Immunopathology — MCQs

A 31-year-old man with AIDS complains of difficulty swallowing. Examination of his oral cavity demonstrates whitish membranes covering much of his tongue and palate. Endoscopy also reveals several whitish, ulcerated lesions in the esophagus. These pathologic findings are fundamentally caused by loss of which of the following immune cells?

Q57Medium

A 26-year-old systems analyst presents for evaluation of a bee sting allergy. He describes an episode in which he was stung on the forearm by a bee and, within 5 minutes, experienced pruritus, urticaria, and mild wheezing. What is the primary effector cell involved in this type of immediate hypersensitivity reaction?

Q58Easy

Pathological findings of Sjogren's syndrome include all except:

Q59Easy

C-ANCA is present in which of the following conditions?

Q60Medium

What is true about hyperacute rejection in renal transplant?

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 51: In which condition are plasma cells increased?

A. Rheumatoid arthritis (Correct Answer)
B. Acute appendicitis
C. Bronchitis
D. Bristles of burnt skin

Explanation: ### Explanation **Correct Answer: A. Rheumatoid Arthritis** The presence of plasma cells is a hallmark of **chronic inflammation** [3]. Rheumatoid Arthritis (RA) is a chronic systemic autoimmune disorder characterized by persistent synovial inflammation [1]. In RA, the synovial membrane becomes infiltrated by a "mononuclear infiltrate" consisting of T-lymphocytes, B-lymphocytes, and **plasma cells** [1], [2]. These plasma cells are crucial as they locally produce autoantibodies, such as Rheumatoid Factor (RF) and Anti-Citrullinated Protein Antibodies (ACPA), which contribute to joint destruction [1]. **Why the other options are incorrect:** * **B. Acute Appendicitis:** This is a classic example of **acute inflammation**. The predominant cell type here is the **neutrophil** (polymorphonuclear leukocyte), which responds to bacterial infection and tissue necrosis. * **C. Bronchitis:** While chronic bronchitis involves inflammation, the question typically refers to general acute inflammatory responses unless specified. Even in chronic bronchitis, the cellular infiltrate is mixed, but RA is the classic "high-yield" association for dense plasma cell infiltration in pathology exams. * **D. Bristles of burnt skin:** Thermal injury (burns) primarily results in acute coagulative necrosis and an immediate acute inflammatory response (neutrophils and edema) rather than a plasma cell-rich chronic infiltrate. **High-Yield Clinical Pearls for NEET-PG:** * **Plasma Cell Morphology:** Look for "Cartwheel" or "Clock-face" nuclei and a prominent perinuclear halo (Golgi apparatus). * **Russell Bodies:** Rounded, eosinophilic cytoplasmic inclusions representing accumulated Immunoglobulins within plasma cells. * **Dutcher Bodies:** Similar inclusions found within the nucleus (common in Waldenström macroglobulinemia). * **Other conditions with increased plasma cells:** Multiple Myeloma (malignant proliferation), Syphilis (plasma cell-rich infiltrate is a diagnostic clue), and Rhinoscleroma (Mikulicz cells and plasma cells). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1212-1214. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 107-109.

Question 52: Early complement deficiency can manifest as?

A. Hereditary angioneurotic edema
B. Atypical HUS
C. SLE (Correct Answer)
D. PNH

Explanation: **Explanation:** The correct answer is **SLE (Systemic Lupus Erythematosus)**. **Why SLE is the correct answer:** Early complement components (**C1q, C1r, C1s, C4, and C2**) play a critical role in the clearance of immune complexes and apoptotic debris [1]. In deficiencies of these components, immune complexes are not efficiently solubilized or cleared by the reticuloendothelial system. These persisting complexes deposit in tissues [3], triggering an inflammatory response and a loss of self-tolerance, which leads to the development of **SLE** [2]. Notably, **C1q deficiency** has the strongest association, with >90% of affected individuals developing a lupus-like syndrome. **Why other options are incorrect:** * **Hereditary Angioneurotic Edema:** Caused by a deficiency of **C1 esterase inhibitor**, leading to excessive production of bradykinin. It is not a deficiency of the complement proteins themselves. * **Atypical HUS:** Primarily associated with mutations or deficiencies in **Complement Factor H**, Factor I, or Membrane Cofactor Protein (MCP), which are regulatory proteins of the alternative pathway. * **PNH (Paroxysmal Nocturnal Hemoglobinuria):** An acquired clonal disorder caused by a PIGA gene mutation, leading to a deficiency of GPI-anchored proteins like **CD55 (DAF)** and **CD59 (MIRL)** on RBC membranes, making them susceptible to complement-mediated lysis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common complement deficiency:** C2 deficiency (often asymptomatic or presents with SLE/infections). * **Strongest association with SLE:** C1q deficiency. * **Late complement component deficiency (C5-C9):** Associated with recurrent **Neisseria** infections (failure to form the Membrane Attack Complex). * **C3 deficiency:** Leads to severe, recurrent pyogenic infections and Type II Membranoproliferative Glomerulonephritis (MPGN). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 226. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 228. [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 53: A 55-year-old male presented with dry mouth and rheumatoid arthritis with high titres of anti-SS-A and anti-SS-B antibodies. He was diagnosed with a minor salivary gland tumor. What is the earliest histologic finding in this condition?

