Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 321: After extravasation, leukocytes emigrate in the tissue towards the site of injury. What is this process called?

A. Margination
B. Chemotaxis (Correct Answer)
C. Diapedesis
D. Pavementing

Explanation: ### Explanation The correct answer is **B. Chemotaxis**. **1. Why Chemotaxis is correct:** After leukocytes exit the blood vessels (extravasation), they must navigate through the interstitial tissue to reach the specific site of injury or infection. This **unidirectional movement along a chemical gradient** is called **Chemotaxis** [1], [2]. Both exogenous substances (e.g., bacterial products like N-formylmethionine) and endogenous substances (e.g., Cytokines like IL-8, Complement component C5a, and Leukotriene B4) act as chemoattractants. These substances bind to G protein-coupled receptors on the leukocyte surface, triggering actin polymerization and the formation of filopodia that "pull" the cell toward the stimulus. **2. Why the other options are incorrect:** * **A. Margination:** This is the initial step of leukocyte recruitment where cells move from the central axial column of the blood flow toward the periphery (near the endothelial surface) due to slowed blood flow (stasis) [2]. * **C. Diapedesis (Transmigration):** This refers specifically to the process of leukocytes squeezing through the endothelial intercellular junctions to exit the blood vessel into the perivascular space [2]. It is mediated primarily by **PECAM-1 (CD31)**. * **D. Pavementing:** This is a consequence of intense adhesion where the internal surface of the venule becomes lined by a dense layer of leukocytes, appearing like a "pavement." **3. High-Yield Clinical Pearls for NEET-PG:** * **Most potent endogenous chemoattractants:** LTB4, C5a, IL-8, and Kallikrein. * **Nature of movement:** Chemotaxis involves the reorganization of the **cytoskeleton (actin)** [1]. * **Sequence of Leukocyte Infiltration:** Neutrophils dominate the first 6–24 hours (due to higher concentration in blood and rapid response), while Monocytes/Macrophages replace them after 24–48 hours. (Exception: *Pseudomonas* infections where neutrophils persist for days). **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, pp. 87-89.

Question 322: Which of the following utilizes an oxygen-dependent mechanism for killing or degradation in phagocytosis?

A. H2O2-MPO halide system (Correct Answer)
B. Bactericidal Permeability Increasing Protein (BPI)
C. Lactoferrin
D. Lysozyme

Explanation: Phagocytosis involves two main mechanisms for killing microbes: **Oxygen-dependent** and **Oxygen-independent**. [1] **1. Why Option A is Correct:** The **H₂O₂-MPO-halide system** is the most potent oxygen-dependent bactericidal mechanism in neutrophils. [1] During the "Respiratory Burst," NADPH oxidase converts oxygen into superoxide radicals, which then dismutate into hydrogen peroxide (H₂O₂). [3] **Myeloperoxidase (MPO)**, present in the azurophilic granules of neutrophils, converts H₂O₂ and a halide (usually Chloride) into **hypochlorite (HOCl⁻)**—the active ingredient in household bleach. [1] This highly reactive free radical destroys bacteria via lipid peroxidation and protein oxidation. **2. Why Other Options are Incorrect:** Options B, C, and D are all **Oxygen-independent mechanisms**. These rely on pre-formed proteins stored in leukocyte granules: [2] * **BPI (Bactericidal Permeability Increasing Protein):** Causes phospholipase activation and membrane phospholipid degradation, specifically against Gram-negative bacteria. * **Lactoferrin:** An iron-binding protein that inhibits bacterial growth by sequestering iron (a vital nutrient for microbes). * **Lysozyme:** An enzyme that attacks the muramic acid-N-acetylglucosamine bond in the glycopeptide coat of bacteria (cell wall degradation). [2] **Clinical Pearls for NEET-PG:** * **Chronic Granulomatous Disease (CGD):** Caused by a deficiency in **NADPH oxidase**. Patients cannot produce superoxide radicals, leading to recurrent infections with catalase-positive organisms (e.g., *S. aureus*). * **MPO Deficiency:** Patients usually remain asymptomatic because the H₂O₂ produced is still capable of killing, albeit more slowly. * **Nitroblue Tetrazolium (NBT) Test:** Used to diagnose CGD; a positive test (blue color) indicates intact NADPH oxidase activity, while a negative test (no color) indicates CGD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 91-92. [3] 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. 59.

