Resolution of Inflammation — MCQs
Which of the following helps in cell-to-cell adhesion?
True about Crohn's disease except
Which of the following statements about wound healing is false?
What is the mechanism of secondary healing?
Which mediators are involved in the resolution of inflammation?
Rolling of leucocytes on endothelial cells is mediated by which of the following proteins?
Which statement about macrophages is incorrect?
Arrange the following cellular events of inflammation in the correct sequence: 1. Rolling 2. Cytokine-mediated integrin activation 3. Adhesion 4. Migration
Which of the following statements about C-reactive protein (CRP) is true?
Which feature is most consistent with chronic inflammation?
Resolution of Inflammation Indian Medical PG Practice Questions and MCQs
Question 1: 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 2: True about Crohn's disease except
- A. Transmural
- B. Recurrence is more common
- C. Rectum is involved (Correct Answer)
- D. Fissures are formed
Explanation: ***Rectum is involved*** - While Crohn's disease can affect any part of the gastrointestinal tract from mouth to anus, **rectal involvement is much less common** and often spares the rectum in typical cases, especially when compared to ulcerative colitis. [1] - The disease typically exhibits **skip lesions**, meaning there are healthy segments of the bowel between affected areas, and the rectum is frequently one of these spared regions. [1] *Transmural* - Crohn's disease is characterized by **transmural inflammation**, meaning the inflammation extends through all layers of the bowel wall, from the mucosa to the serosa. [1] - This transmural involvement can lead to complications such as **fistulas, strictures, and abscesses**. *Recurrence is more common* - **Recurrence after surgery is very common** in Crohn's disease, with many patients experiencing disease relapse within a few years post-operation. - This high recurrence rate often necessitates ongoing medical management and sometimes further surgical interventions. *Fissures are formed* - Due to the **transmural inflammation** and chronic nature of Crohn's disease, patients often develop **fissures**, which are deep cracks or excoriations, particularly in the perianal area. - These fissures can be quite painful and complicated by **fistula formation** or abscesses.
Question 3: 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 4: 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 5: 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 6: Rolling of leucocytes on endothelial cells is mediated by which of the following proteins?
- A. Integrins
- B. Transferrin
- C. PECAM-1
- D. Selectins (Correct Answer)
Explanation: **Selectins** - **Selectins** mediate the initial, weak and transient adhesion of **leukocytes** to the **endothelial cells** lining blood vessels [1]. - This interaction slows down the leukocytes, causing them to **roll** along the vascular endothelium as a prerequisite for **extravasation** [1]. *Integrins* - **Integrins** are responsible for the **firm adhesion** of leukocytes to endothelial cells, but not the rolling [1]. - They bind to **ICAM-1 (intercellular adhesion molecule-1)** on endothelial cells, leading to stable arrest of the leukocyte [1]. *PECAM-1* - **PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1)** plays a role in **diapedesis** or **transmigration**, the movement of leukocytes *through* the endothelial cell junctions [1]. - It facilitates the passage of the leukocyte by interacting with PECAM-1 on the endothelial cells, but does not mediate rolling [1]. *Transferrin* - **Transferrin** is an iron-binding protein found in blood plasma that regulates free **iron levels** in the body. - It is crucial for **iron transport** and metabolic processes but has no direct role in leukocyte adhesion or rolling on endothelial cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.
Question 7: 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 8: Arrange the following cellular events of inflammation in the correct sequence: 1. Rolling 2. Cytokine-mediated integrin activation 3. Adhesion 4. Migration
- A. 1,2,3,4 (Correct Answer)
- B. 3,4,1,2
- C. 2,1,4,3
- D. 4,1,2,3
Explanation: ***1,2,3,4*** - The correct sequence of cellular events for leukocyte recruitment during inflammation begins with **rolling** [1], followed by **cytokine-mediated integrin activation** [2], then firm **adhesion** to the endothelium [1], and finally **migration** (diapedesis) into the tissues [3]. - This step-by-step process ensures effective targeting of leukocytes to the site of injury or infection [1]. *3,4,1,2* - This sequence is incorrect as **adhesion** cannot occur before **rolling**, and **migration** is the final step after adhesion, not an early one. - **Cytokine-mediated integrin activation** must precede firm adhesion [1]. *2,1,4,3* - This order is incorrect because **rolling** (1) is the initial interaction that allows leukocytes to slow down on the endothelium [2], and it occurs before **cytokine-mediated integrin activation** (2) which strengthens the binding. - **Migration** (4) is also misplaced as it should be the last step after firm adhesion (3). *4,1,2,3* - This sequence is incorrect as **migration** (4) is the last step in the process, not the first. - **Rolling** (1) initiates the process by transiently interacting with endothelial cells, followed by activation and adhesion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [2] 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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.
Question 9: Which of the following statements about C-reactive protein (CRP) is true?
- A. It is detected by agglutination test.
- B. It is raised in acute pneumococcal infection. (Correct Answer)
- C. It is an antibody.
- D. It is detected by precipitation with carbohydrate.
Explanation: ***It is raised in acute pneumococcal infection.*** - **C-reactive protein (CRP)** is an **acute-phase reactant** whose levels rise rapidly and significantly in response to inflammation and infection [1]. - **Pneumococcal infection** (e.g., pneumonia) is an acute bacterial infection that triggers a strong inflammatory response, leading to increased CRP synthesis by the liver [1]. *It is detected by agglutination test.* - While some tests for CRP can involve **agglutination assays**, this statement describes a method of detection rather than a fundamental property or primary clinical utility of CRP itself. - CRP is more commonly quantified via methods like **nephelometry** or **turbidimetry** in modern laboratories due to their higher sensitivity. *It is an antibody.* - **CRP** is a **pentameric protein** produced by the liver, belonging to the **pentraxin family** of proteins. - It functions as a non-specific innate immune molecule, primarily involved in binding to damaged cells and pathogens to facilitate their clearance, but it does **not possess antigen-specific binding** characteristic of antibodies. *It is detected by precipitation with carbohydrate.* - **CRP** was originally named for its ability to precipitate the **C-polysaccharide** of *Streptococcus pneumoniae*. - However, this historical observation describes a specific interaction rather than the general method by which CRP is clinically detected or its primary biological function. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 109-111.
Question 10: Which feature is most consistent with chronic inflammation?
- A. Hyperemia
- B. Vasodilation
- C. Fibrosis (Correct Answer)
- D. Edema
Explanation: ***Fibrosis*** - **Fibrosis** is the excessive accumulation of connective tissue, often seen as a **scarring process**, which is a hallmark of chronic inflammation as the body attempts to repair damaged tissue. [1] - Unlike acute inflammation, which is characterized by immediate vascular changes and exudation, chronic inflammation involves persistent tissue injury and attempts at repair, leading to **fibroblast proliferation** and collagen deposition. [2] *Hyperemia* - **Hyperemia** is an active process involving increased blood flow to a tissue, which causes it to redden. - It is a prominent feature of **acute inflammation**, contributing to rubor (redness) and calor (heat). *Vasodilation* - **Vasodilation**, the widening of blood vessels, is a key component of the **acute inflammatory response**. - It increases blood flow to the inflamed area, contributing to the cardinal signs of **redness and warmth**. *Edema* - **Edema** refers to the accumulation of excess fluid in the interstitial spaces, often due to increased vascular permeability. - While it can occur in both acute and chronic inflammation, it is a particularly prominent and early feature of **acute inflammation** as fluid rushes to the site of injury. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 103-104. [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. 194-195.
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