NUR 546/NUR546 Exam 2 V3 | Advanced
Pathophysiology Q&A with Rationale |
William Paterson University
1. Which of the following describes the primary mechanism of action of the Renin-
Angiotensin-Aldosterone System (RAAS) in response to decreased blood pressure?
A. Secretion of renin leading to the formation of Angiotensin II and vasoconstriction.
B. Inhibition of renin release to decrease systemic vascular resistance.
C. Stimulation of atrial natriuretic peptide to promote diuresis.
D. Release of nitric oxide to induce systemic vasodilation.
Correct Answer: A
Expert Explanation: The RAAS is activated when there is a drop in blood pressure or fluid
volume. Renin is released from the juxtaglomerular cells and eventually converts
angiotensinogen to Angiotensin I, then II. Angiotensin II is a potent vasoconstrictor and
stimulates aldosterone release, which increases sodium and water reabsorption to raise
blood pressure.
2. A patient with long-term untreated hypertension is at high risk for which cellular
adaptation in the left ventricle?
A. Hypertrophy
B. Atrophy
,C. Hyperplasia
D. Metaplasia
Correct Answer: A
Expert Explanation: Pathologic hypertrophy occurs in the heart muscle as a response to
an increased workload, such as high systemic blood pressure. The myocytes increase in
size to generate more force against the higher afterload. Over time, this adaptation can lead
to decreased compliance and eventually heart failure.
3. Which compensatory mechanism is primarily responsible for the clinical presentation of
pulmonary edema in left-sided heart failure?
A. Peripheral vasoconstriction causing venous congestion.
B. Increased hydrostatic pressure in the pulmonary capillaries.
C. Decreased lymphatic drainage in the lower extremities.
D. Decreased oncotic pressure due to liver congestion.
Correct Answer: B
Expert Explanation: In left-sided heart failure, the left ventricle fails to pump blood
efficiently into the systemic circulation, leading to a backup of blood into the left atrium
and pulmonary veins. This increases the hydrostatic pressure within the pulmonary
capillaries. When hydrostatic pressure exceeds oncotic pressure, fluid is forced into the
interstitial and alveolar spaces of the lungs.
, 4. What is the hallmark morphological feature of Chronic Bronchitis?
A. Destruction of alveolar walls and loss of elastic recoil.
B. Granulomatous inflammation of the lung parenchyma.
C. Presence of Curshmann spirals and Charcot-Leyden crystals.
D. Hypertrophy of mucus-secreting glands in the large airways.
Correct Answer: D
Expert Explanation: Chronic bronchitis is characterized by a productive cough lasting at
least three months over two consecutive years. The primary underlying change is the
hypersecretion of mucus due to the hypertrophy of submucosal glands in the bronchi. This
leads to airway obstruction, impaired ciliary function, and an increased risk of infection.
5. In the pathophysiology of Emphysema, the destruction of elastin is primarily caused by an
imbalance between:
A. Proteases and antiproteases.
B. Th1 and Th2 cytokines.
C. Sympathetic and parasympathetic tone.
D. Sodium and potassium ions.
Correct Answer: A
Expert Explanation: Emphysema involves the permanent enlargement of gas-exchange
airways accompanied by the destruction of alveolar walls. This process is driven by an
Pathophysiology Q&A with Rationale |
William Paterson University
1. Which of the following describes the primary mechanism of action of the Renin-
Angiotensin-Aldosterone System (RAAS) in response to decreased blood pressure?
A. Secretion of renin leading to the formation of Angiotensin II and vasoconstriction.
B. Inhibition of renin release to decrease systemic vascular resistance.
C. Stimulation of atrial natriuretic peptide to promote diuresis.
D. Release of nitric oxide to induce systemic vasodilation.
Correct Answer: A
Expert Explanation: The RAAS is activated when there is a drop in blood pressure or fluid
volume. Renin is released from the juxtaglomerular cells and eventually converts
angiotensinogen to Angiotensin I, then II. Angiotensin II is a potent vasoconstrictor and
stimulates aldosterone release, which increases sodium and water reabsorption to raise
blood pressure.
2. A patient with long-term untreated hypertension is at high risk for which cellular
adaptation in the left ventricle?
A. Hypertrophy
B. Atrophy
,C. Hyperplasia
D. Metaplasia
Correct Answer: A
Expert Explanation: Pathologic hypertrophy occurs in the heart muscle as a response to
an increased workload, such as high systemic blood pressure. The myocytes increase in
size to generate more force against the higher afterload. Over time, this adaptation can lead
to decreased compliance and eventually heart failure.
3. Which compensatory mechanism is primarily responsible for the clinical presentation of
pulmonary edema in left-sided heart failure?
A. Peripheral vasoconstriction causing venous congestion.
B. Increased hydrostatic pressure in the pulmonary capillaries.
C. Decreased lymphatic drainage in the lower extremities.
D. Decreased oncotic pressure due to liver congestion.
Correct Answer: B
Expert Explanation: In left-sided heart failure, the left ventricle fails to pump blood
efficiently into the systemic circulation, leading to a backup of blood into the left atrium
and pulmonary veins. This increases the hydrostatic pressure within the pulmonary
capillaries. When hydrostatic pressure exceeds oncotic pressure, fluid is forced into the
interstitial and alveolar spaces of the lungs.
, 4. What is the hallmark morphological feature of Chronic Bronchitis?
A. Destruction of alveolar walls and loss of elastic recoil.
B. Granulomatous inflammation of the lung parenchyma.
C. Presence of Curshmann spirals and Charcot-Leyden crystals.
D. Hypertrophy of mucus-secreting glands in the large airways.
Correct Answer: D
Expert Explanation: Chronic bronchitis is characterized by a productive cough lasting at
least three months over two consecutive years. The primary underlying change is the
hypersecretion of mucus due to the hypertrophy of submucosal glands in the bronchi. This
leads to airway obstruction, impaired ciliary function, and an increased risk of infection.
5. In the pathophysiology of Emphysema, the destruction of elastin is primarily caused by an
imbalance between:
A. Proteases and antiproteases.
B. Th1 and Th2 cytokines.
C. Sympathetic and parasympathetic tone.
D. Sodium and potassium ions.
Correct Answer: A
Expert Explanation: Emphysema involves the permanent enlargement of gas-exchange
airways accompanied by the destruction of alveolar walls. This process is driven by an
