NEET-PG 2015 Practice Questions

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

Microglial cells. ***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)**.

Q: Elastic fibers of tunica media are secreted by

Smooth muscle. 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]

Q: What primarily forms the core of chylomicrons?

Triglycerides. ***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.

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

Chylomicrons. ***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**

Q: The strongest occupational risk factor for hematological carcinoma is

Benzene. ***Benzene*** - Benzene exposure is recognized as a potent **carcinogen** linked to various hematological malignancies, including **leukemia** [1]. - It affects the **bone marrow**, leading to dysplastic changes and ultimately malignancy. *Nicotine* - Although nicotine is associated with **smoking-related cancers**, it is not directly linked to **hematological carcinomas**. - Its primary role is in causing **lung cancer**, rather than blood cancers. *Lithium* - Lithium is primarily used for **bipolar disorder** and does not have a known link to causing hematological malignancies. - Side effects are more related to **nephrotoxicity** rather than carcinogenic effects. *Alcohol* - Alcohol consumption is primarily associated with **liver cancers** and not specifically linked to hematological carcinomas [2]. - It can contribute to general malignancy development but is not a direct cause of blood cancers. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 286. [2] 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. 217-218.

Q: Which of the following does not predispose to leukemia?

Alcohol. ***Alcohol*** - Alcohol consumption does not have a well-established association with an increased risk of leukemia compared to other factors. - While excessive alcohol can impact overall health, it is not considered a primary risk factor for developing leukemia. *Chemical exposure* - Certain chemicals, such as **benzene** and **formaldehyde**, are known to be **leukemogenic** and can increase the risk of leukemia. [1] - Occupational exposure to these chemicals has been linked to **acute myeloid leukemia (AML)** and other types of leukemia. [1] *Smoking* - Smoking has been clearly associated with an increased risk of **acute myeloid leukemia (AML)** and other hematologic malignancies. [1] - The toxins in tobacco smoke can cause **DNA damage**, contributing to the development of leukemia. *Genetic disorder* - Certain genetic disorders, like **Down syndrome** and **Fanconi anemia**, are associated with an increased risk of leukemia. - Individuals with these genetic predispositions have a higher likelihood of developing various forms of leukemia.

Q: Which protein is defective in dilated cardiomyopathy?

Dystrophin. ***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.

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

Lung. ***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.

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

Granulomatosis with polyangiitis (GPA). ***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.

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

PAF. ***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.

Question 1

Which type of glial cell is derived from mesodermal origin?

Accepted Answer

Microglial cells

Answer

Macroglial cells

Answer

Oligodendrocytes

Answer

Ependymal cells

Question 2

Elastic fibers of tunica media are secreted by

Accepted Answer

Smooth muscle

Answer

Endothelium

Answer

External lamina

Answer

Fibroblast

Question 3

What primarily forms the core of chylomicrons?

Accepted Answer

Triglycerides

Answer

Triglycerides and Cholesterol together

Answer

Free fatty acids

Answer

Triglyceride, Cholesterol and Phospholipids

Question 4

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

Accepted Answer

Chylomicrons

Answer

LDL

Answer

HDL

Answer

VLDL

Question 5

The strongest occupational risk factor for hematological carcinoma is

Accepted Answer

Benzene

Answer

Lithium

Answer

Radiation exposure

Answer

Cigarette smoke

Question 6

Which of the following does not predispose to leukemia?

Accepted Answer

Alcohol

Answer

Smoking

Answer

Chemical exposure

Answer

Genetic disorder

Question 7

Which protein is defective in dilated cardiomyopathy?

Accepted Answer

Dystrophin

Answer

Tropomyosin

Answer

Myosin

Answer

Troponin

Question 8

Lines of Zahn are LEAST likely to be seen in -

Accepted Answer

Lung

Answer

Liver

Answer

Kidney

Answer

Heart

Question 9

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

Accepted Answer

Granulomatosis with polyangiitis (GPA)

Answer

Classical PAN

Answer

Giant cell arteritis

Answer

None of the options

Question 10

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

Accepted Answer

PAF

Answer

NF-kB

Answer

TNF-α

Answer

TGF-β

NEET-PG 2015

Anatomy

Biochemistry

Community Medicine

Pathology