General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1411: Hypertrophy is -

A. Increase in cell number
B. Increase in cell size (Correct Answer)
C. Decrease in cell number
D. Decrease in cell size

Explanation: ***Increase in cell size*** - **Hypertrophy** is defined as an increase in the **size of individual cells** [1], leading to an increase in the size of the organ or tissue [2]. - This cellular adaptation occurs when cells are subjected to increased workload or demand, such as in **muscle cells** in response to exercise or **cardiac myocytes** in hypertension [2]. *Increase in cell number* - An increase in **cell number** is termed **hyperplasia** [1]. - Hyperplasia typically occurs in tissues capable of **mitotic division**, leading to an increase in the overall size of the tissue or organ due to more cells [1]. *Decrease in cell number* - A decrease in **cell number** can result from **atrophy** (loss of cells) or programmed cell death (**apoptosis**). - This process is seen in various physiological or pathological conditions, leading to a reduction in organ size. *Decrease in cell size* - A decrease in the **size of individual cells** is known as **atrophy** [3]. - Atrophy often occurs due to reduced workload, loss of innervation, diminished blood supply, or inadequate nutrition [3]. **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. 85-88. [2] 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. 45-46. [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. 90-91.

Question 1412: Reversible change from one cell type to another is known as -

A. Hypertrophy
B. Dysplasia
C. Hyperplasia
D. Metaplasia (Correct Answer)

Explanation: ***Metaplesia*** - Refers to the **reversible change** from one cell type to another in response to chronic irritation or damage [1][2]. - It often occurs as an adaptive response in **epithelial tissues**, such as in the respiratory tract in smokers [1][2]. *Hypertrophy* - Represents an **increase in cell size** rather than a change in cell type [2]. - It is often a response to increased functional demand, as seen in **cardiac muscle** in athletes. *Hyperplesia* - Refers to an **increase in cell number** within a tissue or organ, not a change in cell type [2]. - Common in conditions such as **benign prostatic hyperplasia** but does not involve differentiation into other cell types. *Dysplasia* - Indicates an **abnormal growth or development** of cells, leading to disordered morphology rather than a transformation into another cell type. - It is often a precursor to cancer but does not signify the reversible nature of metaplasia. **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, p. 49. [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. 85-92.

Question 1413: What causes the brown color of a contusion?

A. Decomposed hemoglobin
B. Bilirubin breakdown products
C. Hemosiderin (Correct Answer)
D. Methemoglobin

Explanation: ***Hemosiderin*** - The brown color of a contusion is primarily due to **hemosiderin**, an iron-storage complex formed from the breakdown of **hemoglobin**. - As red blood cells trapped in the tissue degrade, their iron is released and converted into hemosiderin, which has a distinct reddish-brown to brown hue. *Decomposed hemoglobin* - While hemoglobin does decompose, it breaks down into stages that result in different colors (**biliverdin** for green, **bilirubin** for yellow), before the formation of hemosiderin. - The direct "decomposition" itself isn't the primary cause of the enduring brown color, but rather the subsequent iron deposition. *Bilirubin breakdown products* - **Bilirubin** is formed from the breakdown of **biliverdin**, which gives contusions their yellow color late in the healing process. - This stage precedes or coexists with the brown color, but bilirubin itself is responsible for the yellow, not the brown. *Methemoglobin* - **Methemoglobin** is an oxidized form of hemoglobin that can cause a **bluish-brown** discoloration, often seen in conditions like methemoglobinemia. - While it can manifest in some bruises, it is not the primary or universal cause of the typical brown color of a resolving contusion; that is usually due to iron deposition.

