Which drug is primarily used to promote fetal lung maturity?
At pKa = pH, what is the relationship between the ionic and non-ionic forms of a drug?
Burkholderia cepacia is resistant to which of the following antibiotics?
What is the physiological dose of hydrocortisone (mg/m2/day)?
Which of the following statements about vitamin K is correct?
Anaerobes are resistant intrinsically against which of the following?
Tadalafil should not be given with:
Colonoscopy performed on a 25 year old woman with eating disorder showed dark brown to black pigmentary deposit in the lining of the large intestine. Histopathology of biopsy revealed pigment laden macrophages within the lamina propria. On probing, the woman revealed use of laxatives for 9 months to lose weight. What could be the probable laxative agent that could have caused these findings?
Which drug increases bone formation in osteoporosis?
Mechanism of action of d-tubocurarine is:
NEET-PG 2018 - Pharmacology NEET-PG Practice Questions and MCQs
Question 11: Which drug is primarily used to promote fetal lung maturity?
- A. Folic acid
- B. Dexamethasone (Correct Answer)
- C. Beclomethasone
Explanation: ***Dexamethasone*** - **Dexamethasone** is a synthetic glucocorticoid that rapidly crosses the placenta and stimulates the maturation of fetal lung surfactant production. - It significantly reduces the incidence and severity of **respiratory distress syndrome (RDS)** in preterm infants when administered to the mother. - **Antenatal corticosteroids** (dexamethasone or betamethasone) are given to mothers at risk of preterm delivery between 24-34 weeks of gestation. *Folic acid* - **Folic acid** is a B vitamin crucial for cell growth and DNA synthesis, primarily used to prevent **neural tube defects** in developing fetuses. - It does not have a direct role in promoting fetal lung maturity or surfactant production. *Beclomethasone* - **Beclomethasone** is an inhaled corticosteroid primarily used for the long-term management of **asthma** in children and adults. - While it is a corticosteroid, it is not typically used for systemic administration to the mother to promote fetal lung maturity due to its primary delivery method (inhalation) and limited systemic bioavailability compared to dexamethasone or betamethasone.
Question 12: At pKa = pH, what is the relationship between the ionic and non-ionic forms of a drug?
- A. Absorption of drug is 50% ionic and 50% non-ionic
- B. Conc. of drug is 25% ionic and 75% non-ionic
- C. Conc. of drug is 75% ionic and 25% non-ionic
- D. Conc. of drug is 50% ionic and 50% non-ionic (Correct Answer)
Explanation: ***Conc. of drug is 50% ionic and 50% non-ionic*** - At **pKa = pH**, the concentrations of the **ionized** and **unionized** forms of a drug are equal as per the **Henderson-Hasselbalch equation**. - This means that exactly **half** of the drug molecules are in their charged (ionic) state, and the other half are in their uncharged (non-ionic) state. *Absorption of drug is 50% ionic and 50% non-ionic* - The amount of drug that is absorbed is dependent on the **non-ionic concentration** available at the absorption site, but this option incorrectly states that the *absorption itself* is 50% ionic. - Absorption primarily occurs for the **non-ionic, lipophilic form** as it can more readily cross cell membranes. *Conc. of drug is 75% ionic and 25% non-ionic* - This ratio would occur when the **pH** is either 0.5 units above the pKa for a weak acid or 0.5 units below the pKa for a weak base. - For example, if **pH = pKa + 0.5** (for a weak acid), approximately 75% would be ionic. *Conc. of drug is 25% ionic and 75% non-ionic* - This ratio would occur when the **pH** is either 0.5 units below the pKa for a weak acid or 0.5 units above the pKa for a weak base. - For example, if **pH = pKa - 0.5** (for a weak acid), approximately 25% would be ionic.
Question 13: Burkholderia cepacia is resistant to which of the following antibiotics?
- A. Trimethoprim-sulfamethoxazole
- B. Cefotetan (Correct Answer)
- C. Ceftazidime
- D. Temocillin
Explanation: ***Cefotetan*** - *Burkholderia cepacia* shows **consistent resistance** to second-generation cephalosporins and cephamycins like **cefotetan**. - This organism is intrinsically resistant to **aminoglycosides** (gentamicin, tobramycin) and **polymyxins** (colistin), and shows variable resistance to many beta-lactams. - Among the options provided, cefotetan represents the most consistently ineffective agent. *Ceftazidime* - **Ceftazidime** (third-generation cephalosporin) shows **variable susceptibility** with *B. cepacia*. - While resistance is common, it is **not uniform**, and ceftazidime is sometimes used in **combination therapy** for B. cepacia infections. - Not considered a classic example of intrinsic resistance. *Trimethoprim-sulfamethoxazole* - **TMP-SMX** is the **first-line treatment** for *Burkholderia cepacia* infections. - It demonstrates good activity and is the preferred antimicrobial agent for this organism. - Resistance can develop but is not intrinsic. *Temocillin* - **Temocillin** (carboxypenicillin) has demonstrated activity against *B. cepacia*. - Used particularly in Europe for treating infections caused by this organism. - Not an antibiotic to which *B. cepacia* shows consistent resistance.
