PATHO 370 In Class Quiz 2 Chapters 10 11
13 14 15 Exam Actual Exam 2026/2027 with
Detailed Rationales | Complete Exam-Style
Questions | Pass Guaranteed – A+ Graded
Chapter 10 – Immune System (Autoimmunity, Immunodeficiency, Hypersensitivity) (Questions 1–10)
Q1: A 16-year-old student develops hives, wheezing, and hypotension within minutes of eating
peanuts. Which immunoglobulin and cell type are primarily responsible for initiating this acute
reaction?
A. IgG and neutrophils
B. IgM and macrophages
C. IgE and mast cells [CORRECT]
D. IgA and basophils
Correct Answer: C
Rationale: The best answer is IgE and mast cells. In Type I hypersensitivity, allergen-specific IgE
binds to Fc receptors on mast cells and basophils; re-exposure triggers cross-linking and rapid
degranulation, releasing histamine, leukotrienes, and other mediators that produce the classic
anaphylaxis presentation.
Q2: A patient experiencing anaphylaxis after a bee sting arrives in the emergency department with
severe hypotension and airway edema. What is the first-line medication and its primary mechanism
in this setting?
A. Diphenhydramine to block H2 receptors and reduce gastric acid
B. Corticosteroids to suppress late-phase inflammatory cytokines
C. Epinephrine to cause vasoconstriction and bronchodilation [CORRECT]
D. Albuterol to selectively antagonize muscarinic receptors
Correct Answer: C
Rationale: The best answer is epinephrine. In anaphylaxis, epinephrine is life-saving because it
stimulates alpha-1 receptors to reverse vasodilation and angioedema while beta-2 stimulation
produces bronchodilation; it also blocks further mast cell mediator release.
,Q3: A patient receives a blood transfusion and within minutes develops fever, chills, back pain, and
hemoglobinuria. Which pathophysiologic process best explains this reaction?
A. Pre-formed IgE mediated mast cell degranulation against donor plasma proteins
B. IgG or IgM binding to foreign red blood cell antigens causing complement-mediated intravascular
hemolysis [CORRECT]
C. Immune complex deposition in glomerular basement membranes triggering neutrophil
recruitment
D. Cytotoxic T-lymphocyte recognition of mismatched MHC molecules on donor erythrocytes
Correct Answer: B
Rationale: The best answer is IgG or IgM binding to foreign red blood cell antigens. This describes
an acute hemolytic transfusion reaction, a classic Type II hypersensitivity in which pre-existing
antibodies bind donor RBC surface antigens, fix complement, and cause rapid intravascular
destruction.
Q4: A patient with a recent streptococcal throat infection develops dark, cola-colored urine,
periorbital edema, and elevated blood pressure. Which hypersensitivity mechanism underlies this
post-infectious glomerular injury?
A. IgE-mediated mast cell activation in the glomerular mesangium
B. Direct antibody-mediated lysis of podocytes via anti-GBM antibodies
C. Circulating immune complex deposition with complement activation producing nephritic
syndrome [CORRECT]
D. CD8+ T-cell mediated delayed destruction of the tubular basement membrane
Correct Answer: C
Rationale: The best answer is circulating immune complex deposition. Post-streptococcal
glomerulonephritis represents a Type III hypersensitivity in which bacterial antigen-antibody
complexes deposit in the glomeruli, activate complement, attract neutrophils, and produce the
classic nephritic triad of hematuria, edema, and hypertension.
Q5: A 28-year-old woman presents with a photosensitive malar rash, painless oral ulcers,
symmetric small joint arthritis, and proteinuria. Laboratory studies reveal a positive ANA,
anti-dsDNA, and anti-Smith antibodies. Which mechanism is central to this multisystem autoimmune
disease?
A. Loss of self-tolerance with defective clearance of apoptotic debris and immune complex
formation [CORRECT]
B. Molecular mimicry between streptococcal M protein and cardiac myosin
C. Thymic hyperplasia leading to excessive regulatory T-cell suppression of autoreactive B cells
D. Sequestered antigen exposure from traumatic muscle injury triggering polyclonal activation
Correct Answer: A
, Rationale: The best answer is loss of self-tolerance with defective clearance of apoptotic debris. In
systemic lupus erythematosus, impaired removal of dying cells leads to nuclear antigen exposure,
autoantibody production, and widespread immune complex deposition that drives inflammation in
the skin, joints, kidneys, and serosal surfaces.
