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112 Cards in this Set
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Oldest ester Local anesthetic
Rapidly metabolized to PABA (plasma cholinesterase) pKa 8.9 Poor lipid solubility (no topical effect) Toxicity uncommon Not used clinically in US |
Procaine
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Produced by chloride substitution of the aromatic ring
-increases susceptibility of ester ring to hydrolysis -rapid onset and short duration In plasma t1/2B 21 sec. -can use high concentrations with decreased risk of toxicity -increased toxicity with plasma cholinesterase deficiency pKa 9.0 3%solution used for epidural blockade Preservative problems -sodium bisulfite ^nueral irritation following SAB -ethylenediaminetetracetic acid (EDTA) ^back pain/spasms(EDTA pulls ca+ out) |
2-Chloroprocaine
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Excellent topical anesthetic
Highly lipophilic-rapidly absorbed into bloodstream Available in lyophilized form(frozen and dehydrated) -reconstituted with 10% dextrose, CSF or sterile water for SAB 2-3min half life Used for spinal anesthesia -1.0%solution Epinephrine use with SAB increases duration by 25% Do not administer great than 80-100mg |
Tetracaine
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First agent used for local anesthesia
used for stimulant and euphoric properties second most commonly abused substance in US Most ofen used as topical agent Toxicity r/t vasoconstrictive properties and actions on catecholamine metabolism Can cause hypertension and coronary vasospasm -resulting in ischemia & infarction Blocks catecholamine uptake centrally & peripherally -blocking dopamine reuptake is likely a cause of euphoric effect Hydrolyzed by esterases -b/w 1% & 10% excreted unchanged in urine Use is controversial-safer alternatives -lidocaine & Neosynephrine |
Cocaine
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Lidocaine
Mepivicaine Prilocaine Etidocaine Bupivacaine Ropivacaine |
Amides
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Most widely used LA in the world
marketed premixed with Epi Metabolized by mixed-function oxidases & amidases -De-ethylation of the amino nitrogen leads to monoethylglycine xylidide (MEGX) and glycine xylidide -MEGX may be seizuregenic Toxicity-max 500-600mg or 7mg/kg Acidosis increases toxicity -Decreases plasma protein binding Use of hyperbaric lidocaine for SAB is controversial |
Lidocaine
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Dual ring structure
LA properties similar to lidocaine -slightly less toxic Weak vasoconstrictor Not for OB use -prolonged half life in fetus ^fetus unable to metabolize double ring structure |
Mepivacaine
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Lidocaine analog
-similar in onset & duration Not widely used b/c of association with methemoglobinemia(large doses) -metabolic product is 3- and 5- hydroxytoluidine -potent oxidants of hemoglobin(convert hgb to methemoglobin) Treatment is methylene blue Used primarily with EMLA -5% ___ & lidocaine? |
Prilocaine
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Potent,longer-acting LA
High pKa limits placental transfer Long latency to onset Differential blockade -often good sensory blockade with minimal motor blockade Do not see aura of CNS toxicity prior to cardiovascular collapse Fast-in, slow out kinetics in myocardial tissue 0.75% banned by FDA for use in OB anesthesia for Epidural use ONLY! |
Bupivacaine
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Approved by FDA in 99
S-enantiomer of bupivacaine Similar pharmacokinetic profile to bupivacaine CNS & cardiac toxicity 1/2 of bupivacaine OFF the market |
Levobupivacaine
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Newest LA released by FDA in 96
Chemically similar to bupivacaine & mepivacaine -wanted long acting LA like bupivacaine (with motor sparing) and lower toxicity similar to Mepivacaine) Arrhythmogenicity intermediate b/w Mepivacaine & Bupivacaine Not marketed for spinal anesthesia -used extensively for epidural anesthesia |
Ropivacaine
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Procaine
Chloroprocaine Tetracaine Cocaine Benzocaine |
Esters
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a1,B1, no B2 activity
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Norepinephrine
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Enzymatic breakdown of adrenergic receptors?
