Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 211: Which interleukin is primarily associated with fever and inflammation?

A. Interleukin 1 (Correct Answer)
B. Interleukin 12
C. Interleukin 5
D. Interleukin 2

Explanation: **Explanation:** **Interleukin-1 (IL-1)** is a key pro-inflammatory cytokine produced primarily by activated macrophages [1]. It plays a central role in the acute inflammatory response. * **Mechanism of Fever:** IL-1 acts as an endogenous pyrogen [2]. It travels to the anterior hypothalamus, where it stimulates the synthesis of **Prostaglandin E2 (PGE2)** via the induction of cyclooxygenase (COX) enzymes [2]. PGE2 resets the hypothalamic thermostat to a higher level, resulting in fever [2]. * **Inflammation:** IL-1 increases the expression of adhesion molecules (E-selectin, ICAM-1) on endothelial cells, facilitating leukocyte recruitment to the site of injury [1]. **Analysis of Incorrect Options:** * **B. Interleukin-12:** Primarily involved in the differentiation of naive T-cells into **Th1 cells** and the activation of Natural Killer (NK) cells. It is crucial for cell-mediated immunity against intracellular pathogens. * **C. Interleukin-5:** Produced by Th2 cells; its primary function is the recruitment, activation, and survival of **eosinophils**. It is highly associated with helminthic infections and allergic asthma. * **D. Interleukin-2:** Known as the "T-cell growth factor," it stimulates the proliferation and differentiation of T and B lymphocytes. **High-Yield Clinical Pearls for NEET-PG:** * **The "Big Three" of Acute Inflammation:** IL-1, TNF-̑̑, and IL-6 are the primary mediators of the systemic acute-phase response [2]. * **IL-1 vs. TNF:** While both induce fever and inflammation, **TNF-̑̑** is more strongly associated with septic shock and cachexia (wasting syndrome) [2]. * **Acute Phase Reactants:** IL-6 is the chief stimulator for the hepatic synthesis of acute-phase proteins like C-reactive protein (CRP) and Fibrinogen [2]. * **IL-8** is the major chemotactic factor for neutrophils ("Clean up on aisle 8"). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111.

Question 212: In the healing of a clean wound, by which day is the maximum immediate strength reached?

A. 2 - 3 days
B. 4 - 7 days
C. 10 - 12 days
D. 13 - 18 days (Correct Answer)

Explanation: ### Explanation The correct answer is **D. 13 - 18 days**. **1. Understanding the Concept: Wound Strength Evolution** Wound healing is a dynamic process involving inflammation, proliferation, and remodeling [1]. In a clean wound (healing by primary intention), the tensile strength of the wound evolves in phases: * **Initial Phase (0-3 days):** Strength is negligible as the wound is held together only by a fibrin clot and sutures. * **Proliferative Phase (3-14 days):** Rapid increase in strength occurs due to the deposition of Type III collagen by fibroblasts [2]. * **The "Maximum Immediate" Peak:** By the end of the second week (**Day 13-18**), the wound reaches its **maximum immediate strength** (approximately 10-15% of normal skin). This is a critical milestone because it is the point where sutures are typically removed, and the wound must rely on its own structural integrity [2]. **2. Why the Other Options are Incorrect:** * **A (2-3 days):** The wound is in the inflammatory phase; it has almost no intrinsic strength and relies entirely on sutures. * **B (4-7 days):** Granulation tissue is forming, but collagen deposition is just beginning [1]. Strength is minimal. * **C (10-12 days):** While strength is increasing rapidly, it has not yet reached the peak of the "immediate" phase (the 2-week mark). **3. NEET-PG High-Yield Clinical Pearls:** * **The 70% Rule:** After the initial 2-week peak, strength increases slowly due to collagen cross-linking and the shift from Type III to Type I collagen [2]. It reaches approximately **70-80%** of original strength by 3 months. * **Final Strength:** A scar **never** regains 100% of the original tensile strength of healthy skin; it plateaus at about 70-80% [2]. * **Vitamin C:** Essential for the hydroxylation of proline and lysine; deficiency (Scurvy) leads to poor wound strength and dehiscence. * **Zinc:** A cofactor for collagenase; deficiency impairs the remodeling phase. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 213: Deficiency of late complement factors is associated with which of the following?

