Diabetic Oral Meds-Treatment of diabetes thoroughly covers the right diet, exercise regularly, and then continued with the drugs being taken, or a shot of insulin. In type 1 diabetes require insulin injections, absolutely every day; whereas in type 2 diabetes, sometimes with diet and exercise alone can be normal blood glucose, but generally needs to drink an oral or diabetes tablets, in some cases of type 2 diabetes require insulin injections, or even need to the combination of insulin injections and tablets.
In a country that was already advanced, well thought out efforts of a pancreatic graft to replace the pancreas is damaged, it’s just that the results so far have not been satisfactory. Technological advances today have found a new type of tablet many drugs with encouraging results, as well as an assortment of insulin has been marketed. So besides the numbers increased diabetes incidence, advances in the treatment of diabetes also continues to gallop to anticipate.
In this blog, I will discuss various classes of Oral drugs Anti Diabetes (OAD) or Oral Hypoglycemic Agents (OHA). Up to now know there are five kinds of OAD marketed, every kind of OAD had the different chemical composition and how to lower glucose. Nothing stimulates the pancreas to produce more insulin, others work reduces the resistance to insulin, while others inhibit carbohydrate absorption from the intestine. Type 2 diabetes patients, at the beginning of treatment, usually wear one type of OAD, but more effective for lowering blood glucose, sometimes it takes more than one kind of OAD.
A. The Sulfonylurea
Known to two generations of sulfonylureas, 1st generation consists of tolazamide, asetoheksimid, tolbutamide, and chlorpropamide. The second generation potential hypoglycemic greater among others are glyburide, gliclazide, and glipizide glimepiride.
Mechanism of action
Often called insulin secretagogues, insulin secretion stimulates work of granule-granule cells of Langerhans pancreas beta. Rangsangannya through its interaction with ATP-sensitive K Channels in the membrane of the cells which give rise to β depolarisasi membrane and this State will open the Canal Ca. With the opening of the Canal Ca Ca ions then will go into the cells of β, stimulates granule that contains insulin and insulin secretions will occur with an amount equivalent to the C-peptides. In addition, the sulfonylurea may reduce insulin in hepar klirens.
In the long-term use or large doses can cause hypoglycemia.
The absorption digest is quite effective. Food and State of hyperglycemia can reduce absorbs because it will be more effective when taken 30 minutes before a meal. In the plasma protein-90% bound to plasma albumin especially. This ties the most minor to the greatest and chlorpropamide to glyburide.
Asetoheksamid half of the time is a short but active metabolite, 1-time hidroksiheksamid its beak is longer, approximately 4-5, same as tolazamide and tolbutamide. These preparations should be given in divided doses. About 10% of a metabolite of excretion via the bile and out with feces.
Chlorpropamide in the blood bound to albumin, the beak length, 24-48 hours. The effect is still visible a few days after the medicine is stopped. According to in hepar incomplete, 20% in excretion intact in urine.
Began to work fast, tolbutamide beak about 4-7 hours. 96% of the blood bound to plasma proteins and tolbutamide in hepar converted into karboksitolbutamid. Ekskresinya through the kidneys. 1
Tolazamide absorption more slowly than others. The effect in blood glucose is not yet real for a few hours after the drug is given. Halftime about 7 hours.
Sulfonylurea generation II are generally the potential hipoglikemik 100 x larger than generation i. Despite the short period of its beak, that is 3-5, hipoglikemik effect lasting 12-24 hour. Enough is given once daily.
Glipizide, complete absorption, the 3-4 half an hour. 98% of blood plasma protein bound, its potential 100 x more powerful than tolbutamide, but the effect is similar to a maximum of hypoglycemic sulfonylurea on another. According to in hepar become inactive metabolites, 10% in excretion through the kidney intact.
Glyburide (glibenclamide), the potential is greater than 200 x tolbutamide, the half-life of about 4 hours. According to in hepar. On the single dosing only 25% metabolite in excretion through urine, the remainder through bile. Failure can occur on the use of primary and secondary, with the entire failure of roughly 21% for 1 ½ years.
Because all sulfonylurea metabolized in hepar and in excretion through the kidneys, this material should not be given to patients impaired kidney function or hepar.
The incidence of side effects generation I is 4% and lower to generation II. Hypoglycemia can arise up to the comma. This reaction is more common in elderly patients with impaired renal function and hepar, especially those that use the material with a long working period.
Other side effects i.e. nausea, vomiting, diarrhea, symptoms of hematologic, CNS, eyes, etc. The disorder can be reduced digest channels by reducing the dose, swallowed the drug along with food or medicine divides into some doses. Symptoms of CNS form of vertigo, confused, ataxia, etc. Hematologic symptoms like leucopenia, agranulocytosis. Other side effects i.e. obstructive jaundice, hypothyroidism, which is temporary and is more often caused by chlorpropamide
The tendency of hypoglycemia in the elderly caused by the mechanism of compensation is reduced and food intake is likely to be less. In addition, Hypoglycemia is not recognizable in the elderly due to arise slowly without any sign of acute brain dysfunction can lead to a coma. The decrease in the speed of the excretion of chlorpropamide may be improved hypoglycemia.
An indication of the
In General, good results were obtained in patients diabetes began to arise at the age of 40 years old. The failure of therapy with one of derivate sulfonylurea may be caused by changes in drug pharmacokinetics, for example, the destruction of a drug that is too large.
During therapy, physical examination and laboratory should be conducted on a regular basis.
Drugs that can increase the use of sulfonylurea when hypoglycemia ririko is insulin, alcohol, phenformin, chloramphenicol, anabolic steroids, and fenfluramine clofibrate.
Propanolol and other β blockers inhibit the reaction of flutter, sweating and tremor on hypoglycemia by various reasons so that a State of hypoglycemia are becoming more excellent without being noticed. Sulfonylurea particularly chlorpropamide can lower tolerance of alcohol. This is shown particularly with redness on the face and neck, similar to disulfiram reaction.