The quizzes about Central Nervous System Pharmacology - Part 2

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Central Nervous System Pharmacology- Part 2

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Question 1

A patient i s transported to the emergency A friend who accompanies the patient says “he was experimenting with ‘angel dust’”. What best describes the actions or other characteristics of this recreational drug, more properly know as phencyclidine?

A	Causes i ts peripheral and central effects via antimuscarinic properties
B	Causes s ignificant withdrawal symptoms
C	Has strong opioid receptor-activating activity
D	Has amphetamine-like properties and i s an hallucinogen
E	Overdoses should be treated with flumazenil

Question 1 Explanation:

“Angel dust” is phencyclidine (PCP), an hallucinogen or psychotomimetic with an amphetamine-like mechanism of action. Thus, the problems that arise are due to blockade of neuronal reuptake of such monoamines as dopamine, norepinephrine, and serotonin. The drug does not have central or peripheral muscarinic receptor antagonist activity (a), nor opioid agonist actions (c). A phencyclidine withdrawal syndrome (b) has not been documented consistently humans, largely because it is used episodically and not chronically present in the circulation. In overdose, the treatment of choice for manifestations of drug-induced psychosis is haloperidol, although rapidly acting and highly sedating benzodiazepines may be used instead. Flumazenil (e) is a benzodiazepine receptor antagonist with no use or efficacy in phencyclidine toxicity

Question 2

Package inserts for a drug caution against administering i t concurrent with any other drug that can raise or lower sodium The ri sks are inadequate or excessive effects of the drug, depending on the direction in which sodium concentrations change. This, of course, requires cautious use or avoidance (i f possible) of the common diuretics. To which of the following drugs does this caution or warning apply?

A	Cholestyramine
B	Li thium (eg, l i thium carbonate)
C	Nifedipine
D	Phenylephrine
E	Statin-type cholesterol-lowering drugs

Question 2 Explanation:

In essence, the intensity of effects from any given plasma concentration of lithium is inversely related to sodium concentrations. When sodium concentration falls, the effects of lithium can be intensified to the point of causing toxicity. By way of their actions to increase renal sodium loss, virtually all the common diuretics also reduce renal lithium excretion. It is probably of greatest concern with thiazides or thiazide-like diuretics, which have the greatest potential of all the common diuretics to cause hyponatremia. Cholestyramine (a) is a cholesterol-binding resin. Given concomitantly with an oral diuretic, the most likely outcome would be reduced bioavailability of the diuretic, not increased or decreased cholestyramine effects. Nifedipine (c), a dihydropyridine calcium channel blocker, may cause excessive antihypertensive effects when administered with any diuretic (although combined administration is common and usually problem-free). If excessive effects of nifedipine occur in conjunction with a diuretic, they are most likely blood volume-related, not specifically due to changes of sodium concentrations. Phenylephrine’s (d) vasoconstrictor effects are not likely to be altered appreciably in the presence of a diuretic. The same lack of a clinically significant interaction applies to the statins (e; HMG Co-A reductase inhibitors, eg, atorvastatin).

Question 3

A 31-year-old woman has been treated with fluoxetine for 5 She i s diagnosed with another medical problem and receives one or more drugs that, otherwise, would be suitable and probably problem-free. She i s rushed to the ED with unstable vi tal s igns, muscle rigidity, myoclonus, CNS i rri tability and altered consciousness, and shivering. What add-on drug(s) most l ikely caused these responses?

A	Codeine for cough
B	Loratadine for seasonal allergies
C	Midazolam and fentanyl, used to ease discomfort from endoscopy
D	Sumatriptan for migraine
E	Zolpidem for short-term insomnia

Question 3 Explanation:

This patient probably has the serotonin syndrome. Serotonin is already present in increased amounts in synapses because of blockade of its reuptake by the SSRIs. When sumatriptan (or other triptans used for migraine therapy; they are 5-HT1B/2D agonists) is added, rapid accumulation of serotonin and/or the triptan in the brain can occur. The risk of the serotonin syndrome in SSRI-treated patients is much higher when MAO inhibitors are used concomitantly. Nonetheless, such severe reactions from an SSRI-triptan interaction have been reported. In addition, do not forget that MAO inhibitors can also cause an acute and potentially fatal hypertensive crisis when co-administered with tricyclic/tetracyclic antidepressants (eg, imipramine); such combined use should be avoided. None of the other drugs listed (codeine, a; loratadine or another second-generation antihistamine, b; midazolam or fentanyl—or other benzodiazepines or opioids—c; or zolpidem or the related drug zaleplon, e) interact with fluoxetine or other SSRIs in terms of specifically raising systemic or synaptic serotonin levels.

