Inflammation and Repair Practice Questions

Q: Chediak Higashi syndrome is characterized by the following EXCEPT:

Neutrophilia. **Explanation:** **Chediak-Higashi Syndrome (CHS)** is a rare autosomal recessive disorder caused by a mutation in the **LYST gene** (Lysosomal Trafficking Regulator) [1]. This mutation leads to defective vesicle fusion and protein trafficking [1]. **Why "Neutrophilia" is the correct answer (the exception):** Patients with CHS actually present with **Neutropenia**, not neutrophilia [1]. The defect in lysosomal trafficking interferes with normal hematopoiesis in the bone marrow, leading to ineffective granulopoiesis and the premature destruction of white blood cells. **Analysis of other options:** * **Giant Granules (Option D):** This is the morphological hallmark of CHS. Due to disordered fusion of endosomes and lysosomes, massive, non-functional "giant" granules are seen in neutrophils, eosinophils, and melanocytes [1]. * **Defective Degranulation (Option B):** The giant granules are unable to fuse properly with phagosomes [1]. This prevents the release of hydrolytic enzymes into the phagocytic vacuole. * **Delayed Microbial Killing (Option C):** Because degranulation is impaired, the delivery of bactericidal enzymes to the ingested microbe is delayed or absent, leading to recurrent pyogenic infections [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Tetrad:** 1. Oculocutaneous albinism (melanocyte defect), 2. Recurrent pyogenic infections (staphylococci/streptococci), 3. Progressive neurological defects, 4. Bleeding tendencies (platelet dense body defect) [1]. * **Diagnosis:** Peripheral blood smear showing **giant peroxidase-positive granules** in neutrophils [1]. * **Accelerated Phase:** Most patients eventually enter a "hemophagocytic lymphohistiocytosis" (HLH) phase characterized by hepatosplenomegaly and pancytopenia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Q: Which of the following cytokines is secreted by classically activated macrophages (M1)?

IL-1. **Explanation:** Macrophages can be activated via two distinct pathways: the **Classical (M1)** pathway and the **Alternative (M2)** pathway [1]. **1. Why IL-1 is correct:** Classically activated macrophages (M1) are induced by microbial products (like LPS) and IFN-γ [1]. Once activated, M1 macrophages function as "pro-inflammatory" cells. They secrete potent inflammatory cytokines, primarily **IL-1, IL-12, IL-23, and TNF** [1]. These cytokines serve to recruit more leukocytes and initiate the acute inflammatory response. M1 cells also produce reactive oxygen species (ROS) and nitric oxide (NO) to facilitate microbicidal activity [1]. **2. Why the other options are incorrect:** * **IL-2:** This is a T-cell growth factor primarily secreted by **Th1 cells**, not macrophages. It stimulates the proliferation of T-lymphocytes and NK cells. * **IL-4:** This is the hallmark cytokine of the **Th2 response**. It actually inhibits M1 activation and instead promotes **Alternative (M2) macrophage activation**, which is involved in tissue repair and anti-inflammatory responses [1]. * **IL-3:** This is a hematopoietic growth factor secreted by activated T-cells that stimulates the production of cells in the bone marrow. **High-Yield Clinical Pearls for NEET-PG:** * **M1 (Classical):** Induced by IFN-γ; Pro-inflammatory; Secretes **IL-1, IL-12, TNF**; Involved in inflammation and tissue destruction [1]. * **M2 (Alternative):** Induced by **IL-4, IL-13**; Anti-inflammatory; Secretes **IL-10, TGF-β**; Involved in tissue repair, fibrosis, and wound healing [1]. * **Memory Aid:** **M1** = "Murder" (Microbicidal/Inflammation); **M2** = "Mend" (Repair/Healing). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 104-107.

Q: In the cyclooxygenase (COX) pathway of arachidonic acid metabolism, which of the following products promotes platelet aggregation and vasoconstriction?

