Flashcards in Drugs affecting ANS Deck (51):
1
length of symp fibers
short pre and long post
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length of para fibers
long pre and short post
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three major events at synapse
1. release NT
2. receptor binding and signal transduction
3. termination of NT
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How can you terminate NT?
1. enzymatic degradation
2. reuptake via monoamine transporter
3. diffusion
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where is ACh released?
1. para pre and post ganglionic neurons
2. symp preganglionic neurons
3. symp postganglionic neurons that innervate most sweat glands
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where is N,m receptors found?
NMJ
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binding of ACh N,m receptors
constriction
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were is N,n receptors found?
autonomic ganglion, adrenal medulla, CNS
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binding of ACh at N,n receptors at autonomic ganglionic
propagate AP
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binding of ACh at N,n receptors at adrenal medulla
release EPI and NE
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binding of ACh at N,n receptors in CNS
multiple effects
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where is M1 receptors found?
salivary glands and stomach
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where is M2 receptors found?
cardiac muscle
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where are M3 receptors found?
GI, glands, pupil, bronchiole and bladder and smooth muscle
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where are M4 and M5 receptors located?
CNS
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binding of ACh at M1 receptors on salivary glands and stomach
increase salivary and gastric secretion
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binding of ACh at M2 receptors on cardiac muscle
lower HR
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binding of ACh at M3 receptors on GI
increase gastric emptying and increase gut motility
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binding of ACh at M3 receptors on sweat glands
sweat gland secretion
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binding of ACh at M3 receptors on pupil
miosis (constriction)
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binding of ACh at M3 receptors on smooth muscle in bronchial and bladder
constriction
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what releases EPI?
adrenal medulla
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what releases NE?
adrenal medulla and symp postganglionic neurons
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what releases DA?
symp postganglionic neurons that innervate renal vascular muscle
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where does EPI preferentially binds?
alpha, beta 1-2 receptors
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where does NE preferentially binds?
alpha and beta1,3 receptors
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effect of binding alpha1 on vascular smooth muscle
contraction --> increase bp
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effect of binding alpha2 on some vascular smooth muscle
contraction --> increase bp
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effect of binding beta1 on heart
increase heart rate and force of contraction --> increase bp
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effect of binding beta1 on juxtaglomerular cells
increase renin release --> increase bp
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effect of binding beta2 on vascular smooth muscle
relaxation --> decrease bp
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Lung: β2 →
bronchodilation
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GI: α, β1/2 →
decrease motility
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GI:α, β2 →
sphincter contraction
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Salivary glands: α →
constriction
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Ocular: α1 →
mydriasis (dilation)
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Pancreas: α2 →
lower insulin release
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Pancreas β2 →
increase insulin release
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GU smooth muscle: α1 →
sphincter contraction
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Adipose: α2 →
lower lipolysis
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Adipose: β2,3 →
increase lipolysis
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Hepatic: α1, β2 →
increase glycogenolysis/gluconeogenesis
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what is the major mode of termination of catecholamines
reuptake via transporters
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degrading enzyme found in mitochondrial membrane of most cell types
MAO
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degrading enzyme found in liver, neurons and extracellularly
COMT
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isoform of MAO that degrades serotonin (5HT), DA, NE, E
MAO-A
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isoform of MAO that degrades DA more rapidly (found in blood platelets)
MAO-B
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what does COMT degrade?
DA, NE, EPI
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Where does sympathetic ganglionic fibers originate from?
thoracic-lumbar of spinal cord
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Where does parasympathetic ganglionic fibers originate from?
cranio-sacral of spinal cord
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