Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 151: Which of the following cells are normally in the G0 stage of the cell cycle, hence not proliferating, but are capable of dividing in response to injury?

A. Transitional epithelium of the urinary tract
B. Parenchyma of most solid organs (Correct Answer)
C. Neurons
D. Skeletal muscles

Explanation: This question tests your understanding of the **classification of cells based on their proliferative capacity**, a fundamental concept in tissue repair and regeneration. [4] ### **1. Why the Correct Answer is Right** Cells are categorized into three groups based on their regenerative potential: * **Stable (Quiescent) Cells:** These cells are normally in the **G0 stage** of the cell cycle. They have a low level of replication but can be stimulated to undergo rapid division (re-enter the cell cycle via G1) in response to injury or loss of tissue mass. [1] * **Parenchyma of solid organs** (such as the **liver, pancreas, and kidney**) consists of stable cells. [4] For example, after a partial hepatectomy, the remaining hepatocytes proliferate to restore the organ's mass. [1], [2] Other examples include vascular endothelial cells, fibroblasts, and smooth muscle cells. ### **2. Analysis of Incorrect Options** * **Option A (Transitional epithelium):** These are **Labile Cells**. They are continuously dividing and follow a cycle of constant death and replacement. [3] They do not rest in G0. Other examples include hematopoietic cells in bone marrow and surface epithelia (skin, GI tract). [4] * **Options C & D (Neurons and Skeletal muscles):** These are **Permanent Cells**. They have exited the cell cycle permanently and cannot undergo division in postnatal life. Injury to these tissues results in **scarring (fibrosis)** rather than regeneration. [5] Cardiac muscle is also a permanent cell type. ### **3. High-Yield Clinical Pearls for NEET-PG** * **Regeneration vs. Repair:** Regeneration requires an intact **extracellular matrix (ECM)**. If the ECM is destroyed, even stable cells cannot restore normal architecture, leading to scarring. [2] * **Stem Cells:** Labile tissues are replaced by the proliferation of immature stem cells (e.g., crypts in the intestine, basal layer of the skin). [4] * **Hypertrophy vs. Hyperplasia:** Permanent cells (like the heart) can only undergo **hypertrophy**, whereas stable and labile cells can undergo both **hypertrophy and hyperplasia**. **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. 108-109. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 113. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 111-112.

Question 152: Parasitic inflammation typically shows a predominance of which type of inflammatory cell?

A. Lymphocytes
B. Neutrophils
C. Eosinophils (Correct Answer)
D. Basophils

Explanation: ### Explanation **Correct Answer: C. Eosinophils** **Why it is correct:** Eosinophils are the hallmark cells of parasitic infections, particularly those caused by helminths (worms) [1]. This is mediated by a **Type 2 helper T cell (Th2) response**, which secretes **Interleukin-5 (IL-5)** [3]. IL-5 is the primary cytokine responsible for the recruitment, activation, and survival of eosinophils. Once at the site, eosinophils release **Major Basic Protein (MBP)** and **Eosinophil Cationic Protein (ECP)** from their granules, which are highly toxic to the tough tegument of parasites [2]. **Why other options are incorrect:** * **A. Lymphocytes:** These are the predominant cells in chronic inflammation and viral infections [1]. While they coordinate the immune response against parasites (via Th2 cells), they are not the primary effector cells visualized in the inflammatory infiltrate. * **B. Neutrophils:** These are the "first responders" of **acute inflammation** and are primarily associated with pyogenic (pus-forming) bacterial infections [1]. * **D. Basophils:** While basophils (and mast cells) participate in IgE-mediated allergic reactions often seen alongside parasitic infections, they are present in much smaller numbers compared to eosinophils. **High-Yield Clinical Pearls for NEET-PG:** * **Charcot-Leyden Crystals:** These are hexagonal, bipyramidal crystals derived from the breakdown of eosinophil membranes (specifically **Galectin-10**). They are found in sputum (asthma) or stool (parasitic infections). * **Eosinophilia:** Defined as an absolute eosinophil count **>500 cells/µL**. * **NAACP Mnemonic:** Common causes of eosinophilia include **N**eoplasia, **A**llergy/Asthma, **A**ddison’s disease, **C**onnective tissue disorders, and **P**arasites [1]. * **IL-5** is the most specific growth factor for eosinophils; **Eotaxin** is the most potent chemoattractant [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. 195-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 404-405. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210.

