MCQ Quiz: Pathophysiology of Ischemic Heart Disease

Ischemic Heart Disease (IHD) represents a spectrum of conditions resulting from an imbalance between myocardial oxygen supply and demand, primarily due to atherosclerosis in the coronary arteries. A thorough understanding of the intricate pathophysiological mechanisms underlying IHD is fundamental for PharmD students. This knowledge underpins the ability to comprehend clinical manifestations, diagnostic approaches, and the rationale for various therapeutic interventions aimed at preventing progression and managing symptoms. This MCQ quiz will explore the core pathophysiological processes involved in the development and progression of Ischemic Heart Disease, from endothelial dysfunction and plaque formation to the consequences of myocardial ischemia.

1. The hallmark of Ischemic Heart Disease (IHD) is an imbalance between:

• A. Myocardial glucose supply and fatty acid supply
• B. Myocardial oxygen supply and myocardial oxygen demand
• C. Coronary artery dilation and constriction
• D. Sympathetic and parasympathetic stimulation of the heart

Answer: B. Myocardial oxygen supply and myocardial oxygen demand

2. The most common underlying cause of reduced myocardial oxygen supply in IHD is:

• A. Severe anemia
• B. Coronary artery vasospasm
• C. Atherosclerotic narrowing of coronary arteries
• D. Hypoxemia due to lung disease

Answer: C. Atherosclerotic narrowing of coronary arteries

3. Which of the following is considered the earliest recognizable lesion of atherosclerosis?

• A. Complicated plaque with rupture
• B. Fibrous plaque
• C. Fatty streak
• D. Calcified plaque

Answer: C. Fatty streak

4. The primary lipid component that accumulates in atherosclerotic plaques is derived from:

• A. High-Density Lipoprotein (HDL)
• B. Chylomicrons
• C. Oxidized Low-Density Lipoprotein (LDL)
• D. Triglycerides directly

Answer: C. Oxidized Low-Density Lipoprotein (LDL)

5. “Foam cells” in an atherosclerotic lesion are primarily formed by:

• A. Proliferating smooth muscle cells
• B. Macrophages that have engulfed oxidized LDL
• C. Endothelial cells filled with lipids
• D. Aggregated platelets

Answer: B. Macrophages that have engulfed oxidized LDL

6. Endothelial dysfunction is a key early event in atherogenesis. It is characterized by:

• A. Increased production of nitric oxide (NO) and reduced permeability
• B. Reduced production of NO, increased expression of adhesion molecules, and increased permeability
• C. Enhanced anticoagulant properties
• D. Proliferation of endothelial cells

Answer: B. Reduced production of NO, increased expression of adhesion molecules, and increased permeability

7. Which of the following is a major determinant of myocardial oxygen DEMAND?

• A. Coronary artery diameter
• B. Blood oxygen carrying capacity
• C. Heart rate and myocardial contractility
• D. Diastolic filling time

Answer: C. Heart rate and myocardial contractility

8. Stable angina pectoris is typically caused by myocardial ischemia that occurs when:

• A. A coronary artery plaque ruptures and forms an occlusive thrombus.
• B. Myocardial oxygen demand exceeds supply due to a fixed, significant coronary stenosis during exertion.
• C. Coronary arteries spasm in the absence of significant atherosclerosis.
• D. There is a sudden drop in systemic blood pressure.

Answer: B. Myocardial oxygen demand exceeds supply due to a fixed, significant coronary stenosis during exertion.

9. The pain associated with angina pectoris is believed to be mediated by the accumulation of which substances in the ischemic myocardium?

• A. Oxygen and glucose
• B. Adenosine, bradykinin, and other metabolic products
• C. Catecholamines exclusively
• D. Sodium and potassium ions

Answer: B. Adenosine, bradykinin, and other metabolic products

10. Unstable angina is pathophysiologically distinguished from stable angina primarily by:

• A. The complete absence of atherosclerotic plaque.
• B. Ischemia caused solely by increased myocardial demand.
• C. Disruption of an atherosclerotic plaque with superimposed non-occlusive thrombosis and/or vasospasm.
• D. A fixed stenosis that causes predictable symptoms only at very high exertion.

