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PA26.1-10 | Cardiovascular System — Graded Quiz

Graded 12 questions · Untimed · 2 attempts

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Q1 PA26.1 1 pt

A 55-year-old man with hypertension and type 2 diabetes undergoes carotid endarterectomy. The surgical specimen shows a fibrous plaque with a thin fibrous cap (< 65 µm), a large necrotic lipid core, inflammatory macrophage infiltration at the cap shoulder, and intraplaque haemorrhage. These morphological features are collectively termed the 'vulnerable plaque'. Which mechanism most directly links these features to the risk of acute coronary syndrome rather than stable angina?

A The thick fibrous cap mechanically obstructs the vessel lumen, reducing coronary blood flow during exertion and causing demand ischaemia
B A thin fibrous cap overlying a large lipid core is prone to rupture, exposing thrombogenic subendothelial collagen and lipid core to platelets, triggering acute thrombus formation and complete occlusion
C Intraplaque haemorrhage raises intraluminal pressure, forcing the plaque to grow outward (positive remodelling) and progressively narrow the lumen
D Macrophage foam cell accumulation at the plaque shoulder secretes PDGF, causing smooth muscle proliferation that obstructs the vessel over years

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Q2 PA26.2 1 pt

A 73-year-old hypertensive man presents with sudden-onset tearing pain radiating from the chest to the back. CT aortography reveals a double lumen in the thoracic aorta with an intimal tear just distal to the aortic valve. His blood pressure is 190/110 mmHg. Histological examination of the aortic wall would most likely show which change in the tunica media?

A Atheromatous plaque with lipid core and fibrous cap extending into the media
B Fragmentation of elastic fibres and smooth muscle loss with mucoid/proteoglycan accumulation — cystic medial degeneration (necrosis)
C Acute neutrophilic infiltration of the media with fibrinoid necrosis of the medial smooth muscle cells
D Obliterative endarteritis of the vasa vasorum with treponema-driven adventitial plasma cell infiltration

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Q3 PA26.3 1 pt

A 58-year-old man presents 8 hours after the onset of crushing substernal chest pain. Serial ECGs show evolving ST elevation in leads II, III, and aVF, and troponin T is markedly elevated. Primary PCI achieves TIMI 3 flow. On day 3 post-procedure he develops a new grade 3/6 pansystolic murmur at the lower sternal border, louder on inspiration, with a right ventricular heave. Echocardiography shows a defect in the interventricular septum. Which pathological event best explains the timing and mechanism of this complication?

A Fibrinous pericarditis from epicardial inflammation reaching peak intensity at day 3, causing friction rub mistaken for a murmur
B Liquefactive necrosis of the infarcted myocardium reaching maximum softening (myomalacia cordis) between days 3–7, leading to septal rupture
C Organisation of the infarcted zone by granulation tissue beginning at day 3, causing scar retraction and septal thinning
D Reperfusion injury causing contraction band necrosis of the septal myocardium, resulting in immediate electromechanical failure

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Q4 PA26.5 1 pt

A 60-year-old woman with longstanding mitral stenosis due to rheumatic heart disease develops progressive dyspnoea, orthopnoea, and bilateral ankle oedema. Chest X-ray shows cardiomegaly, upper lobe venous diversion, Kerley B lines, and a double right heart border. Her BNP is 1,200 pg/mL. The Kerley B lines seen on X-ray are best explained by which pathological process in the lung?

A Pulmonary arterial hypertension causing haemosiderin deposition in alveolar macrophages, producing dense interstitial lines
B Transudation of fluid into the interlobular septa secondary to elevated pulmonary venous and capillary pressure from left heart failure
C Fibrous thickening of interlobular septa caused by recurrent episodes of pulmonary oedema over years, producing fixed horizontal lines
D Lymphatic obstruction by tumour emboli causing retrograde filling of interlobular lymphatics, producing linear opacities

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Q5 PA26.6 1 pt

A 14-year-old girl presents with a 2-week history of migratory polyarthritis, a new apical pansystolic murmur, and an erythematous rash on her trunk. Throat culture taken 5 weeks ago grew Group A beta-haemolytic Streptococcus. ASO titre is markedly elevated. Echocardiography shows mitral regurgitation. Which morphological lesion, if found on biopsy of the myocardium, would be pathognomonic of this diagnosis and represent the histological hallmark of the disease?

