Adverse effects anticholinergic

Inhaled anticholinergics are well tolerated with the most common adverse effect being dry mouth. Occasional metallic taste has also been reported with ipratropium. Other anticholinergic adverse effects include constipation, tachycardia, blurred vision, and precipitation of narrow-angle glaucoma symptoms. Urinary retention could be a problem, especially for those with concurrent bladder outlet obstruction. 

Trospium chloride causes the expected anticholinergic adverse effects with increased frequency in patients >75 years old. 

In the presence of phenytoin, the metabolism of disopyramide is increased (reducing its effective concentration) and the accumulation of its metabolites is also increased, thereby increasing the probability of anticholinergic adverse effects. Rifampin also stimulates the hepatic metaboUsm of disopyramide, reducing its plasma concentration. 

Geriatric Considerations - Summary Diphenoxylate is an analog of meperidine and can cause opiate adverse effects. When discontinued, physical dependence and withdrawal symptoms can occur. Adverse GI effects such as constipation, nausea/vomit-ing, and abdominal pain may result from normal doses. Afropine is added to discourage abuse but can cause anticholinergic adverse effects in the older adult. The benefits of f his drug combination for older adulfs are limifed by fhe risk of adverse effects. 

Geriatric Considerations-Summary Adjust dose based on creatinine clearance. Not effective in preventing NSAID-induced gastric ulceration and bleeding proton pump inhibitors should be used for this indication instead. Anticholinergic adverse effects have been observed in older adults taking ranitidine. 

Muscle relaxants and antispasmodics methocarbamol (Robaxin), carisoprodol (Soma), chlorzoxazone (Paraflex), metaxalone (Skelaxin), cyclobenzaprine (Flexeril), and oxybutynin (Ditropan) Do not consider the extended-release Ditropan XL Most muscle relaxants and antispasmodic drugs are poorly tolerated by elderly patients, because these cause anticholinergic adverse effects, sedation, and weakness. Additionally, their effectiveness at doses tolerated by elderly patients is questionable. High... 

Orphenadrine (Norflex) Causes more sedation and anticholinergic adverse effects than safer alternatives. High... 

Certain antipsychotics and antidepressants block central and peripheral muscarinic cholinergic receptors, producing many anticholinergic adverse effects, such as ... 

This agent is not sedating, has a low incidence of anticholinergic adverse effects, does not cause weight gain, has no effects on intracardiac conduction, and has no significant safety risk beyond seizures in overdoses. 

Patients with cardiovascular disorders or those predisposed to anticholinergic adverse effects (e.g., elderly or diabetic patients) probably do best on drugs low in these effects (e.g., an SSRI, venlafaxine, or bupropion). 

Blockade of cholinergic receptors, which can result in a variety of peripheral anticholinergic adverse effects and memory impairment... 

The major advantages of SSRIs over the tricyclic antidepressants are their less pronounced anticholinergic adverse effects and lack of severe cardiotoxicity. However, some studies have shown some degree of nervousness or agitation, sleep disturbances, gastrointestinal symptoms, and perhaps sexual adverse effects more commonly in patients treated with SSRIs than in those treated with tricyclic antidepressants. SSRIs may also be associated with an increased risk of suicide, particularly in children under 16 (9). 

There have been frequent reports of anticholinergic adverse effects, including dry mouth (7,9,13), blurred vision (4,9), and difficulty in micturition (18). 

The anticholinergic drug clidinium is best known as a component of Librax (chlordiazepoxide 5 mg plus clidinium bromide 2.5 mg) the dose used is sufficient to produce typical anticholinergic adverse effects. Since here it is combined with a benzodiazepine, it is most unwise to allow patients taking Librax to drive motor vehicles or to ingest alcohol. 

Abuse of antihistamines in Scandinavia has been found in schoolchildren, and particularly involved diphenhydramine (alone or in combination with caffeine). As a consequence such formulations were changed from over-the-counter to prescription-only status (7,8). Abuse of diphenhydramine with drug-seeking behavior and anticholinergic adverse effects have been reported in five children and adolescents with chronic hematological or oncological diseases (5). 

Emepronium bromide is an anticholinergic drug. Doses of 200 mg tds (sometimes with a double dose in the evenings) are useful in relieving urinary frequency. It causes the expected milder anticholinergic adverse effects. 

A 5-10 mg oral dose of the anticholinergic drug isopropamide iodide produces typical anticholinergic adverse effects. In patients with ZoUinger-Ellison syndrome the combination of cimetidine plus isopropamide 20-40 mg/day was generally more effective in suppressing acid secretion than cimetidine alone (1). 

The 25-mg dose of the anticholinergic drug mepenzolate bromide, often given several times a day for gastrointestinal disorders, is sufficient to cause anticholinergic adverse effects, but the compound may itself be a cause... 

Procyclidine is an anticholinergic drug (1). The usual oral dose, which lies between 20 and 30 mg/day, is likely to produce only mild anticholinergic adverse effects, but involuntary movements, with chewing and sucking, have been described in some patients (SEDA-1, 120). Even small doses have produced toxic confusional states when procyclidine was combined with phenothiazines for schizophrenia. Procyclidine is more hkely to produce sedation than stimulation. 

Emerging evidence suggests that the high incidence of adverse effects, especially dry mouth, of oxybutynin IR, and to a lesser extent oxybutynin extended-release (XL) and oxybutynin transder-mal system (TDS), may be largely due to the active metabolite, A-desethyloxybutynin (DEO). This metabofite is generated by extensive first-pass metabolism in the liver and upper gastrointestinal tract. ° Since many of the adverse effects seen with oxybutynin are felt to be related to the primary hepatic metabolite DEO, the lower DEO plasma concentrations seen with oxybutynin TDS and oxybutynin XL (which are due to reduced first-pass metabolism) compared to those of oxybutynin IR may explain their lesser propensity to cause dry mouth and other anticholinergic adverse effects. 

The expected anticholinergic adverse effects occur with trospium chloride as well. Of interest, the freqnency of these events is increased in patients 75 years old and older compared to yonnger subjects. This is believed to be pharmacodynamic in nature (i.e., increased sensitivity) and not pharmacokinetic. There are no data at present to support the hypothesis that trospium chloride is less neurotoxic than non-quaternary-ammoninm anticholinergics (based on the hypothesis of rednced transit across the blood-brain barrier of trospium chloride due to its positive electrical charge on the qnaternary nitrogen). Available dmg-dmg interaction data are clearly inadeqnate. 

Procyclidine may reduce the antipsychotic effectiveness of haloperidol and phenothiazines, possibly by direct CNS antagonism related to its anticholinergic properties. Haloperidol and phenothiazine exert their effects in part by blocking the hyperactivity of dopaminergic transmission in the mesocortical and mesolimbic systems. Concomitant use with phenothiazine derivatives, especially thioridazine having pronounced anticholinergic effects, also increases the risk of anticholinergic adverse effects. Paralytic ileus may result from concomitant use with phenothiazines or tricyclic antidepressants. Concomitant use with alcohol and other CNS depressants increases procyclidine s sedative effects. 

Concomitant nse with amantadine may amplify trihexyphenidyl s anticholinergic adverse effects, causing confusion and haUncinations. Concomitant use with haloperidol or phenothiazines may decrease the antipsychotic effectiveness of these drugs, possibly from direct CNS antagonism concomitant phenothiazine nse also increases the risk of anticholinergic adverse effects. 

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