General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 741: All of the following are pyrogenic cytokines, except?

A. Interleukin 18 (IL-18) (Correct Answer)
B. Interleukin 6 (IL-6)
C. Tumor Necrosis Factor (TNF)
D. Interferon alpha (IFN-a)

Explanation: **Explanation:** The regulation of body temperature occurs in the hypothalamus. **Pyrogens** are substances that induce fever by stimulating the synthesis of **Prostaglandin E2 (PGE2)** in the anterior hypothalamus, which resets the thermostatic set-point to a higher level [1]. **Why IL-18 is the correct answer:** While **Interleukin-18 (IL-18)** belongs to the IL-1 family, its primary physiological role is the induction of Interferon-gamma (IFN-̳) and the activation of Th1 responses and NK cells. Unlike its close relative IL-1̢, IL-18 does not possess significant endogenous pyrogenic activity and is not typically involved in the systemic inflammatory response that triggers fever [2]. **Analysis of Incorrect Options:** * **TNF and IL-1:** These are the "master" endogenous pyrogens. They act directly on the hypothalamic vascular endothelium to induce PGE2 [1]. * **Interleukin 6 (IL-6):** A potent endogenous pyrogen that acts downstream of TNF and IL-1. It is a major inducer of the acute-phase response in the liver [1]. * **Interferon alpha (IFN-̱):** Known to be pyrogenic, which explains the common "flu-like symptoms" (fever, chills, myalgia) experienced by patients receiving Interferon therapy for Hepatitis or malignancies. **NEET-PG High-Yield Pearls:** 1. **Exogenous Pyrogens:** The most common is **LPS (Lipopolysaccharide/Endotoxin)** from Gram-negative bacteria, which triggers the release of endogenous cytokines. 2. **Endogenous Pyrogens:** The primary mediators are **IL-1, TNF, IL-6, and IFNs.** [1] 3. **Mechanism of Action:** Pyrogens → OVLT (Organum Vasculosum of Lamina Terminalis) in the hypothalamus → PGE2 release → Increased cAMP → Thermostat reset. 4. **Antipyretics:** Drugs like Aspirin and NSAIDs reduce fever by inhibiting **Cyclooxygenase (COX)**, thereby blocking PGE2 synthesis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201.

Question 742: Amyloidosis deposition most commonly occurs in which of the following structures?

A. Renal vessels (Correct Answer)
B. Knee joints
C. Skin
D. Cornea

Explanation: **Explanation:** **Amyloidosis** is a disorder of protein misfolding where insoluble fibrillar proteins deposit in the extracellular space [1]. The **kidney** is the most common and clinically significant organ involved in systemic amyloidosis (both AL and AA types). **Why Renal Vessels are Correct:** Within the kidney, amyloid deposition typically begins in the **glomeruli**, but it also frequently involves the **interstitial arterioles and renal arteries**. In fact, vascular involvement is a hallmark of systemic amyloidosis [2]. Deposition in the renal vessels and glomerular basement membrane leads to increased permeability, resulting in nephrotic syndrome, and eventually, renal failure—the most common cause of death in systemic amyloidosis. **Analysis of Incorrect Options:** * **Knee joints:** While $\beta_2$-microglobulin amyloidosis (associated with long-term dialysis) can affect joints and synovium [3], it is not the "most common" site compared to renal involvement in systemic forms. * **Skin:** Cutaneous involvement occurs in primary systemic amyloidosis (AL) or localized lichen amyloidosis, but it is less frequent and less clinically significant than renal deposition. * **Cornea:** Lattice corneal dystrophy is a form of localized amyloidosis, but it is a rare, organ-specific condition. **NEET-PG High-Yield Pearls:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red** [2]. * **Morphology:** On H&E stain, it appears as extracellular, amorphous, eosinophilic (pink) material [2]. * **Most common organ involved:** Kidney. * **Most common site of biopsy:** Rectal biopsy or Abdominal fat pad aspiration (due to high sensitivity and ease). * **Cardiac involvement:** Common in AL type; leads to restrictive cardiomyopathy. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 269-270.