Answer: C. Disruption of an atherosclerotic plaque with superimposed non-occlusive thrombosis and/or vasospasm.

11. Which component of an atherosclerotic plaque contributes most to its vulnerability and risk of rupture?

• A. A thick, intact fibrous cap
• B. A large, calcified core
• C. A thin fibrous cap overlying a large lipid-rich necrotic core with inflammatory cells
• D. Predominance of smooth muscle cells

Answer: C. A thin fibrous cap overlying a large lipid-rich necrotic core with inflammatory cells

12. Myocardial stunning refers to:

• A. Irreversible myocardial cell death due to prolonged ischemia.
• B. Chronic ventricular dysfunction due to persistent hypoperfusion, which is reversible if blood flow is restored.
• C. Prolonged systolic dysfunction of viable myocardium that occurs after a brief period of severe ischemia, even after reperfusion.
• D. An electrical abnormality causing arrhythmias.

Answer: C. Prolonged systolic dysfunction of viable myocardium that occurs after a brief period of severe ischemia, even after reperfusion.

13. Myocardial hibernation is characterized by:

• A. Acute myocardial necrosis.
• B. Persistent myocardial dysfunction in the presence of chronically reduced coronary blood flow, which can recover if blood flow is restored.
• C. A temporary increase in myocardial contractility.
• D. Inflammation of the pericardium.

Answer: B. Persistent myocardial dysfunction in the presence of chronically reduced coronary blood flow, which can recover if blood flow is restored.

14. In the event of a coronary artery occlusion, myocardial cell death typically begins in which region of the heart wall?

• A. Epicardium
• B. Mid-myocardium
• C. Subendocardium
• D. Pericardium

Answer: C. Subendocardium

15. The transition from reversible myocardial ischemia to irreversible injury (infarction) is primarily dependent on:

• A. The patient’s age
• B. The severity and duration of the ischemia
• C. The level of HDL cholesterol
• D. The presence of collateral circulation only

Answer: B. The severity and duration of the ischemia

16. An ST-segment elevation myocardial infarction (STEMI) is most commonly caused by:

• A. Severe but incomplete coronary artery occlusion.
• B. Complete and persistent thrombotic occlusion of a coronary artery.
• C. Coronary artery vasospasm without underlying atherosclerosis.
• D. Microvascular dysfunction.

Answer: B. Complete and persistent thrombotic occlusion of a coronary artery.

17. Non-ST-segment elevation myocardial infarction (NSTEMI) typically involves:

• A. Complete occlusion of a major coronary artery leading to transmural infarction.
• B. Severe coronary artery stenosis or a non-occlusive thrombus leading to subendocardial infarction.
• C. No actual myocardial necrosis, only prolonged ischemia.
• D. Ischemia due to valvular heart disease.

Answer: B. Severe coronary artery stenosis or a non-occlusive thrombus leading to subendocardial infarction.

18. The release of cardiac biomarkers like troponin into the bloodstream after an MI is due to:

• A. Increased synthesis by healthy cardiomyocytes.
• B. Leakage from damaged and necrotic cardiomyocyte membranes.
• C. Active secretion by ischemic but viable cells.
• D. Breakdown of atherosclerotic plaques.

Answer: B. Leakage from damaged and necrotic cardiomyocyte membranes.

19. Which of the following inflammatory cells plays a critical role in all stages of atherosclerosis, from fatty streak formation to plaque rupture?

• A. Neutrophils
• B. Eosinophils
• C. Macrophages
• D. Basophils

Answer: C. Macrophages

20. The “coronary flow reserve” is the ability of the coronary circulation to:

• A. Maintain constant flow despite changes in perfusion pressure.
• B. Increase blood flow above basal levels in response to increased myocardial demand.
• C. Divert blood flow from healthy to ischemic areas.
• D. Store oxygen for later use.

