General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 501: What is the percentage of atropine present in atropine drops?

A. 2%
B. 3%
C. 1% (Correct Answer)
D. 4%

Explanation: ***1%*** - Atropine eye drops are commonly formulated as a **1% solution** for ophthalmic use. - This concentration is effective for achieving **cycloplegia** (paralysis of the ciliary muscle) and **mydriasis** (pupil dilation) in clinical settings [2]. *2%* - A **2% concentration** is not the standard formulation for atropine eye drops. - Using a higher concentration than necessary could increase the risk of systemic side effects without providing significant additional therapeutic benefit [1]. *3%* - Atropine eye drops are generally not manufactured or prescribed in a **3% concentration**. - While stronger, such a concentration would be unusual and potentially lead to more pronounced or prolonged effects and adverse reactions. *4%* - A **4% concentration** of atropine eye drops is significantly higher than the standard and is not typically used due to the increased risk of systemic absorption and side effects. - High concentrations increase the likelihood of adverse effects such as **tachycardia**, dry mouth, and blurry vision.

Question 502: All statements regarding ketamine are true except –

A. Raised ICT do not respond to CO2 level (Correct Answer)
B. Psychomimetic emergence
C. May be arrhythmogenic
D. Vasodilator and negative inotropic effect

Explanation: ***Raised ICT do not respond to CO2 level*** - While ketamine generally **increases intracranial pressure (ICP)**, the statement that it *does not respond to CO2 levels* is incorrect. - Changes in arterial CO2 levels directly influence cerebral blood flow and, consequently, ICP, regardless of ketamine administration. Hyperventilation to lower PCO2 is still used to reduce ICP, even if ketamine is used. *Psychomimetic emergence* - **Psychomimetic emergence phenomena** (e.g., vivid dreams, hallucinations, delirium) are a well-known side effect of ketamine, particularly in adults. - This effect is due to ketamine's interaction with the **NMDA receptor** and other neurotransmitter systems. *May be arrhythmogenic* - Ketamine can cause **tachycardia** and **hypertension** due to sympathetic nervous system stimulation, which may lead to or exacerbate arrhythmias, especially in patients with pre-existing cardiac conditions. - Although it has a direct myocardial depressant effect *in vitro*, its *in vivo* effects are usually dominated by **sympathetic stimulation**, which can be arrhythmogenic. *Vasodilator and negative inotropic effect* - While ketamine has a direct **vasodilatory** and **negative inotropic effect** on cardiac muscle *in vitro* or in isolated heart preparations, these actions are typically overridden *in vivo* by its potent **sympathetic stimulating effects**. - *In vivo*, the net effect is usually **increased heart rate, blood pressure, and cardiac output**, due to catecholamine release and reuptake inhibition.

Question 503: All of the following are true about "Imiquimod" except:

A. Antitumor activity
B. Indirect antiviral activity
C. Direct antiviral activity (Correct Answer)
D. It releases cytokines

Explanation: ***Direct antiviral activity*** - Imiquimod is a **Toll-like receptor 7 (TLR7) agonist** that primarily works by **stimulating the immune system** to produce cytokines, which then fight viral infections and cancerous cells. - It does not directly inhibit viral replication or destroy viral particles; its action is entirely **immune-mediated**. *Antitumor activity* - Imiquimod stimulates the local immune response, leading to the production of interferons and other cytokines that can inhibit the growth of **tumor cells**, such as in basal cell carcinoma. - This activity is **indirect**, as it relies on the host immune system rather than direct cytotoxic effects on cancer cells. *Indirect antiviral activity* - As a TLR7 agonist, imiquimod prompts immune cells to release significant amounts of **cytokines** like interferon-alpha, which have potent antiviral effects. - This **enhances the body's natural defense mechanisms** against viral infections, such as those causing genital warts. *It releases cytokines* - Imiquimod's mechanism of action involves binding to **Toll-like receptor 7 (TLR7)** on immune cells like macrophages and dendritic cells. - This binding triggers a signaling cascade that results in the robust production and release of various **pro-inflammatory and anti-viral cytokines**, including interferons and TNF-alpha.

Question 504: Which of the following statements about EMLA is true?