Thromboxane A2. The correct answer is **Thromboxane A2 (TXA2)**. Arachidonic acid is released from membrane phospholipids by phospholipase A2 [1] and metabolized via two major pathways: the Cyclooxygenase (COX) pathway and the Lipoxygenase (LOX) pathway. 1. **Why Thromboxane A2 is correct:** TXA2 is synthesized primarily in platelets via the COX pathway. It is a potent **vasoconstrictor** and a powerful **inducer of platelet aggregation** [1]. It acts in physiological antagonism to Prostacyclin (PGI2), which is a vasodilator and inhibitor of aggregation. The balance between TXA2 and PGI2 is critical for maintaining vascular homeostasis. 2. **Why other options are incorrect:** * **C5a:** This is a component of the Complement System (Anaphylatoxin). Its primary roles are chemotaxis for neutrophils and increasing vascular permeability [1]; it is not a product of the COX pathway. * **Leukotriene B4 (LTB4):** While derived from arachidonic acid, it is a product of the **Lipoxygenase (LOX) pathway**. It is a potent chemotactic agent for neutrophils but does not cause platelet aggregation [1]. * **C1 activators:** These are proteins involved in the initiation of the Classical Complement pathway, unrelated to arachidonic acid metabolism. **NEET-PG High-Yield Pearls:** * **Aspirin's Mechanism:** Low-dose aspirin irreversibly inhibits COX-1, shifting the balance toward PGI2 (antithrombotic) by inhibiting TXA2 synthesis in platelets (which cannot regenerate the enzyme) [1]. * **Chemotaxis Mnemonic:** "Big B" (**LTB4**), **C5a**, and **IL-8** are the primary "attractants" for neutrophils. * **Vasodilation:** Prostaglandins **PGI2, PGE1, PGE2, and PGD2** are primarily vasodilators [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.

Question 1

"CACHECTIN" is produced by?

Accepted Answer

macrophage

Answer

neutrophils

Answer

basophils

Answer

eosinophils

Question 2

Serum amyloid A protein levels are increased in which of the following conditions?

Accepted Answer

Ankylosing spondylitis

Answer

Alzheimer’s disease

Answer

Chronic renal failure

Answer

Malignant hypertension

Question 3

Chediak Higashi syndrome is characterized by the following EXCEPT:

Accepted Answer

Neutrophilia

Answer

Defective degranulation

Answer

Delayed microbial killing

Answer

Giant granules

Question 4

All of the following are false regarding vascular leakage in acute inflammation, except:

Accepted Answer

A hallmark of acute inflammation is increased permeability in the post-capillary venules.

Answer

Chemical mediators such as histamine play a role in delayed vascular leakage.

Answer

Transcytosis is not a contributing factor to vascular leakage.

Answer

In most cases, vascular leakage starts several hours after injury.

Question 5

Serotonin, a mediator of inflammation, is secreted/released by which of the following cells?

Accepted Answer

Platelets

Answer

Leukocytes

Answer

Endothelial cells

Answer

Mast cells

Question 6

In a granuloma, epithelioid cells and giant cells are derived from which cell type?

Accepted Answer

Monocyte-macrophages

Answer

T lymphocytes

Answer

B lymphocytes

Answer

Mast cells

Question 7

Which of the following cytokines is secreted by classically activated macrophages (M1)?

Accepted Answer

IL-1

Answer

IL-2

Answer

IL-4

Answer

IL-3

Question 8

Which of the following is an exogenous pyrogen?

Accepted Answer

Lipopolysaccharide

Answer

TNF-a

Answer

Neurotropic factor

Answer

IL-6

Question 9

In the cyclooxygenase (COX) pathway of arachidonic acid metabolism, which of the following products promotes platelet aggregation and vasoconstriction?

Accepted Answer

Thromboxane A2

Answer

C5a

Answer

Leukotriene B4

Answer

C1 activators

Question 10

The healing of an extraction socket where flaps are approximated occurs by which type of intention?

Accepted Answer

Primary intention

Answer

Secondary intention

Answer

Tertiary intention

Answer

Any of the above

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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