Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 31: Poor wound healing may be due to all of the following factors except?

A. Smoking
B. Excessive tension on sutures
C. Young age (Correct Answer)
D. Diabetes

Explanation: **Explanation** Wound healing is a complex biological process influenced by both local and systemic factors [1]. The correct answer is **Young age** because, in contrast to the other options, youth is generally associated with an enhanced capacity for tissue regeneration, robust collagen synthesis, and efficient vascular supply. **Why "Young age" is the correct answer:** Advanced age is a known risk factor for poor wound healing due to reduced metabolic activity, diminished epidermal turnover, and slower collagen synthesis. Conversely, young individuals typically have optimal physiological reserves, ensuring faster and more effective wound repair. **Analysis of Incorrect Options:** * **Smoking:** Nicotine is a potent vasoconstrictor that reduces distal perfusion and causes tissue hypoxia. Additionally, carbon monoxide increases carboxyhemoglobin levels, further reducing oxygen delivery to the healing tissue. * **Excessive tension on sutures:** This is a local factor. High tension compresses local capillaries, leading to ischemia, wound dehiscence (splitting open), and increased risk of necrosis [1]. * **Diabetes Mellitus:** This is one of the most significant systemic causes of impaired healing [1]. It leads to microangiopathy (poor blood flow), impaired neutrophil function (increased infection risk), and decreased collagen synthesis due to hyperglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **Most important systemic factor:** Diabetes Mellitus [1]. * **Most important local factor:** Infection (prolongs the inflammatory phase) [1]. * **Nutritional deficiency:** Vitamin C deficiency (Scurvy) leads to poor collagen cross-linking (proline/lysine hydroxylation failure) [1]. * **Glucocorticoids:** Impair healing by inhibiting TGF-β and decreasing collagen synthesis (leads to weak scars) [1]. * **Zinc deficiency:** Impairs epithelialization and fibroblast proliferation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 116-117, 119-121.

Question 32: Which of the following selectins is expressed in both platelets and endothelium?

A. Selectin P (Correct Answer)
B. Selectin L
C. Selectin E
D. None of the above

Explanation: **Explanation:** Selectins are a family of cell surface adhesion molecules characterized by an extracellular lectin domain. They play a critical role in the "rolling" phase of leukocyte recruitment during acute inflammation [2]. **1. Why Selectin P is correct:** **Selectin P (CD62P)** is unique because it is stored pre-formed in specific granules and can be rapidly redistributed to the cell surface upon stimulation by mediators like thrombin or histamine. It is expressed in: * **Platelets:** Stored in **α-granules** [1]. * **Endothelium:** Stored in **Weibel-Palade bodies**. Its dual presence in both platelets and endothelial cells makes it the correct answer. **2. Why the other options are incorrect:** * **Selectin L (CD62L):** This is expressed exclusively on **Leukocytes** (neutrophils, monocytes, and lymphocytes) [2]. It is located at the tips of microvilli and is shed from the cell surface after activation. * **Selectin E (CD62E):** This is expressed exclusively on **Endothelial cells** [2]. Unlike Selectin P, it is not stored in granules; its expression is induced by cytokines like IL-1 and TNF-α through de novo protein synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rolling" Phase:** Selectins mediate weak, transient tethering (rolling), whereas **Integrins** (LFA-1, VLA-4) mediate firm adhesion [2]. * **Ligands:** All selectins bind to sialylated oligosaccharides (e.g., **Sialyl-Lewis X**) found on glycoprotein backbones. * **Deficiency:** A deficiency in Sialyl-Lewis X leads to **Leukocyte Adhesion Deficiency Type 2 (LAD II)**, characterized by recurrent infections and a lack of pus formation. * **Mnemonic:** **L**-selectin (Leukocytes), **E**-selectin (Endothelium), **P**-selectin (Platelets & Phospholipids/Endothelium). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 33: A woman who is allergic to cats visits a neighbor who has several cats. During the visit, she inhales cat dander, and within minutes, she develops nasal congestion with abundant nasal secretions. Which of the following substances is most likely to produce these findings?