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Monoamine oxidase (MAO)
Catechol-O-methyltransferase (COMT)in the liver |
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Postsynaptic receptors constrict vascular smooth muscle? (more venous)
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alpha 2
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Located on postsynaptic effector cells(vascular smooth muscle)
Responses are typically excitatory |
Alpha 1 receptors
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Differential blockade of LA's
small fibers get blocked before large fibers,name the order? |
C fibers-->Adelta->Agamma-->Abeta-->Aalpha
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Alpha receptors->G-protein->PLC->PIP2->IP3->IP3receptor->Ca+ release
cause contraction of bld vessels -renal, splanchnic, skin, skeletal muscles,radial muscle of iris,uterus,sphincters of GIT,urinary bladder, uterus ?receptors |
Alpha 1
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Pre/Postsynpatic a receptors cuase contraction
coronary vessels a1,a2 receptors result in contraction of bld vessels may be more a function of a2 more than a1 stimulation |
Postsynaptic a1
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Pre/postsynaprs produce a
adrenergic receptors produce vasoDILATION inhibition of NE release |
Presynaptic a2 (peripheral vasculature)
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receptors cause vasodilation
G-protein->activates AC->increased conversion of AMP->cAMP relaxation of bld vessels, ciliary muscle, tracheal & bronchial muscles, urinary bladder, gallbladder, GIT, & uterus |
B2 receptors
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Postsynaptic
coupled to Gs found in renal and splanchnic vascular beds ?receptors |
D1 receptors
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similar to a2
coupled to Gi/o inhibit presynaptic release of NE ?receptors |
D2 receptors
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Activates a G-protein->L-type Ca+ channel
allows Ca+influx causes an increase in chronotropy, dromotropy, & inotropy ?receptors |
B1
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a receptor activation inhibits neurotransmitter release
NE and ACh G-protein mediated inhibits AMP-->cAMP opens K+ channels increasing efflux inhibits L-& N-type Ca+ chs decreasing Ca+ influx |
A2
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on vasculature smooth muscle these receptors are activated at lower concentrations of circulating epinephrine
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B2
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Sympathomimetic drug that inhibits neuronal transport of catecholamines
blocks reuptake of NE into nerve terminal, more NE remains in synaptic cleft |
Cocaine
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a & b receptor activity
incr. chronotropy, dromotropy, inotropy incr. myocardial workload and O2 consumption large doses may result in PVCs,tachycardia, or fibrillation -may be exaggerated by certain anesthetic agents or MI -dysrhythmic effects may be antagonized by b-adrenergic receptor antagonists Small doses may decrease BP-B2 receptors more sensitive to low dosages than a1 relaxes bronchial smooth muscle insulin release inhibited(a2 mech), glucagon secretion is enhanced B1 & B2 activation Glycogenolysis is stimulated in most tissues B1 & B2 *B2>B1>A1 |
Epinephrine
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Chemical mediator released by mammalian adrenergic nerves
10-20% of adrenal medullary release -alpha1 adrenergic agonist -some B1 effect,no B2 effect may be as high as 97% in pheochromocytoma -systolic & diastolic BPs are increased - CO is unchanged /decreased, -reflex vagal response, -coronary bld flow increased -elevation in BP, -increased myocardial contractility from B1 |
Endogenous Catecholamine
Norepinephrine |
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Indirect & direct acting effects sympathomimetic drug acts by displacing NE from nerve terminals
predominantly act at a & B1 receptors |
Ephedrine
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Precursor of NE
effects are mediated through D1 receptors low doses primarily activated D1 receptors in renal & mesenteric bld vessels moderate dosages act on B1 receptors also causes NE release at infusion rates above 5mg/kg/min(indirect effect) |
Endogenous catecholmine
Dopamine |
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a1/2, b1/2?
In the heart: increased contractility increased automaticity increased conduction velocity |
Beta 1
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a1/2, b1/2?
In the bld vessels:arterior constriction venoconstriction In the iris:radial muscle contraction |
Alpha 1
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a1/2, b1/2:
In skeletal muscle & liver: arteriolar dilatation In the bld vessels: venodilation In the bronchioles: dilatation In the GI tract & urinary bladder: decreased motility In the uterus: relaxation |
Beta 2
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Drug?
In the bld vessels: arteriolar dilatation in the kidney & mesentery |
Dopamine
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a1/2, b1/2?
Metabolic functions: In the liver: gluconeogenesis, glycogenolysis |
Alpha, Beta 2
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a1/2,b1/2?
