Immunopathology — MCQs
On this page
A 40-year-old man with a 10-year history of HIV infection presents with newly diagnosed Kaposi sarcoma involving the skin and a 7-kg weight loss in the past 6 months. His HIV-1 RNA viral load is currently 60,000 copies/mL. Which of the following types of cells is most depleted in his lymph nodes?
A clinical study is performed in which the subjects are children 1 to 4 years old who have had multiple infections with viral, fungal, and parasitic diseases. Compared with a normal control group, these children do not have thymic cells that bear markers of cortical lymphocytes. Which of the following karyotypic abnormalities is most likely to be seen in the children in this study?
Which of the following can provide the "second signal" to a B-cell bound by a specific antigen?
A 40-year-old man presents with yellow skin and sclerae, abdominal tenderness, and dark urine. Physical examination reveals jaundice and mild hepatomegaly. Laboratory studies show elevated serum bilirubin (3.1 mg/dL), decreased serum albumin (2.5 g/dL), and prolonged prothrombin time (17 seconds). Serologic tests reveal antibodies to hepatitis B core antigen (IgG anti-HBcAg). The serum is also positive for HBsAg and HBeAg. What glycoprotein on virally infected hepatocytes provides a target for cell-mediated cytotoxicity in this patient?
Which antibody is known to cross the placenta?
Which of the following cells does HIV primarily affect?
Which of the following is NOT a pro-inflammatory cytokine?
Which of the following is NOT a pro-inflammatory cytokine?
What type of ANCA is most commonly associated with Wegener's granulomatosis?
Secondary amyloidosis is a complication of which condition?
Immunopathology Indian Medical PG Practice Questions and MCQs
Question 261: A 40-year-old man with a 10-year history of HIV infection presents with newly diagnosed Kaposi sarcoma involving the skin and a 7-kg weight loss in the past 6 months. His HIV-1 RNA viral load is currently 60,000 copies/mL. Which of the following types of cells is most depleted in his lymph nodes?
- A. CD4+ lymphocyte (Correct Answer)
- B. CD8+ lymphocyte
- C. CD19+ lymphocyte
- D. Macrophage
Explanation: The patient presents with advanced HIV infection, evidenced by a high viral load and an AIDS-defining illness (**Kaposi sarcoma**, caused by HHV-8) [1]. The hallmark of HIV pathogenesis is the progressive depletion of **CD4+ T-lymphocytes** [2]. **Why CD4+ lymphocyte is correct:** HIV specifically targets cells expressing the CD4 molecule and chemokine coreceptors (CCR5 or CXCR4). The virus infects CD4+ T-cells, leading to their destruction via direct viral cytolysis, syncytia formation, and apoptosis [1]. In the lymph nodes, HIV replicates extensively within the follicular dendritic cell network, leading to the eventual collapse of the node architecture and profound depletion of the CD4+ T-cell population [2]. This depletion is the primary cause of the profound immunodeficiency seen in AIDS [1]. **Why the other options are incorrect:** * **CD8+ lymphocyte:** These are cytotoxic T-cells. While their function may eventually become exhausted, their numbers often initially increase or remain relatively stable compared to the dramatic loss of CD4+ cells [2]. * **CD19+ lymphocyte:** These are B-cells. While HIV causes B-cell dysregulation (leading to hypergammaglobulinemia), they are not the primary target of the virus and are not the "most depleted" cell type. * **Macrophage:** Macrophages express CD4 and act as reservoirs for HIV. They are resistant to the cytopathic effects of the virus; therefore, they are infected but not significantly depleted [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Normal CD4+ count:** 500–1500 cells/mm³. * **AIDS Diagnosis:** CD4+ count **<200 cells/mm³** or the presence of an AIDS-defining illness (e.g., Kaposi Sarcoma, PCP pneumonia, Esophageal Candidiasis) [3]. * **Coreceptors:** **CCR5** is essential for early (macrophage-tropic) infection; **CXCR4** is associated with late-stage (T-cell-tropic) progression [1]. * **Kaposi Sarcoma:** Associated with **HHV-8**; histologically characterized by spindle cells and slit-like vascular spaces [4]. **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. 258-259. [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, pp. 262-263.
Question 262: A clinical study is performed in which the subjects are children 1 to 4 years old who have had multiple infections with viral, fungal, and parasitic diseases. Compared with a normal control group, these children do not have thymic cells that bear markers of cortical lymphocytes. Which of the following karyotypic abnormalities is most likely to be seen in the children in this study?
