Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 81: Diapedesis primarily occurs in?

A. Arterioles
B. Venules (Correct Answer)
C. Capillaries
D. None of the above

Explanation: **Explanation:** **Diapedesis** (also known as transmigration) is the process by which leukocytes squeeze between endothelial cells to exit the bloodstream and enter the extravascular space [1]. This process occurs primarily in the **post-capillary venules** [1][2]. **Why Venules are the Correct Answer:** 1. **Hemodynamics:** Blood flow is slower in venules compared to arterioles, allowing leukocytes to marginate and roll along the endothelium. 2. **Receptor Density:** Post-capillary venules express the highest concentration of adhesion molecules (like PECAM-1/CD31) and respond most robustly to chemical mediators (like histamine and bradykinin) that increase vascular permeability [2][3]. 3. **Structural Properties:** The endothelial junctions in venules are less "tight" than those in the arterial system, making them the preferred site for cellular exit during acute inflammation [1][2]. **Why Other Options are Incorrect:** * **Arterioles:** These are high-pressure resistance vessels with thick muscular walls. The high shear stress and rapid flow prevent leukocyte attachment and transmigration. * **Capillaries:** While some gas and nutrient exchange occurs here, the lack of specific adhesion molecule expression and the narrow diameter make them less significant for leukocyte diapedesis compared to venules [1]. **High-Yield NEET-PG Pearls:** * **CD31 (PECAM-1):** The primary molecule responsible for diapedesis. It is expressed on both leukocytes and endothelial cell junctions [3]. * **Sequence of Events:** Margination → Rolling (Selectins) → Adhesion (Integrins) → **Diapedesis (PECAM-1)** → Chemotaxis [3]. * **Exception:** In the **lungs**, leukocyte recruitment occurs primarily in the **capillaries** rather than the venules. * **Clinical Correlation:** Defects in diapedesis/adhesion lead to **Leukocyte Adhesion Deficiency (LAD)**, characterized by delayed umbilical cord separation and recurrent bacterial infections without pus formation [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. 188-189. [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. 187-188. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 82: Wound healing is the summation of which of the following processes?

A. Coagulation
B. Matrix synthesis
C. Angiogenesis
D. Fibrolysis (Correct Answer)

Explanation: **Explanation:** Wound healing is a complex, dynamic process that aims to restore tissue integrity after injury. It is classically divided into four overlapping phases: **Hemostasis, Inflammation, Proliferation, and Remodeling.** [1] **Why "Fibrolysis" is the Correct Answer:** The question asks for the "summation" of processes involved. While the initial phases focus on building tissue (coagulation, fibroplasia, and angiogenesis), the final and longest phase is **Remodeling**. During this stage, the provisional matrix (rich in Type III collagen) is broken down and replaced by stronger Type I collagen [2]. This process of breaking down excess fibrin and collagen to refine the scar is known as **fibrolysis** (or fibrinolysis/matrix degradation). Without fibrolysis, the wound would result in excessive scarring or keloid formation [3]. It represents the "maturation" step that completes the healing cycle. **Analysis of Incorrect Options:** * **A. Coagulation:** This is merely the *initial* step (Hemostasis) to stop bleeding; it does not encompass the entire healing process. * **B. Matrix synthesis:** This occurs during the proliferative phase [1]. While essential, synthesis alone without subsequent remodeling (degradation) does not result in a functional scar. * **C. Angiogenesis:** This is the formation of new blood vessels to provide nutrients to the healing tissue [1]. It is a *component* of the proliferative phase, not the final summation. **High-Yield Clinical Pearls for NEET-PG:** * **Collagen Switch:** In early wound healing, **Type III collagen** is predominant; in the final scar, **Type I collagen** (high tensile strength) is predominant [2]. * **Key Enzyme:** **Matrix Metalloproteinases (MMPs)** are the primary enzymes responsible for fibrolysis and remodeling. They require **Zinc** as a cofactor. * **Tensile Strength:** At 1 week (suture removal), wound strength is ~10% [2]. It reaches a maximum of **70-80%** of original strength by 3 months; it rarely reaches 100% [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-119. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121. [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. 106-107.

