Immunopathology — MCQs
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Which of the following is NOT a disorder of phagocytosis?
Molecular mimicry is an explanation for which of the following?
Erythroblastosis fetalis is an example of which type of hypersensitivity reaction?
A patient on treatment with penicillin developed pallor, but without shortness of breath, urticaria, or wheezing. Investigations revealed antibodies against penicillin in his blood. What is the most likely type of hypersensitivity reaction that occurred in this patient?
Asthma is classified as which type of hypersensitivity reaction?
Immunopathology Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is NOT a disorder of phagocytosis?
- A. Job's syndrome
- B. Chediak-Higashi syndrome
- C. Myeloperoxidase deficiency
- D. Wiskott-Aldrich syndrome (Correct Answer)
Explanation: The correct answer is **Wiskott-Aldrich syndrome (WAS)** because it is primarily a **combined B-cell and T-cell immunodeficiency**, not a primary disorder of phagocytosis [1]. It is an X-linked recessive condition caused by a mutation in the *WASP* gene, which affects the actin cytoskeleton in hematopoietic cells [1]. This leads to the classic triad of **Thrombocytopenia** (with small platelets), **Eczema**, and **Recurrent infections**. **Analysis of other options (Disorders of Phagocytosis):** * **Job’s Syndrome (Hyper-IgE Syndrome):** A defect in JAK-STAT signaling (STAT3 mutation) leading to impaired neutrophil chemotaxis. It is characterized by "Cold" staphylococcal abscesses, retained primary teeth, and high IgE. * **Chediak-Higashi Syndrome:** A defect in vesicle fusion (LYST gene mutation) [2]. It results in impaired phagolysosome formation [2]. Key findings include giant cytoplasmic granules in neutrophils and partial albinism [2]. * **Myeloperoxidase (MPO) Deficiency:** The most common inherited defect of phagocytes. It involves a failure to produce Hypochlorous acid (HOCl), though most patients remain asymptomatic unless they have co-existing diabetes (predisposing to *Candida* infections). **NEET-PG High-Yield Pearls:** 1. **Phagocytosis Steps:** Remember the sequence: Chemotaxis → Opsonization → Ingestion → Killing (Oxidative burst). 2. **Nitroblue Tetrazolium (NBT) Test:** Used for Chronic Granulomatous Disease (CGD); it remains **negative** (colorless) in CGD due to NADPH oxidase deficiency. 3. **Wiskott-Aldrich Mnemonic:** **TIE** (Thrombocytopenia, Infections, Eczema). 4. **Small Platelets:** WAS is one of the few conditions where platelet size is decreased on a peripheral smear. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 250-251. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.
Question 2: Molecular mimicry is an explanation for which of the following?
- A. Immune tolerance
- B. Autoimmune disorders (Correct Answer)
- C. Hypersensitivity
- D. Immunosuppression
Explanation: ### Explanation **Molecular Mimicry** is a key mechanism in the pathogenesis of **Autoimmune Disorders** [1]. It occurs when there is a structural similarity between the antigens of an infectious agent (bacteria or virus) and the host’s self-antigens. When the immune system mounts a response against the pathogen, the cross-reactive antibodies or T-cells mistakenly attack the host’s own tissues, leading to loss of self-tolerance and subsequent tissue damage [1]. **Why the other options are incorrect:** * **Immune Tolerance:** This is the state of unresponsiveness to an antigen. Molecular mimicry represents a *failure* of tolerance, specifically a breakdown in peripheral tolerance. * **Hypersensitivity:** While autoimmunity involves hypersensitivity reactions (Types II, III, or IV), "Hypersensitivity" is a broad category describing exaggerated immune responses to *exogenous* antigens (like pollen or drugs). Molecular mimicry specifically explains the *trigger* for attacking *endogenous* (self) antigens [1]. * **Immunosuppression:** This refers to a reduced activation or efficacy of the immune system (e.g., HIV or chemotherapy). Molecular mimicry involves an *overactive* and misdirected immune response. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Example:** **Rheumatic Heart Disease.** Antibodies against the M-protein of *Streptococcus pyogenes* cross-react with cardiac myosin, leading to carditis. * **Guillain-Barré Syndrome (GBS):** Lipopolysaccharides of *Campylobacter jejuni* mimic gangliosides in peripheral nerves. * **Type 1 Diabetes:** Potential mimicry between Coxsackie B virus antigens and islet cell antigens (GAD65) [1]. * **Ankylosing Spondylitis:** Associated with *Klebsiella* species cross-reacting with HLA-B27. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 219-226.
Question 3: Erythroblastosis fetalis is an example of which type of hypersensitivity reaction?
- A. Type I
- B. Type II (Correct Answer)
- C. Type III
- D. Type IV
Explanation: **Explanation:** **Erythroblastosis Fetalis (Hemolytic Disease of the Newborn)** is a classic example of **Type II Hypersensitivity**, also known as **Cytotoxic Hypersensitivity**. **Why Type II is correct:** Type II reactions are mediated by **IgG or IgM antibodies** directed against antigens present on the surface of specific cells or tissues [2]. In Erythroblastosis Fetalis, maternal IgG antibodies (produced after prior sensitization) cross the placenta and bind to Rh antigens on the fetal Red Blood Cells (RBCs) [1]. This leads to RBC destruction via two mechanisms: 1. **Opsonization and Phagocytosis** by splenic macrophages [2]. 2. **Complement-mediated lysis** [2]. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE** and mast cell degranulation (e.g., Anaphylaxis, Asthma) [3]. * **Type III (Immune-Complex):** Involves deposition of **antigen-antibody complexes** in tissues, leading to inflammation (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type IV (Delayed):** Cell-mediated immunity involving **T-lymphocytes**, not antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Antibody-dependent cellular cytotoxicity (ADCC) is a key component of Type II reactions. * **Prevention:** Administer **Anti-D (RhoGAM)** to Rh-negative mothers at 28 weeks and within 72 hours of delivery to prevent sensitization [1]. * **Diagnosis:** The **Direct Coombs Test** is used to detect antibodies already bound to the baby's RBCs, while the **Indirect Coombs Test** checks the mother's serum for anti-Rh antibodies. * **Other Type II Examples:** Myasthenia Gravis, Graves' Disease, Goodpasture Syndrome, and Rheumatic Fever [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213.