A. Endothelial cells
B. Basophils
C. Lymphocytes (Correct Answer)
D. Eosinophils

Explanation: ### Explanation **Correct Answer: C. Lymphocytes** The clinical presentation of dry mouth (xerostomia), rheumatoid arthritis (a common associated connective tissue disease), and the presence of **anti-SS-A (Ro)** and **anti-SS-B (La)** antibodies confirms a diagnosis of **Sjögren Syndrome** [1]. In Sjögren Syndrome, the primary pathogenic mechanism is a **Type IV hypersensitivity reaction** (cell-mediated immunity). The earliest histological hallmark is the **periductal lymphocytic infiltration** of the exocrine glands (salivary and lacrimal) [1]. These infiltrates consist primarily of CD4+ T-helper cells and some B cells. As the disease progresses, these lymphocytes form lymphoid follicles with germinal centers, eventually leading to the destruction of the glandular acini and fibrosis [1]. **Analysis of Incorrect Options:** * **A. Endothelial cells:** While angiogenesis may occur in chronic inflammation, endothelial proliferation is not the primary or earliest diagnostic feature of this autoimmune process. * **B. Basophils:** These are involved in Type I hypersensitivity and systemic anaphylaxis; they play no significant role in the pathogenesis of Sjögren Syndrome. * **D. Eosinophils:** These are typically associated with parasitic infections or allergic responses (Type I hypersensitivity) and are not a characteristic finding in the lymphocytic sialadenitis of Sjögren’s. **Clinical Pearls for NEET-PG:** * **Diagnostic Gold Standard:** Lip biopsy (minor salivary gland biopsy) showing focus scores of lymphocytes (≥50 lymphocytes per 4 $mm^2$). * **Antibody Specificity:** Anti-SS-B is more specific for Sjögren Syndrome than Anti-SS-A. * **Malignancy Risk:** Patients have a **40-fold increased risk** of developing **B-cell MALT Lymphoma** (Marginal Zone Lymphoma) due to chronic B-cell stimulation [1]. * **Schirmer Test:** Used clinically to quantify decreased lacrimal gland secretion (keratoconjunctivitis sicca). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 234-236.

Question 54: RA antibody causes which type of hypersensitivity?

A. Type 1
B. Type 2
C. Type 3 (Correct Answer)
D. India ink

Explanation: **Explanation:** **Rheumatoid Arthritis (RA)** is primarily characterized by a **Type 3 Hypersensitivity** reaction [1]. The hallmark of RA is the production of **Rheumatoid Factor (RF)**, which is an autoantibody (usually IgM) directed against the Fc portion of the patient's own IgG. These antibodies bind to circulating IgG to form **immune complexes** [1]. These complexes deposit in the synovial membranes of joints, activating the complement system and recruiting neutrophils, leading to chronic inflammation and tissue destruction [1]. **Analysis of Options:** * **Type 1 (Incorrect):** This is IgE-mediated hypersensitivity involving mast cell degranulation (e.g., Anaphylaxis, Asthma, Atopy). * **Type 2 (Incorrect):** This involves antibodies (IgG/IgM) binding directly to fixed antigens on cell surfaces or tissues (e.g., Myasthenia Gravis, Goodpasture syndrome). While some RA-associated antibodies (like anti-CCP) exist, the systemic and joint manifestations are classically driven by immune complex deposition (Type 3). * **Type 3 (Correct):** Mediated by soluble **antigen-antibody (immune) complexes** that deposit in tissues, causing complement activation and vasculitis [1]. * **India Ink (Incorrect):** This is a laboratory negative stain used to identify *Cryptococcus neoformans*; it is not a type of hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Most Specific Marker for RA:** Anti-Cyclic Citrullinated Peptide (anti-CCP) antibodies. * **Most Sensitive/Screening Marker:** Rheumatoid Factor (RF). * **Joint Involvement:** Classically involves small joints of hands (PIP, MCP) and feet, sparing the DIP joints. * **Extra-articular manifestations:** Rheumatoid nodules, Caplan syndrome (RA + Pneumoconiosis), and Felty syndrome (RA + Splenomegaly + Neutropenia). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216.

