Linitis plastica is a type of ?
What are Councilman bodies and in which condition are they typically observed?
Gastric carcinoma is associated with all of the following EXCEPT:
Centrilobular necrosis of the liver may be seen with?
Trophozoites in stool are characteristically seen in which of the following conditions?
ABO isoantibodies are of which class?
The most common subtype of Non-Hodgkin's lymphoma in India is:
The most common translocation seen in patients with Multiple Myeloma is:
What is a watershed infarct in the brain?
Renal stones which are laminated and irregular in outline are
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 51: Linitis plastica is a type of ?
- A. Benign ulcer
- B. GIST
- C. Manifestation of gastric cancer (Correct Answer)
- D. Plastic-like appearance of stomach lining
Explanation: ***Diffuse carcinoma of stomach*** - Linitis plastica is a specific type of **gastric cancer** characterized by **thickening of the stomach wall**, leading to a rigid, non-distensible abdomen [1]. - It often presents with **significant weight loss** and **early satiety**, distinguishing it from other stomach conditions. *Benign ulcer* - Benign ulcers do not cause the **extensive wall thickening** or **desmoplastic response** seen in linitis plastica [1]. - They typically heal with treatment and are associated with typical ulcer symptoms, unlike the progressive nature of linitis plastica. *Plastic like lining of stomach* - While linitis plastica describes a **plastic-like appearance**, it is not classified as a mere lining change but rather a sign of underlying **malignancy** [1]. - This option misrepresents it as a benign condition rather than a serious **stomach adenocarcinoma**. *GIST* - Gastrointestinal stromal tumors (GIST) are **soft tissue tumors** of mesenchymal origin, differing fundamentally from the **invasive** characteristics of linitis plastica [2]. - GISTs typically present with **mass lesions** in the GI tract, not the diffuse rigidity seen in linitis plastica [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779.
Question 52: What are Councilman bodies and in which condition are they typically observed?
- A. Wilson's disease
- B. Ballooning degeneration of hepatocytes
- C. Acute viral hepatitis (Correct Answer)
- D. Alcoholic liver disease
Explanation: **Option G*****Acute viral hepatitis*** - Councilman bodies are **characteristic histological findings** in acute viral hepatitis, associated with apoptotic hepatocytes [1]. - They represent **necrosis** of liver cells, which is commonly seen during the acute phase of viral infections affecting the liver [1]. *Alcoholic cirrhosis* - While liver damage is present, Councilman bodies are not typical; they are more associated with acute conditions rather than the chronic nature of cirrhosis. - **Fibrosis** and **bridging necrosis** are evident in alcoholic cirrhosis, distinct from the **acute necrotic changes** seen in viral hepatitis. *Ballooning of cells - Damaged cells show diffuse swelling known as ballooning degeneration.* - Ballooning degeneration indicates **cellular swelling**, often noted in conditions like steatosis or alcoholic liver disease, but does not lead to the formation of Councilman bodies. - These changes are different from the **pyknotic or karyolytic changes** associated with Councilman bodies in acute infections. *Hepatic cell necrosis - The necrosis is usually focal or centirzonal.* - This refers to various types of necrosis in the liver but does not specifically indicate the presence of Councilman bodies, which are linked with apoptotic cells. - While necrosis is common in hepatic pathology, Councilman bodies are particularly associated with **viral hepatitis**. *Wilson's disease* - Although it causes liver damage, it typically results in **copper accumulation** and associated features, not specifically Councilman bodies in its pathology. - The findings in Wilson's disease include **hepatocellular degeneration** without the distinct apoptotic features seen in **acute viral hepatitis**. Option F*Autoimmune hepatitis* - This condition may cause liver cell damage and necrosis but does not typically show Councilman bodies in its histological profile. - It primarily shows **interface hepatitis** and **lymphocytic infiltration**, contrasting with the **apoptotic bodies** seen in acute viral scenarios. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 386-387.
