Case Protocols

Question 1

(CP3) A 52 year-old woman suddenly developed breathlessness the day after laparoscopic cholecystectomy. The patient, who was previously otherwise well, had a strong family history of ischaemic heart disease and smoked 20 cigarettes per day. Examination revealed an obese, distressed woman with obvious tachypnoea and a non-productive cough. Auscultation of her chest revealed decreased air entry at the right base.

Vitals: HR 122, BP 100/60, RR 30, temp 37.8, urinalysis NAD

1. What is your provisional diagnosis, and what is the differential diagnosis of acute respiratory distress in this woman?

Answer 1

Provisional diagnosis: PE
Differential diagnosis: 
•	Respiratory causes: pneumonia, atelectasis, pneumothorax, foreign body aspiration, ARDS, asthma
•	Cardiovascular causes: MI, APO
•	Other: panic attack

Question 2

(CP3) A 52 year-old woman suddenly developed breathlessness the day after laparoscopic cholecystectomy. The patient, who was previously otherwise well, had a strong family history of ischaemic heart disease and smoked 20 cigarettes per day. Examination revealed an obese, distressed woman with obvious tachypnoea and a non-productive cough. Auscultation of her chest revealed decreased air entry at the right base.

2. What factors predisposed her to this disease?

Answer 2

Stasis
•	Recent surgery and resulting bed rest – immobility
Changes to vessel wall
•	Smoking (endothelial dysfunction)
•	Atherosclerosis? (FHx of IHD)
Hypercoagulable state
•	Recent surgery – inflammation
•	Smoking
•	Obesity
•	Age

Question 3

3. (CP3: PE) What investigations would you perform to substantiate your diagnosis? Describe the ECG changes likely to be present in this case and explain why they occur.

Answer 3

• CTPA. If CTPA is relatively contraindicated, eg from renal impairment, contrast allergy, very young, would consider VQ scan instead.
• Others:
o Bloods: FBC, CRP, UECs, LFTs, coags. NOT D-dimer
o Bedside: ECG, lower limb Doppler US
o Imaging: CXR

ECG changes might include
• Tachycardia: the most common sign
• Signs of right heart strain – PEs can obstruct the pulmonary vasculature, causing pulmonary hypertension and right heart strain. On ECG, signs of right heart strain include:
o T wave inversion in the right praecordial leads and inferior leads
o Right axis deviation
o Dominant R wave in V1
o The classic ECG sign of PE: S1Q3T3

Question 4

4. (CP3: PE) CXR: area of opacification at the right base, together with a small right pleural effusion. What pathological process may have produced this appearance?

Answer 4

Opacification: pulmonary infarction. Embolus -> lodges distally and causes occlusion -> ischaemia -> infarction of area supplied by that artery, with endothelial damage resulting in haemorrhage -> irritation of the pleural by the haemorrhage, inflammation and infarction -> pleural effusion.

Question 5

5. (CP3: PE) ABGs: how would you interpret them and are they compatible with your diagnosis?
   pH 7.50, PaO2 61, PaCO2 30, bicarb 26, base excess -1, O2 sats 90%

Answer 5

Interpretation: hypoxaemia; decreased O2 saturation; respiratory alkalosis. They are compatible – PE caused bronchoconstriction -> V/Q mismatch -> hypoxaemia -> decreased Hb O2 saturation -> tachypnoea -> hypocapnia -> respiratory alkalosis.

Question 6

6. (CP3: PE with haemodynamic instability D1 post-lap chole) What drug therapy would you think most likely is needed? What are the principles of establishing therapy with this drug? How would you monitor this therapy?

Answer 6

Drug therapy:
Resus and supportive care: O2, ventilatory and haemodynamic support if required.
Treatment
• Consider thrombolysis (t-PA: alteplase) as massive PE has caused haemodynamic instability but avoid because she just had surgery.
• Anticoagulation:
o Short-term: heparin or LMWH. Monitor heparin with APTT, monitoring of clexane not required because dose-response relationship more reliable. For minimum of 6 days, until INR > 2 for 2 consecutive days.
o Long-term: warfarin with bridging clexane. Monitor with INR – give clexane for minimum of 6 days, and until INR > 2 for 2 consecutive days. Warfarin for 3 months – patient has VTE risk factors.
o Other options include NOACs eg dabigatran, rivaroxaban

Question 7

7. (CP3: PE

A 52 year-old woman suddenly developed breathlessness the day after laparoscopic cholecystectomy. The patient, who was previously otherwise well, had a strong family history of ischaemic heart disease and smoked 20 cigarettes per day. Examination revealed an obese, distressed woman with obvious tachypnoea and a non-productive cough. Auscultation of her chest revealed decreased air entry at the right base.

THEN Patient gets central chest pain, increasing dyspnoea, cyanosis, hypotension, elevated JVP and dies.)

Outline the sequence of events that occurred in this woman from the time of presentation until death, and suggest the likely cause of death.