A. Bradykinin
B. Complement C5a
C. Histamine (Correct Answer)
D. Interleukin-1 (IL-1)

Explanation: **Explanation:** The clinical scenario describes a classic **Type I Hypersensitivity reaction** (Immediate Hypersensitivity) [2], [2]. When a sensitized individual is exposed to an allergen (cat dander), IgE antibodies bound to mast cells trigger degranulation [1], [2]. **Why Histamine is correct:** Histamine is the primary preformed mediator released from mast cell granules during the immediate phase (within minutes). It acts on H1 receptors to cause **vasodilation** (leading to congestion) and **increased vascular permeability**, which results in edema and the production of abundant serous nasal secretions [2]. **Analysis of Incorrect Options:** * **A. Bradykinin:** While it causes vasodilation and pain, it is primarily involved in the kinin cascade and hereditary angioedema [3], not the acute IgE-mediated allergic response to inhaled allergens. * **B. Complement C5a:** Known as an "anaphylatoxin," C5a can trigger mast cell degranulation, but it is a product of the complement cascade typically seen in infections or Type II/III reactions, rather than the primary driver of acute allergic rhinitis. * **C. Interleukin-1 (IL-1):** This is a pro-inflammatory cytokine produced by macrophages. It mediates the "acute phase response" (fever, lethargy) and acts over hours to days, not minutes [2]. **High-Yield NEET-PG Pearls:** * **Timeframe:** Type I reactions occur within 5–30 minutes (Immediate phase). * **Key Cells:** Mast cells and Basophils [2]. * **Late Phase:** Driven by **Leukotrienes** (C4, D4, E4) and Cytokines, occurring 2–24 hours later [2]. * **Eosinophils:** Recruited by Eotaxin and IL-5; they are the hallmark of the late-phase allergic response [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 687-689. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 210-212. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101.

Question 34: What is the difference between primary and secondary wound healing?

A. More granulation tissue and fibrosis are seen in secondary healing. (Correct Answer)
B. Scarring is more cosmetic in secondary healing.
C. Secondary healing occurs faster.
D. Surgical wounds commonly heal by secondary healing.

Explanation: **Explanation:** Wound healing is categorized based on the nature and characteristics of the injury. **1. Why Option A is Correct:** **Secondary healing (healing by second intention)** occurs when there is extensive tissue loss, ragged edges, or infection (e.g., large ulcers, abscesses) [1]. Because the wound edges are not approximated, the body must fill the large defect from the bottom up. This requires a significantly larger volume of **granulation tissue** to bridge the gap [1]. Consequently, the inflammatory response is more intense, and the resulting **fibrosis (collagen deposition)** is more extensive, leading to a larger scar [1]. **2. Why Other Options are Incorrect:** * **Option B:** Secondary healing results in larger, irregular, and often contracted scars [2]. **Primary healing** (e.g., a clean surgical incision) produces a fine, linear, and more cosmetic scar [2]. * **Option C:** Primary healing is much faster because the edges are closely apposed. Secondary healing is a **prolonged process** due to the need for extensive tissue regeneration and wound contraction [2]. * **Option D:** Clean, uninfected **surgical incisions** closed with sutures heal by **primary intention** [2]. Secondary healing is reserved for contaminated or large open wounds [1]. **High-Yield NEET-PG Pearls:** * **Wound Contraction:** This is a hallmark of secondary healing, mediated by **myofibroblasts** [3]. It can reduce the wound size by up to 90% [1]. * **Tensile Strength:** At the end of 1 week (suture removal), wound strength is ~10%. It reaches ~70-80% by 3 months but **never** returns to 100% of original strength. * **Type of Collagen:** Initially, Type III collagen is deposited; it is later replaced by the stronger **Type I collagen** during 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] 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. 106-107. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 105-106.

Question 35: A 25-year-old woman sustains a deep, open laceration over her right forearm in a motorcycle accident. During the next 3 months, the wound heals with the formation of a linear scar. Which of the following nutritional factors is required for proper collagen assembly in the scar tissue?

