Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 381: Characteristic of acute inflammation is

A. Vasoconstriction
B. Platelet aggregation
C. Vasodilation and increase permeability (Correct Answer)
D. Infiltration by neutrophils

Explanation: ***Vasodilation and increased permeability*** - **Vasodilation** leads to increased blood flow, causing **heat** and **redness**, which are cardinal signs of acute inflammation [1]. - Increased vascular **permeability** allows plasma proteins and fluid to leak into the interstitial space, resulting in **swelling** (edema) [2]. - These are the **primary and fundamental vascular changes** that define acute inflammation and enable all subsequent events [2]. - These changes occur **immediately** and are **sustained** throughout the inflammatory process [3]. *Vasoconstriction* - **Vasoconstriction** is only a transient, initial response lasting seconds to minutes, not a characteristic and sustained feature of acute inflammation. - Its purpose is primarily to **limit blood loss** in case of injury, and is quickly followed by vasodilation. *Platelet aggregation* - While **platelet aggregation** can occur at sites of vascular injury during inflammation, it is not a defining characteristic of the inflammatory process itself. - The main role of platelets is in **hemostasis** and clot formation, which is secondary to endothelial injury rather than a primary inflammatory response. *Infiltration by neutrophils* - **Neutrophil infiltration** is indeed a hallmark **cellular characteristic** of acute inflammation and is the predominant cell type in the first 24-48 hours [4]. - However, neutrophil migration **depends on** the prior vascular changes (vasodilation and increased permeability) to occur [4]. - When choosing THE most characteristic feature, **vascular changes** are more fundamental as they represent the **initiating and enabling events** that make cellular infiltration possible [2], [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. 185-186. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [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. 187-188. [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. 188-189.

Question 382: A 45 year old patient presents with history of fever, night sweats and weight loss. On X-ray, a mass in apical lobe of lung is seen. On histopathology, it was found to have caseous necrosis. What is the likely underlying process involved -

A. Acute decrease in blood supply
B. Hypersensitivity reaction with modified macrophages, lymphocytes and giant cells (Correct Answer)
C. Decreased supply of growth factors
D. Enzymatic degeneration

Explanation: ***Hypersensitivity reaction with modified macrophages, lymphocytes and giant cells*** - This describes the formation of a **granuloma** [1], [3] with **caseous necrosis**, which is the hallmark of **tuberculosis (TB)** [1]. - The symptoms of fever, night sweats, and weight loss (known as **B symptoms**) are classic for TB [2], and the apical lung mass with caseous necrosis on histopathology confirms the diagnosis [1]. *Acute decrease in blood supply* - An acute decrease in blood supply, or **ischemia**, primarily causes **coagulative necrosis** in most tissues, not caseous necrosis. - While ischemia can lead to tissue damage, it doesn't typically involve the characteristic granulomatous inflammation seen here. *Decreased supply of growth factors* - A decreased supply of growth factors is more associated with **atrophy** or **apoptosis**, where cells shrink or undergo programmed cell death. - It does not explain the presence of a macroscopic lung mass, fever, night sweats, weight loss, or caseous necrosis. *Enzymatic degeneration* - **Enzymatic degeneration** is primarily seen in **liquefactive necrosis**, particularly in infections and brain infarcts, where enzymes digest the dead tissue, forming a viscous fluid. - Caseous necrosis is histologically distinct and characterized by a cheesy, friable appearance due to the incomplete enzymatic digestion of dead cells within a granuloma [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 319-320. [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. 198-200.