Question 4

A 72-year-old woman with a long history of anxiety that has been treated with diazepam decides to triple her daily dose because of increasing fearfulness about “environmental ” Two days after her attempt at self-prescribing, she i s found extremely lethargic and nonresponsive, with markedly obtunded reflexes and reactions to painful stimuli. Respirations are 8/min and shallow. What drug should be given to reverse these s igns and symptoms?

A	Dextroamphetamine
B	Flumazenil
C	Naltrexone
D	Physostigmine
E	Pralidoxime

Question 4 Explanation:

Flumazenil is a competitive antagonist of benzodiazepines at the GABA receptor. Repeated administration is necessary because of its short half-life relative to that of most benzodiazepines—especially diazepam, which forms many long-lasting active metabolites. Dextroamphetamine (a) is a CNS stimulant that will increase the patient’s level of consciousness, but it is not indicated for this use. High doses probably be needed to overcome the intense benzodiazepine effects, and they may cause dangerous CNS and cardiovascular responses rather than simply “normalizing” variables depressed by the diazepam. Naltrexone (c) specifically antagonizes the effects of opioid agonists on μ and κ receptors and is used to diagnose or treat opioid overdoses; it has no benzodiazepine receptor-blocking activity. Physostigmine (d) is a lipophilic acetylcholinesterase inhibitor that may be a life-saving intervention for severe poisoning with many drugs (a key exception being tricyclic antidepressants) having significant antimuscarinic (atropine-like) actions. Pralidoxime (e) is a cholinesterase reactivator used in the adjunctive management of poisoning with such “irreversible” cholinesterase inhibitors as the organo-phosphate insecticides and many “nerve gases” (soman, sarin, VX).

Question 5

A patient who has been treated for Parkinson disease for about a year presents with purplish, mottled changes to her What drug i s the most l ikely cause of this cutaneous response?

A	Amantadine
B	Bromocriptine
C	Levodopa (alone)
D	Levodopa combined with carbidopa
E	Pramipexole

Question 5 Explanation:

This cutaneous response, called livedo reticularis, is characteristically associated with amantadine. Recall that this seldom-used antiparkinson drug probably works by releasing endogenous dopamine and blocking its neuronal reuptake. Livedo reticularis is not associated with levodopa (used alone or with carbidopa; c or d), nor with the dopamine agonists bromocriptine (d) or pramipexole (e; a newer and generally preferred drug for starting treatment of mild parkinsonian signs and symptoms). (You might also recall that amantadine is also used for prophylaxis of some strains of influenza virus infections. The mechanism of action in this setting is not well understood.)

Question 6

A young boy who has been treated for epilepsy for a year i s referred to a periodontist for evaluation and probable treatment of massive overgrowth of his gingival ti Some teeth are almost completely covered with hyperplastic ti ssue. Which drug was the most l ikely cause of the oral pathology?

A	Carbamazepine
B	Lorazepam
C	Phenobarbital
D	Phenytoin
E	Valproic acid

Question 6 Explanation:

For many years, phenytoin has been cited as a classic example of a drug that can cause gingival hyperplasia. (Among oral surgeons and dentists, it is often referred to as Dilantin® hyperplasia, in recognition of phenytoin’s common proprietary name.) The mechanism is unknown, but we suspect the drug alters collagen metabolism in the gingival tissues. Although phenytoin isn’t the only drug associated with potential gingival hyperplasia (verapamil is another common one), it is the only one listed as a choice. Note that phenobarbital, which is still used as an alternative to phenytoin for seizures, does not cause gingival hyperplasia. It is precisely because of the low gingival hyperplasia risk that phenobarbital is sometimes prescribed for children with responsive seizure disorders in lieu of phenytoin.

Question 7

A patient with undiagnosed coronary artery disease i s given a Shortly thereafter she develops intense tightness and “crushing discomfort” of her chest. An ECG reveals ST-segment changes indicative of acute myocardial i schemia. Which drug most l ikely caused this reaction?

A	Clozapine
B	Pentazocine
C	Phenytoin
D	Sumatriptan
E	Zolpidem

Question 7 Explanation:

The serotonin receptor agonist actions of the “triptans,” including the prototype, sumatriptan, can trigger intense vasoconstriction in various vascular beds. The cerebral vasoconstrictor effects of these drugs contribute importantly to the relief they afford in migraine headaches. However, coronary vasospasm can occur also; it may be particularly intense and potentially life-threatening in patients with coronary vasospastic disease (ie, variant or Prinzmetal angina), for whom the triptans are contraindicated. None of the other drugs listed have any significant coronary (or other) vasoconstrictor effects. Indeed, some such as phenytoin and zolpidem (a benzodiazepine-like hypnotic) may cause slight cardiovascular changes (eg, afterload reduction) that would actually reduce the degree of myocardial ischemia and the risk of angina.

