Fibrosis and Repair — MCQs
Wound contraction can be most effectively minimized by:
Fibroblasts in healing wound are derived from -
Which of the following helps in cell-to-cell adhesion?
Which of the following is NOT a pathological manifestation of chronic alcoholism?
Which of the following statements about wound healing is false?
What is the mechanism of secondary healing?
Which vitamin is known to inhibit wound healing?
Which statement about macrophages is incorrect?
Which of the following type of collagen is present in healing and granulation tissue?
Which is NOT a feature of chronic inflammation?
Fibrosis and Repair Indian Medical PG Practice Questions and MCQs
Question 1: Wound contraction can be most effectively minimized by:
- A. Allowing secondary granulation
- B. Full thickness grafting (Correct Answer)
- C. Split skin graft
- D. Dressing with placenta
Explanation: ***Full thickness grafting*** - **Full-thickness skin grafts** include the epidermis and full dermis, which contains **fewer myofibroblasts** than split-thickness grafts, thus minimizing contraction. - The greater amount of dermal tissue acts as a **mechanical barrier** to prevent excessive wound contraction, providing a more stable and aesthetically pleasing result. *Allowing secondary granulation* - Healing by **secondary intention** involves substantial granulation tissue formation, which is rich in **myofibroblasts** and leads to significant wound contraction. - This method of healing is often used for infected or contaminated wounds but results in the **most contraction**. *Split skin graft* - **Split-thickness skin grafts** contain only a portion of the dermis, making them prone to **moderate to significant wound contraction**. - While better than secondary intention, the thin dermal layer provides less resistance to the contractile forces of the **myofibroblasts**. *Dressing with placenta* - **Placental tissue dressings** can promote wound healing by providing growth factors and a scaffold for regeneration. - However, they do not inherently prevent or minimize **wound contraction** in the same way that a full-thickness graft mechanically does, as they do not replace the entire dermal layer.
Question 2: Fibroblasts in healing wound are derived from -
- A. Epithelium
- B. Endothelium
- C. Local mesenchyme (Correct Answer)
- D. Bone marrow
Explanation: ***Local mesenchyme*** - Fibroblasts, crucial for synthesizing **collagen** and other extracellular matrix components in wound healing, are primarily derived from resident **mesenchymal cells** in the local connective tissue [1]. - These undifferentiated mesenchymal cells proliferate and differentiate into fibroblasts to aid in tissue repair [4]. - This is the **major source** of fibroblasts in wound healing. *Bone marrow* - While bone marrow-derived **circulating fibrocytes** can contribute to wound healing, they represent a minor source compared to local mesenchymal cells [2]. - These circulating progenitor cells can migrate to wound sites and differentiate into fibroblasts, but this is a supplementary mechanism. *Epithelium* - **Epithelial cells** primarily provide a protective barrier and regenerate the surface lining; they do not differentiate into fibroblasts [3]. - Their main role in wound healing is **re-epithelialization** to close the wound surface. *Endothelium* - **Endothelial cells** form the lining of blood vessels and are involved in angiogenesis (new blood vessel formation) during wound healing. - While some endothelial cells may undergo **endothelial-to-mesenchymal transition (EndoMT)** to become myofibroblasts, the primary source of fibroblasts is the local mesenchyme. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115. [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. 104-105. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113. [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. 105-106.
Question 3: Which of the following helps in cell-to-cell adhesion?
- A. Interleukins
- B. Interferons
- C. E-Cadherin (Correct Answer)
- D. Matrix metalloproteinases
Explanation: ***E-Cadherin*** - E-Cadherin is a **cell adhesion molecule** that plays a crucial role in maintaining the structure of tissues by promoting **cell-to-cell adhesion** [1]. - It is mainly involved in the **adherens junctions**, helping cells stick together, especially in epithelial tissues. *Matrix metallo proteinase* - Matrix metallo proteinases (MMPs) are enzymes that degrade **extracellular matrix** components, rather than promoting adhesion between cells. - They are involved in **tissue remodeling** and **wound healing**, not in direct cell-to-cell interactions. *Interleukins* - Interleukins are a group of **cytokines** that mediate **immune responses**, but they do not facilitate direct cell adhesion. - Their primary function involves **cell signaling** and communication, rather than adhesion processes. *Interferons* - Interferons are signaling proteins involved in the **immune defense against viral infections** and do not have a role in cell-to-cell adhesion. - They primarily act to induce an **antiviral state** in neighboring cells and modulate the immune response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 314-315.
Question 4: Which of the following is NOT a pathological manifestation of chronic alcoholism?
