Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 411: What is the maximum tensile strength of a healed wound compared to the original tissue?

A. 70-80% of original strength (Correct Answer)
B. 100% of original strength
C. 50% of original strength
D. None of the options

Explanation: ***70-80% of original strength*** - A healed wound, even under optimal conditions, can only achieve a maximum of **70-80%** of the tensile strength of the original **uninjured tissue** [1]. - This is because the repair process involves the formation of **fibrous scar tissue** which differs structurally from the original tissue, particularly in the organization and type of collagen fibers. *100% of original strength* - This option is incorrect because healed wounds, even completely mature ones, rarely regain the **full strength** of the original tissue [1]. - The replacement of damaged tissue with **scar tissue** inherently limits perfect functional and structural restoration. *50% of original strength* - While tensile strength gradually increases during wound healing, it typically exceeds **50%** as the wound matures. - This value is often seen in the **early stages** of healing but not as the maximum achievable strength. *None of the options* - This option is incorrect because **70-80% of original strength** is a well-established range for the maximum tensile strength of a healed wound. - This range reflects the physiological limitations of **scar tissue remodeling** and collagen deposition. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 412: Which mediators are involved in the resolution of inflammation?

A. TNF Alfa, IL-1, and CRP
B. IL-10, IL-1 receptor antagonist, and TGF-β
C. Interferon-gamma and IL-12
D. Resolvins, protectins, and lipoxins (Correct Answer)

Explanation: ***Resolvins, protectins, and lipoxins*** - These are **specialized pro-resolving mediators (SPMs)** derived from omega-3 and omega-6 polyunsaturated fatty acids that actively promote the resolution phase of inflammation. - **Lipoxins** (from arachidonic acid) inhibit neutrophil chemotaxis and promote macrophage-mediated clearance of apoptotic cells. - **Resolvins** (from EPA and DHA) actively terminate inflammatory signals, reduce neutrophil infiltration, and enhance bacterial clearance. - **Protectins** promote resolution by limiting neutrophil recruitment and enhancing clearance of inflammatory debris. - These mediators represent the **endogenous "stop signals"** that actively resolve inflammation rather than simply suppressing it. *IL-10, IL-1 receptor antagonist, and TGF-β* - While these have **anti-inflammatory** effects, they are not classified as primary resolution mediators. - **IL-10** inhibits pro-inflammatory cytokine synthesis and suppresses immune responses (immunosuppressive rather than pro-resolving). - **IL-1 receptor antagonist (IL-1Ra)** blocks IL-1 signaling, preventing inflammation amplification. - **TGF-β** promotes tissue repair and has immunosuppressive functions. - These are **anti-inflammatory mediators** that prevent or dampen inflammation, distinct from specialized pro-resolving mediators that actively orchestrate the resolution process. *TNF-alpha, IL-1, and CRP* - **TNF-alpha** and **IL-1** are classic **pro-inflammatory cytokines** that initiate and amplify inflammation. - **CRP (C-reactive protein)** is an acute-phase reactant and biomarker of inflammation, not a mediator of resolution. *Interferon-gamma and IL-12* - **IFN-γ** and **IL-12** promote **Th1 immune responses** and cellular immunity. - These are pro-inflammatory mediators involved in host defense against intracellular pathogens, not resolution of inflammation.

Question 413: What is the sequence of events in acute inflammation?

A. Transient vasoconstriction - Stasis - Vasodilatation - Increased permeability
B. Transient vasoconstriction - Vasodilatation - Increased permeability - Stasis (Correct Answer)
C. Transient vasoconstriction - Vasodilatation - Stasis - Increased permeability
D. Vasodilatation - Stasis - Transient vasoconstriction - Increased permeability

