Adrenergic Flashcards
Norepinephrine: Class
Pharm: direct acting adrenergic agonist
Ther: vasopressor/vasoconstrictor
Norepi: PD
-stimulates peripheral alpha1 adrenoceptors –> venoconstriction, vasoconstriction, cardiac stimulation.
incr CO, incr SVR, incr MAP.
decr blood flow to skin/muscle/kidney
-stimulates B1 receptors in heart, incr HR and contractility.
Norepi: PK
F = 100%
IV only
metabolized by COMT and MAO, mainly in liver
matabolites excreted in urine
half life 1-2 min (titrate quickly by IV)
crosses placenta but not BBB
Norepi: tox
excessive vasoconstriction in mesenteric vessels and peripheral arterioles --> ischemia, infarct, gangrene. reflex bradycardia (in resp to high MAP)
Norepi: monitor
BP, HR, infusion site, evidence of extravasation
Norepi: special issues
correct volume depletion before giving
careful with infusion site because of extravasation
continuous monitoring of BP in ICU
caution in peds/gers
Norepi v Epi: which has more activity on B receptors?
Epi
Epi: classes
direct acting adrenergic agonist
vasopressor, cardiac stimulant, bronchodilator
adjunct to local anesthetics, anti-anaphylaxis
epi: PD
alpha1 adrenergic receptors -> veno and vaso constriction
B1 leading to tachy and incr contractility
B2 -> bronchodilation
stabilizes mast cells!
Epi: PK
IV = immediate IM = variable SC 5-15 min inh 1-5 min opthalmic topical metabolized by COMT and renally excreted
Epi: tox
excessive vasoconstriction, HTN, hemorrhagic stroke, angina, arrhythmias,
risk of excessive HTN in pts taking propanolol
Epi: special issues
drug of choice in anaphylaxis
useful/added to local anesthetics because of vasoconstriction: limits blood loss, increases duration of anesthetic.
Epi: monitor
BP, HR, rhythm, infusion site, extravasation
Dopamine: class
direct acting non-selective adrenergic and dopaminergic agonist
catecholamine
inotropic agent and vasopressor
Dopamine: PD
activates Beta1 AR and Alpha1 receptors at different concentrations
Acts on D1 receptors in renal vessels (relax) and incr renal flow
Dopamine: PK
IV only
acts within minutes
half life = just minutes –> continuous infusion
Dopamine: tox
ectopy (disturbance of heart rhythm). tachycardia, angina
nausea
Dopamine: special issues
correct hypovolemia before giving
administer thru large vein and monitor patient
Dobutamine: class
adrenergic
cardiac stimulant
very sim to Dopamine
Dobutamine: PD
sim to Dopamine but with less ability to cause vasoconstriction
more specific for Beta1 receptors
Isoproterenol: class
non-selective B-AR agonist
Rx for bradycardia
Isoproterenol: PD
vasodilator, incr HR
Isoproterenol: tox
tachycardia, BP, arrhythmias
General receptor action at molecular level: Alpha1
Works through PLC/PIP2 –> IP3, incr Ca2+ intracellularly, which incr contractility
General receptor action at molec level: Beta1
GPCR, Gs so ATP –> cAMP via increased activity of Adenylyl cyclase –> incr PKA, incr Ca in cell –> incr contractilty
Phenylephrine: class
relatively pure Alpha1-AR agonist
Phenylephrine: PD
potent constrictor, nasal decongestant, mydriatic (dilates pupil) with no affect on accomodation, BP maint during surgery.
Phenylephrine: PK
not inactivated by COMT
causes release of Ca2+ from SR -> incr contractility
give intranasally or topically (eye)
half life = 3h
Phenylephrine: tox
HTN, reflex bradycardia
Clonidine: class
central alpha-2 agonist
antihypertensive, adjunct to Rx of opioid withdrawal, prophylaxis of migraine
Clonidine: PD
stimulates alpha-2 adrenoceptors in brainstem, thereby leading to down-regulation of sympathetic output
Clonidine: PD
Onset 1 h, duration 8 h, F~85%, also available as cutaneous patch
Clonidine: tox
withdraw gradually because of risk of rebound HTN; risk of bradycardia in sinus node disease; lethargy, fatigue, depression
Clonidine: interactions
additive effects with most other antihypertensives; additive sedation with other CNS drugs
Clonidine: special considerations
Pregnancy class C; avoid in patients with renal insufficiency If pt has first or 2nd AV block, do not give. Give an EKG to most patients to make sure no block, no LVH.
