Flu-like symptoms are a side effect of which anti-TB drug?
All of the following are known adverse effects of thalidomide, except:
Where does the oxidation of drugs mainly take place?
In primary open-angle glaucoma, pilocarpine eye drops lower intraocular pressure primarily by acting on which of the following?
All of the following are characteristic features of treatment of iron deficiency anemia with oral iron supplements, except which of the following?
From which part of the Papaver somniferum plant does the latex, commonly referred to as 'milk', exude?
Which of the following substances is commonly known as an arrow poison used by indigenous South American tribes?
In the context of pharmacology, what is the term 'Mickey Finn' commonly associated with?
Best method of treatment for methyl alcohol poisoning is:
When alcohol is consumed with aerated soft drinks -
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 91: Flu-like symptoms are a side effect of which anti-TB drug?
- A. Rifampicin (Correct Answer)
- B. Isoniazid
- C. Pyrazinamide
- D. Ethambutol
Explanation: ***Rifampicin*** - **Flu-like syndrome** (fever, chills, myalgia, and headache) is a dose-dependent side effect of **rifampicin**, particularly with intermittent dosing. - This reaction is due to **immunological mechanisms**, involving antibodies against rifampicin. *Isoniazid* - The most significant side effect of isoniazid is **hepatotoxicity**, which can range from mild elevated liver enzymes to severe hepatitis. - It can also cause **peripheral neuropathy**, particularly in malnourished patients or those with risk factors, preventable with pyridoxine (vitamin B6) supplementation. *Pyrazinamide* - **Hepatotoxicity** is a major concern with pyrazinamide, often leading to elevated liver enzymes and, in some cases, severe liver damage. - It frequently causes **hyperuricemia**, which can precipitate acute gouty arthritis due to decreased excretion of uric acid. *Ethambutol* - The most characteristic adverse effect of ethambutol is **optic neuritis**, causing decreased visual acuity, red-green color blindness, and visual field defects. - Regular **ophthalmological monitoring** is crucial during treatment to detect this reversible side effect early.
Question 92: All of the following are known adverse effects of thalidomide, except:
- A. DVT
- B. Neuropathy
- C. Teratogenicity
- D. Diarrhoea (Correct Answer)
Explanation: ***Diarrhoea*** - **Diarrhoea** is generally *not* considered a common or significant adverse effect of thalidomide. Constipation is more frequently reported. - While individual reactions vary, thalidomide's primary adverse effect profile does not typically include diarrhoea. *Teratogenicity* - **Teratogenicity** is the most notorious adverse effect of thalidomide, causing severe birth defects like **phocomelia** (shortened or absent limbs) in infants exposed during pregnancy. - Due to this, stringent **risk evaluation and mitigation strategies (REMS)** are in place for thalidomide use. *DVT* - Thalidomide is known to increase the risk of **venous thromboembolism (VTE)**, including **deep vein thrombosis (DVT)** and pulmonary embolism, especially in patients with multiple myeloma. - Prophylactic anticoagulation is often recommended for patients receiving thalidomide, particularly in combination with corticosteroids. *Neuropathy* - **Peripheral neuropathy** is a common and dose-limiting adverse effect of thalidomide, often presenting as numbness, tingling, and pain in the hands and feet. - It can be progressive and potentially irreversible, requiring careful monitoring and dose adjustments.
Question 93: Where does the oxidation of drugs mainly take place?
- A. Smooth ER (Correct Answer)
- B. Rough ER
- C. Cytoplasm
- D. Nucleus
Explanation: **Smooth ER** - The **smooth endoplasmic reticulum (SER)** is rich in enzymes, particularly the **cytochrome P450 system**, which is primarily responsible for phase I **oxidation reactions** of many drugs and xenobiotics [1]. - These oxidative reactions typically **increase the polarity** of drugs, making them easier to excrete [1]. *Nucleus* - The nucleus primarily contains the cell's **genetic material** (DNA) and is involved in **gene expression** and replication. - It does not contain the necessary enzymatic machinery for the major oxidative metabolism of drugs. *Rough ER* - The **rough endoplasmic reticulum (RER)** is characterized by the presence of **ribosomes** and is mainly involved in the **synthesis, folding, modification, and transport of proteins** destined for secretion or insertion into membranes [2]. - While it plays a role in protein synthesis, it is not the primary site for drug oxidation. *Cytoplasm* - The cytoplasm contains various organelles and is the site of many metabolic pathways, including **glycolysis** and some **phase II drug metabolism** (e.g., glucuronidation, sulfation) [1]. - However, the bulk of phase I **oxidative drug metabolism** does not occur in the general cytoplasm but rather within the smooth ER due to the concentration of relevant enzymes there [1].
Question 94: In primary open-angle glaucoma, pilocarpine eye drops lower intraocular pressure primarily by acting on which of the following?
