(b) ventricular arrythmias are the life threatening ones, and lidocaine is particularly effective for this kind of arrhythmia when given parenterally in an emergency situation. It has a very rapid onset of action when given IV, which is obviously important in an
emergency. The others all also have antiarrythmic action, mostly used for supraventricular tachyarrythmias

(b) the issue is obviously that the patient may bleed excessively, a situation that would cause problems during dental surgical procedures. Dentist should consult with the patient’s physician about stopping the Coumadin for a few days. Options (a) and (e) might be appropriate in an emergency situation, but that is not what we are dealing with here. Option (c) would take longer to reduce (PT) than just stopping the Coumadin. Finally, heparin is not a Coumadin antagonist, but an anticoagulant in its own right.
Guidelines into what adjustments to make in Coumadin therapy prior to dental treatment have changed since this type of question was written – the safest bet is to consult physician – depending on patient’s status, it could be that no adjustment should be made at all, certainly not for minor surgery anyways.

(b) the rule is ..04 mg of epi max in CV patients. The easiest way to figure this one out is to remember you shouldn’t give more than 2.2 carpules of xylocaine with 1:100,000 epi – your usual choice as a local anesthetic. Two carpules is 3.6 cc. This eliminates options (c) and (d), since they would be safe but not maximal. Since 1:50,000 is twice as concentrated as 1:100,000, 1 cc of 1:50,000 (option (a)) is the same as 2 cc of 1:100,000 so still not close to max, so (b) has to be the right answer. Of course, you could have just remembered, 1:100,000 equals .01 mg per cc, so 1:50,000 equals .02 mg per cc, so (b) would equal the max of .04 mg.

(a) memorize, memorize. Most are anticonvulsants, but diazepam is drug of choice. Chlorpromazine is an antipsychotic, not an anticonvulsant. Phenytoin, is an anticonvulsant, and is one of the answers to the question “which of the following causes gingival hyperplasia?” Don’t forget diazepam is also given for antianxiety and sedation.

(a) enteral means via GI tract-only route listed that goes directly into GI tract is (a) oral.

(e) propranolol is the prototype nonspecific beta adrenergic receptor blocker. In angina, the goal is to reduce the oxygen demands of the heart, since it can’t get enough. (a) and (b) are useful actions in angina, but are the way that nitroglycerin and calcium channel blockers work, not propranolol, which acts to decrease cardiac output and contractility (so (c) is obviously wrong- this is an action that is needed in heart failure patients, not angina)

(a) bradycardia is a reflexive slowed heart rate, controlled by vagal input to the heart, and is cholinergically mediated, which means you need a cholinergic receptor blocker to reduce the vagal effect. Atropine is the only drug listed which is a cholinergic agent. They threw in epinephrine as a tease, because if you knew bradycardia was cardiac slowing, you might be tempted to think epi, which usually speeds up the heart, would be the right answer- but you’ve got to block the vagal input, epi won’t work.

(a) nonionized forms of drugs cross membranes more readily and are highly lipid soluble, and tend to get stored in fat tissue from where they are only slowly released. Thus highly ionized drugs, which are less lipid soluble don’t get stored in fatty tissue and are
subject to more rapid excretion.

(c) one of the things you had to memorize about atropine, the prototype anticholinergic drug was don’t use it with glaucoma patients, as it will increase intraocular pressure, which is already the problem with glaucoma patients. Drugs in categories (b) and
(d) are actually used to treat glaucoma, so they are obviously not contraindicated. Obviously, (a) wouldn’t help either.

(c) platelet aggregation is controlled by two factors, prostacyclin, which decreases it, and thromboxane, which enhances it. Low dose aspirin blocks the latter, so (c) is right, (a) is the mechanism of action of corticosteroid drugs, (d) is the mechanism of action of
anticoagulant drugs like coumadin.

(b) memorize – this is the sign you look for to tell the patient is adequately sedated.

(b) even if you didn’t know that nitrous can alter the patient’s sense of reality (that’s why you don’t give it alone in your office, they might fantasize that you had your way with them when you didn’t!) by elimination (b) has to be the right answer since (a) and (c) are indications for the use of nitrous

(d) for bronchodilation you want a potent beta-2 adrenergic receptor agonist- of the drugs listed (d) is the best. Isoproterenol is a nonspecific beta agonist. Methoxamine and phenylephrine are alpha- 1 agonists, amphetamine is an indirect acting agonist that causes the release of norepinephrine, which is less potent at beta receptors than isoproterenol.

