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Antihistamines adrenergics

Because of their limited effects on allergic symptoms, decongestants often are used in combination with antihistamines.8 Many antihistamines are available in fixed-dose combinations with pseudoephedrine, which enhances the reduction in nasal congestion and allows for the patient convenience of one tablet. Optimally, therapy should be initiated with an antihistamine alone, adding the adrenergic agent only if nasal congestion does not resolve with antihistamine monotherapy. Use of separate antihistamine and pseudoephedrine also permits independent dose titration.4,11,12... [Pg.931]

Topical and systemic decongestants are sympathomimetic agents that act on adrenergic receptors in the nasal mucosa to produce vasoconstriction, shrink swollen mucosa, and improve ventilation. Decongestants work well in combination with antihistamines when nasal congestion is part of the clinical picture. [Pg.915]

Antihistaminic Anti-alphai Adrenergic Anticholinergic Serotonergic... [Pg.52]

Primarily an alpha-adrenergic agonist, indora-mine in a dose of 50 mg/d has also antihistamine and antidopamine properties. [Pg.699]

Trazodone shows significant blockade of peripheral a-adrenergic receptors and moderate antihistamine properties that may account for priapism and somnolence, respectively. Trazodone is almost entirely devoid of anticholinergic activity (Cusack et al., 1994). [Pg.301]

In pharmacodynamic interactions, the pharmacological effect of a drug is changed by the action of a second drug at a common receptor or bioactive site. For example, low-potency antipsychotics and tertiary amine TCAs have anticholinergic, antihistaminic, a-adrenergic antagonist, and quinidine-Kke effects. Therefore, concurrent administration of chlorpromazine and imipramine results in additive sedation, constipation, postural hypotension, and depression of cardiac conduction. [Pg.9]

Olanzapine is metabolized by several pathways and is therefore unlikely to be affected by concurrent administration of other medications. Because olanzapine does not appear to inhibit any cytochrome P450 enzymes, it should not increase the availability of other medications through inhibition of such enzymes. Additive pharmacodynamic effects are expected if olanzapine is combined with medications that also have anticholinergic, antihistaminic, or aj-adrenergic side effects. [Pg.119]

Quetiapine is metabolized by hepatic CYP 3A3/4. Concurrent administration of cytochrome P450-inducing drugs, such as carbamazepine, decreases blood levels of quetiapine. In such circumstances, increased doses of quetiapine are appropriate. Quetiapine does not appreciably affect the pharmacokinetics of other medications. Pharmacodynamic effects are expected if quetiapine is combined with medications that also have antihistaminic or a-adrenergic side effects. Because of its potential for inducing hypotension, quetiapine also may enhance the effects of certain antihypertensive agents. [Pg.121]

ANS They have varying degree of a adrenergic blocking activity. They also have weak anti-cholinergic, Hj-antihistaminic and anti 5-HT actions as well. [Pg.96]

Fexofenadine inhibited antigen-induced bronchospasm and histamine release from mast cells. No anticholinergic or alpha adrenergic-receptor blocking effects were observed. Moreover, no sedative or other CNS effects were observed. Fexofenadine does not cross the blood-brain barrier. It inhibits skin wheal and flare responses produced by histamine injection. Following single and twice daily oral administration, antihistaminic effects occurred within 1 hour, achieved a maximum at 2-3 hours, and lasted a minimum of 12 hours. [Pg.219]

The medical management of other childhood anxiety disorders has included the use of BZDs, antihistamines, b -adrenergic blockers, and clonidine (152,... [Pg.281]

Venlafaxine is a weak inhibitor of NET, whereas desvenlafaxine, duloxetine, and milnacipran are more balanced inhibitors of both SERT and NET. Nonetheless, the affinity of most SNRIs tends to be much greater for SERT than for NET. The SNRIs differ from the TCAs in that they lack the potent antihistamine, -adrenergic blocking, and anticholinergic effects of the TCAs. As a result, the SNRIs tend to be favored over the TCAs in the treatment of MDD and pain syndromes because of their better tolerability. [Pg.661]

FIGURE 11—7. This figure represents an icon of a conventional antipsychotic drug. Such drugs generally have at least four actions blockade of dopamine 2 receptors (D2) blockade of muscarinic-cholinergic receptors (Ml) blockade of alpha 1 adrenergic receptors (alpha 1) and blockade of histamine receptors (antihistaminic actions [HI ). [Pg.409]

FIGURE 6-27. Shown here is an icon of a tricyclic antidepressant (TCA). These drugs are actually five drugs in one (1) a serotonin reuptake inhibitor (SRI) (2) a norepinephrine reuptake inhibitor (NRI) (3) an anticholinergic/antimuscarinic drug (Ml) (4) an alpha adrenergic antagonist (alpha) and (5) an antihistamine (HI). [Pg.658]


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See also in sourсe #XX -- [ Pg.2 ]




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