Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 281: What types of cells are predominant in the early phase of inflammation?

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

Explanation: **Explanation:** In the sequence of events in **acute inflammation**, the cellular response is characterized by the recruitment of leukocytes to the site of injury. **Neutrophils** (Polymorphonuclear leukocytes) are the first responders and the predominant cell type during the **early phase (first 6–24 hours)** [1], [2]. **Why Neutrophils?** Neutrophils are the most numerous leukocytes in the blood and respond rapidly to chemotactic stimuli (like C5a, LTB4, and bacterial products) [1], [2]. They have a short half-life (dying via apoptosis within 24–48 hours), which is why they dominate the early, acute stage [2]. **Analysis of Incorrect Options:** * **A. Macrophages:** These are the dominant cells in **chronic inflammation** and the late phase of acute inflammation (appearing after 24–48 hours) [1], [2]. They replace neutrophils to clear debris and initiate repair. * **B. Basophils:** These are involved in allergic reactions and systemic anaphylaxis but are not the primary cells in general acute inflammation. * **C. Mast cells:** These resides in tissues and act as "sentinels." While they trigger inflammation by releasing histamine, they are not the predominant infiltrating cell population. **High-Yield Clinical Pearls for NEET-PG:** * **Exception to the Rule:** In **Pseudomonas** infections, neutrophils remain the predominant cell type for several days. In **viral infections**, lymphocytes are often the first responders [1]. In **hypersensitivity/parasitic** reactions, eosinophils may dominate. * **Chemotactic agents for Neutrophils:** Remember the mnemonic **"B-C-A-L"**: Bacterial products, C5a, Arachidonic acid metabolites (LTB4), and IL-8. * **Adhesion Molecules:** Neutrophil "rolling" is mediated by **Selectins**, while "firm adhesion" is mediated by **Integrins** (ICAM-1/VCAM-1) [1], [2]. **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. 192-193.

Question 282: Which of the following factors does NOT inhibit wound healing?

A. Hypoxia
B. Hyperthermia (Correct Answer)
C. Hyperglycemia
D. Infection

Explanation: Wound healing is a complex biological process divided into inflammatory, proliferative, and remodeling phases. It is influenced by various local and systemic factors. [1] **Why Hyperthermia is the correct answer:** Unlike the other options, **Hyperthermia** (elevated body temperature) does not typically inhibit wound healing. In fact, controlled local warmth can sometimes improve perfusion and oxygen delivery to the tissue. In contrast, it is **Hypothermia** that is known to inhibit healing by causing vasoconstriction and reducing the partial pressure of oxygen at the wound site. **Analysis of Incorrect Options:** * **Hypoxia (A):** Oxygen is critical for collagen synthesis (prolyl and lysyl hydroxylase enzymes are oxygen-dependent) and for the oxidative burst in neutrophils to kill bacteria. Hypoxia is one of the most common causes of delayed healing. [2] * **Hyperglycemia (C):** Common in Diabetes Mellitus, it leads to impaired neutrophil function (chemotaxis and phagocytosis), glycosylation of the basement membrane, and poor microcirculation, significantly delaying repair. [1], [2] * **Infection (D):** This is the **single most important local cause** of delayed wound healing. It prolongs the inflammatory phase and causes continuous tissue injury through the release of toxins and degradative enzymes. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Most important systemic factor:** Diabetes Mellitus. [1] * **Most important local factor:** Infection. [1] * **Nutritional deficiency:** Vitamin C deficiency (Scurvy) inhibits collagen cross-linking; Zinc deficiency inhibits cell proliferation and metalloproteinases. [1] * **Glucocorticoids:** Inhibit healing by reducing TGF-̢ production and weakening the scar (anti-inflammatory effect). [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 116-117. [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. 110-111.

Question 283: Which of the following occurs in chronic granulomatous disease?

