full recovery without treatment
Progressive
II
15-30%
Compensated shock.
Presents with tachycardia, reduced pulse pressure but
maintained vital organ perfusion. May present with
tachypnoea. Urinary output is satisfactory.
III
30-40%
Failure of compensation.
Falling BP despite high pulse rate. Failing perfusion of vital
organs. Cold periphery, reduced urine output.
IV
>40%
Irreversible.
Life-threatening. Volume replacement cannot restore
patient to normal. Anuria.
Irreversible
PBL 1 – Blood on the Road – Shock – Card 1 of 3
c) One of the major short term compensations for hypovolaemic shock
is the baroreceptor reflex.
Outline its mechanism of increasing mean arterial pressure. (2 marks)
PBL 1 – Blood on the Road – Shock – Card 2 of 3
c)
Marking
0.5 mark
0.5 mark
0.5 mark
0.5 mark
PBL 1 – Blood on the Road – Shock – Card 2 of 3
d) Outline, with the aid of a diagram if necessary, how the Renin-
d) Outline, with the aid of a diagram if necessary, how the ReninAngiotensin-Aldosterone system acts to restore and preserve mean
arterial pressure in patients who have or are undergoing sustained
hypovolaemia due to blood loss. (3 marks)
PBL 1 – Blood on the Road – Shock – Card 3 of 3
d) Decrease in blood volume leads to decrease in MAP -> decreased
renal BP and/or GFR -> Renin released from juxtaglomerular cells/
kidneys [0.5]converts angiotensinogen to angiotensin I -> Angiotensin I
to Angiotensin II via action of ACE [0.5]
Angiotensin II acts on:
1. Adrenal cortex to release aldosterone -> Na retention and K
excretion in kidneys -> water retention [0.5]
2. Posterior pituitary gland -> ADH -> water retention [0.5]
3. Vasculature -> vasoconstriction -> increased total peripheral
resistance -> increase MAP [0.5]
1 and 2 increase blood volume -> increase venous return-> increase SV
-> increase CO -> increase MAP [0.5]
PBL 1 – Blood on the Road – Shock – Card 3 of 3
You are a seasoned physician who has decided to get some much-needed
exercise by walking to your next appointment. Whilst passing through the
park you notice a huge bee hive and a man lying in close proximity who
starts to yell in an anxious tone, “Help me! I am having a anaphylactic
attack” you quickly run to his assistance. Upon initial assessment you
notice he is pale and sweaty and a few minutes later he loses
consciousness. As you are on your way to a home-visit you whip out your
trusty sphygmomanometer and stethoscope. Checking his vital signs you
notice his pulse rate is raised and systolic blood pressure is significantly
decreased.
1. What kind of shock is this man experiencing? (1 marks)
2. What is the definition of shock? In this particular type of shock what
physiological change is responsible for decrease is blood pressure? (2
marks)
3. How is a decrease in arterial blood pressure sensed in the body and
explain 2 immediate compensatory mechanisms utilised to rectify
homeostasis ? (3 marks)
4. You search through the man’s pockets, find an Epipen, and administer
him an emergency dose of adrenaline. Why is this the preferred treatment
for an anaphylactic reaction? (1 mark)
PBL 1 – Blood on the Road – Anaphylactic Shock
1) Distributive
2) Shock is defined as a decrease in tissue perfusion. Decreased total
peripheral resistance, causing fluid shift from blood vessels into
extracellular space and therefore decreasing volume in vessels, ultimately
leading to decreased blood pressure.
3) Baroreceptors located in the aortic arch and carotid sinus sense a
change in the arterial pressure and initiate a sympathetic nervous system
response that leads to: (any two of the following)
• Increased cardiac output due to increased cardiac contractility
• Increased cardiac output due to increased heart rate
• Increased total peripheral resistance due to sympathetic constriction of
arterioles
• Increased venous return as a result of increased venous
tone/venoconstriction
• Increased respiratory rate leading to increase venous return and
therefore cardiac output (respiratory pump).
4) Adrenaline causes immediate and widespread vasoconstriction
PBL 1 – Blood on the Road – Anaphylactic Shock
Screening for diabetes using glycated haemoglobin (HbA1c) offers
potential advantages over fasting glucose or oral glucose tolerance testing.
This has found to be especially true in populations of high diabetes
prevalence, such as Indigenous Australians. A current article about HbA1c
reports the sensitivity to be 73% and its specificity to be 98%.
1. (a) The Australian Bureau of Statistics estimates that 6% of Indigenous
people have diabetes mellitus type II. Therefore determine the likelihood of
an indigenous patient having diabetes, if their glycated hemoglobin test
comes back positive (>7%). Show your working in a 2x2 table. (3 marks)
1. (b) For patients with a positive test, what is your next step clinically? (1
mark)
2. List four (4) other very common conditions, which are prevalent in
Indigenous populations. (2 marks)
Population Health – Screening Diabetes
1 (a):
From the information above:
Prevalence = 0.06
Sensitivity = 0.73
Specificity = 0.98
Positive predicted value
= proportion of people with a positive
result that are diseased
= 44/62
= 0.71 (71%)
Diseased
Not
Diseased
HbA1c
Test
Positive
(0.73 x 60)
= 44
(940 922)
= 18
(44 + 18)
= 62
HbA1c
Test
Negative
(60 - 44)
= 16
(0.98 x
940)
= 922
(16 + 922)
= 938
(0.06 x
1000)
= 60
(1000 60)
= 940
1000
An indigenous patient has a 71% chance of having diabetes if their glycated haemoglobin test
comes back positive.
1 (b): confirm the diagnosis with a more specific test (or more accurate test). (1 mark) 0 mark
if they say repeat the test - as HbA1c not subject to significant variability (reflects BSL over a
3 month period), so no regression to the mean.
2. (1/2 mk each up to 2 marks)
Cardiovascular conditions (MI, hypertension, rheumatic heart disease)
Respiratory conditions
Kidney disease
Cancer
Infectious diseases
Ear and eye problems
Population Health – Screening Diabetes
You are a GP working in a small family practice in Brisbane. Michelle a 45 year old mother of
three presents to you with her youngest son - Bob. She is very concerned as she has heard
that a boy at her son’s school recently contracted hepatitis and so wishes to ensure that Mike
is fully vaccinated.
a) (2 marks) Use the TWO key words listed below to write a short paragraph describing your
understanding of how vaccination works.
-
antibody and exposure to pathogen
b) (1.5 marks) List 3 factors that contribute to a “good” vaccine
Michelle has been told by a friend that if many of the children in her son’s class are
vaccinated that she need not bother getting Bob vaccinated.
c) (2 marks) Discuss your understanding of the term ‘herd immunity’ including the risks and
benefits for individuals who are not vaccinated.
d) (1 mark) It comes to light that the infected child at Bob’s school had contracted Hepatitis A.
Other than vaccination, what two (2) precautions should the school take to avoid
transmission to other students?