Question 14: What is the physiological dose of hydrocortisone (mg/m2/day)?
- A. 20-25 mg/m²/day
- B. 15-18 mg/m²/day
- C. 10-12 mg/m²/day (Correct Answer)
- D. 8-10 mg/m²/day
Explanation: ***10-12 mg/m²/day*** - This range represents the typical **physiological replacement dose** of hydrocortisone, mimicking the body's natural cortisol production. - This dose is used for patients with **adrenal insufficiency** to maintain normal metabolic functions without causing significant side effects. *8-10 mg/m²/day* - This dose is slightly on the lower side of the accepted physiological range and might not be sufficient for complete replacement in all individuals. - While close, it is not the most commonly cited optimal physiological dose for hydrocortisone replacement. *15-18 mg/m²/day* - This dose is typically considered above the physiological replacement level and may begin to cause **mild corticosteroid side effects** with prolonged use. - It might be used for short periods or in specific conditions, but not as a standard physiological replacement. *20-25 mg/m²/day* - This dose is well above the physiological range and would be considered a **pharmacological dose** often used for its anti-inflammatory or immunosuppressive effects. - Prolonged use at this dose would likely lead to significant **corticosteroid side effects** such as Cushingoid features, osteoporosis, and hyperglycemia.
Question 15: Which of the following statements about vitamin K is correct?
- A. All of the options are true
- B. Vitamin K acts as an anticoagulant
- C. Prolonged use of antimicrobials can lead to vitamin K deficiency (Correct Answer)
- D. The recommended dietary allowance for vitamin K is 200-300 micrograms per day
Explanation: ### Prolonged use of antimicrobials can lead to vitamin K deficiency - Long-term use of **broad-spectrum antimicrobials** can reduce the populations of gut bacteria that synthesize **vitamin K**, leading to a deficiency [1]. - This is particularly relevant because a significant portion of the body's vitamin K supply, especially **K2 (menaquinone)**, comes from microbial production in the intestines [1]. ### Vitamin K acts as an anticoagulant - Vitamin K is essential for the synthesis of **coagulation factors II, VII, IX, and X**, as well as protein C and S [3]; therefore, it is a **procoagulant**, not an anticoagulant [2]. - **Anticoagulants** like **warfarin** work by *inhibiting* vitamin K's action, thereby preventing the activation of these clotting factors [2], [3]. ### All of the options are true - This statement is incorrect because, as explained above, vitamin K is a **procoagulant**, not an anticoagulant. - The other statements also contain inaccuracies regarding vitamin K's function and recommended daily allowance. ### The recommended dietary allowance for vitamin K is 200-300 micrograms per day - The recommended daily allowance (RDA) for vitamin K in adults is significantly lower, typically **90 micrograms per day for women** and **120 micrograms per day for men**, not 200-300 micrograms [1]. - Excessive intake of vitamin K is generally not a concern as it has low toxicity due to its limited storage in the body.
Question 16: Anaerobes are resistant intrinsically against which of the following?
- A. Aminoglycosides (Correct Answer)
- B. Azithromycin
- C. Metronidazole
- D. Beta lactam antibiotics
Explanation: ***Aminoglycosides*** - **Aminoglycosides** require an **oxygen-dependent transport system** to enter bacterial cells. [3] - Since **anaerobes** thrive in low-oxygen environments, this transport system is inactive, making them intrinsically resistant to aminoglycosides. [3] *Azithromycin* - **Azithromycin** (a macrolide) inhibits protein synthesis by binding to the 50S ribosomal subunit. - Many anaerobes are susceptible to **azithromycin**, making it an effective treatment for certain anaerobic infections. *Metronidazole* - **Metronidazole** is a potent prodrug that requires reduction by **anaerobic metabolism** to become active. [1], [2] - Its mechanism of action involves creating **cytotoxic free radicals** that damage DNA, making it highly effective against most anaerobes. [2] *Beta lactam antibiotics* - **Beta-lactam antibiotics**, such as **penicillins** and **cephalosporins**, interfere with bacterial cell wall synthesis. - While some anaerobes are susceptible, others have developed resistance mechanisms like producing **beta-lactamase enzymes**, but they are not intrinsically resistant across the board. [4]
Question 17: Tadalafil should not be given with:
- A. Vasodilators (Correct Answer)
- B. Antibiotics
- C. Vasoconstrictors
- D. Valproate
Explanation: ***Vasodilators*** - Tadalafil is a **phosphodiesterase-5 (PDE5) inhibitor** that causes **vasodilation** by increasing cGMP levels, leading to smooth muscle relaxation. - Combining tadalafil with other **vasodilators**, particularly **nitrates**, can lead to a severe and potentially life-threatening drop in **blood pressure (hypotension)**. *Antibiotics* - While some antibiotics, particularly macrolides or azoles, can inhibit **CYP3A4** and increase tadalafil levels, this interaction is typically managed by dose adjustments rather than an absolute contraindication. - The primary concern with administering antibiotics and tadalafil concurrently is **pharmacokinetic interactions**, not a direct pharmacodynamic synergy leading to acute, severe adverse effects. *Vasoconstrictors* - Vasoconstrictors have an effect **opposite** to tadalafil, as they narrow blood vessels. - There is generally no contraindication for co-administration, and in fact, tadalafil's **vasodilatory effects** could potentially **counteract** some of the vasoconstriction, although concurrent use is not typically recommended for erectile dysfunction. *Valproate* - **Valproate** is an **anticonvulsant** and mood stabilizer, and there is no significant or clinically relevant drug interaction established with tadalafil. - It does not share common metabolic pathways or pharmacodynamic effects that would lead to dangerous interactions with tadalafil.
