Pharmacology Practice Test 23
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 23rd 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 23
Idiosyncratic reaction of a drug is?
- A type of hypersensitivity reaction
- A type of drug antagonism
- Unpredictable, inherent, qualitatively abnormal reaction to a drug
- Quantitatively exaggerated response
Explanation: Answer reason: Idiosyncrasy is a genetically determined, unpredictable and qualitatively abnormal response to a drug, distinct from hypersensitivity or exaggerated normal action.
Therapeutic index (TI) is?
- A ratio used to evaluate the safety and usefulness of a drug for indication
- A ratio used to evaluate the effectiveness of a drug
- A ratio used to evaluate the bioavailability of a drug
- A ratio used to evaluate the elimination of a drug
Explanation: Answer reason: Therapeutic index is the ratio TD50 (or LD50) to ED50, expressing the drug’s safety margin relative to its desired effect; thus it evaluates safety and usefulness for an indication.
Local anesthetics produce?
- Analgesia, amnesia, loss of consciousness
- Blocking pain sensation without loss of consciousness
- Alleviation of anxiety and pain with an altered level of consciousness
- A stupor or somnolent state
Explanation: Answer reason: Local anesthetics block nerve impulse conduction (sodium channels) at the site, preventing pain perception while preserving consciousness. Other options describe general anesthesia, sedation, or stupor.
For therapeutic application local anesthetics are usually made available as salts for the reasons of?
- Less toxicity and higher potency
- Higher stability and greater lipid solubility
- Less local tissue damage and more potency
- More stability and greater water solubility
Explanation: Answer reason: Local anesthetics are weak bases and are formulated as hydrochloride salts to increase aqueous solubility and chemical stability for therapeutic use.
Which of the following statements is not correct for local anesthetics?
- In a tissue they exist either as an uncharged base or as a cation
- A charged cationic form penetrates biologic membranes more readily than an uncharged form
- Local anesthetics are much less effective in inflamed tissues
- Low pH in inflamed tissues decreases the dissociation of nonionized molecules
Explanation: Answer reason: Unionized (base) local anesthetic crosses lipid membranes; the cationic form is less membrane-permeable. Low pH increases ionized fraction, making LAs less effective. Therefore option B is the incorrect statement.
Which one of the following statements about the metabolism of local anesthetics is incorrect?
- Metabolism of local anesthetics occurs at the site of administration
- Metabolism occurs in the plasma or liver but not at the site of administration
- Ester group of anesthetics like procaine, are metabolized systemically by pseudocholinesterase
- Amides such as lidocaine, are metabolized in the liver by microsomal mixed function oxidases
Explanation: Answer reason: Local anesthetics are primarily metabolized systemically—esters by plasma pseudocholinesterase and amides by hepatic microsomal enzymes—not at the injection site, making option A the incorrect statement.
The primary mechanism of action of local anesthetics is?
- Activation of ligand-gated potassium channels
- Blockade of voltage-gated sodium channels
- Stimulation of voltage-gated N-type calcium channels
- Blockade the GABA-gated chloride channels
Explanation: Answer reason: Local anesthetics reversibly block voltage-gated Na+ channels in neuronal membranes, preventing action potential initiation and propagation, which produces loss of sensation.
Indicate the route of local anesthetic administration, which is associated with instillation within epidural or subarachnoid spaces?
- Topical anesthesia
- Infiltrative anesthesia
- Regional anesthesia
- Spinal anesthesia
Explanation: Answer reason: Spinal anesthesia involves injecting local anesthetic into the subarachnoid (intrathecal) space; neuraxial techniques also include epidural. The other options do not involve epidural or subarachnoid spaces.
The choice of a local anesthetic for specific procedures is usually based on?
- The duration of action
- Water solubility
- Capability of rapid penetration through the skin or mucosa with limited tendency to diffuse away from the site of application
- All of the above
Explanation: Answer reason: Selection of a local anesthetic depends on multiple drug properties including duration of action, water solubility, and ability to penetrate tissues without excessive diffusion; hence all listed factors apply.
Correct statements concerning cocaine include all of the following, EXCEPT?