Question 323: Which of the following is a chemotactic factor?

A. Prostaglandins
B. Prostacyclins
C. Thromboxane
D. Leukotrienes (Correct Answer)

Explanation: **Explanation:** **1. Why Leukotrienes are correct:** Chemotaxis is the process by which inflammatory cells (like neutrophils) move toward a site of injury along a chemical gradient [3]. **Leukotriene B4 (LTB4)** is one of the most potent endogenous chemotactic agents. It is produced via the Lipoxygenase (LOX) pathway of arachidonic acid metabolism [1]. LTB4 acts by increasing calcium levels and activating intracellular signaling pathways that lead to the reorganization of the cytoskeleton, allowing the leukocyte to migrate [2]. **2. Why the other options are incorrect:** All other options are products of the **Cyclooxygenase (COX) pathway**, which primarily regulate vascular tone and platelet aggregation rather than cell migration [3]: * **Prostaglandins (PGE2, PGD2):** These are primarily involved in causing **vasodilation** and increasing vascular permeability. They also mediate pain and fever [1]. * **Prostacyclins (PGI2):** Produced by vascular endothelium, PGI2 is a potent **vasodilator** and an **inhibitor of platelet aggregation** [1]. * **Thromboxane (TXA2):** Produced by platelets, it is a potent **vasoconstrictor** and promotes **platelet aggregation** [1]. **3. NEET-PG High-Yield Clinical Pearls:** * **Mnemonic for Chemotactic Factors:** **"C-B-I-L"** (pronounced "Civil") * **C:** **C5a** (Complement component) * **B:** **Bacterial products** (e.g., N-formyl methionine) * **I:** **IL-8** (Interleukin-8) * **L:** **LTB4** (Leukotriene B4) [3] * **Exogenous vs. Endogenous:** Bacterial products are the most common *exogenous* chemoattractants, while C5a, LTB4, and IL-8 are the most important *endogenous* ones [3]. * **Drug Link:** Zileuton inhibits the LOX pathway, thereby reducing the production of chemotactic leukotrienes in conditions like asthma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [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. 190-191. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 324: What is most important for diapedesis?

A. PECAM (Correct Answer)
B. Selectin
C. Integrin
D. Mucin-like glycoprotein

Explanation: Leukocyte extravasation is a multi-step process involving rolling, adhesion, and transmigration [1]. **Diapedesis** (transmigration) refers specifically to the movement of leukocytes through the endothelial junctions to reach the extravascular space [1]. **1. Why PECAM is correct:** **PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1)**, also known as **CD31**, is the primary molecule responsible for diapedesis [1]. It is expressed on both the surface of leukocytes and at the intercellular junctions of endothelial cells. Through homophilic binding (PECAM-PECAM interaction), it facilitates the "squeezing" of the leukocyte through the basement membrane [1]. **2. Why other options are incorrect:** * **Selectins (E, P, and L-selectin):** These mediate the initial **Rolling** phase [1]. They have low-affinity interactions with Sialyl-Lewis X ligands, allowing the leukocyte to slow down. * **Integrins (e.g., LFA-1, VLA-4):** These are responsible for **Firm Adhesion** and crawling [1]. They bind to ligands like ICAM-1 and VCAM-1 on the endothelium after being activated by chemokines. * **Mucin-like glycoproteins (e.g., GlyCAM-1, PSGL-1):** These serve as the ligands for selectins and are involved in the **Rolling** phase. **High-Yield Clinical Pearls for NEET-PG:** * **CD31** is the most sensitive and specific marker for **vascular tumors** (e.g., Angiosarcoma). * **Leukocyte Adhesion Deficiency (LAD) Type 1** is caused by a defect in the **\u03b22-integrin (CD18)**, leading to impaired firm adhesion and recurrent infections without pus formation [1]. * **LAD Type 2** is a defect in **Sialyl-Lewis X**, affecting the rolling phase. * **Sequence of migration:** Neutrophils dominate the first 6\u201324 hours, followed by Monocytes/Macrophages after 24\u201348 hours (Exception: *Pseudomonas* infections where neutrophils persist longer). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 325: Which is a vasoconstricting mediator?