Answer 7

Second saddle embolus (or extension of initial PE) -> pulmonary hypertension -> right heart strain -> right heart failure (cor pulmonale) -> MI/right heart rupture -> cardiac tamponade -> hypotension, hypoperfusion

Question 8

8. (CP3: PE

A 52 year-old woman suddenly developed breathlessness the day after laparoscopic cholecystectomy. The patient, who was previously otherwise well, had a strong family history of ischaemic heart disease and smoked 20 cigarettes per day. Examination revealed an obese, distressed woman with obvious tachypnoea and a non-productive cough. Auscultation of her chest revealed decreased air entry at the right base.

THEN Patient gets central chest pain, increasing dyspnoea, cyanosis, hypotension, elevated JVP and dies.)

Is a post-mortem examination mandatory in this case, and if so, why?

Answer 8

Yes – mandatory under Coroner’s Act if death

Question 9

9. (CP3: PE

A 52 year-old woman suddenly developed breathlessness the day after laparoscopic cholecystectomy. The patient, who was previously otherwise well, had a strong family history of ischaemic heart disease and smoked 20 cigarettes per day. Examination revealed an obese, distressed woman with obvious tachypnoea and a non-productive cough. Auscultation of her chest revealed decreased air entry at the right base.

THEN Patient gets central chest pain, increasing dyspnoea, cyanosis, hypotension, elevated JVP and dies.)

Outline the major pathological findings you would expect at autopsy.

Answer 9

• Lung:
o Medium PE: thromboembolus in artery with wedge-shaped haemorrhagic infarction in R lower lobe in corresponding lung tissue
o Large PE in pulmonary artery bifurcation
o Fibrinous pleural exudate
o Potentially also COPD changes due to smoking
• Heart
o RV failure (probably won’t see dilation as the process was acute)
o Atherosclerosis (FHx of IHD)
• Legs
o DVT (more likely in the proximal leg vein rather than distal): large propagating red thrombus

Question 10

10. (CP3: PE) If the patient had survived, what long-term complications might she have developed?

Answer 10

• Chronic thromboembolic pulmonary hypertension -> cor pulmonale
• Recurrent VTE
• Post-thrombotic syndrome: chronic obstruction of venous outflow and destruction of venous valves -> venous insufficiency and venous hypertension

Question 11

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

1. Is a coronial autopsy necessary in this case, and if so, why? What legal obligations must be satisfied before performing an autopsy under these circumstances?

Answer 11

Yes, because within 24 hours of administration of anaesthetic. The coroner must be notified of the death and no death certificate may be issued.

Question 12

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

2. What is the likely pathological basis of his intermittent calf pain, and what may have occurred to precipitate the nocturnal calf pain present in the days before his death?

Answer 12

Underlying pathology: atherosclerosis of the lower limb arteries -> stenosed arteries
Movement -> increased metabolic demand -> insufficient blood supply to calf muscles -> ischaemia -> anaerobic metabolism -> lactic acid -> pain
Sudden onset of rest pain = more significant occlusion of a vessel, usually because of a thrombus forming on a ruptured or fissured plaque. Less commonly, could be thromboembolus from the aorta (eg aortic aneurysm), haemorrhage into the plaque.

Question 13

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

3. Describe the abnormalities you would expect to find at autopsy in the blood vessels of the abdomen and legs.

Answer 13

Extensive atherosclerotic plaques in aorta, iliac, femoral, popliteal arteries.
- R femoral: significant narrowing of lumen
- L popliteal: thrombus overlying a plaque
- Could have
o AAA
o Atherosclerosis at origin of renal and coeliac arteries
o DVTs

Question 14

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

4. How might the finding of atherosclerosis involving the origin of the right renal artery explain the development of hypertension at the age of 55?

Answer 14

Atherosclerosis -> renal artery stenosis -> reduced pressure in the glomerular capillaries -> macula densa detects this and causes the release of renin from the juxtaglomerular apparatus -> hypertension (through water and sodium retention, peripheral vasoconstriction)
INTERESTINGLY: due to the stenosed artery, the kidney with the renal artery stenosis that’s causing the hypertension will be relatively spared from the effects (nephrosclerosis)

Question 15

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

5. What factors predispose to atherosclerotic peripheral vascular disease?

Answer 15

Predisposing factors: non-modifiable
-	Genetic abnormalities
-	Family history
-	Increasing age
-	Male gender
Modifiable
-	Hyperlipidaemia
-	Hypertension
-	Diabetes
-	Inflammation
-	Cigarette smoking

Question 16

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

6. Which organs are likely to undergo pathological changes as a result of long-standing hypertension and what is the nature of the changes in each of those organs?

