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AdrenergicsI-IV
lectures 11-14 taussig
| Question | Answer |
|---|---|
| tachyphylaxis | phenomenon of NE depletion from neuron stores after repeated use of sympathomimetics |
| tyramine | uptaken by NE transporter, stimulates NE release from neurons = sympathomimetic. present in foods like cheese and wine, caution with MAOIs |
| amphetamine | long acting sympathomimetic that enters neuron via NE transporter and stimulates NE and dopamine release; SBP/DBP up and HR down by reflex; effects: euphoria, resp stimulation, appetite suppression (tolerance after 2-3 wks), etc. used for ADHD tx |
| ephedrine | sympathomimetic amine uptaken via NE transporter, stimulates NE and dopamine release. both alpha and beta agonist |
| methylphenidate (Ritalin) | CNS stimulant uptaken via NE transporter in neurons, causes release of NE from neurons. used for ADHD to improve attn through catecholamines' actions. drug holidays when possible to avoid insomnia and anorexia |
| effect of an alpha2 antagonist | removal of inhibition of symp = enhanced sympathetic outflow centrally and peripherally = vasoconstriction and cardiac stimulation |
| phenoxybenzamine | non-selective alpha1,2 blocker irreversibly aklylates alpha receptors AND stops catecholamine uptake into sympathetic neurons. long lasting (3-4 days), used to treat pheochromocytoma or to prep pts for surg |
| phentolamine | reversible nonselective alpha1,2 blocker used acutely to block action of catecholamines. EPI REVERSAL, if epi added after = vasodilation and hypotension, fall in BP (depressor response) |
| effect of alpha1 blockers | stops smooth muscle contraction = vasodilation, pooling of blood peripherally and induced BP drop. little tachycardia b/c alpha2 isn't being blocked |
| prazosin (Minipress) terazosin, doxazosin, tamsulosin (Flomax) | potent & selective alpha1 blockers for primary systemic HTN. prazosin - 3 hr half-life, given 2-3x/day. side effects: marked postural hypotension, betters lipid profiles` |
| tamsulosin (Flomax) action | blocks alpha1a receptors on smooth muscle in bladder and prostate, relieves retention and improves urine flow |
| effect of beta blockers | decreased inotropy, chronotropy and dromotropy (CO goes down) while initially causing increased PVR b/c of blocking beta2 effects. PVR returns to baseline long-term. stops renin secretion (beta1 effect) |
| adverse effects of beta blockers | mask tachycardia associated with hypoglycemia, life-threatening bronchoconstriction in asthma/COPD pts, increases triglycerides, bradyarrhythmias, may induce heart failure, sleep distrubances and depression, lowers exercise tolerance |
| propranolol (Inderal) | nonselective beta1,2 blocker, very lipophilic and enters CNS readily. causes small drop in BP, slight increase in LVCF and transient increased HR |
| metoprolol (Lopressor) | beta1 selective antagonist, wide genetic variation in metabolism rates |
| atenolol (Tenormin) | beta1 selective antagonist with longer half-life than metoprolol, limited penetration into CNS |
| carvedilol (Coreg) | racemic mixture with nonselective beta block and alpha1 blocking activity, used for HTN and maybe now CHF? |
| therapeutic uses of beta blockers | HTN, good for those with angina, tachyarrhythmias or used in combination with vasodilators that would cause reflex tachycardia, early after MI to prevent v-fib and cardiac rupture, aortic dissection, hyperthyroidism |
| diseases that would make beta blocker use a poor choice in certain pts | DM (masks tachycardia in hypoglycemic episode) asthma (no favorable beta2 bronchodilation) PVD (stops favorable beta2 vessel dilation) bradyarrhythmias (decreases dromotropy) |
| combo of drugs to treat hypertensive pts with mild to moderate heart failure | metoprolol or carvedilol in combo with ACE inhibitor-diuretic combo |
| methyldopa | prodrug that's converted to alpha-methylNE in then neuron and released upon stimulation; called false NT b/c it it's NE, but has good alpha2 agonist effects (like clonidine) |
| pheochromocytomas secrete epi/norepi the most? | epinephrine |
| What is the biphasic effect seen with TCA and cocaine use with respect to the adrenergic synapse? | short-term: NE effect is potentiated b/c it's not cleared away from synapse longer-term: once NE diffuses out, stores are all depleted and responses to cocaine and NE will be blunted |
Created by:
sirprakes
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