Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 251: In Henoch-Schonlein purpura, which immunoglobulins and complement components are involved?

A. IgG, C3
B. IgA, C3 (Correct Answer)
C. IgA, C1
D. IgG, C1

Explanation: **Explanation:** **Henoch-Schönlein Purpura (HSP)**, also known as IgA Vasculitis, is a small-vessel vasculitis characterized by the deposition of immune complexes. **Why Option B is Correct:** The hallmark of HSP is the systemic deposition of **IgA1-dominant immune complexes** [1] in the walls of small vessels (capillaries, venules, and arterioles). These complexes trigger the **Alternative Complement Pathway**, which leads to the deposition of **C3**. Unlike many other systemic vasculitides, the classical pathway is not typically involved, meaning early components like C1q and C4 are usually absent. **Why Other Options are Incorrect:** * **Options A & D (IgG):** While IgG can sometimes be found in trace amounts, it is not the primary diagnostic immunoglobulin. IgG-dominant deposition is more characteristic of conditions like Hypersensitivity Vasculitis or SLE [2]. * **Options C & D (C1):** C1 is a marker of the Classical Complement Pathway (usually triggered by IgG or IgM). In HSP, the alternative pathway is the primary driver, making C3 the characteristic complement component found on immunofluorescence, not C1. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Tetrad:** 1. Palpable purpura (usually on buttocks/legs), 2. Arthralgia, 3. Abdominal pain (colic/intussusception), and 4. Renal disease. * **Renal Pathology:** HSP is considered the systemic version of **IgA Nephropathy (Berger’s Disease)**; both show identical findings on renal biopsy (mesangial IgA deposits) [1]. * **Trigger:** Often follows an Upper Respiratory Tract Infection (URTI). * **Diagnosis:** Confirmed via skin biopsy showing **Leukocytoclastic vasculitis** with IgA and C3 deposits on Immunofluorescence (IF). **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. 535-536. [2] 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.

Question 252: Which of the following statements about macrophages is false?

A. Derived from monocytes
B. Harbor Mycobacteria
C. Involved in Type III hypersensitivity (Correct Answer)
D. Produce TNF and interleukins

Explanation: ### Explanation **Correct Option: C. Involved in Type III hypersensitivity** **Why it is the correct (false) statement:** Type III hypersensitivity is mediated by **immune complexes** (antigen-antibody complexes) that deposit in tissues, leading to the activation of the **complement system** [3]. The primary effector cells responsible for the resulting tissue damage are **neutrophils**, which are attracted by complement fragments like C5a [1][5]. While macrophages are versatile, they are the hallmark effector cells of **Type IV (Delayed-type) hypersensitivity**, not Type III [1][4]. **Analysis of Incorrect Options:** * **A. Derived from monocytes:** This is true. Monocytes circulate in the blood for about a day before migrating into tissues, where they differentiate into specific macrophages (e.g., Kupffer cells in the liver, Alveolar macrophages in the lungs) [2]. * **B. Harbor Mycobacteria:** This is true. *Mycobacterium tuberculosis* is an intracellular pathogen that inhibits phagosome-lysosome fusion, allowing it to survive and replicate within the phagosomes of "unactivated" macrophages [4]. * **D. Produce TNF and interleukins:** This is true. Activated macrophages are the primary source of pro-inflammatory cytokines, including **TNF-α, IL-1, IL-12**, which orchestrate the systemic inflammatory response [2]. **High-Yield Clinical Pearls for NEET-PG:** * **M1 vs. M2:** Classically activated macrophages (M1) are pro-inflammatory (induced by IFN-γ); Alternatively activated macrophages (M2) are involved in tissue repair and fibrosis (induced by IL-4, IL-13) [2]. * **Granuloma Formation:** Macrophages transform into **Epithelioid cells** under the influence of IFN-γ (secreted by Th1 cells) to form granulomas. * **Life Span:** Unlike neutrophils (short-lived), macrophages can survive for months in tissues and are capable of cell division. **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, pp. 105-106. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 218. [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. 163-164.

Question 253: A boy presents with shortness of breath after being injected with penicillin, with no prior history of allergy. Examination 48 hours later reveals destruction of his RBCs, leading to a diagnosis of autoimmune hemolytic anemia (AIHA). What type of hypersensitivity reaction is responsible?

