Anesthesiology
4 questionsPhase II block is seen with:
What is the drug of choice for reversing muscle relaxants after anesthesia?
What is the primary clinical use of Sugammadex in anesthesia?
Which anaesthetic agent has maximum MAC ?
NEET-PG 2013 - Anesthesiology NEET-PG Practice Questions and MCQs
Question 471: Phase II block is seen with:
- A. SCh infusion (Correct Answer)
- B. Single dose SCh
- C. Mivacurium
- D. None of the options
Explanation: ***SCh infusion*** - A **prolonged infusion or high dose** of succinylcholine (SCh) can lead to a **Phase II block**, a desensitizing block resembling that of a non-depolarizing neuromuscular blocker. - This occurs due to the **persistent presence of SCh** at the neuromuscular junction, which initially depolarizes the endplate (Phase I) but eventually leads to **receptor desensitization** and repolarization, preventing further muscle contraction. *Single dose SCh* - A **single bolus dose of succinylcholine** typically produces a **Phase I block**, characterized by initial muscle fasciculations followed by flaccid paralysis due to persistent depolarization of the motor endplate. - It resolves relatively quickly as **succinylcholine is rapidly hydrolyzed** by pseudocholinesterase, usually not leading to a prolonged desensitization characteristic of Phase II. *Mivacurium* - **Mivacurium** is an intermediate-acting, **non-depolarizing neuromuscular blocker**. - Its mechanism of action involves **competitively binding to nicotinic acetylcholine receptors** at the neuromuscular junction, thereby preventing acetylcholine from binding and initiating muscle contraction, which is fundamentally different from a Phase II block caused by prolonged depolarization. *None of the options* - This option is incorrect because **SCh infusion** is a recognized cause of Phase II block. - The phenomenon of Phase II block is a well-established pharmacological response to **excessive and prolonged exposure** to depolarizing neuromuscular blockers like succinylcholine.
Question 472: What is the drug of choice for reversing muscle relaxants after anesthesia?
- A. Pralidoxine
- B. Neostigmine (Correct Answer)
- C. Atropine
- D. None of the options
Explanation: ***Neostigmine*** - **Neostigmine** is an **acetylcholinesterase inhibitor** that increases the amount of acetylcholine at the neuromuscular junction, thereby reversing the effects of non-depolarizing muscle relaxants. - It is often co-administered with an **anticholinergic agent** like atropine or glycopyrrolate to counteract its muscarinic side effects (e.g., bradycardia, increased secretions). *Pralidoxine* - **Pralidoxine (2-PAM)** is an **oxime cholinesterase reactivator** used primarily to treat organophosphate poisoning. - It works by regenerating acetylcholinesterase that has been inhibited by organophosphates, which is not the mechanism of action required for reversing typical muscle relaxants. *Atropine* - **Atropine** is an **anticholinergic drug** that blocks muscarinic acetylcholine receptors. - While it is often given with neostigmine to counteract muscarinic side effects like bradycardia, it does not directly reverse the neuromuscular blockade caused by muscle relaxants. *None of the options* - This option is incorrect because **neostigmine** is a well-established and commonly used drug for reversing non-depolarizing muscle relaxants.
Question 473: What is the primary clinical use of Sugammadex in anesthesia?
- A. Organophosphate poisoning
- B. Reversal of NM blockers (Correct Answer)
- C. Treatment of local anaesthetic poisoning
- D. Treatment of central anticholinergic syndrome
Explanation: ***Reversal of NM blockers*** - **Sugammadex** is a modified gamma-cyclodextrin that specifically encapsulates steroidal **neuromuscular blocking agents (NMBAs)** like **rocuronium** and **vecuronium**. - This encapsulation rapidly inactivates the NMBAs, leading to a dose-dependent and swift **reversal of neuromuscular blockade**. *Organophosphate poisoning* - Organophosphate poisoning is treated with **atropine** to block muscarinic effects and **pralidoxime** to reactivate inhibited acetylcholinesterase. - Sugammadex has no role in antagonizing the effects of **organophosphates** or regenerating acetylcholinesterase. *Treatment of local anaesthetic poisoning* - Local anesthetic systemic toxicity (LAST) is primarily managed with supportive care, including airway management, and the administration of **lipid emulsion therapy**. - Sugammadex does not bind to local anesthetics and therefore has no efficacy in treating local anesthetic poisoning. *Treatment of central anticholinergic syndrome* - Central anticholinergic syndrome is typically treated with **physostigmine**, an acetylcholinesterase inhibitor that can cross the blood-brain barrier. - Sugammadex is not an anticholinergic antagonist and does not affect the central nervous system to reverse anticholinergic effects.
