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Quizzes > Quizzes for Business > Healthcare

Cardiovascular Pathology Knowledge Test

Assess Your Cardiac Pathology Mastery Today

Difficulty: Moderate
Questions: 20
Learning OutcomesStudy Material
Colorful paper art depicting a heart for Cardiovascular Pathology Knowledge Test quiz

Ready to challenge your skills with this cardiac pathology quiz? Joanna Weib invites you to tackle 15 questions on cardiovascular lesions, infarction patterns and vascular disease. Ideal for medical students, pathology trainees or clinicians seeking to strengthen diagnostic acumen. After completion, you can tweak the quiz in our editor to suit your learning needs. Explore the Pathology Knowledge Assessment Quiz, dive into the Cardiovascular Physiology Knowledge Test, or browse all quizzes.

Which histologic feature is characteristic of a fatty streak in early atherosclerosis?
Hyaline arteriolosclerosis
Foam cells in the intima
Medial necrosis
Calcification of the media
Fatty streaks are composed of lipid-laden macrophages (foam cells) within the intima, marking the earliest visible sign of atherosclerosis. They lack calcification and medial necrosis which are features of more advanced lesions.
The most common primary benign cardiac tumor in adults is:
Myxoma
Rhabdomyoma
Papillary fibroelastoma
Angiosarcoma
Cardiac myxoma is the most frequent primary benign heart tumor in adults, typically found in the left atrium. Rhabdomyomas are more common in children, and angiosarcoma is malignant.
Which histopathologic change is the earliest detectable on light microscopy after myocardial infarction?
Coagulative necrosis with hypereosinophilic fibers
Scar formation
Neutrophil infiltration
Granulation tissue formation
Within 4 - 24 hours post-infarction, coagulative necrosis appears with hypereosinophilic myocytes and loss of nuclei. Neutrophils peak later (1 - 3 days), granulation tissue forms after ~7 days, and scar formation is even later.
Calcific aortic stenosis in the elderly is characterized by:
Libman-Sacks vegetations
Myxomatous degeneration of valve chordae
Deposition of hydroxyapatite crystals in valve leaflets
Fibrinous verrucae on valve leaflets
Calcific aortic stenosis features progressive deposition of calcium hydroxyapatite in valve leaflets, leading to stiffness. Myxomatous degeneration describes mitral valve prolapse, Libman-Sacks in SLE, and fibrinous verrucae in rheumatic heart disease.
The presence of Aschoff bodies in myocardial tissue is diagnostic of:
Infective endocarditis
Takotsubo cardiomyopathy
Acute rheumatic myocarditis
Viral myocarditis
Aschoff bodies, granulomatous nodules with Anitschkow cells, are specific for acute rheumatic myocarditis. Infective endocarditis has vegetations, viral myocarditis shows lymphocytic infiltrate, and Takotsubo is characterized by contraction band necrosis.
Three to seven days after myocardial infarction, the predominant histological finding is:
Hypertrophy of myocardium
Macrophage-mediated phagocytosis of dead myocytes
Neutrophilic infiltration
Scar formation
Between 3 and 7 days post-infarction, macrophages infiltrate the tissue to phagocytose necrotic myocytes. Neutrophils predominate earlier. Scar formation occurs later.
Which feature distinguishes rheumatic mitral stenosis from mitral annular calcification histologically?
Presence of fibrous fusion of commissures
Libman-Sacks vegetations on atrial surface
Calcium deposition in annulus alone
Myxomatous degeneration of leaflets
Rheumatic mitral stenosis shows fibrous commissural fusion and leaflet thickening. Mitral annular calcification is limited to the annulus, myxomatous degeneration causes prolapse, and Libman-Sacks vegetations are seen in SLE.
A vulnerable atherosclerotic plaque is most likely to rupture when it exhibits:
Complete endothelial integrity
Predominantly calcified core
Thick fibrous cap and small lipid core
Thin fibrous cap and large lipid-rich necrotic core
Vulnerable plaques prone to rupture have a thin fibrous cap and large lipid-rich necrotic core, leading to exposure of thrombogenic material. Thick caps, calcification, and intact endothelium are more stable features.
Myxomatous degeneration of the mitral valve is characterized by:
Vegetations along the line of closure
Replacement of collagen by mucoid material in the spongiosa
Fibrinoid necrosis within valve tissue
Calcific nodules on the valve leaflets
In myxomatous degeneration, connective tissue in the spongiosa layer is replaced by mucopolysaccharide-rich mucoid material, causing leaflet thickening and prolapse. Calcific nodules, vegetations, and fibrinoid necrosis are features of other pathologies.
Which vascular lesion is hallmarked by onion-skin hyperplasia of smooth muscle cells?
Hyperplastic arteriolosclerosis due to malignant hypertension
Thromboangiitis obliterans
Aneurysm formation in syphilitic aortitis
Hyaline arteriosclerosis
Malignant hypertension causes hyperplastic arteriolosclerosis, characterized by onion-skin concentric smooth muscle proliferation. Hyaline arteriosclerosis shows homogeneous thickening, syphilitic aneurysm has vasa vasorum endarteritis, and thromboangiitis obliterans is an inflammatory thrombosis of medium vessels.
