Inflammation and Repair Practice Questions

Q: Which is a vasoconstricting mediator?

Thromboxane-A2. **Explanation:** The correct answer is **Thromboxane-A2 (TXA2)**. This question tests your knowledge of arachidonic acid metabolites (eicosanoids) and their specific roles in the inflammatory response and vascular hemodynamics. **1. Why Thromboxane-A2 is correct:** TXA2 is primarily produced by platelets via the cyclooxygenase (COX) pathway. It is a potent **vasoconstrictor** and a powerful **platelet aggregator** [1]. Its physiological role is to promote clot formation and limit blood loss at the site of vascular injury, acting in direct opposition to prostacyclin. **2. Why the other options are incorrect:** * **Prostacyclin (PGI2):** Produced by vascular endothelium, it is a potent **vasodilator** and an inhibitor of platelet aggregation [1]. It maintains vascular patency. * **PG D2:** Along with PGE2 and PGF2α, PGD2 is a major prostaglandin produced by mast cells that causes **vasodilation** and increases vascular permeability (edema) [1]. * **Lipoxins (LXA4, LXB4):** These are anti-inflammatory mediators that function in the **resolution** of inflammation. They inhibit neutrophil chemotaxis and adhesion, and typically cause vasodilation. **Clinical Pearls for NEET-PG:** * **The "Push-Pull" Mechanism:** Remember the balance between **TXA2** (Platelet-derived; Pro-thrombotic/Vasoconstrictor) and **PGI2** (Endothelial-derived; Anti-thrombotic/Vasodilator) [1]. An imbalance often leads to thrombosis or hypertension. * **Aspirin:** Low-dose aspirin irreversibly inhibits COX-1 in platelets, reducing TXA2 levels, which explains its use as a cardioprotective/anti-platelet agent. * **Other Vasoconstrictors to remember:** Leukotrienes (C4, D4, E4), Endothelin, and Angiotensin II [1]. * **Other Vasodilators to remember:** Nitric Oxide (NO), Histamine, and Bradykinin. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-97.

Q: Which of the following are anti-inflammatory mediators?

Lipoxins. **Explanation:** The process of inflammation is tightly regulated by a balance between pro-inflammatory and anti-inflammatory mediators [1]. The resolution of inflammation is an active process, not merely a passive decay of signals. **1. Why Lipoxins are correct:** Lipoxins (specifically LXA4 and LXB4) are derivatives of arachidonic acid produced via the **lipoxygenase pathway**. Unlike leukotrienes, lipoxins serve as "stop signals" for inflammation [1]. They inhibit neutrophil chemotaxis and adhesion to the endothelium, while simultaneously stimulating the recruitment of non-phlogistic (non-inflammatory) monocytes and macrophages to clear apoptotic debris. This dual action promotes the **resolution phase** of inflammation. **2. Why the other options are incorrect:** * **Thromboxane (TXA2):** A potent pro-inflammatory mediator produced by platelets. It causes vasoconstriction and promotes platelet aggregation. * **Prostaglandins (e.g., PGE2, PGD2):** These are classic pro-inflammatory mediators that cause vasodilation, increase vascular permeability, and mediate pain and fever [1]. * **Interleukins:** While some interleukins (like IL-10) are anti-inflammatory, the term "Interleukins" generally refers to a broad class of cytokines (like IL-1 and IL-6) that are predominantly pro-inflammatory in the context of acute inflammation [1]. **High-Yield NEET-PG Pearls:** * **Pro-resolving mediators:** Besides Lipoxins, keep an eye out for **Resolvins, Protectins, and Maresins** (derived from omega-3 fatty acids) [1]. * **Anti-inflammatory Cytokines:** The most important ones to remember are **IL-10** and **TGF-β**. * **Switch Mechanism:** During inflammation, there is a "class switch" where the production of pro-inflammatory leukotrienes (LTB4) shifts to anti-inflammatory lipoxins to initiate healing. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.

Question 1

After extravasation, leukocytes emigrate in the tissue towards the site of injury. What is this process called?

Accepted Answer

Chemotaxis

Answer

Margination

Answer

Diapedesis

Answer

Pavementing

Question 2

Which of the following utilizes an oxygen-dependent mechanism for killing or degradation in phagocytosis?

Accepted Answer

H2O2-MPO halide system

Answer

Bactericidal Permeability Increasing Protein (BPI)

Answer

Lactoferrin

Answer

Lysozyme

Question 3

Which of the following is a chemotactic factor?

Accepted Answer

Leukotrienes

Answer

Prostaglandins

Answer

Prostacyclins

Answer

Thromboxane

Question 4

What is most important for diapedesis?

Accepted Answer

PECAM

Answer

Selectin

Answer

Integrin

Answer

Mucin-like glycoprotein

Question 5

Which is a vasoconstricting mediator?

Accepted Answer

Thromboxane-A2

Answer

Prostacyclin

Answer

PG D2

Answer

Lipoxins

Question 6

All of the following enzymes may contribute to generating free oxygen radicals within neutrophils for killing intracellular bacteria, except?

Accepted Answer

Glutathione Peroxidase

Answer

Superoxide Dismutase

Answer

Fenton's reaction

Answer

NADPH oxidase

Question 7

The tensile strength of a healing wound starts to increase after which period?

Accepted Answer

3 to 4 days

Answer

Immediate suture of the wound

Answer

7 to 10 days

Answer

6 months

Question 8

What is the most important source of histamine?

Accepted Answer

Mast cells

Answer

Eosinophils

Answer

Neutrophils

Answer

Macrophages

Question 9

All of the following are mediators of inflammation, except:

Accepted Answer

Myeloperoxidase

Answer

Tumour necrosis factor-alpha (TNF-alpha)

Answer

Interleukin-1

Answer

Prostaglandins

Question 10

Which of the following are anti-inflammatory mediators?

Accepted Answer

Lipoxins

Answer

Thromboxane

Answer

Prostaglandins

Answer

Interleukins

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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