SYMPATHOMIMETIC DRUGS Flashcards by lindsey france

Natural Catecholamines what are they called? what are 3 examples?

endogenous

EPI
NE
Dopamine

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Synthetic catecholamine

Isoproterenol

Dobutamine

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Synthetic non-catecholamine (Indirect acting)

Ephedrine
Mephentermine
Amphetamine
Metaraminol

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Synthetic non-catecholamine (Direct acting)

Phenylephrine

Methoxamine

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what medication inhibits the transport of dopamine into the synaptic vesicle

reserpine

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what does dopamine become when it enters the vesicle

norepinephrine

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which 2 drugs blocks the release of NE from the presynaptic cell membrane

guanethidine and bretylium

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how is NE released from the cell membrane

exocytosis from the Ca++ influx

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once NE is released it binds to the receptors activating what

adenylate cyclase

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once NE activates adenylate cyclase what does it do next

opening of ion channel/ formation of cAMP

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once NE channels are open and camp is activated what is the last step

contraction of arterial smooth muscles, increase heart rate and contractility

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removal of NE. what inhibits reuptake

cocaine and TCA

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what metabolizes NE

COMT (PLASMA) and MAO (synaptic cleft)

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what are Adrenergic Receptors

a1, a2, b1, b2, b3

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what are cholinergic receptors

nicotinic and muscarinic receptors

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a1 Receptors

located where?

vascular smooth muscle of skin

splanchnic regions

GIT

bladder sphincter

radial muscle of iris

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a1 Receptors what is their effect?

Produce excitation (contraction of vascular smooth muscles)

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a1 Receptors what are they equally sensitive to?

NE and EPi

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a1 receptor arterial vasoconstriction leads to what CV effects ?

increase SVR, LV afterload, and BP

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a1 receptor venous vasoconstriction causes what effect ?

increase venous return, increase SV, increase CO

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a1 receptor stimulation inhibit what

insulin secretion and lipolysis

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a1 receptor m/a

formation of IP3 and increased intracellular calcium

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a1 receptor pre synaptic or post synaptic?

postsynaptic adrenergic

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a2 receptors location?

presynaptic membrane & postsynaptic in brainstem, walls of GIT, platelets, and fat cells

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a2 receptors are postsynaptic in?

brainstem, platelets, fat cells, and walls of GIT

a2 receptors produce

inhibition of NE release and synthesis (relaxation and dilatation) blocks Ca entry

a2 receptors produce what type of feed back loop

-ve

a2 receptors inhibit what

sympathetic outflow in brain stem

a2 receptors produce

sedation and analgesia in substantia gelatinosa

a2 receptors m/a

inhibition of adenylate cyclase, decrease camp and decreases ca entry

b1 receptors are located where

sa node and av node ventricular muscle

b1 receptors produce

excitation, increase hr, increase conduction, increase contractility, and increase cardiac output.

b1 receptors are sensitive to

NE and EPI

b1 receptors m/a

activation of adenylate cyclase and increase camp

b2 receptors location

smooth muscle of skeletal muscle blood vessel bronchial smooth muscle walls of GIT and bladder

b2 receptors produce what?

relaxation (dilation of vascular smooth muscle, dilation of bronchioles, relaxation of the pregnant uterus- tocolysis)

b2 receptors also produce increase

bg calorigenesis | glycogenolysis and gluconeogenesis

b2 receptors m/a

activation of adenylate cyclase and increase cAMP (same as b1)

b3 receptors located where

gallbladder and adipose tissue

b3 receptor function

unknown function

nicotinic receptors located where

autonomic ganglia (Nn) of the sympathetic and parasympathetic neuromuscular junction(n1) and adrenal medulla (n2) the receptors at these locations are similar but no identical

nicotinic receptors are activated by

ach or nicotine

nicotinic receptors produce

excitation

cholinergic receptors nicotinic receptors ganglion blockers examples and what do they do

hexamthonium trimethaphan block the nicotinic receptors for Ach in autonomic ganglia but not at the NMH

cholinergic receptors nicotinic receptors m/a

opening of Na+ and K+ channels

cholinergic muscarinic receptors - location

in heart (m2) smooth muscle (m3) (except vascular smooth muscle) and glands(m3)

cholinergic receptors muscarinic receptors -activated by

Ach and muscarine

cholinergic receptors muscarinic receptors are inhibitory

in heart (decrease heart rate decrease conduction velocity in AV node)

cholinergic receptors muscarinic receptors are excitatory

in smooth muscle and glands increase motility and increase secretion

cholinergic receptors muscarinic receptors are blocked by

atropine

cholinergic receptors muscarinic receptors mediate

sux induced bradycardia

cholinergic receptors muscarinic receptors m/a in heart? in smooth muscles?

in heart sa node: inhibition of adenylate cyclase leads to opening k channels, slowing rate of phase 4 depolarization and decrease heart rate. in smooth muscles and glands: formation of IP3 and increase intracellular Ca++

cAMP Mechanism receptors

B1 &B2 & A2

receptors couples with ion channels

cholinergic nicotinic

IP3 mechanism receptor

A1 receptor | cholinergic muscarinic

Nitric Oxide utilizes this second messanger

cGMP

Epinephrine mechanism application

Direct general agonist (a1, a2, b1, b2) Anaphylaxis, glaucoma (open angle) asthma, hypotension with LA

Norepinephrine mechanism application

a1, a2, b1 hypotension decrease renal perfusion organ ischemia

isoproterenol mechanism application

B1=B2 av block (rare)

dopamine mechanism application

D1=D2 >b>a shock increase renal perfusion and GFR heart failure

dobutamine mechanism application

b1>b2 shock and CHF

amphetamine mechanism application

indirect general agonist releases stored catecholamines narcolepsy, obesity, adhd

ephedrine mechanism application

indirect general agonist, releases stored catecholamines nasal decongestants urinary incontinence hypotension hypotension with epidural/spinal anesthesia

phenylephrine mechanism application

a1>a2 pure a agonist pupil dilation vasoconstrictor increase SVR increase MAP nasal decongestant

albuterol, terbutaline

B2>b1 asthma & premature labor

cocaine mechanism application

indirect general agonist uptake inhibitor causes vasoconstriction and local anesthesia

clonidine & a-methyl dopa

centrally acting a2 agonist, decrease central sympathetic outflow hypertension, decrease MAC, increase Anesthesia/analgesia

Nonselective Beta 1 Beta 2 antagonist (propranolol) what effect ok K+ level?

Hypokalemia prevention . ( explanation) By blocking beta 2 .Prevents the Beta 2 activation of Na/K pump which causes K+ to move inside inside cell. Prevent the K movement inside cell, prevents hypokalemia.

Cardioselfrive Beta 1 antagonist ( atenolol ) effect of K+level

Cause hypokalemia