Saturday, June 29, 2013
DIABETES Symptoms
Labels:
DIABETES,
diabetes incipides,
diabetes melitus,
diabetic nephropathy,
diabetic retinopathy,
drugindex,
drugs,
drugsinindia,
HOME REMEDIES,
medicin in india,
MEDICINE,
symptoms,
type 1 diabetes,
type 2 diabetes
Location:
Kerala, India
Friday, June 28, 2013
LOSARTAN POTASSIUM
Losartan is an angiotensin II receptor antagonist drug used mainly to treat high blood pressure (hypertension). Losartan was the first angiotensin II receptor antagonist to be marketed. Losartan potassium is available in JAN AUSHADHI price 11 RS for 10 tab available as generic form.
As with all angiotensin II type 1 receptor (AT1) antagonists, losartan is indicated for the treatment of hypertension. It may also delay progression of diabetic nephropathy, and is also indicated for the reduction of renal disease progression in patients with type 2 diabetes, hypertension and microalbuminuria (>30 mg/24 hours) or proteinuria (>900 mg/24 hours).
Although clinical evidence shows calcium channel blockers and thiazide-type diuretics are preferred first-line treatments for most patients (from both efficacy and cost points of view), an angiotensin II receptor antagonist such as losartan is recommended as first-line treatment in patients under the age of 55 who cannot tolerate an ACE inhibitor. The LIFE study demonstrated losartan was significantly superior to atenolol in the primary prevention of adverse cardiovascular events (myocardial infarction or stroke), with a significant reduction in cardiovascular morbidity and mortality for a comparable reduction in blood pressure. A study hints that losartan has a beneficial effect on mitochondria by reversing age related dysfunction in maintaining normal blood pressure and cellular energy usage. The maximal effects on blood pressure usually occur within 3–6 weeks upon starting losartan.
Losartan is also available as hydrochlorothiazide/losartan, a combination drug with a low dose thiazide diuretic to achieve an additive antihypertensive effect.
(2-butyl-4-chloro-1-{[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl}-1H-imidazol-5-yl)methanol
Mechanism of action and pharmacological actions
Losartan is a selective, competitive angiotensin II receptor type 1 (AT1) receptor antagonist, reducing the end organ responses to angiotensin II. Losartan administration results in a decrease in total peripheral resistance (afterload) and cardiac venous return (preload) All of the physiological effects of angiotensin II, including stimulation of release of aldosterone, are antagonized in the presence of losartan. Reduction in blood pressure occurs independently of the status of the renin-angiotensin system. As a result of losartan dosing, plasma renin activity increases due to removal of the angiotensin II feedback.
Losartan is a uricosuric. Because losartan can cause hyperkalemia, potassium supplements or salt substitutes containing potassium should not be used without appropriate monitoring by a physician.
Pharmacokinetics
Losartan is well absorbed following oral administration and undergoes significant first-pass metabolism to produce 5-carboxylic acid metabolite, designated as EXP3174. This metabolite is a long-acting (6 to 8 hr), noncompetitive antagonist at the AT1 receptor, and contributes to the pharmacological effects of losartan. EXP3174 is 10-40 times more potent in blocking AT1 receptors than losartan. Losartan's bioavailability is about 32%.
Metabolism is primarily by cytochrome P450 isoenzymes CYP2C9 and CYP3A4. Peak plasma concentrations of losartan and E-3174 occur about one hour and three to four hours, respectively, after an oral dose. Both losartan and E-3174 are more than 98% bound to plasma proteins. Losartan is excreted in the urine, and in the feces via bile, as unchanged drug and metabolites. About 4% of an oral dose is excreted unchanged in urine, and about 6% is excreted in urine as the active metabolite. The terminal elimination half lives of losartan and E-3174 are about 1.5 to 2.5 hours and 3 to 9 hours, respectively.
BRANDS
Alsartan - aristo, angilo-nitro, Czartan- macleods,giftan - systopic, Lara alkem, Lo - east west
Lopt - rhine, lopar , lomax, lopo, lorsave, lortan, losa, losacar, losaday, losaden, losagard, losain, losak, losakind, losamax, losamed, losan, losanorm, losapot,
Losar, losariv, losartan, losartas, losatrust, losatec, losavas, losavik, losacard, loscom, loset, losin , losit, losium, lopsi, lostat, lossi, lot, lotak, lotace, loza
Omnitan, nusar, osart, presartan , repace resilo , revas, rigard, saan, tozaar, vazortan, zaart, zargo, zilos, zortan, zyltan
As with all angiotensin II type 1 receptor (AT1) antagonists, losartan is indicated for the treatment of hypertension. It may also delay progression of diabetic nephropathy, and is also indicated for the reduction of renal disease progression in patients with type 2 diabetes, hypertension and microalbuminuria (>30 mg/24 hours) or proteinuria (>900 mg/24 hours).
Although clinical evidence shows calcium channel blockers and thiazide-type diuretics are preferred first-line treatments for most patients (from both efficacy and cost points of view), an angiotensin II receptor antagonist such as losartan is recommended as first-line treatment in patients under the age of 55 who cannot tolerate an ACE inhibitor. The LIFE study demonstrated losartan was significantly superior to atenolol in the primary prevention of adverse cardiovascular events (myocardial infarction or stroke), with a significant reduction in cardiovascular morbidity and mortality for a comparable reduction in blood pressure. A study hints that losartan has a beneficial effect on mitochondria by reversing age related dysfunction in maintaining normal blood pressure and cellular energy usage. The maximal effects on blood pressure usually occur within 3–6 weeks upon starting losartan.
Losartan is also available as hydrochlorothiazide/losartan, a combination drug with a low dose thiazide diuretic to achieve an additive antihypertensive effect.
