Pharmacology Practice Test 25
Pharmacology NCLEX Practice Test
Pharmacology is a key topic within the NCLEX test plan, located under Nursing Science → Clinical Foundations → Pharmacology. This section details drug mechanisms, safe administration, and patient education across nursing specialties. Each test contains 50 questions designed to mirror the difficulty and variety of the real exam.
This is the 25th part of the Pharmacology series. To explore all practice tests under this topic, use the “Back to Main Topic” button at the end of the page.
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Pharmacology Practice Test 25
Which of the following antipsychotic drugs has the high risk of potentially fatal agranulocytosis and risk of seizures at high doses?
- Haloperidol
- Risperidone
- Clozapine
- Chlorpromazine
Explanation: Answer reason: Clozapine uniquely carries a significant risk of agranulocytosis and dose-related seizures compared with other antipsychotics listed.
Which of the following statements is correct for lithium?
- Stimulate dopamine and beta-adrenergic receptors
- Decrease catecholamine-related activity
- Stimulate the development of dopamine receptor supersensitivity
- Decrease cholinergic activity
Explanation: Answer reason: Lithium reduces catecholaminergic neurotransmission (e.g., decreases norepinephrine and dopamine release/second-messenger signaling). It does not stimulate dopamine or beta receptors, does not promote dopamine receptor supersensitivity, and does not decrease cholinergic activity.
The principal mechanism of action of antidepressant agents is?
- Stabilization of dopamine and beta-adrenergic receptors
- Inhibition of the storage of serotonin and epinephrine in the vesicles of presynaptic nerve endings
- Blocking epinephrine or serotonin reuptake pumps
- Stimulation of alfa2-norepinephrine receptors
Explanation: Answer reason: Most antidepressants (SSRIs, SNRIs, TCAs) act by inhibiting serotonin and/or norepinephrine reuptake transporters, increasing synaptic monoamines.
Which of the following antidepressants is an unselective MAO blocker and produces extremely long-lasting inhibition of the enzyme?
- Moclobemide
- Tranylcypromine
- Selegiline
- Fluoxetine
Explanation: Answer reason: Tranylcypromine is a nonselective, irreversible MAO inhibitor causing long-lasting enzyme inhibition. Moclobemide is reversible MAO-A selective, selegiline is MAO-B selective, and fluoxetine is an SSRI.
The principal mechanism of MAO inhibitor action is?
- Blocking the amine reuptake pumps, which permits to increase the concentration of the neurotransmitter at the receptor site
- Blocking a major degradative pathway for the amine neurotransmitters, which permits more amines to accumulate in presynaptic stores
- Inhibition the storage of amine neurotransmitters in the vesicles of presynaptic nerve endings
- Antagonism of alfa2-norepinephrine receptors
Explanation: Answer reason: MAO inhibitors block monoamine oxidase, the enzyme that degrades monoamine neurotransmitters, increasing their presynaptic stores and synaptic availability. They do not block reuptake, inhibit vesicular storage, or antagonize alpha2 receptors.
The irreversible MAO inhibitors have a very high risk of developing?
- Respiratory depression
- Cardiovascular collapse and CNS depression
- Hypertensive reactions to tyramine ingested in food
- Potentially fatal agranulocytosis
Explanation: Answer reason: Irreversible MAOIs inhibit tyramine metabolism; dietary tyramine can trigger massive catecholamine release, causing hypertensive crisis. The other options are not characteristic MAOI risks (e.g., agranulocytosis is associated with clozapine).
Which of the following features do MAO inhibitors and tricyclic antidepressants have in common?
- Act postsynaptically to produce their effect
- Can precipitate hypotensive crises if certain foods are ingested
- Increase levels of biogenic amines
- Are useful for the manic phase of bipolar disorder
Explanation: Answer reason: Both MAOIs and TCAs raise synaptic monoamine (NE/5-HT) levels—MAOIs inhibit enzymatic breakdown, while TCAs inhibit reuptake. They do not act postsynaptically, tyramine reactions cause hypertensive (not hypotensive) crises and TCAs/MAOIs are not treatments for acute mania.
Tricyclic antidepressants are?
- Highly selective serotonin reuptake inhibitors
- Monoamine oxidase inhibitors
- Selective norepinephrine reuptake inhibitors
- Mixed norepinephrine and serotonin reuptake inhibitors
Explanation: Answer reason: TCAs inhibit the reuptake of both norepinephrine and serotonin at presynaptic terminals, unlike SSRIs, MAOIs, or selective NE reuptake inhibitors.
