Anatomy
1 questionsElastic fibers of tunica media are secreted by
NEET-PG 2015 - Anatomy NEET-PG Practice Questions and MCQs
Question 291: 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
1 questionsWhat is the classification of Carcinoembryonic Antigen (CEA)?
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 291: What is the classification of Carcinoembryonic Antigen (CEA)?
- A. Glycoprotein (Correct Answer)
- B. Lipoprotein
- C. Phosphoprotein
- D. Nucleoprotein
Explanation: ***Glycoprotein*** - Carcinoembryonic Antigen (CEA) is classified as a **glycoprotein** due to its structure, which consists of both **carbohydrate** and **protein** components. - This glycosylation is crucial for its function as a cell adhesion molecule and its recognition in diagnostic assays. *Lipoprotein* - **Lipoproteins** are complexes of lipids and proteins that function primarily in **lipid transport** in the blood. - CEA's primary role and structure are not related to lipid transport or being predominantly lipid-based. *Phosphoprotein* - A **phosphoprotein** is a protein that has been **covalently modified by the addition of a phosphate group**, a process crucial for cell signaling. - While proteins can be phosphorylated, the defining characteristic and major classification of CEA is its extensive glycosylation rather than phosphorylation state. *Nucleoprotein* - **Nucleoproteins** are proteins that are **structurally associated with nucleic acids** (DNA or RNA), such as histones or ribosomal proteins. - CEA does not have a structural or functional association with nucleic acids.
Internal Medicine
2 questionsMajor contribution to cachexia with advanced cancer?
What is the primary effect of beta blockers in the management of thyroid storm?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 291: Major contribution to cachexia with advanced cancer?
- A. Tumor-necrosis-factor (TNF) (Correct Answer)
- B. Histamine
- C. Interferon
- D. Clathrin
Explanation: ***Tumor-necrosis-factor (TNF)*** - **Tumor necrosis factor (TNF-α)** is a prominent cytokine involved in the pathogenesis of cancer cachexia, leading to muscle wasting and weight loss [1]. - It induces inflammation, increases **catabolism**, and reduces anabolism, contributing significantly to the metabolic dysfunction seen in cancer patients [1]. *Histamine* - **Histamine** is primarily known for its role in allergic reactions and inflammatory responses, but it is not a major direct driver of cachexia. - While it can be released in various inflammatory conditions, its direct contribution to the severe muscle wasting and metabolic changes of cachexia is limited compared to other cytokines. *Interferon* - **Interferons (IFNs)** are cytokines typically associated with antiviral responses and immune modulation, which can have diverse effects on metabolism. - While some interferons can indirectly contribute to systemic inflammation and fatigue, they are not considered a primary or major direct mediator of muscle catabolism and fat loss characteristic of cancer cachexia. *Clathrin* - **Clathrin** is a protein involved in the formation of clathrin-coated vesicles, essential for **endocytosis** and intracellular trafficking. - It has no direct role in the systemic metabolic dysregulation or muscle wasting associated with cancer cachexia.
Question 292: What is the primary effect of beta blockers in the management of thyroid storm?
- A. Increases metabolism of thyroxine
- B. Blocks thyroxine receptors
- C. Decreases synthesis of thyroxine
- D. Provides rapid relief of symptoms (Correct Answer)
Explanation: Detailed management of thyrotoxic crisis (thyroid storm) is a medical emergency where patients should be given propranolol, either oral or intravenous, to manage life-threatening symptoms [1]. ***Provides rapid relief of symptoms*** - Beta blockers primarily address the **adrenergic manifestations** of thyroid storm, such as **tachycardia**, **tremors**, anxiety, and palpitations [1]. - By blocking **beta-adrenergic receptors**, they provide rapid symptomatic relief and reduce cardiovascular stress, without affecting hormone levels [2]. Thyroid hormones normally increase the expression of genes for beta-adrenergic receptors and G-proteins, leading to increased heart rate and force of contraction [2]. *Increases metabolism of thyroxine* - Beta blockers do not increase the **metabolism** or breakdown of thyroxine; their action is primarily on the **peripheral effects** of thyroid hormones. - While some beta blockers like **propranolol** can inhibit the peripheral conversion of T4 to T3, this is a secondary effect and not their primary role in providing rapid symptomatic relief [1]. *Blocks thyroxine receptors* - Beta blockers do not block **thyroxine receptors**; thyroid hormones exert their effects by binding to intracellular receptors, not adrenergic receptors [2]. - Their action is on the **adrenergic system**, which is overstimulated by the high levels of thyroid hormones. *Decreases synthesis of thyroxine* - Beta blockers do not directly decrease the **synthesis of thyroxine** by the thyroid gland. - That action is performed by **antithyroid drugs** like methimazole and propylthiouracil, which inhibit hormone production [1].
