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PA5.1-6 | Hemodynamic Disorders — Graded Quiz

Graded 12 questions · Untimed · 2 attempts

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Q1 PA5.1 1 pt

A 65-year-old man with congestive cardiac failure and a serum albumin of 18 g/L presents with bilateral pitting leg oedema, ascites, and a pleural effusion. A pleural tap yields 350 mL of straw-coloured fluid: protein 12 g/L, LDH 80 U/L (serum LDH 200 U/L). Which Starling force disturbances are operative, and how do they differ from oedema caused by bacterial cellulitis of the left leg?

A CCF/hypoalbuminaemia: raised capillary hydrostatic pressure + reduced plasma oncotic pressure → transudate. Cellulitis: inflammatory mediators increase vascular permeability → exudate confined to the infected leg
B CCF/hypoalbuminaemia: reduced lymphatic drainage from hepatic congestion → transudate. Cellulitis: lymphatic obstruction by bacteria → exudate in the affected limb
C CCF/hypoalbuminaemia: inflammatory cytokines released by failing myocardium increase systemic vascular permeability → exudate. Cellulitis: localised hydrostatic rise from venous obstruction → transudate
D Both conditions produce transudate; the protein content differs only because cellulitis causes haemorrhage into the interstitium, diluting the protein concentration

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Q2 PA5.2 1 pt

At autopsy of a 74-year-old woman who died of chronic right ventricular failure from COPD, the liver is enlarged, dark red, with a nutmeg pattern on cross-section. Histology shows: dilated central veins and sinusoids, centrilobular hepatocyte dropout, and preserved periportal hepatocytes. Which mechanism BEST explains the centrilobular predilection and the ultimate fate of this liver with prolonged right heart failure?

A Portal hypertension preferentially increases pressure in the portal triads, causing periportal haemorrhage and zone 1 necrosis with central sparing
B Venous back-pressure from the right heart is transmitted to hepatic veins and central veins, causing zone 3 (centrilobular) congestion and relative hypoxia; prolonged congestion leads to cardiac cirrhosis
C Arterial insufficiency from reduced cardiac output preferentially affects the hepatic artery, which supplies zone 1 (periportal) hepatocytes, causing centrilobular sparing
D Bile acid accumulation from intrahepatic cholestasis due to hepatic venous compression causes centrilobular hepatocyte apoptosis via bile salt toxicity

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Q3 PA5.3 1 pt

A 42-year-old woman, 6 weeks post-Caesarean section, presents acutely with right-sided pleuritic chest pain, haemoptysis, and a D-dimer of 4,200 ng/mL. CT pulmonary angiogram confirms a large saddle pulmonary embolus. She is anticoagulated with unfractionated heparin. Histology of the embolus (if surgically retrieved) would show Lines of Zahn. Which statement BEST explains what Lines of Zahn represent and why they are clinically significant?

A Lines of Zahn are alternating bands of red fibrin and pale fibrin formed by turbulent blood flow during clot propagation; their presence confirms the clot is postmortem
B Lines of Zahn are alternating pale platelet-fibrin layers and dark red cell-rich layers formed in flowing blood within a living vessel; their presence proves the thrombus formed antemortem in a venous or cardiac site
C Lines of Zahn are concentric layers of fibrin deposited during repeated episodes of organised thrombus formation; they indicate chronic recurrent embolism rather than a single acute event
D Lines of Zahn are formed by alternating leukocyte layers separated by erythrocyte bands; they are specific to arterial thrombi and absent in venous thrombi

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Q4 PA5.3 1 pt

A 55-year-old obese woman is admitted for an elective cholecystectomy. She takes the oral contraceptive pill and has a family history of unprovoked DVT in her father. Pre-operatively she is found to have a prothrombin gene G20210A mutation. Forty-eight hours post-operatively she develops acute dyspnoea and hypoxia. CT-PA confirms bilateral pulmonary emboli. Which component of Virchow's Triad is MOST directly implicated by the prothrombin G20210A mutation specifically?

A Endothelial injury — the mutation causes endothelial dysfunction, exposing subendothelial collagen and initiating platelet adhesion
B Stasis — the mutation causes red cell rigidity that impairs microcirculatory flow in post-operative patients, promoting stasis-related thrombus formation
C Hypercoagulability — the mutation leads to increased prothrombin levels (factor II), enhancing thrombin generation and shifting the coagulation balance toward clot formation
D Stasis combined with hypercoagulability — the mutation inhibits protein C activation, causing stasis by reducing venous tone, and simultaneously impairing anticoagulation

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Q5 PA5.3 1 pt

A 68-year-old man with known peripheral artery disease presents to the emergency department with sudden onset of a cold, pulseless, pale, and painful right leg 4 hours after onset. Doppler shows absence of flow in the superficial femoral artery. Thrombectomy retrieves a 6 cm organised-appearing pale firm thrombus with visible laminations. Histology shows fibrous tissue ingrowth with capillary channels within the thrombus. Which fate of a thrombus does this finding represent, and what is the MOST clinically relevant consequence in the arterial setting?

