NSG 530 Exam 1, 2, 3 & 4 | Advanced
Pathophysiology – Wilkes | 2025 Verified
Questions & Answers, Questions with
Explanations
Q1: When antibodies are formed against red blood cell antigen systems, the blood
cells are destroyed by:
A. Complement-mediated cell lysis
B. Phagocytosis by macrophages
C. Phagocytosis in the spleen
D. Neutrophil granules and toxic oxygen products
Answer: C) Phagocytosis in the spleen
Explanation: In hemolytic disease of the newborn and transfusion reactions,
antibody-coated RBCs are removed primarily by splenic macrophages via Fc
receptors, not complement lysis.
Q2: Soluble antigens that activate neutrophils lead to tissue damage through:
A. Complement-mediated lysis
B. Phagocytosis by macrophages
C. Mast cell degranulation
D. Neutrophil granules and toxic oxygen products
Answer: D) Neutrophil granules and toxic oxygen products
Explanation: Soluble immune complexes trigger neutrophil respiratory burst and
granule release, causing proteolytic and oxidative tissue injury.
Q3: How are target cells destroyed in a type II hypersensitivity reaction?
A. Complement-mediated cell lysis
B. Phagocytosis by macrophages
,C. Neutrophil granules and toxic oxygen products
D. Natural killer cells
Answer: A) Complement-mediated cell lysis
Explanation: Type II hypersensitivity involves IgG/IgM binding to cell surface
antigens, activating classical complement pathway and membrane attack complex
(MAC) formation.
Q4: Graves disease (hyperthyroidism) is an example of which hypersensitivity
type?
A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Answer: B) Type II hypersensitivity
Explanation: Graves disease is caused by autoantibodies that stimulate the TSH
receptor, a type II cytotoxic reaction that results in thyroid hormone
overproduction.
Q5: Type III hypersensitivity reactions result from:
A. Antibodies coating mast cells, causing degranulation
B. Antibodies binding to soluble antigens, forming immune complexes deposited
in tissues
C. Tc cells directly attacking cellular targets
D. Antibodies binding to antigens on cell surfaces
Answer: B) Antibodies binding to soluble antigens, forming immune
complexes deposited in tissues
Explanation: Soluble antigen-antibody complexes lodge in vessel walls, glomeruli,
or joints, triggering complement-mediated inflammation (e.g., serum sickness,
lupus nephritis).
Q6: A patient with a bee sting develops wheezing and hypotension within minutes.
This is most consistent with:
,A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Answer: A) Type I hypersensitivity
Explanation: IgE-mediated mast cell degranulation causes rapid release of
histamine and leukotrienes, leading to bronchospasm and vasodilation
(anaphylaxis).
Q7: Contact dermatitis from poison ivy is an example of:
A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Answer: D) Type IV hypersensitivity
Explanation: Poison ivy causes delayed-type hypersensitivity mediated by memory
T cells and macrophages, peaking at 48-72 hours.
Q8: Which cytokine is primarily responsible for fever induction during
inflammation?
A. Interleukin-2 (IL-2)
B. Interleukin-1 (IL-1)
C. Interferon-gamma (IFN-γ)
D. Tumor necrosis factor-beta (TNF-β)
Answer: B) Interleukin-1 (IL-1)
Explanation: IL-1 acts on the hypothalamus to produce prostaglandin E2, raising
the thermostatic set point and causing fever.
Q9: A patient with rheumatoid arthritis has joint inflammation mediated by
immune complexes. This is classified as:
, A. Type I
B. Type II
C. Type III
D. Type IV
Answer: C) Type III
Explanation: Rheumatoid arthritis involves immune complex deposition in
synovial joints, activating complement and recruiting neutrophils.
Q10: Which cell type is the primary mediator of chronic inflammation?
A. Neutrophil
B. Eosinophil
C. Macrophage
D. Basophil
Answer: C) Macrophage
Explanation: Macrophages dominate chronic inflammation, secreting growth
factors, cytokines, and proteases that cause tissue remodeling and granuloma
formation.
Q11: The classic sign of rubor (redness) during inflammation is caused by:
A. Increased vascular permeability
B. Vasodilation
C. Leukocyte emigration
D. Clotting factor activation
Answer: B) Vasodilation
Explanation: Vasodilation increases blood flow to the injured area, causing redness
(rubor) and warmth (calor).
