Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 101: Which pair of organs is involved in Goodpasture's syndrome?

A. Kidney and intestine
B. Kidney and heart
C. Kidney and lungs (Correct Answer)
D. Kidney and liver

Explanation: **Explanation:** **Goodpasture’s Syndrome** (Anti-GBM Disease) is a classic example of a **Type II Hypersensitivity reaction**. It is characterized by the formation of autoantibodies against the **alpha-3 chain of Type IV collagen** [3]. 1. **Why Kidney and Lungs?** Type IV collagen is a major structural component of basement membranes. The specific target antigen (NC1 domain of the $\alpha$3 chain) is highly expressed in the **Glomerular Basement Membrane (GBM)** of the kidneys and the **Alveolar Basement Membrane** of the lungs [1]. The binding of these antibodies triggers the complement cascade, leading to: * **Kidneys:** Rapidly Progressive Glomerulonephritis (RPGN) with "crescent" formation [2]. * **Lungs:** Alveolar hemorrhage, presenting as hemoptysis [1], [2]. 2. **Why other options are incorrect:** * **Intestine, Heart, and Liver:** While these organs contain basement membranes, they do not express the specific $\alpha$3(IV) collagen isoform targeted in Goodpasture’s syndrome. Therefore, they are not primary sites of immune-mediated damage in this condition. **High-Yield Clinical Pearls for NEET-PG:** * **Immunofluorescence (IF):** Shows a characteristic **Linear IgG deposition** along the basement membranes (unlike the "lumpy-bumpy" granular pattern seen in Post-Streptococcal Glomerulonephritis) [3], [4]. * **Demographics:** Typically affects young adult males [2]. * **Clinical Triad:** Diffuse alveolar hemorrhage (hemoptysis), glomerulonephritis (hematuria/renal failure), and anti-GBM antibodies [2]. * **HLA Association:** Strongly associated with **HLA-DR2** [2]. * **Treatment:** Plasmapheresis (to remove circulating antibodies) and immunosuppressants [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 322-323. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 537-538. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 526-527. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909.

Question 102: Sago spleen is seen in which condition?

A. Infarction
B. Amyloidosis (Correct Answer)
C. Chronic venous congestion
D. Tuberculosis

Explanation: **Explanation:** **Sago spleen** is a classic morphological manifestation of **Amyloidosis** involving the spleen [1]. The term is derived from the resemblance of the splenic surface to "sago" (tapioca-like) grains [3]. 1. **Why Amyloidosis is correct:** In amyloidosis, the pattern of splenic involvement depends on the anatomical site of protein deposition: * **Sago Spleen:** Amyloid is deposited primarily in the **splenic follicles (white pulp)**. On gross examination, these appear as translucent, pale, 1–2 mm granules against a normal background. * **Lardaceous Spleen:** Amyloid is deposited in the **splenic sinuses and red pulp**, leading to large, map-like deposits and significant splenomegaly with a firm, waxy consistency [3]. 2. **Why other options are incorrect:** * **Infarction:** Splenic infarcts typically present as wedge-shaped, pale areas (anemic infarcts) due to the occlusion of the splenic artery or its branches. * **Chronic Venous Congestion (CVC):** Seen in portal hypertension, this leads to a "Congestive Splenomegaly" or **"Siderotic Spleen"** characterized by Gamna-Gandy bodies (fibrosiderotic nodules). * **Tuberculosis:** Splenic TB usually presents as "Miliary Tuberculosis," showing multiple small, yellowish-white, firm granulomas, or as large cold abscesses. **High-Yield Pearls for NEET-PG:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red** [2]. * **Sago Spleen = White Pulp** involvement. * **Lardaceous Spleen = Red Pulp** involvement. * The most common protein in systemic amyloidosis involving the spleen is usually AL (Primary) or AA (Secondary) amyloid [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-266. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [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. 135-136.

Question 103: Which marker is characteristic of Natural Killer (NK) cells?

