100+ Free CMSA Diploma in Allergology Dip Allerg(SA) Practice Questions

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Key Facts: CMSA Diploma in Allergology Dip Allerg(SA) Exam

Written + clinical

Exam Format

CMSA Dip Allerg(SA) Regulations

3-hour papers

Written Paper Duration

CMSA Examination Regulations

R18 950

Exam Fee

CMSA Fee Schedule

Annual (Sem 2)

Sitting Frequency

CMSA Examination Calendar

CMSA

Exam Body

Colleges of Medicine of SA — College of Family Physicians

The CMSA Dip Allerg(SA), awarded by the College of Family Physicians (fee R18 950), uses three-hour written papers (OSCE, long questions, and short questions/MCQs) plus a clinical examination. This free bank provides 100 high-yield practice MCQs as a study aid; it does not replicate the OSCE, long-answer, or clinical components.

Sample CMSA Diploma in Allergology Dip Allerg(SA) Practice Questions

Try these sample questions to test your CMSA Diploma in Allergology Dip Allerg(SA) exam readiness. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1Which subunit combination constitutes the high-affinity IgE receptor (FcεRI) expressed on human mast cells and basophils, and which chains contain Immunoreceptor Tyrosine-based Activation Motifs (ITAMs) essential for intracellular signal transduction?

A.Disulfide-linked Alpha (α) homodimer, Beta (β) chain, and Gamma (γ) monomer; ITAMs are present on all three chains

B.Alpha (α) homodimer and Beta (β) heterodimer; ITAMs are present exclusively on the α chain

C.Single transmembrane Alpha (α) chain and two Beta (β) chains; ITAMs are present on the α and β chains

D.Alpha (α) chain, Beta (β) chain, and a disulfide-linked Gamma (γ) homodimer; ITAMs are present on the β and γ chains

Explanation: The high-affinity IgE receptor (FcεRI) on mast cells and basophils is a tetrameric complex composed of one IgE-binding alpha (α) chain, one signal-amplifying beta (β) chain, and a disulfide-linked gamma (γ2) homodimer. Signal transduction relies on ITAMs located on the cytoplasmic tails of both the β chain and the γ chains, which become phosphorylated by Lyn kinase upon antigen-mediated receptor cross-linking.

2During T-cell dependent B-cell activation, which key cytokine signals via the STAT6 pathway to induce heavy chain class switch recombination to Immunoglobulin E (IgE)?

A.Interleukin-4 (IL-4)

B.Interleukin-5 (IL-5)

C.Interleukin-10 (IL-10)

D.Interferon-gamma (IFN-γ)

Explanation: Interleukin-4 (IL-4) and Interleukin-13 (IL-13) bind to heterodimeric IL-4 receptor complexes on B cells, triggering Janus kinase (JAK1/JAK3) activation and phosphorylation of Signal Transducer and Activator of Transcription 6 (STAT6). Phosphorylated STAT6 homodimers translocate to the nucleus to activate germline Cε transcription, directing immunoglobulin class switch recombination to IgE.

3Which mediator is stored preformed within human mast cell secretory granules and released immediately upon FcεRI cross-linking?

A.Leukotriene C4 (LTC4)

B.Interleukin-13 (IL-13)

C.Prostaglandin D2 (PGD2)

D.Histamine

Explanation: Histamine, tryptase, chymase, carboxypeptidase A3, and heparin are preformed mediators packaged within ionic complexes inside mast cell secretory granules, released within minutes of degranulation. In contrast, LTC4 and PGD2 are newly synthesized lipid mediators produced via arachidonic acid metabolism, and cytokines like IL-13 are synthesized de novo over hours.

4According to the Coombs and Gell classification of hypersensitivity reactions, which immunologic mechanism defines a Type I hypersensitivity reaction?

A.Sensitized T-lymphocyte antigen recognition leading to cytokine release and delayed macrophage activation

B.IgG or IgM antibody binding to fixed cell-surface antigens causing complement-mediated cytotoxicity

C.Immune complex deposition in vascular beds triggering neutrophil activation and complement consumption

D.IgE antibody-mediated soluble antigen binding on tissue mast cells leading to immediate mediator release

Explanation: Type I (immediate) hypersensitivity is mediated by allergen binding to specific IgE antibodies bound to FcεRI receptors on mast cells and basophils, resulting in rapid degranulation and release of histamine, leukotrienes, and prostaglandins within minutes of exposure.

5Which surface phenotype and master transcription factor characterize peripheral Regulatory T cells (Tregs) that actively maintain peripheral immune tolerance and suppress allergen-specific Th2 responses?

