OK I know a guy who says hes using a prescip. diueretic for his Blood Pressure. I was wondering if anyone has used this for comp and the results and doses. He said the clinical name is HYDROCLORTIAZIC.... best spelling there :D
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OK I know a guy who says hes using a prescip. diueretic for his Blood Pressure. I was wondering if anyone has used this for comp and the results and doses. He said the clinical name is HYDROCLORTIAZIC.... best spelling there :D
????
I have never used it. I am sure it woudl work but I prefer to use Potassium sparring diuretics. The thiazide type of diuretics deplete it causing the possibility of cramping up..
can you offset this by potassium loading? I used a natural herbal one last year and I didnt really notice any extra loss of water retention
Yes alot of people do use pottassium supps for replenishing it but keep in mind that to much pottasium can kill (cause cardiac arrest)you not sure what the amount is probablly different for everyone but I would definetly check around on i.
wo didnt know that. thanks man ill check it out.
Hydrochlorothiazide is a diuretic and antihypertensive. It is the 3,4-dihydro derivative of chlorothiazide. Its chemical name is 6-chloro-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. Its empirical formula is C7H8ClN3O4S2.
It is a white, or practically white, crystalline powder with a molecular weight of 297.72, which is slightly soluble in water, but freely soluble in sodium hydroxide solution.
Hydrochlorothiazide is supplied as 25 mg, 50 mg and 100 mg tablets for oral use.
Each tablet contains the following inactive ingredients: calcium phosphate, FD&C Yellow 6, gelatin, lactose, magnesium stearate, starch and talc.
Found on Rx-List
diuretic
1. Increasing urine secretion. SEE: diuresis. 2. An agent that increases urine output.Diuretics are used to treat hypertension, congestive heart failure, and edema. Common side effects of these agents are potassium depletion, low blood pressure, dehydration, and hyponatremia.
The def. of Diuretic
SIDE EFFECTS
The following adverse reactions have been reported and within each category, are listed in order of decreasing severity.
Body as a Whole: Weakness.
Cardiovascular: Hypotension including orthostatic hypotension (may be aggravated by alcohol, barbiturates, narcotics or antihypertensive drugs).
Digestive: Pancreatitis, jaundice (intrahepatic cholestatic jaundice), diarrhea, vomiting, sialadenitis, cramping, constipation, gastric irritation, nausea, anorexia.
Hematologic: Aplastic anemia, agranulocytosis, leukopenia, hemolytic anemia, thrombocytopenia.
Hypersensitivity: Anaphylactic reactions, necrotizing angiitis (vasculitis and cutaneous vasculitis), respiratory distress including pneumonitis and pulmonary edema, photosensitivity, fever, urticaria, rash, purpura.
Metabolic: Electrolyte imbalance (see PRECAUTIONS), hyperglycemia, glycosuria, hyperuricemia.
Musculoskeletal: Muscle spasm.
Nervous System/Psychiatric: Vertigo, paresthesias, dizziness, headache, restlessness.
Renal: Renal failure, renal dysfunction, interstitial nephritis. (See WARNINGS.)
Skin: Erythema multiforme including Stevens-Johnson syndrome, exfoliative dermatitis including toxic epidermal necrolysis, alopecia.
Special Senses: Transient blurred vision, xanthopsia.
Urogenital: Impotence.
Whenever adverse reactions are moderate or severe, thiazide dosage should be reduced or therapy withdrawn.
DRUG INTERACTIONS
When given concurrently the following drugs may interact with thiazide diuretics.
Alcohol, barbiturates, or narcotics: potentiation of orthostatic hypotension may occur.
Antidiabetic drugs: (oral agents and insulin) - dosage adjustment of the antidiabetic drug may be required.
Other antihypertensive drugs: additive effect or potentiation.
Cholestyramine and colestipol resins: Absorption of hydrochlorothiazide is impaired in the presence of anionic exchange resins. Single doses of either cholestyramine or colestipol resins bind the hydrochlorothiazide and reduce its absorption from the gastrointestinal tract by up to 85 and 43 percent, respectively.
Corticosteroids, ACTH: intensified electrolyte depletion, particularly hypokalemia.
Pressor amines (e.g., norepinephrine): possible decreased response to pressor amines but not sufficient to preclude their use.
Skeletal muscle relaxants, nondepolarizing (e.g., tubocurarine): possible increased responsiveness to the muscle relaxant.
Lithium: generally should not be given with diuretics. Diuretic agents reduce the renal clearance of lithium and add a high risk of lithium toxicity. Refer to the package insert for lithium preparations before use of such preparations with Hydrochlorothiazide.
