General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1421: 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.

Question 1422: Maximum collagen deposition in wound healing is seen at -

A. End of third week (Correct Answer)
B. End of first week
C. End of 2 months
D. End of second week

Explanation: ***End of third week*** - By the end of the **third week**, the proliferative phase of wound healing is well underway, characterized by significant **collagen deposition**. [1] - At this stage, **Type III collagen** is initially laid down, which is later replaced by stronger **Type I collagen**, contributing to increasing wound strength. *End of first week* - The first week primarily involves the **inflammatory phase** and the initial stages of **proliferation**, with minimal new collagen deposition. [2] - While some **fibroblasts** are present, the amount of collagen synthesized is still relatively low. *End of second week* - Collagen synthesis is ongoing during the second week, but the **peak deposition rate** and overall amount of collagen accumulated are typically not as high as at the end of the third week. - The wound is gaining strength, but further increase in collagen content and remodeling is yet to occur. *End of 2 months* - By 2 months, the wound is in the **remodeling phase**, where the total collagen content might be substantial but the *rate of new collagen synthesis* has slowed down. - At this stage, there is a balance between **collagen synthesis** and **degradation**, and the collagen fibers are being reorganized and cross-linked to further improve tensile strength. **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, p. 115.

Question 1423: In systemic senile amyloidosis, there is deposition of?

A. AA
B. AL
C. Beta - 2- microglobulin
D. ATTR (Correct Answer)

Explanation: ***ATTR*** - In systemic senile amyloidosis, there is typical deposition of **ATTR** amyloid, which is derived from **transthyretin**, a protein produced by the liver [1]. - This condition occurs predominantly in **older adults**, leading to systemic effects and involvement of various organs such as the heart and kidneys [1]. *AL* - AL amyloidosis is characterized by the deposition of **light chain immunoglobulins**, not typically associated with senile amyloidosis [2]. - AL amyloidosis is more related to **multiple myeloma** and other plasma cell disorders [2]. *Beta - 2- microglobulin* - This refers to a component often seen in conditions like **chronic kidney disease**, leading to **beta-2-microglobulin amyloidosis**, not systemic senile amyloidosis. - It generally does not cause systemic amyloidosis linked with age-related changes in proteins. *AA* - AA amyloidosis is due to **serum amyloid A protein**, typically associated with chronic inflammatory states, rather than senile amyloidosis. - It is mainly seen in conditions like **rheumatoid arthritis** and chronic infections, differing from the aged-related mechanism in ATTR. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 266. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267.

Question 1424: Which of the following statements regarding cell aging is true?

A. Free radicals cause cellular damage.
B. Mitochondrial content decreases with age.
C. Cell size typically decreases with aging.
D. Lipofuscin accumulates in cells with aging. (Correct Answer)

Explanation: ***Lipofuscin accumulation in the cell*** - The accumulation of **lipofuscin** is a well-documented marker of cellular aging, representing oxidative stress and damage [1]. - Lipofuscin, often termed "age pigment," visibly increases in long-lived cells, indicating past cellular injury and degradation processes [1]. *Free radicals injury* - While **free radicals** do contribute to cellular aging, the statement is too broad; their injury is one of many factors, not a definitive marker of aging itself [3]. - Free radicals cause oxidative damage, but **lipofuscin** specifically denotes accumulated cellular debris over time [1]. *Mitochondria are increased* - Aging often leads to **mitochondrial dysfunction**, with a decrease in number and efficiency, rather than an increase. - Increased mitochondria would suggest enhanced metabolism, which contrasts with the characteristics of aging. *Size of cell increased* - Generally, cellular aging is associated with **cellular atrophy** rather than an increase in size, which might occur in specific conditions like hypertrophy [2]. - The **increase in cell size** is not a characteristic feature of aging, as older cells frequently undergo degeneration [2]. **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. 75. [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. 47-49. [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. 100-101.

Question 1425: Which of the following is/are characteristic pathological findings in asthma?