Question 55: Which thyroid carcinoma is associated with calcitonin amyloid deposition?

A. Papillary
B. Follicular
C. Anaplastic
D. Medullary (Correct Answer)

Explanation: **Explanation:** **1. Why Medullary Thyroid Carcinoma (MTC) is correct:** Medullary thyroid carcinoma arises from the **Parafollicular C-cells** [3], which are neuroendocrine cells responsible for secreting **Calcitonin**. In MTC, there is an overproduction of calcitonin. This excess hormone undergoes conformational changes and polymerizes into insoluble fibrils, which deposit within the tumor stroma as **amyloid** [2]. On histopathology, this is seen as extracellular eosinophilic material that shows **Apple-green birefringence** under polarized light when stained with **Congo Red**. **2. Why other options are incorrect:** * **Papillary Carcinoma:** This is the most common thyroid cancer. It is characterized by nuclear features (Orphan Annie eyes, grooves, pseudoinclusions) and **Psammoma bodies** (laminated calcifications), not amyloid. * **Follicular Carcinoma:** This tumor is derived from follicular cells and is characterized by capsular or vascular invasion [2]. It does not secrete calcitonin and therefore lacks amyloid deposits. * **Anaplastic Carcinoma:** This is a highly aggressive, undifferentiated tumor seen in the elderly. It presents with rapid growth and pleomorphic cells [2] but does not have a specific association with amyloid. **3. High-Yield Clinical Pearls for NEET-PG:** * **Genetic Association:** MTC is associated with **RET proto-oncogene** mutations (MEN 2A and 2B syndromes) [1]. * **Staining:** Calcitonin immunostaining is the gold standard for diagnosis. * **Tumor Marker:** Serum calcitonin levels are used for both diagnosis and monitoring postoperative recurrence [1]. * **Amyloid Type:** The specific type of amyloid in MTC is classified as **A-Cal** (procalcitonin-derived). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 430-431. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 424-426.

Question 56: A 31-year-old man with AIDS complains of difficulty swallowing. Examination of his oral cavity demonstrates whitish membranes covering much of his tongue and palate. Endoscopy also reveals several whitish, ulcerated lesions in the esophagus. These pathologic findings are fundamentally caused by loss of which of the following immune cells?

A. B lymphocytes
B. Helper T lymphocytes (Correct Answer)
C. Killer T lymphocytes
D. Monocytes/macrophages

Explanation: ### Explanation **Correct Option: B. Helper T lymphocytes** The clinical presentation describes **Oral and Esophageal Candidiasis** (thrush) in a patient with AIDS [1]. The fundamental defect in HIV/AIDS is the infection and subsequent depletion of **CD4+ Helper T lymphocytes** [3]. * **Mechanism:** HIV uses the CD4 molecule as a primary receptor to enter cells. Helper T cells are the "conductors" of the immune system; they secrete cytokines (like IFN-γ and IL-2) that activate macrophages and cytotoxic T cells. * **Mucocutaneous Defense:** Protection against mucosal fungal infections like *Candida* relies heavily on **Th17 cells** (a subset of Helper T cells). When CD4+ counts drop (typically below 200 cells/mm³ [3]), the body loses its ability to prevent the overgrowth of commensal fungi, leading to invasive mucosal disease [2]. **Incorrect Options:** * **A. B lymphocytes:** While B cell function is indirectly impaired due to lack of T-cell help, B cells primarily handle extracellular bacterial infections through antibody production [4]. They are not the primary defense against *Candida*. * **C. Killer T lymphocytes (CD8+):** These cells are essential for killing virally infected cells and tumor cells. While they remain active longer than CD4 cells in HIV, their loss is not the *primary* cause of the initial opportunistic infections. * **D. Monocytes/macrophages:** HIV can infect these cells (acting as reservoirs), but their depletion is not the hallmark of AIDS. Neutrophils, rather than macrophages, are the primary cells that prevent *systemic* (disseminated) candidiasis. **NEET-PG High-Yield Pearls:** * **CD4 Count <200:** Threshold for defining AIDS and the typical point where esophageal candidiasis appears [3]. * **Th1 vs Th17:** Th1 cells (via IFN-γ) are crucial for intracellular pathogens (e.g., *M. tuberculosis*), while Th17 cells are crucial for fungal/extracellular bacterial defense at mucosal surfaces. * **Esophageal Candidiasis:** It is considered an **AIDS-defining illness**, unlike simple oral thrush [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 394-395. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 736-737. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 259-260. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 258.