Question 83: What is the typical timeframe for a wound site to regain its normal tensile strength?

A. One week
B. Two weeks
C. Two months
D. None of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **None of the above** because a healed wound **never** regains its original, pre-injury tensile strength [1]. **1. Understanding the Concept:** Tensile strength is the capacity of a tissue to withstand pulling forces. When a wound heals, the original Type I collagen is initially replaced by Type III collagen (granulation tissue), which is later remodeled back into Type I. However, the structural arrangement and cross-linking of the new collagen fibers never perfectly replicate the original architecture. Even after extensive remodeling (which can last for a year or more), the maximum tensile strength of a scar plateaus at approximately **70% to 80%** of that of unwounded skin [1]. **2. Analysis of Incorrect Options:** * **One week (A):** At the end of the first week, when sutures are typically removed, the wound has only about **10%** of the strength of normal skin [1]. * **Two weeks (B):** While collagen synthesis is active, the tensile strength is still minimal and insufficient to withstand significant stress. * **Two months (C):** By the end of the third month (approx. 90 days), tensile strength reaches its peak plateau of roughly 70-80% [1]. It does not improve significantly beyond this point and never reaches 100%. **3. NEET-PG High-Yield Pearls:** * **Collagen Switch:** Granulation tissue is characterized by **Type III collagen**; mature scars are characterized by **Type I collagen**. * **Timeline of Strength:** * 1 week: 10% [1] * 3 months: 70-80% (Plateau) [1] * **Vitamin C:** Essential for the hydroxylation of proline and lysine residues; deficiency leads to poor collagen cross-linking and wound dehiscence. * **Zinc:** A necessary cofactor for **Matrix Metalloproteinases (MMPs)**, which are crucial for the remodeling phase of wound healing. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 84: What inflammatory cell will be seen after 2 days of acute appendicitis?

A. Neutrophil
B. Eosinophil
C. Monocyte (Correct Answer)
D. Lymphocyte

Explanation: In acute inflammation, the cellular infiltrate follows a predictable chronological sequence, which is a high-yield concept for NEET-PG. [1] **Explanation of the Correct Answer (C):** The cellular response in acute inflammation is divided into two phases: 1. **First 6–24 hours:** Neutrophils predominate. They are the first responders because they are more numerous in the blood, respond more rapidly to chemokines, and attach more firmly to adhesion molecules (like P-selectin and E-selectin). [1] 2. **24–48 hours (Day 2):** Neutrophils undergo apoptosis and disappear. They are replaced by **Monocytes** (which become macrophages in tissue). [1] Monocytes survive longer, can proliferate in the tissues, and are responsible for phagocytosing debris and initiating the repair process. Therefore, at the 48-hour mark (2 days), the predominant cell seen is the monocyte/macrophage. [2] **Analysis of Incorrect Options:** * **A. Neutrophil:** These are the hallmark of the *early* acute phase (first 24 hours). [1] By day 2, their numbers significantly decline. * **B. Eosinophil:** These are typically associated with Type I hypersensitivity reactions (allergies) or parasitic infections, not the standard progression of acute appendicitis. * **D. Lymphocyte:** These are the hallmark of *chronic* inflammation or specific viral infections. They appear much later in the timeline unless the inflammation becomes chronic. **Clinical Pearls for NEET-PG:** * **Exception to the Rule:** In **Pseudomonas** infections, neutrophils persist for several days. In **viral** infections, lymphocytes may be the first cells to arrive. * **Morphology:** Neutrophils are "polymorphonuclear," while monocytes have a "kidney-shaped" nucleus. * **Key Chemotactic Factors:** C5a, LTB4, and IL-8 are the primary recruiters for neutrophils. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 89. [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. 192-193.

Question 85: All of the following are true regarding vasodilation in acute inflammation, except?

