Past Papers · SAQ
Hypersensitivity, Anaphylaxis & Adrenaline
2026A Q20
Exam questiona) Classify hypersensitivity reactions and provide a brief outline of the immunological mechanisms underlying each type (20% of marks).
b) Explain the immunological basis of anaphylaxis (50% of marks).
c) Outline the pharmacology of adrenaline relevant to its use in the management of anaphylaxis (30% of marks).
CICMWrecks answer
Master answer
Open Adrenaline in the Pharmacopeia
a) Classification of hypersensitivity reactions (20%)
| Type | Mechanism | Examples |
|---|---|---|
| I — Immediate | IgE-mediated mast-cell/basophil activation and mediator release after sensitisation | Anaphylaxis, atopy |
| II — Antibody-mediated | IgG/IgM directed against cell-surface or matrix antigen → complement, opsonisation, ADCC or receptor dysfunction | Transfusion reaction, autoimmune haemolysis, Goodpasture syndrome |
| III — Immune complex | Circulating antigen-antibody complexes deposit in tissues → complement activation and neutrophilic inflammation | SLE, serum sickness, vasculitis |
| IV — Delayed | T-cell mediated; cytokine-driven inflammation and/or direct cytotoxicity | Contact dermatitis, granulomatous inflammation |
b) Immunological basis of anaphylaxis (50%)
1. Sensitisation
- Initial allergen exposure → antigen presentation to CD4+ T helper cells.
- Th2-type cytokine signalling promotes B-cell class switching to allergen-specific IgE.
- IgE binds high-affinity FcεRI receptors on mast cells and basophils, producing a sensitised state.
2. Activation on re-exposure
- Allergen cross-links adjacent IgE–FcεRI complexes on mast cells/basophils.
- This triggers intracellular signalling, calcium influx and degranulation, with rapid synthesis of additional lipid mediators and cytokines.
3. Mediator release and physiological effects
| Mediator | Important effects |
|---|---|
| Histamine | Vasodilation, ↑ vascular permeability, bronchoconstriction, pruritus/urticaria |
| Leukotrienes C4/D4/E4 | Potent bronchoconstriction, vascular permeability and mucosal oedema |
| Prostaglandin D2 | Bronchoconstriction and vasodilation |
| Platelet-activating factor | Vasodilation, permeability, bronchoconstriction; contributes to shock severity |
| Tryptase | Marker of mast-cell activation; contributes to inflammatory/protease pathways |
| Cytokines / TNF | Recruit and activate inflammatory cells; contribute to later-phase amplification |
| Serotonin and other mediators | Additional vascular, bronchial and platelet effects |
- The systemic result is vasoplegia + capillary leak → reduced venous return and distributive shock, plus airway oedema and bronchospasm.
- Amplification: recruited inflammatory cells and newly synthesised mediators sustain the response.
- Biphasic anaphylaxis: recurrence may occur after initial resolution due to ongoing/renewed mediator production despite no further allergen exposure.
c) Adrenaline pharmacology relevant to anaphylaxis (30%)
| Target / property | Relevant effect in anaphylaxis |
|---|---|
| α1 | Gq → PLC/IP3/Ca2+ → vasoconstriction: restores SVR/BP and reduces mucosal oedema |
| β1 | Gs → ↑ cAMP → ↑ inotropy and chronotropy: supports cardiac output |
| β2 | Gs → ↑ cAMP → bronchodilation; also inhibits further mast-cell/basophil mediator release |
| Route / dose | IM is first-line: 10 micrograms/kg (maximum 500 micrograms) into the lateral thigh; repeat dosing may be required. IV infusion is titratable in severe/refractory shock in a monitored setting. |
| Onset / offset | Rapid onset; very short plasma half-life because of uptake and metabolism → repeated IM doses or infusion may be required |
| Metabolism | Rapid metabolism by COMT and MAO; inactive metabolites excreted in urine |
Why adrenaline is uniquely effective: it simultaneously reverses vasodilation/capillary leak consequences, supports cardiac output, relieves bronchospasm and suppresses ongoing mediator release.
Exam focus
- Keep Type I–IV classification brief: it is only 20%.
- For anaphylaxis, explicitly structure sensitisation → activation → mediator release, then mention amplification and biphasic response.
- For adrenaline, explain the α1 / β1 / β2 effects in direct relation to anaphylaxis, plus IM delivery and short duration.
Quick reference
Summary
| Feature | High-yield point |
|---|---|
| Type I | IgE-mediated mast-cell/basophil activation |
| Anaphylaxis sequence | Sensitisation → IgE/FcεRI cross-linking → degranulation → mediator release |
| Key mediators | Histamine, leukotrienes, PGD2, PAF, tryptase and cytokines |
| Adrenaline | α1 reverses vasoplegia/oedema; β1 supports cardiac output; β2 bronchodilates and inhibits mediator release |
| Delivery | IM 10 micrograms/kg (max 500 micrograms); short half-life means repeat dosing or infusion may be required |
Past papers
Exam appearances
| Exam | Exact exam wording | Candidate success |
|---|---|---|
| 2026A Q20 | a) Classify hypersensitivity reactions and provide a brief outline of the immunological mechanisms underlying each type (20% of marks). b) Explain the immunological basis of anaphylaxis (50% of marks). c) Outline the pharmacology of adrenaline relevant to its use in the management of anaphylaxis (30% of marks). | 51% |