Inflammation and Repair — MCQs

A 59-year-old man experiences acute chest pain and is rushed to the emergency room. Laboratory studies and ECG demonstrate an acute myocardial infarction; however, coronary artery angiography performed 2 hours later does not show evidence of thrombosis. Intravascular thrombolysis that occurred in this patient was mediated by plasminogen activators that were released by which of the following cells?

Q134Easy

Granulation tissue comprises of:

Q135Medium

A histological section of lung tissue shows a predominantly eosinophilic inflammatory infiltrate. Which of the following conditions is most likely responsible?

Q136Easy

VEGF is involved in all of the processes of angiogenesis except:

Q137Medium

Which of the following mediators are involved in the resolution of inflammation?

Q138Easy

What can cause edema?

Q139Easy

Which of the following is a hallmark of chronic inflammation?

Q140Easy

Which of the following statements regarding hypertrophic scars is true?

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 131: What is chemotaxis?

A. Unidirectional increase in movement (Correct Answer)
B. Random movement increase
C. Margination of leucocytes
D. Increase of leucocytes

Explanation: **Explanation:** **Chemotaxis** is defined as the **unidirectional movement** of leukocytes toward a chemical gradient [1], [2]. After exiting the circulation (diapedesis), leukocytes migrate through the interstitial tissue toward the site of injury or infection [2]. This movement is purposeful and directed, guided by substances known as **chemoattractants** [2]. * **Why Option A is correct:** Chemotaxis is not random; it is a vector-based movement where cells sense a concentration gradient and move from an area of lower concentration to an area of higher concentration of the chemoattractant [1], [2]. * **Why Option B is incorrect:** Random movement (increased speed without direction) is termed **chemokinesis**, which is distinct from the directional nature of chemotaxis. * **Why Option C is incorrect:** **Margination** refers to the process where leukocytes move to the periphery of the blood vessel lumen (near the endothelium) due to stasis and changes in laminar flow [3]. * **Why Option D is incorrect:** An increase in the number of leukocytes is termed **leukocytosis**, which is a systemic response to inflammation, not a cellular movement mechanism. **High-Yield Clinical Pearls for NEET-PG:** 1. **Exogenous Chemoattractants:** The most common are bacterial products, particularly those with **N-formylmethionine** termini. 2. **Endogenous Chemoattractants:** The "Big Four" to remember are: * **C5a** (Complement component) [1] * **Leukotriene B4 (LTB4)** * **IL-8** (Chemokine) * **Bacterial lipids/Soluble gases** 3. **Mechanism:** Chemoattractants bind to **G-protein coupled receptors (GPCRs)** on the leukocyte surface, leading to actin polymerization at the "leading edge" (lamellipodia) of the cell. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 190-191. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Migration in the tissues toward a chemotactic stimulus, pp. 86-87.

Question 132: All of the following are seen in acute inflammation except:

A. Vasodilatation
B. Neutrophil migration
C. Granuloma formation (Correct Answer)
D. Increased vascular permeability

Explanation: ### Explanation The correct answer is **C. Granuloma formation**. **1. Why Granuloma formation is the correct answer:** Granuloma formation is a hallmark of **chronic inflammation**, specifically chronic granulomatous inflammation. It is a protective mechanism where the body attempts to wall off an offending agent that is difficult to eradicate (e.g., *Mycobacterium tuberculosis*, foreign bodies, or fungi). It involves a collection of activated macrophages (epithelioid cells), lymphocytes, and multinucleated giant cells. Since the question asks for features of **acute inflammation**, granuloma formation is the "except" as it represents a delayed, persistent immune response. **2. Analysis of Incorrect Options (Features of Acute Inflammation):** * **Vasodilatation (A):** One of the earliest manifestations of acute inflammation, primarily affecting arterioles [1]. It leads to increased blood flow, causing redness (*rubor*) and heat (*calor*) [4]. * **Neutrophil migration (B):** Neutrophils are the "first responders" and the characteristic cell type of acute inflammation [2]. They migrate to the site of injury via chemotaxis within the first 6–24 hours [2]. * **Increased vascular permeability (D):** This is the hallmark of acute inflammation, leading to the escape of protein-rich fluid (exudate) into the extravascular tissue, resulting in edema (*tumor*) [1]. The most common mechanism is endothelial cell contraction [3]. **3. NEET-PG Clinical Pearls:** * **Cardinal Signs:** Remember Celsus’ four signs (Rubor, Calor, Tumor, Dolor) and Virchow’s fifth sign (Functio Laesa) [4]. * **Cellular Shift:** Acute inflammation is dominated by **Neutrophils** (first 24 hours), while Chronic inflammation is dominated by **Macrophages, Lymphocytes, and Plasma cells**. * **Vascular Hallmark:** The most common mechanism of increased vascular permeability in acute inflammation is **endothelial cell contraction** (immediate transient response) [3]. * **Granuloma Components:** Look for "Epithelioid cells" (activated macrophages) as the diagnostic feature of a granuloma in pathology slides. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [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. [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. [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. 185-186.