Non-steroidal Anti-inflammatory Drugs: In some patients, the administration of a non-steroidal anti-inflammatory agent can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing and thiazide diuretics. Therefore, when Hydrochlorothiazide and non-steroidal anti-inflammatory agents are used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is obtained.
More Info
Aldactazide: (spironolactone and hydrochlorothiazide)
This drug is a diuretic combination containing Aldactone and a thiazide. It is often used by pre - contest bodybuilders to drop excess water. For some bodybuilders it works very well. It is most often taken for just the last three to five days before a show. The Aldactone prohibits the release of aldosterone, a hormone produced by the adrenal gland. This hormone is partially responsible for the amount of electrolytes and fluid body retains. Combined with the stronger thiazide diuretic this drug is a perfect combination for some. Average dosage was one tablet taken to times daily for three days before a show. This item rarely shows up on the black market. But it is often prescribed by the athletes’ doctor.
Aldactone oral tablets contain 25 mg, 50 mg, or 100 mg of the aldosterone antagonist spironolactone, 17-hydroxy-7alpha-mercapto-3-oxo-17alpha-pregn-4-ene-21-carboxylic acid gamma-lactone acetate. Spironolactone is practically insoluble in water, soluble in alcohol, and freely soluble in benzene and in chloroform. Inactive ingredients include calcium sulfate, corn starch, flavor, hydroxypropyl methylcellulose, iron oxide, magnesium stearate, polyethylene glycol, povidone, and titanium dioxide.
Mechanism of Action
Aldactone (spironolactone) is a specific pharmacologic antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. Aldactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Aldactone acts both as a diuretic and as an antihypertensive drug by this mechanism. It may be given alone or with other diuretic agents which act more proximally in the renal tubule.
Aldosterone Antagonist Activity
Increased levels of the mineralocorticoid, aldosterone, are present in primary and secondary hyperaldosteronism. Edematous states in which secondary aldosteronism is usually involved include congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. By competing with aldosterone for receptor sites, Aldactone provides effective therapy for the edema and ascites in those conditions. Aldactone counteracts secondary aldosteronism induced by the volume depletion and associated sodium loss caused by active diuretic therapy.
Aldactone is effective in lowering the systolic and diastolic blood pressure in patients with primary hyperaldosteronism. It is also effective in most cases of essential hypertension, despite the fact that aldosterone secretion may be within normal limits in benign essential hypertension.
Through its action in antagonizing the effect of aldosterone, Aldactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
Aldactone has not been demonstrated to elevate serum uric acid, to precipitate gout, or to alter carbohydrate metabolism.
Pharmacokinetics
Spironolactone is rapidly and extensively metabolized. Sulfur-containing products are the predominant metabolites and are thought to be primarily responsible, together with spironolactone, for the therapeutic effects of the drug. The following pharmacokinetic data were obtained from 12 healthy volunteers following the administration of 100 mg of spironolactone (Aldactone film-coated tablets) daily for 15 days. On the 15th day, spironolactone was given immediately after a low-fat breakfast and blood was drawn thereafter.
Accumulation Factor:
AUC (0-24 hr,
day 15) / AUC
(0-24 hr, day 1) Mean Peak Serum Concentration Mean (SD) Post-Steady State Half-Life
7-alpha-(thiomethyl) spirolactone (TMS) 1.25 391 ng/mL at 3.2 hr 13.8 hr (6.4) (terminal)
6-beta-hydroxy-7-alpha-(thiomethyl) spirolactone (HTMS) 1.50 125 ng/mL at 5.1 hr 15.0 hr (4.0) (terminal)
Canrenone (C) 1.41 181 ng/mL at 4.3 hr 16.5 hr (6.3) (terminal)
Spironolactone 1.30 80 ng/mL at 2.6 hr Approximately 1.4 hr (0.5) (beta half-life)
The pharmacological activity of spironolactone metabolites in man is not known. However, in the adrenalectomized rat the antimineralocorticoid activities of the metabolites C, T.S. and HTMS, relative to spironolactone, were 1.10, 1.28, and 0.32, respectively. Relative to spironolactone, their binding affinities to the aldosterone receptors in rat kidney slices were 0.19, 0.86, and 0.06, respectively.
In humans the potencies of TMS and 7-alpha-thiospirolactone in reversing the effects of the synthetic mineralocorticoid, fludrocortisone, on urinary electrolyte composition were 0.33 and 0.26, respectively, relative to spironolactone. However, since the serum concentrations of these steroids were not determined, their incomplete absorption and/or first-pass metabolism could not be ruled out as a reason for their reduced in vivo activities.
