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NSG 530 Advanced Pathophysiology Newest Exam
Preparation With Complete Questions And Correct
Answers With Rationales Already Graded A+Brand
New Version!!
Question 1
When antibodies are formed against red blood cell antigens of the Rh
system, 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 Rh incompatibility, antibodies target Rh-positive red
blood cells, and these cells are typically cleared from circulation through
phagocytosis by macrophages in the spleen. The spleen's
reticuloendothelial system recognizes antibody-coated erythrocytes and
removes them from circulation. This is the primary mechanism of
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hemolytic disease of the newborn due to Rh incompatibility.
Complement-mediated lysis is less common in Rh reactions because IgG
antibodies do not efficiently activate the classical complement pathway
to completion.
Question 2
When soluble antigens from infectious agents enter circulation, tissue
damage is a result of:
A) Complement-mediated cell lysis
B) Phagocytosis by macrophages
C) Phagocytosis in the spleen
D) Neutrophil granules and toxic oxygen products
Answer: D) Neutrophil granules and toxic oxygen products
Explanation: Soluble antigens can activate neutrophils, which release
their granules containing cytotoxic substances including proteolytic
enzymes, defensins, and reactive oxygen species. This process
contributes to tissue injury and inflammation during immune complex
deposition. Neutrophils are the primary effector cells in acute
inflammatory responses to circulating immune complexes, and their
release of toxic products causes collateral tissue damage.
Question 3
How are target cells destroyed in a type II hypersensitivity reaction?
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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 antibodies (IgG or IgM)
binding to target cell surface antigens, which activates the complement
system. This leads to direct lysis of the cell through membrane attack
complexes (MAC). Additionally, complement activation generates C3b,
which promotes opsonization and phagocytosis, and C5a, which recruits
inflammatory cells.
Question 4
Graves disease (hyperthyroidism) is an example of which type of
hypersensitivity reaction?
A) Modulation
B) Antibody-dependent cell-mediated cytotoxicity
C) Neutrophil-mediated damage
D) Complement-mediated lysis
Answer: A) Modulation
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Explanation: Graves' disease is a type II hypersensitivity reaction where
autoantibodies (thyroid-stimulating immunoglobulins) bind to and
stimulate the thyroid-stimulating hormone (TSH) receptor, leading to
excessive thyroid hormone production and hyperthyroidism. Rather
than destroying cells, these antibodies modulate receptor function by
mimicking TSH action, resulting in unregulated thyroid stimulation.
Question 5
Type III hypersensitivity reactions are a result of which of the following?
A) Antibodies coating mast cells by binding to receptors that signal its
degranulation
B) Formation of antigen-antibody complexes that deposit in tissues
C) T-cell mediated cytotoxicity directed against self-antigens
D) Antibodies binding to cell surface receptors and altering function
Answer: B) Formation of antigen-antibody complexes that deposit in
tissues
Explanation: Type III hypersensitivity involves the formation of soluble
immune complexes (antigen-antibody complexes) that deposit in
various tissues, including blood vessels, glomeruli, and joints. These
deposits activate the complement system, recruit neutrophils, and cause
tissue damage through inflammation. Classic examples include systemic
lupus erythematosus and serum sickness.
NSG 530 Advanced Pathophysiology Newest Exam
Preparation With Complete Questions And Correct
Answers With Rationales Already Graded A+Brand
New Version!!
Question 1
When antibodies are formed against red blood cell antigens of the Rh
system, 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 Rh incompatibility, antibodies target Rh-positive red
blood cells, and these cells are typically cleared from circulation through
phagocytosis by macrophages in the spleen. The spleen's
reticuloendothelial system recognizes antibody-coated erythrocytes and
removes them from circulation. This is the primary mechanism of
,2|Page
hemolytic disease of the newborn due to Rh incompatibility.
Complement-mediated lysis is less common in Rh reactions because IgG
antibodies do not efficiently activate the classical complement pathway
to completion.
Question 2
When soluble antigens from infectious agents enter circulation, tissue
damage is a result of:
A) Complement-mediated cell lysis
B) Phagocytosis by macrophages
C) Phagocytosis in the spleen
D) Neutrophil granules and toxic oxygen products
Answer: D) Neutrophil granules and toxic oxygen products
Explanation: Soluble antigens can activate neutrophils, which release
their granules containing cytotoxic substances including proteolytic
enzymes, defensins, and reactive oxygen species. This process
contributes to tissue injury and inflammation during immune complex
deposition. Neutrophils are the primary effector cells in acute
inflammatory responses to circulating immune complexes, and their
release of toxic products causes collateral tissue damage.
Question 3
How are target cells destroyed in a type II hypersensitivity reaction?
,3|Page
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 antibodies (IgG or IgM)
binding to target cell surface antigens, which activates the complement
system. This leads to direct lysis of the cell through membrane attack
complexes (MAC). Additionally, complement activation generates C3b,
which promotes opsonization and phagocytosis, and C5a, which recruits
inflammatory cells.
Question 4
Graves disease (hyperthyroidism) is an example of which type of
hypersensitivity reaction?
A) Modulation
B) Antibody-dependent cell-mediated cytotoxicity
C) Neutrophil-mediated damage
D) Complement-mediated lysis
Answer: A) Modulation
, 4|Page
Explanation: Graves' disease is a type II hypersensitivity reaction where
autoantibodies (thyroid-stimulating immunoglobulins) bind to and
stimulate the thyroid-stimulating hormone (TSH) receptor, leading to
excessive thyroid hormone production and hyperthyroidism. Rather
than destroying cells, these antibodies modulate receptor function by
mimicking TSH action, resulting in unregulated thyroid stimulation.
Question 5
Type III hypersensitivity reactions are a result of which of the following?
A) Antibodies coating mast cells by binding to receptors that signal its
degranulation
B) Formation of antigen-antibody complexes that deposit in tissues
C) T-cell mediated cytotoxicity directed against self-antigens
D) Antibodies binding to cell surface receptors and altering function
Answer: B) Formation of antigen-antibody complexes that deposit in
tissues
Explanation: Type III hypersensitivity involves the formation of soluble
immune complexes (antigen-antibody complexes) that deposit in
various tissues, including blood vessels, glomeruli, and joints. These
deposits activate the complement system, recruit neutrophils, and cause
tissue damage through inflammation. Classic examples include systemic
lupus erythematosus and serum sickness.
