Quinethazone

Fibrous crystals from 50% acetone

WHITE TO YELLOWISH WHITE, CRYSTALLINE POWDER

less than 1 mg/mL at 67.1 °F (NTP, 1992)

Sol in acetone, alcohol.

1 G SOL IN 20 ML POLYETHYLENE GLYCOL 300

1 G SOL IN 125 ML PROPYLENE GLYCOL

1 G SOL IN 500 ML ALCOHOL

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Pharmaceuticals

482 to 486 °F (NTP, 1992)

250-252 °C

251 °C

Fibrous crystals or white powder. (NTP, 1992)

Solid

SYMPTOMS: Symptoms of exposure to this compound may include allergies, skin rashes, thirst, epigastric pain, anorexia, gastric irritation, nausea, vomiting, diarrhea, constipation, photosensitivity, dryness, headache, muscle spasm, weakness, inflammation of the salivary gland, loss of libido, paresthesia, acute pancreatitis, pneumonitis, jaundice and other blood disorders. Other symptoms include cramping, hyperglycemia, glycosuria, vertigo, xanthopsia, leukopenia, thrombocytopenia, agranulocytosis, aplastic anemia, purpura, urticaria, necrotizing angiitis and restlessness.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

C - Cardiovascular system

QC - Cardiovascular system

Quinethazone is a thiazide diuretic used to treat hypertension. It inhibits Na⁺/Cl^- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue.

As a diuretic, quinethazone inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like quinethazone also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of quinethazone is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.

...BENZOTHIADIAZIDES HAVE DIRECT EFFECT ON RENAL TUBULAR TRANSPORT OF SODIUM & CHLORIDE INDEPENDENT OF CARBONIC ANHYDRASE INACTIVATION. ...HAVE PARALLEL DOSE-RESPONSE CURVES & COMPARABLE MAX CHLORURETIC EFFECTS. /BENZOTHIADIAZIDES/

RENAL ACTIONS OF THIAZIDE DIURETICS DECR EXTRACELLULAR FLUID & PLASMA VOL, CARDIAC OUTPUT, & TOTAL EXCHANGEABLE SODIUM IN INDIVIDUALS WITHOUT ANY EVIDENCE OF CARDIAC FAILURE. ...SODIUM & WATER DEPLETION...BASIS FOR ANTIHYPERTENSIVE EFFECT. ...DIURETIC THIAZIDES RELAX PERIPHERAL ARTERIOLAR SMOOTH MUSCLE. /BENZOTHIADIAZIDES/

Decreased plasma volume and decreased extracellular fluid volume; decreased cardiac output initially, followed by decreased total peripheral resistance with normalization of cardiac output ... /from table/

Thiazide diuretics increase urinary excretion of sodium and water by inhibiting sodium reabsorption in the early distal tubules. They increase the rate of delivery of tubular fluid and electrolytes to the distal sites of hydrogen and potassium ion secretion, while plasma volume contraction increases aldosterone production. The increased delivery and increase in aldosterone levels promote sodium reabsorption at the distal tubules, thus increasing the loss of potassium and hydrogen ions. /Thiazide diuretics/