A. Folic acid
B. Thiamine
C. Vitamin A
D. Vitamin C (Correct Answer)

Explanation: **Explanation:** The correct answer is **Vitamin C (Ascorbic Acid)**. **1. Why Vitamin C is correct:** Wound healing involves the synthesis and deposition of collagen. For stable collagen fibers to form, the pro-collagen polypeptide chains must undergo **hydroxylation of proline and lysine residues**. This post-translational modification is catalyzed by the enzymes *prolyl hydroxylase* and *lysyl hydroxylase*, both of which require **Vitamin C as a necessary cofactor**. Hydroxylation allows for the formation of hydrogen bonds that stabilize the collagen triple helix. Without Vitamin C, collagen fibers lack tensile strength, leading to impaired wound healing and "scurvy." **2. Why the other options are incorrect:** * **Folic acid (A):** Essential for DNA synthesis and red blood cell maturation. Deficiency leads to megaloblastic anemia but does not directly affect collagen cross-linking. * **Thiamine (B):** Also known as Vitamin B1, it acts as a cofactor for enzymes in carbohydrate metabolism (e.g., pyruvate dehydrogenase). Deficiency causes Beriberi or Wernicke-Korsakoff syndrome. * **Vitamin A (C):** While Vitamin A is important for epithelialization and modulating collagenase activity to prevent excessive scarring, it is not the primary cofactor required for the biochemical assembly (hydroxylation) of the collagen molecule itself. **Clinical Pearls for NEET-PG:** * **Collagen Type:** The initial scar tissue (granulation tissue) contains **Type III collagen**, which is eventually replaced by the stronger **Type I collagen** in the mature scar [1]. [2]. * **Zinc Deficiency:** Another high-yield nutritional factor; Zinc is a cofactor for **matrix metalloproteinases (MMPs)**, which are essential for collagen remodeling. * **Scurvy:** Characterized by "corkscrew hair," gingival bleeding, and poor wound healing due to defective collagen synthesis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [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. 106-107.

Question 36: Granuloma is characterized by all of the following except:

A. A specific type of chronic inflammation
B. Accumulation of modified macrophages
C. Initiated by a number of infectious and non-infectious agents
D. A reaction of acute inflammation (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is the Correct Answer:** Granulomatous inflammation is a distinctive pattern of **chronic inflammation** [2], not acute inflammation. While acute inflammation is characterized by vascular changes, edema, and predominantly neutrophilic infiltration, a granuloma represents a cellular attempt to contain an offending agent that is difficult to eradicate [1], [4]. It is a Type IV (delayed-type) hypersensitivity reaction driven by T-lymphocytes and macrophages [5]. **2. Analysis of Incorrect Options:** * **Option A:** Correct statement. Granuloma is a specific subtype of chronic inflammation characterized by a focal collection of "epithelioid" cells [1], [4]. * **Option B:** Correct statement. The hallmark of a granuloma is the **epithelioid macrophage** [1]. These are "modified" macrophages that have increased secretory capacity but reduced phagocytic activity, appearing histologically with abundant pink cytoplasm and slipper-shaped nuclei [1]. * **Option C:** Correct statement. Granulomas are triggered by diverse agents [4]: * *Infectious:* Tuberculosis (caseating), Leprosy, Syphilis [2], Cat-scratch disease. * *Non-infectious:* Sarcoidosis (non-caseating), Berylliosis [4], and foreign bodies (sutures, talc) [3]. **3. High-Yield NEET-PG Pearls:** * **The Key Cytokine:** **IFN-γ** (Interferon-gamma) is the most important cytokine for granuloma formation; it is secreted by Th1 cells to activate macrophages [1]. * **TNF-α:** Essential for maintaining the structural integrity of a granuloma. Anti-TNF drugs (like Infliximab) can cause the breakdown of granulomas, leading to the reactivation of latent TB. * **Langhans Giant Cells:** Formed by the fusion of epithelioid cells; characterized by nuclei arranged in a "horseshoe" pattern at the periphery [1]. * **Caseating vs. Non-caseating:** Caseous necrosis (cheese-like) is the hallmark of *Mycobacterium tuberculosis*, whereas Sarcoidosis typically presents with non-caseating granulomas containing **Schaumann bodies** and **Asteroid bodies** [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360. [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. 196-197. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 198-200. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 218.