Explanation: ***Transient vasoconstriction → Vasodilatation → Increased permeability → Stasis*** - This sequence accurately reflects the **initial phase** of acute inflammation where **vasoconstriction** briefly occurs for tissue protection, followed by **vasodilatation** that enhances blood flow [3]. - **Increased permeability** allows plasma proteins to exit the bloodstream, crucial for inflammatory responses [1], while **stasis** occurs as blood flow slows, facilitating leukocyte adhesion [2]. *Transient vasoconstriction → Stasis → Vasodilatation → Increased permeability* - This option incorrectly places **stasis** before **vasodilatation**, as stasis occurs only after blood flow has increased. - **Vasodilatation** is essential for increased blood flow, which precedes stasis, making this sequence incorrect. *Transient vasoconstriction → Vasodilatation → Stasis → Increased permeability* - Although it includes **vasodilatation** and **transient vasoconstriction**, it incorrectly suggests that **stasis** occurs before the increase in vascular permeability. - **Increased permeability** is a critical event after vasodilatation [1], thus this order is not accurate. *Vasodilatation → Stasis → Transient vasoconstriction → Increased permeability* - This sequence is incorrect as it starts with **vasodilatation**, neglecting the initial protective phase of **transient vasoconstriction**. - **Transient vasoconstriction** is the first event, making this option inaccurate as it misrepresents the order of events in acute inflammation. **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] 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. 186-187. [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. 185-186.

Question 414: What is the final stage of pneumonia characterized by the resolution of lung inflammation?

A. Congestion (early stage)
B. Red hepatization (middle stage)
C. Gray hepatization (late stage)
D. Resolution (Correct Answer)

Explanation: ***Resolution*** - The terminal stage of pneumonia is characterized by the **resolution** phase, where the inflammatory process subsides and lung tissue begins to heal [1][2]. - During this phase, clinical symptoms improve, and the lungs return to normal function after patient recovery [2]. *Congestion* - This phase occurs early in pneumonia, presenting with increased vascularity and **fluid accumulation** in alveoli before infection resolution [1][3]. - It involves **edema** and a lack of significant resolution, contrary to the final stages of pneumonia [3]. *Red hepatization* - This stage typically happens during the acute phase of pneumonia, where the alveoli fill with **exudate**, giving a liver-like appearance to the lung [1][3]. - It is characterized by **reddish-brown** consolidation, not the output of the terminal stage [3]. *Gray hepatization* - This phase follows red hepatization and involves the breakdown of red cells, presenting a grayish appearance, indicating ongoing inflammation [1][3]. - It does not signify resolution; patients are still in the acute infectious stage during this phase [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-712. [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. 193-194. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.

Question 415: Macrophages are converted to epithelioid cells by which cytokine?

A. TNF-α
B. TGF-β
C. IFN-γ (Correct Answer)
D. IL-4

Explanation: ***IFN-γ: A cytokine involved in classical macrophage activation*** - **Interferon-gamma (IFN-γ)** is a key cytokine produced by activated T cells and NK cells that plays a crucial role in activating macrophages and converting them into **epithelioid cells** [1]. - This conversion is essential for the formation of **granulomas**, a hallmark of chronic inflammatory responses, particularly in infections like tuberculosis [1]. *TNF-α: A cytokine involved in granuloma maintenance* - **Tumor Necrosis Factor-alpha (TNF-α)** is vital for the **formation and maintenance** of granulomas, but it is not directly responsible for the initial conversion of macrophages to epithelioid cells. - While TNF-α helps to **organize and contain** the infection within the granuloma, IFN-γ drives the phenotypic change of macrophages. *TGF-β: A cytokine involved in tissue remodeling* - **Transforming Growth Factor-beta (TGF-β)** is predominantly involved in **tissue repair, fibrosis, and immune regulation**, promoting extracellular matrix production. - It does not primarily induce the differentiation of macrophages into epithelioid cells; rather, it often plays a role in the later stages of granuloma development, contributing to **fibrotic encapsulation** [1]. *IL-4: A cytokine involved in alternative macrophage activation* - **Interleukin-4 (IL-4)** is a characteristic cytokine that drives **alternative macrophage activation (M2 pathway)**, leading to roles in allergic responses and tissue repair [1]. - The M2 phenotype is distinct from the classically activated (M1) phenotype associated with epithelioid cell formation, which is driven by IFN-γ. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 416: 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 417: Which of the following does not belong to the family of selectins?

A. P selectin
B. L selectin
C. A selectin (Correct Answer)
D. E selectin

Explanation: ***A selectin*** - ***A selectin*** is not a recognized member of the selectin family, which includes other specific types. - The known selectins are **E-selectin**, **L-selectin**, and **P-selectin**, demonstrating a distinct classification [1]. *E selectin* - E selectin is a specific type of selectin expressed on **endothelial cells** activated by cytokines [1]. - It plays a crucial role in **leukocyte adhesion** during inflammation, distinguishing it as part of the selectin family [1]. *L selectin* - L selectin is involved in the **homing** of leukocytes to lymph nodes and forms part of the selectin family [1]. - Responsible for the initial tethering and rolling of leukocytes on **venular endothelium** [1]. *P selectin* - P selectin is found on platelets and endothelial cells and is critical in the **aggregation** of platelets and leukocytes. - It is also an established member of the selectin family, involved in **inflammatory responses** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.

