Showing posts with label drugs. Show all posts
Showing posts with label drugs. Show all posts
Monday, July 1, 2013
DIABETIC KETO ACIDOSIS
Labels:
amino acid,
Blood Vessels,
DIABETES,
Diabetic ketoacidosis,
drugs,
fat cell,
fatty acid,
gluconeogenesis,
glucose,
glycerol,
glycogenolysis,
indian medicine,
ketoacidocis,
liver,
MEDICINE,
muscle cell
Location:
Kerala, India
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
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:
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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,
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MEDICINE,
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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.
Labels:
9 week pregnancy,
9weeks,
baby,
drugs,
drugsinindia,
drugsinindia.com,
pregnancy,
pregnancy care
Location:
Kerala, India
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
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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.
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Monday, May 20, 2013
ENALAPRIL
Enalapril (Envas) is an angiotensin converting enzyme (ACE) inhibitor used in the treatment of hypertension and some types of chronic heart failure. ACE converts the peptide hormone angiotensin I to angiotensin II. One of the actions of angiotensin II is the vasoconstriction of blood vessels resulting in an increase in blood pressure. ACE inhibitors such as enalapril prevent this effect. Enalapril has been shown to lower the death rate in systolic heart failure. Enalapril was the first member of the group known as the dicarboxylate-containing ACE inhibitors.
Enalapril is an ACE inhibitor. ACE stands for angiotensin converting enzyme.
Enalapril is used to treat high blood pressure (hypertension) and congestive heart failure.
Enalapril is also used to treat a disorder of the ventricles (the lower chambers of the heart that allow blood to flow out of the heart). This disorder can decrease the heart's ability to pump blood to the bod
chemically described as (S)-1-[N-[1-(ethoxycarbonyl)-3-phenylpropyl]-L-alanyl]-L-proline, (Z)-2-butenedioate salt (1:1). Its empirical formula is C20H28N2O5•C4H4O4, and its structural formula is:

Enalapril Dosing Information
Usual Adult Dose for Diabetic Nephropathy:
Initial dose (oral): 5 mg orally once a day.
Maintenance dose (oral): 10 to 40 mg orally per day in 1 to 2 divided doses.
Intravenous: 1.25 to 5 mg every 6 hours.
Usual Adult Dose for Hypertension:
Initial dose (oral): 5 mg orally once a day.
Maintenance dose (oral): 10 to 40 mg orally per day in 1 to 2 divided doses.
Intravenous: 1.25 to 5 mg every 6 hours.
Usual Adult Dose for Hypertensive Emergency:
Initial dose (oral): 5 mg orally once a day.
Maintenance dose (oral): 10 to 40 mg orally per day in 1 to 2 divided doses.
Intravenous: 1.25 to 5 mg every 6 hours.
Usual Adult Dose for Congestive Heart Failure:
Initial dose (oral): 2.5 mg orally once a day.
Maintenance dose (oral): 2.5 to 20 mg orally twice a day.
Doses should be titrated upward, as tolerated, over a period of a few days or weeks.
The maximum daily dose is 40 mg in divided doses.
Intravenous: 1.25 to 5 mg every 6 hours.
Usual Adult Dose for Left Ventricular Dysfunction:
Initial dose (oral): 2.5 mg orally twice a day.
Maintenance dose (oral): 20 mg orally in divided doses.
If possible, the dose of any concomitant diuretic should be reduced which may diminish the likelihood of hypotension.
Intravenous: 1.25 to 5 mg every 6 hours.
Usual Pediatric Dose for Hypertension:
Hypertension:
Oral:
Children 1 month to 17 years: Initial: 0.08 mg/kg/day (up to 5 mg) in 1 to 2 divided doses. Adjust dosage based on patient response.
Doses greater than 0.58 mg/kg (40 mg) have not been evaluated in pediatric patients
IMPORTANT INFORMATION
Do not use enalapril if you are pregnant. Stop using and tell your doctor right away if you become pregnant.
