NURS 661: ADVANCED PATHOPHYSIOLOGY & THERAPEUTICS
EXAM QUESTIONS AND 100% VERIFIED ANSWERS RECENTLY
UPDATED
275 QUESTIONS AND ANSWERS
1. Q: What is the primary mechanism underlying atherosclerosis? A:
Atherosclerosis is primarily caused by endothelial dysfunction leading to lipid
accumulation, inflammatory cell infiltration, smooth muscle cell proliferation,
and formation of fibrous plaques in arterial walls.
2. Q: Explain the Frank-Starling mechanism and its clinical significance. A:
The Frank-Starling mechanism states that stroke volume increases with
increased venous return (preload) due to optimal sarcomere length. Clinically, it
explains how the heart adapts to varying venous return and is impaired in heart
failure.
3. Q: What are the key differences between systolic and diastolic heart
failure? A: Systolic HF (HFrEF) involves reduced ejection fraction (<40%)
with impaired contractility. Diastolic HF (HFpEF) has preserved ejection
fraction (≥50%) but impaired ventricular filling due to stiffness or relaxation
abnormalities.
4. Q: Describe the pathophysiology of hypertensive crisis. A: Hypertensive
crisis involves acute severe BP elevation (>180/120 mmHg) causing end-organ
damage through autoregulation failure, endothelial dysfunction,
microangiopathy, and inflammatory responses leading to cerebral, cardiac, or
renal complications.
5. Q: What is the mechanism of action of ACE inhibitors in heart failure?
A: ACE inhibitors block conversion of angiotensin I to II, reducing
vasoconstriction, aldosterone secretion, and ventricular remodeling while
improving endothelial function and reducing afterload.
,6. Q: Explain the pathophysiology of atrial fibrillation. A: AF involves
disorganized atrial electrical activity from multiple reentrant circuits, often
triggered by pulmonary vein ectopy, leading to irregular ventricular response
and increased thromboembolism risk due to atrial stasis.
7. Q: What causes the S3 gallop in heart failure? A: S3 gallop results from
rapid ventricular filling against a stiff, volume-overloaded ventricle during early
diastole, indicating elevated filling pressures and ventricular dysfunction.
8. Q: Describe the compensatory mechanisms in heart failure. A:
Compensatory mechanisms include: neurohormonal activation (RAAS, SNS),
ventricular remodeling (hypertrophy, dilation), increased heart rate, and fluid
retention to maintain cardiac output.
9. Q: What is the pathophysiology of cardiogenic shock? A: Cardiogenic
shock occurs when cardiac output is inadequate to meet metabolic demands
despite adequate preload, typically due to >40% LV dysfunction, leading to
hypoperfusion and multiorgan failure.
10. Q: Explain the mechanism of cardiac tamponade. A: Cardiac tamponade
occurs when pericardial pressure equals or exceeds cardiac filling pressures,
impairing venous return and diastolic filling, leading to equalization of
pressures and reduced cardiac output.
11. Q: What are the cellular mechanisms of myocardial ischemia? A:
Ischemia causes ATP depletion, anaerobic metabolism, lactate accumulation,
cellular acidosis, calcium overload, membrane dysfunction, and ultimately cell
death if prolonged.
12. Q: Describe the pathophysiology of mitral regurgitation. A: Mitral
regurgitation involves retrograde flow from LV to LA during systole due to
valve dysfunction, causing volume overload, LA dilation, pulmonary
congestion, and eventual LV dysfunction.
13. Q: What is the mechanism of aortic stenosis pathophysiology? A: Aortic
stenosis creates outflow obstruction, increasing LV pressure, causing concentric
hypertrophy, eventual diastolic dysfunction, and symptoms of angina, syncope,
and heart failure.
14. Q: Explain the pathophysiology of deep vein thrombosis. A: DVT results
from Virchow's triad: venous stasis, endothelial injury, and hypercoagulability,
leading to thrombus formation typically in deep leg veins with risk of
pulmonary embolism.
, 15. Q: What causes orthostatic hypotension? A: Orthostatic hypotension
results from impaired baroreceptor response, reduced blood volume,
medications, or autonomic dysfunction preventing adequate vasoconstriction
and heart rate increase upon standing.
