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130 Cards in this Set
- Front
- Back
epinephrine
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EPI; adrenaline
endogenous, non-selective agonist treat: cardiac arrest acute anaphylactic reactions acute attacks of allergy-induced ashtma |
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norepinephrine (NE;adrenaline)
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agonist
limited therapeutic value, short duration treatment of shock |
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intropin
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(dopamine)
endogenous, non-selective adrenergic agonist binds B1 in heart treat: shock |
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isoproterenol (isuprel)
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non selective B agonist (very potent)
vasodilation chronotropy adverse reactions: tachycardia, BP, arrhythmias |
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neosynephrine
is used to treat? |
phenylephrine
a1 agonist constrictor! similar to NE but less potent not inactivated by COMT Treat: nasal congestion side effects: mydriatic, hypertensive |
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clonidine (catapress)
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a2 agonist
acute hypertensive response follwoed by hypotension treat? hypertension menopausal flushing, migraine side effects: dry mouth, sedation, contact dermatitis Alpha 2 receptors on on the presynaptic neuron. When stimulated they inhibited the ongoing release of NE from the adrenergic receptor |
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dobutamine (Dobutrex)
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B1 agonist
acts on B1 in heart increase force more than rate treats: cardiogenic shock |
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the rate-limiting step in the formation of NE
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Tyrosine is transported by Na into the neuron and hydroxylated to DOPA by tyrosine hydroxylase then it will DOPA will be decarboxylated to form dopamine
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which adrenergic receptor inhibits histamine release by mast cells
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beta 2
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NE is methylated to yield
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EPI
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COMT
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catechol O-methyltransferase - it metabolizes NE
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what are the three ways NE is removed
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1. diffuse out of synaptic space
2. metabolized by COMT 3. recaptured by uptake system |
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two mechanisms for replensishing nerve terminal NE stores
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denovo synthesis
reuptake |
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monoamine oxidase (MAO)
in what cell organelle is it present? |
important in the metabolism of catecholamines
present in the neuronal mitochondria |
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The inactive products of NE matabolism detected in urine.
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vanillylmandelic acid, metanephrine and normetanephrine
so you can detect in urine (one way to detect a catecholamine secreting tumor) |
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phaeochromocytoma
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tumor of the adrenal gland secreting too many catecholamines
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in terms of responding to epi, NE, and isoproterenol the alpha are most receptive to
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epi>NE>isoproternenol
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The action and mechanism of G protein signalling from alpha 1 adrenergic R
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(post synaptic)
phospholipase C, IP3, release of Ca+ from the SR smooth muscle contraction |
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The action of alpha 2
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(pre synaptic)
NE cycles back around and causes feedback inhibition of ongoing release of NE from stimulated adrenergic neuron |
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which adrenergic receptors cause glycogenolysis in the liver
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alpha 1 and Beta 2
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B Receptors respond most to epi, NE, or isoproterenol
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isoproterenol > epi > NE
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affinity of B1 an B2 for epi vs. NE
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B1 the affinity is equal
B2 has higher affinity for epi |
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alpha 1 causes what
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vasoconstriction (increase TPR, increase BP
(blood vessels, bronchi, uterus, sphincter, seminal tract, iris (mydriases) |
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four major actions of alpha 2
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inhibition of NE release
inhibition of insulin release vasoconstriction of b. vessels relax GI tract smooth muscle |
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activation of B1 increases
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HR and contractility
conduction velocity increase AV node |
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activation of Beta 2 has what effect on smooth muslce so f airwys and uterus
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relaxes smooth muscle
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epi causes powerful bronchidilation by acting on what receptors where
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B2
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Epi has what effect on the liver
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increases glycogenolysis in the liver via B2 and can cause hyperglycemia.
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what effect does Epi have on the pancreas
and via what receptor |
decreases release of insulin via the A2 effect
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why is albuterol used over epi in the treatment of chronic asthma?
