NSG 5140 Advanced Pathophysiology Final Exam:
South College NSG 5140 Final Exam – 100 Verified
Pathophysiology Questions| PDF
1. A patient with a spinal cord injury at C5 develops autonomic dysreflexia. The
underlying pathophysiology is:
A) Excessive parasympathetic outflow below the lesion
B) Massive sympathetic discharge in response to a noxious stimulus below the lesion
C) Loss of all reflexes below the lesion
D) Destruction of sympathetic preganglionic neurons
Answer: B
Rationale: Autonomic dysreflexia occurs in patients with spinal cord injuries at or
above T6. A noxious stimulus (e.g., bladder distention) triggers a massive sympathetic
response below the lesion, causing severe hypertension, headache, and sweating. The
baroreflex triggers bradycardia and vasodilation above the lesion but cannot overcome
the sympathetic storm.
2. The hallmark of nephritic syndrome that distinguishes it from nephrotic syndrome is:
A) Massive proteinuria >3.5 g/day
B) Lipiduria
C) Hematuria with red blood cell casts and hypertension
D) Hypoalbuminemia
Answer: C
Rationale: Nephritic syndrome is characterized by acute onset of hematuria, red cell
casts, mild-to-moderate proteinuria, azotemia, oliguria, and hypertension due to
glomerular inflammation. Nephrotic syndrome features heavy proteinuria (>3.5 g/day),
hypoalbuminemia, edema, hyperlipidemia, and lipiduria.
3. In cystic fibrosis, the defect in the CFTR protein primarily affects which ion transport?
A) Sodium reabsorption only
B) Chloride secretion and sodium absorption
C) Potassium secretion
D) Calcium absorption
Answer: B
Rationale: The CFTR gene encodes a cAMP-regulated chloride channel. Defects impair
chloride secretion and lead to excessive sodium absorption through ENaC channels,
,drawing water out of the lumen and producing thick, viscous mucus in the lungs,
pancreas, and other organs.
4. A patient with a blood pressure of 220/130 mmHg, retinal hemorrhages, and
papilledema has malignant hypertension. The immediate danger is:
A) Coronary artery spasm
B) Fibrinoid necrosis of arterioles and cerebral edema
C) Left ventricular dilation
D) Aortic dissection
Answer: B
Rationale: Malignant hypertension causes acute endothelial damage, leading to
fibrinoid necrosis of arterioles, particularly in the kidneys, brain, and retina. This can result
in hypertensive encephalopathy, cerebral edema, and renal failure. Papilledema is a key
sign. While aortic dissection is a risk, the direct immediate pathology is microvascular
damage.
5. Which of the following is an example of a tumor suppressor gene that, when mutated,
predisposes to hereditary breast and ovarian cancer?
A) RAS
B) MYC
C) BRCA1
D) HER2/neu
Answer: C
Rationale: BRCA1 and BRCA2 are tumor suppressor genes involved in DNA double-
strand break repair by homologous recombination. Loss-of-function mutations
significantly increase the risk of breast, ovarian, and other cancers. RAS and MYC are
oncogenes, HER2/neu is an oncogene with amplification.
6. Which complement component is most commonly deficient and associated with
recurrent bacterial infections and autoimmune disease (systemic lupus erythematosus)?
A) C3
B) C2
C) C5
D) C9
Answer: B
Rationale: C2 deficiency is the most common complement deficiency in Western
populations, often associated with SLE-like illness or increased susceptibility to
encapsulated bacterial infections. C3 deficiency leads to severe, recurrent pyogenic
infections. C5-C9 deficiencies predispose to Neisseria infections.
, 7. A patient with untreated sleep apnea develops elevated PaCO2 and a compensated
respiratory acidosis. The compensatory mechanism is:
A) Increased ventilation
B) Decreased renal bicarbonate reabsorption
C) Increased renal bicarbonate reabsorption and generation
D) Decreased hydrogen ion secretion
Answer: C
Rationale: Chronic respiratory acidosis (elevated PaCO2) is compensated by the
kidneys, which increase bicarbonate reabsorption and generate new bicarbonate, raising
the serum HCO3- level. This restores pH toward normal. Acute respiratory acidosis shows
no renal compensation (normal HCO3-).
8. In atherosclerosis, the earliest visible lesion is the:
A) Fibrous plaque
B) Complicated lesion
C) Fatty streak
D) Calcified nodule
Answer: C
Rationale: Fatty streaks are the earliest grossly visible lesions of atherosclerosis,
composed of lipid-laden macrophages (foam cells) and T lymphocytes in the intima. They
can appear in childhood. Fibrous plaques and complicated lesions develop later.
9. A patient with acute leukemia has a white blood cell count of 150,000/µL. They are at
risk for leukostasis, which primarily causes:
A) Severe infection
B) Microvascular occlusion and intracranial hemorrhage
C) Hemolysis
D) Deep vein thrombosis
Answer: B
Rationale: Hyperleukocytosis (usually >100,000/µL in AML) causes leukostasis, where
blast cells plug microvasculature in the brain and lungs, leading to intracranial
hemorrhage, respiratory failure, and neurological symptoms. It is a medical emergency
requiring rapid cytoreduction.
10. Which is the major autoantibody in systemic lupus erythematosus (SLE) that
correlates with disease activity and lupus nephritis?