A Propagation — the thrombus extends distally; the fibrous ingrowth represents extension into collateral vessels preserving some distal flow
B Organisation and recanalisation — fibroblasts and capillaries grow into the thrombus; while some flow may be restored, the lumen remains significantly narrowed and ischaemia persists
C Resolution — thrombolytic enzymes have partially lysed the clot; the capillary ingrowth reflects fibrinolysis restoring full laminar flow
D Embolisation — the laminated layers detach and travel to the femoral bifurcation; the fibrous tissue left behind is organised thrombus remnant

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Q6 PA5.4 1 pt

A 28-year-old woman at 34 weeks gestation presents with sudden onset of severe dyspnoea, cyanosis, and cardiovascular collapse immediately after membranes rupture. She develops haemorrhage from venepuncture sites and from the uterus. Lab: PT 45 seconds (control 12), aPTT >120 seconds, fibrinogen <0.5 g/L, D-dimer markedly elevated, platelets 28,000/μL. She dies despite resuscitation. At autopsy, which pathological finding would MOST directly explain the combination of haemorrhage and thrombosis?

A Amniotic fluid embolism causing direct mechanical occlusion of the pulmonary microvasculature, triggering haemorrhage via right heart failure
B Disseminated intravascular coagulation (DIC) — amniotic fluid activates the extrinsic coagulation pathway, causing systemic microthrombi that consume clotting factors and platelets, leading to simultaneous microthrombosis and haemorrhage
C Massive pulmonary embolism from a paradoxical DVT, causing right heart failure and secondary DIC from poor cardiac output
D Thrombotic thrombocytopenic purpura (TTP) precipitated by pregnancy, causing platelet microthrombi in pulmonary vessels and systemic consumption coagulopathy

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Q7 PA5.5 1 pt

A 70-year-old man with known coronary artery disease presents with 4 hours of crushing central chest pain. ECG shows ST elevation in V1–V4. He is taken for primary PCI, which restores TIMI-3 flow. Six hours later, his troponin peaks at 18,000 ng/L. Echocardiogram shows an anterior wall motion abnormality. Twenty-four hours later, gross pathology of the infarcted zone (if biopsied) would show: which finding, and at what histological stage does the infarct lie?

A No gross change yet; wavy myofibres and contraction bands are the first histological sign at 24 hours
B Pale, slightly soft zone (coagulative necrosis) on gross examination; histology shows neutrophilic infiltration beginning, with preserved ghost myofibres and early cytoplasmic eosinophilia
C Yellow, soft, haemorrhagic zone with well-formed granulation tissue (capillaries + fibroblasts) replacing the necrotic core
D Dense grey-white fibrous scar replacing the full-thickness myocardium — classic of healed transmural infarction

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Q8 PA5.4 1 pt

A 19-year-old male motorcyclist sustains multiple long-bone fractures and internal haemorrhage in a road traffic accident. He receives 6 units of packed red cells and 4 L of crystalloid. Forty-eight hours later, he develops progressive breathlessness, hypoxaemia (PaO2/FiO2 ratio 180), bilateral pulmonary infiltrates on CXR, and no evidence of left heart failure. BAL fluid shows foamy macrophages and proteinaceous debris. Which type of embolism is MOST likely responsible, and through what mechanism does it cause the pulmonary injury?

A Thromboembolism — DVT from lower limb immobility embolises to the pulmonary vasculature, causing haemorrhagic infarction
B Fat embolism — marrow fat from fractured long bones enters systemic veins, reaches pulmonary capillaries, is hydrolysed to free fatty acids by lipases, causing endothelial injury and ARDS
C Air embolism — air introduced during IV fluid resuscitation accumulates in the right ventricle, causing outflow obstruction and bilateral pulmonary infiltrates
D Amniotic fluid embolism — although male, the massive transfusion introduced foreign proteins that trigger a DIC-like picture causing ARDS

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Q9 PA5.6 1 pt

A 64-year-old woman with septic shock from a ruptured appendix is intubated and placed on vasopressors. Despite aggressive resuscitation, her mean arterial pressure (MAP) remains 58 mmHg and her serum lactate rises from 2.8 to 6.4 mmol/L over 4 hours. Urine output falls to 10 mL/hour and her creatinine doubles. Which stage of shock does the RISING LACTATE specifically indicate, and which organ system is at greatest risk of irreversible failure?