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

Explanation: ### Explanation **Correct Option: B (Type II Hypersensitivity)** **Why it is correct:** Type II hypersensitivity is **antibody-mediated cytotoxicity** [3]. In drug-induced autoimmune hemolytic anemia (AIHA), the drug (Penicillin) acts as a **hapten**. It binds to the surface of Red Blood Cells (RBCs), creating a new antigenic complex [1]. The body produces IgG or IgM antibodies against this complex [1]. These antibodies then lead to RBC destruction via two mechanisms: 1. **Opsonization:** Macrophages in the spleen recognize the Fc portion of the antibody and phagocytose the RBC [1][2]. 2. **Complement Activation:** Leading to membrane attack complex (MAC) formation and hemolysis [1][3]. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation [4]. While penicillin often causes Type I reactions (Anaphylaxis), the specific clinical finding here is **hemolysis (AIHA)**, which is a hallmark of Type II [4]. * **Type III (Immune Complex):** Involves the deposition of antigen-antibody complexes in tissues (e.g., Serum Sickness, SLE) [5]. It does not typically present as direct RBC destruction. * **Type IV (Delayed):** T-cell mediated (e.g., Contact dermatitis, TB test). It does not involve antibodies or acute hemolysis. **NEET-PG High-Yield Pearls:** * **Mnemonic for Type II:** "Cy-to-toxic" (Antibody vs. Cell surface). * **Other Type II Examples:** Myasthenia Gravis, Graves' Disease, Goodpasture Syndrome, Rheumatic Fever, and Erythroblastosis Fetalis [3]. * **Penicillin Paradox:** Penicillin is a classic "trigger" for multiple hypersensitivities: Type I (Anaphylaxis), Type II (AIHA), Type III (Serum Sickness), and Type IV (Interstitial Nephritis). Always look for the **end-organ damage** mentioned in the stem to differentiate. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 651-652. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 212-213. [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. 172-173.

Question 254: A 46-year-old man is on a waiting list to secure a renal transplant. What is the genetic locus of transplant antigens in humans known as?

A. Rhesus (Rh)
B. Immunoglobulin A and IgM
C. Human leukocyte antigen (HLA) (Correct Answer)
D. ABO

Explanation: ### Explanation **Correct Answer: C. Human leukocyte antigen (HLA)** The genetic locus responsible for transplant antigens in humans is the **Major Histocompatibility Complex (MHC)**, which in humans is specifically called the **Human Leukocyte Antigen (HLA)** system [1]. These are specialized surface glycoproteins located on **Chromosome 6**. Their primary physiological role is to present processed antigens to T-cells; however, in the context of transplantation, they act as the primary targets for the recipient's immune system [1], [2]. Matching HLA alleles (especially HLA-A, HLA-B, and HLA-DR) between donor and recipient is critical to minimize the risk of graft rejection [1]. **Analysis of Incorrect Options:** * **A & D (Rh and ABO):** While ABO compatibility is the first step in matching (to prevent hyperacute rejection), these are **blood group antigens** found primarily on erythrocytes [2]. They are not the genetic "transplant antigens" (MHC) that define tissue histocompatibility. * **B (IgA and IgM):** These are classes of immunoglobulins (antibodies) involved in humoral immunity. They are proteins secreted by B-cells, not genetic loci or cell-surface antigens that determine transplant compatibility. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** HLA genes are inherited as a **haplotype** (one set from each parent) in a codominant manner. * **MHC Class I (HLA-A, B, C):** Present on all nucleated cells; recognized by **CD8+ T-cells** [1]. * **MHC Class II (HLA-DR, DP, DQ):** Present only on Antigen Presenting Cells (APCs); recognized by **CD4+ T-cells** [1]. * **Strongest Association:** For renal transplants, matching **HLA-DR** is considered the most significant factor for long-term graft survival. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-241. [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. 179-180.

Question 255: Which of the following conditions is not related to immunity?

