Inflammation and Repair — MCQs

An 8-year-old girl with asthma presents with respiratory distress, a history of allergies and upper respiratory tract infections, and wheezing associated with exercise. Which of the following preformed substances, released from mast cells and platelets, results in increased vascular permeability in the lungs?

Q238Medium

Which of the following is activated by the binding of chemotactic agents to leukocyte membrane receptors?

Q239Easy

Macrophages are converted to epithelioid cells by which cytokine?

Q240Medium

Vascular dilation in the inflammatory response is mediated by all the following EXCEPT?

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 231: Which of the following is not an inflammatory mediator?

A. Tumor necrosis factor
B. Integrin (Correct Answer)
C. Interleukin
D. Interferons

Explanation: **Explanation:** The correct answer is **Integrin** because it is an **adhesion molecule**, not a chemical mediator of inflammation. [1] **1. Why Integrin is the correct answer:** Inflammatory mediators are soluble substances (like cytokines or amines) that initiate or amplify the inflammatory response. [1] Integrins, however, are **transmembrane glycoproteins** expressed on the surface of leukocytes. [1] Their primary role is to mediate the **firm adhesion** of leukocytes to the vascular endothelium (by binding to ligands like ICAM-1 and VCAM-1) during the process of leukocyte extravasation. [1] They are structural components of the cell membrane, not secreted signaling molecules. **2. Analysis of incorrect options:** * **Tumor Necrosis Factor (TNF):** A major pro-inflammatory cytokine produced mainly by macrophages. [1] It stimulates the expression of adhesion molecules on endothelium and induces the systemic acute-phase response. [1] * **Interleukins (IL):** A large group of cytokines (e.g., IL-1, IL-6, IL-8) that serve as key mediators. [1] IL-1 works with TNF to activate endothelium, while IL-8 acts as a potent chemoattractant. [1] * **Interferons (IFN):** Specifically IFN-gamma is a critical mediator in chronic inflammation, responsible for activating macrophages and enhancing their phagocytic ability. **High-Yield Clinical Pearls for NEET-PG:** * **LAD Type 1:** Caused by a deficiency in **beta2-integrins** (CD11/CD18), leading to impaired leukocyte adhesion, delayed umbilical cord separation, and recurrent bacterial infections without pus formation. * **Activation:** Integrins on resting leukocytes are in a low-affinity state; they are converted to a **high-affinity state** by chemokines during the "rolling" phase of recruitment. [1] * **Key Mediators of Vasodilation:** Histamine and Prostaglandins. [1] * **Key Mediators of Pain:** Bradykinin and Prostaglandins (PGE2). [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-101.

Question 232: A granulomatous inflammatory reaction is seen in all of the following EXCEPT:

A. Mycobacterium tuberculosis
B. Mycobacterium leprae
C. Yersinia pestis
D. Mycoplasma (Correct Answer)

Explanation: **Explanation:** The core concept tested here is the distinction between **granulomatous inflammation** (a specific form of chronic inflammation) and **acute/non-specific inflammation**. [1] **Why Mycoplasma is the correct answer:** *Mycoplasma pneumoniae* typically causes **atypical pneumonia**, characterized by an interstitial inflammatory infiltrate consisting primarily of **lymphocytes and plasma cells**, rather than granulomas. It lacks a cell wall and does not trigger the Type IV hypersensitivity reaction required for granuloma formation. **Why the other options are incorrect:** * **Mycobacterium tuberculosis:** The classic cause of **caseating granulomas** [4]. The cell wall contains mycolic acids that resist digestion, leading to a T-cell mediated response and epithelioid cell aggregation [1]. * **Mycobacterium leprae:** Causes leprosy, characterized by either **tuberculoid granulomas** (well-formed) or **lepromatous lesions** (foamy macrophages/histiocytes), both of which fall under the spectrum of granulomatous disease. * **Yersinia pestis:** While it causes bubonic plague (necrosis), it is also associated with **sarcoid-like granulomas** in certain chronic presentations. Note: *Yersinia enterocolitica* is a more common cause of mesenteric lymph node granulomas. **NEET-PG High-Yield Pearls:** 1. **Definition of a Granuloma:** A focal collection of **epithelioid histiocytes** (activated macrophages with abundant pink cytoplasm) surrounded by a rim of lymphocytes [1],[2]. 2. **Common Granulomatous Diseases (Mnemonic: SUGAR):** **S**arcoidosis, **U**nknown (Berylliosis), **G**raft vs Host/Granulomatosis with polyangiitis, **A**ctinomycosis/Cat-scratch disease, **R**heumatoid nodules/Syphilis. 3. **Non-infectious causes:** Sarcoidosis (non-caseating), Berylliosis, and Foreign body reactions (sutures, talc) [2], [3]. 4. **Stains:** Always remember **Ziehl-Neelsen (ZN) stain** for Mycobacteria and **Gomori Methenamine Silver (GMS)** for fungal granulomas. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 198-200. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 196-197. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 384-385.