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albuterol which is a selective b2 agonist is used to treat chronic astham because of longer duration of action and minimal cardialc stimulatory effect.
epi is non selective and would stimulate increase HR via B1 |
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why might epidecrease airway resistance in asthma
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action on alpha 1 to contstrict mucosal vessels
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what adrenergic receptor causes K+ release
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Alpha 1
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Dopamine (Intropin) is used to treat and what receptor is stimulated in this treatment
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shock
activates B1 in heart |
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what agonist is
isoproterenol (isuprel) what are the effects |
non-selective B agonist
vasodilation adverse reactions: tachycardia, BP, arrhythmias |
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phenyleprhine (neosynephrine)
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alpha 1 agonist
note: not inactivated by COMT |
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phenylephrine is used to treat
two side effects? |
nasal congestions
note: it causes mydriasis (excessive dilatio nof pupil) and hypertension |
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clonidine (catapress)
used to treat adverse effects |
alpha 2 agonist
used to treat hypertension due to actionin CNS (also used to treat menopausal flushing, migraine) dry mouth, sedation, contact dermatitis |
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explain the paradoxical effect of clonidine in terms of the acute hypertensive response followed by hypotension
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it stimulates alpha 1 a little which increases BP bt over all decreases BP due to the alpha 2 receptor in the CNS (brainstem) which inhibit the release of NE
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Dobutamine (Dobutrex)
to treat |
Beta 1 agonist
treats cardiogenic shock note: increases inotropy but not HR that much so it does not increase O2 demand |
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the advantage of Dobutamine over other sympathomimetic drugs
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does not increase HR only inotropy so it does not increase O2 demand
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albuterol (Ventolin)
is a bronchodilator what are the adverse reactions |
B2 agonist
adverse reactions: tachycardia, tremor, tolerance |
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ephedrine
mechanism of action |
indirect acting agonist
increases NE release, prolonged duration and potent CNS stimulant |
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ephedrine is used to treat what two things
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nasal decongestant and hypotension
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indirect adrenergic agonists cause their effect by what mechanism
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increase the release of NE
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amphetamine is what kind of drug?
used to treat? |
it is indirect agonist (increases release of stored catecholamines)
treat: obesity (appetite control), narcolepsy, ADD |
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tyramine is what kind of drug and is found in high conc where
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it is indirect acting agonist
found in high concentration in fermented food. it is metabolized by liver MAO so MAO inhibtors could lead to increase in tyramine and severe hypertension |
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what is the difference between catecholamines and noncatecholamines in terms of theree duration and administration
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catecholamines: epi, NE, isoproterenol, Dopamine, Dobutamine
catecholamines have rapid onset and brief duration and cant be administered orally. noncatecholamines have longer duration and can be administered orally |
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cocaine is what kind of drug
what is the mechanism? |
indirect acting adrenergic agonist
inhibits NE and dopamine reuptake |
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what adrenergic receptor causes K+ release
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Alpha 1 (liver and salivary gland
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three mechanisms by which sympatholytic drugs block adrenergic receptor action
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1. decrease sympathetic outflow
2. suppress nerve terminal NE (inhibit synthesis, deplete granule, suppress release of NE) 3. Block postsynaptic receptors |
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irreversible adrenergic antagonists attach how
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covalently
the block is insurmoutable and not overcome by NE e.g phenoxybezamine |
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reversible competitive antagonists is different from irreversible adrenergic antagonists hoq
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the antagonist can dissociate from receptor.
they produce equilibrium blockade block disappears as free drug is metabolized |
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alpha adrenergic blocking agents have a profound effect on?
they may result in reflex? |
blood pressure. causes decrease in peripheral vascular resistance and might result in reflex tachycardia
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phentolamine (Regitine)
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reversible alpha adrenergic blocker
nonselective |
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phenoxybenzamine (Dibenzyline)
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irreversible alpha adrenergic blocker
used in peripheral vasospasm. used to treat pheochromocytoma and Raynauds disease |
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name a alpha 2 adrenergic antagonist
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they are not clinically useful.