(2-butyl-4-chloro-1-{[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl}-1H-imidazol-5-yl)methanol
Mechanism of action and pharmacological actions
Losartan is a selective, competitive angiotensin II receptor type 1 (AT1) receptor antagonist, reducing the end organ responses to angiotensin II. Losartan administration results in a decrease in total peripheral resistance (afterload) and cardiac venous return (preload) All of the physiological effects of angiotensin II, including stimulation of release of aldosterone, are antagonized in the presence of losartan. Reduction in blood pressure occurs independently of the status of the renin-angiotensin system. As a result of losartan dosing, plasma renin activity increases due to removal of the angiotensin II feedback.
Losartan is a uricosuric. Because losartan can cause hyperkalemia, potassium supplements or salt substitutes containing potassium should not be used without appropriate monitoring by a physician.
Pharmacokinetics
Losartan is well absorbed following oral administration and undergoes significant first-pass metabolism to produce 5-carboxylic acid metabolite, designated as EXP3174. This metabolite is a long-acting (6 to 8 hr), noncompetitive antagonist at the AT1 receptor, and contributes to the pharmacological effects of losartan. EXP3174 is 10-40 times more potent in blocking AT1 receptors than losartan. Losartan's bioavailability is about 32%.
Metabolism is primarily by cytochrome P450 isoenzymes CYP2C9 and CYP3A4. Peak plasma concentrations of losartan and E-3174 occur about one hour and three to four hours, respectively, after an oral dose. Both losartan and E-3174 are more than 98% bound to plasma proteins. Losartan is excreted in the urine, and in the feces via bile, as unchanged drug and metabolites. About 4% of an oral dose is excreted unchanged in urine, and about 6% is excreted in urine as the active metabolite. The terminal elimination half lives of losartan and E-3174 are about 1.5 to 2.5 hours and 3 to 9 hours, respectively.
BRANDS
Alsartan - aristo, angilo-nitro, Czartan- macleods,giftan - systopic, Lara alkem, Lo - east west
Lopt - rhine, lopar , lomax, lopo, lorsave, lortan, losa, losacar, losaday, losaden, losagard, losain, losak, losakind, losamax, losamed, losan, losanorm, losapot,
Losar, losariv, losartan, losartas, losatrust, losatec, losavas, losavik, losacard, loscom, loset, losin , losit, losium, lopsi, lostat, lossi, lot, lotak, lotace, loza
Omnitan, nusar, osart, presartan , repace resilo , revas, rigard, saan, tozaar, vazortan, zaart, zargo, zilos, zortan, zyltan
Tuesday, June 25, 2013
LABETALOL
Labetalol is a mixed alpha/beta adrenergic antagonist, which is used to treat high blood pressure.
(RS)-2-hydroxy-5-{1-hydroxy-2-[(1-methyl-3-phenylpropyl)amino]ethyl}benzamide
Brands - Normodyne, Trandate
Ab-Lol - from Steadfast , Cebalol - from Health Biotech, Evabet - from Celon, Gravidol - from Mercury Labs, Labesol- from SG Pharma, Labeta - from Geo Pharma, Labil - from Celon (Revilon),
Lobet - from Samarth, Normadate - from GSK ,
Pih - from Dewcare, Talobet - from Celon , Tiplab- from United Biotech ,
Indications
It has a particular indication in the treatment of pregnancy-induced hypertension which is commonly associated with pre-eclampsia.
It is also used to treat chronic and acute hypertension of pheochromocytoma and hypertensive crisis.
Administration
Labetalol is available in 100, 200, and 400 mg tablets and intravenously (available as Trandate) in 5 mg/ml solution. Adults taking tablets usually start with 100 mg twice daily, with a maximum of 2.4 g/day. In cases of emergency, dosage might be higher. Intravenous (IV) doses are usually started at 20 mg over two minutes. Additional doses of 40 mg, then 80 mg may be administered every ten minutes as needed. Additional 80 mg doses can be given to a total maximum dose of 300 mg. Additionally, labetalol can be administered by IV infusion at a rate of 2 mg/minute, with a maximum dose of 300 mg.
Side effects
Side effects may include:
Drowsiness
Fatigue
Weakness
Difficulty sleeping
Diminished sexual function
Orthostatic hypotension (due to alpha receptor blockade)
Scalp tingling
Drug eruption similar to lichen planus
A rare but potentially lethal side effect is respiratory distress.
Contra indications
Labetalol has relative contraindications for use in patients with asthma, congestive heart failure, any degree of heart block, bradycardia, or those in cardiogenic shock.
Chemistry
For adrenergic agents, when the substituent on the amine nitrogen is greater in size than a t-butyl group, then the molecule typically is found to have receptor affinity without intrinsic activity, and is therefore an antagonist. Labetalol has two chiral carbons and consequently exists as four stereoisomers. Two of these isomers, the (S,S)- and (R,S)- forms are inactive. The third, the (S,R)-isomer, is a powerful α1 blocker. The fourth isomer, the (R,R)-isomer, is a mixed nonselective β blocker and selective α1 blocker.
Labetalol acts by blocking alpha and beta adrenergic receptors, resulting in decreased peripheral vascular resistance without significant alteration of heart rate or cardiac output. The β:α antagonism of labetalol is approximately 3:1.
Mechanism of action
Labetalol combines both selective, competitive, alpha-1-adrenergic blocking and nonselective, competitive, beta-adrenergic blocking activity in a single substance. In man, the ratios of alpha- to beta- blockade have been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) administration, respectively. The principal physiologic action of labetalol is to competitively block adrenergic stimulation of β-receptors within the myocardium (β1-receptors) and within bronchial and vascular smooth muscle (β2-receptors), and α1-receptors within vascular smooth muscle. This causes a decrease in systemic arterial blood pressure and systemic vascular resistance without a substantial reduction in resting heart rate, cardiac output, or stroke volume, apparently because of its combined α- and β-adrenergic blocking activity.
