Which of the following antiglaucoma medications can cause drowsiness?
Drug of choice for open angle glaucoma:
Which prostaglandin inhibitor is used in the treatment of patent ductus arteriosus (PDA)?
Which drug is used to keep the patent ductus arteriosus (PDA) open?
Which local anaesthetic is known to cause methemoglobinemia?
In pseudocholinesterase deficiency, which drug should be used cautiously?
In ophthalmology, if a patient is allergic to aminoesters, which local anesthetic can be safely used?
Which drug is most commonly associated with causing exanthema?
Which drug is most commonly associated with causing fixed drug eruptions?
Which drug would be most appropriate for treating a patient with suspected chlamydia-gonorrhea coinfection?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 121: Which of the following antiglaucoma medications can cause drowsiness?
- A. Brimonidine (Correct Answer)
- B. Latanoprost
- C. Dorzolamide
- D. Timolol
Explanation: ***Brimonidine*** - **Brimonidine** is an **alpha-2 adrenergic agonist** [1] that can cause central nervous system depression, leading to side effects such as **drowsiness** and fatigue. - This systemic side effect is more common with the topical ophthalmic formulation due to systemic absorption. *Latanoprost* - **Latanoprost** is a **prostaglandin analog** that primarily works by increasing uveoscleral outflow, and its side effects are mainly localized to the eye (e.g., iris color change, eyelash growth). - It does not typically cause systemic side effects like drowsiness because its systemic absorption is minimal. *Dorzolamide* - **Dorzolamide** is a **topical carbonic anhydrase inhibitor** [1] that reduces aqueous humor production, and its most common side effects include local ocular irritation and a bitter taste. - While systemic carbonic anhydrase inhibitors can cause fatigue and drowsiness, the topical formulation has very limited systemic absorption, making drowsiness uncommon. *Timolol* - **Timolol** is a **non-selective beta-blocker** [1] that reduces aqueous humor production and can cause systemic side effects such as bradycardia, bronchospasm, and hypotension. - While some beta-blockers can cause fatigue, **drowsiness** as a prominent side effect is less common compared to alpha-2 agonists.
Question 122: Drug of choice for open angle glaucoma:
- A. Acetazolamide
- B. Latanoprost (Correct Answer)
- C. Brimonidine
- D. Timolol
Explanation: ***Latanoprost*** - **Prostaglandin F2α analogs** like latanoprost are generally considered **first-line therapy** for open-angle glaucoma due to their efficacy and once-daily dosing. - They work by **increasing uveoscleral outflow** of aqueous humor, thereby lowering intraocular pressure (IOP). *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production. - It is typically used for **acute angle-closure glaucoma** or when initial treatments fail, often due to systemic side effects with long-term use. *Timolol* - **Timolol** is a **non-selective beta-blocker** that reduces aqueous humor production. - While effective, it is often a second-line agent or used in combination due to potential systemic side effects like **bronchospasm** and **bradycardia**. *Brimonidine* - **Brimonidine** is an **alpha-2 adrenergic agonist** that reduces aqueous humor production and increases uveoscleral outflow. - It is typically used as a second-line agent or in combination therapy due to potential side effects like **ocular pruritus** and **allergic conjunctivitis**.
Question 123: Which prostaglandin inhibitor is used in the treatment of patent ductus arteriosus (PDA)?
- A. PGE-2
- B. Misoprostol
- C. Indomethacin (Correct Answer)
- D. Dinoprostone
Explanation: ***Indomethacin*** - **Indomethacin** is a non-steroidal anti-inflammatory drug (**NSAID**) that inhibits **prostaglandin synthesis**, particularly **prostaglandin E2 (PGE2)**. - **PGE2** helps keep the **ductus arteriosus** open in utero; by inhibiting its production, indomethacin facilitates the closure of a **patent ductus arteriosus (PDA)** in neonates. *Misoprostol* - **Misoprostol** is a **prostaglandin E1 (PGE1) analog** and is used to induce labor, treat gastric ulcers, and for medical abortions. - It would work to **maintain** rather than close the **ductus arteriosus** if used in a neonate with a heart defect requiring patency. *Dinoprostone* - **Dinoprostone** is a **prostaglandin E2 analog** used for cervical ripening and labor induction. - It is not used for closing a **PDA**; its prostaglandin agonistic action would likely keep the **ductus arteriosus open**. *PGE-2* - **Prostaglandin E2 (PGE2)** is a naturally occurring prostaglandin that helps maintain the patency of the **ductus arteriosus** in the fetus. - Administering **PGE2** would keep the **ductus arteriosus open**, which is the opposite of the desired effect when treating a **PDA**.
