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130 Cards in this Set

  • Front
  • Back
EPI; adrenaline

endogenous, non-selective agonist

cardiac arrest
acute anaphylactic reactions
acute attacks of allergy-induced ashtma
norepinephrine (NE;adrenaline)

limited therapeutic value, short duration

treatment of shock
endogenous, non-selective adrenergic agonist

binds B1 in heart
treat: shock
isoproterenol (isuprel)
non selective B agonist (very potent)

adverse reactions: tachycardia, BP, arrhythmias

is used to treat?

a1 agonist

similar to NE but less potent
not inactivated by COMT
Treat: nasal congestion
side effects: mydriatic, hypertensive
clonidine (catapress)
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
dobutamine (Dobutrex)
B1 agonist

acts on B1 in heart
increase force more than rate

treats: cardiogenic shock
the rate-limiting step in the formation of NE
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
which adrenergic receptor inhibits histamine release by mast cells
beta 2
NE is methylated to yield
catechol O-methyltransferase - it metabolizes NE
what are the three ways NE is removed
1. diffuse out of synaptic space
2. metabolized by COMT
3. recaptured by uptake system
two mechanisms for replensishing nerve terminal NE stores
denovo synthesis
monoamine oxidase (MAO)

in what cell organelle is it present?
important in the metabolism of catecholamines

present in the neuronal mitochondria
The inactive products of NE matabolism detected in urine.
vanillylmandelic acid, metanephrine and normetanephrine
so you can detect in urine
(one way to detect a catecholamine secreting tumor)
tumor of the adrenal gland secreting too many catecholamines
in terms of responding to epi, NE, and isoproterenol the alpha are most receptive to
The action and mechanism of G protein signalling from alpha 1 adrenergic R
(post synaptic)

phospholipase C, IP3, release of Ca+ from the SR

smooth muscle contraction
The action of alpha 2
(pre synaptic)

NE cycles back around and causes feedback inhibition of ongoing release of NE from stimulated adrenergic neuron
which adrenergic receptors cause glycogenolysis in the liver
alpha 1 and Beta 2
B Receptors respond most to epi, NE, or isoproterenol
isoproterenol > epi > NE
affinity of B1 an B2 for epi vs. NE
B1 the affinity is equal
B2 has higher affinity for epi
alpha 1 causes what
vasoconstriction (increase TPR, increase BP

(blood vessels, bronchi, uterus, sphincter, seminal tract, iris (mydriases)
four major actions of alpha 2
inhibition of NE release
inhibition of insulin release
vasoconstriction of b. vessels
relax GI tract smooth muscle
activation of B1 increases
HR and contractility
conduction velocity
increase AV node
activation of Beta 2 has what effect on smooth muslce so f airwys and uterus
relaxes smooth muscle
epi causes powerful bronchidilation by acting on what receptors where
Epi has what effect on the liver
increases glycogenolysis in the liver via B2 and can cause hyperglycemia.
what effect does Epi have on the pancreas
and via what receptor
decreases release of insulin via the A2 effect
why is albuterol used over epi in the treatment of chronic asthma?
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
why might epidecrease airway resistance in asthma
action on alpha 1 to contstrict mucosal vessels
what adrenergic receptor causes K+ release
Alpha 1
Dopamine (Intropin) is used to treat and what receptor is stimulated in this treatment

activates B1 in heart
what agonist is
isoproterenol (isuprel)
what are the effects
non-selective B agonist

adverse reactions: tachycardia, BP, arrhythmias
phenyleprhine (neosynephrine)
alpha 1 agonist

note: not inactivated by COMT
phenylephrine is used to treat

two side effects?
nasal congestions

note: it causes mydriasis (excessive dilatio nof pupil) and hypertension
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
explain the paradoxical effect of clonidine in terms of the acute hypertensive response followed by hypotension
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
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
the advantage of Dobutamine over other sympathomimetic drugs
does not increase HR only inotropy so it does not increase O2 demand
albuterol (Ventolin)

is a bronchodilator what are the adverse reactions
B2 agonist

adverse reactions: tachycardia, tremor, tolerance

mechanism of action
indirect acting agonist

increases NE release, prolonged duration and potent CNS stimulant
ephedrine is used to treat what two things
nasal decongestant and hypotension
indirect adrenergic agonists cause their effect by what mechanism
increase the release of NE
amphetamine is what kind of drug?