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alpha 1 adrenergic selective blockers can be used to treat
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hypertension and BPH
caues vasodilation and reduction in arterial pressure no decrease in cardiac function and no reflex tachycardia |
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Prazosin (Minipress)
type? treats? adverse reaction |
alpha 1 adrenergic antagonist
treats hypertension 'first dose' effect of postural hypotension so be careful when giving to elderly or someoneon diuretic |
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what is a partial adrenergic agonist
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a drug which blocks receptor partially so that some sympathetic activity still occurs
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by what mechanism does beta blockers have a local anesthetic action
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effects Na channels
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beta blockers are absorbed well after oral administration and their peak concetration takes how long
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1-3 hours
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why might you not want to stop a beta blocker immediately
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you will cause upregulation of receptors - so you want to taper off
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what three diseases should you beware of when using beta blockers
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airways disease (blocking B2 in lungs of susceptible pts causes contraction of bronchiolar smmoth muscle)
diabetes (decrease in glycogenolysis and decreased glucagon section. hypglycemia may result if insulin is injected) heart failure (dont stop suddenly) |
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Propranolol is what kind of drug
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Beta adrenergic non selective blocker
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propranolol is used to treat
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hypertension (decrase CO)
glaucoma (decrease the secretion of acqeous humor) migraine (lipiphilic - enters CNS) hyperthyroidism (thyroid hormone is a sympathetic stimualtor) angina (decrease O2 demand) MI |
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why might you combine a beta blocker with a diuretic
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reduced blood pressure - decrease renal perfusion - increase in na retention - increase BP
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Timolol (blocadren)
treat/ |
Beta adrenergic non selective blocker
treat:open angle glaucoma note: low lipophilicity, no membrane stabilization. |
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Pindolol (Visken)
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non selective beta adrenergic blocker
(partial agonist activity) |
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why might pindolol be good for a pt who is subject to bradycardia
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partial agonist activty
smaller reductions in resting HR. |
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Sotalol (Betapace)
used to treat |
non selective Beta adrenergic antagonist
atrial and ventricular tacharrhythmias |
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how does sotalol work
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beta non selective antagonists
prolongs cardiac action potential blocks K+ channels. |
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Metoprolol (Lopressor)
to treat |
Beta 1 antagonist
hypertension, ischemic heart disease |
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why might you choose metoprolol when treating someone with a kidney problem
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notable hepatic biotransferation - get rid of via liver
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Atenolol (tenormin)
treat: why good for someone with hepatitis? |
Beta 1 adrenergic antagonist
treat hypertension renal excretion |
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Labetalol (Normodyne, Trandate
treat? |
antagonizes B1,B2,A1
treat? hypertension, CHF, pheochromocytoma) |
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Carvedilol (Corea)
treat? |
blocks alpha1, B1,B2
improves survival of pts with heart failure note: has antioxident effects |
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explain all the places where aCh works
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1. preganglionic to adrenal medulla, and autonomic ganglion (sym and para)
2. Post ganglionic parasympathetic ganglion 3. post ganglionic sympathetics to sweat glands 3. neurons at NMJ |
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the receptors at the postganglionic terminus of parasympathetic fibers are called
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muscarinic
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why dont we cuse AcH therapeutically
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1. cannot penetrate membranes
2. multiplicity of actions 3. rapid inactivation |
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a fall in blood pressure mediated by muscarinc receptors on vascular smooth muscle happens via what mechanism
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Nitric oxide synthase is activated to generate NO from arginine
NO activates guanylate cyclase to produce cGMP cGMP binds myosin light chains and relaxes muscle vasodilation |
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actions of muscarinic receptors
DUMBBELS |
Diarrhea
Urination Miosis Bradycardia Bronchorrea (increase secretions and Bronchoconstriction) Emesis Lacrimation sweating |
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Pseudo ChE
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plasma ChE found in blood doesnt usually serve any purpose and people w/o this usually have no problems until they are given a drug
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Methacholine
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muscarinic agaonist
used to challenge somone who is suspected to have asthma |
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bethanecol
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muscarini agonist
used to relieve GI dysmotility replaced metoclopramide (acts upstream on the neuron to release ACh at the terminus) |
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pilocarpine
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muscarinic agonist
relive narrow angle glaucoma (used topically) opens canal of Schlemm and causes a drop in intraocular pressure as a result of increased drainage of aqueous humor. causes contraction of ciliary mscle and causes miosis (contraction of pupil) dilation of the pupil tends to make narrow angle even worse. |
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how might you get flaccid paralysis with ACh
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too mcuh ACh - receptor repolarizes and becomes refractory to further depolarization (depolarization-desensitizatoin blockage)
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what effects does nicotine have on the nicotinic receptos (sym or para?)
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nicotine depolarizes ganglia resulting first in stimulation and then paralysis of all ganlgio
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the signs of nicotine poisoning are due to
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sympathetic discharge from adrenals and possibly sympathetic ganglia
at high doses though you get a decrease in BP due to ganglionic block, and paralysis |
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three classes of ChE inhibitors
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1. Edrophonium
2. Carbamate ChE 3. Organophosphate |
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a ChE inhibitor that does not form a covalent bond w/ the enzyme. it is highly charded and does not cross the BB
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Edropphonium
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uses of Edrophonium
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diagnosis of myasthenia gravis because effects are dissapated in minutes
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myasthenia gravis involves what problem
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Ab from thymus attack motor end plates in periphery causing impairment of neurotransmission -
muscle weakness and rapid muslce fatique |
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physostigmine
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a carbamate ChE inhibitor
used occasionally to treat CNS signs of muscarinic blocker uncharged and lipid so crosses BBB - which is dangerous (myasthenia gravis is just a peripheral disease) |
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why do carbamate ChE last a long time
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they bind covatlently to the ezyme and leave behind a carbamoyl residue that hydrolysis over hours.
