Sympathetic / Adrenergic Flashcards
Andrenergic transmission steps
Synthesis Uptake into vesicles Release Binding to Receptor Removal
Rate limiting step in the synthesis
Hydroxylation of tyrosine
Inhibitors of synthesis
Metyrosine and
Carbidopa
Inhibits transport into vesicle
Reserpine
Facilitates release of NE
Calcium
Block release of NE
Guanethedine
Bertylium
Causes release of NE
M - methamphetamine
E - Ephedrine
T - tyramine
A - amphetamine
Removal
Methylaed by
COMT
catechol o-methyltransferase
COMT destroys
Catecholamines
Epi, NE, dopamine
Removal
Oxidized by
MAO
monoamine oxidase
MAO destroys
Monoamines
NE, dopamine, serotonin
Inhibits reuptake
Cocaine
TCA (tricyclic antidepressants)
Urine metabolites
Vanillylmandelic acid
Metanephrine
Normethanephrine
Alpha 1
B - blood vessel - vasoconstriction P - pili arrector muscle - constriction S - spinchter P - constriction G - glands
Alpha 2
Preganglionic - central
Postganglionic - peripheral
Beta islet cells of pancreas
Beta 1
Heart
Kidney
Beta 2
B - bronchus U - uterus B - blood vessel S - contraction P - pancreas; stimulates INSULIN RELEASE M - metabolism
Beta 3
Adipose tissue
Dopamine 1
BV of Renal Mesenteric Coronary Cerebral vascular Beds VASODILATION
Dopamine 2
CNS
STIMULATION
Sub-groups of DIRECT ADRENERGIC AGONISTS
Catecholamines
Non-catecholamines
Unique feature of catecholamines
3,4-dihydroxybenzene group
Catecholamines
Metabolized by COMT and MAO
ineffective orally
Polar
Do not readily penetrate the CNS
Has the HIGHEST potency in activeting the alpha and beta receptors
Catecholamines
Non-catecholamines
LONGER HALF-LIVES
increased lipid solubility, thus greater access to CNS
[SUBSTITUTION ON THE BENZENE RING]
Absence of ONE OR BOTH -OH GRP IN THE CATECHOL
Without other substitutions
Reduce potency
Increase BA after PO
prolongs duration of action
Increase distribution to the CNS
[SUBSTITUTION ON THE ALPHA CARBON]
Blocks oxidation by MAO
prolongs action
Ephedrine, amphetamine
Other name for alpha methyl cmpds
Phenylisopropylamine
[SUBSTITUTION ON THE BETA CARBON]
Substitution of a hydroxyl group of the beta carbon
Decreases activity with the CNS bec of decreased lipid solubility
Enhances agonist activity for both alpha and beta receptors
Directly bind to adrenergic receptors
Direct acting sympathomimetics
Alpha 1 blockers
3 PM Phenylephrine Phenylpropanolamjne Pseudoephedrine Methoxamine
Causes intense vasoconstriction
For hypotensive emergencies
PHENYLEPHRINE
Alpha 1 agonist
OTC nasal decongestant
PHENYLPROPANOLAMINE
alpha 1 agonist
Alpha 2 agonist aka
Symphatolytics
Symphatoplegics
Alpha 2 agonists
Sir Charles
C - colonidine
M - methyldopa
G - guanabenz and guanfacine
Used for paroxysmal atrial tachycardia
Methoxamine
Decreases preganglionic sympathetic outflow
Leads to decreased BP
Clonidine
Methyldopa
Causes ORTHOSTATIC HYPERTENSION
All alpha 2 agonist but in methyldopa (mild only)
Methyldopa is converted to _________ which is a potent alpha 2 agonist
Alpha methyl norepinephrine
For gestational hypertension
Methyldopa
Has a false-positive result in Coomb’s test
Methyldopa
Clinical use of BETA 2 AGONISTS (-olols)
For ASTHMA
Reduce uterine contractions in premature labor
terbutaline
Ritodrine
Beta 2 agonists
The only beta 1 and 2 agonist
Isoproterenol
Causes intense vasodilation
Reduces mean arterial pressure
Prevent bronchospasm
Stimulates heart more than Epi due to direct effects
Has adverse effects similar to epinephrine
Isoproterenol
Alpha and beta agonists
Epinephrine
Norepinephrine
Dopamine
Dobutamine
Drug of choice for ANAPHYLAXIS
Alpha and Beta agonist
Epinephrine
Epinephrine has _____ onset but ______ duration of action
Rapid
Brief
Used only when intense vasoconstriction is necessary (septic shock)
Norepinephrine
Derivative of dopamine but DOES NOT bind to dopamine receptors
Dobutamine
Increases cardiac output with little change in the heart rate
For congestive heart failure
Dobutamine
Cause NE release from presynaptic terminals but do not bind to adrenergic receptors
Indirect acting
Indirect acting adrenergic agonist
Tyramine
Amphetamine, methamphetamine
Not a clinically useful Drug
Can cause hypertension in depressed patients taking MAOI
Tyramine
For NARCOLEPSY,
ADHD
Apetite suppression
Parkinson’s disease
Amphetamine
Methamphetamine
Displace NE from pre-synaptic terminals and bind to adrenergic receptors
Mixed
Causes narcolepsy
Amphetamine & methamphetamine (indirect acting)
Ephedrine (mixed)
Mixed adrenergic agonists
Ephedrine
Metaraminol
Has longer duration of action but less potent than epi
Poor Substrate for COMT and MAO
Ephedrine
For SHOCK
when Infusion of NE or dopamine is not possible
Acute hypotension
Metaraminol
Benign prostatic hyperplasia (BPH)
Alpha 1 blockers (zosin)
First dose phenomenon
Alpha 1 blockers (zosin)
Treats erectile dysfunction (impotence)
Yohimbine
Alpha 2 blocker
Alpha 1 and 2 blockers
Phenoxybenzamine PO
Irrev
Slow onset, long duration 24 hrs
Phentolamine IV
ReV
Rapid onset, short half-life 4 hrs
Hypertension due to
- PHEOCHROMOCYTOMA
- inatake of MAOIs or symphatomimetics
Alpha 1 and 2 blockers
Vasospasm in reynaud’s syndrome
Alpha 1 and 2 blockers
Lowers BP
Triggers ASTHMA
Beta 1 and 2 blockers
For hypertensive patients with impaired pulmonary function
Beta 1 blockers
Beta 1 and 2 blockers
Propanolol Nadolol Timolol Sotalol Labetalol and carvedilol
Causes arrhythmias and fasting hypoglycemia due to decreased glycogenolysis
Propanolol
For angina pectoris
Requires only one dose per day
Nadolol
Only beta-blocker for the eye (open-angle glaucoma)
Timolol
Has action potential prolonging actions
Sotalol
Maintenance of sinus rhythm in patients with atrial fibrillation
Sotalol
For diabetic hypertensive patients who are receiving insulin or oral hypoglycemic agents
Beta 1 blockers
Indirect-acting adrenergic antagonists
Guanethidine
Reserpine