,NSG3850/NSG 3850 Exam 2 | Pathophysiology for
1. A patient with a history of stable angina reports that chest pain now occurs with minimal exertion
and lasts longer than 15 minutes. Which pathophysiological change best explains this progression?
A) Complete occlusion of a coronary artery by a thrombus
B) Rupture of an atherosclerotic plaque with partial thrombosis
C) Fixed atherosclerotic narrowing without plaque disruption
D) Transient vasospasm of a non-diseased coronary artery
Correct Answer: Rupture of an atherosclerotic plaque with partial thrombosis
Rationale: Unstable angina results from plaque rupture with superimposed partial thrombosis, leading
to reduced coronary blood flow without complete occlusion. Complete occlusion causes acute
myocardial infarction. Fixed narrowing without disruption characterizes stable angina. Vasospasm
without atherosclerosis is Prinzmetal's angina, not a progression from stable disease.
2. A patient with acute myocardial infarction develops a new holosystolic murmur at the cardiac apex
that radiates to the axilla. Which complication is most likely?
A) Ventricular septal rupture
B) Papillary muscle rupture
C) Free wall rupture
D) Pericarditis
Correct Answer: Papillary muscle rupture
Rationale: Papillary muscle rupture causes acute mitral regurgitation, producing a holosystolic
murmur at the apex radiating to the axilla. Ventricular septal rupture produces a harsh holosystolic
murmur at the left sternal border. Free wall rupture causes cardiac tamponade without a
characteristic murmur. Pericarditis produces a friction rub.
3. A patient with heart failure has an ejection fraction of 30% and complains of orthopnea and
paroxysmal nocturnal dyspnea. Which hemodynamic abnormality is the primary cause of these
symptoms?
A) Decreased systemic vascular resistance
B) Increased left ventricular end-diastolic pressure
,C) Decreased right ventricular stroke volume
D) Increased pulmonary vascular resistance
Correct Answer: Increased left ventricular end-diastolic pressure
Rationale: Reduced ejection fraction leads to increased left ventricular end-diastolic pressure, which is
transmitted backward to the pulmonary circulation, causing pulmonary congestion and symptoms of
orthopnea and paroxysmal nocturnal dyspnea. Decreased systemic vascular resistance is not the
primary cause. Right ventricular dysfunction and increased pulmonary vascular resistance are
consequences or separate issues.
4. A patient with chronic hypertension develops a sustained elevation in systemic vascular resistance.
Which compensatory mechanism initially maintains cardiac output in this setting?
A) Decreased heart rate
B) Increased stroke volume
C) Increased myocardial contractility
D) Decreased venous return
Correct Answer: Increased myocardial contractility
Rationale: In early hypertension, increased afterload is initially compensated by increased myocardial
contractility (Frank-Starling mechanism) to maintain stroke volume and cardiac output. Heart rate
typically increases, not decreases. Stroke volume may be maintained but is not the primary
compensatory mechanism. Venous return is not decreased; it may be increased.
5. A patient with pericarditis presents with chest pain that is relieved by sitting forward and worsens
with inspiration. Which pathophysiological process is responsible for this pain pattern?
A) Myocardial ischemia from reduced coronary flow
B) Inflammation of the parietal pericardium with friction
C) Aortic dissection involving the pericardial sac
D) Pulmonary embolism with pleural irritation
Correct Answer: Inflammation of the parietal pericardium with friction
, Rationale: Pericarditis involves inflammation of the pericardial layers, with friction between the
visceral and parietal pericardium. Leaning forward reduces the contact and friction, relieving pain,
while inspiration increases it. Myocardial ischemia is not position-dependent. Aortic dissection causes
tearing pain. Pulmonary embolism causes pleuritic pain but is not relieved by sitting forward.
6. A patient with aortic stenosis develops syncope during exertion. Which pathophysiological
mechanism explains this symptom?
A) Fixed obstruction to left ventricular outflow causing inadequate cerebral perfusion
B) Decreased systemic vascular resistance from vasodilation
C) Increased vagal tone leading to bradycardia
D) Embolization of aortic valve vegetations to the brain
Correct Answer: Fixed obstruction to left ventricular outflow causing inadequate cerebral perfusion
Rationale: In aortic stenosis, the fixed obstruction limits the increase in cardiac output during
exertion, leading to inadequate cerebral perfusion and syncope. Vasodilation is not the primary
mechanism. Bradycardia is not characteristic. Embolization is a complication of infective endocarditis,
not aortic stenosis.
7. A patient with chronic venous insufficiency has edema, skin hyperpigmentation, and stasis ulcers
above the medial malleolus. Which pathophysiological mechanism is primarily responsible for these
findings?
A) Arterial insufficiency with tissue hypoxia
B) Venous hypertension with capillary leakage
C) Lymphatic obstruction with protein-rich fluid
D) Neuropathic changes from diabetes
Correct Answer: Venous hypertension with capillary leakage
Rationale: Chronic venous insufficiency causes venous hypertension, which increases capillary
hydrostatic pressure, leading to leakage of fluid and hemosiderin (causing hyperpigmentation) and
eventual stasis ulcers. Arterial insufficiency causes pale, cool extremities. Lymphatic obstruction
causes non-pitting edema. Neuropathic changes cause ulcers on pressure points.
