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44 Cards in this Set
- Front
- Back
M1 receptor MOA
Found where? |
MOA: Forms IP3 and DAG -> ↑ [Ca] intracellularly
Find in CNS |
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M2 receptor MOA
Found where? |
Opens K+ channels -> hyperpolarization, also inhibits adenylyl cyclase
find in myocardium |
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M3 receptor MOA
Found where? |
Forms IP3 and DAG -> ↑ [Ca] intracellularly
Find in Blood vessels, GI tract |
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Nicotinic NN MOA & Location
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in ganglia
opens Na/K channels -> depolarization |
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Nicotinic NM MOA & Location
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in Skeletal muscle
opens Na/K channels -> depolarization |
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α1 Adrenergic Receptor MOA
Found where? |
MOA: Forms IP3 and DAG via GPCR -> ↑ [Ca] intracellularly
Find: mainly post-synaptic (smooth muscles especially) |
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α2 Adrenergic Receptor MOA
Found where? |
inhibits adenylyl cyclase (↓ cAMP): Hyperpolarizes
Find: pre-synaptic adrenergic nerve terminals, smooth muscle |
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β1 Adrenergic Receptor MOA
Found where? |
MOA: Stim adenylyl cyclase via GPCR (↑ cAMP)
Find: Heart, lipocytes, brain, ciliary body |
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β2 Adrenergic Receptor MOA
Found where? |
MOA: Stim adenylyl cyclase via GPCR (↑ cAMP)
Find: Postsynaptic: smooth muscle & cardiac |
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β3 Adrenergic Receptor MOA
Found where? |
MOA: Stim adenylyl cyclase via GPCR (↑ cAMP)
Find: Fat cells (TAG -> Fatty acids) |
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Dopamine D1 MOA
Find where? |
MOA: Stim adenylyl cyclase via GPCR (↑ cAMP)
Find: Brain effector tissues, esp. smooth muscle of renal vascular bed |
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Dopamine D2 MOA
Find where? |
inhibits adenylyl cyclase (↓ cAMP) & open K+ channels (Hyperpolarizes)
Find: Brain effector tissues - smooth muscle presynaptic nerve terminals |
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Hemicholinium
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inhibits transport of choline into neuron (for creation of acetylation)
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Botulinum toxin
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Blocks release of Ach
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Rate limiting step of ACH synth
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Acetyl + choline
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Rate limiting step of Norepinephrine synthesis
inhibited by? |
Hydroxylation of Tyrosine by Tyrosine Hydroxylase
Inhibited by Methyl-tyrosine |
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Reserpine
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inhibits transport of choline into neuron (for creation of acetylcholine)
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Guanethidine
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inhibits release of Norepinephrine
|
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Bretylium
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inhibits release of Norepinephrine
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Cocaine
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inhibits reuptake of Norepinephrine
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imipramine
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inhibits reuptake of Norepinephrine
|
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Norepinephrine metabolized by
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COMT & MAO
(Catechol-O-Methyltransferase & MonoAmine Oxidase - MAO in mitochondria) |
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Tyramine
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Increase release of Norepinephrine
|
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Amphetamine
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Increase release of Norepinephrine
|
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Drugs that inhibits release of Norepinephrine
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Guanethidine or Bretylium
|
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Drugs that inhibit reuptake of Norepinephrine
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Cocaine & imiprimine
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Drugs that Increase release of norepinephrine
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Tyramine & amphetamine
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Catecholamines: What ones do we know?
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Norepinephrine, epinephrine
|
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Organs w/ Dual innervation
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Eye, Heart, Bronchial, Stomach, Intestine
|
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Organs dominated by Sympathetic tone:
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Vascular smooth mm
Low sympathetic tone -> dilate/relax, ↓ TPR, BP |
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Organs dominated by parasympathetic tone:
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heart, eyes, GI tract, urinary bladder
|
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Effect of Muscarinic Agonists on eye
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1) Contract circular fibers (constrict pupil)
2) relax lens for near vision 3) improve drainage |
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Effect of Muscarinic Antagonists on eye
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1) Dilate pupil
2) Occlude Canal of Schlemm 3) Raise IOP |
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Iris muscle receptor types and actions
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Parasympathetic Receptor = M3 (Circular smooth mm = spincter)
Sympathetic = α1 (Radial Smooth mm = Dilator) |
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Ciliary body receptor types and actions
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Parasympathetic receptor = M3 (ciliary body)
stim -> Accomodation (near vision) Block -> Cycloplegia (blurred vision) Sympathetic to SM: Stim -> Relaxation for Far vision, Block -> Minimal effect |
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PS effects on IOP
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PS Stim: Contract circular muscle of iris -> ↓ occlusion of canal -> ↑ Drainage
PS Block: Dilate pupil -> ↓ drainage (occludes canal) -> ↑ IOP |
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Bladder innervation (Somatic and Autonomic)
Receptor types (Symp and PS) Effects fo stim and block of PS or Symp |
Somatic: Striated muscles of EXTERNAL SPHINCTER
Autonomic: PS stim -> contract detrusor, relax Trigone/Sphincter (M3) -> micturation (Inhib PS: -> Urinary retention) Symp Stim -> contracts trig/sphincter, relax detrusor (α1, β2) -> urinary retention (Inhib Symp. -> minimal effect) |
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GI effects from: PS Stim or Inhib
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PS stim -> ↑ GI motility, tone, relax sphincters, ↑ exocrine gland secretion, increase peristalsis
Inhib PS -> Constipation |
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GI effects from: Symp stim or Inhib
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Symp Stim -> 1)Stim β2 -> relax GI smooth muscle 2) Via presynaptic α2 receptors in submucosal plexus -> ↓ ACH release -> ↓ GI Motility 3) Contract sphincters (α1) -> Constipation
Symp Inhib -> Minimal effect |
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Metabolic effects of Symp Stim
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↑ Glycogenolysis: (β2, α), ↑ Gluconeogensis (β2, α) in liver
↓ Insulin secretion (α2) but may ↑ (β-2) inhibition is PREDOMINANT effect -> ↑ plasma [Glucose] ↑ Lipolysis (β3) in adipose tissue -> breakdown of triglycerides to FFA Inhibition of sympathetic activity (β) ↓ gluconeogenesis & Lipolysis -> ↓glucose & FFA (PS NOT involved) |
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Heart Sympathetic Innervation
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β1: 1) SA -> ↑ HR, 2) AV -> ↑ conduction, 3) Ventricle -> ↑ contractility
NO Vagus innervation of Ventricle |
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Heart Parasympathetic Innervation
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VAGUS: Atria, SA, AV nodes: PS Dominates
Stim -> ↓HR, Conductivity Inhib -> ↑HR, Conductivity |
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Blood Vessels Autonomic Innervation and receptors
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Skin & viscera: Symp: (α1) Stim -> Vasoconstrict, ↑ TPR
Inhib -> Vasodilate (↓TPR) Arterioles in Skeletal muscle (β2): Stim -> vasodilate (↑ Blood flow) NO PS innervation but M3 present (respond to Cholinergic Agonist: dilate) |
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Baroreceptor Reflex
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↑BP -> ↑ Vagal activity (↑Baroreceptor firing), ↓ Symp activity ->
↓HR & ↓CO & ↑ Vasodilation ↓BP -> ↓vagal, ↑Symp -> ↑HR, ↑ vasoconstriction, ↑ TPR e.g. Block PS -> Postural reflex -> hypotension -> fainting |