Question 383: Regeneration is characterized by:

A. Granulation tissue
B. Repairing by different type of tissue
C. Cellular proliferation is largely regulated by biochemical factors
D. Repairing by same type of tissue (Correct Answer)

Explanation: ***Repairing by same type of tissue*** - **Regeneration** involves the replacement of damaged cells and tissues with cells of the **same type**, leading to a complete restoration of normal structure and function [1]. - This process is seen in tissues with high proliferative capacity, like the **epidermis** or the **liver**, following injury [2]. *Granulation tissue* - **Granulation tissue** is characteristic of **repair by fibrosis** (scar formation), not regeneration [1]. - It consists of proliferating fibroblasts, new blood vessels (angiogenesis), and inflammatory cells, which eventually mature into a fibrous scar. *Repairing by different type of tissue* - The replacement of damaged tissue with a **different type of tissue** (typically fibrous connective tissue) is known as **repair by fibrosis** or **scar formation** [1]. - This occurs when the tissue's regenerative capacity is limited or when the injury is severe, resulting in the loss of normal tissue architecture and function [3]. *Cellular proliferation is largely regulated by biochemical factors* - While **cellular proliferation** is indeed regulated by **biochemical factors** (growth factors, cytokines) in both regeneration and repair, this statement describes a mechanism common to cellular growth and healing in general, not a defining characteristic unique to regeneration [1]. - This regulation guides both the replacement with original tissue (regeneration) and scar formation, so it's not specific enough to define regeneration alone. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 113.

Question 384: A young lady presented with bilateral nodular lesions on shins. She was also found to have bilateral hilar lymphadenopathy on chest X-ray. Mantoux test reveals indurations of 5 mms. Skin biopsy would reveal:

A. Vasculitis
B. Non caseating Granuloma (Correct Answer)
C. Caseating Granuloma
D. Malignant cells

Explanation: ***Non-caseating Granuloma*** - This clinical presentation of **bilateral nodular lesions on shins** (**erythema nodosum**) [1] and **bilateral hilar lymphadenopathy** is highly suggestive of **sarcoidosis**. [2] - **Sarcoidosis** is characterized by the presence of **non-caseating granulomas** in affected tissues, including the skin (erythema nodosum) and lymph nodes. [2] *Vasculitis* - While vasculitis can cause skin lesions, the characteristic presentation of erythema nodosum is a form of **panniculitis** (inflammation of subcutaneous fat) rather than true vasculitis. - Vasculitis typically involves inflammation and damage to **blood vessel walls**, which is not the primary histological finding in sarcoidosis-associated skin lesions. *Caseating Granuloma* - **Caseating granulomas** are the hallmark of **tuberculosis** and certain fungal infections, and they involve central necrosis ("caseation"). - The positive Mantoux test (5 mm induration) is equivocal; while it could indicateMycobacterium exposure, the overall constellation of findings points away from active TB as the primary diagnosis, which would typically show caseating granulomas. *Malignant cells* - This clinical picture does not align with a primary malignancy. While malignancies can cause various skin lesions or lymphadenopathy, the specific combination strongly suggests an inflammatory or granulomatous disease. - Skin biopsies would reveal **granulomatous inflammation** rather than malignant cellular proliferation in this context. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 641-642. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.

Question 385: Granulomas in lymph nodes are seen in all of the following infections EXCEPT:

A. Histoplasmosis
B. Brucellosis
C. Staph Aureus (Correct Answer)
D. TB

Explanation: ***Staph Aureus*** - *Staphylococcus aureus* typically causes **suppurative (pus-forming)** infections leading to **abscesses** and **pyogenic inflammation**, not granulomas [2], [3]. - Lymph node involvement with *S. aureus* usually manifests as **acute lymphadenitis** with neutrophil infiltration, not organized granulomatous structures [2]. *Histoplasmosis* - **Histoplasmosis**, caused by *Histoplasma capsulatum*, is a fungal infection that commonly forms **granulomas** in affected tissues, including lymph nodes [1]. - These granulomas often resemble those seen in tuberculosis and can be **caseating or non-caseating** [1]. *Brucellosis* - **Brucellosis**, caused by *Brucella* species, is a zoonotic bacterial infection that classically forms **non-caseating granulomas** in multiple organs including lymph nodes, liver, and spleen. - The granulomas are characterized by epithelioid histiocytes and may contain multinucleated giant cells. *TB* - **Tuberculosis (TB)**, caused by *Mycobacterium tuberculosis*, is the classic example of an infection that forms **caseating granulomas** in affected lymph nodes [3]. - These granulomas are characterized by **central caseous necrosis** surrounded by epithelioid histiocytes, lymphocytes, and Langhans giant cells [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 717. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 592-593. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 379-380.