Clonidine: monitor
follow BP and HR, fatigue
Ibuprofen: class
NSAID
Analgesic, anti-pyretic (fever), anti-inflammatory, anti-gout, anti-dysmennorhea
Ibuprofen: PD
involves inhibition of prostaglandin synthetics via COX1 and COX2
Ibuprofen: PK
F =80%
some excreted unchanged in urine
extensive metabolism in liver
half life 2-4 h
Ibuprofen: tox
“allergies” to aspirin
use caution in pts with renal compromise, ulcer disease
causes fluid retention in CHF patients
Ibuprofen: special considerations
more side effects in geriatrics
Ibuprofen: interactions
with warfarin, aspirin, diuretics, anti-hypertensives
Albuterol: Class
pharmacologic class: selective β-2 AR agonist (SABA: short acting beta2 agonist)
Therapeutic class: bronchodilator for asthma/COPD
Albuterol: PD
binds to beta-2 receptors and relaxes smooth muscle of airway, causing bronchodilation
Albuterol: tox
tachycardia, tremor, tolerance
Albuterol: mechanism of delivery
nebulizer or MDI
Amphetamine: classes
indirectly-acting adrenergic agonist. sympathomimetic
CNS stimulant ==> used for appetite suppression, ADHD, and narcolepsy.
Amphetamine: PD
release of biogenic amines from storage (noradrenaline) Alpha1 -> vasoconstiction, inc BP Beta2 -> bronchodilation Beta1 -> inc HR CNS stimulant
Amphetamine: PK
plasma half life approx 12h
excreted unchanged in urine
Amphetamine: tox
restlessness, tremor, irritability, insomnia, dependency, tolerance, inc BP, tachycardia, psychosis if excessive dose
Amphetamine: special issues
tolerance, dependance, addiction can develop (unlike ephedrine)
Ephedrine: class
Pharmacologic class: Indirect adrenergic, stimulates NE and dopamine release
Therapeutic class: decongestant, anti-hypotension
Also potent CNS stimulants used for ADHD and appetite suppression
Ephedrine: PD
↑ NE and dopamine release and direct effects on α and β
Ephedrine: PK
Prolonged duration of action
Ephedrine: tox
HTN, tachyphylaxis
insomnia
Ephedrine: special
ephedrine-containing herbal products have been banned in the US, Pseudoephedrine is a restricted OTC substance because it can be used to make meth
Pseudophedrine: class
Pharmacologic class: Indirect adrenergic, stimulates NE and dopamine release
Therapeutic class: decongestant only (not antihypotension as is Ephedrine)
Also potent CNS stimulants used for ADHD and appetite suppression
Pseudophedrine: PD
↑ NE and dopamine release and direct effects on α and β
Pseudophedrine: PK
Prolonged duration of action
Pseudophedrine: tox
HTN, tachyphylaxis
insomnia
Pseudophedrine: special
ephedrine-containing herbal products have been banned in the US, Pseudoephedrine is a restricted OTC substance because it can be used to make meth
Tyramine: class
Pharmacologic class: indirectly-acting adrenergic agonist, stimulates NE and dopamine release
Therapeutic class: None.
Tyramine: PD
↑ Release of biogenic amines from storage, including dopamine in the CNS
Tyramine: PK
Byproduct of tyrosine metabolism ==> metabolized by liver MAO
Tyramine: tox
Can cause MAOI hypertensive crisis
Tyramine: special issues
use of MAO inhibitors and severe HTN, and tachypylaxis
Tyramine: interactions
caution with MAO inhibitors ==> can cause HTNsive crisis
Cocaine: class
Pharmacologic class: indirect-acting agonist via blocking Uptake 1 pathway leading to inc NA effects (vasoconstriction)
Therapeutic class: CNS stimulant, musical inspiration, song title by Eric Clapton
Local anesthetic, vasoconstrictor, drug of abuse
Cocaine: PD
blocks NE and dopamine reuptake via Uptake 1 pathway
Shorter lasting than amphetamine, more intense
Cocaine: PK
Smoked, snorted or injected for rapid effect
Cocaine: tox
Hypertension, AMI, arrhythmias, seizures. if snorted can lead to nasal septal necrosis due to vasoconstriction
Phentolamine: class
alpha blocker (reversible) Hypertensive crisis
Phentolamine: PD
blocks both Alpha1 and Alpha2.
Alpha1: block smooth muscle contraction -> vasodilation and postural hypotension
Alpha2: block leads to tachycardia and inc CO
Phentolamine: adverse effects
postural hypotension, tachycardia
Phenoxybenzamine: PD
blocks both Alpha1 and Alpha2.