Fluoxetine has fewer adverse effects because of?
- Mixed norepinephrine and serotonin reuptake inhibition
- Depleted stores of amine neurotransmitters
- Minimal binding to cholinergic, histaminic, and alfa-adrenergic receptors
- All of the above
Explanation: Answer reason: SSRIs like fluoxetine have low affinity for muscarinic, histamine H1, and alpha-1 adrenergic receptors, so they cause fewer anticholinergic, sedative, and orthostatic effects. The other options are incorrect.
Sedation, peripheral atropine-like toxicity (e.g. Cycloplegia, tachycardia, urinary retention, and constipation), orthostatic hypotension, arrhythmias, weight gain and sexual disturbances are possible adverse effects of?
- Sertaline
- Amitriptyline
- Phenelsine
- Bupropion
Explanation: Answer reason: The listed adverse effects—sedation, strong anticholinergic effects, orthostatic hypotension, arrhythmias, weight gain, sexual dysfunction—are classic for tricyclic antidepressants, especially amitriptyline. SSRIs like sertraline and atypicals like bupropion do not prominently cause these anticholinergic or cardiac effects; MAOIs (phenelzine) have different profiles.
Which of the following drugs is least likely to be prescribed to patients with prostatic hypertrophy, glaucoma, coronary and cerebrovascular disease?
- Amitriptyline
- Paroxetine
- Bupropion
- Fluoxetine
Explanation: Answer reason: Amitriptyline (a TCA) has strong anticholinergic effects that can worsen BPH and narrow-angle glaucoma and has cardiotoxic/arrhythmogenic potential, making it unsafe in coronary/cerebrovascular disease. SSRIs and bupropion are safer choices.
The mechanism of fluoxetine action includes?
- Selective inhibition of serotonine uptake in the CNS
- Little effect on central norepinephrine or dopamine function
- Minimal binding to cholinergic, histaminic, and alfa-adrenergic receptors
- All of the above
Explanation: Answer reason: Fluoxetine is an SSRI that selectively inhibits serotonin reuptake, has minimal effects on NE/DA systems, and shows little affinity for cholinergic, histaminic, or alpha-adrenergic receptors; therefore all statements are correct.
Anxiolytic agents should?
- Relieve pain
- Reduce anxiety and exert a calming effect
- Improve mood and behavior in patient with psychotic symptoms
- Produce drowsiness, encourage the onset and maintenance of a state of sleep
Explanation: Answer reason: Anxiolytics primarily decrease anxiety and produce a calming effect (e.g., via GABAergic enhancement). Analgesia, antipsychotic effects, or hypnotic induction are not their primary indication.
Indicate the mechanism of hypnotic benzodiazepine action?
- Increasing the duration of the GABA-gated Cl- channel openings
- Directly activating the chloride channels
- Increasing the frequency of Cl- channel opening events
- All of the above
Explanation: Answer reason: Benzodiazepines bind to GABA-A receptors and increase the frequency of chloride channel opening; barbiturates increase duration and benzodiazepines do not directly open the channel, so option C is correct.
Which of the following disadvantages does not limit using benzodiazepines as antianxiety agents?
- Tendency to develop psychologic dependence
- A high risk of drug interactions based on liver enzyme induction
- Synergic CNS depression with concomitant use of other drugs
- The formation of active metabolites
Explanation: Answer reason: Benzodiazepines generally do not induce hepatic enzymes; enzyme induction and related high interaction risk are characteristic of barbiturates. The other options are true disadvantages of benzodiazepines.
In contrast to benzodiazepines, buspirone?
- Interact directly with gabaergic system
- Has more marked hypnotic, anticonvulsant, or muscle relaxant properties
- Causes less psychomotor impairment and does not affect driving skills
- Has maximal abuse liability
Explanation: Answer reason: Buspirone (5‑HT1A partial agonist) lacks GABAergic, hypnotic, anticonvulsant, and muscle‑relaxant effects and has minimal psychomotor impairment and low abuse potential, so it does not impair driving compared with benzodiazepines.
Which of the following sedative-hypnotic drugs does not potentiate the CNS depressant effects of ethanol, phenothiazines, or tricyclic antidepressants?
- Buspirone
- Phenobarbital
- Diazepam
- Chloralhydrate
Explanation: Answer reason: Buspirone is a non-sedating anxiolytic (5-HT1A partial agonist) and does not have additive CNS depressant effects with alcohol or other sedatives, unlike phenobarbital, diazepam, and chloral hydrate.