Question 124: Which drug is used to keep the patent ductus arteriosus (PDA) open?
- A. PGE1 (Correct Answer)
- B. PGI2
- C. PGH2
- D. PGF2α
Explanation: ***PGE1*** - **Prostaglandin E1** (**PGE1**, alprostadil) is used to maintain the patency of the **ductus arteriosus** in neonates with certain congenital heart defects [1], [2]. - It acts as a **vasodilator** on the smooth muscle of the ductus, preventing its closure and allowing for adequate blood flow prior to surgical correction [1], [2]. *PGI2* - **Prostaglandin I2** (**PGI2**, prostacyclin) is a potent **vasodilator** and **platelet aggregation inhibitor** [1]. - While it has cardiovascular effects, it is primarily used for conditions like **pulmonary hypertension** and not for maintaining ductal patency [1]. *PGF2̑* - **Prostaglandin F2̑** (**PGF2̑**) is involved in processes such as **uterine contractions** and **bronchoconstriction** [1], [2]. - It does not play a role in maintaining the patency of the ductus arteriosus. *PGH2* - **Prostaglandin H2** (**PGH2**) is an immediate precursor in the synthesis of various other prostaglandins and thromboxanes. - It is not directly administered as a drug to maintain ductal patency but is an intermediate in their synthesis.
Question 125: Which local anaesthetic is known to cause methemoglobinemia?
- A. Procaine
- B. Prilocaine (Correct Answer)
- C. Ropivacaine
- D. Etidocaine
Explanation: ***Prilocaine*** - **Prilocaine** is metabolized into **ortho-toluidine**, which can oxidize hemoglobin to **methemoglobin**, especially at higher doses or in susceptible individuals. - **Methemoglobinemia** symptoms include **cyanosis**, **dyspnea**, and in severe cases, central nervous system depression, due to reduced oxygen-carrying capacity of blood. *Procaine* - **Procaine** is an ester-type local anesthetic. It is metabolized to **para-aminobenzoic acid (PABA)**, which can cause allergic reactions, but it is not associated with methemoglobinemia. - It has a relatively **short duration of action** and is less commonly used now compared to amide-type local anesthetics. *Etidocaine* - **Etidocaine** is an amide-type local anesthetic that is known for its **long duration of action** and high potency. - While it can cause systemic toxicity with high doses due to its cardiac and neurological effects, **methemoglobinemia** is not a characteristic side effect. *Ropivacaine* - **Ropivacaine** is an amide-type local anesthetic similar to bupivacaine, known for its **motor-sparing effect** and use in regional anesthesia. - It is associated with a lower risk of **cardiotoxicity** compared to bupivacaine but does not cause methemoglobinemia.
Question 126: In pseudocholinesterase deficiency, which drug should be used cautiously?
- A. Succinylcholine (Correct Answer)
- B. Barbiturates
- C. Gallamine
- D. Halothane
Explanation: ***Succinylcholine*** - **Succinylcholine** is primarily metabolized by **pseudocholinesterase** (also known as butyrylcholinesterase). - In individuals with **pseudocholinesterase deficiency**, the metabolism of succinylcholine is significantly delayed, leading to **prolonged neuromuscular blockade** and extended paralysis. *Barbiturates* - **Barbiturates** are mainly metabolized by the **hepatic cytochrome P450 system** and do not depend on pseudocholinesterase for their breakdown. - Their metabolism would not be significantly affected by pseudocholinesterase deficiency. *Halothane (an inhalational anesthetic)* - **Halothane** is primarily metabolized by the **hepatic cytochrome P450 system** and excreted via the lungs. - Its metabolism is unrelated to **pseudocholinesterase activity**. *Gallamine (a neuromuscular blocker)* - **Gallamine** is a **nondepolarizing neuromuscular blocker** that is primarily eliminated by **renal excretion** as an unchanged drug. - Its metabolism and elimination are independent of **pseudocholinesterase**.
Question 127: In ophthalmology, if a patient is allergic to aminoesters, which local anesthetic can be safely used?
- A. Procaine
- B. Cocaine
- C. Prilocaine (Correct Answer)
- D. Tetracaine
Explanation: **Local anesthetics are classified into two chemical groups: esters (aminoesters) and amides. Allergies to esters typically do not cross-react with amides.** ***Prilocaine*** - **Prilocaine** is an **amide-type local anesthetic**, and allergies to **aminoesters** typically do not cross-react with **amides**. - It is a safe alternative in patients with a known allergy to **ester-type local anesthetics**. *Cocaine* - **Cocaine** is an **ester-type local anesthetic**, sharing a similar chemical structure with **aminoesters**. - Patients allergic to **aminoesters** are likely to experience a **cross-reaction** with **cocaine**. *Procaine* - **Procaine** is a classic **ester-type local anesthetic** (an aminoester). - An allergy to aminoesters directly implies an allergy to **procaine** due to its chemical classification. *Tetracaine* - **Tetracaine** is also an **ester-type local anesthetic** (an aminoester). - It is contraindicated in patients with an allergy to **aminoesters** due to the high risk of **allergic reaction**.