- Cocaine is often used for nose and throat procedures
- Limited use because of abuse potential
- Myocardial depression and peripheral vasodilatation
- Causes sympathetically mediated tachycardia and vasoconstriction
Explanation: Answer reason: Cocaine blocks norepinephrine reuptake, producing sympathetic stimulation with tachycardia and vasoconstriction and is used topically for ENT procedures; it is limited by abuse potential. It does not cause myocardial depression with peripheral vasodilation, making option C the exception.
Procaine has all of the following properties EXCEPT?
- It has ester linkage
- Its metabolic product can inhibit the action of sulfonamides
- It readily penetrates the skin and mucosa
- It is relatively short-acting
Explanation: Answer reason: Procaine is an ester local anesthetic metabolized to PABA (which antagonizes sulfonamides) and is short-acting. It has poor topical efficacy and does not readily penetrate skin or mucous membranes.
Correct statements concerning lidocaine include all of the following EXCEPT?
- It is an universal anesthetic
- It has esteratic linkage
- It widely used as an antiarrhythmic agent
- It is metabolized in liver
Explanation: Answer reason: Lidocaine is an amide-type local anesthetic (not an ester), is used as a class IB antiarrhythmic, and is metabolized in the liver. Therefore the statement that it has ester linkage is incorrect.
Correct statements concerning bupivacaine include all of the following EXCEPT?
- It has low cardiotoxicity
- It has amide linkage
- It is a long-acting drug
- An intravenous injection can lead to seizures
Explanation: Answer reason: Bupivacaine is an amide local anesthetic that is long-acting and notably more cardiotoxic than others; IV/intravascular injection can cause CNS toxicity including seizures. Therefore the statement that it has low cardiotoxicity is incorrect.
The symptoms of mushroom poisoning include all of the following EXCEPT?
- Salivation, lacrimation, nausea, vomiting
- Dryness of mouth, hyperpyrexia, hallucination
- Headache, abdominal colic
- Bradycardia, hypotension and shock
Explanation: Answer reason: Typical mushroom (muscarine) poisoning is cholinergic with salivation, lacrimation, GI upset, bradycardia and hypotension. Dry mouth and hyperpyrexia are anticholinergic features, thus the exception.
Bethanechol has all of the following properties EXCEPT?
- It is extremely resistant to hydrolysis
- Purely muscarinic in its action
- It is used for abdominal urinary bladder distention
- It exerts both nicotinic and muscarinic effects
Explanation: Answer reason: Bethanechol is a direct muscarinic agonist with minimal to no nicotinic activity, is resistant to hydrolysis by cholinesterase, and is used to treat urinary retention/GI atony. Therefore the statement that it exerts both nicotinic and muscarinic effects is false.
Which of the following cholinomimetics is a plant derivative with lower potency than nicotine but with a similar spectrum of action?
- Lobeline
- Pilocarpine
- Carbochol
- Acetylcholine
Explanation: Answer reason: Lobeline is a plant alkaloid from Lobelia with nicotinic agonist activity similar to nicotine but less potent. The other options are not plant-derived nicotinic agonists with this profile.
What are two major side effects of haloperidol (Haldol) the nurse should anticipate?
- Blood dyscrasia and extrapyramidal symptoms.
- Hearing loss and unsteady gait.
- Nystagmus and vertical gaze palsy.
- Alteration in level of consciousness and increased confusion.
Explanation: Answer reason: Haloperidol is a typical antipsychotic that commonly causes extrapyramidal symptoms due to dopamine blockade and may also cause blood dyscrasias, making option A correct.
The mechanism of action of indirect-acting cholinomimetic agents is?
- Binding to and activation of muscarinic or nicotinic receptors
- Inhibition of the hydrolysis of endogenous acetylcholine
- Stimulation of the action of acetylcholinesterase
- Releasing acetylcholine from storage sites
Explanation: Answer reason: Indirect-acting cholinomimetics are acetylcholinesterase inhibitors; they increase acetylcholine by preventing its breakdown.
Cholinesterase inhibitors do not produce?
