General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 551: What is the mechanism of action of Iloprost?

A. Thromboxane synthetase antagonist
B. PGI 2 analogue (Correct Answer)
C. Thromboxane receptor antagonist
D. PGE 1 analogue

Explanation: ***Thromboxane receptor antagonist*** - This statement is incorrect. **Iloprost** is an analogue of **prostacyclin (PGI2)**, not a thromboxane receptor antagonist. - It works by mimicking the effects of natural prostacyclin, leading to **vasodilation** and **inhibition of platelet aggregation**. *Thromboxane synthetase antagonist* - **Thromboxane synthetase inhibitors** prevent the production of thromboxane A2, a potent vasoconstrictor and platelet aggregator. - While this is a different mechanism from iloprost, drugs like **dazoxiben** act this way to achieve similar clinical effects of reduced vasoconstriction and platelet aggregation. *PGE 1 analogue* - **PGE1 analogues** (like **alprostadil**) are primarily used to maintain patent ductus arteriosus in neonates or for erectile dysfunction. - While PGE1 also has vasodilatory and antiplatelet effects, **iloprost** specifically mimics **PGI2**. *PGI 2 analogue* - This is the **correct mechanism of action** for **Iloprost**. Iloprost is a stable synthetic analogue of **prostacyclin (PGI2)**. - By activating **prostacyclin receptors**, it causes **vasodilation** (especially in the pulmonary and systemic vasculature) and potent **inhibition of platelet aggregation**.

Question 552: Tibolone is a ?

A. Natural steroidal hormone
B. Natural non-steroidal hormone
C. Synthetic steroid hormone (Correct Answer)
D. Synthetic non-steroidal hormone

Explanation: ***Synthetic steroid hormone*** - **Tibolone** is a **synthetic steroid** with **estrogenic, progestogenic, and weak androgenic properties** used for hormone therapy in postmenopausal women. - Its structure is derived from **nortestosterone**, making it a synthetic compound rather than naturally occurring. *Natural steroidal hormone* - Natural steroidal hormones like **estrogen** and **progesterone** are produced endogenously by the body and have specific steroidal molecular structures. - Tibolone is not a naturally occurring hormone but is manufactured in a lab. *Natural non-steroidal hormone* - Natural non-steroidal hormones typically include peptides (e.g., insulin) or amines (e.g., thyroid hormones). - Tibolone's chemical structure is clearly steroidal, not non-steroidal. *Synthetic non-steroidal hormone* - Synthetic non-steroidal hormones are compounds like **diethylstilbestrol** (DES) that mimic hormone action but lack the steroid nucleus. - Tibolone possesses a distinct steroid backbone, classifying it as a synthetic steroid.

Question 553: Mechanism of action of Niclosamide is:

A. Inhibition of substrate level phosphorylation
B. Inhibition of proton efflux pumps
C. Increase production of free radicals
D. Inhibition of mitochondrial oxidative phosphorylation (Correct Answer)

Explanation: ***Inhibition of mitochondrial oxidative phosphorylation*** - **Niclosamide** is an **uncoupler of oxidative phosphorylation**, leading to **ATP depletion** in the parasite. - This effectively starves the parasite of energy, particularly **tapeworms**, which are highly dependent on this pathway. *Inhibition of substrate level phosphorylation* - **Substrate-level phosphorylation** is a metabolic pathway that directly phosphorylates ADP to ATP using high-energy intermediate molecules, not the primary target of niclosamide. - While it contributes to ATP production, its inhibition is not the primary mechanism of action for **niclosamide**. *Inhibition of proton efflux pumps* - **Proton efflux pumps** (e.g., proton pumps in gastric cells) are generally not the direct target for anthelmintic drugs like niclosamide. - This mechanism is characteristic of drugs like **proton pump inhibitors** (PPIs) used to reduce stomach acid. *Increase production of free radicals* - Some antiparasitic drugs act by increasing **oxidative stress** and **free radical production**, leading to parasite death. - However, for **niclosamide**, the primary mechanism is the disruption of **ATP synthesis** through uncoupling.

Question 554: Highest cannabinoid content of cannabis is found in which part of the plant?

A. Root
B. Resin (Correct Answer)
C. Seed
D. Stem

Explanation: ***Resin*** - The **resin** (often called **kief** or hashish when processed) is a sticky, viscous substance produced by glandular trichomes, which are most abundant on the female cannabis flower. - This resin contains the highest concentration of **cannabinoids**, including **THC** (tetrahydrocannabinol), which is responsible for the plant's psychoactive effects. *Root* - The **root** of the cannabis plant contains very minimal amounts of cannabinoids. - Its primary function is in nutrient and water absorption, and anchoring the plant. *Seed* - **Cannabis seeds** are rich in oils, proteins, and omega fatty acids, but they contain negligible amounts of psychoactive cannabinoids. - They are primarily used for cultivation or as a nutritional food source (hemp seeds). *Stem* - The **stem** of the cannabis plant mainly consists of fibrous material and woody tissue. - While it may contain trace amounts of cannabinoids, the concentration is significantly lower compared to the resinous parts.

