Which drug would be most appropriate for treating a patient with suspected chlamydia-gonorrhea coinfection?
Which of the following statements about Selective Estrogen Receptor Modulators (SERMs) is correct?
The mechanism by which ergometrine stops postpartum hemorrhage is that it:
Which local anaesthetic is known to cause methemoglobinemia?
Depot preparations are administered by ?
True about MDMA:
Which of the following is used in the second-line management of strychnine poisoning?
Knockout drops are:
Acrodynia, or Pink disease, occurs in poisoning with which of the following substances?
Oximes are contraindicated in which poisoning:
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 131: 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.
Question 132: Which of the following statements about Selective Estrogen Receptor Modulators (SERMs) is correct?
- A. Act as agonists on estrogen receptors.
- B. Some SERMs can act as both agonists and antagonists on estrogen receptors. (Correct Answer)
- C. Used to reduce the risk of hot flushes and thromboembolism.
- D. Act as antagonists on estrogen receptors.
Explanation: ***Some SERMs can act as both agonists and antagonists on estrogen receptors.*** - **SERMs** (Selective Estrogen Receptor Modulators) exert tissue-specific effects, meaning they can act as an **estrogen receptor agonist** in some tissues while acting as an **antagonist** in others. - This **selective mechanism** allows them to confer beneficial estrogenic effects where desired (e.g., bone) and anti-estrogenic effects where unwanted (e.g., breast tissue). *Act as agonists on estrogen receptors.* - This statement is incomplete because while some SERMs can act as **agonists** in certain tissues (e.g., affecting bone density), they are not pure agonists across all tissues. - Their defining characteristic is their **selective action**, exhibiting mixed agonist and antagonist effects depending on the tissue. *Used to reduce the risk of hot flushes and thromboembolism.* - SERMs like **tamoxifen** and **raloxifene** can actually **increase the risk** of both hot flushes and thromboembolism. - **Hot flushes** occur due to their **anti-estrogenic effects** on the hypothalamus, which disrupts thermoregulation. - **Thromboembolism** risk is increased due to their **estrogenic (agonist) effects** on hepatic synthesis of coagulation factors. *Act as antagonists on estrogen receptors.* - This statement is also incomplete because, while some SERMs exhibit **antagonist activity** in certain tissues (e.g., the breast), they simultaneously act as **agonists** in other tissues (e.g., bone or endometrium). - A pure antagonist would block estrogen receptors in all tissues, which is not the defining feature of SERMs.
Question 133: The mechanism by which ergometrine stops postpartum hemorrhage is that it:
- A. Induces platelet aggregation
- B. Promotes coagulation
- C. Causes vasoconstriction of uterine arteries
- D. Increases tone of uterine muscle (Correct Answer)
Explanation: ***Increases tone of uterine muscle*** - **Ergometrine** is an **ergot alkaloid** that directly stimulates **uterine smooth muscle contractions**. - These sustained contractions lead to **compression of blood vessels within the myometrium**, thereby reducing blood flow and controlling **postpartum hemorrhage**. *Causes vasoconstriction of uterine arteries* - While ergometrine does have some generalized **vasoconstrictive effects**, its primary mechanism of action in controlling postpartum hemorrhage is not mainly through direct vasoconstriction of large uterine arteries. - The crucial effect is the **sustained uterine contraction** which mechanically occludes blood vessels, rather than chemical constriction of the vessels themselves. *Induces platelet aggregation* - Ergometrine does not primarily act by inducing **platelet aggregation**; this is a function of specific clotting factors and platelet activators. - Its therapeutic effect against hemorrhage is mediated through its action on **uterine contractility**, not on the cellular components of coagulation. *Promotes coagulation* - Ergometrine does not directly promote the **coagulation cascade** or enhance the formation of fibrin clots. - Its mechanism of action is distinct from agents that affect intrinsic or extrinsic pathways of coagulation.
Question 134: 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 135: Depot preparations are administered by ?
