(d) – (a) is wrong- botulinum toxin does this. (b) is wrong – hemicholinium works this way. (c) is wrong – ACh is broken down almost instantaneously, so it is almost impossible to enhance its destruction. (e) is wrong-these drugs don’t have any actions of their own, they just prevent ACh effects by blocking receptors: atropine and propantheline are postganglionic muscarinic receptor blockers-thus the answer is (d).

(b) – neostigmine is a cholinesterase inhibitor like physostigmine. These differ from the insecticides and nerve gases listed below in that they are reversible and can be used clinically; the latter are irreversible.

(d) memory – you and the bugs die from too much cholinergic stimulation

(3) drugs which potentiate cholinergic stimulation can do so by being either direct acting cholinergic agonists, acting on the cholinergic receptor, or by indirectly increasing the duration of action Ach by preventing its enzymatic degradation. Methacholine and pilocarpine are direct-acting cholinergic agonists, whereas neostigmine acts indirectly. Scopolamine is a muscarinic antagonist like atropine, and will reduce or block cholinergic action via direct receptor antagonism. Pralidoxime is a chemical antidote used to regenerate AchE after nerve gas or insecticide exposure.

(c) see above! What you need in this situation is a chemical that will help regenerate AchE that has been bound irreversibly by the organophosphate insecticide or nerve gas. Pralidoxime does just that – it knocks the insecticide off the enzyme, allowing it to again be able to break down Ach. As for the other alternatives: atropine is a competitive muscarinic cholinergic receptor blocker, phenytoin is an anticonvulsant, propantheline isProBanthine, an synthetic atropine like drug used to dry salivation and as an antispasmodic agent, and Phenobarbital is a barbiturate anticonvulsant. We listed the anticonvulsants to throw you off since you think that some one might experience convulsions after organophosphate exposure

(c) ganglionic blockers, being so unspecific in their action (they would have both anticholinergic and antiadrenergic action) aren’t used clinically anymore, so I wouldn’t think they would still ask you about them, but if you must know… mecamylamine, hexamethonium, etc. are ganglionic blockers. Curarine is a nicotinic receptor blocker that causes muscular paralysis, edrophonium is an anticholinesterase used to treat myasthenia gravis, succinylcholine is a depolarizing neuromuscular junction blocker used for short term paralysis, gallamine is another long acting neuromuscular junction blocker for paralysis. Remember, these paralysis producing drugs all act via nicotinic receptor at the neuromuscular junction – some , like curare, are competitive receptor blockers, while the other class, like succinylcholine, are called depolarizing blockers – they don’t themselves block the nicotinic receptor from being stimulated b y curare, but stimulate the receptor so much that it depolarizes, and while in this state it cannot be stimulated by the Ach and thus paralysis results.

(c) this is the reverse of question 2 in the preceding column

(b) the action will be prolonged because neostigmine prevents its breakdown by AchE! Its action would be blocked by atropine or scopolamine

(e) a strange and amazing truth! Denerevated means the skeletal muscle is not receiving neural input, and thus stimulating a cholinergic neuron to release Ach which would then stimulate the NMJ can’t happen. But if you inject a drug
which can stimulate the nicotinic receptors directly then you can see an effect on the muscle. Neostigmine is one of those anticholinesterases that can act like Ach at nicotinic receptors, in addition to prolonging the action of Ach itself by blocking the acetylcholinesterase that is trying to break the Ach down.

(e) What is needed is a skeletal muscle relaxant. This requires a drug that acts at the neuromuscular junction. Of those listed, only succinylcholine (e) is in this category. (a) atropine is a cholinergic (Muscarinic) receptor blocker, (b) epinephrine is an adrenergic agonist, and (c) diazepam is a benzodiazepine, and (d) is an anticholinesterase.

(c) salivation is typically considered to be a cholinergic response. Xerostomia is too little saliva and thus one could use a cholinergic agonist to stimulate more saliva secretion (assuming there is functional salivary gland tissue, which may not be the case in patients that have been subject to radiation therapy!) From the list, only neostigmine would produce a cholinergic effect, since it is an indirect acting cholinergic agonist. Of the others, atropine and scopolamine are cholinergic antagonists, and are actually used to reduce salivation, mecamylamine is a ganglionic blocker (not the action we desire, too non-specific, and a blocker at that!). Ephedrine is a mixed acting adrenergic agonist.