Metabolic functions: Fat lipolysis |
Beta 1 & 3
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a1/2,b1/2?
Metabolic functions: In the pancreas, decreased insulin secretion |
Alpha 2
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a1/2,b1/2?
Metabolic functions: In the kidney, renin secretion |
Beta 1
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Presynaptic a2 adrenergic receptors produce what in the peripheral vasculature?
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vasoDILATION by inhibition of NE release
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Postsynaptic a1 and a2 result in ? of the bld vessels
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Contraction/vasoconstriction
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B2 receptors cause this in smooth muscle & glandular tissue receptors?
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Vasodilation
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Postsynaptic B2 also found in myocardium and mediate?
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Contraction
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Sympathetic amines with hydroxyl substitutions at positions 3 and 4 of the benzene ring are termed?
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Catecholamines
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How is Epi synthesized?
(steps) |
Tyrosine is taken into the cell & acted on to become Dopa
Dopa gets acted on & becomes Dopamine Dopamine gets made into Nor-epi Nor-epi gets made into Epi |
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G-protein mediated
adenyl cyclase is activated AMP converted to cAMP ?receptors |
B1 & B2
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Activates a G-protein--> L-type Ca+channel
allows Ca+ influx causes an increase in chronotropy, dromotropy, & inotropy ?receptors |
B1
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Presynaptically activation inhibits neurotransmitter release
NE and ACh G-protein mediated inhibits AMP-->cAMP Opens K+ channels increasing efflux Inhibits L-& N-type Ca+ channels decreasing Ca+ influx ?receptors |
a2
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What occurs initially with the administration of Epi?
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B2 effect on musculature will cause a small DECREASE in BP initially then increase
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Insulin release is inhibited (a2 mechanism, some B2)
Glucagon secretion is enhanced by B1 & B2 activation Glycogenolysis is stimulated in most tissues (B1 & B2) (drug?) |
Epinephrine
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Non-selective B-adrenergic agonist
low alpha affinity CVS- -Decr. peripheral vascular resistance (skeletal muscle, -renal & mesenteric vascular beds) -CO is increased due to positive inotropic and chronotropic effects -May lead to palpitations and ischemia Relaxes smooth muscle- -prevents/ relieves bronchoconstriction In asthma its effects are augmented by inhibition of antigen-induced inflammatory mediators -shared by other B2 agonists |
Isoproterenol
Non-endogenous Sympathetic Amine |
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Synthetic dopamine analog
Predominantly B1 effect +isomer 10x more potent as B agonist -also has a ANTAGONISTIC properties Does not act at dopaminergic receptors 2.5-10mg/kg/min for increasing CO More prominent inotrope than chronotrope used for low output state When you need to flog the heart this is a good drug |
Dobutamine-Non-edogenous sympathetic amine
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Non-endogenous sympathetic amine
Used for short-term cardiac decompensation states(low output states) -after cardiac surgery, acute MI, or CHF can increase size of infarct(b/c increases MVO2) -In severe CHF, down regulation of B-adrenergic receptors may hamper its effectiveness Facilitates AV conduction may cause ventricular ectopy 2 min HL |
Dobutamine
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Used primarily to treat asthma
and to arrest premature labor (tocolytic action) side effects are often r/t B1 stimulation -pts with CAD/ myocardial ischemia are at risk for adverse cardiac event -also increased for pts taking MAO inhibitors or TCAs |
Beta 2 selective adrenergic Agonists
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Metaproterenol (alupent, Metaprel)
Terbutaline(Brethine) |
B2 selective adrenergic agonists
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B2 selective bronchodilator
can be adm. SC -0.25mg (can be repeated after 15min) May be administered in status asthmaticus Rapid onset and effects last 3-6hrs -also given to arrest premature labor as a tocolytic agent(decreases uterine tone) |
