100+ Free CMSA Cert Allergology(SA) Phys Practice Questions

Explanation: Cross-linking of FcεRI-bound IgE by multivalent allergen aggregates the receptors, leading to rapid activation of the receptor-associated Src-family tyrosine kinase Lyn. Lyn phosphorylates immunoreceptor tyrosine-based activation motifs (ITAMs) located on the intracellular domains of the FcεRI β and γ subunits. This creates docking sites for the tandem SH2 domains of Syk kinase, which is subsequently activated and propagates down-stream signaling including PLCγ activation, calcium influx, and degranulation.

Explanation: Th2 cell differentiation requires extracellular IL-4 binding to the IL-4 receptor alpha complex, which activates STAT6 phosphorylation and nuclear translocation. STAT6 directly drives expression of GATA-3 (GATA binding protein 3), the master transcription factor for Th2 cell fate. GATA-3 transactivates the Th2 cytokine locus (encoding IL-4, IL-5, and IL-13) while repressing Th1-promoting gene networks.

Explanation: Upon activation, mast cells mobilize membrane phospholipids via phospholipase A2 (PLA2) to release arachidonic acid. Arachidonic acid is metabolized via the 5-lipoxygenase pathway into Leukotriene C4 (LTC4) and via the cyclooxygenase-2 (COX-2) pathway into Prostaglandin D2 (PGD2). In contrast, histamine, beta-tryptase, heparin, chymase, and carboxypeptidase A3 are preformed mediators pre-stored inside secretory granules.

Explanation: Under the expanded Gell and Coombs classification, delayed T-cell-mediated reactions (Type IV) are subclassified: Type IVa (Th1/monocytes), Type IVb (Th2/eosinophils), Type IVc (CD8+ cytotoxic T cells/keratinocyte apoptosis), and Type IVd (T cells/neutrophils via CXCL8). DRESS syndrome is classic Type IVb mediated by drug-specific Th2 cells secreting IL-4, IL-5, and IL-13, leading to tissue eosinophilia. SJS/TEN is Type IVc, Serum Sickness is Type III (immune complex deposition), and AGEP is Type IVd.

Explanation: Hereditary Angioedema (HAE) is caused by autosomal dominant mutations in the SERPING1 gene. HAE Type I (85% of cases) is characterized by reduced synthesis of C1-INH, resulting in low C1-INH antigen levels and low functional activity. HAE Type II (15% of cases) is caused by dysfunctional C1-INH protein; levels of C1-INH antigen are normal or elevated, but C1-INH functional activity is markedly depressed (<50%). Both types exhibit low C4 levels. Low C1q indicates Acquired Angioedema (AAE).

Explanation: Major Basic Protein (MBP-1) constitutes over 50% of the core of eosinophil secondary granules. It has a calculated isoelectric point (pI) exceeding 11 due to an abundance of arginine residues. Its high positive charge allows it to bind non-specifically to negatively charged cell membrane phospholipids, causing membrane disruption, desquamation of bronchial epithelial cells, and tissue cytotoxicity in allergic inflammation.

Explanation: FOXP3+ Tregs constitutively express high levels of CTLA-4 (CD152). CTLA-4 binds CD80 (B7-1) and CD86 (B7-2) on dendritic cells with significantly higher affinity than CD28. Tregs physically capture and remove CD80/CD86 from the dendritic cell surface via trans-endocytosis, thereby depriving naive T cells of essential costimulatory signals required for activation and differentiation into Th2 cells.

Explanation: When mucosal barrier integrity is disrupted by allergens, pollutants, or pathogens, injured epithelial cells release three key alarmins: TSLP, IL-33, and IL-25. These alarmins bind to their respective receptors on ILC2s (TSLPR, ST2, and IL-17RB). Upon activation, ILC2s rapidly produce vast amounts of Th2 cytokines (IL-5, IL-13, and IL-9) independently of T-cell receptor antigen recognition.

Explanation: Pru p 3 is the major non-specific lipid transfer protein (nsLTP) of peach. nsLTPs are extremely stable proteins resistant to both heat denaturation and gastric enzymatic digestion. Sensitization to Pru p 3 is associated with true, severe systemic food allergy (including anaphylaxis) and can trigger symptoms even with cooked or processed foods. In contrast, Pru p 1 (PR-10) and Pru p 4 (profilin) are heat-labile and digestible, causing mild localized Oral Allergy Syndrome.

Explanation: Cross-reactive Carbohydrate Determinants (CCDs) are N-glycans containing core α(1,3)-fucose and β(1,2)-xylose linkages found in plant proteins, insect venoms, and helminths, but absent in humans. Anti-CCD IgE antibodies bind strongly to extract-based in vitro allergen assays, generating positive sIgE values. However, anti-CCD IgE has very low biological activity and rarely induces mast cell degranulation, leading to clinically irrelevant false-positive laboratory results.