NEET-PG 2012 — Pathology
69 Previous Year Questions with Answers & Explanations
Malignancy in pheochromocytoma is indicated by:
Renal papillary necrosis is almost always associated with one of the following conditions:
What is the histological appearance of the brain in Creutzfeldt-Jakob disease?
Thorium-induced tumor is which of the following?
Transitional cell carcinoma of the bladder is associated with which of the following?
What occurs during the stage of Grey hepatization?
Li–Fraumeni syndrome is associated with mutations in which of the following genes?
What change is seen in the vessels during the initial stage of Raynaud's phenomenon?
Which of the following conditions can lead to pulmonary infarction?
Maximum collagen deposition in wound healing is seen at -
NEET-PG 2012 - Pathology NEET-PG Practice Questions and MCQs
Question 1: Malignancy in pheochromocytoma is indicated by:
- A. Mitotic figures
- B. Capsular invasion
- C. Metastasis (Correct Answer)
- D. Vascular invasion
Explanation: ***Metastasis*** - The definitive criterion for diagnosing **malignancy in pheochromocytoma** is the presence of **metastatic disease**, meaning tumor cells have spread to sites where chromaffin tissue is not normally found. - The distinction between benign and malignant pheochromocytomas often cannot be made based on histological features alone. *Mitotic figures* - While increased **mitotic activity** can be a feature indicating aggressive tumor behavior, it is not a standalone definitive criterion for malignancy in pheochromocytoma. - Benign pheochromocytomas can occasionally show mitotic figures, and their presence alone does not confirm malignancy. *Capsular invasion* - **Capsular invasion** suggests an aggressive tumor but is not a definitive indicator of malignancy in pheochromocytoma. - Tumors that exhibit capsular invasion without distant spread are still considered to have uncertain malignant potential rather than overt malignancy. *Vascular invasion* - Similar to capsular invasion, **vascular invasion** indicates an increased risk of metastasis but is not a conclusive sign of malignancy. - The presence of tumor cells within blood vessels raises suspicion, but true malignancy is only confirmed by the presence of distant metastases.
Question 2: Renal papillary necrosis is almost always associated with one of the following conditions:
- A. Diabetes-mellitus
- B. Analgesic-nephropathy (Correct Answer)
- C. Chronic pyelonephritis
- D. Post streptococcal GN
Explanation: ***Analgesic-nephropathy*** - Chronic use of certain analgesics (especially **phenacetin**, aspirin, and NSAIDs) can lead to **ischemia** and damage to the renal papillae, causing **papillary necrosis**. - This condition is considered the **classic** cause of renal papillary necrosis and is the most frequently emphasized in medical education. - Analgesic nephropathy shows a very **strong and direct association** with papillary necrosis as a hallmark feature. *Diabetes-mellitus* - **Diabetes mellitus** is actually one of the **most common causes** of renal papillary necrosis in clinical practice, particularly when complicated by **infection** or **ischemia** [1]. - While clinically very common, it causes papillary necrosis through multiple mechanisms and is often associated with coexisting factors like **pyelonephritis** [1], [2] or NSAID use. - In the context of "almost always associated," analgesic nephropathy has a more direct and consistent association. *Chronic pyelonephritis* - **Chronic pyelonephritis** involves recurrent bacterial infections of the kidney parenchyma and can lead to scarring and kidney damage. - While it is indeed a recognized cause of **papillary necrosis** (part of the POSTCARDS mnemonic), it is not as consistently associated as analgesic nephropathy [2]. *Post streptococcal GN* - **Post-streptococcal glomerulonephritis (PSGN)** is an immune-mediated inflammatory kidney disease that typically follows a **streptococcal infection**. - It primarily affects the **glomeruli** and does **not** cause necrosis of the renal papillae, making this option incorrect. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 543-544. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 937-940.
Question 3: What is the histological appearance of the brain in Creutzfeldt-Jakob disease?