16. Q: Describe the pathophysiology of pulmonary edema. A: Pulmonary
edema occurs when pulmonary capillary pressure exceeds oncotic pressure
(cardiogenic) or from increased capillary permeability (non-cardiogenic),
causing alveolar fluid accumulation.
17. Q: What is the mechanism of sudden cardiac death? A: Sudden cardiac
death typically results from ventricular arrhythmias (VT/VF) due to ischemia,
structural heart disease, or inherited channelopathies causing electrical
instability.
18. Q: Explain the pathophysiology of endocarditis. A: Endocarditis involves
microbial infection of heart valves or endocardium, typically on abnormal
valves, causing vegetation formation, valve destruction, embolic phenomena,
and systemic infection.
19. Q: What causes the murmur in aortic regurgitation? A: Aortic
regurgitation creates a high-pitched, blowing diastolic murmur due to retrograde
flow from aorta to LV during diastole, best heard at left sternal border.
20. Q: Describe the pathophysiology of pericarditis. A: Pericarditis involves
pericardial inflammation from various causes (viral, autoimmune, malignant),
leading to chest pain, friction rub, and potential complications like effusion or
constriction.
21. Q: What is the mechanism of coronary artery spasm? A: Coronary
spasm involves smooth muscle contraction causing transient vessel occlusion,
often triggered by endothelial dysfunction, increased calcium sensitivity, or
autonomic imbalance.
22. Q: Explain the pathophysiology of heart block. A: Heart block results
from conduction system disease affecting AV node, bundle of His, or bundle
branches, causing delayed or absent impulse transmission from atria to
ventricles.
23. Q: What causes the symptoms of heart failure? A: HF symptoms result
from reduced cardiac output (fatigue, weakness) and fluid retention (dyspnea,
edema) due to neurohormonal activation and elevated filling pressures.
24. Q: Describe the pathophysiology of hypertrophic cardiomyopathy. A:
HCM involves genetic mutations causing myocyte hypertrophy, myofibrillar
EXAM QUESTIONS AND 100% VERIFIED ANSWERS RECENTLY
UPDATED
275 QUESTIONS AND ANSWERS
1. Q: What is the primary mechanism underlying atherosclerosis? A:
Atherosclerosis is primarily caused by endothelial dysfunction leading to lipid
accumulation, inflammatory cell infiltration, smooth muscle cell proliferation,
and formation of fibrous plaques in arterial walls.
2. Q: Explain the Frank-Starling mechanism and its clinical significance. A:
The Frank-Starling mechanism states that stroke volume increases with
increased venous return (preload) due to optimal sarcomere length. Clinically, it
explains how the heart adapts to varying venous return and is impaired in heart
failure.
3. Q: What are the key differences between systolic and diastolic heart
failure? A: Systolic HF (HFrEF) involves reduced ejection fraction (<40%)
with impaired contractility. Diastolic HF (HFpEF) has preserved ejection
fraction (≥50%) but impaired ventricular filling due to stiffness or relaxation
abnormalities.
4. Q: Describe the pathophysiology of hypertensive crisis. A: Hypertensive
crisis involves acute severe BP elevation (>180/120 mmHg) causing end-organ
damage through autoregulation failure, endothelial dysfunction,
microangiopathy, and inflammatory responses leading to cerebral, cardiac, or
renal complications.
5. Q: What is the mechanism of action of ACE inhibitors in heart failure?
A: ACE inhibitors block conversion of angiotensin I to II, reducing
vasoconstriction, aldosterone secretion, and ventricular remodeling while
improving endothelial function and reducing afterload.
,6. Q: Explain the pathophysiology of atrial fibrillation. A: AF involves
disorganized atrial electrical activity from multiple reentrant circuits, often
triggered by pulmonary vein ectopy, leading to irregular ventricular response
and increased thromboembolism risk due to atrial stasis.
7. Q: What causes the S3 gallop in heart failure? A: S3 gallop results from
rapid ventricular filling against a stiff, volume-overloaded ventricle during early
diastole, indicating elevated filling pressures and ventricular dysfunction.