Question 8

Nitrous oxide i s a common component in the technique of balanced It i s used in conjunction with such other drugs as a halogenated hydrocarbon volatile l iquid anesthetic, and usually included as 80% of the total inspired gas mixture. Which phrase best summarizes why nitrous oxide cannot be used alone for general anesthesia?

A	Almost total lack of analgesic activity, regardless of concentration
B	Inspired concentrations >10% tend to profound cardiac negative inotropic effects
C	MAC (minimum alveolar concentration) i s >100%
D	Methemoglobinemia occurs even with low inspired concentrations
E	Such great solubility in blood that i ts effects take an extraordinarily long time to develop
F	Very high frequency of bronchospasm

Question 8 Explanation:

Recall that nitrous oxide has a MAC (minimum alveolar concentration) of about 105%. Achieving that concentration in an inspired gas mixture is physically impossible at normal atmospheric pressure. Even if we could safely give pure nitrous oxide (we obviously cannot), and we rounded-off the MAC to 100%, the drug would (1) cause abolition of a painful response in only 50% of subjects (this is one element of the definition of MAC), and (2) be lethal, since 100% nitrous oxide means no (0%) oxygen at normal atmospheric pressures. This very effective analgesic gas is poorly soluble in the blood, so equilibration between alveolar and blood concentration and the onset of its central effects are quite rapid. Even at the usual concentrations (typically 80% of the inspired gas mixture), and whether used only with air (as in many aspects of dental practice) or with other inhaled agents (common in surgery), nitrous oxide causes little or no bronchospasm nor significant cardiac depression.

Question 9

A patient develops a severe and rapidly worsening adverse response to a The physician orders prompt administration of antipyretics, IV hydration, and bromocriptine or dantrolene to manage symptoms and hopefully to prevent a fatal outcome. Which drug or drug group most l ikely caused these adverse responses?

A	Benzodiazepines, especially those used as hypnotics
B	Chlorpromazine
C	Levodopa
D	Phenytoin
E	SSRIs

Question 9 Explanation:

The question described common and necessary interventions for managing neuroleptic malignant syndrome, which is characteristically associated with older antipsychotics—chlorpromazine and other “low potency” antipsychotics to a degree, but occurs more so with haloperidol (butyrophe-none). Signs and symptoms include muscle tetany/rigidity, profound fever, rapid swings of heart rate, rhythm, blood pressure (autonomic instability), electrolyte abnormalities, and dehydration. None of the other agents are associated with this syndrome, whether acutely or with long-term therapy or at therapeutic or toxic plasma levels, nor would the interventions described be indicated.ression.

Question 10

Ropinirole i s a relatively new drug that recently was approved to treat what’s commonly called restless leg syndrome (also known as Ekbom syndrome). The drug works as a dopamine receptor agonist in certain parts of the Given this mechanism of action, what other disorder i s , most l ikely, another indication for this drug?

A	Daytime anxiety
B	Hypersomnia (excessive s leepiness)
C	Parkinson disease
D	Schizophrenia
E	Status epilepticus
F	Treatment of severe pain

Question 10 Explanation:

This is a question about a drug you may not have learned about explicitly, but given the description of its mechanism, which should be quite familiar, you should have no problem arriving at the right answer. Ropinirole (a related drug is pramipexole) directly activates striatal dopamine receptors. It is one of several “dopaminergic” drugs that can be used to initiate therapy of early Parkinson disease. (With the availability of ropinirole, pramipexole, and some related drugs, we now hold-off on prescribing such older drugs as levodopa when parkinsonian signs and symptoms are in the early stages). Dyskinesias and hypotension are relatively common side effects, as also applies to alternatives such as levodopa and bromocriptine. Ropinirole also causes drowsiness or sleepiness; either would render the drug not ideal for managing daytime anxiety (a), but anxiety management is not an indication for the drug, nor is hypersomnia (b). Ropinirole’s dopaminergic action may exacerbate signs and symptoms of schizophrenia (d); like many other antiparkinson drugs it may lower the seizure threshold in patients with epilepsy, and so would be irrational for managing status epilepticus (e). It has no clinically useful analgesic activity (f)

Question 11

A patient in the neurology unit at your hospital develops status epilepticus, and at the time there i s no good information about the What drug should be given fi rst for the fastest suppression of the seizures?