A. CD 34
B. CD 56 (Correct Answer)
C. CD 1
D. CD 45

Explanation: **Explanation:** **Natural Killer (NK) cells** are a subset of innate lymphoid cells that play a critical role in the rejection of tumors and virally infected cells [2], [3]. They are morphologically identified as large granular lymphocytes. * **Correct Answer (B) CD 56:** This is the classic marker used to identify NK cells in clinical practice and flow cytometry. CD 56 (also known as Neural Cell Adhesion Molecule or NCAM) is expressed by all NK cells. Another highly specific marker often associated with NK cells is **CD 16** (an Fc receptor for IgG), which mediates antibody-dependent cellular cytotoxicity (ADCC). **Analysis of Incorrect Options:** * **A. CD 34:** This is a marker for **hematopoietic stem cells** and vascular endothelium. It is used to identify precursor cells in the bone marrow and is a key marker in diagnosing Acute Myeloid Leukemia (AML). * **C. CD 1:** This family of markers (specifically CD1a) is characteristic of **Langerhans cells** and cortical thymocytes [1]. It is a high-yield marker for diagnosing Langerhans Cell Histiocytosis (LCH). * **D. CD 45:** Known as the **Leukocyte Common Antigen (LCA)**, this is expressed on all white blood cells (leukocytes). While NK cells are CD45 positive, it is not a specific marker for them as it is also found on B cells, T cells, and granulocytes. **High-Yield NEET-PG Pearls:** * **NK Cell Definition:** They are defined immunophenotypically as **CD3 negative** and **CD56/CD16 positive**. * **Mechanism:** NK cells kill target cells that show "missing self" (downregulation of MHC Class I molecules) [2]. * **Granules:** They contain **Perforins** (create pores) and **Granzymes** (induce apoptosis). * **Cytokine:** **IL-15** is essential for the development and maturation of NK cells [2]. **References:** [1] 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. 598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201. [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. 164-165.

Question 104: Granuloma formation is seen in which type of hypersensitivity reaction?

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

Explanation: ### Explanation **Correct Answer: D. Type IV Hypersensitivity** **Mechanism of Granuloma Formation:** Granuloma formation is a classic example of **Type IV (Delayed-type) Hypersensitivity**, specifically the **cell-mediated** subtype [1]. It occurs when an antigen is persistent and cannot be easily degraded by macrophages [3]. 1. **Sensitization:** CD4+ T-cells (Th1) recognize the antigen presented by macrophages [1]. 2. **Activation:** Th1 cells secrete cytokines, primarily **Interferon-gamma (IFN-̳)** [1], [2]. 3. **Transformation:** IFN-̳ activates macrophages, transforming them into **Epithelioid cells** [2]. These cells can fuse to form **Multinucleated Giant Cells** (e.g., Langhans giant cells) [2]. 4. **Sequestration:** A rim of lymphocytes and fibroblasts surrounds these cells, forming a granuloma to wall off the offending agent [2]. **Why Other Options are Incorrect:** * **Type I (Immediate):** Mediated by **IgE** and mast cell degranulation (e.g., Anaphylaxis, Asthma). It involves eosinophils, not granulomas. * **Type II (Antibody-mediated):** Involves **IgG/IgM** binding to cell surface antigens leading to complement activation or ADCC (e.g., Myasthenia gravis, Rheumatic fever). * **Type III (Immune-complex):** Caused by deposition of **antigen-antibody complexes** in tissues, leading to vasculitis and fibrinoid necrosis (e.g., SLE, Arthus reaction). **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Cytokine:** IFN-̳ is the most critical cytokine for granuloma formation [2]. * **TNF-̑:** Essential for maintaining the structural integrity of a granuloma (Anti-TNF drugs can cause breakdown of old TB granulomas). * **Caseating vs. Non-caseating:** Tuberculosis shows central caseous necrosis; Sarcoidosis and Berylliosis typically show non-caseating granulomas [3]. * **Schistosomiasis:** A unique example where a granuloma forms around helminth eggs (Th2 mediated) [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [3] 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. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 218-219.

Question 105: Which of the following cell types is most commonly associated with chronic allergic asthma?

