Inflammation and Repair Practice Questions

Q: Charcot Leyden crystals are derived from which type of cell?

Eosinophils. **Explanation:** **Correct Answer: B. Eosinophils** Charcot-Leyden crystals (CLCs) are hexagonal, bipyramidal, needle-like structures that serve as a hallmark of eosinophilic inflammation. They are composed of the protein **Galectin-10**, which is a lysophospholipase binding protein found in the cytoplasm of **eosinophils**. When eosinophils undergo degranulation or cell death (lysis), Galectin-10 is released and crystallizes to form these characteristic structures. **Analysis of Incorrect Options:** * **A. Macrophages:** While macrophages are involved in chronic inflammation and may phagocytose CLCs, they do not produce the Galectin-10 protein required to form them. * **C. Basophils:** Although basophils contain some Galectin-10, the concentration is significantly lower than in eosinophils. Clinically, CLCs are almost exclusively diagnostic of eosinophilic processes. * **D. Neutrophils:** Neutrophils are associated with acute bacterial inflammation and produce different markers, such as myeloperoxidase. They do not form CLCs. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Significance:** The presence of CLCs in clinical samples (sputum, stool, or tissue) indicates an **eosinophil-rich exudate**. * **Associated Conditions:** * **Bronchial Asthma:** Found in the sputum (often alongside Curschmann spirals). * **Parasitic Infections:** Found in the stool (e.g., *Entamoeba histolytica*, *Ascariasis*, or Hookworm infections). * **Allergic Rhinitis/Sinusitis:** Found in nasal secretions. * **Morphology:** They appear as slender, colorless, "double-pointed" needles that stain purplish-red with trichrome stains.

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

Charcot Leyden crystals are derived from which type of cell?

Accepted Answer

Eosinophils

Answer

Macrophages

Answer

Basophils

Answer

Neutrophils

Question 2

Which of the following is NOT a chemokine?

Accepted Answer

Histamine

Answer

IL-8

Answer

IL-1

Answer

Eotaxin

Question 3

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 4

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 5

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 6

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 7

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 8

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 9

Which of the following are anti-inflammatory mediators?

Accepted Answer

Lipoxins

Answer

Thromboxane

Answer

Prostaglandins

Answer

Interleukins

Question 10

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

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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