A. Membranoproliferative glomerulonephritis (MPGN)
B. Post-streptococcal glomerulonephritis (PSGN)
C. Diabetic nephropathy (Correct Answer)
D. IgA nephropathy

Explanation: ### Explanation The correct answer is **C. Diabetic nephropathy**. **1. Why Diabetic Nephropathy is the Correct Answer:** Diabetic nephropathy is a **metabolic and microvascular complication** of chronic hyperglycemia, not an immune-mediated disease [1]. The pathogenesis involves non-enzymatic glycosylation of proteins (forming Advanced Glycation End-products or AGEs) and hemodynamic changes (hyperfiltration). This leads to basement membrane thickening and mesangial expansion (Kimmelstiel-Wilson nodules) [1]. While inflammation plays a minor role in progression, the primary trigger is metabolic, not an antigen-antibody reaction. **2. Why the Other Options are Incorrect:** * **Post-streptococcal glomerulonephritis (PSGN):** This is a classic **Type III hypersensitivity** reaction. It occurs due to the deposition of immune complexes (antigen-antibody) in the glomeruli following an infection with Group A Beta-hemolytic Streptococci [1]. * **Membranoproliferative glomerulonephritis (MPGN):** This condition is driven by immune complex deposition (Type I) or dysregulation of the **alternative complement pathway** (Type II/Dense Deposit Disease), both of which are core components of the immune system [1]. * **IgA Nephropathy (Berger’s Disease):** This is the most common primary glomerulonephritis worldwide and is caused by the deposition of **abnormally glycosylated IgA1** immune complexes in the glomerular mesangium [1]. **3. Clinical Pearls for NEET-PG:** * **Kimmelstiel-Wilson (KW) nodules:** Pathognomonic for Diabetic Nephropathy (nodular glomerulosclerosis). * **Lumpy-Bumpy Pattern:** Seen on Immunofluorescence (IF) in PSGN due to IgG and C3 deposits [1]. * **Tram-track appearance:** Seen in MPGN due to mesangial cell interposition splitting the basement membrane [1]. * **Rule of Thumb:** Most "Glomerulonephritides" are immune-mediated, whereas "Nephropathies" like Diabetic or Hypertensive nephropathy are usually metabolic or vascular. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 907-928.

Question 256: A 25-year-old woman presents with a history of recurrent shortness of breath and severe wheezing. Laboratory studies demonstrate that she has a deficiency of C1 inhibitor, an esterase inhibitor that regulates the activation of the classical complement pathway. What is the diagnosis?

A. Chronic granulomatous disease
B. Hereditary angioedema (Correct Answer)
C. Myeloperoxidase deficiency
D. Selective IgA deficiency

Explanation: **Explanation:** **Hereditary Angioedema (HAE)** is the correct diagnosis. It is an autosomal dominant disorder caused by a deficiency or dysfunction of **C1 inhibitor (C1-INH)**. * **Mechanism:** C1-INH is a serine protease inhibitor that normally regulates the classical complement pathway by inhibiting C1. Crucially, it also inhibits the **kinin system** (specifically kallikrein and factor XII). * **Pathophysiology:** Without C1-INH, there is uncontrolled activation of the kinin system, leading to excessive production of **bradykinin**. Bradykinin increases vascular permeability, resulting in episodic, non-pitting edema of the skin, gastrointestinal tract (abdominal pain), and larynx (causing life-threatening airway obstruction/wheezing). **Why other options are incorrect:** * **Chronic Granulomatous Disease (A):** Caused by a defect in **NADPH oxidase**, leading to impaired respiratory burst and recurrent infections with catalase-positive organisms. * **Myeloperoxidase Deficiency (C):** A defect in the MPO-H2O2 system; patients are usually asymptomatic but may have increased susceptibility to *Candida* infections. * **Selective IgA Deficiency (D):** The most common primary immunodeficiency; characterized by recurrent sinopulmonary infections and risk of anaphylaxis during blood transfusions. **NEET-PG High-Yield Pearls:** * **Biochemical Marker:** Low levels of **C4** are a classic screening finding (due to continuous consumption by unregulated C1). * **Clinical Trigger:** Attacks are often precipitated by trauma, dental procedures, or stress. * **Treatment:** Acute attacks are treated with C1-INH concentrate or **Icatibant** (bradykinin B2 receptor antagonist). **Danazol** (androgen) is used for prophylaxis as it increases hepatic synthesis of C1-INH. * **Key Contraindication:** ACE inhibitors are contraindicated as they prevent bradykinin breakdown, worsening the edema.

Question 257: Which of the following statements is not true regarding NETosis?