A. Myeloperoxidase deficiency
B. Defective H2O2 production (Correct Answer)
C. Defective polymerization
D. Defective phagocytosis

Explanation: **Explanation:** **Chronic Granulomatous Disease (CGD)** is a primary immunodeficiency caused by a genetic defect in the **NADPH oxidase enzyme complex**. This enzyme is responsible for the "respiratory burst," which converts molecular oxygen into superoxide radicals ($O_2^-$). These radicals are subsequently converted into **Hydrogen Peroxide ($H_2O_2$)**. In CGD, the absence of NADPH oxidase leads to a failure in producing $H_2O_2$, preventing the formation of the potent bactericidal agent HOCl (hypochlorous acid). Consequently, phagocytes can ingest but cannot kill certain microbes. **Analysis of Options:** * **Option B (Correct):** Defective $H_2O_2$ production is the hallmark of CGD due to the failure of the oxidative burst. * **Option A:** Myeloperoxidase (MPO) deficiency is a separate condition where $H_2O_2$ is produced normally, but its conversion to HOCl is impaired. * **Option C:** Defective polymerization of actin is seen in **Wiskott-Aldrich Syndrome** or specific neutrophil actin deficiencies, affecting motility. * **Option D:** Phagocytosis (the ingestion of particles) is typically **normal** in CGD; the defect lies in the intracellular killing (microbicidal activity) after ingestion. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked recessive** (CYBB gene mutation). * **Organisms:** Patients are susceptible to **Catalase-positive organisms** (e.g., *S. aureus, Aspergillus, Nocardia, Serratia*). These organisms neutralize their own $H_2O_2$, leaving the neutrophil with no oxidative means to kill them. * **Diagnosis:** The classic test is the **Nitroblue Tetrazolium (NBT) dye test** (remains colorless/negative in CGD). The modern gold standard is the **Dihydrorhodamine (DHR) flow cytometry test**. * **Pathology:** Characterized by the formation of granulomas throughout the body as the immune system attempts to wall off unkilled bacteria [1]. **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. 198-200.

Question 284: Formation of granulation tissue is due to?

A. Thrombosed vessels
B. Budding of new capillaries (Correct Answer)
C. Mucosal proliferation
D. Infiltration of cells

Explanation: **Explanation:** **Granulation tissue** is the hallmark of the early stages of wound healing by secondary intention [2]. It derives its name from its pink, soft, granular appearance on the surface of wounds [1]. **Why Option B is correct:** The core process in the formation of granulation tissue is **angiogenesis** (neovascularization) [3]. This involves the **budding of new capillaries** from pre-existing vessels. These new vessels are "leaky" due to incomplete inter-endothelial junctions, allowing the passage of plasma proteins and cells into the extravascular space [2]. Along with these capillaries, there is a proliferation of **fibroblasts** and the deposition of an edematous extracellular matrix [2]. **Why the other options are incorrect:** * **A. Thrombosed vessels:** These represent vascular occlusion and ischemia, which hinder healing rather than promote tissue repair. * **C. Mucosal proliferation:** This refers to epithelial regeneration, which occurs *over* the granulation tissue but is not the defining component of the granulation tissue itself. * **D. Infiltration of cells:** While inflammatory cells (especially macrophages) are present in granulation tissue, "infiltration" is a generic term [2]. The specific structural framework of granulation tissue is defined by its vascular and fibroblastic components [1]. **NEET-PG High-Yield Pearls:** * **Components of Granulation Tissue:** 1. New capillaries (Angiogenesis), 2. Fibroblasts, 3. Edematous ECM, 4. Inflammatory cells (mainly Macrophages) [2]. * **Growth Factors:** **VEGF** (Vascular Endothelial Growth Factor) is the most important cytokine for the angiogenesis seen in granulation tissue. **TGF-β** is the most important for collagen synthesis [3]. * **Granulation Tissue vs. Granuloma:** Do not confuse them. A *granuloma* is a collection of epithelioid macrophages (chronic inflammation), whereas *granulation tissue* is a vascularized tissue involved in repair [1]. **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. 105-106. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-116.