Question 53: Gastric carcinoma is associated with all of the following EXCEPT:
- A. Over expression of C-met
- B. Inactivation of p53
- C. Over expression of C-erb
- D. Activation of RAS (Correct Answer)
Explanation: ***Activation of RAS*** - **RAS mutations** are relatively uncommon in gastric carcinoma compared to other gastrointestinal malignancies. While KRAS mutations can occur in approximately 10-15% of gastric cancers (particularly intestinal type), they are **far less frequent** than in **pancreatic adenocarcinoma** (~90%) or **colorectal carcinoma** (~40%). - In the context of gastric carcinoma, RAS pathway alterations are **not considered a major oncogenic driver** compared to the other molecular changes listed, making this the **LEAST characteristically associated** alteration. *Inactivation of p53* - **Inactivation of the p53 tumor suppressor gene** is one of the most frequent molecular events in gastric carcinoma, occurring in approximately **50-60% of cases**. - Loss of p53 function leads to genomic instability, uncontrolled cell proliferation, and resistance to apoptosis, contributing significantly to **tumorigenesis** and **poor prognosis**. *Over expression of C-met* - **Overexpression of C-MET**, a receptor tyrosine kinase for hepatocyte growth factor (HGF), is commonly observed in gastric carcinoma (30-40% of cases) and is strongly linked to **tumor growth**, **invasion**, and **metastasis**. - C-MET amplification and overexpression promote cell proliferation, survival, migration, and angiogenesis, making it an important **therapeutic target** in advanced gastric cancer. *Over expression of C-erb* - **Overexpression of C-erbB-2 (HER2/neu)** is found in approximately **10-20% of gastric adenocarcinomas**, particularly the intestinal type. - HER2 amplification or overexpression is a significant **prognostic and predictive biomarker**, and is specifically targeted by **trastuzumab** (Herceptin) therapy in HER2-positive advanced gastric cancer, improving survival outcomes.
Question 54: Centrilobular necrosis of the liver may be seen with?
- A. Arsenic
- B. Ethanol
- C. CCl4 (Correct Answer)
- D. Phosphorus
Explanation: ***CCl4*** - **Carbon tetrachloride (CCl4)** is the **classic and prototypical** hepatotoxin that causes **centrilobular (zone 3) necrosis**. - The **centrilobular zone (zone 3)** is particularly vulnerable due to its high concentration of **cytochrome P450 enzymes**, which metabolize CCl4 into **toxic free radicals (trichloromethyl radicals)**. - This is the **most characteristic** cause of centrilobular necrosis in toxicology and is the preferred answer for exam purposes. *Ethanol* - **Ethanol** can also cause **centrilobular necrosis** in **alcoholic hepatitis**, as zone 3 is most susceptible to hypoxic injury and oxidative stress. - However, alcoholic liver disease presents with a **spectrum of changes** including steatosis (earliest), hepatitis with ballooning degeneration and Mallory-Denk bodies, and eventual cirrhosis. - While centrilobular necrosis occurs in alcoholic hepatitis, **CCl4 remains the prototype** for pure centrilobular necrosis in exam contexts. *Phosphorus* - **Elemental phosphorus** toxicity causes **periportal (zone 1) necrosis**, which is the opposite pattern from centrilobular necrosis. - It also causes widespread fatty change and hemorrhagic necrosis within the liver. *Arsenic* - **Arsenic poisoning** causes **diffuse/generalized hepatocellular necrosis** and cholestasis, rather than the specific centrilobular pattern. - Chronic exposure is associated with non-cirrhotic portal fibrosis and portal hypertension.
Question 55: Trophozoites in stool are characteristically seen in which of the following conditions?