- A. Trisomy 21
- B. 22q11.2 deletion syndrome (Correct Answer)
- C. Philadelphia chromosome (t(9;22))
- D. Philadelphia chromosome variant (t(15;17))
Explanation: ### Explanation **Correct Option: B. 22q11.2 deletion syndrome** The clinical presentation of recurrent viral, fungal, and parasitic infections in a young child suggests a **T-cell deficiency** [3]. The absence of thymic cortical lymphocytes indicates **thymic hypoplasia or aplasia**. This is the hallmark of **DiGeorge Syndrome**, which is caused by a microdeletion at **chromosome 22q11.2** [1], [2]. This deletion leads to the maldevelopment of the **3rd and 4th pharyngeal pouches**, which are embryological precursors to the thymus and parathyroid glands [1]. Without a functional thymus, T-cells cannot mature, leading to profound cell-mediated immunodeficiency. **Analysis of Incorrect Options:** * **A. Trisomy 21 (Down Syndrome):** While associated with increased infections and leukemia, it does not typically present with primary thymic aplasia. * **C. Philadelphia chromosome (t(9;22)):** This translocation creates the *BCR-ABL* fusion gene, characteristic of Chronic Myeloid Leukemia (CML) and some cases of ALL, not primary immunodeficiency. * **D. Philadelphia chromosome variant (t(15;17)):** This is actually the translocation for **Acute Promyelocytic Leukemia (APL - M3)**, involving the *PML-RARA* gene. --- ### High-Yield Clinical Pearls for NEET-PG: * **CATCH-22 Mnemonic for DiGeorge Syndrome:** * **C**ardiac defects (Interrupted aortic arch, Truncus arteriosus, Tetralogy of Fallot). * **A**bnormal facies (Low-set ears, cleft palate). * **T**hymic aplasia (T-cell deficiency → recurrent infections). * **C**left palate. * **H**ypocalcemia (due to parathyroid hypoplasia → tetany) [1]. * **Diagnosis:** Gold standard is **FISH** (Fluorescence In Situ Hybridization) to detect the 22q11.2 microdeletion [2]. * **Radiology:** Look for the "absence of thymic shadow" on a pediatric chest X-ray. **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. 167-168. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 173. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 248-249.
Question 263: Which of the following can provide the "second signal" to a B-cell bound by a specific antigen?
- A. Epstein-Barr virus
- B. Endotoxin
- C. Antigen-specific T-cells (Correct Answer)
- D. Plasma cells
Explanation: ### Explanation B-cell activation typically requires two distinct signals to prevent accidental immune responses against self-antigens. This process is central to the **humoral immune response** [1]. **1. Why the Correct Answer is Right:** * **Signal 1:** Occurs when the B-cell receptor (surface IgM/IgD) binds to its specific **antigen** [2]. * **Signal 2 (The Second Signal):** For T-cell dependent antigens, the B-cell internalizes the antigen and presents it via **MHC Class II** to a **Helper T-cell (CD4+)**. The interaction between **CD40** on the B-cell and **CD40L (CD154)** on the T-cell provides the essential "second signal." This triggers B-cell proliferation, isotype switching, and affinity maturation [1]. **2. Analysis of Incorrect Options:** * **A. Epstein-Barr Virus (EBV):** EBV is a polyclonal B-cell activator that binds to the **CD21** receptor. While it can drive B-cell proliferation, it bypasses the physiological "second signal" mechanism and is associated with oncogenesis (e.g., Burkitt Lymphoma). * **B. Endotoxin (LPS):** This is a classic **T-independent antigen**. At high concentrations, it can activate B-cells without T-cell help, but it does not provide the physiological "second signal" required for memory cell formation or class switching [2]. * **D. Plasma Cells:** These are the terminally differentiated end-products of B-cell activation. They secrete antibodies but do not provide activation signals to naive B-cells. **3. NEET-PG High-Yield Pearls:** * **CD40-CD40L Interaction:** Deficiency in this interaction leads to **Hyper-IgM Syndrome** (failure of isotype switching). * **T-Independent Antigens:** Polysaccharides (like pneumococcal capsule) do not require T-cell help but produce a weaker response (mostly IgM, no memory) [2]. * **B-cell Markers:** CD19, CD20, and CD21 (CR2—the receptor for EBV). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 206-207. [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. 161-162.
Question 264: A 40-year-old man presents with yellow skin and sclerae, abdominal tenderness, and dark urine. Physical examination reveals jaundice and mild hepatomegaly. Laboratory studies show elevated serum bilirubin (3.1 mg/dL), decreased serum albumin (2.5 g/dL), and prolonged prothrombin time (17 seconds). Serologic tests reveal antibodies to hepatitis B core antigen (IgG anti-HBcAg). The serum is also positive for HBsAg and HBeAg. What glycoprotein on virally infected hepatocytes provides a target for cell-mediated cytotoxicity in this patient?