While looking for more information on the Internet, Michelle has come across a newly
available saliva dipstick test for Hepatitis A. The test has a reported sensitivity of 84% and a
sensitivity of 45%.
e) (2 marks) Define the terms sensitivity and specificity
Population Health – Hep. B Vaccination
a) Vaccination is a process that exposes the adaptive immune system to antigen (1/2 mk) . This allows
memory lymphocytes to produce a strong secondary immune response (1/2 mk) with specific antibodies
(1/2 mk) immediately upon expose to the pathogen (1/2 mk).
b)
-
Activation of both T and B lymphocyte memory cells
Cost effective
Antigenically stable ie will not revert to virulent form
Easily and wildly available
Safe (non toxic etc)
Activation of antigen-presenting cells.
Generation of Th and Tc cells to multiple epitopes MHC polymorphism.
c) Herd immunity is when the number of immune individuals in the population reduce the number of
susceptible hosts, protecting the unimmunised, those too young to be immunised and those for whom
immunisation hasn't been effective (1 mark) . Because many vaccines carry some small risk of adverse
reaction, it is most beneficial to the individual to be unvaccinated in a population that is fully vaccinated,
given that there are insufficient susceptible individuals to maintain effective transmission, however, as the
number of unvaccinated individuals in the population increases it is of most benefit to be vaccinated from
disease (1 mark)
d) Hep A is is transmitted in a faecal oral manner, therefore precautions that can be taken by the school are
to ensure child hygiene including promoting regular hand washing (1/2 mk) and avoiding sharing food (1/2
mk) or water bottles (1/2 mk) or other appropriate answer
[Two responses for 1 mark]
e)
Sensitivity = probability of positive test in diseased person TP/TP+FN (1 mk)
Specificity = probability of negative test in healthy person TN/TN+FP (1 mk)
Population Health – Hep. B Vaccination
As a general practitioner with UQ’s Student Health Services,
you are alarmed to realize that there has been a significant
increase in the number of suspected Hepatitis B cases
diagnosed at the Clinic.
Q1. With regards to this illness, define primary illness
prevention and give an example of a primary prevention
activity (1.5 marks)
Q2. With regards to this illness, define secondary illness
prevention and give an example of a secondary prevention
activity (1.5 marks)
Q3. With regards to this illness, define tertiary illness
prevention and give an example of a tertiary prevention
activity (1.5 marks)
Population Health – Hep. B
Q1.
- To prevent the initial occurrence of an illness by identifying and addressing
precursor conditions and behaviours that result in chronic hepatitis. (1 mark)
- Primary prevention focuses on modifiable factors through the promotion of
healthy behaviours, and environments eg. immunisation (1/2 mk) OR counselling to
encourage individual behaviour change (1/2 mk) OR use of universal precautions in
health care settings ( 1⁄2 mk)
Q2.
- To stop or slow Hep B by early detection and appropriate treatment (1 mark)
- Specific to Hepatitis B - screening programs (1/2 mk) OR other approp answer
- Early detection allows for earlier treatments that limit progression and prevents
complications and or resultant disability, early detection also prevents spread of
new infections and protects the public.
Q3.
- To reduce the re-occurrence and establishment of chronic illness (1 mk)
- Targets individuals with chronic hepatitis focusing on effective treatment of
disease symptoms and limiting progression, complication and disabilities. This
includes the management of lifestyle behaviours that can worsen the disease.(1/2
mk) OR
- healthy eating, physical activity, cessation of smoking, limiting alcohol (1/2mk)
Population Health – Hep. B
PART A)
Health determinants are factors that help to explain and predict trends
in health and explain why some groups have better or worse health
than others.
List three (3) social determinants of health and give an example of how
that determinant could negatively affect health. (3 marks)
PART B)
Define primary, secondary and tertiary prevention and give an example
of each in relation to the prevention of Cardiovascular Disease. (3
marks)
Population Health – Health Determinants & Prevention
PART A) (Three marks total)
PART B)
Each social determinant of health listed is
worth 1⁄2 mark, as is each example.
Note: examples are numerous; all
reasonable examples are to be marked as
correct.
1⁄2 mark for definition and 1⁄2 mark for one example.
Note: examples are numerous; all reasonable
examples are to be marked as correct.
Social Determinant
(1/2 mark)
Example (1/2 mark)
Low socioeconomic
status
Poorer access to healthcare leading
to poorer health outcomes
High levels of stress
Stress is a risk factor for many
conditions, including cardiovascular
disease (one of the major burdens
on the health system)
Poor conditions
during childhood
Lower achievement in school and
lack of tertiary education result in
higher morbidity and poorer health
outcomes as compared to those
with a tertiary education
Unemployment
Increased mental and physical
illness
Social exclusion and
isolation
Depression and mental illnesses
Definition (1/2 mark)
Example (1/2 mark)
Primary Prevention:
Measures undertaken to
avoid the development or
initial occurrence of a
disease.
Stop smoking, regular
exercise, reduction of salt in
diet, healthier diet (less fried
foods and more
fruits/vegetables), weight
control (lose weight if
overweight/obese)
Secondary prevention:
Measures aimed to stop
or slow an existing illness
by early
detection and appropriate
treatment.
Blood cholesterol testing,
testing for hypertension,
screening for diabetes and/or
insulin resistance.
Tertiary prevention: :
Measures that reduce the
negative impacts of a
disease and reduce the
re-occurrence and
establishment of chronic
illness.
Anti-hypertensive drug
therapy, anti- coagulant
therapy, lowering blood
cholesterol (Statin therapy),
lifestyle modification
Population Health – Health Determinants & Prevention
John is referred to you by his GP for hypertension. You suspect
pheochromocytoma, which is a neoplasm of chromaffin cells in the
adrenal medulla, which synthesize and release catecholamines.
1. List 4 features of John’s history that might help confirm your
hypothesis (2 marks).
2. Give 4 other possible causes of secondary hypertension (2
marks).
Renal – Hypertension
1.
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Weight loss
Tremors
Sweats
Flank pain
Palpitations
Anxiety
Headache
Facial flushing
Abdominal pain
Increased appetite
Sense of impending doom
Visual disturbances
Dypsnea
Constipation
History of fainting
2.
Give 4 other possible causes of secondary
hypertension (2 marks – half mark each).
