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253 Cards in this Set
- Front
- Back
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Ganglia
somatic - autonomic - |
Ganglia:
somatic - none autonomic - one synapse outside CNS |
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Myelination
somatic - autonomic - |
Myelination
somatic - heavy autonomic - none/light (slow conduction) |
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Sectioning
somatic - autonomic - |
Sectioning
somatic - sectioning --> paralysis & atrophy autonomic - sectioning --> independent activity/supersensitivity |
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Sectioning
somatic - autonomic - |
Sectioning
somatic - motor end plate autonomic - extensive ramifications and varicosities, but no specialized regions of contact on neuroeffector cells |
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varicosities
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sites of transmitters release
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Distributions
PNS - SNS - |
Distributions
PNS - selective SNS - widespread |
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Type of discharge
PNS - SNS - |
Type of discharge
PNS - discrete SNS - diffuse |
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Function
PNS - SNS - |
Function
PNS - resting and digesting SNS - fight or flight |
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PNS (craniosacral) cell bodies of first order neurons located in...
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midbrain
medulla sacral cord |
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PNS (craniosacral) cell bodies of second order neurons located in ...
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innervated organ (except in head)
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SNS (thoracocolumbar) cell bodies of first order neurons are located in...
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intermediolateral (IML) column of spinal cord, T1 - L2/3
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SNS cell bodies of second order neurons are located in...
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chain ganglia (paravertebral)
visceral (prevertebral) or terminal ganglia |
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white rami communicantes
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preganglionic myelinated fibers
exit with the ventral roots of spinal nerves |
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gray rami communicantes
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non-myelinated, second order neurons (post-ganglionic)
join spinal nerves to peripheral structures |
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in what gland do the SNS and PNS have the SAME function?
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Both SNS and PNS increase secretion from salivary glands
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Structures innervated exclusively by the SNS
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spleen
ventricular cardiac muscle radial muscle in the iris limbs (smooth muscle and glands of) |
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structures innervated exclusively by the PNS
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bronchial smooth muscle
ciliary muscle in the eye circular muscle in the iris |
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Sites of direct control of the SNS and PNS on the GI tract
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GI sphincters
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What part of GI tract is not directly controled by SNS and PNS (but is under control of enteric system)
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gut smooth muscle and mucosa
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Describe the SNS' patterns of activity
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continuously active
degree of activity varies from moment to moment & from organ to organ (sympathetic tone) sympathoadrenal system can discharge as a unit in response to threat can discharge discretely to regulate vascular tone and glandular secretions |
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2 examples of when the SNS can discharge discretely to regulate vascular tone and glandular secretions
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an increase in body temp increases blood flow in skin and sweating
baroreceptor reflex: moving from a reclining to a standing position causes vasoconstriction in lower limbs |
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Type of adrengergic receptor in IRIS
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alpha-1
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action of sympathoadrenal system or adrenergic receptor agonists on IRIS
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mydriasis
(contraction of radial muscle) |
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action of parasympathetic nervous system or cholinergic agonists on iris
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miosis
(contraction of sphincter muscle) |
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Parasympathetic action on ciliary muscle
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constriction
(for near vision) |
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Autonomic action on nasopharyngeal glands
SNS or PNS? |
PNS stimulates nasopharyngeal glands
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Type of adrenergic receptor in salivary glands
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alpha-1
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Action of SNS on salivary glands
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stimulation of thick, mucinous saliva
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Action of PNS on salivary glands
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stimulation of profuse, watery saliva
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Type of adrenergic receptor in sweat gands
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alpha-1
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Action of adrenergic receptor agonists on sweat gands
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stimulation of glads (palms and forehead during stress)
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Action of sympathetic cholinergic stimulation on sweat gands
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stimulation of gland
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Type of adrenergic receptor in S.A. node
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beta-1
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Effect of SNS on S.A. node
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increase heart rate
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Effect of PNS on S.A. node
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decrease heart rate
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Conduction velocity is mediated by which type of adrenergic receptor?
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beta-1
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SNS action on conduction velocity in heart
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increase in atria, AV node, His-Purkinje fibers
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PNS action on conduction velocity
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decrease in AV node
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force of contraction in atria mediated by which adrenergic receptor type?
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beta-1
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force of contration in ventricles mediated by which adrenergic receptor type?