- A. Ascariasis
- B. Strongyloidiasis
- C. Allergic colitis
- D. Eosinophilic gastroenteritis
Explanation: **Note:** This question has significant issues. Trophozoites in stool are characteristically seen in **protozoal infections** such as *Entamoeba histolytica* (amoebiasis), *Giardia lamblia*, or *Balantidium coli* [1][2] - none of which are listed as options. ***None of the given options is medically accurate*** for characteristic trophozoites in stool. However, if forced to choose from these options: *Ascariasis* - **Ascariasis** is caused by the nematode *Ascaris lumbricoides* - Diagnosis is by identifying **ova (eggs)** in stool, not trophozoites - Trophozoites are protozoal forms, not associated with helminthic infections [2] *Strongyloidiasis* - Caused by *Strongyloides stercoralis* (nematode) - Typically diagnosed by finding **rhabditiform or filariform larvae** in stool - Not characterized by trophozoites in routine stool examination *Eosinophilic gastroenteritis* - Inflammatory condition with **eosinophilic infiltration** of GI tract - Not a parasitic infection - No trophozoites present - diagnosis is by endoscopic biopsy showing eosinophils *Allergic colitis* - Inflammatory condition related to **food allergies** (common in infants) - Presents with blood and mucus in stool with eosinophilia - Not an infectious process - no trophozoites present **Clinical Pearl:** Trophozoites (motile feeding stage of protozoa) in stool are diagnostic of **acute intestinal protozoal infections** like amoebiasis or giardiasis, where they must be identified in fresh, warm stool samples as they rapidly deteriorate [1][2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 364-365. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 801-802.
Question 56: ABO isoantibodies are of which class?
- A. IgG
- B. IgM (Correct Answer)
- C. IgD
- D. IgA
Explanation: ***IgM*** - Naturally occurring **ABO isoantibodies** are predominantly of the **IgM class**. - These **pentameric antibodies** are highly effective at causing **agglutination** of incompatible red blood cells, which is crucial in transfusion reactions [1]. *IgG* - While IgG antibodies can be formed against ABO antigens (e.g., in hemolytic disease of the newborn), the **naturally occurring isoantibodies** are primarily IgM. - IgG antibodies are **monomeric** and can cross the **placenta**, which is a key difference from the primary IgM ABO antibodies. *IgD* - **IgD** antibodies are primarily found on the surface of **B cells** and play a role in B cell activation. - They are **not a primary mediator** of ABO isoantibody response or red blood cell agglutination. *IgA* - **IgA** antibodies are predominantly found in **mucosal secretions** and play a role in mucosal immunity. - While some IgA may be present, it is **not the predominant class** for naturally occurring ABO isoantibodies involved in transfusion reactions. **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. 154-155.
Question 57: The most common subtype of Non-Hodgkin's lymphoma in India is:
- A. Diffuse small cell lymphocytic lymphoma
- B. Diffuse large B cell lymphoma (Correct Answer)
- C. Follicular lymphoma
- D. Burkitt's lymphoma
Explanation: ***Diffuse large B cell lymphoma*** - It is the most common subtype of **Non-Hodgkin's lymphoma** observed in India, reflecting a higher prevalence in the population. - Characterized by **aggressive clinical behavior** [1] and typically presents as a rapidly enlarging mass, often involving lymph nodes or extranodal sites. *Burkitt's lymphoma* - This subtype is known for its **high proliferation rate** and is more common in specific demographics, such as children and immunocompromised individuals. - It typically presents with **jaw lesions** or abdominal masses, which is not typical in the broader Indian population. *Diffuse small cell lymphocytic lymphoma* - More accurately classified as **chronic lymphocytic leukemia** (CLL), it is not the most common subtype of Non-Hodgkin's lymphoma. - Characterized by a **milder clinical course** and presents with lymphocytosis in peripheral blood, lacking aggressive features. *Follicular lymphoma* - This is usually a **low-grade lymphoma** associated with **indolent behavior** and may not be the most commonly diagnosed subtype in India. - It typically involves multiple lymph nodes and is characterized by **nodular patterns on histology**, making it less prevalent than diffuse large B cell lymphoma. Follicular lymphoma is rare in Asian populations [2]. **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. 563-564. [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. 602-604.