1. A patient with a history of stable angina reports that chest pain now occurs with minimal exertion
and lasts longer than 15 minutes. Which pathophysiological change best explains this progression?
A) Complete occlusion of a coronary artery by a thrombus
B) Rupture of an atherosclerotic plaque with partial thrombosis
C) Fixed atherosclerotic narrowing without plaque disruption
D) Transient vasospasm of a non-diseased coronary artery
Correct Answer: Rupture of an atherosclerotic plaque with partial thrombosis
Rationale: Unstable angina results from plaque rupture with superimposed partial thrombosis, leading
to reduced coronary blood flow without complete occlusion. Complete occlusion causes acute
myocardial infarction. Fixed narrowing without disruption characterizes stable angina. Vasospasm
without atherosclerosis is Prinzmetal's angina, not a progression from stable disease.
2. A patient with acute myocardial infarction develops a new holosystolic murmur at the cardiac apex
that radiates to the axilla. Which complication is most likely?
A) Ventricular septal rupture
B) Papillary muscle rupture
C) Free wall rupture
D) Pericarditis
Correct Answer: Papillary muscle rupture
Rationale: Papillary muscle rupture causes acute mitral regurgitation, producing a holosystolic
murmur at the apex radiating to the axilla. Ventricular septal rupture produces a harsh holosystolic
murmur at the left sternal border. Free wall rupture causes cardiac tamponade without a
characteristic murmur. Pericarditis produces a friction rub.
3. A patient with heart failure has an ejection fraction of 30% and complains of orthopnea and
paroxysmal nocturnal dyspnea. Which hemodynamic abnormality is the primary cause of these
symptoms?
A) Decreased systemic vascular resistance
B) Increased left ventricular end-diastolic pressure
,C) Decreased right ventricular stroke volume
D) Increased pulmonary vascular resistance
Correct Answer: Increased left ventricular end-diastolic pressure
Rationale: Reduced ejection fraction leads to increased left ventricular end-diastolic pressure, which is
transmitted backward to the pulmonary circulation, causing pulmonary congestion and symptoms of
orthopnea and paroxysmal nocturnal dyspnea. Decreased systemic vascular resistance is not the
primary cause. Right ventricular dysfunction and increased pulmonary vascular resistance are
consequences or separate issues.
4. A patient with chronic hypertension develops a sustained elevation in systemic vascular resistance.
Which compensatory mechanism initially maintains cardiac output in this setting?
A) Decreased heart rate
B) Increased stroke volume
C) Increased myocardial contractility
D) Decreased venous return
Correct Answer: Increased myocardial contractility
Rationale: In early hypertension, increased afterload is initially compensated by increased myocardial
contractility (Frank-Starling mechanism) to maintain stroke volume and cardiac output. Heart rate
typically increases, not decreases. Stroke volume may be maintained but is not the primary
compensatory mechanism. Venous return is not decreased; it may be increased.
5. A patient with pericarditis presents with chest pain that is relieved by sitting forward and worsens
with inspiration. Which pathophysiological process is responsible for this pain pattern?
A) Myocardial ischemia from reduced coronary flow
B) Inflammation of the parietal pericardium with friction
C) Aortic dissection involving the pericardial sac
D) Pulmonary embolism with pleural irritation
Correct Answer: Inflammation of the parietal pericardium with friction
, Rationale: Pericarditis involves inflammation of the pericardial layers, with friction between the
visceral and parietal pericardium. Leaning forward reduces the contact and friction, relieving pain,
while inspiration increases it. Myocardial ischemia is not position-dependent. Aortic dissection causes
tearing pain. Pulmonary embolism causes pleuritic pain but is not relieved by sitting forward.
6. A patient with aortic stenosis develops syncope during exertion. Which pathophysiological
mechanism explains this symptom?
A) Fixed obstruction to left ventricular outflow causing inadequate cerebral perfusion
B) Decreased systemic vascular resistance from vasodilation
C) Increased vagal tone leading to bradycardia
D) Embolization of aortic valve vegetations to the brain
Correct Answer: Fixed obstruction to left ventricular outflow causing inadequate cerebral perfusion
Rationale: In aortic stenosis, the fixed obstruction limits the increase in cardiac output during
exertion, leading to inadequate cerebral perfusion and syncope. Vasodilation is not the primary
mechanism. Bradycardia is not characteristic. Embolization is a complication of infective endocarditis,
not aortic stenosis.
7. A patient with chronic venous insufficiency has edema, skin hyperpigmentation, and stasis ulcers
above the medial malleolus. Which pathophysiological mechanism is primarily responsible for these
findings?
A) Arterial insufficiency with tissue hypoxia
B) Venous hypertension with capillary leakage
C) Lymphatic obstruction with protein-rich fluid
D) Neuropathic changes from diabetes
Correct Answer: Venous hypertension with capillary leakage
Rationale: Chronic venous insufficiency causes venous hypertension, which increases capillary
hydrostatic pressure, leading to leakage of fluid and hemosiderin (causing hyperpigmentation) and
eventual stasis ulcers. Arterial insufficiency causes pale, cool extremities. Lymphatic obstruction
causes non-pitting edema. Neuropathic changes cause ulcers on pressure points.