A	Carbamazepine
B	Lorazepam
C	Phenobarbital
D	Phenytoin
E	Valproic acid

Question 11 Explanation:

Intravenous lorazepam is generally regarded as the drug of choice for initial treatment of status epilepticus. (It has surpassed diazepam because of a faster onset of action and less venous irritation, among other things.) Lorazepam, like the benzodiazepines in general, increases the apparent affinity of the inhibitory neurotransmitter GABA for binding sites on brain cell membranes. This increases the frequency of chloride channel opening, which then leads to inhibited target nerve activity. It is essential to note that IV lorazepam’s anticonvulsant effects are relatively short lived; if only lorazepam was given for status the seizures would stop quickly (almost immediate onset of action), but there is a great risk of seizure reappearance as the drug is eliminated quickly and blood concentrations fall (too short a duration of action). Therefore, immediately after giving the lorazepam either phenytoin or fosphenytoin should be given to provide longer seizure suppression and “coverage” because lorazepam’s effect wanes so quickly. Compared with lorazepam, phenytoin’s onset of action is too slow, but the duration of action is much longer. Why not just give phenytoin or fosphenytoin and skip the lorazepam? Recall that the longer status epilepticus persists, the greater the risk of brain damage or death. Our goal is to terminate the seizures as fast as possible. As noted above, phenytoin or fosphenytoin have onsets of action that aren’t fast enough to achieve the goal of prompt seizure suppression. Lorazepam works quickly, and that’s why we give it first. None of the other drugs listed in the question are appropriate for initial therapy of status epilepticus, despite their widespread use for oral therapy of seizure disorders long-term.

Question 12

A patient has had a documented severe allergic reaction to ester-type local What other drug i s a member of the ester class, and so would be the most l ikely to provoke an allergic or anaphylactic reaction i f this patient received i t?

A	Bupivacaine
B	Lidocaine
C	Mepivacaine
D	Pri locaine
E	Tetracaine

Question 12 Explanation:

First, a learning “trick” for how to tell whether a local anesthetic (one you’ve learned about, or not) is an ester or amide. Look at the drug’s generic name; if there are two occurrences of the letter “i” in it, it’s an amide; if not, it’s an ester. Thus, we have such esters as cocaine, chlor(o)procaine, procaine itself, and tetracaine, which is the correct answer for this question. The others I listed are amides. This may seem like a picky question, or perhaps a tricky one, if you’ve been taught the main properties of only one or two prototypic local anesthetics—eg, lidocaine as the prototype amide and prototype local anesthetic overall, procaine as the prototype of the ester class—and perhaps a third drug, benzocaine, an ester that is suitable only for topical administration because it is largely insoluble and can’t be given safelyor effectively by other routes. Nonetheless, there are a couple of important points here, and they revolve around a fundamental difference between amides and esters, and so knowing the class to which a particular local anesthetic belongs: (1) allergic reactions of various severities are more common with esters than with amides; (2) there is classe-based cross-reactivity, meaning that if a patient has had a true immunologic reaction to any ester, he or she is at risk for a similar reaction from subsequent exposure to any ester; and (3) there is no cross-reactivity between esters and amides, such that use of an amide in an “ester-sensitive” patient is not likely to pose problems of allergenicity. As a final aside, if you ask a group of people “how many of you have received Novocain before?” you’ll get a lot yes responses. And most of them will be incorrect. Novocain is the most widely known brand name for the generic drug, procaine. Truth is, procaine is such a poor local anesthetic (low potency, short duration, allergenicity, etc) in comparison with drugs like lidocaine that it’s almost never used nowadays (not available in the United States), in fact hasn’t seen much use for decades. Before then, however, it was basically the only choice when an injectable local anesthetic was needed, and the name Novocain persisted as a ubiquitous (but incorrectly applied) name for many local anesthetics that came out later. If a patient younger than about 40 years old reports a Novocain allergy, be careful how you interpret that information. Chances are good that someone inappropriately told them they were getting Novocain when the drug was actually something else. And be sure that if you’re going to give someone a dose of a local anesthetic you don’t call it Novocain when, in fact, it’ll surely be something else. Names matter.

Question 13

A 66-year-old woman i s diagnosed with Alzheimer disease, with symptoms being described as mild-to-moderate. What pharmacologic approach i s generally considered the most fruitful in terms of alleviating symptoms of early Alzheimer and probably s lowing the course of the underlying brain pathology?