(c) Neuromuscular transmission requires the action of acetylcholine at the nicotinic receptors on the neuromuscular junction endplate. The two drugs used clinically to do this are curare and succinylcholine. Curare is a nicotinic receptor blocker, succinylcholine acts to overstimulate the receptor, thereby causing its subsequent depolarization of the neuron and a block of muscle activity. (e) is how spider venoms and snake toxins work, not succinylcholine. (a) would enhance neuromuscular action, and is actually made use of clinically with myasthenia gravis patients. (d) isn’t possible.

(c) the only definition which covers all three drugs. (a) applies only to pentobarbital, (b) applies only to meperidine, and (d) applies only to diazepam.

(b) obviously – drug has to be absorbed before any of the other actions can take place. The others would determine duration of action, not onset.

(b) they ask a variant of this question every single year, so I would suggest you look at the many different wordings of this question and know that they are just testing the factoid that inflamed tissue has a lower pH, which results in reduced availability of the free base form needed to cross the neural membrane.

(a) if its excreted or detoxified, it ain’t going to get to its active site to have an effect. Same if it is bound to plasma proteins – it has to be free to get distributed to active site

(b) most likely because it is titratable and thus can be used to provide just enough of an effect to calm the anxious child. (c), (d), and (e) are sedative regimens that would probably induce deeper sedation than nitrous, and that much sedation doesn’t seem to be called for here. Naloxone is a drug used to reverse the effects of too much morphine.

(c) Titratability is the primary advantage of iv drug administration. Onset is very fast, not gradual, since it doesn’t have to be absorbed, so (d) is out. (a) and (b) are not possible.

(c) this is the exception, since the purpose of drug metabolism is to change the drug into an excretable form, which is water soluble, ionized. Making it lipid soluble and nonionized would make it stay longer in the body. The other statements are true.

(b) memorize, memorize. Buspirone is used to relieve anxiety – it is not a benzodiazepine like diazepam and alprazolam (BDZs may not be that sedating, but can cause impairment of psychomotor skills), and not a strong sedative like chloral hydrate

(c) vitamin K is stored in the liver – this is decreased by cirrhosis – the result is deficiencies in prothrombin dependent coagulation factors

(d) locals don’t have actions (a), (b), or (c)! Nervous patients, however, do salivate more.

(c) a sympathomimetic drug is going to potentially activate both alpha and beta receptors, so you would need a pairing of drugs which blocks those receptors. Prazosin, an alpha-1 blocker, and propranolol, a non-specific beta-blocker, are the only pair that block both types sympathetic/adrenergic receptors. Atropine is a muscarinic blocker (anticholinergic), phenoxybenzamine is an alpha-blocker, but curare is a neuromuscular junction blocker. Amphetamine is a sympathomimetic drug, not a blocker or sympatholytic drug.

(b) same drugs just different salts, which primarily affects absorption from GI tract. Pen G, due to lousy absorption when taken orally, is usually injected. Pen G is hardly used in dentistry anymore, so we would expect these kinds of questions to disappear.

(d) since you use tetracycline everyday, you have committed all this stuff to memory, right? We would hope, since hardly anyone outside periodontists hardly uses tetracyclines anymore in dentistry that they would not ask you a lot of questions about tetracyclines, but if they do, you’re ready, right?

(d) because it will also cause the anticholinergic effect of mydriasis, or papillary dilation

(a) ah, the classic cocaine is a local anesthetic question! So once again, all locals except for cocaine are vasodilatory, that’s why most require the addition of epinephrine.

(d) If you need to get some antibiotic in the crevicular fluid, tetracycline is apparently the one – must be something to do with gums, since periodontists use tetracyclines a lot.

(b) memorize that list of opioid analgesic potencies. It would go propoxyphene

(d) by process of elimination: herpangina is a viral condition, angina pectoris is heart pain caused by lack of oxygen, apthous stomatitus is canker sores – these are not the result of a bacterial infection, so that leaves (d) gingivitis

(d) each one of these drugs has a side effect that they may use in the stem of this question, and give you the same list of drugs: the effects are polymixin- renal necrosis, chloramphenicol- bone marrow depression, amphotericin B –nephrotoxicity

(c) efficacy sounds like it might have something to do with effect, doesn’t it? Didn’t I make you memorize potency vs. efficacy? Potency is how much drug does it take to produce an effect, and efficacy is now much of an effect is a drug capable of producing.

(c) if you are addicted to formaldehyde, you are dead! Same with the others.

(a) xerostomia is an anticholinergic effect. All the drugs listed except opioids are unfortunately strongly anticholinergic, in addition to their desired mechanism of action.

