Pharmacology Practice Test 24
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 24th 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 24
Characteristics of phentolamine include all of the following EXCEPT?
- Reduction in peripheral resistance
- Stimulation of responses to serotonin
- Tachycardia
- Stimulation of muscarinic, H1 and H2 histamine receptors
Explanation: Answer reason: Phentolamine is a nonselective alpha-adrenergic antagonist that lowers peripheral resistance and commonly causes reflex tachycardia. It antagonizes serotonin responses rather than stimulating them and also has actions that can stimulate muscarinic and histamine (H1, H2) receptors or promote histamine effects.
The principal mechanism of phentolamine-induced tachycardia is?
- Antagonism of presynaptic alfa2 receptors enhances norepinephrine release, which causes cardiac stimulation via unblocked beta receptors
- Baroreflex mechanism
- Direct effect on the heart by stimulation of beta1 receptors
- Inhibition of transmitter reuptake at noradrenergic synapses
Explanation: Answer reason: Phentolamine blocks both alpha1 and presynaptic alpha2 receptors. Alpha2 blockade increases norepinephrine release, which then stimulates cardiac beta1 receptors, producing tachycardia; this effect predominates over reflex causes.
The main reason for using alfa-receptor antagonists in the management of pheochromocytoma is?
- Inhibition of the release of epinephrine from the adrenal medulla
- Blockade of alfa2 receptors on vascular smooth muscle results in epinephrine stimulation of unblocked alfa2 receptors
- Direct interaction with and inhibition of beta2 adrenoreceptors
- Antagonism to the release of renin
Explanation: Answer reason: Alpha blockade prevents catecholamine-induced vasoconstriction and produces epinephrine reversal, where unopposed beta2 effects predominate. Among the options, choice B reflects the rationale for alpha-antagonist use in pheochromocytoma.
Indicate adrenoreceptor antagonist agents, which are used for the management of pheochromocytoma?
- Selective beta2-receptor antagonists
- Nonselective beta-receptor antagonists
- Indirect-acting adrenoreceptor antagonist drugs
- Alfa-receptor antagonists
Explanation: Answer reason: Pheochromocytoma causes excess catecholamine release; initial pharmacologic management is alpha-adrenergic blockade (e.g., phenoxybenzamine, phentolamine). Beta blockers are only added after alpha blockade and are not primary; selective beta2 antagonists and indirect-acting agents are not indicated.
Which of the following statements is not correct?
- There are at least three subtypes of alfa1 receptors, designated alfa1a, alfa1b and alfa1d
- ALFA1a subtype mediates prostate smooth muscle contraction
- ALFA1b subtype mediates vascular smooth muscle contraction
- ALFA1a subtype mediates both vascular and prostate smooth muscle contraction
Explanation: Answer reason: Alpha1A receptors mediate prostate smooth muscle contraction; alpha1B receptors primarily mediate vascular smooth muscle contraction. Therefore the statement that alpha1A mediates both vascular and prostate contraction is incorrect.
Subtype-selective alfa1 receptor antagonists such as tamsulosin, terazosin, alfusosin are efficacious in?
- Hyperthyroidism
- Cardiac arrhythmias
- Benign prostatic hyperplasia (BPH)
- Asthma
Explanation: Answer reason: Alpha-1 selective antagonists relax smooth muscle in the prostate and bladder neck, improving urinary flow; they are indicated for BPH, not for hyperthyroidism, arrhythmias, or asthma.
Which of the following alfa receptor antagonists is useful in reversing the intense local vasoconstriction caused by inadvertent infiltration of norepinephrine into subcutaneous tissue during intravenous administration?
- Propranolol
- Phentolamine
- Tamsulosin
- Ergotamine
Explanation: Answer reason: Phentolamine is a nonselective alpha-adrenergic antagonist used to infiltrate around norepinephrine extravasation sites to produce local vasodilation and reverse ischemia. Propranolol is a beta-blocker, tamsulosin targets alpha1A for BPH, and ergotamine causes vasoconstriction.
Characteristics of beta-blocking agents include all of the following EXCEPT?
