Acute Inflammation: Cellular Events — MCQs
Which of the following helps in cell-to-cell adhesion?
Most effective bactericidal system within phagocytes is-
A major step in the pathogenesis of listeriosis is?
A patient with chronic granulomatous disease is most likely to have a defect in which enzyme?
What is the main feature of chemotaxis as observed in white blood cells?
Arrange the following cellular events of inflammation in the correct sequence: 1. Rolling 2. Cytokine-mediated integrin activation 3. Adhesion 4. Migration
Increased vascular permeability in acute inflammation is due to what?
Which of the following is/are characteristic features of chronic inflammation?
Which of the following statements about C-reactive protein (CRP) is true?
Which statement about macrophages is incorrect?
Acute Inflammation: Cellular Events 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: Most effective bactericidal system within phagocytes is-
- A. Cationic basic protein mediated
- B. Reactive oxygen metabolite mediated (Correct Answer)
- C. Lysozyme mediated
- D. Lactoferrin mediated
Explanation: ***Reactive oxygen metabolite mediated*** - The production of **reactive oxygen metabolites** (like superoxide, hydrogen peroxide, and hydroxyl radicals) through the **respiratory burst** is a highly potent mechanism for killing phagocytosed bacteria. - These highly reactive molecules cause **oxidative damage** to bacterial components, leading to their degradation and death. *Cationic basic protein mediated* - **Cationic proteins** (e.g., defensins) have antimicrobial properties by damaging bacterial membranes, but they are generally less potent than reactive oxygen species in overall bacterial killing within phagocytes. - While important, they contribute to a broader array of antimicrobial mechanisms but are not considered the *most effective* single system. *Lysozyme mediated* - **Lysozyme** primarily targets bacterial **peptidoglycan**, breaking down bacterial cell walls, especially in gram-positive bacteria. - It is an important antimicrobial enzyme, but its effectiveness is limited against many gram-negative bacteria with outer membranes and it is generally less destructive than the radical-forming reactive oxygen species. *Lactoferrin mediated* - **Lactoferrin** primarily acts by **chelating iron**, which is an essential nutrient for bacterial growth, thereby inhibiting bacterial proliferation. - While important for bacteriostasis, its direct bactericidal activity is often limited compared to the direct damaging effects of reactive oxygen species.
Question 3: A major step in the pathogenesis of listeriosis is?
- A. The antiphagocytic activity of the L. monocytogenes capsule
- B. The release of hyaluronidase by L. monocytogenes, which contributes to its dissemination from local sites
- C. The formation of antigen-antibody complexes with resultant complement activation and tissue damage
- D. The survival and multiplication of L. monocytogenes within mononuclear phagocytes and host epithelial cells (Correct Answer)
Explanation: ***The survival and multiplication of L. monocytogenes within mononuclear phagocytes and host epithelial cells*** - **Listeria monocytogenes** is a **facultative intracellular bacterium** that primarily infects and replicates within **macrophages** and epithelial cells. This intracellular survival helps it evade the host immune system and spread from cell to cell. - Its ability to induce its own uptake (**internalin-mediated uptake**), escape the phagosome (via **listeriolysin O**), and move within the cytoplasm (via **ActA protein** for actin polymerization) are key to its pathogenesis and evasion of humoral immunity. *The antiphagocytic activity of the L. monocytogenes capsule* - While some bacteria use capsules for antiphagocytic activity, **Listeria monocytogenes** is not known for having a significant capsule as a primary virulence factor. - Its main strategy for evading phagocytosis involves **intracellular survival** rather than external camouflage. *The release of hyaluronidase by L. monocytogenes, which contributes to its dissemination from local sites* - **Hyaluronidase** is an enzyme produced by some bacteria to break down hyaluronic acid in connective tissue, aiding in spread, but it is not a major virulence factor for **Listeria monocytogenes**. - Listeria primarily disseminates through its **intracellular movement** and cell-to-cell spread, rather than extensive extracellular enzyme activity for tissue degradation. *The formation of antigen-antibody complexes with resultant complement activation and tissue damage* - This mechanism describes **Type III hypersensitivity reactions**, which involve the deposition of immune complexes leading to inflammation and tissue damage. - While immune responses occur during listeriosis, this particular mechanism is not a major or primary step in the **pathogenesis** of the initial infection and spread of **Listeria monocytogenes**.