Question 1414: Caseous necrosis is seen in -

A. Tuberculosis (Correct Answer)
B. CMV infection
C. Treponemal infection
D. Staphylococcal infection

Explanation: ***Tuberculosis*** - **Caseous necrosis** is the **pathognomonic** and **most characteristic** form of necrosis seen in **tuberculosis (TB)** caused by *Mycobacterium tuberculosis* [1]. - It appears as a **cheesy, friable, granular material** in the center of **tuberculous granulomas** (tubercles) [1], [2]. - The unique **lipid-rich cell wall** of *M. tuberculosis* combined with the host's **type IV hypersensitivity reaction** results in this distinctive pattern of tissue destruction [2]. - This is a **classic histopathological hallmark** of TB and is essential for diagnosis [2]. *Treponemal infection* - **Syphilis**, caused by *Treponema pallidum*, causes **gummatous necrosis**, NOT caseous necrosis [3]. - Gummas have a **rubbery consistency** and different histological appearance compared to the cheesy, friable caseous necrosis. - While syphilis produces granulomatous inflammation, the necrosis pattern is distinctly different from TB [3]. *CMV infection* - **Cytomegalovirus (CMV)** infection typically causes **coagulative necrosis** with **cytopathic effects** (enlarged cells with intranuclear and intracytoplasmic inclusions - "owl's eye" appearance) [3]. - Does NOT produce caseous necrosis. *Staphylococcal infection* - **Staphylococcal infections** (e.g., *Staphylococcus aureus*) cause **liquefactive necrosis** leading to **abscess formation** [3]. - Dead cells are enzymatically digested into **liquid pus**, completely different from the solid, cheesy appearance of caseous necrosis. **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, p. 55. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Question 1415: Which of the following cell types is classified as a labile cell?

A. Liver parenchymal cells
B. Vascular smooth muscle cells
C. Surface epithelium (Correct Answer)
D. Neurons

Explanation: ***Surface epithelium*** - Surface epithelium is classified as **labile tissue**, meaning it undergoes constant regeneration due to its high turnover rate [1]. - Cells in this tissue are typically found in areas that experience frequent damage or abrasion, such as the skin and lining of the intestines. *Cardiac cell* - Cardiac cells are considered **permanent cells**, as they do not undergo significant regeneration after injury or damage. - Damage to cardiac cells typically leads to **fibrosis** rather than repair of the original tissue. *Liver parenchymal cell* - Liver parenchymal cells are categorized as **stable cells**, which can regenerate but do so under specific circumstances, such as injury. - They have a slower turnover rate compared to labile cells and do not constantly renew under normal conditions. *Vascular endothelial cells* - Vascular endothelial cells are considered **stable cells** as well, typically maintaining a stable population but capable of regeneration following injury. - They do not have the same rapid turnover and regeneration capability as labile cells do, especially under normal physiological conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115.

Question 1416: Amyloidosis is associated with all of the following conditions except?

A. Chronic bronchitis (Correct Answer)
B. Osteomyelitis
C. Bronchiectasis
D. Tuberculosis

Explanation: ***Chronic bronchitis*** - Chronic bronchitis is primarily characterized by **inflammation of the airways** and **excess mucus production**, not typically associated with amyloidosis [1]. - Amyloidosis more commonly relates to chronic inflammatory states but does not directly result from the long-term exposure seen in chronic bronchitis [1]. *Tuberculosis* - Tuberculosis can lead to chronic inflammation, which may precipitate **secondary amyloidosis** due to persistent infection [1]. - It often causes systemic effects, including weight loss and fever, which can result in **amyloid deposition** [1]. *Osteomyelitis* - Osteomyelitis, as a chronic bone infection, can trigger an inflammatory response leading to **secondary amyloidosis** [1]. - The ongoing inflammation can result in the accumulation of amyloid proteins in the bone and surrounding tissues [1]. *Bronchiectasis* - Bronchiectasis often results from persistent lung infections leading to chronic inflammation, which can cause **amyloid deposition** [1,3]. - It is associated with recurrent lung infections and can lead to systemic complications, including amyloidosis [1,3]. **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. 135-136. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 269-270.

Question 1417: In which condition are Michaelis Gutmann bodies typically seen?

A. Xanthogranulomatous
B. Pyelonephritis
C. Malakoplakia (Correct Answer)
D. Nail patella syndrome

Explanation: ***Malakoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic histological features of malakoplakia, representing calcified concretions containing **iron and calcium** within macrophages. - These are formed around **partially digested bacteria** within defective macrophages, appearing as basophilic inclusions with a "target-like" or "owl's eye" appearance. - Malakoplakia is a chronic granulomatous inflammatory condition most commonly affecting the **urinary tract** (bladder, kidney), but can occur in other organs. *Xanthogranulomatous* - This condition is characterized by an infiltrate of **lipid-laden macrophages** (xanthoma cells, foam cells) and occasional giant cells, but **not** Michaelis-Gutmann bodies. - It most commonly affects the kidney (**xanthogranulomatous pyelonephritis**) and is a destructive inflammatory process with a mass-like appearance. *Pyelonephritis* - Refers to **inflammation of the kidney and renal pelvis**, usually due to bacterial infection (commonly E. coli). - Histologically, it is characterized by acute or chronic inflammatory cells, neutrophil infiltration, and potential abscess formation, **without** Michaelis-Gutmann bodies. *Nail patella syndrome* - This is a **genetic disorder** (autosomal dominant) affecting primarily the **nails, bones** (absent/hypoplastic patella, elbow dysplasia), and sometimes the kidneys (glomerular disease). - It is associated with developmental abnormalities and has **no association** with Michaelis-Gutmann bodies or malakoplakia.

