NURS 676 ADVANCED PATHOPHYSIOLOGY UPDATED AND EXPANDED COMPILATION OF
EXAM QUESTIONS AND ANSWERS BASED ON THE NEWEST EDUCATIONAL STANDARDS
AND EXAMINATION FORMATS
1. What is the primary pathophysiology of heart failure? The heart's
inability to pump sufficient blood to meet the body's metabolic demands,
resulting from impaired contractility, increased afterload, or abnormal filling.
2. What distinguishes systolic from diastolic heart failure? Systolic HF
involves reduced ejection fraction (<40%) with impaired contractility. Diastolic
HF has preserved ejection fraction (>50%) with impaired ventricular relaxation
and filling.
3. What is the Frank-Starling mechanism? The relationship between
ventricular stretch and contractile force; increased preload stretches cardiac
muscle fibers, resulting in stronger contraction up to a physiologic limit.
4. How does chronic hypertension lead to left ventricular hypertrophy?
Persistent increased afterload causes compensatory myocyte hypertrophy and
fibrosis, leading to concentric LVH and eventual diastolic dysfunction.
5. What is the pathophysiology of atherosclerosis? Endothelial injury leads to
LDL accumulation, inflammatory response, foam cell formation, and fibrous
plaque development, eventually causing vessel stenosis or rupture.
6. What causes the chest pain in angina pectoris? Myocardial ischemia from
inadequate oxygen supply relative to demand, causing anaerobic metabolism
and accumulation of pain-producing metabolites like lactate and adenosine.
7. What differentiates stable from unstable angina? Stable angina is
predictable, occurring with exertion and relieved by rest. Unstable angina is
unpredictable, occurs at rest, represents plaque instability, and signals high MI
risk.
8. What is the pathophysiology of acute myocardial infarction? Complete
coronary artery occlusion (usually from plaque rupture and thrombosis) causes
prolonged ischemia leading to irreversible myocardial cell death and necrosis.
9. What are the complications of acute MI? Arrhythmias, cardiogenic shock,
papillary muscle rupture, ventricular septal defect, free wall rupture,
pericarditis, heart failure, and ventricular aneurysm.
,10. What is the role of troponin in MI diagnosis? Troponin is a cardiac-
specific protein released during myocardial cell death; elevated levels indicate
myocardial injury and are highly sensitive and specific for MI.
11. What causes the murmur in aortic stenosis? Turbulent blood flow across
the narrowed aortic valve during systole, creating a crescendo-decrescendo
systolic murmur.
12. What is the pathophysiology of mitral regurgitation? Incomplete mitral
valve closure allows backflow of blood from the left ventricle to the left atrium
during systole, causing volume overload.
13. How does rheumatic fever cause valvular disease? Molecular mimicry
between streptococcal antigens and cardiac tissue triggers autoimmune
inflammation, leading to valvular scarring, stenosis, and regurgitation.
14. What is the pathophysiology of infective endocarditis? Bacterial
colonization of damaged endocardium or valves creates vegetations, causing
valve destruction, systemic emboli, and immune complex deposition.
15. What causes the symptoms of aortic dissection? Tear in the aortic intima
allows blood to enter the media, creating a false lumen that can compress true
lumen or branch vessels, causing ischemia and pain.
16. What is Virchow's triad? Three factors promoting thrombosis: endothelial
injury, venous stasis, and hypercoagulability.
17. How does atrial fibrillation increase stroke risk? Uncoordinated atrial
contraction causes blood stasis in the atria, particularly the left atrial appendage,
promoting thrombus formation and embolic stroke.
18. What is the pathophysiology of hypertrophic cardiomyopathy? Genetic
mutations in sarcomeric proteins cause asymmetric septal hypertrophy, leading
to LV outflow obstruction and diastolic dysfunction.
19. What causes pericardial tamponade? Rapid fluid accumulation in the
pericardial space compresses the heart, impairs diastolic filling, and reduces
cardiac output.
20. What is Beck's triad in cardiac tamponade? Hypotension, jugular venous
distension, and muffled heart sounds.
