Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 421: First cell to migrate into a wound due to chemotaxis to start the process of wound healing is -

A. Lymphocyte
B. Macrophage
C. Platelet
D. Neutrophil (Correct Answer)

Explanation: ***Neutrophil*** - Neutrophils are the **first responders** in the wound healing process, rapidly migrating to the site due to **chemotactic signals** [1,2]. - Their primary role includes **phagocytosing pathogens** and debris, facilitating the subsequent healing phases. *Lymphocyte* - Lymphocytes typically arrive later in the healing process and are mainly involved in **immune response** rather than initial wound healing. - They play a significant role in **adaptive immunity** but do not participate in the **early inflammatory phase**. *Platelet* - While platelets aggregate at the wound site and are crucial for **clot formation**, they do not migrate into the wound through chemotaxis like neutrophils [1]. - Their primary function is to initiate the **hemostatic response** rather than directly phagocytosing debris. *Macrophage* - Macrophages are important for **later stages** of wound healing, clearing debris and coordinating tissue repair, but they arrive after neutrophils. - They are involved in the **remodeling phase** and are not the first cells to respond to the wound. **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. 188-189. [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 422: The principal cell in a granuloma is

A. Lymphocyte
B. Histiocyte (Correct Answer)
C. Giant cell
D. Langerhans

Explanation: ***Histiocyte*** - Histiocytes are the principal **macrophages** in a granuloma, playing a key role in the **immune response** [1][2]. - They are responsible for phagocytosis and the formation of **epithelioid cells**, which are typical of granulomatous inflammation [1]. *Giant cell* - While giant cells are present in granulomas, they are formed from the **fusion of macrophages** and are not the principal cell type [1]. - Their presence signifies a chronic inflammatory response but does not define the granuloma itself. *Langhans* - Langhans giant cells are a specific type of giant cell that may be found in granulomas, particularly in conditions like **tuberculosis** [1]. - They are characterized by a **multi-nucleated** appearance but are not the principal cell in granuloma formation [1]. *Lymphocyte* - Lymphocytes are part of the **adaptive immune response** and may be present in granulomas, but they are not the main cell type [1][3]. - Their role is more of a supportive function, typically acting later in the inflammatory response rather than in granuloma formation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [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. 198-200. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 360-362.

Question 423: All of the following are mediators of acute inflammation, except which one?

A. Kallikrein
B. Angiotensin (Correct Answer)
C. Prostaglandin E2
D. C3a

Explanation: ***Angiotensin*** - Angiotensin is primarily involved in **blood pressure regulation** and **fluid balance**, not in mediating acute inflammation [1]. - It does not participate in the **vascular or cellular responses** characteristic of acute inflammatory processes. *Prostaglandin E2* - Prostaglandin E2 is a key **mediator of inflammation** [1][2], promoting vasodilation and increasing **vascular permeability** [3]. - It contributes to pain and fever during the **inflammatory response** [1]. *Kallikrein* - Kallikrein plays a significant role in activating the **bradykinin** system, which enhances vascular permeability during inflammation. - It is involved in the **kallikrein-kinin system**, thus participating actively in acute inflammatory processes. *C 3a* - C 3a is a fragment of the complement system involved in the **anaphylatoxin** response, promoting inflammation [4]. - It contributes to **chemotaxis** [1] and enhances vascular permeability [4], making it a mediator in acute inflammation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100.

Question 424: Which of the following is not a stage in the progression of community-acquired pneumonia?

A. Liquefaction necrosis (Correct Answer)
B. Grey hepatization
C. Edema
D. Red hepatization

Explanation: ***Liquefaction necrosis*** - **Liquefaction necrosis** is a type of necrosis that typically results from **bacterial infection** or **ischemia** of brain tissue, where dead cells digest and form a viscous fluid. - While pneumonia involves inflammation and tissue damage, widespread **liquefaction necrosis** of lung tissue is **not a characteristic stage** in its typical progression. *Edema* - The **edema stage** (also called congestion) is the **first stage** of lobar pneumonia, characterized by vascular engorgement, intra-alveolar fluid, and scattered neutrophils [1], [2]. - This stage involves the outpouring of a proteinaceous exudate and often some red blood cells and neutrophils into the alveolar spaces [2]. *Grey hepatization* - The **grey hepatization stage** follows red hepatization, marked by the breakdown of red blood cells and the accumulation of fibrin and neutrophils [1]. - During this stage, the lung appears firmer and grayish due to the breakdown of capillaries and the continued presence of fibrin-rich exudate [1], [2]. *Red hepatization* - The **red hepatization stage** is the **second stage** of lobar pneumonia, where the lung appears red and firm due to massive extravasation of red blood cells, neutrophils, and fibrin into the alveoli [1], [2]. - This stage reflects an intense inflammatory response, leading to consolidation of the lung tissue [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-715. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.

Question 425: Which of the following statements about acute rheumatic fever is false?

