General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1351: White infarcts are seen in which of the following?

A. Heart
B. Kidney
C. All of the options
D. Spleen (Correct Answer)

Explanation: ***Spleen*** - The spleen is the **classic example** of an organ that develops **white (anemic) infarcts** [1] - White infarcts occur in **solid organs with end-arterial blood supply** and limited collateral circulation [1] - Splenic infarcts appear as **pale, wedge-shaped areas** of coagulative necrosis [1], [2] - Typically caused by **embolic events** (e.g., infective endocarditis, atrial fibrillation, hypercoagulable states) [3], [4] - The dense parenchyma prevents blood extravasation, resulting in pale appearance [1] *Kidney* - While the kidney also develops white infarcts due to its end-arterial circulation, the **spleen** is the more classic textbook example [1] - Renal infarcts similarly present as pale, wedge-shaped areas but are less frequently emphasized in standard teaching [1], [2] *Heart* - Myocardial infarctions **initially present as RED (hemorrhagic) infarcts**, not white infarcts - This occurs due to reperfusion through anastomotic channels and hemorrhage into necrotic tissue [1] - The heart only develops pale appearance **after several days** when blood is resorbed - Therefore, heart is **not** a typical site for white infarcts *All of the options* - Incorrect because the heart characteristically develops **red infarcts**, not white infarcts **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [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. 148-149. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 136-137. [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. 145-146.

Question 1352: Thymus gland abscess seen in congenital syphilis is called:

A. Politzer's abscess
B. Douglas abscess
C. Fouchier's abscess
D. Dubois' abscess (Correct Answer)

Explanation: ***Dubois' abscess*** - **Dubois' abscesses** are characteristic microscopic foci of necrosis and granulomatous inflammation that occur in the **thymus gland** in cases of **congenital syphilis**. - They are a specific pathological finding associated with **early congenital syphilis**, reflecting the systemic dissemination of *Treponema pallidum*. *Politzer's abscess* - **Politzer's abscess** is a term mainly associated with an abscess in the external or middle ear, often following **otitis media**. - It has no known association with **congenital syphilis** or the **thymus gland**. *Douglas abscess* - A **Douglas abscess** refers to a collection of pus in the **rectouterine pouch** (pouch of Douglas) in females, or the rectovesical pouch in males. - This is typically a complication of **pelvic inflammatory disease** or appendicitis and is unrelated to the thymus or syphilis. *Fouchier's abscess* - **Fouchier's abscess** is an older term sometimes used to describe an **epidural abscess**, particularly in the spine. - This condition involves an infection within the spinal canal and is not linked to the thymus or congenital syphilis.

Question 1353: Fibroblasts in healing wound are derived from -

A. Epithelium
B. Endothelium
C. Local mesenchyme (Correct Answer)
D. Bone marrow

Explanation: ***Local mesenchyme*** - Fibroblasts, crucial for synthesizing **collagen** and other extracellular matrix components in wound healing, are primarily derived from resident **mesenchymal cells** in the local connective tissue [1]. - These undifferentiated mesenchymal cells proliferate and differentiate into fibroblasts to aid in tissue repair [4]. - This is the **major source** of fibroblasts in wound healing. *Bone marrow* - While bone marrow-derived **circulating fibrocytes** can contribute to wound healing, they represent a minor source compared to local mesenchymal cells [2]. - These circulating progenitor cells can migrate to wound sites and differentiate into fibroblasts, but this is a supplementary mechanism. *Epithelium* - **Epithelial cells** primarily provide a protective barrier and regenerate the surface lining; they do not differentiate into fibroblasts [3]. - Their main role in wound healing is **re-epithelialization** to close the wound surface. *Endothelium* - **Endothelial cells** form the lining of blood vessels and are involved in angiogenesis (new blood vessel formation) during wound healing. - While some endothelial cells may undergo **endothelial-to-mesenchymal transition (EndoMT)** to become myofibroblasts, the primary source of fibroblasts is the local mesenchyme. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115. [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. 104-105. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113. [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. 105-106.

Question 1354: Which of these cells is most radio-resistant?