Answer 16

Changes include:
- Hyaline arteriolosclerosis: pink hyaline thickening of arteriolar walls, loss of underlying structural detail, luminal narrowing
- Brain:
o cerebral haemorrhage
o lipohyalinosis of small perforators - with or without Charcot-Bouchard aneurysms
- Kidneys
o Vascular disease: intimal thickening and luminal narrowing
o Glomerulosclerosis
o Tubulo-intestinal atrophy and fibrosis
- Heart:
o Macroscopic: concentric left ventricular hypertrophy, typically without ventricular dilation until late.
o Microscopic: wider transverse diameter of myocytes and there’s prominent nuclear enlargement and hyperchromasia (‘boxcar nuclei’) and intercellular fibrosis
- Aorta and muscular arteries: atherosclerosis, cystic medial necrosis of the aorta
- Eyes (not sure lol)

Question 17

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

7. What do you consider to be the most likely cause(s) of death in this case?

Answer 17

MI: complicated by ventricular arrhythmia
Others: arrhythmia just from LVH, massive PE, stroke (massive cerebral/pontine haemorrhage or thrombotic occlusion of basilar artery)

Question 18

(CP38: PVD
You are an “on-call” surgical resident asked to see a 73 year-old man who died in his sleep 12 hrs after undergoing surgery to bypass an occluded right popliteal artery. You have not seen him previously. His wife, who is very keen for you to sign the death certificate, tells you that he was known to have suffered from intermittent claudication in the right leg for the previous six months, with recent onset of nocturnal pain in the right calf. He had received treatment for systemic hypertension for the past 18 years, and had a history of angina for the past 2 years.)

8. What factors may have increased the risk of myocardial infarction in the perioperative period?

Answer 18

Periop hypotension: from blood loss, decreased oral intake, decreased venous return caused by mechanical ventilation, anaesthetic agents causing vasodilation
Periop hypoxia: opioids, pulmonary atelectasis
 

Question 19

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

1. What is your provisional diagnosis?

Answer 19

MI

DDx: angina, unstable angina, aortic dissection, pericarditis, pleurisy (pneumonia, PE, pneumothorax), oesophageal reflux/spasm, pancreatitis?, musculoskeletal

Question 20

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

2. What cardiovascular risk factors are present and what additional risk factors should be assessed?

Answer 20

Present risk factors: DM, obese, hypertensive, age > 50y, male, hx of angina
Additional risk factors: dyslipidaemia, smoking, alcohol, CKD, diet, physical activity, depression, FHx, FHx, familial hypercholesterolaemia

Question 21

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

3. Outline the investigations you would perform, the costs, and the results you would expect?

Answer 21

• Hx
• Exam: esp vitals, murmur, pericardial rub, signs of heart failure
• Bedside: BSL, ECG (ST elevation/depression, T wave inversion, pathological Q waves)
• Bloods: trops (raised), FBC, CRP, UEC, LFTs (NAD), ABGs, fasting lipids?
• Imaging: CXR (NAD), echo, coronary angiography?

Question 22

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

4. The ECG was consistent with an acute anterior myocardial infarction. What abnormalities would have been present on the ECG, and what is the pathological basis of these changes? What is the significant of the biochemical abnormalities shown below (mildly raised urea, Cr; raised BSLs; raised CK-MB; raised trops)?

Answer 22

ECG changes (in leads V1-V4)
• Earliest change: peaked T wave (localised hyperkalaemia)
• ST elevation: reflects a certain kind of damage current thing (over time returns to isoelectric line)
• T wave inversion: due to the electrical window? So don’t see repolarisation of the dead myocardium, see through it to the opposite thing happening behind it?
• Pathological Q waves: is it because the part of the myocardium shown by the lead is dead so you see a longer depolarisation of the R ventricle?
Biochemistry:
• Urea and creatinine mildly raised: some renal impairment/muscle breakdown?
• Raised BSLs: hyperglycaemic state likely reflecting poor glycaemic control
• Raised CK-MB: cardiac enzyme released from dead cardiomyocytes
• Raised troponin I: cardiac enzyme released from dead cardiomyocytes

Question 23

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

5. Outline the likely sequence of events leading to this man’s clinical presentation.

Answer 23

-Development of atherosclerotic plaques in the coronary arteries – contributed to by hypertension (damages endothelium), diabetes (damages endothelium again and accelerates atherosclerosis) and dyslipidaemia
-Atherosclerotic plaque ruptures – exposing underlying collagen and potentially necrotic core -> thrombogenic materials cause formation of a thrombus
-Occlusion of the artery sufficient to cause infarction in the myocardium supplied by it
-Chest pain
Other causes of MI include: coronary artery dissection, increased O2 demand (arrhythmias) or decreased supply (coronary artery spasm, coronary artery embolus, anaemia, hypertension/hypotension), PCI, stent thrombosis, CABG

Question 24

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

6. What are the important principles of the emergency management of this man’s evolving myocardial infarction? What are the mechanisms of action of the drugs that would be administered?