- Bradycardia, no change or modest fall in blood pressure
- Increased strength of muscle contraction, especially in muscles weakened by myasthenia gravis
- Miosis and reduction of intraocular pressure
- Dramatic hypertension and tachycardia
Explanation: Answer reason: Cholinesterase inhibitors increase acetylcholine, producing parasympathomimetic effects: bradycardia, miosis with reduced intraocular pressure, and improved neuromuscular transmission in myasthenia gravis. They do not cause dramatic hypertension and tachycardia, which are sympathetic responses.
Indicate the organophosphate cholinesterase inhibitor, which can be made up in an aqueous solution for ophthalmic use and retains its activity within a week?
- Physostigmine
- Edrophonium
- Echothiophate
- Neostigmine
Explanation: Answer reason: Echothiophate is an organophosphate acetylcholinesterase inhibitor used topically in glaucoma; it can be prepared in aqueous ophthalmic solution and remains active for about a week. The other options are not organophosphates.
Which of the following cholinomimetics is a drug of choice for reversing the effects of nondepolarizing neuromuscular relaxants?
- Echothiophate
- Physostigmine
- Edrophonium
- Pilocarpine
Explanation: Answer reason: Reversal of nondepolarizing neuromuscular blockade is achieved with acetylcholinesterase inhibitors; edrophonium is a short-acting agent used for this purpose. The other options are used for glaucoma or anticholinergic toxicity, not NM block reversal.
The symptoms of excessive stimulation of muscarinic receptors include all of the following EXCEPT?
- Abdominal cramps, diarrhea
- Increased salivation, excessive bronchial secretion
- Miosis, bradycardia
- Weakness of all skeletal muscles
Explanation: Answer reason: Muscarinic receptor overstimulation causes parasympathomimetic effects such as GI hyperactivity, salivation/bronchial secretions, miosis, and bradycardia. Skeletal muscle weakness is mediated by nicotinic receptors at the neuromuscular junction, not muscarinic.
The toxic effects of a large dose of nicotine include all of the following EXCEPT?
- Hypotension and bradycardia
- Convulsions, coma and respiratory arrest
- Skeletal muscle depolarization blockade and respiratory paralysis
- Hypertension and cardiac arrhythmias
Explanation: Answer reason: Nicotine toxicity causes prominent nicotinic stimulation with hypertension and arrhythmias, CNS excitation with seizures/coma, and at high doses depolarizing neuromuscular blockade leading to respiratory paralysis. Hypotension and bradycardia are not typical, making them the exception.
Indicate the drug, which is rapidly and fully distributed into CNS and has a greater effect than most other antimuscarinic agents?
- Atropine
- Scopolamine
- Homatropine
- Ipratropium
Explanation: Answer reason: Scopolamine is a tertiary, highly lipophilic antimuscarinic that rapidly crosses the blood–brain barrier and produces strong CNS effects. Atropine and homatropine have less CNS effect at therapeutic doses, and ipratropium is quaternary and poorly penetrates the CNS.
The mechanism of atropine action is?
- Competitive ganglion blockade
- Competitive muscarinic blockade
- Competitive neuromuscular blockade
- Noncompetitive neuromuscular blockade
Explanation: Answer reason: Atropine is a competitive antagonist at muscarinic acetylcholine receptors, producing competitive muscarinic blockade rather than ganglionic or neuromuscular blockade.
Atropine causes?
- Miosis, a reduction in intraocular pressure and cyclospasm
- Mydriasis, a rise in intraocular pressure and cycloplegia
- Miosis, a rise in intraocular pressure and cycloplegia
- Mydriasis, a rise in intraocular pressure and cyclospasm
Explanation: Answer reason: Atropine is an antimuscarinic that blocks M3 receptors in the iris sphincter and ciliary muscle, causing mydriasis and cycloplegia; it can increase intraocular pressure. Cyclospasm and miosis are cholinergic effects, not produced by atropine.
Atropine is now rarely used for the treatment of peptic ulcer because of?
- Slow gastric empting and prolongation of the exposure of the ulcer bed to acid
- Low efficiency and necessity of large doses
- Adverse effects
- All of the above
Explanation: Answer reason: Antimuscarinic therapy like atropine delays gastric emptying, is relatively ineffective for ulcer healing requiring large doses, and causes significant anticholinergic adverse effects; therefore all listed reasons apply.