Question 153: What is the main cell responsible for scar contraction?

A. Myofibroblast (Correct Answer)
B. Fibroblast
C. Epithelial cell
D. Elastin

Explanation: **Explanation:** The correct answer is **Myofibroblast** [1], [2]. **1. Why Myofibroblasts are correct:** Scar contraction is a critical phase of wound healing, particularly in healing by secondary intention [1]. **Myofibroblasts** are specialized cells that appear in the wound during the second week of healing. They possess features of both fibroblasts (synthetic capacity) and smooth muscle cells (contractile capacity) [2]. They contain bundles of **alpha-smooth muscle actin (α-SMA)**, which allows them to exert contractile force, pulling the edges of the wound together and reducing the overall surface area of the resulting scar [1], [2]. **2. Why other options are incorrect:** * **Fibroblast:** While fibroblasts are the primary cells responsible for synthesizing collagen and extracellular matrix (ECM) to provide structural integrity, they lack the specialized contractile apparatus (α-SMA) required for significant wound contraction [2]. * **Epithelial cell:** These cells are involved in **re-epithelialization** (covering the wound surface) rather than the contraction of the underlying connective tissue. * **Elastin:** This is a structural protein of the ECM that provides elasticity and recoil to tissues. It is not a cell and does not have active contractile properties. **Clinical Pearls for NEET-PG:** * **Healing by Secondary Intention:** Wound contraction is a hallmark of secondary intention; it can reduce the wound size by up to 5%–10% of its original size [1]. * **Contracture:** Excessive contraction by myofibroblasts leads to a pathological deformity called a **contracture**, commonly seen after severe burn injuries, limiting joint mobility. * **TGF-β:** This is the most important cytokine for the differentiation of fibroblasts into myofibroblasts. **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.

Question 154: Sialyl-Lewis X is linked to which of the following?

A. Selectin (Correct Answer)
B. ICAM
C. CD31
D. VCAM

Explanation: **Explanation:** The correct answer is **Selectin**. This question tests the molecular basis of leukocyte adhesion, specifically the **Rolling phase**. **1. Why Selectin is correct:** Rolling is the initial step of leukocyte recruitment, mediated by the **Selectin** family of adhesion molecules [1]. Selectins (E-selectin on endothelium, P-selectin on endothelium/platelets, and L-selectin on leukocytes) bind to specific carbohydrate ligands. **Sialyl-Lewis X** is the essential oligosaccharide ligand found on the surface of neutrophils and monocytes that binds to E-selectin and P-selectin [1]. This low-affinity interaction allows leukocytes to "roll" along the vessel wall. **2. Why other options are incorrect:** * **ICAM-1 (Option B) & VCAM-1 (Option D):** These belong to the **Immunoglobulin (Ig) Superfamily**. They are involved in the **Firm Adhesion** phase [3]. Their ligands are **Integrins** (e.g., LFA-1 binds to ICAM-1; VLA-4 binds to VCAM-1), not Sialyl-Lewis X. * **CD31 (Option C):** Also known as **PECAM-1** (Platelet Endothelial Cell Adhesion Molecule). It is primarily involved in **Diapedesis** (transmigration), where the leukocyte squeezes through the endothelial junctions [2]. **NEET-PG High-Yield Pearls:** * **Leukocyte Adhesion Deficiency (LAD) Type 2:** Caused by a genetic defect in fucosyltransferase, leading to the absence of **Sialyl-Lewis X** [2]. Clinical features include recurrent bacterial infections and impaired wound healing, but *without* the umbilical cord delay seen in LAD-1. * **P-selectin** is stored in **Weibel-Palade bodies** of endothelial cells and alpha-granules of platelets. * **L-selectin** is unique because it is expressed on the leukocyte itself (ligand is GlyCam-1 on HEVs). **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. Inflammation and Repair, p. 89.

