Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 161: Myasthenia gravis is associated with which of the following conditions?

A. Thymoma
B. Thymic carcinoma
C. Thymic hyperplasia (Correct Answer)
D. Lymphoma

Explanation: **Explanation:** Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder caused by antibodies against the post-synaptic acetylcholine receptors (AChR). The thymus plays a central role in the pathogenesis of MG, as it is the site where T-cell tolerance is lost [2]. **1. Why Thymic Hyperplasia is Correct:** Approximately **65-75%** of patients with Myasthenia Gravis exhibit **Thymic Follicular Hyperplasia** (presence of germinal centers in the thymic medulla) [1]. This is the most common thymic abnormality associated with MG. These germinal centers contain B-cells that produce the pathogenic AChR antibodies. **2. Analysis of Incorrect Options:** * **Thymoma (Option A):** While there is a strong association, only about **10-15%** of MG patients have a thymoma [1]. Conversely, about 30% of patients with a thymoma develop MG. While high-yield, it is statistically less common than hyperplasia. * **Thymic Carcinoma (Option B):** This is a rare, aggressive malignancy of the thymus [1]. Unlike thymomas, thymic carcinomas are rarely associated with paraneoplastic autoimmune syndromes like MG. * **Lymphoma (Option C):** While Hodgkin lymphoma can occur in the mediastinum, it is not a classic association with the pathogenesis of Myasthenia Gravis [1]. **Clinical Pearls for NEET-PG:** * **Most common thymic lesion in MG:** Thymic Hyperplasia (65-75%). * **Age Distribution:** Hyperplasia is more common in younger females; Thymoma is more common in older patients (40-60 years). * **Antibody Profile:** 85% of patients are AChR-antibody positive. In seronegative cases, look for **MuSK (Muscle-Specific Kinase) antibodies**. * **Edrophonium (Tensilon) Test:** Historically used for diagnosis (shows rapid, transient improvement in muscle strength). * **Treatment:** Acetylcholinesterase inhibitors (Pyridostigmine), immunosuppressants, and **Thymectomy** (which often provides clinical improvement even in the absence of a thymoma). **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. 571-574. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 634.

Question 162: Chediak-Higashi syndrome is characterized by a defect in which of the following?

A. Lysosome fusion (Correct Answer)
B. T-cells
C. B-cells
D. Complement

Explanation: **Explanation:** **Chediak-Higashi Syndrome (CHS)** is an autosomal recessive disorder caused by a mutation in the **LYST gene** (Lysosomal Trafficking Regulator). This mutation leads to a defect in **microtubule-dependent phagosome-lysosome fusion** [1]. 1. **Why Option A is Correct:** The defect in the LYST protein prevents the proper trafficking and fusion of lysosomes with phagosomes [1]. This results in the formation of **giant lysosomal granules** in various cells (neutrophils, melanocytes, and platelets) because the organelles cannot be properly distributed or fused, leading to impaired intracellular killing of bacteria [1]. 2. **Why Other Options are Incorrect:** * **B & C (T-cells and B-cells):** CHS is primarily a defect of phagocytes (innate immunity) and natural killer (NK) cells. While it causes severe immunodeficiency, it is not a primary T-cell (e.g., DiGeorge) or B-cell (e.g., Bruton’s) deficiency. * **D (Complement):** Complement deficiencies (like C3 or C5-C9 defects) involve opsonization or membrane attack complex issues, not intracellular trafficking. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Pathognomonic **giant granules** in neutrophils on peripheral smear [1]. * **Clinical Triad:** 1. **Partial Albinism** (melanocytes cannot transfer pigment granules to keratinocytes) [1]. 2. **Recurrent Pyogenic Infections** (Staph and Strep due to impaired chemotaxis/killing) [1]. 3. **Neurological symptoms** (peripheral neuropathy) [1]. * **Associated Feature:** Mild bleeding tendency due to defective dense granules in platelets [1]. * **Complication:** Risk of "Accelerated Phase" (Hemophagocytic Lymphohistiocytosis - HLH). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Question 163: In acute solid organ Graft versus Host Disease, which of the following is not a characteristic feature?