A. Hereditary angioneurotic edema
B. Systemic lupus erythematosus
C. Recurrent infections, particularly with Neisseria species (Correct Answer)
D. Hemolytic uremic syndrome

Explanation: **Explanation:** The complement system is a vital component of innate immunity. The **late complement factors (C5–C9)** are responsible for the formation of the **Membrane Attack Complex (MAC)** [1]. 1. **Why Option C is correct:** The MAC is essential for the lysis of thin-walled bacteria. **Neisseria species** (*N. meningitidis* and *N. gonorrhoeae*) have thin cell walls and are uniquely susceptible to MAC-mediated killing. Therefore, a deficiency in C5, C6, C7, C8, or C9 leads to a significantly increased risk of recurrent, disseminated Neisserial infections. 2. **Why other options are incorrect:** * **Option A (Hereditary angioneurotic edema):** This is caused by a deficiency of **C1 esterase inhibitor**, leading to unregulated activation of the complement pathway and excessive production of bradykinin. * **Option B (SLE):** Deficiencies in **early complement components (C1, C2, C4)** are strongly associated with SLE-like autoimmune syndromes because these factors are necessary for the clearance of immune complexes. [2] * **Option C (Hemolytic Uremic Syndrome):** Atypical HUS is associated with mutations or deficiencies in **Factor H, Factor I, or Membrane Cofactor Protein (CD46)**, which are regulators of the alternative pathway [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common complement deficiency:** C2 deficiency (often asymptomatic or presents with SLE-like features). * **C3 deficiency:** Most severe; leads to recurrent pyogenic infections (S. pneumoniae, H. influenzae) and Type III hypersensitivity reactions. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Caused by a deficiency of **DAF (CD55)** and **MIRL (CD59)**, which normally protect RBCs from MAC-mediated lysis [3]. * **CH50 Assay:** Used to screen for classical pathway deficiencies; it will be low/zero in late component deficiencies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [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. 162-163. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 534-535.

Question 214: Which of the following is not an activator of the alternate complement system?

A. Factor H
B. IgA
C. Bacteria
D. Immune complex (Correct Answer)

Explanation: To master the complement system for NEET-PG, it is essential to distinguish between the triggers of the three major pathways: Classical, Alternative, and Lectin [1]. ### **Explanation** The **Classical Pathway** is primarily activated by **Immune Complexes** (Antigen-Antibody complexes involving IgG or IgM) [1]. Therefore, Option D is the correct answer as it does not activate the alternative pathway. **Why the other options are incorrect (Activators of the Alternative Pathway):** * **Bacteria (Option C):** The alternative pathway is an innate immune response triggered directly by microbial surface molecules like Endotoxins (LPS) and polysaccharides [1]. * **IgA (Option B):** While the classical pathway requires IgG/IgM, the alternative pathway can be triggered by aggregated **IgA** and occasionally IgE [1]. * **Factor H (Option A):** This is a regulatory protein of the alternative pathway [3]. While it acts as an inhibitor to prevent over-activation on host cells, it is an integral component of the alternative system's machinery [3]. (Note: Some examiners consider Factor H a "component" rather than an "activator," but in the context of this question, the Immune Complex is the definitive classical trigger). ### **High-Yield Clinical Pearls for NEET-PG** 1. **C3:** This is the common point where all three pathways converge [2]. 2. **C5b-9:** Known as the **Membrane Attack Complex (MAC)**, responsible for cell lysis [2]. 3. **C3a, C5a (Anaphylatoxins):** Trigger histamine release; **C5a** is also a potent chemotactic agent for neutrophils [2], [3]. 4. **C3b:** Acts as an **Opsonin** (enhances phagocytosis) [1], [2]. 5. **Deficiency:** C3 deficiency is the most severe as it cripples all pathways, leading to recurrent pyogenic infections. MAC deficiency (C5-C9) specifically predisposes to *Neisseria* infections. **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 help important aspects., pp. 162-163. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100. [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.