Question 743: Teuton giant cells are seen in which of the following conditions?

A. Sarcoidosis
B. Tuberculosis
C. Foreign body granuloma
D. Xanthoma (Correct Answer)

Explanation: **Explanation:** **Touton giant cells** (also known as xanthelasmic giant cells) are the hallmark histological feature of **Xanthomas**. These are specialized multinucleated giant cells formed by the fusion of macrophages (histiocytes). **Why Xanthoma is correct:** The underlying mechanism involves the accumulation of lipids [1]. In Touton giant cells, nuclei form a complete or partial ring around a central area of homogeneous eosinophilic cytoplasm. Crucially, the **peripheral cytoplasm** outside the ring of nuclei appears **foamy or vacuolated** due to the presence of processed lipids (cholesterol) [1]. This characteristic "wreath-like" arrangement is diagnostic of lesions with high lipid content, such as xanthomas, xanthogranulomas, and fat necrosis. **Why other options are incorrect:** * **Sarcoidosis:** Characterized by non-caseating granulomas containing **Langhans giant cells** and specific inclusions like **Asteroid bodies** and **Schaumann bodies**. * **Tuberculosis:** Features caseating granulomas with **Langhans giant cells**, where nuclei are arranged in a peripheral "horseshoe" pattern. * **Foreign body granuloma:** Contains **Foreign body giant cells**, where nuclei are disorganized and scattered randomly throughout the cytoplasm. **High-Yield Clinical Pearls for NEET-PG:** * **Touton Giant Cell:** Central eosinophilic cytoplasm + Ring of nuclei + Peripheral foamy cytoplasm. * **Langhans Giant Cell:** Peripheral horseshoe nuclei (seen in TB, Sarcoidosis). * **Foreign Body Giant Cell:** Haphazard/scattered nuclei. * **Aschoff Cells:** Found in Rheumatic Heart Disease (Anitschkow cells are the mononuclear precursors). * **Warthin-Finkeldey Cells:** Multinucleated giant cells seen in Measles. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 73-74.

Question 744: In Langerhans cell histiocytosis, what is the characteristic abnormality seen on microscopy?

A. Birbeck granules (Correct Answer)
B. Foamy macrophages
C. Giant cells
D. Plasma cells

Explanation: **Explanation:** **Langerhans Cell Histiocytosis (LCH)** is a proliferative disorder of dendritic cells (Langerhans cells). The hallmark diagnostic feature seen on electron microscopy is the **Birbeck granule** [1]. 1. **Why Birbeck granules are correct:** These are unique, pentalaminar, rod-shaped cytoplasmic organelles with a central striated line and a bulbous end, giving them a characteristic **"tennis racket" appearance** [1]. They contain the protein **Langerin (CD207)**, which is involved in antigen processing. Their presence is pathognomonic for Langerhans cells [1]. 2. **Why other options are incorrect:** * **Foamy macrophages:** These are lipid-laden macrophages commonly seen in atherosclerosis, xanthomas, or Niemann-Pick disease, but not characteristic of LCH. * **Giant cells:** While multinucleated giant cells can be seen in various granulomatous inflammations (like TB or Sarcoidosis), they are not the defining feature of LCH. * **Plasma cells:** These are seen in chronic inflammation and Multiple Myeloma. While LCH lesions have an inflammatory background (including eosinophils), plasma cells are not the diagnostic hallmark. **High-Yield Clinical Pearls for NEET-PG:** * **Immunohistochemistry (IHC) Markers:** LCH cells are characteristically positive for **S100, CD1a, and Langerin (CD207)** [1]. * **Morphology:** On light microscopy, cells show "coffee-bean" nuclei (grooved nuclei) [1]. * **Clinical Presentation:** Often presents as "punched-out" lytic bone lesions (especially in the skull) and skin rashes. * **Eosinophilic Granuloma:** This is the most common and benign form of LCH, typically presenting as a solitary bone lesion. **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. 630.

Question 745: Apoptosis does not occur by the normal caspase pathway in which of the following?