Question 155: The complex process of leukocyte extravasation includes all EXCEPT?

A. Rolling
B. Adhesion
C. Migration
D. Phagocytosis (Correct Answer)

Explanation: ### Explanation Leukocyte extravasation (or recruitment) is the process by which white blood cells move from the vessel lumen to the site of injury in the interstitial tissue [1]. This is a multi-step cascade occurring primarily in the **post-capillary venules** [2]. **Why Phagocytosis is the Correct Answer:** Phagocytosis is the process of engulfing and degrading microbes or debris. While it is a crucial function of leukocytes (especially neutrophils and macrophages) during inflammation, it occurs **after** the leukocyte has already exited the blood vessel and reached the site of injury [1]. Therefore, it is not a step in the extravasation process itself. **Analysis of Other Options:** * **A. Rolling:** This is the initial step where leukocytes slow down and "roll" along the endothelial surface [1]. It is mediated by the **Selectin** family (L-selectin on leukocytes; E and P-selectin on endothelium). * **B. Adhesion:** Following rolling, leukocytes bind firmly to the endothelium [1]. This is mediated by **Integrins** (like VLA-4 and LFA-1) on leukocytes binding to ligands like VCAM-1 and ICAM-1 on endothelial cells. * **C. Migration (Diapedesis):** Also known as transmigration, this is the step where leukocytes squeeze through the endothelial junctions. It is primarily mediated by **PECAM-1 (CD31)** [1]. **High-Yield NEET-PG Pearls:** 1. **Sequence of Extravasation:** Margination → Rolling → Adhesion → Transmigration (Diapedesis) → Chemotaxis [1]. 2. **LAD-1 (Leukocyte Adhesion Deficiency Type 1):** Caused by a defect in **Integrins** (CD18 subunit), leading to impaired firm adhesion and recurrent infections without pus formation [1]. 3. **LAD-2:** Caused by a defect in **Sialyl-Lewis X** (ligand for selectins), leading to impaired rolling. 4. **Chemotaxis:** The most potent chemoattractants for neutrophils are **C5a, LTB4, IL-8, and bacterial products** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [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. 188-189.

Question 156: When sutures are removed from an incisional surgical wound at the end of one week, what is the approximate wound strength compared to unwounded skin?

A. 50%
B. 80%
C. 1%
D. 10% (Correct Answer)

Explanation: This question tests your knowledge of the kinetics of wound healing and the recovery of tensile strength in primary intention healing. ### **Explanation of the Correct Answer** Wound strength is a function of collagen synthesis exceeding degradation and the subsequent cross-linking of collagen fibers. * **At 1 week:** When sutures are typically removed, the wound strength is approximately **10%** of that of unwounded skin [1]. At this stage, the wound is primarily held together by epithelialization and the initial deposition of Type III collagen, which has not yet undergone significant remodeling or cross-linking. ### **Analysis of Incorrect Options** * **C (1%):** This represents the strength immediately after the incision is made and sutured. At this point, the strength is provided almost entirely by the sutures themselves, not the tissue. * **A (50%) & B (80%):** These values are achieved much later. By the end of the **4th week**, strength increases rapidly [1]. By **3 months (90 days)**, the wound reaches its plateau of approximately **70–80%** of the strength of original skin [1]. Note that a scar rarely, if ever, regains 100% of the strength of unwounded skin. ### **High-Yield NEET-PG Pearls** * **The "10-70-80" Rule:** Remember 10% at 1 week, and 70–80% at 3 months [1]. * **Collagen Switch:** During the early phase (granulation tissue), **Type III collagen** is predominant. During remodeling (maturation), it is replaced by **Type I collagen**, which provides greater tensile strength. * **Vitamin C & Copper:** These are essential cofactors for collagen cross-linking (prolyl hydroxylase and lysyl oxidase, respectively). Deficiency leads to poor wound healing and decreased tensile strength. * **Plateau:** Wound strength typically maxes out at 70–80% by 3 to 6 months; it does not continue to improve indefinitely [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 157: Which of the following leukotrienes aids in leukocyte adhesion?