Question 4: A patient with chronic granulomatous disease is most likely to have a defect in which enzyme?
- A. Superoxide dismutase
- B. Catalase
- C. Myeloperoxidase
- D. NADPH oxidase (Correct Answer)
Explanation: ***NADPH oxidase*** - **Chronic granulomatous disease (CGD)** is characterized by a defect in **NADPH oxidase**, an enzyme critical for the formation of **superoxide radicals**. - Without a functional **NADPH oxidase**, phagocytes cannot mount a **respiratory burst** to kill certain bacteria and fungi, leading to recurrent infections and granuloma formation. *Superoxide dismutase* - This enzyme converts **superoxide** into **hydrogen peroxide** and oxygen, an essential step in detoxifying reactive oxygen species. - A defect here would lead to an accumulation of superoxide, but is not the primary cause of the susceptibility to specific infections seen in CGD. *Catalase* - **Catalase** breaks down **hydrogen peroxide** into water and oxygen, protecting cells from oxidative damage. - While important for reducing oxidative stress, its deficiency is not responsible for the impaired microbial killing in CGD, rather, it's involved in the *breakdown* of products generated by NADPH oxidase. *Myeloperoxidase* - **Myeloperoxidase (MPO)** combines **hydrogen peroxide** with chloride ions to produce **hypochlorous acid (bleach)**, a potent microbicidal agent. - Although crucial for killing, MPO can only function if NADPH oxidase first produces sufficient hydrogen peroxide; thus, its deficiency presents differently than CGD.
Question 5: What is the main feature of chemotaxis as observed in white blood cells?
- A. Increased random movement of neutrophils
- B. Increased adhesiveness to intima
- C. Increased phagocytosis
- D. Unidirectional locomotion of neutrophils (Correct Answer)
Explanation: ***Unidirectional locomotion of neutrophils*** - **Chemotaxis** refers to the **directional movement** of cells, such as neutrophils, towards a chemical attractant. - This process is crucial for recruiting immune cells to sites of infection or inflammation. *Increased random movement of neutrophils* - While neutrophils do exhibit random movement, **chemotaxis** specifically describes **directed movement** along a chemical gradient, not merely an increase in random motion. - **Random movement** without a specific direction does not effectively guide immune cells to a specific target. *Increased adhesiveness to intima* - **Adhesion to the intima** (endothelial cells) is an initial step in the process of leukocyte extravasation, allowing cells to roll and stick to vessel walls. - However, it is primarily mediated by adhesion molecules and is distinct from the **directional migration** defined by chemotaxis. *Increased phagocytosis* - **Phagocytosis** is the process by which cells engulf pathogens or cellular debris. - While essential for immune function, it is a separate function that occurs **after** the cell has migrated to its target via chemotaxis.
Question 6: 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 7: 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 8: Which of the following is/are characteristic features of chronic inflammation?
- A. Infiltration of neutrophils
- B. Tissue fibrosis and lymphocyte infiltration (Correct Answer)
- C. Increased blood flow (hyperemia)
- D. Presence of fluid accumulation (edema) in tissues
Explanation: ***Tissue fibrosis and lymphocyte infiltration*** - **Chronic inflammation** is characterized by the persistent presence of lymphocytes, plasma cells, and macrophages as the predominant inflammatory cells [1]. - **Tissue fibrosis** (scarring) and destruction are hallmarks of chronic inflammation as the body attempts to repair ongoing damage, often leading to loss of organ function [1]. *Infiltration of neutrophils* - **Neutrophils** are the primary inflammatory cells seen in **acute inflammation**, being the first responders to injury or infection [2]. - Their presence typically signifies an active, recent inflammatory process, usually resolving within hours to days. *Increased blood flow (hyperemia)* - **Hyperemia** is a classic sign of **acute inflammation**, contributing to the **redness and warmth** observed at the site. - While some vascular changes can persist in chronic inflammation, pronounced and primary hyperemia is characteristic of the acute phase. *Presence of fluid accumulation (edema) in tissues* - **Edema** primarily results from increased vascular permeability, a key feature of **acute inflammation**, causing swelling [2]. - While some edema may be present in chronic inflammation due to persistent vascular leakage, it is a dominant feature of acute inflammatory responses. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 109-110. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 103-104.
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 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.
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