- They occupy beta receptors and competitively reduce receptor occupancy by catecholamines or other beta agonists
- They do not cause hypotension in individuals with normal blood pressure
- They induce depression and depleted stores of catecholamines
- They can cause blockade in the atrioventricular node
Explanation: Answer reason: Beta blockers are competitive antagonists at beta receptors, typically do not lower BP in normotensive individuals, and slow AV nodal conduction. They do not deplete catecholamine stores; that is characteristic of drugs like reserpine. Thus option C is the exception.
Beta-receptor antagonists have all of the following cardiovascular effects EXCEPT?
- The negative inotropic and chronotropic effects
- Acute effects of these drugs include a fall in peripheral resistance
- Vasoconstriction
- Reduction of the release of renin
Explanation: Answer reason: Beta-blockers decrease heart rate and contractility, reduce renin release (β1), and nonselective agents can cause peripheral vasoconstriction via β2 blockade. Acutely they tend to increase or maintain peripheral resistance; a fall in peripheral resistance occurs only with chronic use. Thus option B is the exception.
Beta-blocking agents have all of the following effects except?
- Increase plasma concentrations of HDL and decrease of VLDL
- Bronchoconstriction
- Decrease of aqueous humor production
- "membrane-stabilizing" action
Explanation: Answer reason: Nonselective beta-blockers can cause bronchoconstriction, reduce aqueous humor production, and some have membrane-stabilizing (quinidine-like) action. They tend to lower HDL and raise VLDL/triglycerides; therefore an increase in HDL with a decrease in VLDL is not an effect.
Propranolol has all of the following cardiovascular effects EXCEPT?
- It decreases cardiac work and oxygen demand
- It reduces blood flow to the brain
- It inhibits the renin secretion
- It increases the atrioventricular nodal refractory period
Explanation: Answer reason: Propranolol, a nonselective beta blocker, decreases heart rate and contractility (reducing cardiac work and O2 demand), inhibits renin release via beta-1 blockade, and increases AV nodal refractory period (Class II antiarrhythmic effect). It does not significantly reduce cerebral blood flow due to autoregulation.
Propranolol-induced adverse effects include all of the following EXCEPT?
- Bronchoconstriction
- “supersensitivity” of beta-adrenergic receptors (rapid withdrawal)
- Hyperglycemia
- Sedation, sleep disturbances, depression and sexual dysfunction
Explanation: Answer reason: Propranolol (nonselective β-blocker) can cause bronchoconstriction, CNS effects (sedation, sleep issues, depression, sexual dysfunction), and rebound due to β-receptor upregulation after abrupt withdrawal. It more typically masks and can prolong hypoglycemia rather than cause hyperglycemia; thus hyperglycemia is the exception.
Which of the following drugs is a nonselective beta-blocker without intrinsic sympathomimetic or local anesthetic activity and used for the treatment of life-threatening ventricular arrhythmias?
- Propranolol
- Oxprenolol
- Sotalol
- Atenolol
Explanation: Answer reason: Sotalol is a nonselective beta-blocker with no intrinsic sympathomimetic or local anesthetic (membrane-stabilizing) activity and has class III antiarrhythmic effects, making it useful for life-threatening ventricular arrhythmias.
Characteristics of carvedilol include all of the following EXCEPT?
- It is a beta1-selective antagonist
- It has both alfa1-selective and beta-blocking effects
- It attenuates oxygen free radical-initiated lipid peroxidation
- It inhibits vascular smooth muscle mitogenesis
Explanation: Answer reason: Carvedilol is a nonselective beta-blocker with additional alpha1-blocking activity and antioxidant/antiproliferative properties. Therefore, it is not beta1-selective.
Beta-blocker-induced adverse effects include all of the following EXCEPT?
- Bronchoconstriction
- Depression of myocardial contractility and excitability
- "supersensitivity" of beta-receptors associated with rapid withdrawal of drugs
- Hyperglycemia
Explanation: Answer reason: Beta-blockers can cause bronchoconstriction, decrease myocardial contractility, and lead to receptor upregulation with abrupt withdrawal. They more commonly cause or mask hypoglycemia rather than hyperglycemia; therefore hyperglycemia is not a typical adverse effect.
Hypnotic drugs should?