Question 133: A 59-year-old man experiences acute chest pain and is rushed to the emergency room. Laboratory studies and ECG demonstrate an acute myocardial infarction; however, coronary artery angiography performed 2 hours later does not show evidence of thrombosis. Intravascular thrombolysis that occurred in this patient was mediated by plasminogen activators that were released by which of the following cells?

A. Cardiac myocytes
B. Endothelial cells (Correct Answer)
C. Macrophages
D. Segmented neutrophils

Explanation: **Explanation** The correct answer is **Endothelial cells (Option B)**. **Mechanism of Fibrinolysis** The patient experienced a "spontaneous thrombolysis," a natural protective mechanism to restore blood flow. The key enzyme responsible for degrading a fibrin clot is **Plasmin**. Plasmin is derived from its inactive precursor, **Plasminogen**, through the action of **Plasminogen Activators (PAs)** [1]. The most important physiological activator is **Tissue-type Plasminogen Activator (t-PA)**. t-PA is primarily synthesized and secreted by **vascular endothelial cells** [1]. When endothelial cells are stimulated by stasis or occlusion, they release t-PA, which binds to fibrin and converts plasminogen into active plasmin, thereby dissolving the thrombus. **Analysis of Incorrect Options:** * **A. Cardiac myocytes:** These cells are the victims of ischemia in MI; they do not produce fibrinolytic enzymes. * **C. Macrophages:** While they participate in chronic inflammation and wound healing (phagocytosis), they are not the primary source of systemic plasminogen activators in acute thrombosis. * **D. Segmented neutrophils:** These are the first cells to arrive at the site of infarction (within 6–24 hours) to initiate inflammation, but they do not mediate the intravascular thrombolytic pathway. **High-Yield NEET-PG Pearls:** * **t-PA vs. Urokinase:** t-PA (from endothelium) is the major activator in the blood; Urokinase-like PA (u-PA) is found primarily in plasma and various tissues. * **Therapeutic Correlation:** Recombinant t-PA (Alteplase, Reteplase) is used clinically as "clot-busters" in acute MI and ischemic stroke [1]. * **Inhibitor:** **PAI-1** (Plasminogen Activator Inhibitor) is also released by endothelial cells to regulate this process and prevent excessive bleeding. * **Diagnostic Marker:** D-dimer is a specific breakdown product of fibrin degradation by plasmin, used to rule out DVT/PE. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 130-132.

Question 134: Granulation tissue comprises of:

A. Fibroblasts
B. Small blood vessels
C. Macrophages
D. All of the above (Correct Answer)

Explanation: **Explanation:** Granulation tissue is the hallmark of the **proliferative phase of wound healing**, typically appearing 3 to 5 days after injury [2]. It is a specialized, temporary tissue that serves as a scaffold for the formation of a permanent scar. **Why "All of the above" is correct:** The histological composition of granulation tissue is characterized by three primary components: 1. **Fibroblasts (Option A):** These cells migrate to the site of injury and proliferate to synthesize collagen (primarily Type III initially) and extracellular matrix (ECM) components [1]. 2. **Small blood vessels (Option B):** Through the process of **angiogenesis** (neovascularization), new, thin-walled, delicate capillaries are formed [1]. This gives granulation tissue its characteristic pink, soft, and granular appearance. 3. **Macrophages (Option C):** These are the dominant inflammatory cells in granulation tissue. They clear debris, fibrin, and pathogens while secreting growth factors (like TGF-β and VEGF) that drive fibroblast activity and angiogenesis [2]. **Analysis of Options:** While each individual component (A, B, and C) is a vital constituent, selecting any single one would be incomplete. Granulation tissue is defined by the *coexistence* of these elements within an edematous extracellular matrix [2]. **High-Yield NEET-PG Pearls:** * **Granulation Tissue vs. Granuloma:** Do not confuse them. A granuloma is a collection of epithelioid macrophages (chronic inflammation), whereas granulation tissue is related to wound healing [1]. * **Key Growth Factor:** **TGF-β** is the most important cytokine for synthesis and deposition of connective tissue proteins [2]. * **Clinical Appearance:** It is characterized by "bleeding on touch" due to the fragility of the newly formed, leaky capillaries [2]. * **Evolution:** Over time, it matures into a **scar** as cellularity and vascularity decrease and collagen content increases (Type III collagen is replaced by Type I) [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.

