Inflammation and Repair Practice Questions

Q: Which of the following eicosanoids cause vasoconstriction and increase vascular permeability?

Leukotriene C4. **Explanation:** The correct answer is **Leukotriene C4 (LTC4)**. Eicosanoids are lipid mediators derived from arachidonic acid via two main pathways: the Cyclooxygenase (COX) pathway and the Lipoxygenase (LOX) pathway [1]. **1. Why Leukotriene C4 is correct:** LTC4, along with LTD4 and LTE4 (collectively known as cysteinyl leukotrienes), are produced via the 5-LOX pathway. These mediators are potent triggers of **smooth muscle contraction**. In the vascular system, they cause **vasoconstriction**, while in the microcirculation, they induce endothelial cell contraction, leading to increased **vascular permeability** (venular leakage) [1]. They are significantly more potent than histamine in inducing these effects [1]. **2. Why the other options are incorrect:** * **Prostacyclin (PGI2):** Produced by vascular endothelium, it is a potent **vasodilator** and inhibitor of platelet aggregation [1]. * **Thromboxane A2 (TXA2):** Produced by platelets, it causes potent vasoconstriction and promotes platelet aggregation, but it does **not** increase vascular permeability [1]. * **PGE1:** Prostaglandins of the E series (PGE1 and PGE2) are primarily **vasodilators** and are involved in inducing pain and fever [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Vasodilation:** PGI2, PGE1, PGE2, PGD2 [1]. * **Vasoconstriction:** TXA2, LTC4, LTD4, LTE4 [1]. * **Increased Vascular Permeability:** LTC4, LTD4, LTE4 (Cysteinyl leukotrienes) [1]. * **Chemotaxis:** LTB4 is the "gold standard" chemotactic agent among eicosanoids (along with IL-8, C5a, and bacterial products) [1]. * **Aspirin-induced Asthma:** Caused by the shunting of arachidonic acid from the COX pathway to the LOX pathway, leading to an overproduction of bronchoconstrictive leukotrienes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.

Q: Which of the following is NOT a pro-inflammatory cytokine?

Interleukin-10. ### Explanation Cytokines are signaling molecules that regulate the immune response. They are broadly categorized into **pro-inflammatory** (promoting inflammation) and **anti-inflammatory** (limiting inflammation and promoting tissue repair). **Why Interleukin-10 (IL-10) is the correct answer:** IL-10 is a potent **anti-inflammatory cytokine**. Its primary role is to terminate the inflammatory response and prevent host tissue damage. It acts by inhibiting the synthesis of pro-inflammatory cytokines (like IL-1, IL-6, and TNF-α) and suppressing the antigen-presenting capacity of macrophages and dendritic cells by downregulating MHC Class II expression. **Analysis of Incorrect Options:** * **Interleukin-1 (IL-1):** A classic pro-inflammatory cytokine produced by macrophages. It is a primary mediator of the acute phase response and is responsible for inducing **fever** (endogenous pyrogen). * **Interleukin-6 (IL-6):** A major pro-inflammatory cytokine that stimulates the liver to produce **Acute Phase Reactants** (like CRP and Fibrinogen). It also plays a key role in the transition from innate to adaptive immunity. * **TNF-Alpha (Tumor Necrosis Factor):** A "master regulator" of inflammation. It promotes leukocyte adhesion, activates endothelial cells, and is a key mediator in the pathogenesis of **septic shock**. **NEET-PG High-Yield Pearls:** * **Anti-inflammatory cytokines:** Remember the duo **IL-10 and TGF-β** (Transforming Growth Factor-beta). * **Pro-inflammatory cytokines:** The "Big Three" are **IL-1, IL-6, and TNF-α**. * **IL-8** is the primary chemotactic factor for neutrophils ("Clean up on aisle 8"). * **IL-12** drives the differentiation of Th1 cells, bridging innate and adaptive immunity.

Q: Rubor (redness) during inflammation is primarily due to:

Dilatation of the arterioles. ### Explanation **Correct Answer: D. Dilatation of the arterioles** **Mechanism:** The cardinal signs of inflammation (Rubor, Calor, Tumor, Dolor, and Functio Laesa) are initiated by chemical mediators like histamine, bradykinin, and prostaglandins. **Rubor (redness)** and **Calor (heat)** are primarily caused by **active hyperemia**. This occurs when inflammatory mediators cause the smooth muscles of the **arterioles** to relax, leading to vasodilation. This increases blood flow to the capillary bed, resulting in the characteristic redness and warmth seen in inflamed tissues. **Analysis of Incorrect Options:** * **A & B (Decreased Oncotic Pressure):** Oncotic pressure (primarily maintained by albumin) governs fluid movement between compartments. A decrease in oncotic pressure contributes to **Tumor (edema)** by allowing fluid to leak into the interstitium, but it does not cause the redness associated with Rubor. * **C (Constriction of the capillaries):** Capillaries lack smooth muscle and do not "constrict" in the traditional sense. Furthermore, any reduction in blood flow (vasoconstriction) would lead to pallor (whiteness), not rubor. **High-Yield Clinical Pearls for NEET-PG:** * **Triple Response of Lewis:** Includes **Flush** (capillary dilatation), **Flare** (arteriolar dilatation via axon reflex), and **Wheal** (exudation/edema). * **Sequence of Hemodynamic Changes:** Transient vasoconstriction (seconds) → Persistent arteriolar vasodilation → Increased vascular permeability (leading to stasis). * **Key Mediator:** Histamine is the most important mediator for the immediate transient phase of increased vascular permeability.

