NSG 3850 PATHOPHYSIOLOGY FOR
NURSES II - EXAM 1 REVIEW
QUESTIONS AND ANSWERS
1. A patient with chronic kidney disease (CKD) presents with a serum potassium level of 6.2
mEq/L. Which physiological mechanism is primarily responsible for the risk of cardiac
dysrhythmias in this patient?
A. Increased resting membrane potential, leading to hypopolarization
B. Decreased resting membrane potential making cells less excitable
C. Rapid repolarization due to decreased sodium-potassium pump activity
D. Increased calcium influx into the myocardial cells
Answer: A
Conceptual Explanation: Hyperkalemia increases the resting membrane potential,
bringing it closer to the threshold for depolarization (hypopolarization). This makes the
heart more excitable initially but eventually impairs repolarization, leading to potentially
fatal dysrhythmias.
,2. Which compensatory mechanism is activated by the kidneys in response to a sustained
decrease in mean arterial pressure (MAP)?
A. Inhibition of the juxtaglomerular apparatus
B. Release of Atrial Natriuretic Peptide (ANP)
C. Decrease in Antidiuretic Hormone (ADH) secretion
D. Activation of the Renin-Angiotensin-Aldosterone System (RAAS)
Answer: D
Conceptual Explanation: Low MAP triggers the RAAS to conserve sodium and water and
cause vasoconstriction via Angiotensin II, thereby increasing blood volume and pressure.
3. A patient is diagnosed with Right-Sided Heart Failure. Which clinical manifestation is a
direct result of increased systemic venous hydrostatic pressure?
A. Peripheral edema and jugular venous distention
B. Orthopnea and paroxysmal nocturnal dyspnea
C. Pulmonary edema and crackles
D. Pink frothy sputum
Answer: A
Conceptual Explanation: Right-sided heart failure causes blood to back up into the
systemic circulation, increasing hydrostatic pressure in the peripheral veins and leading to
edema and JVD. Pulmonary symptoms are characteristic of left-sided failure.
, 4. In the pathogenesis of Atherosclerosis, what is the significance of ‘foam cells’?
A. They are smooth muscle cells that have migrated to the adventitia
B. They are platelets that have adhered to the damaged endothelium
C. They are macrophages that have engulfed oxidized LDL cholesterol
D. They represent the final stage of fibrous plaque calcification
Answer: C
Conceptual Explanation: Foam cells are formed when macrophages ingest oxidized LDL.
These cells accumulate in the arterial wall, contributing to the formation of the fatty streak,
the earliest lesion of atherosclerosis.
5. During an acute asthma attack, the ‘late-phase’ response (occurring 4-8 hours after the
initial trigger) is primarily characterized by:
A. Rapid bronchospasm caused by histamine release
B. Inflammatory cell infiltration and mucosal edema
C. Increased cAMP production leading to bronchodilation
D. Immediate IgE-mediated mast cell degranulation
Answer: B
Conceptual Explanation: The late-phase response involves the recruitment of eosinophils,
neutrophils, and lymphocytes, which cause persistent airway inflammation, edema, and
mucus production, unlike the early phase which is mainly bronchospasm.
NURSES II - EXAM 1 REVIEW
QUESTIONS AND ANSWERS
1. A patient with chronic kidney disease (CKD) presents with a serum potassium level of 6.2
mEq/L. Which physiological mechanism is primarily responsible for the risk of cardiac
dysrhythmias in this patient?
A. Increased resting membrane potential, leading to hypopolarization
B. Decreased resting membrane potential making cells less excitable
C. Rapid repolarization due to decreased sodium-potassium pump activity
D. Increased calcium influx into the myocardial cells
Answer: A
Conceptual Explanation: Hyperkalemia increases the resting membrane potential,
bringing it closer to the threshold for depolarization (hypopolarization). This makes the
heart more excitable initially but eventually impairs repolarization, leading to potentially
fatal dysrhythmias.
,2. Which compensatory mechanism is activated by the kidneys in response to a sustained
decrease in mean arterial pressure (MAP)?
A. Inhibition of the juxtaglomerular apparatus
B. Release of Atrial Natriuretic Peptide (ANP)
C. Decrease in Antidiuretic Hormone (ADH) secretion
D. Activation of the Renin-Angiotensin-Aldosterone System (RAAS)
Answer: D
Conceptual Explanation: Low MAP triggers the RAAS to conserve sodium and water and
cause vasoconstriction via Angiotensin II, thereby increasing blood volume and pressure.
3. A patient is diagnosed with Right-Sided Heart Failure. Which clinical manifestation is a
direct result of increased systemic venous hydrostatic pressure?
A. Peripheral edema and jugular venous distention
B. Orthopnea and paroxysmal nocturnal dyspnea
C. Pulmonary edema and crackles
D. Pink frothy sputum
Answer: A
Conceptual Explanation: Right-sided heart failure causes blood to back up into the
systemic circulation, increasing hydrostatic pressure in the peripheral veins and leading to
edema and JVD. Pulmonary symptoms are characteristic of left-sided failure.
, 4. In the pathogenesis of Atherosclerosis, what is the significance of ‘foam cells’?
A. They are smooth muscle cells that have migrated to the adventitia
B. They are platelets that have adhered to the damaged endothelium
C. They are macrophages that have engulfed oxidized LDL cholesterol
D. They represent the final stage of fibrous plaque calcification
Answer: C
Conceptual Explanation: Foam cells are formed when macrophages ingest oxidized LDL.
These cells accumulate in the arterial wall, contributing to the formation of the fatty streak,
the earliest lesion of atherosclerosis.
5. During an acute asthma attack, the ‘late-phase’ response (occurring 4-8 hours after the
initial trigger) is primarily characterized by:
A. Rapid bronchospasm caused by histamine release
B. Inflammatory cell infiltration and mucosal edema
C. Increased cAMP production leading to bronchodilation
D. Immediate IgE-mediated mast cell degranulation
Answer: B
Conceptual Explanation: The late-phase response involves the recruitment of eosinophils,
neutrophils, and lymphocytes, which cause persistent airway inflammation, edema, and
mucus production, unlike the early phase which is mainly bronchospasm.