Compared with atropine, scopolamine has all of the following properties EXCEPT?
- More marked central effect
- Less potent in decreasing bronchial, salivary and sweat gland secretion
- More potent in producing mydriasis and cycloplegia
- Lower effects on the heart, bronchial muscle and intestines
Explanation: Answer reason: Scopolamine (hyoscine) has greater CNS effects than atropine and, peripherally, shows relatively less effect on the heart, bronchial smooth muscle, and intestines while being a strong mydriatic/cycloplegic. It is not less potent than atropine at inhibiting bronchial, salivary, and sweat secretions, so option B is the incorrect statement.
The atropine poisoning includes all of the following symptoms EXCEPT?
- Mydriasis, cycloplegia
- Hyperthermia, dry mouth, hot and flushed skin
- Agitation and delirium
- Bradicardia, orthostatic hypotension
Explanation: Answer reason: Atropine toxicity is anticholinergic: mydriasis, cycloplegia, hyperthermia with hot dry skin, tachycardia, agitation and delirium. Bradycardia and orthostatic hypotension are not typical, so they are the exception.
The applications of the ganglion blockers have disappeared because of all of the following reasons EXCEPT?
- Orthostatic hypotension
- Lack of selectivity
- Homeostatic reflexes block
- Respiratory depression
Explanation: Answer reason: Ganglionic blockers are obsolete mainly due to nonselective autonomic blockade and loss of reflex control, leading to marked adverse effects such as orthostatic hypotension and blockade of homeostatic (baroreceptor) reflexes. Respiratory depression is not a characteristic reason for their abandonment.
The systemic effects of hexamethonium include all of the following EXCEPT?
- Reduction of both peripheral vascular resistance and venous return
- Partial mydriasis and loss of accommodation
- Constipation and urinary retention
- Stimulation of thermoregulatory sweating
Explanation: Answer reason: Hexamethonium is a ganglionic blocker that reduces sympathetic and parasympathetic tone. It causes vasodilation with decreased PVR and venous return, mydriasis with cycloplegia, and decreased GI/GU motility. It blocks sympathetic cholinergic innervation to sweat glands, leading to anhidrosis—not stimulation of sweating.
Agents that produce neuromuscular blockade act by inhibiting?
- Interaction of acetylcholine with cholinergic receptors
- Release of acetylcholine from prejunctional membrane
- Packaging of acetylcholine into synaptic vesicles
- Reuptake of acetylcholine into the nerve ending
Explanation: Answer reason: Most neuromuscular blockers (nondepolarizing agents) cause paralysis by competitively blocking nicotinic cholinergic receptors at the neuromuscular junction, preventing acetylcholine from interacting with them. The other options are not the primary mechanism.
Depolarizing agents include all of the following properties EXCEPT?
- Interact with nicotinic receptor to compete with acetylcholine without receptor activation
- React with the nicotinic receptor to open the channel and cause depolarisation of the end plate
- Cause desensitization, noncompetitive block manifested by flaccid paralysis
- Cholinesterase inhibitors do not have the ability to reverse the blockade
Explanation: Answer reason: Depolarizing neuromuscular blockers are nicotinic receptor agonists that open the channel and depolarize the end plate; they may lead to desensitization and are not reversed by cholinesterase inhibitors. Competitive antagonism without receptor activation describes nondepolarizing agents, so option A is the exception.
All of the following drugs increase the effects of depolarizing neuromuscular blocking agents EXCEPT?
- Aminoglycosides
- Antiarrhythmic drugs
- Nondepolarizing blockers
- Local anesthetics
Explanation: Answer reason: Aminoglycosides, certain antiarrhythmics (e.g., quinidine), and local anesthetics can potentiate depolarizing neuromuscular blockade by reducing acetylcholine release or membrane excitability. Nondepolarizing blockers do not increase succinylcholine’s depolarizing effect and can antagonize phase I block, making them the exception.
Which of the following diseases can augment the neuromuscular blockade produced by nondepolarizing muscle relaxants?
