Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 221: Hyperacute rejection of renal transplant is which type of hypersensitivity reaction?

A. Type I hypersensitivity reaction
B. Type II hypersensitivity reaction (Correct Answer)
C. Type III hypersensitivity reaction
D. Type IV hypersensitivity reaction

Explanation: **Explanation:** **Hyperacute rejection** occurs within minutes to hours after transplantation [1]. It is a classic example of a **Type II Hypersensitivity Reaction** (Antibody-mediated) [2]. * **Mechanism:** It is mediated by **pre-formed cytotoxic antibodies** (IgG or IgM) in the recipient's serum that recognize antigens on the donor vascular endothelium. These antigens are typically ABO blood group antigens or HLA Class I molecules. * **Pathophysiology:** Once the graft is perfused, these antibodies bind to the endothelium, activating the **complement system** and the coagulation cascade [1]. This leads to diffuse thrombosis, fibrinoid necrosis of vessel walls, and ischemic necrosis of the graft (appearing cyanotic and mottled) [1]. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis) [2]. It plays no role in graft rejection. * **Type III (Immune-complex):** Involves deposition of antigen-antibody complexes in tissues (e.g., SLE, Serum Sickness) [2]. While some chronic rejection features involve complexes, hyperacute rejection is direct antibody binding. * **Type IV (Cell-mediated):** Mediated by T-cells. This is the primary mechanism for **Acute Rejection** (Type IVa/IVb), not hyperacute [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Characterized by "Arthus-like" reaction in vessels and neutrophilic infiltration [1]. * **Prevention:** Can be prevented by **Cross-matching** (testing recipient serum against donor lymphocytes). * **Key Association:** Often seen in multiparous women or patients with previous blood transfusions (due to prior sensitization). * **Treatment:** There is no effective treatment once it starts; the graft must be removed immediately [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 222: Which of the following conditions is primarily a T-cell mediated disease?

A. Asthma
B. Myasthenia gravis
C. Systemic Lupus Erythematosus (SLE)
D. Sarcoidosis (Correct Answer)

Explanation: **Explanation:** The correct answer is **Sarcoidosis**. This condition is a classic example of a **Type IV (Delayed-type) Hypersensitivity reaction** [1]. The pathogenesis involves an exaggerated cellular immune response to an unknown antigen, leading to the formation of **non-caseating granulomas** [2]. This process is driven by **CD4+ T-helper cells (Th1)**, which secrete cytokines like IL-2 and Interferon-gamma (IFN-γ) to activate macrophages and recruit more T-cells [3]. **Analysis of Incorrect Options:** * **Asthma:** This is primarily a **Type I Hypersensitivity** reaction. It is mediated by IgE antibodies and mast cell degranulation in response to allergens, though Th2 cells play a role in the chronic phase. * **Myasthenia Gravis:** This is a **Type II Hypersensitivity** reaction. It is caused by autoantibodies (B-cell mediated) directed against acetylcholine receptors at the neuromuscular junction. * **Systemic Lupus Erythematosus (SLE):** This is the prototype for **Type III Hypersensitivity**. It involves the formation of immune complexes (antigen-antibody) that deposit in tissues, causing systemic inflammation. **NEET-PG High-Yield Pearls:** * **Sarcoidosis Marker:** Elevated **Serum ACE (Angiotensin-Converting Enzyme)** levels and hypercalcemia (due to 1-alpha hydroxylase activity in macrophages). * **Kveim-Siltzbach Test:** Historically used for diagnosis (skin reaction to sarcoid tissue injection). * **Radiology:** Bilateral hilar lymphadenopathy and interstitial infiltrates. * **Pathology:** Look for **Schaumann bodies** (laminated calcium-protein concretions) and **Asteroid bodies** (stellate inclusions) within giant cells. **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] 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. 198-200. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 223: Which of the following is NOT true about graft-versus-host reaction?

