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Auto Pharm Meds
ANS Pharmacology Drugs
| Question | Answer |
|---|---|
| What drugs are Direct Acting Muscarinic Agonist Choline Esters? | Betanechol, Carbachol, Methacholine |
| What drugs are Direct Acting Muscarinic Agonists? | Muscarine, Pilocarpine |
| What drug is a Muscarinic Antagonist that treats diarrhea? | Atropine |
| What drug is a Muscarinic Antagonist that treats nausea? | Scopolamine |
| What are the differences between Atropine & Scopolamine? | Atropine stimulates the heart, has minor CNS effects, and the L-isomer is Hyoscyamine. Scopolamine has strong CNS effects b/c it crosses the BBB & causes drowsiness, L-isomer is hyoscine. |
| What Direct Acting Muscarinic Agonist is the best to treat urinary retention? | Betanechol b/c it doesn't stimulate Nicotinic Receptors |
| What Direct Acting Muscarinic Agonists treat glaucoma? | Carbachol, Pilocarpine |
| What are the natural alkaloids of Direct Acting Muscarinic Agonists? | Muscarine, Pilocarpine |
| What are 2 drugs that are Muscarinic Antagonists that treat COPD? | Ipratropium, Tiotropium |
| Why can Tiotropium be used to treat asthma along with COPD? | Tiotropium is M3-R selective. M3 specifically bronchodilates. |
| What do Methscopolamine Br & Homatropine Methylbromide treat? | GI spasms & IBS |
| What is Glycopyrrolate used for? | Anesthesia - anti-Vagal |
| What does Pirenzepine treat? | Acid-peptic disorders, ulcers. M1&M4 selective |
| What drugs are Muscarinic Antagonists that treat urinary incontinence? | Darifenacin, Oxybutynin, Tolterodine |
| What are the differences between the urinary incontinence Muscarinic Antagonists? | Darifenacin is M3 selective & also treats fecal incontinence. Oxybutynin & Tolterodine aren't selective, relax the detrusor mm. |
| What Muscarinic Antagonists treat Parkinson's? How are they able to do this? | Benztropine, Trihexyphenidyl, Biperiden, Procyclidine. They are able to cross the BBB. |
| What Muscarinic Antagonists are receptor selective? | Tiotropium, Pirenzepine, Darifenacin |
| What are the side effects of stimulating Muscarinic Receptors? | Parasympathetic effects: SLUDGE, bradycardia, bronchoconstriction, hypotension, miosis |
| What are the side effects of blocking Muscarinic Receptors? | Sympathetic effects: tachycardia, hypertension, bronchodilation, constipation, urinary retention, mydriasis, cyclopegia, dry mouth |
| What is the SNS exception for NT & Receptor? | Sweat glands. ACh-R are stimulated. |
| What Muscarinic Receptors stimulate? | M1, 3, 5. Use Phospholipase C (PLC) as a 2nd messenger. |
| What Muscarinic Receptors inhibit? | M2, 4. Inhibit adenylate cyclase, open K+ & close Ca2+ channels. |
| What drugs are Cholinesterase Inhibitors (Indirect Cholinergic Agonists) that treat glaucoma? | Echothiophate, DFP |
| What Cholinesterase Inhibitors (Indirect Cholinergic Agonists) treat Myasthenia Gravis? | Neostigmine, Pyridostigmine, Ambenonium, Edrophonium |
| How is Edrophonium used? | If administered to patient & they feel better, diagnosis of MG. If already diagnosed: if administered & feel better pt is underdosed; if administered & feel worse pt is overdosed. |
| Physostigmine, Tacrine, Donepezil, Galantamine are what type of drugs & what do they treat? | They are Cholinesterase Inhibitors (Indirect Cholinergic Agonists) that can cross BBB, and they treat Alzheimer's |
| Parathion, Malathion, Sevin, Chlorpyriphos are what? | Cholinesterase Inhibitors (Indirect Cholinergic Agonists) that are used as bug poisons |
| Sarin, Soman, VX are what? | Cholinesterse Inhibitors (Indirect Cholinergic Agonists) that are used as human poisons |
| What is a side effect of inhibiting Acetylcholinesterase? | An increase in skeletal muscle contractions (fasciculations) |
| How do quaternary amines inhibit AChE, and what is an example drug? | They bind to AChE for a very short amount of time & just go away. Edrophonium is an example |