Question 215: Which mechanism of increased vascular permeability in the inflammatory process is characterized by direct endothelial injury to venules, capillaries, and arterioles?

A. Immediate transient response
B. Immediate sustained response (Correct Answer)
C. Endothelial cell retraction
D. None of the above

Explanation: **Explanation:** The correct answer is **Immediate sustained response**. This mechanism of increased vascular permeability is characterized by **direct injury** to the endothelial cells, leading to cell necrosis and detachment. **1. Why "Immediate sustained response" is correct:** In cases of severe injury (e.g., major burns, severe bacterial infections, or direct trauma), the damage is so intense that it affects all levels of the microvasculature, including **venules, capillaries, and arterioles** [1]. Because the endothelium is physically destroyed, the leakage begins immediately and persists for several hours or days until the vessels are repaired or thrombosed—hence the term "sustained." **2. Why other options are incorrect:** * **A. Immediate transient response:** This is the most common mechanism, mediated primarily by **histamine**, bradykinin, and leukotrienes [1], [2]. It involves the contraction of endothelial cells, creating gaps. Crucially, it affects **only venules** (not capillaries or arterioles) and lasts for a short duration (15–30 minutes) [1]. * **C. Endothelial cell retraction:** This refers to the reversible opening of interendothelial junctions mediated by cytokines like **TNF and IL-1**. It is a delayed response (taking 4–6 hours to develop) and is distinct from the direct necrotizing injury seen in the sustained response. **High-Yield Clinical Pearls for NEET-PG:** * **Vessel Involvement:** Immediate transient = Venules only; Immediate sustained = Venules, Capillaries, and Arterioles. * **Delayed Prolonged Leakage:** A classic NEET-PG favorite; this occurs in **sunburns** (UV radiation) or thermal injury, starting after 2–12 hours and involving venules and capillaries [1]. * **Most common mechanism** of vascular leakage in inflammation is **endothelial cell contraction** (Immediate transient response). **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. 187-188. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 216: Epithelioid cells are seen in all of the following conditions except?

A. Tuberculosis
B. Granulation tissue (Correct Answer)
C. Syphilis
D. Sarcoidosis

Explanation: **Explanation:** The presence of **epithelioid cells** is the hallmark of **granulomatous inflammation**, a specific pattern of chronic inflammation [1]. Epithelioid cells are modified activated macrophages that resemble epithelial cells (having abundant pink cytoplasm and indistinct cell borders) [1]. **1. Why Granulation Tissue is the correct answer:** Granulation tissue is a feature of **healing and repair**, not granulomatous inflammation. It consists of a proliferation of new thin-walled, delicate capillaries (angiogenesis), fibroblasts, and an edematous extracellular matrix. While it contains inflammatory cells (like macrophages), it does **not** contain epithelioid cells or form granulomas. **2. Analysis of Incorrect Options:** * **Tuberculosis (A):** The classic example of granulomatous inflammation. It features "caseating granulomas" containing epithelioid cells, Langhans giant cells, and central necrosis [1]. * **Syphilis (C):** Tertiary syphilis is characterized by the **Gumma**, which is a type of granuloma containing epithelioid cells, plasma cells, and central necrotic tissue. * **Sarcoidosis (D):** Characterized by "non-caseating granulomas" composed of tightly packed epithelioid cells [2]. **Clinical Pearls for NEET-PG:** * **Definition:** Epithelioid cells are activated by **IFN-gamma** (secreted by Th1 cells) [1]. * **Key Marker:** CD68 is a common marker for macrophages and epithelioid cells. * **Granulation Tissue vs. Granuloma:** Do not confuse these. Granulation tissue = Healing; Granuloma = Chronic Inflammation. * **Schumann bodies and Asteroid bodies:** High-yield inclusions often seen in the giant cells of Sarcoidosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [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. 198-200.

Question 217: Delayed prolonged vascular leakage can result from which of the following?