A. The question asks for an untrue statement regarding graft-versus-host reaction.
B. Bile duct damage
C. Intrahepatic cholestasis
D. None of the above statements are untrue (i.e., all are true about GvHD) (Correct Answer)

Explanation: **Explanation:** Graft-versus-Host Disease (GvHD) occurs when immunocompetent T-cells from a donor graft recognize the recipient’s (host) HLA antigens as foreign and initiate an immune attack [1]. This is most common in allogeneic bone marrow or hematopoietic stem cell transplants. **Why Option D is Correct:** In GvHD, the liver is a primary target organ. The immune-mediated attack specifically targets the **epithelium of the bile ducts**. This leads to: 1. **Bile duct damage:** Direct destruction of small bile ducts by donor T-lymphocytes. 2. **Intrahepatic cholestasis:** As a result of ductal damage and inflammation, bile flow is obstructed within the liver, leading to clinical jaundice and elevated alkaline phosphatase levels. Since both statements B and C are classic pathological features of hepatic GvHD, none of the provided statements are untrue. **Analysis of Other Options:** * **Bile duct damage:** This is a hallmark of chronic GvHD. Histology typically shows lymphocytic infiltration of the portal tracts and destruction of the biliary epithelium. * **Intrahepatic cholestasis:** This is the functional consequence of the biliary damage. It is one of the clinical criteria used to grade the severity of GvHD. **High-Yield Clinical Pearls for NEET-PG:** * **Prerequisites (Billingham’s Criteria):** 1. Graft must contain immunologically competent cells. 2. Host must possess antigens foreign to the donor. 3. Host must be immunocompromised (cannot reject the graft). * **Target Organs:** Skin (maculopapular rash/dermatitis), Liver (cholestasis/jaundice), and GI tract (bloody diarrhea) [1]. * **Acute vs. Chronic:** Acute GvHD occurs within 100 days; Chronic GvHD occurs after 100 days and often mimics autoimmune diseases like Scleroderma or Sjögren’s syndrome. * **Graft-versus-Leukemia effect:** In leukemia patients, a mild GvHD is often beneficial as donor cells also attack residual cancer cells. **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. 182-183.

Question 224: Arthus reaction is what type of hypersensitivity reaction?

A. Localized immune complex reaction (Correct Answer)
B. Antigen-antibody reaction
C. Complement-mediated reaction
D. Antibody-mediated reaction

Explanation: The **Arthus reaction** is a classic example of **Type III Hypersensitivity**, specifically categorized as a **localized immune complex reaction**. [1], [2] It occurs when an antigen is injected into the skin of an individual who already has high levels of circulating IgG antibodies. These antibodies diffuse into the tissues and form localized antigen-antibody complexes that precipitate in the walls of small blood vessels, leading to vasculitis, localized edema, and tissue necrosis. [1], [3] **Why the correct answer is right:** * **Option A:** The Arthus reaction is defined by the *local* formation of immune complexes at the site of antigen entry (e.g., skin). [1], [2] Unlike systemic Type III reactions (like Serum Sickness), the pathology is confined to the injection site, making "localized immune complex reaction" the most precise description. [3] **Why the incorrect options are wrong:** * **Option B:** While it involves antigens and antibodies, this is too generic. All hypersensitivity types (except Type IV) are antigen-antibody reactions. * **Option C:** Although the Arthus reaction *activates* the complement system (C5a, C3a), the primary initiating event is the formation of immune complexes. [1] "Complement-mediated" is a mechanism within the reaction, not the classification of the reaction itself. * **Option D:** This term usually refers to Type II Hypersensitivity, where antibodies bind to antigens on specific cell surfaces or tissues (e.g., Autoimmune Hemolytic Anemia), rather than forming complexes with soluble antigens. **High-Yield Clinical Pearls for NEET-PG:** * **Time Frame:** Occurs within 4–12 hours (Intermediate). * **Key Mediator:** Neutrophils (recruited by C5a) are the primary cells causing tissue damage. [1] * **Histology:** Characterized by **Fibrinoid Necrosis** of the vessel walls. * **Clinical Example:** A "booster" vaccination (like Tetanus) in a person with high pre-existing titers can trigger a painful, localized Arthus reaction. **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. 172-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.

Question 225: In the immunofluorescence method to detect antinuclear antibodies, which of the following rat tissues is commonly used?

