Hypersensitivity Reactions — MCQs
All of the following forces are involved in antigen-antibody reactions, except:
Which among the following is an example of type I hypersensitivity reaction?
A 32 year old man presents with a 3-month history of weight loss, night sweats, a productive cough with blood-tinged sputum, anorexia, general malaise, and a low grade fever. A PPD skin test shows > 10 mm of induration. If the area of induration were biopsied, which of the following type of reactive cells would be found?
Which type of hypersensitivity reaction is characterized by immune complex formation?
A child has a rash. His family history is positive for asthma. What could be the most probable diagnosis?
In a case of glomerulonephritis (GN), C3 is normal in all the following except?
Which of the following substances is primarily synthesized and secreted by mast cells?
Which is the best investigation to confirm diagnosis of anaphylaxis?
Which of the following best denotes classical complement pathway activation in immune inflammatory conditions?
All of the following are features of Goodpasture syndrome, except for which of the following?
Hypersensitivity Reactions Indian Medical PG Practice Questions and MCQs
Question 1: All of the following forces are involved in antigen-antibody reactions, except:
- A. Electrostatic bond
- B. Hydrogen bond
- C. Covalent bond (Correct Answer)
- D. Van der Waals forces
Explanation: ***Covalent bond*** - **Covalent bonds** are strong, irreversible bonds that involve the sharing of electrons between atoms. - Antigen-antibody interactions are predominantly **non-covalent** and reversible, allowing for dynamic binding and release. *Vander Waal's forces* - **Van der Waals forces** are weak attractive forces that arise from temporary fluctuations in electron distribution, creating transient dipoles. - They are crucial in antigen-antibody binding, especially when the molecules are in **close proximity**, contributing to overall affinity. *Electrostatic bond* - **Electrostatic (ionic) bonds** occur between oppositely charged groups on the antigen and antibody surfaces. - These interactions are significant for **initial recognition** and overall binding stability, particularly at appropriate pH levels. *Hydrogen bond* - **Hydrogen bonds** form between a hydrogen atom covalently linked to an electronegative atom (like oxygen or nitrogen) and another electronegative atom. - They play a vital role in the **specificity and strength** of antigen-antibody interactions by providing numerous weak, directional contacts.
Question 2: Which among the following is an example of type I hypersensitivity reaction?
- A. Graves' disease
- B. Pernicious anemia
- C. Arthus reaction
- D. Casoni's test (Correct Answer)
Explanation: ***Casoni's test*** - Casoni's test is a **diagnostic skin test** for **hydatid disease** (echinococcosis), involving intradermal injection of **hydatid cyst fluid antigen**. - A positive reaction produces an **immediate wheal and flare response** (within 15-30 minutes), which is a classic manifestation of **Type I hypersensitivity** mediated by **IgE antibodies** and **mast cell degranulation** [1], [2]. - Among the given options, Casoni's test is the correct answer because it **demonstrates/elicits** a Type I hypersensitivity reaction as part of its diagnostic mechanism. *Arthus reaction* - The Arthus reaction is a localized **Type III hypersensitivity** reaction caused by pre-formed IgG antibodies forming **immune complexes** with antigens injected intracutaneously. - It results in **vasculitis**, **edema**, **necrosis**, and **erythema** at the injection site, typically appearing **3-8 hours** after antigen exposure (delayed, not immediate). *Graves' disease* - Graves' disease is an **autoimmune disorder** causing **hyperthyroidism**, due to **stimulatory autoantibodies** (TSI - thyroid-stimulating immunoglobulins) against the **TSH receptor** [1]. - It is classified as a **Type II hypersensitivity** reaction, where antibodies bind to cell surface receptors leading to abnormal cell stimulation rather than destruction [1]. *Pernicious anemia* - Pernicious anemia is a **Type II hypersensitivity** reaction where autoantibodies target **intrinsic factor** or **gastric parietal cells**, leading to **vitamin B12 malabsorption** and subsequent megaloblastic anemia. - This antibody-mediated destruction or interference with normal cell function is characteristic of Type II hypersensitivity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-213. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 171-172.