You should not use enalapril if you have ever had angioedema.
If you have diabetes or kidney disease, you may not be able to take enalapril if you are taking medication that contains aliskiren. Tell your doctor about all medicines you use.
Enalapril can cause kidney problems. Call your doctor at once if you have swelling, rapid weight gain, little or no urinating, or if you feel short of breath.
Enalapril can affect your heart or your electrolyte levels. Call your doctor if you have chest pain, pounding heartbeats or fluttering in your chest, a slow heart rate or weak pulse, a tingly feeling, muscle weakness, or muscle tightness or contraction.
Before taking enalapril
You should not use enalapril if you have ever had angioedema, or if you are allergic to enalapril or to any other ACE inhibitor (benazepril, captopril, fosinopril, lisinopril, moexipril, perindopril, quinapril, ramipril, trandolapril).
To make sure enalapril is safe for you, tell your doctor if you have:
kidney disease (or if you are on dialysis);
liver disease;
heart disease or congestive heart failure (unless you are taking enalapril for this condition);
diabetes; or
a history of blood clot or stroke (including "mini-stroke").
FDA pregnancy category D. Do not use enalapril if you are pregnant. Stop using this medication and tell your doctor right away if you become pregnant. Enalapril can cause injury or death to the unborn baby if you take the medicine during your second or third trimester. Use effective birth control while taking this medication.
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Wednesday, May 15, 2013
HOME REMEDIES FOR HAIR FALL TREATMENT 3
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Tuesday, May 14, 2013
BASIC SKIN CARE TIPS
Skin of our body can be considered as important as any other vital organ in the human system. The Skin and muscles provide an important shelter to the inner organs which are delicate and need to be protected. Apart from its utility in the body system, skin contributes to a large extent to the outer appearance and the beauty of an individual. Who doesn't want a clean and glowing skin that magnifies the a beauty or attractiveness of a person. A healthy and glowing skin is also the indication of the healthy state of the body. Mentioned here in the article, are a few basic skin care tips that should be kept in mind to have healthy skin and a beautiful appearance.
Regular washing of the skin
This is the very basic and logically obvious method to maintain a good skin that is to keep it clean. You should wash your skin on a daily basis as part of your bath or otherwise with suitable cleaning agents.
It is not necessary always to use expensive and fancy skin care products to be used daily, rather the experts advice that a mild and scentless cleansing agent must be used on a daily basis which will get you rid of the dirt, germs and dead skin accumulated over it. The cleansing soap is preferred to have moisturizing qualities as well.
Deodorant body soaps and antibacterial soaps should not be used for a regular use.
Moisturizing the skin
With our day to day activities and exposure to pollution, Sun and harsh weather conditions like rain etc , our skin tends to lose the much needed miniaturization needed to keep it healthy and breathing.
It is easy to moisturize your skin and is as simple as rubbing the moisturizer after you take bath to the body. Again, there is not need to go after very costly products and you can chose a average priced but good quality solution available in the market for daily use.
If you have oily skin and have concerns due to the same then you can try using the products that don't cause clogging of the pores , they are known as non comedogenic products.
Use Sunscreen for skin protection
We all know the ill effects that the Sun's UV rays can have on our skin. These are the harmful rays that can cause major skin diseases as grave as skin cancer. It is recommended by the dermatologists to use Sun screens to effectively protect the skin against these hazardous effects.
Dermatologists suggest that whatever be the weather condition, be it rainy, sunny or even during snowfall we should ensure the use sun protection. The UV rays are present in abundance in the environment and are often reflected by these agents on to our skin. This exposure to UV rays for a long time may cause skin diseases like wrinkles, moles and discoloration.
Use Skin care products of a trusted brand which provides UVA and UVB level of protection and is SPF 15 or more.
Skin Care for Acne Prone skin
If you are prone to acne breakouts, then you need to handle the cleansing differently and with greater care.
Use cleanser products specially formulated for acne affected skin conditions. These products generally have an agent named as benzyl peroxide which is helpful in cleaning the soars caused due to acne.
