Made available through the combined efforts of Brady Bouchard, Brett Burrett , Cameron Curtis, Meg O’Connell, & M

2. Made available through the combined efforts of Brady Bouchard, Brett Burrett, Cameron Curtis, Meg O’Connell, & Maximilian Stephens.

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) Respiratory – Flow-volume – Card 1 of 3

4. Jenny is likely to have asthma.(0.5 marks) • decreased PEF • scooped out shape following PEF • unaffected inspiration (i.e normal PIF) • (0.5 marks for providing any two of the above reasons or other reasonable answers) Respiratory – Flow-volume – Card 1 of 3

5. b. Based on the flow-volume curve above, superimpose onto the normal vitalograph below, a curve that Jenny is highly likely to produce. Be sure to include key points such as FEV1, FVC and note if there is any change of the FEV1/FVC ratio.(1 mark) Respiratory – Flow-volume – Card 2 of 3

6. Respiratory – Flow-volume – Card 2 of 3

7. c. In the table below is the arterial blood gas report which you ordered. With respect to gas exchange in the lungs, what information can be deduced from: PaCO2(1 mark) PAO2– PaO2(1 mark) Respiratory – Flow-volume – Card 3 of 3

8. c. PaCO2 is low (hypocapnia) so Jenny is hyperventilating.(1 mark) Alveolar-arterial oxygen difference is elevated, suggesting VQ mismatch (perfusion of underventilated alveoli).(1 mark) Respiratory – Flow-volume – Card 3 of 3

9. 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

10. Student must mention four of the following (0.5 marks each): • Sputum • Haemoptysis • Dyspnoea • Cough • Wheeze • Chest pain • Fever • Hoarseness • Night sweats Respiratory – Respiratory Disease

11. 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. 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

12. (4 marks total) • James is hypocapnic(0.5 marks) • Due to hyperventilation resulting in CO2 being blown off. • James is hypoxic (0.5 marks) • Respiratory alkalosis with partial metabolic compensation (2 marks) • The kidney's are excreting more bicarbonate out of the body to release H+ and partially compensate the respiratory alkalosis by lowering pH. • However only partial compensation as the pH has not completely returned to within normal ranges yet. • There is a large Alveolar arterial oxygen difference (0.5 marks) • Due to a high amount of physiological shunting (0.5 marks) • b) Type I respiratory failure (1 mark) • c) (2 marks) Respiratory – Acute Asthma

13. 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”. Briefly explain the role of glucocorticoids in the treatment of asthma.(1 mark) 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

14. Glucocorticoids reduce airway inflammation (0.5 marks), and decrease airway hyper-responsiveness (0.5 marks). 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

15. 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”. What are the two main aims of asthma therapy delivered by “puffers”?(1 mark) Mungo is on Salbutamol and Fluticasone. What are their mechanisms of action?(5 marks) Respiratory – Asthma Therapy

16. Prevention (0.5 marks) and relief (0.5 marks) (5 marks total): Salbutamol is a B2 agonist (0.5 marks), which acts on the beta-2 adrenergic receptors of bronchioles (0.5 marks), causing bronchodilation(0.5 marks). This is used in circumstances of bronchoconstriction (0.5 marks), such as an acute asthma attack (0.5mk) (or excerbation of asthma). Fluticasone is a corticosteroid (0.5 marks) used for prevention (0.5 marks) of asthmatic attacks. Corticosteroids act to inhibit inflammation (0.5 marks) by a variety of mechanisms, including inhibition of COX expression, down-regulation of pro-inflammatory mediators such as interleukin-(IL)-1, 3, and 5 (or other acceptable alternate answer) (0.5 marks). Preventive medications must be taken regularly by people with asthma in order to prevent attacks (0.5 marks) Respiratory – Asthma Therapy

17. 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) Respiratory – Respiratory Failure

