Immunopathology — MCQs
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Hematoxylin bodies are seen in which of the following conditions?
Which of the following statements regarding Wiskott-Aldrich syndrome is TRUE?
A 12-year-old boy presents with a 5-day history of sore throat. His temperature is 38.7°C (103°F). Physical examination reveals inflamed tonsils and swollen cervical lymph nodes. Trafficking and recirculation of blood-borne lymphocytes through the cervical lymph nodes in this patient occurs primarily at which of the following locations?
Severe combined immunodeficiency is seen with which precursor cell type?
Which of the following is found in DiGeorge syndrome?
Myasthenia gravis is associated with which of the following?
What condition is characterized by the pathognomonic lesion known as a tophus?
Which immunoglobulin has the highest molecular weight?
Graft between members of the same species but of different genetic constitution is known as:
A patient presents with a history of episodic painful edema of the face and larynx, associated with abdominal pain, particularly during periods of stress. Which of the following is likely to be deficient?
Immunopathology Indian Medical PG Practice Questions and MCQs
Question 201: Hematoxylin bodies are seen in which of the following conditions?
- A. Systemic Lupus Erythematosus (SLE) (Correct Answer)
- B. Polyarteritis Nodosa (PAN)
- C. Disseminated Intravascular Coagulation (DIC)
- D. Wegener's Granulomatosis
Explanation: **Explanation:** **Hematoxylin bodies** (also known as **Gross bodies**) are the only pathognomonic histological feature of **Systemic Lupus Erythematosus (SLE)**. 1. **Why SLE is correct:** The underlying mechanism involves **Type II and Type III hypersensitivity**. In SLE, antinuclear antibodies (ANAs) attack the nuclei of damaged cells [1]. This interaction causes the chromatin to denature, forming a homogenous, smudgy, purplish-blue mass known as a Hematoxylin body [2]. These bodies are essentially the tissue equivalent of the **LE cell** found in blood or bone marrow (which is a neutrophil that has ingested a hematoxylin body) [2]. They are most commonly found in the heart (Libman-Sacks endocarditis), kidneys, and lymph nodes. 2. **Why other options are incorrect:** * **Polyarteritis Nodosa (PAN):** Characterized by **fibrinoid necrosis** of medium-sized arteries. It does not involve the specific ANA-induced nuclear denaturation seen in SLE. * **DIC:** A consumptive coagulopathy characterized by widespread **microthrombi** (fibrin clots) in small vessels, not nuclear degradation products. * **Wegener’s Granulomatosis (GPA):** Defined by a triad of necrotizing granulomas, vasculitis, and glomerulonephritis. The hallmark is **c-ANCA** positivity, not hematoxylin bodies. **High-Yield Clinical Pearls for NEET-PG:** * **LE Cell:** A neutrophil that has engulfed a denatured nucleus [2]. While classic, it is now rarely used for diagnosis (replaced by ANA titers). * **Wire-loop lesions:** Seen in Lupus Nephritis (Class IV) due to subendothelial immune complex deposits [3]. * **Libman-Sacks Endocarditis:** Characterized by small, sterile vegetations on *both* sides of the heart valves. * **Onion-skin lesions:** Concentric splenic arterial fibrosis seen in SLE. **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. 230. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 232.
Question 202: Which of the following statements regarding Wiskott-Aldrich syndrome is TRUE?
- A. Primary defect is a B cell defect.
- B. Primary defect is a T cell defect.
- C. Associated with WASP gene mutation. (Correct Answer)
- D. Defect in phagocytosis.