Question 233: Which of the following hormones has the greatest effect on granulation tissue in wound healing?

A. Antidiuretic hormone (ADH)
B. Estrogen
C. Cortisol (Correct Answer)
D. Parathormone

Explanation: **Explanation:** **Why Cortisol is the Correct Answer:** Glucocorticoids, specifically **Cortisol**, have a profound inhibitory effect on wound healing [1]. They are well-known for antagonizing the inflammatory response and impairing the formation of **granulation tissue**. Cortisol achieves this through several mechanisms: 1. **Inhibition of TGF-β:** It decreases the production of Transforming Growth Factor-beta, which is essential for collagen synthesis. 2. **Fibroblast Inhibition:** It reduces fibroblast proliferation and activity, leading to decreased collagen deposition. 3. **Anti-angiogenic effects:** It inhibits the formation of new blood vessels (neovascularization), a hallmark of granulation tissue. 4. **Weakened Scar:** The resulting scar has poor tensile strength and is prone to dehiscence. **Why the Other Options are Incorrect:** * **A. Antidiuretic hormone (ADH):** Primarily regulates water reabsorption in the renal collecting ducts and has no significant physiological role in tissue repair or granulation. * **B. Estrogen:** Generally promotes wound healing by accelerating re-epithelialization and modulating the inflammatory response. It does not inhibit granulation tissue like cortisol does. * **D. Parathormone (PTH):** Primarily regulates calcium and phosphate homeostasis by acting on bone and kidneys; it does not directly influence the cellular dynamics of soft tissue wound healing. **NEET-PG High-Yield Pearls:** * **Clinical Correlation:** Patients on long-term steroids (e.g., for SLE or Asthma) or those with Cushing’s syndrome exhibit delayed wound healing and thin, fragile skin [2]. * **Vitamin Connection:** Vitamin C deficiency (Scurvy) also impairs granulation tissue by preventing the hydroxylation of proline and lysine residues in collagen. * **Granulation Tissue Components:** Defined by the triad of **Fibroblasts**, **Capillaries** (Angiogenesis), and **Inflammatory cells** (mainly Macrophages). Do not confuse "Granulation tissue" with "Granuloma" (a form of chronic inflammation). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 420-421. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1127-1129.

Question 234: Which of the following is a preformed mediator of inflammation?

A. Serotonin (Correct Answer)
B. Prostaglandin
C. Dopamine
D. Leukotrienes

Explanation: ### Explanation Chemical mediators of inflammation are classified into two main categories based on their origin: **Cell-derived** and **Plasma-derived** [3]. Cell-derived mediators are further divided into **preformed** (stored in secretory granules) and **newly synthesized** (produced on demand) [3]. **Why Serotonin is Correct:** **Serotonin (5-hydroxytryptamine)** is a **preformed** vasoactive amine [1]. It is primarily stored in the granules of **platelets** and certain neuroendocrine cells (e.g., enterochromaffin cells) [1]. During inflammation, platelet aggregation triggers the release of serotonin, which causes increased vascular permeability and vasodilation (similar to histamine) [2]. **Analysis of Incorrect Options:** * **Prostaglandins (B) and Leukotrienes (D):** These are **newly synthesized** mediators derived from **Arachidonic Acid** metabolism [1]. They are produced via the Cyclooxygenase (COX) and Lipoxygenase (LOX) pathways, respectively, only after a cell is activated [4]. * **Dopamine (C):** While a catecholamine and neurotransmitter, dopamine is not a primary mediator of the inflammatory response. **High-Yield NEET-PG Pearls:** * **The Two Preformed Mediators:** Only **Histamine** (Mast cells, Basophils) and **Serotonin** (Platelets) are considered major preformed cell-derived mediators [3]. * **Histamine** is the first mediator to be released during the immediate transient phase of increased vascular permeability. * **Plasma-derived mediators** (e.g., Complement proteins, Kinins, Coagulation factors) are produced by the **liver** and circulate in an inactive precursor form [3]. * **Memory Aid:** "Preformed = **H**istamine & **S**erotonin" (Think: **H**ot **S**tuff is ready to go). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.

