,NSG 530 Exam 2 Advanced Pathophysiology Questions And Answers
2026/2027 Wilkes University
Q1. Breakdown of self-tolerance permits autoreactive lymphocytes
to persist. What is the most direct consequence of this defect?
A) Failure to recognize all microbial antigens
B) Immune responses directed against host tissues
C) Complete loss of complement activation
D) Elimination of antibody production
Correct Answer: B) Immune responses directed against host tissues
Rationale: Self-tolerance normally eliminates or suppresses lymphocytes
capable of reacting strongly with host antigens. When central or peripheral
tolerance fails, autoreactive B and T lymphocytes can become activated and
produce inflammatory responses against normal tissues.
Q2. Which mechanism contributes substantially to tissue injury in
systemic lupus erythematosus?
A) Permanent suppression of B-cell activity
B) Absence of circulating immunoglobulins
C) Loss of all complement proteins
D) Deposition of antigen-antibody immune complexes in tissues
Correct Answer: D) Deposition of antigen-antibody immune complexes in
tissues
Rationale: SLE involves production of numerous autoantibodies.
Autoantibodies bind self-antigens and form circulating immune complexes
that can deposit in tissues, activate complement, and generate inflammation
affecting organs such as the kidneys, skin, joints, lungs, and nervous system.
Q3. Impaired clearance of apoptotic cellular debris can promote SLE
because it produces what effect?
A) Prolonged exposure of the immune system to nuclear self-antigens
B) Elimination of autoreactive B lymphocytes
C) Decreased availability of antigen-presenting material
, D) Permanent inhibition of type I interferon production
Correct Answer: A) Prolonged exposure of the immune system to nuclear
self-antigens
Rationale: Defective removal of apoptotic material increases exposure to
DNA, RNA, histones, and other intracellular molecules. These self-antigens
can activate autoreactive lymphocytes and innate nucleic-acid sensing
pathways, promoting autoantibody production and chronic inflammation.
Q4. A person with SLE develops glomerular inflammation associated
with deposition of immune complexes. Which hypersensitivity
mechanism most closely explains this process?
A) Immediate IgE-mediated mast-cell activation
B) Antibody-mediated stimulation of a cell-surface receptor
C) Immune-complex-mediated tissue injury
D) Direct cytotoxic T-cell destruction only
Correct Answer: C) Immune-complex-mediated tissue injury
Rationale: Type III hypersensitivity occurs when antigen-antibody
complexes deposit in tissues and activate complement and inflammatory
cells. This mechanism contributes importantly to manifestations such as
lupus nephritis and some forms of vasculitis.
Q5. Why may serum complement concentrations decrease during
active immune-complex disease?
A) Complement components are consumed during inflammatory activation
B) The liver permanently stops producing complement
C) Complement proteins are converted directly into antibodies
D) Complement is transferred from plasma into erythrocytes
Correct Answer: A) Complement components are consumed during
inflammatory activation
Rationale: Immune complexes activate the complement cascade. Extensive
ongoing activation consumes circulating complement proteins, so reduced
complement concentrations can accompany active immune-complex-
mediated inflammation.
2026/2027 Wilkes University
Q1. Breakdown of self-tolerance permits autoreactive lymphocytes
to persist. What is the most direct consequence of this defect?
A) Failure to recognize all microbial antigens
B) Immune responses directed against host tissues
C) Complete loss of complement activation
D) Elimination of antibody production
Correct Answer: B) Immune responses directed against host tissues
Rationale: Self-tolerance normally eliminates or suppresses lymphocytes
capable of reacting strongly with host antigens. When central or peripheral
tolerance fails, autoreactive B and T lymphocytes can become activated and
produce inflammatory responses against normal tissues.
Q2. Which mechanism contributes substantially to tissue injury in
systemic lupus erythematosus?
A) Permanent suppression of B-cell activity
B) Absence of circulating immunoglobulins
C) Loss of all complement proteins
D) Deposition of antigen-antibody immune complexes in tissues
Correct Answer: D) Deposition of antigen-antibody immune complexes in
tissues
Rationale: SLE involves production of numerous autoantibodies.
Autoantibodies bind self-antigens and form circulating immune complexes
that can deposit in tissues, activate complement, and generate inflammation
affecting organs such as the kidneys, skin, joints, lungs, and nervous system.
Q3. Impaired clearance of apoptotic cellular debris can promote SLE
because it produces what effect?
A) Prolonged exposure of the immune system to nuclear self-antigens
B) Elimination of autoreactive B lymphocytes
C) Decreased availability of antigen-presenting material
, D) Permanent inhibition of type I interferon production
Correct Answer: A) Prolonged exposure of the immune system to nuclear
self-antigens
Rationale: Defective removal of apoptotic material increases exposure to
DNA, RNA, histones, and other intracellular molecules. These self-antigens
can activate autoreactive lymphocytes and innate nucleic-acid sensing
pathways, promoting autoantibody production and chronic inflammation.
Q4. A person with SLE develops glomerular inflammation associated
with deposition of immune complexes. Which hypersensitivity
mechanism most closely explains this process?
A) Immediate IgE-mediated mast-cell activation
B) Antibody-mediated stimulation of a cell-surface receptor
C) Immune-complex-mediated tissue injury
D) Direct cytotoxic T-cell destruction only
Correct Answer: C) Immune-complex-mediated tissue injury
Rationale: Type III hypersensitivity occurs when antigen-antibody
complexes deposit in tissues and activate complement and inflammatory
cells. This mechanism contributes importantly to manifestations such as
lupus nephritis and some forms of vasculitis.
Q5. Why may serum complement concentrations decrease during
active immune-complex disease?
A) Complement components are consumed during inflammatory activation
B) The liver permanently stops producing complement
C) Complement proteins are converted directly into antibodies
D) Complement is transferred from plasma into erythrocytes
Correct Answer: A) Complement components are consumed during
inflammatory activation
Rationale: Immune complexes activate the complement cascade. Extensive
ongoing activation consumes circulating complement proteins, so reduced
complement concentrations can accompany active immune-complex-
mediated inflammation.