Question 58: The most common translocation seen in patients with Multiple Myeloma is:
- A. t(14;16)
- B. t(4;14)
- C. t(11;14) (Correct Answer)
- D. t(14;20)
Explanation: ***t(11;14)*** - This translocation is the **most common cytogenetic abnormality** found in patients with multiple myeloma, occurring in approximately 15-20% of cases. - It results in the juxtaposition of the **IgH gene on chromosome 14** with the **cyclin D1 gene on chromosome 11**, leading to overexpression of cyclin D1. *t(4;14)* - This translocation, occurring in about 5-10% of patients, is associated with a **poor prognosis** in multiple myeloma. - It involves the IgH gene on chromosome 14 and the **FGFR3 and MMSET genes on chromosome 4**, leading to their upregulation. *t(14;16)* - This translocation is also associated with a **poor prognosis** and is less common than t(11;14) or t(4;14), found in about 2-5% of cases. - It involves the **IgH gene on chromosome 14** and the **c-MAF gene on chromosome 16**, leading to overexpression of c-MAF. *t(14;20)* - This translocation is **rarely observed** in multiple myeloma patients, typically occurring in less than 1% of cases. - It involves the **IgH gene on chromosome 14** and the **MAFB gene on chromosome 20**, which can also contribute to disease progression.
Question 59: What is a watershed infarct in the brain?
- A. Occurs in the border zones between major arteries (Correct Answer)
- B. Occurs in the areas supplied by only one artery
- C. Occurs in the terminal portion of main arteries
- D. Occurs only in areas with complete arterial occlusion
Explanation: ***Occurs in the border zones between major arteries*** - A **watershed infarct** or **border zone infarct** arises in areas where the **perfusion** from two different arterial territories meets [1]. - These areas are particularly vulnerable to ischemia during periods of **systemic hypoperfusion**, as blood flow is lowest at the "watershed" of these overlapping supply zones [1]. *Occurs in the areas supplied by only one artery* - Infarcts in areas supplied by only one artery are typically seen in **lacunar strokes**, affecting **deep penetrating arteries** and not necessarily watershed areas [2]. - These are often due to occlusion of a single, small perforating artery, leading to a **discrete, localized lesion**. *Occurs only in areas with complete arterial occlusion* - Watershed infarcts result from **systemic hypoperfusion** rather than complete arterial occlusion [1]. - They occur when global reduction in cerebral blood flow affects the **most vulnerable border zones**, even without complete vessel occlusion. - Complete arterial occlusions typically cause **territorial infarcts** in the distribution of that specific artery. *Occurs in the terminal portion of main arteries* - Infarcts in the terminal portions of main arteries are more consistent with **embolic or thrombotic events** directly occluding that specific artery. - A watershed infarct is distinct as it results from a **global reduction in cerebral blood flow**, affecting the *most distal* and *least well-perfused regions*. **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. 150-151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1266-1268.
Question 60: Renal stones which are laminated and irregular in outline are
- A. Uric acid
- B. Calcium oxalate (Correct Answer)
- C. Struvite
- D. Cystine
Explanation: ***Calcium oxalate*** - **Calcium oxalate stones** are the most common type of kidney stones and characteristically present with a **laminated** (layered) and **irregular, spiculated outline** due to their crystalline structure - They are typically **radio-opaque** on X-rays due to their calcium content - The irregular outline distinguishes them from other stone types *Uric acid* - **Uric acid stones** are often **smooth**, hard, and **yellowish-brown** in appearance - They are **radio-lucent** on standard X-rays and are associated with conditions like gout or acidic urine - Their smooth surface contrasts with the irregular calcium oxalate stones *Struvite* - **Struvite stones** (magnesium ammonium phosphate) are strongly associated with **urinary tract infections** (UTIs) and can form **staghorn calculi**, filling the renal pelvis - They tend to be **friable** and have a **smooth or glistening** surface, often growing quite large - Associated with urease-producing bacteria *Cystine* - **Cystine stones** are caused by a genetic disorder affecting amino acid transport and generally appear **smooth, waxy, and hexagonal crystal-shaped** - They are typically **moderately radio-opaque** but less dense than calcium stones - The smooth, waxy appearance differs from the irregular calcium oxalate stones