Question 555: What is the typical maintenance dose of Levetiracetam in pediatric patients?

A. 10 - 20 mg/kg/day
B. 20 - 30 mg/kg/day
C. 30 - 40 mg/kg/day (Correct Answer)
D. 40 - 50 mg/kg/day

Explanation: ***30 - 40 mg/kg/day*** - Levetiracetam is often initiated with a lower dose (e.g., 10-15 mg/kg/day) and **titrated upwards** to achieve seizure control. - The typical maintenance dose for Levetiracetam, especially in pediatric patients, is generally considered to be in the range of **30-40 mg/kg/day** administered in two divided doses. *10 - 20 mg/kg/day* - This range is more typical for the **initial starting dose** of Levetiracetam, rather than the maintenance dose. - While sometimes used as a maintenance dose in specific adult cases or for mild seizure control, it is often considered **sub-therapeutic** for many patients. *20 - 30 mg/kg/day* - This dose range can be an **intermediate dose** during titration, or a maintenance dose for some patients, but it is generally at the lower end of the effective maintenance range. - Many patients require a higher dose to achieve **optimal seizure control** without intolerable side effects. *40 - 50 mg/kg/day* - Doses in this range are often associated with an **increased risk of side effects**, such as somnolence, asthenia, and behavioral changes [1]. - While some patients may require these higher doses under careful supervision, they are generally **above the typical maintenance dose** and should be considered only when lower doses are ineffective.

Question 556: Tachyphylaxis is seen with which of the following drugs?

A. Pethidine
B. Phenoxybenzamine
C. Phentolamine
D. Ephedrine (Correct Answer)

Explanation: ***Ephedrine*** - **Ephedrine** is an indirectly acting sympathomimetic that releases stored norepinephrine from nerve terminals [1, 3]. This can lead to **tachyphylaxis** (rapidly decreasing response to repeated doses) as **norepinephrine stores** become depleted [2, 3]. - Due to the depletion of **neurotransmitter stores**, subsequent doses become less effective until stores are replenished [2, 3]. *Pethidine* - **Pethidine** is an opioid analgesic; its primary mechanism of action involves agonizing opioid receptors. - It does not typically exhibit **tachyphylaxis** through neurotransmitter depletion, but rather can lead to tolerance with chronic use. *Phenoxybenzamine* - **Phenoxybenzamine** is a non-selective, **irreversible alpha-adrenergic receptor blocker**. - Its mechanism involves long-lasting blockade of receptors, and **tachyphylaxis** is not a characteristic feature of its pharmacodynamics. *Phentolamine* - **Phentolamine** is a non-selective, **reversible alpha-adrenergic receptor blocker**. - While it has a shorter duration of action compared to phenoxybenzamine, its effects are reversible and it does not typically cause **tachyphylaxis** through neurotransmitter depletion.

Question 557: Which of the following drug classes is not typically considered a first-line treatment for chronic pain management?

A. Opioids
B. Antiepileptics
C. Serotonergic drugs
D. Dopamine antagonist (Correct Answer)

Explanation: ***Dopamine antagonist*** - **Dopamine antagonists** (e.g., metoclopramide, haloperidol) are primarily used for treating conditions like **psychosis, nausea, and vomiting**, and are **not used for chronic pain management**. - While dopamine pathways can influence pain perception, directly blocking dopamine receptors is not a recognized approach for managing chronic pain and can cause significant adverse effects (extrapyramidal symptoms, sedation). - This is the **correct answer** as they are definitively not first-line (or even considered) for chronic pain. *Opioids* - While **opioids** can be effective for moderate to severe pain, **current guidelines do NOT recommend them as first-line for chronic non-cancer pain** due to risks of addiction, tolerance, and limited long-term efficacy. - However, they may be considered in specific circumstances after other treatments fail, so they are not the best answer here since dopamine antagonists are never used. - First-line options are typically non-opioid analgesics (NSAIDs, acetaminophen) for nociceptive pain. *Antiepileptics* - **Antiepileptics** (e.g., **gabapentin, pregabalin**) are **first-line treatments for neuropathic chronic pain**. - They work by modulating voltage-gated calcium channels and reducing neurotransmitter release, which helps calm overactive nerve signals. - Widely recommended in guidelines for diabetic neuropathy, postherpetic neuralgia, and other neuropathic conditions. *Serotonergic drugs* - **Serotonergic drugs**, particularly **SNRIs** (e.g., **duloxetine, venlafaxine**) and **tricyclic antidepressants** (e.g., amitriptyline), are **first-line agents for several chronic pain conditions**. - Used for fibromyalgia, chronic musculoskeletal pain, and neuropathic pain. - They enhance descending inhibitory pain pathways by increasing serotonin and norepinephrine at the spinal cord level.