- Myasthenia gravis
- Burns
- Asthma
- Parkinsonism
Explanation: Answer reason: Myasthenia gravis reduces functional nicotinic receptors at the neuromuscular junction, making patients highly sensitive to nondepolarizing blockers and augmenting their effect. Burns typically cause resistance; asthma and parkinsonism do not increase blockade.
Characteristics of epinephrine include all of the following EXCEPT?
- It is synthesized into the adrenal medulla
- It is synthesized into the nerve ending
- It is transported in the blood to target tissues
- It directly interacts with and activates adrenoreceptors
Explanation: Answer reason: Epinephrine is synthesized primarily in the adrenal medulla, circulates in the bloodstream to target tissues, and activates adrenoceptors. Synthesis in sympathetic nerve endings characterizes norepinephrine, not epinephrine; therefore that statement is the exception.
Indirect action includes all of the following properties EXCEPT?
- Displacement of stored catecholamines from the adrenergic nerve ending
- Inhibition of reuptake of catecholamines already released
- Interaction with adrenoreceptors
- Inhibition of the release of endogenous catecholamines from peripheral adrenergic neurons
Explanation: Answer reason: Indirect-acting agents modify synaptic catecholamine levels (release, reuptake inhibition, or altering release) without binding to adrenoceptors. Direct action involves receptor interaction, so this is the exception.
Which of the following statements is not correct?
- ALFA receptors increase arterial resistence, whereas beta2 receptor promote smooth muscle relaxation
- The skin and splanchnic vessels have predominantly alfa receptors
- Vessels in a skeletal muscle may constrict or dilate depending on whether alfa or beta2 receptors are activated
- Skeletal muscle vessels have predominantly alfa receptors and constrict in the presence of epinephrine and norepinephrine
Explanation: Answer reason: Skeletal muscle vasculature contains significant beta2 receptors; epinephrine (especially at low doses) causes beta2-mediated vasodilation, while alpha activation (e.g., by norepinephrine) causes vasoconstriction. Thus stating they are predominantly alpha and constrict with both catecholamines is incorrect.
Which of the following statement is not correct?
- Alfa agonists cause miosis
- Alfa agonists cause mydriasis
- Beta antagonists decrease the production of aqueous humor
- Alfa agonists increase the outflow of aqueous humor from the eye
Explanation: Answer reason: Alpha agonists (e.g., phenylephrine via α1) cause mydriasis, not miosis. Beta blockers reduce aqueous humor production; α2 agonists reduce production and can increase outflow.
Alfa-receptor stimulation includes all of the following effects EXCEPT?
- Relaxation of gastrointestinal smooth muscle
- Contraction of bladder base, uterus and prostate
- Stimulation of insulin secretion
- Stimulation of platelet aggregation
Explanation: Answer reason: Alpha-adrenergic stimulation causes GI smooth muscle relaxation (mainly via alpha2), contraction of bladder neck/uterus/prostate (alpha1), and promotes platelet aggregation (alpha2). It inhibits, not stimulates, insulin secretion; beta2 stimulates insulin release.
Which of the following statements is not correct?
- Epinephrine acts on both alfa- and beta-receptors
- Norepinephrine has a predominantly beta action
- Methoxamine has a predominantly alfa action
- Isoprenaline has a predominantly beta action
Explanation: Answer reason: Norepinephrine is primarily an alpha-adrenergic agonist (with some beta1 activity), not predominantly beta. The other statements are correct: epinephrine acts on both alpha and beta receptors; methoxamine is mainly alpha; isoprenaline is predominantly beta.
Epinephrine produces all of the following effects EXCEPT?
- Positive inotropic and chronotropic actions on the heart (beta1 receptor)
- Increase peripheral resistance (alfa receptor)
- Predominance of alfa effects at low concentration
- Skeletal muscle blood vessel dilatation (beta2 receptor)
Explanation: Answer reason: At low concentrations epinephrine’s beta effects predominate (beta1 cardiac stimulation, beta2 vasodilation in skeletal muscle). Alpha effects predominate at higher concentrations. Therefore option C is the exception; the other statements are true.
Compared with epinephrine, norepinephrine produces all of the following effects EXCEPT?