You have to be gentle in cleaning your skin as being rough may cause burst those acne breakouts aggravating the problem. Use only non-comedogenic moisturizers.
SKIN CARE TIPS 1
Among the things you will find out are:
1. What causes dry skin.
2. How to prevent dry skin.
3. How to manage dry skin.
You will be given important "Skin Tips," and you will learn how to care for your skin from the inside out. You will learn about Stevens Skin Softener Cream and how it can help you manage your dry skin problem, and you will find out different ways you can qualify to get your Stevens Cream "FREE!".
But first, here are many Skin Care Tips from A to Z
I trust you will find them helpful...
Aging Skin
The thickened skin texture associated with middle age is caused by cellular build up. It responds very well to
mild, abrasive daily cleansing with beauty grains such
as finely ground corn meal, ground sun flowers or almonds. Massage gently to cleanse and stimulate.
Beautiful Skin
To make or keep your skin beautiful, it's best to work from the inside.
Eating the right kind of food can do you more good than any medicine, and go a long way in helping your body's own healing forces. Eat a balanced diet that includes raw foods, plenty of yellow and orange vegetables (they contain beta carotene - a precursor to vitamin A). Foods high in sulfur such as garlic, onions, asparagus and eggs. Include fruits, seeds, grains and nuts.
Dry Skin
Blend together one ounce safflower oil, one ounce
avocado oil and two ounces of sesame oil. Apply this to your dry skin areas.
Facial Mask
An excellent facial mask can be made with stewed and mashed apricots. Apply to your freshly cleaned face and leave for 20 minutes or longer. Rinse away with warm water, and blot dry. One application will help sallow, dead skin tones, but applying this 3 or 4 times a week will do wonders.
Tea Tree Oil for Fungal Infection
If you suffer from fungal infections of the nail, the most effective natural anti fungal is tea tree oil. Apply to the nails and surrounding skin twice daily, in the morning and at bedtime
Using Honey Treatments
Honey applied under a dry dressing every two or thee days promotes rapid healing of ulcers and burns.
Itchy Skin
Try the following. A compress made with skim milk or powdered milk or soak the affected area in a colloidal bath made with oatmeal, corn- starch or baking soda.
Homemade Skin Lotion
The following body lotion is easy to make, and can be used after bathing. Mix one teaspoonful of honey, one teaspoon of lemon juice and a half cup of water. Massage into your skin after bathing.
Mayonnaise for Dry Facial
If you have a tendency towards dry facial skin, a gentle daily massage with mayonnaise will do wonders. You can use lemon juice, egg and safflower or other such oil to make your own dry skin lotion.
Oily Skin
Here is a cleansing stimulating facial treatment that is very helpful for those with oily skin. Mash together the pulp of one garden ripe tomato and enough fuller's earth (should find it at most pharmacies) to make a smooth paste. Rub it into your skin and leave it on until it dries completely (note: do not apply to eye area). Rinse with warm water, then splash your face with cold water. Blot dry.
Treating Large Pores
If you have large pores that resemble little holes on your skin, the following steps may be helpful. Stop using commercial products on your skin. Instead, use homemade skin cleansers. Splash warm water onto your face and pour half a handful of stone-ground cornmeal into your wet palm. Massage the moistened meal into your entire face area, adding water as needed. Another homemade cleanser can be made by adding a few drops of lemon or lime juice or apple cider vinegar to milk (use powdered skim milk if your skin is oily).
Soak yarrow (check health food stores or botanical supply stores for this herb) in water overnight, and apply this astringent several times a day - less frequently if your skin is dry.
Avoid all creams. Use an unsaturated vegetable oil if you need to (e.g. vitamin E oil).
Rashes
Whether it's diaper rash, chicken pox, measles, insect bites or hives, corn starch can provide relief. For measles and chicken pox, bathe in a tub of water to which a large handful of cornstarch has been added. For the other rashes rub the cornstarch on as a powder.
