Inflammation and Repair — MCQs
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A 25-year-old woman develops a sore, red, hot, swollen left knee. She has no history of trauma and no familial history of joint disease. Fluid aspirated from the joint space shows an abundance of segmented neutrophils. Aspirin is effective in relieving symptoms of acute inflammation in the patient because it inhibits which of the following enzymes?
What are the most important growth factors in angiogenesis?
Which of the following is not a negative acute-phase reactant?
Important components of collagen synthesis, wound strength, and contraction include all of the following EXCEPT?
Which cell is involved in the immediate phase of wound healing?
Which of the following are considered slow mediators of inflammation?
What is a characteristic feature of acute inflammation?
Which of the following is NOT an action of bradykinin?
Endothelial activation refers to which of the following processes?
A 54-year-old male presents with severe chest pain. ECG shows acute myocardial infarction. He was given thrombolytic therapy with tPA. His serum creatine kinase levels increased after this therapy. Which event most likely occurred?
Inflammation and Repair Indian Medical PG Practice Questions and MCQs
Question 101: A 25-year-old woman develops a sore, red, hot, swollen left knee. She has no history of trauma and no familial history of joint disease. Fluid aspirated from the joint space shows an abundance of segmented neutrophils. Aspirin is effective in relieving symptoms of acute inflammation in the patient because it inhibits which of the following enzymes?
- A. Cyclooxygenase (Correct Answer)
- B. Myeloperoxidase
- C. Phospholipase A2
- D. Protein kinase C
Explanation: ### Explanation **Correct Answer: A. Cyclooxygenase** The clinical presentation of a red, hot, swollen joint with an abundance of neutrophils indicates **acute inflammation** [4]. The cardinal signs of inflammation (rubor, calor, tumor, dolor) are largely mediated by **Prostaglandins (PG)** [3], [4], specifically PGE2, which causes vasodilation and increases pain sensitivity [2], [3]. **Cyclooxygenase (COX)** is the enzyme responsible for converting arachidonic acid into Prostaglandins and Thromboxanes [1], [2]. **Aspirin** is a Non-Steroidal Anti-Inflammatory Drug (NSAID) that irreversibly inhibits COX-1 and COX-2 [1], [2]. By blocking this pathway, Aspirin reduces the production of PGE2, thereby relieving pain and reducing inflammation. **Analysis of Incorrect Options:** * **B. Myeloperoxidase (MPO):** Found in neutrophil granules, MPO converts hydrogen peroxide to hypochlorous acid (HOCl) to kill bacteria. Inhibiting it would impair microbial killing but not the inflammatory process itself. * **C. Phospholipase A2:** This enzyme releases arachidonic acid from membrane phospholipids [1]. While **Corticosteroids** inhibit this enzyme (via lipocortin), Aspirin acts further downstream on the COX enzyme. * **D. Protein kinase C:** This is an intracellular signaling molecule involved in various cellular responses, including the oxidative burst, but it is not the target of Aspirin. **High-Yield Pearls for NEET-PG:** * **Aspirin Mechanism:** Irreversible acetylation of the serine residue in the active site of COX. * **Prostaglandin E2 (PGE2):** Key mediator of **Pain** and **Fever** [3]. * **Leukotrienes (LTB4):** A product of the Lipoxygenase (LOX) pathway; it is a potent **chemotactic agent** for neutrophils [2], [3]. Aspirin does *not* inhibit LOX; in fact, blocking COX can shunt arachidonic acid toward the LOX pathway (leading to Aspirin-induced asthma). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 95. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [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.
Question 102: What are the most important growth factors in angiogenesis?