Answer: B. Increase blood flow above basal levels in response to increased myocardial demand.

21. Prinzmetal’s (variant) angina is caused by episodic myocardial ischemia due to:

• A. Fixed high-grade coronary stenosis
• B. Rupture of an atherosclerotic plaque
• C. Spasm of a coronary artery
• D. Increased heart rate during exercise

Answer: C. Spasm of a coronary artery

22. What is the primary mechanism by which hypertension contributes to the pathophysiology of IHD?

• A. It directly causes coronary artery vasospasm.
• B. It promotes endothelial dysfunction, increases shear stress, and enhances atherosclerosis development.
• C. It leads to a decrease in myocardial oxygen demand.
• D. It improves coronary collateral circulation.

Answer: B. It promotes endothelial dysfunction, increases shear stress, and enhances atherosclerosis development.

23. How does smoking contribute to the pathophysiology of IHD?

• A. It increases HDL cholesterol levels.
• B. It causes endothelial dysfunction, promotes a prothrombotic state, and introduces carbon monoxide.
• C. It primarily leads to coronary vasodilation.
• D. It reduces platelet aggregation.

Answer: B. It causes endothelial dysfunction, promotes a prothrombotic state, and introduces carbon monoxide.

24. Diabetes mellitus accelerates atherosclerosis and IHD primarily through mechanisms involving:

• A. Reduced blood glucose levels.
• B. Enhanced nitric oxide production.
• C. Endothelial dysfunction, oxidative stress, advanced glycation end-product formation, and a pro-inflammatory state.
• D. Decreased platelet reactivity.

Answer: C. Endothelial dysfunction, oxidative stress, advanced glycation end-product formation, and a pro-inflammatory state.

25. The process of “cardiac remodeling” after a myocardial infarction refers to changes in:

• A. The electrical conduction system only.
• B. The size, shape, and function of the ventricle due to scar formation and neurohormonal activation.
• C. The coronary artery anatomy only.
• D. The patient’s lifestyle habits.

Answer: B. The size, shape, and function of the ventricle due to scar formation and neurohormonal activation.

26. Which neurohormonal systems are typically activated after a myocardial infarction and contribute to adverse remodeling?

• A. Only the parasympathetic nervous system
• B. The renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system
• C. Only the natriuretic peptide system
• D. The kinin-kallikrein system

Answer: B. The renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system

27. The initial cellular response to myocardial ischemia (within minutes) involves:

• A. A shift to aerobic metabolism and increased ATP production.
• B. A shift to anaerobic metabolism, lactate accumulation, and ATP depletion.
• C. Apoptosis of all affected cells.
• D. Rapid formation of collateral vessels.

Answer: B. A shift to anaerobic metabolism, lactate accumulation, and ATP depletion.

28. The “no-reflow” phenomenon, sometimes observed after reperfusion therapy for MI, refers to:

• A. Re-occlusion of the infarct-related artery due to new thrombus.
• B. Inability to restore microvascular perfusion despite reopening the epicardial coronary artery.
• C. Excessive bleeding from the reperfused area.
• D. A sudden surge in blood pressure upon reperfusion.

Answer: B. Inability to restore microvascular perfusion despite reopening the epicardial coronary artery.

29. Reperfusion injury can occur when blood flow is restored to ischemic myocardium, paradoxically causing further damage due to:

• A. Insufficient oxygen delivery.
• B. Production of reactive oxygen species, calcium overload, and inflammation.
• C. Persistent anaerobic metabolism.
• D. Activation of anti-inflammatory pathways.

Answer: B. Production of reactive oxygen species, calcium overload, and inflammation.