Terbutaline (Brethine)
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Considered to be relatively B2 selective
Effects last from minutes to several hrs B2 selective Adrenergic Agonists |
Metaproterenol(Alupent, Metaprel)
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Longer acting B2 selective Adrenergic Agonist
Significant bronchodilation within 15min effects last 3-4hrs |
Albuterol(Salbutamol)
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a1 selective Adrenergic Agonists
Direct acting a1-selective agonist Longer acting than phenylephrine(30-60min) not available any more May cause reflex slowing HR |
Methoxamine
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a1-selective Adrenergic Agonist
Direct acting Activates B1 adrenergic receptors at high concentrations It's Epinephrine minus a hydroxyl group at position 4 Reflexively decr. HR by baroreceptors IV duration 5-10min Bolus doses 40-100mg Infusion rate 10-20mg/kg/min Metab. in liver by MAO Used for vasoconstriction when CO is adequate Nasal decongestant(prior to nasotracheal intubation) added to LA to prolong SAB |
Phenylephrine
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a1-selective Adrenergic Agonists
Direct and indirect acting 100 alpha agonist causes release of NE |
Mephentermine & Metaraminol
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Reduce sympathetic outflow from the CNS & lower arterial pressure generally
Reduce presynaptic NE release Affect CO & PVR Reduce anesthetic requirements Sudden discontinuation may cause withdrawal symptoms Sedation & xerostomia are common |
a2-selective Adrenergic agonists
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a2-selective agonists
Patients may display symptomatic bradycardia/sinus arrest(individuals with SA or AV nodal disease) Developed as topical vasoconstricting decongestant Will cause hypotension, sedation, & bradycardia Imidazoline compound with a2 agonist properties IV infusion causes an acute rise in BP(activates postsynaptic a2 receptors in vasculature) -initial incr. in Bp Has analgesic effects -stimulates PSNS outflow -elimination HF of about 12 hrs -transdermal delivery system allow SS in 3-4 days |
Clonidine(Catapress)
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a2-selective Adrenergic Agonists
Highly selective a2 agonist properties reduces anesthetic requirements -may be used to induce anesthesia itself -may be used as a premedicant for sedation (IM 2.5mg/kg) Has analgesic effects |
Dexmedetomidine
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a2-selective Adrenergic Agonist
Prodrug -metabolized by Laromatic amino acid decarboxylase(LAAD) to a-methylnorepinephrine in the brain activates central a2 receptors and lower BP similar to clonidine a-methylnorepinephrine is taken up by adrenergic neurons and stored in secretory vesicles -a-methyLNE is then released instead of NE Used as a antiHTN decr. in BP maximal 6-8hrs after ingestion |
Methyldopa
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Adrenergic Agonists
-CNS stimulant action racemic formulation has peripheral indirect a & b effects(causes CV excitiation) -Releases biogenic amines from storage sites in nerve terminals -activates RAS(can cause psychosis, 5-HT mediated) -anorectic, locomotor stimulant(DA mediated) |
Amphetamine & Dextromphetamine
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Adrenergic Agonist
an a and b adrenergic agonist(direct acting) has an indirect effect as well increases CO & HR usually increases BP Potent CNS stimulant-crosses BBB excreted unchanged in urine HL 3-6hrs |
Ephedrine
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Sympathomimetic drugs:
Sympathetic blockade from SAB causing hypotension, what 2 drugs would you use? |
Ephedrine
Phenylephrine |
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Sympathomimetic drugs:
Cardiac arrest increases diastolic pressure & CoBF? |
Epinephrine and a agonist
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Sympathomimetic drugs:
asthma |
B2 agonists are drugs of choice in acute episode
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Sympathomimetic drugs:
Allergic reactions |
Epi is drug of choice for serious, acute hypersensitivity reactions
shock and anaphylaxis Epi may also activate B2 agonists that suppress mast cell release of vasoactive mediators (histamine,leukotrienes) |
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Sympathomimetic drugs:
weight reduction? |
Phenteramine & fenfluramine
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a1/2?
