HLA is located on ?
What is the major fibril protein associated with Primary Amyloidosis?
What is a hamartoma?
All are growth promoting oncogenes except ?
Which of the following conditions is least associated with tumor suppressor genes?
Curschmann's spirals are seen in which condition?
Which of the following is a primary pleural tumor?
What is the primary mechanism involved in the pathogenesis of acute proliferative glomerulonephritis?
Which of the following are examples of trinucleotide repeat mutations?
According to WHO/ISN classification, which class of lupus nephritis shows a membranous pattern in SLE?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 21: HLA is located on ?
- A. Short arm of chr-6 (Correct Answer)
- B. Long arm of chr-6
- C. Short arm of chr-3
- D. Long arm of chr-3
Explanation: ***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.
Question 22: What is the major fibril protein associated with Primary Amyloidosis?
- A. Immunoglobulin Light Chain (Correct Answer)
- B. Amyloid Associated protein (AA)
- C. Procalcitonin (PCT)
- D. Transthyretin (TTR)
Explanation: ***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.
Question 23: What is a hamartoma?
- A. Malignant tumor
- B. Metastatic tissue
- C. Hemorrhage in vessel
- D. Developmental malformation (Correct Answer)
Explanation: ***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.
Question 24: All are growth promoting oncogenes except ?
- A. FGF
- B. PDGF
- C. TGF-α
- D. TGF-β (Correct Answer)
Explanation: ***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.
Question 25: Which of the following conditions is least associated with tumor suppressor genes?
- A. Neurofibromatosis
- B. Retinoblastoma
- C. Acute Myeloid Leukemia (AML) (Correct Answer)
- D. Breast cancer
Explanation: ***Multiple endocrine neoplasia*** - This syndrome involves mutations in **proto-oncogenes** like RET rather than tumor suppressor genes. - The condition is mainly characterized by the presence of **multiple endocrine tumors** rather than a failure of tumor suppression. *Retinoblastoma* - Associated with mutations in the **RB1 tumor suppressor gene**, leading to uncontrolled cell proliferation [1] [2]. - Classic example of **loss of function** in a tumor suppressor gene resulting in cancer, specifically in early childhood [1] [2]. *Neurofibromatosis* - Caused by mutations in **NF1** or **NF2 genes**, both of which function as tumor suppressors. - Leads to benign tumors such as **neurofibromas** and other neurogenic tumors due to malfunction in tumor suppression. *Breast cancers* - Often related to mutations in tumor suppressor genes such as **BRCA1** and **BRCA2**, which increase cancer risk [2]. - Implicated in the hereditary form of breast and ovarian cancers due to their roles in DNA repair and cell cycle regulation [2]. **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. 227-228. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-302.
Question 26: Curschmann's spirals are seen in which condition?
- A. Bronchiectasis
- B. Chronic bronchitis
- C. Wegener's granulomatosis
- D. Bronchial asthma (Correct Answer)
Explanation: ***Bronchial asthma*** - **Curschmann's spirals** are spiral-shaped mucus plugs found in the sputum of patients with **bronchial asthma**. - They represent casts from small bronchi and are formed from **mucus and cellular debris** within the airways during an asthmatic exacerbation. *Bronchiectasis* - Characterized by **permanent abnormal dilation** of the bronchi due to chronic inflammation and infection, leading to productive cough and recurrent respiratory infections. - While it involves mucous production, it is typically associated with **purulent sputum** due to bacterial colonization, not necessarily Curschmann's spirals. *Chronic bronchitis* - Defined clinically by a **chronic productive cough** for at least three months in each of two successive years, without other causes. - Involves mucus hypersecretion and inflammation, but **Curschmann's spirals are not a characteristic finding** compared to asthma. *Wegener's granulomatosis (Granulomatosis with Polyangiitis)* - This is a systemic **vasculitis** affecting small to medium-sized blood vessels, typically involving the upper and lower respiratory tracts and kidneys. - Its pulmonary manifestations include **nodules, cavities, and diffuse alveolar hemorrhage**, and sputum findings are related to inflammation and bleeding, not Curschmann's spirals.
Question 27: Which of the following is a primary pleural tumor?
