Where can i purchase Physostigmine?
im planning on taking a very large recreational dose of Diphenhydramine for some studies i am doing (i assure you i do not just want to get high, ive taken a hobby of archiving and studying the chemestry of the inebriated and intoxicated human mind) and ive been doing my homework on it and Physostigmine is the cure for a benadryl overdose. and also with a dose of 600mg of Diphenhydramine with me being 16, 6 foot, 140 lbs; how much of the anti drug would i need in case of overdose? i know im only 16 but i have an IQ of 147 and i know this is something i shouldnt be doing but i have made up my mind, so save your fingers some strein and don't bother telling me not to do it.
How is Physostigmine Synthesized?
Physostigmine (also known as eserine) is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor obtained from the Calabar bean. By interfering with the metabolism of acetylcholine, physostigmine indirectly stimulates both nicotinic and muscarinic receptors. The chemical was synthesized for the first time in 1935 by the chemists Percy Lavon Julian and Josef Pikl. Clinical Uses Physostigmine is used to treat glaucoma and delayed gastric emptying. Because it is a tertiary amine, it can cross the blood-brain barrier and so it is also used to treat the central nervous system effects of atropine, scopolamine and other anticholinergic drug overdoses. Possible side effects include depression. Overdose can cause a cholinergic syndrome. Physostigmine is available in the U.S. under the trade names Antilirium, Eserine Salicylate, Isopto Eserine, and Eserine Sulfate. Intravenous injection of physostigmine (0.5mg-2mg) can be used to reverse GHB overdose, although careful control of dose is needed to avoid convulsions; often a small dose of an anticonvulsant such as diazepam is administered first to counteract the lowering of seizure threshold from the physostigmine.
Physostigmine treatment?
I'm afraid I can't give you a clinical answer of the side effects but I can tell you the mechanism of the two drugs and hopefully that will help. Both drugs affect the activity of the neurotransmitter acetylcholine (ACh). Physostigmine blocks the enzyme which breaks ACh down (acetylcholine esterase), therefore, the action of ACh is enhanced and lasts longer. Atropine blocks the muscarinic ACh receptors, if ACh cannot bind to these receptors, it cannot produce a response. This would overcome the effects of physostigmine because despite increased ACh concentration or duration of effect, the ACh molecule can do nothing if it cannot bind to the receptors. ACh also binds to nicotinic ACh receptors which are not blocked by atropine so this may explain how physostigmine (which would work in all parts of the body) cannot be completely overcome by atropine. This nicotinic receptors are found in the brain and at the synapse between nerve and muscle, whereas muscarinic receptors (the ones atropine blocks) are mostly found at smooth muscle (e.g. intestines) and cardiac muscle (heart). Hope that helps and wasn't too complicated or too patronising (I don't know your level of understanding) :-)
Why do we give atropine preceeding to neostigmine in a snake bite as a specific treatment?
To be specific:Only when the whole blood clotting time is more than 20 mins and signs of envenomation e.g ptosis and external opthalmoplegia i.e. diplopia are there, we consider it a neurotoxic snake bite.A cobra bite acts on post synaptically on the neuromuscular junction causing paralysis. In these cases anti cholinesterases such as neostigmine are helpful and are given in large doses to act on the nicotinic receptors. While neostigmine will also act on the muscarinic receptors, so to counteracts its muscarinic side effects like bradycardia, sweating, lacrimation atropine is given in relatively small doses.Ofcourse, Polyvalent ASV is given along with which is implied.Hope that clears the confusion.
What is the drug that causes mydriasis as well as loss of corneal reflex?
As far as I know there is no topical agent that will cause mydriasis and loss of corneal reflex.I have came across this platform called Saturo Global which does clinical pharmacology as a service in an online portal which allows it's user to track, view and download eCopy of documents. It's also provides other services like Patent search etc,. Know more: Saturo Global - Landscape search,Patent tracking,Trademark curation,Patent Indexing,Journal Indexing
What drug works against poison?
It’s ANTIDOTE.Different poisons have different Antidotes. Some Antidotes are mentioned on the packaging of the Poison. Doctors use Pralidoxime chloride and Atropine Injections for Organophosphate Insecticide poisonings. Anti Snake Venom in the form of Injection is used for Snake bites. Physostigmine is used for Atropa belladona (deadly nightshade) poisoning. Ethyl alcohol is used for Methyl alcohol poisoning.Calcined magnesia in milk or water is given in cases of Mineral acid poisoning like Sulfuric Acid. Common soap (hard or soft), chalk, or even mortar from the wall mixed in water may be given, until magnesia can be obtained. Ingested poisons are frequently treated by the oral administration of activated charcoal, which adsorbs the poison and flushes it from the digestive tract, thereby removing a large part of the toxin.AntidoteList of Antidotes in above link.
If Physostigmine inhibits the breakdown of acetylcholine, then could it serve as a nootropic?
No.Nootropic like piracetam+choline only increase acetycholine level to normal hence doesnt cause much side effect.But drugs like physostigmine and Donepezil inhibit a chemical that break down acetycholine hence increase Acetycholine to disastrous level in normal people.But remember excess acetycholine inhibits other neurotransmitter like dopamine and serotonin which are normal for healthy brain function.Resource->1-Internet.2-Self experiment.
How do poisons affect the neurotransmitter acetylcholine and cause death?
Nerve gases like sarin block acetylcholine esterase, the enzyme that breaks ACh down into choline and acetate. This extends the time that the postsynaptic receptors are exposed to ACh. At the neuromuscular junction, this causes a persistent depolarization in the muscle that prevents sodium channels from recovering from inactivation. Thus, the muscle cannot fire any more action potentials and will not contract. If it affects your diaphragm muscle, that's fatal pretty quickly. Sarin's action is irreversible, so it is truly a poison. But physicians may administer similar drugs (physostigmine is one) that do the same thing but are reversible. However, an overdose of these will have the same effect. Muscle relaxants are also drugs that affect the neuromuscular junction. They can be used safely by anesthesiologists, but would be fatal if administered to a person who was not breathing with the help of a ventilator. There are 2 forms of these drugs 1) depolarizing (succinylcholine) which binds to the postsynaptic ACh receptor and causes a persistent depolarization of the muscle. 2) nondepolarizing (curare) which binds to the postsynaptic ACh receptor and prevents ACh from binding. The channels do not open and, again, there is paralysis. There is an irreversible form of this as well. alpha-bungarotoxin, found in snake venom, will bind to the receptors and prevent channel opening. Some forms of snail toxins (conotoxins) will do the same. Its a scary world out there ....
Antidotes for drugs?
ok, im in nursing school and i have a tone of drugs i have been looking up and im having trouble finding antidotes or antagonist! the only ones that are shown in my drug book are the drugs that provide an analgesic opiod reaction and they are antagonized by Narcan. if any of you out there can give me a web site or something i would so appreciate it! thanks for your help!