Which of the following benzodiazepines is more likely to cause "hangover" effects such as drowsiness, dysphoria, and mental or motor depression the following day?
- Oxazepam
- Triazolam
- Clorazepat
- Lorazepam
Explanation: Answer reason: Next-day hangover effects are most common with long-acting benzodiazepines that form active metabolites. Clorazepate is a prodrug converted to desmethyldiazepam with a long half-life, leading to residual sedation; the others are shorter-acting.
Which dosage of benzodiazepines for 60-90 days may produce severe withdrawal symptoms?
- 50-60 mg/d
- Less than 400 mg/d
- More than 800 mg/d
- Less than 40 mg/d
Explanation: Answer reason: Severe benzodiazepine withdrawal is associated with prolonged high-dose use, typically over about 40 mg/day diazepam equivalents for 2–3 months. A dose of 50–60 mg/day for 60–90 days fits this high‑risk range.
Flumazenil is used to?
- Reverse the CNS depressant effects of hypnotic benzodiazepines overdose
- Hasten recovery following use of hypnotic benzodiazepines in anesthetic and diagnostic procedure
- Reverse benzodiazepine-induced respiratory depression
- All of the above
Explanation: Answer reason: Flumazenil, a benzodiazepine receptor antagonist, reverses benzodiazepine effects including CNS depression and respiratory depression, and is used to hasten recovery after procedural sedation or overdose.
Flumazenil given intravenously?
- Has intermediate onset and duration of action about 2 hours
- Acts rapidly but has a short half-life
- Has an effect lasting 3-5 hours
- Has duration of action longer than 6 hours
Explanation: Answer reason: IV flumazenil, a benzodiazepine antagonist, has rapid onset within minutes and a short elimination half-life (~40–80 minutes), leading to possible resedation.
Inhaled anesthetics and intravenous agents having general anesthetic properties?
- Directly activate GABAA receptors
- Facilitate GABA action but have no direct action on GABAA receptors
- Reduce the excitatory glutamatergic neurotransmission
- Increase the duration of opening of nicotine-activated potassium channels
Explanation: Answer reason: Volatile anesthetics and several IV general anesthetics (e.g., propofol, etomidate, barbiturates) enhance and at sufficient concentrations directly activate GABAA chloride channels. Option B describes benzodiazepines, not general anesthetics; C may occur but is not the principal shared mechanism; D is incorrect for nicotinic channels.
An ideal anesthetic drug would?
- Induces anesthesia smoothly and rapidly and secure rapid recovery
- Posses a wide margin of safety
- Be devoid of adverse effects
- All of the above
Explanation: Answer reason: An ideal anesthetic would provide smooth rapid induction with quick recovery, have a wide safety margin, and lack adverse effects; therefore all statements are correct.
Sevoflurane has largely replaced halothane and isoflurane as an inhalation anesthetic of choice because?
- Induction of anesthesia is achieved more rapidly and smoothly
- Recovery is more rapid
- It has low post- anesthetic organ toxicity
- All of the above
Explanation: Answer reason: Sevoflurane’s low blood–gas solubility provides rapid, smooth induction and quick recovery, and it has relatively low postanesthetic organ toxicity compared with halothane and isoflurane—making all statements correct.
Which of the following inhalants lacks sufficient potency to produce surgical anesthesia by itself and therefore is commonly used with another inhaled or intravenous anesthetic?
- Halothane
- Sevoflurane
- Nitrous oxide
- Desflurane
Explanation: Answer reason: Nitrous oxide has very high MAC (~105%) and therefore low potency; it cannot produce surgical anesthesia alone and is used as an adjunct to other agents.
Which of the following inhaled anesthetics causes centrally mediated sympathetic activation leading to a rise in blood pressure and heart rate?
- Desflurane
- Sevoflurane
- Nitrous oxide
- Isofurane
Explanation: Answer reason: Desflurane can trigger centrally mediated sympathetic stimulation, especially with rapid increases in concentration, causing tachycardia and hypertension; the others do not typically raise BP and HR this way.
Unlike inhaled anesthetics, intravenous agents such as thiopental, etomidate, and propofol?
- Have a faster onset and rate of recovery
- Provide a state of conscious sedation
- Are commonly used for induction of anesthesia
- All of the above
Explanation: Answer reason: IV induction agents are highly lipophilic, producing rapid onset and quick recovery; propofol (and IV agents in appropriate dosing) is used for procedural/conscious sedation; and these drugs are standard for induction of general anesthesia. Therefore, all statements are correct.
