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?
Maximum collagen deposition in wound healing is seen at -
Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?
What laboratory findings are associated with common variable hypogammaglobulinemia?
Which of the following does not belong to the family of selectins?
In which type of Hodgkin's Lymphoma are lacunar cells typically observed?
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: 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 7: Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?
- A. Thrombocytopenia
- B. PT elevation
- C. Fibrinogen decreased
- D. Normal aPTT (Correct Answer)
Explanation: ***Normal APTT*** - In Disseminated Intravascular Coagulation (**DIC**), **APTT** is typically **prolonged** due to consumption of clotting factors [1]. - The presence of normal APTT indicates that coagulation pathways are not significantly affected, which is contrary to what is seen in DIC. *Fibrinogen decreased* - **Decreased fibrinogen levels** are common in DIC, reflecting its consumption during the coagulation process [1]. - This depletion is linked to the increased clotting and is a hallmark of DIC, making this statement false in the context of the question. *Thrombocytopenia* - **Thrombocytopenia** occurs in DIC as platelets are consumed during the formation of microclots [1]. - A significant drop in platelet count is a key feature of DIC, therefore this statement does not align with the "except" clause. *PT elevation* - Prothrombin Time (**PT**) is usually **elevated** in DIC due to the consumption of clotting factors [1]. - This reflects the ongoing activation of the coagulation cascade, supporting the exclusion in the question context. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.
Question 8: What laboratory findings are associated with common variable hypogammaglobulinemia?
- A. Low serum immunoglobulin levels (Correct Answer)
- B. Decreased B cell count
- C. Increased B cell count
- D. Neutropenia
Explanation: ***Low serum immunoglobulin levels*** - **Common variable hypogammaglobulinemia (CVID)** is characterized by significantly **low levels of IgG, IgA, and/or IgM** due to impaired B cell differentiation into plasma cells. - This deficiency in antibodies is the hallmark of the disorder, explaining the increased susceptibility to infections. *Decreased B cell count* - While CVID involves impaired B cell function, the **B cell counts** in the peripheral blood are typically **normal** or sometimes even elevated [1]. - The problem lies in their inability to differentiate and produce adequate antibodies, not in their numerical presence [1]. *Increased B cell count* - An increased B cell count is not a characteristic finding in CVID; peripheral B cell numbers are usually normal [1]. - If B cell counts are significantly increased, other conditions such as certain **lymphoproliferative disorders** should be considered. *Neutropenia* - **Neutropenia** (low neutrophil count) is not a primary diagnostic feature of CVID, although it can occur in some patients with autoimmune complications. - The defining laboratory finding is the **deficiency of immunoglobulins**, leading to recurrent infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 249-250.
Question 9: Which of the following does not belong to the family of selectins?
- A. P selectin
- B. L selectin
- C. A selectin (Correct Answer)
- D. E selectin
Explanation: ***A selectin*** - ***A selectin*** is not a recognized member of the selectin family, which includes other specific types. - The known selectins are **E-selectin**, **L-selectin**, and **P-selectin**, demonstrating a distinct classification [1]. *E selectin* - E selectin is a specific type of selectin expressed on **endothelial cells** activated by cytokines [1]. - It plays a crucial role in **leukocyte adhesion** during inflammation, distinguishing it as part of the selectin family [1]. *L selectin* - L selectin is involved in the **homing** of leukocytes to lymph nodes and forms part of the selectin family [1]. - Responsible for the initial tethering and rolling of leukocytes on **venular endothelium** [1]. *P selectin* - P selectin is found on platelets and endothelial cells and is critical in the **aggregation** of platelets and leukocytes. - It is also an established member of the selectin family, involved in **inflammatory responses** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.
Question 10: In which type of Hodgkin's Lymphoma are lacunar cells typically observed?
- A. Mixed cellularity type
- B. Lymphocyte predominant type
- C. Nodular Sclerosis type (Correct Answer)
- D. All of the options
Explanation: ***Nodular Sclerosis Type*** - **Lacunar cells** are characteristically seen in **Nodular Sclerosis Hodgkin lymphoma**, which is the most common subtype [1][3]. - These cells are large **Reed-Sternberg cells** with a distinctive morphology, typically found in **fibrous areas** of the lymph node [1]. *Mixed cellularity type* - This subtype is associated with a diverse cell population but does not primarily feature **lacunar cells** [2][4]. - It predominantly contains **Reed-Sternberg cells** without the specific morphology seen in nodular sclerosis [2]. *Lymphocyte predominant* - Lymphocyte predominant type mainly consists of **lymphocytes** with few Reed-Sternberg cells, and lacks **lacunar cells** [5]. - The histology is significantly different, exhibiting a more lymphocytic composition and not the classic lucent spaces [5]. *All of the above* - This option is incorrect as neither **Mixed cellularity** nor **Lymphocyte predominant** types contain **lacunar cells** [2][4][5]. - Lacunar cells are a distinctive feature solely of the **Nodular Sclerosis type** in Hodgkin lymphoma [1]. **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, p. 616. [2] 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. 616-618. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 558-559. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560. [5] 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, p. 618.