A patient has Cushing syndrome due to an adrenal tumor. Which drug should be given?
Which of the following drugs is useful in acute attack of gout ?
What is the drug of choice for the treatment of kala-azar?
XDR-TB is defined as resistance to which of the following drug combinations?
The mechanism by which ergometrine stops postpartum hemorrhage is that it:
Which of the following medications is not typically used for the treatment of erectile dysfunction?
All are symptoms of morphine withdrawal except?
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?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 121: A patient has Cushing syndrome due to an adrenal tumor. Which drug should be given?
- A. Ketoconazole (Correct Answer)
- B. Spironolactone
- C. Hydrocortisone
- D. Dexamethasone
Explanation: ***Ketoconazole*** - **Ketoconazole** is an antifungal agent that also inhibits several enzymes involved in **steroidogenesis**, including 17α-hydroxylase and 11β-hydroxylase. - This action helps to reduce the overproduction of **cortisol** in Cushing syndrome caused by an adrenal tumor. *Hydrocortisone* - **Hydrocortisone** is a glucocorticoid itself and would exacerbate the symptoms of **Cushing syndrome** by adding to the already elevated cortisol levels. - It is used for **cortisol replacement therapy** in conditions like Addison's disease, where cortisol levels are low. *Dexamethasone* - **Dexamethasone** is a potent synthetic glucocorticoid used to suppress **ACTH production** in cases of ACTH-dependent Cushing's syndrome (e.g., Cushing's disease) or to diagnose Cushing's syndrome. - In an adrenal tumor, which is **ACTH-independent**, dexamethasone would not reduce cortisol production but could instead worsen the hypercortisolism. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** and a weak antiandrogen, primarily used for conditions like hyperaldosteronism, heart failure, and hirsutism. - It has no direct effect on the overproduction of **cortisol** from an adrenal tumor in Cushing syndrome.
Question 122: Which of the following drugs is useful in acute attack of gout ?
- A. Furosemide
- B. Sulfinpyrazone
- C. Allopurinol
- D. Piroxicam (Correct Answer)
Explanation: ***Piroxicam*** - **Piroxicam** is a **non-steroidal anti-inflammatory drug (NSAID)**, which are the first-line treatment for acute gout attacks. - NSAIDs work by inhibiting **prostaglandin synthesis**, thereby reducing inflammation and pain associated with the acute crystal-induced arthritis. *Furosemide* - **Furosemide** is a loop diuretic that can **raise uric acid levels** by increasing reabsorption in the renal tubules. - Therefore, it would exacerbate **gout** and is contraindicated during an acute attack. *Sulfinpyrazone* - **Sulfinpyrazone** is a **uricosuric agent** used for chronic gout management to increase uric acid excretion. - It is **not used for acute attacks** as it can precipitate or worsen an attack by mobilizing uric acid crystals. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for long-term management of hyperuricemia and chronic gout. - Starting allopurinol during an **acute attack** can worsen or prolong the attack by causing rapid changes in serum uric acid levels.
Question 123: What is the drug of choice for the treatment of kala-azar?
- A. Amphotericin B
- B. Quinine
- C. Paromomycin
- D. Liposomal Amphotericin B (Correct Answer)
Explanation: ***Liposomal Amphotericin B*** - It is currently considered the **drug of choice** for treating **visceral leishmaniasis (kala-azar)** due to its high efficacy and better tolerability profile compared to conventional amphotericin B. - The **liposomal formulation** allows for targeted delivery to macrophages, where *Leishmania* parasites reside, reducing systemic toxicity. *Amphotericin B* - While effective against *Leishmania*, conventional **Amphotericin B deoxycholate** is associated with significant **nephrotoxicity** and other severe side effects. - It is generally reserved for cases where liposomal amphotericin B is unavailable or as an alternative in specific clinical situations. *Quinine* - **Quinine** is an **antimalarial drug** primarily used for the treatment of *Plasmodium falciparum* malaria. - It has no significant efficacy against *Leishmania* species, which are the causative agents of kala-azar. *Paromomycin* - **Paromomycin** is an **aminoglycoside antibiotic** that can be used as an alternative treatment for visceral leishmaniasis, especially in combination therapies. - Although effective, it is generally not considered the first-line **drug of choice** globally, and its efficacy can vary by region.
