Cardiovascular Pathology MCQs: Rheumatic Fever, AAA, HTN

Question 1

A 58-year-old male smoker with hypertension, crushing chest pain 2 hrs, ST-elevation in leads V1–V4. Which artery is MOST likely occluded?

Accepted Answer

Left anterior descending artery (LAD) — V1–V4 = anterior/anteroseptal leads → territory of the LAD - RCA → inferior leads (II, III, aVF); LCx → lateral leads (I, aVL, V5–V6) ---

Question 2

72-year-old male, longstanding HTN, AAA 6.2 cm. Which layer MOST affected, and key mechanism?

Accepted Answer

Media — destruction of elastin and collagen by matrix metalloproteinases (MMPs) — AAA pathogenesis centers on the media : chronic inflammation (often atherosclerosis-driven) upregulates MMPs that degrade elastin/collagen, weakening the wall and allowing dilation - (E) describes Marfan-type dissection pathology, not typical atherosclerotic AAA ---

Question 3

50-year-old, sudden cardiac death, heart 560g, concentric LV wall thickening, normal-sized chamber. Most likely hemodynamic cause?

Accepted Answer

Chronic systemic hypertension (pressure overload) — Concentric hypertrophy with normal chamber size = pressure overload (hypertension, aortic stenosis) - Volume overload lesions (MR, AR, VSD) cause eccentric hypertrophy with chamber dilation ---

Question 4

66-year-old female, T2DM, exertional dyspnea, EF preserved (55%), impaired diastolic filling. Best explanation? - Classic HFpEF picture in diabetes: diabetic cardiomyopathy causes myocardial fibrosis/hypertrophy → stiff, poorly compliant ventricle → impaired relaxation despite preserved EF ---

Accepted Answer

Myocardial fibrosis and hypertrophy causing impaired ventricular relaxation

Question 5

35-year-old male, Marfan syndrome, aortic dissection ascending aorta to iliacs. Which layer does the dissection plane travel through?

Accepted Answer

Within the outer third of the media — Marfan-associated dissection results from cystic medial degeneration (loss of elastin/smooth muscle, mucoid pools) - The dissection plane classically splits within the outer third of the media ---

Question 6

60-year-old, chronic renal failure, calcific deposits in the media of muscular arteries, "tram-track" on X-ray. Best description? - Mönckeberg sclerosis: calcification of the media of muscular arteries, common in elderly/diabetics/CKD; does not narrow the lumen (unlike atherosclerosis) ---

Accepted Answer

Mönckeberg medial calcific sclerosis

Question 7

48-year-old, infective endocarditis on a previously damaged (rheumatic) valve. Most common cause of subacute bacterial endocarditis?

Accepted Answer

Streptococcus viridans (S. sanguinis) — Low-virulence oral streptococci ( viridans group ) classically infect already-damaged/deformed valves → indolent, subacute course - S. aureus causes acute IE, often on normal valves ---

Question 8

Which plaque change is MOST directly responsible for converting stable angina to an acute coronary syndrome?

Accepted Answer

Plaque rupture or erosion with superimposed thrombosis — ACS results from acute plaque disruption (rupture/erosion) exposing thrombogenic core material → superimposed thrombus → sudden flow-limiting or occlusive event ---

Question 9

25-year-old female, dyspnea, hemoptysis, leg edema, PA pressure 58/25, PCWP 8 (normal), PVR markedly elevated, plexiform lesions, BMPR2 mutation. Diagnosis? - Normal PCWP (rules out Group 2/left heart cause) + BMPR2 mutation + plexiform lesions = classic for Group 1 (idiopathic/hereditary) PAH ---

Accepted Answer

Group 1 PAH — idiopathic/hereditary pulmonary arterial hypertension

Question 10

68-year-old, fever, new murmur, splinter hemorrhages 3 weeks after dental extraction, aortic valve vegetation. Which sign is caused by septic emboli specifically?

Accepted Answer

Janeway lesions (painless hemorrhagic macules on palms/soles) — Janeway lesions result directly from septic microemboli lodging in the skin - Osler nodes and Roth spots are immune complex-mediated , not embolic ---

Question 11

70-year-old, exertional syncope/angina/dyspnea (classic triad), harsh systolic ejection murmur, calcified aortic valve, mean gradient 52 mmHg. Most likely underlying pathology?

Accepted Answer

Calcific (senile/degenerative) aortic stenosis of a trileaflet valve — In an elderly patient, the classic mechanism is age-related "wear-and-tear" calcific degeneration of a normal trileaflet valve - Bicuspid valve calcification (B) presents earlier, typically 50s–60s rather than 70s+ ---

Question 12

40-year-old female, MVP, leaflets thick/rubbery/balloon into LA, myxomatous expansion of the spongiosa. This material is PRIMARILY:

Accepted Answer

Proteoglycans and glycosaminoglycans (dermatan sulfate) — Myxomatous degeneration = excess accumulation of proteoglycans/GAGs (especially dermatan sulfate) in the spongiosa layer, weakening the valve's structural collagen framework ---

Question 13

30-year-old male with AIDS, fever/night sweats/weight loss, cardiac mass, spindle cells with slit-like vascular spaces and surrounding RBCs. Most likely diagnosis?