- A. Platelet-derived growth factor (PDGF)
- B. Transforming growth factor alpha (TGF-α)
- C. Transforming growth factor beta (TGF-β)
- D. Angiotensin I (Ang I) (Correct Answer)
Explanation: **Explanation:** Angiogenesis (neovascularization) is a critical step in chronic inflammation and wound healing, involving the formation of new blood vessels from pre-existing ones. [1] **Why Angiopoietins are correct:** While **VEGF (Vascular Endothelial Growth Factor)** is the primary inducer of angiogenesis, **Angiopoietins (Ang 1 and Ang 2)** are essential for the maturation and stabilization of these new vessels. [1] Ang 1 interacts with the **Tie2 receptor** on endothelial cells to recruit peri-endothelial cells (pericytes and smooth muscle cells), ensuring the structural integrity of the vessel. [1] Without Ang 1, new vessels remain fragile and prone to leakage. **Analysis of Incorrect Options:** * **A. PDGF:** While PDGF is involved in the recruitment of smooth muscle cells to the vessel wall, its primary role in repair is stimulating the migration and proliferation of fibroblasts and smooth muscle cells. [1] * **B. TGF-α:** This is structurally related to EGF (Epidermal Growth Factor) and is primarily involved in the proliferation of epithelial cells and hepatocytes; it is not a primary driver of angiogenesis. * **C. TGF-β:** This is a potent fibrogenic agent. It stimulates collagen synthesis and inhibits collagen degradation, making it the most important cytokine for **scar formation (fibrosis)** rather than the initiation of angiogenesis. [1] **NEET-PG High-Yield Pearls:** * **VEGF:** Most important growth factor for *initiating* angiogenesis and increasing vascular permeability (Notch signaling pathway). [1] * **FGF-2 (bFGF):** Stimulates proliferation of endothelial cells and migration of macrophages/fibroblasts. [2] * **HIF-1 (Hypoxia-inducible factor):** The transcription factor that triggers VEGF production in response to low oxygen. [2] * **Metalloproteinases (MMPs):** Essential for degrading the basement membrane to allow for vessel "sprouting." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-116. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 313-314.
Question 103: Which of the following is not a negative acute-phase reactant?
- A. Albumin
- B. Transthyretin
- C. Ferritin (Correct Answer)
- D. Transferrin
Explanation: **Explanation:** Acute-phase reactants (APRs) are proteins whose plasma concentrations change by at least 25% in response to inflammation, triggered primarily by cytokines like IL-6, IL-1, and TNF-alpha [1]. They are categorized into **Positive APRs** (levels increase) and **Negative APRs** (levels decrease). **Why Ferritin is the correct answer:** **Ferritin** is a **Positive Acute-Phase Reactant**. During inflammation, the body sequesters iron to withhold it from microbes (which require iron for growth). Consequently, ferritin levels rise significantly during acute or chronic inflammation, infection, or malignancy [2]. Therefore, it is not a negative APR. **Analysis of Incorrect Options (Negative APRs):** Negative APRs decrease during inflammation because the liver prioritizes the synthesis of positive APRs (like CRP and Fibrinogen) to aid the immune response. * **Albumin (Option A):** The most common negative APR. Its synthesis decreases to conserve amino acids for positive APRs. * **Transthyretin (Option B):** Also known as Pre-albumin; its levels drop rapidly during acute inflammation and malnutrition. * **Transferrin (Option D):** This iron-transport protein decreases during inflammation (unlike ferritin, which increases), contributing to the "Anemia of Chronic Disease" [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Most sensitive marker:** C-Reactive Protein (CRP) is the most commonly used positive APR to monitor acute inflammation [1]. * **ESR vs. CRP:** ESR is an indirect measure of APRs (mainly fibrinogen), whereas CRP is a direct measurement. * **The "Rule of T's":** Most negative APRs start with 'T'—**T**ransferrin, **T**ransthyretin (Pre-albumin), and **T**ranscortin (along with Albumin and Retinol-binding protein). * **Hepcidin:** A positive APR that inhibits ferroportin, leading to the iron sequestration seen in Anemia of Chronic Disease [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 109-111. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 657-662.
Question 104: Important components of collagen synthesis, wound strength, and contraction include all of the following EXCEPT?
- A. Fibroblasts
- B. Myofibroblasts
- C. Vitamin C
- D. Vitamin D (Correct Answer)
Explanation: ### Explanation The correct answer is **Vitamin D**, as it does not play a direct role in collagen synthesis, wound contraction, or the mechanical strength of a healing wound. **1. Why Vitamin D is the Correct Answer:** While Vitamin D is essential for calcium homeostasis and bone mineralization, it is not a cofactor for the enzymes involved in collagen formation. Wound healing primarily depends on protein synthesis, enzymatic cross-linking, and cellular contraction—processes where Vitamin D has no established primary role. **2. Analysis of Other Options:** * **Fibroblasts (A):** These are the "workhorse" cells of wound healing. They migrate to the wound site to synthesize the extracellular matrix (ECM) and type III collagen, which is later replaced by type I collagen [3]. * **Myofibroblasts (B):** These are modified fibroblasts containing alpha-smooth muscle actin [1]. They are responsible for **wound contraction**, which reduces the surface area of the injury [2]. * **Vitamin C (C):** This is a critical cofactor for the enzymes **prolyl and lysyl hydroxylase**. These enzymes hydroxylate proline and lysine residues, a step necessary for the cross-linking and stabilization of the collagen triple helix. Deficiency leads to Scurvy and poor wound healing. **3. High-Yield Clinical Pearls for NEET-PG:** * **Collagen Types:** Type III collagen is found in early granulation tissue; Type I collagen provides the final tensile strength in scars. * **Tensile Strength:** At the end of 1 week (suture removal), wound strength is ~10% [1]. It reaches a maximum of **70-80%** by 3 months; it never returns to 100% [1]. * **Zinc Deficiency:** Another common "EXCEPT" distractor; Zinc is a cofactor for **Matrix Metalloproteinases (MMPs)**, which are essential for remodeling the scar. * **Glucocorticoids:** These inhibit wound healing by decreasing TGF-beta production and weakening the scar. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121. [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. 105-106. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119.