Answer 24

Principles: restore blood supply to the ischaemic myocardium as soon as possible to salvage the myocardium
Emergency management
O2, IV access, aspirin, morphine, nitrates
• Vasodilating the coronary arteries: with glyceryl trinitrate(forms nitric oxide, which causes vasodilation)
• Preventing further development of the thrombus: with antiplatelet agent aspirin (COX inhibitor, prevent formation of thromboxane A2 from arachidonic acid, which is involved in platelet activation and aggregation) and potentially clopidogrel as well (ADP-receptor blocker -> reduces platelet aggregation)
• Firstline: PCI (if PCI available within 60-90 minutes)
• If not: thrombolysis: with t-PA eg tenectoplase/reteplase/alteplase (activates plasminogen into plasmin, which breaks apart the fibrin meshwork that stabilises a thrombus)
o Absolute contraindications: active bleeding, bleeding diathesis, significant head/facial trauma in past 3 months, suspected aortic dissection, any history of ICH, known malignant intracranial lesion or structural cerebral vascular lesion
o Relative contraindications: current use of anticoagulants, recent major surgery, traumatic/prolonged CPR, recent internal bleeding, active peptic ulcer, severe HTN, recent ischaemic stroke, dementia, pregnancy
Additional supportive care would involve
• Analgesia eg morphine (activates mu opioid receptors to modulate ascending pain transmission)
• Anti-emetics eg metoclopramide

Question 25

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

ECG: ant infarct

7. Which arteries, and what areas of these, are likely to be diseased? Describe the sequential changes that occur in the myocardium following infarction.

Answer 25

The coronary arteries are likely to be diseased – given that the infarction was of the anterior myocardium, the left anterior descending artery is likely to be involved and have the atherosclerotic plaque that underwent rupture – mostly common the first 2cm. The site of infarct would be the anterior wall of the LV near apex, anterior portion of the ventricular septum, apex (circumferentially)
Changes in the myocardium following infarction:
(Macroscopic)
- First day: in the first 12 hours you’d see minimal changes. Then you’ll start to see dark mottling due to the stagnated trapped blood over the next 12 hours.
- First week: the area becomes sharply defined, yellow coloured, soft
- Second week: the yellow area becomes surrounded by a red tan area (vascular granulation tissue)
- First month: you get scarring (grey-white) – from the border (the remaining vasculature) inwards
- Two months: scar complete
(Microscopic)
- First day: first 12 hours you see early coagulative necrosis, oedema, haemorrhage and wavy fibres. The next 12 hours you see more signs of coagulative necrosis (pyknosis of nuclei) plus the neutrophils coming in to take case of it
- First week: you’ll see the loss of nuclei and striations (cells without cell-doing stuff in them), disintegration of myofibrils, and the neutrophils have died
- Second week: clearing up the dead stuff (phagocytosis) and making new stuff (granulation tissue)
- First month: scarring (collagen deposition)
- Two months: dense collagenous scar

Question 26

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

8. What complications might develop in the first 48 hours after admission?

Answer 26

In first 48 hours: arrhythmias (tachys, bradys, stunned myocardium) and SCD, cardiogenic shock
After that, complications include pericarditis, cardiac rupture, cardiac failure, false aneurysm, thromboembolism, papillary muscle dysfunction, infarct extension, recurrent ischaemia and infarction

Question 27

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

9. On the 4th hospital day, the patient developed severe chest pain lasting 60 minutes, requiring morphine for relief. What is the likely cause of this chest pain?

Answer 27

Second MI. (DDx: reperfusion injury, re-infarction, arrhythmia, PE)

Question 28

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

On the 4th hospital day, the patient developed severe chest pain lasting 60 minutes, requiring morphine for relief.

10. The patient’s pain persisted and examination revealed pallor and diaphoresis, blood pressure 80/40 mm Hg, heart rate 110/min with frequent ventricular ectopic beats (VEBs), S3 and S4 gallop rhythm and oliguria. What is the most likely diagnosis? Explain the pathophysiological basis of this condition.

Answer 28

Cardiogenic shock – the MI causes pump failure (if at least 40% of LV myocardial muscle mass is lost) to produce sufficient cardiac output, leading to inadequate organ perfusion. Alternatively structural damage (eg MR secondary to papillary muscle rupture, free wall rupture or VSD) can cause it.

Question 29

CP9

A 58 year-old man presented to his local GP with a two hour history of severe chest pain. The pain had commenced while running, and was initially associated with nausea, vomiting and agitation. The patient had experienced similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of Type 1 diabetes mellitus.
On examination the man was distressed, diaphoretic and mildly obese. Blood pressure was 165/105 mm Hg, pulse rate 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Basal crepitations were audible over both lungs.

On the 4th hospital day, the patient developed severe chest pain lasting 60 minutes, requiring morphine for relief.

The patient’s pain persisted and examination revealed pallor and diaphoresis, blood pressure 80/40 mm Hg, heart rate 110/min with frequent ventricular ectopic beats (VEBs), S3 and S4 gallop rhythm and oliguria.

Despite appropriate treatment the patient died on the fifth hospital day. What is the likely cause of death? Does this man require an autopsy under the Coroner’s Act? Outline the pathological findings expected at autopsy.