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beta-1
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effect of SNS stimulation on heart force of contraction
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increase
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effect of PNS stimulation on atrial force of contraction
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decrease
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effect of PNS stimulation on ventricle force of contraction
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none
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type of receptor that mediates stimulation of skin and mucosa arterioles
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alpha-1
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Effect of SNS or adrenergic agonist on skin and mucosa arterioles
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constriction
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Effect of PNS or cholinergic agonist on sin and mucosa arteriole
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dilation
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Skeletal muscle arteriole adrenergic receptor types
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alpha-1
beta-2 |
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Effect of alpha adrenergic receptor agonist stimulation on skeletal muscle arterioles
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constriction
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Effect of beta adrenergic receptor agonist stimuliation on skeletal muscle arterioles
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dilation
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Effect of cholinergic agonists/PNS on all arterioles
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dilation
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Types of adrenergic receptors on visceral arterioles
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alpha-1
beta-2 |
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Effect of alpha adrenergic receptor agonists on visceral arterioles
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constriction
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effect of beta adrenergic receptor agonists on visceral arterioles
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dilation
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types of adrenergic recptors on veins
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alpha-1
alpha-2 beta-2 |
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action of alpha adrenergic receptor agonists on veins
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constriction
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action of beta adrenergic receptor agonist on veins
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dilation
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effect of cholinergic/PNS stimulation on veins
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none
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type of adrenergic receptors on bronchioles
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beta-2
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effect of beta adrenergic agonists or SNS on bronchioles
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bronchodilation
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effect of PNS/cholinergic agonists on bronchioles
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constriction
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types of adrenergic receptors in GI tract
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alpha-2
beta-2, beta-3 |
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effect of alpha adrenergic stimulation on GI tract
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inhibit ACh release from enteric neurons
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effect of PNS/cholinergic agonists on GI tract
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increased tone
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effect of beta adrenergic agonists on GI tract
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relaxation
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type of adrenergic recepto in GI sphincters
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alpha-1
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effect of SNS on GI sphincters
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contraction
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effect of PNS of GI sphincters
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relaxation
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type of adrenergic receptor on gall bladder
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beta-2
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effect of SNS on gall bladder
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relaxation
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effect of PNS on gall bladder
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contraction
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type of adrenergic receptor on gall bladder
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beta-2
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type of adrenergic receptor on splenic capsule
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alpha-1
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action of SNS on splenic capsule
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constriction
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type of adrenergic receptor on detrusor muscle
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beta-2
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type of adrenergic receptor on trigone and sphincter
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alpha-1
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Effect of SNS or adrenergic stimulation on urinary bladder (detrusor, trigone and sphincter)
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relaxation (minor effect)
contraction |
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effect of PNS/cholinergic on urinary bladder
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contraction
relaxation |
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type of adrenergic receptor uterus (pregnant)
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beta-2
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type of adrenergic receptor male sex organs
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alpha-1
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action of SNS/adrenergic on male sex organs
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ejaculation and porstate capsule contraction
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action of PNS/cholinergic on male sex organs
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erection
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type of adrenergic receptors on piloerector muscles
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alpha-1
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type of adrenergic receptor that mediates muscle and liver glycogenolysis (carb metabolism)
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beta-2
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type of adrenergic receptor that mediates lipolysis (release of fatty acids)
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beta-3
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type of adrenergic receptor that mediates renin secretion
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beta-1
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Effect of SNS/adrenergic stimulation on renin secretion
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increase
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effect of PNS/cholinertic stimuliation on renin secretion
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NONE
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type of adrenergic receptor on beta cells of pancreas (insulin secretion)
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alpha-2
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type of adrenergic receptor on alpha cells of pancreas (glucagon secretion)
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beta-2
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action of SNS on insulin secretion
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decrease
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action of SNS on glucagon secretion
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increase
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action of PNS on insulin secretion
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increase
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action of PNS on glucagon secretion
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none
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type of adrenergic receptor in Na/K ATPase in skeletal muscle
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beta-2
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effect of SNS stimulation on Na/K ATPase in skeletal muscle
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transports K+ into muscle cells
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type of adrenergic receptors on mast cells
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beta-2
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effect of beta adrenergic agonists on histamine release (mast cells)
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decrease
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action of trimethaphan
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blocks transmission in autonomic ganglia
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how does trimethaphan influence baroreceptor neurons?
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??
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how does trimethaphan influence preganglionic sympathetic neurons?
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??