18. Respiratory – Respiratory Failure

19. 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. What is the most likely diagnosis (1 mark)? Explain the major pathophysiological effects of this condition (2 marks) 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) How do the flow volume loop on spirometry testing differ between obstructive and restrictive airway disease? (3 marks) Respiratory – Respiratory Pathology

20. 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). Low PaO2and 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 marks): Respiratory – Respiratory Pathology

21. 1 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) Explain what sort of appearance the hand/wrist might take on if the radial nerve had a distal lesion.(3 Marks) MSK – Ulnar Claw

22. 1. • a. • Distal lesion = finger flexors/extensors acting without medial two lumbricals • Medial two lumbricals have ulnar nerve innervation • Action of lumbricals is to extend IP joints but flex MCP joints. • Proximal lesion = also lose medial Flex. Dig. Prof. • Extension predominates and extends fingers (less “claw-like”) • 1. • b. • Appearance is wrist drop • Because radial nerve supplies all wrist extensors • Without extensors, gravity+flexors flex the wrist MSK – Ulnar Claw

23. 1. • Laceration causes parasthesia over central proximal palm between thenar/hypothenar – what nerve was lesioned?(1 Mark) • Upper limb injury involving alcohol/violence/lacerations. Other than fractures, what else should you see in X-ray?(0.5 Marks) • Wrist injury with lacerations. You suture lacerations without physical exam. What have you neglected?(1 Mark) • Why is this important? Likely Sequalae? • Describe 1 difficulty arising from assessing drunken patient in terms of wrist injury/parasthesia/history? MSK – Wrist Injury

24. 1. • Palmar cutaneous branch of the median nerve • Foreign bodies/objects • Checking anatomical snuffbox for occult scaphoid fracture • 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 • Consciousness/Pain/Range of Motion/Parasthesia MSK – Wrist Injury

25. 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. Based on her age/sex describe most likely mechanisms behind the osteoporosis (4 Marks) List 4 modifiable risk factors for osteoporosis (2 Marks) MSK – Osteoporosis

26. 1. 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. Excessive alcohol, smoking, calcium/vitamin D deficient diet, lack of exercise/sedentary lifestyle, poorly controlled diabetes mellitus, having small thin stature. MSK – Osteoporosis

27. 1. 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) What effect does renal failure have on vitamin D levels? List two (2) consequences of this effect.(2 Marks) 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

28. 1. • PTH is detected by osteoblasts. Osteoblasts then  RANLK:OPG ratio which increases osteoclast maturation/activity. osteoclast activity  bone resorption serum Ca2+  bone density • Renal failure  activated vitamin D. Secondary hyperparathyroidism, hypocalcaemia, hyperphosphataemia (due to the kidney failure, not PTH) • Bisphosphonates: apoptoseosteoclasts • Oestrogen replacement (HRT): decreases osteoclastic activity indirectly through osteoblasts or directly by  chemical mediators like IL-6 • Selective oestrogen receptor modulators: e.g. raloxifene (same as above) • Calcitriol/Vit. D: increased absorption of calcium and phsophates in gut and kidney • Calcitonin: inhibits osteoclasts • Intermittent rPTH (Teriparatide): activates osteoblasts>osteoclasts • Strontium ranelate:  bone formation via osteoblasts and  OPG which osteoclasts MSK – Renal Osteodystrophy

29. What type of joint is the hip joint? Provide both general and specific classification(2 Marks) What are the major anatomical features contributing to the stability of the hip joint?(3 Marks) List the normal movements of the hip joint(3 Marks) What important anatomical structures related to hip joint might be damaged by dislocation? List 4 (2 Marks) List 4 other signs or symptoms that are associated with dislocation of hip joint(2 Marks) MSK – Hip Dislocation

30. Ball and socket, synovial joint Surrounding musculature, shape of acetabulum/head of femur, fibrous capsule Flexion, extension, adduction, abduction, internal/medial rotation, external/lateral rotation Ligament of head of femur, bony rim of acetabulum, fibrous capsule, sciatic nerve, circumflex arteries Pain, pain exacerbated by movement, parasthesia, deformity, swelling, loss of function, altered gait, positive trendelenburg sign MSK – Hip Dislocation