Question 128: Which drug is most commonly associated with causing exanthema?
- A. Atropine
- B. Phenytoin
- C. Sulfonamide (Correct Answer)
- D. All of the options
Explanation: ***Sulfonamide*** - **Sulfonamides** are among the **most common causes** of drug-induced exanthema (maculopapular/morbilliform rash). - They account for a significant proportion of cutaneous adverse drug reactions, with exanthema being the most frequent presentation. - The mechanism typically involves a **delayed hypersensitivity reaction** (Type IV) to the drug or its metabolites. - **Classic presentation:** Symmetrical, erythematous, maculopapular rash appearing 7-14 days after drug initiation. *Phenytoin* - **Phenytoin** can cause exanthematous eruptions, but it is more notably associated with **severe cutaneous adverse reactions** such as: - **DRESS syndrome** (Drug Reaction with Eosinophilia and Systemic Symptoms) - **Stevens-Johnson syndrome (SJS)** and **Toxic Epidermal Necrolysis (TEN)** - While exanthema can occur, **sulfonamides** are more frequently implicated in simple morbilliform rashes. *Atropine* - **Atropine** is an anticholinergic agent primarily causing **predictable pharmacological effects**: - Dry mouth, mydriasis, tachycardia, urinary retention - **Allergic skin reactions** with atropine are rare and not a characteristic adverse effect. - Atropine is **not recognized** as a common cause of exanthema. *All of the options* - This is incorrect because **atropine** is not commonly associated with exanthema. - While both sulfonamides and phenytoin can cause exanthema, only **sulfonamides** are considered among the **most common** causes.
Question 129: Which drug is most commonly associated with causing fixed drug eruptions?
- A. Aminoglycoside
- B. Sulfonamide (Correct Answer)
- C. Erythromycin
- D. None of the options
Explanation: ***Sulfonamide*** - **Sulfonamides**, particularly **sulfamethoxazole-trimethoprim**, are frequently implicated in causing fixed drug eruptions. - A fixed drug eruption characteristically recurs at the **same cutaneous site** each time the offending drug is administered. *Aminoglycoside* - **Aminoglycosides** are broad-spectrum antibiotics known for potential **ototoxicity** and **nephrotoxicity**. - While they can cause various adverse reactions, fixed drug eruptions are **not a common association** with this drug class. *Erythromycin* - **Erythromycin** is a macrolide antibiotic primarily associated with **gastrointestinal side effects**, such as nausea and abdominal cramping. - Although drug eruptions can occur, fixed drug eruptions are **not typically linked** to erythromycin. *None of the options* - This option is incorrect because **sulfonamides** are well-documented causes of fixed drug eruptions. - Therefore, there is a specific drug class listed that is strongly associated with this condition.
Question 130: Which drug would be most appropriate for treating a patient with suspected chlamydia-gonorrhea coinfection?
- A. Ciprofloxacin
- B. Nalidixic acid
- C. Doxycycline (Correct Answer)
- D. Norfloxacin
Explanation: ***Doxycycline*** - **Doxycycline** is a highly effective treatment for **chlamydia**, and its broad-spectrum activity also covers potential **gonorrhea coinfection** when used as part of a dual therapy regimen. - It is often prescribed alongside a **single dose of ceftriaxone** for presumed gonorrhea coinfection, as ceftriaxone targets gonorrhea while doxycycline targets chlamydia. *Ciprofloxacin* - **Ciprofloxacin** is a **fluoroquinolone** antibiotic, which is generally not recommended as first-line treatment for uncomplicated **gonorrhea** or **chlamydia** due to increasing resistance. - It has activity against *Neisseria gonorrhoeae*, but its effectiveness against *Chlamydia trachomatis* is suboptimal compared to macrolides or tetracyclines. *Norfloxacin* - **Norfloxacin** is another **fluoroquinolone** with a narrower spectrum of activity than ciprofloxacin and is primarily used for **urinary tract infections**. - It has **poor efficacy against chlamydia** and is not a recommended treatment for either organism in this context. *Nalidixic acid* - **Nalidixic acid** is a first-generation **quinolone** with a very limited spectrum, used mainly for **gram-negative urinary tract infections**. - It has **no significant activity against chlamydia** or gonorrhea and is therefore inappropriate for treating this suspected coinfection.