Adrenergic Receptor Antagonists Flashcards
(33 cards)
alpha1 antagonist
(Remember: alpha1 located vascular smooth muscle: blood vessel, sphincters, bronchi; Iris, Pilomotor sm, Prostate, Uterus, Heart) ANTAGONIST so.. relax miosis bladder/prostate relax
alpha2 antagonist
(remember: located on platelets, presynaptic: neg feedback, CNS, GI)
ANTAGONIST so…
Increased NE from nerve terminals
blocking neg feed back
Phentolamine
class, causes, uses, does, DOA
nonselective alpha blocker
causes vasodilation, decrease BP, increased HR/CO
used in: Hypertensive emergencies, pheocromocytoma or autonomic dysreflexia, local infiltration for extravascular admin of sympathomimetics
(*not first choice for HTN bc get increase HR)
30-70 mcg/kg IV
Onset 2 minutes; DOA 10-15min
Phenoxybenzamine
receptors, causes/uses, e1/2t,
binds covalently
more alpha1 than 2 (less tachyc)
decreased SVR, vasodilation
pro-drug w/1hr onset time:LONG acting E1/2, 24hrs
used for: pheochromocytoma, Raynaud’s disease
Prazosin
receptors, uses, CV effects
Selective alpha1 blocker (minimal alpha2)
Control BP in pheochromocytoma
Less reflexive tachycardia (remember alpha2 is inhibitory to NE release)
Yohimibine
receptors, uses
Alpha2 selective blocker
Increases the release of NE from post-synaptic neuron
Used w/ orthostatic hypotension (pt that needs more SNS for postural changes) impotence
Terazosin and tamulosin
receptors uses
selective alpha 1
long acting
effective in prostatic smooth muscle relaxation
Beta adrenergic antagonist
remember beta1 located: Heart, kidneys
beta2 located: visceral sm:resp,uterine, vascular, GI, GU; mast cells, skeletal muscles, liver, pancreas, adrenergic nerve terminal
ANTAGONIST
improve O2 supply and demand balance
bronchospasm (2)
vasoconstriction in skeletal muscle, PVD symptoms increase
decreased renin release (indirect way of decreasing BP)
Beta-adrenergic receptor antagonist MOA
Selective binding to beta receptors (influence inotropy, chronotropy)
Large doses of agonists will completely overcome antagonism
Chronic use is associated with increase in the # of receptors (up-regulation) so have massive response bc of all the receptors
beta agonist derivatives
beta isoproterenol
substitution on benzene ring
possessing some sympathomimetic effects
Propranolol
class, receptors
how to give
prototype no selective pure antagonist equal B1 and 2 give in stepwise manner until goal lf 55-60 HR
Propranolol cardiac effects
Decreased HR, contractility, CO
especially during exercise and sympathetic outflow
Blockade of β2 receptors-increased PVR, increased coronary vascular resistance
*decreased HR and CO oxygen demand is lowered, compensating for the increased PVR
Sodium retention due to renal
system response to drop in CO
Propranolol pharmacokinetics
goes through firsts effect (90-95%)
therefore PO dose much larger
0.05mg/kg IV or 1-10mg *give slowly q5min
protein bound 90-95%
metablized in liver E1/2 2-3hrs–will be increased in low hepatic blood flow states
decrease clearance of amide LA due to a drop in hepatic blood flow/metabolism inhibition
decrease pulm 1st pass effect of fentanyl
Timolol receptor, use
Non selective beta blocker
Used to tx glaucoma-decreases intraocular pressure by ↓ production of aqueous humor
Eye drops can cause ↓BP, ↓HR and ↑ airway resistance (can get systemicly absorption)
Nadolol receptor, metabolism
Non selective beta blocker
No significant metabolism (renal/biliary elimination)
E1/2t of 20-40hrs take 1X daily *LONG 1/2life
Metoprolol
receptor, causes, first pass, dose, e1.2t
Selective beta 1 blocker (better for asthma than propranolol bc selective) Prevents inotropy and chronotropy Selectivity is dose related About 60% goes thru first pass effect PO 50-400mg IV 1-15 mg E1/2t of 3-4hrs
Atenolol
receptor, causes, metabolism, e1.2t
Most selective beta 1 antagonist and thought to have the least CNS
effects (polar, doesn’t cross BBB)
E1/2t is 6-7hrs
Not metabolized in liver, excreted via renal system (polar), sticks around active until kidney gets rid of it.
therefore E1/2t is increased in renal disease
Very useful in cardiac patients with CAD
Betaxolol
e1/2t, use, receptor
Cardioselective beta 1 blocker
E1/2t is 11-22hrs
Single dose daily for HTN
Topical useful for glaucoma, with less risk of brochospasm than Timolol,
so good alternative choice in asthmatics with glaucoma
Esmolol
class, receptor, dose, infusion, e1/2t, hydrolyzed
Selective beta 1 antagonist
Rapid onset, short acting ( good for hemodynamic response to noxious stimuli)
dose: 0.5mg/kg IV (10-180mg IV)
DOA= <15mins
Can start infusion 50-300 mcg/kg/min
Small does: effects HR without decreasing BP significantly
In doses used, it does not occupy sufficient beta receptors to cause negative inotropy (decreased contractility)
E1/2t is 9 min
rapidly hydrolyzed by plasma esterases
*not the same as the cholinesterase that does succ, so no effect on such
Beta blockers side effects
CV: decrease HR, Contractility, BP
worsens PVD (block of beta-2 vasodilation)
Airway: bronchospasm
Metabolism: alter carbohydrate and fat metabolism, mask the increase in HR caused by hypoglycemic
Distribution of ec K: inhibit uptake of K into skeletal muscles
Interaction with anesthetics: may have ↓BP with IAs
Nervous system: fatigue, lethargy
N/V/D
Beta blockers relative contrindications
Pre-existing AV heart block or cardiac failure
Reactive Airway Disease
Diabetes Mellitus (without BS monitoring)
Hypovolemia
Clinical uses of B-blockers
HTN mgmt Angina decrease mortality in tx of post MI periop/postop of pts at risk of MI suppression of tachyarrythmias prevention of excessive SNS activity (stage fright)
Labetalol
receptors, metabolism, CO effects, dose, SE
Selective at alpha 1, beta 1 and 2 receptors; more beta 7:1 (no alpha 2 so still get neg feedback)
Metabolism conjugation of glucuronic acid; <5% in the urine
E1/2t of 5-8 hrs, prolonged in liver disease
↓ BP, SVR, HR.
CO is unaffected
Maximum drop in BP is 5-10 min after given
Dose 0.1-0.5mg/kg IV
Usually 5mg at a time for mild hypertension in the OR
Can cause orthostatic hypotension, bronchospasm, heart block, CHF, bradycardia
Antimuscarinic MOA, natural vs semi-synthetic
Competitively antagonize Ach at muscarinic receptors ONLY
Cation portion of the drug fits into Ach’s place on mus receptor and reversibly inhibits Ach binding
**Allow sympathetic responses to predominate
This competitive inhibition can be reversed if Ach concentration is ↑
Natural (atropine & scopolamine) are tertiary amines – alkaloids of belladonna plants (can get into brain)
Semi-synthetic (glycopyrrolate/Robinal) - quaternary ammonium derivative (canNOT get into brain)