Question 105: Which cell is involved in the immediate phase of wound healing?
- A. Platelets (Correct Answer)
- B. Fibroblasts
- C. Basophils
- D. Macrophages
Explanation: **Explanation:** Wound healing is a complex, overlapping process traditionally divided into four phases: **Hemostasis, Inflammation, Proliferation, and Remodeling.** **Why Platelets are correct:** The **immediate phase** of wound healing is **Hemostasis** [2]. Upon injury, blood vessels constrict and **platelets** are the first cells to arrive at the site [1]. They aggregate to form a primary hemostatic plug and release clotting factors to form a fibrin clot [1], [2]. Crucially, platelets degranulate, releasing growth factors like **PDGF** (Platelet-Derived Growth Factor) and **TGF-̢**, which act as chemoattractants for the inflammatory cells that follow [1]. **Why the other options are incorrect:** * **Fibroblasts:** These are the hallmark cells of the **Proliferative phase**. They typically appear 3–5 days after injury to synthesize collagen and extracellular matrix [5]. * **Macrophages:** These are the dominant cells of the **late inflammatory phase** (appearing around 48–72 hours) [4]. While essential for debridement and orchestrating the transition to repair, they are not the "immediate" responders [5]. * **Basophils:** These cells are involved in allergic reactions and type I hypersensitivity; they do not play a primary or diagnostic role in the standard timeline of wound healing. **High-Yield NEET-PG Pearls:** * **Order of cell arrival:** Platelets (Seconds) → Neutrophils (24–48 hrs) → Macrophages (48–72 hrs) → Fibroblasts (3–5 days) [4], [5]. * **Key Growth Factor:** **PDGF** is the most important factor for initiating the migration and proliferation of fibroblasts and smooth muscle cells [4]. * **Tensile Strength:** At the end of 1 week, wound strength is ~10%. It reaches a maximum of **70–80%** by 3 months; it never returns to 100% of original strength. * **Type III vs. Type I Collagen:** Early granulation tissue is rich in Type III collagen, which is later replaced by Type I collagen during remodeling [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 126-128. [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. 105-106. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115.
Question 106: Which of the following are considered slow mediators of inflammation?
- A. Leukotrienes (Correct Answer)
- B. Prostaglandins
- C. Interleukins
- D. Vasoactive amines
Explanation: **Explanation:** The correct answer is **Leukotrienes (Option A)**. Leukotrienes (specifically LTC4, LTD4, and LTE4) are known as the **Slow-Reacting Substances of Anaphylaxis (SRS-A)**. Unlike preformed mediators like histamine, leukotrienes are synthesized *de novo* from arachidonic acid via the lipoxygenase pathway [1]. They are significantly more potent than histamine in inducing vascular permeability and bronchospasm [1], but their action is characterized by a slower onset and a more sustained, prolonged effect. **Analysis of Incorrect Options:** * **Vasoactive Amines (Option D):** Histamine and serotonin are "preformed" mediators stored in mast cell granules [1]. They are the first mediators released during an injury, causing an immediate (but short-lived) vascular response. * **Prostaglandins (Option B):** While also derived from arachidonic acid (cyclooxygenase pathway), they primarily mediate vasodilation, pain, and fever [1]. They do not share the specific "slow-reacting" nomenclature associated with the leukotriene-mediated bronchoconstriction. * **Interleukins (Option C):** These are cytokines (e.g., IL-1, TNF) that primarily mediate the systemic acute phase response and chronic inflammatory cell recruitment [1]. Their timeline is generally much later (hours) compared to the immediate/sub-acute chemical mediators. **High-Yield NEET-PG Pearls:** * **Potency:** Leukotrienes are 100–1000 times more potent than histamine in causing bronchoconstriction. * **Chemotaxis:** LTB4 is a highly potent chemoattractant for neutrophils (Remember: **B**4 for "**B**e there" – recruitment) [1]. * **Clinical Link:** Leukotriene receptor antagonists (e.g., Montelukast) are used in asthma to block these slow-reacting mediators [1]. * **Triple Response of Lewis:** Mediated primarily by histamine (Vasoactive amine), not leukotrienes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.