A Compensated (non-progressive) shock — lactate rises as the liver compensates by switching to anaerobic metabolism to spare glucose for the brain
B Progressive (decompensated) shock — lactate rise indicates tissue hypoperfusion beyond compensatory capacity; the kidney is at greatest risk due to its high oxygen extraction fraction and susceptibility to hypoxic tubular necrosis
C Irreversible shock — lactate >6 mmol/L is the threshold for irreversible mitochondrial failure; no organ can be salvaged at this lactate level
D Progressive shock — lactate rise reflects hepatic failure specifically; the brain is at greatest risk because lactate crosses the blood-brain barrier and inhibits neuronal ATP synthesis

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Q10 PA5.1 1 pt

A 45-year-old man with decompensated alcoholic cirrhosis is admitted with tense ascites, jaundice (bilirubin 185 μmol/L), and bilateral pitting ankle oedema. Serum albumin is 21 g/L and his INR is 2.4. He has a serum-ascites albumin gradient (SAAG) of 18 g/L. Echocardiography shows normal cardiac function. Which mechanism PRIMARILY drives his ascites, and why is SAAG >11 g/L the diagnostic threshold?

B Portal hypertension raises capillary hydrostatic pressure in the splanchnic bed; SAAG >11 g/L reflects the hydrostatic (not oncotic) pressure differential, as serum albumin minus ascites albumin correlates with portal pressure
A Hypoalbuminaemia reduces oncotic pressure systemically; SAAG >11 g/L is diagnostic because the difference reflects the degree of oncotic pressure deficit across the peritoneal membrane
C Inflammatory peritoneal exudate from alcoholic hepatitis; SAAG <11 g/L would be expected in this patient due to high ascites protein from inflammation
D Lymphatic obstruction from a cirrhotic liver impairs thoracic duct drainage; SAAG >11 g/L reflects the high protein content of chylous ascites

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Q11 PA5.3 1 pt

At autopsy of a 78-year-old man who died of acute MI, the pathologist identifies a firm, grey-white structure attached to the left ventricular mural wall at the site of a recent infarct. Microscopically it shows alternating pale and dark layers (Lines of Zahn), fibrin, red cells, and areas of early fibrous organisation at the edges. A second specimen from the right ventricle shows a uniform dark red gelatinous clot with a yellow upper layer separating spontaneously from the wall. Which statement CORRECTLY distinguishes these two findings?

A Both are antemortem thrombi; the different appearances reflect the age of each thrombus (LV older, RV newer)
B The LV specimen is an antemortem mural thrombus (Lines of Zahn, fibrous organisation, firm attachment); the RV specimen is a postmortem clot (uniform currant-jelly/chicken-fat separation, no attachment, no Lines of Zahn)
C Both are postmortem clots; the LV appears pale and layered because haemolysis of trapped red cells alters the colour in postmortem fixation
D The LV specimen is a paradoxical embolus from a DVT crossing the interatrial septum; the RV specimen is an antemortem platelet thrombus from right ventricular infarction

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Q12 PA5.2 1 pt

A 72-year-old man with a 3-week history of progressive dyspnoea, bilateral ankle oedema, and orthopnoea is admitted. CXR shows bilateral pleural effusions, cardiomegaly, and perihilar haziness. The HS-troponin is mildly elevated. BNP is 1,840 pg/mL. On examination he has elevated JVP, bilateral basal crepitations, and tender hepatomegaly. The liver biopsy shows centrilobular congestion and haemorrhagic necrosis, with preservation of periportal hepatocytes. Which SINGLE structural abnormality in the cardiovascular system BEST links all the findings — elevated JVP, bilateral oedema, pleural effusions, and centrilobular hepatic necrosis?

A Left ventricular systolic dysfunction — reduced forward flow raises left atrial pressure, causing pulmonary venous hypertension and pulmonary oedema; retrograde pressure causes JVP elevation
B Right ventricular failure (from any cause) — inadequate right ventricular output → venous congestion propagates through the systemic venous system: elevated JVP → hepatic venous congestion → centrilobular necrosis; raised systemic venous pressure → bilateral oedema + pleural effusion
C Pulmonary arterial hypertension — high PA pressure overloads the right ventricle; the right ventricle dilates, impairing left ventricular filling via ventricular interdependence, causing biventricular failure and hepatic congestion
D Constrictive pericarditis — pericardial thickening restricts all cardiac chambers equally; elevated venous pressure is transmitted equally to pulmonary and systemic venous systems, causing both pulmonary oedema and systemic oedema simultaneously

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