| How do carbamates inhibit AChE, and what is an example drug? | They bind to AChE, and break into 2 pieces. 1 piece stays attached to the esteratic site until it's hydrolyzed by water. At this point it will go away. This is intermediate to long acting. Example drugs are neostigmine & physostigmine |
| How do organophosphates inhibit AChE, and what is an example drug? | They bind to the esteratic site & 1 isopropyl group leaves after being hydrolyzed. This causes the OP to stay bound and this is irreversible. An example is DFP |
| If given an OP, how would you stop the permanent "killing" of AChE? | Administer 2-PAM before the OP is hydrolyzed. 2-PAM will bind to the OP & fill the anionic site. The combined molecules can then go away |
| Why would you treat glaucoma with a Muscarinic Agonist? | M3 stimulation promotes drainage by contracting the ciliary & iris muscles (miosis) |
| Why would you treat glaucoma with a B2 Antagonist? | B2 promotes the production of the aqueous humor, so if it's blocked, there will be no fluid buildup |
| Why would you treat glaucoma with an A2 Agonist? | A2 helps drainage & reduce fluid buildup |
| What are the drugs that are Ganglionic Blockers & used to treat acute dissecting aortic aneurysm? | Hexamethonium, Mecamylamine, Tetraethylammonium |
| Succinylcholine, Pancuronium, Tubocurarine, Atracurium, Doxacurium are all what type of drugs & what do they do? | They are Nicotinic Blockers used for paralysis that don't cross BBB |
| Nicotinic Blockers are typically competitive non-depolarizing. What makes Succinylcholine special? | It causes many little depolarizations until the muscle can't respond anymore. At this point it becomes non-depolarizing & the muscles can't reset. Lasts about 8 mins |
| What are some B1 Agonists? | Dopamine, Dobutamine, Isoproterenol, Epi |
| Dopamine is a B1 Agonist. What does it do? | Stimulates NE release & improves renal blood flow |
| Dobutamine is a B1 Agonist. What does it do? | It helps in the treatment of CHF. It increases CO by increasing contractility |
| Isoproterenol is a B1 Agonist. What does it do? | Cardiac stimulation |
| Epi is a B1 Agonist in low doses. What does it do? | Cardiac stimulation |
| What do B1 Receptors do? | Most prominent effect is cardiac stimulation. It also stimulates renin release & promotes production of the aqueous humor |
| What effect does Isoproterenol have on B2-R? | Bronchodilation & vasodilation |
| What B2 Agonist drugs are used to treat asthma & COPD? | Albuterol, Terbutaline, Salmeterol, Formoterol |
| What B2 Agonist asthma/COPD drugs are short acting? | Albuterol & Terbutaline |
| Ritodrine is a B2 Agonist. What does it do? | Prevent premature labor |
| Epi has an effect on B2-R at low doses. What does it do? | Bronchodilation & vasodilation |
| What effects do B2-R have? | Most prominent effect is bronchodilation. It also has BPULSE effects. |
| You can remember what effects B2-R have by 2B's & PULSE. What do these stand for? | Blood vessel dilation, Bronchodilation, Pancreas (insulin), Uterus (relaxation), Liver (glycogenolysis), Skeletal mm (inc contractility), Eye (mydriasis) |
| MAO & COMT degrade monoamines & catecholamines. What are their main methods of doing this? | MAO - deamination, COMT - methylation |
| What are some things about COMT? | Widely distributed, degrades circulating catecholamines |
| What are some things about MAO? | Metabolizes monoamines, MAO-A (other places) & MAO-B (blood platelets) |
| A1 Agonists use G-Protein coupling. What is the sequence of events? | A1-R is activated, which activates the G-protein. In turn, this activates PLC to cleave PIP2 into IP3 & DAG. IP3 stimulates the ER to release Ca2+, & the Ca2+ activates things. |
| What do B-R & A2-R do to adenylyl cyclase? | They do opposite things. B-R stimulate cAMP & A2-R inhibit cAMP from being formed. |
| What do A1-R do? | Predominately vasoconstriction, which causes an increase in BP; urinary retention, prostate contraction, mydriasis, stimulate ejaculation |