Absorption
Completely absorbed (100%) from the gastrointestinal tract with peak plasma levels occurring 1 to 2 hours after oral administration. The absolute bioavailability of labetalol is increased when administered with food.
Toxicity
LD50 = 66 mg/kg (Rat, IV). Side effects or adverse reactions include dizziness when standing up, very low blood pressure, severely slow heartbeat, weakness, diminished sexual function, fatigue
Drug Interactions
In one survey, 2.3% of patients taking labetalol HCl in combination with tricyclic antidepressants experienced tremor, as compared to 0.7% reported to occur with labetalol HCl alone. The contribution of each of the treatments to this adverse reaction is unknown but the possibility of a drug interaction cannot be excluded.
Drugs possessing beta-blocking properties can blunt the bronchodilator effect of beta-receptor agonist drugs in patients with bronchospasm; therefore, doses greater than the normal antiasthmatic dose of beta-agonist bronchodilator drugs may be required.
Cimetidine has been shown to increase the bioavailability of labetalol HCl. Since this could be explained either by enhanced absorption or by an alteration of hepatic metabolism of labetalol HCl, special care should be used in establishing the dose required for blood pressure control in such patients.
Synergism has been shown between halothane anesthesia and intravenously administered labetalol HCl. During controlled hypotensive anesthesia using labetalol HCl in association with halothane, high concentrations (3% or above) of halothane should not be used because the degree of hypotension will be increased and because of the possibility of a large reduction in cardiac output and an increase in central venous pressure. The anesthesiologist should be informed when a patient is receiving labetalol HCl.
Labetalol HCl blunts the reflex tachycardia produced by nitroglycerin without preventing its hypotensive effect. If labetalol HCl is used with nitroglycerin in patients with angina pectoris, additional antihypertensive effects may occur.
Care should be taken if labetalol is used concomitantly with calcium antagonists of the verapamil type.
(RS)-2-hydroxy-5-{1-hydroxy-2-[(1-methyl-3-phenylpropyl)amino]ethyl}benzamide
Brands - Normodyne, Trandate
Ab-Lol - from Steadfast , Cebalol - from Health Biotech, Evabet - from Celon, Gravidol - from Mercury Labs, Labesol- from SG Pharma, Labeta - from Geo Pharma, Labil - from Celon (Revilon),
Lobet - from Samarth, Normadate - from GSK ,
Pih - from Dewcare, Talobet - from Celon , Tiplab- from United Biotech ,
Indications
It has a particular indication in the treatment of pregnancy-induced hypertension which is commonly associated with pre-eclampsia.
It is also used to treat chronic and acute hypertension of pheochromocytoma and hypertensive crisis.
Administration
Labetalol is available in 100, 200, and 400 mg tablets and intravenously (available as Trandate) in 5 mg/ml solution. Adults taking tablets usually start with 100 mg twice daily, with a maximum of 2.4 g/day. In cases of emergency, dosage might be higher. Intravenous (IV) doses are usually started at 20 mg over two minutes. Additional doses of 40 mg, then 80 mg may be administered every ten minutes as needed. Additional 80 mg doses can be given to a total maximum dose of 300 mg. Additionally, labetalol can be administered by IV infusion at a rate of 2 mg/minute, with a maximum dose of 300 mg.
Side effects
Side effects may include:
Drowsiness
Fatigue
Weakness
Difficulty sleeping
Diminished sexual function
Orthostatic hypotension (due to alpha receptor blockade)
Scalp tingling
Drug eruption similar to lichen planus
A rare but potentially lethal side effect is respiratory distress.
Contra indications
Labetalol has relative contraindications for use in patients with asthma, congestive heart failure, any degree of heart block, bradycardia, or those in cardiogenic shock.
Chemistry
For adrenergic agents, when the substituent on the amine nitrogen is greater in size than a t-butyl group, then the molecule typically is found to have receptor affinity without intrinsic activity, and is therefore an antagonist. Labetalol has two chiral carbons and consequently exists as four stereoisomers. Two of these isomers, the (S,S)- and (R,S)- forms are inactive. The third, the (S,R)-isomer, is a powerful α1 blocker. The fourth isomer, the (R,R)-isomer, is a mixed nonselective β blocker and selective α1 blocker.
Labetalol acts by blocking alpha and beta adrenergic receptors, resulting in decreased peripheral vascular resistance without significant alteration of heart rate or cardiac output. The β:α antagonism of labetalol is approximately 3:1.
Mechanism of action
Labetalol combines both selective, competitive, alpha-1-adrenergic blocking and nonselective, competitive, beta-adrenergic blocking activity in a single substance. In man, the ratios of alpha- to beta- blockade have been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) administration, respectively. The principal physiologic action of labetalol is to competitively block adrenergic stimulation of β-receptors within the myocardium (β1-receptors) and within bronchial and vascular smooth muscle (β2-receptors), and α1-receptors within vascular smooth muscle. This causes a decrease in systemic arterial blood pressure and systemic vascular resistance without a substantial reduction in resting heart rate, cardiac output, or stroke volume, apparently because of its combined α- and β-adrenergic blocking activity.
Absorption
Completely absorbed (100%) from the gastrointestinal tract with peak plasma levels occurring 1 to 2 hours after oral administration. The absolute bioavailability of labetalol is increased when administered with food.
Toxicity
LD50 = 66 mg/kg (Rat, IV). Side effects or adverse reactions include dizziness when standing up, very low blood pressure, severely slow heartbeat, weakness, diminished sexual function, fatigue
Drug Interactions
In one survey, 2.3% of patients taking labetalol HCl in combination with tricyclic antidepressants experienced tremor, as compared to 0.7% reported to occur with labetalol HCl alone. The contribution of each of the treatments to this adverse reaction is unknown but the possibility of a drug interaction cannot be excluded.
