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Nrsg 310 Pathophysiology 1 Exam 2 Immune Disorders & Reactions Practice Questions And Correct Answers Plus Rationales| Instant Download

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Practice questions on immune disorders and reactions for Pathophysiology 1 Exam 2. Covers hypersensitivity types I through IV, SLE, myasthenia gravis, Graves disease, transplant rejection, chronic granulomatous disease, anaphylaxis, and central tolerance. Each question includes the correct answer with a rationale explaining the pathophysiology, so you can review why each option is right or wrong before exam day.

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, Question 1
Which mechanism best explains the delayed onset (24-72 hours) of a positive
purified protein derivative (PPD) skin test in a patient with prior
Mycobacterium tuberculosis exposure?
A. IgE-mediated mast cell degranulation with histamine release
B. Immune complex deposition in dermal capillaries
C. CD4+ Th1 cell-mediated macrophage activation and cytokine release
D. Complement-mediated cytotoxic damage to infected keratinocytes
Correct Answer: C - CD4+ Th1 cell-mediated macrophage
activation and cytokine release


RATIONALE
The PPD test is a classic example of type IV delayed-type
hypersensitivity, mediated by sensitized CD4+ Th1 lymphocytes that
release IFN- and other cytokines, recruiting and activating
macrophages. This cellular response peaks at 24-72 hours.
IgE-mediated reactions (type I) occur within minutes, immune
complex deposition (type III) typically peaks at 4-10 hours, and
complement-mediated cytotoxicity (type II) is not the primary
mechanism here.

Question 2
A patient with systemic lupus erythematosus (SLE) has a low C3 and C4,
elevated anti-dsDNA, and active urinary sediment. Which pathophysiologic
process best explains these findings?
A. Type II hypersensitivity with antibody-mediated destruction of
glomerular basement membrane
B. Type III hypersensitivity with immune complex deposition in
glomeruli and complement consumption
C. Type IV hypersensitivity with T-cell infiltration of renal interstitium
D. Direct cytotoxic T-cell killing of podocytes
Correct Answer: B - Type III hypersensitivity with immune

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,complex deposition in glomeruli and complement consumption




RATIONALE
SLE nephritis is primarily a type III hypersensitivity reaction where
circulating immune complexes (anti-dsDNA with DNA) deposit in
glomeruli, activating complement and causing consumption of C3 and
C4. The low complement levels and active sediment reflect this
ongoing immune complex-mediated inflammation. Type II involves
antibodies against fixed tissue antigens, type IV is T-cell mediated,
and direct CTL killing of podocytes is not the primary mechanism.

Question 3
Which statement best describes the role of central tolerance in preventing
autoimmunity?
A. It eliminates self-reactive T cells in the thymus via negative selection
B. It suppresses autoreactive T cells in peripheral tissues via Tregs
C. It promotes B-cell differentiation into plasma cells in bone marrow
D. It enhances complement-mediated clearance of apoptotic cells
Correct Answer: A - It eliminates self-reactive T cells in the
thymus via negative selection


RATIONALE
Central tolerance occurs in primary lymphoid organs: in the thymus,
developing T cells that strongly recognize self-antigens undergo
negative selection (apoptosis), eliminating autoreactive T cells.
Peripheral tolerance involves Tregs and anergy. B-cell differentiation
and complement clearance are not central tolerance mechanisms.

Question 4
A patient with chronic granulomatous disease (CGD) is at increased risk for
which type of infection, and what is the underlying defect?
A. Encapsulated bacteria; defect in antibody production
B. Catalase-positive organisms; defect in NADPH oxidase and respiratory


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, burst

C. Viral infections; defect in T-cell receptor signaling
D. Fungal infections; defect in complement C3
Correct Answer: B - Catalase-positive organisms; defect in
NADPH oxidase and respiratory burst


RATIONALE
CGD is caused by defective NADPH oxidase, impairing the
respiratory burst and killing of catalase-positive organisms (e.g.,
Staphylococcus aureus, Aspergillus). This leads to recurrent abscesses
and granulomas. Antibody production, T-cell signaling, and
complement C3 are not primarily defective in CGD.

Question 5
Which finding is most consistent with hyperacute rejection of a kidney
transplant?
A. Gradual rise in creatinine over months with interstitial fibrosis
B. Immediate anuria with thrombotic occlusion of graft vessels within
minutes to hours
C. Fever and graft tenderness at 2 weeks post-transplant with lymphocytic
infiltration
D. Development of donor-specific antibodies at 1 year with proteinuria
Correct Answer: B - Immediate anuria with thrombotic occlusion
of graft vessels within minutes to hours


RATIONALE
Hyperacute rejection is mediated by preformed recipient antibodies
against donor antigens, leading to complement activation, endothelial
damage, and rapid thrombotic occlusion of graft vessels, often within
minutes to hours. This presents as immediate anuria and graft failure.
Acute rejection occurs days to weeks, and chronic rejection occurs
over months to years.




Page 4

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