- Reduce anxiety and exert a calming effect
- Induce absence of sensation
- Produce drowsiness, encourage the onset and maintenance of sleep
- Prevent mood swings in patients with bipolar affective disorders
Explanation: Answer reason: Hypnotics are medications that induce sleep by promoting drowsiness and facilitating the onset and maintenance of sleep. The other options describe anxiolytics, anesthetics, or mood stabilizers.
Which of the following factors can influence the biodisposition of hypnotic agents?
- Alterations in the hepatic function resulting from a disease
- Old age
- Drug-induced increases or decreases in microsomal enzyme activities
- All of the above
Explanation: Answer reason: Hepatic disease, advanced age, and enzyme induction or inhibition all affect metabolism and clearance, thereby altering biodisposition of hypnotic agents.
Indicate the mechanism of barbiturate action (at hypnotic doses)?
- 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: At therapeutic hypnotic doses, barbiturates enhance GABA-A activity by prolonging the duration of chloride channel opening. Increasing frequency is characteristic of benzodiazepines, and direct channel activation occurs only at very high/toxic doses.
Imidazopyridines are?
- Partial agonists at brain 5-TH1A receptors
- Selective agonists of the BZ1 (omega1) subtype of BZ receptors
- Competitive antagonists of BZ receptors
- Nonselective agonists of both BZ1 and BZ2 receptor subtypes
Explanation: Answer reason: Imidazopyridines such as zolpidem act selectively at the BZ1 (omega-1) subtype of the benzodiazepine site on GABA-A receptors, producing hypnotic effects with minimal anxiolysis or muscle relaxation.
All of the hypnotic drugs induce?
- Increase the duration of REM sleep
- Decrease the duration of REM sleep
- Do not alter the duration of REM sleep
- Increase the duration of slow wave sleep
Explanation: Answer reason: Most hypnotic agents suppress REM sleep, reducing its duration; withdrawal can cause REM rebound.
Which of the following hypnotic benzodiazepines is more likely to cause "hangover" effects such as drowsiness, dysphoria, and mental or motor depression the following day?
- Temazepam
- Triazolam
- Flurazepam
- None of the above
Explanation: Answer reason: Flurazepam is a long-acting benzodiazepine with active metabolites, leading to next-day sedation and hangover effects. Temazepam is intermediate-acting and triazolam is short-acting, so they have less daytime residual effects.
Which of the following statements is correct for zolpidem?
- Causes minor effects on sleep patterns
- The risk of development of tolerance and dependence is less than with the use of hypnotic benzodiazepines
- Has minimal muscle relaxing and anticonvulsant effects
- All of the above
Explanation: Answer reason: Zolpidem, a non-benzodiazepine hypnotic, preserves sleep architecture, has lower tolerance/dependence risk than benzodiazepines, and lacks significant muscle relaxant or anticonvulsant effects—thus all statements are correct.
The mechanism of action of antiseizure drugs is?
- Enhancement of GABAergic (inhibitory) transmission
- Diminution of excitatory (usually glutamatergic) transmission
- Modification of ionic conductance
- All of the above mechanisms
Explanation: Answer reason: Antiseizure drugs work by enhancing inhibitory GABA transmission, reducing excitatory glutamatergic transmission, and altering ionic conductances (e.g., Na+, Ca2+ channels), so all listed mechanisms are correct.
Select the appropriate consideration for phenytoin?
- It blocks sodium channels
- It binds to an allosteric regulatory site on the GABA-BZ receptor and prolongs the openings of the Cl-channels
- It effects on Ca2+ currents, reducing the low-threshold (T-type) current
- It inhibits GABA-transaminase, which catalyzes the breakdown of GABA
Explanation: Answer reason: Phenytoin is an antiepileptic that blocks voltage-gated sodium channels to limit repetitive neuronal firing. The other options describe mechanisms of benzodiazepines/barbiturates (GABA-A modulation), ethosuximide (T-type Ca2+ channel), and vigabatrin/valproate (GABA transaminase inhibition).
Barbiturates are used in the emergency treatment of status epilepticus in infants and children because of?