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how does trimethaphan influence postganglionic sympathetic neurons?
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??
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how does trimethaphan influence preganglionic vagal neurons?
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??
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how does trimethaphan influence postganglionic vagal neurons?
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??
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Consequent of a drug that increases BP, what happens to...
SNS activity? Vagus activity? HR? |
SNS activity decreases
vagus activity increases HR decreases |
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Consequent of a drug that reduces BP, what happens to...
SNS activity? vagus activity? HR? |
SNS activity increases
vagus activity decreases HR increases |
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General trend of baroreceptor reflex with respect to BP increase/decrease drugs?
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baroreceptor reflex acts to attempt to compensate for changes in blood pressure (opposing reactions)
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effect of phenylephrine on...
blood vessels baroreceptor activity PNS activity SNS activity |
phenylephrine -->
vasoconstriction increased baroreceptor activity increased PNS decreased SNS |
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effect of histamine on
blood vessels baroreceptor activity PNS activity SNS activity |
histamine:
vasodilation |
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Effect of ganglionic blockade on arterioles
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vasodilation
increased peripheral blood flow hypotension |
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Effect of ganglionic blockade on veins
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dilation
peripheral pooling of blood decreased venous return decreased cardiac output |
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Effect of ganglionic blockade on heart
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tachycardia
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Effect of ganglionic blockade on iris
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mydriasis
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Effect of ganglionic blockade on ciliary muscle
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cycloplegia - focus to far vision
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Effect of ganglionic blockade on GI tract
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Reduced tone and motility; constipation;
decreased gastric and pancreatic secretions |
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Effect of ganglionic blockade on urinary bladder
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urine retention
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Effect of ganglionic blockade on salivary glands
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xerostomia (dry mouth)
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Effect of ganglionic blockade on sweat glands
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anhidrosis
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3 sources of NE release
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some neurons in the CNS
from adrenal medulla from most postganglionic SNS neurons |
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ACh is released from...
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motor neurons to skeletal muscle
preganglionic neurons of SNS & PNS postganglionic neurons of PNS some post ganglionic in SNS (e.g.: to sweat glands) some neurons in CNS |
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Low concentrations of nicotine _____ ganglion cells
High concentrations of nicotine ____ ganglion cells |
Low concentrations of nicotine STIMULATE ganglion cells
High concetnrations of nicotine PARALYZE ganglion cells |
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Muscarine mimics the effects of ____
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PNS stimulation
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Actions of ACh at organs innvervated by ______ and _____ are muscarinic
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postganglionic PNS
cholinergic SNS |
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nAChR
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"ionotropic" (ligand gated - control Na+ [Ca2+] channels)
depolarization --> excitation rapid onset/short duration located on skeletal muscle and neurons |
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mAChR
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metabotropic (G-protein coupled)
inhibition or excitation depending on location slow onset/long duration |
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AChE
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acetylcholinesterase - degrades ACh
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ChAT
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choline acetyltransferase -
synthesizes ACh from AcCoA + choline |
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carbachol
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cholinergic agonist - enhances or mimics ACh
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physostigmine
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AChE inhibitor
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hemicholinium
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inhibits ACh synthesis
(blocks transport of choline into neuron) |
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botulinum toxin
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inhibits ACh release (targets SNARE proteins)
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organism that secretes botulinum toxin
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Clostridium botulinum:
spore-forming, anaerobic bacterium |
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4 symptoms of botulism
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pupillary dysfuntion
dysphagia descending falccid paralysis respiratory distress |
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what do botulism toxins bind?
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1st: transport sites on cholinergic nervet terminal (endocytosed)
2nd: proteases cleave SNARE proteins on synaptic vesicles and neuronal membrane |
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How long does recovery from botulism take?