• Renal artery stenosis
• Renin-secreting tumours
• Glomerulonephritis
• Coarctation of the aorta
• Obstructive sleep apnea
• Also accept, obesity, oral contraceptive pill
and pyelonephritis
• Diabetic nephropathy
• Adult polycystic disease
• Primary aldosteronism
• Cushing’s syndrome
• Pregnancy
Renal – Hypertension
A. Outline the short-term mechanism by which decreased blood
pressure is detected and restored by the kidneys (3)
B. Name two classes of anti-hypertensive medications you would
prescribe to a hypertensive patient with co-morbid asthma and give
one example of each (2)
C. Name two classes of diuretics that can cause hypokalaemia, where
and how each acts and how hypokalaemia can occur (3)
Renal – Blood Pressure
A. A decrease in BP leads to decreased Na+ concentration at the macula densa and renin
release from juxtaglomerular apparatus cells (1/2) Renin stimulates the conversion of
Angtiotensiniogen to Angiotensin I and angiotensin converting enzyme converts Angiotensin
I to Angiotensin II (1/2) Angiotensin II has numerous effects that help increase blood pressure
including: Aldosterone release from the adrenal gland (1/2), vasopressin release from the
anterior pituitary (1/2), vasoconstriction (1/2), promotion of thirst (1/2)
Any other effects of Angiotensin II that contribute to increasing blood pressure also receive
1⁄2 mark (up to a total of 2 marks) but any non-related effects do not receive any marks.
B.
α-1 adrenoceptor antagonists e.g. Prazosin
Angiotensin II receptor antagonists e.g. Candasartan, Losartan
Calcium channel blockers e.g. Nifedipine, Verapamil
Diuretics e.g. Frusemide, Hydrochlorothiazide, Spironalactone, Amiloride
1⁄2 point for each class of drug (any two of the 4 listed) and 1⁄2 point for each matching drug
example (1⁄2 mark also given for other correctly matched drug examples not listed here)
C.
Loop Diuretics ( 1⁄2 ) -> Inhibit the Na/K/2Cl symporter in the Loop of Henle (1⁄2)
Thiazide Diuretics ( 1⁄2 ) -> Inhibit the Na/Cl symporter in the Distal Convoluted Tubule (1⁄2)
Decreased Na+ reabsorption increases the Na+ concentration in the distal nephron. This
results in increased exchange of Na+ and K+, with Na+ reabsorbed and K+ excreted into the
lumen, in the distal tubule, thus increased K+ loss into the urine and hypokalaemia (1)
Renal – Blood Pressure
i) Describe the main function/s of the following regions of the nephron (e.g.
secretion of protons etc) with a brief explanation of how these functions are
achieved (e.g. transporters, specific cell types etc) (1-2 sentences each) (5
marks)
a. Proximal convoluted tubule
b. Descending limb of the loop of Henle
c. Ascending limb of the loop of Henle
d. Distal convoluted tubule
e. Collecting duct
ii) With reference to their sites of action, explain the differences between
the effects of loop diuretics (e.g. frusemide) and thiazides (e.g.
hydrochlorothiazide) (1-2 sentences each) (3 marks)
iii) Which diuretic would you prescribe in a patient with hypokalemia?
Why? (1-2 sentences) (2 marks)
Renal – Nephron
i) 1 mark for each of (a) to (e)
a) The major function of the proximal tubule is to reduce the volume of the tubular fluid without varying its osmolarity from
that of glomerular filtrate. It is also the only site of reabsorption for glucose and amino acids (via sodium symporters), and
secretion of some drugs occurs at the distal end. NB: the answer may include reabsorption of potassium, urea and phosphate
(under the influence of parathyroid hormone). Must mention volume reduction, glucose and anion reabsorption and sodium
symporters.
b) The descending limb of the loop of Henle is highly permeable to water, and this segment produces concentrated tubular
fluid (up to 1400mOsmol) thanks to the high concentration of urea and sodium in the medullary interstitium. NB: answer may
include that water is transported across the epithelium via AQP1. Must include mention of concentrated tubular fluid and the
effect of the high-osmolarity medullary interstitium.
c) The thick ascending limb of the loop of Henle is impermeable to water, and undertakes active reabsorption of sodium,
potassium and chloride via the Na/K/Cl symporter. The thin ascending limb has similar properties to the descending limb of
the loop of Henle.
d) The distal convoluted tubule undertakes active uptake of solutes, via the Na/Cl cotransporter and the Na/Ca antiporter on
the apical surface, diluting the tubular fluid under the influence of aldosterone. This segment also regulates plasma pH by
controlling the degree of bicarbonate reuptake and proton secretion into the fluid and is sensitive to vasopressin insertion of
aquaporins for water reabsorption.
e) The primary function of the collecting duct is to react to the presence or absence of vasopressin by inserting or removing
aquaporins (AQP2) to promote or restrict water reabsorption down the concentration gradient created by urea reabsorption
from the loop of Henle.
ii) Frusemide acts on the Na/K/Cl symporter (1/2 mk) in the ascending limb of the loop of Henle (1/2 mk), which when inhibited
prevents the reabsorption of these solutes (1/2 mk). Thiazides act upon the Na/Cl symporter (1/2 mk) in the distal convoluted
tubule (1/2 mk), which plays a smaller role in the reuptake of solutes, and hence has a less- pronounced diuretic effect. (1/2
mk)
ii) Aldosterone acts to increase the secretion of potassium into the tubular fluid; therefore spironalactone (1 mark) as an
aldosterone-antagonist (1/2 mk) increases potassium reabsorption and reduces its secretion (1/2 mk). This would be an
appropriate treatment for a hypokalemic patient.
Renal – Nephron
Mr. Wayne, 52, is brought into the emergency department by his wife. Upon examination, Mr. Wayne is
breathing rapidly. He has also been experiencing increased thirst, and has been urinating very frequently.
Further history taken reveals that Mr. Wayne has insulin-dependent diabetes, and has not been taking his
insulin shots for a few days due to his hectic work schedule, but he figured ‘It was OK every now and then’.
A blood test shows the following serum values:
Na = 156 (135-145)
K = 6.0 (3.5-5)
PCO2 = 17 (40-60)
Cl = 118 (95-105)
HCO3 = 6 (22-26)
Blood pH = 7.0 (7.35-7.45)
A urine dipstick test afterwards shows a positive sign for ketone bodies and glucose.