(d) I guess since Dentists deal with so much spit, they think this kind of question should be on every test! Again, if you wish to reduce salivation, you want to give a drug that has an anticholinergic action. The usual suspects, atropine and scopolamine are not in this list, so it’s not so easy. So what can you remove by elimination? Well, that depends that you know what some of the other drugs are, doesn’t it? Diazepam is valium, and while it will reduce your patient’s anxiety, it doesn’t do much to make them stop salivating – might even make it worse like the barbiturate sedatives do! Promethazine is an antihistamine used for IM sedation. Looks to me so far that they have thrown in a lot of drugs used in a sedation context, and expect you to know which one is in the mix to control salivation. Physostigmine is an anticholinesteras – why is that in this list? Diphenhydramine is Benadryl, a very sedating antihistamine that is used as a sedation agent. In a previous question I discussed propantheline as Pro-Banthine, a synthetic atropine type drug – so this would work to dry up the oral cavity. What I don’t like about this question is that the antihistamines are also anticholinergic and will have a drying action. I guess the distinction from propantheline is that it doesn’t cause sedation, so is more selective for just drying up excessive salivation – so if you want only that effect and not the sedative action as well, a drug like propantheline is better.

(b) well, this is just the opposite way of asking what was asked in the other questions given here! If anticholinergic agents are useful to reduce salivation, only an idiot couldn’t figure out that a cholinergic agent would be useful to induce salivation!

(3) you are probably thinking, who the hell ever heard of meprobamate and methantheline, or for that matter, chlorpromazine! Well, these are drugs that may have been useful in the olden days, but would be probably replace in this
type of questions by more modern equivalents. But of course you should figure out that atropine (b), being the prototype anticholinergic drug has to be one of the answers. So option 5 has to bee incorrect, since it does not include atropine. Now only the most corrupt dentist would prescribe codeine to reduce salivation, so #4 should also be incorrect – that leaves 1, 2, or 3. So see, you didn’t even have to recognize that chlorpromazine is an antipsychotic drug. So what is meprobamate – if we can eliminate that one then we are down to only option 3 as a possible answer. Meprobamate happens to be an antianxiety, skeletal muscle relaxant drug sometimes used by dentists to treat muscle spasms associated with TMD – also has use for external sphincter spasticity – imagine! But it doesn’t seem to have anticholinergic activity that is significant enough to cause significant reduction of saliva. Methantheline, in contrast, is Banthine, a synthetic version of atropine! So option 3, atropine and methantheline are the drugs for this purpose.

(d) a ganglionic blocker, since it acts by preventing cACh from stimulating nicotinic receptors at the ganglia level will have both anticholinergic and antiadrenergic effects. Options a, b, c, and e are symptoms of cholinergic stimulation, and thus can’t be right. Option (d), the remaining answer, is an antiadrenergic effect, arising from decreases in sympathetic tone to the vasculature

(b) – Atropine and scopolamine are muscarinic cholinergic receptor blockers. Just knowing that eliminates all the alternatives except (b). But you should also remember that heart rate is kept under tight reflexive control: any sudden increase in HR usually stimulates baroreceptors to send a signal to the vagus nerve to stimulate the heart to slow it back down. This reflex is cholinergically mediated, and will be blocked by cholinergic blockers such as atropine. Even when given in the absence of higher than normal heart rate, atropine will block the normal cholinergic control over the heart, leaving the sympathetic system in charge with a resulting tachycardia.

(a) – The first thing you have to know is that a cholinomimetic drug is one that mimics the action of acetylcholine, the endogenous neurotransmitter in the parasympathetic or cholinergic nervous system. The acronym for remembering the effects of cholinergic stimulation is SLUD, or increased salivation, lacrimation, defecation, and urination. The heart is the exception in that activity or heart rate is decreased (bradycardia)- thus since the question asks for an effect which does not occur with cholinergic stimulation, that leaves (a) as the only possibility. Miosis, not mydriasis, occurs with cholinergic stimulation.