Spironolactone and its metabolites are more than 90% bound to plasma proteins. The metabolites are excreted primarily in the urine and secondarily in bile.
The effect of food on spironolactone absorption (two 100-mg Aldactone tablets) was assessed in a single dose study of 9 healthy, drug-free volunteers. Food increased the bioavailability of unmetabolized spironolactone by almost 100%. The clinical importance of this finding is not known.
SIDE EFFECTS
The following adverse reactions have been reported and within each category (body system), are listed in order of decreasing severity.
Digestive: Gastric bleeding, ulceration, gastritis, diarrhea and cramping, nausea, vomiting.
Endocrine: Gynecomastia (see PRECAUTIONS), inability to achieve or maintain erection, irregular menses or amenorrhea, postmenopausal bleeding. Carcinoma of the breast has been reported in patients taking spironolactone but a cause and effect relationship has not been established.
Hematologic: Agranulocytosis.
Hypersensitivity: Fever, urticaria, maculopapular or erythematous cutaneous eruptions, anaphylactic reactions, vasculitis.
Nervous system/psychiatric: Mental confusion, ataxia, headache, drowsiness, lethargy.
Liver/biliary: A very few cases of mixed cholestatic/hepatocellular toxicity, with one reported fatality, have been reported with spironolactone administration.
DRUG INTERACTIONS
ACE inhibitors: Concomitant administration of ACE inhibitors with potassium-sparing diuretics has been associated with severe hyperkalemia.
Alcohol, barbiturates, or narcotics: Potentiation of orthostatic hypotension may occur.
Corticosteroids, ACTH: Intensified electrolyte depletion, particularly hypokalemia, may occur.
Pressor amines (eg, norepinephrine): Spironolactone reduces the vascular responsiveness to norepinephrine. Therefore, caution should be exercised in the management of patients subjected to regional or general anesthesia while they are being treated with Aldactone.
Skeletal muscle relaxants, nondepolarizing (eg, tubocurarine): Possible increased responsiveness to the muscle relaxant may result.
Lithium: Lithium generally should not be given with diuretics. Diuretic agents reduce the renal clearance of lithium and add a high risk of lithium toxicity.
Nonsteroidal anti-inflammatory drugs (NSAIDs): In some patients, the administration of an NSAID can reduce the diuretic, natriuretic, and antihypertensive effect of loop, potassium-sparing and thiazide diuretics. Combination of NSAIDs, eg, indomethacin, with potassium-sparing diuretics has been associated with severe hyperkalemia. Therefore, when Aldactone and NSAIDs are used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is obtained.
Digoxin: Spironolactone has been shown to increase the half-life of digoxin. This may result in increased serum digoxin levels and subsequent digitalis toxicity. It may be necessary to reduce the maintenance and digitalization doses when spironolactone is administered, and the patient should be carefully monitored to avoid over- or underdigitalization.
Drug/Laboratory Test Interactions
Several reports of possible interference with digoxin radioimmunoassays by spironolactone, or its metabolites, have appeared in the literature. Neither the extent nor the potential clinical significance of its interference (which may be assay-specific) has been fully established.
WARNINGS
Spironolactone has been shown to be a tumorigen in chronic toxicity studies in rats (see
PRECAUTIONS
). Aldactone should be used only in those conditions described under INDICATIONS AND USAGE. Unnecessary use of this drug should be avoided.
Potassium supplementation, either in the form of medication or as a diet rich in potassium, should not ordinarily be given in association with Aldactone therapy. Excessive potassium intake may cause hyperkalemia in patients receiving Aldactone (see
PRECAUTIONS
: General). Aldactone should not be administered concurrently with other potassium-sparing diuretics. Aldactone, when used with ACE inhibitors or indomethacin, even in the presence of a diuretic, has been associated with severe hyperkalemia. Extreme caution should be exercised when Aldactone is given concomitantly with these drugs.
Aldactone should be used with caution in patients with impaired hepatic function because minor alterations of fluid and electrolyte balance may precipitate hepatic coma.
Lithium generally should not be given with diuretics (see DRUG INTERACTIONS).
PRECAUTIONS
General
All patients receiving diuretic therapy should be observed for evidence of fluid or electrolyte imbalance, eg, hypomagnesemia, hyponatremia, hypochloremic alkalosis, and hyperkalemia.
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 the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, and gastrointestinal disturbances such as nausea and vomiting. Hyperkalemia may occur in patients with impaired renal function or excessive potassium intake and can cause cardiac irregularities, which may be fatal. Consequently, no potassium supplement should ordinarily be given with Aldactone.