Q12: A patient has a positive tuberculin skin test. This indicates:
A. Active tuberculosis infection
B. Previous exposure and type IV hypersensitivity memory
Pathophysiology – Wilkes | 2025 Verified
Questions & Answers, Questions with
Explanations
Q1: When antibodies are formed against red blood cell antigen systems, the blood
cells are destroyed by:
A. Complement-mediated cell lysis
B. Phagocytosis by macrophages
C. Phagocytosis in the spleen
D. Neutrophil granules and toxic oxygen products
Answer: C) Phagocytosis in the spleen
Explanation: In hemolytic disease of the newborn and transfusion reactions,
antibody-coated RBCs are removed primarily by splenic macrophages via Fc
receptors, not complement lysis.
Q2: Soluble antigens that activate neutrophils lead to tissue damage through:
A. Complement-mediated lysis
B. Phagocytosis by macrophages
C. Mast cell degranulation
D. Neutrophil granules and toxic oxygen products
Answer: D) Neutrophil granules and toxic oxygen products
Explanation: Soluble immune complexes trigger neutrophil respiratory burst and
granule release, causing proteolytic and oxidative tissue injury.
Q3: How are target cells destroyed in a type II hypersensitivity reaction?
A. Complement-mediated cell lysis
B. Phagocytosis by macrophages
,C. Neutrophil granules and toxic oxygen products
D. Natural killer cells
Answer: A) Complement-mediated cell lysis
Explanation: Type II hypersensitivity involves IgG/IgM binding to cell surface
antigens, activating classical complement pathway and membrane attack complex
(MAC) formation.
Q4: Graves disease (hyperthyroidism) is an example of which hypersensitivity
type?
A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Answer: B) Type II hypersensitivity
Explanation: Graves disease is caused by autoantibodies that stimulate the TSH
receptor, a type II cytotoxic reaction that results in thyroid hormone
overproduction.
Q5: Type III hypersensitivity reactions result from:
A. Antibodies coating mast cells, causing degranulation
B. Antibodies binding to soluble antigens, forming immune complexes deposited
in tissues
C. Tc cells directly attacking cellular targets
D. Antibodies binding to antigens on cell surfaces
Answer: B) Antibodies binding to soluble antigens, forming immune
complexes deposited in tissues
Explanation: Soluble antigen-antibody complexes lodge in vessel walls, glomeruli,
or joints, triggering complement-mediated inflammation (e.g., serum sickness,
lupus nephritis).
Q6: A patient with a bee sting develops wheezing and hypotension within minutes.
This is most consistent with:
,A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Answer: A) Type I hypersensitivity
Explanation: IgE-mediated mast cell degranulation causes rapid release of
histamine and leukotrienes, leading to bronchospasm and vasodilation
(anaphylaxis).
Q7: Contact dermatitis from poison ivy is an example of:
A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Answer: D) Type IV hypersensitivity
Explanation: Poison ivy causes delayed-type hypersensitivity mediated by memory
T cells and macrophages, peaking at 48-72 hours.
Q8: Which cytokine is primarily responsible for fever induction during
inflammation?
A. Interleukin-2 (IL-2)
B. Interleukin-1 (IL-1)
C. Interferon-gamma (IFN-γ)
D. Tumor necrosis factor-beta (TNF-β)
Answer: B) Interleukin-1 (IL-1)
Explanation: IL-1 acts on the hypothalamus to produce prostaglandin E2, raising
the thermostatic set point and causing fever.
Q9: A patient with rheumatoid arthritis has joint inflammation mediated by
immune complexes. This is classified as:
, A. Type I
B. Type II
C. Type III
D. Type IV
Answer: C) Type III
Explanation: Rheumatoid arthritis involves immune complex deposition in
synovial joints, activating complement and recruiting neutrophils.
Q10: Which cell type is the primary mediator of chronic inflammation?
A. Neutrophil
B. Eosinophil
C. Macrophage
D. Basophil
Answer: C) Macrophage
Explanation: Macrophages dominate chronic inflammation, secreting growth
factors, cytokines, and proteases that cause tissue remodeling and granuloma
formation.
Q11: The classic sign of rubor (redness) during inflammation is caused by:
A. Increased vascular permeability
B. Vasodilation
C. Leukocyte emigration
D. Clotting factor activation
Answer: B) Vasodilation
Explanation: Vasodilation increases blood flow to the injured area, causing redness
(rubor) and warmth (calor).
Q12: A patient has a positive tuberculin skin test. This indicates:
A. Active tuberculosis infection
B. Previous exposure and type IV hypersensitivity memory