30. The fibrous cap of an atherosclerotic plaque is primarily composed of:

• A. Cholesterol crystals and foam cells
• B. Smooth muscle cells, collagen, and elastin
• C. Aggregated platelets and fibrin
• D. Endothelial cells and red blood cells

Answer: B. Smooth muscle cells, collagen, and elastin

31. How does high HDL cholesterol exert a protective effect against atherosclerosis?

• A. By directly inhibiting HMG-CoA reductase.
• B. By promoting reverse cholesterol transport from peripheral tissues to the liver.
• C. By increasing LDL oxidation.
• D. By stimulating platelet aggregation.

Answer: B. By promoting reverse cholesterol transport from peripheral tissues to the liver.

32. Which statement accurately describes the role of platelets in the pathophysiology of acute coronary syndromes?

• A. They primarily cause vasodilation.
• B. They adhere to ruptured plaques, activate, and aggregate to form a thrombus.
• C. They are responsible for clearing cholesterol from plaques.
• D. They release nitric oxide, preventing thrombosis.

Answer: B. They adhere to ruptured plaques, activate, and aggregate to form a thrombus.

33. The degree of coronary artery stenosis becomes hemodynamically significant (limiting flow during increased demand) typically when the lumen diameter is reduced by at least:

• A. 10-20%
• B. 20-30%
• C. 50-70%
• D. 95-100% (which would be critical stenosis or occlusion)

Answer: C. 50-70% (Some sources say >70% for symptoms at rest, but >50% can be significant with demand).

34. “Collateral circulation” in the heart refers to:

• A. The main epicardial coronary arteries.
• B. A network of small, pre-existing or newly formed vessels that can provide alternative blood flow to ischemic myocardium.
• C. The lymphatic drainage of the heart.
• D. The venous system returning blood from the myocardium.

Answer: B. A network of small, pre-existing or newly formed vessels that can provide alternative blood flow to ischemic myocardium.

35. What is the effect of increased myocardial wall tension (due to increased preload or afterload) on myocardial oxygen demand?

• A. It decreases oxygen demand.
• B. It increases oxygen demand.
• C. It has no effect on oxygen demand.
• D. It primarily affects oxygen supply.

Answer: B. It increases oxygen demand. (LaPlace’s Law)

36. The progression of an atherosclerotic plaque involves the migration and proliferation of which cell type from the media into the intima?

• A. Endothelial cells
• B. Smooth muscle cells
• C. Neutrophils
• D. Red blood cells

Answer: B. Smooth muscle cells

37. Which of these is a key pro-inflammatory cytokine involved in atherosclerosis?

• A. Interleukin-10 (IL-10)
• B. Tumor Necrosis Factor-alpha (TNF-α)
• C. Transforming Growth Factor-beta (TGF-β)
• D. Erythropoietin

Answer: B. Tumor Necrosis Factor-alpha (TNF-α)

38. Pathological Q waves on an ECG are most indicative of:

• A. Acute pericarditis
• B. Previous transmural myocardial infarction (scar tissue)
• C. Atrial fibrillation
• D. Coronary vasospasm

Answer: B. Previous transmural myocardial infarction (scar tissue)

39. The vulnerability of an atherosclerotic plaque to rupture is more dependent on its __________ than its __________.

• A. Size; composition
• B. Composition and inflammatory state; degree of stenosis
• C. Location; size
• D. Degree of stenosis; lipid content

Answer: B. Composition and inflammatory state; degree of stenosis

40. What is the primary consequence of ATP depletion in ischemic myocardial cells regarding ion pumps?

• A. Increased activity of Na+/K+-ATPase, leading to hyperpolarization.
• B. Failure of Na+/K+-ATPase, leading to intracellular Na+ and Ca2+ accumulation and K+ loss.
• C. Enhanced SERCA pump activity, leading to excessive Ca2+ sequestration.
• D. Opening of ATP-sensitive K+ channels, causing repolarization.

Answer: B. Failure of Na+/K+-ATPase, leading to intracellular Na+ and Ca2+ accumulation and K+ loss.

41. Angiotensin II contributes to adverse cardiac remodeling post-MI by promoting:

• A. Vasodilation and natriuresis.
• B. Apoptosis of viable cardiomyocytes.
• C. Fibroblast proliferation, collagen deposition, and myocyte hypertrophy.
• D. Inhibition of the sympathetic nervous system.