- They significantly decrease of oxygen utilization by the brain, protecting cerebral edema and ischemia
- Short onset and duration of action
- They do not have effect on sleep architecture
- All of the above
Explanation: Answer reason: Barbiturates (e.g., phenobarbital) lower cerebral metabolic rate and oxygen consumption, providing neuroprotection in status epilepticus. They do not have short onset/duration and they alter sleep architecture, so only option A is correct.
The mechanism of vigabatrin's action is?
- Direct action on the GABA receptor-chloride channel complex
- Inhibition of GABA aminotransferase
- NMDA receptor blockade via the glycine binding site
- Inhibition of GABA neuronal reuptake from synapses
Explanation: Answer reason: Vigabatrin irreversibly inhibits GABA transaminase, increasing brain GABA. It does not act directly on GABA-A receptors, block NMDA, or inhibit GABA reuptake.
Tiagabine?
- Blocks neuronal and glial reuptake of GABA from synapses
- Inhibits GABA-T, which catalyzed the breakdown of GABA
- Blocks the T-type Ca2+ channels
- Inhibits glutamate transmission at AMPA/kainate receptors
Explanation: Answer reason: Tiagabine is an antiepileptic that inhibits GABA reuptake via GAT-1, increasing synaptic GABA. GABA-T inhibition is vigabatrin, T-type Ca2+ blockade is ethosuximide, and AMPA/kainate inhibition is topiramate.
The mechanism of valproate action is?
- Facilitation glutamic acid decarboxylase, the enzyme responsible for GABA synthesis and inhibition of GABA aminotransferase, the enzyme responsible for the breakdown of GABA (enhance GABA accumulation)
- Inhibition of voltage sensitive Na+ channels
- Inhibition of low threshold (T-type) Ca2+ channels
- All of the above
Explanation: Answer reason: Valproate enhances GABA by increasing glutamic acid decarboxylase activity and inhibiting GABA transaminase, and it also blocks voltage-gated Na+ channels and T-type Ca2+ channels.
Indicate the antiseizure drug, which is a sulfonamide derivative, blocking Na+ channels and having additional ability to inhibit T-type Ca2+ channels?
- Tiagabine
- Zonisamide
- Ethosuximide
Explanation: Answer reason: Zonisamide is a sulfonamide derivative that blocks voltage-gated Na+ channels and also inhibits T-type Ca2+ channels. Tiagabine is a GABA reuptake inhibitor; ethosuximide targets T-type Ca2+ channels but is not a sulfonamide.
Mu (μ) receptors are associated with?
- Analgesia, euphoria, respiratory depression, physical dependence
- Spinal analgesia, mydriasis, sedation, physical dependence
- Dysphoria, hallucinations, respiratory and vasomotor stimulation
- Analgesia, euphoria, respiratory stimulation, physical dependence
Explanation: Answer reason: Mu opioid receptor activation classically causes analgesia and euphoria but also respiratory depression and physical dependence; other options include mydriasis or respiratory stimulation, which are incorrect for μ.
Kappa and delta agonists?
- Inhibit postsynaptic neurons by opening K+ channels
- Close a voltage-gated Ca2+ channels on presynaptic nerve terminals
- Both a and b
- Inhibit of arachidonate cyclooxygenase in CNS
Explanation: Answer reason: Opioid receptor agonists (kappa and delta) are Gi/o-coupled; they open postsynaptic K+ channels causing hyperpolarization and close presynaptic voltage-gated Ca2+ channels to reduce neurotransmitter release. They do not inhibit cyclooxygenase.
Indicate the opioid analgesic, which has 80 times analgesic potency and respiratory depressant properties of morphine, and is more effective than morphine in maintaining hemodynamic stability?
- Fentanyl
- Pentazocine
- Meperidine
- Nalmefene
Explanation: Answer reason: Fentanyl is approximately 80–100 times more potent than morphine, has significant respiratory depressant effects, and is preferred for better hemodynamic stability compared with morphine.
The relief produced by intravenous morphine in dyspnea from pulmonary edema is associated with reduced?
- Perception of shortness of breath
- Patient anxiety
- Cardiac preload (reduced venous tone) and afterload (decreased peripheral resistance)
- All of the above
Explanation: Answer reason: IV morphine in acute pulmonary edema decreases anxiety and the perceived dyspnea and causes venodilation lowering preload, with some reduction in afterload, thus all listed effects are true.