- A. All of the options
- B. Trabecular meshwork
- C. Ciliary epithelium
- D. Longitudinal fibres of the ciliary muscle (Correct Answer)
Explanation: ***Longitudinal fibres of the ciliary muscle***- Pilocarpine is a **muscarinic agonist** that contracts the **longitudinal fibers of the ciliary muscle** [1, 3].- This contraction pulls on the **scleral spur**, separating the **trabecular meshwork** sheets, which increases conventional **aqueous humor outflow** [2, 3].*Trabecular meshwork*- While the **trabecular meshwork** is the site where aqueous humor exits the eye, pilocarpine primarily acts on the ciliary muscle to **indirectly affect** the meshwork's outflow facility [2, 3].- Pilocarpine does not directly alter the structure or function of the trabecular meshwork cells.*Ciliary epithelium*- The **ciliary epithelium** is responsible for **aqueous humor production** [1, 2].- Pilocarpine primarily affects **outflow**, not production, through its action on the ciliary muscle [1, 2].*All of the options*- Pilocarpine does not act on **all** these structures; its primary mechanism is through the ciliary muscle to enhance outflow.- It has no direct significant effect on **ciliary epithelium** or direct action on the **trabecular meshwork** itself.
Question 95: All of the following are characteristic features of treatment of iron deficiency anemia with oral iron supplements, except which of the following?
- A. Bioavailability is enhanced with vitamin C
- B. The proportion of iron absorbed reduces as hemoglobin improves
- C. The reticulocyte count should begin to increase within 7-10 days and peak at 2-4 weeks; this suggests good response to treatment
- D. The treatment should be discontinued immediately once hemoglobin normalizes to prevent side effects of iron (Correct Answer)
Explanation: ***The treatment should be discontinued immediately once hemoglobin normalizes to prevent side effects of iron*** - Treatment of **iron deficiency anemia** with oral iron supplements should continue for at least **3-6 months** after hemoglobin normalizes to replenish **iron stores**. - Premature cessation can lead to a rapid **recurrence of anemia** due to depleted iron reserves, despite normal hemoglobin levels. *Bioavailability is enhanced with vitamin C* - **Ascorbic acid (vitamin C)** creates an acidic environment in the stomach and reduces ferric iron (Fe3+) to ferrous iron (Fe2+), which is more readily absorbed. - This enhancement of **ferrous iron absorption** is a common practice to improve the efficacy of oral iron supplements. *The proportion of iron absorbed reduces as hemoglobin improves* - The body's **iron absorption mechanism** is tightly regulated by **hepcidin**, a hormone that increases when iron stores are sufficient. - As hemoglobin levels improve and iron stores are replenished, hepcidin levels rise, leading to a **decrease in iron absorption** to prevent iron overload. *The reticulocyte count should begin to increase in two weeks and peak in 4 weeks this suggests good response to treatment* - An increase in **reticulocyte count** by approximately **7-10 days** and peaking around **2-4 weeks** after starting iron therapy indicates that the bone marrow is effectively responding to the increased iron availability by producing new red blood cells. - This **reticulocytosis** is an early and reliable sign of a positive treatment response before a significant rise in hemoglobin is observed.
Question 96: From which part of the Papaver somniferum plant does the latex, commonly referred to as 'milk', exude?
- A. Leaf of the plant
- B. Root of the plant
- C. Seeds of the plant
- D. Unripe capsule of the plant (Correct Answer)
Explanation: ***Unripe capsule of the plant*** - The **latex** (or 'milk') containing **opioid alkaloids** like morphine and codeine is primarily harvested by incising the **unripe seed capsules** of the *Papaver somniferum* plant. - This milky sap is then collected and dried to produce **crude opium**. *Leaf of the plant* - The leaves of *Papaver somniferum* do not contain significant amounts of the latex and are not the primary source of **opium alkaloids**. - While some **alkaloids** might be present in trace amounts, they are not extracted commercially from the leaves. *Root of the plant* - The roots of the poppy plant are not known to exude latex or to be a significant source of medically relevant **opioid alkaloids**. - Their primary function is absorption of water and nutrients, and anchoring the plant. *Seeds of the plant* - While the dried seeds are used for culinary purposes (poppy seeds), they contain very low levels of **opioid alkaloids** compared to the latex. - The latex is produced within the **capsule** before the seeds fully mature.
Question 97: Which of the following substances is commonly known as an arrow poison used by indigenous South American tribes?