| What does an A2-R do? | It lowers BP by inhibiting ACh from being released by presynaptic cells in the SNS |
| What receptors inhibit NE from being released by presynaptic cells in the PSNS? | M2- & M4-R |
| What effect does NE have on A1-R? | Vasoconstriction |
| What effect does NE have on B1-R? | Cardiac stimulation at high doses. Body will initiate reflex bradycardia via baroreceptors so the HR & heart work will be lowered. This is dangerous b/c there is already vasoconstriction with A1-R & stimulation of B1-R can also cause vasoconstriction |
| What kind of effect does Epi have on A1-R at high doses? | Vasoconstriction |
| Pseudophedrine, Phenylephrine, Oxymetazoline, Tetrahydrozaline are decongestants. What type of drugs are they? | A1 Agonists b/c A1-R inhibit respiratory tract secretions |
| Methoxamine & Mephenteramine are A1 Agonists. What would they treat? | Hypotension |
| Metaraminol is a A1 Agonist. What does it treat? | Paroxysmal supraventricular tachycardia |
| What A1 Agonist is used to treat postural/orthostatic hypotension? | Midodrine |
| Amphetamine, Methamphetamine, Phentermine aren't really A1 Agonists, but they have Alpha effects for what? | Weight loss |
| A2 Agonists are used to treat what? | Hypertension, mm spasms, glaucoma |
| What A2 Agonist drugs are used to treat hypertension? | Clonidine, Guanabenz, Guanfacine |
| Tizanidine is an A2 Agonist. What does it treat? | Muscle spasms |
| What A2 Agonists are used to treat glaucoma? | Apraclonidine & Brimonidine |
| There are 2 A1 Antagonist drugs used to treat pheochromocytoma. What are they? | Phenoxybenzamine & Phentolamine |
| What is the difference between Phenoxybenzamine & Phentolamine? | Phentolamine has a bigger reflex tachycardia b/c it binds to both A1- & A2-R |
| Prazosin & Doxazosin are what type of drugs & what do they treat? | A1 Antagonists, hypertension |
| Terazosin & Tamsulosin are A1 Antagonists. What do they treat? | BPH, they cause vasodilation |
| Yohimbine is an A2 Antagonist. What is it used for? | Sexual dysfunction |
| B1 Blockers are good for a lot of things. Name some. | Antihypertensive, prophylaxis for migraines, tx of glaucoma, reduce sense of situational stress |
| Why can't you just stop taking Beta Blockers cold turkey? | There is serious risk of rebound hypertension & receptor up-regulation on the heart which can cause a MI |
| Exposure to agonists cause... | Receptor down-regulation (there is a lot of NT or whatever around, there's no need for extra receptors) |
| Exposure to antagonists cause... | Receptor up-regulation (there isn't a lot of NT or whatever around, & all the receptors scramble to pick up what little is there) |
| What are the Selective B1 Antagonists? | Acebutolol, Atenolol, Esmolol, Metoprolol |
| What are the Non-Selective Beta Blockers? | Labetalol, Nadolol, Pindolol, Propranolol, Timolol |
| What drugs exhibit Intrinsic Sympathomimetic Activity (ISA)? | Acebutolol, Labetalol, Pindolol |
| Why wouldn't you give someone with asthma Propranolol as a Beta Blocker? | Propranolol is non-selective, so it'll antagonize B2-R which causes bronchoconstriction. |
| Why is Metoprolol special? | It is B1-R selective (cardioselective) |
| What Beta Blocker is the prototype? | Propranolol |
| What Beta Blocker blocks B-R & A1-R? | Labetalol |
| Why would giving someone Esmolol orally be a bad idea? | It has a half-life of 10 minutes |
| What is the half-life of Propranolol? | 3.5-6H b/c of high lipid solubility |
| Pindolol has ISA. What does this do? | Pindolol is a partial agonist. It will stimulate B-R a little while also inhibiting the B-R so HR won't drop too low |
| What are the main effects of the Beta Blockade? | Decreases HR & contractility, inhibits gluconeogenesis & glycogenlysis, inhibits renin release, decreases intraocular pressure |
Created by:
Naychan07
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