NEET-PG 2015

1414 Questions — Page 40 of 142

Anatomy

2 questions

Q391

Which type of glial cell is derived from mesodermal origin?

Q392

Elastic fibers of tunica media are secreted by

NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs

Question 391: Which type of glial cell is derived from mesodermal origin?

A. Macroglial cells
B. Microglial cells (Correct Answer)
C. Oligodendrocytes
D. Ependymal cells

Explanation: ***Microglial cells*** - **Microglial cells** are unique among glial cells as they originate from **mesoderm**, specifically from **monocyte/macrophage precursors** in the bone marrow [1]. - They function as the **immune cells of the central nervous system (CNS)**, scavenging for plaques, damaged neurons, and infectious agents [1]. *Macroglial cells* - This is a broad category that includes **astrocytes, oligodendrocytes, and ependymal cells**, all of which are derived from **neuroectoderm**, not mesoderm [1]. - They perform various supportive roles but are distinct in origin from microglial cells [1]. *Oligodendrocytes* - **Oligodendrocytes** are derived from **neuroectoderm** and are responsible for forming the **myelin sheath** around axons in the CNS [2]. - Myelination is crucial for rapid and efficient nerve impulse conduction. *Ependymal cells* - **Ependymal cells** are derived from **neuroectoderm** and line the **ventricles of the brain** and the **central canal of the spinal cord**. - They play a role in the production and circulation of **cerebrospinal fluid (CSF)**.

Question 392: Elastic fibers of tunica media are secreted by

A. Endothelium
B. Smooth muscle (Correct Answer)
C. External lamina
D. Fibroblast

Explanation: Correct: Smooth muscle - Smooth muscle cells within the tunica media are primarily responsible for synthesizing and secreting elastic fibers along with collagen and proteoglycans [1] - This extracellular matrix provides elasticity and structural integrity to blood vessels, allowing them to stretch and recoil with blood flow [1] - In elastic arteries (like the aorta), smooth muscle cells produce fenestrated elastic membranes that are characteristic of the tunica media Incorrect: Endothelium - Endothelial cells form the innermost lining of blood vessels (tunica intima) and are involved in regulating vascular tone, blood clotting, and inflammation [1] - They do not typically secrete the bulk of elastic fibers found in the tunica media Incorrect: External lamina - The external lamina (or external basal lamina) is an extracellular matrix layer, not a cellular component that secretes elastic fibers - It is actually secreted by the smooth muscle cells themselves and serves as structural support around individual muscle cells Incorrect: Fibroblast - Fibroblasts are connective tissue cells that primarily produce collagen and other extracellular matrix components in many tissues - While they contribute to the tunica adventitia (outermost layer), the tunica media's elastic fibers are primarily produced by smooth muscle cells [1]

Biochemistry

2 questions

Q391

What primarily forms the core of chylomicrons?

Q392

Transport of lipids from the intestine to other tissues is by -

NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs

Question 391: What primarily forms the core of chylomicrons?

A. Triglycerides and Cholesterol together
B. Triglycerides (Correct Answer)
C. Free fatty acids
D. Triglyceride, Cholesterol and Phospholipids

Explanation: ***Triglycerides*** - Chylomicrons are primarily responsible for transporting **dietary triglycerides** from the intestines to other tissues. - Their large core, composed mainly of **triglycerides**, allows efficient transport of these hydrophobic molecules. *Triglycerides and Cholesterol together* - While **cholesterol** is present in chylomicrons, it is less abundant than **triglycerides** and primarily exists as **cholesterol esters** in the core. - The core is not an equal mixture; **triglycerides** overwhelmingly dominate the volume. *Free fatty acids* - **Free fatty acids** are transported in the blood primarily bound to **albumin**, not within the core of chylomicrons. - Chylomicrons typically carry **esterified fatty acids** as part of triglycerides. *Triglyceride, Cholesterol and Phospholipids* - **Phospholipids** form the outer monolayer of the chylomicron, along with apoproteins, making them **amphipathic**. - They do not constitute a core component but rather the **surface interface** with the aqueous environment.

Question 392: Transport of lipids from the intestine to other tissues is by -

A. Chylomicrons (Correct Answer)
B. LDL
C. HDL
D. VLDL

Explanation: ***Chylomicrons*** - **Chylomicrons** are the **largest lipoprotein particles** that transport **dietary (exogenous) lipids** from the **intestine** to peripheral tissues - They are synthesized in **intestinal enterocytes** after fat absorption and enter the bloodstream via the **lymphatic system (thoracic duct)** - They carry **triglycerides (85-95%), cholesterol, phospholipids, and fat-soluble vitamins** (A, D, E, K) - **Apolipoprotein B-48** is the characteristic structural protein of chylomicrons - After delivering triglycerides to tissues (via lipoprotein lipase), chylomicron remnants are taken up by the **liver** *LDL (Low-Density Lipoprotein)* - LDL transports **cholesterol from the liver to peripheral tissues** (not from intestine) - It carries **endogenous cholesterol**, not dietary lipids from the intestine - Often called "**bad cholesterol**" due to its role in atherosclerosis - Contains **Apolipoprotein B-100** *HDL (High-Density Lipoprotein)* - HDL performs **reverse cholesterol transport** - moving excess cholesterol from peripheral tissues **back to the liver** - It does **not transport lipids from the intestine** to tissues - Called "**good cholesterol**" for its protective cardiovascular role - Contains **Apolipoprotein A-I and A-II** *VLDL (Very-Low-Density Lipoprotein)* - VLDL is synthesized in the **liver** (not intestine) and transports **endogenous triglycerides** to peripheral tissues - It carries lipids **from the liver**, not from the intestine - VLDL is converted to IDL and then LDL after losing triglycerides - Contains **Apolipoprotein B-100**

Community Medicine

1 questions

Q391

The strongest occupational risk factor for hematological carcinoma is

Internal Medicine

1 questions

Q391

Which of the following does not predispose to leukemia?