A. Occurs within 100 days of transplantation
B. Skin is the most common organ involved
C. Preformed antibodies are involved (Correct Answer)
D. May lead to cholestatic jaundice

Explanation: **Explanation:** **Graft-versus-Host Disease (GVHD)** occurs when immunologically competent donor T-cells (the graft) recognize the recipient’s (the host) HLA antigens as foreign and mount an immune attack [1]. **Why Option C is the Correct Answer:** Preformed antibodies are the hallmark of **Hyperacute Rejection** [2], not GVHD. In GVHD, the primary mediators are **donor T-lymphocytes** (specifically CD4+ and CD8+ T-cells) that react against host tissues [1]. GVHD is a cell-mediated (Type IV) hypersensitivity reaction, whereas preformed antibodies involve a Type II hypersensitivity mechanism. **Analysis of Incorrect Options:** * **Option A:** Acute GVHD is classically defined as occurring **within 100 days** of transplantation [1]. Beyond 100 days, it is classified as Chronic GVHD, which mimics autoimmune disorders like systemic sclerosis. * **Option B:** The **skin** is indeed the most common and often the first organ involved, typically presenting as a maculopapular rash (often starting on the palms, soles, and neck) [1]. * **Option D:** The gastrointestinal tract and liver are primary targets [1]. In the liver, the destruction of small bile ducts leads to **cholestatic jaundice** and elevated alkaline phosphatase. **High-Yield Clinical Pearls for NEET-PG:** * **Prerequisites for GVHD (Billingham’s Criteria):** 1. Graft must contain immunocompetent cells. 2. Host must be immunocompromised. 3. Host must express antigens foreign to the donor. * **Common Settings:** Most common in Allogeneic Bone Marrow/Stem Cell Transplants; can also occur in solid organ transplants rich in lymphoid tissue (e.g., Liver) or non-irradiated blood transfusions in immunocompromised patients. * **Target Organs:** Skin (Rash), Liver (Jaundice), and GI tract (Bloody diarrhea) [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. 182-183. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242.

Question 164: MAST cells play a central role in the development of which type of hypersensitivity reaction?

A. Immediate (Correct Answer)
B. Antibody mediated
C. Cell mediated
D. Immune complex mediated

Explanation: **Explanation:** **Type I Hypersensitivity (Immediate)** is primarily mediated by **IgE antibodies** and **Mast cells** [1]. Upon first exposure to an allergen, IgE is produced and binds to high-affinity FcεRI receptors on the surface of mast cells (sensitization) [3]. Upon re-exposure, the allergen cross-links the IgE, triggering mast cell **degranulation** [2]. This releases primary mediators like **histamine** (causing vasodilation and increased permeability) and secondary mediators like leukotrienes and prostaglandins, leading to the clinical manifestations of allergy or anaphylaxis [4]. **Analysis of Incorrect Options:** * **Option B (Antibody-mediated/Type II):** Involves IgG or IgM antibodies binding to antigens on specific cell surfaces or tissues (e.g., Autoimmune Hemolytic Anemia, Myasthenia Gravis), leading to complement activation or ADCC, not mast cell degranulation [1]. * **Option C (Cell-mediated/Type IV):** This is a delayed-type reaction mediated by **T-lymphocytes** (CD4+ and CD8+) and macrophages, not antibodies or mast cells (e.g., Mantoux test, Contact dermatitis). * **Option D (Immune complex-mediated/Type III):** Caused by the deposition of antigen-antibody (IgG/IgM) complexes in tissues, leading to complement recruitment and neutrophil-mediated damage (e.g., SLE, Post-streptococcal glomerulonephritis). **High-Yield Clinical Pearls for NEET-PG:** * **Mast Cell Markers:** CD117 (c-kit) and Tryptase (used clinically to diagnose systemic mastocytosis or confirm anaphylaxis). * **Eosinophils:** Recruited in the "Late Phase" of Type I reactions by Eosinophilic Chemotactic Factor (ECF-A) released by mast cells [4]. * **Preformed Mediators:** Histamine, Heparin, and Serine Proteases (Tryptase). * **Newly Synthesized Mediators:** Leukotrienes (C4, D4, E4)—which are 1000x more potent than histamine in causing bronchospasm [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212.

Question 165: For each patient with a specific medical condition, select the most likely immune dysfunction.