Question 3: A 32 year old man presents with a 3-month history of weight loss, night sweats, a productive cough with blood-tinged sputum, anorexia, general malaise, and a low grade fever. A PPD skin test shows > 10 mm of induration. If the area of induration were biopsied, which of the following type of reactive cells would be found?
- A. Eosinophil
- B. T lymphocyte (Correct Answer)
- C. B lymphocyte
- D. Mast cell
Explanation: ***T lymphocyte*** - The clinical picture (weight loss, night sweats, productive cough with blood-tinged sputum, positive PPD) is highly suggestive of **tuberculosis**, a **Type IV hypersensitivity reaction** [1], [2]. - **Type IV hypersensitivity reactions** are cell-mediated, involving the activation of **T lymphocytes**, which migrate to the site of antigen exposure (like a PPD test site or a tuberculous granuloma) and release cytokines, leading to induration and inflammation [1], [2]. *Eosinophil* - **Eosinophils** are primarily involved in allergic reactions and defense against parasitic infections [3]. - They are not the predominant reactive cells in a **Type IV hypersensitivity** response like that seen in tuberculosis [1]. *Mast cell* - **Mast cells** play a critical role in immediate hypersensitivity reactions (Type I), releasing histamine and other mediators [4]. - They are not the primary cells involved in the delayed-type hypersensitivity response elicited by tuberculin purified protein derivative (PPD) [2]. *B lymphocyte* - **B lymphocytes** are responsible for humoral immunity by producing antibodies [3]. - While they contribute to overall immune responses, they are not the main effector cells in a cell-mediated **Type IV hypersensitivity reaction** characteristic of a positive PPD test [1], [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 218. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 195-196. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.
Question 4: Which type of hypersensitivity reaction is characterized by immune complex formation?
- A. Type-I
- B. Type-II
- C. Type-III (Correct Answer)
- D. Type-IV
Explanation: ***Type-III*** - Immune complex hypersensitivity reactions involve the formation of **antigen-antibody complexes** that deposit in tissues, leading to inflammation [1]. - This type includes conditions like **systemic lupus erythematosus** and **serum sickness**, characterized by tissue damage due to these complexes [2][3]. *Type-II* - Type-II hypersensitivity is mediated by **IgG or IgM antibodies** that target cell surface antigens, leading to cytotoxic effects. - Examples include **hemolytic anemia** and **Graves' disease**, which do not involve immune complex deposition. *Type-IV* - Type-IV hypersensitivity is a **delayed-type** reaction mediated by **T cells**, not antibodies, responsible for conditions like **contact dermatitis** [4]. - It does not involve the formation of immune complexes, unlike Type-III reactions [1]. *Type-I* - Type-I hypersensitivity is an **immediate allergic reaction** mediated by **IgE antibodies**, resulting in conditions like **asthma** and **anaphylaxis**. - This type is characterized by activation of **mast cells** and **basophils**, distinct from immune complex mechanisms. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 172-173. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174.
Question 5: A child has a rash. His family history is positive for asthma. What could be the most probable diagnosis?
- A. Seborrheic dermatitis
- B. Atopic dermatitis (Correct Answer)
- C. Allergic contact dermatitis
- D. Erysipelas
Explanation: ***Atopic dermatitis*** - The presence of a rash in a child with a family history of **asthma** strongly suggests atopic dermatitis, as it is part of the **atopic triad** (eczema, asthma, allergic rhinitis). - Atopic dermatitis often presents with **erythematous, pruritic patches** and plaques, commonly affecting flexural areas like the antecubital and popliteal fossae, as well as the face and neck in younger children. *Seborrheic dermatitis* - This condition typically presents with **greasy, yellowish scales** on an erythematous base, often affecting areas rich in sebaceous glands such as the scalp, face (nasolabial folds), and chest. - While it can occur in infants, it does not have the strong association with a family history of asthma seen in atopic dermatitis. *Allergic contact dermatitis* - This rash results from an **exposure to an allergen**, leading to a localized, erythematous, and pruritic eruption, often with vesicles or bullae, at the site of contact. - The history does not provide information about a specific allergen exposure, and while it could produce a similar-looking rash, the family history of asthma points more strongly to atopic diathesis. *Erysipelas* - Erysipelas is a superficial skin infection, usually caused by *Streptococcus pyogenes*, presenting as a **well-demarcated, intensely erythematous, warm, and painful rash** with a raised border. - This is an **acute bacterial infection** and would typically be accompanied by systemic symptoms like fever and chills, which are not mentioned in the child's presentation.