A) Anti-Ro (SSA)
B) Anti-La (SSB)
C) Anti-dsDNA
D) Anti-centromere
South College NSG 5140 Final Exam – 100 Verified
Pathophysiology Questions| PDF
1. A patient with a spinal cord injury at C5 develops autonomic dysreflexia. The
underlying pathophysiology is:
A) Excessive parasympathetic outflow below the lesion
B) Massive sympathetic discharge in response to a noxious stimulus below the lesion
C) Loss of all reflexes below the lesion
D) Destruction of sympathetic preganglionic neurons
Answer: B
Rationale: Autonomic dysreflexia occurs in patients with spinal cord injuries at or
above T6. A noxious stimulus (e.g., bladder distention) triggers a massive sympathetic
response below the lesion, causing severe hypertension, headache, and sweating. The
baroreflex triggers bradycardia and vasodilation above the lesion but cannot overcome
the sympathetic storm.
2. The hallmark of nephritic syndrome that distinguishes it from nephrotic syndrome is:
A) Massive proteinuria >3.5 g/day
B) Lipiduria
C) Hematuria with red blood cell casts and hypertension
D) Hypoalbuminemia
Answer: C
Rationale: Nephritic syndrome is characterized by acute onset of hematuria, red cell
casts, mild-to-moderate proteinuria, azotemia, oliguria, and hypertension due to
glomerular inflammation. Nephrotic syndrome features heavy proteinuria (>3.5 g/day),
hypoalbuminemia, edema, hyperlipidemia, and lipiduria.
3. In cystic fibrosis, the defect in the CFTR protein primarily affects which ion transport?
A) Sodium reabsorption only
B) Chloride secretion and sodium absorption
C) Potassium secretion
D) Calcium absorption
Answer: B
Rationale: The CFTR gene encodes a cAMP-regulated chloride channel. Defects impair
chloride secretion and lead to excessive sodium absorption through ENaC channels,
,drawing water out of the lumen and producing thick, viscous mucus in the lungs,
pancreas, and other organs.
4. A patient with a blood pressure of 220/130 mmHg, retinal hemorrhages, and
papilledema has malignant hypertension. The immediate danger is:
A) Coronary artery spasm
B) Fibrinoid necrosis of arterioles and cerebral edema
C) Left ventricular dilation
D) Aortic dissection
Answer: B
Rationale: Malignant hypertension causes acute endothelial damage, leading to
fibrinoid necrosis of arterioles, particularly in the kidneys, brain, and retina. This can result
in hypertensive encephalopathy, cerebral edema, and renal failure. Papilledema is a key
sign. While aortic dissection is a risk, the direct immediate pathology is microvascular
damage.
5. Which of the following is an example of a tumor suppressor gene that, when mutated,
predisposes to hereditary breast and ovarian cancer?
A) RAS
B) MYC
C) BRCA1
D) HER2/neu
Answer: C
Rationale: BRCA1 and BRCA2 are tumor suppressor genes involved in DNA double-
strand break repair by homologous recombination. Loss-of-function mutations
significantly increase the risk of breast, ovarian, and other cancers. RAS and MYC are
oncogenes, HER2/neu is an oncogene with amplification.
6. Which complement component is most commonly deficient and associated with
recurrent bacterial infections and autoimmune disease (systemic lupus erythematosus)?
A) C3
B) C2
C) C5
D) C9
Answer: B
Rationale: C2 deficiency is the most common complement deficiency in Western
populations, often associated with SLE-like illness or increased susceptibility to
encapsulated bacterial infections. C3 deficiency leads to severe, recurrent pyogenic
infections. C5-C9 deficiencies predispose to Neisseria infections.
, 7. A patient with untreated sleep apnea develops elevated PaCO2 and a compensated
respiratory acidosis. The compensatory mechanism is:
A) Increased ventilation
B) Decreased renal bicarbonate reabsorption
C) Increased renal bicarbonate reabsorption and generation
D) Decreased hydrogen ion secretion
Answer: C
Rationale: Chronic respiratory acidosis (elevated PaCO2) is compensated by the
kidneys, which increase bicarbonate reabsorption and generate new bicarbonate, raising
the serum HCO3- level. This restores pH toward normal. Acute respiratory acidosis shows
no renal compensation (normal HCO3-).
8. In atherosclerosis, the earliest visible lesion is the:
A) Fibrous plaque
B) Complicated lesion
C) Fatty streak
D) Calcified nodule
Answer: C
Rationale: Fatty streaks are the earliest grossly visible lesions of atherosclerosis,
composed of lipid-laden macrophages (foam cells) and T lymphocytes in the intima. They
can appear in childhood. Fibrous plaques and complicated lesions develop later.
9. A patient with acute leukemia has a white blood cell count of 150,000/µL. They are at
risk for leukostasis, which primarily causes:
A) Severe infection
B) Microvascular occlusion and intracranial hemorrhage
C) Hemolysis
D) Deep vein thrombosis
Answer: B
Rationale: Hyperleukocytosis (usually >100,000/µL in AML) causes leukostasis, where
blast cells plug microvasculature in the brain and lungs, leading to intracranial
hemorrhage, respiratory failure, and neurological symptoms. It is a medical emergency
requiring rapid cytoreduction.
10. Which is the major autoantibody in systemic lupus erythematosus (SLE) that
correlates with disease activity and lupus nephritis?
A) Anti-Ro (SSA)
B) Anti-La (SSB)
C) Anti-dsDNA
D) Anti-centromere