NEET-PG 2013 — Pathology

Q: Clear cell variety of renal cell carcinoma is related to a gene located on which chromosome?

3. ***3*** - The **clear cell variety of renal cell carcinoma** (RCC) is associated with **mutations in the VHL gene**, which is located on chromosome **3** [1]. - This gene plays a crucial role in the **regulation of angiogenesis**, and its inactivation leads to tumor development. *22* - Chromosome **22** is associated with other disorders but not specifically with clear cell RCC or its genetic mutations. - Renal cell carcinoma primarily relates to **chromosome 3**, not chromosome 22 [1]. *X* - The **X chromosome** has other oncogenes and tumor suppressor genes but is not linked to clear cell RCC specifically. - Mutations in the **VHL gene** on chromosome 3 are the key factors, not those found on the X chromosome. *20* - Chromosome **20** does not contain significant genes linked to clear cell renal cell carcinoma. - The notable genetic association is with chromosome **3**, specifically the VHL gene [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959. [Practice more Pathology PYQs on OnCourse]

Q: Job's syndrome is which of the following types of immunodeficiency disease?

Disorder of phagocytosis. ***Disorder of phagocytosis*** - Job's syndrome (Hyper-IgE syndrome) is primarily classified as a **disorder of phagocytosis** due to defective **neutrophil chemotaxis** - The hallmark feature is **impaired neutrophil migration** to sites of infection, leading to recurrent **staphylococcal skin abscesses** and **pneumonias with pneumatocele formation** - Caused by **STAT3 mutations** (autosomal dominant form), which affect multiple immune pathways but clinically manifest predominantly as phagocyte dysfunction - Classic triad: **elevated IgE** (>2000 IU/mL), **recurrent skin and lung infections**, and **characteristic facies** *Cellular immunodeficiency* - While STAT3 mutations do affect T-cell function (particularly Th17 differentiation), the **primary clinical manifestation** is phagocyte dysfunction - Pure cellular immunodeficiencies like **DiGeorge syndrome** present with viral and fungal infections, which are not the predominant feature in Job's syndrome - The classification is based on the **dominant clinical defect**, which in Job's syndrome is impaired neutrophil chemotaxis *humoral immunodeficiency* - Despite markedly elevated IgE levels, patients have relatively preserved **antibody production** against most pathogens - Humoral deficiencies like **X-linked agammaglobulinemia** present with low immunoglobulin levels and recurrent encapsulated bacterial infections - The elevated IgE in Job's syndrome is a consequence of dysregulated cytokine signaling, not a primary antibody production defect *Disorder of complement* - Complement disorders result from defects in the **complement cascade proteins** (C1-C9) - These typically present with recurrent **Neisseria infections** or autoimmune phenomena like SLE - Job's syndrome does not involve complement pathway defects and presents with characteristic staphylococcal infections [Practice more Pathology PYQs on OnCourse]

Q: Heart failure cells are

Pigmented alveolar macrophages. ***Pigmented alveolar macrophages*** - These macrophages engulf **hemosiderin** (iron-rich pigment from degraded red blood cells) that leaks into the alveoli due to increased capillary pressure in left-sided **heart failure**. - The presence of **hemosiderin-laden macrophages** in the sputum or lung tissue is diagnostic for chronic pulmonary congestion caused by heart failure. *Lipofuscin granules in cardiac cells* - **Lipofuscin** is a "wear-and-tear" pigment that accumulates in aging cells, including cardiac cells. - While present in older hearts, its presence does not specifically indicate **heart failure** or represent "heart failure cells" in the described context. *Pigmented pancreatic acinar cells* - Pancreatic acinar cells primarily produce digestive enzymes and are not typically associated with **pigment accumulation** in the context of heart failure. - Pigmentation in pancreatic cells would suggest other pathologies, such as **hemochromatosis** affecting the pancreas. *Pigment cells seen in liver* - The liver can accumulate various pigments, such as **hemosiderin** in hemochromatosis or **bilirubin** in cholestasis. - While liver congestion can occur in right-sided heart failure, the specific "heart failure cells" refer to the **pulmonary macrophages**. [Practice more Pathology PYQs on OnCourse]

Q: Which of the following cancers is associated with osteolytic metastases?