A. Can be used for intubation
B. Faster acting
C. Used only in children
D. Mixture of local anesthetics (Correct Answer)

Explanation: ***Mixture of local anesthetics*** - **EMLA** (Eutectic Mixture of Local Anesthetics) is a cream composed of a 1:1 mixture of **lidocaine** and **prilocaine**. - This eutectic mixture has a lower melting point than its individual components, allowing it to penetrate the skin more effectively for **topical anesthesia**. *Can be used for intubation* - EMLA is a **topical anesthetic cream** designed for skin surface application rather than mucosal surfaces or deep tissue. - Its slow onset and limited depth of penetration make it **unsuitable for intubation**, which requires rapid and profound anesthesia of the airway. *Faster acting* - EMLA requires an application time of **at least 60 minutes** (and sometimes longer for deeper anesthesia) to achieve maximal effect. - This **slow onset** is a significant limitation and is much slower than injected local anesthetics or other rapid-acting topical agents. *Used only in children* - EMLA is indeed **commonly used in children** to reduce pain from venipuncture, vaccinations, and minor procedures. - However, it is also widely used in **adults** for similar indications, such as before IV insertions, laser treatments, or skin biopsies.

Question 505: Pertussis toxin acts by all of the following mechanisms except ?

A. Increase cyclic AMP
B. Acts through G alpha subunit
C. ADP ribosylation of proteins associated with receptors
D. Increased calcium release from sarcoplasmic reticulum (Correct Answer)

Explanation: ***Increased calcium release from sarcoplasmic reticulum*** - Pertussis toxin does NOT directly cause increased calcium release from the sarcoplasmic reticulum. - While increased cAMP can have downstream effects on calcium signaling, **direct calcium release from SR is not a characteristic mechanism** of pertussis toxin action. - This is the exception among the listed mechanisms. *Acts through G alpha subunit* - Pertussis toxin primarily acts by **ADP-ribosylating** the αi subunit of **G proteins** (Gαi), effectively inhibiting its function. - This inhibition leads to the **inactivation of Gi proteins**, preventing them from inhibiting adenylate cyclase. - This is the PRIMARY mechanism of pertussis toxin. *Increase cyclic AMP* - The inhibition of Gi proteins by pertussis toxin leads to **constitutive activation of adenylate cyclase**. - This results in a **sustained increase in intracellular cyclic AMP (cAMP)** levels. - This is a well-established consequence of pertussis toxin action. *ADP ribosylation of proteins associated with receptors* - Pertussis toxin specifically acts as an **ADP-ribosyltransferase**, transferring an ADP-ribose group from NAD+ to target proteins. - This modification occurs on the **alpha-inhibitory subunit (Giα)** of heterotrimeric G proteins, which are associated with various cell surface receptors. - This is the molecular mechanism by which pertussis toxin exerts its effects.

Question 506: Anti-inflammatory action of steroids is due to

A. Inhibition of lipoxygenase
B. Inhibition of phospholipase A2 (Correct Answer)
C. Inhibition of cyclooxygenase
D. Increased activity of lipoprotein lipase

Explanation: ***Inhibition of phospholipase A2*** - Steroids exert their potent anti-inflammatory effects primarily by inducing the synthesis of **lipocortin-1 (annexin-1)**, which then inhibits **phospholipase A2 (PLA2)** activity. - This inhibition of PLA2 prevents the release of **arachidonic acid** from cell membrane phospholipids, thereby blocking the entire cascade of downstream inflammatory mediators, including prostaglandins, thromboxanes, and leukotrienes. *Inhibition of lipoxygenase* - While leukotrienes (products of the lipoxygenase pathway) are inflammatory mediators, steroids achieve their effect upstream by blocking the precursor (arachidonic acid) rather than directly inhibiting **lipoxygenase**. - **Zileuton** is an example of a drug that directly inhibits lipoxygenase. *Inhibition of cyclooxygenase* - Steroids do not directly inhibit **cyclooxygenase (COX) enzymes**; this is the primary mechanism of action for **NSAIDs (Nonsteroidal Anti-inflammatory Drugs)** like ibuprofen and aspirin. - By inhibiting COX, NSAIDs primarily block the synthesis of prostaglandins and thromboxanes, but not leukotrienes. *Increased activity of lipoprotein lipase* - Increased activity of **lipoprotein lipase (LPL)** by steroids is related to their metabolic effects, such as promoting fat deposition and contributing to steroid-induced dyslipidemia, rather than their anti-inflammatory action. - LPL's role is in the metabolism of triglycerides in lipoproteins, which is distinct from the inflammatory cascade.

Question 507: Which drug does not lead to osteoporosis?