Question 4: A patient on treatment with penicillin developed pallor, but without shortness of breath, urticaria, or wheezing. Investigations revealed antibodies against penicillin in his blood. What is the most likely type of hypersensitivity reaction that occurred in this patient?
- A. Type I hypersensitivity
- B. Type II hypersensitivity (Correct Answer)
- C. Type III hypersensitivity
- D. Type IV hypersensitivity
Explanation: ### Explanation **Why Type II Hypersensitivity is Correct:** This scenario describes **Drug-Induced Hemolytic Anemia**, a classic example of Type II (Antibody-mediated/Cytotoxic) hypersensitivity. In this mechanism, penicillin acts as a **hapten**; it binds to the surface of red blood cells (RBCs) [1]. The immune system then produces IgG or IgM antibodies against this drug-protein complex. These antibodies bind to the RBCs, leading to their destruction via the complement system or phagocytosis by splenic macrophages (opsonization) [2]. The clinical presentation of **pallor** without systemic anaphylactic symptoms (like wheezing or urticaria) points specifically to targeted cell destruction rather than a systemic allergic response [1]. **Why the Other Options are Incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation. It would typically present with urticaria, angioedema, wheezing, or anaphylaxis. The question specifically excludes these symptoms. * **Type III (Immune-Complex):** Involves the deposition of antigen-antibody complexes in tissues (e.g., Serum Sickness) [3]. It usually presents with fever, joint pain, and rashes, rather than isolated pallor/anemia. * **Type IV (Delayed):** T-cell mediated and does not involve antibodies. Examples include contact dermatitis or the Mantoux test. **High-Yield Clinical Pearls for NEET-PG:** * **Coombs Test:** The Direct Antiglobulin Test (DAT) is the gold standard for diagnosing Type II drug-induced hemolysis (detects IgG/complement on the RBC surface) [1]. * **Common Triggers:** Besides Penicillin, other drugs causing Type II reactions include **Quinidine** (thrombocytopenia) and **Methyldopa** (autoimmune hemolytic anemia) [1]. * **Mnemonic for Hypersensitivity (ACID):** * **A** - **A**naphylactic (Type I) * **C** - **C**ytotoxic (Type II) * **I** - **I**mmune Complex (Type III) * **D** - **D**elayed-type (Type IV) **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 651-652. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215.
Question 5: Asthma is classified as which type of hypersensitivity reaction?
- A. Type I hypersensitivity (Correct Answer)
- B. Type II hypersensitivity
- C. Type III hypersensitivity
- D. Type IV hypersensitivity
Explanation: **Explanation:** **Type I Hypersensitivity (Immediate Hypersensitivity)** is the correct answer. Bronchial asthma (specifically atopic asthma) is mediated by an **IgE-dependent mechanism** [2]. Upon exposure to an allergen, Th2 cells stimulate B-cells to produce IgE, which binds to the surface of **mast cells** [3]. Subsequent exposure leads to antigen cross-linking of IgE, causing mast cell degranulation and the release of mediators like histamine, leukotrienes (C4, D4, E4), and prostaglandins [1]. This results in smooth muscle contraction (bronchospasm), mucosal edema, and mucus hypersecretion [5]. **Why other options are incorrect:** * **Type II (Antibody-mediated):** Involves IgG or IgM antibodies binding to fixed antigens on cell surfaces or tissues (e.g., Goodpasture syndrome, Myasthenia gravis) [2]. * **Type III (Immune complex-mediated):** Caused by the deposition of antigen-antibody complexes in tissues, leading to complement activation (e.g., SLE, Post-streptococcal glomerulonephritis) [2]. * **Type IV (Cell-mediated/Delayed):** Mediated by T-lymphocytes rather than antibodies. It typically takes 48–72 hours to manifest (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Key Cytokines:** Th2 cells produce **IL-4** (stimulates IgE switch), **IL-5** (activates eosinophils), and **IL-13** (stimulates mucus secretion) [3]. * **Curschmann Spirals & Charcot-Leyden Crystals:** Classic microscopic findings in the sputum of asthmatic patients. * **Late-phase reaction:** Occurs 2–24 hours after exposure, primarily driven by **eosinophils** recruited by IL-5 [4]. * **Drug-induced Asthma:** Aspirin-induced asthma is a non-immune variant involving the cyclooxygenase pathway, not Type I hypersensitivity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212.
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Cells and Tissues of the Immune System
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Innate Immunity
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Adaptive Immunity
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Hypersensitivity Reactions
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Autoimmune Diseases
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Immunodeficiency Disorders
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Transplantation Immunopathology
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Immune Response to Infections
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Immunologic Laboratory Techniques
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Tumor Immunology
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