Neuroleptanalgesia has all of the following properties EXCEPT?
- Droperidol and fentanyl are commonly used
- It can be used with nitrous oxide to provide neuroleptanesthesia
- Hypertension is a common consequence
- Confusion and mental depression can occur as adverse effects
Explanation: Answer reason: Neuroleptanalgesia (droperidol + fentanyl) commonly causes hypotension, not hypertension; it may be combined with N2O for neuroleptanesthesia and can cause confusion/depression.
Ketamine anesthesia is associated with?
- Cardiovascular stimulation
- Increased cerebral blood flow, oxygen consumption and intracranial pressure
- Disorientation, sensory and perceptual illusions, and vivid dreams following anesthesia
- All of the above
Explanation: Answer reason: Ketamine stimulates the sympathetic nervous system (↑HR/BP), increases cerebral blood flow and intracranial pressure, and commonly causes emergence phenomena such as disorientation and vivid dreams—thus all statements are correct.
All of the following drugs destroy disulfide bonds of proteoglycans, which causes depolymerization and reduction of viscosity of sputum, EXCEPT?
- Acetylcysteine
- Ambroxol
- Desoxiribonuclease
- Bromhexin
Explanation: Answer reason: N-acetylcysteine, ambroxol, and bromhexine reduce sputum viscosity partly by disrupting disulfide bonds in mucoproteins. Desoxiribonuclease (DNase) decreases viscosity by cleaving extracellular DNA, not by breaking disulfide bonds; therefore it is the exception.
Select the drug stimulating the protective function of the mucous barrier and the stability of the mucous membrane against damaging factors?
- De-nol
- Sucralfate
- Misoprostol
- Omeprazole
Explanation: Answer reason: Misoprostol, a PGE1 analog, increases gastric mucus and bicarbonate secretion and mucosal blood flow, enhancing the mucosal barrier. Sucralfate and bismuth (De-nol) primarily coat ulcers; omeprazole reduces acid without stimulating mucus production.
All of the following statements regarding cardiac glycosides are true EXCEPT?
- They inhibit the activity of the Na+/K+-ATPase
- They decrease intracellular concentrations of calcium in myocytes
- They increase vagal tone
- They have a very low therapeutic index
Explanation: Answer reason: Cardiac glycosides (e.g., digoxin) inhibit Na+/K+-ATPase, increasing intracellular Na+, reducing Na+/Ca2+ exchange, and thereby increasing intracellular Ca2+. They also increase vagal tone and have a narrow therapeutic index. Thus the statement that they decrease intracellular calcium is false.
All of the following statements regarding cardiac glycosides are true EXCEPT?
- Digoxin is a mild inotrope
- Digoxin increases vagal tone
- Digoxin has a longer half-life than digitoxin
- Digoxin acts by inhibiting the Na+/K+ ATPase
Explanation: Answer reason: Digitoxin has a longer half-life than digoxin; the other statements about digoxin’s positive inotropy, vagotonic effect, and Na+/K+ ATPase inhibition are correct.
In very severe digitalis intoxication the best choice is to use?
- Lidocaine
- Digibind (Digoxin immune fab)
- Oral potassium supplementation
- Reducing the dose of the drug
Explanation: Answer reason: Life-threatening digoxin toxicity is treated with digoxin-specific antibody fragments (Digibind/DigiFab), which rapidly bind and neutralize digoxin. Other options are adjuncts or inappropriate as definitive therapy.
All of the following statements regarding cardiac glycoside-induced ventricular tachyarrhythmias are true EXCEPT?
- Lidocaine is a drug of choice in treatment
- Digibind should be used in life-threatening cases
- They occur more frequently in patients with hyperkalemia than in those with hypokalemia
- They are more likely to occur in patients with a severely damaged heart
Explanation: Answer reason: Digoxin-induced ventricular arrhythmias are precipitated by hypokalemia; hyperkalemia does not increase risk in this context. Lidocaine and Digoxin-immune Fab are accepted treatments, and severe structural heart disease increases susceptibility.
All of the following statements regarding inhibitors of type III phosphodiesterase are true EXCEPT?
- They raise cAMP concentrations in cardiac myocytes
- They reduce afterload
- They show significant cross-tolerance with beta-receptor agonists
- They are associated with a significant risk for cardiac arrhythmias
Explanation: Answer reason: PDE3 inhibitors (e.g., milrinone) increase cAMP in cardiac myocytes and vascular smooth muscle, producing inotropy and vasodilation that decreases afterload. They carry a notable risk of arrhythmias. They do not exhibit cross-tolerance with beta-agonists, making option C the false statement.