Answer 29

Likely cause of death: cardiogenic shock -> insufficient cerebral perfusion pressure
Autopsy: yes - death in hospital
Pathological findings expected at autopsy
- Heart:
o Macro: sharply-defined area of yellow infarction, potentially with red border (reflecting granulation tissue), potentially mechanical complications (papillary muscle rupture, free wall rupture, VSD)
o Micro: coagulative necrosis and early granulation tissue border
o Coronary artery atherosclerosis/thrombosis
- Other organs (as a result of shock)
o Lung: pulmonary oedema
o GI: infarction
o Kidneys: ATN
o Liver: hepatocellular infarction
- Changes associated with the comorbidities
o Atherosclerosis: in other arteries
o Diabetes: hyaline arteriolosclerosis, nephropathy, retinopathy, foot ulcers, (neuropathy?)
o Hypertension – hypertrophy of vascular smooth muscle, hyaline arteriolosclerosis …

Question 30

CP33
A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

1. What further information would you seek from the history and physical examination?

Answer 30

History
- Characterise sx: changes over time
- Associated sx: pain, STI changes
- Sx of cancer: weight loss, fever, night sweats, chills, malaise, anorexia, lymphadenopathy
o Sx of lung metastases: SOB, cough, haemoptysis, chest pain
o Sx of other mets: bone pain
- Sx of beta-hCG and AFP secretion: gynaecomastia, changes in secondary sex characteristics
- Hx of trauma
- PMHx
o Infections: UTI, STI, TB, mumps
o Nature of surgical treatment for undescended testis
Examination
- Confirm side and site of tumour
- Is the mass confined to the scrotum
- Tenderness
- Scrotal wall thickening/oedema (invasive tumour or infective)
- Testicular size –is the tumour part of the testicle or separate?

Question 31

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

2. What are the common causes of a scrotal mass lesion, and what do you think is the most likely diagnosis in this case?

Answer 31

DDx
- Hernia: most common scrotal mass, but unlikely in this case because can get above it
- Hydrocoele: second most common scrotal mass, but unlikely because not transilluminable
- Varicocoele: more common on the left, unlikely because would feel like ‘bag of worms’ rather than a mass and can’t get above it (extends up the cord)
- Haematoma (haematocoele?): if history of trauma or surgery, often associated with scrotal oedema
- Epididymal cysts: cysts in the epididymis itself rather than in the tunica vaginalis, but can feel the testicle separate
- Epididymoorchitis: mumps, other
- Torsion: sudden onset pain, predisposed to by a abnormal lie (need to fix both testes)
- Testicular cancer
o Seminoma linked to undescended testes
o Commonest in ages 15-35 – germ cell tumours and seminomas commonest tumours in this age group
o Other tumours include teratomas, lymphomas

Question 32

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

3. Outline the investigations you would perform and give reasons for each of the tests.

Answer 32

Confirming PDx
-	Testicular U/S
-	Tumour markers: beta-hCG, AFP, LDH
Others
-	Bloods
o	FBC
o	UEC
o	LFTs
-	Imaging
o	CT chest abdo pelvis
o	PET scan
-	Histopath
o	Biopsy: excisional biopsy (orchidectomy) via an inguinal route

Question 33

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

4. Histopathological assessment of an excisional biopsy of the left testis via the inguinal route confirmed that the mass was a seminoma of the testis. By what route (s) do testicular tumours metastasise?

Answer 33

Testicle: embryologically starts at the urogenital ridge and descends along the posterior abdominal wall along the inguinal canal into the scrotum.
Hence:
- Lymphatic spread: retroperitoneal: para-aortic nodes -> thoracic and supraclavicular nodes
- Haematogenous spread: to lung and other organs

Question 34

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

Histopathological assessment of an excisional biopsy of the left testis via the inguinal route confirmed that the mass was a seminoma of the testis.

5. What hormonal effects might be produced by testicular tumours?

Answer 34

Human gonadotrophins
Beta-hCG
- Elevated in 50% of patients with germ cell tumours
- 25% of seminomas
- 100% choriocarcinomas – can indicate a chorionic component to tumour
- Half life 24-36 ours
- May be biologically active and cause gynaecomastia
AFP
- Yolk sac derived tumours
- Secreted by 50-70% of testicular germ cell tumours
- Half life about 4.5 days
LDH
- Primarily elevated due to the bulk of tumour

Question 35

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

Histopathological assessment of an excisional biopsy of the left testis via the inguinal route confirmed that the mass was a seminoma of the testis.

6. What are the main types of testicular tumours and how do they differ in terms of prognosis?

Answer 35

Germ cell tumours (90% of testicular tumours)
-	Seminomas
o	Predictable lymphatic spread
o	Very sensitive to chemo and radiotherapy
-	Non-seminoma
o	Teratomas
o	Embryonal carcinomas
o	Yolk sac tumour
o	Trophoblastic tumours
	Choriocarcinoma
	Other trophoblastic
o	Mixed
Non-germ cell
-	Leydig
-	Sertoli
-	Gonadoblastoma
-	Adenocarcinoma of rete testis
Gonadal stromal tumours
Mesenchymal neoplasms

Question 36

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

Histopathological assessment of an excisional biopsy of the left testis via the inguinal route confirmed that the mass was a seminoma of the testis.