used to treat?
it is indirect agonist (increases release of stored catecholamines)

treat: obesity (appetite control), narcolepsy, ADD
tyramine is what kind of drug and is found in high conc where
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
what is the difference between catecholamines and noncatecholamines in terms of theree duration and administration
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
cocaine is what kind of drug

what is the mechanism?
indirect acting adrenergic agonist

inhibits NE and dopamine reuptake
what adrenergic receptor causes K+ release
Alpha 1 (liver and salivary gland
three mechanisms by which sympatholytic drugs block adrenergic receptor action
1. decrease sympathetic outflow
2. suppress nerve terminal NE (inhibit synthesis, deplete granule, suppress release of NE)
3. Block postsynaptic receptors
irreversible adrenergic antagonists attach how

the block is insurmoutable and not overcome by NE

e.g phenoxybezamine
reversible competitive antagonists is different from irreversible adrenergic antagonists hoq
the antagonist can dissociate from receptor.

they produce equilibrium blockade

block disappears as free drug is metabolized
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
phentolamine (Regitine)
reversible alpha adrenergic blocker

phenoxybenzamine (Dibenzyline)
irreversible alpha adrenergic blocker

used in peripheral vasospasm. used to treat pheochromocytoma and Raynauds disease
name a alpha 2 adrenergic antagonist
they are not clinically useful.
alpha 1 adrenergic selective blockers can be used to treat
hypertension and BPH

caues vasodilation and reduction in arterial pressure

no decrease in cardiac function and no reflex tachycardia
Prazosin (Minipress)

adverse reaction
alpha 1 adrenergic antagonist

treats hypertension
'first dose' effect of postural hypotension
so be careful when giving to elderly or someoneon diuretic
what is a partial adrenergic agonist
a drug which blocks receptor partially so that some sympathetic activity still occurs
by what mechanism does beta blockers have a local anesthetic action
effects Na channels
beta blockers are absorbed well after oral administration and their peak concetration takes how long
1-3 hours
why might you not want to stop a beta blocker immediately
you will cause upregulation of receptors - so you want to taper off
what three diseases should you beware of when using beta blockers
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)
Propranolol is what kind of drug
Beta adrenergic non selective blocker
propranolol is used to treat
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)
why might you combine a beta blocker with a diuretic
reduced blood pressure - decrease renal perfusion - increase in na retention - increase BP
Timolol (blocadren)

Beta adrenergic non selective blocker

treat:open angle glaucoma

note: low lipophilicity, no membrane stabilization.
Pindolol (Visken)
non selective beta adrenergic blocker

(partial agonist activity)
why might pindolol be good for a pt who is subject to bradycardia
partial agonist activty

smaller reductions in resting HR.
Sotalol (Betapace)

used to treat
non selective Beta adrenergic antagonist

atrial and ventricular tacharrhythmias
how does sotalol work
beta non selective antagonists

prolongs cardiac action potential

blocks K+ channels.
Metoprolol (Lopressor)

to treat
Beta 1 antagonist

hypertension, ischemic heart disease
why might you choose metoprolol when treating someone with a kidney problem
notable hepatic biotransferation - get rid of via liver
Atenolol (tenormin)


why good for someone with hepatitis?
Beta 1 adrenergic antagonist

treat hypertension

renal excretion
Labetalol (Normodyne, Trandate

antagonizes B1,B2,A1

treat? hypertension, CHF, pheochromocytoma)
Carvedilol (Corea)

blocks alpha1, B1,B2

improves survival of pts with heart failure

note: has antioxident effects
explain all the places where aCh works
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
the receptors at the postganglionic terminus of parasympathetic fibers are called
why dont we cuse AcH therapeutically
1. cannot penetrate membranes
2. multiplicity of actions
3. rapid inactivation
a fall in blood pressure mediated by muscarinc receptors on vascular smooth muscle happens via what mechanism
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

actions of muscarinic receptors

Bronchorrea (increase secretions and Bronchoconstriction)
Pseudo ChE
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
muscarinic agaonist