8. Q: Describe the compensatory mechanisms in heart failure. A:
Compensatory mechanisms include: neurohormonal activation (RAAS, SNS),
ventricular remodeling (hypertrophy, dilation), increased heart rate, and fluid
retention to maintain cardiac output.
9. Q: What is the pathophysiology of cardiogenic shock? A: Cardiogenic
shock occurs when cardiac output is inadequate to meet metabolic demands
despite adequate preload, typically due to >40% LV dysfunction, leading to
hypoperfusion and multiorgan failure.
10. Q: Explain the mechanism of cardiac tamponade. A: Cardiac tamponade
occurs when pericardial pressure equals or exceeds cardiac filling pressures,
impairing venous return and diastolic filling, leading to equalization of
pressures and reduced cardiac output.
11. Q: What are the cellular mechanisms of myocardial ischemia? A:
Ischemia causes ATP depletion, anaerobic metabolism, lactate accumulation,
cellular acidosis, calcium overload, membrane dysfunction, and ultimately cell
death if prolonged.
12. Q: Describe the pathophysiology of mitral regurgitation. A: Mitral
regurgitation involves retrograde flow from LV to LA during systole due to
valve dysfunction, causing volume overload, LA dilation, pulmonary
congestion, and eventual LV dysfunction.
13. Q: What is the mechanism of aortic stenosis pathophysiology? A: Aortic
stenosis creates outflow obstruction, increasing LV pressure, causing concentric
hypertrophy, eventual diastolic dysfunction, and symptoms of angina, syncope,
and heart failure.
14. Q: Explain the pathophysiology of deep vein thrombosis. A: DVT results
from Virchow's triad: venous stasis, endothelial injury, and hypercoagulability,
leading to thrombus formation typically in deep leg veins with risk of
pulmonary embolism.
, 15. Q: What causes orthostatic hypotension? A: Orthostatic hypotension
results from impaired baroreceptor response, reduced blood volume,
medications, or autonomic dysfunction preventing adequate vasoconstriction
and heart rate increase upon standing.
16. Q: Describe the pathophysiology of pulmonary edema. A: Pulmonary
edema occurs when pulmonary capillary pressure exceeds oncotic pressure
(cardiogenic) or from increased capillary permeability (non-cardiogenic),
causing alveolar fluid accumulation.
17. Q: What is the mechanism of sudden cardiac death? A: Sudden cardiac
death typically results from ventricular arrhythmias (VT/VF) due to ischemia,
structural heart disease, or inherited channelopathies causing electrical
instability.
18. Q: Explain the pathophysiology of endocarditis. A: Endocarditis involves
microbial infection of heart valves or endocardium, typically on abnormal
valves, causing vegetation formation, valve destruction, embolic phenomena,
and systemic infection.
19. Q: What causes the murmur in aortic regurgitation? A: Aortic
regurgitation creates a high-pitched, blowing diastolic murmur due to retrograde
flow from aorta to LV during diastole, best heard at left sternal border.
20. Q: Describe the pathophysiology of pericarditis. A: Pericarditis involves
pericardial inflammation from various causes (viral, autoimmune, malignant),
leading to chest pain, friction rub, and potential complications like effusion or
constriction.
21. Q: What is the mechanism of coronary artery spasm? A: Coronary
spasm involves smooth muscle contraction causing transient vessel occlusion,
often triggered by endothelial dysfunction, increased calcium sensitivity, or
autonomic imbalance.
22. Q: Explain the pathophysiology of heart block. A: Heart block results
from conduction system disease affecting AV node, bundle of His, or bundle
branches, causing delayed or absent impulse transmission from atria to
ventricles.
23. Q: What causes the symptoms of heart failure? A: HF symptoms result
from reduced cardiac output (fatigue, weakness) and fluid retention (dyspnea,
edema) due to neurohormonal activation and elevated filling pressures.
24. Q: Describe the pathophysiology of hypertrophic cardiomyopathy. A:
HCM involves genetic mutations causing myocyte hypertrophy, myofibrillar