- A. Mesothelioma (Correct Answer)
- B. Myxoma
- C. Lipoma
- D. None of the options
Explanation: ***Mesothelioma*** - Mesothelioma is a **primary malignant tumor** of the pleura [1], commonly associated with **asbestos exposure** [2]. - It typically presents with symptoms like **pleuritic chest pain**, dyspnea, and pleural effusion. *Myxoma* - Myxoma is a **benign tumor** primarily found in the **heart**, particularly in the left atrium, not in the pleura. - It does not arise from pleural tissue and lacks the **malignant characteristics** of mesothelioma. *All* - This option suggests that multiple tumors can be primary pleural tumors, which is incorrect as only mesothelioma is recognized as such. - Other tumors like myxoma and lipoma do not originate in the pleura and thus cannot be classified as primary pleural tumors. *Lipoma* - Lipoma is a **benign tumor** made up of adipose tissue [3] and is typically found in *subcutaneous tissue*, not the pleural cavity. - It does not have the malignant potential or association with pleural disease that characterizes mesothelioma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 728-729. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 339-340. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1222.
Question 28: What is the primary mechanism involved in the pathogenesis of acute proliferative glomerulonephritis?
- A. Immune complex mediated (Correct Answer)
- B. T-cell mediated cytotoxicity
- C. Direct antibody-mediated injury
- D. Type IV hypersensitivity reaction
Explanation: ***Immune complex mediated*** - The pathogenesis of **acute proliferative glomerulonephritis** is primarily caused by **immune complexes** that deposit in the glomeruli, leading to inflammation [1]. - This is typically associated with **post-streptococcal infections**, where the body's immune response generates complexes that affect kidney function [1]. *Cytotoxic T-cell mediated* - This mechanism involves T-cells directly damaging cells, which is not the primary cause of **acute proliferative glomerulonephritis**. - It is more relevant in conditions like **viral infections** or **transplant rejection**, rather than immune complex diseases. *Antibody mediated* - While antibodies play a role in various diseases, acute proliferative glomerulonephritis is primarily mediated by **immune complexes**, not just antibodies alone [1]. - This oes not account for the presence of **complexes formed from antigens**, which is crucial in the pathogenesis [1]. *Cell-mediated (Type IV)* - Type IV hypersensitivity involves delayed-type hypersensitivity, typically seen in **tuberculosis** or **contact dermatitis**, not in acute glomerulonephritis. - The inflammation in this case is due to **immune complexes**, rather than a purely cell-mediated response [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-916.
Question 29: Which of the following are examples of trinucleotide repeat mutations?
- A. Friedreich ataxia
- B. Fragile X syndrome
- C. Huntington's chorea
- D. All of the options (Correct Answer)
Explanation: ***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.
Question 30: According to WHO/ISN classification, which class of lupus nephritis shows a membranous pattern in SLE?
- A. Diffuse proliferative pattern
- B. Membranous pattern (Correct Answer)
- C. Mesangial pattern involvement
- D. Focal proliferative pattern
Explanation: ***Membranous pattern*** - This corresponds to **Class V lupus nephritis** in the WHO/ISN classification, characterized by widespread immune complex deposition along the **glomerular basement membrane (GBM)**. - The subepithelial immune deposits lead to GBM thickening, creating the characteristic membranous pattern on light microscopy. - This pattern resembles idiopathic membranous nephropathy but occurs in the context of SLE. *Mesangial pattern involvement* - This refers to **Class I (minimal mesangial LN)** or **Class II (mesangial proliferative LN)**, where immune deposits are primarily confined to the mesangium. - There is minimal or no involvement of the glomerular capillary walls, distinguishing it from the membranous pattern. *Diffuse proliferative pattern* - This is **Class IV lupus nephritis**, the most severe form characterized by widespread **endocapillary and/or extracapillary proliferation** involving ≥50% of glomeruli. - The primary feature is cellular proliferation (mesangial, endocapillary, epithelial crescents), not the subepithelial immune deposits typical of membranous pattern. *Focal proliferative pattern* - This corresponds to **Class III lupus nephritis**, involving **endocapillary or extracapillary proliferation** in <50% of glomeruli. - Distinguished by focal (not diffuse) involvement and active proliferation rather than the membranous pattern seen in Class V.