A. Kidney
B. Brain
C. Liver (Correct Answer)
D. Stomach

Explanation: ### Explanation **Correct Answer: C. Liver** In the Indirect Immunofluorescence (IIF) method for detecting Antinuclear Antibodies (ANA), the substrate must provide a rich source of nuclei. Historically, **rodent (rat or mouse) liver or kidney sections** were the standard substrates used in clinical laboratories. The **rat liver** is preferred because its hepatocytes have large, prominent nuclei with a relatively uniform distribution of autoantigens [1]. When a patient's serum containing ANAs is applied to the liver section, the antibodies bind to these nuclei, which are then visualized using fluorescein-conjugated anti-human globulin. While modern laboratories have largely shifted to **HEp-2 cells** (human epithelial cell line) due to their higher sensitivity and ability to show mitotic figures, rat liver remains a classic, high-yield answer for traditional substrate questions [1]. **Analysis of Incorrect Options:** * **A. Kidney:** While rat kidney sections can be used (often in a composite block with liver and stomach), the liver is the primary and most common choice for ANA specifically due to the high density of hepatocyte nuclei [1]. * **B. Brain:** Brain tissue is not used for routine ANA screening as it lacks the necessary cellular density and contains specialized antigens (like Ma2 or NMDA) more relevant to paraneoplastic or autoimmune encephalitis panels. * **D. Stomach:** Rat stomach sections are primarily used to detect **Anti-Smooth Muscle Antibodies (ASMA)**, which are characteristic of Autoimmune Hepatitis (Type 1), rather than general ANA [2]. **NEET-PG High-Yield Pearls:** * **Gold Standard:** IIF on **HEp-2 cells** is currently the "Gold Standard" for ANA screening because HEp-2 cells are larger, have more prominent nucleoli, and express more antigens (like Ro/SSA) than rodent tissues [1]. * **Screening Dilution:** ANA is typically considered positive at a titer of **1:160** or higher in symptomatic patients [1]. * **Pattern Association:** Remember the associations: **Rim/Peripheral pattern** = Anti-dsDNA (Specific for SLE); **Centromere pattern** = Limited Scleroderma (CREST syndrome) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 226-228. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 845-846.

Question 226: Severe Combined Immunodeficiency (SCID) is due to deficiency of which of the following?

A. Adenosine deaminase
B. JAK 3
C. Recombinase - activating genes (RAG)
D. Any of the above (Correct Answer)

Explanation: **Explanation:** Severe Combined Immunodeficiency (SCID) is a heterogeneous group of genetic disorders characterized by the failure of both **humoral (B-cell)** and **cell-mediated (T-cell)** immunity [1]. Because the defects occur at the level of the common lymphoid progenitor or early lymphocyte development, multiple genetic mutations can lead to this phenotype. * **Adenosine Deaminase (ADA) Deficiency:** This is the second most common cause of SCID (and the most common autosomal recessive form). ADA deficiency leads to the accumulation of toxic metabolites (deoxyadenosine and dATP) which are particularly lethal to developing T and B lymphocytes [1]. * **JAK3 Mutation:** Janus Kinase 3 (JAK3) is a signaling molecule downstream of the common gamma chain ($\gamma$c) receptor. A mutation here mimics X-linked SCID, preventing cytokine signaling (IL-2, IL-4, IL-7, etc.) required for lymphocyte maturation. * **RAG 1/2 Mutations:** Recombinase-activating genes are essential for **V(D)J recombination**. Without RAG, lymphocytes cannot rearrange their antigen receptor genes, leading to a total absence of mature T and B cells. Since all three mechanisms result in the clinical syndrome of SCID, **"Any of the above"** is the correct choice. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Type:** X-linked SCID (due to mutation in the **IL-2 receptor common gamma chain**). * **Morphology:** Characterized by a **hypoplastic/vestigial thymus** (lacking Hassall’s corpuscles) and depleted lymphoid tissue in lymph nodes and spleen. * **Clinical Presentation:** Recurrent severe infections (fungal, viral, bacterial), chronic diarrhea, and failure to thrive in infancy [2]. * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the treatment of choice; ADA deficiency is also a candidate for gene therapy [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 246-248. [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. 167-168.

Question 227: Adenosine deaminase deficiency is seen in which of the following diseases?

