General Pharmacology — MCQs
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Which of the following causes an increase in cAMP levels?
Bradycardia is common after the injection of
A 67-year-old man with Parkinson disease has experienced an increasingly dry mouth for the past 3 months, and this interferes with eating and swallowing. He has noted dry eyes as well. On physical examination, he has minimal tremor at rest; there are no other abnormal findings. Laboratory studies show no detectable autoantibodies. Which of the following is the most likely cause for his findings?
NO acts on platelets through what mechanism?
Which substance reduces the regional arterial resistance of the mesentery and kidney vessels?
Which of the following is not an alkaloid?
Which vitamin is known to inhibit wound healing?
Which of the following vaccines is classified as a killed vaccine?
MgCl2 is added to polio vaccine for what purpose?
Which of the following medications does not cause hirsutism?
General Pharmacology Indian Medical PG Practice Questions and MCQs
Question 631: Which of the following causes an increase in cAMP levels?
- A. Alpha (α) receptor
- B. Somatostatin
- C. Beta (β) receptor (Correct Answer)
- D. Acetylcholine
Explanation: ***Beta (β) receptor*** - **Beta-adrenergic receptors** (β1, β2, β3) are G-protein coupled receptors that, when activated, couple to **Gs proteins**, leading to the activation of **adenylyl cyclase**. - **Adenylyl cyclase** then catalyzes the conversion of **ATP to cAMP**, thereby increasing intracellular cAMP levels and triggering downstream signaling pathways. *Alpha (α) receptor* - **Alpha-1 adrenergic receptors** (α1) typically couple to **Gq proteins**, leading to the activation of **phospholipase C**, which increases **intracellular calcium** and activates protein kinase C, not cAMP. - **Alpha-2 adrenergic receptors** (α2) couple to **Gi proteins**, which inhibit adenylyl cyclase, thereby **decreasing cAMP levels**. *Somatostatin* - **Somatostatin receptors** are G-protein coupled receptors that primarily couple to **Gi proteins**. - Activation of **Gi proteins** leads to the **inhibition of adenylyl cyclase**, resulting in a **decrease in cAMP levels**. *Acetylcholine* - **Acetylcholine** acts on **muscarinic** and **nicotinic receptors**. Muscarinic receptors (M2 and M4) couple to **Gi proteins**, which **decrease cAMP production**. - Other muscarinic receptors (M1, M3, M5) couple to **Gq proteins**, leading to increased **intracellular calcium**, not cAMP.
Question 632: Bradycardia is common after the injection of
- A. Succinylcholine
- B. Fentanyl (Correct Answer)
- C. Atropine
- D. Adrenaline
Explanation: ***Fentanyl*** - Fentanyl is an **opioid analgesic** that **consistently and commonly** causes **bradycardia** [1] by directly stimulating the **vagal nerve** nuclei in the brainstem. - This effect is mediated through increased **parasympathetic activity**, reliably slowing the heart rate. - Bradycardia is a **predictable and dose-dependent** side effect of fentanyl administration. *Succinylcholine* - Succinylcholine is a **depolarizing neuromuscular blocker** that **can** cause **bradycardia**, particularly with **repeat dosing**, in **children**, or with **higher doses** due to stimulation of **muscarinic receptors** at the SA node. - However, its cardiac effects are **variable and context-dependent** - it can also cause **tachycardia** in some patients due to sympathetic ganglion stimulation. - The bradycardia is **less predictable** compared to fentanyl. *Atropine* - Atropine is an **anticholinergic drug** that acts as a **muscarinic receptor antagonist**, therefore it typically causes **tachycardia**, not bradycardia [2]. - It works by blocking the effects of **acetylcholine** on the **vagus nerve**, thereby increasing heart rate. *Adrenaline* - Adrenaline (epinephrine) is a **sympathomimetic drug** that stimulates **alpha and beta-adrenergic receptors**. - Its primary cardiac effects are **increased heart rate**, **contractility**, and **blood pressure**, directly opposing bradycardia.
Question 633: A 67-year-old man with Parkinson disease has experienced an increasingly dry mouth for the past 3 months, and this interferes with eating and swallowing. He has noted dry eyes as well. On physical examination, he has minimal tremor at rest; there are no other abnormal findings. Laboratory studies show no detectable autoantibodies. Which of the following is the most likely cause for his findings?