A. Curschmann spirals
B. Charcot-Leyden crystals
C. Occlusion of bronchi and bronchioles by mucus
D. All of the options (Correct Answer)

Explanation: ***All of the above*** - Asthma is associated with various pathological findings, including **Charcot-Leyden crystals** and **Curschmann spirals** during bronchial inflammation [1]. - These findings represent the underlying **eosinophilic** and **mucous** hypersecretion processes commonly seen in asthma [2,3]. *Charcot-Leyden crystals* - These **crystals** are associated with **eosinophilic** inflammation, but their presence alone is not definitive for asthma diagnosis [2]. - They are often found in **sputum** of asthmatic patients but are not the only indicator of asthma presence. *Curschmann spirals* - These **spirals** indicate **mucous plugging** of bronchi and are indeed seen in asthma, but signify only one aspect of the condition [1,3]. - They highlight the **mucosal** response in asthma rather than providing a comprehensive view of the disease. *Occlusion of bronchi and bronchioles by mucus* - **Mucus** production leading to **bronchial obstruction** occurs in asthma, but this statement is too narrow to encompass the condition's entirety [1]. - While it is a common feature, it does not consider the immunological or inflammatory elements intrinsic to asthma. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 328-329. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 329-330.

Question 1426: Which of the following is a characteristic feature of Down syndrome?

A. Trisomy 18
B. Robertsonian translocation involving chromosome 21
C. Trisomy 21 (Correct Answer)
D. Trisomy 13

Explanation: ***Trisomy 21*** - **Down syndrome** is the most common autosomal chromosome abnormality and is characterized by the presence of an extra copy of chromosome 21 [1, 2]. - This extra genetic material leads to the characteristic physical features, intellectual disability, and medical conditions associated with the syndrome [1, 2]. *Trisomy 18* - **Trisomy 18**, also known as **Edwards syndrome**, is a serious chromosomal disorder distinct from Down syndrome [2]. - It is characterized by severe developmental problems, including **heart defects**, **kidney malformations**, and **severe intellectual disability**, with generally a much shorter life expectancy [2, 3]. *Robertsonian translocation involving chromosome 21* - A **Robertsonian translocation** involving chromosome 21 is a cause of Down syndrome, but it is not the characteristic feature itself; rather, it is a specific **chromosomal rearrangement** that can lead to an extra copy of chromosome 21 material [1, 2]. - This specific type of translocation accounts for only a small percentage (2-3%) of all Down syndrome cases, while **Trisomy 21** (nondisjunction) is the most common cause [1, 2]. *Trisomy 13* - **Trisomy 13**, also known as **Patau syndrome**, is a distinct chromosomal disorder characterized by the presence of an extra copy of chromosome 13 [2]. - It is associated with severe birth defects, including **cleft lip/palate**, **polydactyly**, and severe neurological problems, and is usually fatal within the first year of life [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 170-171. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.

Question 1427: Which protein is primarily affected by mutations in Marfan's syndrome?

A. Collagen I
B. Collagen IV
C. Fibrillin I (Correct Answer)
D. Fibrillin II

Explanation: ***Fibrillin I*** - Marfan's syndrome is caused by a mutation in the **FBN1 gene**, which encodes the protein **fibrillin I**, crucial for connective tissue integrity [1]. - Clinical manifestations include **skeletal abnormalities**, **cardiovascular issues**, and **ocular problems**, linking the mutation to its phenotypic features [1]. *Collagen I* - While collagen is important for connective tissue, **collagen I** mutations are associated with disorders like **osteogenesis imperfecta**, not Marfan's syndrome. - This oes not account for the significant **fibrillin deficiency** noted in Marfan's patients. *Fibrillin II* - **Fibrillin II** does exist but is not the causative factor in Marfan's syndrome; mutations in this protein relate to different syndromes like **Congenital Contractural Arachnodactyly**. - The primary influence in Marfan's is due to the defect in **fibrillin I**, not fibrillin II. *Collagen IV* - Mutations in **collagen IV** are linked to diseases such as **Alport syndrome**, primarily affecting renal function and hearing, rather than the hallmark features of Marfan's. - This type of collagen is more critical for **basement membranes**, differentiating it from the connective tissue role of fibrillin I in Marfan's. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 35-36.

