Inflammation and Repair — MCQs
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A 28-year-old female patient presents with patches of burns and swelling of the arm. Histopathological findings reveal swelling of the endoplasmic reticulum, blebs from the cell membrane, loss of microvilli, presence of myeloid bodies, and no changes in the nucleus. Which type of cell injury is seen in this patient?
Maximum tensile strength is recovered in a wound area during what period after an injury?
Which of the following factors most significantly impairs wound healing?
In cellular events of acute inflammation, all of the following are observed EXCEPT:
Fever is primarily caused by which of the following cytokines?
All of the following vascular changes are observed in acute inflammation, except?
All of the following statements about Xanthogranulomatous inflammation are true, except:
A patient presents with chest pain and dies within 12 hours of arrival. Autopsy performed 5 days later reveals necrosis in the myocardium. What type of necrosis is observed?
Prostaglandins are produced by which of the following cell types?
Which of the following is true about thromboxane-A2?
Inflammation and Repair Indian Medical PG Practice Questions and MCQs
Question 1: A 28-year-old female patient presents with patches of burns and swelling of the arm. Histopathological findings reveal swelling of the endoplasmic reticulum, blebs from the cell membrane, loss of microvilli, presence of myeloid bodies, and no changes in the nucleus. Which type of cell injury is seen in this patient?
- A. Irreversible cell injury
- B. Autolysis
- C. Pyroptosis
- D. Reversible cell injury (Correct Answer)
Explanation: ### Explanation The correct answer is **D. Reversible cell injury**. **1. Why Reversible Cell Injury is Correct:** The histopathological features described—**swelling of the endoplasmic reticulum (ER)**, **plasma membrane blebbing**, **loss of microvilli**, and the presence of **myeloid bodies** (whorled phospholipid masses)—are classic hallmarks of reversible cell injury [1]. The most critical clue in the question is the **absence of nuclear changes**. In reversible injury, the cell undergoes hydropic change (cellular swelling) due to the failure of energy-dependent ion pumps, but the nucleus remains intact, allowing the cell to return to homeostasis if the stimulus is removed [1]. **2. Why Other Options are Incorrect:** * **A. Irreversible cell injury:** This is characterized by severe mitochondrial dysfunction and **nuclear changes** (pyknosis, karyorrhexis, or karyolysis) and rupture of the lysosomal and plasma membranes. * **B. Autolysis:** This refers to the self-digestion of a cell by its own hydrolytic enzymes, typically occurring post-mortem or as a late stage of necrosis. * **C. Pyroptosis:** This is a form of programmed cell death associated with inflammation (mediated by Caspase-1 and IL-1), characterized by cell swelling and membrane rupture, but it involves distinct biochemical pathways not suggested by the simple morphological changes listed. **3. NEET-PG Clinical Pearls:** * **Earliest change in reversible injury:** Cellular swelling (Hydropic change/Vacuolar degeneration) [1]. * **Earliest change in irreversible injury:** Mitochondrial membrane damage/Amorphous densities in mitochondria. * **Myeloid bodies:** These are derived from damaged cellular membranes (organelles) and can be seen in both reversible and irreversible injury, but their presence alongside an intact nucleus points toward reversibility. * **Key differentiator:** If you see "Pyknosis" or "Mitochondrial Vacuolization," think Irreversible. If you see "ER swelling" or "Blebbing," think Reversible. **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. 49-61.
Question 2: Maximum tensile strength is recovered in a wound area during what period after an injury?
- A. 1 to 2 weeks
- B. 3 to 4 weeks (Correct Answer)
- C. 6 months
- D. 1 year
Explanation: ### Explanation The recovery of tensile strength in a healing wound is a dynamic process involving collagen synthesis and structural remodeling. **Why Option B is Correct:** Tensile strength increases most rapidly during the **3rd and 4th weeks** (21–28 days) post-injury [1]. This period marks the transition from the proliferative phase to the remodeling phase. During this time, there is a significant increase in collagen cross-linking and a shift from Type III collagen (granulation tissue) to Type I collagen (mature scar tissue). By the end of the first month, the wound typically regains approximately **20–30%** of its original strength. **Analysis of Incorrect Options:** * **Option A (1 to 2 weeks):** At the end of the first week, wound strength is only about **10%** of unwounded skin [1]. While collagen deposition has begun, the structural integrity is still minimal. * **Options C & D (6 months to 1 year):** While the wound continues to gain strength through remodeling for several months, the *rate* of recovery plateaus. Even after a year, a scar typically reaches a maximum of **70–80%** of the original tensile strength; it rarely, if ever, returns to 100% [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Collagen Switch:** Granulation tissue is characterized by **Type III collagen**, which is eventually replaced by the stronger **Type I collagen** in mature scars. * **Vitamin C:** Essential for the hydroxylation of proline and lysine residues; deficiency leads to poor tensile strength and wound dehiscence (Scurvy). * **Zinc:** A necessary cofactor for metalloproteinases (MMPs) which are crucial for the remodeling phase. * **Timeline Summary:** * 24 hours: Neutrophils appear. * 3 days: Macrophages predominate; granulation tissue starts. * 5 days: Peak of neovascularization [1]. * **3–4 weeks: Maximum rate of tensile strength recovery.** **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-121.
