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66 Cards in this Set
- Front
- Back
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Peripheral Nervous system 2 parts
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afferent
efferent |
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Peripheral Efferent system
2 parts |
Somatic Nervous System
Autonomic Nervous System |
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Somatic Nervous System controls
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skeletal muscle
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Autonomic Nervous System controls
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homeostasis
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2 parts of autonomic system
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SNS
PNS |
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-Autonomic Nervous System
3 types of cells |
skeletal
cardiac exocrine |
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Adrenergic Neurotransmitter is
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Norepinephrine
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Norepinephrine responsible for most Adrenergic activity of the SNS with the exception of
3X |
exocrine
sweat . glands and some blood vessels |
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norepinephrine released where
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postganglionic sympathetic fibers at end organ tissues
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norepinephrine Synthesized in the __________ and packaged into vesicles of ____________
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cytoplasm
vesicles in the sympathetic postganglionic fibers |
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Norepinephrine -Released by
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exocytosis
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Norepinephrine terminated by 3 mechanisms
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1. re uptake of post ganglion nerve endings
2. diffusion from the receptor site 3. metabolism by monamine oxidase and catecholitransferoxidase |
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Prolonged adrenergic activation leads
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to desensitization and hyporesponsiveness to further stimulation .
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Adrenergic Receptors divided into two general categories
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alpha 1 and 2
beta 1 and 2 |
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Alpha-1 receptors located
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postsynaptic adrenoreceptors located in smooth muscle
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Alpha-1 receptors postsynaptic adrenoreceptors located in smooth muscle including:
6 places |
eye
lung blood vessels uterus gut GU system |
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Alpha-1 receptors activation
(how it works) |
increases intracellular calcium ion concentration leading to muscle contraction
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Alpha-1 receptors associated with
5X (smooth muscles constriction) |
mydriasis (excessive dilation of the pupil)
bronchoconstriction vasoconstriction uterine contraction contraction of sphincter in GI and GU |
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Alpha-1 receptors
and insulin |
Stimulates glycogenolysis and gluconeogenesis leading to INCREASE in blood glucose levels
(formation and breakdown) |
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Alpha-1 receptors and myocardium
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alpha 1 causes vasoconstriction
(biggest response you will see) increases PVR increasing BP |
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Alpha-2 receptors located on
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presynaptic nerve terminals
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Alpha-2 receptors when activated
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decreases the entry of calcium ion into the neuronal terminal, thus limiting subsequent exocytosis of storage vesicles containing Norepinephrine (NE)
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Alpha-2 receptors stimulation
2 things you will see |
sedation
reduces sympathetic outflow (vasodolation and lowering BP) opposite alpha 1 |
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Beta-1 receptors located
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postsynaptic membranes in the heart
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Beta-1 receptors activate
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adenyl cyclase
Converts ATP to cAMP and initiates a kinase phosphorylation cascade |
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Beta-1 receptor stim
results in |
cardiac stimulation
(increase HR, conduction, contractility) |
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Beta-2 receptors located
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postsynaptic adrenoreceptors of smooth muscles and gland cells
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Beta-2 receptors stim
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relax smooth muscle leading to:
broncodilation vasodilation relaxation of the uterus, bladder, and gut |
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Beta-2 receptors stim and insulin
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gIycogenolysis, gluconeogenesis and insulin release stimulated I
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Beta·2 receptors activates
pump |
sodium/potassium pump
·this drives K+ intracellular and can induce hypokalemia and dysrhythmias I |
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Pharmacologic Agents
Sympathomimetics |
facilitate or mimic the SNS
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Pharmacologic Agents
Sympatholytics |
block or reduce the action of SNS
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Adrenergic Agonists interact
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lnteract with varying specificity at alpha & beta adrenoreceptors
(may overlap which complicate the prediction of the clinical effect) |
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Direct Agonist
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binds to receptor
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Direct Agonist
enervation or depletion of NE |
DOES NOT prevent the activity of these drugs
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indirect Agonist
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increase endogenous neurotransmitter release
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indirect action includes:
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increased release of NE
decreased reuptake of NE |
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indirect Agonist:
Denervation or depletion of NE |
BLUNTS the pharmacologic responses
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Diffferentiation between direct and indirect mechanism of action
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Important in patients who have abnormal endogenous Norepinephrine stores as with some antihypertensive medications or Monamine Oxidase Inhibitors
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Catecholamines short-acting b/c metabolism by:
2X |
monoamine oxidase
catecholomethyltransferase |
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someone on a MOA inhibitor and have hypotension you treat them with a
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direct agonist
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patient taking Monamine Oxidase inhibitor or Tricyclic Antidepressant may demonstrate
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exaggerated response to catecholamines .
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3 naturally occurring Catecholamines
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epinephrine
norephinephrine dopamine |
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2 synthetic catecholamines
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dobutamine
isoproterenol |
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MAOi and NE
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prevent the breakdown
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Tricyclic Antidepressent and NE, serotonin
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prevent the reuptake of NE and serotonin
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Epinephrine -released from
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adrenal medula
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Epinephrine natural functions include:
5X |
myocardial contractility
HR vascular and bronchial smooth muscle tone glandular secretion metabolic process (glycogenelysis and lipolysis) |
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most potent activator of Alpha-adrenergic receptors
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Epinephrine
2-10x more active than NE . |
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Epinephrine direct stimulation of
receptor? |
beta-1 receptors
alpha-1 beta-2 |
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Epinephrine clinical doses
Principal pharmacologic treatment for: 3X |
anaplyxis
vfib prolong duration of local anesthetics |
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Epinephrine Dosage
emergency (shock, allergic reaction) |
-IV bolus 0.5-1.0 mg, q 3-5min
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Epinephrine
continuous infusion |
-Rate of 2-20 mcg/min
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Norepinephrine
alpha vs beta |
alpha greater than beta
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Norepinephrine is a
receptor type |
Direct alpha-1
Intense arterial and venous vasoconstriction : |
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Norepinephrine and CO
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May contribute to increase in BP, but elevated afterload and reflex bradycardia prevent elevation in CO
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Norepinephrine clinical uses:
may be also used with |
to Increase B/P
used with an alpha blocker (phentolamine) to take advantage of beta activity without profound vasoconstriction |
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Norepinephrine dosage Infusion
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rate of 2-20 mcg/min
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Norepinephrine Bolus
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0.1 mcg/kg
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Dopamine class
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nonselective direct and indirect adrenergic agonist
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Dopamine receptor
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alpha & beta adrenergic agonist
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Dopamine small doses, <3 mcg/kg/min
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Dopaminergic receptors
activator of dopaminergic promotes diureses |
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Dopamine moderate doses. 3-8 mcg/kg/min
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beta stim
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Dopamine higher doses, 8·20 meg/kg/min
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alpha 1 stim
increases peripheral vasc resistance decreases renal blood flow |
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Dopamine has indirect effects due to
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NE release at > 20 meg/kg/min
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epinephrine dilution
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10 mcg per 1ml
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