- Similar effects on beta1 receptors in the heart and similar potency at an alfa receptor
- Decrease the mean pressure below normal before returning to the control value
- Significant tissue necrosis if injected subcutaneously
- Increase both diastolic and systolic blood pressure
Explanation: Answer reason: Norepinephrine strongly activates alpha1 and beta1 receptors but has minimal beta2 activity. It increases both systolic and diastolic BP and can cause tissue necrosis if injected subcutaneously; it has similar beta1 and alpha potency to epinephrine. A fall of mean pressure below normal (epinephrine reversal via beta2 vasodilation) is not produced by norepinephrine.
Which of the following direct-acting drugs is a relatively pure alpha agonist, an effective mydriatic and decongestant and can be used to raise blood pressure?
- Epinephrine
- Norepinephrine
- Phenylephrine
- Ephedrine
Explanation: Answer reason: Phenylephrine is a direct-acting selective alpha-1 agonist used as a mydriatic and nasal decongestant and increases blood pressure via vasoconstriction. Epinephrine and norepinephrine act on multiple receptors, and ephedrine is mixed-acting, not a relatively pure alpha agonist.
Characteristics of methoxamine include all of the following EXCEPT?
- It is a direct-acting alfa1-receptor agonist
- It increases heart rate, contractility and cardiac output
- It causes reflex bradycardia
- It increases total peripheral resistance
Explanation: Answer reason: Methoxamine is a direct-acting alpha1 agonist that causes peripheral vasoconstriction, increasing total peripheral resistance and blood pressure, which leads to reflex bradycardia. It does not increase heart rate or cardiac output—thus option B is the exception.
Characteristics of dobutamine include all of the following EXCEPT?
- It is a relatively beta1-selective synthetic catecholamine
- It is used to treat bronchospasm
- It increases atrioventricular conduction
- It causes minimal changes in heart rate and systolic pressure
Explanation: Answer reason: Dobutamine is a predominantly beta1-adrenergic agonist used as an inotrope in acute heart failure and shock. It is not a bronchodilator; beta2 agonists (e.g., albuterol) treat bronchospasm. The other statements are characteristic of dobutamine.
Characteristics of salmeterol include all of the following EXCEPT?
- It is a potent selective beta2 agonist
- It causes uterine relaxation
- It stimulates heart rate, contractility and cardiac output
- It is used in the therapy of asthma
Explanation: Answer reason: Salmeterol is a long-acting, selective beta2-adrenergic agonist used for asthma; beta2 activation causes bronchodilation and uterine relaxation. Significant stimulation of heart rate, contractility, and cardiac output is a beta1 effect and is not characteristic of salmeterol at therapeutic doses.
Compared with epinephrine, ephedrine produces all of the following features EXCEPT?
- It is a direct-acting sympathomimetic
- It has oral activity
- It is resistant to MAO and has much longer duration of action
- Its effects are similar, but it is less potent
Explanation: Answer reason: Ephedrine is a mixed-acting sympathomimetic (primarily indirect by releasing norepinephrine with some direct receptor activity). It is orally active, not metabolized by COMT and relatively resistant to MAO, giving a longer duration, and its effects are similar to epinephrine but less potent. Thus calling it purely direct-acting is incorrect.
The adverse effects of sympathomimetics include all of the following EXCEPT?
- Drug-induced parkinsonism
- Cerebral hemorrhage or pulmonary edema
- Myocardial infarction
- Ventricular arrhythmias
Explanation: Answer reason: Sympathomimetics can cause severe cardiovascular and cerebrovascular events such as hypertension leading to cerebral hemorrhage, pulmonary edema, myocardial infarction, and ventricular arrhythmias. Drug-induced parkinsonism is associated with dopamine antagonists (e.g., antipsychotics), not sympathomimetics.
The principal mechanism of action of adrenoreceptor antagonists is?
- Reversible or irreversible interaction with adrenoreceptors
- Depletion of the storage of catecholamines
- Blockade of the amine reuptake pumps
- Nonselective MAO inhibition
Explanation: Answer reason: Adrenergic receptor antagonists act by blocking adrenergic receptors—usually via reversible competitive antagonism; some (e.g., phenoxybenzamine) are irreversible. The other options describe indirect sympatholytics or MAO inhibition, not receptor antagonism.
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