Inflammation and Repair Practice Questions

Q: Which of the following is seen in Chediak-Higashi syndrome?

All of the above. **Explanation:** **Chediak-Higashi Syndrome (CHS)** is a rare autosomal recessive disorder caused by a mutation in the **LYST (Lysosomal Trafficking Regulator) gene**. This defect disrupts protein trafficking, leading to the failure of phagosome-lysosome fusion. 1. **Why Option D is correct:** * **Presence of large granules (Option C):** This is the hallmark of CHS. Due to disordered intracellular trafficking, lysosomes and secretory granules fuse uncontrollably, forming **giant azurophilic granules** visible in neutrophils, melanocytes, and platelets. * **Defective microbial killing (Option B):** Although bacteria are ingested normally, the inability of phagosomes to fuse with lysosomes prevents the delivery of bactericidal enzymes. This leads to recurrent pyogenic infections (e.g., *Staphylococcus aureus*). * **Neutropenia (Option A):** Giant granules damage the precursor cells in the bone marrow, leading to ineffective hematopoiesis and intramedullary destruction of neutrophils. **Clinical Pearls for NEET-PG:** * **Classic Tetrad:** 1. **Partial Oculocutaneous Albinism** (melanin trapped in giant melanosomes). 2. **Recurrent Pyogenic Infections** (respiratory and skin). 3. **Progressive Neuropathy** (peripheral and cranial). 4. **Bleeding Tendency** (due to defective dense granules in platelets). * **Peripheral Smear:** Look for "Giant Lysosomal Granules" in granulocytes. * **Accelerated Phase:** Most patients eventually develop a "hemophagocytic lymphohistiocytosis" (HLH)-like syndrome characterized by hepatosplenomegaly and pancytopenia.

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

Which of the following is seen in Chediak-Higashi syndrome?

Accepted Answer

All of the above

Answer

Neutropenia

Answer

Defective microbial killing

Answer

Presence of large granules in neutrophils

Question 2

What is the most important role of bradykinin in acute inflammation?

Accepted Answer

Increase in vascular permeability

Answer

Vasodilation

Answer

Mediation of pain

Answer

Bronchoconstriction

Question 3

Which among the following is the hallmark of acute inflammation?

Accepted Answer

Vasodilation and increase in permeability

Answer

Vasoconstriction

Answer

Stasis

Answer

Leukocyte margination

Question 4

Scar formation is part of the normal healing process following injury. Which of the following tissues has the ability to heal without scar formation?

Accepted Answer

Bone

Answer

Liver

Answer

Skin

Answer

Muscle

Question 5

In the lipoxygenase pathway, which of the following arachidonic acid products promotes platelet aggregation and vasoconstriction?

Accepted Answer

Thromboxane A2

Answer

C5a

Answer

Leukotriene B4

Answer

Complement activators

Question 6

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 7

Which of the following are anti-inflammatory mediators?

Accepted Answer

Lipoxins

Answer

Thromboxane

Answer

Prostaglandins

Answer

Interleukins

Question 8

A full-thickness wound that is not sutured heals by what process?

Accepted Answer

Secondary healing

Answer

Primary healing

Answer

Delayed primary healing

Answer

Reepithelization

Question 9

All of the following can trigger sensors of cell damage in the cytoplasm, except:

Accepted Answer

Increased intracellular potassium ion concentration

Answer

Adenosine triphosphate

Answer

Deoxyribonucleic acid

Answer

Uric acid

Question 10

Which cytokine is responsible for activating macrophages and their conversion into epithelioid cells or giant cells?

Accepted Answer

Interferon-gamma (IFN-gamma)

Answer

Interleukin-2 (IL-2)

Answer

Interleukin-17 (IL-17)

Answer

Tumor Necrosis Factor-alpha (TNF-alpha)

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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