All of the options. ***All of the options*** - **Lung**, **kidney**, and **thyroid** cancers are all known to frequently produce **osteolytic bone metastases** [1]. - These cancers release factors that stimulate **osteoclast activity**, leading to bone destruction rather than new bone formation. *Lung* - **Non-small cell lung cancer** often metastasizes to bone and commonly causes **osteolytic lesions** [2]. - Bone metastases are a frequent complication, particularly in advanced stages, and are associated with **pain** and **pathological fractures**. *Kidney* - **Renal cell carcinoma** is notorious for causing highly vascularized and often **osteolytic metastases** in bone [1]. - These lesions can be aggressive, leading to significant **bone destruction** and **hypercalcemia**. *Thyroid* - **Follicular thyroid carcinoma** and, less commonly, **papillary thyroid carcinoma** are known to cause **osteolytic bone metastases** [1]. - Thyroid cancer metastases in bone can be slow-growing but are typically **destructive** and may cause **pain** or **fractures**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725. [Practice more Pathology PYQs on OnCourse]

Q: Which of the following is not seen in Aschoff bodies?

Polymorphonuclear cells. ***Polymorphonuclear cells*** - **Aschoff bodies** are associated with rheumatic fever and typically contain **lymphocytes and macrophages**, not polymorphonuclear cells [1]. - The presence of **PMNs** would suggest an acute inflammatory response, which is not characteristic of Aschoff bodies. *Giant cells* - **Giant cells**, formed by the fusion of macrophages, can be found within Aschoff bodies. - They are indicative of **chronic inflammation**, presenting in conditions like rheumatic heart disease. *Aschoff cells* - **Aschoff cells** are a specific type of macrophage found within Aschoff bodies and are hallmark features of rheumatic fever [1]. - These cells are derived from activated macrophages and participate in **granulomatous inflammation**. *Fibroblasts* - **Fibroblasts** can also be present in Aschoff bodies, contributing to the **fibrous tissue** formation during the healing process. - They are involved in tissue repair and are found in various inflammatory conditions, including rheumatic fever. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566. [Practice more Pathology PYQs on OnCourse]

74 Previous Year Questions with Answers & Explanations

Questions

Clear cell variety of renal cell carcinoma is related to a gene located on which chromosome?

Job's syndrome is which of the following types of immunodeficiency disease?

Heart failure cells are

Which of the following cancers is associated with osteolytic metastases?

Which of the following is not seen in Aschoff bodies?

Which of the following is not a myeloproliferative disorder?

Which immunohistochemical marker is primarily associated with glomus tumors?

Which one of the following stains is specific for amyloid?

Irreversible injury in myocardium occurs at ?

Q10

Dystrophic calcification is seen in

NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs

Question 1: Clear cell variety of renal cell carcinoma is related to a gene located on which chromosome?

A. X
B. 22
C. 20
D. 3 (Correct Answer)

Explanation: ***3*** - The **clear cell variety of renal cell carcinoma** (RCC) is associated with **mutations in the VHL gene**, which is located on chromosome **3** [1]. - This gene plays a crucial role in the **regulation of angiogenesis**, and its inactivation leads to tumor development. *22* - Chromosome **22** is associated with other disorders but not specifically with clear cell RCC or its genetic mutations. - Renal cell carcinoma primarily relates to **chromosome 3**, not chromosome 22 [1]. *X* - The **X chromosome** has other oncogenes and tumor suppressor genes but is not linked to clear cell RCC specifically. - Mutations in the **VHL gene** on chromosome 3 are the key factors, not those found on the X chromosome. *20* - Chromosome **20** does not contain significant genes linked to clear cell renal cell carcinoma. - The notable genetic association is with chromosome **3**, specifically the VHL gene [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 958-959.

Question 2: Job's syndrome is which of the following types of immunodeficiency disease?