7. Why is percutaneous biopsy of suspected testicular tumours usually contraindicated?

Answer 36

Potentially opens a new lymphatic field – scrotal skin drains to the inguinal lymph nodes.

Question 37

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

Histopathological assessment of an excisional biopsy of the left testis via the inguinal route confirmed that the mass was a seminoma of the testis.
8. Outline the factors incriminated in the pathogenesis of testicular neoplasms. Which factors might be relevant in this case?

Answer 37

Risk factors
- Undescended testis – relevant in this case (both testes are at the same risk)
o Risk is 10-40% higher than normal population
o Higher site related to greater risk fo malignancy eg groin vs intrabdominal
o Contralateral testicle at equal risk
o If find undescended testis late – remove (can monitor the other)
- Intersex – testicular dysgenesis, androgen insensitivity syndrome
- Previous history, family history
- In most cases no cause/predisposing factor is found
o Only 10% of men with testicular tumours have history of cryptoorchidism
o Intersex with gonadal dysgenesis risk may be 10-25%
o Familial germ cell tumour accounts for 1-2% of all cases

Question 38

CP33

A 36 year old businessman sought medical advice because of a painless swelling in the left side of his scrotum, which had been present for three weeks. He was otherwise well apart from a history of surgical treatment for an undescended left testis as a child. Examination revealed a 5 x 3 centimetre, non-tender, firm mass at the upper pole of the left testis. It was possible to get above the lesion and it did not transilluminate.

Histopathological assessment of an excisional biopsy of the left testis via the inguinal route confirmed that the mass was a seminoma of the testis.

9. Compare and contrast the histological features of seminomas and teratomas.

Answer 38

Seminoma: Large uniform cells with round nuclei with conspicuous nucleoli, clear glycogen-rich cytoplasm and distinct cell borders, Separated in sheets and columns but no tubular formation, Variable lymphatic infiltrate

Teratoma: Very variable appearance: heterogenous collection of differentiated cells or organoid structures

Question 39

CP37
A 36 year-old man presented to the Emergency Department with severe right loin pain. The pain had been present “on and off” for the past six hours, with each attack of pain lasting approximately 30 minutes. The patient recalled a similar episode of pain six months previously that had resolved spontaneously. Examination revealed a distressed man, pale and tachycardic. The abdomen was soft and non-tender, and no other abnormalities were detected on physical examination.
Vitals: tachy, hypertensive
Urinalysis: prot + blood ++

1. What are your provisional and differential diagnoses?

Answer 39

PDx: renal colic
-	Renal calculi
-	Blood clots secondary to RCC, TCC, analgesic nephropathy, polycystic kidney disease
-	Necrotic papillae
-	Tumour tissue
DDx:
-	Pyelonephritis
-	Pancreatitis
-	Crohn’s, UC
-	Infective gastroenteritis
-	Mesenteric ischaemia
-	Appendicitis
-	Choledocholithiasis, cholecystitis
-	Leaking AAA
-	Hepatitis

Question 40

CP37
A 36 year-old man presented to the Emergency Department with severe right loin pain. The pain had been present “on and off” for the past six hours, with each attack of pain lasting approximately 30 minutes. The patient recalled a similar episode of pain six months previously that had resolved spontaneously. Examination revealed a distressed man, pale and tachycardic. The abdomen was soft and non-tender, and no other abnormalities were detected on physical examination.
Vitals: tachy, hypertensive
Urinalysis: prot + blood ++

2. What investigations would you perform while the patient is in the Emergency Department to confirm your diagnosis?

Answer 40

Gold standard: CT KUB (non-contrast)
Others:
-	Urine: urinalysis, urine MCS
-	Bloods: FBC, CRP, lipase, ABGs
-	Imaging: consider abdo US if CT unhelpful

Question 41

CP37
A 36 year-old man presented to the Emergency Department with severe right loin pain. The pain had been present “on and off” for the past six hours, with each attack of pain lasting approximately 30 minutes. The patient recalled a similar episode of pain six months previously that had resolved spontaneously. Examination revealed a distressed man, pale and tachycardic. The abdomen was soft and non-tender, and no other abnormalities were detected on physical examination.
Vitals: tachy, hypertensive
Urinalysis: prot + blood ++

3. An abdominal helical CT scan showed a 5mm radiodense lesion 2cm lateral to the body of the fifth lumbar vertebra. What might produce such an appearance?

Answer 41

There are apparently a number of things:

• Renal calculus (calcium oxalate)
• Calcification of blood vessel wall
• Phlebolith
• Calcified mesenteric lymph node (if had TB)
• Tablets in the bowel
• Faecoliths

Question 42

CP37
A 36 year-old man presented to the Emergency Department with severe right loin pain. The pain had been present “on and off” for the past six hours, with each attack of pain lasting approximately 30 minutes. The patient recalled a similar episode of pain six months previously that had resolved spontaneously. Examination revealed a distressed man, pale and tachycardic. The abdomen was soft and non-tender, and no other abnormalities were detected on physical examination.
Vitals: tachy, hypertensive
Urinalysis: prot + blood ++

An abdominal helical CT scan showed a 5mm radiodense lesion 2cm lateral to the body of the fifth lumbar vertebra.