A. Liver
B. Muscle
C. Neurons (Correct Answer)
D. Skin

Explanation: **Explanation:** The correct answer is **Neurons (Option C)**. While apoptosis is the programmed cell death mechanism across most tissues, **neurons** exhibit a unique variation. In mature neurons, the traditional caspase-dependent pathway is often suppressed as a survival mechanism to prevent the loss of these non-renewable cells. Instead, neuronal cell death frequently occurs via **caspase-independent pathways**, involving the release of **AIF (Apoptosis Inducing Factor)** and **Endonuclease G** from the mitochondria. These factors translocate directly to the nucleus to cause DNA fragmentation and chromatin condensation without requiring the activation of the executioner caspases (Caspase-3, 6, or 7). **Analysis of Incorrect Options:** * **A. Liver:** Hepatocytes undergo classic apoptosis via both intrinsic (mitochondrial) and extrinsic (death receptor) pathways [1], [2], heavily involving Caspase-3 (e.g., in viral hepatitis or Councilman bodies). * **B. Muscle:** Both skeletal and cardiac muscles utilize standard caspase pathways during development and in pathological states like atrophy or heart failure [3]. * **D. Skin:** Keratinocytes rely on caspase activation for normal turnover and during the formation of the cornified envelope (a specialized form of programmed cell death). **NEET-PG High-Yield Pearls:** * **Executioner Caspases:** Caspase-3, 6, and 7 (Caspase-3 is the most common). * **Initiator Caspases:** Caspase-8 and 10 (Extrinsic); Caspase-9 (Intrinsic) [1]. * **AIF (Apoptosis Inducing Factor):** A flavoprotein that moves from mitochondria to the nucleus to cause DNA damage *without* caspase involvement. * **Councilman Bodies:** Eosinophilic apoptotic hepatocytes seen in Yellow Fever and Viral Hepatitis. * **Psammoma Bodies:** Result from single-cell necrosis/apoptosis followed by dystrophic calcification. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 67. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-64.

Question 746: A deficiency of which one of the listed enzymes is most likely to be associated with the formation of multiple pale yellow, hard, round stones within the gallbladder?

A. 1-a-hydroxylase
B. 7-a-hydroxylase (Correct Answer)
C. 11-hydroxylase
D. 17-hydroxylase

Explanation: **Explanation:** The question describes the formation of **cholesterol gallstones** (pale yellow, hard, and round) [1]. The pathogenesis of these stones involves the supersaturation of bile with cholesterol, which occurs when there is either an excess of cholesterol or a deficiency of bile salts. **Why 7-α-hydroxylase is correct:** 7-α-hydroxylase is the **rate-limiting enzyme** in the synthesis of bile acids from cholesterol. * A deficiency or inhibition of this enzyme leads to decreased production of bile acids (cholic acid and chenodeoxycholic acid). * Bile acids are essential for solubilizing cholesterol in the gallbladder. * Reduced bile acid levels result in bile becoming supersaturated with cholesterol, leading to its precipitation and the formation of cholesterol stones. **Why the other options are incorrect:** * **1-α-hydroxylase (Option A):** This enzyme is located in the kidneys and converts 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D (Calcitriol). Its deficiency leads to Vitamin D-dependent rickets. * **11-β-hydroxylase (Option C):** This enzyme is involved in adrenal steroidogenesis. Deficiency leads to Congenital Adrenal Hyperplasia (CAH), characterized by hypertension and virilization. * **17-α-hydroxylase (Option D):** This enzyme is required for the synthesis of cortisol and sex hormones. Deficiency leads to CAH with hypertension and primary amenorrhea/delayed puberty. **High-Yield Clinical Pearls for NEET-PG:** * **The "4 F’s" Risk Factors:** Female, Fat, Fertile, and Forty. * **Fibrates Connection:** Fibrates (e.g., Gemfibrozil) inhibit 7-α-hydroxylase, which is why they increase the risk of gallstones. * **Estrogen:** Increases cholesterol synthesis by upregulating HMG-CoA reductase, also predisposing to stones. * **Pigment Stones:** Associated with chronic hemolysis (black stones) or biliary infections (brown stones), not cholesterol metabolism [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 882.

