Inflammation and Repair Practice Questions

Q: What molecule is most important for diapedesis?

PECAM. **Explanation:** The process of leukocyte extravasation (migration from blood to tissue) occurs in four distinct stages: Rolling, Activation, Adhesion, and Diapedesis. **1. Why PECAM-1 is correct:** **PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1)**, also known as **CD31**, is the primary molecule responsible for **Diapedesis** (transendothelial migration). It is expressed on both the surface of leukocytes and at the intercellular junctions of endothelial cells. Through homophilic binding (PECAM-1 binding to PECAM-1), it acts like a "zipper," allowing the leukocyte to squeeze through the tight junctions of the vessel wall into the extravascular space. **2. Why the other options are incorrect:** * **Selectins (E, P, and L-selectins):** These mediate the initial **Rolling** phase. They create weak, transient bonds that slow down the leukocyte. * **Integrins (e.g., LFA-1, VLA-4):** These are responsible for **Stable Adhesion** (firm attachment). They bind to ligands like ICAM-1 and VCAM-1 on the endothelium, stopping the leukocyte's movement. * **Mucin-like glycoproteins (e.g., GlyCAM-1, PSGL-1):** These act as ligands for selectins and are involved in the initial tethering and rolling phase. **Clinical Pearls for NEET-PG:** * **CD31** is the most specific marker for **endothelial cells** and is used to identify vascular tumors (e.g., Angiosarcoma). * **Leukocyte Adhesion Deficiency (LAD) Type 1** is caused by a defect in **Integrins** (specifically the ̢2 chain of CD18), leading to impaired firm adhesion and recurrent infections without pus formation. * **LAD Type 2** is caused by a defect in **Sialyl-Lewis X** (ligand for selectins), impairing the rolling phase.

Q: Which of the following cytokines is not pyrogenic?

Interleukin-4 (IL-4). **Explanation:** The core concept here is the distinction between **pro-inflammatory (pyrogenic)** and **anti-inflammatory** cytokines. Pyrogens are substances that induce fever by acting on the hypothalamus to increase the set-point of body temperature, primarily through the induction of Prostaglandin E2 (PGE2). **Why Interleukin-4 (IL-4) is the correct answer:** IL-4 is a classic **anti-inflammatory cytokine** produced by Th2 cells. Its primary roles include promoting B-cell differentiation into IgE-producing plasma cells and inhibiting the production of pro-inflammatory cytokines. Because it antagonizes the inflammatory response, it does not induce fever and is therefore **not pyrogenic**. **Analysis of Incorrect Options (Pro-inflammatory Pyrogens):** * **IL-1 (Interleukin-1):** Often called the "endogenous pyrogen," it is the most potent inducer of fever. It stimulates the anterior hypothalamus to produce PGE2. * **TNF-α (Tumor Necrosis Factor-alpha):** A major mediator of acute inflammation and septic shock. It induces fever both directly and by stimulating the release of IL-1. * **IL-6 (Interleukin-6):** A key mediator of the acute-phase response. It acts as a pyrogen and is the primary stimulus for the liver to produce C-reactive protein (CRP). **High-Yield Clinical Pearls for NEET-PG:** * **Endogenous Pyrogens:** IL-1, IL-6, TNF-α, and IFN-γ. * **Exogenous Pyrogen:** Lipopolysaccharide (LPS) from Gram-negative bacteria is the most common example; it triggers the release of endogenous pyrogens. * **Mechanism of Fever:** Cytokines → Hypothalamic vascular endothelium → COX-2 activation → PGE2 release → Increased thermoregulatory set-point. * **Anti-inflammatory Cytokines:** IL-4, IL-10, and TGF-β (Think: "IL-10 and 4 keep the inflammation on the floor").

Q: Caseous necrosis in granuloma is typically not found in which of the following conditions?

Leprosy. **Explanation:** The core concept tested here is the distinction between **caseating** and **non-caseating** granulomas. **Why Leprosy is the correct answer:** In **Leprosy (Hansen’s disease)**, particularly the Tuberculoid spectrum, the characteristic lesion is a **non-caseating granuloma**. While both Tuberculosis and Leprosy are caused by Mycobacteria, the granulomas in Leprosy typically show epithelioid cells and Langhans giant cells *without* central cheesy (caseous) necrosis. In Lepromatous leprosy, granulomas are even less organized, consisting mainly of "foamy macrophages" (Virchow cells) packed with bacilli. **Analysis of Incorrect Options:** * **Tuberculosis (A):** This is the prototype of caseating granulomatous inflammation. The central area of the granuloma undergoes "cheese-like" necrosis due to the delayed-type hypersensitivity reaction against *M. tuberculosis*. * **Histoplasmosis (C):** Fungal infections, especially Histoplasmosis and Coccidioidomycosis, frequently mimic Tuberculosis by producing granulomas with central caseous necrosis. * **Cytomegalovirus (D):** While CMV typically presents with "Owl’s eye" intranuclear inclusions rather than classic granulomas, the question asks where caseous necrosis is *typically not found*. In the context of granulomatous diseases, Leprosy is the classic "non-caseating" example compared to TB. (Note: Some examiners include CMV as a distractor; however, in standard pathology, Leprosy is the definitive answer for non-caseating granulomas among Mycobacterial diseases). **High-Yield Clinical Pearls for NEET-PG:** * **Caseating Granulomas:** Tuberculosis, Histoplasmosis, Coccidioidomycosis, Syphilis (Gumma). * **Non-Caseating Granulomas:** Sarcoidosis (most common association), Leprosy, Cat-scratch disease (stellate), Crohn’s disease, Berylliosis, and Foreign body reactions. * **Key Histology:** Look for "Schumann bodies" and "Asteroid bodies" in Sarcoidosis (non-caseating).