- A. Neuronophagia
- B. Micro abscess
- C. Demyelination
- D. Spongiform changes (Correct Answer)
Explanation: ***Spongiform changes*** - The hallmark histological feature of **Creutzfeldt-Jakob disease (CJD)** is **spongiform degeneration**, characterized by vacuolation of neuronal cell bodies [1]. - It results in a **spongy appearance** of the affected brain regions, particularly in the **cerebral cortex** and **basal ganglia** [1]. *Neuronophagia (can occur in various contexts, not specific to CJD)* - Neuronophagia refers to the phagocytic activity involving **dying neurons**, which can occur in various conditions but is not a defining feature of CJD [2]. - It indicates the presence of **inflammation** or a response to neuronal injury rather than specific changes seen in CJD. *Demyelination (associated with multiple sclerosis)* - Demyelination is primarily associated with conditions like **multiple sclerosis** and is characterized by loss of **myelin sheaths** around neurons. - This is not related to CJD, which involves **prion protein accumulation** and subsequent neuronal degeneration. *Micro abscess (indicative of bacterial infections)* - Micro abscesses indicate localized collections of **pus** typically seen in **bacterial infections**, which is incongruent with the pathophysiology of CJD. - In CJD, there are no signs of **inflammation** or **neutrophilic infiltration** associated with abscess formation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1284-1286. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256.
Question 4: Thorium-induced tumor is which of the following?
- A. Angiosarcoma of liver (Correct Answer)
- B. Lymphoma
- C. Renal cell carcinoma
- D. Astrocytoma
Explanation: ***Angiosarcoma of liver*** - Thorium exposure is specifically linked to the development of **angiosarcoma of the liver**, often seen in individuals with a history of thorium dioxide injection [1]. - This type of tumor arises from **vascular endothelial cells** and is highly aggressive, often leading to significant morbidity. *Lymphoma* - Lymphoma is associated with **immune system factors** and typically arises from lymphoid tissues, which do not correlate with thorium exposure. - **Hematological malignancies** such as lymphoma do not have a documented direct association with thorium as a causative agent. *Astrocytoma* - Astrocytomas originate from **glial cells** in the brain and are primarily influenced by genetic predispositions rather than environmental carcinogens like thorium. - There is no established relationship between **thorium exposure** and the incidence of brain tumors such as astrocytomas. *Renal cell carcinoma* - Renal cell carcinoma is commonly linked to **smoking, obesity**, and genetic factors rather than thorium exposure. - It does not have a recognized connection to thorium, which is more specifically associated with liver tumors. **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. 216-217.
Question 5: Transitional cell carcinoma of the bladder is associated with which of the following?
- A. Malaria
- B. Schistosomiasis
- C. None of the options (Correct Answer)
- D. Ascariasis
Explanation: ***Schistosomiasis*** - Schistosomiasis, particularly from *Schistosoma haematobium*, is a well-known risk factor for **transitional cell carcinoma of the bladder** due to chronic irritation and inflammation [1]. - The association arises due to the **presence of eggs in the bladder**, leading to calcification and eventually cancer development. *Malaria* - Malaria is primarily associated with **hemolytic anemia** and does not have a direct correlation with **bladder cancer**. - Its causative agents, *Plasmodium* species, do not typically lead to **urological malignancies** like transitional cell carcinoma. *Ascarasis* - Ascarasis, caused by *Ascaris lumbricoides*, primarily affects the **intestines** and is more associated with gastrointestinal issues. - There is no significant link between ascarasis and the **development of bladder cancer**. *Any of d above* - As this option suggests all listed conditions, it incorrectly implies that **malaria** and **ascarasis** are linked to bladder cancer, which they are not. - Transitional cell carcinoma is specifically associated with **schistosomiasis**, making this option misleading. **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. 968-970.
Question 6: What occurs during the stage of Grey hepatization?
- A. Accumulation of fibrin (Correct Answer)
- B. Red blood cells fill the alveoli
- C. White blood cells fill the alveoli
- D. Bacteria fill the alveoli
Explanation: ***Accumulation of fibrin*** - Grey hepatization is characterized by the **presence of fibrinous exudate** in the alveoli, indicating significant lung pathology, usually in cases of pneumonia [1,2]. - This stage follows red hepatization and reflects the **progression of inflammation** within the lung tissue [1,2]. *RBC's fill the alveoli* - This occurs during the **red hepatization** stage, where RBCs invade alveoli, not grey hepatization [1,2]. - **Grey hepatization** is marked by **fibrinous deposits** instead of erythrocytes [1,2]. *Organisms fill the alveoli* - While organisms, such as bacteria, can be present, they are more characteristic of the **initial infection phase** rather than grey hepatization [1]. - This stage reflects more on the **inflammatory response** than the presence of pathogens. *WBC's fill the alveoli* - The infiltration of **WBCs (like neutrophils)** represents an earlier inflammatory process, usually preceding grey hepatization [1,2]. - In grey hepatization, the focus is on the **accumulation of fibrin**, not directly on WBC infiltration [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-712. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.