A.CD8+ CD28+ T-bet+

B.CD3+ CD56+ RORγt+

C.CD4+ CD25+ FoxP3+

D.CD4+ CD127+ GATA3+

Explanation: Regulatory T cells (Tregs) are characterized by surface expression of CD4 and high-affinity IL-2 receptor alpha chain (CD25), alongside expression of the master transcription factor Forkhead Box P3 (FoxP3). Tregs maintain allergen tolerance by secreting immunosuppressive cytokines (IL-10 and TGF-β) and expressing CTLA-4 to downregulate co-stimulatory molecules on antigen-presenting cells.

6Which chemokine receptor expressed on human eosinophils specifically binds Eotaxin-1 (CCL11), Eotaxin-2 (CCL24), and Eotaxin-3 (CCL26) to mediate selective eosinophil tissue homing?

A.CCR7

B.CCR3

C.CCR5

D.CXCR4

Explanation: CCR3 is a G-protein coupled receptor abundantly expressed on eosinophils (as well as basophils and Th2 cells). It acts as the primary receptor for the eotaxin family (CCL11, CCL24, CCL26) and RANTES (CCL5), driving selective recruitment and transendothelial migration of eosinophils into inflamed allergic tissues.

7Epithelial cell injury caused by environmental allergens triggers the release of epithelial-derived 'alarmins' that activate Group 2 Innate Lymphoid Cells (ILC2s). Which triad of cytokines represents these key epithelial alarmins?

A.IL-1β, TNF-α, and IL-6

B.TSLP, IL-33, and IL-25

C.IL-12, IL-18, and IFN-γ

D.IL-2, IL-7, and IL-15

Explanation: Thymic Stromal Lymphopoietin (TSLP), Interleukin-33 (IL-33), and Interleukin-25 (IL-25 / IL-17E) are epithelial-derived cytokines released in response to barrier disruption, proteases, or micro-organisms. They directly stimulate ILC2s via ST2 (IL-33R), IL-17RB (IL-25R), and TSLPR, triggering antigen-independent secretion of massive amounts of IL-5 and IL-13.

8Which complement cleavage fragments act as potent anaphylatoxins, binding G-protein coupled receptors on mast cells and basophils to induce degranulation independent of IgE?

A.C1q and C1r

B.C3b and C4b

C.C5b and C6

D.C3a and C5a

Explanation: C3a and C5a (and to a lesser extent C4a) are small peptide fragments generated during complement cascade activation. They function as anaphylatoxins that bind specific receptors (C3aR and C5aR/CD88) on mast cells, basophils, and granulocytes, stimulating smooth muscle contraction, vascular permeability, and mast cell degranulation via non-IgE mechanisms.

9What structural category and cluster of differentiation designation define the low-affinity IgE receptor (FcεRII), which regulates serum IgE levels and antigen presentation?

A.Integrin alpha subunit; CD11b

B.C-type lectin protein; CD23

C.Immunoglobulin superfamily receptor; CD16

D.G-protein coupled receptor; CD32

Explanation: FcεRII (CD23) is a transmembrane C-type (calcium-dependent) lectin protein, distinguishing it from most Fc receptors which belong to the immunoglobulin superfamily. It exists in membrane-bound and soluble forms (sCD23) on B cells, macrophages, and follicular dendritic cells, playing key roles in regulating IgE synthesis and IgE-mediated antigen presentation.

10Activation of vascular endothelial H1 histamine receptors during acute allergic reactions leads to microvascular leakage and edema through which intracellular signaling pathway?

A.Gq/11 protein coupling -> Phospholipase C (PLC) activation -> IP3/DAG production -> increased intracellular Ca2+

B.Gi protein coupling -> Adenylate cyclase inhibition -> decreased cAMP -> hyperpolarization

C.Gs protein coupling -> Adenylate cyclase activation -> increased cAMP -> Protein Kinase A (PKA) activation

D.JAK/STAT pathway activation -> STAT3 phosphorylation -> nuclear gene transcription

Explanation: Histamine H1 receptors are Gq/11-protein coupled receptors. Receptor binding activates Phospholipase C (PLC), which cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers calcium release from the endoplasmic reticulum, leading to endothelial cell contraction, intercellular gap formation, and tissue edema.

About the CMSA Diploma in Allergology Dip Allerg(SA) Exam

The Diploma in Allergology of South Africa (Dip Allerg(SA)) is a prestigious postgraduate clinical qualification awarded by the Colleges of Medicine of South Africa. It validates specialized expertise in diagnosing and managing allergic diseases, including asthma, allergic rhinitis, food allergy, anaphylaxis, drug hypersensitivity, atopic dermatitis, and chronic urticaria across paediatric and adult populations.