A. Common variable immunodeficiency
B. Severe combined immunodeficiency (Correct Answer)
C. Chronic granulomatous disease
D. Nezelof syndrome

Explanation: **Severe Combined Immunodeficiency (SCID)** is a group of rare disorders characterized by the profound deficiency of both T-cell and B-cell functions [1]. **Adenosine Deaminase (ADA) deficiency** is the second most common cause of SCID (autosomal recessive inheritance), accounting for approximately 15% of cases. * **Pathophysiology:** ADA is an enzyme responsible for the breakdown of adenosine and deoxyadenosine. In its absence, **deoxyadenosine triphosphate (dATP)** accumulates within lymphocytes. High levels of dATP are toxic; they inhibit ribonucleotide reductase, thereby stalling DNA synthesis and leading to lymphocyte apoptosis. This results in a near-total lack of cell-mediated and humoral immunity. **Analysis of Incorrect Options:** * **Common Variable Immunodeficiency (CVID):** Characterized by low serum levels of IgG, IgA, and IgM due to B-cell differentiation defects, not ADA deficiency. * **Chronic Granulomatous Disease (CGD):** A defect in phagocyte function (NADPH oxidase deficiency) leading to an inability to kill catalase-positive organisms. * **Nezelof Syndrome:** An older term for a type of combined immunodeficiency where T-cell defect is prominent but B-cells may be present; however, it is not specifically defined by ADA deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of SCID:** X-linked SCID (mutation in the **IL-2 receptor gamma chain**). * **Radiology:** A classic sign of SCID is the **absence of a thymic shadow** on a chest X-ray. * **Treatment:** ADA deficiency was the first disease treated with **gene therapy** [2]. Other treatments include bone marrow transplant and enzyme replacement therapy (PEG-ADA). * **Clinical Presentation:** Recurrent severe infections (fungal, viral, bacterial), failure to thrive, and chronic diarrhea in infancy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 246-247. [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. 167-168.

Question 228: Patch test is a type of:

A. Immediate hypersensitivity
B. Antibody mediated hypersensitivity
C. Immune complex mediated hypersensitivity
D. Delayed type hypersensitivity (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Delayed type hypersensitivity** The **Patch Test** is the gold standard diagnostic tool for **Allergic Contact Dermatitis**, which is a classic example of **Type IV (Delayed-type) Hypersensitivity** [1]. * **Mechanism:** This reaction is cell-mediated, not antibody-mediated [3]. It involves **T-lymphocytes** (specifically Th1 and CD8+ cells) [1]. Upon exposure to an allergen (hapten), sensitized T-cells release cytokines that recruit macrophages, leading to inflammation [1]. * **Timing:** The reaction is "delayed" because it takes **48 to 72 hours** for T-cell recruitment and cytokine production to manifest as a visible skin reaction (erythema/vesicles) [2], [3]. --- ### Why other options are incorrect: * **Option A (Immediate Hypersensitivity/Type I):** Mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Urticaria) [4], [5]. The **Skin Prick Test**, not the patch test, is used to diagnose Type I reactions [5]. * **Option B (Antibody-mediated/Type II):** Involves **IgG or IgM** antibodies binding to antigens on cell surfaces (e.g., Autoimmune hemolytic anemia, Pemphigus vulgaris) [4]. * **Option C (Immune complex-mediated/Type III):** Caused by the deposition of **antigen-antibody complexes** in tissues (e.g., SLE, Arthus reaction, Serum sickness) [4]. --- ### NEET-PG High-Yield Pearls: * **Type IV Hypersensitivity Examples:** Mantoux test (Tuberculin), Contact Dermatitis (Nickel, Poison Ivy), Graft rejection (Cellular), and Granuloma formation (Sarcoidosis, TB) [1]. * **Patch Test vs. Skin Prick Test:** * **Patch Test:** Read at 48–96 hours (Type IV) [1]. * **Skin Prick Test:** Read at 15–20 minutes (Type I) [5]. * **Key Cells:** The **Langerhans cell** is the primary antigen-presenting cell in the skin involved in the sensitization phase of the patch test [1]. **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. 174-175. [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] 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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [5] 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 229: On which cell type are IgE receptors primarily found?