- A. Piecemeal necrosis (Correct Answer)
- B. Microvesicular fatty changes
- C. Central hyaline sclerosis
- D. Ballooning degeneration
Explanation: ***Piecemeal necrosis*** - Piecemeal necrosis is not a common manifestation of chronic alcoholism but is instead more typical of **autoimmune hepatitis** or **chronic viral hepatitis**. - Chronic alcoholism primarily leads to different types of liver damage, such as **steatosis** or **apoptosis**, rather than piecemeal necrosis. *Balloning degeneration* - Balloning degeneration reflects **swelling** of hepatocytes, often associated with **alcoholic liver disease** and represents liver cell injury [1]. - It is a recognized feature seen in chronic alcohol exposure indicating the effect of toxicity on liver cells [1]. *Microvesicular fatty changes* - Microvesicular fatty changes, characterized by small fat vacuoles in liver cells, can be induced by chronic alcohol use and is commonly noted in **steatosis** [2]. - This finding is also seen in conditions like **reye syndrome** and is closely related to alcohol-induced liver injury. *Central hyaline sclerosis* - Central hyaline sclerosis refers to fibrosis and is often related to chronic liver disease but is not a direct pathological manifestation seen in chronic alcoholism. - However, chronic alcohol abuse contributes to **cirrhosis**, which can lead to various forms of liver scarring, but this is not specific to alcohol alone [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 389-390. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-850. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 848.
Question 5: Which of the following statements about wound healing is false?
- A. Inhibited by diabetes mellitus (DM)
- B. Inhibited by foreign body
- C. Hematomas promote wound healing (Correct Answer)
- D. Inhibited by infection
Explanation: ***Hematomas promotes wound healing*** - Hematomas (localized collections of **blood outside blood vessels**) actually **inhibit wound healing** by acting as a medium for bacterial growth and increasing tissue tension. - This statement is **false** because hematomas interfere with proper tissue apposition and oxygen delivery, which are crucial for successful wound repair [3]. *Inhibited by diabetes mellitus (DM)* - **Diabetes mellitus** impairs various stages of wound healing due to **poor glycemic control**, leading to compromised immune function, neuropathy, and reduced blood flow [1]. - This often results in **delayed wound closure** and increased risk of infection [2]. *Inhibited by foreign body* - The presence of a **foreign body** in a wound can lead to a persistent inflammatory response, impeding tissue repair and increasing the likelihood of chronic infection. - This sustained inflammation prevents the orderly progression through the phases of wound healing, thus **inhibiting the process**. *Inhibited by infection* - **Infection** in a wound significantly delays healing by causing ongoing inflammation, tissue destruction, and increased metabolic demands [1]. - Bacteria compete for nutrients and produce toxins that harm host cells, preventing proper **granulation tissue formation** and **epithelialization**. **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] 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 6: What is the mechanism of secondary healing?
- A. Neovascularization
- B. Scab formation
- C. Granuloma formation
- D. Granulation tissue (Correct Answer)
Explanation: ***Granulation tissue*** - **Secondary intention healing** involves the formation of abundant **granulation tissue** to fill the tissue defect [1]. - Granulation tissue consists of new **capillaries**, **fibroblasts**, and inflammatory cells, which lay the groundwork for wound closure [2]. *Neovascularization* - **Neovascularization** is the specific process of forming new blood vessels within the wound, which is a component of granulation tissue formation, but not the overall healing mechanism [2]. - While essential for delivering nutrients and oxygen, it's a sub-process rather than the primary mechanism for secondary healing itself. *Scab formation* - **Scab formation** is an initial protective mechanism, primarily associated with superficial wounds and not the intrinsic mechanism of tissue repair and closure in secondary healing. - A scab primarily protects the underlying wound from infection and desiccation while healing occurs beneath it. *Granuloma formation* - **Granuloma formation** is a specific type of chronic inflammatory response characterized by collections of macrophages, often seen in persistent infections or foreign body reactions, not typical secondary wound healing [2]. - It indicates a **cell-mediated immune response** to a non-degradable stimulus, aiming to wall off the offending agent. **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. 105-107.
Question 7: Which vitamin is known to inhibit wound healing?
