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Chlorsulfonamidodihydrobenzothiadiazine Dioxide Nombres de marca, Chlorsulfonamidodihydrobenzothiadiazine Dioxide Analogos

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  • Chlorsulfonamidodihydrobenzothiadiazine Dioxide Formula quimica

    C7H8ClN3O4S2

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide RX enlace

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

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide FDA hoja

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide MSDS (hoja de seguridad de materiales)

    Chlorsulfonamidodihydrobenzothiadiazine_Dioxide MSDS

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Sintesis de referencia

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

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Peso molecular

    297.741 g/mol

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Punto de fusion

    274 oC

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide H2O Solubilidad

    0,7 mg / ml

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Estado

    Solid

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide LogP

    -0.268

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Formas de dosificacion

    Tablet (oral)

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Indicacion

    Para el tratamiento de la hipertensión arterial y tratamiento del edema.

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Farmacologia

    Las tiazidas como hidroclorotiazida promover la pérdida de agua del cuerpo (diuréticos). Inhiben la Na + / Cl-reabsorción de los túbulos contorneados distales de los riñones. Las tiazidas también causan pérdida de potasio y un aumento del ácido úrico sérico. Las tiazidas se utilizan a menudo para tratar la hipertensión, pero sus efectos hipotensores no son necesariamente debido a su actividad diurética. Las tiazidas han demostrado para prevenir hipertensión, la morbilidad y la mortalidad, aunque el mecanismo no se entiende completamente. Tiazidas producen vasodilatación por activación de los canales activados por el calcio potasio (gran conductancia) en vascular músculo liso y la inhibición de varios anhidrasas carbónico en el tejido vascular.

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Absorcion

    50-60%

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Toxicidad

    Los signos y síntomas más comunes observados son los causados por la pérdida de electrólitos (hipopotasemia, hipocloremia, hiponatremia) y deshidratación como resultado de diuresis excesiva. Si la digital también ha ha administrado, la hipopotasemia puede acentuar las arritmias cardíacas. La DL50 oral de hidroclorotiazida es mayor de 10 g / kg en el ratón y la rata.

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Informacion de Pacientes

    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.

    Chlorsulfonamidodihydrobenzothiadiazine Dioxide Organismos afectados

    Humanos y otros mamíferos