- A. Subcutaneous route
- B. Intravenous route
- C. Intramuscular route
- D. Both subcutaneous and intramuscular route (Correct Answer)
Explanation: ***Both subcutaneous and intramuscular route*** - **Depot preparations** are designed for **sustained release** of medication over an extended period - This is achieved by forming a 'depot' in the tissue, often facilitated by a viscous vehicle or sparingly soluble form of the drug - Both **subcutaneous** and **intramuscular** tissues can sustain depot formulations effectively - **SC depot examples:** Insulin glargine, contraceptive implants (Nexplanon), leuprolide acetate - **IM depot examples:** Haloperidol decanoate, medroxyprogesterone acetate (Depo-Provera), paliperidone palmitate, long-acting risperidone *Subcutaneous route* - While some **depot preparations** are administered **subcutaneously**, it is not the *only* route for all depot formulations - The **subcutaneous tissue** offers relatively low blood flow, suitable for slow absorption - Alone, this option is incomplete as many depot preparations require IM administration *Intramuscular route* - Many **depot preparations** are given **intramuscularly** due to the muscle tissue's vascularity and tissue volume - The **muscle tissue** provides an excellent site for drug reservoir formation - Alone, this option is incomplete as some depot preparations are given subcutaneously *Intravenous route* - **Intravenous administration** is used for immediate and rapid drug delivery directly into the bloodstream - This route is **unsuitable for depot preparations** which require sustained release over time - No 'depot' can be formed with IV route as the drug is immediately diluted and distributed throughout the body
Question 136: True about MDMA:
- A. It is a cocaine congener
- B. Methadone is used to treat withdrawal symptoms
- C. Ecstasy is another name for it (Correct Answer)
- D. Causes parkinsonism like syndrome
Explanation: Ecstasy is another name for it - MDMA (3,4-methylenedioxymethamphetamine) is widely known by its street name, Ecstasy [1]. - This name refers to its profound empathogenic effects and sense of well-being it often induces. It is a cocaine congener - MDMA is an amphetamine derivative and acts primarily on serotonin, dopamine, and norepinephrine systems, distinct from cocaine's primary action as a reuptake inhibitor [1], [2]. - While both MDMA and cocaine are stimulants, their chemical structures and primary mechanisms of action are different; MDMA is a substituted amphetamine [1]. Methadone is used to treat withdrawal symptoms - Methadone is an opioid agonist primarily used in the management of opioid dependence and withdrawal symptoms [3]. - MDMA withdrawal symptoms are typically managed with supportive care, focusing on symptom relief and psychological support, as there is no specific pharmacological treatment like methadone for MDMA withdrawal [3]. Causes parkinsonism like syndrome - While MDMA can cause neurotoxicity, particularly affecting serotonergic neurons, it is not typically associated with a direct parkinsonism-like syndrome [2]. - Parkinsonism is primarily linked to dopaminergic system damage, often seen with certain neuroleptics or drugs like MPTP, not MDMA.
Question 137: Which of the following is used in the second-line management of strychnine poisoning?
- A. Physostigmine
- B. Naloxone
- C. Barbiturates (Correct Answer)
- D. Diazepam
Explanation: ***Barbiturates*** - As a **second-line treatment**, barbiturates like phenobarbital are used to control **refractory seizures** and muscle spasms in strychnine poisoning when benzodiazepines are insufficient. - They enhance the effect of **GABA**, leading to central nervous system depression and muscle relaxation. *Physostigmine* - This is an **acetylcholinesterase inhibitor** and is primarily used to reverse the anticholinergic effects of certain poisonings, not strychnine. - It would worsen seizures by increasing **acetylcholine**, which can cause tremors and convulsions. *Naloxone* - Naloxone is an **opioid antagonist** used to reverse opioid overdose, which presents with respiratory depression and pinpoint pupils. - It has no role in treating strychnine poisoning, which primarily causes **muscle spasms** and seizures. *Diazepam* - Diazepam, a **benzodiazepine**, is the **first-line treatment** for seizures and muscle spasms in strychnine poisoning. - It works by enhancing the effects of **GABA** at the GABA-A receptor, thereby reducing neuronal excitability.