21. How does the RAAS system contribute to heart failure? Decreased
cardiac output activates RAAS, causing vasoconstriction, sodium/water
, retention, and increased afterload, which initially compensates but eventually
worsens HF.
22. What is the role of BNP in heart failure? Brain natriuretic peptide is
released by ventricular myocytes in response to stretch; it promotes natriuresis
and vasodilation, serving as a diagnostic and prognostic marker.
23. What causes peripheral edema in right heart failure? Elevated right
atrial pressure increases systemic venous pressure, forcing fluid from capillaries
into interstitial space due to increased hydrostatic pressure.
24. What is the mechanism of nitrate therapy in angina? Nitrates are
converted to nitric oxide, causing venodilation (reduced preload) and coronary
vasodilation, reducing myocardial oxygen demand.
25. How do beta-blockers benefit post-MI patients? They reduce myocardial
oxygen demand by decreasing heart rate, contractility, and blood pressure,
while also stabilizing cardiac membranes and reducing arrhythmias.
26. What is Prinzmetal's angina? Variant angina caused by coronary artery
vasospasm, typically occurring at rest and showing ST elevation on ECG.
27. What causes the S3 heart sound in heart failure? Rapid ventricular filling
in early diastole against a stiff, volume-overloaded ventricle creates vibrations
heard as an S3 gallop.
28. What is the pathophysiology of cardiogenic shock? Severe impairment of
cardiac output (usually from massive MI) leads to inadequate tissue perfusion,
hypotension, and end-organ dysfunction despite adequate intravascular volume.
29. How does chronic kidney disease affect cardiovascular risk? CKD
causes fluid overload, hypertension, dyslipidemia, anemia, calcification, and
inflammatory states, all increasing cardiovascular morbidity and mortality.
30. What is the mechanism of statin-induced muscle injury? Statins inhibit
CoQ10 synthesis and may disrupt muscle cell membranes, leading to myalgia,
myositis, or rarely rhabdomyolysis.
31. What causes orthostatic hypotension? Failure of autonomic reflexes to
maintain blood pressure during position change, resulting from volume
depletion, autonomic neuropathy, or medications.
EXAM QUESTIONS AND ANSWERS BASED ON THE NEWEST EDUCATIONAL STANDARDS
AND EXAMINATION FORMATS
1. What is the primary pathophysiology of heart failure? The heart's
inability to pump sufficient blood to meet the body's metabolic demands,
resulting from impaired contractility, increased afterload, or abnormal filling.
2. What distinguishes systolic from diastolic heart failure? Systolic HF
involves reduced ejection fraction (<40%) with impaired contractility. Diastolic
HF has preserved ejection fraction (>50%) with impaired ventricular relaxation
and filling.
3. What is the Frank-Starling mechanism? The relationship between
ventricular stretch and contractile force; increased preload stretches cardiac
muscle fibers, resulting in stronger contraction up to a physiologic limit.
4. How does chronic hypertension lead to left ventricular hypertrophy?
Persistent increased afterload causes compensatory myocyte hypertrophy and
fibrosis, leading to concentric LVH and eventual diastolic dysfunction.
5. What is the pathophysiology of atherosclerosis? Endothelial injury leads to
LDL accumulation, inflammatory response, foam cell formation, and fibrous
plaque development, eventually causing vessel stenosis or rupture.
6. What causes the chest pain in angina pectoris? Myocardial ischemia from
inadequate oxygen supply relative to demand, causing anaerobic metabolism
and accumulation of pain-producing metabolites like lactate and adenosine.
7. What differentiates stable from unstable angina? Stable angina is
predictable, occurring with exertion and relieved by rest. Unstable angina is
unpredictable, occurs at rest, represents plaque instability, and signals high MI
risk.
8. What is the pathophysiology of acute myocardial infarction? Complete
coronary artery occlusion (usually from plaque rupture and thrombosis) causes
prolonged ischemia leading to irreversible myocardial cell death and necrosis.
9. What are the complications of acute MI? Arrhythmias, cardiogenic shock,
papillary muscle rupture, ventricular septal defect, free wall rupture,
pericarditis, heart failure, and ventricular aneurysm.