Question 235: A 54-year-old man presents with poor wound healing following laparoscopic hernia repair, despite small incision size. Further history reveals a diet deficient in vitamin C. Which extracellular matrix component's synthesis is most significantly affected by vitamin C deficiency?

A. Collagen (Correct Answer)
B. Elastin
C. Fibronectin
D. Integrin

Explanation: **Explanation:** The correct answer is **Collagen**. Vitamin C (ascorbic acid) is an essential cofactor for the enzymes **prolyl hydroxylase** and **lysyl hydroxylase**. These enzymes are responsible for the hydroxylation of proline and lysine residues during the post-translational modification of pre-procollagen. Hydroxyproline is critical for stabilizing the collagen triple helix via hydrogen bonding. In Vitamin C deficiency (Scurvy), collagen remains unstable and is easily degraded, leading to defective osteoid formation, capillary fragility, and poor wound healing [2]. **Analysis of Incorrect Options:** * **B. Elastin:** While elastin contains some hydroxyproline, its synthesis is not as heavily dependent on Vitamin C as collagen. Elastin relies more on desmosine and isodesmosine cross-links mediated by lysyl oxidase (which requires Copper). * **C. Fibronectin:** This is an adhesive glycoprotein that binds ECM components to cells. Its synthesis is not directly regulated by Vitamin C-dependent hydroxylation. * **D. Integrin:** These are transmembrane receptors that facilitate cell-extracellular matrix adhesion [1]. They are proteins, but their synthesis does not involve the specific hydroxylation steps characteristic of collagen. **NEET-PG High-Yield Pearls:** * **Hydroxylation** occurs in the **Rough Endoplasmic Reticulum (RER)**. * **Copper deficiency** affects **Lysyl Oxidase**, leading to impaired cross-linking of both collagen and elastin (seen in Menkes syndrome). * **Type I Collagen** is the most abundant and is the primary collagen involved in late-stage wound healing and scar formation [3]. * **Scurvy Clinical Triad:** Perifollicular hemorrhage, corkscrew hairs, and bleeding gums. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 32-34. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 116-117. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 236: A 5-year-old boy punctures his thumb with a rusty nail. Four hours later, the thumb appears red and swollen. Which of the following serum proteins activates the complement, coagulation, and fibrinolytic systems at the site of injury?

A. Bradykinin
B. Hageman factor (Correct Answer)
C. Kallikrein
D. Plasmin

Explanation: **Explanation:** The correct answer is **Hageman Factor (Factor XII)**. This scenario describes the early stages of acute inflammation following a mechanical injury. **Why Hageman Factor is correct:** Hageman factor (Factor XII) is a serum protein synthesized by the liver that circulates in an inactive form. It is activated upon contact with negatively charged surfaces, such as **exposed subendothelial collagen** (following the nail puncture), basement membranes, or bacterial endotoxins. Once activated (XIIa), it acts as a central "hub" for four interrelated mediator systems [1]: 1. **Kinin System:** Converts prekallikrein to kallikrein, eventually producing bradykinin [1]. 2. **Clotting System:** Activates the intrinsic coagulation pathway (Factor XI → XIa) [1]. 3. **Fibrinolytic System:** Converts plasminogen to plasmin [1]. 4. **Complement System:** Activates C3 to C3a (anaphylatoxin) [1]. **Why other options are incorrect:** * **A. Bradykinin:** A product of the kinin system that causes vasodilation, increased vascular permeability, and **pain** [2]. It does not activate the other systems; it is an end-effector. * **C. Kallikrein:** An intermediate enzyme that cleaves HMWK to produce bradykinin. While it can further activate Factor XII (autocatalysis), it is not the primary initiator of all four systems. * **D. Plasmin:** The primary enzyme of the fibrinolytic system responsible for lysing fibrin clots. While it can activate C3, it is a downstream product rather than the initial activator. **High-Yield NEET-PG Pearls:** * **The "Linker":** Factor XIIa is the key link between inflammation and coagulation [1]. * **Pain Mediators:** Remember **P**rostaglandin (PGE2) and **B**radykinin mediate **P**ain [2]. * **Vascular Permeability:** Histamine is the primary mediator of the immediate transient response (15–30 mins), whereas Hageman factor-driven systems sustain the inflammatory response. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 189-190. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 237: An 8-year-old girl with asthma presents with respiratory distress, a history of allergies and upper respiratory tract infections, and wheezing associated with exercise. Which of the following preformed substances, released from mast cells and platelets, results in increased vascular permeability in the lungs?

