NR507 ADVANCED
PATHOPHYSIOLOGY FINAL EXAM
REVIEW QUESTIONS AND ANSWERS
1. A patient presents with severe dehydration and a high serum osmolarity. Which hormone
is primarily responsible for increasing water reabsorption in the collecting ducts of the
kidneys?
A. Aldosterone
B. Atrial Natriuretic Peptide
C. Angiotensin II
D. Antidiuretic Hormone (ADH)
Answer: D
Conceptual Explanation: Antidiuretic Hormone (ADH) acts on the V2 receptors in the
collecting ducts to increase water permeability through aquaporin-2 channels, thereby
increasing water reabsorption.
2. Which of the following describes the mechanism of Myasthenia Gravis?
A. Autoimmune destruction of the myelin sheath in the CNS
B. Antibody-mediated destruction of acetylcholine receptors at the neuromuscular junction
,C. Degeneration of dopaminergic neurons in the substantia nigra
D. Loss of lower motor neurons in the anterior horn of the spinal cord
Answer: B
Conceptual Explanation: Myasthenia Gravis is a Type II hypersensitivity reaction where
IgG antibodies block or destroy acetylcholine receptors, leading to muscle weakness.
3. In the development of atherosclerosis, what is the primary role of oxidized LDL?
A. It is engulfed by macrophages to form foam cells within the tunica intima
B. It stimulates the release of nitric oxide to dilate vessels
C. It inhibits the migration of smooth muscle cells
D. It prevents platelet aggregation on the endothelial surface
Answer: A
Conceptual Explanation: Oxidized LDL is toxic to endothelial cells and is taken up by
macrophages via scavenger receptors, leading to foam cell formation and the development
of fatty streaks.
4. A patient with chronic kidney disease (CKD) develops secondary hyperparathyroidism.
What is the underlying cause?
A. Hyperphosphatemia and decreased activation of Vitamin D
B. Vitamin D toxicity
C. Hypercalcemia and hypophosphatemia
, D. Direct stimulation of the parathyroid gland by urea
Answer: A
Conceptual Explanation: In CKD, the kidneys fail to excrete phosphate and activate
Vitamin D. Hypocalcemia (due to low Vitamin D) and hyperphosphatemia both stimulate
the parathyroid glands to secrete PTH.
5. What is the pathophysiological hallmark of Multiple Sclerosis?
A. Plaque formation and axonal loss in the peripheral nervous system
B. Demyelination of central nervous system neurons followed by gliosis
C. Depletion of gamma-aminobutyric acid (GABA) in the basal ganglia
D. Accumulation of amyloid-beta proteins in the cerebral cortex
Answer: B
Conceptual Explanation: Multiple Sclerosis is an autoimmune inflammatory disease
characterized by demyelination of the CNS, which leads to nerve impulse slowing and
eventual axonal damage.
6. During an asthma attack, the late-phase response (4-8 hours after exposure) is primarily
driven by:
A. Immediate mast cell degranulation and histamine release
B. Activation of the sympathetic nervous system
C. Infiltration of eosinophils, neutrophils, and lymphocytes
PATHOPHYSIOLOGY FINAL EXAM
REVIEW QUESTIONS AND ANSWERS
1. A patient presents with severe dehydration and a high serum osmolarity. Which hormone
is primarily responsible for increasing water reabsorption in the collecting ducts of the
kidneys?
A. Aldosterone
B. Atrial Natriuretic Peptide
C. Angiotensin II
D. Antidiuretic Hormone (ADH)
Answer: D
Conceptual Explanation: Antidiuretic Hormone (ADH) acts on the V2 receptors in the
collecting ducts to increase water permeability through aquaporin-2 channels, thereby
increasing water reabsorption.
2. Which of the following describes the mechanism of Myasthenia Gravis?
A. Autoimmune destruction of the myelin sheath in the CNS
B. Antibody-mediated destruction of acetylcholine receptors at the neuromuscular junction
,C. Degeneration of dopaminergic neurons in the substantia nigra
D. Loss of lower motor neurons in the anterior horn of the spinal cord
Answer: B
Conceptual Explanation: Myasthenia Gravis is a Type II hypersensitivity reaction where
IgG antibodies block or destroy acetylcholine receptors, leading to muscle weakness.
3. In the development of atherosclerosis, what is the primary role of oxidized LDL?
A. It is engulfed by macrophages to form foam cells within the tunica intima
B. It stimulates the release of nitric oxide to dilate vessels
C. It inhibits the migration of smooth muscle cells
D. It prevents platelet aggregation on the endothelial surface
Answer: A
Conceptual Explanation: Oxidized LDL is toxic to endothelial cells and is taken up by
macrophages via scavenger receptors, leading to foam cell formation and the development
of fatty streaks.
4. A patient with chronic kidney disease (CKD) develops secondary hyperparathyroidism.
What is the underlying cause?
A. Hyperphosphatemia and decreased activation of Vitamin D
B. Vitamin D toxicity
C. Hypercalcemia and hypophosphatemia
, D. Direct stimulation of the parathyroid gland by urea
Answer: A
Conceptual Explanation: In CKD, the kidneys fail to excrete phosphate and activate
Vitamin D. Hypocalcemia (due to low Vitamin D) and hyperphosphatemia both stimulate
the parathyroid glands to secrete PTH.
5. What is the pathophysiological hallmark of Multiple Sclerosis?
A. Plaque formation and axonal loss in the peripheral nervous system
B. Demyelination of central nervous system neurons followed by gliosis
C. Depletion of gamma-aminobutyric acid (GABA) in the basal ganglia
D. Accumulation of amyloid-beta proteins in the cerebral cortex
Answer: B
Conceptual Explanation: Multiple Sclerosis is an autoimmune inflammatory disease
characterized by demyelination of the CNS, which leads to nerve impulse slowing and
eventual axonal damage.
6. During an asthma attack, the late-phase response (4-8 hours after exposure) is primarily
driven by:
A. Immediate mast cell degranulation and histamine release
B. Activation of the sympathetic nervous system
C. Infiltration of eosinophils, neutrophils, and lymphocytes
