Acute and Chronic Inflammation — MCQs
Which of the following does not cause granulomatous inflammation?
The characteristic cell of a granulomatous reaction is:
Which of the following is/are characteristic features of chronic inflammation?
Which is NOT a feature of chronic inflammation?
Stellate granulomas are seen in
Which of the following is least associated with the mediation of inflammation?
Which of the following amyloid forms is seen in secondary amyloidosis associated with chronic diseases?
Which of the following is the most important infiltrate in rheumatoid arthritis?
What is the drug of choice for the treatment of acute gout in patients in whom NSAIDs are contraindicated?
Strawberry gallbladder is seen in:
Acute and Chronic Inflammation Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following does not cause granulomatous inflammation?
- A. Sarcoidosis
- B. Tuberculosis
- C. Pneumonia (Correct Answer)
- D. Histoplasmosis
Explanation: ***Pneumonia*** - **Pneumonia**, in its typical bacterial form, usually causes an **acute inflammatory response** with neutrophil infiltration in the alveoli [1], [2]. - While some atypical pneumonias can have chronic or granulomatous features, the term "pneumonia" alone generally refers to acute inflammation without granulomas. *Sarcoidosis* - **Sarcoidosis** is characterized by distinctive **non-caseating granulomas** in multiple organs, most commonly the lungs, lymph nodes, and skin [3], [4]. - The formation of these granulomas is a hallmark of the disease and is crucial for diagnosis [3]. *Tuberculosis* - **Tuberculosis** is classically characterized by the formation of **caseating granulomas** (tubercles) with central necrosis, surrounded by epithelioid macrophages and giant cells [2]. - The host immune response to *Mycobacterium tuberculosis* is primarily granulomatous, aiming to contain the infection. *Histoplasmosis* - **Histoplasmosis**, a fungal infection caused by *Histoplasma capsulatum*, often leads to the formation of **granulomas**, both caseating and non-caseating [2]. - The granulomatous response is an essential part of the host's defense mechanism against this intracellular pathogen. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701. [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. 198-200.
Question 2: The characteristic cell of a granulomatous reaction is:
- A. Plasma cell
- B. Epithelioid cell (Correct Answer)
- C. Lymphocyte
- D. Eosinophil
Explanation: ***Epithelioid cell*** - Epithelioid cells are activated **macrophages** that are a hallmark of granulomatous inflammation, forming the core of the granuloma [1]. - These cells are characterized by their large size, abundant cytoplasm, and **epithelial-like appearance**, crucial for tuberculous and other granulomatous diseases [1,2]. *Eosinophil* - Eosinophils are primarily involved in **allergic reactions** and **parasitic infections**, not granulomatous reactions. - While present in some conditions (like asthma), they do not contribute to the **formation of granulomas**. *Lymphocyte* - Lymphocytes are involved in **adaptive immunity** but are not the main cell type in granulomatous reactions. - They contribute to inflammation but do not form the characteristic structures seen in **granulomas** [1]. *Plasma cell* - Plasma cells are differentiated **B cells** responsible for producing antibodies, not associated with granulomatous inflammation. - Their roles are more aligned with humoral immunity rather than the **granulomatous response**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.
Question 3: 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 4: 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.
Question 5: Stellate granulomas are seen in
- A. Sarcoidosis
- B. Cat scratch disease (Correct Answer)
- C. Cryptococcosis
- D. Histoplasmosis
Explanation: ***Cat scratch disease*** - **Stellate granulomas** are a characteristic histological feature of **Cat scratch disease**, caused by **Bartonella henselae**. - These granulomas are composed of macrophages, lymphocytes, and neutrophils arranged in a **star-shaped or stellate pattern**, often with central necrosis. *Sarcoidosis* - Sarcoidosis is characterized by **non-caseating granulomas**, which are typically well-formed and discrete [2], [3]. - However, they do not usually have the distinct **stellate (star-shaped) morphology** seen in cat scratch disease [3]. *Cryptococcosis* - Cryptococcosis is a fungal infection that typically presents with **granulomas containing yeasts** within macrophages. - The granulomas formed in cryptococcosis are not classically described as **stellate granulomas**. *Histoplasmosis* - Histoplasmosis is another fungal infection that can cause granuloma formation, usually with **caseous necrosis** similar to tuberculosis [1]. - The granulomas in histoplasmosis do not exhibit the **stellate architectural pattern** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 717. [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. The Lung, pp. 700-701.
Question 6: 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 7: Which of the following amyloid forms is seen in secondary amyloidosis associated with chronic diseases?