A	Activate a population of serotonin receptors
B	Block dopamine release or receptor activation
C	Inhibit acetylcholinesterase
D	Inhibit MAO
E	Dissolve cerebral vascular thrombi

Question 13 Explanation:

Initial recommended therapy includes use of acetylcholinesterase inhibitors (donepezil, tacrine, galantamine, rivastigmine; all are reversible cholinesterase inhibitors). These drugs are not cures, but they appear to slow symptoms of brain neurodegeneration in some patients. None appears to be invariably superior to any other. Their actions almost certainly involve activation of central muscarinic receptors—indirectly, by inhibiting metabolism of ACh released from viable nerves, of course—in part because drugs with central antimuscarinic actions reduce their efficacy. Tacrine is noteworthy, compared with the other drugs noted in the answer, because it causes a higher incidence of cholinesterase inhibition in the periphery: more and more disturbing symptoms typical characteristic of increased (and indirect, due to cholinesterase inhibition) muscarinic effects on the gut, bladder, airways, etc. Activating serotonin receptors (a) or blocking dopaminergic effects (b) are not suitable or effective therapies for Alzheimer. Selegiline (MAO-B inhibitor, d) and high doses of vitamin E (antioxidant) apparently slow neurodegenerative processes, but so far there are no convincing data that they slow cognitive decline, and they are not first-line therapies. Thrombolytic drugs (e) are not indicated, as the signs and symptoms of Alzheimer are not due to clots or other vaso-obstructive causes.

Question 14

Trihexyphenidyl i s prescribed as an adjunct to other drugs being used to manage a patient with Parkinson What i s the most l ikely purpose or action of this drug as part of the overall drug treatment plan?

A	To counteract sedation that i s l ikely to be caused by the other medications
B	To help correct further the dopamine-ACh imbalance that accounts for parkinsonian s igns and symptoms
C	To manage cutaneous allergic responses that are so common with “typical” anti-parkinson drugs
D	To prevent the development of manic/hypomanic responses to other antiparkinson drugs
E	To reverse tardive dyskinesias i f the parkinsonism was induced by an antipsychotic drug

Question 14 Explanation:

Recall that in idiopathic parkinsonism the signs and symptoms generally reflect an imbalance between the opposing effects of dopamine and of ACh in the brain’s striatum. More specifically, dopaminergic influences are, or at least appear to be, outweighing the effects of muscarinic cholinergic activity. There are two basic ways to manage this: (1) enhance dopaminergic activity; and/or (2) diminish the central muscarinic influences. Trihexyphenidyl (and the related drug benztropine) do the latter. They cause significant antimuscarinic (atropinelike) actions in the CNS—hence, these drugs have been classified as “centrally acting antimuscarinics.” These drugs are quite lipophilic and enter the CNS well (this accounts for the drug’s marked sedative effects, too) to block muscarinic receptors there. That helps adjust the dopamine-ACh imbalance that appears to be a main biochemical underpinning of parkinsonism. Diphenhydramine can be used instead of trihexyphenidyl or benztropine, but it causes more drowsiness in most patients. Nonetheless, none of these drugs is used to counteract CNS depression caused by other antiparkinson drugs. Diphenhydramine does help alleviate cutaneous allergy symptoms (eg, urticaria; d), but those are rare with any of the common antiparkinson drugs (I did not specify which “other” drug was given). None of these drugs affect manic/hypomanic episodes that might occur with, say, high doses of levodopa. They do not reverse antipsychotic-induced tardive dyskinesias (e); no drug does that effectively

Question 15

A few years ago the FDA granted approval to market a new prescription drug (“drug X”) that will be administered in the form of a dermal patch (apply the patch to intact skin, the drug i s absorbed from there). Drug X belongs to a very old class of drugs that, when given by i ts usual route, orally, can interact with foods such as cheese and processed meats (and certain breads, other foods, and alcoholic beverages) leading to an interaction that can elevate blood pressure to severe and sometimes fatal levels. After more than a decade of testing, the FDA approved i ts use for adults. In i ts lowest dose, no dietary restriction(s) are required. Based on this information, how i s drug X most l ikely classified and what i s i ts most l ikely cl inical use?