A. humoral immunodeficiency
B. Disorder of phagocytosis (Correct Answer)
C. Cellular immunodeficiency
D. Disorder of complement

Explanation: ***Disorder of phagocytosis*** - Job's syndrome (Hyper-IgE syndrome) is primarily classified as a **disorder of phagocytosis** due to defective **neutrophil chemotaxis** - The hallmark feature is **impaired neutrophil migration** to sites of infection, leading to recurrent **staphylococcal skin abscesses** and **pneumonias with pneumatocele formation** - Caused by **STAT3 mutations** (autosomal dominant form), which affect multiple immune pathways but clinically manifest predominantly as phagocyte dysfunction - Classic triad: **elevated IgE** (>2000 IU/mL), **recurrent skin and lung infections**, and **characteristic facies** *Cellular immunodeficiency* - While STAT3 mutations do affect T-cell function (particularly Th17 differentiation), the **primary clinical manifestation** is phagocyte dysfunction - Pure cellular immunodeficiencies like **DiGeorge syndrome** present with viral and fungal infections, which are not the predominant feature in Job's syndrome - The classification is based on the **dominant clinical defect**, which in Job's syndrome is impaired neutrophil chemotaxis *humoral immunodeficiency* - Despite markedly elevated IgE levels, patients have relatively preserved **antibody production** against most pathogens - Humoral deficiencies like **X-linked agammaglobulinemia** present with low immunoglobulin levels and recurrent encapsulated bacterial infections - The elevated IgE in Job's syndrome is a consequence of dysregulated cytokine signaling, not a primary antibody production defect *Disorder of complement* - Complement disorders result from defects in the **complement cascade proteins** (C1-C9) - These typically present with recurrent **Neisseria infections** or autoimmune phenomena like SLE - Job's syndrome does not involve complement pathway defects and presents with characteristic staphylococcal infections

Question 3: Heart failure cells are

A. Lipofuscin granules in cardiac cells
B. Pigmented alveolar macrophages (Correct Answer)
C. Pigmented pancreatic acinar cells
D. Pigment cells seen in liver

Explanation: ***Pigmented alveolar macrophages*** - These macrophages engulf **hemosiderin** (iron-rich pigment from degraded red blood cells) that leaks into the alveoli due to increased capillary pressure in left-sided **heart failure**. - The presence of **hemosiderin-laden macrophages** in the sputum or lung tissue is diagnostic for chronic pulmonary congestion caused by heart failure. *Lipofuscin granules in cardiac cells* - **Lipofuscin** is a "wear-and-tear" pigment that accumulates in aging cells, including cardiac cells. - While present in older hearts, its presence does not specifically indicate **heart failure** or represent "heart failure cells" in the described context. *Pigmented pancreatic acinar cells* - Pancreatic acinar cells primarily produce digestive enzymes and are not typically associated with **pigment accumulation** in the context of heart failure. - Pigmentation in pancreatic cells would suggest other pathologies, such as **hemochromatosis** affecting the pancreas. *Pigment cells seen in liver* - The liver can accumulate various pigments, such as **hemosiderin** in hemochromatosis or **bilirubin** in cholestasis. - While liver congestion can occur in right-sided heart failure, the specific "heart failure cells" refer to the **pulmonary macrophages**.

Question 4: Which of the following cancers is associated with osteolytic metastases?

A. Lung
B. Kidney
C. Thyroid
D. All of the options (Correct Answer)

Explanation: ***All of the options*** - **Lung**, **kidney**, and **thyroid** cancers are all known to frequently produce **osteolytic bone metastases** [1]. - These cancers release factors that stimulate **osteoclast activity**, leading to bone destruction rather than new bone formation. *Lung* - **Non-small cell lung cancer** often metastasizes to bone and commonly causes **osteolytic lesions** [2]. - Bone metastases are a frequent complication, particularly in advanced stages, and are associated with **pain** and **pathological fractures**. *Kidney* - **Renal cell carcinoma** is notorious for causing highly vascularized and often **osteolytic metastases** in bone [1]. - These lesions can be aggressive, leading to significant **bone destruction** and **hypercalcemia**. *Thyroid* - **Follicular thyroid carcinoma** and, less commonly, **papillary thyroid carcinoma** are known to cause **osteolytic bone metastases** [1]. - Thyroid cancer metastases in bone can be slow-growing but are typically **destructive** and may cause **pain** or **fractures**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725.