A. LTB4 (Correct Answer)
B. LTD4
C. LTE4
D. LTC4

Explanation: **Explanation:** Leukotrienes are potent inflammatory mediators derived from arachidonic acid via the **5-lipoxygenase pathway**. **Why LTB4 is correct:** **LTB4 (Leukotriene B4)** is primarily a potent **chemoattractant** and activator of neutrophils [1]. Its role in leukocyte adhesion is critical; it induces the expression of **integrins** (specifically CD11/CD18) on the surface of leukocytes, which allows them to bind firmly to ICAM-1 on the vascular endothelium [1]. Beyond adhesion, LTB4 also stimulates chemotaxis, the release of lysosomal enzymes, and the generation of reactive oxygen species (ROS) [1]. **Why the other options are incorrect:** * **LTC4, LTD4, and LTE4:** These are collectively known as **cysteinyl leukotrienes** (or the "slow-reacting substance of anaphylaxis"). Their primary functions are related to smooth muscle contraction and vascular permeability [1]. They cause intense **bronchospasm** (important in asthma pathogenesis) and increased **venular permeability** (leading to edema), but they do not play a direct role in leukocyte adhesion or chemotaxis [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Chemotactic Agents "Big Four":** Remember the mnemonic **"C-B-I-L"** for the most important chemoattractants: **C**5a, **B**4 (LTB4), **I**L-8, and **L**PS (Bacterial products). * **Aspirin-Exacerbated Respiratory Disease (AERD):** Inhibiting COX-1 shunts arachidonic acid toward the lipoxygenase pathway, increasing leukotriene production, which leads to bronchospasm. * **Pharmacology Link:** **Zileuton** inhibits 5-lipoxygenase (preventing LTB4/C4/D4/E4 synthesis), while **Montelukast** blocks the receptors for cysteinyl leukotrienes (LTC4/D4/E4). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.

Question 158: Which of the following is NOT a known effect of transforming growth factor?

A. Promotes fibroblast proliferation
B. Promotes endothelial cell proliferation
C. Induces chemotaxis of fibroblasts
D. Activates macrophages (Correct Answer)

Explanation: **Explanation:** Transforming Growth Factor-beta (TGF-̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢̢β) is a multifunctional cytokine that plays a pivotal role in tissue repair and fibrosis. Its primary function is to act as a **growth inhibitor** for most epithelial cells and leukocytes, while being a potent **fibrogenic agent**. **Why "Activates Macrophages" is the correct answer:** TGF-β is actually a potent **anti-inflammatory** cytokine. It inhibits lymphocyte proliferation and suppresses the activation of macrophages (deactivating them). This helps in limiting the inflammatory response once the repair process begins [1]. In contrast, the primary activator of macrophages is **Interferon-gamma (IFN-γ)** [2]. **Analysis of other options:** * **A & C (Fibroblast effects):** TGF-β is the most important cytokine for synthesis and deposition of connective tissue. It is a powerful chemoattractant for fibroblasts and stimulates them to proliferate and secrete collagen and fibronectin [1]. * **B (Endothelial cell proliferation):** While TGF-β can inhibit endothelial proliferation *in vitro*, in the complex environment of wound healing, it promotes angiogenesis indirectly and regulates the formation of the extracellular matrix required for new vessel stability [1]. (Note: Some texts highlight its role in stimulating VEGF). **High-Yield NEET-PG Pearls:** 1. **TGF-β Source:** Produced by platelets, macrophages, and endothelial cells. 2. **Dual Role:** It is "growth-inhibitory" for epithelial cells but "growth-stimulatory" for mesenchymal cells (fibroblasts) [1]. 3. **Clinical Significance:** Excessive TGF-β activity is linked to pathological fibrosis (e.g., Liver Cirrhosis, Pulmonary Fibrosis, and Systemic Sclerosis). 4. **Signaling:** It signals through **Serine/Threonine kinase receptors** and **SMAD proteins**. **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. 105-106.