A. Mast cell (Correct Answer)
B. NK cell
C. B cell
D. T cell

Explanation: **Explanation:** The correct answer is **Mast cell**. **1. Why Mast cells are correct:** Mast cells (and basophils) express high-affinity receptors for the Fc portion of IgE, known as **FcεRI** [1]. When an allergen binds to the IgE already attached to these receptors, it causes "cross-linking," leading to immediate degranulation [2]. This releases mediators like histamine, proteases, and chemotactic factors, which are central to **Type I Hypersensitivity** reactions (e.g., anaphylaxis, asthma). **2. Why the other options are incorrect:** * **NK cells:** These cells primarily express **CD16** (FcγRIII), a receptor for **IgG**, which mediates Antibody-Dependent Cellular Cytotoxicity (ADCC). They do not typically express IgE receptors. * **B cells:** While B cells produce IgE after class-switching (stimulated by IL-4), they do not primarily function via IgE surface receptors [2]. They express BCRs (IgM/IgD) and low-affinity IgG receptors (FcγRIIB) for feedback inhibition. * **T cells:** T cells recognize antigens presented by MHC molecules via the T-cell receptor (TCR) [2]. They do not express Fc receptors for antibody binding. **3. High-Yield Clinical Pearls for NEET-PG:** * **FcεRI vs. FcεRII:** Mast cells and Basophils have **high-affinity** receptors (FcεRI) [1]. B cells and macrophages express **low-affinity** receptors (FcεRII or CD23). * **Location:** Mast cells are found in connective tissue (skin, mucosal surfaces), while basophils are the circulating counterparts in the blood [1]. * **Eosinophils:** These also play a role in IgE-mediated immunity (especially against helminths) but are characterized by MBP (Major Basic Protein) release [3]. * **Omalizumab:** A monoclonal antibody used in severe asthma that works by binding to circulating IgE, preventing it from attaching to the FcεRI on mast cells. **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] 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. 155-156. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689.

Question 230: Intravascular hemolysis is mediated by which immunoglobulin?

A. IgA
B. IgD
C. IgE
D. IgG (Correct Answer)

Explanation: Intravascular hemolysis occurs when red blood cells (RBCs) are destroyed directly within the blood vessels. This process is primarily mediated by **IgG** (and sometimes IgM) [3]. **Why IgG is correct:** In the context of immune-mediated hemolysis, IgG antibodies (specifically IgG1 and IgG3) are potent activators of the classical complement pathway [4]. When IgG binds to RBC surface antigens, it triggers the complement cascade up to the formation of the **Membrane Attack Complex (MAC: C5b-C9)** [4]. The MAC creates pores in the RBC membrane, leading to osmotic lysis directly within the circulation (intravascular hemolysis) [4]. This is typically seen in conditions like Acute Hemolytic Transfusion Reactions or severe Autoimmune Hemolytic Anemia (AIHA). **Why other options are incorrect:** * **IgA:** Primarily involved in mucosal immunity (secretory IgA). It does not fix complement via the classical pathway and is not a primary mediator of hemolysis. * **IgD:** Found on the surface of B-cells; its systemic effector functions are minimal and it plays no role in RBC destruction. * **IgE:** Mediates Type I hypersensitivity reactions (allergies and helminth infections) by binding to mast cells and basophils. It does not cause hemolysis. **NEET-PG High-Yield Pearls:** * **Warm AIHA:** Mediated by **IgG**; usually results in **extravascular hemolysis** (splenic sequestration), but can cause intravascular hemolysis if complement activation is robust [1]. * **Cold AIHA:** Mediated by **IgM**; often leads to intravascular hemolysis via C3b opsonization and MAC formation [2]. * **Direct Coombs Test:** The gold standard for diagnosing immune-mediated hemolysis; it detects IgG or C3b bound to the surface of RBCs [1], [3]. * **Key finding:** Intravascular hemolysis is characterized by low haptoglobin, hemoglobinuria, and hemosiderinuria [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [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. 154-155. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 651-652. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651.

Practice by Chapter

Cells and Tissues of the Immune System

Practice Questions

Innate Immunity

Practice Questions

Adaptive Immunity

Practice Questions

Hypersensitivity Reactions

Practice Questions

Autoimmune Diseases

Practice Questions

Immunodeficiency Disorders

Practice Questions

Transplantation Immunopathology

Practice Questions

Immune Response to Infections

Practice Questions

Immunologic Laboratory Techniques

Practice Questions

Tumor Immunology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free