Question 5: Which of the following is not seen in Aschoff bodies?

A. Aschoff cells
B. Fibroblasts
C. Giant cells
D. Polymorphonuclear cells (Correct Answer)

Explanation: ***Polymorphonuclear cells*** - **Aschoff bodies** are associated with rheumatic fever and typically contain **lymphocytes and macrophages**, not polymorphonuclear cells [1]. - The presence of **PMNs** would suggest an acute inflammatory response, which is not characteristic of Aschoff bodies. *Giant cells* - **Giant cells**, formed by the fusion of macrophages, can be found within Aschoff bodies. - They are indicative of **chronic inflammation**, presenting in conditions like rheumatic heart disease. *Aschoff cells* - **Aschoff cells** are a specific type of macrophage found within Aschoff bodies and are hallmark features of rheumatic fever [1]. - These cells are derived from activated macrophages and participate in **granulomatous inflammation**. *Fibroblasts* - **Fibroblasts** can also be present in Aschoff bodies, contributing to the **fibrous tissue** formation during the healing process. - They are involved in tissue repair and are found in various inflammatory conditions, including rheumatic fever. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 566.

Question 6: Which of the following is not a myeloproliferative disorder?

A. Acute myeloid leukemia (Correct Answer)
B. Chronic myeloid leukemia
C. Essential thrombocytosis
D. Polycythemia vera

Explanation: ***Acute myeloid leukemia*** - *Acute myeloid leukemia (AML)* is a **myeloid neoplasm** characterized by the rapid proliferation of myeloid cells and is classified as an acute leukemia, not a myeloproliferative disorder. - It involves **highly abnormal cells** that impede normal blood cell production, contrasting with chronic myeloproliferative disorders which have a more gradual progression. *Essential thrombocytosis* - This is a true **myeloproliferative disorder** characterized by an **increase in platelet count** and is due to the increased production of megakaryocytes in the bone marrow [1]. - Patients can present with thrombotic or hemorrhagic complications, supporting its classification as a myeloproliferative neoplasm. *Chronic myeloid leukemia* - Chronic myeloid leukemia (CML) is another type of **myeloproliferative disorder**, arising from a genetic mutation leading to excessive production of myeloid cells. - It is associated with the **Philadelphia chromosome** and typically presents in a chronic phase with variable leukocytosis. *Polycythemia vera* - Polycythemia vera is a **myeloproliferative neoplasm** characterized by hyperproduction of red blood cells, often accompanied by leukocytosis and thrombocytosis [1]. - It is associated with mutations in the **JAK2 gene**, leading to increased erythropoiesis and elevation of hemoglobin levels, confirming its classification [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615.

Question 7: Which immunohistochemical marker is primarily associated with glomus tumors?

A. Cytokeratin
B. S-100
C. CD-57
D. CD-34 (Correct Answer)

Explanation: ***CD-34*** (Marked answer, but controversial) - **IMPORTANT NOTE:** This association is **contested** in modern pathology literature. - Glomus tumors are derived from modified smooth muscle cells of the glomus body and typically show **smooth muscle actin (SMA)** and **vimentin positivity**. - **CD34** is an endothelial marker; while glomus tumors have prominent vascularity, the **neoplastic glomus cells themselves** are generally **CD34-negative**. - The correct positive markers are **SMA, vimentin, and caldesmon** - none of which are options here. - Among the given options, CD-34 may show positivity in the **vascular endothelium** within the tumor, but this does not represent the tumor cells. *CD-57* - **CD57** (HNK-1) is associated with neural differentiation, particularly in peripheral nerve sheath tumors like **schwannoma** or **neurofibroma**. - Glomus tumors lack neural differentiation and are **CD57-negative**. *Cytokeratin* - **Cytokeratin** is a marker for epithelial cells and carcinomas. - Glomus tumors are mesenchymal smooth muscle tumors and are **cytokeratin-negative**. *S-100* - **S-100** protein marks neural crest-derived cells, melanomas, and schwannomas. - Glomus tumors originate from modified smooth muscle cells, not neural crest, and are typically **S-100-negative** (though rare cases may show focal weak positivity).