Question 107: What is a characteristic feature of acute inflammation?
- A. Vasoconstriction
- B. Vascular stasis
- C. Margination of leucocytes
- D. Vasodilation and increased vascular permeability (Correct Answer)
Explanation: **Explanation:** Acute inflammation is the immediate and early response to injury, characterized by three major components: alterations in vascular caliber, structural changes in microvasculature, and emigration of leukocytes [1]. **Why Option D is Correct:** The hallmark of acute inflammation is **vasodilation** (induced by mediators like histamine and nitric oxide) and **increased vascular permeability** [1], [2]. Vasodilation increases blood flow (causing redness and heat), while increased permeability allows protein-rich fluid (exudate) to move into extravascular tissues, leading to edema [1]. This is the most fundamental vascular change that facilitates the delivery of inflammatory cells to the site of injury. **Analysis of Incorrect Options:** * **A. Vasoconstriction:** While transient vasoconstriction of arterioles occurs immediately after injury (lasting seconds), it is a fleeting reflex and not a characteristic sustained feature of the inflammatory process [1]. * **B. Vascular Stasis:** Stasis (slowing of blood flow) does occur as a *consequence* of fluid loss and increased blood viscosity, but it is a secondary phenomenon rather than the primary defining characteristic [1]. * **C. Margination of Leucocytes:** This is a cellular event where leukocytes move toward the endothelial surface [4]. While essential, it is part of the cellular phase, whereas the question focuses on the primary vascular hallmark of the acute response. **High-Yield Clinical Pearls for NEET-PG:** * **Cardinal Signs:** Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), and Functio Laesa (loss of function) [5]. * **Most Common Mechanism of Increased Permeability:** Endothelial cell contraction leading to intercellular gaps (occurs primarily in post-capillary venules) [3]. * **Sequence of Leukocyte Extravasation:** Margination → Rolling (Selectins) → Adhesion (Integrins) → Transmigration (PECAM-1) → Chemotaxis [2]. **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. [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. 186-187. [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. 185-186.
Question 108: Which of the following is NOT an action of bradykinin?
- A. Vasodilation
- B. Bronchodilation (Correct Answer)
- C. Increased vascular permeability
- D. Pain
Explanation: **Explanation:** Bradykinin is a potent inflammatory mediator belonging to the kinin system. It is formed from high-molecular-weight kininogen (HMWK) through the action of the enzyme kallikrein. **Why Bronchodilation is the correct answer:** Bradykinin is a potent **bronchoconstrictor**, not a bronchodilator. It acts on the smooth muscles of the bronchial tree, leading to airway narrowing [1]. This is clinically significant in patients taking ACE inhibitors (which prevent bradykinin breakdown), often resulting in a dry cough or exacerbation of asthma. **Analysis of Incorrect Options:** * **A. Vasodilation:** Bradykinin is one of the most powerful endogenous vasodilators [1]. It acts by stimulating the release of nitric oxide (NO) and prostacyclin from endothelial cells, leading to a drop in blood pressure. * **C. Increased vascular permeability:** Similar to histamine, bradykinin causes contraction of endothelial cells in post-capillary venules, creating gaps that allow fluid and proteins to leak into the extravascular space (edema) [1], [3]. * **D. Pain:** Bradykinin is a primary mediator of pain [1], [2]. It sensitizes nociceptors (pain receptors) and lowers the threshold for pain activation, often acting synergistically with prostaglandins. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolism:** Bradykinin is inactivated by **Angiotensin-Converting Enzyme (ACE)**. Therefore, ACE inhibitors lead to increased bradykinin levels, causing the classic side effects of **dry cough** and **angioedema**. * **Hageman Factor (Factor XII):** The kinin system is triggered by the activation of Factor XII, linking the coagulation cascade to inflammation. * **C1 Esterase Inhibitor Deficiency:** This leads to **Hereditary Angioedema** due to the overproduction of bradykinin. **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, 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 109: Endothelial activation refers to which of the following processes?