Question 1428: In amyloidosis, beta pleated sheets can be directly visualized at the molecular level using:

A. Electron microscope
B. X-ray crystallography (Correct Answer)
C. Congo red stain
D. Cryo-electron microscopy

Explanation: ***Congo red stain*** - Congo red stain is **specific** for detecting amyloid deposits, showing a characteristic **apple-green birefringence** under polarized light [1]. - The presence of **beta-pleated sheets** is a key feature of the amyloid fibrils that this stain highlights, confirming amyloidosis [1]. *Spiral electron microscope* - The **spiral electron microscope** is not a standard technique used for identifying amyloid structures or deposits. - It does not provide the **specificity** required to visualize amyloid-related beta-pleated sheets. *Electron microscope* - While electron microscopy can visualize amyloid fibrils [2], it does not specifically confirm the **beta-pleated sheet** structure like Congo red does. - This technique requires more complex preparations and does not have the same **ease of interpretation** for diagnosing amyloidosis. *X-ray crystallography* - X-ray crystallography is primarily used to determine the **three-dimensional** structure of crystalline substances, not specific to amyloid detection. - It does not provide direct evidence of **amyloid deposits** like Congo red staining does. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [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. 135-136.

Question 1429: Which of the following statements about apoptosis is not true?

A. Cellular swelling (Correct Answer)
B. Nuclear compaction
C. Intact cell membrane
D. Formation of apoptotic bodies

Explanation: ***Cellular swelling*** - **Apoptosis**, or programmed cell death, is characterized by cell shrinkage, not cellular swelling. - **Cellular swelling** is typically seen in **necrosis**, which is an uncontrolled form of cell death often due to injury. *Nuclear compaction* - **Nuclear compaction**, or **pyknosis**, is a hallmark feature of apoptosis where the nucleus condenses and fragments. - This process is crucial for the organized dismantling of the cell during programmed cell death. *Intact cell membrane* - In apoptosis, the **cell membrane** generally remains intact until the very late stages, preventing the release of cellular contents and subsequent inflammation. - This intactness differentiates apoptosis from necrosis, where the cell membrane ruptures early. *Formation of apoptotic bodies* - The cell fragments into small, membrane-bound structures called **apoptotic bodies**, which are then readily engulfed by phagocytes. - This mechanism allows for the efficient removal of dying cells without triggering an inflammatory response.

Question 1430: Which enzymes are primarily responsible for the degeneration of the basement membrane?

A. Oxidases
B. Elastases
C. Hydroxylases
D. Metalloproteinases (Correct Answer)

Explanation: ***Metalloproteinases*** - **Matrix metalloproteinases (MMPs)** are a family of **zinc-dependent endopeptidases** that degrade various components of the **extracellular matrix (ECM)**, including the **basement membrane**. - Their activity is crucial in processes such as **tissue remodeling** and **wound healing**, and also in pathological conditions like **cancer invasion** and **metastasis** where basement membrane degradation is a key step. - **Type IV collagenase** (MMP-2 and MMP-9) specifically targets type IV collagen, the major structural component of basement membranes. *Oxidases* - Oxidases are enzymes that catalyze **oxidation-reduction reactions** involving molecular oxygen as the electron acceptor. - While they can indirectly contribute to tissue damage by generating **reactive oxygen species (ROS)**, their primary role is not the direct enzymatic degradation of the basement membrane. *Elastases* - Elastases are a type of **serine protease** that specifically break down **elastin**, a key component of elastic fibers in connective tissue. - While the basement membrane contains some proteins that might be affected, elastases are not the primary enzymes responsible for its general degradation. *Hydroxylases* - Hydroxylases are enzymes that catalyze the addition of a **hydroxyl group (-OH)** to a substrate. - They are involved in various metabolic pathways, including **collagen synthesis** (e.g., prolyl hydroxylase, lysyl hydroxylase), but they do not directly degrade the basement membrane.

Practice by Chapter

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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Tissue Repair and Wound Healing

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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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