Explanation: **Explanation:** **Wiskott-Aldrich Syndrome (WAS)** is an X-linked recessive primary immunodeficiency characterized by the triad of **thrombocytopenia (with small platelets), eczema, and recurrent infections.** 1. **Why Option C is Correct:** The primary defect lies in a mutation of the **WASP gene** located on the short arm of the X chromosome (Xp11.23) [1]. This gene encodes the **Wiskott-Aldrich Syndrome Protein (WASP)**, which is expressed in hematopoietic cells. WASP is a key regulator of the **actin cytoskeleton**. Defective WASP leads to impaired assembly of actin filaments, which are essential for cell signaling, migration, and the formation of the "immunological synapse" between T cells and antigen-presenting cells [1]. 2. **Why Other Options are Incorrect:** * **Options A & B:** WAS is not primarily a B-cell or T-cell defect in isolation; it is a **combined immunodeficiency**. While both cell types are affected, the root cause is the cytoskeletal protein defect, not a primary failure of lymphocyte maturation (like in XLA or DiGeorge syndrome). * **Option D:** While the actin defect can affect the movement of phagocytes, the hallmark of the disease is the failure of lymphocyte activation and platelet production, rather than a primary defect in the phagocytic machinery (like Chronic Granulomatous Disease). **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked Recessive (mostly affects males). * **Platelet Morphology:** Unique finding of **microthrombocytopenia** (small platelets with low counts). This is a classic "buzzword" for WAS. * **Laboratory Findings:** Characteristically shows **Low IgM**, Normal/High IgG, and **Elevated IgA and IgE** [1]. * **Mnemonic (WATER):** **W**iskott-**A**ldrich, **T**hrombocytopenia, **E**czema, **R**ecurrent infections. * **Complications:** Increased risk of B-cell lymphomas and autoimmune hemolytic anemia [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 250-251.
Question 203: A 12-year-old boy presents with a 5-day history of sore throat. His temperature is 38.7°C (103°F). Physical examination reveals inflamed tonsils and swollen cervical lymph nodes. Trafficking and recirculation of blood-borne lymphocytes through the cervical lymph nodes in this patient occurs primarily at which of the following locations?
- A. Afferent lymphatic vessel
- B. Efferent lymphatic vessel
- C. Hassall corpuscles
- D. High endothelial venules (Correct Answer)
Explanation: ### Explanation **Correct Option: D. High Endothelial Venules (HEVs)** The patient is presenting with acute tonsillitis and reactive lymphadenopathy. The primary site for the entry of circulating (blood-borne) lymphocytes into the lymph node parenchyma is the **High Endothelial Venule (HEV)** [1]. HEVs are specialized post-capillary venous swellings found in the **paracortex** of lymph nodes [2] (and other secondary lymphoid organs like Peyer’s patches, but not the spleen). They are lined by plump, cuboidal endothelial cells rather than the typical flat endothelium. These cells express specific adhesion molecules called **addressins** (e.g., PNAd) that bind to L-selectin on naive T and B cells, facilitating their "homing" and extravasation from the blood into the lymphoid tissue [1]. **Analysis of Incorrect Options:** * **A. Afferent lymphatic vessel:** These vessels carry lymph and **antigen-presenting cells** (like dendritic cells) from the peripheral tissues into the subcapsular sinus of the lymph node, not blood-borne lymphocytes [1]. * **B. Efferent lymphatic vessel:** This is the exit route for lymphocytes to return to the systemic circulation via the thoracic duct [1]. It is not the site of entry for blood-borne cells. * **C. Hassall corpuscles:** These are concentric epithelial structures found in the **thymus medulla**, not in lymph nodes. They are involved in T-cell maturation, not lymphocyte trafficking during an infection. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** HEVs are located in the **paracortex** (the T-cell zone) [2]. * **Morphology:** Cuboidal/Plump endothelium (unique for venules). * **Molecular Mechanism:** L-selectin (on lymphocyte) + CD34/GlyCAM-1 (on HEV) = Rolling. LFA-1 (on lymphocyte) + ICAM-1 (on HEV) = Firm Adhesion/Diapedesis. * **Exception:** The **Spleen** does not have HEVs; lymphocytes enter the spleen through the marginal zone sinuses. **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. 160-161. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 553-554.
Question 204: Severe combined immunodeficiency is seen with which precursor cell type?
