Internal Medicine
1 questionsWhat 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 501: 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].
Obstetrics and Gynecology
1 questionsWhich drug is contraindicated before delivery of the baby (during first and second stages of labor)?
NEET-PG 2015 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 501: Which drug is contraindicated before delivery of the baby (during first and second stages of labor)?
- A. Mifepristone
- B. Oxytocin
- C. Misoprostol
- D. Ergometrine (Correct Answer)
Explanation: ***Ergometrine*** - **Ergometrine** is a potent uterotonic agent that causes **tetanic (sustained) uterine contractions**. - It is **absolutely contraindicated before delivery of the baby** (during first and second stages of labor) because: - Sustained contractions lead to **fetal hypoxia** and **fetal distress** by reducing placental blood flow - Risk of **uterine rupture** due to excessive uterine tone - **Obstructed labor** and **cervical lacerations** from forcing delivery against sustained contraction - Ergometrine is **only used after delivery of the baby** in the third stage for active management and prevention of postpartum hemorrhage. *Mifepristone* - **Mifepristone** is an antiprogesterone used for medical abortion in early pregnancy or cervical ripening before labor induction. - It is not relevant during active labor as it acts by blocking progesterone receptors, not by causing immediate uterine contractions. *Oxytocin* - **Oxytocin** is the drug of choice for induction and augmentation of labor. - It causes **rhythmic, intermittent contractions** that allow for adequate placental perfusion between contractions. - Safe to use during first and second stages when properly monitored. *Misoprostol* - **Misoprostol** is a prostaglandin E1 analog used for cervical ripening and labor induction. - Can be used before and during labor for induction, though requires careful monitoring. - Unlike ergometrine, it does not cause sustained tetanic contractions when used in appropriate doses.
Pharmacology
8 questionsWhat is the primary mechanism of action of zonisamide?
Buprenorphine is a partial agonist at which opioid receptor?
Which of the following drugs is not used in the treatment of akathisia?
Where is the benzodiazepine binding site located on GABA receptors?
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?
Which of the following is an aromatase inhibitor?
Which antithyroid drug is preferred during the first trimester of pregnancy due to relatively lower placental transfer?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 501: What is the primary mechanism of action of zonisamide?
- A. GABA receptors
- B. Cl- channels
- C. Sodium channels (Correct Answer)
- D. T-type calcium channels
Explanation: ***Sodium channels (Correct Answer)*** - Zonisamide's primary mechanism involves **blocking voltage-sensitive sodium channels**, which stabilizes neuronal membranes and inhibits repetitive neuronal firing. - This action helps to prevent the propagation of **seizure activity** in the brain. *GABA receptors* - While zonisamide has some weak effects on GABA, it is not its **primary mechanism of action** for antiepileptic efficacy. - Drugs like **benzodiazepines** and **barbiturates** primarily act by enhancing GABAergic transmission. *T-type calcium channels* - Zonisamide also blocks T-type calcium channels, contributing to its broad-spectrum antiepileptic activity, but this is a **secondary mechanism** compared to its sodium channel blockade. - **Ethosuximide** is a classic example of a drug primarily acting on T-type calcium channels, especially for absence seizures. *Cl- channels* - Zonisamide does not primarily act on **chloride channels**; these are often modulated by GABA receptors. - Drugs that act directly on chloride channels are not typically used as **antiepileptics** in the same way.
Question 502: 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 503: 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 504: Where is the benzodiazepine binding site located on GABA receptors?
- A. β-subunit
- B. δ-subunit
- C. γ-subunit (Correct Answer)
- D. α-subunit
Explanation: ***γ-subunit*** - The **benzodiazepine binding site** is located at the interface between the **α and γ subunits** of the GABA-A receptor, with the **γ-subunit (especially γ2) being essential** for benzodiazepine sensitivity. - The presence of the **γ2 subunit** is **mandatory** for benzodiazepine binding - receptors lacking this subunit are **insensitive to benzodiazepines**. - Benzodiazepines bind to this site and act as **positive allosteric modulators**, increasing the frequency of **chloride channel opening** in response to GABA. - This is the **standard answer** for NEET-PG and medical PG examinations in India. *α-subunit* - The **α-subunit** contributes to forming the benzodiazepine binding pocket at the α-γ interface. - Different **α-subunit isoforms** (α1, α2, α3, α5) determine the pharmacological profile and tissue distribution of benzodiazepine effects. - However, the **α-subunit alone** cannot bind benzodiazepines without the γ-subunit. *β-subunit* - The **β-subunit** contains the primary binding site for **GABA** itself. - It does not participate in benzodiazepine binding but is crucial for the receptor's overall function and GABAergic signaling. *δ-subunit* - The **δ-subunit** replaces the γ-subunit in certain GABA-A receptor subtypes that mediate **tonic inhibition**. - Receptors containing **δ-subunits** are **insensitive to benzodiazepines** but sensitive to neurosteroids and certain general anesthetics. - This is a key distinguishing feature between phasic (γ-containing) and tonic (δ-containing) GABA-A receptors.
Question 505: 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 506: 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.
Question 507: Which of the following is an aromatase inhibitor?
- A. Letrozole (Correct Answer)
- B. Tamoxifen
- C. Danazol
- D. Taxane
Explanation: ***Letrozole*** - **Letrozole** is a commonly used **aromatase inhibitor**, which works by blocking the enzyme **aromatase** that converts androgens into estrogens [1]. - This reduction in estrogen levels is crucial in treating **hormone-sensitive breast cancers** [1]. *Tamoxifen* - **Tamoxifen** is a **selective estrogen receptor modulator (SERM)**, not an aromatase inhibitor [2]. - It acts by blocking estrogen receptors in breast tissue while potentially stimulating them in other tissues like bone and uterus [2]. *Danazol* - **Danazol** is a synthetic androgen that suppresses the hypothalamic-pituitary-gonadal axis, leading to **decreased estrogen production**. - It works by inhibiting gonadotropin release and directly inhibiting ovarian steroidogenesis, rather than blocking the aromatase enzyme directly. *Taxane* - **Taxanes** are a class of **chemotherapy drugs** that interfere with cell division by stabilizing microtubules. - They are used to treat various cancers, including breast cancer, but do not act as aromatase inhibitors.
Question 508: Which antithyroid drug is preferred during the first trimester of pregnancy due to relatively lower placental transfer?
- A. Carbimazole
- B. Propylthiouracil (Correct Answer)
- C. Both
- D. None of the options
Explanation: ***Propylthiouracil*** - **Propylthiouracil (PTU)** is the preferred antithyroid drug during the **first trimester** of pregnancy because it crosses the placenta less readily than methimazole/carbimazole. - While it still crosses the placenta, its lower placental transfer and association with fewer fetal anomalies in early pregnancy make it a safer initial choice, especially to minimize the risk of **fetal embryopathy** associated with methimazole. *Carbimazole* - **Carbimazole** (which is metabolized to methimazole) can cross the placenta more easily than PTU and has been associated with **fetal anomalies**, particularly in the first trimester. - Its use is generally avoided during the first trimester due to concerns about congenital malformations such as **aplasia cutis** and **esophageal atresia**. *Both* - While both drugs can cross the placenta to some extent, their safety profiles and recommended use during pregnancy differ significantly. - Carbimazole (methimazole) has a higher risk of teratogenicity in the first trimester compared to PTU. *None of the options* - This option is incorrect because propylthiouracil is indeed known to cross the placenta and is commonly used in pregnancy, especially during the first trimester. - The choice of antithyroid drug is a critical consideration in managing hyperthyroidism in pregnancy.