General Pathology Practice Questions

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

Xanthoma. **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.

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

Birbeck granules. **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.

Q: Which cytokine enhances NK cell activity?

Interleukin-2 (IL-2). **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.

Q: What is the clinical evidence of dentinogenesis imperfecta?

Defective dentine and obliterated pulp chamber. **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.

Question 1

All of the following are pyrogenic cytokines, except?

Accepted Answer

Interleukin 18 (IL-18)

Answer

Interleukin 6 (IL-6)

Answer

Tumor Necrosis Factor (TNF)

Answer

Interferon alpha (IFN-a)

Question 2

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

Accepted Answer

Renal vessels

Answer

Knee joints

Answer

Skin

Answer

Cornea

Question 3

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

Accepted Answer

Xanthoma

Answer

Sarcoidosis

Answer

Tuberculosis

Answer

Foreign body granuloma

Question 4

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

Accepted Answer

Birbeck granules

Answer

Foamy macrophages

Answer

Giant cells

Answer

Plasma cells

Question 5

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

Accepted Answer

Neurons

Answer

Liver

Answer

Muscle

Answer

Skin

Question 6

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?

Accepted Answer

7-a-hydroxylase

Answer

1-a-hydroxylase

Answer

11-hydroxylase

Answer

17-hydroxylase

Question 7

Which cytokine enhances NK cell activity?

Accepted Answer

Interleukin-2 (IL-2)

Answer

Interleukin-1 (IL-1)

Answer

Tumor Necrosis Factor (TNF)

Answer

Transforming Growth Factor-beta (TGF-b)

Question 8

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

Accepted Answer

Hyperacute Rejection

Answer

Acute cellular (T cell-mediated) rejection

Answer

Acute antibody-mediated rejection

Answer

Chronic Rejection

Question 9

Which pair of oncogenes is activated by translocation?

Accepted Answer

ABL and C-MYC

Answer

SIS and HST-1

Answer

HGF and L-MYC

Answer

TGF and CDK-4

Question 10

What is the clinical evidence of dentinogenesis imperfecta?

Accepted Answer

Defective dentine and obliterated pulp chamber

Answer

Defective enamel and dentine

Answer

Increased rate of caries

Answer

Oligodontia

General Pathology — MCQs

General Pathology — MCQs

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