All of the following statements concerning angiotensin converting enzyme (ACE) inhibitors are true EXCEPT?
- They act by inhibiting the ability of renin to convert angiotensinogen to angiotensin I.
- Enalapril is a prodrug that is converted to an active metabolite
- They reduce secretion of aldosterone
- They can produce hyperkalemia in combination with a potassium-sparing diuretic
Explanation: Answer reason: ACE inhibitors block angiotensin-converting enzyme, preventing conversion of angiotensin I to angiotensin II; they do not inhibit renin. The other statements are correct.
All of the following effects of ACE inhibitors may be useful in treating heart failure EXCEPT?
- They decrease afterload
- They increase circulating catecholamine levels
- They reduce reactive myocardial hypertrophy
- They increase myocardial beta-1 adrenergic receptor density
Explanation: Answer reason: ACE inhibitors lower afterload and limit remodeling via RAAS blockade and reduced sympathetic activity. Increasing circulating catecholamines would worsen heart failure and is not an effect of ACE inhibitors.
All of the following statements concerning the use of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure are true EXCEPT?
- They improve hemodynamics by decreasing afterload
- They can increase plasma cholesterol levels
- They may slow the progression of heart failure by preventing myocardial and vascular remodeling
- They are effective first-line agents in the treatment of chronic heart failure
Explanation: Answer reason: ACE inhibitors reduce afterload, slow adverse remodeling, and are first-line therapy in chronic heart failure. They do not increase plasma cholesterol; they have a neutral or favorable metabolic profile, making option B the false statement.
All of the following statements regarding verapamil are true EXCEPT?
- It blocks L-type calcium channels
- It increases heart rate
- It relaxes coronary artery smooth muscle
- It depresses cardiac contractility
Explanation: Answer reason: Verapamil, a non-dihydropyridine calcium channel blocker, decreases SA/AV nodal conduction and myocardial contractility. It relaxes vascular smooth muscle and blocks L-type calcium channels. Therefore, it does not increase heart rate; it decreases it.
All these drug groups useful in angina both decrease myocardial oxygen requirement (by decreasing the determinations of oxygen demand) and increase myocardial oxygen delivery (by reversing coronary arterial spasm), EXCEPT?
- Nitrates and nitrite drugs (Nitroglycerin, Isosorbide dinitrate)
- Calcium channel blockers (Nifedipine, Nimodipine)
- Beta-adrenoceptor-blocking drugs (Atenolol, Metoprolol)
- Potassium channel openers (Minoxidil)
Explanation: Answer reason: Beta-blockers reduce myocardial oxygen demand (↓HR and contractility) but do not increase oxygen delivery or relieve coronary spasm. Nitrates, calcium channel blockers, and potassium channel openers increase coronary flow and can relieve spasm.
This drug group useful in angina decreases myocardial oxygen requirement (by decreasing the determinations of oxygen demand) and does not increase myocardial oxygen delivery (by reversing coronary arterial spasm)?
- Nitrates and nitrite drugs (Nitroglycerin, Isosorbide dinitrate)
- Myotropic coronary dilators (Dipyridamole)
- Potassium channel openers (Minoxidil)
- Beta-adrenoceptor-blocking drugs (Atenolol, Mtoprolol)
Explanation: Answer reason: Beta-blockers lower myocardial oxygen demand by reducing heart rate and contractility and do not increase oxygen delivery via coronary vasodilation or relief of spasm. Nitrates and other vasodilators can increase delivery by relieving spasm.
This drug group useful in angina increase myocardial oxygen delivery (by reversing coronary arterial spasm) and does not decrease myocardial oxygen requirement (by decreasing the determinants of oxygen demand)?
- Beta-adrenoceptor-blocking drugs (Atenolol, Metoprolol)
- Myotropic coronary dilators (Dipyridamole)
- Calcium channel blockers (Nifedipine, Nimodipine)
- Potassium channel openers (Minoxidil)
Explanation: Answer reason: Myotropic coronary vasodilators increase coronary flow (relieve spasm) but do not reduce determinants of myocardial O2 demand. Beta-blockers and calcium channel blockers decrease O2 demand, and potassium channel openers like minoxidil are not antianginal.
Which of the following nitrates and nitrite drugs is used for prevention of angina attack?