A. Prostacyclin
B. Thromboxane-A2 (Correct Answer)
C. PG D2
D. Lipoxins

Explanation: **Explanation:** The correct answer is **Thromboxane-A2 (TXA2)**. This question tests your knowledge of arachidonic acid metabolites (eicosanoids) and their specific roles in the inflammatory response and vascular hemodynamics. **1. Why Thromboxane-A2 is correct:** TXA2 is primarily produced by platelets via the cyclooxygenase (COX) pathway. It is a potent **vasoconstrictor** and a powerful **platelet aggregator** [1]. Its physiological role is to promote clot formation and limit blood loss at the site of vascular injury, acting in direct opposition to prostacyclin. **2. Why the other options are incorrect:** * **Prostacyclin (PGI2):** Produced by vascular endothelium, it is a potent **vasodilator** and an inhibitor of platelet aggregation [1]. It maintains vascular patency. * **PG D2:** Along with PGE2 and PGF2α, PGD2 is a major prostaglandin produced by mast cells that causes **vasodilation** and increases vascular permeability (edema) [1]. * **Lipoxins (LXA4, LXB4):** These are anti-inflammatory mediators that function in the **resolution** of inflammation. They inhibit neutrophil chemotaxis and adhesion, and typically cause vasodilation. **Clinical Pearls for NEET-PG:** * **The "Push-Pull" Mechanism:** Remember the balance between **TXA2** (Platelet-derived; Pro-thrombotic/Vasoconstrictor) and **PGI2** (Endothelial-derived; Anti-thrombotic/Vasodilator) [1]. An imbalance often leads to thrombosis or hypertension. * **Aspirin:** Low-dose aspirin irreversibly inhibits COX-1 in platelets, reducing TXA2 levels, which explains its use as a cardioprotective/anti-platelet agent. * **Other Vasoconstrictors to remember:** Leukotrienes (C4, D4, E4), Endothelin, and Angiotensin II [1]. * **Other Vasodilators to remember:** Nitric Oxide (NO), Histamine, and Bradykinin. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-97.

Question 326: All of the following enzymes may contribute to generating free oxygen radicals within neutrophils for killing intracellular bacteria, except?

A. Superoxide Dismutase
B. Fenton's reaction
C. NADPH oxidase
D. Glutathione Peroxidase (Correct Answer)

Explanation: ### Explanation The killing of intracellular bacteria by neutrophils primarily occurs through the **Respiratory Burst**, a process that generates **Reactive Oxygen Species (ROS)** [2], [4]. **Why Glutathione Peroxidase is the Correct Answer:** Glutathione Peroxidase is an **antioxidant enzyme**, not a pro-oxidant [1]. Its primary role is to **neutralize** free radicals (specifically hydrogen peroxide) into water, thereby protecting the cell from oxidative damage [1], [2]. Since the question asks for enzymes that *contribute to generating* radicals for bacterial killing, Glutathione Peroxidase is the exception as it performs the opposite function (scavenging). **Analysis of Other Options:** * **NADPH Oxidase (Option C):** This is the "initiator" enzyme located in the phagosome membrane [4]. It converts Oxygen ($O_2$) into the **Superoxide radical** ($\cdot O_2^-$) [2]. A deficiency in this enzyme leads to **Chronic Granulomatous Disease (CGD)**. * **Superoxide Dismutase (Option A):** This enzyme converts the superoxide radical into **Hydrogen Peroxide** ($H_2O_2$) [2], [3]. While $H_2O_2$ is a precursor to more potent radicals, it is itself a ROS involved in the killing pathway. * **Fenton’s Reaction (Option B):** Though not an enzyme itself, this chemical reaction involves the transition of $H_2O_2$ to the highly reactive **Hydroxyl radical** ($\cdot OH$) in the presence of ferrous iron ($Fe^{2+}$) [2]. It is a major contributor to free radical-mediated injury and bacterial killing. ### High-Yield Clinical Pearls for NEET-PG: 1. **MPO-Halide System:** The most potent bactericidal mechanism in neutrophils is the conversion of $H_2O_2$ to **Hypochlorite** (HOCl/Bleach) by the enzyme **Myeloperoxidase (MPO)** [4]. 2. **CGD Diagnosis:** Use the **Nitroblue Tetrazolium (NBT) test** (negative/colorless in CGD) or the more modern **Dihydrorhodamine (DHR) flow cytometry** test. 3. **Antioxidant Trio:** Remember the three main enzymes that scavenge free radicals: **SOD** (neutralizes superoxide), **Catalase**, and **Glutathione Peroxidase** (both neutralize $H_2O_2$) [2]. **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. 59-60. [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. 59. [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. 100-101. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91.