Question 418: Which of the following vasoactive amines is primarily involved in inflammation?

A. Histamine (Correct Answer)
B. Epinephrine
C. Norepinephrine
D. Serotonin

Explanation: ***Histamine*** - Released by **mast cells and basophils** [1], histamine plays a crucial role in the inflammatory response, causing **vasodilation** [1] and increased vascular permeability [1]. - It is a key mediator in allergic reactions and contributes to symptoms like **reddening** and **swelling** at the site of inflammation. *All* - This option incorrectly implies that **all listed substances** are vasoactive amines involved in inflammation, which is not true. - Only **histamine** is primarily related to the inflammation process among the options given [1]. *Angiotensin* - Angiotensin primarily affects **blood pressure regulation** and fluid balance, not directly involved in inflammation like histamine. - It works through the **renin-angiotensin system**, primarily altering vascular tone rather than mediating inflammatory responses. *Renin* - Renin is an enzyme that activates the **renin-angiotensin system** but does not act as a vasoactive amine in inflammation [1]. - Its role is primarily in **blood pressure regulation** and fluid homeostasis, rather than direct involvement in the inflammatory process. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85, 93-94, 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95.

Question 419: Increased vascular permeability in acute inflammation is due to what?

A. Histamine (Correct Answer)
B. IL-2
C. TGF-β
D. FGF-2

Explanation: ***Histamine*** - Histamine is a key **mediator** released during acute inflammation that causes **increased vascular permeability** by inducing **contraction of endothelial cells** [1][2]. - Its release contributes to the hallmark signs of inflammation, including **swelling** and **redness** [2]. *IL 2* - IL 2 primarily functions as a **growth factor** for T cells, not directly influencing vascular permeability in acute inflammation. - It is more involved in the **adaptive immune response** rather than in the acute phase of inflammation. *TGF beta* - TGF beta is primarily involved in **fibrosis** and **tissue repair** and does not play a direct role in increasing vascular permeability during acute phases. - It acts more as an **anti-inflammatory** cytokine rather than a pro-inflammatory mediator. *FGF* - Fibroblast growth factor (FGF) is mainly involved in **angiogenesis** and wound healing rather than direct modulation of vascular permeability during acute inflammation. - It does not contribute to **edema formation** associated with acute inflammatory responses. **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 420: Increased permeability in acute inflammation is due to all except?

A. Lytic enzymes (Correct Answer)
B. Cytokines
C. Endothelial cell contraction
D. Endothelial injury

Explanation: ***Lytic enzymes*** - **Lytic enzymes** play a role in the breakdown of tissue and are not primarily responsible for increased vascular permeability in acute inflammation [2]. - They are more involved in tissue destruction rather than facilitating permeability changes [2]. *Cytokines* - **Cytokines** are crucial mediators in the inflammatory response and increase vascular permeability by affecting endothelial function. - They promote the expression of adhesion molecules and induce other inflammatory mediators, contributing to permeability. *Endothelial injury* - **Endothelial injury** directly contributes to increased permeability by damaging the endothelial barrier, allowing fluid and proteins to leak into tissues. - It often occurs due to various insults, such as infections, toxins, and mechanical stress during inflammation. *Cell contraction* - **Cell contraction** refers to the retraction of endothelial cells, which leads to increased gaps in the endothelium and enhances permeability [1]. - This mechanism is induced by inflammatory mediators like histamine and contributes significantly to acute inflammation [1,2]. **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. 187-189. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Practice by Chapter

Acute Inflammation: Vascular Events

Practice Questions

Acute Inflammation: Cellular Events

Practice Questions

Chemical Mediators of Inflammation

Practice Questions

Chronic Inflammation

Practice Questions

Granulomatous Inflammation

Practice Questions

Systemic Effects of Inflammation

Practice Questions

Wound Healing

Practice Questions

Tissue Regeneration

Practice Questions

Fibrosis and Repair

Practice Questions

Resolution of Inflammation

Practice Questions

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