Drugs possessing beta-blocking properties can blunt the bronchodilator effect of beta-receptor agonist drugs in patients with bronchospasm; therefore, doses greater than the normal antiasthmatic dose of beta-agonist bronchodilator drugs may be required.
Cimetidine has been shown to increase the bioavailability of labetalol HCl. Since this could be explained either by enhanced absorption or by an alteration of hepatic metabolism of labetalol HCl, special care should be used in establishing the dose required for blood pressure control in such patients.
Synergism has been shown between halothane anesthesia and intravenously administered labetalol HCl. During controlled hypotensive anesthesia using labetalol HCl in association with halothane, high concentrations (3% or above) of halothane should not be used because the degree of hypotension will be increased and because of the possibility of a large reduction in cardiac output and an increase in central venous pressure. The anesthesiologist should be informed when a patient is receiving labetalol HCl.
Labetalol HCl blunts the reflex tachycardia produced by nitroglycerin without preventing its hypotensive effect. If labetalol HCl is used with nitroglycerin in patients with angina pectoris, additional antihypertensive effects may occur.
Care should be taken if labetalol is used concomitantly with calcium antagonists of the verapamil type.
Labels:
Ab-lol,
cebalol,
DRUG,
drugindex,
drugs,
drugsinindia,
gravidol,
labeta,
Labetalol,
lobet,
medicin in india,
study of drugs in india
Location:
Kerala, India
Thursday, June 20, 2013
IRBESARTAN
Irbesartan is an angiotensin II receptor antagonist used mainly for the treatment of hypertension. Irbesartan was developed by Sanofi Research (now part of sanofi-aventis). It is jointly marketed by sanofi-aventis and Bristol-Myers Squibb under the trade names Aprovel, Karvea, and Avapro.
2-butyl-3-({4-[2-(2H-1,2,3,4-tetrazol-5-yl)phenyl]phenyl}methyl)-1,3-diazaspiro[4.4]non-1-en-4-one
INDICATION
As with all angiotensin II receptor antagonists, irbesartan is indicated for the treatment of hypertension. Irbesartan may also delay progression of diabetic nephropathy and is also indicated for the reduction of renal disease progression in patients with type 2 diabetes, hypertension and microalbuminuria or proteinuria
Combination with diuretic
Irbesartan is also available in a combination formulation with a low dose thiazide diuretic, invariably hydrochlorothiazide, to achieve an additive antihypertensive effect. Irbesartan/hydrochlorothiazide combination preparations are marketed under similar trade names to irbesartan preparations, including Irda, CoIrda, CoAprovel, Karvezide, Avalide and Avapro HCT.
Heart failure
A large randomized trial following 4100+ men and women with heart failure and normal ejection fraction over 4+ years found no improvement in study outcomes or survival with irbesartan as compared to placebo.
2-butyl-3-({4-[2-(2H-1,2,3,4-tetrazol-5-yl)phenyl]phenyl}methyl)-1,3-diazaspiro[4.4]non-1-en-4-one
INDICATION
As with all angiotensin II receptor antagonists, irbesartan is indicated for the treatment of hypertension. Irbesartan may also delay progression of diabetic nephropathy and is also indicated for the reduction of renal disease progression in patients with type 2 diabetes, hypertension and microalbuminuria or proteinuria
Combination with diuretic
Irbesartan is also available in a combination formulation with a low dose thiazide diuretic, invariably hydrochlorothiazide, to achieve an additive antihypertensive effect. Irbesartan/hydrochlorothiazide combination preparations are marketed under similar trade names to irbesartan preparations, including Irda, CoIrda, CoAprovel, Karvezide, Avalide and Avapro HCT.
Heart failure
A large randomized trial following 4100+ men and women with heart failure and normal ejection fraction over 4+ years found no improvement in study outcomes or survival with irbesartan as compared to placebo.
INDAPAMIDE
Indapamide is a thiazide-like diuretic drug marketed by Servier, generally used in the treatment of hypertension, as well as decompensated cardiac failure. The US trade name for indapamide is Lozol. Indapamide is marketed as Natrilix outside the US, and as Insig in Australia. Combination preparations with perindopril (an ACE inhibitor antihypertensive) are also available.
It is described as a thiazide-like diuretic.
4-chloro-N-(2-methyl-2,3-dihydroindol-1-yl)- 3-sulfamoyl-benzamide
INDICATION AND DOSE
Hypertension and edema due to congestive heart failure. Indapamide has been proven in the HYVET trial to reduce stroke and all cause mortality when given with or without perindopril to people over the age of 80 for the treatment of hypertension
The adult dosage is 1.25 to 5 mg, orally and once daily, usually in the morning.
CONTRA INDICATIONS
Indapamide is contraindicated in known hypersensitivity to sulfonamides, severe renal failure, hepatic encephalopathy or severe hepatic failure and hypokalemia (low blood potassium levels).
There is insufficient safety data to recommend indapamide use in pregnancy or breastfeeding.
INTERACTIONS
Caution is advised in the combination of indapamide with lithium and nonantiarrhythmic drugs causing wave-burst arrhythmia (astemizole, bepridil, IV erythromycin, halofantrine, pentamidine, sultopride, terfenadine, vincamine).
BRANDS - NATRILIX, LAZOL
What are the possible side effects of indapamide (Lozol)?
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.
Stop using this medication and call your doctor at once if you have a serious side effect such as:
dry mouth, thirst, nausea, vomiting;
feeling weak, drowsy, restless, or light-headed;
fast or uneven heartbeat; or
muscle pain or weakness.