Q6: A patient with chronic fatigue, weight loss, and heat intolerance has a diffusely enlarged
thyroid and exophthalmos. TSH is suppressed and free T4 is elevated. Which autoantibody and
target explain the pathophysiology?
A. Anti-thyroglobulin and anti-thyroperoxidase destroying thyroid follicular cells
B. TSH receptor-stimulating antibodies causing unregulated thyroid hormone production
[CORRECT]
C. Anti-insulin antibodies blocking glucose uptake in skeletal muscle
D. Anti-acetylcholine receptor antibodies impairing neuromuscular transmission
Correct Answer: B
Rationale: The best answer is TSH receptor-stimulating antibodies. Graves disease is caused by
IgG autoantibodies that bind and activate the TSH receptor on thyroid follicular cells, driving
uncontrolled hormone synthesis and release, which produces hyperthyroidism and the
characteristic ophthalmopathy.
Q7: A child with recurrent sinopulmonary infections since infancy is found to have extremely low
serum levels of all immunoglobulin classes. Genetic testing reveals a mutation in the BTK gene.
Which pathogen susceptibility pattern is most consistent with this disorder?
A. Intracellular bacterial and fungal infections due to defective macrophage activation
B. Encapsulated bacterial infections due to inability to generate opsonic antibodies [CORRECT]
C. Opportunistic viral and protozoal infections due to absent CD4+ T-cell function
D. Disseminated mycobacterial infections due to defective interferon-gamma signaling
Correct Answer: B
Rationale: The best answer is encapsulated bacterial infections. Bruton X-linked
agammaglobulinemia results from defective B-cell maturation and profound antibody deficiency;
without opsonizing antibodies, patients are uniquely vulnerable to encapsulated organisms like
Streptococcus pneumoniae and Haemophilus influenzae.
Q8: A patient with HIV presents with dyspnea, nonproductive cough, and hypoxemia. Chest imaging
shows diffuse bilateral ground-glass opacities. The organism most likely responsible is an
opportunistic pathogen rarely seen in immunocompetent hosts. Which statement accurately
describes the underlying immunologic defect?
A. Depletion of CD4+ T-helper cells below 200 cells/mm³ predisposing to Pneumocystis jirovecii
pneumonia [CORRECT]
B. Loss of CD8+ cytotoxic T-cell surveillance permitting uncontrolled Epstein-Barr virus replication
13 14 15 Exam Actual Exam 2026/2027 with
Detailed Rationales | Complete Exam-Style
Questions | Pass Guaranteed – A+ Graded
Chapter 10 – Immune System (Autoimmunity, Immunodeficiency, Hypersensitivity) (Questions 1–10)
Q1: A 16-year-old student develops hives, wheezing, and hypotension within minutes of eating
peanuts. Which immunoglobulin and cell type are primarily responsible for initiating this acute
reaction?
A. IgG and neutrophils
B. IgM and macrophages
C. IgE and mast cells [CORRECT]
D. IgA and basophils
Correct Answer: C
Rationale: The best answer is IgE and mast cells. In Type I hypersensitivity, allergen-specific IgE
binds to Fc receptors on mast cells and basophils; re-exposure triggers cross-linking and rapid
degranulation, releasing histamine, leukotrienes, and other mediators that produce the classic
anaphylaxis presentation.
Q2: A patient experiencing anaphylaxis after a bee sting arrives in the emergency department with
severe hypotension and airway edema. What is the first-line medication and its primary mechanism
in this setting?
A. Diphenhydramine to block H2 receptors and reduce gastric acid
B. Corticosteroids to suppress late-phase inflammatory cytokines
C. Epinephrine to cause vasoconstriction and bronchodilation [CORRECT]
D. Albuterol to selectively antagonize muscarinic receptors
Correct Answer: C
Rationale: The best answer is epinephrine. In anaphylaxis, epinephrine is life-saving because it
stimulates alpha-1 receptors to reverse vasodilation and angioedema while beta-2 stimulation
produces bronchodilation; it also blocks further mast cell mediator release.
,Q3: A patient receives a blood transfusion and within minutes develops fever, chills, back pain, and
hemoglobinuria. Which pathophysiologic process best explains this reaction?
A. Pre-formed IgE mediated mast cell degranulation against donor plasma proteins
B. IgG or IgM binding to foreign red blood cell antigens causing complement-mediated intravascular
hemolysis [CORRECT]
C. Immune complex deposition in glomerular basement membranes triggering neutrophil
recruitment
D. Cytotoxic T-lymphocyte recognition of mismatched MHC molecules on donor erythrocytes
Correct Answer: B
Rationale: The best answer is IgG or IgM binding to foreign red blood cell antigens. This describes
an acute hemolytic transfusion reaction, a classic Type II hypersensitivity in which pre-existing
antibodies bind donor RBC surface antigens, fix complement, and cause rapid intravascular
destruction.