In infective endocarditis, vegetations on valve leaflets consist primarily of:
Platelet-fibrin aggregates with microorganisms
Lipid-laden macrophages
Organized smooth muscle cells
Mucoid connective tissue
Infective endocarditis vegetations are composed of fibrin, platelets, and colonies of microorganisms, often with inflammatory cells. Lipid-laden macrophages characterize atherosclerosis, and mucoid tissue is seen in myxomatous degeneration.
After myocardial infarction, papillary muscle dysfunction is most likely to occur due to rupture occurring in which period?
After complete scar formation
2 - 4 weeks post-infarction
Within the first 4 hours
3 - 7 days post-infarction
Papillary muscle rupture most commonly occurs 3 - 7 days post-infarction, when macrophages have weakened the necrotic tissue. It is rare very early or after scar maturation.
Which cardiac tumor is strongly associated with tuberous sclerosis in infants?
Rhabdomyoma
Papillary fibroelastoma
Fibroma
Cardiac myxoma
Cardiac rhabdomyomas are the most common pediatric cardiac tumors and are strongly linked with tuberous sclerosis. Myxomas occur in adults, fibroelastomas are incidental, and fibromas are less common.
In hypertensive vascular disease, hyaline arteriolosclerosis is characterized by:
Atherosclerotic plaque deposition
Fibrinoid necrosis of the vessel wall
Concentric laminated smooth muscle hyperplasia
Homogenous pink hyaline thickening of arteriolar walls
Hyaline arteriolosclerosis, seen in benign hypertension and diabetes, shows uniform, homogeneous, pink (hyaline) thickening of arteriolar walls. Concentric smooth muscle hyperplasia defines hyperplastic arteriolosclerosis, fibrinoid necrosis is malignant hypertension, and atherosclerosis affects larger vessels.
Which histologic feature is most consistent with healed myocardial infarction?
Dense collagenous scar
Wavy fibers with neutrophils
Contraction band necrosis
Granulation tissue with abundant capillaries
A healed myocardial infarct is characterized by a dense collagenous scar replacing necrotic myocytes. Wavy fibers and neutrophils reflect early MI, contraction bands are in reperfusion injury, and granulation tissue is seen in the intermediate healing phase.
Which mechanism best explains myocardial reperfusion injury after ischemia?
Generation of reactive oxygen species causing cell membrane damage
Decreased calcium influx into cells
Activation of neutrophils leading to collagen deposition
Upregulation of anti - apoptotic factors
Reperfusion injury is largely due to the sudden influx of oxygen generating reactive oxygen species that damage cell membranes and organelles. Neutrophils contribute but collagen deposition is part of healing, not injury; calcium influx increases, and anti-apoptotic factors are not upregulated.
Papillary fibroelastoma on heart valves is histologically characterized by:
Sheets of atypical endothelial cells
Avian nest - like branching fronds of connective tissue with elastin
Myxoid stroma with stellate cells
Lamellated concentric calcifications
Papillary fibroelastoma shows frond-like projections resembling a sea-anemone, composed of a central core of dense connective tissue rich in elastin and lined by endothelium. Myxoid stroma and stellate cells describe myxoma; concentric calcifications are calcific sclerosis; atypical endothelial cells could suggest angiosarcoma.
Which finding is most characteristic of Takayasu arteritis in the aorta?
Fibrinoid necrosis of vasa vasorum
Thrombosis of small cutaneous vessels
Deposition of immune complexes in glomeruli
Mononuclear granulomatous inflammation with giant cells throughout the vessel wall
Takayasu arteritis is a granulomatous panarteritis affecting medium and large arteries, with mononuclear cell infiltrates and giant cells present in the arterial wall. Fibrinoid necrosis of vasa vasorum is syphilitic aortitis; immune complexes in glomeruli reflect renal disease; cutaneous small vessel thrombosis indicates thromboangiitis obliterans.
Histopathological hallmark of hypertrophic cardiomyopathy includes:
Concentric ventricular hypertrophy with uniform fibers
Subendocardial fibrosis without myocyte disarray
Fatty infiltration of right ventricular free wall
Widespread myocyte hypertrophy with disorganized cell alignment and interstitial fibrosis
Hypertrophic cardiomyopathy shows marked myocyte hypertrophy, disarray of muscle fibers, and interstitial fibrosis. Concentric hypertrophy suggests pressure overload, fatty infiltration characterizes ARVC, and subendocardial fibrosis alone lacks disarray.
Loeffler endocarditis is defined by:
Eosinophil-mediated endomyocardial fibrosis with thrombus formation
Viral inclusion bodies in cardiomyocytes
Macrophage infiltration of myocardium forming Aschoff bodies
Lymphocytic myocarditis with giant cells
Loeffler endocarditis (endomyocardial fibrosis) involves eosinophilic infiltration causing myocardial damage, fibrosis, and intracardiac thrombi. Aschoff bodies are rheumatic, lymphocytic infiltration suggests viral myocarditis, and inclusion bodies also reflect viral infections.
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Learning Outcomes