Less serious side effects may include:
dizziness;
headache; or
mild skin rash.
This is not a complete...
What are the precautions when taking indapamide (Lozol)?
Before taking indapamide, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.
Before using this medication, tell your doctor or pharmacist your medical history, especially of: diabetes, gout, kidney problems, liver disease, a certain nerve surgery (sympathectomy).
This drug may make you dizzy. Do not drive, use machinery, or do any activity that requires alertness until you are sure you can perform such activities safely. Limit alcoholic beverages.
Saturday, June 15, 2013
HYDROCHLORTHIAZIDE
Hydrochlorothiazide, abbreviated HCTZ, HCT, or HZT, is a diuretic drug of the thiazide class that acts by inhibiting the kidneys' ability to retain water. This reduces the volume of the blood, decreasing blood return to the heart and thus cardiac output and, by other mechanisms, is believed to lower peripheral vascular resistance.
Hydrochlorothiazide is a calcium-sparing diuretic, meaning it can help the body get rid of excess water while still keeping calcium.
6-chloro-1,1-dioxo-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide
use
Hydrochlorothiazide is frequently used for the treatment of hypertension, congestive heart failure, symptomatic edema, diabetes insipidus, renal tubular acidosis, and the prevention of kidney stones.
It is also sometimes used for hypercalciuria, Dent's disease and Ménière's disease. For diabetes insipidus, the effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and reducing the urine output.
Thiazides are also used in the treatment of osteoporosis. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation.
ADVERSE EFFECTS
Hypokalemia, an occasional side effect, can be usually prevented by potassium supplements or by combining hydrochlorothiazide with a potassium-sparing diuretic.
Hypomagnesemia
Hyponatremia
Hyperuricemia
High blood sugar
Hyperlipidemia
Hypercalcemia
Headache
Nausea/vomiting
Photosensitivity
Weight gain
Gout
Pancreatitis
MECHANISM OF ACTION
Hydrochlorothiazide belongs to thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na) reabsorption in the distal convoluted tubule. The major site of action in the nephron appears on an electroneutral Na+-Cl- co-transporter by competing for the chloride site on the transporter. By impairing Na transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss. Thiazides increase the reabsorption of calcium in this segment in a manner unrelated to sodium transport. Additionally, by other mechanisms, HCTZ is believed to lower peripheral vascular resistance.
Prohibited use in sport
Hydrochlorothiazide was detected in the urine of the Russian cyclist Alexandr Kolobnev during the 2011 Tour de France. Kolobnev was the only cyclist to leave the 2011 race in connection with adverse findings at a doping control. While Hydrochlorothiazide is not itself a performance-enhancing drug, it may be used to mask the use of performance-enhancing drugs, and is classed by the World Anti-Doping Agency as a "specified substance". Kolobnev was subsequently cleared of all charges of intentional doping.
BRANDS - AQUAZIDE 12.5,25, HYDRAZIDE, Hydrodiuril,Aquazide H,Dichlotride, BENICAR HydroSaluric, Hydrochlorot, Microzide, Esidrex, and Oretic.
Hydrochlorothiazide is a calcium-sparing diuretic, meaning it can help the body get rid of excess water while still keeping calcium.
6-chloro-1,1-dioxo-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide
use
Hydrochlorothiazide is frequently used for the treatment of hypertension, congestive heart failure, symptomatic edema, diabetes insipidus, renal tubular acidosis, and the prevention of kidney stones.
It is also sometimes used for hypercalciuria, Dent's disease and Ménière's disease. For diabetes insipidus, the effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and reducing the urine output.
Thiazides are also used in the treatment of osteoporosis. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation.
ADVERSE EFFECTS
Hypokalemia, an occasional side effect, can be usually prevented by potassium supplements or by combining hydrochlorothiazide with a potassium-sparing diuretic.
Hypomagnesemia
Hyponatremia
Hyperuricemia
High blood sugar
Hyperlipidemia
Hypercalcemia
Headache
Nausea/vomiting
Photosensitivity
Weight gain
Gout
Pancreatitis
MECHANISM OF ACTION
Hydrochlorothiazide belongs to thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na) reabsorption in the distal convoluted tubule. The major site of action in the nephron appears on an electroneutral Na+-Cl- co-transporter by competing for the chloride site on the transporter. By impairing Na transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss. Thiazides increase the reabsorption of calcium in this segment in a manner unrelated to sodium transport. Additionally, by other mechanisms, HCTZ is believed to lower peripheral vascular resistance.
Prohibited use in sport
Hydrochlorothiazide was detected in the urine of the Russian cyclist Alexandr Kolobnev during the 2011 Tour de France. Kolobnev was the only cyclist to leave the 2011 race in connection with adverse findings at a doping control. While Hydrochlorothiazide is not itself a performance-enhancing drug, it may be used to mask the use of performance-enhancing drugs, and is classed by the World Anti-Doping Agency as a "specified substance". Kolobnev was subsequently cleared of all charges of intentional doping.
BRANDS - AQUAZIDE 12.5,25, HYDRAZIDE, Hydrodiuril,Aquazide H,Dichlotride, BENICAR HydroSaluric, Hydrochlorot, Microzide, Esidrex, and Oretic.
Labels:
abbreviated HCTZ,
calcium-sparing diuretic,
diuretic,
drugs,
HCT,
hydrochlorothiazide,
is a diuretic drug of the thiazide class that acts .aquazide,
medicin in india,
or HZT,
tab,
tablet
Location:
Kerala, India
Friday, June 14, 2013
FRUSEMIDE
Furosemide or frusemide is a loop diuretic used in the treatment of congestive heart failure and edema. It is most commonly marketed by Sanofi under the brand name Lasix, PRICE OF FRUSEMIDE 40 IN JAN AUSHADHI STORE just 4 rs for 10 tab, It has also been used to prevent Thoroughbred and Standardbred race horses from bleeding through the nose during races.