- A. CD4
- B. CD8
- C. Class I HLA molecules (Correct Answer)
- D. Class II HLA molecules
Explanation: The clinical presentation and serology (HBsAg+, HBeAg+, IgG anti-HBcAg) indicate **Chronic Active Hepatitis B**. In viral hepatitis, the liver injury is not caused by the virus itself (HBV is not cytopathic) but by the host’s immune response against infected hepatocytes [1]. **1. Why Class I HLA is correct:** Cytotoxic T Lymphocytes (CTLs), which are **CD8+ T cells**, are the primary effectors of cell-mediated immunity against viral infections. For a CTL to recognize and kill a virally infected cell, the viral antigens must be processed and presented on the cell surface in association with **Class I HLA molecules (HLA-A, B, or C)**. This "MHC restriction" ensures that CD8+ cells specifically target intracellular pathogens. The TCR (T-cell receptor) on the CD8+ cell binds the HLA I-antigen complex, leading to hepatocyte apoptosis via perforins and granzymes. **2. Why incorrect options are wrong:** * **CD4:** This is a surface marker for Helper T cells, which recognize antigens presented by Class II HLA molecules. They coordinate the immune response but do not directly provide the "target" for cytotoxicity. * **CD8:** This is the marker on the effector T cell (the "attacker"), not the glycoprotein on the target hepatocyte. * **Class II HLA molecules:** These are primarily expressed on professional antigen-presenting cells (APCs) like macrophages and B cells, not on hepatocytes. They present exogenous antigens to CD4+ Helper T cells. **Clinical Pearls for NEET-PG:** * **MHC Restriction:** CD8+ = MHC I; CD4+ = MHC II (Rule of 8: 8\u00D71=8; 4\u00D72=8). * **HBV Pathogenesis:** The "ground-glass" appearance of hepatocytes in chronic HBV is due to the accumulation of HBsAg in the endoplasmic reticulum [1]. * **HBeAg:** Its presence signifies high viral replication and high infectivity [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 838-845.
Question 265: Which antibody is known to cross the placenta?
- A. IgG1 (Correct Answer)
- B. IgG4
- C. IgA
- D. IgD
Explanation: **Explanation:** The ability of antibodies to cross the placenta is a crucial mechanism of passive immunity, protecting the fetus and neonate. This transport is mediated by the **neonatal Fc receptor (FcRn)** located on placental syncytiotrophoblasts, which specifically binds the Fc portion of the **IgG** molecule [2]. **1. Why IgG1 is correct:** Among the four subclasses of IgG (IgG1, IgG2, IgG3, and IgG4), **IgG1** is the most efficiently transported across the placenta. While all IgG subclasses cross the placenta to some extent, the efficiency follows the order: **IgG1 > IgG3 > IgG4 > IgG2**. IgG1 is the most abundant subclass and plays a vital role in opsonization and neutralizing toxins. **2. Why the other options are incorrect:** * **IgG4:** While it does cross the placenta, its transport efficiency is lower than that of IgG1. In the context of a single best answer for placental transfer, IgG1 is the superior choice. * **IgA:** This is the primary secretory antibody found in colostrum and breast milk. It does **not** cross the placenta; instead, it provides mucosal immunity to the infant post-delivery via breastfeeding. * **IgD:** This antibody is primarily found on the surface of B-lymphocytes and does not cross the placental barrier. **High-Yield Clinical Pearls for NEET-PG:** * **IgG** is the *only* immunoglobulin class that crosses the placenta (providing "Natural Passive Immunity") [2]. * **IgM** cannot cross the placenta due to its large pentameric size [1], [3]. Therefore, the presence of IgM in a neonate’s blood indicates an **in utero infection** (e.g., TORCH infections), as it represents the fetus's own immune response. * **Rh Incompatibility:** The pathogenesis of Erythroblastosis Fetalis involves maternal **IgG** antibodies (specifically anti-D) crossing the placenta to attack fetal RBCs [1], [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470. [2] 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. 165-167. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.
Question 266: Which of the following cells does HIV primarily affect?
