Hypersensitivity Reactions — MCQs
Which of the following substances can lead to fixed drug eruptions?
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 is associated with cell-mediated immunity?
Which of the following best explains the development of intravascular hemolysis in a 54-year-old woman who was given type A Rh+ blood by mistake, despite being a type B Rh+ patient, after a blood transfusion following an automobile accident?
In glomerulus subendothelial deposits are seen in?
"Isomorphic response" can be a feature of the following except
Which is the best investigation to confirm diagnosis of anaphylaxis?
All of the following are features of Goodpasture syndrome, except for which of the following?
All of the following forces are involved in antigen-antibody reactions, except:
A 42 year-old female patient presents with cough, low-grade fever, and hemoptysis. Investigations reveal a cavitary lesion on her right lung apex, which on biopsy reveals caseous necrosis. The underlying pathophysiology is:
Hypersensitivity Reactions Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following substances can lead to fixed drug eruptions?
- A. Na fluorititanate
- B. Phenolphthalein (Correct Answer)
- C. Magnesium oxide
- D. CaSO4
Explanation: ***Phenolphthalein*** - **Phenolphthalein** is a common cause of fixed drug eruptions, often found in laxatives. - Exposure to the drug can cause recurrent, well-demarcated skin lesions in the exact same location each time it is ingested [1]. *Na fluorititanate* - This compound is not commonly associated with causing fixed drug eruptions. - It is primarily used in industrial applications, such as ceramics and enamels. *Magnesium oxide* - **Magnesium oxide** is a common antacid and laxative, but it is rarely implicated in fixed drug eruptions. - Its adverse effects usually involve gastrointestinal symptoms rather than cutaneous reactions. *CaSO4* - **Calcium sulfate (CaSO4)**, or gypsum, is primarily used in construction and as a filler in pharmaceuticals. - It is not recognized as a common causative agent for fixed drug eruptions.
Question 2: 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 3: Which type of hypersensitivity is associated with cell-mediated immunity?
- A. Type 2
- B. Type 3
- C. Type 4 (Correct Answer)
- D. Type 1
Explanation: ***Type 4*** - Cell-mediated immunity primarily involves **T-lymphocytes** [1], essential for targeting and eliminating **intracellular pathogens** like viruses. - It plays a crucial role in **delayed-type hypersensitivity reactions** [2], making it vital for the adaptive immune response. *Type 3* - Type 3 immune responses are primarily associated with **immune complex-mediated** diseases and not directly with cell-mediated immunity. - This type involves primarily **B-cells** and antibodies in the response against antigens. *Type 2* - Type 2 immunity mainly concerns the activation of **B-lymphocytes** and antibody production against **extracellular pathogens** like bacteria. - It is characterized by **IgE-mediated responses** [3], particularly in allergic reactions, rather than cell-mediated actions. *Type 1* - Type 1 responses are associated with **Th1 cells** [2] and are more specifically linked to **autoimmunity and cell-mediated pathways**, but represent only a part of the broader cell-mediated immunity. - This type mainly focuses on clearance of **intracellular pathogens** but is not synonymous with the entire process of cell-mediated immunity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [3] 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 of the following best explains the development of intravascular hemolysis in a 54-year-old woman who was given type A Rh+ blood by mistake, despite being a type B Rh+ patient, after a blood transfusion following an automobile accident?
- A. Direct cytotoxic T-cell mediated lysis
- B. Antibody-mediated complement fixation (Correct Answer)
- C. Immune complex mediated hemolysis
- D. Antibody-dependent cellular cytotoxicity
Explanation: ***Antibody-mediated complement fixation*** - Intravascular hemolysis occurs when type B blood is transfused with type A blood, triggering **IgM antibodies** to activate **complement**, leading to the destruction of transfused red blood cells [1][2]. - This mechanism is rapid and results in **hemolytic transfusion reactions**, which are life-threatening and present shortly after the transfusion [1]. *Antibody-dependent cellular cytotoxicity* - This process primarily involves **IgG antibodies** targeting cells for destruction by **NK cells** or macrophages, rather than complement activation. - It usually leads to **extravascular hemolysis** rather than intravascular hemolysis caused by complement. *Delayed-type hypersensitivity* - This immune response is mediated by **T cells** and typically occurs days to weeks after exposure, not immediately as seen in transfusion reactions. - It does not directly lead to **hemolysis** but rather to tissue damage due to cellular immunity. *Immune complex disease* - Characterized by **formation of immune complexes** leading to inflammation and sometimes tissue damage, but not specifically linked to immediate hemolytic reactions. - This mechanism is more relevant in conditions like **serum sickness**, rather than the direct hemolysis observed in this transfusion scenario. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.
