Immunopathology Cat: Hypersensitivity & OmpathStudy

MOUNT KENYA UNIVERSITY — MEDICAL SCHOOL Programme: Bachelor of Medicine and Bachelor of Surgery, Year 3 Assessment: Mid Semester 1 — CAT 1 Unit Code: MBPA 3414 — Immunopathology Date: 13th October 2025 Time: 22 minutes Reg No: BMS/2023/.. --- Q1. A 25-year-old patient develops anaphylaxis within 15 minutes of receiving the influenza vaccine. Which mechanism BEST explains this reaction? A. Complement-mediated cytotoxicity via IgG antibodies B. IgE-mediated mast cell degranulation and histamine release C. Immune complex deposition in blood vessel walls D. T-cell mediated delayed-type hypersensitivity E. Direct complement activation by vaccine Answer: B Rapid (minutes) onset is the hallmark of Type I hypersensitivity. C and D take hours-to-days; A and E don't cause immediate anaphylaxis. Q2. In Type I hypersensitivity reactions, which mediator is primarily responsible for the late-phase response occurring 4-12 hours after initial exposure? A. Histamine B. Tryptase C. Leukotrienes C4, D4, and E4 D. Prostaglandin D2 E. Platelet-activating factor Answer: C Leukotrienes drive the sustained late-phase inflammation. Histamine (A) and tryptase (B) act in the immediate phase (preformed mediators). Q3. A patient with a known egg allergy is considering influenza vaccination. The contraindication is MOST likely due to which vaccine component? A. Aluminum hydroxide adjuvant B. Thimerosal preservative C. Ovalbumin protein residues D. Formaldehyde stabilizers E. Gelatin excipients Answer: C Vaccines grown in egg-based culture retain trace ovalbumin, the actual allergen in egg allergy. Q4. Which of the following best describes the sensitization phase in Type I hypersensitivity? A. Immediate degranulation of mast cells upon first antigen exposure B. Asymptomatic IgE production and binding to mast cell Fc receptors C. Formation of circulating immune complexes D. Activation of complement cascade E. T-cell proliferation and cytokine release Answer: B Sensitization is the silent priming step (first exposure); symptoms only occur on re-exposure once IgE is already bound. Q5. Cross-reactivity in Type I hypersensitivity reactions can occur due to: A. Identical molecular weights of different antigens B. Similar epitope structures on different proteins C. Same route of antigen administration D. Identical complement activation pathways E. Same HLA class II presentation Answer: B IgE recognises shared/similar epitopes across structurally related allergens (e.g., latex-fruit syndrome), not molecular weight or delivery route. Q6. A newborn develops severe hemolytic anemia 24 hours after birth. The mother is Rh-negative and this is her second pregnancy with an Rh-positive fetus. This condition exemplifies which type of hypersensitivity mechanism? A. IgE-mediated immediate hypersensitivity B. IgG-mediated antibody-dependent cellular cytotoxicity C. Immune complex-mediated complement activation D. T-cell mediated delayed hypersensitivity E. Complement-independent antibody binding Answer: B Maternal IgG anti-D crosses the placenta and coats fetal RBCs, marking them for destruction — a Type II hypersensitivity mechanism, not IgE- (A) or immune-complex-driven (C). Q7. In Type II hypersensitivity, tissue damage occurs through all of the following mechanisms EXCEPT: A. Complement-dependent cytolysis B. Antibody-dependent cellular cytotoxicity (ADCC) C. Antibody interference with cellular function D. Mast cell degranulation and histamine release E. Fc receptor-mediated phagocytosis Answer: D Mast cell degranulation is a Type I mechanism, not Type II. A, B, C, E are all recognised Type II tissue damage pathways. Q8. Goodpasture's syndrome involves Type II hypersensitivity targeting which specific antigen? A. Glomerular basement membrane collagen IV B. Pulmonary surfactant protein C. Complement component C3 D. Immunoglobulin heavy chains E. Platelet glycoprotein IIb/IIIa Answer: A Anti-GBM antibodies specifically target the alpha-3 chain of type IV collagen in the glomerular (and alveolar) basement membrane. Q9. Which immunoglobulin classes are PRIMARILY involved in Type II hypersensitivity reactions? A. IgE and IgA B. IgG and IgM C. IgA and IgD D. IgM and IgE E. IgG and IgA Answer: B These classes fix complement and mediate cytotoxic/opsonising Type II reactions. IgE (A, D) is Type I-specific. Q10. Drug-induced thrombocytopenia through hapten-carrier mechanism represents which immunopathological process? A. Type I immediate hypersensitivity B. Type II antibody-mediated cytotoxicity C. Type III immune complex disease D. Type IV delayed hypersensitivity E. Mixed Type I and Type IV reaction Answer: B The drug (hapten) binds platelet surface proteins, and antibodies against this drug-platelet complex destroy the platelets — classic Type II. Q11. Arthus reaction following tetanus vaccination is characterized by which pathophysiological sequence? A. IgE binding → mast cell degranulation → vasodilation B. IgG immune complexes → complement activation → neu