Question 386: Michaelis-Gutmann bodies are seen in

A. Malacoplakia (Correct Answer)
B. Thimble Bladder
C. Transitional cell carcinoma of bladder
D. Interstitial cystitis

Explanation: ***Malacoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic, spherical, intracytoplasmic or extracellular concretions that stain positive with **Perls' Prussian blue stain** (due to their iron content). - Malacoplakia is a specific type of **granulomatous inflammation** [2] that most commonly affects the urinary tract, particularly the bladder. *Thimble Bladder* - This term refers to a **small, contracted bladder** often seen in end-stage **tuberculosis** [3] or interstitial cystitis [1], but it is not characterized by Michaelis-Gutmann bodies. - It describes a morphological feature rather than a specific microscopic inclusion [4]. *Transitional cell carcinoma of bladder* - This is a common **malignant tumor** of the bladder lining, characterized by atypical transitional epithelial cells, not Michaelis-Gutmann bodies. - Diagnosis involves histopathological examination revealing **dysplastic urothelial cells** with varying degrees of invasion. *Interstitial cystitis* - Characterized by **chronic bladder pain** and urinary frequency without infection, often associated with submucosal hemorrhages (glomerulations) and sometimes **Hunner's ulcers** [1]. - It is a diagnosis of exclusion and does not involve the formation of Michaelis-Gutmann bodies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 966-967. [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 Diseases Of The Urinary And Male Genital Tracts, pp. 494-495. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 972-973.

Question 387: Onion peel appearance of splenic capsule is seen in

A. Scleroderma
B. SLE (Correct Answer)
C. Rheumatoid arthritis
D. Sjögren's syndrome

Explanation: ### SLE [1] - The **onion peel appearance** of the splenic capsule is a characteristic histological finding in **Systemic Lupus Erythematosus (SLE)**. - It results from **concentric perivascular fibrosis** and **lamellar thickening** around central arterioles in the spleen, a manifestation of autoimmune damage [1]. *Scleroderma* - **Scleroderma** is characterized by excessive **collagen deposition** and fibrosis in tissues, which would not typically manifest as an "onion peel" appearance in the spleen. - While it can affect connective tissue throughout the body, splenic involvement is usually not described with this specific histological finding. *Rheumatoid arthritis* - **Rheumatoid arthritis** primarily affects synovial joints and is associated with **chronic inflammation** and pannus formation. - Splenic changes in RA, if present (e.g., Felty's syndrome), involve splenomegaly due to lymphoid hyperplasia, not concentric perivascular fibrosis. *Sjögren's syndrome* - **Sjögren's syndrome** is an autoimmune disease primarily affecting **exocrine glands**, leading to dry eyes and mouth. - While systemic manifestations can occur, the characteristic "onion peel" splenic changes are not associated with Sjögren's syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 685-686.

Question 388: In a patient with gouty arthritis, synovial fluid aspiration will show which of the following:

A. Calcium pyrophosphate crystals
B. Polymorphonuclear leukocytosis
C. Monosodium urate crystals (Correct Answer)
D. Mononuclear leukocytosis