- A. Alcohol ingestion
- B. Anticholinergic drug use (Correct Answer)
- C. Candidiasis
- D. Sialadenitis with blockage of salivary duct
Explanation: ***Anticholinergic drug use***- Many medications used to treat **Parkinson disease** have **anticholinergic effects**, which can lead to **dry mouth (xerostomia)** and **dry eyes (xerophthalmia)** due to reduced glandular secretions [1].- The patient's presentation of worsening dry mouth and dry eyes aligns well with the side effects of such medications.*Alcohol ingestion*- While chronic alcohol use can contribute to **dehydration** and indirectly affect salivary production, it is typically not the primary cause of such pronounced and progressive symptoms in this context, nor does it commonly cause dry eyes.- The patient's symptoms are more consistent with a direct pharmacological effect rather than general dehydration from alcohol.*Candidiasis*- Oral candidiasis usually presents with **white plaques** on the oral mucosa, **soreness**, or difficulty swallowing due to pain, not primarily dry mouth and dry eyes.- The physical examination did not reveal any other abnormal findings, making candidiasis less likely as the primary cause.*Sialadenitis with blockage of salivary duct*- **Sialadenitis** (inflammation of salivary glands) or salivary duct obstruction typically causes **pain**, **swelling**, and localized tenderness in the affected gland, often exacerbated by eating.- This condition generally affects salivation but does not explain the concurrent dry eyes, making it an unlikely sole cause for both symptoms.
Question 634: NO acts on platelets through what mechanism?
- A. Adenosine
- B. cGMP (Correct Answer)
- C. cAMP
- D. TXA2
Explanation: ***cGMP (inhibits platelet activation)*** - **Nitric oxide (NO)** diffuses into platelets and activates **guanylate cyclase**, leading to an increase in intracellular **cyclic guanosine monophosphate (cGMP)**. - Elevated **cGMP** levels then activate protein kinase G, which phosphorylates various proteins involved in platelet signaling, ultimately inhibiting **platelet activation**, adhesion, and aggregation. *cAMP (modulates platelet function through other pathways)* - While **cAMP** also plays a role in inhibiting platelet aggregation, it is primarily generated through the activation of **adenylyl cyclase** by agents like **prostacyclin (PGI2)**, not directly by NO. - NO's direct effect on platelets is mediated by **cGMP**, not **cAMP**. *Adenosine (vasodilator)* - **Adenosine** is a nucleoside known for its **vasodilatory** properties and can also influence platelet function, but it is not the primary mechanism by which NO acts on platelets. - **Adenosine** exerts its effects by activating specific **purinergic receptors** on the platelet surface, distinct from NO's intracellular signaling pathway. *TXA2 (a mediator of platelet aggregation and vasoconstriction)* - **Thromboxane A2 (TXA2)** is a potent **pro-aggregatory** and **vasoconstrictive** eicosanoid produced by platelets through the **cyclooxygenase pathway**. - NO's action on platelets is to *antagonize* the effects of **TXA2**, promoting **platelet inhibition** rather than mediating it.
Question 635: Which substance reduces the regional arterial resistance of the mesentery and kidney vessels?
- A. A) Dopamine (Correct Answer)
- B. B) Dobutamine
- C. D) Isoprenaline
- D. C) Noradrenaline
Explanation: **Dopamine** - **Low doses of dopamine** activate **D1 receptors** in the renal and mesenteric vascular beds, leading to **vasodilation** and increased blood flow. - This specific action makes dopamine useful in situations where improved renal and mesenteric perfusion is desired, such as in certain types of **shock** [1]. *Dobutamine* - Primarily acts as a **beta-1 adrenergic agonist**, increasing myocardial contractility and heart rate. - It has **minimal effect** on mesenteric or renal vascular resistance at therapeutic doses. *Noradrenaline* - Also known as **norepinephrine**, it is a potent **alpha-1 adrenergic agonist** that causes **vasoconstriction** in most vascular beds, including the mesenteric and renal arteries [1]. - This action would increase, not decrease, regional arterial resistance. *Isoprenaline* - Primarily a **non-selective beta-adrenergic agonist** with significant **beta-1** and **beta-2** effects. - While it causes vasodilation in some vascular beds (due to beta-2 activation), it does not specifically target and reduce resistance in the mesenteric and renal vessels in the same way as low-dose dopamine.
Question 636: Which of the following is not an alkaloid?
- A. Physostigmine
- B. Morphine
- C. Aspirin (Correct Answer)
- D. Atropine
Explanation: ***Aspirin*** - **Aspirin** (acetylsalicylic acid) is a synthetic derivative of **salicylic acid**, a non-alkaloid compound. - Alkaloids are generally naturally occurring organic compounds containing **nitrogen atoms** in a heterocyclic ring system, while aspirin does not fit this chemical structure definition. *Morphine* - **Morphine** is a naturally occurring **alkaloid** derived from the opium poppy [1]. - It contains a **nitrogen atom** within a heterocyclic ring, making it a classic example of an alkaloid [1]. *Physostigmine* - **Physostigmine** is an **alkaloid** obtained from the Calabar bean plant. - It contains a **nitrogen atom** as part of its molecular structure and is classified as a cholinergic alkaloid. *Atropine* - **Atropine** is a naturally occurring **alkaloid** found in plants of the Solanaceae family, like deadly nightshade [2], [3]. - Its chemical structure includes a **nitrogen atom** within a heterocyclic ring system, consistent with the definition of an alkaloid [2].
Question 637: Which vitamin is known to inhibit wound healing?