Softening your skin
Avocado oil used regularly is an excellent skin softener. It is rich in vitamins and minerals, especially the skin vitamins A, C and E.
Teenagers
Many teenagers have to deal with embarrassing skin problems. taking supplements of zinc and Vitamin A will go a long way in helping them relieve these problems.
Leg Ulcers
Leg ulcers are more likely to develop in persons with poor circulation, thrombophlebitis and/or varicose veins. To speed healing, apply vitamin E oil to the sore and bandage it lightly with a sterile gauze pad. Change the bandage daily until the sore is healed.
Vitamins and Your Skin
Vitamins are essential to the health of your skin, especially vitamins A, B, C and E. Vitamin E is especially helpful to improve your complexion when applied externally.
Winter Care
The air inside your house can get very dry in the winter. This will play a major part in aggravating your dry skin condition. To add humidity to the dry air in your house, put a little extra water in the kettle when you're boiling water. Leave the kettle on the burner as it cools. It will continue to steam for 10 to 15 minutes, making your life a whole lot more comfortable.
Zinc for Acne
Not enough zinc, caused by a diet high in refined carbohydrates may be the chief cause of acne. Zinc is necessary for processing carbohydrates, but it is removed when cane is refined into white sugar, and wheat is refined into white flour. Eat more foods rich in zinc, including soybeans, whole grains, sunflower seeds, and a small amount of raw nuts daily. Zinc also has antibacterial activity, and is a necessary element in the oil-producing glands of the skin.
Sunday, May 12, 2013
DRY SKIN SOLUTIONS
Avoid These Dry Skin Mistakes Today
Your Skin is the largest organ "on" your body. In fact, that is the first thing people notice about you. That is why, from time immemorial, the care of the skin has been the preoccupation of many.
Your skin is 70% water, and many skin problems are associated with dry skin. That is why many skin preparations are made, using the concept of preventing moisture from leaving the skin. They therefore use occlusive agents, that is ingredients that clog your pores, thus theoretically sealing moisture in.
There is a problem with this approach however, and I'll explain shortly, but first...
Let's Learn About Your Skin. How it is Made, and How it Actually Works.
Your skin consists of two distinct layers: The outer layer, the epidermis, consists of dry mature cells and forms the protective layer. The inner layer or dermis consists of collagen. This gives the skin strength and flexibility. The dermis also contains the sweat glands, nerves, blood capillaries hair follicles and sebaceous glands.
Your skin is an important, vital, living, dynamic organ without which you could not survive. Among its many functions, it regulates your body temperature, and through its more than 2,000,000 sweat pores, is an organ of excretion. Your skin should also be allowed to breathe.
With this background, it's easy to understand why the following ingredients do NOT belong on your skin:
Mineral Oil A mixture of refined liquid hydrocarbons derived from petroleum. Mineral oil is the stabilizing ingredient of many skin care products. Mineral oil forms an occlusive film on your skin, blocking your pores, and interfering with normal skin respiration. It may, therefore, not only harm your skin but be a contributing cause of blemishes.
Petroleum
(Petrolatum) Petroleum products such as Vaseline, etc., do not penetrate your skin, but sit on the surface blocking natural respiration, excretion, and absorption of other nutrients. It is also an occlusive agent, and should be avoided.
Lanolin Derived from sheep wool, Lanolin is a common lubricating ingredient in many cosmetics and creams. In addition t being occlusive, it has been proven to cause allergic reactions in skin of sensitive people.
Solvent Solvent alcohols in the form of propyl of isopropyp are drying to your skin
Collagen This animal product is added to cosmetics as a moisturizing agent. The molecules are too large to penetrate your skin. They therefore clog your pores, and in some cases cause allergic reactions.
Here's an interesting exercise. Check your skin care products now and see how many of them have one or more or the above offending products. You may be surprised.
Other ingredients to avoid are:
Artificial Colors Known to cause allergic reactions in some people.
ARTIFICIAL FRAGRANCES Known to create allergic skin reactions and photosensitivity in some people.