Question 5: In glomerulus subendothelial deposits are seen in?
- A. Goodpasture syndrome (linear IgG deposits in the basement membrane)
- B. MPGN type I (subendothelial deposits) (Correct Answer)
- C. MPGN type II (intramembranous deposits)
- D. IgA nephropathy (mesangial IgA deposits)
Explanation: ***MPGN type I*** - **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1]. - This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1]. *Good pasture syndrome* - Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits. - Typically, it presents with **crescent formation** in the glomeruli rather than deposits. *MPGN type II* - Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1]. - It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology. *IgA nephropathy* - Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially. - It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.
Question 6: "Isomorphic response" can be a feature of the following except
- A. Tinea (Correct Answer)
- B. Warts
- C. Molluscum contagiosum
- D. Psoriasis
Explanation: ***Tinea*** - The **isomorphic response (Koebner phenomenon)** refers to the development of new skin lesions in areas of trauma due to an immunological process. - This phenomenon is **not typically seen in tinea** (fungal infections). - While tinea can spread to new areas, this occurs through **direct fungal inoculation and contact spread**, not through the true Koebner mechanism. *Warts* - **Warts** caused by human papillomavirus (HPV) can exhibit the **isomorphic response**. - Trauma to the skin can lead to **viral inoculation** in that area, resulting in new wart formation along lines of trauma. - This is a well-recognized example of Koebner phenomenon in viral infections. *Molluscum contagiosum* - **Molluscum contagiosum** (poxvirus infection) can demonstrate the **isomorphic response**. - **Scratching or rubbing** can spread the virus to new areas through autoinoculation. - New lesions develop along the lines of trauma, consistent with Koebner phenomenon. *Psoriasis* - **Psoriasis** is the **classic and most well-known** condition exhibiting the isomorphic response or Koebner phenomenon. - New psoriatic plaques appear in areas of **skin injury** (scratches, cuts, burns, surgical incisions, friction). - Seen in approximately **25-50%** of psoriasis patients.
Question 7: 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 8: 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.
Question 9: 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 10: A 42 year-old female patient presents with cough, low-grade fever, and hemoptysis. Investigations reveal a cavitary lesion on her right lung apex, which on biopsy reveals caseous necrosis. The underlying pathophysiology is:
- A. Type 4 hypersensitivity reaction (Correct Answer)
- B. Sudden cut off of blood supply
- C. Enzyme degradation
- D. Fibrinoid deposition
Explanation: ***Type 4 hypersensitivity reaction*** - **Caseous necrosis**, characteristic of **tuberculosis**, is mediated by a **Type 4 hypersensitivity reaction** to the mycobacterial antigens [1], [3]. - This delayed-type hypersensitivity involves activated **macrophages** and **T-lymphocytes** forming **granulomas** with central caseous necrosis [2], [4]. *Sudden cut off of blood supply* - This mechanism typically leads to **coagulative necrosis** (e.g., in myocardial infarction), where the tissue architecture is preserved for some time. - **Infarction** due to loss of blood supply generally does not result in the distinct cheesy, crumbly appearance of caseous necrosis. *Enzyme degradation* - This mechanism describes **liquefactive necrosis**, where dead cells are digested by hydrolytic enzymes, resulting in a viscous fluid. - Liquefactive necrosis is common in bacterial infections and central nervous system infarcts, which is not consistent with the morphology of caseous necrosis. *Fibrinoid deposition* - **Fibrinoid necrosis** involves immune complex deposition in arterial walls, leading to leakage of plasma proteins and fibrin. - This type of necrosis is characteristic of **vasculitis** and immunologic reactions in vessels, not the widespread tissue destruction seen in caseous necrosis. **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. Inflammation and Repair, p. 109. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 380. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384.
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