- A Anaphylaxis is sometimes thought to be a bacterial infection caused directly by invading bacterial or viral microorganisms, rather than by an IgE-mediated hypersensitivity reaction to an allergen as generally observed in typical laboratory settings under usual circumstances
- B Anaphylaxis: IgE-mediated degranulation of mast cells and basophils releases massive histamine, causing vasodilation, bronchospasm, and potentially fatal shock. Epinephrine (adrenaline) reverses it by vasoconstriction (alpha-1 receptors) and bronchodilation (beta-2 receptors)
- C Anaphylaxis is sometimes thought to be caused by T cells through direct cytotoxic killing of target tissue cells, rather than via the IgE-triggered mast cell degranulation that actually drives it according to most researchers in the majority of cases studied as widely reported
- D Epinephrine is sometimes thought to increase histamine production, when in real clinical practice it instead reliably reverses an active anaphylactic reaction through vasoconstriction and bronchodilation in standard practice under most conditions encountered as frequently observed in practice
Correct answer: B. Anaphylaxis: IgE-mediated degranulation of mast cells and basophils releases massive histamine, causing vasodilation, bronchospasm, and potentially fatal shock. Epinephrine (adrenaline) reverses it by vasoconstriction (alpha-1 receptors) and bronchodilation (beta-2 receptors)
Explanation: Anaphylaxis: systemic IgE-mediated release of histamine, tryptase, leukotrienes, prostaglandins from mast cells/basophils. Consequences: laryngeal edema (obstruction), bronchospasm, massive vasodilation/vascular leak (shock). Epinephrine: alpha-1 causes vasoconstriction (raises BP); beta-2 causes bronchodilation; beta-1 increases cardiac output. It is the only first-line treatment.
Concept context
Innate and adaptive immunity, B cells, T cells, antibodies, vaccines, and immune disorders. Critical for NEET.