NEET-PG 2013 - Pathology Practice Questions

Q: HLA is located on ?

Short arm of chr-6. ***Short arm of chr-6*** - The **Human Leukocyte Antigen (HLA)** complex, crucial for immune recognition, is located on the **short arm of chromosome 6**. [1] - This region, specifically 6p21.3, contains highly polymorphic genes encoding MHC (Major Histocompatibility Complex) proteins. [2] *Long arm of chr-6* - The **long arm of chromosome 6** contains many genes, but the primary HLA complex is not located here. - Genes on the long arm are involved in various cellular functions, but not central to immune recognition via HLA. *Short arm of chr-3* - Genes on **chromosome 3**, including its short arm, are not associated with the primary HLA complex. - Chromosome 3 is known for genes related to conditions such as von Hippel-Lindau disease. *Long arm of chr-3* - The **long arm of chromosome 3** is not the location for the HLA complex. - This region contains genes involved in diverse cellular processes and disease associations, but not immune recognition via HLA molecules. **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. 55-56. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-240.

Q: What is the major fibril protein associated with Primary Amyloidosis?

Immunoglobulin Light Chain. ***AL*** - In Primary Amyloidosis, **AL amyloid** is derived from immunoglobulin light chains produced by **plasma cell dyscrasias** [1]. - This type of amyloidosis is commonly associated with conditions like **multiple myeloma** or monoclonal gammopathy [1]. *Transthyretin* - This protein is associated with **Familial Amyloid Polyneuropathy** and **Senile Systemic Amyloidosis**, not Primary Amyloidosis. - Transthyretin amyloidosis (ATTR) results from **mutations** or **aging**, contributing to different clinical presentations than AL. *AA* - AA amyloidosis is secondary and occurs due to **chronic inflammatory** conditions, such as rheumatoid arthritis or chronic infections. - It is not the main fibril protein in **Primary Amyloidosis**, which is specifically linked to **light chains**. *Procalcitonin* - Procalcitonin is a **biomarker** used primarily for diagnosing bacterial infections, particularly sepsis, and is not involved in amyloidogenesis. - It does not relate to amyloidosis and is not a component of amyloid fibrils. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267.

Q: What is a hamartoma?

Developmental malformation. ***Development malformation*** - A **hamartoma** is a type of **benign tumor** that consists of an overgrowth of mature cells, representing a **developmental malformation** [1]. - It is formed from tissues that are normally present in the affected organ but are disorganized, leading to a characteristic appearance. *Malignant tumor* - Hamartomas are classified as **benign tumors** [1], not malignant, as they do not invade surrounding tissues or metastasize. - Despite being a growth, they do not exhibit the aggressive characteristics of malignant tumors. *Hemorrhage in vessel* - Hemorrhage refers to bleeding within a vessel and is unrelated to the definition or nature of a **hamartoma**. - Hamartomas do not consist of blood or bleeding; instead, they involve disorganized tissue growth. *Metastatic tissue* - Metastatic tissue refers to cancerous cells that have spread from their original site, which contrasts with the **non-cancerous** nature of hamartomas [1]. - Hamartomas do not involve the spread of cancer cells, but rather a **local abnormality** in tissue arrangement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-482.

Q: All are growth promoting oncogenes except ?

TGF-β. ***TGF-p*** - **TGF-p (Transforming Growth Factor beta)** is primarily known as a **growth inhibitory** factor rather than a promoting oncogene. - It plays a crucial role in **cell differentiation**, **apoptosis**, and inhibits cell proliferation, counteracting the effects of other oncogenes. *TGF-a* - **TGF-a (Transforming Growth Factor alpha)** is a **growth factor** that stimulates cell proliferation and is involved in various cancers [1][2]. - It binds to the **EGF receptor**, promoting growth and tumor development. *PDGF* - **PDGF (Platelet-Derived Growth Factor)** acts as a potent **mitogen** for connective tissue cells and is involved in wound healing and tumor growth [2][4]. - It plays a central role in promoting cell proliferation and migration, contributing to cancer progression [4]. *FGF* - **FGF (Fibroblast Growth Factor)** promotes mitosis and is crucial in **angiogenesis**, wound healing, and several developmental processes [2]. - Its overexpression is linked to various tumors, making it a significant oncogenic growth promoter [2][3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 30-31. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 292. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32.