Question 37: What cytokine is produced by Th1 cells?

A. IL-1
B. IL-2 (Correct Answer)
C. IL-4
D. IL-5

Explanation: **Explanation:** The differentiation of CD4+ T-helper cells into specific subsets (Th1, Th2, Th17) is a fundamental concept in immunology and inflammation. **Th1 cells** are primarily involved in cell-mediated immunity and the activation of macrophages [1]. They are induced by IL-12 and IFN-̳. Once activated, Th1 cells characteristically produce **IL-2**, **IFN-̳**, and **TNF-̲** [1], [2]. * **IL-2 (Correct Answer):** Acts as a potent T-cell growth factor, stimulating the proliferation of T-lymphocytes (autocrine and paracrine) and increasing the activity of Natural Killer (NK) cells [2]. **Analysis of Incorrect Options:** * **IL-1 (Option A):** This is a pro-inflammatory cytokine primarily produced by **macrophages** and monocytes, not Th1 cells. It is responsible for inducing fever and activating vascular endothelium. * **IL-4 (Option C):** This is the signature cytokine of **Th2 cells**. It promotes B-cell differentiation into IgE-producing plasma cells and inhibits Th1 differentiation. * **IL-5 (Option D):** Also produced by **Th2 cells**, it is crucial for the activation, recruitment, and persistence of **eosinophils**, often seen in helminthic infections and allergic reactions. **High-Yield Clinical Pearls for NEET-PG:** * **Th1 vs. Th2 Balance:** Th1 cells drive **Type IV hypersensitivity** and granuloma formation (e.g., Tuberculosis) [2]. Th2 cells drive **Type I hypersensitivity** (Atopy/Asthma). * **Key Th1 Cytokine:** **IFN-̳** is the most potent activator of macrophages (classical pathway/M1) [1]. * **Transcription Factors:** Th1 differentiation is governed by **T-bet**, while Th2 is governed by **GATA-3**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 206. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218.

Question 38: Which mediator of acute inflammation is NOT derived from a cell?

A. Histamine
B. Kinins (Correct Answer)
C. Leukotrienes
D. Cytokines

Explanation: Chemical mediators of inflammation are classified into two categories based on their origin: **cell-derived** and **plasma-derived**. [2] ### Why Kinins is the Correct Answer **Kinins (e.g., Bradykinin)** are **plasma-derived mediators**. They are produced by the proteolytic cleavage of high-molecular-weight kininogen (HMWK) in the plasma, a process triggered by the activation of **Hageman Factor (Factor XII)**. [2] Bradykinin is a potent mediator that increases vascular permeability, causes vasodilation, and is specifically responsible for inducing **pain** during acute inflammation. [1] ### Why the Other Options are Incorrect * **A. Histamine:** This is a cell-derived mediator. It is pre-formed and stored in the granules of **mast cells**, basophils, and platelets. It is one of the first mediators released during the immediate transient phase of increased vascular permeability. [1] * **C. Leukotrienes:** These are cell-derived mediators synthesized de novo from **arachidonic acid** via the lipoxygenase pathway in leukocytes (neutrophils and macrophages). [1] * **D. Cytokines:** These are cell-derived proteins (e.g., TNF, IL-1) produced primarily by activated macrophages, lymphocytes, and endothelial cells to modulate the immune response. [1] ### NEET-PG High-Yield Pearls * **Factor XII (Hageman Factor)** is the central link between four plasma systems: the Kinin system, the Clotting system, the Fibrinolytic system, and the Complement system. [2] * **Pain Mediators:** The two primary mediators responsible for pain in inflammation are **Bradykinin** and **Prostaglandins (PGE2)**. [1] * **Plasma-derived mediators** (Kinins, Complement, Coagulation factors) usually circulate as inactive precursors (zymogens) that require proteolytic cleavage for activation. [2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101. [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. 189-190.

Question 39: Myositis ossificans is an example of which of the following pathological processes?

