made available through the combined efforts of brady bouchard, brett burrett , cameron curtis,...

Made available through the combined efforts of

Brady Bouchard, Brett Burrett, Cameron Curtis,

Meg O’Connell, & Maximilian Stephens.

Respiratory – Flow-volume – Card 1 of 3

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)


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)


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)


c. In the table below is the arterial blood gas report which you ordered.

Parameter

Units Result Reference

PaO2 mmHg 50 80-100PaCO2 mmHg 30 36-44pH 7.5 7.35-7.45HCO3- mM 24 21-28PAO2 – 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)


c.i. PaCO2 is low (hypocapnia) so Jenny is

hyperventilating.(1 mark)

ii. Alveolar-arterial oxygen difference is elevated, suggesting VQ mismatch (perfusion of underventilated alveoli).(1 mark)

Respiratory – Respiratory Disease

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 – Acute Asthma

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 37FiO2 0.21

Bar Pressure

758

pH 7.46 7.35 – 7.45PaCO2 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 volume-time 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 – 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 Therapy

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 – Respiratory Failure

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

Definition(1 mark each)

Hypoxaemia without hypercapnia

Typically caused by a ventilation/perfusion (V/Q) mismatch

Hypercapnia (usually with hypoxaemia)

Underlying causes:•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

Blood Gases• PaO2• PaCO2• PAO2 – PaO2(1 mark each)

• Low (< 60 mmHg)• Normal/low (< 45 mmHg)• Increased

• Low• High (> 50 mmHg)• Decreased

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

•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 Pathology

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

MSK – Ulnar Claw

1a. 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 – Wrist Injury

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 nerveb. Foreign bodies/objectsc. Checking anatomical snuffbox for occult

scaphoid fractured. 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 – Osteoporosis

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 resorptionAge: 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 – Renal Osteodystrophy

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 – Hip Dislocation

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 joint2. Surrounding musculature, shape of

acetabulum/head of femur, fibrous capsule3. 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 – Shoulder Injury

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

Reproductive – Menstrual Cycle

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 – Down Syndrome – Card 1 of 2

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)


1a)46: Normal no. of chromosomes/46 chromosomesXY: Maleder(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


Down syndrome cont’d on back


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 – Pregnancy

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 (Lh-hCG 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 – Fertility

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 analysisFemale: mid-luteal progesterone or basal body temp. chart

Reproductive – Male Reproductive System

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

Cardiovascular – MI – Card 1 of 2

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. List three (3) physiological signs or symptoms of an MI (1.5 marks)2. 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)

3. 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)


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)

• 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

• Creatine kinase-MB isoenzyme (CK-MB)• 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 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 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


Answer to Question 3 on reverse.


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 – Atherosclerosis

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 TPRAtherosclerosis 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 – Dyspnoea

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).OR2) 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 – 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 Measures cardiac activity along the frontal plane.

2 Left leg

3 Left leg

aVF L1 leads Left leg

aVL L2 leads

aVR L3 leads

Lead Electrode Location Rationale for use

V1 4th intercostal space at the right sternal border

V2

V3 Midway between V2 and V4

V4 Measures cardiac electrical activity through the chest wall’s depth

V5 5th intercostal space in the anterior axillary line

V6 5th intercostal space in the mid-axillary line

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 Measures cardiac activity along the frontal plane.

2 Right arm Left leg

3 Left arm Left leg

aVF L1 leads Left leg Measures cardiac electrical activity along the frontal plane

aVL L2 leads Left arm

aVR L3 leads Right arm

Lead Electrode Location Rationale for use

V1 4th intercostal space at the right sternal border

Measures cardiac electrical activity along a horizontal plane across the chest

V2 4th intercostal space at the left sternal border

V3 Midway between V2 and V4

V4 5th intercostal space in midclavicular line

Measures cardiac electrical activity through the chest wall’s depth

V5 5th intercostal space in the anterior axillary line

V6 5th intercostal space in the mid-axillary line

Cardiovascular – ECG Trace

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)

PBL 1 – Blood on the Road – Femoral Artery

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 incompensating 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 II2. Vasopressin (ADH)3. Noradrenaline4. Adrenaline5. 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 kidneys3. Noradrenaline/Adrenaline – increases peripheral vascular tone and inotropic effects and rate of contractility on the heart4. 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 solutions2. 2. cost3. 3. increase risk of oedema4. 4. increase risk of anaphylaxis

PBL 1 – Blood on the Road – Shock – Card 1 of 3

a) What is the physiological definition of shock? (1 mark)

b) Briefly list and define the stages of shock. (2 marks)


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 parametersCompensations 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.

Irreversible IV >40% Irreversible.Life-threatening. Volume replacement cannot restore patient to normal. Anuria.


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)


d) Outline, with the aid of a diagram if necessary, how the Renin-Angiotensin-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)


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 – Anaphylactic Shock

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

Population Health – Screening Diabetes

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 = 0.06Sensitivity = 0.73Specificity = 0.98

Positive predicted value= proportion of people with a positiveresult that are diseased= 44/62= 0.71 (71%)

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 conditionsKidney diseaseCancerInfectious diseasesEar and eye problems

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

Population Health – Hep. B Vaccination

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

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 – Health Determinants & Prevention

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)

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.

