Amphetamines may impair the ability of the patient to engage in potentially hazardous activities such as operating machinery or vehicles; the patient should therefore be cautioned accordingly.
Acidifying agents - Gastrointestinal acidifying agents (guanethidine,reserpine, glutamic acid HCl,ascorbic acid, fruit juices, etc.) lower absorption of amphetamines.
Urinary acidifying agents -(ammonium chloride, sodium acid phosphate, etc.) Increase the concentration of the ionized species of the amphetamine.
Primary excretion - Both Groups of agents lower blood levels and efficacy of amphetamines.
Adrenergic blockers - Adrenergic blockers are inhibited by amphetamines.
Alkalinizing agents -Gastrointestinal alkalinizing agents (sodium bicarbonate, etc.)increase absorption of amphetamines. Urinary alkalinizing agents (acetazolamide, some thiazides) increase the concentration of the non-ionized species of the amphetamine molecule, thereby decreasing urinary excretion. Both groups of agents increase blood levels and therefore potentate the actions of amphetamines.
Antidepressants, tricyclic - Amphetamines may enhance the activity of tricyclic or sympathomimetic agents; d-amphetamine with desipramine or protriptyline and possibly other tricyclics cause striking and sustained increases in the concentration of d-amphetamine in the brain; cardiovascular effects can be potentiated.
MAO inhibitors - MAO antidepressants, as well as a metabolite of furazolidone, slow amphetamine metabolism. This slowing potentiates amphetamines, increasing their effect on the release of norepinephrine and other monoamines from adrenergic nerve endings, this can cause headaches and other signs of hypertensive crisis. A variety of neurological toxic effects and malignant hyperpyrexia can occur, sometimes with fatal results.
Antihistamines - Amphetamines may counteract the sedative effect of antihistamines.
Antihypertensives - Amphetamines may antagonize the hypotensive effects of antihypertensives.
Chlorpromazine - Chlorpromazine blocks dopamine and norepinephrine receptors, thus inhibiting the central stimulant effects of amphetamines, and can be used to treat amphetamine poisoning.
Ethosuximide - Amphetamines may delay intestinal absorption of ethosuximide.
Haloperidol - Haloperidol blocks dopamine receptors, thus inhibiting the central stimulant effects of amphetamines.
Lithium carbonate - The anorectic and stimulatory effects of amphetamines may be inhibited by lithium carbonate.
Meperidine - Amphetamines pone the analgesic effect of meperidine.
Methenamine therapy - Urinary excretion of amphetamines is increased, and efficacy is reduced, by acidifying agents used in methenamine therapy.
Norepinephrine - Amphetamines enhance the adrenergic effect of norepinephrine.
Phenobarbital - Amphetamines may delay intestinal absorption of phenobarbital; co-administration of phenobarbital may produce a synergistic anticonvulsant action.
Phenytoin - Amphetamines may delay intestinal absorption of phenytoin; co-administration of phenytoin may produce a synergistic anticonvulsant action.
Propoxyphene - In cases of propoxyphene overdose, amphetamine CNS stimulation is potentiated and fatal convulsions can occur.
Veratrum alkaloids - Amphetamines inhibit the hypotensive effect of veratrum alkaloids.
Drug/Laboratory Test Interactions
Amphetamines can cause a significant elevation in plasma corticosteroid levels. This increase is greatest in the evening.
Amphetamines may interfere with urinary steroid determinations.
Advanced arteriosclerosis, symptomatic cardiovascular disease, moderate to severe hypertension, hyperthyroidism, known hypersensitivity or idiosyncrasy to the sympathomimetic amines, glaucoma. Agitated states. Patients with a history of drug abuse. During or within 14 days following the administration of monoamine oxidase inhibitors (hypertensive crises may result).