Question 474: Which anaesthetic agent has maximum MAC ?
- A. Ether
- B. Methoxyfluorane
- C. Halothane
- D. Nitrous Oxide (N2O) (Correct Answer)
Explanation: ***Nitrous Oxide (N2O)*** - **Nitrous Oxide** has the highest **minimum alveolar concentration (MAC)** of all commonly used inhalational anesthetics, approximately 104%. - A high MAC indicates **low potency**, meaning that a large concentration is required to achieve anesthetic effects. *Ether* - **Ether** has a MAC of about 1.92%, which is significantly lower than that of Nitrous Oxide. - Its use has largely been replaced due to its flammability, slow induction, and recovery times. *Methoxyfluorane* - **Methoxyfluorane** is known for having a very low MAC, around 0.16%, making it the most potent inhalational anesthetic. - Due to its high potency and significant nephrotoxicity, its use is now very limited. *Halothane* - **Halothane** has a MAC of approximately 0.75%. - While it was a widely used inhalational anesthetic, it has largely been replaced due to concerns about **halothane hepatitis** and arrhythmogenicity.
Biochemistry
1 questionsWhat is the role of Anandamide in the human body?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 471: What is the role of Anandamide in the human body?
- A. Opioid
- B. D2 blocker
- C. Cannabinoid neurotransmitter (Correct Answer)
- D. CCK1 antagonist
Explanation: ***Cannabinoid neurotransmitter*** - **Anandamide** is an **endogenous cannabinoid neurotransmitter** that binds to **CB1** and **CB2 receptors**. - It plays a role in **pain modulation**, **appetite stimulation**, and **memory regulation**. *Opioid* - **Opioids** bind to **opioid receptors** (mu, delta, kappa) and are known for their **analgesic** and **euphoric effects**. - Examples include **morphine** and **endorphins**, which are chemically distinct from anandamide and have different receptor targets. *CK 1 antagonist* - This option refers to a **cholecystokinin 1 (CCK1) receptor antagonist**, which would block the effects of **CCK**. - **CCK** is a hormone involved in **digestion** and **satiety**, and its role is unrelated to anandamide. *D2 blocker* - A **D2 blocker** is an agent that antagonizes the **dopamine D2 receptor**. - These are typically **antipsychotic medications** that modulate **dopamine pathways** in the brain, unrelated to the function of anandamide.
Pharmacology
5 questionsWhich of the following is a benzylisoquinoline muscle relaxant?
Which medication increases insulin secretion from beta cells?
Which of the following antidiabetic drugs (other than insulin) is indicated as adjunct therapy for the management of both type I and type II diabetes mellitus?
Which of the following statements about sitagliptin is false?
What is a potential risk associated with the use of thiazolidinediones in the treatment of type 2 diabetes?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 471: Which of the following is a benzylisoquinoline muscle relaxant?
- A. Rocuronium
- B. Doxacurium (Correct Answer)
- C. Pancuronium
- D. Vecuronium
Explanation: ***Doxacurium*** - **Doxacurium** is a long-acting, non-depolarizing neuromuscular blocker classified as a **benzylisoquinoline** compound [1]. - These agents are known for their minimal cardiovascular effects and lack of histamine release in therapeutic doses [1]. *Vecuronium* - **Vecuronium** is an **aminosteroid** non-depolarizing neuromuscular blocker [2]. - It is known for its intermediate duration of action and minimal cardiovascular effects [1]. *Rocuronium* - **Rocuronium** is also an **aminosteroid** non-depolarizing neuromuscular blocker [2]. - It has a rapid onset of action, making it suitable for rapid sequence intubation, and can be reversed by **sugammadex**. *Pancuronium* - **Pancuronium** is an **aminosteroid** non-depolarizing neuromuscular blocker with a long duration of action [1]. - It is associated with a vagolytic effect that can cause an increase in **heart rate** and **blood pressure** [1].
Question 472: Which medication increases insulin secretion from beta cells?
- A. Metformin
- B. Repaglinide (Correct Answer)
- C. Pioglitazone
- D. Pramlintide
Explanation: ***Repaglinide*** - This medication is a **meglitinide analog** that stimulates **insulin release** from pancreatic beta cells by closing ATP-sensitive potassium channels. - Its fast onset and short duration of action make it particularly useful for controlling **postprandial glucose** excursions. *Metformin* - This medication primarily works by **decreasing hepatic glucose production** and improving insulin sensitivity in peripheral tissues. - It does **not directly stimulate insulin secretion** from beta cells; thus, it carries a lower risk of hypoglycemia compared to sulfonylureas or meglitinides. *Pramlintide* - This is an **amylin analog** that works by slowing gastric emptying, suppressing postprandial glucagon secretion, and increasing satiety. - It is an **injectable medication** used as an adjunct to insulin therapy and does not directly enhance insulin secretion from beta cells. *Pioglitazone* - This drug is a **thiazolidinedione** that improves insulin sensitivity in target tissues (e.g., muscle, fat, liver) by activating **peroxisome proliferator-activated receptor-gamma (PPAR-γ)**. - While it improves the body's response to insulin, it does **not directly stimulate insulin secretion** from the beta cells.