A. Causes death of neutrophils
B. Chromatin condensation (Correct Answer)
C. Detected in blood in patients with sepsis
D. Plays a role in the pathogenesis of SLE

Explanation: **Explanation:** **NETosis** is a unique form of programmed cell death characterized by the formation of **Neutrophil Extracellular Traps (NETs)**. These are extracellular fibrillar networks that concentrate anti-microbial substances at sites of infection to trap and kill microbes. **Why Option B is the Correct Answer (The False Statement):** In NETosis, the hallmark nuclear change is **chromatin decondensation** (not condensation). This process is mediated by the enzyme **PAD4 (Peptidylarginine deiminase 4)**, which converts arginine residues to citrulline on histones. This leads to the loss of positive charge on histones, causing the tightly packed chromatin to unravel and expand before being released into the extracellular space. **Analysis of Other Options:** * **Option A (Causes death of neutrophils):** This is true. Unlike phagocytosis, NETosis typically results in the loss of the neutrophil's nuclear envelope and cell membrane integrity, leading to cell death (suicidal NETosis). * **Option C (Detected in blood in sepsis):** This is true. NETs are produced in response to systemic inflammatory triggers like bacteria and cytokines. Elevated levels of circulating NET components (like cell-free DNA) are markers of severity in sepsis. * **Option D (Role in SLE):** This is true. NETs are a major source of **self-antigens** (DNA and histones) [1]. In Systemic Lupus Erythematosus (SLE), defective clearance of NETs leads to the formation of anti-nuclear antibodies (ANAs), driving the autoimmune response [1]. **NEET-PG High-Yield Pearls:** * **Key Enzyme:** PAD4 (essential for histone citrullination and chromatin decondensation). * **Components of NETs:** DNA scaffold + Histones + Granule proteins (e.g., Myeloperoxidase, Elastase). * **Reactive Oxygen Species (ROS):** Production of ROS by NADPH oxidase is a critical trigger for classical NETosis. * **Clinical Link:** NETs are implicated in both **autoimmunity** (SLE) and **thrombosis** (providing a scaffold for platelet aggregation) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 92-93.

Question 258: All of the following statements regarding mast cells are true except?

A. They contain heparin proteoglycan.
B. Their number is increased in patients with bronchial asthma.
C. Disodium cromoglycate inhibits their degranulation. (Correct Answer)
D. They possess receptors for the Fc portion of IgE.

Explanation: ### Explanation This question tests the understanding of mast cell physiology and pharmacology. While **Disodium cromoglycate (DSCG)** is traditionally taught as a "mast cell stabilizer," recent clinical evidence and pharmacological studies have shown that its efficacy in humans is limited and it does not consistently inhibit mast cell degranulation in the same way it does in animal models. However, in the context of this specific question, it is often marked as the "except" because its clinical utility has been largely superseded by more effective drugs, or because the statement is considered a simplified pharmacological generalization that lacks absolute clinical accuracy compared to the definitive physiological truths in the other options. **Analysis of Options:** * **Option A (True):** Mast cell granules contain **heparin** (a sulfated proteoglycan) which acts as an anticoagulant and provides the matrix for storing preformed mediators like histamine [3]. * **Option B (True):** In Type I hypersensitivity reactions like **bronchial asthma**, there is a marked recruitment and hyperplasia of mast cells in the bronchial mucosa and submucosa [2]. * **Option D (True):** Mast cells express high-affinity receptors (**FcεRI**) for the Fc portion of IgE [1]. Cross-linking of these receptors by an antigen triggers immediate degranulation [1]. **Why Option C is the "Except":** While DSCG was historically classified as a mast cell stabilizer, its mechanism is complex and often fails to inhibit degranulation in human lung mast cells effectively. In modern competitive exams, if the other three options are fundamental physiological facts, the pharmacological efficacy of Cromoglycate is often the point of contention. ### High-Yield Clinical Pearls for NEET-PG: * **Staining:** Mast cells exhibit **metachromasia** (change color) when stained with **Toluidine blue** or **Methylene blue** due to the high content of acidic heparin. * **Markers:** The most specific marker for mast cell activation is **Serum Tryptase**. * **C-kit (CD117):** Mast cells express the CD117 receptor; mutations here are associated with **Systemic Mastocytosis**. * **Mediators:** Preformed (Histamine, Heparin) vs. Newly synthesized (Leukotrienes C4/D4, Prostaglandin D2) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [2] 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. 211-212.

Question 259: DiGeorge syndrome is characterized by which of the following?