Along with some other diuretics, furosemide is also included on the World Anti-Doping Agency's banned drug list due to its alleged use as a masking agent for other drugs.
4-chloro-2-(furan-2-ylmethylamino)- 5-sulfamoylbenzoic acid
use
Furosemide is primarily used for the treatment of hypertension and edema. It is the first-line agent in most people with edema due to congestive heart failure. It is also used for hepatic cirrhosis, renal impairment, nephrotic syndrome, in adjunct therapy for cerebral/pulmonary edema where rapid diuresis is required (IV injection), and in the management of severe hypercalcemia in combination with adequate rehydration.
ADVERSE EFFECTS
Although disputed, it is considered ototoxic: "usually with large parenteral doses and rapid administration and in renal impairment". Furosemide also can lead to gout due to hyperuricemia. Hyperglycemia is also a common side effect.
The tendency, as for all loop diuretics, to cause low potassium levels (hypokalemia) has given rise to combination products, either with potassium itself (e.g. Lasix-K) or with the potassium-sparing diuretic amiloride (Co-amilofruse).
What are the precautions when taking furosemide (Lasix)?
Before taking furosemide, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.
Before using this medication, tell your doctor or pharmacist your medical history, especially of: kidney problems, liver problems, inability to make urine, gout, lupus.
If you have diabetes, furosemide may affect your blood sugar level. Check your blood sugar level regularly as directed and share the results with your doctor. Your doctor may need to adjust your diabetes medication or diet.
What happens if I miss a dose?
Furosemide is sometimes used only once, so you may not be on a dosing schedule. If you are using the medication regularly, take the missed dose as soon as you remember. Skip the missed dose if it is almost time for your next scheduled dose. Do not take extra medicine to make up the missed dose.
What happens if I overdose?
Seek emergency medical attention or call the Poison Help line at 1-800-222-1222.
Overdose symptoms may include feeling very thirsty or hot, heavy sweating, or hot and dry skin.
What should I avoid while taking furosemide?
Avoid getting up too fast from a sitting or lying position, or you may feel dizzy. Get up slowly and steady yourself to prevent a fall.
Avoid becoming dehydrated. Follow your doctor's instructions about the type and amount of liquids you should drink while you are taking furosemide.
Labels:
congestive heart failure,
diuretic,
drugs,
edema,
FRUSEMIDE,
FUROSEMIDE,
indian medicine,
inj,
lasix,
loop diuretic,
medicin in india,
MEDICINE,
sanofi,
tab
Sunday, June 9, 2013
9 WEEK PREGNANCY
- From crown to rump your baby measures at 2.2-3cm or 1-1¼ inch, the size of a medium green olive.
- This week your baby is looking less like a tadpole and more human - the tail at the bottom is shrinking and disappearing and the face is more rounded.
- Hands and feet continue to form along with the fingers, toes and elbows.
- Internal organs such as testes and ovaries start to develop this week but the external genitals don't have noticeable male or female characteristics yet.
- The eyelids almost cover the eyes now, the intestines are growing longer and the pancreas, bile ducts, gall bladder and anus have formed.
8 WEEKS OF PREGNANCY
- From crown to rump your baby measures at 1.4-2cm or ½-¾ inch, the size of a pinto bean.
- From week 8 your baby graduates from being an embryo to being a fetus literally meaning the ‘little one’.
- The rudiments of all the vital body parts are in place now - all the main internal organs are already present.
- Baby now has the beginnings of a recognizably human face with nostrils, lips and a mouth with a tongue.
- Your baby is now covered with a thin layer of skin cells but is still translucent.
- Baby has already started moving around inside the uterus although you are not able to feel a thing.
- Toes and fingers begin to form although they are webbed; paddle shaped foot and hand areas are clearly present.
- Initially the arms develop faster than the legs - similarly after birth baby will develop hand and arm control faster than leg control.
- Baby's eyelids are beginning to form and until that completes, the eyes will appear open.
- The digestive tract especially the intestines are continuing to grow.
- Ten dental buds have formed in each jaw - these will become baby teeth.
- Heart function is now more fully developed with the heart pumping about 150 beats a minute (twice the adult rate).
Labels:
8weeks,
8weeks of pregnancy,
DRUG,
drugindex,
drugsinindia,
drugsinindia.com,
fetal growth,
fetal images,
fetal stages,
medicin in india,
MEDICINE
Location:
Kerala, India
7 TH WEEK OF PREGNANCY
- From crown to rump at the start of the week your baby measures at 4-5mm or 0.16-0.2 inch, the size of a small raspberry.
- This week your baby goes through an incredible growth spurt; it no longer looks like a blastocyst.
- Intestines are developing, the heart chambers are forming and the brain hemispheres are growing.
- Other changes are the dark spots where the eyes and the nostrils are to be, are forming; the color in the irises are now visible and the lenses of the baby's eyes are forming.
- Pits that mark the ears and protruding buds that will eventually become the arms and legs begin to appear.
- The appendix is now present along with the pancreas.
- The skull is still transparent and the baby's brain is continuing in its venture to become more complex.
Saturday, June 8, 2013
6 TH WEEK OF PREGNANCY
- From crown to rump your baby measures at 2-4mm or 0.08-0.16 inch, the size of a small lentil.
- This week marks the beginning of the embryonic period which spans from the 6th to 10th weeks of pregnancy or the 4th to 8th weeks of fetal development.
- Growth is rapid this week with your baby resembling a tadpole with a tail but no brain.
- It is already 10,000 times larger than the fertilized egg; it doesn't have gender characteristics yet.
- Over the next 5 months, more than 100 billion neurons will be formed in the brain, laying the necessary groundwork for a lifetime of learning.