31. 1. Name the rotator cuff muscles.(2 Marks) Describe one clinical test to assess the function or integrity of the glenohumeral joint, with reason for test.(2 Marks) What type of joint is the glenohumeraljont?(1 Mark) MSK – Shoulder Injury

32. 1a) Supraspinatus, infraspinatus, teres minor, subscapularis • 1b) • Apley’s scratch: patient instructed to scratch opposite shoulder anteriorly (adduction), behind neck (external rotation, adduction), behind back (internal rotation, adduction) • Hawkin’s Kennedy: flex arm and forearm 90° then internally rotate. Tests impingement of local structures e.g. nerve • Apprehension: arm abducted to 90° and externally rotated. Joint pushed anteriorly. Tests impending dislocation • Empty can/rotator cuff: abduct to 90° externally rotated-test abduction power. Repeat at 30° internally rotated. Tests supraspinatus tear. • Winged scapula: patient pushes with both hands arms length against wall. Tests serratus anterior. • 1c) Ball and socket, synovial joint MSK – Shoulder Injury

33. 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

34. 1a) • Menstrual • Proliferative • Secretory • 1b) • Follicle-stimulating hormone (FSH): Increased FSH levels stimulate several primordial follicles to develop into primary follicles and then into secondary follicles. • Luteinising Hormone (LH): Increased LH levels cause a rupture of the mature Graafian follicle and expulsion of a secondary oocyte. Reproductive – Menstrual Cycle

35. 1a) Interpret each element of the following karyotype: 46,XY, der(14;21)(q10;q10)mat,+21 (2 Marks) 1b) The above karyotype is an example of Robertsonian translocation. Name and briefly explain the other two mechanisms by which Down syndrome can occur. (2 Marks) 1c) List five (5) signs of Down syndrome that you may see on general observation. (2.5 Marks) 1d) List one (1) psycho-social implication of Down syndrome for the i) Child ii) Teenager iii) Adult (1.5 Marks) Reproductive – Down Syndrome – Card 1 of 2

36. 1a) 46: Normal no. of chromosomes/46 chromosomes XY: Male der(14;21)(q10;q10)mat: Breakage and reunion have occurred at band 14q10 and band 21q10 in the centromeric regions of maternal chromosomes 14 and 21 +21: gain of chromosome 21/trisomy 21/extra copy of 21 1b) 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 Mosaic: Mitotic nondisjunction of chromosome 21 in an early stage of embryogenesis Reproductive – Down Syndrome – Card 1 of 2

37. Down syndrome cont’d on back Reproductive – Down Syndrome – Card 2 of 2

38. 1c) simian crease (single palmar crease), flat facial profile, epicanthic folds, oblique eye fissures, macroglossia, large gap between 1st and 2nd toes, microgenia, Brushfield spots, small ears 1d) i) slow cognitive development/difficulties learning speech ii) social gap from peers, self discovery, social isolation iii) independent living, employment, death of carers/parents Reproductive – Down Syndrome – Card 2 of 2

39. 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

40. 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 – Pregnancy

41. 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

42. 1a) No, couple cannot be defined as infertile. Infertility is defined as 12 months of unsuccessful regular unprotected sexual intercourse. • 1b) Reduced or abnormal sperm count (from Klienfelter’s), ductus deferens obstruction (from scarring from infection) • 1c) Ovulatory disorder (extreme mental or physical stress  hypothalamus), tubal disease (from damage from previous ectopic pregnancy) • 1d) Male: semen analysis • Female: mid-luteal progesterone or basal body temp. chart Reproductive – Fertility

43. 1a) Describe 1 function of: • Testes: • Epididymis: • Seminal vesicle: • Prostate gland: • Bulbourethral gland: Reproductive – Male Reproductive System