use to TREAT myasthenia gravis |
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Neostigmine
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Treat myasthenia gravis
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why is neostigmine designed with a quaternary ammonium group
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keep it out of the CNS
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myasthenic crisis vs. cholinergic crisis
how would you distinguish? |
too littel neostigmine would lead to myasthenic crisis and too much would result in depolarization-desensitization blockade (cholinergic crisis)
give edrophonium. if it has not effct then you have given too much neostigmine. |
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the group of ChE inhibitors that included insecticides parathion, malathion and nerve gases sarin and soman
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organophosphate ChE inhibitors
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mechanism of organophosphate ChE inhiboros
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react covalently w/ esteratic site and leave behingd phophorylated enzyem that requires hundresn of hours hydrolyze
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Pralidoxime's effect on ChE inhibors
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given to counter act the phosphorylating effect of organophosphate ChE inhibitors but contraindicated in carbamate ChE inhibtor poisoning
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the transmemebrane muscarinic receptors linked to phospholipase C
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M1 , 3, 5
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The muscarinic receptor linked in an inhibitory manner with adenyl cyclase
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M2 and M4
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M2 Receptor is found where
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stomach and heart
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M3 R is found where
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glands
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which Muscarinic Receptors are found on nerves, CNS
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1, 4, 5
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dicyclomine
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muscarinic receptor antagonist which is a antispasmodic
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benztropine
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muscarinic R antagonist used to treat Parkinsons
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gallamine
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muscarinic Receptor antagonist used as a MNJ blocker
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atropine effect on the eye
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muscarinic R blocker so causes dilation for days (mydriasis)
could be dangerous for pts with narrow angle glaucoma |
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what kind of channel are the Nicotinic Receptors
|
Na+/K+
at ganglia (two subunits) at NMJ (5 subunits) there are some semi-selective antagonists |
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perenzipine
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M1 muscarinic antagonist
reduces gastric acid secreation treat: peptic ulcer |
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Atropine effect on urinary system
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causes urinary retention
good to treat enuresis (involuntary voiding of urine) |
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scopolamine
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an muscarinic receptor antagonists which treats motion sickness.
but blocks short term memory ! |
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the only depolarizing blocker at the MNJ in clinical use
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Succinylcholine
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the effects of succinylcholine
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continued binding to nicotinic receptor causes continue depolarization and receptor is incapable of transmitting further impulses. causes flaccid paralysis
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succinylcholine is cleared by
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plasma ChE, so pts lacking enzyme are paralyzed for many hours instead of 5 to 7 minutes
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first muscle to be come flaccid with succinylcholine
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chest and abdomen
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why might succinylcholine cause hyperthermia w/ muscle rigitity
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uncontrolled release of Ca++ from SR
treat hyperthermia with ice bath |
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treat muscle rigidity caused by succinylcholine overdose with
|
dantrolen (blocks release of Ca2
|
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what two things synergize with succinylcholine
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anesthetic gases
aminoglycoside antibiotics |
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nondepolarizing blocker at NMJ
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curare
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used in surgery back in the day. thought to have CNS analgesic effects because children would not cry out during procedures but turned out it does not effect CNS
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curare
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a aminosterol which is a competitive nondepolarizing MNJ blocker and cleared by RENAL excretion
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pancuronium
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two aminosterols which are competitive nondepolarizing MNJ blockers which are cleared by LIVER metabolism
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rocuronium
vercuronium |
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a benzoisoquinolinium and a competitive nondepolarizing MNJ blocker which is cleared by liver and plasma esterases
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cistracurium
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with nondepolariing competitive cholinergice blockers what size muscles are affected first
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small (opposite succinylcholine)
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what would you give a patient to reverse the effects of a nondepolarizing competitive cholinergic blockes
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neostigmine
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the only one ganglionic cholinergic blocker in clinical use and is nondepolarizing competitive
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Trimethaphan
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uses of trimethaphan
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blocks cholinergic receptors
used for controlling hypertensive crises or surgery for aortic aneurysm effects dissipated in minutes; cleared by the liver |
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how does the botulinum toxin work
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ACh vesicles cant dock properly and neurotransmitter cant be released
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