Question 327: The tensile strength of a healing wound starts to increase after which period?

A. Immediate suture of the wound
B. 3 to 4 days (Correct Answer)
C. 7 to 10 days
D. 6 months

Explanation: ### Explanation The tensile strength of a healing wound is a measure of its capacity to resist rupture. The correct answer is **3 to 4 days** because this marks the transition from the inflammatory phase to the **proliferative phase** [1]. **1. Why Option B is Correct:** During the first 48–72 hours (Lag Phase), the wound has negligible strength, relying entirely on sutures. Around **day 3 to 4**, fibroblasts begin to migrate into the wound site [1] and initiate **Type III collagen synthesis**. This deposition of collagen fibers is the primary driver for the initial increase in tensile strength. **2. Why Incorrect Options are Wrong:** * **Option A (Immediate):** At the time of suturing, the wound has 0% intrinsic strength; it is held together solely by mechanical hardware [1]. * **Option C (7 to 10 days):** By the end of the first week, tensile strength increases rapidly (reaching about 10% of original strength), but the *start* of the increase occurs much earlier (day 3-4) [1]. * **Option D (6 months):** This is near the end of the remodeling phase. While strength continues to increase through collagen cross-linking and the switch from Type III to Type I collagen, it peaks at roughly 70–80% of original skin strength by 3 months and plateaus [1]. **NEET-PG High-Yield Pearls:** * **Timeline of Strength:** 10% at 1 week; 70–80% at 3 months (it never reaches 100%) [1]. * **Collagen Switch:** Initial repair uses **Type III collagen** (granulation tissue); it is later replaced by **Type I collagen** (mature scar) for greater strength. * **Key Nutrient:** Vitamin C is essential for the hydroxylation of proline and lysine residues in collagen; deficiency leads to poor wound healing and scurvy [1]. * **Most Important Cell:** The **Macrophage** is the "director" of wound healing, transitioning the wound from inflammation to repair [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-121.

Question 328: What is the most important source of histamine?

A. Mast cells (Correct Answer)
B. Eosinophils
C. Neutrophils
D. Macrophages

Explanation: **Explanation:** **Histamine** is a potent vasoactive amine and the first mediator to be released during an acute inflammatory response. **Why Mast Cells are the Correct Answer:** Mast cells are the **most important and richest source** of histamine [2]. They are widely distributed in connective tissues, particularly near blood vessels [1]. Histamine is pre-formed and stored in the granules of mast cells. It is released via degranulation in response to various stimuli, including physical injury, binding of IgE antibodies (Type I Hypersensitivity), and complement fragments (C3a and C5a, known as anaphylatoxins) [1], [2]. Once released, histamine causes arteriolar dilation and increased vascular permeability (venular gaps) [3]. **Why Other Options are Incorrect:** * **Eosinophils:** While eosinophils contain various enzymes (like Major Basic Protein), they are not a primary source of histamine. In fact, they contain **histaminase**, an enzyme that degrades histamine to help limit the inflammatory response. * **Neutrophils:** These are the hallmark of acute inflammation and contain lysosomal enzymes and reactive oxygen species, but they do not store or produce significant amounts of histamine. * **Macrophages:** These cells are central to chronic inflammation and secrete cytokines (TNF, IL-1), but they are not a source of histamine. **High-Yield Clinical Pearls for NEET-PG:** * **Other Sources:** Besides mast cells, **basophils** (in the blood) and **platelets** also contain histamine [1]. * **Mechanism of Action:** Histamine acts primarily on **H1 receptors** on microvascular endothelial cells to cause contraction and interendothelial gaps [3]. * **Inhibitor:** Epinephrine is the physiological antagonist of histamine and is the drug of choice for anaphylaxis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [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 329: All of the following are mediators of inflammation, except:

A. Tumour necrosis factor-alpha (TNF-alpha)
B. Interleukin-1
C. Myeloperoxidase (Correct Answer)
D. Prostaglandins

Explanation: **Explanation:** The core concept in this question is distinguishing between **mediators of inflammation** and **microbicidal enzymes**. **Why Myeloperoxidase (MPO) is the correct answer:** Myeloperoxidase is an enzyme found in the azurophilic (primary) granules of neutrophils. It is not a mediator that initiates or regulates the inflammatory response; rather, it is an **effector molecule**. During the "respiratory burst," MPO converts hydrogen peroxide ($H_2O_2$) and halide ions (like $Cl^-$) into hypochlorous acid ($HOCl$), a potent oxidizing agent that kills ingested microbes [2]. It acts downstream of the inflammatory process. **Analysis of Incorrect Options:** * **TNF-alpha & Interleukin-1 (IL-1):** These are the "master cytokines" of acute inflammation [1]. Produced primarily by activated macrophages, they mediate systemic acute-phase responses (fever, sleep, decreased appetite) and induce endothelial cells to express adhesion molecules [2]. * **Prostaglandins:** These are lipid mediators derived from arachidonic acid via the cyclooxygenase (COX) pathway [1]. They are classic mediators responsible for vasodilation, pain, and fever [2]. **High-Yield Clinical Pearls for NEET-PG:** * **MPO Deficiency:** The most common inherited defect of phagocytosis; however, most patients are asymptomatic because other killing mechanisms remain intact. * **Vascular Permeability:** Histamine is the most important mediator of the immediate transient response (contraction of endothelial cells) [2]. * **Pain Mediators:** Prostaglandin $E_2$ ($PGE_2$) and Bradykinin are the primary mediators of pain in inflammation [2]. * **Chemotaxis:** The most potent chemotactic factors are $C5a$, $LTB_4$, $IL-8$, and bacterial products (N-formyl methionine) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 330: Which of the following are anti-inflammatory mediators?

A. Lipoxins (Correct Answer)
B. Thromboxane
C. Prostaglandins
D. Interleukins

Explanation: **Explanation:** The process of inflammation is tightly regulated by a balance between pro-inflammatory and anti-inflammatory mediators [1]. The resolution of inflammation is an active process, not merely a passive decay of signals. **1. Why Lipoxins are correct:** Lipoxins (specifically LXA4 and LXB4) are derivatives of arachidonic acid produced via the **lipoxygenase pathway**. Unlike leukotrienes, lipoxins serve as "stop signals" for inflammation [1]. They inhibit neutrophil chemotaxis and adhesion to the endothelium, while simultaneously stimulating the recruitment of non-phlogistic (non-inflammatory) monocytes and macrophages to clear apoptotic debris. This dual action promotes the **resolution phase** of inflammation. **2. Why the other options are incorrect:** * **Thromboxane (TXA2):** A potent pro-inflammatory mediator produced by platelets. It causes vasoconstriction and promotes platelet aggregation. * **Prostaglandins (e.g., PGE2, PGD2):** These are classic pro-inflammatory mediators that cause vasodilation, increase vascular permeability, and mediate pain and fever [1]. * **Interleukins:** While some interleukins (like IL-10) are anti-inflammatory, the term "Interleukins" generally refers to a broad class of cytokines (like IL-1 and IL-6) that are predominantly pro-inflammatory in the context of acute inflammation [1]. **High-Yield NEET-PG Pearls:** * **Pro-resolving mediators:** Besides Lipoxins, keep an eye out for **Resolvins, Protectins, and Maresins** (derived from omega-3 fatty acids) [1]. * **Anti-inflammatory Cytokines:** The most important ones to remember are **IL-10** and **TGF-β**. * **Switch Mechanism:** During inflammation, there is a "class switch" where the production of pro-inflammatory leukotrienes (LTB4) shifts to anti-inflammatory lipoxins to initiate healing. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-101.

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

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Fibrosis and Repair

Practice Questions

Resolution of Inflammation

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