Question 3: Which of the following factors most significantly impairs wound healing?
- A. Cortisol (Correct Answer)
- B. Growth hormone
- C. Thyroxin
- D. Adrenaline
Explanation: **Explanation:** **Correct Answer: A. Cortisol** Glucocorticoids (Cortisol) are well-known inhibitors of wound healing [1]. They exert their inhibitory effects through multiple mechanisms: 1. **Anti-inflammatory effect:** They inhibit the production of inflammatory mediators and cytokines (like TGF-β), which are essential for initiating the repair process. 2. **Decreased Collagen Synthesis:** Cortisol inhibits fibroblast proliferation and reduces the synthesis of collagen, leading to poor tensile strength in the wound [1]. 3. **Inhibition of Angiogenesis:** It slows down the formation of new blood vessels (granulation tissue). *Clinical Note:* In surgical patients, high doses of steroids are often associated with wound dehiscence [2]. **Incorrect Options:** * **B. Growth Hormone (GH):** GH generally promotes healing by stimulating the production of Insulin-like Growth Factor-1 (IGF-1), which enhances protein synthesis and cellular proliferation. * **C. Thyroxin:** Thyroid hormones are essential for normal metabolic activity. While not a primary driver of wound repair, thyroxin deficiency (hypothyroidism) can lead to delayed healing, but it does not "impair" it in the active inhibitory sense that cortisol does. * **D. Adrenaline:** While adrenaline causes local vasoconstriction (which might transiently reduce blood flow), it does not have a significant systemic inhibitory effect on the cellular mechanisms of wound repair compared to steroids. **High-Yield NEET-PG Pearls:** * **Most important systemic factor** impairing wound healing: **Diabetes Mellitus** (due to microangiopathy and impaired neutrophil function) [1]. * **Most important local factor** impairing wound healing: **Infection**. * **Nutritional deficiency:** Vitamin C deficiency (Scurvy) leads to impaired collagen cross-linking (proline/lysine hydroxylation), causing wound breakdown. * **Zinc deficiency:** Inhibits DNA polymerase and RNA polymerase, significantly delaying epithelialization and fibroblast proliferation. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 423-424.
Question 4: In cellular events of acute inflammation, all of the following are observed EXCEPT:
- A. Complement involved in chemotaxis
- B. ICAM involved in adhesion of leukocytes
- C. PECAM involved in activation of leukocytes (Correct Answer)
- D. Selectins involved in margination and rolling
Explanation: ### Explanation The cellular events of acute inflammation follow a highly regulated sequence: Margination, Rolling, Adhesion, Transmigration (Diapedesis), and Chemotaxis [1]. **Why Option C is the correct answer (The "EXCEPT"):** **PECAM-1 (CD31)** is a molecule expressed on both leukocytes and endothelial cells. Its primary role is to facilitate **Transmigration (Diapedesis)**—the process where leukocytes squeeze through endothelial intercellular junctions to reach the extravascular space [1]. It is **not** primarily involved in the "activation" of leukocytes. Leukocyte activation is triggered by specific stimuli like bacterial products (LPS), cytokines (TNF, IL-1), and chemokines binding to G-protein coupled receptors [2]. **Analysis of Incorrect Options:** * **Option A (Complement in Chemotaxis):** Correct statement. **C5a** is a potent chemoattractant that guides leukocytes toward the site of injury [3]. * **Option B (ICAM in Adhesion):** Correct statement. Firm adhesion is mediated by **Integrins** (LFA-1, MAC-1) on leukocytes binding to **Ig-superfamily** ligands like **ICAM-1** and VCAM-1 on the endothelium [2]. * **Option D (Selectins in Rolling):** Correct statement. Rolling is the initial loose tethering mediated by **Selectins** (P-selectin, E-selectin, and L-selectin) binding to Sialyl-Lewis X ligands [2]. **High-Yield Clinical Pearls for NEET-PG:** * **LAD Type 1:** Deficiency of **Integrins** (specifically CD18/β2 chain), leading to impaired adhesion and delayed umbilical cord separation [1]. * **LAD Type 2:** Deficiency of **Sialyl-Lewis X**, leading to impaired rolling. * **Chemotactic Agents:** Remember the "Big Four": **C5a, LTB4, IL-8, and Bacterial products** (N-formyl methionine). * **CD31:** Also used as an immunohistochemical marker for vascular tumors (e.g., Angiosarcoma). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [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. 190-191.