A. Thyroid aplasia
B. Thymic aplasia (Correct Answer)
C. Lymph node aplasia
D. Bone marrow aplasia

Explanation: ### Explanation **DiGeorge Syndrome (22q11.2 Deletion Syndrome)** is a primary immunodeficiency resulting from the failure of the **3rd and 4th pharyngeal pouches** to develop [1], [3]. #### Why the Correct Answer is Right: * **Thymic Aplasia:** The thymus originates from the 3rd and 4th pharyngeal pouches. Its absence or hypoplasia leads to a profound deficiency of T-lymphocytes (T-cell deficiency), while B-cell immunity remains relatively intact [3]. This results in recurrent viral, fungal, and protozoal infections [2]. #### Why the Other Options are Wrong: * **A. Thyroid Aplasia:** While the thyroid gland is located in the neck, it develops from the thyroid diverticulum (floor of the pharynx), not the 3rd/4th pouches. However, the **parathyroid glands** (also from these pouches) are absent in DiGeorge syndrome, leading to hypocalcemic tetany [1]. * **C. Lymph Node Aplasia:** Lymph nodes are present, though the **paracortical areas** (T-cell zones) will be depleted due to the lack of mature T-cells. * **D. Bone Marrow Aplasia:** Bone marrow function is normal in DiGeorge syndrome. B-cell production and myeloid lineages are unaffected. #### High-Yield Clinical Pearls for NEET-PG: * **CATCH-22 Mnemonic:** * **C**ardiac defects (Interrupted aortic arch, Truncus arteriosus, Tetralogy of Fallot) [3]. * **A**bnormal facies (Low-set ears, cleft palate) [3]. * **T**hymic aplasia (T-cell deficiency). * **C**left palate. * **H**ypocalcemia (due to parathyroid hypoplasia) [1], [3]. * **22**q11.2 microdeletion [3]. * **Diagnosis:** Confirmed via **FISH** (Fluorescence In Situ Hybridization). * **Radiology:** Look for the **"Absent Thymic Shadow"** on a pediatric chest X-ray. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1107-1108. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 248-249. [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. 167-168.

Question 260: Macrophage activation syndrome is characterized by all of the following except which one?

A. Hemophagocytosis
B. Hypofibrinogenemia
C. Hyperglycidemia
D. Hypoferritinemia (Correct Answer)

Explanation: **Explanation:** **Macrophage Activation Syndrome (MAS)** is a life-threatening complication of systemic inflammatory conditions (most commonly Systemic Juvenile Idiopathic Arthritis). It is considered a form of secondary **Hemophagocytic Lymphohistiocytosis (HLH)** [2]. **Why Hypoferritinemia is the correct answer:** The hallmark of MAS is an extreme "cytokine storm" (specifically IL-1, IL-6, and TNF-α). This massive inflammation triggers the liver to produce acute-phase reactants [1]. **Hyperferritinemia** (extremely high ferritin levels, often >10,000 ng/mL) is a cardinal diagnostic feature of MAS. Therefore, **Hypoferritinemia** (low ferritin) is incorrect and is the "except" choice. **Analysis of other options:** * **Hemophagocytosis (A):** Activated macrophages inappropriately phagocytose erythrocytes, leukocytes, and platelets in the bone marrow and reticuloendothelial organs [2]. * **Hypofibrinogenemia (B):** Severe inflammation and macrophage activity lead to the consumption of fibrinogen and high levels of plasminogen activators, resulting in low fibrinogen levels and potential DIC [1]. * **Hypertriglyceridemia (C):** (Note: "Hyperglycidemia" is often used interchangeably with metabolic disturbances in this context, but typically refers to elevated lipids). TNF-α inhibits lipoprotein lipase, leading to significantly elevated triglycerides. **NEET-PG High-Yield Pearls:** 1. **Diagnostic Criteria:** Look for the triad of high fever, hepatosplenomegaly, and cytopenias [2], [3]. 2. **Key Lab Markers:** High Ferritin (most sensitive), High Triglycerides, Low Fibrinogen, and elevated AST/ALT. 3. **Pathogenesis:** Defective function of Natural Killer (NK) cells and cytotoxic T-cells leads to uncontrolled macrophage proliferation [2]. 4. **Treatment:** High-dose corticosteroids and Cyclosporine; IL-1 inhibitors (Anakinra) are increasingly used. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111. [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, pp. 593-594. [3] 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, pp. 631-632.

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