- A. Amyloid light chain
- B. ATTR
- C. Amyloid beta (Aβ)
- D. AA amyloid (Correct Answer)
Explanation: ***Amyloid Associated Protein*** - This form is particularly linked with **secondary amyloidosis**, commonly seen in conditions like chronic infections or inflammatory diseases [1]. - It is derived from **serum amyloid A (SAA)** protein, which elevates in response to inflammation, leading to the accumulation of amyloid fibrils [1][2]. *ATTR* - Stands for **transthyretin amyloidosis**, associated with genetic mutations or aging, not typically related to chronic secondary causes. - Involves proteins that primarily affect the **heart** and **nervous system**, particularly distinct from secondary amyloid deposits. *Amyloid light chain* - Primarily associated with **primary amyloidosis (AL)**, resulting from monoclonal plasma cell disorders, differing from the context of chronic diseases. - Characterized by deposition of **light chains from immunoglobulins**, rather than the **serum amyloid A** found in secondary amyloidosis [1]. *Beta 2 Amyloid* - Refers to **beta-amyloid** peptide associated with **Alzheimer's disease**, unrelated to secondary amyloidosis or chronic inflammatory states. - It is associated more with **neurological** pathologies, specifically the formation of plaques, rather than systemic amyloid deposition. **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. 136-140. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 267-268.
Question 8: Which of the following is the most important infiltrate in rheumatoid arthritis?
- A. Dendritic cells
- B. CD4+ Helper cells
- C. Macrophages (Correct Answer)
- D. Neutrophils
Explanation: ***Macrophages*** - **Macrophages** are crucial in rheumatoid arthritis synovium due to their role in producing **pro-inflammatory cytokines** like TNF-̑, IL-1, and IL-6, which drive joint destruction [1], [2]. - They also contribute to the **pannus formation** and degrade cartilage and bone through the release of proteases [1]. *Dendritic cells* - While present in the synovium, **dendritic cells primarily function as antigen-presenting cells**, initiating T-cell responses. - Their direct contribution to tissue damage and chronic inflammation is less prominent than that of macrophages. *CD4+ Helper cells* - **CD4+ T helper cells** orchestrate the immune response by activating B cells and macrophages, but they are not the primary effector cells causing direct tissue damage [3]. - They secrete cytokines that promote inflammation but do not directly participate in tissue degradation. *Neutrophils* - **Neutrophils are abundant in the synovial fluid** during acute flares, contributing to inflammation and breakdown of cartilage through the release of enzymes. - However, their role in the chronic, sustained synovial inflammation and tissue destruction characteristic of RA is less significant compared to macrophages. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 677-678. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.
Question 9: What is the drug of choice for the treatment of acute gout in patients in whom NSAIDs are contraindicated?
- A. Colchicine (Correct Answer)
- B. Allopurinol
- C. Paracetamol
- D. Febuxostat
Explanation: ***Colchicine*** * **Colchicine** is a highly effective anti-inflammatory agent for acute gout flares, particularly when initiated early in the attack. * It is often the drug of choice when **NSAIDs are contraindicated** due to renal, gastrointestinal, or cardiovascular issues. *Allopurinol* * **Allopurinol** is a **xanthine oxidase inhibitor** used for long-term **gout prophylaxis** by reducing uric acid levels, not for acute attacks. * Initiating allopurinol during an acute flare can sometimes *exacerbate* the attack by transiently shifting uric acid levels. *Febuxostat* * **Febuxostat** is another **xanthine oxidase inhibitor** used for **chronic management of hyperuricemia** in gout patients, similar to allopurinol. * It is not indicated for the **acute treatment of gout** due to its mechanism of action, which focuses on reducing uric acid production over time. *Paracetamol* * **Paracetamol (acetaminophen)** is an **analgesic** and **antipyretic** but possesses very limited anti-inflammatory properties. * It is generally **ineffective** for the intense inflammatory pain and swelling characteristic of an acute gout attack.
Question 10: Strawberry gallbladder is seen in:
- A. Porcelain gallbladder
- B. Cholesterosis (Correct Answer)
- C. Necrosis of gallbladder
- D. Gallbladder carcinoma
Explanation: ***Cholesterosis*** - **Cholesterosis** of the gallbladder is often referred to as \"**strawberry gallbladder**\" due to the presence of **cholesterol deposits** within the gallbladder mucosa, which appear as yellowish spots against the red mucosal lining. - This characteristic gross pathological appearance results from **lipid-laden macrophages** (foam cells) in the lamina propria, creating a stippled yellow appearance on the red background. - It is a **benign condition** typically discovered incidentally and is associated with cholesterol metabolism disorders. *Porcelain gallbladder* - **Porcelain gallbladder** is characterized by extensive **calcification** of the gallbladder wall, making it rigid and porcelain-like on imaging and gross examination. - It is associated with a higher risk of **gallbladder carcinoma** and does not involve the \"strawberry\" appearance or cholesterol deposits. *Necrosis of gallbladder* - **Necrosis of the gallbladder** implies tissue death, typically due to severe inflammation (e.g., **gangrenous cholecystitis**) or ischemia. - This condition presents with severe acute symptoms, perforation risk, and does not produce the characteristic \"strawberry\" appearance. *Gallbladder carcinoma* - **Gallbladder carcinoma** is a malignant tumor arising from the gallbladder epithelium, often associated with chronic cholecystitis and cholelithiasis. - It presents as a **mass lesion** or diffuse wall thickening and does not produce a \"strawberry\" appearance.
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