A. B-cell deficiency/dysfunction
B. Mixed T- and B-cell deficiency/dysfunction (Correct Answer)
C. T-lymphocyte deficiency/dysfunction
D. Neutropenia

Explanation: The correct answer is **Mixed T- and B-cell deficiency/dysfunction (Option B)**. ### **Explanation** Mixed immune deficiencies, such as **Severe Combined Immunodeficiency (SCID)** and **Wiskott-Aldrich Syndrome**, involve defects in both humoral (B-cell) and cell-mediated (T-cell) immunity [1]. Because T-cells are essential for B-cell activation and isotype switching, a primary T-cell defect often results in secondary B-cell dysfunction [1], [2]. Patients typically present early in life with a broad susceptibility to bacterial, viral, fungal, and protozoal infections, along with failure to thrive. ### **Analysis of Incorrect Options** * **A. B-cell deficiency:** These primarily manifest after 6 months of age (once maternal IgG wanes). They result in recurrent infections with **encapsulated bacteria** (e.g., *S. pneumoniae*, *H. influenzae*) but usually maintain normal defense against viruses and fungi [3]. * **C. T-lymphocyte deficiency:** These present with infections by **intracellular pathogens**, opportunistic fungi (e.g., *Candida*, *Pneumocystis jirovecii*), and viruses. While severe, pure T-cell defects are rarer than combined defects in clinical scenarios [2]. * **D. Neutropenia:** This leads to skin abscesses, mouth ulcers, and life-threatening infections with **Staphylococci** or Gram-negative bacteria (e.g., *Pseudomonas*), rather than a global failure of the adaptive immune system. ### **NEET-PG High-Yield Pearls** * **SCID (Most Severe):** Most common form is **X-linked** (IL-2 receptor gamma chain mutation). The autosomal recessive form is often due to **Adenosine Deaminase (ADA) deficiency** [2]. * **Wiskott-Aldrich Syndrome Triad:** Thrombocytopenia (small platelets), Eczema, and Recurrent infections (T and B cell defect) [4]. * **Ataxia-Telangiectasia:** Defect in the **ATM gene** (DNA repair), leading to cerebellar ataxia, telangiectasia, and IgA deficiency [4]. * **DiGeorge Syndrome:** CATCH-22; specifically involves thymic hypoplasia leading to T-cell deficiency [5]. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 247-248. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 248-249. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 250-251. [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. 167-168.

Question 166: Which of the following is NOT a feature of antiphospholipid antibody syndrome?

A. Bleeding disorder (Correct Answer)
B. Recurrent fetal loss
C. Thrombotic disorder
D. Coagulation disorder

Explanation: **Explanation:** Antiphospholipid Antibody Syndrome (APS) is an autoimmune prothrombotic state characterized by the presence of antiphospholipid antibodies (e.g., Lupus anticoagulant, Anti-cardiolipin, and Anti-β2-glycoprotein I) [1]. **Why "Bleeding disorder" is the correct answer:** Despite the paradoxical name "Lupus Anticoagulant" and the fact that these antibodies prolong the Activated Partial Thromboplastin Time (aPTT) *in vitro*, APS is clinically a **thrombotic disorder**, not a bleeding disorder [1], [2]. The antibodies interfere with phospholipids in the laboratory assay, mimicking a deficiency of clotting factors, but in the human body, they induce a hypercoagulable state by activating platelets and endothelial cells [1]. **Analysis of incorrect options:** * **B. Recurrent fetal loss:** This is a hallmark clinical criterion for APS [2]. It occurs due to placental infarction, spiral artery thrombosis, and inflammation-mediated placental dysfunction [2]. * **C. Thrombotic disorder:** APS is defined by both arterial and venous thrombosis [2]. Common manifestations include Deep Vein Thrombosis (DVT), stroke, and pulmonary embolism [2]. * **D. Coagulation disorder:** APS is classified as an acquired coagulation disorder (specifically a thrombophilia) because it involves an abnormality in the regulation of the coagulation cascade. **High-Yield Clinical Pearls for NEET-PG:** * **The Paradox:** Prolonged aPTT *in vitro* + Thrombosis *in vivo* [1]. * **Mixing Study:** In APS, the prolonged aPTT does **not** correct when mixed with normal plasma (indicating the presence of an inhibitor/antibody). * **VDRL False Positivity:** Patients often show a false-positive test for Syphilis because the reagin antibodies cross-react with the cardiolipin used in the VDRL antigen [1]. * **Catastrophic APS (Asherson’s Syndrome):** A rare, life-threatening form involving multi-organ failure due to small vessel occlusion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 134-135. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 626-627.