A Caseous granuloma with Langhans giant cells and peripheral lymphocytes in the myocardial interstitium
B Aschoff body: perivascular granuloma with central fibrinoid necrosis, Aschoff giant cells (caterpillar/owl-eye nuclei), and surrounding lymphocytes and plasma cells
C Myocyte necrosis with contraction bands and an interstitial polymorphonuclear neutrophilic infiltrate
D Replacement fibrosis of myocardial fibres with sparse lymphocytic infiltrate and no giant cells

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Q6 PA26.7 1 pt

A 28-year-old intravenous drug user presents with a 10-day history of high-grade fever, rigors, and a new loud pansystolic murmur at the left lower sternal border that increases on inspiration. Blood cultures grow Staphylococcus aureus. Echocardiography reveals vegetations on the tricuspid valve with evidence of right heart volume overload. Which complication is most likely to occur specifically due to the right-sided location of these vegetations?

A Splenic infarcts from septic emboli reaching the systemic circulation via the aorta
B Pulmonary septic emboli causing multiple peripheral lung cavities and abscesses
C Stroke from paradoxical embolism through a patent foramen ovale
D Renal infarction from septic emboli via the systemic arterial circulation

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Q7 PA26.9 1 pt

A 6-week-old infant is referred for failure to thrive and feeding difficulties. On examination there is a loud continuous 'machinery' murmur below the left clavicle, bounding pulses, and a wide pulse pressure. Echocardiography reveals a large patent ductus arteriosus (PDA) with left-to-right shunting. The parents ask why the baby has become breathless and sweaty during feeds but is not cyanosed. Which pathophysiological explanation best accounts for the absence of cyanosis in this infant with a significant cardiac shunt?

A The ductus arteriosus connects the pulmonary artery to the descending aorta distal to the left subclavian artery, so desaturated blood does not reach the coronary arteries or brain
B The left-to-right direction of shunting delivers oxygenated blood from the aorta back into the pulmonary artery, adding volume load to the pulmonary circulation without mixing desaturated blood into the systemic circulation
C The pulmonary vascular resistance in neonates is naturally high, which prevents any desaturated blood from crossing into the aorta and mixing with systemic circulation
D The ductus connects the ascending aorta to the right pulmonary artery, allowing oxygenated blood to recirculate only through the right lung without reaching the systemic arterial circulation

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Q8 PA26.8 1 pt

A 35-year-old man presents with a 2-year history of progressive dyspnoea and a family history of sudden cardiac death in his father at age 38 and his paternal uncle at age 42. Echocardiography shows asymmetric septal hypertrophy (septum 22 mm, posterior wall 10 mm) with systolic anterior motion of the mitral valve (SAM) and a dynamic left ventricular outflow tract gradient of 55 mmHg at rest. Genetic testing reveals a missense mutation in the MYH7 gene (encoding beta-myosin heavy chain). Why does this particular lesion cause dynamic — rather than fixed — obstruction of the left ventricular outflow tract?

A The hypertrophied septum forms a fixed anatomical narrowing that progressively worsens with increasing ventricular filling over decades
B During systole, the hypertrophied septum bulges into the LVOT; the Venturi effect draws the elongated mitral valve leaflet anteriorly (SAM) to further narrow the outflow tract in a load- and heart-rate-dependent manner
C Myocyte disarray causes electrical re-entry that produces intermittent systolic non-compaction of the septal myocardium, dynamically narrowing the outflow tract
D The MYH7 mutation causes abnormal AV node conduction with intermittent left bundle branch block, dynamically changing the septal activation sequence and outflow geometry

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Q9 PA26.5 1 pt

A 70-year-old woman with known dilated cardiomyopathy (EF 20%) and longstanding biventricular failure is admitted with massive ascites, peripheral oedema, and jaundice. Liver biopsy shows congestion of hepatic sinusoids with hepatocyte atrophy and eosinophilic change at the central vein zones, giving a mottled 'nutmeg' appearance on gross inspection. Her INR is 2.1 despite no anticoagulation. Which pathological mechanism best explains the coagulopathy and the centrilobular pattern of liver injury in this patient?