A. Caused by release of histamine
B. First affects arterioles and followed by opening of capillaries (Correct Answer)
C. Vasodilation leads to extravasation of fluid from microvasculature, leading to edema
D. Vasodilation occurs notably due to the action of histamine on vascular smooth muscle

Explanation: ### Explanation **1. Why Option B is the Correct Answer (The Exception)** In acute inflammation, the vascular response follows a specific chronological order. While vasodilation is indeed one of the earliest manifestations, it is often preceded by a **transient, inconstant vasoconstriction** of arterioles (lasting only seconds). Following this, vasodilation occurs, first involving the **arterioles** and then leading to the **opening of new capillary beds** in the area [1]. The statement in Option B is technically a true description of the process; however, in the context of standard NEET-PG pathology (based on Robbins), the question often hinges on the fact that vasodilation is the *result* of mediator action, but the *very first* vascular event is transient vasoconstriction. Furthermore, if the option implies that vasodilation is the "first" event overall, it ignores the initial neurogenic/chemical reflex of constriction. **2. Analysis of Other Options** * **Option A & D:** These are **true**. Histamine is the primary mediator of the early phase of increased vascular permeability and vasodilation [2]. It acts directly on the **vascular smooth muscle** cells, causing them to relax, which results in increased blood flow (hyperemia) [1]. * **Option C:** This is **true**. Vasodilation increases hydrostatic pressure and is accompanied by increased vascular permeability [1]. This allows protein-rich fluid (exudate) to move into the extravascular tissues, resulting in **edema**, a hallmark of acute inflammation [3]. **3. Clinical Pearls & High-Yield Facts** * **Sequence of Hemodynamic Changes:** Transient vasoconstriction → Persistent Vasodilation → Increased Permeability → Stasis → Leukocytic Margination. * **Histamine Source:** Primarily stored in **Mast cell granules**; released in response to physical injury, Type I hypersensitivity, or complement fragments (C3a, C5a) [2]. * **Triple Response of Lewis:** Induced by firm stroking of the skin, involving: 1. Red spot (capillary dilation), 2. Flare (arteriolar dilation), 3. Wheal (exudation/edema) [2]. * **Stasis:** As fluid leaves the vessels, RBCs become more concentrated, increasing blood viscosity and slowing flow, which allows leukocytes to settle (margination) along the endothelium. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [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. 187-188.

Question 86: Which vasoactive amine is involved in inflammation?

A. Histamine (Correct Answer)
B. Renin
C. Angiotensin
D. All of the above

Explanation: **Explanation:** **1. Why Histamine is Correct:** Histamine is a primary **vasoactive amine** stored in the preformed granules of **mast cells**, basophils, and platelets [1]. During the early phase of acute inflammation, it is released in response to stimuli such as physical injury, IgE-mediated immune reactions, or anaphylatoxins (C3a, C5a) [1]. Its primary action is to cause **vasodilation** of arterioles and **increased vascular permeability** in venules by creating endothelial gaps [2]. This process is the hallmark of the "exudative" phase of inflammation [2]. **2. Why Other Options are Incorrect:** * **Renin:** This is a proteolytic enzyme secreted by the juxtaglomerular cells of the kidney. Its primary role is in the **Renin-Angiotensin-Aldosterone System (RAAS)** to regulate blood pressure and fluid balance, not to mediate acute inflammatory responses. * **Angiotensin:** Angiotensin II is a potent **vasoconstrictor** involved in systemic blood pressure regulation. While it has some minor roles in chronic tissue remodeling, it is not classified as a primary vasoactive amine of acute inflammation. **3. NEET-PG High-Yield Pearls:** * **Vasoactive Amines:** There are only two major ones to remember—**Histamine** and **Serotonin** (5-HT) [1]. * **Serotonin Source:** In humans, serotonin is primarily found in **platelets** and enterochromaffin cells [1]. It acts similarly to histamine during inflammation. * **Triple Response of Lewis:** Histamine is the mediator responsible for this phenomenon (Flush, Flare, and Wheal) [1]. * **Inactivation:** Histamine is rapidly inactivated by **histaminase**, which explains why its effects are short-lived and occur early in the inflammatory process. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [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. 187-188.

Question 87: What is the major source for histamine released during inflammation?