Answer: C. Fibroblast proliferation, collagen deposition, and myocyte hypertrophy.

42. The “lipid hypothesis” of atherosclerosis states that:

• A. All dietary lipids are directly incorporated into plaques.
• B. Elevated levels of plasma cholesterol, particularly LDL-C, are a primary cause of atherosclerosis.
• C. HDL cholesterol is the main atherogenic lipoprotein.
• D. Triglycerides are more important than cholesterol in plaque formation.

Answer: B. Elevated levels of plasma cholesterol, particularly LDL-C, are a primary cause of atherosclerosis.

43. Matrix metalloproteinases (MMPs) secreted by inflammatory cells within an atherosclerotic plaque contribute to plaque instability by:

• A. Promoting collagen synthesis and thickening the fibrous cap.
• B. Degrading extracellular matrix components, thereby weakening the fibrous cap.
• C. Inhibiting platelet aggregation.
• D. Reducing the size of the lipid core.

Answer: B. Degrading extracellular matrix components, thereby weakening the fibrous cap.

44. The development of stable angina symptoms is most closely related to:

• A. The absolute size of the coronary plaque.
• B. The degree to which a fixed plaque limits coronary flow reserve during exertion.
• C. The presence of a non-occlusive thrombus.
• D. The level of C-reactive protein.

Answer: B. The degree to which a fixed plaque limits coronary flow reserve during exertion.

45. Which of the following is a compensatory mechanism that can initially help maintain myocardial perfusion in the presence of a developing coronary stenosis?

• A. Decreased heart rate
• B. Vasodilation of downstream resistance vessels (arterioles)
• C. Increased blood viscosity
• D. Reduced myocardial contractility

Answer: B. Vasodilation of downstream resistance vessels (arterioles)

46. The transition from unstable angina to NSTEMI is primarily differentiated by:

• A. The presence of ST-segment elevation on ECG in NSTEMI.
• B. Evidence of myocardial necrosis (e.g., elevated cardiac troponins) in NSTEMI.
• C. The duration of chest pain (longer in NSTEMI).
• D. The location of the affected coronary artery.

Answer: B. Evidence of myocardial necrosis (e.g., elevated cardiac troponins) in NSTEMI.

47. Atherosclerotic plaques tend to form preferentially at which locations in the coronary arteries?

• A. Straight, non-branching segments with laminar flow.
• B. Sites of arterial branching, bifurcations, and curvatures where blood flow is turbulent or disturbed.
• C. The distal ends of all coronary arteries equally.
• D. Within the capillaries of the myocardium.

Answer: B. Sites of arterial branching, bifurcations, and curvatures where blood flow is turbulent or disturbed.

48. What is the role of vasoconstrictors like endothelin-1 in the context of endothelial dysfunction and IHD?

• A. They are primarily protective by maintaining vascular tone.
• B. Their production is decreased in endothelial dysfunction, leading to excessive vasodilation.
• C. Their local overproduction can contribute to vasoconstriction and reduced myocardial perfusion.
• D. They primarily act to reduce platelet aggregation.

Answer: C. Their local overproduction can contribute to vasoconstriction and reduced myocardial perfusion.

49. Myocardial oxygen extraction from coronary blood is normally very high, even at rest. This implies that increased oxygen demand must be primarily met by:

• A. Increasing the percentage of oxygen extracted from the blood.
• B. Increasing coronary blood flow.
• C. Shifting to anaerobic metabolism.
• D. Utilizing stored oxygen reserves in myocytes.

Answer: B. Increasing coronary blood flow.

50. The healing process after a myocardial infarction involves the replacement of necrotic tissue with:

• A. Regenerated functional cardiomyocytes
• B. Adipose tissue
• C. Fibrous scar tissue
• D. New collateral blood vessels primarily

Answer: C. Fibrous scar tissue