The patient’s pain settled with analgesia and he was discharged four hours later. Biochemistry results are shown opposite. (Na slightly low, urea up, Cr up, Ca up, urate up) What is the significance of these results? What further information do you require to interpret them correctly?

Answer 42

Raised urea and Cr, low Na – dehydration secondary to being unwell (renal colic often associated with vomiting)
Low Na because dry -> thirsty -> drink water -> water retention -> low Na
Raised calcium, urate – could be the cause of the stone
Other information to know: albumin (was the calcium standard or corrected?)
Causes of hypercalcaemia: hyperparathyroidism, malignancy, lymphoma, sarcoidosis, dietary vitamin D excess

Question 43

CP37
A 36 year-old man presented to the Emergency Department with severe right loin pain. The pain had been present “on and off” for the past six hours, with each attack of pain lasting approximately 30 minutes. The patient recalled a similar episode of pain six months previously that had resolved spontaneously. Examination revealed a distressed man, pale and tachycardic. The abdomen was soft and non-tender, and no other abnormalities were detected on physical examination.
Vitals: tachy, hypertensive
Urinalysis: prot + blood ++

An abdominal helical CT scan showed a 5mm radiodense lesion 2cm lateral to the body of the fifth lumbar vertebra.

The patient’s pain settled with analgesia and he was discharged four hours later.

5. The next day the patient passed a stone 5mm in diameter with an irregular, ‘mulberry’ shape. What would you expect chemical analysis of the stone to reveal? What are the main types of calculi?

Answer 43

Chemical analysis: expect calcium oxalate or calcium phosphate (most common, radio-opaque, more likely to occur in males over 30)
Main types of stones
- Calcium oxalate
- Calcium oxalate and calcium phosphate
- Magnesium ammonium phosphate (struvite) – partially radioopaque
- Uric acid
- Cystine

Question 44

CP37
A 36 year-old man presented to the Emergency Department with severe right loin pain. The pain had been present “on and off” for the past six hours, with each attack of pain lasting approximately 30 minutes. The patient recalled a similar episode of pain six months previously that had resolved spontaneously. Examination revealed a distressed man, pale and tachycardic. The abdomen was soft and non-tender, and no other abnormalities were detected on physical examination.
Vitals: tachy, hypertensive
Urinalysis: prot + blood ++

An abdominal helical CT scan showed a 5mm radiodense lesion 2cm lateral to the body of the fifth lumbar vertebra.

The patient’s pain settled with analgesia and he was discharged four hours later. Biochemistry results are shown opposite.

The next day the patient passed a stone 5mm in diameter with an irregular, ‘mulberry’ shape.

6. What complications of nephrolithiasis are present in this patient, and what other complications can occur?

Answer 44

Present: renal colic, acute kidney injury
Others: ureteric obstruction, infection, local inflammation -> ulceration -> scarring -> stricture

Question 45

7. What are the major factors implicated in the pathogenesis of renal calculi?

Answer 45

• High urinary concentration of those minerals
  o Calcium: excessive calcium absorption from the gut which is promptly excreted in the urine, sometimes exacerbated by a defect in renal calcium reabsorption)
  o Uric acids: gout, diseases involving excessive cell turnover (eg leukaemia)
  o Cystine: genetic defect in renal transport of certain amino acids including cystine
• Stasis (eg chronic obstruction)
• Infection (nidus for crystallization)
• Nucleation by epithelial debris, bacteria, ‘matrix’ mucoprotein
• Persistently alkaline urine (calcium and triple phosphate stones) or acidic urine (uric acid and cystine stones)
• Lack of inhibitors of crystal growth and aggregation eg nephrocalcin, pyrophosphate, citrate

Question 46

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++
1. What is the likely cause of this man’s illness?

Answer 46

Hepatitis
- Viral
- Alcoholic
- Drug-induced
- CT disease
- Autoimmune
- Metabolic: haemochromatosis, alpha-1 antitrypsin
DDx of hepatomegaly
- Hepatitis: infective (viral, bacterial, fungal), alcoholic steatohepatitis, NASH, drug-induced, ischaemic, autoimmune
- Storage disorders: haemochromatosis, alpha-1 antitrypsin, lipid and glycogen storage disorders
- Infiltrative: benign tumours, malignant cancer, TB, sarcoidosis
- Impaired venous outflow: Budd-Chiari syndrome, sinusoidal outflow obstruction, right heart failure
- Biliary tract: primary biliary sclerosis, primary sclerosing cholangitis

Question 47

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

2. Which viruses commonly cause this clinical picture, and what further information would you seek in the history and physical examination?