- A. B-cells
- B. Helper T cells (Correct Answer)
- C. Suppressor T-cells
- D. Cytotoxic T-cells
Explanation: ### **Explanation** **Correct Answer: B. Helper T cells** **Mechanism of Action:** The Human Immunodeficiency Virus (HIV) primarily targets cells expressing the **CD4 molecule** on their surface. The viral envelope glycoprotein **gp120** binds with high affinity to the CD4 receptor [2]. While macrophages and dendritic cells also express CD4, the **CD4+ Helper T cells** are the primary targets for viral replication and subsequent destruction [1]. This leads to a progressive decline in the CD4+ T-cell count, resulting in profound immunosuppression (AIDS) [1]. **Analysis of Incorrect Options:** * **A. B-cells:** HIV does not directly infect B-cells as they lack the CD4 receptor. However, B-cell function is indirectly impaired because they require "help" from Helper T cells for effective antibody production and class switching. * **C. Suppressor T-cells & D. Cytotoxic T-cells:** Both of these are **CD8+ T-cells**. HIV does not infect these cells because they do not express the CD4 receptor. In early HIV infection, the number of CD8+ cells may actually increase as the body attempts to control the viral load, leading to an **inverted CD4:CD8 ratio** (normal is ~2:1). **High-Yield Clinical Pearls for NEET-PG:** * **Co-receptors:** Binding requires co-receptors: **CCR5** (found on macrophages/T-cells, important in early infection) and **CXCR4** (found on T-cells, important in late infection) [2]. * **Genetic Resistance:** Individuals with a homozygous **CCR5-Δ32 mutation** are resistant to HIV infection. * **Diagnosis:** The hallmark of progression to AIDS is a **CD4+ T-cell count < 200 cells/mm³**. * **Viral Entry:** **gp120** is for attachment; **gp41** is for fusion and entry [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 253-259. [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. 170-171.
Question 267: Which of the following is NOT a pro-inflammatory cytokine?
- A. IL-1
- B. IL-10 (Correct Answer)
- C. IL-6
- D. TNF Alpha
Explanation: ### Explanation The inflammatory response is tightly regulated by a balance between **pro-inflammatory** and **anti-inflammatory** cytokines [1]. **Why IL-10 is the correct answer:** **IL-10** is a potent **anti-inflammatory cytokine**. Its primary role is to terminate the inflammatory response and prevent tissue damage caused by overactive immunity. It achieves this by: * Inhibiting the synthesis of pro-inflammatory cytokines (like IL-1, IL-6, and TNF). * Downregulating the expression of MHC Class II and co-stimulatory molecules on macrophages and dendritic cells. * Inhibiting the "oxidative burst" in macrophages. **Why the other options are incorrect:** * **IL-1:** A classic pro-inflammatory cytokine produced by macrophages [1]. It induces fever (endogenous pyrogen), activates vascular endothelium, and stimulates the production of acute-phase reactants. * **IL-6:** A major mediator of the acute-phase response [1]. It stimulates the liver to produce C-reactive protein (CRP) and promotes the differentiation of B-cells into plasma cells. * **TNF-Alpha:** The "master regulator" of inflammation [1]. It promotes leukocyte adhesion, activates neutrophils, and in high concentrations, can lead to septic shock and cachexia. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-inflammatory Cytokines:** Remember the mnemonic **"TGF-̢ and IL-10"**—these are the two primary "brakes" of the immune system. * **Pyrogenic Cytokines:** IL-1, IL-6, and TNF-̡ are the primary cytokines responsible for inducing fever [1]. * **IL-8:** Specifically functions as a potent **chemotactic factor** for neutrophils ("Clean up on aisle 8") [1]. * **IL-12:** Essential for the differentiation of T-cells into **Th1 cells**, linking innate and adaptive immunity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-99.
Question 268: Which of the following is NOT a pro-inflammatory cytokine?
- A. IL-8
- B. IL-11
- C. IL-1
- D. PAF (Correct Answer)
Explanation: ### Explanation The core of this question lies in the biochemical classification of inflammatory mediators. While all options listed are involved in the inflammatory process, the question specifically asks for a **cytokine** [1]. **Why PAF is the Correct Answer:** **Platelet-Activating Factor (PAF)** is a potent phospholipid-derived mediator (a lipid mediator), not a cytokine [1]. It is synthesized by the action of phospholipase A2 on membrane phospholipids. While PAF is highly pro-inflammatory—causing platelet aggregation, vasodilation, and bronchoconstriction—it belongs to the same category as prostaglandins and leukotrienes, rather than the polypeptide category of cytokines [1]. **Analysis of Incorrect Options:** * **IL-1 (Interleukin-1):** A classic "master" pro-inflammatory cytokine produced mainly by macrophages [1]. It induces fever (endogenous pyrogen) and stimulates the expression of adhesion molecules on endothelial cells [1]. * **IL-8 (CXCL8):** A major pro-inflammatory chemokine [1]. Its primary role is the recruitment and activation of **neutrophils** at the site of inflammation [1]. * **IL-11:** A pleiotropic cytokine of the IL-6 family. While it has some anti-inflammatory properties in specific contexts, it is traditionally classified as a pro-inflammatory cytokine involved in the acute phase response and megakaryocyte maturation. **High-Yield Clinical Pearls for NEET-PG:** * **Major Pro-inflammatory Cytokines:** TNF-α, IL-1, IL-6, and Chemokines (like IL-8) [1]. * **Major Anti-inflammatory Cytokines:** **IL-10** and **TGF-β** (Frequently tested). * **Acute Phase Response:** Primarily driven by IL-6 (the chief stimulator of CRP production in the liver). * **PAF Source:** Derived from the cell membranes of neutrophils, monocytes, and endothelium via the remodeling pathway. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.
