Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 431: Granuloma is seen in all conditions except which one?

A. Churg-strauss disease
B. Wegener's granulomatosis
C. Giant cell arteritis
D. Microscopic polyangiitis (Correct Answer)

Explanation: ***Microscopic polyangitis*** - This condition is characterized by **necrotizing vasculitis** without granuloma formation, primarily affecting small vessels [1]. - It typically presents with symptoms such as **glomerulonephritis** and systemic symptoms, distinct from granulomatous diseases. *Giant cell arteritis* - This condition presents with **giant cell formation** and can cause headaches and visual disturbances, featuring granulomatous inflammation [3]. - It predominantly affects older adults and involves the **temporal arteries**, leading to potential complications like blindness. *Churg-strauss disease* - Also known as **eosinophilic granulomatosis with polyangiitis**, this disease exhibits **granulomatous inflammation** along with asthma and eosinophilia. - It typically affects medium to small-sized vessels, leading to organ damage. *Wegner's granulomatosis* - Currently known as **granulomatosis with polyangiitis**, it features **granulomas in the respiratory tract** and affects the kidneys [2]. - Patients may show upper respiratory symptoms like sinusitis, alongside a potential for rapid kidney decline. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 516-517.

Question 432: The most characteristic cells found in a granuloma are?

A. Mast cells
B. Lymphocytes
C. Giant cells (Correct Answer)
D. Neutrophils

Explanation: ***Lymphocytes*** - Lymphocytes are crucial components of granulomas, involved in the immune response and chronic inflammation [1]. - They play a key role in activating macrophages, which form the central structure of the granuloma [1]. *Mast cells* - These cells are primarily involved in allergic responses and the **release of histamine**, not in granuloma formation. - They are not typically a **dominant cell type** seen in granulomatous inflammation. *Neutrophilis* - Neutrophils are usually associated with **acute inflammation** and are not the primary cells in a granuloma, which is characterized by chronic inflammation. - Their presence is more typical in **abscesses** or early inflammatory responses rather than in mature granulomas. *Giant cells* - While giant cells can be present in granulomas, they are formed from the fusion of macrophages and are a secondary feature rather than the most frequently found cells [1][2]. - Granulomas are primarily composed of **lymphocytes and macrophages**, making giant cells less predominant [1]. **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, pp. 360-362.

Question 433: Granulation tissue is replaced by connective tissue in what stage of wound healing?

A. 7 days (Correct Answer)
B. 14 days
C. 21 days
D. 1 month

Explanation: ***21 days*** - Granulation tissue formation is prominent until about **21 days**, after which it starts to reorganize into fibrous connective tissue [1][2]. - In this stage, collagen deposition increases, contributing to **wound strength** and integrity [2]. *1 month* - By this time, connective tissue maturation continues but the primary transition from granulation tissue typically completes by **21 days** [2]. - It may lead to overestimation of healing progression as remodeling may still be ongoing. *14 days* - At **14 days**, granulation tissue is still present and not yet fully replaced by connective tissue [1]. - This stage primarily involves **vascularization** and **inflammatory responses**, not complete fibrous change [1]. *7 days* - This early phase is characterized by **hemostasis** and **inflammation**, with granulation tissue just beginning to form [1]. - Significant connective tissue replacement has not yet occurred, as the wound healing process is still at the initial stages. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 434: Skin lesions in meningococcal meningitis are due to

A. Endotoxin (Correct Answer)
B. Direct vascular damage
C. Bacterial exotoxin
D. Immune-mediated reaction

Explanation: ***Endotoxin*** - The skin lesions (petechiae and purpura) seen in **meningococcal meningitis** are primarily caused by the release of **endotoxin** from *Neisseria meningitidis* [1]. - Endotoxin, specifically **lipopolysaccharide (LPS)**, activates the coagulation cascade and triggers a systemic inflammatory response, leading to vascular damage, microthrombosis, and hemorrhage in the skin [1], [2]. *Bacterial exotoxin* - **Exotoxins** are proteins secreted by bacteria that can cause a wide range of effects, but are not the primary cause of the characteristic hemorrhagic skin lesions in meningococcal meningitis. - While some bacterial infections involve exotoxins causing skin manifestations (e.g., scarlet fever), the severe purpuric rash of meningococcal disease is specifically linked to endotoxin. *Immune-mediated reaction* - While the host immune response plays a role in the overall pathology of meningococcal disease, the initial and prominent skin lesions are directly due to the **toxic effects of endotoxin** rather than purely immune-complex deposition [5]. - Immune-mediated reactions usually involve antigen-antibody complexes or cell-mediated responses, which manifest differently from the rapid hemorrhagic changes seen here [5]. *Direct vascular damage* - While there is **direct damage to blood vessels**, this damage is *mediated by endotoxin* [3]. - Endotoxin causes endothelial cell injury, leading to increased vascular permeability, platelet aggregation, and the formation of thrombi, resulting in the visible skin lesions [3], [4]. **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. 63-64. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 708-709. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 671-672. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 142. [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. 65-66.