A	Amphetamine-like agent for ADD/ADHD
B	Barbiturates used for daytime anxiety
C	Benzodiazepine for anxiety and s leep
D	MAO inhibitor for depression
E	Morphine-like analgesic for severe/chronic pain

Question 15 Explanation:

Many drugs (but not amphetamines, a; barbiturates, b; benzodiazepines, c; or morphine or related opioid analgesics, e) participate in significant interactions with certain foods or beverages. However, when you read phrases along the lines of those noted in the question—“severe and sometimes fatal hypertension from consuming such foods as cheeses and processed meats”—you should automatically be thinking of the older, nonselective (MAO A/B) monoamine oxidase inhibitors. These drugs have been used for severe hypertension or depression, but due to the potentially lethal interactions with tyramine-containing foods or beverages, their use has dwindled because the risks were too great. (Nonetheless, you need to know your pharmacology for such drugs as pargyline, phenelzine, and tranylcypromine.) Recall that tyramine is a catecholamine-releasing drug with sympathomimetic actions in its own right. When we consume tyramine-rich foods or beverages much of that sympathomimetic is metabolized by hepatic MAO before it reaches the systemic circulation (first-pass metabolism), and so its effects are slight. In the presence of a nonselective MAO inhibitor, however, the metabolic inactivation does not occur and significant amounts of the drug reach the circulation to cause more intense and potentially very intense effects that involve adrenergic receptor activation. In addition, catecholaminergic (eg, adrenergic) nerves in the MAO-treated patient can be considered “loaded” with an abundance of the neurotransmitter due to inhibited intraneuronal metabolism of the neurotransmitter. Although the neurotransmitter may not be released physiologically, in response to an action potential (at least in the peripheral sympathetic nervous system), it can be released by such drugs as tyramine or by such drugs as pseudoephedrine and ephedrine (mixed-acting sympathomimetics) or amphetamines (indirect-acting sympathomimetics), which can then trigger possibly fatal hypertensive crisis, profound cardiac stimulation, and the consequences thereof. These problems led to the development of MAO inhibitors (eg, selegiline) that have preferential effects on MAO in the brain (MAO-B) and far less an effect on MAO forms in the liver and peripheral nervous system (MAO-A). Nonetheless, as stated in the question, there is a new nonselective MAO inhibitor that has just been approved for use, for depression, in the form of a transdermal delivery system (skin patch).

Question 16

The pediatrician writes a prescription for a combination (of several drugs) product that contains dextromethorphan, which i s an i somer of a codeine The patient i s a 12-year-old boy. What i s the most l ikely purpose for which the drug was prescribed?

A	Control mild-moderate pain after the lad broke his wrist playing soccer
B	Manage diarrhea caused by food-borne bacteria
C	Provide sedation because the child has ADD/ADHD
D	Suppress severe cough associated with a bout of influenza
E	Treat nocturnal bed-wetting

Question 16 Explanation:

Dextromethorphan is, indeed, chemically related to codeine, but it lacks many effects you probably associate with codeine or other opioids, except one: it has excellent antitussive activity. This cough-suppressant effect presumably occurs via some ill-defined central mechanism, but does not involve agonist actions on opioid receptors. (Some have speculated that the mechanism involves suppression of the afferent limb of the 10th cranial nerve, but don’t memorize that!) Dextromethorphan does not have analgesic effects (a); alter gut motility (b); or have effects on the bladder musculature that might relieve nocturia. Very high doses of dextromethorphan can cause CNS depression, but regardless of the dose it is not used as a sedative or other agent for controlling symptoms of ADD/ADHD. Finally, unlike codeine and most other opioids, dextromethorphan lacks significant addictive properties or potential.

Question 17

Many legal jurisdictions have imposed various restrictions on over-the-counter sale of products, mainly oral decongestants, that contain That i s because pseudoephedrine can be rather easily used to synthesize which highly psychoactive and abuse-prone drug?

A	Methamphetamine
B	Morphine
C	Oxycodone
D	Pentazocine
E	Phencyclidine (PCP)

Question 17 Explanation:

Whether you have learned or read about this specifically in a pharmacology class or text, for medicolegal and societal (and board-related?) reasons you should be aware of the growing problem of illicit “meth labs” that use pseudoephedrine (“pseudo”) as the starting point for a rather easy chemical synthesis of this highly addictive and dangerous CNS stimulant. None of the other drugs listed can be synthesized using this common indirect-acting sympathomimetic as a starting point

Question 18

The anesthesiologist prepares to administer several drugs to a patient as part of normal pre- and intraoperative What drug lacks, as i ts normal spectrum of action, the ability to cause generalized CNS depression or the patient’s level of consciousness, or lacks any intrinsic analgesic effects?