A. Fibroblasts
B. Vascular endothelial cells
C. Early precursor cells of erythroblastic series
D. Muscle cells (Correct Answer)

Explanation: ***Muscle cells*** - Muscle cells are **terminally differentiated** [1] and have a very **low mitotic rate**, making them highly radio-resistant. - Their primary function as contractile units does not require rapid cell division, reducing their susceptibility to radiation-induced damage. *Fibroblasts* - While generally considered relatively radio-resistant compared to hematopoietic cells, **fibroblasts** maintain a capacity for proliferation and collagen synthesis. - This proliferative capacity makes them more susceptible to radiation damage than terminally differentiated cells like muscle cells in the context of tissue repair and fibrosis. *Vascular endothelial cells* - **Vascular endothelial cells** are crucial for maintaining vessel integrity [2] and have a moderate proliferative capacity, particularly during angiogenesis or repair. - Damage to these cells by radiation can lead to vascular permeability issues and long-term tissue damage [2]. *Early precursor cells of erythroblastic series* - **Early precursor cells** in the erythroblastic series are highly proliferative and undifferentiated, making them extremely **radio-sensitive** [2]. - Radiation exposure severely impacts **bone marrow production** and can lead to significant cytopenia due to the death of these rapidly dividing cells [2]. **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. 78-79. [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. 111-113.

Question 1355: Which of the following is most susceptible to ionizing radiation?

A. Nerve cells
B. Small lymphocytes (Correct Answer)
C. Epithelial cells
D. Mature bone

Explanation: ***Small lymphocytes*** - **Lymphocytes** are highly sensitive to **ionizing radiation** due to their rapid proliferation and vulnerability during DNA synthesis [1]. - Exposure to radiation can lead to rapid **apoptosis** (programmed cell death) of lymphocytes, causing **lymphocytopenia** [1]. *Nerve cells* - **Nerve cells** are generally considered **radioresistant** because they are terminally differentiated and do not undergo cell division. - Their primary function is transmission of electrical impulses, which is not immediately disrupted by typical radiation doses. *Epithelial cells* - **Epithelial cells** (e.g., skin, gut lining) are moderately sensitive to radiation, primarily due to their **high turnover rate** [1]. - However, they are generally less sensitive than lymphocytes, and their damage often requires higher doses or prolonged exposure [1]. *Mature bone* - **Mature bone** is highly resistant to radiation because its cells (osteocytes) are largely quiescent and the extracellular matrix is inert [1]. - Significant damage to bone typically occurs at very high doses, affecting the more sensitive **bone marrow** stem cells within it rather than the mature bone itself [1]. **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. 111-114.

Question 1356: Liver after transplant enlarges by -

A. Increase in number of cells
B. Increase in size of cell
C. Both (Correct Answer)
D. None of the options

Explanation: ***Both*** - Liver regeneration after transplant involves both an **increase in the number of hepatocytes (hyperplasia)** through cell division and an increase in the **size of individual cells (hypertrophy)** [1],[2]. - This combined process allows the transplanted liver to rapidly grow and adapt to the metabolic demands of the recipient, restoring full liver function [1]. *Increase in number of cells* - While **hepatocyte proliferation (hyperplasia)** is a crucial component of liver regeneration, it is not the sole mechanism for post-transplant liver enlargement [1],[3]. - Relying only on an increase in cell number would disregard the immediate compensatory increase in cell size that also contributes significantly to organ growth. *Increase in size of cell* - **Hepatocyte hypertrophy** does contribute to early liver enlargement after transplant, as cells increase in volume to enhance metabolic capacity [2]. - However, this process alone is insufficient for the complete functional recovery and growth of the liver, which also requires an increase in the total number of cells [1]. *None of the options* - This option is incorrect because liver enlargement after transplant is a well-documented biological phenomenon. - The liver possesses a remarkable capacity for regeneration, and its response to transplantation includes measurable growth that is vital for survival [1],[3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-115. [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. 87-88. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 382-383.

Question 1357: Type of necrosis seen in case of burn:

A. Coagulative necrosis. (Correct Answer)
B. Liquefactive necrosis.
C. Caseous necrosis.
D. Both coagulative and liquefactive.

Explanation: ***Coagulative necrosis.*** [1] - Burn injuries cause **protein denaturation** due to heat, leading to **cell death** where the cellular architecture is preserved for some time [1]. - This is the **primary and characteristic** type of necrosis directly resulting from thermal injury [1]. - The coagulation of intracellular proteins results in an **infarcted area** that appears firm and opaque [1]. *Both coagulative and liquefactive.* - While coagulative necrosis is the primary type, liquefactive necrosis may occur **secondarily** if there is superimposed infection or tissue breakdown. - However, the question asks for the type of necrosis **seen in case of burn**, which refers to the **primary pathological process** caused by thermal injury itself. - The characteristic and predominant pattern is **coagulative**, not both simultaneously. *Liquefactive necrosis.* - **Liquefactive necrosis** is characterized by the dissolution of dead cells into a viscous liquid mass due to enzymatic digestion. - Typically seen in **bacterial abscesses**, **brain infarcts**, and **hypoxic death of CNS tissue**. - This is not the primary type of necrosis directly caused by thermal injury of a burn. *Caseous necrosis.* - **Caseous necrosis** is a distinct form of cell death associated with specific granulomatous diseases, most notably **tuberculosis**. - Results in cheese-like, friable dead tissue with loss of cellular architecture. - Not characteristic of burn injuries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 51-55.