Assessment

Three-hour written papers covering Basic Mechanisms of Allergy & Immunology (20%), Allergic Rhinitis, Conjunctivitis & Asthma (30%), Food Allergy & Gastrointestinal Manifestations (20%), Anaphylaxis, Drug Allergy & Hymenoptera Venom (15%), and Atopic Dermatitis, Urticaria & Diagnostic Testing (15%), followed by a clinical examination.

Time Limit

Three-hour written papers plus a clinical examination.

Passing Score

Candidates must pass the written component before proceeding to the clinical examination; standard-set cut score applied per CMSA Senate policy.

Exam Fee

R18 950 (Colleges of Medicine of South Africa (CMSA), College of Family Physicians)

CMSA Diploma in Allergology Dip Allerg(SA) Exam Content Outline

20%

Basic Mechanisms of Allergy & Immunology

IgE synthesis, FcεRI signaling, mast cell & basophil biology, Th2 immune responses, cytokines, eosinophil physiology, complement, and epithelial barrier function.

30%

Allergic Rhinitis, Conjunctivitis & Asthma

ARIA rhinitis guidelines, GINA asthma steps, ocular allergy (VKC, AKC, PAC), FeNO, spirometry, allergen immunotherapy (SCIT/SLIT), and biologic therapies.

20%

Food Allergy & Gastrointestinal Manifestations

IgE vs non-IgE food allergy, FPIES, EoE, component-resolved diagnostics (CRD), oral food challenges, milk/egg tolerance, LEAP guidelines, and alpha-gal syndrome.

15%

Anaphylaxis, Drug Allergy & Hymenoptera Venom

Acute epinephrine management, serum tryptase, biphasic anaphylaxis, drug hypersensitivity (DRESS, SJS/TEN, beta-lactam, aspirin/NSAID), and venom immunotherapy.

15%

Atopic Dermatitis, Urticaria & Diagnostic Testing

Filaggrin mutations, atopic eczema management, chronic spontaneous urticaria guidelines, skin prick testing, patch testing, intradermal testing, and BAT.

How to Pass the CMSA Diploma in Allergology Dip Allerg(SA) Exam

What You Need to Know

Passing score: Candidates must pass the written component before proceeding to the clinical examination; standard-set cut score applied per CMSA Senate policy.
Assessment: Three-hour written papers covering Basic Mechanisms of Allergy & Immunology (20%), Allergic Rhinitis, Conjunctivitis & Asthma (30%), Food Allergy & Gastrointestinal Manifestations (20%), Anaphylaxis, Drug Allergy & Hymenoptera Venom (15%), and Atopic Dermatitis, Urticaria & Diagnostic Testing (15%), followed by a clinical examination.
Time limit: Three-hour written papers plus a clinical examination.
Exam fee: R18 950

Keys to Passing

Work through all 100 available questions
Review every answer and explanation
Track weak areas and revisit them
Use our AI tutor for tough concepts

CMSA Diploma in Allergology Dip Allerg(SA) Study Tips from Top Performers

1Master component-resolved diagnostics (CRD) for peanut (Ara h 2), egg (Gal d 1), and wheat (Tri a 19/Omega-5 gliadin) to differentiate high-risk anaphylaxis from low-risk pollen cross-reactivity.

2Understand the step-down and step-up GINA 2023/2024 asthma guidelines emphasizing air-way anti-inflammatory reliever therapy (ICS-formoterol).

3Memorize emergency epinephrine dosing, serum tryptase diagnostic kinetics (1.2 x baseline + 2 ng/mL), and hereditary angioedema management algorithms (C1-INH concentrate, Icatibant).

Frequently Asked Questions

What is the exam format for the CMSA Dip Allerg(SA)?

The exit examination uses three-hour written papers (OSCE, long questions, and short questions/MCQs) plus a clinical examination. It is not a single computer-based MCQ paper.

What is the examination fee for the Dip Allerg(SA)?

The CMSA examination fee is R18 950, payable upon application to the Colleges of Medicine of South Africa (College of Family Physicians).

Which guidelines form the core basis of the Dip Allerg(SA) examination?

The exam relies on guidelines from the Allergy Society of South Africa (ALLSA), GINA (Global Initiative for Asthma), ARIA (Allergic Rhinitis and its Impact on Asthma), EAACI, and WAO (World Allergy Organization).