,10. What is the role of troponin in MI diagnosis? Troponin is a cardiac-
specific protein released during myocardial cell death; elevated levels indicate
myocardial injury and are highly sensitive and specific for MI.
11. What causes the murmur in aortic stenosis? Turbulent blood flow across
the narrowed aortic valve during systole, creating a crescendo-decrescendo
systolic murmur.
12. What is the pathophysiology of mitral regurgitation? Incomplete mitral
valve closure allows backflow of blood from the left ventricle to the left atrium
during systole, causing volume overload.
13. How does rheumatic fever cause valvular disease? Molecular mimicry
between streptococcal antigens and cardiac tissue triggers autoimmune
inflammation, leading to valvular scarring, stenosis, and regurgitation.
14. What is the pathophysiology of infective endocarditis? Bacterial
colonization of damaged endocardium or valves creates vegetations, causing
valve destruction, systemic emboli, and immune complex deposition.
15. What causes the symptoms of aortic dissection? Tear in the aortic intima
allows blood to enter the media, creating a false lumen that can compress true
lumen or branch vessels, causing ischemia and pain.
16. What is Virchow's triad? Three factors promoting thrombosis: endothelial
injury, venous stasis, and hypercoagulability.
17. How does atrial fibrillation increase stroke risk? Uncoordinated atrial
contraction causes blood stasis in the atria, particularly the left atrial appendage,
promoting thrombus formation and embolic stroke.
18. What is the pathophysiology of hypertrophic cardiomyopathy? Genetic
mutations in sarcomeric proteins cause asymmetric septal hypertrophy, leading
to LV outflow obstruction and diastolic dysfunction.
19. What causes pericardial tamponade? Rapid fluid accumulation in the
pericardial space compresses the heart, impairs diastolic filling, and reduces
cardiac output.
20. What is Beck's triad in cardiac tamponade? Hypotension, jugular venous
distension, and muffled heart sounds.
21. How does the RAAS system contribute to heart failure? Decreased
cardiac output activates RAAS, causing vasoconstriction, sodium/water
, retention, and increased afterload, which initially compensates but eventually
worsens HF.
22. What is the role of BNP in heart failure? Brain natriuretic peptide is
released by ventricular myocytes in response to stretch; it promotes natriuresis
and vasodilation, serving as a diagnostic and prognostic marker.
23. What causes peripheral edema in right heart failure? Elevated right
atrial pressure increases systemic venous pressure, forcing fluid from capillaries
into interstitial space due to increased hydrostatic pressure.
24. What is the mechanism of nitrate therapy in angina? Nitrates are
converted to nitric oxide, causing venodilation (reduced preload) and coronary
vasodilation, reducing myocardial oxygen demand.
25. How do beta-blockers benefit post-MI patients? They reduce myocardial
oxygen demand by decreasing heart rate, contractility, and blood pressure,
while also stabilizing cardiac membranes and reducing arrhythmias.
26. What is Prinzmetal's angina? Variant angina caused by coronary artery
vasospasm, typically occurring at rest and showing ST elevation on ECG.
27. What causes the S3 heart sound in heart failure? Rapid ventricular filling
in early diastole against a stiff, volume-overloaded ventricle creates vibrations
heard as an S3 gallop.
28. What is the pathophysiology of cardiogenic shock? Severe impairment of
cardiac output (usually from massive MI) leads to inadequate tissue perfusion,
hypotension, and end-organ dysfunction despite adequate intravascular volume.
29. How does chronic kidney disease affect cardiovascular risk? CKD
causes fluid overload, hypertension, dyslipidemia, anemia, calcification, and
inflammatory states, all increasing cardiovascular morbidity and mortality.
30. What is the mechanism of statin-induced muscle injury? Statins inhibit
CoQ10 synthesis and may disrupt muscle cell membranes, leading to myalgia,
myositis, or rarely rhabdomyolysis.
31. What causes orthostatic hypotension? Failure of autonomic reflexes to
maintain blood pressure during position change, resulting from volume
depletion, autonomic neuropathy, or medications.