(d) BDZs are better than narcotics or barbiturates because they don’t cause anywhere near the problem with respiratory depression that those two do. Phenothiazines have more side effects.

(c) naloxone is an example of a “pure” competitive receptor antagonist – such a drug binds to a receptor with high affinity, but has no intrinsic activity. If it did it would be an agonist.

(a) why would you care which one is the least likely? Actually, because if it binds covalently, that is a non-reversible situation that can’t be overcome – you get a long-lasting drug effect that can only be overcome by making new receptors. Some antagonists work this way.

(a) easy – the only “transmitter” listed is acetylcholine. You don’t have to have any idea what the question is about (I don’t!) as long as you recognize that there is only one transmitter listed – the others kinda sound the same – cholinesterase is the enzyme that breaks acetylcholine down, acetylsalicylic acid is aspirin, have no idea what hydroxycholine is

(a) miconazole and amphotericin B you should recognize, I hope, as antifungals, so your choice is between (a) and (b). Novobiocin sounds like an antibiotic, which it actually is, so guess (a)

(c) mydriasis is papillary dilation, which is a hallmark effect of anticholinergic drugs, and why they are used in eye exams

(a) see the words “definitely” and CONTRAINDICATED – why do you think they worded it that way? This means worst case scenario, which would be someone who has had an anaphylactic reaction to penicillin, which is an immediate type reaction

c) this is one of those questions where they give you five drugs as possible answers, and can create 5 different questions just by changing the question regarding mechanism of action. So (a) is an alpha-1 blocker, (b) alpha-2 agonist that decreases sympathetic outflow from CNS, (d) is a direct acting vasodilator, and (e) is a type I calcium channel
blocker

(c) hey, this is the question everybody missed on the exam! Don’t you wish you had learned it then?

(d) So they don’t get hypokalemia

(d) they all sound pretty serious, don’t they. I mean hypotensive shock, liver damage, cancer, stroke, immunosuppression – fortunately only (d) is a real risk with oral contraceptive therapy – would you take one if you were gonna get all of those bad things?

(a) these are all opioid receptors – only mu and kappa are involved in analgesia, mu at the supraspinal level and kappa at the spinal level (the receptor that pentazocine (Talwin), the mixed acting agonist/antagonist acts on

(a) you are looking for an ester – ester pairing. Only (a) meets this criterion. procaine, benzocaine and tetracaine are esters, lidocaine, prilocaine and mepivacaine are amides. Amides, unlike esters are not by rule cross-allergenic

(c) memorize this picky little fact please!

(e) They will ask you questions about drugs that you don’t normally use every day. Actions a, c, and d are all clinically useful actions of the phenothiazines, which you might remember were discussed under the category of antipsychotic drugs. But wait- Promethazine (Phenergan) is used in dentistry as a sedative, often in combination with Demerol because it reduces the nausea associated with the use of the opioid and also potentiates its analgesic effect, allowing lower dose to be used, thus again reducing the potential for adverse side effects. Alpha adrenergic effects are an adverse side effect.

(c) It does not act via (a), which is how cromolyn (Intal) works, or by (d) which is how antihistamines work.

(b) candidiasis is a fungal infection that needs to be treated with an antifungal agent like nystatin. (a) and (c) are antiviral drugs used to treat HIV, while chlorhexidine is a antimicrobial mouthwash

(c) antibiotic therapy won’t be very effective if you don’t incise and drain first. (a) and (b) are palliative actions the patient can take at home, not actions for the dentist.

Remember, cocaine is an indirect acting adrenergic agonist, acting by causing the release of adrenergic neurotransmitters as well as blocking their reuptake, thereby prolonging their activity. The other drugs listed are just local anesthetics that don’t have this action – they just block sodium influx into the neuron.

(d) Patients using corticosteroids for arthritis often develop ulcers because these drug block prostaglandin action in the stomach, thereby increasing acid secretion while decreasing the protective mucosal barrier of the stomach.

(d) the first three are all signs that the patient is getting too much nitrous.

(b) sedation does not decrease the local anesthetic requirement, the patient will still feel pain. Sedatives, with the exception of nitrous oxide, have no analgesic effect -barbiturate sedatives may make the patient more sensitive to pain.

(b) only benzodiazepines are actually classified as antianxiety drugs, although other drugs, such as opioids have antianxiety actions in addition to their other clinically useful actions. (b) lorazepam is the only BDZ listed. Methohexital is a barbiturate – these are classified as sedatives. Haloperidol is an antipsychotic, pentazocine an opioid, and phenylpropanolamine is a decongestant used in cold medications.