NEET-PG 2013 - Pathology Practice Questions

Q: In glomerulus subendothelial deposits are seen in?

MPGN type I (subendothelial deposits). ***MPGN type I*** - **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1]. - This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1]. *Good pasture syndrome* - Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits. - Typically, it presents with **crescent formation** in the glomeruli rather than deposits. *MPGN type II* - Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1]. - It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology. *IgA nephropathy* - Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially. - It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.

Q: Amyloidosis is associated with all of the following conditions except?

Chronic bronchitis. ***Chronic bronchitis*** - Chronic bronchitis is primarily characterized by **inflammation of the airways** and **excess mucus production**, not typically associated with amyloidosis [1]. - Amyloidosis more commonly relates to chronic inflammatory states but does not directly result from the long-term exposure seen in chronic bronchitis [1]. *Tuberculosis* - Tuberculosis can lead to chronic inflammation, which may precipitate **secondary amyloidosis** due to persistent infection [1]. - It often causes systemic effects, including weight loss and fever, which can result in **amyloid deposition** [1]. *Osteomyelitis* - Osteomyelitis, as a chronic bone infection, can trigger an inflammatory response leading to **secondary amyloidosis** [1]. - The ongoing inflammation can result in the accumulation of amyloid proteins in the bone and surrounding tissues [1]. *Bronchiectasis* - Bronchiectasis often results from persistent lung infections leading to chronic inflammation, which can cause **amyloid deposition** [1,3]. - It is associated with recurrent lung infections and can lead to systemic complications, including amyloidosis [1,3]. **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. 135-136. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 269-270.

Q: Which of the following is a sign of reversible injury in alcoholic liver disease?

Cytoplasmic vacuole. ***Cytoplasmic vacuole*** - The presence of **cytoplasmic vacuoles** in liver cells indicates fatty change, which is a **reversible injury** in alcoholic liver disease [1][2]. - This injury allows the liver to recover if **alcohol consumption** is ceased, highlighting its reversible nature [1]. *Nuclear karyolysis* - **Nuclear karyolysis** signifies severe cellular damage and necrosis, indicating an irreversible process [2]. - This feature involves the dissolution of the nucleus, which does not align with reversible injury. *Loss of cell membrane* - Loss of the **cell membrane** indicates irreversible damage, leading to cell death rather than a reversible condition [2]. - This change is associated with significant cellular impairment, contrary to the concept of recovery. *Pyknosis* - **Pyknosis**, the condensation of chromatin in the nucleus, suggests irreversible cellular injury and impending necrosis [2]. - It is often a precursor to cell death and is not indicative of reversible damage in liver pathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-850. [2] 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. 51-53.

Q: Which of the following are examples of trinucleotide repeat mutations?

All of the options. ***All of the options*** - **Fragile X syndrome**, **Friedreich ataxia**, and **Huntington's chorea** are all well-known examples of genetic disorders caused by trinucleotide repeat expansions [1]. - The mutations involve an abnormal increase in the number of repetitions of a specific three-nucleotide sequence in the DNA [1]. *Fragile X syndrome* - This condition is caused by an expansion of the **CGG repeat** in the **FMR1 gene** on the X chromosome [1]. - The expansion leads to hypermethylation and silencing of the gene, impairing the production of fragile X mental retardation protein [1]. *Friedreich ataxia* - This is an autosomal recessive neurodegenerative disorder caused by an expansion of the **GAA repeat** in an intron of the **frataxin gene (FXN)**. - The repeat expansion interferes with transcription, leading to reduced frataxin protein levels. *Huntington's chorea* - This is an autosomal dominant neurodegenerative disorder caused by an expansion of the **CAG repeat** in the **huntingtin gene (HTT)**. - The expanded polyglutamine tract in the huntingtin protein leads to protein misfolding and neuronal damage, particularly in the striatum [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 177-181.

Q: Trophozoites in stool are characteristically seen in which of the following conditions?

**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.

Q: ABO isoantibodies are of which class?

IgM. ***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.

Q: The most common subtype of Non-Hodgkin's lymphoma in India is:

Diffuse large B cell lymphoma. ***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.

Q: In Articular cartilage, most active chondrocytes are seen in ?

Zone 2. ***Zone 2*** - This is the **transitional (or middle) zone**, where chondrocytes are numerous and more metabolically active, responsible for synthesizing major components of the extracellular matrix. - Chondrocytes here are typically **ovoid or round**, arranged somewhat randomly, and are involved in maintaining the cartilage structure. *Zone 1* - This is the **superficial (or tangential) zone**, where chondrocytes are **flattened** and oriented parallel to the articular surface. - Their primary role is to resist shear forces, and they are generally less metabolically active compared to those in the transitional zone. *Zone 3* - This is the **deep (or radial) zone**, characterized by **columnar arrangements** of chondrocytes. [1] - While these chondrocytes are metabolically active and synthesize matrix components, they are generally less active than those in the transitional zone and are more involved in resisting compressive forces. *Zone 4* - This is the **calcified zone**, directly adjacent to subchondral bone, where chondrocytes are **sparse** and often hypertrophic prior to eventual calcification. - This zone acts as an interface between cartilage and bone, and its chondrocytes have significantly reduced metabolic activity once calcification occurs. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1184.