Question 7: Li–Fraumeni syndrome is associated with mutations in which of the following genes?
- A. Gene RB1
- B. Gene BRCA1
- C. Gene P21
- D. Gene TP53 (Correct Answer)
Explanation: ***Gene TP53*** - Li-Fraumeni syndrome is a rare, inherited cancer susceptibility syndrome associated with germline mutations in the **TP53 tumor suppressor gene**. - The **TP53 gene** encodes the p53 protein, which plays a critical role in cell cycle arrest, DNA repair, and initiation of apoptosis in response to cellular stress, thus preventing tumor formation. *Gene P21* - The **p21 gene** (CDKN1A) is a cyclin-dependent kinase inhibitor that acts downstream of p53, mediating p53-induced cell cycle arrest. - While p21 is involved in the p53 pathway, mutations in p21 itself are not the primary cause of Li-Fraumeni syndrome. *Gene RB1* - The **RB1 gene** encodes the retinoblastoma protein, a tumor suppressor involved in cell cycle regulation, particularly in controlling passage from G1 to S phase. - Mutations in **RB1** are primarily associated with hereditary retinoblastoma and osteosarcoma, not Li-Fraumeni syndrome. *Gene BRCA1* - The **BRCA1 gene** is a tumor suppressor gene involved in DNA repair, especially homologous recombination. - Germline mutations in **BRCA1** are strongly associated with hereditary breast and ovarian cancer syndrome, not Li-Fraumeni syndrome.
Question 8: What change is seen in the vessels during the initial stage of Raynaud's phenomenon?
- A. No pathological changes (functional vasospasm only) (Correct Answer)
- B. Thrombosis
- C. Fibrinoid necrosis
- D. Hyaline sclerosis
Explanation: ***No pathological changes (functional vasospasm only)*** - Raynaud's phenomenon, particularly **primary Raynaud's** (Raynaud's disease), is characterized by **functional vasospasm** of arterioles, especially in fingers and toes, in response to cold or stress [1]. - In its initial stages, there are no structural changes or pathological alterations within the vessel walls; the vasoconstriction is entirely **functional** [1]. *Thrombosis* - **Thrombosis** involves the formation of a blood clot within a vessel, obstructing blood flow. - While severe Raynaud's can, in rare cases, lead to digital ischemia and microthrombosis, it is **not the primary or initial change** seen in typical Raynaud's phenomenon. *Fibrinoid necrosis* - **Fibrinoid necrosis** is a type of vascular damage associated with severe autoimmune diseases or malignant hypertension, where fibrin and plasma proteins deposit in the vessel wall. - This is a **structural, irreversible change** and is not characteristic of the initial, functional vasospasm seen in Raynaud's phenomenon. *Hyaline sclerosis* - **Hyaline sclerosis** is a change in small arteries and arterioles, often seen in benign essential hypertension or as part of the aging process, where the vessel wall thickens and becomes hyaline (glassy) due to plasma protein leakage and fibrosis. - This represents a **chronic structural change** and is not the acute, intermittent, functional vasoconstriction defining the initial stage of Raynaud's. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 520-522.
Question 9: Which of the following conditions can lead to pulmonary infarction?
- A. Saddle embolus at bifurcation
- B. Arterioles being blocked
- C. None of the above.
- D. Blockage of 2nd and 3rd generation end arteries (Correct Answer)
Explanation: ***None*** - Indicates that all the listed options do indeed contribute to **pulmonary infarction**. - **Pulmonary infarction** typically occurs due to vascular obstruction; thus, this choice signifies all other options are related. [1] *Saddle embolus at bifurcation* - A **saddle embolus** can cause significant blockage at the **pulmonary artery bifurcation**, leading to acute pulmonary infarction. [2] - This type of embolism can severely reduce blood supply to both lungs, directly contributing to infarction. [3] *Arterioles are blocked* - Obstruction of **small arterioles** can lead to localized ischemia and subsequent infarction in the pulmonary region. [1] - This phenomenon is consistent with the pathophysiology of pulmonary infarction, hence it is a contributing factor. *Blockage of 2nd and 3rd gen end arteries* - Infarction can occur if there is blockage of the **2nd and 3rd generation of pulmonary arteries**, leading to compromised blood flow. [1] - These smaller branches play a critical role in perfusing lung tissue, and their blockage can result in pulmonary infarction. [4] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 137-138. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 323-324. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 705-706.
Question 10: 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.