A. Burns
B. X-rays
C. Exposure to the sun
D. All of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. All of the above.** **Underlying Medical Concept:** Vascular leakage (increased vascular permeability) is a hallmark of acute inflammation [2]. While most stimuli cause an "immediate transient response" (lasting 15–30 minutes), certain types of injuries result in a **Delayed Prolonged Response** [3]. This pattern is characterized by a lag period of 2 to 12 hours, after which leakage begins and lasts for several hours or even days. This occurs due to direct cell injury resulting in delayed endothelial cell apoptosis or sublethal damage. **Analysis of Options:** * **A. Burns:** Mild to moderate thermal injury is the classic example of a delayed response [3]. While severe burns cause immediate damage, moderate heat leads to leakage that develops after a few hours. * **B. X-rays:** Ionizing radiation causes DNA damage and cellular stress that manifests as delayed vascular leakage, often seen in radiation dermatitis [1], [3]. * **C. Exposure to the sun:** Ultraviolet (UV) radiation causes the most common form of delayed prolonged leakage—the **sunburn** [3]. The erythema and increased permeability typically peak 12–24 hours after exposure. **High-Yield NEET-PG Pearls:** 1. **Immediate Transient Response:** Most common pattern; mediated by **Histamine**, Bradykinin, and Leukotrienes; affects only **venules** [2]. 2. **Delayed Prolonged Response:** Caused by thermal, UV, or X-ray injury; involves both **capillaries and venules** [3]. 3. **Immediate Sustained Response:** Occurs in severe injuries (e.g., major burns/infections) where endothelial necrosis causes leakage in all vessels (arterioles, capillaries, and venules) until the vessel is thrombosed or repaired [1]. 4. **Mechanism of Delayed Leakage:** It is primarily due to direct endothelial injury and subsequent retraction or apoptosis, not just chemical mediators [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 437-438. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [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 218: Which of the following pattern recognition receptors recognize products of necrotic cells?

A. Toll-like receptors (TLRs)
B. NOD-like receptors (NLRs) (Correct Answer)
C. Lectin type receptors
D. Retinoic acid-inducible gene-I-like receptors (RLRs)

Explanation: **Explanation:** The recognition of cell injury and microbes is the first step in the inflammatory response. This is mediated by **Pattern Recognition Receptors (PRRs)**, which identify Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Associated Molecular Patterns (DAMPs) [4]. **Why NOD-like receptors (NLRs) are correct:** NLRs are cytosolic receptors that specifically recognize **DAMPs** (products of necrotic or damaged cells) such as uric acid, ATP, reduced intracellular potassium, and DNA [1]. Upon activation, NLRs signal through a multi-protein complex called the **inflammasome**, which activates **Caspase-1**. This enzyme cleaves precursor forms of Interleukin-1 (IL-1) into its active form, inducing inflammation [1]. **Why the other options are incorrect:** * **Toll-like receptors (TLRs):** These are found on plasma membranes and endosomes. While they can recognize some endogenous proteins, they are primarily known for recognizing **PAMPs** (e.g., LPS, bacterial DNA, viral RNA) [3]. * **Lectin type receptors (C-type lectins):** These are located on the plasma membranes of macrophages and dendritic cells. They specifically detect **fungal glycans** and terminal sugars on microbial surfaces [2]. * **RIG-I-like receptors (RLRs):** These are cytosolic receptors that specifically detect **viral RNA**, playing a crucial role in the antiviral interferon response. **High-Yield NEET-PG Pearls:** * **Gout Connection:** The crystals of uric acid in Gout are recognized by the **NLRP3 inflammasome**, leading to IL-1 mediated joint inflammation [1]. * **Gain-of-function mutations** in NLRs cause "Autoinflammatory syndromes" (e.g., Familial Mediterranean Fever). * **IL-1** is the primary cytokine mediator of fever and the acute phase response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 83-84. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 142. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 81.

Question 219: What is the most common mechanism of phagocytosis by lysosomes?

