Hypersensitivity and allergic reactions: mechanisms and therapy MCQs With Answer

Introduction: This quiz collection on Hypersensitivity and Allergic Reactions: Mechanisms and Therapy is tailored for M.Pharm students preparing for Advanced Pharmacology-II. It consolidates core concepts — immunologic mechanisms (Types I–IV), cellular and molecular mediators, diagnostic approaches, and pharmacotherapeutic strategies including antihistamines, corticosteroids, leukotriene modifiers, biologics, immunotherapy and emergency management of anaphylaxis. Questions emphasize mechanistic depth, clinically relevant drug actions, adverse reaction pathways (e.g., SJS/TEN, DRESS), and modern interventions such as monoclonal antibodies and plasmapheresis. Use these 20 MCQs with answers to test understanding, reinforce learning, and identify topics needing further review.

Q1. Which mechanism best describes immediate (Type I) hypersensitivity leading to classical allergic reactions?

• IgG-mediated complement activation causing cell lysis
• Antigen-specific IgM binding leading to immune-complex deposition
• IgE cross-linking of FcεRI on mast cells leading to histamine and mediator release
• Delayed T‑cell mediated cytotoxicity against target tissues

Correct Answer: IgE cross-linking of FcεRI on mast cells leading to histamine and mediator release

Q2. Which mediator is primarily stored in mast cell granules and is responsible for early vasodilation, increased vascular permeability and pruritus?

• Leukotriene C4
• Histamine
• Interleukin-4
• Bradykinin

Correct Answer: Histamine

Q3. Montelukast exerts its therapeutic effect in asthma and allergic rhinitis primarily by which mechanism?

• Inhibition of cyclooxygenase-2 reducing prostaglandin synthesis
• Blocking cysteinyl leukotriene type 1 (CysLT1) receptors
• Neutralizing circulating IgE
• Competitive antagonism at histamine H1 receptors

Correct Answer: Blocking cysteinyl leukotriene type 1 (CysLT1) receptors

Q4. What is the principal mechanism of action of omalizumab in allergic asthma?

• Small-molecule antagonist of the CysLT1 receptor
• Monoclonal anti-IgE antibody that binds circulating IgE preventing FcεRI binding
• Inhibitor of phospholipase A2 reducing eicosanoid synthesis
• Blocker of histamine H2 receptors to reduce gastric acid and allergy symptoms

Correct Answer: Monoclonal anti-IgE antibody that binds circulating IgE preventing FcεRI binding

Q5. In the initial prehospital management of an adult with anaphylaxis, the recommended first-line drug and dosing is:

• Intravenous hydrocortisone 100 mg
• Subcutaneous epinephrine 0.5 mg of 1:10,000 dilution
• Intramuscular epinephrine 0.3–0.5 mg of 1:1,000 (1 mg/mL) concentration
• Inhaled albuterol nebulization only

Correct Answer: Intramuscular epinephrine 0.3–0.5 mg of 1:1,000 (1 mg/mL) concentration

Q6. Type II hypersensitivity reactions are best characterized by which pathogenic mechanism?

• Immune complex deposition in vessel walls activating complement
• Antibody-mediated cytotoxicity where IgG or IgM binds cell-surface antigens causing complement-mediated lysis or phagocytosis
• IgE-mediated mast cell degranulation producing bronchospasm
• Delayed-type T-cell mediated granuloma formation

Correct Answer: Antibody-mediated cytotoxicity where IgG or IgM binds cell-surface antigens causing complement-mediated lysis or phagocytosis

Q7. Serum sickness following administration of foreign protein or some drugs is best explained by which immunopathology?

• Type I IgE-mediated immediate hypersensitivity
• Type II antibody-dependent cellular cytotoxicity (ADCC)
• Type III immune-complex mediated vasculitis with complement activation
• Type IV delayed T-cell mediated contact dermatitis

Correct Answer: Type III immune-complex mediated vasculitis with complement activation

Q8. Hypersensitivity pneumonitis (extrinsic allergic alveolitis) involves which combination of immune mechanisms?

• Pure IgE-mediated airway constriction without cellular infiltration
• Type II cytotoxic reactions against alveolar epithelium
• Combination of type III immune-complex deposition and type IV T‑cell mediated alveolar inflammation
• Autoantibody formation against surfactant proteins exclusively

Correct Answer: Combination of type III immune-complex deposition and type IV T‑cell mediated alveolar inflammation

Q9. The predominant cytotoxic mechanism implicated in Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) induced by drugs is:

• Complement-mediated neutrophil recruitment causing pustular lesions
• Drug‑specific CD8+ cytotoxic T cells releasing granulysin and perforin/granzyme causing widespread keratinocyte apoptosis
• IgE-mediated mast cell activation leading to epidermal detachment
• B-cell mediated immune complex deposition in the epidermis

Correct Answer: Drug‑specific CD8+ cytotoxic T cells releasing granulysin and perforin/granzyme causing widespread keratinocyte apoptosis

Q10. Which diagnostic test is most appropriate to confirm an IgE-mediated immediate hypersensitivity to a specific inhalant allergen?