Q: Which of the following statements is true regarding light microscopy findings in minimal change disease?

No significant changes are seen under light microscopy.. ***No change seen*** - In minimal change disease, **light microscopy** typically shows no significant changes, which is a key characteristic of the condition [1]. - The disease primarily affects the **podocytes** leading to **nephrotic syndrome**, while light microscopy does not reveal any abnormalities [1]. *Loss of foot process seen* - Loss of foot processes is actually observed under **electron microscopy**, not light microscopy. - Light microscopy remains normal, differentiating minimal change disease from other glomerular diseases. *IgA deposits seen* - IgA deposits are associated with **IgA nephropathy**, which is a different condition characterized by mesangial deposition. - Minimal change disease does not have **immunofluorescence** findings, and thus shows no such deposits on light microscopy [1]. *Anti GBM Abs seen* - Anti-GBM antibodies are characteristic of **Goodpasture syndrome**, which presents with significant changes in glomerular structure. - In minimal change disease, there are no **anti-GBM antibodies** or major changes visible under light microscopy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.

Q: Gastric carcinoma is associated with all of the following EXCEPT:

Activation of RAS. ***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.

Q: Linitis plastica is a type of ?

Manifestation of gastric cancer. ***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.

Q: Centrilobular necrosis of the liver may be seen with?

CCl4. ***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 1

Which of the following statements about wound healing is false?

Accepted Answer

Hematomas promote wound healing

Answer

Inhibited by diabetes mellitus (DM)

Answer

Inhibited by foreign body

Answer

Inhibited by infection

Question 2

HLA is located on ?

Accepted Answer

Short arm of chr-6

Answer

Long arm of chr-6

Answer

Short arm of chr-3

Answer

Long arm of chr-3

Question 3

What is the major fibril protein associated with Primary Amyloidosis?

Accepted Answer

Immunoglobulin Light Chain

Answer

Amyloid Associated protein (AA)

Answer

Procalcitonin (PCT)

Answer

Transthyretin (TTR)

Question 4

What is a hamartoma?

Accepted Answer

Developmental malformation

Answer

Malignant tumor

Answer

Metastatic tissue

Answer

Hemorrhage in vessel

Question 5

All are growth promoting oncogenes except ?

Accepted Answer

TGF-β

Answer

FGF

Answer

PDGF

Answer

TGF-α

Question 6

Which of the following statements is true regarding light microscopy findings in minimal change disease?

Accepted Answer

No significant changes are seen under light microscopy.

Answer

Foot process effacement is observed under electron microscopy, not light microscopy.

Answer

Anti-GBM antibodies are associated with Goodpasture syndrome, not minimal change disease.

Answer

IgA deposits are characteristic of IgA nephropathy, not minimal change disease.

Question 7

Gastric carcinoma is associated with all of the following EXCEPT:

Accepted Answer

Activation of RAS

Answer

Over expression of C-met

Answer

Inactivation of p53

Answer

Over expression of C-erb

Question 8

Linitis plastica is a type of ?

Accepted Answer

Manifestation of gastric cancer

Answer

Benign ulcer

Answer

GIST

Answer

Plastic-like appearance of stomach lining

Question 9

Centrilobular necrosis of the liver may be seen with?

Accepted Answer

CCl4

Answer

Arsenic

Answer

Ethanol

Answer

Phosphorus

Question 10

What are Councilman bodies and in which condition are they typically observed?

Accepted Answer

Acute viral hepatitis

Answer

Wilson's disease

Answer

Ballooning degeneration of hepatocytes

Answer

Alcoholic liver disease

NEET-PG 2013 — Pathology