Question 138: Knockout drops are:
- A. Chloral hydrate (Correct Answer)
- B. Kerosene
- C. Paraldehyde
- D. Turpentine
Explanation: ***Chloral hydrate*** - **Chloral hydrate** is a sedative-hypnotic substance historically used as "knockout drops" due to its quick action in inducing sleep or unconsciousness. - Its use has largely been replaced by safer alternatives due to its narrow therapeutic index and potential for respiratory depression and cardiac arrhythmias. *Kerosene* - **Kerosene** is a flammable hydrocarbon liquid primarily used as fuel or solvent, not as a sedative or hypnotic agent. - Ingestion of kerosene is highly toxic and can cause chemical pneumonitis and gastrointestinal irritation. *Paraldehyde* - **Paraldehyde** is an older sedative and hypnotic drug, but it is not typically referred to as "knockout drops." - It has a very pungent odor and taste, which would make surreptitious administration difficult, and is generally avoided in modern medical practice. *Turpentine* - **Turpentine** is a distillate of pine resin used as a solvent or cleaner, and historically as a liniment or anthelminthic. - It is highly toxic if ingested and can cause severe gastrointestinal distress, kidney damage, and central nervous system depression, but it is not a sedative-hypnotic.
Question 139: Acrodynia, or Pink disease, occurs in poisoning with which of the following substances?
- A. Lead
- B. Thallium
- C. Arsenic
- D. Mercury (Correct Answer)
Explanation: ***Mercury*** - **Acrodynia**, also known as **Pink disease**, is a rare and severe form of **mercury poisoning**, primarily affecting infants and young children. - Key symptoms include **pinkish-red rash** on the hands and feet, hypertension, irritability, profuse sweating, and muscle weakness. *Lead* - **Lead poisoning** typically presents with symptoms such as **abdominal pain**, constipation, developmental delay, and a **lead line on the gums**. - It does not cause the characteristic rash or other symptoms associated with acrodynia. *Thallium* - **Thallium poisoning** is known for causing **hair loss (alopecia)**, excruciating neuropathic pain, gastrointestinal disturbances, and neurological symptoms. - While it is a neurotoxic heavy metal, its clinical picture is distinct from acrodynia. *Arsenic* - **Arsenic poisoning** can manifest with dermatological signs like **hyperpigmentation** and **hyperkeratosis**, as well as gastrointestinal and neurological symptoms. - It does not produce the pinkish rash, irritability, or hypertension typical of acrodynia.
Question 140: Oximes are contraindicated in which poisoning:
- A. Diazinon
- B. Carbamate (Correct Answer)
- C. Phorate
- D. Malathion
Explanation: ***Carbamate*** - Traditionally, oximes were considered **contraindicated** in carbamate poisoning based on concerns they could worsen the **cholinergic crisis** by reactivating carbamylated acetylcholinesterase. - Carbamates spontaneously **decarbamylate** from acetylcholinesterase within minutes to hours, so their inhibition is typically **short-lived and reversible**. - **Clinical relevance**: While modern evidence suggests oximes are more likely **ineffective** rather than harmful in carbamate poisoning, they are generally **not recommended** as they provide no therapeutic benefit. For exam purposes, particularly in historical contexts (NEET 2012-2013), carbamate poisoning is the answer for oxime contraindication. *Diazinon* - Diazinon is an **organophosphate**, and oximes like pralidoxime are **strongly indicated** for reactivating **acetylcholinesterase** inhibited by organophosphates. - Oximes are a crucial part of recommended antidotal therapy alongside **atropine** for severe organophosphate poisoning. - Must be administered early (within 24-48 hours) before **aging** of the phosphorylated enzyme occurs. *Phorate* - Phorate is a highly toxic **organophosphate pesticide**, and oximes are **indicated** for treatment of phorate poisoning. - Oximes work by **dephosphorylating** (nucleophilic attack on) the acetylcholinesterase enzyme, which has been inhibited by the organophosphate, restoring its catalytic function. *Malathion* - Malathion is an **organophosphate insecticide**, and oxime reactivators are **effective** in malathion poisoning. - The mechanism involves **cleaving the phosphate bond** from the serine residue on the acetylcholinesterase enzyme, allowing it to metabolize acetylcholine again and reverse cholinergic toxicity.