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Aldomet

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Aldomet generic
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Mechanism of Action: After crossing the blood-brain barrier, methyldopa is decarboxylated to produce alpha-methylnorepinephrine. This metabolite stimulates central inhibitory alpha-adrenergic receptors, thereby reducing peripheral resistance and lowering blood pressure. Although cardiac output and heart rate are not believed to be affected, conflicting data from studies of long-term therapy and the use of methyldopa in patients with congestive heart failure suggest that cardiac output may be decreased and peripheral resistance unaffected. Methyldopa also may act as a false transmitter, thereby exerting a direct effect on peripheral sympathetic nerves. Blood pressure decreases are greatest when the patient is standing but are also significant when the patient is supine. Postural hypotension has been reported in patients receiving methyldopa.Methyldopa can cause sodium and fluid retention, and tolerance can develop during long-term therapy. As an antihypertensive, reduces LVH and does not worsen glucose tolerance, but does exert detrimental effects on serum lipids. Serum prolactin levels can increase during methyldopa administration.
Absorption: 50% absorbed from the GI tract. Parenteral form, methyldopate hydrochloride, is slowly converted to methyldopa.
Distribution: Crosses the blood-brain barrier. Crosses the placenta; small
amounts enter breast milk.
Metabolism and Excretion: Partially metabolized by the liver, partially excreted
unchanged by the kidneys.
Half-life: 1.7 hr.
TIME/ACTION PROFILE (antihypertensive effect)
ROUTE ONSET PEAK DURATION
PO 4-6 hr 12-24 hr 24-48 hr
IV 4-6 hr unknown 10-16 hr
Contraindicated in: Hypersensitivity; Active liver disease.
Use Cautiously in: Previous history of liver disease; OB: Has been used safely
(may be used for treatment of hypertension in pregnancy); Lactation: Usually compatible with breast feeding; Geri:qrisk of adverse reactions; consider age-related
impairment of hepatic, renal and cardiovascular function as well as other chronic illnesses. Appears on Beers list. May cause bradycardia and exacerbate depression.
Drug-Drug: Additive hypotension with other antihypertensives, acute ingestion
of alcohol, anesthesia, and nitrates. Amphetamines, barbiturates, tricyclic
antidepressants, NSAIDs, and phenothiazines maypantihypertensive effect of
methyldopa.qeffects and risk of psychoses with haloperidol. Excess sympathetic
stimulation may occur with concurrent use of MAO inhibitors or other adrenergics. Mayqlithium toxicity. Additive hypotension and CNS toxicity with levodopa.
Additive CNS depression may occur with alcohol, antihistamines, sedative/hypnotics, some antidepressants, and opioid analgesics. Concurrent use with nonselective beta blockersmay rarely cause paradoxical hypertension
Assessment
● Monitor BP and pulse frequently during initial dose adjustment and periodically
during therapy. Report significant changes.
● Monitor frequency of prescription refills to determine compliance.
● Monitor intake and output ratios and weight and assess for edema daily, especially
at beginning of therapy. Report weight gain or edema; sodium and water retention
may be treated with diuretics.
● Assess patient for depression or other alterations in mental status. Notify health
care professional promptly if these symptoms develop.
● Monitor temperature during therapy. Drug fever may occur shortly after
initiation of therapy and may be accompanied by eosinophilia and hepatic function changes. Monitor hepatic function test if unexplained fever occurs.
● Lab Test Considerations: Monitor renal and hepatic function and CBC before
and periodically during therapy.
● Monitor direct Coombs' test before and after 6 and 12 mo of therapy. May cause a
positive direct Coombs' test, rarely associated with hemolytic anemia.
● May causeqBUN, serum creatinine, potassium, sodium, prolactin, uric
acid, AST, ALT, alkaline phosphatase, and bilirubin concentrations.
● May cause prolonged prothrombin times.
● May interfere with serum creatinine and AST measurements