- A. Pre-B cell
- B. Pre-T cell
- C. Both Pre-B and Pre-T cells (Correct Answer)
- D. NK cell precursor
Explanation: **Explanation:** Severe Combined Immunodeficiency (SCID) is a heterogeneous group of genetic disorders characterized by the **failure of both humoral (B-cell) and cell-mediated (T-cell) immunity** [1]. The fundamental defect in SCID occurs at the level of the **common lymphoid progenitor** or the early differentiation stages of **Pre-B and Pre-T cells** [1]. Because these precursor cells fail to mature, the patient lacks functional peripheral T-lymphocytes and B-lymphocytes. The most common molecular causes include: 1. **X-linked SCID:** Mutation in the γ-chain of cytokine receptors (IL-2, IL-4, IL-7, etc.), halting T-cell and NK-cell maturation [1]. 2. **Autosomal Recessive SCID:** Most commonly due to **Adenosine Deaminase (ADA) deficiency**, which leads to the accumulation of metabolites toxic to both immature B and T-cell precursors [1]. **Analysis of Options:** * **Option A & B:** While both are affected, selecting only one is incomplete. SCID, by definition, involves a "combined" deficit. A defect isolated to Pre-B cells would result in Agammaglobulinemia (e.g., Bruton’s), while an isolated T-cell defect (e.g., DiGeorge Syndrome) is not classified as SCID. * **Option D:** NK cell precursors are often affected in X-linked SCID, but the clinical hallmark of the disease is the combined loss of adaptive immunity (B and T cells) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** The thymus is **hypoplastic/dysplastic** (fetal appearance) and lymph nodes lack germinal centers. * **Clinical Presentation:** Recurrent "opportunistic" infections (Candidiasis, *Pneumocystis jirovecii*, CMV) and failure to thrive within the first few months of life. * **Treatment:** SCID is a pediatric emergency; the definitive treatment is **Hematopoietic Stem Cell Transplantation (HSCT)**. * **Radiology:** Absence of a thymic shadow on a chest X-ray is a classic finding. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 246-249.
Question 205: Which of the following is found in DiGeorge syndrome?
- A. Tetany (Correct Answer)
- B. Eczema
- C. Total absence of T cells
- D. Absent B and T cells
Explanation: **Explanation:** **DiGeorge Syndrome (22q11.2 Deletion Syndrome)** results from a failure in the development of the **3rd and 4th pharyngeal pouches** [2]. This leads to a classic triad of thymic hypoplasia, parathyroid hypoplasia, and congenital heart defects (CATCH-22) [1]. 1. **Why Tetny is Correct:** The failure of the 3rd and 4th pharyngeal pouches leads to **parathyroid hypoplasia**. This causes a deficiency in Parathyroid Hormone (PTH), resulting in **hypocalcemia**. Low serum calcium levels increase neuromuscular excitability, manifesting clinically as **tetany**, seizures, or positive Chvostek/Trousseau signs [1]. 2. **Why Incorrect Options are Wrong:** * **Eczema:** This is a hallmark of **Wiskott-Aldrich Syndrome** (triad: eczema, thrombocytopenia, and recurrent infections), not DiGeorge syndrome. * **Total absence of T cells:** While there is T-cell deficiency due to thymic hypoplasia, it is rarely a "total" absence. Most patients have "Partial DiGeorge Syndrome" with some residual T-cell function [2]. Total absence is more characteristic of Severe Combined Immunodeficiency (SCID) [2]. * **Absent B and T cells:** This describes **SCID** (e.g., ADA deficiency or IL-2RG mutation). In DiGeorge, B-cell numbers are typically normal, though their function (antibody production) may be impaired due to a lack of T-cell help. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic CATCH-22:** **C**ardiac defects (Truncus arteriosus/TOF), **A**bnormal facies, **T**hymic hypoplasia, **C**left palate, **H**ypocalcemia/Hypoparathyroidism, due to **22**q11 deletion [2]. * **Radiology:** Look for the **"Absent Thymic Shadow"** on a pediatric chest X-ray. * **Immunology:** Patients are susceptible to viral, fungal, and protozoal infections due to T-cell deficiency. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1107-1108. [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. 167-168.
Question 206: Myasthenia gravis is associated with which of the following?