Question 269: What type of ANCA is most commonly associated with Wegener's granulomatosis?
- A. cANCA (Correct Answer)
- B. pANCA
- C. Both
- D. None
Explanation: **Wegener’s Granulomatosis** (now officially known as **Granulomatosis with Polyangiitis or GPA**) is a small-vessel vasculitis characterized by a triad of necrotizing granulomas of the respiratory tract, necrotizing vasculitis, and focal necrotizing glomerulonephritis [1]. 1. **Why cANCA is correct:** The hallmark laboratory finding in GPA is the presence of **cANCA (cytoplasmic Antineutrophil Cytoplasmic Antibody)** [1]. On immunofluorescence, cANCA shows a diffuse granular cytoplasmic staining pattern. The primary target antigen for cANCA is **Proteinase-3 (PR3)**, a constituent of neutrophil primary granules. It is highly specific (approx. 95%) for GPA, especially when the disease is active. 2. **Why other options are incorrect:** * **pANCA (perinuclear ANCA):** This pattern shows staining around the nucleus and targets the enzyme **Myeloperoxidase (MPO)**. While pANCA is associated with other vasculitides like **Microscopic Polyangiitis (MPA)** and **Churg-Strauss Syndrome (EGPA)**, it is not the primary marker for GPA [1]. * **Both/None:** These are incorrect because the association between cANCA and GPA is distinct and diagnostic in the context of clinical symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Target Antigen:** cANCA = Anti-PR3; pANCA = Anti-MPO. * **Clinical Triad of GPA:** Upper Respiratory Tract (sinusitis/saddle nose deformity), Lower Respiratory Tract (hemoptysis/cavitation), and Kidneys (RPGN). * **Biopsy Gold Standard:** Shows "geographic necrosis" and poorly formed granulomas. * **Monitoring:** ANCA titers often correlate with disease activity; a rise in titers may predict a relapse. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918.
Question 270: Secondary amyloidosis is a complication of which condition?
- A. Rheumatoid arthritis (Correct Answer)
- B. Plasmacytosis
- C. Multiple myeloma
- D. None of the above
Explanation: **Explanation:** **1. Why Rheumatoid Arthritis (RA) is correct:** Secondary amyloidosis (also known as **AA Amyloidosis**) occurs as a complication of chronic inflammatory conditions, chronic infections, or certain malignancies [1]. In RA, persistent inflammation leads to the sustained release of **Interleukin-1 (IL-1) and Interleukin-6 (IL-6)**. These cytokines stimulate hepatocytes to produce **Serum Amyloid-Associated (SAA) protein**, an acute-phase reactant [3]. Prolonged elevation of SAA leads to its limited proteolysis, forming AA amyloid fibrils that deposit in organs like the kidneys, liver, and spleen [1]. **2. Why the other options are incorrect:** * **Multiple Myeloma & Plasmacytosis:** These are associated with **Primary Amyloidosis (AL Amyloidosis)**. In these plasma cell dyscrasias, there is an overproduction of monoclonal immunoglobulin light chains (usually Lambda). These light chains undergo proteolysis to form AL amyloid fibrils [1]. While they are "secondary" to a disease process, in medical classification, they are strictly categorized as Primary (AL) Amyloidosis. **3. NEET-PG High-Yield Pearls:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red**. * **Most Common Cause:** Globally, RA is the most common cause of AA amyloidosis [1],[2]. In developing countries, chronic infections like Tuberculosis and Bronchiectasis remain significant causes [1]. * **Organ Involvement:** The **Kidney** is the most common and earliest organ involved in AA amyloidosis, often presenting as nephrotic syndrome [1]. * **Precursor Protein:** Remember the mnemonic: **AA** = **A**ssociated with **A**cute phase reactant (SAA); **AL** = **L**ight chains [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. 136-140. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 678-679. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 267-268.
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