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

PART B)

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.

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 earlydetection 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

Renal – Hypertension

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 – Blood Pressure

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. PrazosinAngiotensin II receptor antagonists e.g. Candasartan, LosartanCalcium channel blockers e.g. Nifedipine, VerapamilDiuretics 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 – Nephron

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 tubuleb. Descending limb of the loop of Henlec. Ascending limb of the loop of Henled. Distal convoluted tubulee. 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 – Diabetes

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 AcidosisB) Metabolic AcidosisC) Respiratory AlkalosisD) 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) Sodiumb) Ureac) Glucosed) 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 – Conn’s Syndrome

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 – Thiazides

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 – Hypotensive

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 -> hyponatremiab. Reduced water reabsorption -> hypotension -> collapsec. Decreased K+ loss -> hyperkalemia

I, I D & D – T-Cell Receptor

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 (2.6 – 3.5 x 109)CD8 = 0 (.11 – .96 x 109)B = 0.5 (.02 – .43 x 109)CD3 = .43 (3.4 – 9.6 x 109)NK = .8 (.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 IgAClearly, 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 – Head Cold – Card 1 of 3

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


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 apoptosisOne 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 cellsOne missing or incorrect step will get 1 mark. More than two missing or incorrect steps will get 0 marks


More for answer B on the back.


Other possible answers for B, for full marks:

InnateIFN-/ (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)InnateAntibodies (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):InnateMacrophages: important for phagocytosing virus and activating other immune cells (but not virus-specific)AdaptiveTh1 cells: mostly for activating macrophages to defend against intracellular bacterial infectionsInnate/AdaptiveAntibody-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.


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)


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 synthesisCephalosporins – cell wall synthesisCarbapenems – cell wall synthesis

Glycopeptides – peptidoglycan or cell wall synthesisPolymyxins – cell membraneSulfonamides – enzyme functionQuinolones - DNA replication (or Enzyme function)Aminoglycosides – protein synthesisTetracyclines – protein synthesisMacrolides – protein synthesisCarbacephem – cell division

No need to be more specific, but if correct full marks should be rewarded.

I, I D & D – Hepatitis B

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 thatwould support your hypothesis. (3 marks) (1 each)

b) You receive the results for the liver function testsand virology, however you suspect there may havebeen an error in the testing.

List a key feature of the test results that indicate anerror may have occurred and explain in terms ofphysiology why you think so. (3 marks)

c) Once the patient was diagnosed Hepatitis B, whatprecautions would you advise the patient to reducechances 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 bilirubindue 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 intothe 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 – Immunoglobulins

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 – Inflammation

Create a table contrasting the differences between acute and chronic inflammation taking into account:

1. Cell populations (one example)2. Chemical Mediators (one example)3. Causes (one example)4. 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 chronicInflammation)4. Mast cells (in some types of chronicinflammation)

1. Neutrophils2. Macrophages3. Mast cells

Chemical Mediators

IFN-gammaPlatelet-derived growth factor (PDGF)Transforming growth factor-alpha TGF-alpha)Fibroblast growth factor (FGF)

IL-1, TNFalphaClotting factor – FibrinKininsC3a, C5aHistamineSerotoninPlatelet- activating factorProstaglandinsLeukotrienesNitric oxide

Causes Persistent InfectionLong term exposure to exogenous particles (carbon dust, silica)AtherosclerosisAutoimmune disease (rheumatoid arthritis, SLE)

InfectionsPhysical or chemical damage Foreign bodies (splinters, sutures, dirt)Immune reactions (certain hypersensitivity reactions)

Outcomes FibrosisTissue repairPermanent tissue damageCancer, eg. gastric cancer from chronic gastritis

ResolutionOrganization (Fibrosis)Abscess FormationChronic inflammation – (if the injurious agent persists then chronic inflammation will ensue)

I, I D & D – Bacterial Pneumonia

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)

Gastrointestinal – Stomach

(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 – Crigler-Najjar Syndrome

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 glucuronyl-transferase 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 – Epigastric Pain

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, haematopoiesiswill 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 – Jaundice – Card 1 of 2

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).


(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 (0-50) 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).


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 intra- hepatic 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 carriersince there is no chronic state (0.5 mk)

Gastrointestinal – Ethics – Sterilisation

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 – Duty of Care

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 diagnose2. Duty to treat3. Duty of confidentiality4. Duty to disclose information to patient5. Duty to follow up6. Duty to disclose medical error

Gastrointestinal – Ethics – Informed Consent

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 coercion2) COMPETENCE - Patient has information, weighs their options, and makes an informed decision3) INFORMATION DISCLOSURE - Enough information must be given to the patient to make their decision4) COMPREHENSION - Satisfy that patient appreciates and understands the information given to them0.5 mark per key term of element mentionedAdd 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 values3. choose / select an option4. communicate their choice to others5. act upon choice6. account for / persevere with / stick with choice0.5 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 competent0.5 mark: Term “Gillick competence” cited0.5 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 will 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 – MVA

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 adequately advise.

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