The jury is still out on such chemicals as Retin A, Retinol, and Alpha Hydroxy Acids. A prudent approach is to avoid their use, especially now that something better safer, and more in tune with your skin's normal physiology, is available.
Stevens Skin Softener Cream...a New Approach to Skin Care
Rather than using occlusive agents that clog your pores to prevent moisture from leaving your skin, Stevens Skin Softener Cream is designed to put moisture into your skin.
For this it uses Jojoba oil, Apricot kernel oil, Almond oil, Purcelin oil, Avocado oil and Squalene. Not only do these natural oils take moisture deep into your skin, but Jojoba, Avocado and Almond oils have the same consistency and molecular structure as sebum, your skin's own natural lubricating oil. They therefore also serve to lubricate your skin.
Why is this so important to you?
You see, your skin is 70% water. Sebum, your skin's own natural lubricating oil, functions to lubricate your skin and prevent it from drying out. This natural protection breaks down with many skin problems, and also as you get older. Women especially, experience an estimated 32% reduction per decade in sebum production, after age 20. Do you understand now why everything you have tried for your dry skin has not worked, and why Stevens Skin Softener Cream will? Try It!!!
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EATING DISORDERS
Eating disorders affect millions of teens and young adults around the world. They're most common in cultures that focus on weight and body image and can affect people of all races and ethnic backgrounds. Extreme focus on appearance often leads to poor body image and unhealthy eating behaviors, which can turn into eating disorders such as anorexia nervosa, bulimia, binge eating disorder, or a category called eating disorders not otherwise specified (ED-NOS). Eating disorders have serious health consequences and require treatment. Recovery is likely with the help of specially trained health care providers and a supportive family. We hope this guide will help you understand eating disorders, the different kinds of treatment, and the recovery process.
What are eating disorders?
Eating disorders are complicated medical and psychological conditions that affect a person's physical and emotional health and involve intense emotions and behaviors around food. Eating disorders are very dangerous illnesses and can lead to permanent consequences if left untreated.
The four types of eating disorders are anorexia nervosa, bulimia nervosa, binge eating disorder, and eating disorder not otherwise specified (EDNOS).
Anorexia (pronounced: an-or -rex-e-ah) involves food restriction (limiting or not having certain foods or food groups). People with anorexia drastically limit their food intake and have an intense fear of gaining weight, even though they may be underweight or they are losing a lot of weight
Bulimia (pronounced: bull-e-me-ah) involves cycles of binge eating followed by a purging behavior. People with bulimia will eat an unusually large amount of food in a short period of time and then purge by vomiting, using laxatives, enemas, diuretics, or by exercising excessively as a way to avoid gaining weight.
Binge eating disorder involves eating an unusually large amount of food in a short period of time and feeling a loss of control during this episode. Binge eaters do not purge afterwards, but often feel a lot of shame or guilt about their binge eating.
Eating disorder not otherwise specified (EDNOS) involves some combination of symptoms of the other eating disorders such as an intense fear of weight gain and a preoccupation with food (thinking about food or having food related thoughts most of the day). Many people with EDNOS have symptoms of the other eating disorders, but may not meet the exact criteria, and therefore are diagnosed with EDNOS.
Disordered eating is a term used to describe when someone doesn't have all the symptoms of an eating disorder, but their eating patterns and behaviors put them at risk for developing an eating disorder. For example, anorexia can start when dieting becomes too extreme; binge eating disorder or bulimia can start because dieting often restricts the amount and types of food, so when a diet is broken, it can lead to uncontrollable eating and loss of control around food.
Prevalence rates, or how often eating disorders occur varies with each disorder. While anorexia nervosa and bulimia nervosa are fairly rare, binge eating disorder and EDNOS are slightly more common. A study done in 2011 estimated that 0.3% of Americans between the ages of 13-18 suffer from anorexia, 0.9% from bulimia, and 1.6% from binge eating disorder (Swanson et al. 2011). Estimates of EDNOS differ from study to study, but may be as high as 15%.
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