Q4: A patient with a recent streptococcal throat infection develops dark, cola-colored urine,
periorbital edema, and elevated blood pressure. Which hypersensitivity mechanism underlies this
post-infectious glomerular injury?
A. IgE-mediated mast cell activation in the glomerular mesangium
B. Direct antibody-mediated lysis of podocytes via anti-GBM antibodies
C. Circulating immune complex deposition with complement activation producing nephritic
syndrome [CORRECT]
D. CD8+ T-cell mediated delayed destruction of the tubular basement membrane
Correct Answer: C
Rationale: The best answer is circulating immune complex deposition. Post-streptococcal
glomerulonephritis represents a Type III hypersensitivity in which bacterial antigen-antibody
complexes deposit in the glomeruli, activate complement, attract neutrophils, and produce the
classic nephritic triad of hematuria, edema, and hypertension.
Q5: A 28-year-old woman presents with a photosensitive malar rash, painless oral ulcers,
symmetric small joint arthritis, and proteinuria. Laboratory studies reveal a positive ANA,
anti-dsDNA, and anti-Smith antibodies. Which mechanism is central to this multisystem autoimmune
disease?
A. Loss of self-tolerance with defective clearance of apoptotic debris and immune complex
formation [CORRECT]
B. Molecular mimicry between streptococcal M protein and cardiac myosin
C. Thymic hyperplasia leading to excessive regulatory T-cell suppression of autoreactive B cells
D. Sequestered antigen exposure from traumatic muscle injury triggering polyclonal activation
Correct Answer: A
, Rationale: The best answer is loss of self-tolerance with defective clearance of apoptotic debris. In
systemic lupus erythematosus, impaired removal of dying cells leads to nuclear antigen exposure,
autoantibody production, and widespread immune complex deposition that drives inflammation in
the skin, joints, kidneys, and serosal surfaces.
Q6: A patient with chronic fatigue, weight loss, and heat intolerance has a diffusely enlarged
thyroid and exophthalmos. TSH is suppressed and free T4 is elevated. Which autoantibody and
target explain the pathophysiology?
A. Anti-thyroglobulin and anti-thyroperoxidase destroying thyroid follicular cells
B. TSH receptor-stimulating antibodies causing unregulated thyroid hormone production
[CORRECT]
C. Anti-insulin antibodies blocking glucose uptake in skeletal muscle
D. Anti-acetylcholine receptor antibodies impairing neuromuscular transmission
Correct Answer: B
Rationale: The best answer is TSH receptor-stimulating antibodies. Graves disease is caused by
IgG autoantibodies that bind and activate the TSH receptor on thyroid follicular cells, driving
uncontrolled hormone synthesis and release, which produces hyperthyroidism and the
characteristic ophthalmopathy.
Q7: A child with recurrent sinopulmonary infections since infancy is found to have extremely low
serum levels of all immunoglobulin classes. Genetic testing reveals a mutation in the BTK gene.
Which pathogen susceptibility pattern is most consistent with this disorder?
A. Intracellular bacterial and fungal infections due to defective macrophage activation
B. Encapsulated bacterial infections due to inability to generate opsonic antibodies [CORRECT]
C. Opportunistic viral and protozoal infections due to absent CD4+ T-cell function
D. Disseminated mycobacterial infections due to defective interferon-gamma signaling
Correct Answer: B
Rationale: The best answer is encapsulated bacterial infections. Bruton X-linked
agammaglobulinemia results from defective B-cell maturation and profound antibody deficiency;
without opsonizing antibodies, patients are uniquely vulnerable to encapsulated organisms like
Streptococcus pneumoniae and Haemophilus influenzae.
Q8: A patient with HIV presents with dyspnea, nonproductive cough, and hypoxemia. Chest imaging
shows diffuse bilateral ground-glass opacities. The organism most likely responsible is an
opportunistic pathogen rarely seen in immunocompetent hosts. Which statement accurately
describes the underlying immunologic defect?
A. Depletion of CD4+ T-helper cells below 200 cells/mm³ predisposing to Pneumocystis jirovecii
pneumonia [CORRECT]
B. Loss of CD8+ cytotoxic T-cell surveillance permitting uncontrolled Epstein-Barr virus replication
