Inflammation and Repair Practice Questions

Q: In tuberculosis, which cytokine plays a major role in the conversion of tissue macrophages into epithelioid cells?

Interferon gamma. **Explanation:** The formation of a granuloma in Tuberculosis is a classic example of **Type IV (Delayed-type) Hypersensitivity**. The conversion of macrophages into epithelioid cells is the hallmark of this process. **Why Interferon-gamma (IFN-γ) is correct:** In response to *Mycobacterium tuberculosis* antigens, CD4+ T-cells (Th1 subset) secrete **IFN-γ**. This is the most potent activator of macrophages. Under the chronic influence of IFN-γ, macrophages undergo structural changes: they increase their cytoplasmic volume, develop abundant organelles, and take on a "slipper-shaped" appearance resembling epithelial cells—hence the term **epithelioid cells**. These cells have enhanced bactericidal activity but are primarily secretory and structural in nature. **Analysis of Incorrect Options:** * **Tumor Necrosis Factor (TNF-α):** While TNF-α is crucial for **maintaining** the structural integrity of the granuloma and preventing hematogenous spread, it is not the primary driver of epithelioid transformation. * **Interleukin-12 (IL-12):** This cytokine is secreted by macrophages to stimulate T-cells and NK cells to produce IFN-γ. It acts "upstream" in the pathway. * **Macrophage Chemoattractant Protein (MCP-1):** This chemokine is responsible for the **recruitment** of monocytes from the blood to the site of infection, not their differentiation into epithelioid cells. **High-Yield Clinical Pearls for NEET-PG:** * **Epithelioid cells** are defined by their inability to phagocytose but high secretory capacity. * Fusion of epithelioid cells under the influence of IFN-γ leads to the formation of **Langhans giant cells** (peripheral arrangement of nuclei). * **Key Cytokine Sequence:** IL-12 (from Macrophage) → IFN-γ (from Th1 cell) → Macrophage activation/Epithelioid change. * Anti-TNF drugs (like Infliximab) carry a high risk of **reactivating latent TB** because they disrupt existing granulomas.

Q: In acute inflammation, pain is primarily mediated by which of the following substances?

Bradykinin. **Explanation:** In the process of acute inflammation, the cardinal sign of **Pain (Dolor)** is primarily mediated by **Bradykinin** and **Prostaglandins (PGE2)** [1]. **1. Why Bradykinin is correct:** Bradykinin is a potent inflammatory mediator derived from the kinin system (activated by Hageman factor/Factor XII). It acts directly on nociceptors (pain receptors) in the peripheral nervous system, increasing their sensitivity [1]. While Prostaglandins also cause pain, they primarily act by "sensitizing" the nerve endings to other mediators like Bradykinin [1]. Therefore, Bradykinin is considered the direct chemical mediator of the pain response. **2. Analysis of Incorrect Options:** * **A. Serotonin:** Primarily released by platelets; its main roles are vasoconstriction and acting as a neurotransmitter [1]. It does not play a primary role in the pain of acute inflammation. * **B. Histamine:** Released by mast cells, it is the chief mediator of **vasodilation** and **increased vascular permeability** (leading to redness and swelling/edema), but it does not directly mediate pain [1]. * **C. Cytokines:** While TNF and IL-1 are crucial for the systemic acute phase response (fever, leucocytosis), they do not directly stimulate pain receptors [1]. **3. NEET-PG High-Yield Pearls:** * **Mediators of Vasodilation:** Histamine and Nitric Oxide (NO). * **Mediators of Increased Permeability:** Histamine, Bradykinin, and Leukotrienes (C4, D4, E4) [1]. * **Mediators of Fever:** IL-1, TNF, and Prostaglandins (PGE2) [1]. * **Mediators of Chemotaxis:** C5a, LTB4, and IL-8 [1]. * **Pain Duo:** Remember **Bradykinin** (direct) and **PGE2** (sensitizer) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Q: Wound strength reaches approximately 70% after how much time?