Question 159: Which cell type releases the vasoactive amine that causes vasodilation during inflammation?

A. Plasma cells
B. Lymphocytes
C. Monocytes
D. Mast cells (Correct Answer)

Explanation: **Explanation:** The correct answer is **Mast cells**. **1. Why Mast cells are correct:** In the early stages of acute inflammation, vasodilation is primarily mediated by **Histamine**, a potent vasoactive amine [1]. Mast cells, which are widely distributed in connective tissues near blood vessels, are the richest source of histamine [5]. Upon stimulation (by physical injury, IgE binding, or complement fragments like C3a and C5a), mast cells undergo **degranulation**, releasing preformed histamine [1], [3]. Histamine acts on H1 receptors on endothelial cells, leading to arteriolar vasodilation and increased vascular permeability (forming endothelial gaps) [1], [5]. **2. Why the other options are incorrect:** * **Plasma cells:** These are terminally differentiated B-lymphocytes responsible for synthesizing and secreting **antibodies** (immunoglobulins). They do not store or release vasoactive amines. * **Lymphocytes:** These are the primary cells of the adaptive immune system (T cells and B cells). They are characteristic of **chronic inflammation** and are involved in cytokine production and cell-mediated immunity, not the immediate release of histamine. * **Monocytes:** These circulate in the blood and migrate into tissues to become **macrophages**. While they secrete cytokines (like TNF and IL-1) and arachidonic acid metabolites, they are not the primary source of preformed vasoactive amines like histamine. **3. Clinical Pearls for NEET-PG:** * **Vasoactive Amines:** Histamine and Serotonin are the two main amines. In humans, histamine is the most important; serotonin is primarily found in **platelets** [2]. * **Triple Response of Lewis:** Mediated by histamine, it consists of Flush (capillary dilation), Flare (arteriolar dilation), and Wheal (exudation/edema) [1]. * **Basophils:** These are the circulating counterparts of mast cells and also contain histamine [4]. * **Inactivation:** Histamine is rapidly degraded by **histaminase**, which explains why the immediate transient response of inflammation is short-lived. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95. [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. 163-164. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-211. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.

Question 160: Complete wound strength, in terms of collagen recovery, is regained in what period of time?

A. Never regained (Correct Answer)
B. 1 month
C. 6 months
D. 1 year

Explanation: **Explanation:** The correct answer is **A. Never regained**. [1] The underlying medical concept is that tissue repair in humans occurs via two processes: **regeneration** (replacement by the same cell type) and **healing by fibrosis/scarring**. Skin wounds heal primarily through scarring. While a scar provides structural integrity, it is a fibrous patch rather than a perfect reconstruction of the original dermis. The timeline of wound strength recovery is as follows: * **At 1 week:** Approximately 10% of the strength of unwounded skin. [1] * **At 3 months:** Strength increases rapidly to about 70–80%. [1] * **Long-term:** Wound strength plateaus at roughly **70–80%** of the original tensile strength. It never reaches 100% because the collagen fibers in a scar are thinner and more disorganized compared to the basket-weave pattern of normal dermis. [1] **Why incorrect options are wrong:** * **B, C, and D:** These options suggest that given enough time (1 month to 1 year), the tissue will eventually return to its baseline strength. However, the remodeling phase of wound healing involves a balance of collagen synthesis by myofibroblasts and degradation by Matrix Metalloproteinases (MMPs). This process improves strength significantly but never achieves full recovery. [1] **High-Yield NEET-PG Pearls:** * **Type III Collagen** is synthesized first during the proliferative phase (granulation tissue). * **Type I Collagen** eventually replaces Type III during the remodeling phase to provide more strength. * **Vitamin C** is a critical cofactor for the hydroxylation of proline and lysine residues; deficiency leads to poor wound healing (Scurvy). * **Zinc deficiency** also impairs wound healing as it is a cofactor for MMPs involved in remodeling. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

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

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