Beta-adrenergic blockers causing

BETA-BLOCKERS CYTOTOXICS Imatinib may cause an t in plasma concentrations of metoprolol, propanolol and timolol, with a risk of toxic effects Imatinib is a potent inhibitor of CYP2D6 isoenzymes, which metabolize beta-blockers Monitor for clinical efficacy and toxicity of beta-adrenergic blockers... 

Beta-adrenergic blockers decrease the heart rate, decrease blood pressure, and cause bronchoconstriction. There are two types of beta-adrenergic blockers. 

When used concomitantly, theophylline increases the excretion of lithium. Also, cimetidine, allopurinol (high dose), propranolol, erythromycin, and troleandomycin may cause an increase in serum concentrations of theophylline by decreasing the hepatic clearance. Barbiturates and phenytoin enhance hepatic clearance and hepatic metabolism of theophylline, decreasing plasma levels. Beta-adrenergic blockers exert an antagonistic pharmacologic effect. 

I. Pharmacology. Esmolol is a short-acting, IV, cardioselective beta-adrenergic blocker with no intrinsic sympathomimetic or membrane-depressant activity. In usual therapeutic doses, it causes little or no bronohospasm in patients with asthma. Esmolol produces peak effects within 6-10 minutes of administration of an intravenous bolus. It is rapidly hydrolyzed by red blood cell esterases, with an elimination half-life of 9 minutes therapeutic and adverse effects disappear within 30 minutes after the infusion is discontinued. 

I. Pharmacology. Phentolamine is a competitive presynaptic and postsynaptic alpha-adrenergic receptor blocker that produces peripheral vasodilation. By acting on both venous and arterial vessels, it decreases total peripheral resistance and venous return. It may also stimulate beta-adrenergic receptors, causing cardiac stimulation. Phentolamine has a rapid onset of action (usually 2 minutes) and short duration of effect (approximately 15-20 minutes). 

Deficiency of adrenal medullary catecholamines appears to give no ill effects, and replacement therapy is therefore not used, but adrenal medullary tumours, phaeochromocytomas, secrete excess catecholamines often causing hypertension with dramatic episodes of headache, palpitations, pallor, sweating and anxiety. This condition is normally treated surgically, but preoperative preparation is mandatory to avoid catastrophic effects of surges of catecholamine release. A combination of alpha- and beta-adrenergic receptor blockade is normally used, with drugs such as phenoxybenzamine or doxazosin as alpha-blockers, and propranolol as a non-selective beta-blocker. 

Beta-blockers. There is some evidence that beta-adrenergic blocking drugs such as propranolol can cause bronchoconstriction in some patients. Some selectivity with beta2-adrenergic drugs can minimise this effect but caution should be exercised. 

BETA-BLOCKERS ERGOT DERIVATIVES Three reported cases of arterial vasoconstriction and one of T BP occurred when ergotamine or methysergide was added to propanolol or oxprenolol Ergotamine can cause peripheral vasospasm, and absence of beta-adrenergic activity can t the risk of vasoconstriction Ergot derivatives and beta-blockers are often co-administered without trouble however, monitor BP at least weekly until stable (watch for t BP) and warn patients to stop the ergot derivative and seek medical attention if they develop cold, painful feet... 

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