Question 57: A 26-year-old systems analyst presents for evaluation of a bee sting allergy. He describes an episode in which he was stung on the forearm by a bee and, within 5 minutes, experienced pruritus, urticaria, and mild wheezing. What is the primary effector cell involved in this type of immediate hypersensitivity reaction?

A. Eosinophil
B. Mast cell (Correct Answer)
C. Megakaryocyte
D. Neutrophil

Explanation: ### Explanation **Correct Option: B. Mast cell** The clinical presentation of pruritus, urticaria, and wheezing within minutes of an allergen exposure (bee sting) is a classic example of **Type I Hypersensitivity (Immediate)**. This reaction is mediated by **IgE antibodies** that are pre-bound to the high-affinity FcεRI receptors on the surface of **mast cells** and basophils [1]. Upon re-exposure, the allergen crosses-links these IgE molecules, triggering mast cell degranulation [3]. This releases primary mediators like **histamine**, which causes vasodilation (urticaria) and smooth muscle contraction (wheezing/bronchospasm) [4]. **Analysis of Incorrect Options:** * **A. Eosinophil:** While eosinophils are characteristic of the **late-phase response** of Type I hypersensitivity (recruited by IL-5 and eotaxin), they are not the primary initiators of the immediate reaction [2]. * **C. Megakaryocyte:** These are large bone marrow cells responsible for the production of platelets; they have no direct role in the pathophysiology of acute allergic reactions. * **D. Neutrophil:** These are the hallmark of acute inflammation and Type III hypersensitivity (Arthus reaction). They are not the primary effectors in IgE-mediated allergic responses. **NEET-PG High-Yield Pearls:** * **Sequence of Type I Hypersensitivity:** Sensitization (IgE production) → Re-exposure → Cross-linking of IgE → Mast cell degranulation [3]. * **Preformed Mediators:** Histamine, Proteases (Tryptase - used as a clinical marker for anaphylaxis), and ECF (Eosinophil Chemotactic Factor). * **Newly Synthesized Mediators:** Leukotrienes (C4, D4, E4) are the most potent bronchoconstrictors (1000x more potent than histamine) [4]. * **Th2 Cells:** These are the T-helper cells responsible for secreting **IL-4** (stimulates IgE switch) and **IL-5** (activates eosinophils) [2]. **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 58: Pathological findings of Sjogren's syndrome include all except:

A. Keratoconjunctivitis sicca
B. Glomerular lesion
C. Renal tubular functional defect
D. Salivary gland germinal center lymphocyte deficient (Correct Answer)

Explanation: **Explanation:** Sjogren’s Syndrome is a chronic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands, primarily the lacrimal and salivary glands [1]. **Why Option D is the Correct Answer:** In Sjogren’s syndrome, the hallmark histopathological finding in the salivary glands is a **dense lymphocytic infiltration** (primarily CD4+ T cells and some B cells) [1]. In advanced cases, these lymphocytes organize into **follicles with germinal centers**. Therefore, the glands are **lymphocyte-rich**, not lymphocyte-deficient. The presence of these germinal centers is also a risk factor for the subsequent development of B-cell lymphomas (MALToma) [1]. **Analysis of Incorrect Options:** * **A. Keratoconjunctivitis sicca:** This is a classic clinical and pathological feature resulting from the destruction of lacrimal glands, leading to drying of the corneal epithelium, inflammation, and erosion [2]. * **B. & C. Renal Involvement:** While less common than glandular symptoms, the kidney is a frequent extraglandular site. The most common renal manifestation is **Tubulointerstitial Nephritis**, leading to **Renal Tubular Acidosis (RTA Type I)** or functional defects. Though rare, **Glomerular lesions** (such as membranous nephropathy or MPGN) can occur, especially in secondary Sjogren’s associated with SLE or Cryoglobulinemia. **High-Yield Clinical Pearls for NEET-PG:** * **Serology:** Positive for **Anti-Ro (SS-A)** and **Anti-La (SS-B)** antibodies [1]. * **Diagnostic Test:** Lip biopsy (minor salivary gland biopsy) showing an aggregate of $\ge$ 50 lymphocytes (Focus Score $\ge$ 1). * **Schirmer’s Test:** Used to quantify decreased lacrimation ($<$ 5mm in 5 mins). * **Malignancy Risk:** 40-fold increased risk of **Non-Hodgkin Lymphoma** (specifically B-cell MALT lymphoma) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 234-236. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 236.