Alpha1: block smooth muscle contraction -> vasodilation and postural hypotension
Alpha2: block leads to tachycardia and inc CO
Phenoxybenzamine: class
alpha blocker (IRreversible) Hypertensive crisis
Phenoxybenzamine: adverse effects
postural hypotension, tachycardia
Prazosin: class
a1 blocker
Prazosin: indications
antihypertensive, treatment of BPH, treatment of Raynaud’s syndrome, treatment for kidney stones
Prazosin: PD
blocks alpha-1 receptors on arterioles and veins, thereby inhibiting NE-mediated vasoconstriction and venoconstriction
Prazosin: PK
available po or transdermal; variable oral bioavailability (~60%), onset 2 h, duration 12-24 h
Prazosin: tox
excessive hypotension with passing out, especially orthostatic, especially in patients on diuretics
Prazosin: excr
extensively metabolized in liver
Prazosin: interactions
additive effects with most other antihypertensives, especially diuretics
Prazosin: special
start gradually, and at bedtime, to avoid first-time passing out; male patients with BPH?
Prazosin: monitor
BP, weight, edema
Propanolol: class
b blocker (1 and 2)
Propanolol: indication
Antihypertensive, antianginal, antiarrhythmic, MI
Propanolol: PD
binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system); recent evidence suggests less effective in preventing strokes than other drugs
Prolanolol: PK
available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)
Propanolol: tox
excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)
Propanolol: interactions
additive effects with most other antihypertensives, additive AV block with CEB’s
Propanolol: special
may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)
Propanolol: monitor
BP, HR, exercise tolerance
Timolol: class
same class as propanolol, non-specific b blocker
Timolol: indication
Open angle glaucoma, antihypertensive, MI prevention
Pindolol: class
same as propanolol. nonspecific b blocker & partial agonist
Pindolol: indication
Antihypertensive, antianginal, antiarrhythmic
Pindolol: PD
some degree of beta-1 activation is maintained while the cardiac response to increased sympathetic activity is blunted
Sotalol: class
K channel blocker & b blocker
Sotalol: indication
Antiarrhythmic Class III, antihypertensive
Sotalol: PD
prolongs cardiac action potential; blocks K+ channels
Metoprolol: class
b1 blocker (specific)
Metoprolol: indication
Antihypertensive, antianginal, antiarrhythmic, CHF
Metoprolol: PD
binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system); recent evidence suggests less effective in preventing strokes than other drugs
Metoprolol: PK
available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)
Metoprolol: tox
excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)
Metoprolol: interactions
additive effects with most other antihypertensives, additive AV block with CEB’s
Metoprolol: special
may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)
Metoprolol: monitor
BP, HR, exercise tolerance
Atenolol: class
b1 blocker
Atenolol: indication
Antihypertensive, antianginal, antiarrhythmic, anti-MI
Atenolol: PD
binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system); recent evidence suggests less effective in preventing strokes than other drugs
Atenolol: PK
available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)
Atenolol: tox
excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)
Atenolol: interactions
additive effects with most other antihypertensives, additive AV block with CEB’s
Atenolol: special
may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)
Atenolol: monitor
BP, HR, exercise tolerance
Labetalol: class
a1 and b blocker
Labetaolol: indication
antihypertensive, treatment of CHF, pheochromocytoma
Labetalol: PD
reduces BP by blocking access of NE to beta-receptors and alpha-1 receptors, thereby lowering BP by several different mechanisms; patients differ in degree of beta-blockade vs alpha-blockade
Labetalol: PK
excellent absorption but high first-pass effect, leading to F~25%; onset 1-2 hours after po, 2-5 minutes when given iv; extensively metabolized in liver by IID6
Labetalol: tox
avoid in patient with bradycardia, heartblock, CHF, asthma, shock; use with caution in patients with cardiomyopathy, pheochromocytoma: Pregnancy Class D
Labetalol: interactions
additive effects with most other antihypertensives
Labetalol: special
use reduced doses in patients with impaired liver function; dizziness is most troubling early side effect; most often used for hypertensive crises (as with nitroprusside)
Labetalol: monitor
BP, HR
Carvedilol: class
a1 and b blocker, antioxidant
Carvedilol: indication
CHF
Carvedilol: PD
reduces BP by blocking access of NE to beta-receptors and alpha-1 receptors, thereby lowering BP by several different mechanisms; patients differ in degree of beta-blockade vs alpha-blockade
Carvedilol: PK
excellent absorption but high first-pass effect, leading to F~25%; onset 1-2 hours after po, 2-5 minutes when given iv; extensively metabolized in liver by IID6
Carvedilol: tox
avoid in patient with bradycardia, heartblock, CHF, asthma, shock; use with caution in patients with cardiomyopathy, pheochromocytoma: Pregnancy Class D
Carvedilol: interactions
additive effects with most other antihypertensives
Carvedilol: special
use reduced doses in patients with impaired liver function; dizziness is most troubling early side effect; most often used for hypertensive crises (as with nitroprusside)
Carvedilol: monitor
BP, HR