Primary effects of these drugs are on cardiovascular system inhibit vasoconstriction by sympathomimetic amines vasodilation may be arteriolar or venous |
a1 antagonists
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These agents act peripherally & centrally
activation of these agaonists inhibit NE release in the pontomedullary region (BR stem) inhibit sympathetic outflow and decr. BP |
a2 agonists
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Blockade with selective a2-adrenergic anagonists can increase sympathetic outflow?(drug)
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Yohimbine
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Nonselective a-adrenergic antagonists
haloalkylamine blocks a1 and a2 IRREVERSIBLY Covalently binds to adrenergic receptors* responsiveness requires new receptors to be made inhibits catechol reuptake into nerve terminals causes decrease in SVR and incr. in CO(reflex) hypotension enhanced with b2 agonists in muscle beds Useful in pheochromocytoma and in autonomic hyperreflexia |
Phenoxybenzamine
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Nonselective a adrenergic antagonists
Imidazoline blocks a1,a2 receptors COMPETITIVELY Reversible can also block K+ channels causes release of histamine c/i CAD |
Phentolamine
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a1-adrenergic antagonists
potent a1 receptor antagonist -blocks a1 receptors in arterioles & veins decreases SVR & venous return to heart used very effectively in treating prostatic hypertrophy(decr. tone and better flow) doesnt usually cause increase in HR/CO |
Prazosin (Minipress)
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These drugs used primarily for systemic HTN
drugs tend to improve lipid profiles & glucose-insulin metab. used in CHF -dilate arteries & veins -decr. afterload & preload -long term therapy may not prolong life TURP ias initial therapy is being considered -reduce resistance in some pts -bladder trigone & urethra contribute to blockage |
a1 adrenergic antagonists
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a2-adrenergic antagonists
Indolealkylamine from bark of pausinystalia antagonist at 5-HT receptors marketed as an aphrodisiac |
Yohimbine
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a,b adrenergic antagonist
competitive antagonist a1 & B receptors selective a and nonselective B blocker partial B2 agonist racemic mixture with 4 stereoisomers a1 block leads to arteriolar dilation B1 block leads to decr. in BP by blocking refelx sympathetic stimulation 5x-10x more potent b blocker than a blocker extensively metab.in liver elimination HL 8 hrs 10-80mg every 10min (start at 5-10mg q 10min) |
labetolol
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Decr. chronotropy, inotropy & dromotropy= decr. CO
SVR incr. Some have ability to partically stimulate receptors -these agents have ISA -this property prevents profound bradycardia and decr. likelihood of bronchospasm In HTN pts these lower Bp block renin release caused by SNS stimulation affect cardiac rhythm and automaticity decr. SR, spontaneous & depolarization of ectopic foci usually improve the relationship b/w myocardial oxygen demand & supply Nonselective block bronchial smooth muscle receptors -little effect on pulm. function in healthy individuals -in COPD/ASTHMA may be life threatening |
B-adrenergic antagonists
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Block catecholamines that promote glycogenolsis and mobilize glucose in response to hypoglycemia
block may inhibit hepatic response to insulin-induced hypoglycemia block attenuates the release of free fatty acids from adipose tissue block inhibition of mast-cell degranulation by catecholamines |
Metabolic effects of Beta antagonists
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Non-selective B-adrenergic antagonists
not used much in OR b/c long acting B1 & B2 receptors with equal affinity Highly lipophilic with large Vd Lacks intrinsic sympathomimetic activity adm. IV for management of life-threatening dysrhythmias/to pts under anesthesia 1-3mg ad. slowly Atropine may be used for profound bradycardia |
Propanolol
Nonselective B-adrenergic Antagonist |
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Non-selective B-adrenergic antagonist
interacts with B1& B2 receptors with equal affinity lacks intrinsic sympathomimetic activity excreted largely unchanged in urine exceptionally long HL(20hrs) dont use in OR |
Nadolol
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Selective B-adrenergic antagonist
easy to titrate B1 selective devoid of ISA good oral absorption Poor bioavailabiliy PO(first pass effect) lg individual differences in plasma concentration HL 3-4hrs Nota Bene: only IV b-blocker approved by FDA in treatment of AMI |
Metroprolol
Selective B adrenergic Antagonist |
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B-adrenergic antagonist
B1 relatively selective very short duration t1/2B= 8-9min ester linkage rapidly hydrolyzed onset & cessation rapid peak hemodynapic effect in 6-10min little ISA |
Esmolol
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used for centuries
first comprehensive description in the treatment of CHF comes from purple foxglove plant found in many plants and several toad species usually acting as venoms/toxins These are the only two cardiac glycosides commercially available in the US |
Digitoxin & digoxin
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Characteristic ring structure known as an aglycone