1) What acid-base disorder is Mr. Wayne presenting with? (1 mark)
A) Respiratory Acidosis
B) Metabolic Acidosis
C) Respiratory Alkalosis
D) Metabolic Alkalosis
2) Calculate the Anion Gap for Mr. Wayne and comment on your result. What is the cause of Mr. Wayne’s
anion gap? (Note: The normal range is between 9 and 16) (3 marks)
3) Which of the following does NOT exert an appreciable effect on the osmosis of water? (1 mark)
a) Sodium
b) Urea
c) Glucose
d) Mannitol
4) Briefly explain the process by which insulin-dependent diabetes mellitus leads to glucosuria, and how
this leads to fluid loss in the diabetic patient. (4 marks)
Renal – Diabetes
1) B (1 mark)
2) AG = 156 – (6 + 118) = 32; high, in accordance with the metabolic acidosis (2
marks)
Caused by diabetic ketoacidosis (1 mark)
3) B (1 mark)
4) -> Low levels of insulin leads to hyperglycaemia due to impaired uptake of
glucose in the body -> Increased levels of glucose are filtered by the glomerulus,
and glucose transporters in the proximal tubules reach saturation as a result ->
Glucose remains in the lumen and, as an effective osmole, glucose creates an
osmotic pull on fluid preventing it from being reabsorbed -> As a result, the excess
glucose and fluid held from the osmotic gradient glucose has created are moved
onwards to excretion, resulting in glucosuria and excess fluid being excreted from
the body
(4 marks)
Renal – Diabetes
Conn’s syndrome is an endocrine disorder
brought about by a tumour of the adrenal
cortex that secretes excessive aldosterone in
uncontrolled fashion. Given what you know
about the functions of aldosterone, describe
what would be the most prominent features of
this condition (3 marks)
Renal – Conn’s Syndrome
Hypokalemia/below-normal K+ levels in the blood (0.5 marks) due
to excessive K+ secretion from the kidneys(0.5 marks)
Metabolic alkalosis (increased pH) (0.5 mks) Due to K+ depletion
(0.5 mk)
Hypertension/elevated blood pressure (0.5 marks) due to excessive
sodium and water retention (0.5 marks)
MILD hypernatremia/elevated Na+ levels in the blood (0.5 marks)
due to excessive Na+ reabsorption (0.5 marks)
Any three from four answers for 3 marks
Renal – Conn’s Syndrome
Name one type of condition that thiazides used
to treat (1 marks). How does their action bring
about a change in potassium levels in the
patient's body (4 marks), and what does this
effect have on glucose levels (3 marks)?
Renal – Thiazides
Thiazide diuretics are often used to treat hypertension, oedema, and/or congestive heart
failure (1 mark).
They inhibit the action of Na-Cl symporters in the early distal tubules (1 mark). This leads to
an increased Na+ and Cl- excretion (1 mark). Increased Na+ excretion leads to increased K+
excretion and possibly hypokalemia (1 mark) because the increased distal tubular sodium
concentration stimulates the aldosterone-sensitive sodium pump to exchange more sodium
for potassium (1 mark).
Low potassium levels may result in hyperglycemia (2 marks). This is thought to occur
because decreased potassium intake into beta cells in the pancreas prevents depolarization
of the membrane and the resulting calcium influx which reduces the amount of insulin
released (1 mark).
Renal – Thiazides
Suzy, a 49 year old mother of three, has severe adrenal insufficiency
due to Addison’s disease. She has presented to the emergency
department after collapsing, which was later found to be due to a
hypotensive episode. At the emergency department her blood
pressure was recorded as 90/60mmHg. Blood tests showed
hyperkalaemia and hyponatraemia.
Fully explain this presentation, with reference to the effect of adrenal
steroids on kidney function and blood pressure. (6 marks)
Renal – Hypotensive
Aldosterone secreted from adrenal gland (1/2)
Aldosterone upregulates apical ENaC and basal Na/K ATPase to
increase Na+ reabsorption (1)
With consequent loss of K+ down its electrochemical gradient into
the tubule (1)
Water reabsorption follows Na+ reabsorption by osmosis (1/2)
Adrenal insufficiency reduces plasma aldosterone concentration (3
marks for all 3 points below)
a. Reduced Na+ reabsorption -> hyponatremia
b. Reduced water reabsorption -> hypotension -> collapse
c. Decreased K+ loss -> hyperkalemia
Renal – Hypotensive
Describe the consequences of a T-cell receptor (TCR) deficiency in a
patient with the blood serum results below and explain how the
replacement of haematopoietic tissue would benefit this patient.
(6 marks)
CD4 = 0
CD8 = 0
B = 0.5
CD3 = .43
NK = .8
(2.6 – 3.5 x 109)
(.11 – .96 x 109)
(.02 – .43 x 109)
(3.4 – 9.6 x 109)
(.07 – .53 x 109)
I, I D & D – T-Cell Receptor
In this patient, B cell levels are elevated, while CD3+ (immature T lymphocyte) levels are decreased and mature T lymphocyte
(CD4+ and CD8+) levels are absent. This indicates that while immature T- lymphocytes are being produced in the bone
marrow, during the positive selection process in the thymus, all maturing T cells will be eliminated through apoptosis because
their receptors will not be capable of recognizing antigen presented by self-MHC molecules. The absence of mature T cells in
the patient has significant ramifications for the patient’s ability to defend itself against immune challenges.
Firstly, the absence of cytotoxic T cells (CD8+ cells) impairs the immune system’s ability to induce apoptosis in cells infected
with viruses or other pathogens, tumour cells or cells that are otherwise damaged or dysfunctional. In addition, memory T
cells are not produced and so immunological memory of intracellular pathogens is not present in this patient. Furthermore,
while B lymphocytes levels are elevated, the deficiency of T cells means T-cell dependent B cell activation (by Th2 cells) and
subsequent antibody production will not occur, impacting on humoral immunity and immunological memory, which will
particularly have a detrimental effect in terms of extracellular pathogens such as bacteria. While thymus, independent
antigens such as certain bacterial polysaccharides, including lipopolysaccharide, will not be affected by this, the majority of
antigens presented with MHC-II require co-stimulation by Th2 cells. Thus, the production of memory B cells will not occur and
the immune system will not be able to recognise extracellular pathogens encountered previously.
In addition, the absence of helper T cell function will significantly impair antibody class switching. As the immune system’s
ability to improve the affinity of their antibodies to antigens encountered is greatly hindered, they are unable to produce B
cells that can produce antibody classes such as IgG and IgA
Clearly, the overall impact of this patient’s defective TCR receptor on the integrity of the immune system is massive, and as a
result, this patient will be vulnerable to a range of pathogens, including bacteria, viruses, helminths and protozoa, including
opportunistic pathogens, as well as tumour cells. Without adequate intervention, death due to an infection is likely to occur
within months to a couple of years.
Since the cause of the patient’s T cell deficiency is due to a mutation in the TCR, haematopoetic stem cell replacement is the
only known cure. A bone marrow transplant involves giving the patient high doses of chemotherapy and/or radiation to
eliminate the underlying haematopoetic tissue, resulting in a loss of immune function and enabling a new immune system to
develop from the new haematopoietic stem cells. The stem cells are received via a central venous catheter and from the
bloodstream and the cells make their way to the bone marrow where they become functional and produce immature T and B
cells. It may take months to years for the immune system to mature and provide an adequate level of protection from
numerous infectious processes.
Ultimately, however, if the stem cells take, the immature T lymphocytes produced by the transplanted stem cells will travel to
the thymus , and with a functional T-cell receptor, mature T lymphocytes will be produced through the processes of positive
and negative selection. Consequently, this will enable the cell-mediated branch of the immune system to function through
mature CD8+ cells, the helper T lymphocytes produced will be able to stimulate B cells to mature to antibody- secreting
plasma cells and both memory T and B cells will be able to be produced, enabling the immune system to defend against both
intra- and extracellular pathogens and recognise antigens previously encountered.
