Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
18 Cards in this Set
- Front
- Back
PHENYLEPHRINE |
* Alpha-1 adrenergic agonist * Weak beta effects * Not a substrate for COMT * Primary use: vasoconstrictor * Treat hypotensive states- shock, spinal anesthesia * Nasal decongestant (Neosynephrine)- rhinitis medicamentosa or rebound * Mydriasis |
|
METHOXAMINE |
* Alpha-1 adrenergic agonist * Does not stimulate beta adrenoceptors * Primary use: vasoconstrictor * Treat hypotensive states- shock, spinal anesthesia * Not metabolized by COMT or MAO |
|
CLONIDINE |
* Alpha-2 adrenergic agonist * Direct vasoconstrictor * Indirect antihypertensive agent- central suppression * Rebound hypertension |
|
DOBUTAMINE |
* “Beta-1” adrenergic agonist (not DOR’s) * Stimulates beta-2 and alpha adrenoceptors * Inotropic agent * Vasodilation predominates- preserves renal and G.I. blood flow- heart failure * Tolerance may develop |
|
TERBUTALINE and ALBUTEROL |
* Selective beta-2 agonists (normal doses) * Primary use: broncodilator * Reduced risk of cardiac stimulation * May inhibit mast cell secretion * Not metabolized by COMT or MAO- long duration of action- 4 - 8 hours; 0.5 – 2 hours for ISO * Inhalation helps limit side effects |
|
AMPHETAMINE |
*Indirect Adrenergic Agonist * Enhances NE release * Action similar to NE * Powerful CNS stimulant- Less fatigue, increased alertness- Better physical performance * Appetite suppression * Dependency and tolerance |
|
EPHEDRINE |
*Mixed-Acting Adrenergic Agonist * Indirect: induces NE release * Direct: stimulates alpha and beta adrenoceptors * Bronchodilation due to beta effects- replaced by beta-2 agonists * Urinary incontinence * CNS stimulation * Appetite suppression- more effective combined with caffeine- herbal preparation: Ma huang |
|
METARAMINOL |
*Mixed-Acting Adrenergic Agonist * Direct: stimulates alpha-1 adrenoceptors- weak beta effects (like phenylephrine) * Indirect: replaces NE in storage granules- “false neurotransmitter” * Treat hypotensive states |
|
PHENOXYBENZAMINE |
*Alpha Adrenergic Antagonist * Covalent, irreversible blockade- may require days to recover * Nonselective (slight preference for alpha-1) * Primary use: pheochromocytoma * Urinary obstruction (BPH) * Autonomic hyperreflexia * Side effects- orthostatic hypotension- nasal congestion- ejaculatory dysfunction |
|
PHENTOLAMINE |
*Alpha Adrenergic Antagonist * Nonselective (equal affinity for both) * Competitive blockade * Primary use: pheochromocytoma * Not good general antihypertensive- reflex tachycardia (a-2 block) * erectile dysfunction * Side effects- orthostatic hypotension- reflex cardiac stimulation- nasal congestion |
|
PRAZOSIN |
*Alpha Adrenergic Antagonist * Selective alpha-1 antagonist * Primary use: antihypertensive * Little or no alpha-2 blockade- limited reflex tachycardia * Dilates arterial and venous beds (PDE?)- decreases venous return * May have CNS effects also? * Improve urinary flow in BPH * “First-Dose Phenomenon”- give it at bedtime |
|
PROPRANOLOL |
*Beta Adrenergic Antagonist * Blocks both beta-1 and beta-2 adrenoceptors * Primary uses:- antihypertensive (decreases PVR)….CNS?- ischemic heart disease (depress HR, cont.)- little effect on normal heart or BP at rest * Can lead to bronchoconstriction- limited use in patients with asthma or COPD * Hypoglycemia, especially in diabetics * Hyperthyroidism * Glaucoma * Membrane “stabilizing” effect |
|
METOPROLOL |
* Beta Adrenergic Antagonist * Selective beta-1 blocker * Primary uses:- antihypertensive- ischemic heart disease (depress HR, cont.)- little effect on normal heart or BP at rest * Less tendency for bronchoconstriction |
|
GUANETHIDINE |
*Sympatholytic Agent * Catecholamine depletion- replaces NE in storage vesicles (MAO)- interferes with vesicle release (?) * Powerful antihypertensive- dilates both arterial and venous beds- orally effective – half life 5 days * Little effect on CNS * Orthostatic hypotension * G.I. / diarrhea * Male sexual disturbances * Caution with MAO inhibitors |
|
RESERPINE (snakeroot) |
* Sympatholytic Agent * Catecholamine depletion- inhibits amine uptake into vesicles- irreversible- inhibits DO uptake as well * Blocks NE STORAGE and SYNTHESIS * Long-acting (weeks) and irreversible * CNS effects limit use- depression, sedation, suicide * Inexpensive and Powerful |
|
METHYL TYROSINE |
*Inhibitors of NE Synthesis * Inhibits tyrosine hydroxylase- decreases catecholamines * Pheochromocytoma- preoperative- long-term therapy * Side effects: sympathetic depression * CNS effects- sedation, anxiety |
|
alpha-METHYLDOPA |
*Replaces NE * “False Transmitter”- alpha-methyl-NE: alpha adrenergic agonist- antihypertensive agent- CNS effects: decreased sympathetic activity- alpha-2 adrenoceptors ? * Spares renal blood flow * CNS effects- Sedation– central alpha-2 adrenoceptors * Preferred for hypertension in pregnancy |
|
COCAINE |
*Neuronal Uptake Inhibitor * Inhibits Uptake 1 mechanism * Enhances NE effects at effector sites |