Concomitant administration of potassium-sparing diuretics and ACE inhibitors or nonsteroidal anti-inflammatory drugs (NSAIDs), eg, indomethacin, has been associated with severe hyperkalemia.
If hyperkalemia is suspected (warning signs include paresthesia, muscle weakness, fatigue, flaccid paralysis of the extremities, bradycardia and shock) an electrocardiogram (ECG) should be obtained. However, it is important to monitor serum potassium levels because mild hyperkalemia may not be associated with ECG changes.
If hyperkalemia is present, Aldactone should be discontinued immediately. With severe hyperkalemia, the clinical situation dictates the procedures to be employed. These include the intravenous administration of calcium chloride solution, sodium bicarbonate solution and/or the oral or parenteral administration of glucose with a rapid-acting insulin preparation. These are temporary measures to be repeated as required. Cationic exchange resins such as sodium polystyrene sulfonate may be orally or rectally administered. Persistent hyperkalemia may require dialysis.
Reversible hyperchloremic metabolic acidosis, usually in association with hyperkalemia, has been reported to occur in some patients with decompensated hepatic cirrhosis, even in the presence of normal renal function.
Dilutional hyponatremia, manifested by dryness of the mouth, thirst, lethargy, and drowsiness, and confirmed by a low serum sodium level, may be caused or aggravated, especially when Aldactone is administered in combination with other diuretics, and dilutional hyponatremia may occur in edematous patients in hot weather; appropriate therapy is water restriction rather than administration of sodium, except in rare instances when the hyponatremia is life-threatening.
Aldactone therapy may cause a transient elevation of BUN, especially in patients with preexisting renal impairment. Aldactone may cause mild acidosis.
Gynecomastia may develop in association with the use of spironolactone; physicians should be alert to its possible onset. The development of gynecomastia appears to be related to both dosage level and duration of therapy and is normally reversible when Aldactone is discontinued. In rare instances some breast enlargement may persist when Aldactone is discontinued.
Information for Patients
Patients who receive Aldactone should be advised to avoid potassium supplements and foods containing high levels of potassium including salt substitutes.
Laboratory Tests
Periodic determination of serum electrolytes to detect possible electrolyte imbalance should be done at appropriate intervals, particularly in the elderly and those with significant renal or hepatic impairments.
Drug Interactions
See DRUG INTERACTIONS section.
Drug/Laboratory Test Interactions
Several reports of possible interference with digoxin radioimmunoassays by spironolactone, or its metabolites, have appeared in the literature. Neither the extent nor the potential clinical significance of its interference (which may be assay-specific) has been fully established.
hyperkalemia
An excessive amount of potassium in the blood. SEE: hypokalemia.
ETIOLOGY: This condition usually is caused by inadequate excretion of potassium or the shift of potassium from tissues. Causes of inadequate secretion include acute renal failure, severe chronic renal failure, renal tubular disorders, hypoaldosteronism, and decreased renin secretion due to kidney disease or drugs (e.g., nonsteroidal anti-inflammatory agents, diuretics) that inhibit potassium excretion. The shift of potassium from tissues occurs in tissue damage due to trauma, hemolysis, digitalis poisoning, acidosis, and insulin deficiency.
SYMPTOMS: Hyperkalemia is often a symptomless condition until very high levels of potassium are present in the blood. The precise level at which cardiac or skeletal muscle toxicities arise varies greatly from patient to patient. Eventually, muscular weakness, electrocardiographic abnormalities (such as peaked T waves), and intractable cardiac rhythm disturbances may result.
PREVENTION: To help prevent hyperkalemia, patients who use salt substitutes containing potassium should be advised to discontinue them if urine output decreases. Predisposed patients, especially those with poor urinary output or taking oral or intravenous potassium supplements, require regular laboratory testing to assess their serum potassium levels.
TREATMENT: Mild hyperkalemia can be treated by eliminating its cause, often a medication or a potassium source in the diet or dietary supplement (e.g., potassium chloride taken as a salt substitute). Severe or progressive hyperkalemia can be treated with infusions of calcium gluconate, sodium bicarbonate, or insulin and glucose, or by the administration of potassium-binding resins orally or rectally. Hemodialysis also is effective.
NURSING-IMP: Cardiac rhythm and serum potassium and other electrolyte levels are monitored. Intake and output are recorded. Prescribed drugs are given and their effects on potassium levels are promptly evaluated. A dietician is consulted to recommend optimal quantities of potassium in foods and fluids. Safety measures are implemented for the patient with muscle weakness. If the patient requires transfused blood, only fresh blood may be used, since older blood contains potassium released by hemolysis.
There I think I cleared up my own question. Just in case anyone else has some.