- A. Hypergammaglobulinemia
- B. Thymoma (Correct Answer)
- C. Squamous cell carcinoma
- D. Hepatic adenoma
Explanation: **Explanation:** **Myasthenia Gravis (MG)** is an autoimmune neuromuscular disorder characterized by muscle weakness and fatigability caused by autoantibodies against the **postsynaptic acetylcholine receptors (AChR)** at the neuromuscular junction [1], [2]. **Why Thymoma is the Correct Answer:** The thymus plays a central role in the pathogenesis of MG. Approximately **75% of MG patients** have thymic abnormalities. Of these, 65% show **thymic follicular hyperplasia** (germinal centers in the medulla), and **10-15% have a Thymoma** (a tumor of the thymic epithelial cells). The thymus is believed to be the site where self-tolerance is lost, leading to the production of AChR antibodies. **Analysis of Incorrect Options:** * **A. Hypergammaglobulinemia:** While MG is antibody-mediated, it does not typically present with a generalized increase in all gamma globulins (unlike conditions like Multiple Myeloma or Sarcoidosis). * **C. Squamous cell carcinoma:** This is not classically associated with MG. However, **Small Cell Carcinoma of the lung** is strongly associated with **Lambert-Eaton Myasthenic Syndrome (LEMS)**, which is the primary differential diagnosis for MG [3]. * **D. Hepatic adenoma:** This is a benign liver tumor associated with oral contraceptive use and has no clinical link to MG. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Type II Hypersensitivity reaction [1]. * **Clinical Feature:** Ptosis and diplopia (extraocular muscle involvement) are often the earliest signs [3]. Weakness worsens with activity and improves with rest. * **Diagnosis:** Edrophonium (Tensilon) test (historically), Ice pack test, and repetitive nerve stimulation (shows **decremental response**). * **Management:** Acetylcholinesterase inhibitors (Pyridostigmine) and **Thymectomy** (often curative or leads to remission even in the absence of a tumor). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 733-734.
Question 207: What condition is characterized by the pathognomonic lesion known as a tophus?
- A. Multiple myeloma
- B. Cystinosis
- C. Gout (Correct Answer)
- D. Eale's disease
Explanation: **Explanation:** **Correct Answer: C. Gout** A **tophus** (plural: tophi) is the pathognomonic hallmark of chronic tophaceous gout [1]. It represents a large, clinical aggregate of **monosodium urate (MSU) crystals** surrounded by an intense inflammatory response [2]. Under microscopy, a tophus consists of a central core of needle-shaped crystals (showing strong negative birefringence under polarized light) surrounded by a granulomatous reaction involving macrophages, lymphocytes, and foreign-body giant cells [2]. Common sites include the olecranon bursa, Achilles tendon, and the helix of the ear. **Why other options are incorrect:** * **Multiple Myeloma:** Characterized by "punched-out" lytic bone lesions and the presence of Bence-Jones proteins. It does not form tophi. * **Cystinosis:** A lysosomal storage disorder characterized by the accumulation of cystine crystals in various organs (kidneys, eyes). These are distinct from urate tophi. * **Eale’s Disease:** An idiopathic peripheral retinal vasculitis. While it involves inflammation, it is an ophthalmological condition unrelated to crystal deposition or tophus formation. **High-Yield Clinical Pearls for NEET-PG:** * **Crystal Morphology:** MSU crystals are **needle-shaped** and **strongly negatively birefringent** (yellow when parallel to the slow axis of the compensator) [1]. * **Pseudogout:** Caused by Calcium Pyrophosphate Deposition (CPPD); crystals are **rhomboid-shaped** and **weakly positively birefringent**. * **Radiology:** Tophi appear as "punched-out" erosions with overhanging edges (Martel’s sign) on X-rays [2]. * **Gold Standard Diagnosis:** Identification of MSU crystals in synovial fluid using polarized light microscopy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1218. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1218-1220.
Question 208: Which immunoglobulin has the highest molecular weight?
- A. IgG
- B. IgA
- C. IgM (Correct Answer)
- D. IgD
Explanation: **Explanation:** The molecular weight of an immunoglobulin is determined by its basic structure (monomer vs. polymer) and the weight of its heavy chains. **Why IgM is the correct answer:** IgM is the largest antibody in the human body [1]. While it can exist as a monomer on the surface of B cells, it primarily circulates in the plasma as a **pentamer** (five units joined by a J-chain). Due to this pentameric structure, it has a molecular weight of approximately **900,000 to 970,000 Daltons** [1]. This "macroglobulin" status prevents it from crossing the placenta but makes it highly efficient at agglutination and complement activation [1]. **Why the other options are incorrect:** * **IgG (Option A):** The most abundant antibody, but it exists only as a monomer. Its molecular weight is ~150,000 Da. * **IgA (Option B):** Exists as a monomer in serum (~160,000 Da) and a dimer in secretions (~385,000 Da). Even in its dimeric form, it is significantly smaller than IgM. * **IgD (Option C):** Exists only as a monomer with a molecular weight of ~180,000 Da. **High-Yield NEET-PG Pearls:** 1. **Valency:** IgM has a theoretical valency of 10 (10 antigen-binding sites), though steric hindrance usually limits it to 5 [1]. 2. **First Responder:** IgM is the first antibody produced in a primary immune response [1]. 3. **Intravascular Distribution:** Due to its high molecular weight, IgM is largely confined to the intravascular compartment (80% is found within blood vessels). 4. **Sedimentation Coefficient:** IgM is often referred to as **19S** antibody, whereas IgG is **7S**. **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. 154-155.