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weeks to months (requires sprouting of new nerve terminals)
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BOTOX
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botulinum toxin A
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MYOBLOC
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botulinum toxin B
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3 indications for injecting BOTOX/MYOBLOC into skeletal muscles
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prevent disabling and painful involuntary muscle spasms
to treat strabismus cosmetic purposes |
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2 indications for injecting smooth muscles/glands with BOTOX/MYOBLOC
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to treat achalasia
to treat axillary or palmar hyperhidrosis |
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Biosynthesis pathway of catecholamines
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Tyrosine --> DOPA --> dopamine --> NE --> epi
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4 enzymes involved in biosynthesis pathway of catecholamines
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Tyrosine hydroxylase
DOPA decarboxylase Dopamine beta-hydroxylase Phenylethanolamine N-methyltransferase |
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Rate limiting step of catecholamine synthesis
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Tyrosine --> DOPA
catalyzed by Tyrosine hydroxylase |
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amine agonists
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phenylephrine
isoproterenol |
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block reuptake of NE
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cocaine
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release NE
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amphetamine
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NE antagonists
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phentolamine
propranolol |
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block release of NE
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guanethidine
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inhibit synthesis of NE
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alpha-methyltyrosine
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deplete NE
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reserpine
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false NE transmitter
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alpha-MDOPA
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these conditions involve catecholamines as part of routine management
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bronchial asthma
peripheral vascular disease congested mucous membranes local anesthetic tx allergies essential HTN |
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these conditions involve catecholamines as part of emergency management
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hypotension, shock
superficial hemorrhage anaphylactic reaction supraventricular tachycardia opthalmic disorders acute asthmatic attacks |
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direct-acting alpha-agonists
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NE
epi phenylephrine clonidine brimonidine |
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direct-acting beta-agonists
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epi
isoproterenol terbutaline albuterol dobutamine ritodrine salmeterol dopamine |
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indirect-acting adrenergic drugs
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tyramine
amphetamine ephedrine MDMA (ecstasy) cocaine methylphenidate |
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Drugs interacting with DA receptors
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dopamine
haloperidol |
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Drugs that inhibit catecholamine metabolism
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phenelzine
entacapone |
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Cholinergic antagonists
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atropine
tripmethaphan curare |
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Is carbachol a substrate of AChE?
Clinical significance? |
No - not degraded by AChE.
Therefore, more clinically useful than ACh because much longer-acting. |
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What ACh receptor(s) does carbachol act on?
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muscarinic
nicotinic |
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What ACh receptors does bethanechol act on?
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muscarinic only
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Selective, muscarinic agonist
|
Bethanechol
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2 cholinergic agonists
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carbachol
bethanechol |
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Which cholinergic antagonist acts at muscarinic receptors?
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atropine
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Which cholinergic antagonist acts on nicotinic nerve receptors?
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trimethaphan
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Which cholinergic antagonist acts on nicotinic muscle receptors?
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curare
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Why does it take hours for hemicholinium to produce its effect?
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It inhibits ACh synthesis, and there is already a store of ACh that has to be used up before synthesis inhibition will show an effect.
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Where is the enzyme Dopamine beta-hydroxylase found?
What does it catalyze? |
In synaptic vesicles that uptake DA.
Converts DA to NE in the synaptic vesicle. |
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Where is the enzyme phenylethanolamine N-methyltransferase found?
What does it catalyze? |
adrenal medulla
converts NE to epi |
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DOPA decarboxylase, aka:
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aromatic L-amino acid decarboxylase
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What causes synaptic vesicle to associate with neuron membrane?
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Action potential --> Ca2+ influx --> synaptic vesicle association with membrane
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With respect to NE, what is "Uptake 1"?
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Uptake 1 - channel protein that mediates reuptake of NE from synapse
major way NE is removed from synapse |
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With respect to NE, what is "Uptake 2"
|
NE going into target nerve from synapse
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Outside the neuron, DA is metabolized via ____
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deamination
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Which amine agonist acts at alpha-1 receptors?
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phenylephrine
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Which amine agonist acts at beta-1 receptors?
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isoproterenol
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Which amine antagonist acts at alpha-1 receptors?
|
phentolamine
|
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which amine antagonist acts at beta-1 receptors?
|
propranolol
|
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What tissue was used to demonstrate that adrenergic agonists cause contraction?
What were these receptors called? What was the relative efficacy of NE, epi and isoproterenol? |
arteriole stripes
alpha-1 E < NE <<< isoproterenol |
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What were adrenergic receptors causing cardiac contraction called?
What were the relative efficacies of NE, E, and I? |
beta-1
I < E < NE |
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What tissue was used to demonstrate that adrenergic agonists can cause relaxation?