- A. Aberration of the anatomy of the vessel wall
- B. Irreversible changes in the functional state of the vessel wall
- C. Smooth muscle proliferation
- D. Increased expression of adhesion molecules for leukocyte recruitment (Correct Answer)
Explanation: ### Explanation **Endothelial activation** is a critical physiological response of the vascular endothelium to inflammatory stimuli (such as TNF, IL-1, and bacterial products) [1]. It represents a **functional shift** from a quiescent, anti-coagulant state to a pro-inflammatory and pro-coagulant state. **Why Option D is Correct:** The hallmark of endothelial activation is the **upregulation of cell adhesion molecules (CAMs)** [1]. To facilitate leukocyte recruitment to the site of injury, activated endothelial cells express: * **Selectins (E-selectin and P-selectin):** Mediate initial "rolling" [4]. * **Integrin Ligands (ICAM-1 and VCAM-1):** Mediate "firm adhesion." Additionally, activated cells secrete chemokines and change their shape to allow for paracellular transmigration (diapedesis) [2]. **Analysis of Incorrect Options:** * **Option A:** Endothelial activation is a **functional and phenotypic change**, not primarily an anatomical aberration or structural defect of the vessel wall [3]. * **Option B:** The process is generally **reversible**. Once the inflammatory stimulus is removed, the endothelium can return to its basal, non-activated state. * **Option C:** While smooth muscle proliferation occurs in chronic inflammation and atherosclerosis (often triggered by growth factors like PDGF), it is a secondary response and not the definition of endothelial activation itself [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Triggers:** The most potent cytokines for endothelial activation are **TNF** and **IL-1** [3]. * **Weibel-Palade Bodies:** These are storage granules in endothelial cells containing **P-selectin** and **Von Willebrand Factor (vWF)**. Their rapid translocation to the surface is the earliest sign of activation. * **Nitric Oxide (NO):** In a healthy state, NO inhibits endothelial activation; its loss (endothelial dysfunction) is a precursor to atherosclerosis [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 502-503. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Migration in the tissues toward a chemotactic stimulus, pp. 86-87.
Question 110: A 54-year-old male presents with severe chest pain. ECG shows acute myocardial infarction. He was given thrombolytic therapy with tPA. His serum creatine kinase levels increased after this therapy. Which event most likely occurred?
- A. Reperfusion injury (Correct Answer)
- B. Cellular regeneration
- C. Chemical injury
- D. Increased synthesis of creatine kinase
Explanation: ### Explanation **1. Why Reperfusion Injury is Correct:** The clinical scenario describes a classic case of **Ischemia-Reperfusion Injury**. When blood flow is restored (via thrombolytics like tPA) to previously ischemic myocardial tissue, it paradoxically leads to further damage [1]. This occurs because the sudden influx of oxygen and nutrients triggers the production of **Reactive Oxygen Species (ROS)**, mitochondrial permeability transition, and increased leukocyte infiltration. The **increase in serum creatine kinase (CK)** after therapy is a hallmark sign. Reperfusion causes further membrane damage (via lipid peroxidation), allowing intracellular enzymes like CK and LDH to leak into the bloodstream more rapidly than they would have with ischemia alone. **2. Why the Other Options are Incorrect:** * **B. Cellular Regeneration:** Myocytes are permanent cells; they do not undergo regeneration. Myocardial injury heals by scarring (fibrosis), not by the replacement of functional muscle cells. * **C. Chemical Injury:** While tPA is a drug, it does not cause direct chemical toxicity to the myocardium. The injury is a result of the physiological consequences of restored blood flow. * **D. Increased synthesis of CK:** The rise in CK levels is due to the **leakage** of pre-existing enzymes through damaged cell membranes, not due to new protein synthesis by the dying myocytes. **3. NEET-PG High-Yield Pearls:** * **Mechanism of ROS:** The main source of ROS during reperfusion is **Xanthine Oxidase** and infiltrated neutrophils. * **Morphological Sign:** Reperfusion injury is often characterized histologically by **Contraction Band Necrosis** [1] (due to massive calcium influx causing hypercontraction of myofibrils). * **Clinical Correlation:** This explains why "Time is Muscle"—the longer the ischemia, the more severe the potential reperfusion injury, though reperfusion remains the standard of care to salvage viable tissue [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 554-556.
Practice by Chapter
Acute Inflammation: Vascular Events
Practice Questions
Acute Inflammation: Cellular Events
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Chemical Mediators of Inflammation
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Chronic Inflammation
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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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