Question 209: Graft between members of the same species but of different genetic constitution is known as:
- A. Xenograft
- B. Autograft
- C. Allograft (Correct Answer)
- D. Isograft
Explanation: ### Explanation The correct answer is **Allograft**. In immunopathology, transplantations are classified based on the genetic relationship between the donor and the recipient. This classification is crucial for understanding the risk of graft rejection and the necessity of immunosuppression. **1. Why Allograft is Correct:** An **Allograft** (also called a homograft) is a transplant between two genetically different individuals of the **same species** (e.g., human to human) [1]. Because the donor and recipient have different Major Histocompatibility Complex (MHC/HLA) molecules, the recipient’s immune system recognizes the graft as "non-self," leading to a potential immune response (rejection). This is the most common type of clinical transplant (e.g., kidney or liver transplant from a deceased or living donor) [1]. **2. Analysis of Incorrect Options:** * **Xenograft:** A graft between members of **different species** (e.g., a pig heart valve transplanted into a human) [1]. These carry the highest risk of hyperacute rejection. * **Autograft:** A graft taken from one part of an individual's body and transplanted to another part of the **same individual** (e.g., skin graft for burns or CABG using the saphenous vein). There is no risk of rejection. * **Isograft (Syngeneic graft):** A graft between **genetically identical** individuals (e.g., monozygotic/identical twins) [1]. Like autografts, these do not trigger an immune rejection. **High-Yield Clinical Pearls for NEET-PG:** * **HLA Matching:** The most important loci for matching in allografts are **HLA-A, HLA-B, and HLA-DR**. * **Direct Pathway:** Recipient T-cells recognize donor MHC molecules on donor APCs (responsible for acute rejection). * **Indirect Pathway:** Recipient T-cells recognize processed peptides of donor MHC presented by recipient APCs (responsible for chronic rejection). * **Hyperacute Rejection:** Occurs within minutes due to **pre-formed antibodies** (Type II Hypersensitivity) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-244.
Question 210: A patient presents with a history of episodic painful edema of the face and larynx, associated with abdominal pain, particularly during periods of stress. Which of the following is likely to be deficient?
- A. Complement C3
- B. Complement C5
- C. C1 Esterase Inhibitor (Correct Answer)
- D. Properidin
Explanation: **Explanation:** The clinical presentation of episodic, non-pitting edema of the face, larynx, and gastrointestinal tract (causing abdominal pain) triggered by stress or trauma is classic for **Hereditary Angioedema (HAE)**. **Why C1 Esterase Inhibitor is correct:** HAE is caused by an autosomal dominant deficiency or dysfunction of the **C1 esterase inhibitor (C1-INH)**. C1-INH normally regulates the classical complement pathway and the kinin system. Its deficiency leads to the uncontrolled activation of C1 and the kallikrein-kinin cascade. This results in excessive production of **Bradykinin**, a potent vasodilator that increases vascular permeability [1], leading to the characteristic angioedema. **Why other options are incorrect:** * **Complement C3/C5:** Deficiency of these late-pathway components typically presents with increased susceptibility to pyogenic bacterial infections (C3) or disseminated Neisserial infections (C5-C9). They do not cause angioedema. * **Properdin:** This is a positive regulator of the alternative pathway. Its deficiency is X-linked and predisposes individuals to severe meningococcal disease. **High-Yield NEET-PG Pearls:** * **Diagnosis:** Screening shows **low C4 levels** (even between attacks) because C1-INH cannot stop C1 from consuming C4. C1 levels remain normal. * **Management:** Acute attacks are treated with C1-INH concentrate or **Icatibant** (Bradykinin B2 receptor antagonist). * **Contraindication:** **ACE inhibitors** are strictly contraindicated in these patients as they prevent bradykinin breakdown, potentially triggering a fatal laryngeal edema. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.
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