What were these receptors called? What were the relative efficacies of NE, E and I? |
smooth muscle
beta-2 I < E <<< NE |
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Which two adrenergic receptors does NE act on?
|
alpha
beta-1 |
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Which two adrenergic receptors does isoproterenol act on?
|
beta-1
beta-2 |
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What does epinephrine act on?
|
everything
|
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alpha-1 receptor stimulation generally results in ....
for example, leading to (3 things) |
alpha-1 receptor stimulation generally results in contraction of smooth muscle
leading to... - constriction of blood vessels - dilation of pupil (contraction of radial muscle) - contraction of some visceral smooth muscle |
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alpha-2 receptor stimulation of receptors located on NE nerve terminals does what?
|
inhibits release of transmitter (autoreceptor)
|
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alpha-2 receptor stimulation of receptors located on enteric cholinergic neurons does what?
|
reduces release of ACh from these neurons --> relaxes GI smooth muscle
|
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alpha-2 receptor stimulation of pancreatic beta cells does what?
|
reduces secretion of insulin
|
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alpha-2 receptor stimulation of receptors located on neurons in pons-medulla does what?
|
reduces outflow of SNS
|
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alpha-2 receptor stimulation of receptors located on ciliary process does what?
|
reduces secretion of aqueous humor
|
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Activation of beta-2 receptors generally _______, while activation of beta-1 receptors generally ______
|
Activation of beta-2 receptors generally decreases activity of smooth muscle, while activation of beta-1 receptors increases activity of cardiac muscle
|
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Direct-acting sympathomimetics
|
combine directly with a receptor to produce a response, e.g.: Epi
|
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Indirect-acting sympathomimetics
|
release or block reuptake of released NE, e.g.: Tyramine
|
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5 outcomes of activated beta receptors
|
increases heart rate and force of contraction
relaxes visceral smooth muscle (e.g.: urinary bladder) dilates some vlood vessels dilates bronchioles relaxes uterus |
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Effect of denervation on direct and indirect acting sympathomimetics
|
Direct: denervation increases activity
Indirect: denervation decreases activity |
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Effect of reserpine on direct and indirect acting sympathomimetics
|
Direct: no change/either change
Indirect: reserpine decreases activity |
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Effect of uptake 1 blocker on direct and indirect acting sympathomimetics
|
Direct: Uptake 1 Blocker increases activity
Indirect: Uptake 1 Blocker decreases activity |
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3 factors that affect adrenergic receptor sensitivity
|
hormonal milieu (e.g.: pregnancy, thyroid)
chornic drug administration denervation/disease |
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syndrome that exemplifies denervation supersensitivity
|
Horner's syndrome
|
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denervation supersensitivity
|
enhanced response to direct acting sympathomimetics
|
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Early denervation supersensitivity
|
loss of uptake 1 (NET) if drug is substrate
|
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late denervation supersensitivity
|
increase in numbers of receptors (up regulation)
|
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disuses supersensitivity (vs. denervation supersensitivity)
|
super- or sub-sensitivity (down regulation of receptors in response to chronic administration of drugs)
|
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prototype of direct-acting a1, a2, b1, b2 agonists
|
epinephrine
|
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3 effects of epi on the heart
|
increase force of contraction (positive ionotropic effect)
increase rate of contraction (positive chronotropic effect) increased cardiac output (increased force & rate of contraction + INCREASED FILLING TIME) |
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epinephrine-related causes of cardiac dysrhythmias
|
increased rate of conduction through AV node
activation of latent pacemakers |
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2 causes of epinephrine-derived increased coronary blood flow
|
mechanical
metabolic |
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when and where does epinephrine cause vasocontriction
|
vessels with a1 receptors
- precapillary resistance vessels - veins |
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when and where does epinephrine cause vasodilation?
|
b2 receptors
- skeletal muscle - liver |
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effects of epi on BP depend on...?
|
dose
|
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effect of epinephrine on bronchioles
|
b2 receptors
relaxation of bronchiole smooth muscle inhibition of release of bronchoconctrictors and inflammatory mediators from basophils & mast cells |
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effect of epinephrine on urinary bladder
|
heistation of urination
- contraction of smooth muscle in trigone and sphincter (a1) - relaxation of detrusor smooth muscle (modest effect) (b2) |
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effect of epinephrine on pregnant uterus
|
b2 receptor
- relaxation during 3rd trimester |
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effect of epinephrine on GI tract
|
contracts smooth muscle in sphincters (a1)
relaxes GI smooth muscle by: - activating a2 resceptors on cholinergic enteric neurons - activating b2/3 receptors on smooth muscles |
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general, overall metabolic action of epinephrine
|
converts energy stores to usable fuels (glucose, FFA)
|
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epinephrine increases blood concentration of what 5 things?