Rhinorrhea, lacrimation, chills, gooseflesh, hyperventilation, hyperthermia, mydriasis, muscular aches, vomiting, diarrhea, anxiety, and hostility are effects of?
- Tolerance
- Opioid overdosage
- Drug interactions between opioid analgesics and sedative-hypnotics
- Abstinence syndrome
Explanation: Answer reason: The listed autonomic and GI symptoms (rhinorrhea, lacrimation, piloerection, mydriasis, vomiting, diarrhea, anxiety) are classic for opioid withdrawal (abstinence). Overdose would cause miosis and respiratory depression, not these signs.
The diagnostic triad of opioid overdosage is?
- Mydriasis, coma and hyperventilation
- Coma, depressed respiration and miosis
- Mydriasis, chills and abdominal cramps
- Miosis, tremor and vomiting
Explanation: Answer reason: Opioid toxicity classically presents with the triad of CNS depression (coma), respiratory depression, and pinpoint pupils (miosis).
Indicate a partial mu receptor agonist, which has 20-60 times analgesic potency of morphine, and a longer duration of action?
- Pentazocine
- Buprenorphine
- Nalbuphine
- Naltrexone
Explanation: Answer reason: Buprenorphine is a partial mu-opioid receptor agonist with very high potency (about 20–60 times morphine) and prolonged duration due to slow receptor dissociation. Pentazocine and nalbuphine are kappa agonists/mu antagonists, and naltrexone is an opioid antagonist.
Which of the following drugs has weak mu agonist effects and inhibitory action on norepinephrine and serotonin reuptake in the CNS?
- Loperamide
- Tramadol
- Fluoxetine
- Butorphanol
Explanation: Answer reason: Tramadol is a weak mu-opioid receptor agonist and inhibits reuptake of norepinephrine and serotonin. Loperamide acts peripherally on mu receptors, fluoxetine is an SSRI without mu agonism, and butorphanol is primarily a kappa agonist/partial mu antagonist.
Correct statements concerning aspirin include all of the following EXCEPT?
- It inhibits mainly peripheral COX
- It does not have an anti-inflammatory effect
- It inhibits platelet aggregation
- It stimulates respiration by a direct action on the respiratory center
Explanation: Answer reason: Aspirin is an NSAID that irreversibly inhibits COX, producing anti-inflammatory effects and inhibiting platelet aggregation; at high doses it directly stimulates the respiratory center. Therefore the statement that it does not have an anti-inflammatory effect is false.
All of the following are undesirable effects of aspirin EXCEPT?
- Gastritis with focal erosions
- Tolerance and physical addiction
- Bleeding due to a decrease of platelet aggregation
- Reversible renal insufficiency
Explanation: Answer reason: Aspirin (an NSAID) commonly causes gastritis/erosions, bleeding from inhibited platelet aggregation, and can lead to reversible renal insufficiency. It does not produce tolerance or physical dependence, which are characteristic of opioids.
Characteristic findings of salicylism include?
- Headache, mental confusion and drowsiness
- Tinnitus and difficulty in hearing
- Hyperthermia, sweating, thirst, hyperventilation, vomiting and diarrhea
- All of the above
Explanation: Answer reason: Salicylism (aspirin toxicity) commonly presents with tinnitus and hearing changes, CNS symptoms such as headache, confusion, drowsiness, and systemic features including hyperthermia, sweating, thirst, hyperventilation, vomiting, and diarrhea—thus all listed options are correct.
Parkinsonian symptoms and tarditive dyskinesia are caused by blockade dopamine in?
- The nigrostriatal system
- The mesolimbic and mesofrontal systems
- The chemoreceptor trigger zone of the medulla
- The tuberoinfundibular system
Explanation: Answer reason: Extrapyramidal symptoms such as parkinsonism and tardive dyskinesia result from D2 receptor blockade in the nigrostriatal dopamine pathway. Mesolimbic blockade mediates antipsychotic effect, CTZ affects emesis, and tuberoinfundibular blockade causes hyperprolactinemia.
Which of the following statements is true?