Q: Genetic deficiency of myeloperoxidase (MPO) leads to increased susceptibility to infections due to which of the following mechanisms?

Inability to produce hydroxyl halide radicals. The correct answer is **C. Inability to produce hydroxyl halide radicals.** **Mechanism of Action:** Myeloperoxidase (MPO) is a heme-containing enzyme found in the primary (azurophilic) granules of neutrophils. During the "respiratory burst," NADPH oxidase converts oxygen into superoxide ($\text{O}_2^-$), which then dismutates into hydrogen peroxide ($\text{H}_2\text{O}_2$). MPO catalyzes the reaction between $\text{H}_2\text{O}_2$ and a halide (usually chloride) to produce **hypochlorous acid (HOCl)**—a potent hydroxyl halide radical. HOCl is the most effective bactericidal system in neutrophils; thus, MPO deficiency leads to an inability to generate this specific oxidant, resulting in impaired microbial killing. **Analysis of Incorrect Options:** * **A. Defective production of prostaglandin:** Prostaglandin synthesis involves the cyclooxygenase (COX) pathway, which is unrelated to the microbicidal activity of MPO. * **B. Defective rolling of neutrophils:** Rolling is mediated by **selectins** (E, P, and L-selectins). Defects in this process are seen in Leukocyte Adhesion Deficiency (LAD) Type 2. * **D. Inability to produce hydrogen peroxide:** $\text{H}_2\text{O}_2$ production is dependent on **NADPH oxidase** and superoxide dismutase. In Chronic Granulomatous Disease (CGD), there is a failure to produce $\text{H}_2\text{O}_2$, not in MPO deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **MPO Deficiency:** Most patients are clinically asymptomatic except for an increased risk of **disseminated Candidiasis** (especially in diabetics). * **NBT Test:** The Nitroblue Tetrazolium (NBT) test is **normal** (positive) in MPO deficiency because the respiratory burst (superoxide production) is intact. It is **abnormal** (negative) in CGD. * **Dihydrorhodamine (DHR) Flow Cytometry:** Currently the gold standard for screening phagocyte oxidase defects.

Question 1

Which of the following statements regarding wound healing is correct?

Accepted Answer

Wound healing is more rapid in young than in old individuals.

Answer

Wound healing is impaired in anemic patients.

Answer

Wound healing is not impaired by hypoproteinemia.

Answer

Wound healing is stimulated by steroids.

Question 2

Immune granulomas are not seen in which of the following conditions?

Accepted Answer

Silicosis

Answer

Tuberculosis

Answer

Syphilis

Answer

Berylliosis

Question 3

What molecule is most important for diapedesis?

Accepted Answer

PECAM

Answer

Selectins

Answer

Integrins

Answer

Mucin-like glycoproteins

Question 4

What is the first change seen in acute inflammation?

Accepted Answer

Vasoconstriction

Answer

Increased permeability

Answer

Vasodilation

Answer

Neutrophil migration

Question 5

Which of the following cytokines is not pyrogenic?

Accepted Answer

Interleukin-4 (IL-4)

Answer

Interleukin-1 (IL-1)

Answer

Tumor Necrosis Factor-alpha (TNF-a)

Answer

Interleukin-6 (IL-6)

Question 6

Which one of the following impairs epithelialization in wound healing?

Accepted Answer

Basic growth factor (BGF)

Answer

Platelet-derived growth factor (PDGF)

Answer

Fibronectin

Answer

Transforming growth factor (TGF)

Question 7

Caseous necrosis in granuloma is typically not found in which of the following conditions?

Accepted Answer

Leprosy

Answer

Tuberculosis

Answer

Histoplasmosis

Answer

Cytomegalovirus infection

Question 8

Genetic deficiency of myeloperoxidase (MPO) leads to increased susceptibility to infections due to which of the following mechanisms?

Accepted Answer

Inability to produce hydroxyl halide radicals

Answer

Defective production of prostaglandin

Answer

Defective rolling of neutrophils

Answer

Inability to produce hydrogen peroxide

Question 9

A fibroblast in a healing wound contains large quantities of which of the following cell organelles?

Accepted Answer

Rough endoplasmic reticulum

Answer

Nucleoli

Answer

Free non-membranous bound ribosomes

Answer

Smooth endoplasmic reticulum

Question 10

Which of the following chemical mediators of inflammation is an example of a C-X-C or alpha chemokine?

Accepted Answer

Interleukin IL-8

Answer

Lipoxin LXA-4

Answer

Interleukin IL-6

Answer

Monocyte chemoattractant protein MCP-1

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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