Question 285: Increased capillary permeability is caused by all of the following except?

A. Anaphylatoxin
B. 5-hydroxytryptamine
C. Renin (Correct Answer)
D. Histamines

Explanation: **Explanation:** The correct answer is **Renin (Option C)**. Increased capillary permeability is a hallmark of acute inflammation, leading to the formation of protein-rich exudate [1]. This process is mediated by specific chemical mediators that cause endothelial cell contraction or injury [3]. **Why Renin is the correct answer:** Renin is an enzyme secreted by the juxtaglomerular cells of the kidney. Its primary role is to convert Angiotensinogen to Angiotensin I as part of the **Renin-Angiotensin-Aldosterone System (RAAS)**. It is involved in systemic blood pressure regulation and fluid-electrolyte balance, not in the mediation of vascular permeability during inflammation. **Why the other options are incorrect:** * **Histamine (Option D):** The most important mediator of the immediate transient response [3]. It causes contraction of endothelial cells, leading to interendothelial gaps in post-capillary venules [1]. * **5-Hydroxytryptamine (Serotonin) (Option B):** Found in platelet granules, it acts similarly to histamine, causing vasodilation and increased vascular permeability [1]. * **Anaphylatoxins (Option A):** These are the complement fragments **C3a and C5a**. They induce mast cell degranulation, releasing histamine, which subsequently increases capillary permeability [1]. **NEET-PG High-Yield Pearls:** 1. **Mechanism:** The most common mechanism of increased permeability is **endothelial cell contraction** (immediate transient response), affecting only post-capillary venules [3]. 2. **Vasoactive Amines:** Histamine and Serotonin are the first mediators to be released during inflammation [1]. 3. **Leukotrienes:** LTC4, LTD4, and LTE4 are significantly more potent than histamine in increasing vascular permeability [1]. 4. **Bradykinin:** Another potent mediator that increases permeability and is also responsible for the pain (dolor) associated with inflammation [2]. **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. 100-101. [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 286: Replacement of columnar epithelium of the respiratory tract by squamous epithelium is termed as?

A. Hyperplasia
B. Metaplasia (Correct Answer)
C. Hypoplasia
D. None of the above

Explanation: **Explanation:** The correct answer is **Metaplasia**. **1. Why Metaplasia is correct:** Metaplasia is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another differentiated cell type [1]. It is an adaptive response to chronic irritation. In the respiratory tract of chronic smokers, the normal ciliated columnar epithelium is replaced by stratified squamous epithelium [2]. While the squamous cells are more rugged and better able to survive the noxious chemicals in smoke, the change results in the loss of important functions like mucus secretion and ciliary action [1]. **2. Why other options are incorrect:** * **Hyperplasia:** This refers to an increase in the *number* of cells in an organ or tissue, usually resulting in increased volume [3]. It does not involve a change in cell type. * **Hypoplasia:** This refers to the incomplete development or underdevelopment of an organ or tissue, resulting in a lower than normal number of cells (often congenital). * **Dysplasia:** (Though not an option, it is a related concept) This refers to disordered growth and maturation of an epithelium, often a precursor to malignancy [3]. **3. Clinical Pearls for NEET-PG:** * **Most common type:** Squamous metaplasia (e.g., Respiratory tract in smokers, Endocervix due to chronic inflammation) [2]. * **Barrett’s Esophagus:** A classic example of **Columnar metaplasia**, where squamous epithelium of the esophagus is replaced by intestinal-type columnar cells due to acid reflux [4]. * **Mechanism:** Metaplasia does not result from a change in the phenotype of an already differentiated cell; instead, it is the result of a **reprogramming of stem cells** (or undifferentiated mesenchymal cells) [1]. * **Reversibility:** Metaplasia is reversible if the stimulus is removed, but if the irritation persists, it can progress to **Dysplasia** and eventually **Neoplasia** (Cancer) [1], [3]. **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, p. 49. [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. 91-92. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 723. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349.