I, I D & D – T-Cell Receptor
Cletus is 22 years old. He has come to see you because he has a cold
and wants antibiotics to relieve his cold-like symptoms. You suspect
that the causative agent of his symptoms is either a rhinovirus or
coronavirus.
a) List the stages of the general lifecycle of a virus? (1 mark)
b) Fill in the chart below to describe the main mechanisms that help the
body defend against viral infections. Include an example from the
innate immune response and an example from the adaptive immune
response (4 marks).
Main Effector
Mechanism
Innate
Adaptive
I, I D & D – Head Cold – Card 1 of 3
a) Attachment to host cell -> Penetration (will also accept Adsorption or Entry) -> Uncoating > Transcription of viral genes and translation of viral proteins (may come after Replication
step) -> Replication of viral nucleic acid (may come before Transcription/Translation step) ->
Assembly (will also accept Maturation) of viral particle -> Release from host cell
At minimum, must have: Attachment (or Adsorption or Entry) -> Penetration -> Uncoating ->
Transcription and Translation -> Replication -> Assembly (or Maturation) -> Release
Main Effector
Mechanism
Innate
NK Cells (0.5 marks)
NK cells activated by interferon from infected cells or IL-12 from
macrophages -> killing of virus-infected cells induced via activation
signals and lack of inhibitory signals -> release of perforin and
granzyme -> apoptosis of infected cell (1.5 marks)
At minimum must have: activation by cytokines -> activation signals
and lack of inhibitory signals will induce killing -> release of perforin and
granzyme -> host cell apoptosis
One missing or incorrect step will get 1 mk. More than two missing or
incorrect steps will get 0 marks.
Adaptive
Cytotoxic T Cells (0.5 marks)
CTLs activated by APC -> stimulates release of IL-2 causing self
proliferation -> recognition of MHCI bound antigen and costimulation by
CTL Fas ligand binding induces cell killing -> release of perforin and
granzyme cause apoptosis of infected cell (1.5 marks)
At minimum must have: activated by APC -> proliferation ->
recognition of MHCI:antigen complex on infected cells -> release of
perforin and granzyme from CTL -> apoptosis of infected cells
One missing or incorrect step will get 1 mark. More than two missing or
incorrect steps will get 0 marks
I, I D & D – Head Cold – Card 1 of 3
More for answer B on the back.
I, I D & D – Head Cold – Card 2 of 3
Other possible answers for B, for full marks:
Innate
IFN- / (0.5 marks): produced by virally infected cells in response to viral structures (eg.
dsRNA) -> act on self and nearby cells -> increase resistance of viral infection by
degrading mRNA and inhibiting viral protein translation (1.5 marks)
Innate
Antibodies (0.5 marks): produced by activated B plasma cells -> bind viral surface antigen
of extracellular virus causing neutralization -> prevents release of nucleic acid into host
cell (1.5 marks)
Answers that will only get (0.5/1.0 marks):
Innate
Macrophages: important for phagocytosing virus and activating other immune cells (but
not virus-specific)
Adaptive
Th1 cells: mostly for activating macrophages to defend against intracellular bacterial
infections
Innate/Adaptive
Antibody-dependent cell-mediated cytotoxicity: activation of NK cells via binding of Fc
receptor of IgG antibodies; since this is an infection of the upper respiratory tract, the main
active immunoglobulin will be IgA.
I, I D & D – Head Cold – Card 2 of 3
c) What are the main antibodies involved in (i) a primary immune
response against a cold virus and (ii) a secondary immune response
(1 marks).
d) What would you say to Cletus about prescribing antibiotics for a
cold? Explain your clinical reasoning, citing 2 classes of antibiotics
and their targets within the bacterial cell. (3 marks)
I, I D & D – Head Cold – Card 3 of 3
c)
(i) IgM (ii) IgA (0.5 marks for each correct answer)
d) Must include:
• the majority of colds are caused by viruses (0.5 marks)
• viruses have a different structure than bacteria and thus antibiotics are not
effective (0.5 marks)
• antivirals are not used to treat the common cold (not necessary to mention to
get full marks)
• colds generally resolve on their own (not necessary to mention to get full marks)
Any 2 of the following answers would be accepted for 1 mark each:
-Lactams
Pencillins - cell wall synthesis
Cephalosporins – cell wall synthesis
Carbapenems – cell wall synthesis
Glycopeptides – peptidoglycan or cell wall synthesis
Polymyxins – cell membrane
Sulfonamides – enzyme function
Quinolones - DNA replication (or Enzyme function)
Aminoglycosides – protein synthesis
Tetracyclines – protein synthesis
Macrolides – protein synthesis
Carbacephem – cell division
No need to be more specific, but if correct full marks should be rewarded.
I, I D & D – Head Cold – Card 3 of 3
You are an overworked fourth year medical student who is doing an elective placement in the
Emergency Department at a hospital in Thailand. A male Thai patient in his mid thirties
presents with malaise and abdominal discomfort and on physical examination you noted
scleral icterus as one of your findings. You suspect patient to be suffering from Hepatitis B so
you take blood to run liver function tests and for virology.
a) Name three additional signs and symptoms that
would support your hypothesis. (3 marks) (1 each)
b) You receive the results for the liver function tests
and virology, however you suspect there may have
been an error in the testing.
List a key feature of the test results that indicate an
error may have occurred and explain in terms of
physiology why you think so. (3 marks)
c) Once the patient was diagnosed Hepatitis B, what
precautions would you advise the patient to reduce
chances of transmission of the disease? (2) (1 each)
I, I D & D – Hepatitis B
a) Name three additional signs and symptoms that would support your hypothesis.
(3 marks) (1 each)
Nausea, vomiting, anorexia, mild fever, dark urine, hepatomegaly, itching
b) List a key feature of the test results that indicate an error may have occurred and
explain in terms of physiology why you think so. (3 marks)
Level of Bilirubin (conjugated) (1)
A patient suffering hepatitis would have increased levels of conjugated bilirubin
due to the inability of the hepatocytes to secrete conjugated bilirubin (1)
As a result, conjugated bilirubin would build up in the liver and leak back into
the circulation, hence increased levels of conjugated bilirubin (1)
c) Once the patient was diagnosed Hepatitis B, what precautions would you advise
the patient to reduce chances of transmission of the disease? (2) (1 each)
Safe sex Informing past sexual partners Avoidance of IV drug use Screening of
transfused blood Vaccine for family or close partners recommended
I, I D & D – Hepatitis B
Immunoglobulins produced by mature plasma cells have been classified into five isotypes IgG, IgM, IgD, IgE and IgA.