Pathology

4 questions

Q391

Which protein is defective in dilated cardiomyopathy?

Q392

Lines of Zahn are LEAST likely to be seen in -

Q393

Which of the following is a type of small vessel vasculitis?

Q394

Radiotherapy induced radiation pneumonitis is mediated by all of the following cytokines and factors except -

NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs

Question 391: Which protein is defective in dilated cardiomyopathy?

A. Tropomyosin
B. Myosin
C. Troponin
D. Dystrophin (Correct Answer)

Explanation: ***Dystrophin*** - **Dystrophin** is a crucial protein in the **muscle cell membrane** that anchors the cytoskeleton to the extracellular matrix. - Defects in dystrophin lead to sarcolemmal fragility, causing muscle damage and can result in **dilated cardiomyopathy**, especially in conditions like **Duchenne muscular dystrophy** [1]. *Myosin* - **Myosin** is a fundamental **motor protein** involved in muscle contraction, forming the thick filaments. - While mutations in myosin can cause various cardiac conditions, like hypertrophic cardiomyopathy, direct primary defects in myosin are not typically identified as the cause of dilated cardiomyopathy [2]. *Troponin* - **Troponin** is a protein complex that regulates muscle contraction by controlling the interaction between actin and myosin, particularly in response to calcium. - Although troponins are vital for cardiac function and are released during myocardial injury, their primary defect is not typically implicated in the etiology of dilated cardiomyopathy [2]. *Tropomyosin* - **Tropomyosin** is a protein that winds around actin filaments and, along with troponin, regulates the binding of myosin to actin. - While essential for muscle contraction, direct defects in tropomyosin are not a common genetic cause of dilated cardiomyopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.

Question 392: Lines of Zahn are LEAST likely to be seen in -

A. Liver
B. Kidney
C. Heart
D. Lung (Correct Answer)

Explanation: ***Lung*** - **Lines of Zahn are LEAST likely in the lungs** because most pulmonary thrombi are actually **emboli that formed elsewhere** (typically in deep leg veins) and then **lodged in pulmonary vessels**. - These pre-formed thrombi developed in **low-flow venous environments** and therefore **lack the characteristic layered appearance** of Lines of Zahn. - Even when thrombi form in situ in pulmonary vessels, the vascular bed characteristics make Lines of Zahn formation less common compared to other sites. *Heart* - **Mural thrombi** in heart chambers (especially post-MI in left ventricle or in atrial fibrillation) commonly show **Lines of Zahn**. - The **high-flow, turbulent environment** with continuous cardiac contractions creates ideal conditions for alternating platelet-fibrin and RBC layer deposition. - These are classic examples of antemortem thrombi with visible Lines of Zahn. *Liver* - **Portal vein thrombosis** and **hepatic vein thrombosis** (Budd-Chiari syndrome) can exhibit **Lines of Zahn**. - Despite being venous, these vessels have **sufficient flow velocity and turbulence** to allow layered thrombus formation. - Lines of Zahn indicate the thrombus formed during life with flowing blood. *Kidney* - **Renal artery thrombosis** and **renal vein thrombosis** frequently show **Lines of Zahn**. - Both arterial and venous renal circulation have adequate flow dynamics for layered thrombus formation. - These represent antemortem thrombi formed in vessels with active blood flow.

Question 393: Which of the following is a type of small vessel vasculitis?

A. Classical PAN
B. Giant cell arteritis
C. Granulomatosis with polyangiitis (GPA) (Correct Answer)
D. None of the options

Explanation: ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.

Question 394: Radiotherapy induced radiation pneumonitis is mediated by all of the following cytokines and factors except -

A. PAF (Correct Answer)
B. NF-kB
C. TNF-α
D. TGF-β

Explanation: ***PAF*** - **Platelet-activating factor (PAF)** is primarily involved in **anaphylaxis**, **asthma**, and **allergic responses**, mediating inflammation through platelet aggregation and smooth muscle contraction. - While it has pro-inflammatory effects, it is **not a primary mediator** of the specific inflammatory cascade seen in radiotherapy-induced radiation pneumonitis. *TNF-α* - **Tumor Necrosis Factor-alpha (TNF-α)** is a crucial **pro-inflammatory cytokine** that plays a significant role in the initial acute phase of radiation pneumonitis. - It induces **cytotoxicity**, **apoptosis**, and the production of other inflammatory mediators, contributing to lung tissue damage. *TGF-β* - **Transforming Growth Factor-beta (TGF-β)** is a key cytokine involved in the **fibrotic phase** of radiation pneumonitis. - It promotes **fibroblast proliferation**, collagen synthesis, and extracellular matrix deposition, leading to lung scarring. *NF-kB* - **Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB)** is a master **transcription factor** that regulates the expression of numerous genes involved in inflammation and immune responses. - Radiation exposure **activates NF-kB**, leading to the transcription of various pro-inflammatory cytokines, including TNF-α, which contribute to radiation pneumonitis.