Internal Medicine
2 questionsWhich of the following is not a typical feature of haemolytic uremic syndrome?
Which of the following is not an obstructive lung disease?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 361: Which of the following is not a typical feature of haemolytic uremic syndrome?
- A. Splenomegaly (Correct Answer)
- B. Anemia
- C. Renal microthrombi
- D. Hyperkalemia
Explanation: ***Neuro psychiatric disturbances*** - Neuropsychiatric disturbances are not a direct feature of hemolytic uremic syndrome (HUS), which primarily affects renal and hematological systems. - HUS is characterized by a triad of **hemolytic anemia**, **thrombocytopenia**, and **acute renal failure**, without specific neuropsychiatric manifestations [2]. *Anaemia* - **Hemolytic anemia** is a key feature of HUS due to red blood cell destruction [1], [2]. - Patients often exhibit signs of **fatigue and pallor**, distinguishing it from other renal syndromes [3]. *Renal microthrombi* - HUS is characterized by the formation of **microthrombi in renal vasculature**, leading to acute kidney injury [1]. - The presence of these microthrombi is fundamental to the pathology of HUS [1]. *Hyperkalemia* - Renal failure in HUS can lead to **hyperkalemia** due to decreased potassium excretion. - It is a common complication associated with the acute renal failure seen in HUS.
Question 362: Which of the following is not an obstructive lung disease?
- A. Emphysema
- B. Interstitial fibrosis (Correct Answer)
- C. Asthma
- D. Bronchitis
Explanation: ***Interstitial fibrosis*** - **Interstitial fibrosis** is a **restrictive lung disease**, characterized by **reduced lung elasticity** and lung volumes, rather than airway obstruction [1]. - In this condition, the **lung tissue becomes scarred and stiff**, making it difficult to expand fully during inspiration [1]. *Emphysema* - **Emphysema** is a classic **obstructive lung disease** caused by the destruction of the **alveolar walls**, leading to enlarged air spaces and loss of elastic recoil [3]. - This destruction results in **airflow limitation**, particularly during exhalation, as airways collapse prematurely. *Asthma* - **Asthma** is an **obstructive lung disease** characterized by **reversible airway inflammation**, bronchoconstriction, and increased mucus production [2]. - These factors lead to **episodic airflow obstruction**, making it difficult to breathe, especially during exacerbations [2]. *Bronchitis* - **Bronchitis**, particularly **chronic bronchitis**, is an **obstructive lung disease** defined by chronic inflammation of the bronchi. - This inflammation causes **mucus hypersecretion** and narrowing of the airways, leading to persistent cough and airflow limitation.
Pathology
7 questionsAccording to WHO/ISN classification, which class of lupus nephritis shows a membranous pattern in SLE?
What is the primary mechanism involved in the pathogenesis of acute proliferative glomerulonephritis?
Which of the following is a primary pleural tumor?
Curschmann's spirals are seen in which condition?
Which of the following conditions is least associated with tumor suppressor genes?
All are growth promoting oncogenes except ?
What is a hamartoma?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 361: 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.
Question 362: 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 363: 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 364: 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 365: 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 366: 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 367: 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.
Psychiatry
1 questionsWhat is the name of the syndrome associated with the deletion of chromosome 22?
NEET-PG 2013 - Psychiatry NEET-PG Practice Questions and MCQs
Question 361: What is the name of the syndrome associated with the deletion of chromosome 22?
- A. Down syndrome
- B. Di George syndrome (Correct Answer)
- C. Turner syndrome
- D. Klinefelter syndrome
- E. Prader-Willi syndrome
Explanation: ***Di George syndrome*** - Di George syndrome, also known as **22q11.2 deletion syndrome**, is caused by a deletion on the long arm of chromosome 22. - This syndrome is associated with varied clinical features, including **congenital heart defects**, **thymic hypoplasia** (leading to immune deficiencies), **hypocalcemia** due to parathyroid hypoplasia, and characteristic facial features. *Down syndrome* - Down syndrome is caused by a **trisomy of chromosome 21**, meaning there's an extra copy of chromosome 21. - It is characterized by intellectual disability, distinctive facial features, and developmental delays, and is not associated with chromosome 22 deletion. *Turner syndrome* - Turner syndrome is a chromosomal condition affecting females, characterized by the partial or complete absence of one of the **X chromosomes (45, X0)**. - It leads to short stature, ovarian dysfunction, and characteristic physical features, unrelated to chromosome 22. *Klinefelter syndrome* - Klinefelter syndrome is a chromosomal disorder in males resulting from an extra **X chromosome (47, XXY)**. - Individuals often experience hypogonadism, reduced fertility, and abnormal body proportions, which is distinct from a deletion on chromosome 22. *Prader-Willi syndrome* - Prader-Willi syndrome is caused by a **deletion of paternal chromosome 15q11-q13** or maternal uniparental disomy. - It presents with hypotonia, hyperphagia, obesity, intellectual disability, and hypogonadism, unrelated to chromosome 22 deletion.