A. Platelets
B. Mast cells (Correct Answer)
C. Basophils
D. Endothelial cells

Explanation: **Explanation:** Histamine is a potent vasoactive amine and is typically the first mediator released during the early phase of acute inflammation [2], [4]. It causes vasodilation of arterioles and increases the permeability of venules [3], [4]. **Why Mast Cells are the Correct Answer:** Mast cells are considered the **major and richest source** of histamine in the body. They are widely distributed in connective tissues, particularly those adjacent to blood vessels. Histamine is stored in preformed granules within mast cells and is released (degranulation) in response to various stimuli, including physical injury, binding of antibodies (IgE in Type I Hypersensitivity), and complement fragments (C3a and C5a, known as anaphylatoxins) [2]. **Analysis of Incorrect Options:** * **Basophils:** While basophils contain histamine granules and function similarly to mast cells, they are primarily found in the circulation. Mast cells are more abundant in tissues where the inflammatory response typically initiates. * **Platelets:** Platelets contain histamine in their dense granules, but they are a secondary source [1]. Their primary role in inflammation involves the release of serotonin and growth factors during aggregation. * **Endothelial cells:** These cells respond *to* histamine (by contracting to create gaps), but they do not synthesize or store it as a primary mediator [3]. **NEET-PG High-Yield Pearls:** * **First Mediator:** Histamine is the first mediator to be released in acute inflammation [2]. * **Mechanism of Action:** It acts primarily on **H1 receptors** on microvascular endothelial cells. * **Triple Response of Lewis:** Histamine is responsible for the "Wheal, Flare, and Flush" reaction [2]. * **Inactivation:** Histamine is rapidly degraded by the enzyme **histaminase** (diamine oxidase), which limits the duration of its effect. **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] 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. 187-188. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85.

Question 88: What is the earliest feature of reversible cell injury?

A. Amorphous densities
B. Ribosomal detachment
C. Hydropic swelling (Correct Answer)
D. Bleb formation

Explanation: **Explanation:** **Hydropic swelling** (also known as cellular swelling or vacuolar degeneration) is the **earliest and most common manifestation** of reversible cell injury [1]. **Why it is the correct answer:** The fundamental mechanism involves the failure of energy-dependent membrane pumps, specifically the **Na+/K+-ATPase pump** [1]. When a cell is injured (e.g., via hypoxia), ATP production decreases. This leads to an accumulation of intracellular Sodium ($Na^+$) and a loss of Potassium ($K^+$). The resulting increase in intracellular osmotic pressure draws water into the cell, causing the cytoplasm to swell and small clear vacuoles to form within the endoplasmic reticulum [1]. **Analysis of Incorrect Options:** * **B. Ribosomal detachment:** This occurs shortly after swelling as the Rough Endoplasmic Reticulum (RER) dilates. While it is a feature of reversible injury leading to decreased protein synthesis, it follows the initial influx of water [1]. * **D. Bleb formation:** Membrane blebbing and loss of microvilli are later reversible changes resulting from cytoskeletal damage [1]. * **A. Amorphous densities:** The appearance of **large, flocculent, amorphous densities** in the mitochondrial matrix is a hallmark of **irreversible** cell injury (necrosis), signifying permanent mitochondrial dysfunction [1]. **NEET-PG High-Yield Pearls:** * **Light Microscopy:** Hydropic swelling is the first change visible under a light microscope [1]. * **Electron Microscopy:** The very first changes (e.g., loss of microvilli, mitochondrial swelling) are seen here before light microscopic changes appear [1]. * **Organ Level:** Grossly, affected organs (liver, kidney) show increased weight and pallor [1]. * **Point of No Return:** Irreversibility is characterized by two phenomena: inability to reverse mitochondrial dysfunction and profound disturbances in membrane function [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 49-55.

Question 89: Disease or infarction of neurological tissue causes it to be repaired by what?