A. Bradykinin
B. Hageman factor
C. Histamine (Correct Answer)
D. Leukotrienes (SRS-A)

Explanation: **Explanation:** The clinical presentation describes a classic case of **Type I Hypersensitivity** (Atopic Asthma). The key to this question lies in the phrase **"preformed substances."** **1. Why Histamine is Correct:** Histamine is the primary vasoactive amine involved in the immediate phase of inflammation. It is stored in a **preformed state** within the granules of mast cells, basophils, and platelets [3]. Upon IgE-mediated degranulation, histamine is rapidly released, leading to: * Contraction of post-capillary venular endothelial cells (creating gaps). * **Increased vascular permeability** (edema) [1], [3]. * Bronchoconstriction and mucus production [1]. **2. Why the other options are incorrect:** * **Bradykinin (A):** While it increases vascular permeability and causes pain, it is not "preformed" in cells; it is derived from the cleavage of high-molecular-weight kininogen (HMWK) in the plasma [2]. * **Hageman factor (B):** Also known as Factor XII, this is a plasma protein synthesized by the liver. It initiates the kinin, coagulation, and fibrinolytic systems but is not a mediator released from mast cells. * **Leukotrienes (D):** Specifically LTC4, LTD4, and LTE4 (SRS-A), these are potent bronchoconstrictors and increase permeability. However, they are **newly synthesized** from arachidonic acid via the lipoxygenase pathway, not preformed. **NEET-PG High-Yield Pearls:** * **Vasoactive Amines:** Histamine and Serotonin are the two main preformed mediators. * **Mechanism of Permeability:** Histamine causes "immediate transient response" (lasting 15–30 mins) specifically in the **post-capillary venules**. * **Mast Cell Triggers:** Apart from IgE, mast cells can be degranulated by physical stimuli (cold, heat), C3a/C5a (anaphylatoxins), and certain drugs (morphine). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 211-212.

Question 238: Which of the following is activated by the binding of chemotactic agents to leukocyte membrane receptors?

A. Leukotriene B4
B. Histamine
C. Phospholipase C (Correct Answer)
D. Tumor necrosis factor

Explanation: **Explanation:** The binding of chemotactic agents (such as C5a, LTB4, or bacterial products) to **G-protein coupled receptors (GPCRs)** on the leukocyte membrane triggers a complex intracellular signaling cascade. **Why Phospholipase C (PLC) is correct:** When a chemoattractant binds to its receptor, it activates the G-protein, which in turn activates **Phospholipase C**. PLC cleaves membrane-bound Phosphatidylinositol 4,5-bisphosphate (PIP2) into two secondary messengers: 1. **Inositol triphosphate (IP3):** This triggers the release of intracellular calcium from the endoplasmic reticulum. 2. **Diacylglycerol (DAG):** This activates Protein Kinase C (PKC). The resulting increase in cytosolic calcium is crucial for the assembly of cytoskeletal proteins (actin polymerization), which allows the leukocyte to move toward the chemical gradient (chemotaxis) [1]. **Analysis of Incorrect Options:** * **Leukotriene B4 (A):** LTB4 is a potent chemotactic agent itself, not an intracellular signaling enzyme activated by receptor binding [2]. * **Histamine (B):** Histamine is a preformed mediator stored in mast cell granules. It is released primarily via IgE-mediated degranulation, not as a direct result of leukocyte chemotactic signaling. * **Tumor Necrosis Factor (D):** TNF is a cytokine produced by macrophages. While it can induce the expression of adhesion molecules, it is not the immediate intracellular effector of the chemotactic receptor pathway [3]. **NEET-PG High-Yield Pearls:** * **GPCRs** are the most common receptors involved in leukocyte activation and chemotaxis [1]. * The "Respiratory Burst" (via NADPH oxidase) is also triggered by this signaling pathway to produce Reactive Oxygen Species (ROS). * **Exogenous chemoattractants:** Bacterial products (e.g., N-formylmethionine peptides). * **Endogenous chemoattractants:** C5a, LTB4, and IL-8 (CXCL8) [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 190-191. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 95. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 89.

