Chlorsulfonamidodihydrobenzothiadiazine Dioxide
Categoria
Chlorsulfonamidodihydrobenzothiadiazine Dioxide Nombres de marca, Chlorsulfonamidodihydrobenzothiadiazine Dioxide Analogos
- Acuretic
- Aldactazide
- Aldoril
- Apresazide
- Aquarills
- Aquarius
- Bremil
- Caplaril
- Capozide
- Chlorosulthiadil
- Chlorothiazide
- Chlorsulfonamidodihydrobenzothiadiazine Dioxide
- Chlorzide
- Cidrex
- Dichlorosal
- Dichlorotride
- Dichlotiazid
- Dichlotride
- Diclotride
- Dicyclotride
- Dihydrochlorothiazid
- Dihydrochlorothiazide
- Dihydrochlorothiazidum
- Dihydrochlorurit
- Dihydrochlorurite
- Dihydroxychlorothiazidum
- Direma
- Disalunil
- Diu-Melusin
- Diuril
- Drenol
- Dyazide
- Esidrex
- Esidrix
- Esimil
- Fluvin
- HCTZ
- HCZ
- Hidril
- Hidrochlortiazid
- Hidroronol
- Hidrotiazida
- Hydril
- Hydro-Aquil
- Hydro-D
- Hydro-Diuril
- Hydrochlorothiazid
- Hydrochlorothiazide Intensol
- Hydrochlorthiazide
- Hydrodiuretic
- Hydrodiuril
- Hydropres
- Hydrosaluric
- Hydrothide
- Hydrozide
- Hypothiazid
- Hypothiazide
- Hyzaar
- Idrotiazide
- Inderide
- Ivaugan
- Jen-Diril
- Lopressor Hct
- Lotensin Hct
- Maschitt
- Maxzide
- Megadiuril
- Microzide
- Moduretic
- Nefrix
- Neo-Codema
- Neoflumen
- Newtolide
- Oretic
- Palonyl
- Panurin
- Perovex
- Primogyn
- Prinzide
- Ro-Hydrazide
- Servithiazid
- Thiaretic
- Thiuretic
- Thlaretic
- Timolide
- Unipres
- Urodiazin
- Vaseretic
- Vetidrex
- Ziac
- Zide
Chlorsulfonamidodihydrobenzothiadiazine Dioxide Marca los nombres de mezcla
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 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.
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