Question 287: How many hours after injury are activated fibroblasts, myofibroblasts, and capillary sprouts most abundant in a wound?

A. 3 to 6 hours
B. 12 to 24 hours
C. 3 to 5 days (Correct Answer)
D. 8 to 10 days

Explanation: **Explanation:** The question tests the timeline of **Granulation Tissue formation**, a hallmark of the proliferative phase of wound healing. **Why Option C is correct:** By **3 to 5 days**, the process of repair is in full swing. This period is characterized by the peak presence of **granulation tissue**, which histologically consists of [1]: 1. **Fibroblasts and Myofibroblasts:** These cells migrate to the site and proliferate to synthesize collagen and provide wound contraction [2]. 2. **Angiogenesis:** New, leaky capillary sprouts form (driven by VEGF) to provide nutrients and oxygen to the healing tissue [1]. 3. **Extracellular Matrix (ECM):** Initial deposition of Type III collagen occurs during this window. **Why incorrect options are wrong:** * **A (3 to 6 hours):** This is the **Hemostasis phase**. The focus is on platelet aggregation, clot formation, and the release of chemotactic factors. * **B (12 to 24 hours):** This is the **Inflammatory phase**. Neutrophils are the predominant cells at the wound margins, and epithelial cells begin to migrate from the edges, but fibroblast activity is minimal. * **D (8 to 10 days):** This is the **Remodeling/Maturation phase**. By this time, the acute vascular response has subsided, and the wound begins to transition from granulation tissue to a pale scar as Type III collagen is replaced by Type I. **High-Yield NEET-PG Pearls:** * **Granulation Tissue vs. Granuloma:** Do not confuse them [2]. Granulation tissue is a sign of *healing*; a granuloma is a feature of *chronic inflammation*. * **Collagen Switch:** Type III collagen (early/weak) is replaced by Type I collagen (late/strong) during remodeling. * **Wound Contraction:** Mediated specifically by **myofibroblasts**, which contain smooth muscle actin [2]. * **Tensile Strength:** At 1 week, wound strength is ~10% of unwounded skin; it reaches a maximum of ~70-80% by 3 months [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-121. [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 288: Flare response in triple response occurs due to?

A. Vasodilation due to release of secondary mediators (Correct Answer)
B. Chemotaxis and adhesion of leucocytes to the vessel wall
C. Direct vessel injury
D. Increased vascular permeability

Explanation: The **Triple Response of Lewis** is a classic physiological reaction of the skin to mechanical injury, illustrating the vascular changes in acute inflammation. It consists of three distinct stages: 1. **Red Spot (Flush):** Localized vasodilation of capillaries and venules due to direct mechanical stimulation and histamine release. 2. **Flare (The correct answer):** A bright red, irregular area surrounding the red spot. This occurs due to **vasodilation of adjacent arterioles** mediated by an **axon reflex**. When the skin is injured, sensory nerve endings are stimulated, releasing **secondary mediators** (specifically Neuropeptides like Substance P and Calcitonin Gene-Related Peptide/CGRP), which cause widespread vasodilation [1]. 3. **Wheal:** Localized edema (swelling) caused by **increased vascular permeability** of post-capillary venules, leading to exudation of fluid. ### Why the other options are incorrect: * **Option B:** Chemotaxis and adhesion are cellular events of inflammation that occur later; they do not contribute to the immediate vascular "flare." * **Option C:** Direct vessel injury causes the initial "Red Spot," but the "Flare" is a neurogenic response extending beyond the site of direct trauma. * **Option D:** Increased vascular permeability is the mechanism behind the **Wheal** formation, not the Flare. ### NEET-PG High-Yield Pearls: * **Mediator of Triple Response:** Histamine is the primary chemical mediator involved. * **Axon Reflex:** The Flare is unique because it depends on an intact nerve supply (orthodromic and antidromic conduction). * **Sequence:** Red Spot (seconds) → Flare (30-60 seconds) → Wheal (1-5 minutes). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Question 289: Delayed wound healing is seen in all EXCEPT:

A. Malignancy
B. Diabetes
C. Hypertension (Correct Answer)
D. Infection

Explanation: ### Explanation Wound healing is a complex process involving inflammation, proliferation, and remodeling. Factors that delay this process are categorized into **local factors** (e.g., infection, poor blood supply) and **systemic factors** (e.g., nutrition, metabolic status) [1]. **Why Hypertension is the Correct Answer:** Hypertension, in isolation, is **not** a recognized cause of delayed wound healing. While chronic hypertension can lead to atherosclerosis (which impairs perfusion), the condition itself does not directly interfere with the cellular or molecular mechanisms of tissue repair. In contrast, the other options have direct, well-documented inhibitory effects on the healing cascade. **Analysis of Incorrect Options:** * **Malignancy:** Cancer causes delayed healing through multiple mechanisms, including systemic cachexia (protein-energy malnutrition), anemia, and the side effects of treatments like chemotherapy or radiation, which inhibit cell proliferation [2]. * **Diabetes Mellitus:** This is the most common metabolic cause of delayed healing [1]. It leads to compromised microcirculation, impaired neutrophil function (chemotaxis and phago-cytosis), and glycosylation of the basement membrane, which hinders nutrient exchange [3]. * **Infection:** This is the **single most important local cause** of delayed wound healing [1]. Persistent inflammation due to pathogens leads to prolonged tissue injury and prevents the transition to the proliferative phase. **NEET-PG High-Yield Pearls:** * **Vitamin C deficiency (Scurvy):** Leads to defective collagen synthesis (proline/lysine hydroxylation), causing wound dehiscence [1]. * **Zinc deficiency:** Impairs epithelialization and fibroblast proliferation (Zinc is a cofactor for DNA polymerase and MMPs). * **Glucocorticoids:** Delay healing by inhibiting TGF-β and decreasing collagen synthesis [1]. * **Most important systemic factor:** Nutrition (specifically protein deficiency) [1]. * **Most important local factor:** Infection [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 116-117. [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. 88-89. [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. 110-111.

Question 290: Nearly 20% of the normal tensile strength of tissue at the site of a wound is gained after how much time of wound healing?

A. 1 week
B. 2 weeks
C. 3 weeks (Correct Answer)
D. 4 weeks

Explanation: ### Explanation The tensile strength of a healing wound is a function of collagen synthesis, cross-linking, and remodeling. This process follows a predictable timeline that is frequently tested in NEET-PG. **Why Option C is Correct:** At the end of the **first week**, wound strength is only about **3%** of that of unwounded skin. However, there is a rapid acceleration of collagen synthesis and cross-linking over the next two weeks. By the end of **3 weeks (21 days)**, the tensile strength typically reaches approximately **20%** of the original strength [1]. This period marks the transition from the proliferative phase to the remodeling phase. **Analysis of Incorrect Options:** * **Option A (1 week):** At this stage, the wound is primarily held together by a "fibrin glue" and early granulation tissue. Tensile strength is minimal (approx. 3-10%) [1]. * **Option B (2 weeks):** While collagen deposition is active, it has not yet reached the 20% threshold. * **Option D (4 weeks):** By this time, the wound has entered the prolonged remodeling phase. Strength continues to increase, but the 20% milestone is achieved earlier, at the 3-week mark [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Maximum Strength:** A wound never regains 100% of its original tensile strength. It plateaus at approximately **70–80%** after 3 months [1]. * **Collagen Switch:** During healing, **Type III collagen** (early/granulation tissue) is replaced by **Type I collagen** (mature scar) via the action of metalloproteinases (zinc-dependent). * **Suture Removal:** Most skin sutures are removed at 7–10 days because, by then, the wound has enough integrity to stay closed, even though its tensile strength is still low (<10%) [1]. * **Vitamin C & Copper:** Essential for collagen cross-linking; deficiency leads to poor wound healing and decreased tensile strength. **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

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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