Question 558: Which vaccine should not be frozen?

A. OPV
B. Measles
C. HBV (Correct Answer)
D. Yellow fever

Explanation: ***HBV*** - **Hepatitis B vaccine** (HBV) contains an **aluminum adjuvant** (aluminum hydroxide or aluminum phosphate), which is **irreversibly damaged by freezing**. - Freezing causes the adjuvant to form **large aggregates**, leading to loss of **potency and immunogenicity**, rendering the vaccine ineffective. - **WHO and CDC guidelines** strictly prohibit freezing of aluminum-adjuvanted vaccines. *OPV* - **Oral polio vaccine** (OPV) is a **live attenuated vaccine** that is **stable when frozen**. - It is stored at **-20°C for long-term storage** to maintain its **viability over extended periods**. - Freezing is **recommended** for OPV preservation. *Measles* - The **measles vaccine** should ideally be **stored at 2-8°C** and **not frozen** according to standard guidelines. - However, measles vaccine is **more freeze-tolerant** than aluminum-adjuvanted vaccines and some formulations can withstand brief freezing. - **HBV remains the classic answer** for vaccines that should not be frozen due to the aluminum adjuvant sensitivity. *Yellow fever* - The **yellow fever vaccine** is a **live attenuated vaccine** that is **stable when frozen**. - Stored at **-20°C or colder** for long-term storage to preserve its **potency and effectiveness**. - Freezing is **recommended** for yellow fever vaccine preservation.

Question 559: Tocilizumab is an antibody against which interleukin?

A. IL 8
B. IL 2
C. IL 4
D. IL 6 (Correct Answer)

Explanation: ***IL 6*** - **Tocilizumab** is a **monoclonal antibody** specifically designed to target the **interleukin-6 (IL-6) receptor**. - By blocking the IL-6 receptor, tocilizumab inhibits the signaling pathways mediated by IL-6, which plays a crucial role in **inflammation** and immune responses in conditions like **rheumatoid arthritis** and **cytokine release syndrome**. *IL 2* - **Interleukin-2 (IL-2)** is important for the proliferation and differentiation of T cells, and antibodies targeting IL-2 or its receptor (e.g., **daclizumab**) are used in different contexts like **transplant rejection prophylaxis** or **autoimmune diseases**. - Tocilizumab does not directly interact with IL-2. *IL 4* - **Interleukin-4 (IL-4)** is a key cytokine involved in **allergic responses** and the differentiation of **Th2 cells**. - Antibodies targeting IL-4 or its receptor (e.g., **dupilumab**) are used in the treatment of conditions like **atopic dermatitis** and asthma. Tocilizumab is not an anti-IL-4 agent. *IL 8* - **Interleukin-8 (IL-8)**, also known as **CXCL8**, is a **chemokine** primarily involved in the recruitment of neutrophils to sites of infection or inflammation. - While IL-8 is an important mediator of inflammation, tocilizumab does not target IL-8; its action is focused on IL-6.

Question 560: What is the primary mechanism of action of colchicine?

A. Inhibits granulocyte migration (Correct Answer)
B. Inhibits gouty inflammation
C. Inhibits the release of chemotactic factors
D. All of the options

Explanation: ***Inhibits granulocyte migration*** - Colchicine's primary cellular mechanism involves binding to **tubulin**, preventing its polymerization into **microtubules**. - This microtubule disruption specifically affects **neutrophils/granulocytes**, inhibiting their **chemotaxis, migration, and phagocytic activity**, thereby reducing inflammation. - Among the given options, this represents the **most specific mechanism of action** at the cellular level, making it the best answer. - This is the key mechanism tested in medical examinations when the molecular target (tubulin) is not listed as an option. *Inhibits gouty inflammation* - This describes the **clinical effect** or therapeutic outcome, not the mechanism of action. - While colchicine is highly effective in acute **gout**, this option tells us *what* the drug does clinically, not *how* it works at the cellular/molecular level. *Inhibits the release of chemotactic factors* - Colchicine primarily affects the **cellular response to chemotactic factors** (i.e., preventing neutrophil migration toward inflammatory signals) rather than blocking the release of chemotactic factors themselves. - Its mechanism is on the **responding cell** (neutrophil), not on the source of chemotactic signals. *All of the options* - Incorrect because the other options describe either clinical outcomes or secondary effects. - The **inhibition of granulocyte migration** through microtubule disruption is the fundamental cellular mechanism that explains colchicine's anti-inflammatory effects.

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