Question 135: A histological section of lung tissue shows a predominantly eosinophilic inflammatory infiltrate. Which of the following conditions is most likely responsible?

A. Bacterial pneumonia
B. Dirofilaria infestation (Correct Answer)
C. Infectious mononucleosis
D. Tuberculosis

Explanation: ***Dirofilaria infestation*** - **Helminthic infections** like Dirofilaria cause a **type 1 hypersensitivity reaction** with prominent **eosinophilic infiltration** in lung tissue. - **Parasitic antigens** trigger **IL-5 and IL-4** release, leading to **eosinophil recruitment and activation** in the pulmonary parenchyma. *Bacterial pneumonia* - Characterized by **neutrophilic infiltration** rather than eosinophilic, as bacteria trigger **acute inflammatory response**. - **Polymorphonuclear leukocytes (PMNs)** are the predominant cells in **purulent exudate** formation. *Infectious mononucleosis* - Primarily causes **atypical lymphocytic infiltration** with enlarged, activated **T-lymphocytes** (Downey cells). - **Epstein-Barr virus** infection leads to **lymphoid hyperplasia** rather than eosinophilic response. *Tuberculosis* - Characterized by **epithelioid cell granulomas** with **multinucleated giant cells** and **caseous necrosis**. - **Chronic granulomatous inflammation** involves **macrophages and lymphocytes**, not eosinophils.

Question 136: VEGF is involved in all of the processes of angiogenesis except:

A. Migration and proliferation of endothelial cells
B. Capillary sprouting
C. Enhances the production of ECM proteins (Correct Answer)
D. Increased vascular permeability

Explanation: Angiogenesis is a complex process of new blood vessel formation from pre-existing vessels, primarily driven by **Vascular Endothelial Growth Factor (VEGF)**. **Why Option C is the correct answer:** VEGF is primarily a mitogen for endothelial cells, not fibroblasts. The production of Extracellular Matrix (ECM) proteins (like collagen and fibronectin) and the subsequent stabilization of the vessel are functions of **Transforming Growth Factor-beta (TGF-β)** and **Platelet-Derived Growth Factor (PDGF)** [1]. VEGF actually promotes the degradation of the ECM (via matrix metalloproteinases) to allow endothelial cells to migrate. **Analysis of Incorrect Options:** * **Option A (Migration and proliferation):** VEGF is the most important growth factor for the "sprouting" phase of angiogenesis. It binds to VEGFR-2 to trigger the proliferation and migration of endothelial cells toward the site of injury [1]. * **Option B (Capillary sprouting):** This is the hallmark of angiogenesis. VEGF induces the formation of "tip cells" that lead the sprout and "stalk cells" that form the vessel lumen [1]. * **Option D (Increased vascular permeability):** VEGF was originally discovered as "Vascular Permeability Factor" (VPF). It is significantly more potent than histamine in inducing edema by creating fenestrations and increasing the leakiness of new vessels [1]. **NEET-PG High-Yield Pearls:** * **VEGF-A:** The major isoform involved in angiogenesis and vasculogenesis. * **VEGFR-2:** The primary receptor for most VEGF pro-angiogenic effects. * **HIF-1 (Hypoxia-Inducible Factor):** The most important inducer of VEGF production in response to low oxygen [3]. * **Bevacizumab:** A monoclonal antibody against VEGF used in treating various cancers (e.g., colorectal, RCC) and wet macular degeneration [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-119. [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. 88-89. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 313-314.