Question 473: Which of the following antidiabetic drugs (other than insulin) is indicated as adjunct therapy for the management of both type I and type II diabetes mellitus?
- A. Sulphonylureas
- B. Metformin
- C. Acarbose
- D. Pramlintide (Correct Answer)
Explanation: Pramlintide - Pramlintide is an amylin analog indicated as an adjunct therapy to insulin for both type 1 and type 2 diabetes, helping to regulate post-prandial glucose. - It slows gastric emptying, suppresses postprandial glucagon secretion, and promotes satiety, leading to reduced insulin requirements and improved glycemic control. Sulphonylureas - Sulphonylureas primarily stimulate insulin secretion from pancreatic beta cells, making them effective only in Type 2 diabetes where some beta-cell function is preserved [2]. - They are not indicated for Type 1 diabetes because these patients have absolute insulin deficiency due to beta cell destruction. Metformin - Metformin is a biguanide that primarily reduces hepatic glucose production and improves insulin sensitivity in peripheral tissues. - It is a first-line treatment for Type 2 diabetes but is generally not used for Type 1 diabetes as it does not address the fundamental lack of insulin. Acarbose - Acarbose is an alpha-glucosidase inhibitor that works by delaying carbohydrate absorption from the gastrointestinal tract, thus reducing postprandial glucose spikes [1]. - While it can be used in Type 2 diabetes to manage postprandial hyperglycemia, it is not typically indicated as an adjunct for Type 1 diabetes alongside insulin [3].
Question 474: Which of the following statements about sitagliptin is false?
- A. Used in type II diabetes mellitus
- B. Cannot be used orally (Correct Answer)
- C. Used in combination with other oral hypoglycemic agents
- D. All of the above statements are true
Explanation: ***Cannot be used orally*** - This statement is **false** because **sitagliptin** is an **oral medication** approved for the treatment of type 2 diabetes mellitus. - As a **DPP-4 inhibitor**, it is designed to be taken by mouth to increase incretin hormone levels. *Used in type II diabetes mellitus* - This statement is **true** as **sitagliptin** is a commonly prescribed **oral antidiabetic drug** for the management of type 2 diabetes. - It works by inhibiting the enzyme **dipeptidyl peptidase-4 (DPP-4)**, which increases levels of **GLP-1** and **GIP** to enhance insulin secretion and reduce glucagon secretion. *Used in combination with other oral hypoglycemic agents* - This statement is **true** as **sitagliptin** is often used as **add-on therapy** with other oral hypoglycemic agents like **metformin** or a **sulfonylurea** when monotherapy is insufficient. - This combination approach helps achieve better glycemic control by targeting different mechanisms of action. *All of the above statements are true* - This statement is **false** because the first statement "Cannot be used orally" is incorrect. - Since sitagliptin is indeed an oral medication, not all the above statements are true, making this option incorrect.
Question 475: What is a potential risk associated with the use of thiazolidinediones in the treatment of type 2 diabetes?
- A. Heart failure (Correct Answer)
- B. Pulmonary fibrosis
- C. Myocarditis
- D. Renal dysfunction
Explanation: ***Heart failure*** - Thiazolidinediones (TZDs), such as **pioglitazone** and **rosiglitazone**, can cause **fluid retention** and **volume expansion**, which may precipitate or worsen congestive heart failure. - This risk is higher in patients with pre-existing cardiac conditions and is a significant concern for these drugs. *Pulmonary fibrosis* - **Pulmonary fibrosis** is not a known or common adverse effect associated with thiazolidinedione use. - This condition is typically linked to certain other medications (e.g., **amiodarone**, **methotrexate**) or systemic diseases. *Myocarditis* - **Myocarditis**, inflammation of the heart muscle, is not a recognized side effect of thiazolidinediones. - Myocarditis is more commonly caused by viral infections, autoimmune diseases, or hypersensitivity reactions to certain drugs, but not TZDs. *Renal dysfunction* - While TZDs can cause fluid retention, they do not directly cause **renal dysfunction** or damage the kidneys. - In fact, some studies suggest they may have renoprotective effects due to reduced proteinuria, although fluid balance needs careful monitoring in patients with impaired renal function.