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Oral hypoglycemic agents

This document discusses oral hypoglycemic agents (OHAs), which are drugs taken orally to lower blood glucose levels in patients with diabetes. It describes two main types of diabetes and explains how OHAs work to increase insulin secretion, sensitivity, and decrease glucose absorption. The document classifies OHAs and discusses specific drug classes like sulfonylureas including first generation drugs like tolbutamide and second generation drugs like glipizide. It provides details on the mechanisms of action, pharmacokinetics, indications, contraindications and side effects of various OHAs.

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{ ORAL HYPOGLYCEMIC AGENTS ZAINUL KHAN ASSISTANT PROFESSOR AIPR, LUCKNOW
ORAL HYPOGLYCEMIC AGENTS Agents that are given orally to reduce the blood glucose levels in diabetic patients. • Diabetes mellitus type 1 is a disease caused by lack of insulin. Insulin must be used in type 1,which must be injected. • Diabetes mellitus type 2 is a disease of insulin resistance by cells due to several factors. HYPOGLYCEMIC AGENTS WORKS BY: Increasing the amount of insulin secreted by the pancreas. Increasing the sensitivity of target organs to insulin Decreasing the rate at which glucose is absorbed from the gastrointestinal tract. SELECTION OF ANTI DIABETIC DRUGS DEPENDS UP ON: • Nature of the diabetes • Age and situation of the person • Other factors
SYMPTOMS OF HYPERGLYCEMIA • Fatigue • Blurred vision • Weight loss • Fast heart beat • Poor wound heeling • Dry mouth • Dry or itchy skin • Sweating • Irritable • headache
CLASSIFICATION
ORAL HYPOGLYCEMIC DRUGS
SULFONYLUREAS: The drugs of this class is divided into two generations: First Generation: Second Generation: Tolbutamide Glyburide Chlorpropamide Glipizide Tolazamide Glimepiride MECHANISM OF ACTION: Stimulation of insulin from pancreas. Reduce hepatic glucose production. Increase peripheral insulin sensitivity. ADVERSE EFFECTS: Hypoglycemia Weight gain Skin reaction
TOLBUTAMIDE Tolbutamide is a first-generation potassium channel blocker,sulfonylurea oral hypoglycemic medication that acts by increasing the pancreatic insulin secretion. Mechanism of action: Binds to sulphonylureas receptors on beta cells Stimulates release of insulin from beta cells of pancreatic islets By inhibiting the ATP potassium channels on the beta cells which results in depolarization Resulting in calcium influx, and this kinase gets activated and release of insulin containing granules by exocytosis increases.
INDICATION DOSE INITIAL DOSE: 1 to 2 g orally once a day or in divided doses. MAINTENANCE DOSE: 0.25 to 3 g orally once a day or in divided doses. MAXIMUM DOSE: 3 g per day. Non-insulin dependent diabetes if diet alone is not Effective. Recommended when there is great danger of hypoglycemia Has a short duration of action due to its rapid metabolism, so is safe for use in older people.
PHARMACOKINETICS ABSORPTION: Get absorbed in 30 to 60 minutes but can be altered by increased pH. ONSET OF ACTION: It is within one hour & lasts for 6-12 Hrs. DURATION OF ACTION: Short HALF LIFE: 7 Hrs. POTENCY: Twice potent as the related second-generation agent Glipizide SIDE EFFECTS Allergic reactions like itching; red, swollen, blistered, or peeling skin with or without fever, wheezing, tightness in the chest or throat, trouble breathing or talking, unusual hoarseness, or swelling of the mouth, face, lips, tongue, or throat. Dark urine Dark urine Hypoglycemia
GLIPIZIDE Glipizide is an oral rapid- and short-acting anti- diabetic medication from the sulfonylurea class. It is classified as a second-generation sulfonylurea. MECHANISM OF ACTION: Insulin is a hormone secreted from the cells of pancreas. When released into the blood causes cells in the body to remove sugar (glucose) from the blood. It reduces the formation of glucose by the liver. It causes inhibition of hepatic glucose production and reduction in serum glucagon levels.
PHARMACOKINETICS : ABSORPTION: Readily absorbed from GI tract ONSET: 15–30 min DURATION: up to 24 h METABOLISM: Metabolized extensively in liver. ELIMINATION: Excreted mainly in urine with some excretion via bile in faeces. HALF LIFE: 3–5 h. DRUGS OF GLINIDES Repaglinide MOA: Stimulation of pancreatic insulin release. By closing ATP dependent B-cells. INDICATIONS: Type II diabetes mellitus Long term cardiovascular Renal effects CONTRAINDICATIONS: Diabetic ketoacidosis Co-administration with gemfibrozil Known hypersensitivity SIDE EFFECTS: Hypoglycemia Rhinitis Cardiac Ischemia Angina
Nateglinide MECHANISM OF ACTION: • Nateglinide has no impact on insulin discharge without glucose or maybe, it potentiates the impact of extracellular glucose on ATP sensitive potassium channel and also has little impact on insulin levels. • Impacts of nateglinide are most elevated at intermediate glucose level (3 to 10 mmo1/L) and it does not expand the insulin discharge effectively stimulated by high glucose fixations. • (It should be greater than 15 mmo1/L) • Nateglinide seems to be specific for pancreatic B-cells and does not seems to be influence skeletal or cardiovascular muscle or thyroid tissue. PHARMACOKINETICS • ABSORPTION: Nateglinide is rapidly absorbed in the intestine. • ONSET: After 30 min of administration. • DURATION: 1 hour • METABOLISM: Nateglinide is extensively metabolised, primarily by cytochrome P450 2C9. • ELIMINATION: eliminated By Urine (83%) and feces (10%). • HALF LIFE: 1.5 hours
CONTRAINDICATIONS Nateglinide is contraindicated in patients who: Hypersensitivity. Type 1 (namely insulin-dependent) diabetes mellitus. SIDE EFFECT: SERIOUS SIDE EFFECTS: • Seizure (convulsions) • Jaundice (yellowing of the skin or eyes) LESS SERIOUS SIDE EFFECTS: • Runny or stuffy nose, sneezing, cough,cold or • flu symptoms • Diarrheal, nausea • Back pain • Dizziness or • Joint pain or stiffness
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