Explanation: ***Monosodium urate crystals*** - **Gouty arthritis** is pathognomonically characterized by the presence of **monosodium urate (MSU) crystals** in the synovial fluid [1]. - These crystals are typically **needle-shaped** and display **strong negative birefringence** under polarized light microscopy [1]. *Mononuclear leucocytosis* - While present in inflammatory conditions, a predominance of **mononuclear cells** is less typical for acute gout [1]. - **Pseudogout** or even some chronic arthritides are more likely to exhibit this pattern. *Calcium pyrophosphate crystals* - These crystals are characteristic of **pseudogout**, also known as **calcium pyrophosphate deposition disease (CPPD)** [2]. - They are typically **rhomboid-shaped** and show **positive birefringence** [2]. *Polymorphonuclear leukocytosis* - Although there is an inflammatory response with increased **polymorphonuclear leukocytes (PMNs)** in gout, their presence alone is not specific for gout [1]. - **Septic arthritis** also presents with a significant increase in PMNs, and the definitive diagnosis relies on identifying the specific crystals or infectious agents. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1218-1220. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 683-684.

Question 389: In Still's disease the transient cutaneous rash coincides with the fever spike. The rash is due to:

A. Lymphocyte infiltration in the dermis
B. Neutrophil infiltration in the dermis (Correct Answer)
C. Eosinophil infiltration in the dermis
D. None of the options

Explanation: ***Neutrophil infiltration in the dermis*** - The characteristic rash of Still's disease (juvenile idiopathic arthritis systemic onset or adult-onset Still's disease) is a **transient, salmon-pink, macular or maculopapular eruption** that typically appears during **febrile spikes**. - Histologically, this rash is characterized by a **superficial perivascular infiltrate of neutrophils** and sometimes lymphocytes, without significant epidermal changes. *Lymphocyte infiltration in the dermis* - While lymphocytes can be present, the predominant inflammatory cell type associated with the classic rash of Still's disease during fever spikes is the **neutrophil**. - Conditions like chronic dermatitis or viral exanthems are more commonly associated with prominent lymphocytic infiltrates. *Eosinophil infiltration in the dermis* - Eosinophils are typically associated with **allergic reactions**, parasitic infections, or certain drug eruptions. - Their presence is not a primary feature of the rash seen in Still's disease. *None of the options* - This option is incorrect because **neutrophil infiltration** is the recognized histological feature of the rash in Still's disease.

Question 390: Endotoxin shock is initiated by:

A. Endothelial injury
B. Cytokine action (Correct Answer)
C. Peripheral vasodilation
D. Increased vascular permeability

Explanation: ***Cytokine action*** - Endotoxins (specifically **lipopolysaccharides** from Gram-negative bacteria) trigger immune cells to release a cascade of **pro-inflammatory cytokines** (e.g., TNF-α, IL-1) [2]. - These cytokines are the primary mediators responsible for initiating the widespread systemic inflammation and physiological changes characteristic of **endotoxin shock** [1]. *Endothelial injury* - While **endothelial injury** is a significant consequence of **cytokine activity** in endotoxin shock, it is not the initiating event [3]. - Cytokines induce damage to the endothelium, leading to downstream effects such as increased permeability and coagulation activation [3]. *Peripheral vasodilation* - **Peripheral vasodilation** is a key feature of the distributive shock seen in endotoxemia, but it occurs *after* the initial cytokine release. - Inflammatory mediators, including cytokines, cause the relaxation of vascular smooth muscle, leading to widespread vasodilation and hypoperfusion. *Increased vascular permeability* - **Increased vascular permeability** is a crucial part of the pathophysiology of endotoxin shock, causing fluid leakage from vessels into tissues. - This is also a downstream effect, primarily induced by **cytokines** and other inflammatory mediators acting on endothelial cells [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 142. [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. 63-64. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 142-143.

Practice by Chapter

Acute Inflammation: Vascular Events

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Acute Inflammation: Cellular Events

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Chemical Mediators of Inflammation

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Chronic Inflammation

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Granulomatous Inflammation

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Systemic Effects of Inflammation

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Wound Healing

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Tissue Regeneration

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Fibrosis and Repair

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Resolution of Inflammation

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