- A. Vitamin A
- B. Vitamin E (Correct Answer)
- C. Vitamin C
- D. Vitamin B complex
Explanation: ***Vitamin E*** - **High doses** or **supraphysiologic levels** of vitamin E may potentially **impair wound healing** due to anticoagulant effects and possible interference with platelet function. - Excessive vitamin E supplementation (above recommended doses) can increase **bleeding risk** at surgical and wound sites, potentially delaying healing. - **Note:** Physiologic doses of vitamin E do not inhibit wound healing; this refers specifically to excessive supplementation. *Vitamin A* - **Vitamin A** plays a crucial role in wound healing by promoting **epithelial cell differentiation** and collagen synthesis. - It aids in **immune function** and inflammation modulation, both vital for effective wound repair. - Can even counteract steroid-induced impairment of wound healing. *Vitamin C* - **Vitamin C** is essential for **collagen synthesis** and cross-linking, which provides tensile strength to healing wounds. - Acts as an **antioxidant** and is vital for immune function, supporting tissue repair processes. - Deficiency leads to impaired wound healing (scurvy). *Vitamin B complex* - **B vitamins**, particularly **B1 (thiamine)**, **B5 (pantothenic acid)**, and **B6 (pyridoxine)**, are important cofactors in metabolic processes crucial for cell proliferation and tissue repair. - They contribute to energy production and synthesis of proteins and DNA needed for wound healing.
Question 638: Which of the following vaccines is classified as a killed vaccine?
- A. Varicella
- B. BCG
- C. OPV
- D. Meningococcal vaccine (Correct Answer)
Explanation: ***Meningococcal vaccine*** - The meningococcal conjugate and polysaccharide vaccines are **killed vaccines**, containing inactivated bacterial components (polysaccharides) that stimulate an immune response. - They provide protection against *Neisseria meningitidis* and are considered safe for most populations due to their non-live nature. *Varicella* - The varicella vaccine is a **live-attenuated vaccine**, meaning it contains a weakened form of the **varicella-zoster virus**. - This attenuated virus can replicate in the recipient, eliciting a strong and long-lasting immune response, similar to natural infection. *BCG* - The **Bacillus Calmette-Guérin (BCG)** vaccine is a **live-attenuated vaccine** used to prevent tuberculosis. - It contains a weakened strain of **_Mycobacterium bovis_**, which is closely related to *Mycobacterium tuberculosis* but has lost its virulence. *OPV* - The **Oral Polio Vaccine (OPV)** is a **live-attenuated vaccine** that contains weakened but live strains of all three poliovirus serotypes. - It induces strong mucosal immunity in the gut, which is crucial for preventing the wild poliovirus from replicating and spreading.
Question 639: MgCl2 is added to polio vaccine for what purpose?
- A. Vaccine can be kept at higher temperatures (Correct Answer)
- B. Enhances the vaccine's effectiveness
- C. Acts as a preservative
- D. None of the options
Explanation: ***Vaccine can be kept at higher temperatures*** - Magnesium chloride (**MgCl2**) is used in the **oral polio vaccine (OPV)** to provide **thermostability**, allowing the vaccine to withstand higher temperatures. - This property is crucial for vaccine distribution in regions with **limited cold chain infrastructure**, preventing degradation of the live attenuated virus. *Enhances the vaccine's effectiveness* - While vaccine effectiveness is critical, **MgCl2** does not directly enhance the **immunogenicity** or **potency** of the polio antigens. - Its primary role is related to **stabilization** of the viral particles, not improvement of the immune response generated. *Acts as a preservative* - **Preservatives** like 2-phenoxyethanol or thimerosal are added to vaccines to prevent **microbial growth**. - **MgCl2** acts as a **stabilizer**, protecting the viral structure from heat-induced denaturation, which is distinct from preventing bacterial contamination. *None of the options* - This option is incorrect because **MgCl2** does have a specific and important role in stabilizing the polio vaccine, as explained. - Its ability to confer **thermostability** is a well-established property in vaccine formulation.
Question 640: Which of the following medications does not cause hirsutism?
- A. Flutamide (Correct Answer)
- B. Danazol
- C. Phenytoin
- D. Norethisterone
Explanation: ***Flutamide*** - **Flutamide** is an **anti-androgen** that blocks androgen receptors, thereby *reducing* the effects of androgens and preventing hirsutism. - It is used in conditions like prostate cancer to counteract androgenic effects and would not cause increased hair growth. *Norethisterone* - **Norethisterone** is a synthetic progestin that can have **androgenic effects** in some individuals. - These androgenic properties can lead to side effects like **hirsutism**, acne, and oily skin. *Danazol* - **Danazol** is a synthetic androgen that has **pronounced androgenic activity**. - Its androgenic effects are well-known to cause side effects such as **hirsutism**, acne, and deepening of the voice. *Phenytoin* - **Phenytoin** is an anticonvulsant medication that can induce **hirsutism** as a common side effect. - The mechanism is not fully understood but may involve stimulating hair follicle growth.
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