- A. Vitamin A
- B. Vitamin E (Correct Answer)
- C. Vitamin C
- D. Vitamin B complex
Explanation: ***Vitamin E*** - **High doses** or **supraphysiologic levels** of vitamin E may potentially **impair wound healing** due to anticoagulant effects and possible interference with platelet function. - Excessive vitamin E supplementation (above recommended doses) can increase **bleeding risk** at surgical and wound sites, potentially delaying healing. - **Note:** Physiologic doses of vitamin E do not inhibit wound healing; this refers specifically to excessive supplementation. *Vitamin A* - **Vitamin A** plays a crucial role in wound healing by promoting **epithelial cell differentiation** and collagen synthesis. - It aids in **immune function** and inflammation modulation, both vital for effective wound repair. - Can even counteract steroid-induced impairment of wound healing. *Vitamin C* - **Vitamin C** is essential for **collagen synthesis** and cross-linking, which provides tensile strength to healing wounds. - Acts as an **antioxidant** and is vital for immune function, supporting tissue repair processes. - Deficiency leads to impaired wound healing (scurvy). *Vitamin B complex* - **B vitamins**, particularly **B1 (thiamine)**, **B5 (pantothenic acid)**, and **B6 (pyridoxine)**, are important cofactors in metabolic processes crucial for cell proliferation and tissue repair. - They contribute to energy production and synthesis of proteins and DNA needed for wound healing.
Question 8: Which statement about macrophages is incorrect?
- A. Phagocytic cells
- B. M2 type involved in inflammation (Correct Answer)
- C. Activation by IFN-γ
- D. Major cells in chronic inflammation
Explanation: ***M2 type involved in inflammation*** - The M2 macrophages are primarily associated with **anti-inflammatory responses** and tissue repair, not inflammation [1][2]. - They play a role in **wound healing** and **resolution of inflammation**, contrasting with the inflammatory role attributed in the statement [2][3]. *Phagocytic cells* - **Macrophages are indeed phagocytic**, meaning they ingest and eliminate pathogens and debris [1]. - This is a fundamental characteristic of macrophages, playing a crucial role in the **immune response**. *Activation by IFN-y* - **Interferon-gamma (IFN-y)** is known to activate macrophages, particularly enhancing their ability to kill intracellular pathogens [1][2]. - This activation is vital for macrophage's role in **cell-mediated immunity** [1]. *Major cells in chronic inflammation* - Macrophages are significant players in **chronic inflammation**, contributing to tissue remodeling and the persistent inflammatory state [1]. - They secrete various cytokines that maintain the pathological state seen in chronic inflammatory diseases. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 106-107. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115.
Question 9: Which of the following type of collagen is present in healing and granulation tissue?
- A. Type II
- B. Type I
- C. Type III (Correct Answer)
- D. Type IV
Explanation: ***Type III*** - **Type III collagen** is prominently found in **granulation tissue** during the early stages of wound healing [1]. - It provides a **scaffold** for cellular migration and proliferation [2], contributing to the initial strength of the healing tissue. *Type II* - **Type II collagen** is the primary collagen type found in **cartilage**, particularly **hyaline cartilage**. - It is crucial for the **structural integrity** and resilience of articular surfaces, not typically in granulation tissue. *Type I* - **Type I collagen** is the most abundant collagen in the body, providing **tensile strength** to tissues like bone, skin, tendons, and ligaments. - While ultimately replacing type III collagen in mature scar tissue, it is **less prevalent in initial granulation tissue** compared to type III [1]. *Type IV* - **Type IV collagen** is a major component of **basement membranes**, forming a mesh-like network [3]. - It provides **structural support** and acts as a selective filter in tissues such as the kidneys and lungs, but not in healing granulation tissue. **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. With Illustrations By, pp. 32-34.
Question 10: Which is NOT a feature of chronic inflammation?
- A. Mononuclear cells
- B. Neutrophil predominance (Correct Answer)
- C. Fibrosis
- D. Granulation tissue
Explanation: ***Neutrophil predominance*** - **Neutrophil predominance** is characteristic of **acute inflammation**, where these cells are among the first responders to injury or infection [1]. - In chronic inflammation, neutrophils are typically present in much smaller numbers compared to mononuclear cells, or their presence indicates an acute exacerbation [3]. *Mononuclear cells* - **Mononuclear cells**, such as **macrophages**, **lymphocytes**, and **plasma cells**, are the hallmark cellular infiltrates of chronic inflammation [1]. - These cells are responsible for sustained immune responses, tissue destruction, and repair processes [2]. *Fibrosis* - **Fibrosis**, or the deposition of **collagen** by fibroblasts, is a common outcome of chronic inflammation as the body attempts to repair ongoing tissue damage [3]. - It leads to **scarring** and functional impairment of affected organs [4]. *Granulation tissue* - **Granulation tissue** is an early phase of **tissue repair** during chronic inflammation, characterized by the proliferation of **fibroblasts** and new **blood vessels (angiogenesis)** [5]. - It represents the body's effort to fill tissue defects and prepare for eventual fibrous scar formation [5]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 195-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 107-109. [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. 200-202. [5] 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. 194-195.
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