A. TH17
B. TH1
C. TH2 (Correct Answer)
D. TH4

Explanation: ### Explanation **Correct Option: C (TH2)** Chronic allergic asthma is a classic example of a **Type I Hypersensitivity reaction** [2]. The pathogenesis is driven by the activation of **T-Helper 2 (TH2) cells** [1], [3]. Upon exposure to an allergen, TH2 cells secrete a specific profile of cytokines: * **IL-4 & IL-13:** Stimulate B-cells to undergo class switching to produce **IgE** [1]. * **IL-5:** Activates and recruits **eosinophils**, which are the hallmark effector cells of chronic asthmatic inflammation [1]. * **IL-13:** Stimulates mucus secretion from bronchial submucosal glands [1]. **Analysis of Incorrect Options:** * **A. TH17:** These cells produce IL-17 and are primarily involved in the recruitment of neutrophils. While they play a role in "non-atopic" or severe steroid-resistant asthma, they are not the primary drivers of classic allergic asthma. * **B. TH1:** These cells produce Interferon-gamma (IFN-̲̲̲̲̲̲̲̲̲̲̲̲̲̲ ̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲̲ĳ) and are involved in Type IV (delayed-type) hypersensitivity and defense against intracellular pathogens. They generally antagonize the TH2 response. * **D. TH4:** This is not a standard functional subset of T-helper cells. (Note: CD4 refers to the surface marker for all T-helper cells, but the functional subsets are TH1, TH2, TH17, and Treg). **NEET-PG High-Yield Pearls:** * **The "Hygiene Hypothesis":** Suggests that decreased early childhood exposure to infections leads to a TH2-biased immune system, increasing asthma risk. * **Curschmann Spirals & Charcot-Leyden Crystals:** Key microscopic findings in asthmatic sputum. The latter are derived from eosinophil proteins (Galectin-10). * **Airway Remodeling:** Chronic TH2 inflammation leads to subepithelial fibrosis (thickening of the basement membrane) and hypertrophy of bronchial smooth muscle. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210.

Question 106: All of the following are included in the Sydney revision of the Sapporo criteria for Antiphospholipid antibody syndrome EXCEPT:

A. Vascular thrombosis
B. Livedo reticularis (Correct Answer)
C. 3 or more unexplained spontaneous abortions
D. Lupus anticoagulant in plasma

Explanation: The **Sydney revision of the Sapporo criteria** (2006) defines the classification for Antiphospholipid Antibody Syndrome (APS). To be diagnosed with APS, a patient must meet at least **one clinical criterion** and **one laboratory criterion** [1]. ### Why Livedo Reticularis is the Correct Answer **Livedo reticularis** is a common dermatological manifestation of APS (a reticulated, purplish skin discoloration). However, it is considered a **non-criteria manifestation**. While clinically suggestive, it is not specific enough to be included in the formal Sydney/Sapporo diagnostic criteria. ### Explanation of Incorrect Options (Criteria included in the classification): * **Vascular Thrombosis (Option A):** This is a primary clinical criterion. It includes one or more clinical episodes of arterial, venous, or small-vessel thrombosis in any tissue or organ, confirmed by imaging or histopathology [1]. * **Pregnancy Morbidity (Option C):** This clinical criterion includes: * **3 or more** unexplained consecutive spontaneous abortions before the 10th week. * 1 or more unexplained deaths of a morphologically normal fetus at or after the 10th week [1]. * 1 or more premature births before the 34th week due to eclampsia, severe pre-eclampsia, or placental insufficiency. * **Lupus Anticoagulant (Option D):** This is one of the three laboratory criteria [1]. The others are **Anti-cardiolipin antibodies** (IgG/IgM) and **Anti-β2-glycoprotein I antibodies** (IgG/IgM), present on two or more occasions at least 12 weeks apart. ### High-Yield Clinical Pearls for NEET-PG: * **The "Paradox":** In APS, the Lupus Anticoagulant causes a **prolonged aPTT** *in vitro* (acting as an anticoagulant), but it causes **thrombosis** *in vivo* (acting as a procoagulant) [2]. * **False Positive VDRL:** Patients with APS often show a false positive test for Syphilis because the VDRL antigen contains cardiolipin [2]. * **Catastrophic APS (Asherson’s Syndrome):** A rare, life-threatening form involving multi-organ failure due to small vessel occlusion. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 626-627. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 134-135.