Q: In the inflammatory process, what effect do prostaglandins E1 and E2 have?

Vasodilation. **Explanation:** Prostaglandins (PGs) are lipid autacoids derived from arachidonic acid via the cyclooxygenase (COX) pathway [2]. They play a pivotal role in the cardinal signs of inflammation. **1. Why Vasodilation is Correct:** Prostaglandins **PGE1 and PGE2** are potent **vasodilators**. During inflammation, they act on G-protein coupled receptors (EP receptors) on vascular smooth muscle cells, leading to relaxation and increased blood flow (hyperemia) [1]. This vasodilation contributes to the clinical presentation of *rubor* (redness) and *calor* (heat) at the site of injury. Furthermore, they sensitize nociceptors to bradykinin and histamine, mediating inflammatory pain. **2. Analysis of Incorrect Options:** * **B. Increased gastric output:** This is incorrect. PGE2 and PGI2 (Prostacyclin) actually **decrease** gastric acid secretion and increase the production of protective mucus and bicarbonate (cytoprotective effect). * **C. Decreased body temperature:** PGE2 is a major mediator of **fever**. It acts on the anterior hypothalamus to increase the thermoregulatory set-point; therefore, it increases body temperature rather than decreasing it. * **D. Vasoconstriction:** While some eicosanoids like Thromboxane A2 (TXA2) and PGF2-alpha cause vasoconstriction, PGE1 and PGE2 are primarily vasodilatory [1]. **High-Yield NEET-PG Pearls:** * **PGE2** is the primary prostaglandin involved in **fever induction** and **patent ductus arteriosus (PDA)** maintenance. * **Alprostadil** is a PGE1 analogue used clinically to keep the ductus arteriosus open in cyanotic heart disease. * **Misoprostol** (PGE1 analogue) is used for gastric protection against NSAID-induced ulcers and for medical abortion. * **NSAIDs** exert their anti-inflammatory and analgesic effects by inhibiting COX enzymes, thereby reducing the synthesis of PGE2 [2].

Q: The morphological pattern of inflammation shown here is:

Serous. ***Serous*** - Characterized by **watery, protein-poor fluid** with minimal cellular content, typically seen in **blisters** and **vesicles**. - Classic example includes **skin blisters** from burns or allergic reactions, where clear fluid accumulates in tissue spaces. *Fibrinous* - Features **fibrin strands** and **fibrin deposits** creating a mesh-like appearance on tissue surfaces. - Commonly seen in **pericarditis** and **pleuritis**, where fibrin forms a "bread-and-butter" appearance on organ surfaces. *Purulent* - Contains abundant **neutrophils** and **pus formation** with thick, yellowish inflammatory exudate. - Typical of **bacterial infections** like abscesses, where neutrophil infiltration dominates the inflammatory response. *Chronic* - Dominated by **lymphocytes**, **macrophages**, and **plasma cells** rather than acute inflammatory cells. - Develops over **weeks to months** and often involves **tissue destruction** and **fibrosis** formation.

Question 1

Arrange the following steps in order of the events occurring first to last: Margination, Rolling, Stasis, Pavementing?

Accepted Answer

Stasis, Margination, Rolling, Pavementing

Answer

Margination, Rolling, Stasis, Pavementing

Answer

Pavementing, Stasis, Rolling, Margination

Answer

Pavementing, Margination, Rolling, Stasis

Question 2

Which of the following eicosanoids cause vasoconstriction and increase vascular permeability?

Accepted Answer

Leukotriene C4

Answer

Prostacyclin

Answer

Thromboxane A2

Answer

PGE1

Question 3

Which of the following is NOT a pro-inflammatory cytokine?

Accepted Answer

Interleukin-10

Answer

Interleukin 1

Answer

Interleukin 6

Answer

TNF-Alpha

Question 4

Multinucleated giant cells are least likely to be found in which of the following disorders?

Accepted Answer

Streptococcus pneumoniae infection

Answer

Blastomycosis

Answer

Cat scratch fever

Answer

Sarcoidosis

Question 5

Rubor (redness) during inflammation is primarily due to:

Accepted Answer

Dilatation of the arterioles

Answer

Decreased tissue oncotic pressure

Answer

Decreased oncotic pressure in arterioles

Answer

Constriction of the capillaries

Question 6

In the inflammatory process, what effect do prostaglandins E1 and E2 have?

Accepted Answer

Vasodilation

Answer

Increased gastric output

Answer

Decreased body temperature

Answer

Vasoconstriction

Question 7

Esterase inhibitor deficiency causes which of the following conditions?

Accepted Answer

Hereditary angioneurotic edema

Answer

Systemic Lupus Erythematosus (SLE)

Answer

Membranoproliferative Glomerulonephritis (MPGN)

Answer

Omen syndrome

Question 8

A 29-year-old carpenter receives a traumatic laceration to her left arm. Which of the following is the most important factor that determines whether this wound will heal by primary or secondary intention?

Accepted Answer

Apposition of edges

Answer

Depth of wound

Answer

Metabolic status

Answer

Skin site affected

Question 9

The morphological pattern of inflammation shown here is:

Accepted Answer

Serous

Answer

Fibrinous

Answer

Purulent

Answer

Chronic

Question 10

Which of the following statements regarding keloid formation is true?

Accepted Answer

Keloids exhibit increased collagen deposition and vascularity.

Answer

Keloids are characterized by normal levels of growth factors.

Answer

Surgical excision is the primary treatment for keloids.

Answer

Keloid tissue typically remains confined to the original wound site.

Inflammation and Repair — MCQs

Inflammation and Repair — MCQs

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