Question 124: XDR-TB is defined as resistance to which of the following drug combinations?
- A. INH plus rifampicin
- B. Fluoroquinolones plus INH plus amikacin
- C. Fluoroquinolones plus rifampicin plus kanamycin
- D. Fluoroquinolones plus INH plus rifampicin plus amikacin (Correct Answer)
Explanation: **Fluoroquinolones plus INH plus rifampicin plus amikacin** - **Extensively drug-resistant tuberculosis (XDR-TB)** is defined by resistance to the most effective anti-TB drugs: **isoniazid (INH)**, **rifampicin**, any **fluoroquinolone**, and at least one of the three injectable second-line drugs (**amikacin**, **kanamycin**, or **capreomycin**). - This combination signifies a substantial therapeutic challenge due to limited treatment options and a high risk of treatment failure. *INH plus rifampicin* - Resistance to **INH** and **rifampicin** defines **multidrug-resistant tuberculosis (MDR-TB)**, which is a precursor to XDR-TB but not XDR-TB itself. - While serious, MDR-TB is not as extensively resistant as XDR-TB, as it doesn't include resistance to fluoroquinolones and second-line injectables. *Fluoroquinolones plus INH plus amikacin* - This combination is incomplete for the definition of XDR-TB because it omits **rifampicin** from the core definition. - XDR-TB specifically requires resistance to both **INH** and **rifampicin** (defining MDR-TB), in addition to resistance to a fluoroquinolone and one of the injectable second-line drugs. *Fluoroquinolones plus rifampicin plus kanamycin* - This combination is also incomplete for the definition of XDR-TB as it omits **isoniazid (INH)**, which is one of the two most crucial first-line drugs that characterize MDR-TB. - XDR-TB builds upon MDR-TB's resistance to both INH and rifampicin.
Question 125: 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 126: Which of the following medications is not typically used for the treatment of erectile dysfunction?
- A. Beta blockers (Correct Answer)
- B. Papaverine
- C. Sildenafil
- D. PG-E
Explanation: ***Beta blockers*** - **Beta blockers** are primarily used to treat conditions like **hypertension** and **heart disease**. - While they can cause ED as a side effect, they are **not used for its treatment**. *Sildenafil* - **Sildenafil** is a **PDE5 inhibitor** that works by increasing **blood flow to the penis**, facilitating an erection. - It is a **first-line oral medication** widely prescribed for erectile dysfunction. *PG-E* - **PG-E** refers to **Prostaglandin E1** (alprostadil), which can be administered via **intracavernosal injection** or **urethral suppository**. - It directly causes **vasodilation** in the penis, leading to an erection, and is used when oral medications are ineffective or contraindicated. *Papaverine* - **Papaverine** is a **non-specific vasodilator** that can be used as an **intracavernosal injection** for ED. - It works by relaxing **smooth muscle** in the penile arteries, increasing blood flow and inducing an erection, often used in combination with phentolamine.
Question 127: All are symptoms of morphine withdrawal except?
- A. Yawning
- B. Lacrimation
- C. Mydriasis
- D. Fall in BP (Correct Answer)
Explanation: ***Fall in BP*** - **Hypotension (fall in BP)** is **not** typically a symptom of opioid withdrawal; rather, **hypertension** can occur due to sympathetic overdrive. - Opioid withdrawal symptoms are primarily characterized by **hyperactivity** and increased sympathetic nervous system activity. *Mydriasis* - **Mydriasis (dilated pupils)** is a classic symptom of opioid withdrawal, resulting from reduced parasympathetic tone and increased sympathetic activity. - In contrast, opioid intoxication causes **miosis (pinpoint pupils)**. *Yawning* - **Yawning** is a very common and early symptom of opioid withdrawal, often accompanied by feelings of fatigue and restlessness. - It reflects generalized **autonomic dysregulation** during withdrawal. *Lacrimation* - **Lacrimation (tearing)** is another prominent autonomic symptom of opioid withdrawal. - This, along with rhinorrhea, contributes to the **"flu-like" symptoms** experienced during withdrawal.
Question 128: 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 129: 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 130: 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**.