Question 137: Which of the following mediators are involved in the resolution of inflammation?

A. TNF alpha, IL-1 and CRP
B. TNF beta, IL-6 and CRP
C. TNF alpha, IL-10 and IL-1 receptor antagonist (Correct Answer)
D. TNF gamma

Explanation: **Explanation:** The resolution of inflammation is an active process aimed at restoring tissue homeostasis. It involves the neutralization or degradation of pro-inflammatory mediators and the release of anti-inflammatory cytokines. **Why Option C is Correct:** The resolution phase is characterized by a "stop signal" that halts leukocyte infiltration. * **IL-10:** A potent anti-inflammatory cytokine that inhibits the production of TNF and IL-12 by activated macrophages and reduces MHC II expression. [1] * **IL-1 Receptor Antagonist (IL-1ra):** A naturally occurring protein that binds to IL-1 receptors without triggering a signal, effectively blocking the pro-inflammatory actions of IL-1. * **TNF-alpha (in this context):** While primarily pro-inflammatory, TNF-alpha plays a dual role; it is essential for initiating the apoptosis of neutrophils and triggering the transition from a pro-inflammatory to a pro-resolving macrophage phenotype (M2). [1] **Why Other Options are Incorrect:** * **Options A & B:** **IL-1, IL-6, and TNF-alpha** are the primary mediators of the **Acute Phase Response**. [1] They induce fever and stimulate the liver to produce **CRP (C-Reactive Protein)**. These are markers of active inflammation, not resolution. * **Option D:** **IFN-gamma** (often confused with "TNF gamma") is a major macrophage-activating cytokine that promotes chronic inflammation and granuloma formation. [1] **NEET-PG High-Yield Pearls:** 1. **Lipoxins:** These are arachidonic acid metabolites (specifically Lipoxin A4 and B4) that serve as the "molecular brakes" of inflammation by inhibiting neutrophil recruitment. [1] 2. **TGF-beta:** Along with IL-10, TGF-beta is a key anti-inflammatory cytokine involved in limiting the immune response and promoting wound healing/fibrosis. 3. **M2 Macrophages:** These are the "alternative" macrophages responsible for tissue repair and resolution, whereas M1 macrophages are "classical" and pro-inflammatory. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 81-106.

Question 138: What can cause edema?

A. Decreased hydrostatic pressure
B. Sodium retention (Correct Answer)
C. Hyperproteinemia
D. Polycythemia

Explanation: **Explanation:** Edema is defined as the accumulation of excess fluid in the interstitial spaces or body cavities [1]. According to **Starling’s Law**, fluid movement is governed by the balance between hydrostatic pressure (which pushes fluid out of vessels) and plasma colloid osmotic pressure (which pulls fluid back into vessels) [1]. **Why Sodium Retention is Correct:** Sodium is the primary osmotically active solute in the extracellular fluid. **Sodium retention** (often accompanied by water retention) leads to two main consequences [4]: 1. An increase in total blood volume, which raises **capillary hydrostatic pressure**. 2. A dilution of plasma proteins, which lowers **colloid osmotic pressure**. This dual effect forces fluid into the interstitium, causing systemic edema. Common clinical causes include renal failure and congestive heart failure (via activation of the Renin-Angiotensin-Aldosterone System) [1], [2]. **Analysis of Incorrect Options:** * **A. Decreased hydrostatic pressure:** This would actually promote fluid reabsorption into the capillaries, preventing edema. Increased hydrostatic pressure (e.g., in DVT or Heart Failure) is what causes edema [1]. * **C. Hyperproteinemia:** High levels of plasma proteins (like albumin) increase the colloid osmotic pressure, which keeps fluid inside the vessels. It is **hypoproteinemia** (e.g., in Nephrotic syndrome or Cirrhosis) that leads to edema [1], [3]. * **D. Polycythemia:** This refers to an increased concentration of red blood cells. While it increases blood viscosity, it does not inherently disrupt the Starling forces to cause edema [4]. **NEET-PG High-Yield Pearls:** * **Most common cause of localized edema:** Venous obstruction or lymphatic obstruction (Lymphedema) [1], [2]. * **Most common cause of generalized edema (Anasarca):** Cardiac, renal, or hepatic failure [1], [3]. * **Transudate vs. Exudate:** Edema in heart failure is a **transudate** (low protein, low SG), whereas inflammatory edema is an **exudate** (high protein, high SG due to increased vascular permeability) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 124. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 124-126. [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. 126-127. [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. 124-125.