Question 6: In a case of glomerulonephritis (GN), C3 is normal in all the following except?
- A. Goodpasture's syndrome
- B. Diffuse lupus nephritis (Correct Answer)
- C. IgA nephropathy
- D. HSP
Explanation: ***Diffuse lupus nephritis*** - This condition is characterized by **immune complex deposition** in the glomeruli [2], leading to activation of the **classical complement pathway** and consumption of C3, resulting in low C3 levels. [3] - Patients with diffuse lupus nephritis often present with **systemic lupus erythematosus (SLE)** symptoms, and **hypocomplementemia** is a hallmark. [3] *Goodpasture's syndrome* - This is an **autoimmune disease** targeting the **glomerular basement membrane (GBM)** and lung alveolar basement membranes. [1] - It involves **anti-GBM antibodies** directly, rather than widespread immune complex formation and complement consumption, so C3 levels are typically normal. [1] *IgA nephropathy* - Characterized by the deposition of **IgA immune complexes** in the glomeruli. [2] - While there is immune activity, C3 levels are generally **normal** because the alternative complement pathway, which primarily involves C3, is not extensively activated or consumed. *HSP* - **Henoch-Schönlein Purpura (HSP)** is a form of **IgA vasculitis** that can affect the kidneys, causing a glomerulonephritis similar to IgA nephropathy. - Similar to IgA nephropathy, C3 levels are usually **normal** in HSP-associated glomerulonephritis as the primary immune mechanism does not typically involve significant C3 consumption. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 915. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 911. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-911.
Question 7: Which of the following substances is primarily synthesized and secreted by mast cells?
- A. Adrenaline
- B. Acetylcholine
- C. Heparin
- D. Histamine (Correct Answer)
Explanation: ***Histamine*** - **Histamine** is a key mediator of immediate hypersensitivity reactions, primarily synthesized and stored in the **granules of mast cells** and basophils. - Upon activation, mast cells release histamine, which causes **vasodilation**, increased vascular permeability, and smooth muscle contraction, contributing to allergic symptoms. - Histamine is considered the **primary and most important mediator** released by mast cells in allergic and inflammatory responses. *Adrenaline* - **Adrenaline (epinephrine)** is a hormone and neurotransmitter primarily produced by the **adrenal medulla**. - It plays a crucial role in the **"fight or flight" response**, affecting heart rate, blood pressure, and metabolism, and is not associated with mast cell synthesis. *Acetylcholine* - **Acetylcholine** is a major neurotransmitter in the **parasympathetic nervous system** and at neuromuscular junctions. - It is synthesized and released by neurons to transmit signals, and not by mast cells. *Heparin* - **Heparin** is also synthesized and stored in mast cell granules and has anticoagulant properties. - However, while mast cells do produce heparin, **histamine** is considered the **primary and most clinically significant** substance synthesized and secreted by mast cells, particularly in the context of immediate allergic responses. - The question emphasizes "primarily," making histamine the best answer as it is the principal mediator of mast cell-related allergic reactions.
Question 8: Which is the best investigation to confirm diagnosis of anaphylaxis?
