Beta-blockers adverse effects

Eor preventive treatments, the adverse effects of the beta blockers are classical for this class bradycardia, bronchospasm, hypotension, nightmares and depression. Indoramine induces neuropsychiatric effects (sedation, asthenia) and cardiovascular disorders (hypotension). Eluanarizine is strictly contraindicated in patients with Parkinsonism and depression. 

Geriatric Considerations - Summary Systemic absorption of ophthalmic drugs may occur and cause adverse effects in older adults. Since betaxolol is beta-selective, cardiovascular, respiratory and CNS adverse effects occur less frequently than with beta-nonselective topical opthalmics. These effects may still occur therefore close monitoring for systemic side effects is warranted. Betaxolol maybe less effective than the nonselective topical beta-blockers with an average lOP reduction of 18%-26%. Tachyphylaxis may occur after long-term therapy. 

Geriatric Considerations - Summary Carteolol decreases lOP on average 20%-32%. Systemic absorption of ophthalmic drugs may occur and cause adverse effects in older adults. Since carteolol is a nonselective beta-blocker, older adults maybe more... 

Geriatric Considerations - Summary Discontinuation of clonidine is likely to require a slow taper. If the patient is receiving a concomitant beta-blocker, the beta-blocker must be tapered and discontinued before discontinuing clonidine. Clonidine discontinuation in the presence of a beta-blocker can lead to severe hypertension and cardiovascular events due to unopposed alpha-receptor stimulation. CNS effects often preclude its use in older adults. A higher clonidine dose (0.4 mg/day) is generally needed to control peri- or postmenopausal vasomotor symptoms however, adverse effects often make it difficult to achieve effective doses. 

There are few absolute contraindications, but several points should be considered. Medications that produce changes in sinus node or AV nodal conduction may potentiate the cardiovascular adverse effects of the a2 agonists. This may be particularly relevant for concomitant administration of beta-blockers, which, similar to the agonists, have been used to treat aggression. 

Coadministration of beta-blockers can potentiate rebound hypertension upon discontinuation of medications, and it is therefore recommended that the beta-blocker be withdrawn before the tt2 agonist (Physicians Desk Reference, 2001). Tricyclic antidepressants may also produce changes in sinus node and AV conduction, and it is recommended that they be used cautiously in combination with tt2 agonists (Physicians Desk Reference, 2001). However, in child psychiatric practice, there has been debate about whether there are adverse interactions related to concomitant use of tricyclics and tt2 agonists. Finally, the tt2 agonists may potentiate the effects of CNS depressants (e.g., barbiturates) or other medications that produce sedation, so lower doses of each may be warranted. 

Drug interactions Proleukin may affect central nervous system function. Therefore interactions could occur following concomitant administration of psychotropic drugs. Concurrent administration of drugs possessing nephrotoxic, myelotoxic, cardiotoxic, or hepatotoxic effects with Proleukin may increase toxicity in these organ systems. Reduced kidney and liver function secondary to Proleukin treatment may delay elimination of concomitant medications and increase the risk of adverse events from those drugs. Beta-blockers and other antihypertensives may potentiate the hypotension seen with Proleukin. 

Q5 Beta-blockers can have a number of adverse effects. In fact, all drugs used to treat hypertension have some side effects. Beta-adrenoceptor antagonists are... 

In 27 hypertensive patients aged 65 years or more, randomized to continue atenolol treatment for 20 weeks or to discontinue atenolol and start cilazapril, there was a significant improvement in the choice reaction time in the patients randomized to cilazapril (93). This study has confirmed previous reports that chronic beta-blockade can determine adverse effects on cognition in elderly patients. Withdrawal of beta-blockers should be... 

ACEBUTOLOL, ATENOLOL, BETAXOLOL, BISOPROLOL, METOPROLOL, PROPANOLOL CICLOSPORIN t risk of hyperkalaemia Beta-blockers cause an efflux of potassium from cells, and side-effect has been observed during cidosporin therapy Monitor serum potassium levels during co-administration > For signs and symptoms of hyperkalaemia, see Clinical Features of Some Adverse Drug Interactions, Hyperkalaemia... 

BETA-BLOCKERS RITONAVIR, TIPRANAVIR t adverse effects of carvedilol, metoprolol, propanolol and timolol Inhibition of CYP2D6-mediated metabolism of these beta-blockers and CYP2C19-mediated metabolism of propanolol Use an alternative beta-blocker if possible if not, monitor closely... 

Legal claims arising from glaucoma therapy may be divided into three categories adverse effects of beta-blockers, retinal detachments after initiation of miotic therapy, and complications resulting from use of CAIs. 

Until recently, very few systemic drug therapies were implicated in ocular adverse effects in the episclera, sclera, and uvea. Topical ocular medications such as beta-blockers, latanoprost, and corticosteroids as well as other topical ocnlar medications have been associated with uveitis. 

Beta-adrenoceptor blockers. The realisation that the coiuse of chronic heart failure can be adversely affected by activation of the renin-angiotensin-aldosterone and sympathetic nervous systems led to exploration of possible benefit from P-adrenoceptors in a condition where, paradoxically, such drugs can have an adverse effect. Clinical trials have, indeed, shown that bisoprolol, carvedilol or metoprolol lower mortality and decrease hospitalisation when added to diuretics, digoxin and an ACE inhibitor (see below). 

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