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WCU Pathophysiology Exam 2026-2027 BANK
QUESTIONS WITH DETAILED VERIFIED ANSWERS
EXAM QUESTIONS WILL COME FROM HERE (100%
Latest Already Graded A+
QUESTION 1
Which cellular adaptation is characterized by a decrease in cell size and
metabolic activity in response to reduced workload or nutrient supply?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Answer: C. Atrophy is the reduction in cell size and function.
Hypertrophy is an increase in cell size; hyperplasia is an increase in cell
number; metaplasia is a change in cell type.
QUESTION 2
Programmed cell death that does not elicit an inflammatory response is
termed:
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A. Necrosis
B. Apoptosis
C. Pyroptosis
D. Autophagy
Answer: B. Apoptosis is a highly regulated, energy-dependent process of
cell suicide that eliminates damaged cells without triggering
inflammation. Necrosis is uncontrolled cell death that releases cellular
contents and induces inflammation.
QUESTION 3
A 65-year-old patient with chronic heart failure develops bilateral
pitting edema and ascites. This fluid accumulation is most directly
caused by:
A. Decreased plasma oncotic pressure
B. Increased capillary hydrostatic pressure
C. Lymphatic obstruction
D. Sodium retention by the kidneys
Answer: B. Increased capillary hydrostatic pressure, a consequence of
elevated venous pressure in heart failure, forces fluid out of the
capillaries into the interstitial space. While sodium retention and
decreased oncotic pressure contribute, the primary driver in this
scenario is hydrostatic pressure.
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QUESTION 4
Which of the following best describes the pathogenesis of type I
hypersensitivity reactions?
A. Antigen-antibody complexes deposited in tissues
B. T-cell mediated cytotoxicity
C. IgE-mediated mast cell degranulation
D. Antibody-mediated destruction of cell surface receptors
Answer: C. Type I hypersensitivity is an immediate, IgE-mediated
reaction. Allergen cross-links IgE on mast cells, causing degranulation
and release of histamine and other inflammatory mediators.
QUESTION 5
A patient with sepsis is in a state of low systemic vascular resistance
and high cardiac output. This hemodynamic profile is characteristic of:
A. Cardiogenic shock
B. Hypovolemic shock
C. Distributive shock
D. Obstructive shock
Answer: C. Distributive shock, including septic shock, is defined by
profound vasodilation leading to low systemic vascular resistance
despite normal or elevated cardiac output.
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QUESTION 6
The primary genetic defect in cystic fibrosis involves a mutation in the
CFTR gene, leading to:
A. Defective chloride channel function
B. Excessive mucus production
C. Impaired immune cell migration
D. Abnormal surfactant synthesis
Answer: A. The CFTR gene encodes a chloride channel. Dysfunction
results in thick, dehydrated secretions in the lungs, pancreas, and other
organs.
QUESTION 7
In the context of acute inflammation, which vascular change is
responsible for the localized redness and heat?
A. Increased capillary permeability
B. Vasodilation
C. Leukocyte adhesion
D. Platelet aggregation
Answer: B. Vasodilation of arterioles increases blood flow to the area,
causing the classic signs of redness (rubor) and heat (calor).
WCU Pathophysiology Exam 2026-2027 BANK
QUESTIONS WITH DETAILED VERIFIED ANSWERS
EXAM QUESTIONS WILL COME FROM HERE (100%
Latest Already Graded A+
QUESTION 1
Which cellular adaptation is characterized by a decrease in cell size and
metabolic activity in response to reduced workload or nutrient supply?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Answer: C. Atrophy is the reduction in cell size and function.
Hypertrophy is an increase in cell size; hyperplasia is an increase in cell
number; metaplasia is a change in cell type.
QUESTION 2
Programmed cell death that does not elicit an inflammatory response is
termed:
,2|Page
A. Necrosis
B. Apoptosis
C. Pyroptosis
D. Autophagy
Answer: B. Apoptosis is a highly regulated, energy-dependent process of
cell suicide that eliminates damaged cells without triggering
inflammation. Necrosis is uncontrolled cell death that releases cellular
contents and induces inflammation.
QUESTION 3
A 65-year-old patient with chronic heart failure develops bilateral
pitting edema and ascites. This fluid accumulation is most directly
caused by:
A. Decreased plasma oncotic pressure
B. Increased capillary hydrostatic pressure
C. Lymphatic obstruction
D. Sodium retention by the kidneys
Answer: B. Increased capillary hydrostatic pressure, a consequence of
elevated venous pressure in heart failure, forces fluid out of the
capillaries into the interstitial space. While sodium retention and
decreased oncotic pressure contribute, the primary driver in this
scenario is hydrostatic pressure.
,3|Page
QUESTION 4
Which of the following best describes the pathogenesis of type I
hypersensitivity reactions?
A. Antigen-antibody complexes deposited in tissues
B. T-cell mediated cytotoxicity
C. IgE-mediated mast cell degranulation
D. Antibody-mediated destruction of cell surface receptors
Answer: C. Type I hypersensitivity is an immediate, IgE-mediated
reaction. Allergen cross-links IgE on mast cells, causing degranulation
and release of histamine and other inflammatory mediators.
QUESTION 5
A patient with sepsis is in a state of low systemic vascular resistance
and high cardiac output. This hemodynamic profile is characteristic of:
A. Cardiogenic shock
B. Hypovolemic shock
C. Distributive shock
D. Obstructive shock
Answer: C. Distributive shock, including septic shock, is defined by
profound vasodilation leading to low systemic vascular resistance
despite normal or elevated cardiac output.
, 4|Page
QUESTION 6
The primary genetic defect in cystic fibrosis involves a mutation in the
CFTR gene, leading to:
A. Defective chloride channel function
B. Excessive mucus production
C. Impaired immune cell migration
D. Abnormal surfactant synthesis
Answer: A. The CFTR gene encodes a chloride channel. Dysfunction
results in thick, dehydrated secretions in the lungs, pancreas, and other
organs.
QUESTION 7
In the context of acute inflammation, which vascular change is
responsible for the localized redness and heat?
A. Increased capillary permeability
B. Vasodilation
C. Leukocyte adhesion
D. Platelet aggregation
Answer: B. Vasodilation of arterioles increases blood flow to the area,
causing the classic signs of redness (rubor) and heat (calor).