Complete the following table about immunoglobulins by filling in the blank cells (6 marks):
I, I D & D – Immunoglobulins
0.5 mark for each correct entry
for ‘structure’ and ‘serum
abundance’ boxes there is only
one correct answer for all other
boxes there is more than one
answer possible
• ‘distinguishing feature’: any
one of those listed above
are acceptable
• ‘location’: answer needs to
clearly illustrate that test
taker is aware of where that
immunoglobulin is primarily
found
• ‘primary function’: when
more than one function is
listed the first function
always needs to be listed for
a correct response
I, I D & D – Immunoglobulins
Create a table contrasting the differences between acute and chronic
inflammation taking into account:
1.
2.
3.
4.
Cell populations (one example)
Chemical Mediators (one example)
Causes (one example)
Outcome (one example)
I, I D & D – Inflammation
1 mark per cell (8 marks total):
Features
Chronic Inflammation
Acute Inflammation
Cell
Populations
1. Activated macrophages (from circulating monocytes)
2. Lymphocytes (both T and B cells)
3. Eosinophils (in some types of chronic
Inflammation)
4. Mast cells (in some types of chronic
inflammation)
1. Neutrophils
2. Macrophages
3. Mast cells
Chemical
Mediators
IFN-gamma
Platelet-derived growth factor (PDGF)
Transforming growth factor-alpha TGF-alpha)
Fibroblast growth factor (FGF)
IL-1, TNFalpha
Clotting factor – Fibrin
Kinins
C3a, C5a
Histamine
Serotonin
Platelet- activating factor
Prostaglandins
Leukotrienes
Nitric oxide
Causes
Persistent Infection
Long term exposure to exogenous particles (carbon
dust, silica)
Atherosclerosis
Autoimmune disease (rheumatoid arthritis, SLE)
Infections
Physical or chemical damage
Foreign bodies (splinters, sutures, dirt)
Immune reactions (certain hypersensitivity
reactions)
Outcomes
Fibrosis
Tissue repair
Permanent tissue damage
Cancer, eg. gastric cancer from chronic gastritis
Resolution
Organization (Fibrosis)
Abscess Formation
Chronic inflammation – (if the injurious agent
persists then chronic inflammation will ensue)
I, I D & D – Inflammation
Gloria, an 83 year old female, presents at your practice in Keperra (a
suburb of Brisbane). She is complaining of increasing shortness of
breath and an increase work of breathing over the past 5-7 days.
Upon taking her history, you find that she has a productive cough with
green sputum. You suspect a bacterial pneumonia and send a
specimen away for culture and sensitivity (M/C/S); in the meantime you
prescribe doxycycline (a broad spectrum antibiotic) to prevent a
serious infection from developing.
1) You suspect that Gloria might have moderate dementia. List the 3
criteria for establishing competency. (1.5 marks)
2) Explain the mechanisms of the innate immune system in response to
the bacterial infection leading to fluid in the lungs. (3.5 marks)
3)Gloria comes back 3 days later with acute diarrhoea. Explain why
antibiotics can cause diarrhoea. (2 marks)
I, I D & D – Bacterial Pneumonia
Q1) They must be able to:
• Understand the nature and effects of decisions (1⁄2 mark)
• Freely and voluntarily make decisions (1⁄2 mark)
• Communicate the decisions in some way (1⁄2 mark)
Q2)
Acute inflammation is the reaction of living vascularised tissue to infection. (1⁄2
mark) It is a protective physiological response to tissue injury which aims to
destroy, dilute or wall off the injurious agent and initiate repair. (1 mark) Following
the initial tissue damage an increase in vascular calibre (blood flow) occurs. This is
to increase the number of leukocytes which reach the damaged site and results in
the signs of redness and heat. (1⁄2 mark) Rapidly following this increased vascular
permeability occurs. This allows for the migration of the leukocytes from the blood
vessels out into the damaged tissue. This causes swelling. (1⁄2 mark) The main
leukocytes that are involved in the innate immune response are Neutrophils and
Natural killer cells. (1⁄2 mark) The fluid in Gloria’s lungs is mainly caused by the
migration of fluid into the lung tissue when vascular permeability occurs. As the
leukocytes migrate into the lung tissue, so will blood plasma. This fluid would also
contain puss as the Neutrophils begin to die off. (1 mark)
Q3)
Antibiotics can kill off the normal flora in the gut. (1 mark) The result of this is an
imbalance of fluid, nutrients and electrolytes in the gastrointestinal system.
Consequently this leads to diarrhoea. (1 mark)
I, I D & D – Bacterial Pneumonia
(a) What are the cells labelled A? (0.5 marks)
(b) This cell produces a glycoprotein that is
required for the absorption of a particular
substance in the ileum. Name the
glycoprotein, and name the substance whose
absorption is enabled by the glycoprotein. (1
mark)
(c) Failure of absorption of the substance in
(b) causes anaemia. What change (if any)
would be observed in the mean red blood cell
volume? (0.5 marks) Why does failure of
absorption of the substance in (b) cause
anaemia? (1 mark)
(d) Iron deficiency also causes anaemia.
What change (if any) would be observed in
the mean red blood cell volume? (0.5 marks)
Infection by a particular microorganism is the
most common cause of iron deficiency. What
is this microorganism? (0.5 marks) How does
it cause iron deficiency? (0.5 marks) List 3
other causes of iron deficiency. (1.5 marks)
Gastrointestinal – Stomach
(a) Parietal cell (0.5 marks)
(b) The glycoprotein is intrinsic factor. (0.5 marks) It enables the absorption of
vitamin B12. (0.5 marks)
(c) The mean red blood cell volume will increase. (0.5 marks) Malabsorption of
vitamin B12 causes deficiency of vitamin B12. Vitamin B12 is required for the
conversion of dietary folate to an active form which is involved in DNA synthesis.
Thus, vitamin B12 deficiency causes defective DNA synthesis and delayed nuclear
maturation of erythroblasts, causing megaloblastic macrocytic anaemia. (1 mark)
(d) The mean red blood cell volume will decrease. (0.5 marks) The microorganism
that is the most common cause of iron deficiency is hookworm (0.5 marks). It
causes iron deficiency by causing blood loss from the GI tract (0.5 marks). Other
causes of iron deficiency include (0.5 marks for each; maximum of 1.5 marks)
Rapid growth in infancy or adolescence Pregnancy Erythropoietin therapy
Chronic blood loss Menses Acute blood loss Blood donation Phlebotomy
as treatment for polycythemia vera Inadequate diet Malabsorption from disease
(sprue, Crohn’s disease) Malabsorption from surgery (post-gastrectomy) Acute
or chronic inflammation
Gastrointestinal – Stomach
Ruben is a 20 year old male. He was recently diagnosed with Crigler-Najjar
syndrome 10 years ago. Crigler-Najjar syndrome is a complete UDP glucuronyltransferase deficiency.
Ruben’s 22 year old wife, Billie has cholestasis. Compare and contrast Billie and
Ruben’s conditions.
Gastrointestinal – Crigler-Najjar Syndrome
0.5 marks for each correct answer.