A. Metaplasia (Correct Answer)
B. Hyperplasia
C. Hypertrophy
D. Both hypertrophy and hyperplasia

Explanation: **Explanation:** **Myositis ossificans** is a classic example of **connective tissue metaplasia**. Metaplasia is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another differentiated cell type [1]. In this condition, following intramuscular trauma or hemorrhage, mesenchymal stem cells in the soft tissue differentiate into osteoblasts instead of fibroblasts. This results in the formation of **lamellar bone within skeletal muscle**, representing a change from fibrous/muscular tissue to bone. **Analysis of Incorrect Options:** * **Hyperplasia (B):** This refers to an increase in the *number* of cells in an organ or tissue [1]. While cell proliferation occurs during repair [2], the defining feature of myositis ossificans is the change in cell *type*, not just quantity. * **Hypertrophy (C):** This is an increase in the *size* of cells, leading to an increase in the size of the organ (e.g., skeletal muscle growth due to exercise) [1]. It does not involve the formation of new tissue types like bone. * **Both Hypertrophy and Hyperplasia (D):** While these often occur together (e.g., the gravid uterus), they do not explain the ectopic bone formation seen in this pathology [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Metaplasia is not a result of a change in the phenotype of an already differentiated cell; rather, it is a **reprogramming of tissue-specific stem cells** [1]. * **Radiological Sign:** On X-ray, it often shows a characteristic "eggshell calcification" or peripheral mineralization. * **Other Metaplasia Examples:** * **Barrett’s Esophagus:** Squamous to Columnar (most common epithelial metaplasia). * **Vitamin A Deficiency:** Columnar to Squamous in the respiratory tract [1]. * **Note:** Metaplasia is reversible, but if the stimulus persists, it can predispose to malignant transformation (except in myositis ossificans, which is benign) [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. 85-87, 91-92. [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. 87-88.

Question 40: Which of the following factors impairs wound healing?

A. Diabetes mellitus
B. Glucocorticoids
C. Vitamin C deficiency
D. Clot formation (Correct Answer)

Explanation: ### Explanation The correct answer is **D. Clot formation**. **Why Clot Formation is the Correct Answer:** In the context of this question, **clot formation** is a physiological **prerequisite** for wound healing, not an impairment. The formation of a blood clot (composed of fibrin and platelets) provides the initial scaffold for migrating inflammatory cells and fibroblasts [4]. It stops hemorrhage and releases growth factors (like PDGF and TGF-β) that initiate the healing cascade [3]. Therefore, it is a beneficial and necessary step in the repair process. **Analysis of Incorrect Options (Factors that DO Impair Healing):** * **A. Diabetes Mellitus:** This is one of the most important systemic causes of delayed healing [1]. It leads to microangiopathy (reduced perfusion), decreased collagen synthesis, and impaired leukocyte function (chemotaxis and phagocytosis), increasing infection risk [2]. * **B. Glucocorticoids:** Steroids inhibit inflammation and protein synthesis. They decrease the production of TGF-β, leading to poor collagen deposition and weakened scar strength [1]. * **C. Vitamin C Deficiency (Scurvy):** Vitamin C is a vital cofactor for the hydroxylation of proline and lysine residues. Without it, stable collagen cross-linking cannot occur, leading to wound dehiscence [1]. **NEET-PG High-Yield Pearls:** * **Local Factors Impairing Healing:** Infection (Single most important cause), poor blood supply, foreign bodies, and mechanical stress [1]. * **Systemic Factors Impairing Healing:** Nutrition (Protein/Vitamin C deficiency), Metabolic status (Diabetes), and Hormones (Glucocorticoids) [1]. * **Zinc Deficiency:** Also impairs healing as it is a cofactor for DNA polymerase and matrix metalloproteinases (MMPs) involved in remodeling. * **Tensile Strength:** At 1 week, a wound has ~10% of the strength of unwounded skin; it reaches ~70-80% by 3 months but rarely returns to 100%. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 106-107.

Practice by Chapter

Acute Inflammation: Vascular Events

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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

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Tissue Regeneration

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Fibrosis and Repair

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Resolution of Inflammation

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