Question 1418: Which of the following is a sign of reversible injury in alcoholic liver disease?

A. Cytoplasmic vacuole (Correct Answer)
B. Pyknosis (nuclear shrinkage)
C. Loss of cell membrane integrity
D. Nuclear karyolysis (nuclear dissolution)

Explanation: ***Cytoplasmic vacuole*** - The presence of **cytoplasmic vacuoles** in liver cells indicates fatty change, which is a **reversible injury** in alcoholic liver disease [1][2]. - This injury allows the liver to recover if **alcohol consumption** is ceased, highlighting its reversible nature [1]. *Nuclear karyolysis* - **Nuclear karyolysis** signifies severe cellular damage and necrosis, indicating an irreversible process [2]. - This feature involves the dissolution of the nucleus, which does not align with reversible injury. *Loss of cell membrane* - Loss of the **cell membrane** indicates irreversible damage, leading to cell death rather than a reversible condition [2]. - This change is associated with significant cellular impairment, contrary to the concept of recovery. *Pyknosis* - **Pyknosis**, the condensation of chromatin in the nucleus, suggests irreversible cellular injury and impending necrosis [2]. - It is often a precursor to cell death and is not indicative of reversible damage in liver pathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-850. [2] 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. 51-53.

Question 1419: Which of the following translocations is not associated with Down syndrome?

A. t(21;21)
B. t(14;21)
C. t(15;21)
D. t(11;14) (Correct Answer)

Explanation: ***t (11: 14)*** - The **t(11;14) translocation** is commonly associated with **mantle cell lymphoma**, a B-cell non-Hodgkin lymphoma, and is not a cause of Down syndrome. - This translocation leads to the overexpression of the **cyclin D1 gene**, located on chromosome 11, which promotes cell growth and proliferation. *t (14; 21)* - This is a common **Robertsonian translocation** involving chromosomes 14 and 21, which results in an extra copy of chromosome 21 material [1]. - Individuals with this translocation can have **Down syndrome** because their cells end up with the equivalent of three copies of chromosome 21 [1]. *t (21; 21)* - This translocation is another type of **Robertsonian translocation** where two chromosome 21s fuse. - This specific translocation is rare and results in an extra copy of chromosome 21, leading to **Down syndrome** with a high recurrence risk in offspring. *t (15: 21)* - This is a **Robertsonian translocation** involving chromosomes 15 and 21, resulting in an extra copy of chromosome 21 material. - This translocation is a known cause of **Down syndrome** due to the dosage imbalance of genes on chromosome 21 [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 169-172.

Question 1420: A mutation in the transthyretin (TTR) protein causes which of the following types of amyloidosis?

A. Familial Mediterranean fever
B. Dialysis associated amyloidosis
C. Prion protein associated amyloidosis
D. Familial amyloidotic polyneuropathy (Correct Answer)

Explanation: ***Familial amyloidotic polyneuropathy*** - This condition is specifically caused by **mutations in the transthyretin (TTR) protein**, leading to amyloid deposition primarily in nerves [1]. - It presents with **peripheral neuropathy**, including sensory and autonomic symptoms, which align with TTR mutations [1]. *Familial Mediterranean fever* - This is an autoinflammatory disorder caused by mutations in the **MEFV gene**, unrelated to transthyretin. - It is characterized by recurrent **fever, abdominal pain**, and **serositis**, not amyloidosis caused by TTR. *Prion protein associated amyloidosis* - Relates to prion diseases like **Creutzfeldt-Jakob disease**, caused by abnormal **prion proteins** rather than TTR [1]. - Symptoms are usually **neurodegenerative** in nature, not linked to familial amyloidogenic processes. *Dialysis associated amyloidosis* - This form of amyloidosis is due to the accumulation of **beta-2 microglobulin**, not mutations in TTR [1]. - Commonly presents with **joint pain** and carpal tunnel syndrome associated with long-term dialysis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 266.

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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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Molecular Basis of Disease

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