Gastrointestinal – Crigler-Najjar Syndrome
Joseph K., a 52-year-old male, presents to the emergency department with
severe epigastric pain. He says it is relieved somewhat by food and
aggravated by hunger. Endoscopy reveals a peptic ulcer located in the
antrum of the stomach. Further testing reveals the ulcer to be positive for
Helicobacter pylori. Joseph K. has no allergies.
a) Describe the treatment protocol that is the standard first line therapy for
this type of case. Include in your answer a brief mechanism of action of any
drugs mentioned. (3 marks)
b) The enzyme urease is an important virulence factor of H. pylori. Predict
what would happen to H. pylori lacking urease in a human stomach and
explain why you predicted this. (1 marks)
c) H. pylori has been known to cause parietal cell destruction by promoting
autoimmunity and/or chronic gastritis. Explain how this might lead to
pernicious anaemia. (3 marks)
Gastrointestinal – Epigastric Pain
a) The standard treatment is a triple therapy.
____prazole (e.g. omeprazole, pentoprazole) OR proton pump inhibitor (PPI) (0.5 marks). Just PPI is not acceptable.
MOA: PPI irreversibly (covalently) binds to and inhibits the H+/K+ exchanger* (0.5 marks)
*Anti-porter is also acceptable, transporter not acceptable.
Amoxicillin (0.5 marks) Not acceptable: Penicillin, beta-lactam, penicillin derivative. These are not acceptable as the specific drug
needs to be recalled.
MOA: Amoxicillin has a complex MOA, the following answers are acceptable: (0.5 marks)
Inhibits synthesis of the peptidoglycan layer of the cell wall
Amoxicillin binds to transpeptidases OR penicillin-binding proteins and inhibits the crosslinking (transpeptidation) of the
peptidoglycan layer Although it is not necessary to obtain full marks, the student may say these actions could inhibit growth
(bacteriostatic) OR could lead to autolysis (bacteriocydal). Both statements are correct but not detailed enough by themselves to obtain
marks.
Clarithromycin OR clarythromycin (0.5 marks). Not acceptable: macrolide, erythromycin – the specific drug needs to be recalled.
MOA: Binds to 50S subunit of bacterial ribosome and halts/inhibits protein synthesis by effect on translocation (0.5 marks)
Other drug that might be mentioned: metronidazole (binds to DNA to cause strand breakage OR inhibits nucleic acid synthesis) which
can replace either the amoxicillin or the clarithromycin in patients who cannot tolerate these drugs.
Other treatments that might be mentioned: bismuth chelate or sulcrufate. No penalty for mentioning these, but full marks can only be
attained by mentioning the three drugs listed above.
b) Student must mention:
The bacteria would not survive in the acidic environment of the stomach (0.5 marks) Because: (needs one of the following answers)
Urease is needed to break down urea into ammonia (0.5 marks)
Ammonia is a base that will neutralize the acid (0.5 marks) in the local environment surrounding each bacterium. Ammonia becomes
ammonium which is a weaker acid than hydrochloric acid
c) Student can mention:
Parietal cells synthesise/release intrinsic factor (0.5 marks) Intrinsic factor prevents the degradation of vitamin B12 (OR
cobalamin) in the acidic environment of the stomach (0.5 marks) by binding to and protecting B12. (0.5 marks) Without intrinsic
factor, B12 absorption is highly impeded (0.5 marks) B12 is needed for DNA synthesis (0.5 marks), therefore without B12,
haematopoiesis
will be limited and red blood cell (RBC) production slowed (0.5 marks) B12 is needed for folate regeneration, therefore lack of B12
limits RBC production (0.5 marks) Low RBC production leads to anaemia (0.5 marks)
Gastrointestinal – Epigastric Pain
John, a 30 year old patient, arrives at your clinic with symptoms of abdominal pain and
yellowing of the sclera. You suspect he has jaundice.
(a) Fill in the following table on what you would expect to be the key signs of pre- hepatic,
hepatic and post-hepatic jaundice. (2.5 marks - 1/2 mark for each correct answer).
Gastrointestinal – Jaundice – Card 1 of 2
Gastrointestinal – Jaundice – Card 1 of 2
(b) You run a series of serology test and find the following results: AST:
600IU (0-35)
ALT: 400IU (0-40) Alkaline phosphathase: 180 (35-100) Gamma GT: 200 (050) Conjugated Bilirubin: 65umol/L (<7)
Given the above results explain what these markers indicate, what type of
jaundice (Pre-Hepatic, Hepatic, Post Hepatic) the results suggest, and
provide a likely mechanism for this problem. (4 marks)
(c) You also discover John has recently returned from a trip to India, where
he was assisting with volunteering efforts in underprivileged areas. You
note that these areas may be subject to poor hygiene and lack of water
management and this may link back to an exposure to Hepatitis A.
Comment on the mode of transmission, distribution of, and intervention
strategies for Hepatitis A. You note that Hepatitis A is a notifiable disease in
Queensland, why is this and should you be concerned that John could
become a carrier. (2.5 marks – 1/2 mark for each correct answer).
Gastrointestinal – Jaundice – Card 2 of 2
b)
AST and ALT are sensitive markers of liver damage or injury (0.5 mk), Gamma GT and
Alkaline Phosphatase are markers of intra-hepatic or post-hepatic obstruction (0.5 mk),
and conjugated bilirubin is a marker of a liver outflow problem. (0.5 mk)
Thus, the increased levels of AST and ALT indicate there is hepatocyte damage, the
increased levels of Alkaline phosphatase and Gamma GT indicate that there is an intrahepatic or post-hepatic obstruction, and the increased levels of conjugated bilirubin
indicates that there is a outflow problem, either intra-hepatic or post-hepatic. Hence, it is
likely this patient has an intra-hepatic problem. (1 mark)
The likely mechanism is that there is hepatocyte damage, causing inflammation (0.5 mk)
and leading to obstruction of the bile canniculi (0.5 mk). This results in a backflow of
conjugated bilirubin, leading to an increased presence in the blood and the clinical signs of
jaundice. (1 mark)
c)
• Mode of transmission = Faecal Oral (0.5 mk)
• Worldwide distribution, but more prevalent in less developed areas (0.5 mk)
• Intervention strategies: vaccination, good hygiene (0.5 mk for one answer)
• Infectious during incubation period (0.5 mk) however will not become a carrier
since there is no chronic state (0.5 mk)
Gastrointestinal – Jaundice – Card 2 of 2
Susan Z, a 15 year old patient with Down syndrome, comes into your
practice with her parents. Her parents have requested your assistance
for a referral for her to be sterilised. However, Susan is reluctant to
comply.
a) Name the type of competence associated with a minor approaching
the age of 18. [1 mark]
b) How would Susan Z demonstrate her competence to the doctor? [5
marks]
c) Describe the processes involved for involuntary admission. [4 marks]
Gastrointestinal – Ethics – Sterilisation
a) Gillick competence [1 mark]
b) Any five (5) of the following six (6) are applicable.