- D1 postsynaptic receptors are located in striatum
- D2 pre- and postsynaptic receptors are located in striatum and limbic areas
- D4 postsynaptic receptors are located in frontal cortex, mesolimbic system
- All of the above
Explanation: Answer reason: All listed statements accurately describe dopamine receptor subtype distributions: D1 postsynaptic in striatum; D2 both pre- and postsynaptic in striatum and limbic areas; D4 postsynaptic in frontal cortex and mesolimbic system.
Atypical antipsychotic agents (such as clozapine) differ from typical ones?
- In reduced risks of extrapyramidal system dysfunction and tardive dyscinesia
- In having low affinity for D1 and D2 dopamine receptors
- In having high affinity for D4 dopamine receptors
- All of the above
Explanation: Answer reason: Atypical antipsychotics like clozapine cause fewer EPS/tardive dyskinesia due to weaker D2 blockade, show relatively low D1/D2 affinity, and clozapine has higher affinity for D4 receptors; therefore all statements are correct.
Tardive dyskinesia is the result of?
- Degeneration of dopaminergic and cholinergic fibers
- Hyperactive dopaminergic state in the presence of dopamine blockers
- Degeneration of histaminergic fibers
- Supersensitivity of cholinergic receptors in the caudate-putamen
Explanation: Answer reason: Chronic dopamine receptor blockade (e.g., antipsychotics) causes D2 receptor upregulation and supersensitivity, producing a functional hyperdopaminergic state that manifests as tardive dyskinesia.
The strong antiemetic effect of the phenothiazine derivatives is due to dopamine receptor blockade?
- In the chemoreceptor trigger zone of the medulla
- Of the receptors in the stomach
- The medullary vomiting centre
- All of the above
Explanation: Answer reason: Phenothiazine antiemetics (e.g., prochlorperazine) exert their effect primarily by D2 receptor blockade in the area postrema/chemoreceptor trigger zone, not by blocking gastric receptors or the vomiting center directly.
Phenothiazine derivatives are able to?
- Alter temperature-regulating mechanisms producing hypothermia
- Decrease levels of prolactin
- Increase corticotrophin release and secretion of pituitary growth hormone
- Decrease appetite and weight
Explanation: Answer reason: Phenothiazine antipsychotics block hypothalamic dopamine pathways, disrupting thermoregulation and causing hypothermia. They increase (not decrease) prolactin, do not increase ACTH or GH, and commonly cause weight gain rather than loss.
Parkinson's syndrome, acute dystonic reactions, tardive dyskinesia, antimuscarinic actions, orthostatic hypotension, galactorrhea are possible adverse effects of?
- Haloperidol
- Clozapine
- Chlorpromazine
- Risperidone
Explanation: Answer reason: The listed effects—marked antimuscarinic actions and orthostatic hypotension along with EPS and hyperprolactinemia—are characteristic of low‑potency typical antipsychotics, especially chlorpromazine.
Adverse peripheral effects, such as loss of accommodation, dry mouth, tachycardia, urinary retention, constipation are related to?
- Alpha adrenoceptor blockade
- Muscarinic cholinoceptor blockade
- Supersensitivity of the dopamine receptor
- Dopamine receptor blockade
Explanation: Answer reason: These are classic peripheral anticholinergic effects (blurred vision from loss of accommodation, dry mouth, tachycardia, urinary retention, constipation) caused by blockade of muscarinic receptors.
Which of the following phenothiazine derivatives may produce cardiac toxicity, including ventricular arrhythmias, cardiac conduction block, and sudden death?
- Thioridazine
- Chlorpromazine
- Perphenazine
- Fluphenazine
Explanation: Answer reason: Thioridazine, a low-potency phenothiazine, is notably associated with QT prolongation leading to ventricular arrhythmias, conduction block, and sudden death more than the other listed agents.
Which of the following statements is correct for clozapine?
- Has potent anticholinergic activity
- Has high affinity for D1 and D2 dopamine receptors
- Produces significant extrapyramidal toxicity
- Is related to typical antipsychotic agents
Explanation: Answer reason: Clozapine is an atypical antipsychotic with strong anticholinergic effects and low D2 affinity, producing minimal extrapyramidal symptoms and not classified as a typical antipsychotic.
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