Question 747: Which cytokine enhances NK cell activity?

A. Interleukin-1 (IL-1)
B. Tumor Necrosis Factor (TNF)
C. Interleukin-2 (IL-2) (Correct Answer)
D. Transforming Growth Factor-beta (TGF-b)

Explanation: **Explanation:** The correct answer is **Interleukin-2 (IL-2)**. Natural Killer (NK) cells are innate immune lymphocytes that provide the first line of defense against virally infected cells and tumor cells. Their activation and proliferation are heavily dependent on specific cytokines. **IL-2**, primarily secreted by CD4+ T-helper (Th1) cells, acts as a potent growth factor for both T-cells and NK cells [1]. It enhances the cytotoxic capacity of NK cells and induces their differentiation into **Lymphokine-Activated Killer (LAK) cells**, which have superior anti-tumor activity. **Analysis of Options:** * **IL-1 (Option A):** A pro-inflammatory cytokine produced by macrophages. Its primary roles include inducing fever (pyrogen), activating vascular endothelium, and stimulating the synthesis of acute-phase reactants. * **TNF (Option B):** Primarily involved in systemic inflammation, induction of apoptosis, and recruitment of leukocytes. While it works synergistically with other cytokines, it is not the primary enhancer of NK cell activity. * **TGF-β (Option D):** Generally an **immunosuppressive** cytokine. It inhibits lymphocyte proliferation and suppresses NK cell activity, acting as a "brake" on the immune response. **NEET-PG High-Yield Pearls:** * **IL-2, IL-12, IL-15, and Type I Interferons (IFN-α/β)** are the primary stimulators of NK cells [1]. * **IL-12** is the most potent inducer of **IFN-γ** production by NK cells [1]. * NK cells do not require prior sensitization and lack MHC restriction (they follow the "missing self" hypothesis). * **Clinical Correlation:** Recombinant IL-2 (Aldesleukin) has been used in immunotherapy for renal cell carcinoma and melanoma due to its ability to boost NK and T-cell responses. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201.

Question 748: Rejection that may appear within minutes or hours of transplantation is termed as:

A. Hyperacute Rejection (Correct Answer)
B. Acute cellular (T cell-mediated) rejection
C. Acute antibody-mediated rejection
D. Chronic Rejection

Explanation: ### Explanation **Correct Answer: A. Hyperacute Rejection** **Why it is correct:** Hyperacute rejection occurs within **minutes to hours** after transplantation [1]. It is mediated by **pre-formed antibodies** (Type II Hypersensitivity) in the recipient's serum that recognize antigens (usually ABO blood group or HLA) on the donor vascular endothelium. Once the graft is perfused, these antibodies bind, activating the complement system and coagulation cascade. This leads to thrombotic occlusion of the graft vasculature, resulting in ischemic necrosis (the graft turns cyanotic and mottled on the operating table) [1]. **Why the other options are incorrect:** * **B & C. Acute Rejection (Cellular or Antibody-mediated):** These typically occur within **days to weeks** (or months if immunosuppression is reduced) [1]. Acute cellular rejection is mediated by T-cells (Type IV Hypersensitivity), while acute antibody-mediated rejection involves *de novo* synthesis of antibodies against donor HLA [2]. * **D. Chronic Rejection:** This occurs over **months to years**. It is characterized by progressive fibrosis, intimal thickening of blood vessels (arteriosclerosis), and graft atrophy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Hyperacute rejection is a **Type II Hypersensitivity** reaction. * **Morphology:** Grossly, the organ becomes cyanotic/flaccid [1]. Microscopically, look for **fibrinoid necrosis** of vessel walls and neutrophilic infiltration [1]. * **Prevention:** It is prevented by **Cross-matching** (testing recipient serum against donor lymphocytes) before surgery. * **Treatment:** There is no effective treatment; the graft must be removed immediately [1]. * **Key Association:** Often seen in patients with previous blood transfusions, multiple pregnancies, or prior transplants (sensitized patients). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 242.