44. 1a) • Testes: produce sperm/secrete testosterone • Epididymis: matures sperm/stores sperm • Seminal vesicle: supply fructose to sperm/secrete prostaglandins/provide precursors for semen clotting • Prostate gland: secrete alkaline fluid to neutralise vaginal acid/trigger clotting of semen via factors • Bulbourethral gland: secretes lubricating mucus Reproductive – Male Reproductive System

45. 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. • List three (3) physiological signs or symptoms of an MI (1.5 marks) • You order a serum serology test. What are two (2) biochemical markers you would request if you suspect an MI? Describe the limitations of each with respect to time. (3 marks) • In the emergency room, your intern prescribes five (5) drugs for the patient. You raise an eyebrow (up and slightly to the side for maximal ‘constructively critical but not derogatory’ effect), and tell your intern not to prescribe verapamil. • GTN (glyceryl tri-nitrite) • Aspirin • Morphine • Atenolol • Verapamil • a) Describe a fairly detailed mechanism of action for GTN and aspirin, and justify their use in the acute management of myocardial infarction (4 marks) • b) Explain, with reference to their mechanisms of action, why it is dangerous to prescribe β-blockers with Ca2+ channel blockers? (2 marks) Cardiovascular – MI – Card 1 of 2

46. 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 Cardiovascular – MI – Card 1 of 2

47. Answer to Question 3 on reverse. Cardiovascular – MI – Card 2 of 2

48. 3. a. (4 marks) • Glyceryltrinitrate (GTN): GTN is a peripheral vasodilator (1/2 mark) that is metabolised to provide an exogenous source of nitric oxide (NO) (1/2 mk). NO stimulates increased production of cGMP, leading to relaxation of vascular smooth muscle (1/2 mk). This reduces venous return and preload to the heart, reducing myocardial oxygen requirement (1/2 mk). • Aspirin: Low dose aspirin inhibits the cyclo-oxygenase enzyme (1/2 mk) and therefore irreversibly inhibits thromboxane A2 synthesis in platelets (1/2 mk) and prostacyclin synthesis in endothelium (1/2 mark), hence decreasing platelet aggregation and decreasing the risk of myocardial infarction (1/2 mk). • b. (1 mark) • 1⁄2 mark for mentioning AV node block • 1.5 marks for mentioning why: • - β-blockers reduce myocardial workload by preventing the noradrenaline- induced increases in force and rate of contraction, and common adverse effects include bradycardia and AV block. • - Calcium channel blockers block voltage-operated L-type Ca2+ channels, which decreases Ca2+ entry into the AV node, slowing AV node conduction, which decreases heart rate and the force of contraction. • - When used together, the cumulative effects of calcium entry blockers and β- adrenoceptor antagonists can cause complete AV block, so this combination must be used with caution. Adverse effects include bradycardia, AV block, hypotension, peripheral oedema, headaches and nausea. Cardiovascular – MI – Card 2 of 2

49. 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. • Calculate Joseph’s BMI. (1 mark) • 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

50. BMI = weight (kg) / height2(m) = 34.7 • (b) Obesity, hypertension, hypercholesterolemia, smoking, stress (work), sex (male), physical inactivity (0.5 marks each up to 1.5 marks total) • (c) Step 1: Chronic endothelial injury (eg. Hyperlipidemia, hypertension, smoking, toxins, hemodynamic factors, immune reactions, viruses) • Step 2: Endothelial dysfunction (eg. Increased permeability, leukocyte adhesion, monocyte adhesion and emigration) • Step 3: Smooth muscle emigration from media to intima, macrophage activation • Step 4: Fatty streak (Macrophages and smooth muscle cells engulf lipids = foam cells) • Step 5: Smooth muscle proliferation, collagen/ECM deposition, extracellular lipid (1 mark for each step) • (d) BP= CO x TPR • Atherosclerosis increases vascular wall thickness, resulting in a decreased lumen. This then increases the peripheral resistance(1/2) . This causes an increased afterload, resulting in an increased force of contraction required by the heart (1/2). Cardiovascular – Atherosclerosis