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    • Lopressor HCT Formula chimica

    C7H8ClN3O4S2

    Lopressor HCT RX link

    http://www.rxlist.com/cgi/generic/hctz.htm

    Lopressor HCT FDA foglio

    Lopressor HCT DMS (foglio di materiale di sicurezza)

    Lopressor_HCT MSDS

    Lopressor HCT Sintesi di riferimento

    Werner et al. J. Am. Chem. Soc. 82, 1161 (1960)

    Lopressor HCT Peso molecolare

    297.741 g/mol

    Lopressor HCT Temperatura di fusione

    274 oC

    Lopressor HCT H2O Solubilita

    0,7 mg / ml

    Lopressor HCT Stato

    Solid

    Lopressor HCT LogP

    -0.268

    Lopressor HCT Forme di dosaggio

    Tablet (orale)

    Lopressor HCT Indicazione

    Per il trattamento della pressione alta e la gestione di edema.

    Lopressor HCT Farmacologia

    I tiazidici, come l'idroclorotiazide favorire la perdita di acqua dal corpo (diuretici). Essi inibiscono la Na + / Cl-riassorbimento da parte del tubulo contorto distale nei reni. I diuretici tiazidici anche causare la perdita di potassio e un aumento di livelli sierici di acido urico. I diuretici tiazidici sono spesso usati per trattare l'ipertensione, ma i loro effetti ipotensivi non sono necessariamente a causa della loro attività diuretica. I diuretici tiazidici hanno dimostrato di prevenire ipertensione correlata morbilità e mortalità anche se il meccanismo non è completamente nota. I diuretici tiazidici provocare vasodilatazione mediante l'attivazione canali del potassio calcio-attivata (conduttanza di grandi dimensioni) in vascolare muscolatura liscia e inibendo vari carbonica anhydrases nel tessuto vascolare.

    Lopressor HCT Assorbimento

    50-60%

    Lopressor HCT Tossicita

    I segni e sintomi più comuni osservati sono quelli causati dalla deplezione elettrolitica (ipopotassiemia, ipocloremia, iposodiemia) e disidratazione conseguente a diuresi eccessiva. Se il digitale ha anche , l'ipokalemia può accentuare le aritmie cardiache. La DL50 orale di idroclorotiazide è superiore a 10 g / kg nel topo e ratto.

    Lopressor HCT Informazioni paziente

    General

    All patients receiving diuretic therapy should be observed for evidence of fluid or electrolyte
    imbalance: namely, hyponatremia, hypochloremic alkalosis, and hypokalemia. Serum and urine
    electrolyte determinations are particularly important when the patient is vomiting excessively or
    receiving parenteral fluids. Warning signs or symptoms of fluid and electrolyte imbalance,
    irrespective of cause, include dryness of mouth, thirst, weakness, lethargy, drowsiness,
    restlessness, confusion, seizures, muscle pains or cramps, muscular fatigue, hypotension,
    oliguria, tachycardia, and gastrointestinal disturbance such as nausea or vomiting.

    Hypokalemia may develop, especially with brisk diuresis, when severe cirrhosis is present or
    after prolonged therapy.

    Interference with adequate oral electrolyte intake will also contribute to hypokalemia.
    Hypokalemia may cause cardiac arrhythmia and may also sensitize or exaggerate the response of
    the heart to the toxic effects of digitalis (e.g., increased ventricular irritability).
    Hypokalemia may be avoided or treated by use of potassium sparing diuretics or potassium
    supplements such as foods with a high potassium content.

    Although any chloride deficit is generally mild and usually does not require specific treatment
    except under extraordinary circumstances (as in liver disease or renal disease), chloride
    replacement may be required in the treatment of metabolic alkalosis.

    Dilutional hyponatremia may occur in edematous patients in hot weather; appropriate therapy is
    water restriction, rather than administration of salt, except in rare instances when the
    hyponatremia is life threatening. In actual salt depletion, appropriate replacement is the
    therapy of choice.

    Hyperuricemia may occur or acute gout may be precipitated in certain patients receiving thiazides.

    In diabetic patients dosage adjustments of insulin or oral hypoglycemic agents may be required.
    Hyperglycemia may occur with thiazide diuretics. Thus latent diabetes mellitus may become manifest
    during thiazide therapy.

    The antihypertensive effects of the drug may be enhanced in the post-sympathectomy patient.

    If progressive renal impairment becomes evident, consider withholding or discontinuing diuretic therapy.

    Thiazides have been shown to increase the urinary excretion of magnesium; this may result in hypomagnesemia.

    Thiazides may decrease urinary calcium excretion. Thiazides may cause intermittent and slight elevation
    of serum calcium in the absence of known disorders of calcium metabolism. Marked hypercalcemia may be
    evidence of hidden hyperparathyroidism. Thiazides should be discontinued before carrying out tests for
    parathyroid function.

    Increases in cholesterol and triglyceride levels may be associated with thiazide diuretic therapy.

    Laboratory Tests

    Periodic determination of serum electrolytes to detect possible electrolyte imbalance should be done
    at appropriate intervals.

    Lopressor HCT Atto interessato organismi

    Gli esseri umani e altri mammiferi