Question 1358: Necrotizing granulomatous lymphadenopathy is caused by -

A. Cat Scratch Disease (Bartonella henselae)
B. Atypical mycobacterial infection (Correct Answer)
C. Sarcoidosis
D. Kikuchi disease

Explanation: ***Atypical mycobacterial infection*** - Atypical mycobacterial infections, particularly in children, often present with **necrotizing granulomatous lymphadenopathy**, characterized by granulomas with central necrosis [3]. - The necrosis in these granulomas is typically **caseating** and may lead to abscess formation and draining sinuses. *Cat Scratch Disease (Bartonella henselae)* - While Cat Scratch Disease causes **granulomatous lymphadenitis**, the granulomas are usually **non-necrotizing** or show stellate microabscesses rather than widespread necrosis. - Histology often reveals **suppurative granulomas** with neutrophilic microabscesses and Warthin-Starry staining can highlight the bacteria [1]. *Sarcoidosis* - Sarcoidosis is characterized by **non-caseating granulomas**, meaning there is no central necrosis within the granulomatous inflammation [2], [4]. - These granulomas are typically composed of epithelioid histiocytes, multinucleated giant cells, and lymphocytes [4]. *Kikuchi disease* - Kikuchi disease, or **histiocytic necrotizing lymphadenitis**, is characterized by focal areas of **coagulative necrosis** and abundant histiocytes, but it lacks true granuloma formation. - It often presents with cervical lymphadenopathy and fever, and the necrosis is usually associated with prominent karyorrhexis. **References:** [1] 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. [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, p. 360. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Question 1359: Ischemic necrosis in alkali burn corresponds to which stage?

A. Stage II (Correct Answer)
B. Stage I
C. Stage III
D. Stage IV

Explanation: ***Stage II*** - **Ischemic necrosis** in an alkali burn corresponds to Stage II, indicating a more severe and damaging effect on the tissue. - This stage involves significant cell death due to **loss of blood supply**, often seen in deeper tissue penetration by the corrosive agent [1]. *Stage I* - Stage I describes **edema** and **epithelial erosion** without significant tissue necrosis or ischemia [1]. - This stage is typically characterized by superficial damage, good perfusion, and a relatively rapid recovery without permanent scarring. *Stage III* - Stage III represents a severely advanced burn that progresses beyond necrosis to **perforation** of the esophagus or other affected organs. - At this stage, the tissue damage is extensive, leading to a high risk of complications like **mediastinitis** or **peritonitis**. *Stage IV* - While not a universally recognized stage for alkali burns, if used, Stage IV would imply **incurable damage** or **systemic complications** that threaten the patient's life, possibly involving multiple organ failure due to sepsis or other severe sequelae. - This stage would signify irreversible harm beyond localized tissue destruction, often leading to a fatal outcome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 53-56, 61-62.

Question 1360: Crumpled paper appearance of cells is a feature of-

A. Asbestosis
B. GVHD
C. Gaucher disease (Correct Answer)
D. Wilson's disease

Explanation: ***Gaucher disease*** - The **crumpled paper** or **wrinkled tissue paper** appearance is characteristic of **Gaucher cells**, which are macrophages engorged with **glucocerebroside** [1]. - This accumulation results from a deficiency in the enzyme **glucocerebrosidase**, a hallmark of Gaucher disease [1]. *Asbestosis* - Characterized by the presence of **asbestos bodies** (ferruginous bodies), which are asbestos fibers coated with an iron-protein complex, not cells with crumpled appearance [2]. - This condition involves **pulmonary fibrosis** due to asbestos exposure [2]. *GVHD (Graft-versus-host disease)* - Histologically, GVHD is characterized by **lymphocytic infiltration** and damage to target organs like skin, liver, and GI tract, not by storage cells with a crumpled appearance. - It is an immunological reaction occurring after **allogeneic hematopoietic stem cell transplantation**. *Wilson's disease* - Involves excessive accumulation of **copper** in various tissues, particularly the liver, brain, and cornea. - Diagnosed by markers like low **ceruloplasmin** and high urinary copper, and does not involve cells with a storage-related crumpled appearance. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 162-163. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 698-699.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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Accumulations and Deposits

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Acute and Chronic Inflammation

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Hemodynamic Disorders

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Genetic Disorders

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Environmental Pathology

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Nutritional Diseases

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Molecular Basis of Disease

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