Question 167: T cell dependent tubercular antigens stimulate the production of which of the following antibodies?

A. IgM
B. IgG
C. IgG and IgA (Correct Answer)
D. IgG, IgM, IgA, IgE

Explanation: **Explanation:** The correct answer is **C. IgG and IgA**. **Underlying Medical Concept:** The immune response to *Mycobacterium tuberculosis* is primarily cell-mediated, involving T-helper 1 (Th1) cells. However, T-cell dependent antigens also trigger a humoral response. When T-cells recognize tubercular antigens, they release cytokines (like IL-4 and IFN-̳) that induce **B-cell class switching** [1]. In the context of tuberculosis, this results in the production of **IgG** (the primary systemic antibody) and **IgA** (the primary mucosal antibody) [2]. Since *M. tuberculosis* enters via the respiratory tract, secretory IgA plays a crucial role in mucosal defense, while serum IgG reflects the systemic immune activation. **Analysis of Options:** * **Option A (IgM):** IgM is the first antibody produced in a primary immune response [3]. However, it is T-cell independent. T-cell dependent responses specifically lead to class switching away from IgM toward more specialized isotypes [1]. * **Option B (IgG only):** While IgG is a major component of the response, it is incomplete. The mucosal nature of the infection necessitates the production of IgA. * **Option D (IgG, IgM, IgA, IgE):** While IgE is a product of T-cell dependent class switching (Th2 mediated), it is typically associated with Type I hypersensitivity and helminthic infections, not the Type IV delayed-type hypersensitivity characteristic of tuberculosis. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** While antibodies (IgG/IgA) are produced, they are not used for routine diagnosis due to low sensitivity. Sputum microscopy (AFB) and NAAT (CBNAAT/GeneXpert) remain the standards. * **Cytokine Profile:** The protective immunity in TB is driven by **IFN-̳**, which activates macrophages to kill the intracellular bacilli. * **Ghon Complex:** Consists of a parenchymal lung lesion (Ghon focus) plus involved regional lymph nodes. **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. 161-162. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 206-207. [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. 154-155.

Question 168: MALT is most commonly present in which part of the small intestine?

A. Duodenum
B. Jejunum
C. Ileum (Correct Answer)
D. Stomach

Explanation: **Explanation:** **MALT (Mucosa-Associated Lymphoid Tissue)** refers to the organized collection of lymphoid tissue found in the submucosal layers of the gastrointestinal, respiratory, and urogenital tracts. **Why Ileum is the Correct Answer:** The **Ileum** is the site of the highest concentration of MALT in the small intestine, specifically in the form of **Peyer’s Patches** [1]. These are macroscopic aggregates of lymphoid follicles located primarily in the antimesenteric border of the distal ileum [1]. They play a critical role in immune surveillance by sampling intestinal antigens via specialized **M-cells (Microfold cells)** [1]. **Analysis of Incorrect Options:** * **Duodenum & Jejunum:** While lymphoid follicles are scattered throughout the entire gastrointestinal tract, their density increases distally [1]. The duodenum and jejunum contain significantly fewer organized lymphoid aggregates compared to the ileum. * **Stomach:** Under normal physiological conditions, the stomach contains virtually **no MALT** [1]. The presence of MALT in the stomach is considered pathological and is typically an acquired response to chronic inflammation, most commonly due to ***H. pylori* infection**, which can eventually progress to MALToma (marginal zone B-cell lymphoma) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **M-Cells:** These cells lack microvilli and a thick glycocoalyx; they are the entry point for pathogens like *Salmonella* and *Shigella* [1]. * **Homing:** Lymphocytes activated in the MALT express **α4β7 integrin**, which directs them back to the mucosal surfaces. * **MALToma:** The most common site for extranodal lymphoma is the stomach (acquired MALT), and it is strongly associated with the **t(11;18)** translocation [1]. * **IgA Production:** MALT is the primary site for the generation of plasma cells that secrete **Secretory IgA**, the dominant mucosal antibody. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-359.