Answer 47

Viruses
-	Most common viruses: HAV, HBV, HCV, HEV (although would expect a higher rise in transaminases)
-	EBV possible
-	CMV, HSV, VZV only likely to cause symptomatic disease in immunosuppressed people
History and exam
-	Hep risk factors
o	Travel overseas
o	Injecting drug use
o	Needlestick injury
o	Infectious contacts
o	Blood transfusions before some year
-	Contact tracing?
-	Liver disease symptoms and signs
-	Differentials
o	Autoimmune: other autoimmune diseases, FHx
o	Drug-induced: thorough drug history
o	Metabolic: neuro sx

Question 48

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

3. Are the liver function tests shown opposite consistent with your diagnosis? Explain the mechanism of each of the abnormalities.

LFTs: 
bilirubin 120 (2-20) 
ALP 148 (38-126)
AST 642 (

Answer 48

Derangements
- Bilirubin elevated: destruction of hepatocytes releases conjugated bilirubin and also means that unconjugated bilirubin can’t become conjugated -> builds up too; swelling and oedema in the lobule also causes some obstruction of bile canaliculi
- ALP, GGT: mildly elevated
- AST, ALT markedly elevated: released from dead hepatocytes
o Level of transaminase rise: NAFLD

Question 49

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

4. Explain the pathological basis for the presence of bilirubin in the urine.

Answer 49

Increased serum bilirubin (especially conjugated) -> increased filtration and exhaustion of renal reabsorptive capacity -> increased urinary bilirubin
Notes: unconjugated bilirubin is mostly bound to albumin and thus not filtered by the glomerulus. Conjugated bilirubin that is bound to albumin is known as delta-bilirubin.

Question 50

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

5. What serological investigations would be appropriate to make a specific diagnosis in this case?

Answer 50

• HAV:
  o IgM anti-HAV: develops 3-7 weeks after infection, positive at onset of symptoms, peaks during acute or early convalescent phase, remains positive for 4-6 months
• HBV:
  o HBsAg: appears 1-10 weeks after exposure to HBV, prior to onset of symptoms and becomes undetectable 4-6 months after recovery.
  o IgM anti-HBs: may not be detectable until weeks-months after HBsAg becomes undetectable, usually IgG persists for life and reflects immunity. If present along with HBsAg, reflects inability to clear it = carrier.
  o IgM anti-HBc: usually indicates acute infection, but may remain detectable up to 2 years after the acute infection or reflect exacerbation of chronic infection.
  o IF HbsAg persists for more than 6 months -> chronic infection
   HBeAg: reflects active replication
   Serum HBV DNA
• HCV:
  o PCR for HCV-RNA: typically positive by the time the patient is symptomatic
  o IgM anti-HCV: stay high as long as 3-6 months after infection

Question 51

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

6. Compare and contrast hep A, B, C, E infections in terms of their epidemiology (incubation, transmission) and sequelae (fulminant necrosis, chronic hep, carrier state, hepatocellular carcinoma).

Answer 51

ceebs

you should know this

Question 52

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

7. What is the role of the immune response in producing the characteristic features of HBV infection?

Answer 52

HBV is not lethal to hepatocytes, rather it is the immune response which causes hepatocyte damage. CD8 T cells lyse infected cells (which express HBsAg on their cell membranes). When the CD8 T cells don’t recognise HBsAg, they continue to attack nucleocapsid antigens (HBcAg, HBeAg), which causes a chronic disease state. Antibodies against HBeAg prevent replication of the virus.

Question 53

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

8. Five days after admission to hospital, the patient became confused and tremulous. What pathological changes in the liver and likely to be the basis for this clinical deterioration, and what further complications may develop in other organ systems?

Answer 53

Viral hepatitis -> chronic liver disease -> exhaustion of hepatic reserve -> precipitating event -> liver failure - massive destruction of hepatocytes (fulminant viral hepatitis)-> elevated serum urea (may be precipitated by an event such as GI bleed) -> hepatic encephalopathy
Other potential complications
- Infections
- Hypoglycaemia
- Renal failure with no apparent cause (hepato-renal syndrome)
- Coagulopathy
- CV and respiratory function changes

Question 54

CP36
A 24 year-old single man presented to his GP with a two-week history of lethargy, anorexia, nausea and arthralgia. Over the past two days he had noticed darkening of his urine. On examination he was found to have scleral icterus, an enlarged tender liver (16 centimetres liver span) and splenomegaly.
Vitals: febrile
Urinalysis: prot +, blood -ve, bili +++

9. What treatments are available to manage chronic HBV infection, and what are their mechanisms of action?

Answer 54

Options:
- Interferon
o Bind to receptors on host cells, induce production of enzymes inhibiting translation of viral mRNA
- Nucleos(t)ide analogues (entecavir, tenofovir, lamivudine, adefovir dipivoxil, telbivudine)
o Incorporated into DNA formed by reverse transcriptase, but as they lack a 3’OH group, chain termination occurs
o (Nucleoside analogues are phosphorylated to form nucleotide analogues)
Approach
- Treatment naive patients: pegylated interferon, tenofovir, entecavir
- Hx of lamivudine or unspecified nucleos(t)ide analogues: tenofovir