Pharmacology
5 questionsAntidepressant drug used in nocturnal enuresis is:
Buprenorphine is a partial agonist at which opioid receptor?
Which of the following drugs is not used in the treatment of akathisia?
Which of the following statements about glucocorticoids is true?
A 47-year-old woman presents with complaints of nervousness and increased sensitivity to hot weather. She is diagnosed with hyperthyroidism and prescribed propylthiouracil. What is the principal mechanism by which this drug acts?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 291: Antidepressant drug used in nocturnal enuresis is:
- A. Imipramine (Correct Answer)
- B. Fluoxetine
- C. Trazodone
- D. Sertraline
Explanation: ***Imipramine*** - **Imipramine**, a **tricyclic antidepressant (TCA)**, is frequently used off-label for **nocturnal enuresis** in children [1]. - Its mechanism of action in enuresis is thought to involve a combination of anticholinergic effects (which relax the bladder detrusor muscle) and central nervous system effects (which may increase bladder capacity and arousal from sleep) [1]. *Fluoxetine* - **Fluoxetine** is a **selective serotonin reuptake inhibitor (SSRI)** and is primarily used for depression, anxiety disorders, and OCD [2]. - It is not indicated for the treatment of nocturnal enuresis and does not have the same bladder-relaxing or arousal-modulating properties as imipramine in this context. *Trazodone* - **Trazodone** is a **serotonin antagonist and reuptake inhibitor (SARI)**, commonly prescribed for depression and insomnia due to its prominent sedative effects. - It is not used for nocturnal enuresis and its mechanism of action does not confer benefits for bladder control. *Sertraline* - **Sertraline** is another **selective serotonin reuptake inhibitor (SSRI)** used for a wide range of psychiatric conditions, including depression, anxiety, and panic disorder [2]. - Like fluoxetine, it is not an appropriate treatment for nocturnal enuresis and lacks the specific known effects beneficial for this condition.
Question 292: Buprenorphine is a partial agonist at which opioid receptor?
- A. Mu (Correct Answer)
- B. Kappa
- C. Delta
- D. ORL-1
Explanation: ***Mu*** - Buprenorphine primarily acts as a **partial agonist** at the **mu opioid receptor**, providing analgesic effects with a ceiling effect on respiratory depression. - Its partial agonism at the mu receptor contributes to its lower potential for respiratory depression and overdose compared to full mu agonists. *Kappa* - While buprenorphine has some antagonist activity at the kappa receptor, its primary therapeutic action is not at this receptor. - **Kappa receptor agonists** like pentazocine can produce dysphoria and psychotomimetic effects. *Delta* - The delta opioid receptor is involved in analgesia and emotional responses, but buprenorphine has very low affinity and activity at this receptor. - **Delta receptor agonists** are not widely used clinically due to limited efficacy and side effects. *ORL-1* - The ORL-1 (Opioid Receptor-like 1) receptor, also known as the nociceptin receptor, is distinct from classical opioid receptors. - Buprenorphine has **no significant activity** at the ORL-1 receptor, which primarily mediates pain, anxiety, and learning.
Question 293: Which of the following drugs is not used in the treatment of akathisia?
- A. Benzodiazepine
- B. Propranolol
- C. Trihexyphenidyl
- D. Haloperidol (Correct Answer)
Explanation: ***Haloperidol*** - **Haloperidol** is a typical antipsychotic drug known to **cause** or worsen **akathisia**, rather than treat it. - Akathisia is an extrapyramidal symptom, and **first-generation antipsychotics** like haloperidol are frequent culprits due to their strong **D2 receptor blockade**. *Benzodiazepine* - **Benzodiazepines** like lorazepam or clonazepam are often used to treat akathisia due to their **sedative** and **anxiolytic** properties. - They act by enhancing **GABAergic transmission**, which can help calm the motor restlessness associated with akathisia. *Propranolol* - **Propranolol**, a **beta-blocker**, is a first-line treatment for akathisia, particularly effective for its objective motor symptoms. - It works by reducing **adrenergic activity**, which is thought to contribute to the motor restlessness. *Trihexyphenidyl* - **Trihexyphenidyl** is an **anticholinergic** agent primarily used to treat **parkinsonian-like extrapyramidal symptoms** (e.g., dystonia, pseudoparkinsonism). - While sometimes used for generalized EPS, it is **less effective** for the specific motor restlessness of akathisia compared to beta-blockers or benzodiazepines.
Question 294: Which of the following statements about glucocorticoids is true?