|
glucose
lactic acid potassium (transiently - ultimate decrease) FFA & glycerol oxygen consumption & body temp |
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epinephrine-induced metabolic pathways leading to hyperglycemia
|
breakdown of glycogen (glycogenolysis) in liver
reduced secretion of insulin increased secretion of glucagon |
|
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epinephrine-induced metabolic pathways leading to lactic acidemia
|
breakdown of glycogen in muscle
lactic acid converted to glucose in liver |
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what happens to K+ levels consequent of epinephrine?
|
brief increase, followed by more prolonged decrease due to transport of K+ into muscle (epi-activated na/K ATPase)
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epinephrine causes _____ in intraocular pressure
|
decrease
|
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at very high doses, epi can cause _____ or _____ (bad side effects)
|
cerebral hemorrhage
PE |
|
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3 means of epinephrine administration
|
parenterally, inhalation, topically
|
|
|
how is epinephrine NOT given?
|
orally
|
|
|
2 means of epinephrine termination
|
enzymatic destruction (MAO, COMT)
transporters (Uptake 1 "NET" and Uptake 2) |
|
|
COMT inhibitor
|
entacapone
|
|
|
MAO inhibitor
|
pheneizine
|
|
|
3 reasons structural analogs of endogenous catecholamines are used therapeutically
|
oral bioavailability
longer duration of action specificity towards receptor subtakes |
|
|
NE acts on which 3 adrenergic receptors?
|
a1, a2, b1
|
|
|
a1 agonist used to mantain BP during general and spinal anesthesia
|
phenylephrine
|
|
|
effect of isoproterenol on diastolic BP
(also: what receptor) |
b2 receptor - reduces diastolic BP
|
|
|
effect of isoproterenol on heart
(what receptor?) |
b1 receptor - stimulates heart
|
|
|
isoproterenol effect on bronchioles
(what receptor?) |
b2 receptor - bronchodilation
|
|
|
secondary messenger in b2 agonist-induced bronchodilation
|
cAMP
|
|
|
2 qualities for "ideal" asthma/COPD drugs
|
selectively activate b2 receptors
are longer acting (not substrates for COMT, MAO, NET) |
|
|
4 relatively selective b2 agonists
|
terbutaline
albuterol slameterol formoterol |
|
|
ADVAIR
|
Salmeterol
|
|
|
SYMBICORT
|
Formoterol (& budesonide)
|
|
|
BRETHAIRE, BRETHHINE
|
Terbutaline
|
|
|
PROVENTIL
|
albuterol
|
|
|
2 relatively selective b2 agonists used to treat ACTUTE bronchospasm (rapid onset, short duration of action)
|
terbutaline
albuterol |
|
|
2 relatively selective b2 agonists used for maintenance tx for chronic asthma
|
salmeterol
formoterol |
|
|
salmeterol and formoterol should be administered with a ____
|
corticosteroid
|
|
|
effects of retodrine and terbutaline in pregnancy
|
b2 agonists relax uterine smooth msucle during 3rd trimester - can be used to delay delivery in premature labor
|
|
|
4 adverse effects of relatively selective b2 agonists
|
skeletal muscle tremor
tachycardia hyperglycemia hypokalemia |
|
|
relatively selective b1 agonists are administered by i.v. infusion to treat ______
|
low cardiac output
|
|
|
2 relatively selective b1 agonists
|
dopamine
dobutamine |
|
|
dopamine is very short acting (t1/2 = 2 min). why?
|
substrate for NET, MAO, COMT
|
|
|
DA is less likely to casue ____ and _____ than isoproterenol
|
tachycardia, dysrhythmias
|
|
|
at low dose DA increases blood flow in _____
and induces _____ |
renal/mesenteric vascular beds (D1 receptors)
and induces vomiting (D2 receptors in area postrema) |
|
|
at moderate doses, DA has a ______ inotropic effect on heart
|
positive
|
|
|
"inotropic"
|
affecting force of muscle contraction
|
|
|
at high doses, DA causes ______ via a1 receptors
|
vasoconstriction
|
|
|
why does dobutamine have a very short duration of action?
|
substrate for COMT
|
|
|
Dobutamine is different ffrom DA in that it does NOT.... (3 points)
|
increase renal and mesenteric blood flow
activate DA receptors in area postrema release NE (no local ischemia at i.v. injection site) |