A	Droperidol
B	Midazolam
C	Vecuronium
D	Propofol
E	Thiopental

Question 18 Explanation:

Vecuronium is a curare-like nondepolarizing neuromuscular blocker that is used to induce or maintain skeletal muscle paralysis for surgery. (Your learning may have focused on vecuronium; the two drugs, and indeed all other drugs with “curonium” or “curine” in the generic name are similar.) It has no effects on brain functions such as levels of consciousness or sensations such as of pain. The drug prevents activation of nicotinic receptors on skeletal muscle (it is a competitive antagonist), thereby preventing myocyte depolarization and other elements of normal skeletal muscle activation and ultimately causing flaccid paralysis. The onset and duration of this effect depends on the actual drug being administered. Droperidol (a) is a haloperidol-like neuroleptic drug. It causes drowsiness and sedation in its own right. In some instances it is administered with fentanyl to cause neurolept analgesia (a calming effect, indifference to pain and surroundings); or with fentanyl and nitrous oxide for greater pain control (neurolept anesthesia). However, droperidol does not have any clinically useful intrinsic analgesic effects. A limitation to using droperidol for any purpose is its tendency to prolong ventricular repolarization, which renders patients with “long QT syndrome”) at risk of serious arrhythmias (especially torsades). Midazolam (b), propofol (d), and thiopental (e), when given intravenously, cause prompt sedation or loss of consciousness (dose-dependent) and can be used for such purposes as induction of anesthesia or sedation; some are used for a variety of purposes (patients on ventilators, those undergoing endoscopy, or other noninvasive procedures). These drugs lack intrinsic analgesic effects, and should not be used alone for pain control.

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II. Preview all questions below

1.A patient i s transported to the emergency A friend who accompanies the patient says “he was experimenting with ‘angel dust’”. What best describes the actions or other characteristics of this recreational drug, more properly know as phencyclidine?

Causes i ts peripheral and central effects via antimuscarinic properties
Causes s ignificant withdrawal symptoms
Has strong opioid receptor-activating activity
Has amphetamine-like properties and i s an hallucinogen
Overdoses should be treated with flumazenil

2. Package inserts for a drug caution against administering i t concurrent with any other drug that can raise or lower sodium The ri sks are inadequate or excessive effects of the drug, depending on the direction in which sodium concentrations change. This, of course, requires cautious use or avoidance (i f possible) of the common diuretics. To which of the following drugs does this caution or warning apply?

Cholestyramine
Li thium (eg, l i thium carbonate)
Nifedipine
Phenylephrine
Statin-type cholesterol-lowering drugs

3. A 31-year-old woman has been treated with fluoxetine for 5 She i s diagnosed with another medical problem and receives one or more drugs that, otherwise, would be suitable and probably problem-free. She i s rushed to the ED with unstable vi tal s igns, muscle rigidity, myoclonus, CNS i rri tability and altered consciousness, and shivering. What add-on drug(s) most l ikely caused these responses?

Codeine for cough
Loratadine for seasonal allergies
Midazolam and fentanyl, used to ease discomfort from endoscopy
Sumatriptan for migraine
Zolpidem for short-term insomnia

4. A 72-year-old woman with a long history of anxiety that has been treated with diazepam decides to triple her daily dose because of increasing fearfulness about “environmental ” Two days after her attempt at self-prescribing, she i s found extremely lethargic and nonresponsive, with markedly obtunded reflexes and reactions to painful stimuli. Respirations are 8/min and shallow. What drug should be given to reverse these s igns and symptoms?

Dextroamphetamine
Flumazenil
Naltrexone
Physostigmine
Pralidoxime

5. A patient who has been treated for Parkinson disease for about a year presents with purplish, mottled changes to her What drug i s the most l ikely cause of this cutaneous response?

Amantadine
Bromocriptine
Levodopa (alone)
Levodopa combined with carbidopa
Pramipexole

6. A young boy who has been treated for epilepsy for a year i s referred to a periodontist for evaluation and probable treatment of massive overgrowth of his gingival ti Some teeth are almost completely covered with hyperplastic ti ssue. Which drug was the most l ikely cause of the oral pathology?

Carbamazepine
Lorazepam
Phenobarbital
Phenytoin
Valproic acid

7. A patient with undiagnosed coronary artery disease i s given a Shortly thereafter she develops intense tightness and “crushing discomfort” of her chest. An ECG reveals ST-segment changes indicative of acute myocardial i schemia. Which drug most l ikely caused this reaction?

Clozapine
Pentazocine
Phenytoin
Sumatriptan
Zolpidem

8. Nitrous oxide i s a common component in the technique of balanced It i s used in conjunction with such other drugs as a halogenated hydrocarbon volatile l iquid anesthetic, and usually included as 80% of the total inspired gas mixture. Which phrase best summarizes why nitrous oxide cannot be used alone for general anesthesia?