- A. Glucocorticoids directly activate T-helper cells.
- B. Glucocorticoids have no effect on immune cells.
- C. Glucocorticoids downregulate MHC class II expression. (Correct Answer)
- D. Glucocorticoids enhance the activity of cytotoxic T cells.
Explanation: ***Glucocorticoids downregulate MHC class II expression.*** - Glucocorticoids exert **immunosuppressive effects** by reducing the expression of **MHC class II molecules** on antigen-presenting cells. - This downregulation impairs the ability of antigen-presenting cells to activate **CD4+ T-helper cells**, thereby suppressing adaptive immune responses. *Glucocorticoids directly activate T-helper cells.* - Glucocorticoids do not directly activate T-helper cells; rather, they have an **inhibitory effect** on T-cell function and proliferation. - They tend to promote **T-cell apoptosis** and reduce cytokine production, thus dampening T-helper cell responses. *Glucocorticoids have no effect on immune cells.* - This statement is incorrect as glucocorticoids have profound and widespread **immunosuppressive and anti-inflammatory effects** on various immune cells. - They influence the function, proliferation, and survival of **lymphocytes, macrophages, and granulocytes**. *Glucocorticoids enhance the activity of cytotoxic T cells.* - Glucocorticoids generally **suppress immune responses**, including the activity of **cytotoxic T cells (CTLs)**, rather than enhancing it. - They tend to inhibit the production of **interleukins** necessary for CTL activation and proliferation.
Question 295: A 47-year-old woman presents with complaints of nervousness and increased sensitivity to hot weather. She is diagnosed with hyperthyroidism and prescribed propylthiouracil. What is the principal mechanism by which this drug acts?
- A. Reducing the proteolysis of thyroglobulin.
- B. Inhibiting the binding of TSH to its receptor.
- C. Inhibiting the enzyme thyroid peroxidase, which reduces the synthesis of thyroid hormones. (Correct Answer)
- D. Altering the levels of reverse T3 (rT3) in the body.
Explanation: ***Inhibiting the enzyme thyroid peroxidase, which reduces the synthesis of thyroid hormones.*** - **Propylthiouracil (PTU)** is a **thionamide** drug that primarily acts by inhibiting the enzyme **thyroid peroxidase**. - Thyroid peroxidase is crucial for the **organification of iodide** and the **coupling of iodotyrosines** (MIT and DIT) to form T3 and T4, thus reducing the synthesis of thyroid hormones. *Inhibiting the binding of TSH to its receptor.* - This mechanism is characteristic of **TSH receptor antibodies**, which are a cause of hyperthyroidism (e.g., in Graves' disease), rather than the action of an antithyroid drug like PTU. - PTU works at the level of hormone synthesis within the thyroid gland, not at the receptor level for TSH. *Reducing the proteolysis of thyroglobulin.* - While thyroid hormones are stored as part of thyroglobulin, and their release involves proteolysis, this is not the **principal mechanism of action** for PTU. - The main effect of PTU is upstream, preventing the formation of the hormones themselves. *Altering the levels of reverse T3 (rT3) in the body.* - PTU does inhibit the **peripheral conversion of T4 to T3**, which can reduce overall T3 levels and increase rT3, but this is a **secondary mechanism**. - The primary and most significant action for reducing hyperthyroid symptoms is the direct inhibition of thyroid hormone synthesis within the gland.
Physiology
1 questionsWhat does the ST Segment of an ECG correspond to?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 291: What does the ST Segment of an ECG correspond to?
- A. Ventricular depolarization
- B. Plateau phase between ventricular depolarization and repolarization (Correct Answer)
- C. Atrial depolarization
- D. AV Conduction
Explanation: ***Plateau phase between ventricular depolarization and repolarization*** - The **ST segment** represents the electrically neutral period between ventricular depolarization and repolarization, corresponding to the **plateau phase (phase 2)** of the ventricular action potential. - During this phase, the entire ventricular myocardium is depolarized, and there is minimal electrical activity, typically causing the ST segment to be **isoelectric**. *Ventricular depolarization* - This electrical event is represented by the **QRS complex** on the ECG, not the ST segment. - The QRS complex signifies the rapid spread of electrical impulses through the ventricles, leading to their contraction. *Atrial depolarization* - **Atrial depolarization** is represented by the **P wave** on the ECG. - This wave indicates the electrical activation of the atria, which precedes atrial contraction. *AV Conduction* - **AV conduction** time is primarily represented by the **PR interval** on the ECG. - The PR interval measures the time from the beginning of atrial depolarization to the beginning of ventricular depolarization, encompassing the delay at the AV node.