Researchers soon recognized the addictive properties of amphetamines during the middle of the past century. During the Second World War, soldiers used them to stay awake for extended periods of time. Medical professionals prescribed them to treat conditions such as depression and nasal congestion. These effects are produced by increasing dopamine levels in the brain.Īmphetamines were first synthesized in the late 19th century. People use amphetamines illicitly for their pleasurable effects. Some people abuse them to enhance academic or athletic performance, work longer, or stay awake. Using them causes increased alertness and wakefulness. Specific guidelines for dosage adjustments in hepatic impairment are not available.Amphetamines are a class of synthetic drugs that have stimulant properties. Hepatic Dose : Use with caution as elimination of amphetamine is impaired in liver disease. Propoxyphene: In cases of propoxyphene overdosage, amphetamine CNS stimulation is potentiated, and fatal convulsions can occur. Co-administration of phenytoin may produce a synergistic anticonvulsant action.
Phenytoin: Amphetamines may delay intestinal absorption of phenytoin. Phenobarbital: Amphetamines may delay the intestinal absorption of phenobarbital. Norepinephrine: Amphetamines enhance the adrenergic effect of norepinephrine. Methenamine therapy: Urinary excretion of amphetamines is increased, and efficacy is reduced by acidifying agents used in methenamine therapy.
Meperidine: Amphetamines potentiate the analgesic effect of meperidine. Lithium Carbonate: The antiobesity and stimulatory effects of amphetamines may be inhibited by lithium carbonate. Haloperidol: Haloperidol blocks dopamine and norepinephrine reuptake, thus inhibiting the central stimulant effects of amphetamines. 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.Īntihypertensives: Amphetamines may antagonize the hypotensive effects of antihypertensives.Ĭhlorpromazine: Chlorpromazine blocks a dopamine and norepinephrine reuptake, thus inhibiting the central stimulant effects of amphetamines, and can be used to treat amphetamine poisoning.Įthosuximide: Amphetamines may delay intestinal absorption of ethosuximide. MAO Inhibitors: MAO antidepressants, as well as a metabolite of furazolidone, slow amphetamine metabolism. Tricyclic Antidepressants: Amphetamines may enhance the activity of tricyclic or sympathomimetic agents. Urinary alkalinizing agents (acetazolamide, some thiazides) increase the concentration of the non-ionized species of the amphetamine molecules, thereby decreasing urinary excretion. Urinary Acidifying Agents (ammonium chloride, sodium acid phosphate, etc.): Increase the concentration of the ionized species of the amphetamine molecule, thereby increasing urinary excretion.Īdrenergic Blockers: Adrenergic blockers are inhibited by amphetamines.Īlkalinizing agents, Gastrointestinal alkalinizing agents (sodium bicarbonate, etc.): Increase absorption of amphetamines.
Interaction :Īcidifying Agents: Gastrointestinal acidifying agents (guanethidine, reserpine, glutamic acid HCl, ascorbic acid, fruit juices, etc.): Lower absorption of amphetamines. Tachycardia, palpitations, hypertension, cardiomyopathy (on chronic use), psychosis, dizziness, insomnia, euphoria, restlessness, dysphoria, tremor, headaches, motor and phonic tics exacerbation, Tourette’s syndrome, dryness of mouth, unpleasant taste, diarrhea, constipation, anorexia, weight loss, urticaria, impotence, changes in libido. ≥6 years: 5 mg/day initially, increase by 5 mg weekly until optimal response.
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