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

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 2

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

Accepted Answer

Bradykinin

Answer

Serotonin

Answer

Histamine

Answer

Cytokines

Question 3

Which type of cells remain in the G0 phase?

Accepted Answer

Quiescent cells

Answer

Permanent cells

Answer

Labile cells

Answer

Intermitotic cells

Question 4

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 5

Chemotaxis is the main function of which molecule?

Accepted Answer

C5a

Answer

ICAM1

Answer

P-selectin

Answer

IL-5

Question 6

Wound strength reaches approximately 70% after how much time?

Accepted Answer

3 months

Answer

1 week

Answer

1 month

Answer

6 months

Question 7

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 8

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

Question 9

A 28-year-old woman cuts her hand while dicing vegetables in the kitchen. The wound is cleaned and sutured. Five days later, the site of injury contains an abundance of chronic inflammatory cells that actively secrete interleukin-1, tumor necrosis factor-a, interferon- a, numerous arachidonic acid derivatives, and various enzymes. What are these cells?

Accepted Answer

Macrophages

Answer

B lymphocytes

Answer

Plasma cells

Answer

Smooth muscle cells

Question 10

In an experiment, bacteria are inoculated into aliquots of normal human blood treated with an anticoagulant. It is observed that the bacteria are either phagocytized by neutrophils or undergo lysis. Which of the following blood plasma components is most likely to facilitate these effects?

Accepted Answer

Complement

Answer

Fibrin

Answer

Kallikrein

Answer

Plasmin

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

On this page

Practice by Chapter

Want unlimited practice?