- A. Opium
- B. Curare (Correct Answer)
- C. Cannabis
- D. Cyanide
Explanation: ***Curare*** - **Curare** is the traditional name for South American arrow poisons derived from plants, primarily *Chondrodendron tomentosum* and *Strychnos* species - It acts as a **competitive non-depolarizing neuromuscular blocking agent**, blocking nicotinic receptors at the neuromuscular junction - Causes **skeletal muscle paralysis** by competing with acetylcholine, leading to respiratory failure in prey - **Clinical relevance:** Tubocurarine (d-tubocurarine), derived from curare, was historically used as a muscle relaxant in surgery; modern derivatives include atracurium, vecuronium, and rocuronium *Opium* - **Opium** is derived from *Papaver somniferum* (opium poppy) and contains alkaloids like morphine and codeine - Acts on **opioid receptors** in the CNS to produce analgesia and sedation - Not used as an arrow poison by South American tribes; its effects are analgesic rather than paralytic *Cannabis* - **Cannabis** (*Cannabis sativa*) contains psychoactive compounds like THC (tetrahydrocannabinol) - Acts on **cannabinoid receptors** producing psychoactive and analgesic effects - Not used as an arrow poison; lacks the rapid paralytic action needed for hunting *Cyanide* - **Cyanide** inhibits cytochrome c oxidase, blocking cellular respiration and causing rapid cell death - While highly toxic, it is **not the traditional arrow poison** of South American indigenous tribes - Traditional arrow poisons like curare cause neuromuscular paralysis rather than cellular asphyxiation
Question 98: In the context of pharmacology, what is the term 'Mickey Finn' commonly associated with?
- A. Chloroform
- B. Methyl alcohol
- C. Chloral hydrate (Correct Answer)
- D. Ethylene glycol
Explanation: ***Chloral hydrate*** - A "Mickey Finn" is a slang term for a drink **laced with a psychoactive drug or incapacitating agent** given to an unsuspecting person. - Historically, **chloral hydrate** was a common substance used for this purpose due to its rapid sedative-hypnotic effects. *Chloroform* - While chloroform is a potent anesthetic and sedative, it is primarily used as an **inhalant** and is not typically administered orally in drinks. - Ingesting chloroform in large quantities can be **fatal due to severe hepatotoxicity and neurotoxicity**. *Methyl alcohol* - **Methyl alcohol (methanol)** is highly toxic and causes severe metabolic acidosis, blindness, and death, even in small amounts. - It does not induce the quick, incapacitating sedative effects associated with a "Mickey Finn" but rather a **delayed, severe poisoning syndrome**. *Ethylene glycol* - **Ethylene glycol** is an antifreeze agent that is also highly toxic, causing kidney failure and metabolic derangements. - Similar to methanol, its effects are **delayed and severe**, not the immediate incapacitating sedation implied by the term "Mickey Finn."
Question 99: Best method of treatment for methyl alcohol poisoning is:
- A. Calcium gluconate
- B. Ethyl alcohol (Correct Answer)
- C. Amphetamines
- D. 1% Ammonia
Explanation: ***Ethyl alcohol*** - **Ethanol** (ethyl alcohol) acts as a competitive substrate for **alcohol dehydrogenase**, the enzyme responsible for metabolizing **methanol** into toxic metabolites like formaldehyde and formic acid. - By saturating alcohol dehydrogenase, ethanol prevents the formation of these toxic metabolites, allowing methanol to be excreted unchanged. - **Clinical note**: While **fomepizole** (4-methylpyrazole) is now the preferred first-line antidote when available, **ethanol** remains an effective and widely used alternative, especially in resource-limited settings. - **Administration**: IV ethanol is given to maintain blood ethanol concentration of 100-150 mg/dL. *Calcium gluconate* - **Calcium gluconate** is primarily used to treat **hypocalcemia**, ethylene glycol poisoning (for hypocalcemia), or hydrofluoric acid burns. - It has no role in the management of methyl alcohol poisoning as it does not interfere with the metabolism of methanol or its toxic byproducts. *Amphetamines* - **Amphetamines** are central nervous system stimulants used for conditions like ADHD and narcolepsy. - They have no therapeutic benefit or antidotal properties in the context of methanol poisoning. *1% Ammonia* - **Ammonia** is a strong base and is highly corrosive; it has no medical application as an antidote for methanol poisoning. - Administering ammonia would cause direct tissue damage and exacerbate patient harm due to its toxic and caustic properties.
Question 100: When alcohol is consumed with aerated soft drinks -
- A. Effect is enhanced
- B. To reduce hangover risk
- C. Absorption is faster, increasing intoxication risk (Correct Answer)
- D. None of the options
Explanation: ***Absorption is faster, increasing intoxication risk*** - The carbonation in aerated soft drinks speeds up the absorption of alcohol into the bloodstream. - This **faster absorption** leads to a more rapid increase in blood alcohol concentration and can intensify the effects of alcohol, thereby increasing the risk of intoxication. *Effect is enhanced* - While the **effect** might seem to be enhanced due to quicker onset, this option doesn't fully explain the physiological mechanism. - The primary reason for the perceived enhancement is the **accelerated absorption**, not a direct potentiation of alcohol's action. *To reduce hangover risk* - Mixing alcohol with aerated drinks generally **does not reduce hangover risk**; in fact, the rapid absorption can sometimes worsen dehydration and lead to a more severe hangover. - Hangovers are primarily caused by dehydration, acetaldehyde buildup, and other congeners, which are not mitigated by carbonated mixers. *None of the options* - This option is incorrect because the statement about **faster absorption leading to increased intoxication risk** is a well-established physiological effect.