• Be able to recall, retain and receive information
• Integrate information into value system
• Evaluate risks and benefits
• Select a treatment option, giving reasons
• Communicate a decision giving reasons
• Persevere with their decision
c) Any adult can request an admission for a person who reasonably believes that the person’s
illness is of a nature or to an extent that involuntary assessment is necessary [1 mark]
A doctor or authorised medical health practitioner appointed by the Director of Mental Health
(includes nurses or allied health professionals) who have seen the patient within the last 3 days can
recommend the person for involuntary assessment [1 mark]
Once a request or recommendation is made, a health practitioner or an ambulance officer is
authorised to take the person for hospitalisation with police assistance if necessary [1 mark]
The person can be detained for up to 72 hours by a doctor to determine if involuntary treatment is
necessary. Some states require a tribunal to determine if forced hospitalisation would be deemed
necessary. [1 mark]
Gastrointestinal – Ethics – Sterilisation
Geon and Simon were at the bar having a drink at the
Crocodile Dundee in Brisbane. They see a taxi run a red
light and hit Kwai. As first year interns, Simon and Geon
wonder if they have any duty of care towards Kwai.
1) List the considerations that would be taken into account
in determining if Simon and Geon had a legal duty of care
to Kwai. (2 marks)
2) List six (6) duties which doctors have to their patients?
(3 marks)
Gastrointestinal – Ethics – Duty of Care
Part 1 (1.5 marks)
1. They were aware of a risk to Kwai’s health – forseeability of risk (0.5)
2. This risk was not insignificant (0.5)
3. A reasonable person in these circumstances would have acted, and
this would be determined by the probability and likely seriousness of the
harm, the burden involved in providing care, including the fact that Simon
and Geon are interns with medical skills, and the fact that providing care
is socially useful. (1)
Part 2 (3 marks; 0.5 mark each)
1. Duty to diagnose
2. Duty to treat
3. Duty of confidentiality
4. Duty to disclose information to patient
5. Duty to follow up
6. Duty to disclose medical error
Gastrointestinal – Ethics – Duty of Care
1) Jane wishes to obtain birth control from her GP. Describe the elements
of informed consent which must be satisfied? (4 marks)
2) What elements of competence must be satisfied? (3 marks)
3) Jane is a minor; what impact does this have on the concept of
competence? (2 marks)
4) If Jane is a minor and Jane’s parents ask what you talked about in the
visit, what are your obligations? (They are present in the waiting room)
(3.5 marks)
Gastrointestinal – Ethics – Informed Consent
Q1.
1) VOLUNTARINESS - Decision must be made voluntarily and without coercion
2) COMPETENCE - Patient has information, weighs their options, and makes an informed decision
3) INFORMATION DISCLOSURE - Enough information must be given to the patient to make their decision
4) COMPREHENSION - Satisfy that patient appreciates and understands the information given to them
0.5 mark per key term of element mentioned
Add 0.5 mark each if key term is reasonably defined
Q2.
1.
comprehend nature of situation (eg Rx)
2.
evaluate / weigh up risks and benefits in light of values
3.
choose / select an option
4.
communicate their choice to others
5.
act upon choice
6.
account for / persevere with / stick with choice
0.5 marks for each element mentioned (more than one possible synonym)
Q3.
A physician may determine that a minor is mature enough to understand the nature and associated risks of an intervention, therefore
establishing Gillick competence. If such competence is established, parental consent to the intervention is not necessary. If the minor is
deemed not competent, parental consent is required.
0.5 mark: Physician judges minor as competent
0.5 mark: Term “Gillick competence” cited
0.5 mark: Parental consent unnecessary with established competence, or else required.
0.5 mark: Logical, coherent answer.
Q4.
Mature minors/Minors mature enough to consent are medico-legally owed the same duty of confidentiality as adults. The law
recognises the rights of mature minors to make decisions about their medical treatment and to receive confidential health care;
however, the doctor must weigh up certain factors to assess maturity and ensure that confidentiality around such treatment wi ll be in
the young person’s best interests.
Evaluation of maturity must take into account characteristics of the young person, gravity of the proposed treatment, family factors, and
statutory restrictions.
1 mark: Pointing out that mature minors are medico-legally owed the same duty of confidentiality as adults.
1 mark: Explaining that the law recognises the rights of mature minors to make decisions.
1.5 mark: Emphasising the necessity of assessment/evaluation for maturity (1 mark), and mentioning one or more possible factors
which must be taken into account (0.5 marks).
Gastrointestinal – Ethics – Informed Consent
Robert, 31 years of age, is admitted to the emergency department in an unconscious state
following a motor vehicle accident (MVA). Paramedics had stabilised Robert, but his right
hand had been completely crushed in the accident. Physicians tell Robert's wife and
mother (who have arrived at the hospital) that they do not foresee any chance of recovery
of the hand and recommend amputation.
(a) Explain the hierarchy of decision-making in Queensland which is relevant to this
recommended procedure. (3 marks)
Robert's wife gives consent for the amputation. Shortly before surgery, Robert regains
consciousness and demands that the surgeons operate in order to keep his hand. The
surgeon fully explains the seriousness of the situation, the futility of attempting to save the
hand, and the risk of infection if the hand is not removed, together with other risks. Robert
is still adamant and the amputation is not completed, as he was deemed competent,
although no surgery was attempted
(b) What criteria would you use to establish that Robert is competent to make this
decision? (2 marks)
6 months later, Robert dies from an infection that spread from his shattered hand. His wife
is furious and wants to sue the hospital and physician for negligence.
(c) Does she have a valid claim? (1 mark) Why or why not? (2 marks)
Gastrointestinal – Ethics – MVA
a) The hierarchy of decision-making is a list of the individuals, groups or regulations
responsible for decisions involving consent to the treatment of a patient. From most power
to least power the hierarchy of decision-making is as follows:
Competent Patient Advance Health Directive Guardian (if appointed by a statutory
body such as the Guardianship Tribunal) Enduring Power of Attorney Statutory
Health Attorney (Spouse, Long-Term Unpaid Care Giver) which may include the Adult
Guardian
b) A patient is deemed competent through the ability to:
Recall and retain information pertaining to the decision Understand the procedure, its
risks and benefits, and the risks and benefits of not proceeding Consider these options
in the light of one’s own value system Select an option and communicate the decision in
some way Persevere with the decision made
c) No. Negligence is defined by four criteria, all of which must be applicable to the case in
question:
A Duty of Care must be established / owed to the patient A breach must occur in the
standard of care Damage must have occurred The damage must have been a direct
result of a breach in the standard of care.
In this case, the full risks of keeping the hand attached were disclosed. The patient’s
wishes were upheld against medical advice pertaining to the risk that eventuated, so the
damage that occurred was not caused by the failure to adequatelyGastrointestinal
advise. – Ethics – MVA