NUR 546/NUR546 Exam 2 V2 | Advanced
Pathophysiology Q&A with Rationale |
William Paterson University
1. Which mechanism is primarily responsible for the development of pulmonary edema in a
patient with left-sided heart failure?
A. Decreased capillary oncotic pressure
B. Increased pulmonary capillary hydrostatic pressure
C. Increased pulmonary vascular resistance
D. Decreased lymphatic drainage in the lungs
Answer: B
Rationale: Left-sided heart failure results in an inability of the left ventricle to pump blood
efficiently into the systemic circulation. This leads to a backup of blood into the pulmonary
veins and capillaries, significantly raising the hydrostatic pressure. The high pressure
forces fluid out of the vessels and into the alveolar spaces, impairing gas exchange.
2. A patient presents with orthopnea and paroxysmal nocturnal dyspnea. These symptoms
are most characteristic of which condition?
A. Left-sided heart failure
B. Chronic obstructive pulmonary disease
C. Right-sided heart failure
,D. Pulmonary embolism
Answer: A
Rationale: Orthopnea and paroxysmal nocturnal dyspnea are classic signs of pulmonary
congestion associated with left ventricular dysfunction. When the patient lies flat, venous
return increases and fluid shifts into the lungs, exacerbating shortness of breath. These
symptoms reflect the heart’s inability to manage the increased volume in a horizontal
position.
3. Which compensatory mechanism is activated by the kidneys in response to decreased
cardiac output?
A. Inhibition of the sympathetic nervous system
B. Decreased production of erythropoietin
C. Activation of the renin-angiotensin-aldosterone system
D. Increased secretion of atrial natriuretic peptide
Answer: C
Rationale: Decreased cardiac output reduces renal perfusion, which triggers the release of
renin from the juxtaglomerular cells. Renin facilitates the conversion of angiotensinogen to
angiotensin I, which is then converted to angiotensin II by ACE. Angiotensin II causes
vasoconstriction and stimulates aldosterone secretion to increase sodium and water
retention.
, 4. In the pathophysiology of atherosclerosis, what is the initial step that leads to plaque
formation?
A. Endothelial injury
B. Smooth muscle cell proliferation
C. Foam cell accumulation
D. Formation of a fatty streak
Answer: A
Rationale: Endothelial injury is the triggering event that allows lipids and inflammatory
cells to enter the vessel wall. Factors such as hypertension, smoking, and hyperlipidemia
cause damage to the protective inner lining of the artery. This injury initiates an
inflammatory response that ultimately leads to the development of an atherosclerotic
lesion.
5. Which type of shock is characterized by a profound decrease in systemic vascular
resistance (SVR)?
A. Hypovolemic shock
B. Septic shock
C. Cardiogenic shock
D. Obstructive shock
Answer: B
Pathophysiology Q&A with Rationale |
William Paterson University
1. Which mechanism is primarily responsible for the development of pulmonary edema in a
patient with left-sided heart failure?
A. Decreased capillary oncotic pressure
B. Increased pulmonary capillary hydrostatic pressure
C. Increased pulmonary vascular resistance
D. Decreased lymphatic drainage in the lungs
Answer: B
Rationale: Left-sided heart failure results in an inability of the left ventricle to pump blood
efficiently into the systemic circulation. This leads to a backup of blood into the pulmonary
veins and capillaries, significantly raising the hydrostatic pressure. The high pressure
forces fluid out of the vessels and into the alveolar spaces, impairing gas exchange.
2. A patient presents with orthopnea and paroxysmal nocturnal dyspnea. These symptoms
are most characteristic of which condition?
A. Left-sided heart failure
B. Chronic obstructive pulmonary disease
C. Right-sided heart failure
,D. Pulmonary embolism
Answer: A
Rationale: Orthopnea and paroxysmal nocturnal dyspnea are classic signs of pulmonary
congestion associated with left ventricular dysfunction. When the patient lies flat, venous
return increases and fluid shifts into the lungs, exacerbating shortness of breath. These
symptoms reflect the heart’s inability to manage the increased volume in a horizontal
position.
3. Which compensatory mechanism is activated by the kidneys in response to decreased
cardiac output?
A. Inhibition of the sympathetic nervous system
B. Decreased production of erythropoietin
C. Activation of the renin-angiotensin-aldosterone system
D. Increased secretion of atrial natriuretic peptide
Answer: C
Rationale: Decreased cardiac output reduces renal perfusion, which triggers the release of
renin from the juxtaglomerular cells. Renin facilitates the conversion of angiotensinogen to
angiotensin I, which is then converted to angiotensin II by ACE. Angiotensin II causes
vasoconstriction and stimulates aldosterone secretion to increase sodium and water
retention.
, 4. In the pathophysiology of atherosclerosis, what is the initial step that leads to plaque
formation?
A. Endothelial injury
B. Smooth muscle cell proliferation
C. Foam cell accumulation
D. Formation of a fatty streak
Answer: A
Rationale: Endothelial injury is the triggering event that allows lipids and inflammatory
cells to enter the vessel wall. Factors such as hypertension, smoking, and hyperlipidemia
cause damage to the protective inner lining of the artery. This injury initiates an
inflammatory response that ultimately leads to the development of an atherosclerotic
lesion.
5. Which type of shock is characterized by a profound decrease in systemic vascular
resistance (SVR)?
A. Hypovolemic shock
B. Septic shock
C. Cardiogenic shock
D. Obstructive shock
Answer: B