steroid nucleus containing an unsaturated lactone at the C17 position and one or more(sugar) residues at C3 Sugar moiety affects in part the activity by influencing solubility, absorption, distribution, and toxicity |
Cardiac Glycosides
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vascular effects
primary effect is exerted on smaller arterioles & precapillary sphincters various vascular beds respond differently bld flow to skeletal muscles is increased -Primarily a B2 response -in resence on non-selective B-blocker, only vasoconstriction occurs- will have a pressor effect Coronary bld flow is increased -due to relative increase in diastolic filling time -vasocilation from metabolic factors BP increase due to positive inotropic & chronotropic effects -vasoconstiction in some vascular beds B2 receptors more sensitive to low dosages than a2 receptors Respiratory -relaxes bronchial smooth muscle -inhibits release of inflammatory mediators(B2 receptors) insulin release is inhibited(a2) Glucagon secretion is enhanced (B1 & B2) Glycogenolysis is stimulated in most tissues (B1,B2) |
Endogenous Catecholamine
Epinephrine |
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Precursor of NE
effects are mediated through D1 receptors Low doses primarily activate D1 receptors -vascular postjunctional D1 receptors in renal & mesenteric bld vessels -0.5-3.0 mcq/kg Moderate doses act on B1 receptors -3.0-10mcq/kg -also causes NE release at infusion rates above 5mg/kg(indirect effect) Higher dosages 10-20mcq/kg primarily act at a1 receptors -leads to vascular vasoconstriction -low dose increased RBF & GFR Moderate dose increased myocardial contractility & incr. CO High dosages vasoconstriction -benefit to renal may be lost Important central neurotransmitter Peripherally adm. has no central s/e substrate for MAO & COMT HL about 1 min |
Dopamine
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Selective B2 adrenergic agonist developed as tocolytic
(Yutopar) |
Ritodrine
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First drug used for treatment of bronchospasm
Not as B2-selective as other agents |
Isoetharine
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structurally similar to Albuterol
inhalation dosing every 4-6hrs |
Pirbuterol
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H/A, apprehension, abd. pain, tachycardia,arterial BP may arise to that above original BP, symp. occur 18-36 hrs after withdrawal, surgical pts should not be acutely withdrawn
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Sudden discontinuation of a2 agonist withdrawal symptoms
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Sympathomimetic drugs for PSVT?
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Phenylephrine & Methoxamine have been used to increase vagal tone
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Sympathomimetic Drugs used for local vascular effects of a-adrenergic agonists
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Epinephrine(or phenylephrine) + Local anesthetic
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Selective B-adrenergic Antagonist-No ISA
Limited ability to cross BBB |
Atenolol
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Improved consistency & higher oral bioavailability of modern formulations.
-70-80% oral bioavailability elixir & encapsulated gel preparations -Principal tissue reservoir is skeletal muscle (huge reservoir) -Large Vd(4-7L/kg) -Does cross the placenta, drug levels in maternal & umbilical vein bld are similar -With therapeutic plasma concen., 20-30% in the bld is bound to plasma proteins -Used for A-Fib _Higher concen. may cause SB/arrest and/ prolongation of AV conduction/Heart Block -Higher concen. can increase SNS activity(as approach toxicity) -directly affect automaticity in cardiac tissue, actions that contribute to the generation of dysrhythmias -simultaneous non-uniform increase in automaticity & depression of conduction in His-Purkinje & ventricular muscle fibers may lead to VT & Fibrillation |
Digoxin (Lanoxin)
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Crystodigin
Principal cardiac glycoside present in preparation of digitalis leaf Oral bioavailabilitiy is near 100%(known for this) |
Digitoxin
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Methyldopa
Clonidine Dexmedetomidine |
a2 selective agonists
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Epi
Ephedrine |
a, B
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almost pure a1, only at high doses produces an effect on B receptors
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Phenylephrine
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Norepi
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a1, B1
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Fenoldopam
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DA1
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Dopamine
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a, B, DA1, DA2
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Dobutamine
Isoproterenol |
B
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Terbutaline
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B1, B2
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B1 selective Antagonists
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Metoprolol
Atenolol Esmolol Acebutolol |
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Labetolol
Carvedilol |
Selective a1, B1,B2
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Propanolol
Pindolol Timolol Nadolol |
Nonselective B
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Pindolol
Acebutolol |
ISA
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