A. Myeloperoxidase (MPO) (Correct Answer)
B. Hydrogen Peroxide (H2O2)
C. Nitric Oxide (NO)
D. Lactoferrin

Explanation: **Explanation:** The killing of ingested microbes is the final step in phagocytosis, primarily achieved through **Oxygen-Dependent mechanisms**. The most potent and efficient system among these is the **H2O2-MPO-Halide system** [1]. **Why Myeloperoxidase (MPO) is the correct answer:** During the "respiratory burst," NADPH oxidase converts oxygen into superoxide radicals, which then dismutate into Hydrogen Peroxide ($H_2O_2$). In the presence of the enzyme **Myeloperoxidase (MPO)**—found in the azurophilic granules of neutrophils—$H_2O_2$ combines with a halide (usually Chloride) to form **Hypochlorite ($HOCl^-$)** [1]. Hypochlorite is the active ingredient in household bleach and is the most powerful bactericidal agent in the phagolysosome, making MPO the central mediator of this process [1]. **Analysis of Incorrect Options:** * **B. Hydrogen Peroxide ($H_2O_2$):** While $H_2O_2$ is a precursor in the killing process, it is relatively weak on its own. It requires MPO to be converted into the more lethal Hypochlorite. * **C. Nitric Oxide (NO):** Produced by iNOS in macrophages, NO reacts with superoxide to form Peroxynitrite. While important for killing fungi and parasites, it is not the *most common* or primary mechanism compared to the MPO system in neutrophils [1]. * **D. Lactoferrin:** This is an oxygen-independent mechanism found in specific granules. It works by sequestering iron (which bacteria need for growth) rather than direct enzymatic killing [1]. **NEET-PG High-Yield Pearls:** * **MPO Deficiency:** Patients are usually asymptomatic, but may have a predisposition to *Candida albicans* infections. * **NBT Test:** The Nitroblue Tetrazolium test is used to diagnose **Chronic Granulomatous Disease (CGD)**, where there is a deficiency in NADPH oxidase (not MPO). * **Morphology:** MPO gives pus its characteristic **greenish color**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 91-92.

Question 220: Which of the following occurs during scar formation?

A. Deposition of type I and type III collagen
B. Type III collagen replaces type I collagen
C. Type I collagen replaces type III collagen (Correct Answer)
D. None of the above

Explanation: The process of scar formation (fibrosis) is a dynamic sequence involving the replacement of damaged tissue with connective tissue [1]. This process is characterized by a specific transition in the types of collagen deposited. **Why Option C is Correct:** During the early stages of wound healing (specifically the **proliferative phase**), fibroblasts rapidly deposit **Type III collagen** (granulation tissue) [2]. This collagen is thin and flexible but lacks significant tensile strength. As the scar matures during the **remodeling phase**, Type III collagen is degraded by **Matrix Metalloproteinases (MMPs)** and replaced by **Type I collagen** [1]. Type I collagen is the most abundant form in the body and provides high tensile strength, transforming the soft granulation tissue into a firm, pale scar. **Why Other Options are Incorrect:** * **Option A:** While both types are present at different stages, the hallmark of scar *maturation* is the specific shift from III to I, not just the simultaneous deposition of both. * **Option B:** This is the reverse of the physiological process. Type III is "embryonic/early" collagen, whereas Type I is "mature/strong" collagen. Replacing I with III would result in a weaker, unstable wound. **NEET-PG High-Yield Pearls:** * **Collagen Mnemonic:** Type **One** is in **Bone** (and mature scars); Type **Three** is **Reticular** (and granulation tissue). * **Zinc Dependency:** MMPs, which are essential for remodeling (replacing Type III with Type I), are **Zinc-dependent** enzymes. Zinc deficiency can lead to poor wound healing. * **Tensile Strength:** A wound reaches approximately **10%** strength by the end of week 1 and plateaus at about **70-80%** of original strength by 3 months; it rarely regains 100% of its original strength [1]. * **Vitamin C:** Essential for the hydroxylation of proline and lysine residues during collagen synthesis. Deficiency leads to scurvy and wound dehiscence. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119.

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

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

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