Question 169: CANCA is associated with which of the following conditions?

A. Wegener's granulomatosis (Correct Answer)
B. Microscopic polyangiitis
C. Churg-Strauss syndrome
D. Goodpasture syndrome

Explanation: **Explanation:** **c-ANCA (Cytoplasmic Antineutrophil Cytoplasmic Antibody)** is a specific diagnostic marker primarily directed against the enzyme **Proteinase-3 (PR3)** found in the granules of neutrophils [1]. 1. **Why Wegener’s Granulomatosis is correct:** Wegener’s Granulomatosis (now known as **Granulomatosis with Polyangiitis - GPA**) shows a very high correlation with c-ANCA/anti-PR3 [1]. It is characterized by a triad of necrotizing granulomas of the respiratory tract, necrotizing vasculitis of small-to-medium vessels, and renal involvement (focal necrotizing glomerulonephritis) [1],[4]. c-ANCA levels are highly sensitive (>90%) during the active phase of the disease and are used to monitor disease activity [1],[2]. 2. **Why other options are incorrect:** * **Microscopic Polyangiitis (MPA) & Churg-Strauss Syndrome (EGPA):** These are primarily associated with **p-ANCA** (Perinuclear ANCA), which targets the enzyme **Myeloperoxidase (MPO)**. While MPA lacks granulomas, Churg-Strauss is distinguished by eosinophilia and asthma [3]. * **Goodpasture Syndrome:** This is caused by **anti-GBM antibodies** (Type II Hypersensitivity) targeting the alpha-3 chain of Type IV collagen in the lungs and kidneys [3]. It is not an ANCA-associated vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **c-ANCA = Anti-PR3** (Pattern: Diffuse cytoplasmic staining). * **p-ANCA = Anti-MPO** (Pattern: Perinuclear staining). * **GPA Triad:** "C" shape distribution (Nasopharynx, Lungs, Kidneys) + **c**-ANCA. * **Pauci-immune Glomerulonephritis:** A hallmark of ANCA-associated vasculitides (GPA, MPA, EGPA), meaning there is little to no antibody deposition on immunofluorescence [2],[4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 322-323. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537.

Question 170: Which of the following organs is NOT typically affected in Graft-Versus-Host disease?

A. Skin
B. Gastrointestinal tract
C. Liver
D. Lung (Correct Answer)

Explanation: **Explanation:** Graft-Versus-Host Disease (GVHD) occurs when immunologically competent donor T-cells (the graft) recognize the recipient’s (the host) HLA antigens as foreign and mount an immune attack [1]. This typically occurs in the setting of hematopoietic stem cell transplantation. **Why Lung is the Correct Answer:** While the lung can be involved in chronic GVHD (presenting as bronchiolitis obliterans), it is **not** considered a primary or "classic" target organ in the acute phase of the disease. The diagnostic triad for acute GVHD specifically involves the skin, liver, and GI tract [1]. Therefore, among the options provided, the lung is the least typically affected organ. **Analysis of Incorrect Options:** * **Skin (A):** The most common and usually the first organ affected. It typically presents as a maculopapular rash, often starting on the palms, soles, and neck, which can progress to generalized erythroderma [1] or toxic epidermal necrolysis. * **Gastrointestinal Tract (B):** Involvement leads to mucosal ulceration, causing profuse watery or bloody diarrhea [1], abdominal pain, and ileus. * **Liver (C):** Manifests as cholestatic jaundice due to the destruction of small bile ducts, leading to hepatosplenomegaly [1], elevated bilirubin and alkaline phosphatase levels. **High-Yield Clinical Pearls for NEET-PG:** * **Acute GVHD:** Occurs within **100 days** of transplant; primarily affects skin, GI tract, and liver [1]. * **Chronic GVHD:** Occurs after **100 days**; resembles systemic sclerosis (scleroderma-like skin changes) and can involve the lungs (bronchiolitis obliterans) and lacrimal glands (sicca syndrome). * **Prerequisite:** The recipient must be immunocompromised, and the graft must contain live T-lymphocytes. * **Prevention:** Depletion of donor T-cells before transfusion reduces GVHD risk but increases the risk of graft failure and recurrence of leukemia (loss of Graft-Versus-Leukemia effect). **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.

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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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