A. Alcohol
B. Warfarin
C. Thyroxine (Correct Answer)
D. Heparin

Explanation: ***Thyroxine*** - While **thyrotoxicosis** (excessive thyroid hormone levels) can accelerate bone turnover and lead to bone loss, appropriate physiological doses of **thyroxine replacement therapy** for hypothyroidism generally *do not* cause osteoporosis. - Maintaining **euthyroid status** with thyroxine replacement is crucial for overall health and does not significantly increase the risk of osteoporosis when monitored correctly. *Alcohol* - **Chronic alcohol abuse** is a significant risk factor for **osteoporosis** due to its toxic effects on osteoblasts, inhibition of calcium absorption, and nutritional deficiencies. - It also leads to increased cortisol levels and often liver disease, further contributing to **bone loss**. *Warfarin* - Long-term use of **warfarin**, an anticoagulant, has been associated with decreased bone mineral density and an increased risk of **osteoporosis**. - This is primarily due to its antagonistic effect on **vitamin K**, which is essential for the gamma-carboxylation of osteocalcin and other bone matrix proteins. *Heparin* - Both unfractionated and to a lesser extent, **low-molecular-weight heparin**, can induce **osteoporosis** with prolonged use, typically after several months. - Heparin's mechanism of action in bone involves stimulating bone resorption, inhibiting osteoblast activity, and potentially increasing the activity of collagenase.

Question 508: Rapid infusion of insulin causes

A. Hyponatremia
B. Hyperkalemia
C. Hypokalemia (Correct Answer)
D. Hypernatremia

Explanation: ***Hypokalemia*** - Insulin promotes the uptake of **glucose** and **potassium** into cells, primarily via the Na+/K+-ATPase pump. - Rapid infusion of insulin can cause a rapid shift of potassium from the **extracellular space** into the **intracellular space**, leading to hypokalemia. *Hyponatremia* - While insulin can influence fluid balance, it does not directly cause hyponatremia through a rapid shift of sodium. - **Hyponatremia** is more commonly associated with conditions like excessive fluid intake, heart failure, or SIADH. *Hyperkalemia* - **Hyperkalemia** is the opposite of the effect typically seen with insulin administration; insulin is often used to treat hyperkalemia. - Hyperkalemia can be caused by conditions like **kidney failure**, certain medications (e.g., ACE inhibitors), or **rhabdomyolysis**. *Hypernatremia* - Insulin does not directly cause **hypernatremia**. - **Hypernatremia** is usually a result of **dehydration** or excessive sodium intake, leading to a high concentration of sodium in the blood.

Question 509: Which of the following statements best describes an orphan drug?

A. It is a drug which has no therapeutic use
B. It is a drug declared for treatment or prevention of a rare disease (Correct Answer)
C. It is a very cheap drug
D. It is a drug which acts on orphan receptors

Explanation: ***It is a drug declared for treatment or prevention of a rare disease*** - An **orphan drug** is specifically developed to treat or prevent a **rare disease** or condition. - Due to the limited patient population, pharmaceutical companies often receive incentives (like tax credits, fee waivers, or extended market exclusivity) for developing these drugs [1]. *It is a drug which has no therapeutic use* - This statement is incorrect; **orphan drugs** are developed for specific therapeutic uses in rare conditions. - Drugs with no therapeutic use would not undergo the rigorous development and approval processes for market release. *It is a very cheap drug* - This is generally incorrect; **orphan drugs** can often be very expensive due to the high development costs and small patient populations over which these costs are spread. - Their cost is not a defining characteristic, and many are premium-priced. *It is a drug which acts on orphan receptors* - While some drugs may act on **orphan receptors** (receptors whose endogenous ligands are unknown), this is a separate scientific classification and not the definition of an **orphan drug**. - The term **"orphan drug"** relates to the prevalence of the disease it treats, not its pharmacological mechanism.

Question 510: A drug used to prevent niacin-induced flushing is

A. Dexamethasone
B. Aspirin (Correct Answer)
C. Paracetamol
D. Cetirizine

Explanation: ***Aspirin*** - Niacin-induced flushing is mediated by **prostaglandins**, primarily prostaglandin D2 (PGD2), which cause vasodilation. - **Aspirin**, being a non-steroidal anti-inflammatory drug (NSAID) and a cyclooxygenase (COX) inhibitor, blocks the synthesis of prostaglandins, thereby reducing flushing. *Cetirizine* - Cetirizine is a **second-generation H1 antihistamine** primarily used to treat allergic symptoms like rhinitis or urticaria. - It does not significantly affect prostaglandin pathways implicated in niacin-induced flushing. *Dexamethasone* - Dexamethasone is a **corticosteroid** with potent anti-inflammatory and immunosuppressive effects. - While it can broadly reduce inflammation, it is not the primary or most appropriate treatment for niacin-induced flushing, which is better managed with prostaglandin inhibitors. *Paracetamol* - Paracetamol (acetaminophen) is an **analgesic and antipyretic** that works primarily by inhibiting prostaglandin synthesis in the central nervous system. - It has minimal anti-inflammatory effects and does not effectively reduce peripheral prostaglandin production responsible for niacin flush.

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