Pharmacology Synopses 2 Flashcards by X x

Acetyl CoA + Choline via choline acetyl transferase

Ach

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ratelimiting step in Ach formation

availability of choline

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excitation by increasing Na+ and K+ conductances

Ach in skeletal muscle

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excitation by increasing Na+ conductances

Ach in smooth muscle

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inhibition (slowing heartbeat) by increasing K+ conductances

Ach in cardiac muscle

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Acetylcholinesterase

hydrolyzes Ach at postsynaptic membrane

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Butyrocholine esterase

metabolizes Ach analogs in blood and liver

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250 kDa multimeric glycoprotein, related to other ionopore receptors (GABAa)

nicotinic Ach receptor

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80 kDa monomeric glycoprotein, related to G-protein coupled receptors like beta-adrenergic

muscarinic Ach receptor

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skeletal muscle neuromuscular junction receptor type

Ach nicotinic

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main preganglionic to postganglionic synapses receptor type

Ach nicotinic

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all parasympathetic postganglionic cells

Ach, muscarinic

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____ are primary agents for autonomic ganglia, ____ are only effective as adjuncts

nicotinic, muscarinic

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parasympathetic effects: eye

miosis (constriction of pupil)

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parasympathetic effects:heart

decrease in heart rate

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parasympathetic effects: GI tract

increase motility and tone

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parasympathetic effects: bladder

contraction

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parasympathetic effects: glands (sweat, lacrimal, nasopharyngeal, etc)

increased secretion (*sweat glands receive cholinergic sympathetic innervation)

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parasympathetic effects: adrenal medulla

none, but receives direct Ach nicotinic pre-ganglionic innervation

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tissues without nerves, but with muscarinic receptors (many vascular beds)

Ach causes vasodilation

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autonomic effects of parasympathetic system, CNS (if passes blood-brain barrier), slow modulatory electrophysiological effects

muscarinic Ach receptor

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autonomic ganglia and skeletal muscle, symapthetics & parasympathetics, fast electrophysiological effects

nicotinic Ach receptor

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comes from adrenal medulla chromaffin cells, 10-20% of amines secreted

norepinephrine

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comes from adrenal medulla chromaffin cells, 80-90% of amines secreted

epinephrin

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50% of catecholamine content of CNS mammals, interneurons in some sympathetic ganglia

dopamine

rate limiting step in catecholamine production

tyrosine to DOPA via tyrosine hydroxylase

Pumps 90% norepi into storage vesicles

vesicular monoamine transporter (VMAT-2)

norepi in axoplasm does what?

regulates synthesis

takes most NE released from nerves back up into the synaptic terminal

norepinephrine transporter (NET). NET also transports DA and E.

Cocaine and imipramine (tricyclic antidepressant) inhibit

NET

take synaptic NE into other cells

OCTs (organic cation transporters)

metabolize NE in other cells

COMT (catechol-O-methyltransferase)

members of g-protein-linked receptor family, 7 transmembrane passes

adrenergic receptors

Alpha 1 tissues

vascular smooth muscle, liver

Alpha 1 responses

contraction in vascular smooth muscle, glycogenolysis and gluconeogenesis in liver

Alpha 2 tissues

Nerve terminals, vascular smooth muscle

Alpha 2 responses

decreased release of NE in terminals, contraction in vascular smooth muscles

Beta 1 tissues

Heart

Beta 1 responses

increases force and rate of contraction, AV nodal conduction velocity

Beta 2 tissues

smooth muscle (VASCULAR, bronchial, GI and GU), liver

Beta 2 responses

relaxation in smooth muscle, glycogenolysis and gluconeogenesis in liver

act at sympathetic and parasympathetic ganglia, skeletal muscle and perhaps CNS

nicotinic agonists (and antagonists)

structural similarity to Ach allows binding and blocking of AchE

anticholinesterase mode of action

Anti-ACHEs act

at both nicotinic and muscarinic cites

autonomic effects in order of appearance by dose of muscarinic antagonists

1. decreased salivation and sweating. 2. pupil dilation and heart rate increase 3. inhibit micturition, decrease gut motility 4. inhibit gastric secretion

CNS effects of muscarinic antagonists

scopolamine causes drowsiness, amnesia, etc. in clinical doses, excitement, restlessness and hallucination in higher doses. atropine has none

subtype specific: M1

brain (cognition)

subtype specific: M2

Heart

subtype specific: M3

eye

subtype specific: M1/3

salivary glands

subtype specific M2/3

GI tract and bladder

Epinephrin stimulates which receptors

All adrenergic!

Give epi how?

IM or SC, since PO gets degraded in the GI tract by MAO or COMT.

IV epi is dangerous to hypertensive and hyperthyroid because

increases BP (via alpha 1) → cerebral hemorrhage, and increases HR (via beta 1) leads to arrhythmia

reflex brachycardia pronounced with NORepi why?

no beta 2 means no skeletal vasodilation to counteract splanchnic vasoconstriction of alpha 1: increased blood pressure

Are MASTs broken down by COMT?

No. That is why they have a longer half-life

Tyramine (from wine and cheese) + MAO inhibitor

hypertensive crisis due to release of NE stores.

amphetamine, methamphetamine, and cocaine

block NE reuptake

reliance on stored NE causes ____ with meth, tyramine and amphetamine

tachyphylaxis

epi reversal

give epi with alpha antagonists, so only beta effects are agonized.

responsible for BP increase upon standing

Alpha 1, so you'll faint if it is inhibited

blocks alpha 2 only, increases sympathetic tone, HR and BP

Yohimbine (opposite of clonidine)

SA node location

at the junction of the SVC and right atrium

the only way the impulse can get to the ventricle

through AV node and His bundle

After His, impulse enters ___ and propagates through ventricles

Purkinje cells

Does SA node have resting potential?

No. Self-excites.

sinus node has special pacemaker cells that pass current from out to in, creating

funny current

Like SA, AV node depolarizes due to

inward Ca current

Ca current is slow, allowing what

atria to empty into ventricles before ventricles contract

What causes contraction?

Inward Ca current (Ca-->SR-->releases Ca-->contraction)

P on EKG

atrial polarization

QRS on EKG

ventricular depolarization

T on EKG

repolarization

innervate sinus node, atria, and are not in ventricles

parasympathetics

four ways to change heart rate

level of max diastolic potential, rate of funny current, change threshold potential, change slope of pacemaker current via SA node

sympathetic (adrenergic to beta 1) effects on SA node

increases slope of funny current, membrane depolarizes faster, HR increases

parasympathetic effects on SA node

decrease pacemaker current, slow down rate of polarization, decrease HR

sympathetics on AV node

increase inward Ca current, increase nodal action potential, faster conduction

parasympathetics on AV node

decrease AV nodal action potential, slower conductoin

P w/o QRS

AV block, extreme parasympathetic activation

sympathetics enhance inward pacemaker current ____ than they do in the sinus node

parasympathetics don't work on ventricular rhythms, but

they can work on atrial tachycardia

who can change stroke volume?

sympathetics, increase SV. Paras don't affect ventricular muscle

what can weaken contractions but act of the atria only?

Ach.

Cardiac output equation

CO = SV * HR

blood pressure equation

BP = SV *TPR

mean arterial pressure equation

CO * TPR

systolic PP

during contraction

diastolic PP

during relaxation

Pharmacology Synopses 2 Flashcards

(89 cards)