Question 18: Colonoscopy performed on a 25 year old woman with eating disorder showed dark brown to black pigmentary deposit in the lining of the large intestine. Histopathology of biopsy revealed pigment laden macrophages within the lamina propria. On probing, the woman revealed use of laxatives for 9 months to lose weight. What could be the probable laxative agent that could have caused these findings?
- A. Castor oil
- B. Bisacodyl
- C. Senna (Correct Answer)
- D. Sorbitol
Explanation: ***Senna*** - Chronic use of **anthraquinone laxatives** like senna [1] leads to **melanosis coli**, characterized by dark brown pigment in the colon. - Histopathology reveals **pigment-laden macrophages** in the lamina propria, confirming melanosis coli. *Castor oil* - **Castor oil** is a stimulant laxative that acts on the small intestine but does not typically cause **melanosis coli**. - Its primary action is to increase fluid secretion and bowel motility, rather than pigment deposition. *Bisacodyl* - **Bisacodyl** is a stimulant laxative that works locally in the colon to increase fluid and electrolyte secretion and stimulate peristalsis. - It works on different pharmacological mechanisms and typically does not cause the characteristic **pigment-laden macrophages** that define melanosis coli. *Sorbitol* - **Sorbitol** is an osmotic laxative that works by drawing water into the colon, softening stools and promoting bowel movements. - It does not induce the characteristic **darkening of the colonic mucosa** or the specific histological changes observed in melanosis coli.
Question 19: Which drug increases bone formation in osteoporosis?
- A. Teriparatide (Correct Answer)
- B. Calcitonin
- C. Risedronate
- D. Denosumab
Explanation: ***Correct Option: Teriparatide*** - **Teriparatide** is a recombinant form of **parathyroid hormone (PTH)** that, when administered intermittently, stimulates **osteoblast activity** to increase bone formation. - It is an **anabolic agent** specifically designed to build new bone, making it unique among osteoporosis treatments that primarily inhibit bone resorption. - Administered as a **daily subcutaneous injection** for up to 2 years. *Incorrect Option: Calcitonin* - **Calcitonin** is a hormone that inhibits **osteoclast activity**, thereby reducing bone resorption, but does not directly stimulate bone formation. - It may be used for pain relief in acute vertebral fractures but has a minor role in increasing bone density. *Incorrect Option: Risedronate* - **Risedronate** is a **bisphosphonate** that works by inhibiting **osteoclast-mediated bone resorption**, preventing bone breakdown. - It does not directly promote new bone formation; its primary action is to reduce bone turnover. *Incorrect Option: Denosumab* - **Denosumab** is a **monoclonal antibody** that targets and binds to **RANKL**, thereby inhibiting **osteoclast formation, function, and survival**, leading to decreased bone resorption. - Like bisphosphonates, its main mechanism is anti-resorptive, not anabolic.
Question 20: Mechanism of action of d-tubocurarine is:
- A. Competitive, nondepolarizing block at the Nm cholinergic receptor (Correct Answer)
- B. Noncompetitive, depolarizing block at the Nm cholinergic receptor
- C. Non-competitive, nondepolarizing block at the Nm cholinergic receptor
- D. Competitive, depolarizing block at the Nm cholinergic receptor
Explanation: ***Competitive, nondepolarizing block at the Nm cholinergic receptor*** - **d-tubocurarine** acts as a **competitive antagonist** at the **nicotinic muscle (Nm) cholinergic receptors** on the motor endplate. - It competes with **acetylcholine (ACh)** for binding sites, preventing ACh from activating the receptor and causing **muscle paralysis** without depolarization. *Noncompetitive, depolarizing block at the Nm cholinergic receptor* - This describes the mechanism of action of **depolarizing neuromuscular blockers** like **succinylcholine**, which first *depolarize* the motor endplate before causing paralysis. - d-tubocurarine does not cause initial depolarization; it directly blocks the receptor. *Non-competitive, nondepolarizing block at the Nm cholinergic receptor* - While d-tubocurarine is **nondepolarizing**, it is a **competitive antagonist**, not a non-competitive one. - A non-competitive block would involve binding to a different site on the receptor or an associated ion channel, altering receptor function indirectly. *Competitive, depolarizing block at the Nm cholinergic receptor* - This option incorrectly combines the concepts, as **depolarizing blockers** like succinylcholine act initially by **depolarizing** the endplate, whereas d-tubocurarine is purely a **nondepolarizing** agent. - The "competitive" aspect would be true for the binding of ACh to its site on a depolarizing agent, but the effect of d-tubocurarine is simply to block, not depolarize.