(d) because succinylcholine (SUX) is an agonist at nicotinic receptors, so the initial response is muscle stimulation. But the NMJ rapidly depolarizes due to the inability of the plasma cholinesterase to break down the SUX, which isjust two molecules of acetylcholine fused together – the other information has no relevance unless you’re just stuck thinking “gee, I know that SUX has something to do with autonomics but not sure exactly what!”

(5) scopolamine is an anticholinergic drug, and thus will have effects like atropine – effects opposite to those observed from cholinergic stimulation. Remembering SLUD doesn’t work here, though, since none of the responses involve SLUD type reactions. You can memorize the list of therapeutic uses of anticholinergic drugs (easiest way, since the list corresponds roughly to the list in this question, so therefore you should be prepared for any other type of question like this)

(d) organophosphates kill you from too much cholinergic stimulation (SLUD). Option (a) is from nicotinic receptor stimulation, (b) and (c) and (e) are also cholinergic stimulation. Option (d) is an atropine, anticholinergic type reaction and thus doesn’t fit the pattern of responses given.

(e) basically the same question as the preceding question, they just changed organophosphate insecticides to neostigmine. The difference is that neostigmine is a reversible anticholinesterase, whereas insecticides are irreversible. But again, the question just basically wants you to recognize two things – that neostigmine is an indirect acting cholinergic drug and then know what the symptoms of cholinergic stimulation are. But even if you didn’t know those facts you might be able to get if you remember that neostigmine is a drug that is used to reverse the skeletal muscle paralysis produced by drugs of the curare class – the non-depolarizing neuromuscular junction blockers (you did remember this right?)

(2) glandular secretions are generally under cholinergic control, so sweating and salivation are greatly reduced by the anticholinergic drug atropine. So if you can’t salivate or sweat, you very possible will show what kind of symptoms? How about a burning dry mouth and hyperthemia? Nausea and vomiting are cholinergic overdose, as is orthostatic hypotension.

(a) just when you thought you could get by with the anti-SLUD strategy, they then expect you to remember that atropine overdose causes CNS excitation and tachycardia? Actually, that is one of the interesting diffs between atropine and scopolamine, and the reason that scopolamine is used for sedation, while atropine isn’t (b) and (e) are cholinergic stimulation I think, (c) is histamine produced, while I haven’t got a clue what “ptyalism” is – do you? But I do know that if atropine causes dry hot skin because it prevents sweating then (d) can’t be right!

(d) so you gotta know scopolamine is anticholinergic, so ya need a cholinergic agonist, either direct or indirect to overcome its effects. The options in the list are c and (d). Acetylcholine won’t work because it gets broken down way to rapidly by acetylcholinesterase, and thus is useless to inject. Physostigmine will work since it is an indirect acetylcholinesterase.

(d) – while some of these are indeed associated with organophosphate toxicity, the immediate cause of death is due to (d), which results from the stimulation of nicotinic receptors at the neuromuscular junction resulting in paralysis of skeletal muscles.

(c) this is an except question, don’t miss that word! So looking at the list, we got the S (option d) and the L (option b) from SLUD, so we are left with (a), c, and (e) as possibles. (e) results from cholinergic stimulation of the NMJ, so that can’t be it. (a) or bradycardia, can occur from too much cholinergic stimulation of the heart (that’s why atropine is useful in surgery, to reverse the bradycardia that sometimes arises. So, by default, vasoconstriction is the exception we are looking for.

(c) that’s why it is long-acting in patient’s that have a deficiency in this enzyme

(d) again – don’t you wish you had gotten comfortable with this type of terminology during the course? Imagine how many different drugs they might put into this kind of question! Anticholinergics, because they cause xerostomia, are obviously important to know for dentistry. TCAs, H1 antihistamines, opioid analgesics are all drugs that have potent anticholinergic activity, in addition to the prototypes atropine and scopolamine. All of these might turn up in the kind of question “Which of the following causes xerostomia?”