Accepted Answer

Kaposi sarcoma — HHV-8-associated Kaposi sarcoma in an AIDS patient; classic histology is spindle cells forming slit-like vascular spaces with extravasated RBCs ---

Question 14

55-year-old, anterior STEMI 5 yrs ago, LBBB, EF 22%, dilated LV with global hypokinesis, apical thrombus. GREATEST risk for which complication?

Accepted Answer

Systemic thromboembolic events (e.g., stroke) — An established apical mural thrombus poses the greatest immediate risk of systemic embolization (e.g., stroke) - Wall/papillary muscle rupture and tamponade are acute complications (days post-MI), not 5 years later ---

Question 15

62-year-old, 70% RCA stenosis from a stable fibrous plaque. What distinguishes it from a VULNERABLE plaque? - Stable plaques : thick fibrous cap, abundant SMCs/collagen, minimal inflammation - Vulnerable plaques : thin fibrous cap, large lipid core, dense macrophage infiltration — prone to rupture ---

Accepted Answer

Thick fibrous cap with abundant smooth muscle cells and few macrophages

Question 16

5-year-old boy, cyanosis worse with exertion, improves with squatting; VSD + overriding aorta + RVOT obstruction + RVH. Diagnosis, and what determines cyanosis severity?

Accepted Answer

Tetralogy of Fallot — determined by degree of right ventricular outflow obstruction — Classic Tetralogy of Fallot (VSD + overriding aorta + RVOT obstruction + RVH) - Degree of cyanosis correlates with severity of RVOT/pulmonic obstruction — worse obstruction → more right-to-left shunting across the VSD ---

Question 17

50-year-old female, systemic sclerosis, right heart failure, PCWP normal, PVR markedly elevated. Vascular pathology MOST responsible?

Accepted Answer

Pulmonary arteriolar intimal fibrosis and medial hypertrophy (PAH) — Normal PCWP + elevated PVR = precapillary pulmonary hypertension - In scleroderma, this is due to PAH -type small vessel remodeling: intimal fibrosis and medial hypertrophy of pulmonary arterioles (Group 1 PAH associated with connective tissue disease) ---

Question 18

63-year-old, known CAD, new harsh pansystolic murmur + cardiogenic shock 4 days after large inferior MI, severe MR on echo. MOST likely structural cause?

Accepted Answer

Papillary muscle rupture causing acute mitral valve incompetence — Inferior MIs (RCA territory) put the posteromedial papillary muscle (single blood supply) at high risk of rupture, causing acute severe MR — typically 3–7 days post-MI ---

Question 19

72-year-old, constrictive pericarditis, pericardiectomy shows dense fibrous thickening with calcification. Expected hemodynamic feature?

Accepted Answer

Equalization of diastolic pressures across all four cardiac chambers — The rigid, non-compliant pericardium restricts filling equally in all chambers → classic equalization of diastolic pressures (RA = RV = PCWP) ---

Question 20

34-year-old female, 2 weeks exertional dyspnea/ankle swelling, delivered 6 weeks ago, dilated LV EF 30%, lymphocytic myocarditis on biopsy. Most likely mechanism?

Accepted Answer

Autoimmune myocarditis triggered by fetal microchimerism or hormonal changes — Classic peripartum cardiomyopathy — postpartum dilated LV with lymphocytic myocarditis; proposed mechanisms include autoimmune response to fetal microchimeric cells and pregnancy-related hormonal/vascular changes (e.g., prolactin fragments) ---

Question 21

16-year-old male, family history of sudden death, collapses during basketball, asymmetric septal hypertrophy (22mm), no dilation, myofiber disarray. Genetic mutation MOST responsible?

Accepted Answer

Beta-myosin heavy chain (MYH7) or myosin-binding protein C (MYBPC3) mutations — Classic hypertrophic cardiomyopathy (HCM) , autosomal dominant, most commonly caused by sarcomeric protein gene mutations — MYH7 and MYBPC3 are the two most common ---

Question 22

52-year-old, hyperlipidemia, femoral-popliteal bypass, plaque shows central cholesterol clefts and calcification. Why do cholesterol clefts form? - Cholesterol crystals are dissolved by the organic solvents used in histologic tissue processing , leaving behind characteristic needle-shaped empty clefts on H&E ---

Accepted Answer

Cholesterol crystals dissolve during tissue processing, leaving empty spaces

Question 23

42-year-old female, SLE, pleuritic chest pain, friction rub, diffuse saddle-shaped ST elevation, afebrile. Expected pericardial finding?

Accepted Answer

Fibrinous pericarditis with "bread-and-butter" appearance — SLE-associated (and uremic) pericarditis is classically fibrinous , giving the gross "bread-and-butter" shaggy appearance of the pericardial surfaces ---

Cardiovascular Pathology MCQs: Rheumatic Fever, AAA, HTN

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