A Splanchnic arterial vasodilation in portal hypertension reduces hepatic arterial supply, causing ischaemia in the centrilobular zone which receives least arterial blood
B Elevated right-sided venous pressure transmits directly to the hepatic veins and sinusoids; the centrilobular zone (zone 3 of Rappaport) is most distal from the portal supply and most susceptible to passive venous congestion and secondary ischaemia
C Recurrent microthrombi from cardiac thrombus embolise selectively to centrilobular sinusoids, causing patchy infarction with a zone 3 predilection
D Reduced cardiac output decreases hepatic portal blood flow, causing periportal (zone 1) hepatocyte death with preserved centrilobular hepatocytes

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Q10 PA26.10 1 pt

An autopsy is performed on a 48-year-old man who died suddenly during exercise. Gross examination shows a massive, firm, pale yellow tumour measuring 14 × 11 cm in the left atrium, attached by a pedicle to the fossa ovalis and prolapsing intermittently into the mitral orifice during systole. Microscopically, the mass shows stellate and polygonal cells embedded in a loose myxoid stroma with abundant mucopolysaccharides. No significant mitotic activity is seen. Which of the following best explains why this tumour caused syncopal episodes intermittently related to body position during the months before death?

A Tumour emboli from the myxoid stroma occlude small coronary arteries during exercise, causing intermittent myocardial ischaemia and syncope
B A pedunculated mass in the left atrium prolapses into the mitral orifice with changes in body position, intermittently obstructing mitral inflow and causing episodic reduction in cardiac output and syncope
C The myxoid stroma secretes serotonin intermittently, causing episodic systemic vasodilation and syncope in a pattern resembling carcinoid syndrome
D Intermittent arrhythmias from direct tumour infiltration of the AV node cause transient haemodynamic compromise and syncope

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Q11 PA26.4 1 pt

A 78-year-old woman with a 40-year history of poorly controlled hypertension develops acute pulmonary oedema. Her chest X-ray shows bilateral perihilar 'bat-wing' alveolar opacities with an upper lobe venous blood diversion pattern. On examination she has a fourth heart sound (S4) and signs of pulmonary venous hypertension, but the left ventricular ejection fraction is preserved at 62% on echocardiography. Which pathological sequence best explains how decades of hypertension can cause pulmonary oedema with a preserved ejection fraction?

A Hypertension causes progressive right ventricular dilation that eventually pushes the interventricular septum leftward, reducing LV filling and causing diastolic dysfunction with preserved systolic function
B Chronic pressure overload induces concentric LV hypertrophy with increased wall stiffness; the hypertrophied ventricle resists diastolic filling (diastolic dysfunction), raising left atrial pressure and causing pulmonary venous hypertension without systolic impairment
C Hypertension accelerates coronary atherosclerosis, causing repeated silent NSTEMI events that progressively replace contractile myocardium with fibrosis while preserving overall EF by septal compensatory hypercontraction
D Sustained high afterload causes compensatory LV dilation and eccentric hypertrophy with normal systolic shortening fraction but elevated filling pressures due to dilated cardiomyopathy physiology

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Q12 PA26.8 1 pt

A gross pathology specimen from a 66-year-old man who died of biventricular failure shows both ventricles dilated, with a spherical cardiac silhouette and a combined heart weight of 810 g (normal ~300 g). All valves appear structurally normal. The myocardium appears pale, flabby, and diffusely thinned. There is a mural thrombus in the left ventricular apex. The patient had a 30-year history of heavy alcohol use with no coronary artery disease found at autopsy. Which microscopic finding would most specifically point to alcoholic cardiomyopathy rather than idiopathic dilated cardiomyopathy in this specimen?

A Widespread myocyte hypertrophy with disorganised sarcomere architecture (myocyte disarray) involving > 20% of the LV wall
B Interstitial and perivascular fibrosis with myocyte atrophy, vacuolisation, and lipid droplet accumulation within cardiomyocytes (myocyte lipidosis)
C Dense transmural lymphocytic infiltrate with focal myocyte necrosis consistent with active myocarditis pattern
D Extensive replacement fibrosis in a coronary artery territory distribution with thinned, scarred ventricular wall at the apex

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