Question 5: Fever is primarily caused by which of the following cytokines?
- A. Interleukin 3 (IL-3)
- B. Interleukin 6 (IL-6) (Correct Answer)
- C. Interleukin 5 (IL-5)
- D. Interleukin 9 (IL-9)
Explanation: ### Explanation **Correct Answer: B. Interleukin 6 (IL-6)** Fever (pyrexia) is a systemic manifestation of the acute-phase response [1]. It is mediated by **pyrogens**, which can be exogenous (e.g., bacterial LPS) or endogenous (cytokines). The primary endogenous pyrogens are **IL-1, TNF-α, and IL-6** [1]. When these cytokines are released, they travel to the hypothalamus, where they stimulate the enzyme **Cyclooxygenase (COX)** to produce **Prostaglandin E2 (PGE2)** [1][2]. PGE2 acts on the thermoregulatory center of the anterior hypothalamus to "reset" the body's temperature set-point to a higher level. While IL-1 and TNF are potent initiators, **IL-6** is a major systemic mediator that also stimulates the liver to synthesize acute-phase proteins like CRP and Fibrinogen [1]. **Analysis of Incorrect Options:** * **A. IL-3:** Known as a "multilineage colony-stimulating factor," it primarily stimulates the differentiation of hematopoietic stem cells into various myeloid progenitor cells. * **C. IL-5:** This cytokine is crucial for the recruitment, activation, and survival of **eosinophils**. It is a key mediator in Type I hypersensitivity (allergic) reactions and parasitic infections. * **D. IL-9:** Produced by Th9 cells, it is involved in mast cell activation and mucus production in the airways, playing a role in the pathogenesis of asthma. **NEET-PG High-Yield Pearls:** * **The "Big Three" of Acute Inflammation:** IL-1, IL-6, and TNF-α. * **Acute Phase Reactants:** IL-6 is the most potent stimulator of C-Reactive Protein (CRP) production in the liver [1]. * **Mechanism of NSAIDs:** Drugs like Paracetamol and Aspirin reduce fever by inhibiting COX, thereby blocking the synthesis of PGE2. * **IL-8:** Remember this as the primary chemotactic factor for **neutrophils** ("Clean up on aisle 8"). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.
Question 6: All of the following vascular changes are observed in acute inflammation, except?
- A. Vasodilation
- B. Stasis of blood
- C. Increased vascular permeability
- D. Decreased hydrostatic pressure (Correct Answer)
Explanation: In acute inflammation, the vascular response is characterized by a series of changes designed to maximize the movement of plasma proteins and leukocytes out of the circulation and into the site of injury. [1] ### Why "Decreased Hydrostatic Pressure" is the Correct Answer In acute inflammation, there is **increased hydrostatic pressure**, not decreased. Vasodilation of the arterioles leads to an increase in local blood flow (hyperemia). [1] This surge in blood volume within the microvasculature raises the hydrostatic pressure, which, combined with increased permeability, facilitates the movement of fluid into the extravascular space (edema). [1] ### Explanation of Incorrect Options * **A. Vasodilation:** This is one of the earliest manifestations of acute inflammation. It is primarily mediated by histamine and nitric oxide acting on vascular smooth muscle, leading to the characteristic redness (rubor) and warmth (calor). [1], [4] * **B. Stasis of blood:** As fluid leaves the vessels due to increased permeability, the concentration of red blood cells increases, leading to increased blood viscosity. This slows down the blood flow, a phenomenon known as stasis, which allows leukocytes (neutrophils) to marginate along the endothelium. * **C. Increased vascular permeability:** This is the hallmark of acute inflammation. [2] It is mainly caused by endothelial cell contraction (creating "gaps"), leading to the leakage of protein-rich fluid (exudate) into the tissues. [5] ### High-Yield Clinical Pearls for NEET-PG * **Starling’s Law:** Edema in inflammation is caused by **increased hydrostatic pressure** AND **increased vascular permeability** (which leads to decreased osmotic pressure in the vessel). [3] * **Immediate Transient Response:** The most common mechanism of vascular leakage is endothelial cell contraction, affecting **post-capillary venules**. [5] * **Exudate vs. Transudate:** Inflammatory fluid is an **Exudate** (high protein, high specific gravity >1.020), whereas non-inflammatory fluid (e.g., in CHF) is a **Transudate**. [1] **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. 186-187. [4] 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. 185-186. [5] 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 7: All of the following statements about Xanthogranulomatous inflammation are true, except:
- A. Foam cells are seen
- B. Yellow nodules are seen
- C. Multinucleated Giant cells are seen
- D. Associated with Tuberculosis (Correct Answer)
Explanation: **Explanation:** **Xanthogranulomatous inflammation** is a specific form of chronic inflammation characterized by the massive accumulation of lipid-laden macrophages (foam cells), leading to the destruction of the involved organ [1]. **Why Option D is the Correct Answer (The Exception):** Xanthogranulomatous inflammation is **not** associated with Tuberculosis. Tuberculosis is the classic example of **Granulomatous inflammation** (specifically caseating granulomas) caused by *Mycobacterium tuberculosis* [2]. While both terms contain "granulomatous," they are pathologically distinct. Xanthogranulomatous inflammation is most commonly associated with chronic infections caused by **Proteus mirabilis** or **E. coli**, often in the setting of urinary or biliary obstruction [1]. **Analysis of Incorrect Options:** * **Option A (Foam cells):** These are the hallmark of this condition. They are macrophages that have phagocytosed lipids from destroyed cell membranes [1]. * **Option B (Yellow nodules):** Grossly, the affected tissue shows bright yellow, lobulated nodules [1]. The "Xantho-" prefix (Greek for yellow) refers to this characteristic appearance caused by the high lipid content of the foam cells. * **Option C (Multinucleated Giant cells):** Along with foam cells, plasma cells, and lymphocytes, multinucleated giant cells are a standard histological component of the inflammatory infiltrate in this condition [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Site:** Kidney (**Xanthogranulomatous Pyelonephritis - XPN**), often associated with **Staghorn calculi** [1]. * **Second Most Common Site:** Gallbladder (**Xanthogranulomatous Cholecystitis**), which can radiologically mimic gallbladder carcinoma. * **Microscopic Hallmark:** Lipid-laden macrophages are also known as **Xanthoma cells**. * **Differential Diagnosis:** In the kidney, it can be mistaken for Renal Cell Carcinoma (RCC) due to its mass-like appearance [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 939-940. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384.
Question 8: A patient presents with chest pain and dies within 12 hours of arrival. Autopsy performed 5 days later reveals necrosis in the myocardium. What type of necrosis is observed?
- A. Coagulative (Correct Answer)
- B. Fibrinoid
- C. Caseous
- D. Liquefactive
Explanation: **Explanation:** **Why Coagulative Necrosis is Correct:** Coagulative necrosis is the characteristic pattern of cell death seen in **hypoxic/ischemic injury** in all solid organs except the brain [1]. In this clinical scenario, the patient likely suffered a Myocardial Infarction (MI). The hallmark of coagulative necrosis is the preservation of the basic structural outline of the cell for several days, despite the loss of nuclei and cytoplasmic detail (often described as **"tombstone" or "ghost" cells**) [1]. This occurs because the injury denatures not only structural proteins but also the enzymes responsible for proteolysis, thereby delaying autolysis. **Why the other options are incorrect:** * **B. Fibrinoid:** This is typically seen in immune-mediated vascular damage (e.g., Polyarteritis Nodosa) or malignant hypertension, characterized by the deposition of immune complexes and fibrin in arterial walls. * **C. Caseous:** This is a "cheese-like" necrosis characteristic of **Tuberculosis** (granulomatous inflammation) [2]. It represents a combination of coagulative and liquefactive processes but lacks the preserved cell outlines seen in the myocardium. * **D. Liquefactive:** This is seen in **brain infarcts** and bacterial/fungal infections (abscesses). It is characterized by the complete digestion of dead cells, resulting in a liquid viscous mass [1]. **High-Yield Clinical Pearls for NEET-PG:** * **MI Timeline:** While gross changes are not visible within 12 hours, light microscopy begins to show wavy fibers and early coagulative necrosis [3]. * **Exception Rule:** Ischemia in the **Brain** leads to Liquefactive necrosis, not Coagulative [1]. * **Mechanism:** Coagulative necrosis is primarily due to **protein denaturation** [1]. * **Autopsy Note:** The 5-day delay in the autopsy does not change the type of necrosis that occurred at the time of death, though post-mortem autolysis may begin to overlap. **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. 53-55. [2] 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, p. 55. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.