- Nitroglycerin, 2% ointment (Nitrol)
- Nitroglycerin, oral sustained-release (Nitrong)
- Isosorbide mononitrate (Ismo)
- All of the above
Explanation: Answer reason: All listed nitrate formulations are used for angina prophylaxis: topical nitroglycerin ointment, sustained-release oral nitroglycerin, and isosorbide mononitrate.
The following statements concerning mechanism of nitrate beneficial clinical effect are true, EXCEPT?
- Decreased myocardial oxygen requirement
- Relief of coronary artery spasm
- Improved perfusion to ischemic myocardium
- Increased myocardial oxygen consumption
Explanation: Answer reason: Nitrates venodilate and reduce preload/afterload, lowering myocardial O2 demand; they relieve coronary spasm and can improve perfusion to ischemic myocardium. They do not increase myocardial oxygen consumption.
The following statements concerning mechanism of calcium channel blockers' action are true, EXCEPT?
- Therapeutically active agents in this group are capable of releasing nitric oxide (NO) in vascular smooth muscle target tissues
- Calcium channel blockers bind to L-type calcium channel sites
- Calcium channel blockers useful in angina decrease myocardial oxygen requirement (by decreasing the determinations of oxygen demand) and increase myocardial oxygen delivery (by reversing coronary arterial spasm)
- Calcium channel blockers decrease transmembrane calcium current associated in smooth muscle with long-lasting relaxation and in a cardiac muscle with a reduction in contractility
Explanation: Answer reason: Calcium channel blockers act by blocking L-type calcium channels, reducing calcium influx, which relaxes vascular smooth muscle and decreases cardiac contractility. They do not exert their effects by releasing nitric oxide; NO-mediated vasodilation is characteristic of nitrates, not CCBs. The other statements reflect true mechanisms/effects of CCBs.
Which of the following cardiovascular system effects refers to a calcium channel blocker?
- The reduction of peripheral vascular resistance
- The reduction of cardiac contractility and, in some cases, cardiac output
- Relief of coronary artery spasm
- All of the above
Explanation: Answer reason: Calcium channel blockers relax arterial smooth muscle lowering peripheral vascular resistance, depress myocardial contractility (sometimes reducing cardiac output), and relieve coronary vasospasm. Therefore, all listed effects apply.
Which of the following statements concerning beta-adrenoceptor-blocking drugs are true?
- These agents decrease transmembrane calcium current associated in a smooth muscle with long-lasting relaxation and in a cardiac muscle with a reduction in contractility
- These agents has a moderate reflex and vascular dilative action caused by the stimulation of sensitive nerve endings
- Beneficial effects of these agents are related primarily to their hemodynamic effects – decreased heart rate, blood pressure, and contractility – which decrease myocardial oxygen requirements at rest and during exercise
- These agents increase the permeability of K channels, probably ATP-dependent K channels, that results in stabilizing
Explanation: Answer reason: Beta-blockers lower heart rate, blood pressure, and contractility, reducing myocardial oxygen demand (true). Option a describes calcium channel blockers; b describes reflex/vasodilator actions not characteristic of beta-blockers; d refers to K+ channel openers.
Which of the following statements concerning Validol is true?
- Validol has a moderate reflex and vascular dilative action caused by the stimulation of sensitive nerve endings
- At sublingual administration the effect is produced in five minutes and 70% of the preparation is released in 3 minutes
- It is used in cases of angina pectoris, motion sickness, nausea, vomiting when seasick or airsick and headaches due to taking nitrates
- All of the above
Explanation: Answer reason: Validol (menthyl isovalerate with menthol) acts as a reflex coronary vasodilator, has rapid onset when taken sublingually, and is used for mild angina, motion sickness-related nausea/vomiting, and nitrate-induced headaches. Therefore, all listed statements are correct.
Following statements concerning specific bradycardic agents (Falipamil, Alinidine) are true, EXCEPT?
- Bradycardic drugs have a moderate reflex and vascular dilative action caused by the stimulation of sensitive nerve endings
- The predominant effect of bradycardic drugs is a decrease in heart rate without significant changes in arterial pressure
- The protective effect of bradycardic drugs is likely due to a reduced O2 demand
- Specific bradycardic agents are used in the management of a wide range of cardiovascular disorders, including sinus tachyarrhythmias and angina pectoris
Explanation: Answer reason: Specific bradycardic agents primarily lower heart rate with minimal effects on arterial pressure and no significant peripheral vasodilation; reduced heart rate lowers myocardial O2 demand and they are used for sinus tachyarrhythmias and angina. Thus statement A is false.
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