Question 8: Which one of the following stains is specific for amyloid?

A. Congo red (Correct Answer)
B. Von - Kossa
C. Alizarin red
D. Periodic Acid Schiff (PAS)

Explanation: ***Congo red*** - Congo red is a **specific stain for amyloid** that exhibits a characteristic **apple-green birefringence** under polarized light [1]. - It is widely used in **histopathology** to confirm the diagnosis of amyloidosis by staining amyloid deposits [1]. *Periodic Acid schiff (PAS)* - While PAS stain reveals **glycogen** and is useful in identifying certain infections, it is **not specific** for amyloid. - It may also stain various other cellular components like **glucose** and can lead to false positives in different conditions. *Von - Kossa* - This stain is primarily used to detect **calcium deposits**, particularly in cases of **mineralization** in tissues. - It is not applicable to amyloid deposits and does not provide diagnostic information about amyloidosis. *Alzerian red* - Alzerian red cannot be found in literature as a recognized stain; likely a misspelling of a similar term. - It fails to serve any staining purpose related to amyloid or established histological diagnostics. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-269.

Question 9: Irreversible injury in myocardium occurs at ?

A. 30 minutes (Correct Answer)
B. 5 hours
C. 1 minute
D. 1 hour

Explanation: ***30 minutes*** - Irreversible injury to **myocardial cells** typically begins **at approximately 20-30 minutes of ischemia** [1]. - This time frame represents the critical threshold where cellular damage, including **mitochondrial dysfunction** and **sarcolemmal rupture**, becomes too severe for recovery even with reperfusion [2]. - Beyond this point, cells lose membrane integrity and undergo **coagulative necrosis** [2]. *1 minute* - Myocardial cells can tolerate **ischemia** for a short period, with reversible changes occurring within the first few minutes [4]. - At 1 minute, the injury is still entirely **reversible**, and cells can fully recover if blood flow is restored [5]. - Changes at this stage include depletion of ATP and accumulation of metabolites [5]. *1 hour* - While significant **irreversible damage** has occurred by this time, the onset of irreversibility is earlier, around the 20-30 minute mark [1]. - By 1 hour, a substantial portion of the ischemic myocardium would have undergone **necrosis**, but the critical threshold was crossed 30 minutes earlier [2]. *5 hours* - By 5 hours, nearly all myocardial tissue that was subjected to continuous **ischemia** would have experienced **irreversible injury** and necrosis [3]. - This duration is well beyond the initial window for irreversible changes, indicating extensive and widespread cell death [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 140-142. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 554-556. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 548-550. [5] 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. 61-62.

Question 10: Dystrophic calcification is seen in

A. Vitamin A intoxication
B. Atheromatous plaque (Correct Answer)
C. Milk alkali syndrome
D. Hyperparathyroidism

Explanation: ***Atheromatous plaque*** - Dystrophic calcification occurs in **local areas of tissue injury**, like atheromatous plaques, where necrotic debris provides a nidus for calcification [1]. - It's commonly observed in chronic **atherosclerosis**, leading to the deposition of calcium in the damaged arterial walls [1]. *Hyperparathyroidism* - Typically associated with **metastatic calcification** due to elevated calcium levels, not dystrophic calcification [2][3]. - It results in renal, pulmonary, or vascular calcifications rather than calcifications in previously damaged tissues [3]. *Milk alkali syndrome* - Involves **hypercalcemia** and can lead to calcifications, but they are primarily **metastatic** rather than dystrophic [2][3]. - The syndrome results from excess calcium intake and is associated with renal injury rather than tissue necrosis. *Vitamin A intoxication* - Can cause **hyperostosis** and **calcifications**, but these are diffuse and not primarily dystrophic in nature. - The calcifications in this condition do not stem from necrotic tissue but rather are due to toxicity effects on bone metabolism. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 506-507. [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. 134-135. [3] 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. 76-77.