Question 749: Which pair of oncogenes is activated by translocation?

A. SIS and HST-1
B. HGF and L-MYC
C. TGF and CDK-4
D. ABL and C-MYC (Correct Answer)

Explanation: Proto-oncogenes can be converted into oncogenes through various mechanisms, including point mutations, gene amplification, and chromosomal translocations [1]. **Why Option D is Correct:** Translocation is a hallmark mechanism for activating **ABL** and **C-MYC**: * **ABL:** In Chronic Myeloid Leukemia (CML), the *ABL* gene on chromosome 9 translocates to the *BCR* locus on chromosome 22, forming the **Philadelphia chromosome [t(9;22)]** [2]. This creates a BCR-ABL fusion protein with constitutive tyrosine kinase activity [3]. * **C-MYC:** In Burkitt Lymphoma, the *C-MYC* gene on chromosome 8 translocates to the Immunoglobulin Heavy Chain (IgH) locus on chromosome 14 **[t(8;14)]**, leading to overexpression of the MYC transcription factor [1]. **Analysis of Incorrect Options:** * **Option A (SIS and HST-1):** These are growth factors. They are typically overexpressed via autocrine loops or gene amplification, not translocation. * **Option B (HGF and L-MYC):** While *L-MYC* is an oncogene (often amplified in small cell lung cancer), *HGF* is a growth factor. * **Option C (TGF and CDK-4):** *CDK-4* (a cell cycle regulator) is primarily activated by **gene amplification** (e.g., in glioblastomas and sarcomas), not translocation. **High-Yield Clinical Pearls for NEET-PG:** * **N-MYC:** Amplification is a key prognostic marker in **Neuroblastoma**. * **ERBB2 (HER2/neu):** Activated by **amplification** in breast cancer. * **RAS:** Most common oncogene mutation in human tumors; activated by **point mutation**. * **BCL-2:** Activated by **t(14;18)** in Follicular Lymphoma, leading to evasion of apoptosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [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. 225-226. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.

Question 750: What is the clinical evidence of dentinogenesis imperfecta?

A. Defective enamel and dentine
B. Defective dentine and obliterated pulp chamber (Correct Answer)
C. Increased rate of caries
D. Oligodontia

Explanation: **Explanation:** **Dentinogenesis Imperfecta (DI)** is an autosomal dominant disorder of dentin formation caused by mutations in the **DSPP gene** (Dentin Sialophosphoprotein). **Why Option B is Correct:** The hallmark of DI is the formation of abnormal, poorly mineralized dentin. Histologically and radiographically, this manifests as: 1. **Defective Dentin:** The dentin is softer and contains irregular, sparse tubules. 2. **Obliteration of Pulp Chambers:** Because the odontoblasts are functionally deranged, they produce dentin in an accelerated, disorganized manner, eventually filling and completely obliterating the pulp chambers and root canals. This is a classic radiographic sign. **Analysis of Incorrect Options:** * **Option A:** DI primarily affects dentin. While the enamel may flake off easily because the underlying dentino-enamel junction (DEJ) is smooth (lacking the normal scalloping), the **enamel itself is structurally normal**. * **Option C:** Interestingly, teeth with DI actually show a **decreased rate of caries**. This is attributed to the rapid attrition (wear) of the teeth and the absence of patent dentinal tubules, which prevents bacterial invasion. * **Option D:** **Oligodontia** (congenital absence of six or more teeth) is not a feature of DI. DI affects the structure of the teeth that are present, not their number. **High-Yield Clinical Pearls for NEET-PG:** * **Appearance:** Teeth often exhibit a characteristic **translucent, opalescent, or "amber"** color. * **Radiographic Sign:** "Bell-shaped" crowns with cervical constriction and thin, short roots. * **Association:** DI Type I is associated with **Osteogenesis Imperfecta** (look for "blue sclera" in the clinical vignette). DI Type II and III occur in isolation.

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