Almost total lack of analgesic activity, regardless of concentration
Inspired concentrations >10% tend to profound cardiac negative inotropic effects
MAC (minimum alveolar concentration) i s >100%
Methemoglobinemia occurs even with low inspired concentrations
Such great solubility in blood that i ts effects take an extraordinarily long time to develop
Very high frequency of bronchospasm

9. A patient develops a severe and rapidly worsening adverse response to a The physician orders prompt administration of antipyretics, IV hydration, and bromocriptine or dantrolene to manage symptoms and hopefully to prevent a fatal outcome. Which drug or drug group most l ikely caused these adverse responses?

Benzodiazepines, especially those used as hypnotics
Chlorpromazine
Levodopa
Phenytoin
SSRIs

10. Ropinirole i s a relatively new drug that recently was approved to treat what’s commonly called restless leg syndrome (also known as Ekbom syndrome). The drug works as a dopamine receptor agonist in certain parts of the Given this mechanism of action, what other disorder i s , most l ikely, another indication for this drug?

Daytime anxiety
Hypersomnia (excessive s leepiness)
Parkinson disease
Schizophrenia
Status epilepticus
Treatment of severe pain

11. A patient in the neurology unit at your hospital develops status epilepticus, and at the time there i s no good information about the What drug should be given fi rst for the fastest suppression of the seizures?

Carbamazepine
Lorazepam
Phenobarbital
Phenytoin
Valproic acid

12. A patient has had a documented severe allergic reaction to ester-type local What other drug i s a member of the ester class, and so would be the most l ikely to provoke an allergic or anaphylactic reaction i f this patient received i t?

Bupivacaine
Lidocaine
Mepivacaine
Pri locaine
Tetracaine

13. A 66-year-old woman i s diagnosed with Alzheimer disease, with symptoms being described as mild-to-moderate. What pharmacologic approach i s generally considered the most fruitful in terms of alleviating symptoms of early Alzheimer and probably s lowing the course of the underlying brain pathology?

Activate a population of serotonin receptors
Block dopamine release or receptor activation
Inhibit acetylcholinesterase
Inhibit MAO
Dissolve cerebral vascular thrombi

14. Trihexyphenidyl i s prescribed as an adjunct to other drugs being used to manage a patient with Parkinson What i s the most l ikely purpose or action of this drug as part of the overall drug treatment plan?

To counteract sedation that i s l ikely to be caused by the other medications
To help correct further the dopamine-ACh imbalance that accounts for parkinsonian s igns and symptoms
To manage cutaneous allergic responses that are so common with “typical” anti-parkinson drugs
To prevent the development of manic/hypomanic responses to other antiparkinson drugs
To reverse tardive dyskinesias i f the parkinsonism was induced by an antipsychotic drug

15. A few years ago the FDA granted approval to market a new prescription drug (“drug X”) that will be administered in the form of a dermal patch (apply the patch to intact skin, the drug i s absorbed from there).

Drug X belongs to a very old class of drugs that, when given by i ts usual route, orally, can interact with foods such as cheese and processed meats (and certain breads, other foods, and alcoholic beverages) leading to an interaction that can elevate blood pressure to severe and sometimes fatal levels. After more than a decade of testing, the FDA approved i ts use for adults. In i ts lowest dose, no dietary restriction(s) are required.

Based on this information, how i s drug X most l ikely classified and what i s i ts most l ikely cl inical use?

Amphetamine-like agent for ADD/ADHD
Barbiturates used for daytime anxiety
Benzodiazepine for anxiety and s leep
MAO inhibitor for depression
Morphine-like analgesic for severe/chronic pain

16. The pediatrician writes a prescription for a combination (of several drugs) product that contains dextromethorphan, which i s an i somer of a codeine The patient i s a 12-year-old boy. What i s the most l ikely purpose for which the drug was prescribed?

Control mild-moderate pain after the lad broke his wrist playing soccer
Manage diarrhea caused by food-borne bacteria
Provide sedation because the child has ADD/ADHD
Suppress severe cough associated with a bout of influenza
Treat nocturnal bed-wetting

17. Many legal jurisdictions have imposed various restrictions on over-the-counter sale of products, mainly oral decongestants, that contain That i s because pseudoephedrine can be rather easily used to synthesize which highly psychoactive and abuse-prone drug?

Methamphetamine
Morphine
Oxycodone
Pentazocine
Phencyclidine (PCP)

18. The anesthesiologist prepares to administer several drugs to a patient as part of normal pre- and intraoperative What drug lacks, as i ts normal spectrum of action, the ability to cause generalized CNS depression or the patient’s level of consciousness, or lacks any intrinsic analgesic effects?

Droperidol
Midazolam
Vecuronium
Propofol
Thiopental

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