Question 107: Human immunodeficiency virus (HIV) affects the immune response. What is the primary change it brings about?

A. A gammaglobulinemia
B. Defect in cell-mediated immunity (Correct Answer)
C. Defect in complement system
D. Defect in natural killer cells

Explanation: **Explanation:** The hallmark of HIV pathogenesis is the profound depletion of **CD4+ T-lymphocytes** (Helper T-cells) [1]. HIV uses the CD4 molecule as its primary receptor, entering these cells via the gp120 envelope glycoprotein. Since CD4+ T-cells are the "master orchestrators" of the immune system, their destruction leads to a severe **defect in cell-mediated immunity (CMI)** [1]. This deficiency makes the patient highly susceptible to opportunistic infections (e.g., *Pneumocystis jirovecii*, Toxoplasmosis) and specific malignancies (e.g., Kaposi Sarcoma) [1]. **Analysis of Incorrect Options:** * **A. Agammaglobulinemia:** HIV actually causes **polyclonal hypergammaglobulinemia** due to non-specific B-cell activation [2]. However, these antibodies are dysfunctional and ineffective [2][4]. * **C. Defect in complement system:** HIV does not primarily target the complement cascade. While secondary deficiencies can occur in advanced AIDS, it is not the primary mechanism of immunodeficiency. * **D. Defect in natural killer (NK) cells:** While NK cell function may be impaired in late-stage HIV, the primary and defining pathology is the loss of CD4+ T-cells and the resulting CMI defect. **High-Yield Clinical Pearls for NEET-PG:** * **Receptor Dynamics:** HIV requires both the **CD4 receptor** and a co-receptor (**CCR5** on macrophages/T-cells in early infection; **CXCR4** on T-cells in late infection) [1]. * **Inversion of Ratio:** A classic laboratory finding in HIV is the **inversion of the CD4:CD8 ratio** (Normal is ~2:1; in HIV it becomes <1:1). * **Diagnostic Marker:** The **p24 antigen** is the earliest detectable serological marker (window period), while **CD4 count** is the best indicator of disease progression and the risk of opportunistic infections [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 256-257. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 257-258. [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 108: C5a acts as a/an?

A. Opsonin
B. Chemotactic agent (Correct Answer)
C. Membrane Attack Complex (MAC)
D. Vasodilator

Explanation: The complement system is a vital component of innate immunity, consisting of plasma proteins that enhance the ability of antibodies and phagocytic cells to clear pathogens. **C5a** is a potent inflammatory mediator produced during the cleavage of C5 by C5-convertase [1]. **1. Why C5a is a Chemotactic Agent (Correct):** C5a is the most powerful **chemotactic factor** of the complement system [1]. It acts as a chemical attractant that recruits neutrophils, monocytes, eosinophils, and basophils to the site of inflammation [1]. Additionally, it activates the lipoxygenase pathway of arachidonic acid metabolism in these cells, further amplifying the inflammatory response. **2. Analysis of Incorrect Options:** * **A. Opsonin:** This refers primarily to **C3b** (and its derivative iC3b) [3]. Opsonins "coat" microbes to make them more recognizable for phagocytosis by neutrophils and macrophages [4]. * **B. Membrane Attack Complex (MAC):** The MAC is composed of **C5b-C9** [2]. While C5a is a byproduct of C5 cleavage, it is a soluble anaphylatoxin and does not form part of the physical pore-forming complex [2]. * **C. Vasodilator:** While C5a causes vasodilation indirectly (by triggering histamine release from mast cells), it is primarily classified as an **Anaphylatoxin** (along with C3a and C4a) and a chemotactic agent [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Potency Hierarchy:** C5a is significantly more potent than C3a in inducing inflammation. * **Anaphylatoxins:** C3a, C4a, and C5a cause mast cell degranulation, leading to increased vascular permeability and smooth muscle contraction [1], [2]. * **C5a and Neutrophils:** C5a also increases the avidity of **integrins** on the surface of leukocytes, promoting firm adhesion to endothelium during the cellular phase of inflammation. **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. 163-164. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [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. 162-163. [4] 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. 190-191.