Q: What are the common causes of vertebra plana?

All of the options. ***All of the options*** - **Vertebra plana** refers to the severe flattening of a vertebral body, often caused by a destructive lesion, and all listed options are known causes. [5] - While **eosinophilic granuloma** is a classic cause, **metastatic disease** and **tuberculosis** can also lead to significant vertebral collapse. [3], [5] *Eosinophilic granuloma* - This is a benign condition, a form of **Langerhans cell histiocytosis**, which commonly affects children and can cause vertebra plana. [1] - It results from proliferative lesions of **Langerhans cells** that infiltrate the bone, leading to its destruction and collapse. [1] *Metastatic disease* - **Malignant tumors** often spread to the spine, causing osteolytic lesions that weaken the vertebral body. [4], [5] - The destruction caused by metastatic deposits can lead to **vertebral collapse** and associated pain. [5] *Tuberculosis* - **Tuberculosis of the spine (Pott's disease)** is an infectious inflammatory condition that can severely damage vertebral bodies. [2], [3] - The granulomatous inflammation and caseous necrosis can erode the bone, leading to **vertebral collapse** and kyphosis. [2] **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. 630. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1197-1198. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 669-670. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672.

Q: Which of the following is a major feature of Alagille syndrome?

Bile duct paucity. ***Bile duct paucity*** - **Bile duct paucity** is a hallmark histologic finding in Alagille syndrome, leading to **cholestasis** and liver disease. - This results from the reduced number of **intrahepatic bile ducts**, which are crucial for bile flow. *IHBR dilation* - **Intrahepatic biliary radical (IHBR) dilation** is characteristic of biliary obstruction, which is not the primary feature of Alagille syndrome. - Alagille syndrome is primarily a genetic condition leading to **hypoplasia or paucity** of bile ducts, not dilation. *PBC* - **Primary Biliary Cholangitis (PBC)** is an autoimmune disease primarily affecting **small intrahepatic bile ducts**, leading to their destruction and fibrosis [1]. - It is typically seen in middle-aged women and is characterized by **antimitochondrial antibodies (AMA)**, which are not features of Alagille syndrome. *PSC* - **Primary Sclerosing Cholangitis (PSC)** is a chronic cholestatic liver disease characterized by **inflammation and fibrosis** of both intrahepatic and extrahepatic bile ducts [2]. - PSC is strongly associated with **inflammatory bowel disease (IBD)** and **ANCA positivity**, which are distinct from the genetic basis and features of Alagille syndrome [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 864-865. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 865-866.

Question 1

In glomerulus subendothelial deposits are seen in?

Accepted Answer

MPGN type I (subendothelial deposits)

Answer

Goodpasture syndrome (linear IgG deposits in the basement membrane)

Answer

MPGN type II (intramembranous deposits)

Answer

IgA nephropathy (mesangial IgA deposits)

Question 2

Amyloidosis is associated with all of the following conditions except?

Accepted Answer

Chronic bronchitis

Answer

Osteomyelitis

Answer

Bronchiectasis

Answer

Tuberculosis

Question 3

Which of the following is a sign of reversible injury in alcoholic liver disease?

Accepted Answer

Cytoplasmic vacuole

Answer

Pyknosis (nuclear shrinkage)

Answer

Loss of cell membrane integrity

Answer

Nuclear karyolysis (nuclear dissolution)

Question 4

Which of the following are examples of trinucleotide repeat mutations?

Accepted Answer

All of the options

Answer

Friedreich ataxia

Answer

Fragile X syndrome

Answer

Huntington's chorea

Question 5

Trophozoites in stool are characteristically seen in which of the following conditions?

Answer

Ascariasis

Answer

Strongyloidiasis

Answer

Allergic colitis

Answer

Eosinophilic gastroenteritis

Question 6

ABO isoantibodies are of which class?

Accepted Answer

IgM

Answer

IgG

Answer

IgD

Answer

IgA

Question 7

The most common subtype of Non-Hodgkin's lymphoma in India is:

Accepted Answer

Diffuse large B cell lymphoma

Answer

Diffuse small cell lymphocytic lymphoma

Answer

Follicular lymphoma

Answer

Burkitt's lymphoma

Question 8

In Articular cartilage, most active chondrocytes are seen in ?

Accepted Answer

Zone 2

Answer

Zone 1

Answer

Zone 4

Answer

Zone 3

Question 9

What are the common causes of vertebra plana?

Accepted Answer

All of the options

Answer

Eosinophilic granuloma

Answer

Metastatic disease

Answer

Tuberculosis

Question 10

Which of the following is a major feature of Alagille syndrome?

Accepted Answer

Bile duct paucity

Answer

IHBR dilation

Answer

PBC

Answer

PSC

NEET-PG 2013 — Pathology