Question 435: 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 436: Epithelioid granulomatous lesions are found in all of the following diseases except:

A. TB
B. Sarcoidosis
C. Berylliosis
D. Pneumocystis jirovecii (Correct Answer)

Explanation: ***Pneumocystis carinii*** - Epithelioid granulomatous lesions are **not associated** with Pneumocystis carinii (now called **Pneumocystis jirovecii** in humans), which causes opportunistic infections without granulomatous response [1]. - Typically presents as **interstitial pneumonia** with foamy alveolar exudates rather than granulomatous inflammation [1]. *Berylliosis* - This condition is characterized by **granulomatous lung disease**, particularly with **epithelioid granulomas** in the lung tissue [2]. - It's caused by exposure to **beryllium**, often seen in occupational settings [2]. *TB* - Tuberculosis (TB) is well-known for inducing **caseating granulomas**, but it can also show **epithelioid granulomas** in active disease [3]. - Typically starts in the lungs and can disseminate, forming granulomas in various organs [3]. *Sarcoidosis* - Sarcoidosis is defined by the presence of **non-caseating epithelioid granulomas** primarily in the lungs but can affect other organs too [2]. - Commonly linked with **bilateral hilar lymphadenopathy** and respiratory symptoms. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 318-319. [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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321.

Question 437: Vasodilation in acute inflammation is first shown by which blood vessels?

A. Venules
B. Arterioles (Correct Answer)
C. Capillaries
D. Veins

Explanation: ***Arterioles*** - **Arterioles** are the primary sites of **vasodilation** in acute inflammation [1][2], allowing increased blood flow to affected tissues. - They respond rapidly to inflammatory mediators, leading to **decreased vascular resistance** and subsequent hyperemia. *Vein* - While veins can undergo changes in response to inflammation, they typically do not initiate **vasodilation** during acute inflammatory responses. - Their primary role is in **draining blood**, rather than altering flow dynamics significantly in acute conditions. *Capillaries* - Capillaries are where **exudate** occurs, but they do not initiate vasodilation; they primarily facilitate the **exchange** of fluids and nutrients. - Their diameter remains relatively constant; changes primarily occur in arterioles before affecting capillary perfusion. *Venules* - Venules primarily function as sites for **exudation** and are influenced by the arteriolar changes that precede their dilation. - They play a role in **collecting blood** but do not exhibit initial vasodilatory responses 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. 185-186. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 438: The commonest variety of acute inflammation is:

A. Necrotic inflammation
B. Serous inflammation (Correct Answer)
C. Catarrhal inflammation
D. Purulent inflammation

Explanation: ***Catarrhal inflammation*** - It is characterized by the **accumulation of mucus** and is often seen in respiratory infections, making it the commonest type of acute inflammation. - Typical examples include **rhinitis** and **bronchitis**, where the mucosal lining becomes inflamed and exudates are primarily mucus. *Serous inflammation* - Usually presents with a **thin, clear fluid** (serous exudate) accumulation, often seen in blisters or mild reactions [1]. - While common, it is not as prevalent as catarrhal inflammation in respiratory disorders. *Purulent inflammation* - Characterized by the formation of **pus** [2][3], indicating bacterial infection, but is not the most common form observed. - Conditions like **abscesses** or infections like **appendicitis** may see this [2], but they are less frequent in general acute inflammation cases. *Necrotic inflammation* - This type involves **tissue death** and is severe, usually due to ischemia or infection, thus is associated with significant morbidity [1]. - It is less common in the spectrum of acute inflammation compared to catarrhal, which is more mild and prevalent. **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. 191-192. [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. 192-193. [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. 193-194.

Question 439: In the context of tissue repair, which cell type is predominantly found during the proliferative phase of wound healing?

A. Fibroblasts (Correct Answer)
B. Mesenchymal cells
C. Ameloblasts
D. Odontoblasts

Explanation: ***Fibroblasts*** - During the proliferative phase, **fibroblasts** are stimulated to proliferate and migrate into the wound site [1], [2]. - They are responsible for synthesizing and depositing the **extracellular matrix**, including **collagen**, which forms the structural framework of the new tissue [1], [2]. *Mesenchymal cells* - **Mesenchymal cells** are multipotent **stem cells** that can differentiate into various cell types, including fibroblasts, but they are not the predominant cell type actively laying down collagen in the proliferative phase. - While they play a role in providing cells for wound repair, **fibroblasts** are the primary effector cells of collagen production [1]. *Odontoblast* - **Odontoblasts** are specialized cells found in the **dental pulp** that are responsible for forming **dentin**. - They are not involved in general tissue repair processes outside of tooth development or injury. *Ameloblast* - **Ameloblasts** are cells responsible for forming **tooth enamel** during tooth development. - They are not found in general wound healing and are specific to **enamel genesis**. **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. 105-106. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-119.

Question 440: Most important for diapedesis is

A. PECAM (Correct Answer)
B. Selectins
C. Mucin like glycoprotein
D. Integrins

Explanation: ***Platelet Endothelial Cell Adhesion Molecule (PECAM)*** - PECAM plays a crucial role in the process of **diapedesis**, allowing white blood cells to pass through the endothelial barrier [1]. - It is specifically involved in **intercellular junctions**, facilitating the migration of leukocytes during **inflammation** [1]. *Selectins* - Selectins are important for **rolling** of leukocytes on the endothelium but do not directly mediate **diapedesis**. - They are crucial for initial attachment but do not promote the passage through the endothelial cell junctions. *Mucin like glycoprotein* - While mucin like glycoproteins can facilitate **cell adhesion**, they primarily contribute to the **rolling phase** rather than diapedesis itself. - They are not as directly involved in the **transmigration** across the endothelium as PECAM. *Integrins* - Integrins are involved in **firm adhesion** of leukocytes, but do not directly enable **diapedesis** across the endothelium. - They support the binding to the endothelium but play a lesser role compared to PECAM in the actual process of migration. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

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

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