- His heart, the size of poppy seed, is beating on its own
- Your baby at this stage has his own bloodstream with blood circulating already.
- Testes or ovaries at this stage are mere clusters of cells.
- Other major organs continue to develop including liver, kidneys and lungs.
- The head has the beginnings of the eyes, ears and mouth and there are tiny buds which will become arms and legs.
FOSINOPRIL
Fosinopril is an angiotensin converting enzyme (ACE) inhibitor used for the treatment of hypertension and some types of chronic heart failure. Fosinopril is the only phosphinate-containing ACE inhibitor marketed.
(2S,4S)-4-cyclohexyl-1-(2-{[2-methyl-1-(propanoyloxy)propoxy](4-phenylbutyl)phosphoryl}acetyl)pyrrolidine-2-carboxylic acid
Fosinoprilat and Fosinopril
Fosinoprilat proved to have the same problem as enalaprilat and the other carboxylate-containing ACE inhibitors (namely poor oral bioavailability). Addition of a hydrophobic side-chain modulated the ionisation characteristics of the molecule making it more bioavailable. Fosinopril is administered as a prodrug and is converted in vivo to the active form fosinoprilat.
Congestive heart failure and angiotensin II
In congestive heart failure, the ability of the heart to pump enough blood to satisfy the physiological needs of the body is reduced.This condition has a variety of causes, including damaged heart valves, myocardial infarction, hypertension, vitamin B1 deficiency, and genetic mutations. When subsequent blood flow to the kidneys is reduced, the kidneys respond by increasing the secretion of renin from the juxtaglomerular apparatus. Renin converts the inactive angiotensinogen into angiotensin I, which is converted to angiotensin II (AII) by angiotensin converting enzyme (ACE). AII can have negative effects on the cardiovascular system after events such as heart failure and myocardial infarction. AII causes arterial vasoconstriction and hypertension resulting in an increase in afterload, increasing the resistance against which the heart works. Additionally, chronic increase in production of AII is associated with structural changes to the myocardium which reduces the functionality of the heart.
Effects of Fosinopril on treating heart failure
Fosinopril is de-esterified by the liver or gastrointestinal mucosa and is converted to its active form, fosinoprilat. Fosinoprilat competitively binds to ACE, preventing ACE from binding to and converting angiotensin I to angiotensin II. Inhibiting the production of AII lowers peripheral vascular resistance, decreases afterload and decreases blood pressure, thus helping to alleviate the negative effects of AII on cardiac performance. In heart failure patients, fosinopril increases exercise tolerance and lowers the frequency of events associated with worsening heart failure, such as dyspnea, the need for supplemental diuretics, fatigue, and hospitalizations. In a study examining the effects of fosinopril on insulin-like growth factor 1 (IGF-1) and IGF binding protein serum concentrations in high cardiovascular risk patients, a six-month treatment of fosinopril was associated with an elevation in IGF-1. Since a decline in IGF-1 is associated with an increased risk of ischemic heart disease, fosinopril may reduce ischemic risk.
Benefits of Fosinopril
Unlike other ACE inhibitors that are primarily excreted by the kidneys, fosinopril is eliminated from the body via both renal and hepatic pathways. This characteristic of fosinopril makes the drug a safer choice than other ACE inhibitors for heart failure patients with impaired kidney function resulting from poor perfusion as fosinopril can still be eliminated by the liver, preventing accumulation of the drug in the body.
Brands
fovas10 mg,20mg
fosinase 10,20
(2S,4S)-4-cyclohexyl-1-(2-{[2-methyl-1-(propanoyloxy)propoxy](4-phenylbutyl)phosphoryl}acetyl)pyrrolidine-2-carboxylic acid
Fosinoprilat and Fosinopril
Fosinoprilat proved to have the same problem as enalaprilat and the other carboxylate-containing ACE inhibitors (namely poor oral bioavailability). Addition of a hydrophobic side-chain modulated the ionisation characteristics of the molecule making it more bioavailable. Fosinopril is administered as a prodrug and is converted in vivo to the active form fosinoprilat.
Congestive heart failure and angiotensin II
In congestive heart failure, the ability of the heart to pump enough blood to satisfy the physiological needs of the body is reduced.This condition has a variety of causes, including damaged heart valves, myocardial infarction, hypertension, vitamin B1 deficiency, and genetic mutations. When subsequent blood flow to the kidneys is reduced, the kidneys respond by increasing the secretion of renin from the juxtaglomerular apparatus. Renin converts the inactive angiotensinogen into angiotensin I, which is converted to angiotensin II (AII) by angiotensin converting enzyme (ACE). AII can have negative effects on the cardiovascular system after events such as heart failure and myocardial infarction. AII causes arterial vasoconstriction and hypertension resulting in an increase in afterload, increasing the resistance against which the heart works. Additionally, chronic increase in production of AII is associated with structural changes to the myocardium which reduces the functionality of the heart.
Effects of Fosinopril on treating heart failure
Fosinopril is de-esterified by the liver or gastrointestinal mucosa and is converted to its active form, fosinoprilat. Fosinoprilat competitively binds to ACE, preventing ACE from binding to and converting angiotensin I to angiotensin II. Inhibiting the production of AII lowers peripheral vascular resistance, decreases afterload and decreases blood pressure, thus helping to alleviate the negative effects of AII on cardiac performance. In heart failure patients, fosinopril increases exercise tolerance and lowers the frequency of events associated with worsening heart failure, such as dyspnea, the need for supplemental diuretics, fatigue, and hospitalizations. In a study examining the effects of fosinopril on insulin-like growth factor 1 (IGF-1) and IGF binding protein serum concentrations in high cardiovascular risk patients, a six-month treatment of fosinopril was associated with an elevation in IGF-1. Since a decline in IGF-1 is associated with an increased risk of ischemic heart disease, fosinopril may reduce ischemic risk.
