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a1 agonist
a2 agonist
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B1 and B2 agonist
B1 agonist
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B2 agonist
B2 agonist
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B2 agonist
prototype a1 agonist
phenylephrine
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what is a drug that can be used in the ICU to increase peripheral resistance without increasing CO?
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clonidine
action of clonidine
at the neuroeffector junction - on the nerve terminus itself feeds back and binds a2 receptor of the neuron releasing NE and inhibits release of more NE feedback regulator of NE release
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dobutamine
terbutaline
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1. act directly on adrenergic receptors 2. act by promoting release of endogenous NE 3. mixed actions
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1. vasoconstriction increases peripheral resistance and BP 2. venoconstriction decreases capacitance and increases venous pressure and right heart filling pressure 3. contraction of the iris radial (dilator) Definition muscle 24 induces myddriasis 4. constriction of bladder and intestine sphincters venoconstriction decreases capacitance increases venous pressure and right heart filling pressure
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contraction of the iris radial effect of a1 receptor agonists (dilator) muscle on bladder and intestine induces mydriasis
contraction of sphincters
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phenylephrine
BP increase BV are related to heart via baroreceptors constrict vessels --> decrease CO --> decrease HR and SV via baroreceptors reversible
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BP drops initially - a1 receptors cause constriction normal response to getting to stop from crashing up from laying down (getting need more blood - HR and up in the morning)? contractility increase vasoconstrict
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orthostatic HTN and syncope - block normal phys that allows for vasoconstriction problem elderly woman on a1 receptor blocker for HTN can fall and break a hip
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peripheral tone
effect of a1 on veins
don't constrict - stiffen and decrease compliance causes - blood to be increased back to the heart and increase right heart filling pressure and thus preload
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1. increased cardiac contractility and HR 2. increased lipolysis 3. production of renin from the kidneys
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increased renin production from kidneys effects of B1 receptor agonist on peripheral fat increased lipolysis effects of B1 receptor agonist on renin production kidneys are singly innervated by the arterioles that lead to them
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1. relaxation of vascular SM; vasodilation results in decreased peripheral vascular resistance and BP 2. reflexive tachycardia with B2 agonist infusion 3. bronchodilation 4. uterine SM relaxation 5. gluconeogenesis and glycogenolysis Definition in 41 the liver
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reflexive tachycardia
bronchodilation
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uterine SM relaxation
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heart - CO
HR and SV
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increase HR increase contractility (force of contraction) components of SV? preload contractility afterload effects of infusing B1 agonist? afterload - NOT increased with selective B1 agonist preload - not increased directly by B1; determined by veins
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NOT increased
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B2 receptor locations
central BVs
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reflexive bradycardia
reflexive tachycardia
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induces profound constriction of renal BV dangerously reduces renal blood flow problem in patient with low GFR
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NO
degraded by acidic pH
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NO
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B2
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use of epi
emergency management of anaphylactic shock characterized by severe bronchial constriction and CV collapse included as a vasoconstrictor agent in most local anesthetic (procaine-like) preparations
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epi
neuroeffector junction
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NE epi is not released at the neuroeffector junction which what is the physiologically is the physiologically most most important ligand for a2 important location of a2 receptors? why? receptors epi can bind a2 - not its primary role
phenylephrine type
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applied topically to the nasal mucosa - induces increase BP - induces a vasoconstriction to improve vagally-mediated reflex of phenylephrine systemic use air flow slowing the heart in patients works well for stuffy noses with paroxysmal tachycardia and common cold
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isoproterenol
isoproterenol type
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isoproterenol use
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more heart
dobutamine type
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dobutamine use
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patients with dyspnea and anxiety about not being able to breath - often take too much of the drugs
drives Na/K ATPase - can cause hypokalemia and problems that go along with it
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agonist of D1 dopaminergic receptors relaxes SM in renal BV and improves renal blood flow
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inactivation of dopamine
ephedrine orgin
found in many plants used in China for >200 years introduced in West medicine in 1924 as the first orally active sympathomimetic
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ephedrine structure
non-catechol phenylisopropylamine
long
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stimulant
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use of ephedrine
NE - get reflexive bradycardia from peripheral what drug would cause vasoconstriction despite B1 principal use - decongestant slight decrease in HR, activation (from baroreceptor also recommended for increase in systolic, reflex) could be stress incontinence in diastolic, and mean BP, and phenylephrine - same BP women a large increase in peripheral response (maybe larger); HR resistance? reduced more because no B1 action
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what drug would cause slight increase in HR, increase in systolic BP, decrease in diastolic BP, very minimal increase in mean BP, and a slight decrease in peripheral resistance?
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epi - acts on B2 what drug would cause eliminates rise in BP seen significant increase in HR, with NE slight increase in systolic don't get reflexive BP, decrease in diastolic BP, bradycardia seen with NE slight decrease in mean BP, binds B1 - increases HR and a large decrease in B2 actions on BV - primarily peripheral resistance? in liver and skeletal muscle
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isoproterenol - B1 and B2 only; no a big increase in HR no vascoconstrictor response enormous change in peripheral resistance
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CO and BP
peripheral resistance
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increases CO
use of B adrenergic agents to attenuate premature labor, delay delivery, allow fetal maturation thereby - reducing neonatal morbidity and mortality
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what is a common side effect of B-adrenergic tocolytic therapy for treatment of preterm labor?
hypokalemia
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activate Na/K ATPase by what can happen with abrupt increasing cAMP - take K out withdrawal of a B adrenergic of blood and store in cell --> agonist? hypokalemia
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ephedrine actions
tyramine type
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tyramine origin
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tyramine action
enters NE nerve terminal via the amine transporter and causes NE release
octopamine dopamine-B-hydroxylase
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metabolism of tyramine
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amphetamines type
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amphetamines action
facilitate release of NE
NO
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stimulant
cocaine type
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cocaine action
blocks neuronal uptake1 pathway for NE extends half life of NE at synaptic cleft
negative impact can be played out over 72-98 hours after ingested toxicity is potentially several days after use because of long half life