  1. Analyse histopathological features of common cardiovascular lesions
  2. Identify key cellular changes in myocardial infarction
  3. Differentiate various forms of valvular heart disease
  4. Evaluate vascular abnormalities and atherosclerotic plaques
  5. Apply pathological insights to clinical cardiovascular cases
  6. Demonstrate understanding of cardiac tumor pathology

Cheat Sheet

  1. Progression of Coronary Atherosclerosis - Imagine your arteries as bustling highways that start off smooth but gradually develop fatty streaks, then fibrous caps, and finally rigid fibrocalcific plaques that narrow the lanes. Understanding each stage from intimal hyperplasia to advanced calcification helps you predict when and where blockages may occur. Read the full article
  2. Histopathological Features of Myocardial Infarction - Picture heart muscle cells as tiny workers: when blood flow stops, they undergo coagulative necrosis (freezing in place) and signal for inflammatory "cleanup crews" of neutrophils and macrophages. Spotting wavy fibers, nuclear changes, and cell debris under a microscope is like detective work at the cellular level. Read the full article
  3. Valvular Heart Disease Differentiation - Think of your heart valves as doors: in aortic stenosis the hinge thickens and stiffens (often with calcium nodules), while mitral regurgitation leads to floppy, leaky edges and stretched chordae tendineae. Recognizing these unique pathological changes is key to choosing the right treatment strategy. Read the full article
  4. Characteristics of Cardiac Tumors - Cardiac myxomas are benign, gelatinous masses often lurking in the atria, while angiosarcomas are aggressive, irregular blood”vessel tumors that invade surrounding tissues. Learning their histological patterns and clinical warning signs helps you spot these rare but impactful growths. Read the full article
  5. Role of Inflammation in Atherosclerosis - Inflammation isn't just an aftermath - it's a major driver as immune cells, cytokines, and oxidized lipids team up to turn fatty streaks into complex plaques. Grasping how macrophages become foam cells and secrete enzymes deepens your understanding of plaque stability. Read the full article
  6. Plaque Rupture and Thrombosis Mechanisms - Picture a thin fibrous cap as a fragile dam: once weakened by enzymes and cellular stress, it cracks, releasing lipid cores into the bloodstream and triggering clot (thrombus) formation. Knowing this cascade clarifies why some heart attacks strike suddenly. Read the full article
  7. Hypertrophic vs. Dilated Cardiomyopathies - In hypertrophic cardiomyopathy, the heart walls thicken and stiffen (like an overbuilt fortress), whereas in dilated cardiomyopathy the chambers balloon out and weaken (like an overstretched balloon). Spotting these contrasting changes under the microscope aids in precise diagnosis. Read the full article
  8. Histology of Infective Endocarditis - Endocarditis vegetations look like grainy, friable sprouts on valves, teeming with bacteria, fibrin, and inflammatory cells. Recognizing these destructive lesions explains why patients can develop valve perforations and systemic infections. Read the full article
  9. Pathology of Congenital Heart Defects - Ventricular septal defects create a hole between chambers, causing left-to-right blood shunts that overload pulmonary circulation over time. Visualizing this defect helps explain associated symptoms like breathlessness and failure to thrive in infants. Read the full article
  10. Vascular Changes in Hypertension - High blood pressure forces arterioles to remodel: you'll see hyaline "glass-like" thickening or hyperplastic onion-skin layers of smooth muscle. Understanding these changes shows why organs like the kidney and brain are vulnerable to chronic pressure damage. Read the full article
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