Adrenergic Pharmacology Flashcards
Precursor to catecholamines
Tyrosine
Pathway for norepinephrine
Tyrosine–>L DOPA–>Dopamine–>Norepinephrine
a2 stimulation
Results in negative feedback in presynaptic terminal
b2 receptors
Only stimulated by epinephrine, not NE
COMT
Metabolizes NE in synapse
MAO
Make sure that the NE mobile pool that is not recycled into vesicles is destroyed so not too much NE is released
Methyl Tyrosine
Blocks conversion of tyrosine–>L dopa and therefore decreases NE release
MAO inhibitors
Block degradation of excess NE mobile pool in presynaptic cell–can cause excess NE release
a1 effect on blood vessels
Constriction and increased BP
Arterioles: Increased TPR, increased afterload, increased diastolic BP
Veins: Increased preload and increased systolic pressure
a1 effect on eye
Dilation
a1 effect on kidney
Decreased renin release
a1 effect on liver
increased glycogenolysis
Decreased insulin
a1 effect on bladder
Increased sphincter tone and urinary retention
a2 effect
Decreased synthesis and release of NE
B1 effect on heart
Increased HR, Increased conduction velocity, increased contractility, increased SV and increased systolic pressure
B1 effect on kidney
increased renin release
B1 effect on ciliary body in eye
Increased aqueous humor
B2 effect on vessels
Vasodilation, decreased TPR and decreased diastolic pressure
B2 effect on bronchioles
Bronchodilation
B2 effect on uterus
Relaxation–can delay preterm labor
B2 effect on liver
Glycogenolysis and gluconeogenesis
Increased insulin
a1 agonists
Increase in BP with no change in pulse pressure
Does not effect HR but reflex bradycardia may occur due to increase in BP
Phenylephrine
a1 agonist
Can be used for septic shock
Use as a nasal decongestant due to vasoconstriction preventing mucus
a2 agonists
Increase negative feedback so decrease release of NE
Can help with muscle spasticity by causing muscle relaxation
Will decrease insulin so caution in diabetics
Isoproterenol
Beta Agonist
B1=B2
use for bradycardia and heart block (B1) and asthma (B2)
Side effects: tachycardia, hypotension, flushing, headache
Dobutamine
B1 agonist
Use for congestive heart failure management
Side effects: tachycardia due to reflex from vasodilation
Albuterol
B2 agonist
Used for acute asthma
Side effects: palpitations, tremor, anxiety, restlessness
Terbutaline
B2 agonist
Used for premature labor
Salmetrerol
long acting B2 agonist, delayed onset, good for prophylaxis of asthma
Formoterol
Long acting b2 agonist, prompt onset, good for acute and prophylaxis
Norepinephrine always
Activates a1, a2, B1
Increases BP (a1 and B1 causes increased systolic BP and a1 causes slight increase in diastolic BP): increase in pulse pressure
B1 causes increase in HR, however reflex bradycardia will occur due to increased BP
Epinephrine
Effects are dose dependent
Activates a1, a2, B1, B2
Low dose epi
B1 and B2 agonist
Use for anaphylactic shock
High dose epi
a1 and B1 primarily (looks more like NE)…B2 is masked by a1 effects
Use for heart stopping
how to differentiate between high dose epi and NE
Need to block a1 to see if B2 becomes unmasked
Will cause hypotension if it is high dose epi
Effect of low dose epi on HR and BP
B1: increased HR, increased SV, increased CO
B2: decreased TPR, decreased BP
Increased pulse pressure and mean pressure decreases
Effect of medium dose epi on HR and BP
B1: increased HR, increased SV, increased CO
B2: decreased TPR, decreased BP
a1: increased TPR, increased BP
Increased pulse pressure, mean pressure stays constant
Effect of high dose epi on HR and BP
B2 effect masked by a1=increased TPR and increased BP
Potential reflex bradycardia–can make ischemia worse
Uses of NE and epi
Cardiac arrest Adjunct to local anesthetic Hypotension Anaphylaxis: Epi only Asthma: Epi only
Dopamine
Can be used in shock management due to similarity to NE
Low dose dopamine
D1
Vasodilation on renal, coronary, mesenteric vessels
Medium dose dopamine
D1 and B1
Adds inotropic effect to D1 to preserve blood flow to heart and kidneys
High dose dopamine
D1, B1, a1
a1 can help maintain BP
Indirect acting adrenergic receptor agonists: releasers
Displaces NE from mobile pool causing an increase in NE availability
Releasers can interact negatively with
MAO inhibitors and Tyramine rich food
Can cause hypertensive crisis due to too much NE
Examples of reuptake inhibitors of NE
Cocaine and TCAs
a receptor antagonists
Decrease TPR and decreases mean BP
Used to fight hypertension
May cause reflex tachycardia and salt/water retention
B1 receptor antagonists
Decreases HR, SV, and CO: good for anti-arrhythmic and decrease O2 demand and angina
Decreases renin release: good for anti CHF
Decreases aqueous humor production: good for anti glaucoma
B2 receptor antagonists
Aggregates bronchospasm in asthmatics, makes metabolic effects worse in diabetics
General use of beta blockers
Angina, hypertension, post MI
Anti arrhythmic
Glaucoma
Chronic use of beta blockers leads to
Upregulation and tolerance
Important to taper dose to avoid excessive CV effects
Additive bradycardia occurs when
Take beta blocker with calcium channel blocker
Can cause AV block
What can be used in Beta blocker OD
glucagon
Binds to Gs coupled receptors and reverses B blockade toxicity without interfering Beta receptor
1st generation beta blockers
nonselective
N-Z
“-olol”
2nd generation beta blockers
B1 selective
A-M
“-olol”
3rd generation beta blockers
Also act as vasodilators
Nonselective + a1 antagonist: used in CHF
Selective B1 and NO release: used in HTN
Clonidine
a2 agonist
Methyldopa
a2 agonist
Phentolamine
a1 blockers nonselective
Labetalol
A1 + b blocker
Amphetamines
Increase release of NE
Methylphenidate
Increase release of NE
Treatment of ADHD
Atomexetine
Increase release of NE
Treatment of ADHD
Modafinil
Increase release of NE
treatment of narcolepsy
B2 blocking effects
Bronchoconstriction, decreased aqueous humor, impotence
Beta blockers can decrease
Renin
Can be used for hypertension but not first line