Question 109: A patient presented with generalized edema, sweating, flushing, tachycardia, and fever after a bee sting. What type of hypersensitivity reaction is this?

A. T cell mediated cytotoxicity
B. IgE mediated reaction (Correct Answer)
C. IgG mediated reaction
D. IgA mediated hypersensitivity reaction

Explanation: ### Explanation The clinical presentation of generalized edema, tachycardia, flushing, and sweating immediately following a bee sting is characteristic of **Anaphylaxis**, which is a classic example of **Type I Hypersensitivity** [1]. **Why Option B is Correct:** Type I hypersensitivity is an **IgE-mediated reaction**. Upon re-exposure to an allergen (bee venom), specific IgE antibodies already bound to the surface of **mast cells and basophils** cause cross-linking of FcεRI receptors [1]. This triggers immediate degranulation and the release of vasoactive amines like **histamine**. These mediators cause systemic vasodilation (flushing, hypotension), increased vascular permeability (edema), and compensatory tachycardia [1]. **Why Other Options are Incorrect:** * **Option A (T cell mediated):** This refers to **Type IV Hypersensitivity** (Delayed-type). It involves sensitized T lymphocytes and typically takes 48–72 hours to manifest (e.g., Contact dermatitis, Mantoux test). It does not cause immediate systemic anaphylaxis [1]. * **Option C (IgG mediated):** While IgG is involved in Type II (cytotoxic) and Type III (immune-complex) reactions, it is not the primary trigger for acute allergic anaphylaxis [1]. * **Option D (IgA mediated):** IgA is primarily involved in mucosal immunity. While IgA-deficient patients can develop anaphylaxis when receiving blood products (due to anti-IgA antibodies), the reaction itself is still mediated by IgE. **NEET-PG High-Yield Pearls:** * **Key Cells:** Mast cells (tissue) and Basophils (blood) [1]. * **Preformed Mediators:** Histamine, Proteases (Tryptase). *Note: Serum Tryptase levels are used to confirm a diagnosis of anaphylaxis post-event.* * **Newly Synthesized Mediators:** Leukotrienes (C4, D4, E4) – these are 1000x more potent than histamine in causing bronchospasm [1]. * **Treatment of Choice:** Intramuscular Epinephrine (1:1000). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-213.

Question 110: Hyperacute rejection occurs within which timeframe?

A. 12 hours (Correct Answer)
B. 2 weeks
C. 1 month
D. 3 months

Explanation: **Explanation:** **Hyperacute rejection** is a Type II hypersensitivity reaction mediated by **preformed antibodies** (IgG) in the recipient’s serum against the donor’s antigens (typically ABO blood group or HLA antigens). 1. **Why 12 hours is correct:** Hyperacute rejection occurs almost immediately—ranging from **minutes to a few hours** after the graft is vascularized [1]. Because the antibodies are already present, they immediately bind to the vascular endothelium of the graft, triggering the complement cascade, thrombosis, and fibrinoid necrosis [1]. In the context of the options provided, **12 hours** is the most accurate timeframe representing this immediate post-surgical window. 2. **Why the other options are incorrect:** * **2 weeks:** This timeframe is characteristic of **Acute Rejection**. Acute rejection is T-cell mediated (Type IV) or antibody-mediated (Type II) and typically occurs within days to a few weeks (usually <6 months) as the recipient's immune system takes time to recognize and respond to the new antigens [1]. * **1 month & 3 months:** These periods fall under the spectrum of **Acute Rejection** or the beginning of **Chronic Rejection**. Chronic rejection occurs over months to years and is characterized by intimal thickening and fibrosis (arteriosclerosis). **High-Yield NEET-PG Pearls:** * **Mechanism:** Preformed antibodies → Complement activation → Endothelial damage → **Thrombosis and Fibrinoid Necrosis** [1]. * **Gross Appearance:** The kidney rapidly becomes cyanotic, mottled, and flaccid (often described as a "blue kidney") [1]. * **Prevention:** Mandatory **Cross-matching** (mixing recipient serum with donor lymphocytes) before transplantation has made hyperacute rejection rare in modern clinical practice. **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.

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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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