Question 59: C-ANCA is present in which of the following conditions?

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

Explanation: **Explanation:** **Wegener’s Granulomatosis** (now known as Granulomatosis with Polyangiitis - GPA) is the correct answer because it is characteristically associated with **c-ANCA** (cytoplasmic Antineutrophil Cytoplasmic Antibody) [1]. The target antigen for c-ANCA is **Proteinase-3 (PR3)** [1]. GPA is defined by a triad of necrotizing granulomas of the respiratory tract, necrotizing vasculitis of small-to-medium vessels, and renal involvement (crescentic glomerulonephritis) [1]. **Analysis of Incorrect Options:** * **Microscopic Polyangiitis (MPA):** This condition is primarily associated with **p-ANCA** (perinuclear ANCA), where the target antigen is **Myeloperoxidase (MPO)**. Unlike GPA, it lacks granulomatous inflammation [2]. * **Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis):** This is also associated with **p-ANCA** (in about 50% of cases). It is clinically distinguished by bronchial asthma, peripheral eosinophilia, and tissue infiltrates. * **Kawasaki Disease:** This is a large-to-medium vessel vasculitis (mucocutaneous lymph node syndrome) seen in children. It is **not associated with ANCA** [3]; diagnosis is clinical (fever, conjunctivitis, strawberry tongue, and coronary artery aneurysms). **High-Yield Clinical Pearls for NEET-PG:** 1. **c-ANCA (PR3-ANCA):** Highly specific for **Wegener’s Granulomatosis** (GPA) [1]. 2. **p-ANCA (MPO-ANCA):** Associated with **Microscopic Polyangiitis**, **Churg-Strauss**, and **Primary Sclerosing Cholangitis (PSC)**. 3. **Rule of thumb:** If the disease name has "Granulomatosis" without "Eosinophilic," think c-ANCA. If it involves "Microscopic" or "Eosinophilic," think p-ANCA. 4. ANCA titers are useful for monitoring **disease activity** and treatment response in these vasculitides [1]. **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. Diseases of Infancy and Childhood, pp. 518-519. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.

Question 60: What is true about hyperacute rejection in renal transplant?

A. Occurs within a few days of transplant
B. Involves T cells
C. Characterized by blood vessel thrombosis (Correct Answer)
D. Associated with eosinophilic infiltration

Explanation: **Explanation:** **Hyperacute rejection** is a type of transplant rejection that occurs almost immediately (within minutes to hours) after the graft is vascularized [1]. **Why Option C is Correct:** The underlying mechanism is a **Type II Hypersensitivity reaction** mediated by **pre-formed antibodies** (anti-HLA or anti-ABO) in the recipient’s serum. When the donor organ is anastomosed, these antibodies immediately bind to the vascular endothelium of the graft. This triggers the complement cascade, leading to endothelial injury, platelet aggregation, and widespread **fibrinoid necrosis and thrombosis** of the graft capillaries and arterioles [1]. This results in rapid ischemic necrosis, making the kidney appear cyanotic and mottled [1]. **Analysis of Incorrect Options:** * **Option A:** Hyperacute rejection occurs within **minutes to hours**. Rejection occurring within "a few days" is typically **Acute Rejection** (cellular or antibody-mediated) [1]. * **Option B:** It is mediated by **B-cells/Antibodies**, not T-cells. T-cell mediated rejection is the hallmark of Acute Cellular Rejection [2]. * **Option C:** **Eosinophilic infiltration** is a characteristic feature of **Drug-induced Acute Interstitial Nephritis**, not hyperacute rejection. **High-Yield Clinical Pearls for NEET-PG:** * **Gross Appearance:** The kidney becomes soft, flaccid, and "blue" (cyanotic) [1]. * **Prevention:** It is prevented by **Cross-matching** (testing recipient serum against donor lymphocytes) before surgery. * **Treatment:** There is no effective treatment; the graft must be **surgically removed** immediately [1]. * **Key Histology:** Neutrophilic infiltration in peritubular capillaries followed by widespread microvascular thrombosis [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, p. 242.

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Cells and Tissues of the Immune System

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Hypersensitivity Reactions

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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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