• Patch testing with 48–72 hour reading
• Serum IgG antibody titers to the allergen
• Skin prick testing demonstrating immediate wheal-and-flare mediated by IgE
• Bronchoscopy with epithelial biopsy for eosinophils

Correct Answer: Skin prick testing demonstrating immediate wheal-and-flare mediated by IgE

Q11. How do systemic glucocorticoids reduce allergic inflammation at the molecular level?

• By irreversibly inhibiting cyclooxygenase-1 activity
• By upregulating lipocortin-1 (annexin‑1) and inhibiting phospholipase A2, reducing eicosanoid and cytokine synthesis
• By blocking histamine H1 receptors as inverse agonists
• By directly neutralizing free IgE in circulation

Correct Answer: By upregulating lipocortin-1 (annexin‑1) and inhibiting phospholipase A2, reducing eicosanoid and cytokine synthesis

Q12. First-generation antihistamines differ from second-generation H1 antagonists primarily because first-generation agents:

• Are highly selective for peripheral H1 receptors without CNS penetration
• Cross the blood–brain barrier causing sedation due to central H1 receptor antagonism
• Directly inhibit leukotriene biosynthesis
• Act as monoclonal antibodies against histamine

Correct Answer: Cross the blood–brain barrier causing sedation due to central H1 receptor antagonism

Q13. The immunological basis for allergen-specific subcutaneous immunotherapy (SCIT) achieving long-term tolerance includes:

• Permanent depletion of IgA-producing plasma cells in mucosa
• Induction of regulatory T cells and production of blocking IgG4 antibodies shifting response away from Th2
• Selective augmentation of mast cell FcεRI expression
• Irreversible neutralization of allergen by intradermal deposition

Correct Answer: Induction of regulatory T cells and production of blocking IgG4 antibodies shifting response away from Th2

Q14. Which complement pathway is most directly activated by antigen–antibody complexes in type III hypersensitivity?

• Alternative pathway initiated by properdin
• Lectin pathway initiated by mannose-binding lectin
• Classical pathway initiated by IgG or IgM binding to antigen
• Coagulation complement cross‑activation pathway

Correct Answer: Classical pathway initiated by IgG or IgM binding to antigen

Q15. Development of DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms) has a strong association with which drug and HLA allele?

• Carbamazepine and HLA-B*1502
• Allopurinol and HLA-B*5801
• Penicillin and HLA-B*5701
• Sulfonamides and HLA-A*0201

Correct Answer: Allopurinol and HLA-B*5801

Q16. High‑dose intravenous immunoglobulin (IVIG) is effective in some antibody‑mediated autoimmune disorders primarily because it:

• Directly lyses autoantibody-producing B cells via complement activation
• Provides passive IgE to neutralize allergens
• Blocks Fc gamma receptors on phagocytes and supplies anti-idiotypic antibodies to neutralize pathogenic autoantibodies
• Acts as a chemoattractant for neutrophils to clear immune complexes

Correct Answer: Blocks Fc gamma receptors on phagocytes and supplies anti-idiotypic antibodies to neutralize pathogenic autoantibodies

Q17. Aspirin‑exacerbated respiratory disease (AERD) is best managed pharmacologically by which strategy?

• Exclusive use of H2 antihistamines to prevent bronchospasm
• Leukotriene pathway inhibition (e.g., montelukast or zileuton) often combined with aspirin desensitization
• High-dose oral penicillin to eradicate sinonasal bacteria
• Topical capsaicin to reduce nasal hyperreactivity

Correct Answer: Leukotriene pathway inhibition (e.g., montelukast or zileuton) often combined with aspirin desensitization

Q18. Therapeutic plasmapheresis benefits severe antibody-mediated hypersensitivity disease by:

• Increasing production of autoantibodies to promote immune regulation
• Removing circulating pathogenic autoantibodies and immune complexes to rapidly reduce tissue injury
• Stimulating bone marrow to produce regulatory B cells
• Neutralizing complement components in the circulation permanently

Correct Answer: Removing circulating pathogenic autoantibodies and immune complexes to rapidly reduce tissue injury

Q19. Which cytokine is most critical for B-cell class switching to IgE in allergic sensitization?

• Interferon-gamma (IFN-γ)
• Interleukin-2 (IL-2)
• Interleukin-4 (IL-4)
• Transforming growth factor-beta (TGF-β)

Correct Answer: Interleukin-4 (IL-4)

Q20. In a patient with progressive airway compromise due to anaphylactic angioedema, the immediate priority of management is:

• Administer oral antihistamine and observe for several hours
• Immediate intramuscular epinephrine (0.3–0.5 mg adult) and secure airway support
• Start broad-spectrum intravenous antibiotics
• Perform skin testing to identify the allergen before treatment

Correct Answer: Immediate intramuscular epinephrine (0.3–0.5 mg adult) and secure airway support

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