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