Question 9: Prostaglandins are produced by which of the following cell types?
- A. Neutrophils
- B. Endothelium
- C. Macrophages
- D. All of the above (Correct Answer)
Explanation: ### Explanation **Concept Overview:** Prostaglandins (PGs) are lipid-derived mediators of inflammation produced via the **Arachidonic Acid (AA) pathway** [1]. When cell membranes are damaged or stimulated, Phospholipase A2 releases AA from membrane phospholipids. AA is then acted upon by **Cyclooxygenase (COX-1 and COX-2)** enzymes to produce PGs [1]. **Why "All of the Above" is Correct:** The COX enzymes are ubiquitously expressed in almost all nucleated cells, particularly those involved in the inflammatory response. * **Macrophages and Neutrophils:** These are the primary inflammatory cells that produce PGs (specifically PGE2 and PGI2) to induce vasodilation and increase vascular permeability at the site of injury [1]. * **Endothelial Cells:** These cells are a major source of **Prostacyclin (PGI2)**, which acts as a potent vasodilator and inhibitor of platelet aggregation, maintaining vascular patency [1]. **Analysis of Options:** While each cell type listed (Neutrophils, Endothelium, and Macrophages) is a significant producer of prostaglandins, selecting any single one would be incomplete [1]. In the context of acute inflammation, these cells work in concert to release PGs to mediate pain, fever, and vasodilation. **NEET-PG High-Yield Pearls:** * **PGE2:** Known as the "hyperalgesic" prostaglandin; it makes skin hypersensitive to pain and is the primary mediator of **fever** (induced by IL-1 and TNF acting on the hypothalamus). * **PGI2 (Prostacyclin) vs. TXA2 (Thromboxane):** PGI2 (from endothelium) causes vasodilation/inhibits aggregation, while TXA2 (from platelets) causes vasoconstriction/promotes aggregation [1]. The balance between these two is critical for vascular homeostasis. * **Pharmacology Link:** NSAIDs (like Aspirin) work by inhibiting COX enzymes, thereby blocking the synthesis of PGs from all these cell types. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.
Question 10: Which of the following is true about thromboxane-A2?
- A. Vasodilation
- B. Platelet aggregation (Correct Answer)
- C. Potentiation of edema
- D. Formed in endothelium
Explanation: **Explanation:** Thromboxane A2 (TXA2) is a potent eicosanoid derived from the cyclooxygenase (COX) pathway of arachidonic acid metabolism. It is synthesized primarily in **platelets** by the enzyme thromboxane synthase. [1] **Why Option B is correct:** TXA2 is a powerful **platelet aggregator** and a potent **vasoconstrictor**. When a vessel is injured, platelets release TXA2 to facilitate the formation of a primary platelet plug (hemostasis). [1] It acts via the TP receptor to increase intracellular calcium, leading to the activation and recruitment of additional platelets. [1] **Analysis of Incorrect Options:** * **A. Vasodilation:** This is incorrect. TXA2 is a potent **vasoconstrictor**. Vasodilation is caused by its functional antagonist, **Prostacyclin (PGI2)**. * **C. Potentiation of edema:** Edema is typically potentiated by Prostaglandins (PGE2 and PGD2) and Leukotrienes (LTC4, LTD4, LTE4), which increase vascular permeability. TXA2 does not have a primary role in increasing permeability. * **D. Formed in endothelium:** This is incorrect. TXA2 is primarily produced in **platelets**. [1] The vascular **endothelium** is the primary site for the production of **Prostacyclin (PGI2)**. **NEET-PG High-Yield Pearls:** * **The PGI2/TXA2 Balance:** In health, a delicate balance exists between PGI2 (vasodilator/anti-aggregator) and TXA2 (vasoconstrictor/aggregator) to prevent spontaneous thrombosis. * **Aspirin Mechanism:** Low-dose aspirin irreversibly inhibits COX-1 in platelets. Since platelets lack a nucleus, they cannot synthesize new enzymes, leading to a permanent reduction in TXA2 for the life of the platelet (7–10 days). This is the basis for its use as an anti-platelet drug. * **Key Mnemonic:** **T**hromboxane **T**ightens (Vasoconstriction) and **T**ies (Aggregation) platelets together. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.
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
Practice Questions
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