Benefits of Fosinopril
Unlike other ACE inhibitors that are primarily excreted by the kidneys, fosinopril is eliminated from the body via both renal and hepatic pathways. This characteristic of fosinopril makes the drug a safer choice than other ACE inhibitors for heart failure patients with impaired kidney function resulting from poor perfusion as fosinopril can still be eliminated by the liver, preventing accumulation of the drug in the body.
Brands
fovas10 mg,20mg
fosinase 10,20
Labels:
ACE inhibitor,
angiotension 2,
chronic heart failure,
congestive heart failure,
drugindex,
drugs,
drugsinindia,
fosinopril,
Fosinoprila,
FOVAS,
indian medicine,
medicin in india
Location:
India
Sunday, June 2, 2013
CENTRAL NERVOUS SYSTEM
The central nervous system (CNS) is the part of the nervous system that integrates the information that it receives from, and coordinates the activity of, all parts of the bodies of bilaterian animals—that is, all multicellular animals except radially symmetric animals such as sponges and jellyfish. It contains the majority of the nervous system and consists of the brain and the spinal cord. Some classifications also include the retina and the cranial nerves in the CNS. Together with the peripheral nervous system, it has a fundamental role in the control of behavior. The CNS is contained within the dorsal cavity, with the brain in the cranial cavity and the spinal cord in the spinal cavity. In vertebrates, the brain is protected by tDuring early development of the vertebrate embryo, a longitudinal groove on the neural plate gradually deepens and the ridges on either side of the groove (the neural folds) become elevated, and ultimately meet, transforming the groove into a closed tube, the ectodermal wall of which forms the rudiment of the nervous system. This tube initially differentiates into three vesicles (pockets): the prosencephalon at the front, the mesencephalon, and, between the mesencephalon and the spinal cord, the rhombencephalon. (By six weeks in the human embryo) the prosencephalon then divides further into the telencephalon and diencephalon; and the rhombencephalon divides into the metencephalon and myelencephalon.
DEVELOPMENT
As the vertebrate grows, these vesicles differentiate further still. The telencephalon differentiates into, among other things, the striatum, the hippocampus and the neocortex, and its cavity becomes the first and second ventricles. Diencephalon elaborations include the subthalamus, hypothalamus, thalamus and epithalamus, and its cavity forms the third ventricle. The tectum, pretectum, cerebral peduncle and other structures develop out of the mesencephalon, and its cavity grows into the mesencephalic duct (cerebral aqueduct). The metencephalon becomes, among other things, the pons and the cerebellum, the myelencephalon forms the medulla oblongata, and their cavities develop into the fourth ventricle.
Planarians, members of the phylum Platyhelminthes (flatworms), have the simplest, clearly defined delineation of a nervous system into a central nervous system (CNS) and a peripheral nervous system (PNS).Their primitive brain, consisting of two fused anterior ganglia, and longitudinal nerve cords form the CNS; the laterally projecting nerves form the PNS. A molecular study found that more than 95% of the 116 genes involved in the nervous system of planarians, which includes genes related to the CNS, also exist in humans.Like planarians, vertebrates have a distinct CNS and PNS, though more complex than those of planarians.
The CNS of chordates differs from that of other animals in being placed dorsally in the body, above the gut and notochord/spine. The basic pattern of the CNS is highly conserved throughout the different species of vertebrates and during evolution. The major trend that can be observed is towards a progressive telencephalisation: the telencephalon of reptiles is only an appendix to the large olfactory bulb, while in mammals it makes up most of the volume of the CNS. In the human brain, the telencephalon covers most of the diencephalon and the mesencephalon. Indeed, the allometric study of brain size among different species shows a striking continuity from rats to whales, and allows us to complete the knowledge about the evolution of the CNS obtained through cranial endocasts.
Mammals – which appear in the fossil record after the first fishes, amphibians, and reptiles – are the only vertebrates to possess the evolutionarily recent, outermost part of the cerebral cortex known as the neocortex.The neocortex of monotremes (the duck-billed platypus and several species of spiny anteaters) and of marsupials (such as kangaroos, koalas, opossums, wombats, and Tasmanian devils) lack the convolutions – gyri and sulci – found in the neocortex of most placental mammals (eutherians). Within placental mammals, the size and complexity of the neocortex increased over time. The area of the neocortex of mice is only about 1/100 that of monkeys, and that of monkeys is only about 1/10 that of humans. In addition, rats lack convolutions in their neocortex (possibly also because rats are small mammals), whereas cats have a moderate degree of convolutions, and humans have quite extensive convolutions. Extreme convolution of the neocortex is found in dolphins, possibly related to their complex echolocation
Diseases of the central nervous system
There are many central nervous system diseases, including infections of the central nervous system such as encephalitis and poliomyelitis, neurodegenerative diseases such as Alzheimer's disease and amyotrophic lateral sclerosis, autoimmune and inflammatory diseases such as multiple sclerosis or acute disseminated encephalomyelitis, and genetic disorders such as Krabbe's disease, Huntington's disease, or adrenoleukodystrophy. Lastly, cancers of the central nervous system can cause severe illness and, when malignant, can have very high mortality rates.
Specialty professional organizations recommend that neurological imaging of the brain be done only to answer a specific clinical question and not as routine screening.
Labels:
AUTONOMOUS,
brain,
CNS,
CNS DRUGS,
DRUG,
drugs,
drugsinindia,
medicin in india,
MEDICINE,
NERV,
NERVOUS SYSTEM,
PARASYMPATHETIC,
spinal cord,
SYMPATHETIC
Location:
Kerala, India
Subscribe to:
Posts (Atom)