NSG530 / NSG 530 Exam 1 (Latest ):
Advanced Pathophysiology | Questions and Verified
Answers | 100% Correct | Grade A - Wilkes
Question 1
When antibodies are formed against red blood cell antigens of the Rh
system, how are the blood cells destroyed?
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: Antibodies against platelet-specific antigens or against
red blood cell antigens of the Rh system coat those cells at low
density, resulting in their preferential removal by phagocytosis in
the spleen, rather than by complement-mediated lysis. These blood
cells are not destroyed by complement-mediated cell lysis,
phagocytosis by macrophages, neutrophil granules, or toxic oxygen
products.
Question 2
When soluble antigens from infectious agents enter circulation, what is
tissue damage 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: Of the options available, only the components of
neutrophil granules as well as the several toxic oxygen products
produced by these cells, damage the tissue.
Question 3
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: D) Natural killer cells
Explanation: The mechanism that results in a type II hypersensitivity
reaction involves a subpopulation of cytotoxic cells that are not
antigen specific (natural killer [NK] cells). Antibody on the target
cell is recognized by Fc receptors on the NK cells, which releases
toxic substances that destroy the target cell. The other options do
not cause the destruction of target cells related to a type II
hypersensitivity reaction.
,Question 4
Graves' disease (hyperthyroidism) is an example of which type II
hypersensitivity reaction?
A) Modulation
B) Antibody-dependent cell-mediated cytotoxicity
C) Neutrophil-mediated damage
D) Complement-mediated lysis
Answer: A) Modulation
Explanation: The antibody reacts with the receptors on the target
cell surface and modulates the function of the receptor by
preventing interactions with their normal ligands, replacing the
ligand and inappropriately stimulating the receptor or destroying
the receptor. For example, in the hyperthyroidism (excessive
thyroid activity) of Graves disease, autoantibody binds to and
activates receptors for thyroid-stimulating hormone (TSH) (a
pituitary hormone that controls the production of the hormone
thyroxine by the thyroid). Graves disease is not a result of cell-
mediated cytotoxicity, neutrophil-mediated damage, or complement-
mediated lysis.
Question 5
Type III hypersensitivity reactions are a result of which of these?
A) Antibodies coating mast cells by binding to receptors that signal its
, degranulation, followed by the discharge of preformed mediators
B) Antibodies binding to soluble antigens that were released into body
fluids and the immune complexes being deposited in the tissues
C) Tc cells or lymphokine-producing Th1 cells directly attacking and
destroying cellular targets
D) Antibodies binding to the antigen on the cell surface
Answer: B) Antibodies binding to soluble antigens that were released
into body fluids and the immune complexes being deposited in the
tissues
Explanation: Antigen-antibody (immune) complexes that are formed
in the circulation and then deposited later in vessel walls or
extravascular tissues cause most type III hypersensitivity diseases.
Type III hypersensitivity reactions are not the result of antibodies
coating mast cells to signal their degranulation, immune cells
directly attacking and destroying targets, or antibodies binding to
the antigen on the cell surface.
Question 6
A type IV hypersensitivity reaction causes which result?
A) Antibodies coating mast cells by binding to receptors that signal its
degranulation, followed by the discharge of preformed mediators
B) Antibodies binding to soluble antigens that were released into body
fluids and the immune complexes being deposited in the tissues
C) Lymphokine-producing Th1 cells directly attacking and destroying
Advanced Pathophysiology | Questions and Verified
Answers | 100% Correct | Grade A - Wilkes
Question 1
When antibodies are formed against red blood cell antigens of the Rh
system, how are the blood cells destroyed?
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: Antibodies against platelet-specific antigens or against
red blood cell antigens of the Rh system coat those cells at low
density, resulting in their preferential removal by phagocytosis in
the spleen, rather than by complement-mediated lysis. These blood
cells are not destroyed by complement-mediated cell lysis,
phagocytosis by macrophages, neutrophil granules, or toxic oxygen
products.
Question 2
When soluble antigens from infectious agents enter circulation, what is
tissue damage 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: Of the options available, only the components of
neutrophil granules as well as the several toxic oxygen products
produced by these cells, damage the tissue.
Question 3
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: D) Natural killer cells
Explanation: The mechanism that results in a type II hypersensitivity
reaction involves a subpopulation of cytotoxic cells that are not
antigen specific (natural killer [NK] cells). Antibody on the target
cell is recognized by Fc receptors on the NK cells, which releases
toxic substances that destroy the target cell. The other options do
not cause the destruction of target cells related to a type II
hypersensitivity reaction.
,Question 4
Graves' disease (hyperthyroidism) is an example of which type II
hypersensitivity reaction?
A) Modulation
B) Antibody-dependent cell-mediated cytotoxicity
C) Neutrophil-mediated damage
D) Complement-mediated lysis
Answer: A) Modulation
Explanation: The antibody reacts with the receptors on the target
cell surface and modulates the function of the receptor by
preventing interactions with their normal ligands, replacing the
ligand and inappropriately stimulating the receptor or destroying
the receptor. For example, in the hyperthyroidism (excessive
thyroid activity) of Graves disease, autoantibody binds to and
activates receptors for thyroid-stimulating hormone (TSH) (a
pituitary hormone that controls the production of the hormone
thyroxine by the thyroid). Graves disease is not a result of cell-
mediated cytotoxicity, neutrophil-mediated damage, or complement-
mediated lysis.
Question 5
Type III hypersensitivity reactions are a result of which of these?
A) Antibodies coating mast cells by binding to receptors that signal its
, degranulation, followed by the discharge of preformed mediators
B) Antibodies binding to soluble antigens that were released into body
fluids and the immune complexes being deposited in the tissues
C) Tc cells or lymphokine-producing Th1 cells directly attacking and
destroying cellular targets
D) Antibodies binding to the antigen on the cell surface
Answer: B) Antibodies binding to soluble antigens that were released
into body fluids and the immune complexes being deposited in the
tissues
Explanation: Antigen-antibody (immune) complexes that are formed
in the circulation and then deposited later in vessel walls or
extravascular tissues cause most type III hypersensitivity diseases.
Type III hypersensitivity reactions are not the result of antibodies
coating mast cells to signal their degranulation, immune cells
directly attacking and destroying targets, or antibodies binding to
the antigen on the cell surface.
Question 6
A type IV hypersensitivity reaction causes which result?
A) Antibodies coating mast cells by binding to receptors that signal its
degranulation, followed by the discharge of preformed mediators
B) Antibodies binding to soluble antigens that were released into body
fluids and the immune complexes being deposited in the tissues
C) Lymphokine-producing Th1 cells directly attacking and destroying
