Cardiovascular: Palpitations, tachycardia, elevation of blood pressure.

Central Nervous System: Psychotic episodes at recommended doses (rare), overstimulation, restlessness, dizziness, insomnia, euphoria, dyskinesia, dysphoria, tremor, headaches, exacerbation of motor and phonic tics and Tourette's syndrome.

Gastrointestinal: Dryness of the mouth, unpleasant taste, diarrhea, constipation and other gastrointestinal disturbances. Anorexia and weight loss may occur as undesirable effects when amphetamines are used for other than the anorectic effect.

Allergic: Urticaria.

Endocrine: Impotence, changes in libido.

DRUG ABUSE AND DEPENDENCE

Amphetamine sulfate is a Schedule II controlled substance. Amphetamines have been extensively abused. Tolerance, extreme psychological dependence, and severe social disability have occurred. There are reports of patients who have increased the dosage to many times that recommended. Abrupt cessation following prolonged high dosage administration results in extreme fatigue and mental depression; changes are also noted in the sleep EEG.

Manifestations of chronic intoxication with amphetamines include severe dermatosis, marked insomnia, irritability, hyperactivity and personality changed. The most severe manifestation of chronic intoxication is psychosis, often clinically indistinguishable from schizophrenia. This is rare with oral amphetamine.

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 molecule, thereby increasing urinary 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 molecules, thereby decreasing urinary excretion. Both groups of agents increase blood levels and therefore potentiate the action 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.

Antihypertensives: Amphetamines may antagonize the hypotensive effects of antihypertensives.

Chlorpromazine: Chlorpromazine blocks a dopamine and norepinephrine reuptake, thus inhibiting the central stimulant affects of amphetamines, and can be used to treat amphetamine poisoning.

Ethosuximide: Amphetamines may delay intestinal absorption of ethosuximide.

Haloperidol: Haloperidol blocks dopamine and norepinephrine reuptake, thus inhibiting the central stimulant affects of amphetamines.

Lithium Carbonate: The antiobesity and stimulatory effects of amphetamines may be inhibited by lithium carbonate.

Meperidine: Amphetamines potentiate 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 the 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 overdosage, amphetamine CNS stimulation is potentiated and fatal convulsions can occur.

Veratrum Alkaloids: Amphetamines inhibit the hypotensive effect of veratrum alkaloids.

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