A. Focal myocardial fiber necrosis
B. Lymphocytic myocarditis
C. Microthrombi in arteriole (Correct Answer)
D. Aschoff nodule in myocardium

Explanation: ***Microthrombi in arteriole*** - This statement is correct; **microthrombi** are not typically associated with acute rheumatic fever, making this option false. - Acute rheumatic fever primarily involves **immune-mediated processes** rather than direct thrombosis in small vessels [1]. *Focal myocardial fiber necrosis* - In acute rheumatic fever, **focal necrosis** is not a primary characteristic; rather, the condition may show **myocarditis** without extensive necrosis. - Other cardiac manifestations include **Aschoff bodies**, which are collections of immune cells rather than necrotic myocardial tissue [1]. *Aschoff nodule in mycoacardium* - **Aschoff nodules** are pathognomonic for rheumatic fever, occurring in the heart tissue as a result of the autoimmune response [1]. - They are areas of granulomatous inflammation, not typically associated with straightforward necrosis but rather with a reaction to the preceding streptococcal infection [1]. *Lymphocytic myocarditis* - Acute rheumatic fever can lead to **lymphocytic infiltration** in the myocardium, but describing it as myocarditis simplifies the broader range of findings seen in the disease [1]. - The involvement often includes a mixed inflammatory infiltrate, not solely lymphocytic [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567.

Question 426: In acute inflammation, due to the contraction of the endothelial cell cytoskeleton, which of the following occurs?

A. Early transient increase in permeability (Correct Answer)
B. Early permanent increase in permeability
C. Delayed permanent increase in permeability
D. Delayed transient increase in permeability

Explanation: ***Early transient increase in permeability*** - During acute inflammation, the **contraction of the endothelial cell cytoskeleton** leads to a rapid and temporary increase in vascular permeability [1]. - This process allows for the **exudation of fluid and plasma proteins** [1][2], contributing to the inflammatory response. *Early permanent increase in permeability* - Permanent changes in permeability do not occur early; they typically result from **severe injury** or prolonged inflammation. - Early events in inflammation are characterized by a **transient** rather than a permanent change [1]. *Delayed permanent increase in permeability* - Delayed permeability increases occur later in the inflammatory process due to **endothelial cell injury**, not the initial contraction. - This concept relates to more chronic inflammatory processes rather than **acute inflammation**. *Delayed transient increase in permeability* - Delayed transient increases are not typical and **can lead to confusion** regarding cellular responses in acute vs. chronic inflammation. - This oes not accurately represent the **initial response** during 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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85.

Question 427: 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 428: Which of the following is characteristically associated with sarcoidosis?

A. Asteroid bodies
B. Granulomatous inflammation
C. Schaumann bodies
D. Non-caseating granulomas (Correct Answer)

Explanation: ***Grossly bullous appearance*** - This feature is **not typically seen** in sarcoidosis; instead, sarcoidosis usually presents with various tissue infiltrations [1]. - Characteristically, sarcoidosis features **granulomas**, not a bullous skin manifestation [1]. *Asteroid bodies* - Asteroid bodies are **star-shaped inclusions** found within the non-caseating granulomas seen in sarcoidosis. - Their presence supports the diagnosis, indicating **typical histological findings** of the disease. *Non caseating granulomas* - Sarcoidosis is definitively characterized by the presence of **non-caseating granulomas**, which are key diagnostic features [1]. - These granulomas differentiate sarcoidosis from other granulomatous diseases, like tuberculosis [2]. *Schaumann bodies* - Schaumann bodies are **calcium-laden** structures found within the granulomas in sarcoidosis, further supporting the diagnosis. - The presence of these bodies alongside non-caseating granulomas is a classic histopathological finding in sarcoidosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 429: Which of the following is least associated with the mediation of inflammation?

A. Prostaglandins/Interleukins
B. Myeloperoxidase
C. IFN (Correct Answer)
D. TNF

Explanation: ***Myeloperoxidase*** - Myeloperoxidase is primarily an enzyme involved in the **oxidative burst** of neutrophils, not a classic mediator of inflammation. - It plays a role in **microbial killing** but does not directly participate in inflammation mechanisms like cytokines do. *IFN* - Interferons (IFNs) are cytokines crucial in immune responses and have roles in **inflammatory signaling** [1]. - They are produced in response to **viral infections** and activate immune cells, thus mediating inflammation. *Prostaglandins/Interleukins* - Prostaglandins are lipid compounds that promote **vasodilation** and **sensitize pain receptors**, key factors in the inflammatory process [1][2]. - Interleukins are a diverse group of cytokines that play significant roles in **cell signaling** during inflammation [1][3]. *TNF* - Tumor Necrosis Factor (TNF) is a major pro-inflammatory cytokine crucial in promoting systemic inflammation [1]. - It is involved in the activation of other inflammatory mediators and is significant in numerous inflammatory diseases [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 99-100.

Question 430: Who described the four classical features of inflammation?

A. Aulus Cornelius Celsus (Correct Answer)
B. Hippocrates
C. Aristotle
D. Galen

Explanation: ***Aulus Cornelius Celsus*** - Credited with describing the **four classical features of inflammation**: redness, heat, swelling, and pain [1]. - His work **De Medicina** laid the groundwork for understanding inflammation in clinical settings. *Aristotle* - Although a significant figure in early medicine and philosophy, he did not specifically describe the features of inflammation. - His contributions focused more on **natural philosophy** rather than detailed clinical observations of inflammation. *Galen* - A prominent physician whose works expanded upon earlier knowledge, but he did not delineate the four classical features of inflammation. - His emphasis was on **anatomy and physiology**, which laid a foundation for later medical understanding, but not specifically on inflammation. *Hippocrates (contributed to medical knowledge but not specific to inflammation)* - Known as the "Father of Medicine," Hippocrates made pivotal contributions to medicine but did not explicitly describe the classical features of inflammation. - His teachings laid the foundations for **clinical observation** but lacked detail about inflammation's characteristics as outlined by Celsus. **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. 185-186.

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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