used to challenge somone who is suspected to have asthma
muscarini agonist

used to relieve GI dysmotility

replaced metoclopramide (acts upstream on the neuron to release ACh at the terminus)
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.
how might you get flaccid paralysis with ACh
too mcuh ACh - receptor repolarizes and becomes refractory to further depolarization (depolarization-desensitizatoin blockage)
what effects does nicotine have on the nicotinic receptos (sym or para?)
nicotine depolarizes ganglia resulting first in stimulation and then paralysis of all ganlgio
the signs of nicotine poisoning are due to
sympathetic discharge from adrenals and possibly sympathetic ganglia

at high doses though you get a decrease in BP due to ganglionic block, and paralysis
three classes of ChE inhibitors
1. Edrophonium
2. Carbamate ChE
3. Organophosphate
a ChE inhibitor that does not form a covalent bond w/ the enzyme. it is highly charded and does not cross the BB
uses of Edrophonium
diagnosis of myasthenia gravis because effects are dissapated in minutes
myasthenia gravis involves what problem
Ab from thymus attack motor end plates in periphery causing impairment of neurotransmission -

muscle weakness and rapid muslce fatique
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)
why do carbamate ChE last a long time
they bind covatlently to the ezyme and leave behind a carbamoyl residue that hydrolysis over hours.

use to TREAT myasthenia gravis
Treat myasthenia gravis
why is neostigmine designed with a quaternary ammonium group
keep it out of the CNS
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.
the group of ChE inhibitors that included insecticides parathion, malathion and nerve gases sarin and soman
organophosphate ChE inhibitors
mechanism of organophosphate ChE inhiboros
react covalently w/ esteratic site and leave behingd phophorylated enzyem that requires hundresn of hours hydrolyze
Pralidoxime's effect on ChE inhibors
given to counter act the phosphorylating effect of organophosphate ChE inhibitors but contraindicated in carbamate ChE inhibtor poisoning
the transmemebrane muscarinic receptors linked to phospholipase C
M1 , 3, 5
The muscarinic receptor linked in an inhibitory manner with adenyl cyclase
M2 and M4
M2 Receptor is found where
stomach and heart
M3 R is found where
which Muscarinic Receptors are found on nerves, CNS
1, 4, 5
muscarinic receptor antagonist which is a antispasmodic
muscarinic R antagonist used to treat Parkinsons
muscarinic Receptor antagonist used as a MNJ blocker
atropine effect on the eye
muscarinic R blocker so causes dilation for days (mydriasis)

could be dangerous for pts with narrow angle glaucoma
what kind of channel are the Nicotinic Receptors

at ganglia (two subunits)
at NMJ (5 subunits)

there are some semi-selective antagonists
M1 muscarinic antagonist
reduces gastric acid secreation

treat: peptic ulcer
Atropine effect on urinary system
causes urinary retention

good to treat enuresis (involuntary voiding of urine)
an muscarinic receptor antagonists which treats motion sickness.

but blocks short term memory !
the only depolarizing blocker at the MNJ in clinical use
the effects of succinylcholine
continued binding to nicotinic receptor causes continue depolarization and receptor is incapable of transmitting further impulses. causes flaccid paralysis
succinylcholine is cleared by
plasma ChE, so pts lacking enzyme are paralyzed for many hours instead of 5 to 7 minutes
first muscle to be come flaccid with succinylcholine
chest and abdomen
why might succinylcholine cause hyperthermia w/ muscle rigitity
uncontrolled release of Ca++ from SR

treat hyperthermia with ice bath
treat muscle rigidity caused by succinylcholine overdose with
dantrolen (blocks release of Ca2
what two things synergize with succinylcholine
anesthetic gases
aminoglycoside antibiotics
nondepolarizing blocker at NMJ
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
a aminosterol which is a competitive nondepolarizing MNJ blocker and cleared by RENAL excretion
two aminosterols which are competitive nondepolarizing MNJ blockers which are cleared by LIVER metabolism
a benzoisoquinolinium and a competitive nondepolarizing MNJ blocker which is cleared by liver and plasma esterases
with nondepolariing competitive cholinergice blockers what size muscles are affected first
small (opposite succinylcholine)
what would you give a patient to reverse the effects of a nondepolarizing competitive cholinergic blockes
the only one ganglionic cholinergic blocker in clinical use and is nondepolarizing competitive
uses of trimethaphan
blocks cholinergic receptors

used for controlling hypertensive crises or surgery for aortic aneurysm

effects dissipated in minutes; cleared by the liver
how does the botulinum toxin work
ACh vesicles cant dock properly and neurotransmitter cant be released