Question 139: Which of the following is a hallmark of chronic inflammation?

A. Tissue destruction (Correct Answer)
B. Mononuclear infiltration
C. Wound healing and repair
D. All of the above

Explanation: **Explanation:** Chronic inflammation is defined as inflammation of prolonged duration (weeks to months) in which inflammation, tissue injury, and attempts at repair coexist in varying combinations [1]. **Why "Tissue Destruction" is the Hallmark:** While chronic inflammation involves several processes, **tissue destruction** is considered its defining hallmark [1]. It is primarily mediated by the persistent products of mononuclear cells, especially **activated macrophages**. These cells release reactive oxygen species (ROS), NO, and proteases that damage both the offending agent and the host tissue [2]. Unlike acute inflammation, which usually resolves with minimal damage, chronic inflammation is inherently destructive. **Analysis of Other Options:** * **B. Mononuclear infiltration:** This refers to the collection of macrophages, lymphocytes, and plasma cells at the site [1]. While it is a *characteristic* feature, it is the cellular mechanism that leads to the hallmark of destruction. * **C. Wound healing and repair:** This involves angiogenesis (new vessel formation) and fibrosis. While these occur simultaneously with destruction in chronic inflammation, they are the body’s *response* to injury rather than the primary pathological hallmark. * **D. All of the above:** In many textbooks (like Robbins Pathology), chronic inflammation is characterized by all three: mononuclear infiltration, tissue destruction, and attempts at healing [1]. However, in competitive exams like NEET-PG, if forced to choose the single most defining pathological consequence, **tissue destruction** is prioritized. **High-Yield Clinical Pearls for NEET-PG:** * **The "Dominant Cell":** The **Macrophage** is the central figure in chronic inflammation [2]. * **Granulomatous Inflammation:** A specific subtype of chronic inflammation characterized by "epithelioid" macrophages (activated by IFN-γ from Th1 cells). * **Key Cytokines:** TNF-α and IL-1 are crucial for systemic effects, while **IFN-γ** is the major macrophage activator [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 104-105. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 140: Which of the following statements regarding hypertrophic scars is true?

A. Usually occurs across flexural areas (Correct Answer)
B. Does not improve with time
C. Overgrows its boundaries
D. Develops months after surgery

Explanation: ### Explanation **Hypertrophic scars** are a common topic in NEET-PG, often contrasted with keloids. They represent an exuberant but controlled healing response characterized by excessive collagen deposition. **1. Why Option A is Correct:** Hypertrophic scars typically develop in areas of **high skin tension**. Flexural areas (like joints) are subject to constant mechanical stress and movement, which triggers fibroblasts to produce excess collagen [1]. Unlike keloids, which prefer the earlobes and chest, hypertrophic scars are frequently seen across joints and flexural surfaces [1]. **2. Why the Other Options are Incorrect:** * **Option B (Does not improve with time):** This is false. Hypertrophic scars often show **spontaneous regression** or flattening over several months to years [1]. In contrast, keloids rarely regress and may even enlarge over time [1]. * **Option C (Overgrows its boundaries):** This is the classic definition of a **Keloid** [1]. A hypertrophic scar remains **confined to the boundaries** of the original wound [1]. * **Option D (Develops months after surgery):** Hypertrophic scars usually appear **early** (within 4 to 8 weeks) after the initial injury [1]. Keloids, however, can appear months or even years later [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Collagen Type:** Both involve Type I and Type III collagen, but hypertrophic scars have a more organized, **parallel arrangement** of collagen bundles, whereas keloids have thick, disorganized "glassy" (hyalinized) collagen bundles [1]. * **Genetics:** Keloids have a strong genetic predisposition (more common in dark-skinned individuals) [1]; hypertrophic scars do not show a racial predilection. * **Treatment:** Both respond to intralesional steroids (Triamcinolone), but hypertrophic scars have a much better prognosis following surgical excision compared to keloids, which have high recurrence rates [1]. **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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free