A. Fluid
B. Neuroglia (Correct Answer)
C. Proliferation of adjacent nerve cells
D. Blood vessels

Explanation: **Explanation:** In the Central Nervous System (CNS), the process of repair differs significantly from peripheral tissues. While most organs undergo repair via fibrosis (scarring by fibroblasts and collagen), the brain and spinal cord lack significant connective tissue. Instead, they rely on **Neuroglia**, specifically **Astrocytes**, for structural repair. **Why Neuroglia is correct:** When neurological tissue is damaged due to infarction (stroke) or disease, the primary response is **Gliosis** [1]. Astrocytes undergo hypertrophy and hyperplasia, proliferating to form a dense network of cytoplasmic processes [3]. This "glial scar" acts as the CNS equivalent of a fibrous scar, walling off the damaged area and maintaining structural integrity [3]. **Why other options are incorrect:** * **Fluid:** While liquefactive necrosis (common in brain infarcts) initially results in a fluid-filled cavity, the actual *repair* mechanism that replaces or borders the lost tissue is the proliferation of glial cells [2]. * **Proliferation of adjacent nerve cells:** Neurons are considered **permanent cells**. They lack the regenerative capacity to divide and replace lost tissue; once destroyed, they cannot be replenished by mitosis [1]. * **Blood vessels:** While angiogenesis occurs during the healing process (granulation tissue), blood vessels alone do not constitute the definitive repair tissue in the CNS. **NEET-PG High-Yield Pearls:** * **Gliosis** is the most important histopathologic indicator of CNS injury [1]. * **Liquefactive Necrosis:** The brain is the only organ where hypoxic cell death results in liquefactive (rather than coagulative) necrosis [2]. * **Microglia:** These are the resident macrophages of the CNS; they clear debris (Gitter cells) but do not form the structural scar. * **Gemistocytic Astrocytes:** These are activated astrocytes with eosinophilic cytoplasm seen during the early stages of repair. **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. 109-110. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.

Question 90: Which among the following is a vasoconstrictor?

A. Histamine
B. Prostacyclin (PGI2)
C. Bradykinin
D. Thromboxane A2 (TXA2) (Correct Answer)

Explanation: **Explanation:** The correct answer is **Thromboxane A2 (TXA2)**. In the context of inflammation and hemostasis, vasoactive mediators are classified based on their effect on vascular smooth muscle. **Thromboxane A2 (TXA2)** is a potent **vasoconstrictor** and a powerful inducer of platelet aggregation [1]. It is synthesized from arachidonic acid via the cyclooxygenase (COX) pathway, primarily within platelets [1]. Its primary physiological role is to limit blood flow at the site of injury and facilitate the formation of a platelet plug. **Analysis of Incorrect Options:** * **Histamine:** One of the first mediators released during acute inflammation (from mast cell degranulation). It causes **vasodilation** of arterioles and increases the permeability of venules [1]. * **Prostacyclin (PGI2):** Produced by vascular endothelium, it acts as the functional antagonist to TXA2. It is a potent **vasodilator** and an inhibitor of platelet aggregation, maintaining vascular patency. * **Bradykinin:** A peptide of the kinin system that causes significant **vasodilation**, increased vascular permeability, and mediates pain. **High-Yield Clinical Pearls for NEET-PG:** * **Vasoconstrictors to remember:** Thromboxane A2, Leukotrienes (C4, D4, E4), Endothelin, and Angiotensin II [1]. * **Vasodilators to remember:** Histamine, Prostaglandins (PGE2, PGD2, PGF2α, PGI2), Nitric Oxide (NO), and Bradykinin [1]. * **Aspirin Connection:** Low-dose aspirin irreversibly inhibits COX-1 in platelets, reducing TXA2 levels, which explains its clinical use as an anti-platelet/cardioprotective agent. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95.

Practice by Chapter

Acute Inflammation: Vascular Events

Practice Questions

Acute Inflammation: Cellular Events

Practice Questions

Chemical Mediators of Inflammation

Practice Questions

Chronic Inflammation

Practice Questions

Granulomatous Inflammation

Practice Questions

Systemic Effects of Inflammation

Practice Questions

Wound Healing

Practice Questions

Tissue Regeneration

Practice Questions

Fibrosis and Repair

Practice Questions

Resolution of Inflammation

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