Question 239: Macrophages are converted to epithelioid cells by which cytokine?

A. IL-2
B. TNF-α
C. IFN-γ (Correct Answer)
D. TGF-β

Explanation: **Explanation:** The conversion of macrophages into epithelioid cells is the hallmark of **granulomatous inflammation**. This process is primarily mediated by **Interferon-gamma (IFN-γ)** [1]. 1. **Why IFN-γ is correct:** In a Type IV hypersensitivity reaction, CD4+ T-cells (Th1 subset) encounter an antigen and secrete **IFN-γ** [2]. This cytokine is the most potent activator of macrophages [1]. Under its influence, macrophages undergo structural changes: they increase in size, develop abundant eosinophilic cytoplasm, and their nuclei become elongated (resembling epithelial cells), thus becoming **epithelioid cells** [1]. IFN-γ also promotes the fusion of these cells into multinucleated giant cells (e.g., Langhans giant cells) [1]. 2. **Why other options are incorrect:** * **IL-2:** Primarily functions as a T-cell growth factor, stimulating the proliferation of T-lymphocytes and NK cells [1]. * **TNF-α:** While TNF-α is crucial for *maintaining* the integrity of a granuloma (preventing its breakdown), it is not the primary inducer of epithelioid transformation. * **TGF-β:** This is an anti-inflammatory cytokine involved in tissue repair and fibrosis; it inhibits macrophage activation rather than promoting epithelioid change [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Epithelioid cells** are defined by their lack of phagocytic activity but increased secretory capacity. * **Granuloma composition:** A collection of epithelioid cells surrounded by a rim of lymphocytes and fibroblasts [1]. * **Key Marker:** CD68 is a common marker for macrophages and epithelioid cells. * **TNF-α Inhibitors:** Drugs like Infliximab can cause the breakdown of existing granulomas, leading to the reactivation of latent Tuberculosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106, 109. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 173-174.

Question 240: Vascular dilation in the inflammatory response is mediated by all the following EXCEPT?

A. Prostaglandins
B. C3a
C. Leukotrienes (Correct Answer)
D. C5a

Explanation: **Explanation:** The inflammatory response involves a complex interplay of chemical mediators that regulate vascular changes [1]. The correct answer is **Leukotrienes** (specifically $LTC_4$, $LTD_4$, and $LTE_4$) because their primary vascular effect is **vasoconstriction** and increased vascular permeability (venular gaps), rather than vasodilation [2]. **Analysis of Options:** * **Leukotrienes (Correct):** While $LTB_4$ is a potent chemotactic agent, the cysteinyl leukotrienes ($LTC_4, D_4, E_4$) cause intense vasoconstriction and bronchospasm [2]. They do not mediate vasodilation [1]. * **Prostaglandins (Incorrect):** Prostaglandins, specifically $PGI_2$ (Prostacyclin), $PGE_1$, $PGE_2$, and $PGD_2$, are the principal mediators of **vasodilation** during inflammation [2]. They also potentiate the edema-forming effects of other mediators. * **C3a and C5a (Incorrect):** Known as **anaphylatoxins**, these complement fragments trigger mast cell degranulation [1]. This releases **Histamine**, which is the most well-known mediator of early vasodilation and increased capillary permeability. Therefore, they indirectly mediate vascular dilation. **High-Yield Clinical Pearls for NEET-PG:** * **Vasodilation Mediators:** Histamine, Prostaglandins ($PGI_2, PGE_2$), Nitric Oxide (NO), and Bradykinin [1]. * **Increased Permeability Mediators:** Histamine, Bradykinin, Leukotrienes ($LTC_4, D_4, E_4$), and Substance P [2]. * **Chemotaxis Mediators:** $LTB_4$, $C5a$, IL-8, and Bacterial products (N-formyl methionine) [1]. * **Pain Mediators:** Prostaglandins ($PGE_2$) and Bradykinin [1]. * **Fever Mediators:** $IL-1$, $TNF$, and Prostaglandins [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.

Practice by Chapter

Acute Inflammation: Vascular Events

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Acute Inflammation: Cellular Events

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Chemical Mediators of Inflammation

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Chronic Inflammation

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Granulomatous Inflammation

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Systemic Effects of Inflammation

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Wound Healing

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Tissue Regeneration

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Fibrosis and Repair

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Resolution of Inflammation

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