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Pharm ANS drugs
Pharm: ANS drugs
| Question | Answer |
|---|---|
| which adrenergic receptors AREN'T innervated? | Beta-2 |
| receptors causing miosis vs mydriasis in eye | miosis=M3, mydriasis=a1 |
| how to tell if it is a1 or M3 being affected in pupil? | check for cycloplegia (M3) |
| this drug blocks Choline uptake into nerve terminal | Hemicholinium |
| ACh release blocking agent | Botulinum toxin |
| How does Botulinum toxin work? | interacts w/ synaptobrevin to prevent ACh release |
| Muscarinic receptors in Heart: Which type and what function? | type is M2. function is slows heart rate (SA node) and conduction (AV node). NO MUSCLE AFFECTS |
| Where are M1 receptors located? | GIT glands |
| Muscarinic affect on sphincters of GIT | relaxes all but lower esophageal sphincter |
| Do indirect agonists work on blood vessel muscarinic receptors? | NO b/c these receptors (M3) aren't innervated. Function via EDRF. |
| Are muscarinic agonists used in glaucoma? | Yes. ciliary muscle contraction assists in lowering IOP. |
| are there specific agonists/antagonists drugs for M1,M2,M3 | NO. Muscarinic drugs (ag/antag) are nonspecific |
| Locations of nicotinic receptors (3)? | Adrenal medulla (release NE/Epi) Nn, Autonomic Ganglia Nn, Neuromuscular junction (Nm) |
| which are Gq coupled Muscarinic receptors? | M1, M3 (Gq=IP3/DAG/Ca2+) |
| Which are Gi coupled Muscarinic receptors? | M2 (Gi= decreased cAMP) |
| Which are Gs coupled Muscarinic receptors? | NONE. no cAMP producing M receptors. |
| Nicotinic receptor mechanism? | Na/K ion channel coupled. |
| Name the Muscarinic agonists (4) | ACh (duh), BethaneCHOL, MethaCHOLine, Pilocarpine |
| Use of Bethanechol? | Urinary retention/post op ileus |
| Use of Pilocarpine? | glaucoma, xerostomia (dry mouth) |
| Name AChE inhibitors (5 'groups') | Edrophonium, Physostigmine, Neostigmine/Pyridostigmine, Donepezil, Organophosphates (echoTHIOphate, malaTHIOn, paraTHIOn, sarin) |
| Use of Edrophonium? | distinguish between myasthenic crisis and cholinergic crisis |
| what's the difference btwn myasthenic crisis and cholinergic crisis? | myasthenic crisis = not enough ACh, cholinergic crisis= too much ACh |
| Which of the following AChE inh's enters CNS: neostigmin, physostigmine, pyridostigmine? | Physostigmine (tertiary Amine) |
| What AChE inh is used to treat Alzheimers? | Donepezil (CNS entry<--Lipid soluble) |
| ACHE inh poisoning? | DUMBBELSS diarrhea, urination, miosis, bradycardia, bronchoconstrxn, excitation (muscle/cns), lacrimation, salivation, sweating |
| If given atropine for AChE inh poisoning, where will affect of reversal bot be seen? | muscle...requires Pralidoxime |
| can atropine enter CNS? | yes, it's a tertiary amine |
| List of anti-muscarinics (6) | aTROPine, TROPicamide, ipraTROPium, scopolamine, benzTROPine, trihexyphenydyl |
| Use of ipratropium | Asthma/COPD |
| use of scopolamine | motion sickness |
| use of benztropine/trihexyphenidyl? | Parkinsonism and EPS of anti-psychotics |
| What are the only 3 locations that have naturally predominant SANS stimulation | arterioles, veins, sweat glands. If Nn are blocked, this is impt. |
| Antidote for atropine poisoning? | physostigmine |
| in adrenegric neurons, what is role of reserpine? | Blocks vesicle formation (Dopamine entry into vesicle for subsequent formation of NE) |
| function of guanethedine? | blocks NE vesicle release (exocytosis) |
| are a1 receptors present on arterioles or veins? | BOTH. arteriole contraction = increased TPR (afterload), venous contraction = increased preload |
| Renin release control is through which adrenergic receptors? | a1 and B1 |
| which receptor stim causes decreased Renin | a1 |
| which rec stim causes increased renin | B1 |
| Which receptors control insulin release? | a2, B2 |
| which rec stim causes increased insulin | B2 |
| which rec stim causes decreased insulin | a2 |
| affect of B2 stim in Uterus? | relaxation |
| affect of B2 stim in blood vessels? | vasodilation!! (un innervated) |
| effect of D1 rec in kidney? | vasodilation |
| Gq coupled adrenergic rec? | a1 (M1,M3) |
| Gi coupled? | a2, (M2) |
| Gs coupled? | B1, B2, D1 |
| what are the a1 agonists? | Phenylephrine, Methoxamine |
| how will a1 stim affect BP/HR? | increased TPR= incr BP....leads to reflex bradycardia. No change in total pulse pressure |
| what are the a2 agonists? | methyldopa, clonidine |
| uses of a2 agonists? | methyldopa, clonidine used in mild-moderate HTN (cause decr. NE release) |
| which adrenergic agonists stimulates B1=B2? | isoproterenol |
| B1>B2? | dobutamine |
| B2 agonists? | salmeterol, albuterol, terbutaline |
| BP/HR affects of B1 and B2 | B1= incr HR, incr stroke volume, incr CO, incr pulse pressure B2= decr BP (vasodilation) |
| norepinephrine affects what receptors? | a1,a2,B1 (NOT B2!!! therefore NEVER lowers BP) |
| which adrenergic rec causes lower BP? | B2!!!!!!!!!!!! |
| Epinephrine at low, med, high dose | low= isproteranol (B1=B2) med= dobutamine (B1>B2) high= norepinephrine (a1, B1) |
| how to differentiate high dose Epi from NE? | Epi has B2 affects, so if you give a1-block..BP will drop with Epi but not with NE. |
| why Epi given instead of NE during anaphylaxis? | B2 affect of Epi causes bronchodilation! |
| indirect adrenergic agonists mech of action? | Release NE from mobile pool |
| name 3 indirect adrenergic agonists | tyramine (wine/cheese), amphetamines, ephedrine |
| tyramine is metabolized by what enzyme | MAO-A (so if you take MAOi's, your tyramine levels go up and cause hypertensive crisis) |
| what are the non selective alpha blockers? | phentolamine, phenoxybenzamine |
| which non selective alpha blocker is comp inh, which is non comp inh? | comp= phentolamine, noncomp=phenoxybenzamine |
| selective a1 blockers? | prazocin, doxazocin, terazocin, tamsulosin |
| a2 blockers? | yohimbine, mirtazapine |
| which B blockers have B1 selectivity | A-M (acebutolol-->Metoprolol) |
| Which B blocker causes CNS depression | Propranolol |
| Which 2 B blockers have intrinsic sympathomimetic activity | Acebutolol, Pindolol |
| which B blockers have K+ blockade | sotAlol |
| which have combined a1 and B blockade | labetAlol, carvedIlol |
| what opens the angle of glaucoma: miosis or mydriasis? | miosis |
| what types of drugs can be used to cause miosis for closed angle glaucoma? | M agonists, AChE inh's |
| how can aqeous humor produxn be decreased | B blockers |
| what does B1 rec do to Myocyte | cAMP causes phosphorylation of Na+, K+, Ca2+ channels. M2 does opposite. |
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