3 months. **Explanation:** The tensile strength of a healing wound is a function of collagen deposition and remodeling. This process follows a specific chronological pattern: * **Correct Answer (C):** By the end of **3 months**, wound strength reaches approximately **70% to 80%** of the strength of unwounded skin [1]. This is the plateau phase where the rate of strength gain slows down significantly. It is important to note that a scar rarely, if ever, regains 100% of the original tissue strength [1]. **Analysis of Incorrect Options:** * **Option A (1 week):** At the end of the first week (when sutures are typically removed), the wound strength is only about **10%** [1]. This is why wound dehiscence is a risk if excessive tension is applied early. * **Option B (1 month):** Strength increases rapidly over the next few weeks due to collagen cross-linking and the shift from Type III to Type I collagen, but it has not yet reached the 70% threshold [1]. * **Option D (6 months):** While remodeling continues for up to a year, the specific milestone of 70-80% strength is traditionally associated with the 3-month mark in standard pathology texts (Robbins) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Collagen Switch:** In early wound healing (granulation tissue), **Type III collagen** predominates. During maturation/remodeling, it is replaced by **Type I collagen**, which provides greater tensile strength [1]. * **Vitamin C & Copper:** These are essential cofactors for collagen cross-linking (prolyl hydroxylase and lysyl oxidase, respectively). Deficiency leads to poor wound healing. * **The 10% Rule:** Remember that at 1 week, strength is 10% [1]. This is a frequent "distractor" in exams. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Q: Which of the following is NOT an action of platelet-activating factor?

Bronchodilation. **Explanation:** Platelet-activating factor (PAF) is a potent phospholipid-derived mediator released from various cells, including platelets, endothelium, and inflammatory cells (neutrophils, eosinophils, and macrophages). It plays a central role in inflammation and anaphylaxis. **Why Bronchodilation is the Correct Answer:** PAF is a potent **bronchoconstrictor**, not a bronchodilator. In the lungs, it induces smooth muscle contraction and airway hyperreactivity, making it significantly more potent than histamine in triggering asthma-like symptoms. Therefore, Option B is the incorrect action. **Analysis of Incorrect Options:** * **A. Increased capillary permeability:** PAF causes endothelial cell contraction and gap formation, leading to protein leakage and edema. This is a hallmark of the inflammatory response. * **C. Vasodilation:** At low concentrations, PAF induces systemic vasodilation, which can lead to hypotension and shock during anaphylactic reactions. * **D. Erosion of gastric mucosa:** PAF is highly ulcerogenic. It reduces gastric blood flow and stimulates the release of other inflammatory mediators, leading to mucosal damage and ulcer formation. **High-Yield NEET-PG Pearls:** * **Potency:** PAF is 100 to 1,000 times more potent than histamine in causing bronchoconstriction and vasodilation. * **Source:** It is synthesized via the action of **Phospholipase A2** on membrane phospholipids. * **Platelet Effects:** As the name suggests, it causes platelet aggregation and the "release reaction" (degranulation of serotonin and ADP). * **Clinical Link:** PAF antagonists are a subject of research for treating septic shock and inflammatory disorders.

Question 1

What is the pathophysiology of Chronic Granulomatous disease?

Accepted Answer

Decreased oxidative burst

Answer

Defective myeloperoxidase

Answer

Impaired phagocytosis

Answer

Impaired activity of lysozyme

Question 2

Which of the following is NOT a granulomatous disease?

Accepted Answer

Amebiasis

Answer

Leprosy

Answer

Tuberculosis

Answer

Sarcoidosis

Question 3

In tuberculosis, which cytokine plays a major role in the conversion of tissue macrophages into epithelioid cells?

Accepted Answer

Interferon gamma

Answer

Tumor necrosis factor

Answer

Interleukin 12

Answer

Macrophage chemoattractant protein

Question 4

In acute inflammation, pain is primarily mediated by which of the following substances?

Accepted Answer

Bradykinin

Answer

Serotonin

Answer

Histamine

Answer

Cytokines

Question 5

Which type of cells remain in the G0 phase?

Accepted Answer

Quiescent cells

Answer

Permanent cells

Answer

Labile cells

Answer

Intermitotic cells

Question 6

Which of the following is NOT observed during the inflammatory stage of wound healing?

Accepted Answer

Angiogenesis

Answer

Chemotaxis

Answer

Increased capillary permeability

Answer

Cytokine and chemotactic factor release

Question 7

Chemotaxis is the main function of which molecule?

Accepted Answer

C5a

Answer

ICAM1

Answer

P-selectin

Answer

IL-5

Question 8

Wound strength reaches approximately 70% after how much time?

Accepted Answer

3 months

Answer

1 week

Answer

1 month

Answer

6 months

Question 9

Phagocytosis is enhanced when bacteria are coated with complement and Ig. What mechanism best describes this enhanced phagocytosis?

Accepted Answer

C3b and Fc receptor-mediated phagocytosis

Answer

Receptor-mediated endocytosis

Answer

Pseudopod formation

Answer

Myeloperoxidase-mediated destruction

Question 10

Which of the following is NOT an action of platelet-activating factor?

Accepted Answer

Bronchodilation

Answer

Increased capillary permeability

Answer

Vasodilation

Answer

Erosion of gastric mucosa

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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