- A. IgA levels
- B. Serum tryptase (Correct Answer)
- C. IgD levels
- D. Serum precipitins
Explanation: ***Serum tryptase*** - **Serum tryptase** is released from activated mast cells and is a reliable biomarker for confirming anaphylaxis, particularly when measured within 1-3 hours of symptom onset. - Elevated levels help differentiate anaphylaxis from other conditions with similar symptoms, especially when the clinical picture is ambiguous. *IgA levels* - **IgA levels** are relevant in diagnosing conditions like selective IgA deficiency or celiac disease, but they do not play a direct role in confirming acute anaphylaxis. - They reflect long-term immune status rather than immediate hypersensitivity reactions. *IgD levels* - **IgD levels** have no established role in the diagnosis or confirmation of anaphylaxis. - Their physiological function is not fully understood, but they are not used as biomarkers for acute allergic reactions. *Serum precipitins* - **Serum precipitins** are antibodies detected in various hypersensitivity reactions, especially to inhaled antigens, and are not specific for anaphylaxis [1]. - They are primarily associated with conditions like hypersensitivity pneumonitis, reflecting different immunological mechanisms [1].
Question 9: Which of the following best denotes classical complement pathway activation in immune inflammatory conditions?
- A. C2, C4 and C3 decreased (Correct Answer)
- B. C2 and C4 normal, C3 is decreased
- C. C3 normal and C2, C4 decreased
- D. C2, C4, C3 all are elevated
Explanation: ***C2, C4 and C3 decreased*** - Activation of the **classical complement pathway** consumes upstream components C2 and C4, leading to their depletion [2]. - The activation also consumes C3 as all complement pathways converge at C3, thus its levels will also be decreased [1]. *C2 and C4 normal, C3 is decreased* - This pattern is more indicative of **alternate pathway activation** or a C3 deficiency, where classical pathway components (C2, C4) are not primarily involved [3]. - In classical pathway activation, C2 and C4 would be depressed due to their role early in the cascade. *C3 normal and C2, C4 decreased* - While C2 and C4 being decreased is consistent with **classical pathway activation**, the C3 component would also be decreased as it is consumed by the **C3 convertase** [1]. - A normal C3 level would imply either very early or ineffective classical pathway activation, which is unlikely given significant C2 and C4 consumption. *C2, C4, C3 all are elevated* - Elevated levels of complement components typically occur during the **acute phase response** in inflammatory conditions, but this indicates increased production, not consumption due to activation. - Active consumption in an immune inflammatory condition would lead to **decreased serum levels** of these components, not increased levels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 162-163. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535.
Question 10: All of the following are features of Goodpasture syndrome, except for which of the following?
- A. Hemoptysis
- B. Antibody to alpha-3 chain of type IV collagen (COL4A3)
- C. Subendothelial IgG deposits in renal biopsy (Correct Answer)
- D. Linear IgG deposits on the glomerular basement membrane
Explanation: ***Subendothelial IgG deposits in renal biopsy*** - Goodpasture syndrome is characterized by the presence of **anti-glomerular basement membrane antibodies** [1], not subendothelial IgG deposits. - Renal biopsy typically shows a **linear pattern** of IgG deposition along the glomerular basement membrane [2], rather than subendothelial deposits. *Pulmonary haemorrhage* - A hallmark of Goodpasture syndrome [1], resulting from the antibodies targeting the lungs, leading to **alveolar damage**. - Patients often present with **hemoptysis** and signs of respiratory failure due to pulmonary complications [1]. *Glomerular basement membrane is involved* - This syndrome specifically targets the **glomerular basement membrane**, causing **rapidly progressive glomerulonephritis (RPGN)** [1]. - The involvement of the glomerular basement membrane is a significant feature of Goodpasture syndrome. *Antibody to alpha-3 chain of type IV collagen (COL4A3)* - Goodpasture syndrome is associated with antibodies against the **alpha-3 chain of type IV collagen**, crucial for the pathogenesis. - These antibodies lead to damage in both the **renal and pulmonary** systems due to the shared type IV collagen in the basement membranes. Recovery of renal function may follow early intensive plasmapheresis combined with steroids and cytotoxic agents [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 537-538. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 526-527. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 918-919.
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