The document discusses diabetes mellitus, its types, causes, and management, focusing on the role of insulin and anti-diabetic medications like glibenclamide. It covers the physiological mechanisms of insulin, diabetes diagnosis criteria, potential complications, and the classes of oral anti-diabetic agents. Additionally, it highlights the importance of lifestyle management, including diet and exercise, in controlling blood sugar levels for those with diabetes.

1. GLIBENCLAMIDE ANTI-DIABETIC DRUG

2. DIABETES MELLITUS Diabetes Mellitus Is Due To A Disorder Of Carbohydrate, protein And Lipid Metabolism As A Result Of An Absolute Or Deficiency In Metabolically Active Insulin. IN OLDER DAYS Diabetes = Over Abundant Urine Or Melting of flesh in urine MELLITUS = Sweet As Honey

3. TYPES OF DIABETES MELLITUS Improper Working Of Pancreas Is Diabetes Mellitus. SO TYPES ARE DIABETES MELLITUS TYPE-I = IDDM DIABETES MELLITUS TYPE-II = NIDDM DIABETES TYPE-II a = NORMAL WEIGHT OR THIN DIABETES DIABETES TYPE-II b = OVER WEIGHT DIABETES ABOUT 80% OF TYPE 2 DIABETES ARE OVERWEIGHT

4. 60 g 18 cm Below liver Under stomach Acinar cells Islets of langerhans

5. Acinar cell makes bulk of pancreas and make digestive enzymes Islets of langerhans are only 1-2%of pancreas

6. They are responsible for the release of insulin and somastatin and glucagon. Beta cells are for insulin

7. INSULIN 51 amino acids in chain Orally rapidly destroyed Half-life 7-10 minutes C-peptide s s A-chain

8. INSULIN SECRETION 10 5 0 1 2 Insulin secretion FOOD INSULIN EFFECT 25-50 UNITS OR 1-2 mg OF INSULIN IS SECRETED EACH DAY

9. INSULIN EFFECTS SUGAR CONSUMING GLUCOSE TRANSPORT FUNCTIONTHROUGH THE CELL MEMEBRANE TO THE MUSCLE AND FAT CELLS GLYCOGEN FORMATION FROM GLUCOSE IN LIVER & MUSCLES FORMATION OF FATS FROMGLUCOSE INSULIN PREVENTS THE ACTION OF LIPOLYTIC HARMONES

10. SUGAR-PROVIDING Absorption of carbohydrates in the intestine Glycogenolysis = glucose molecules come from glycogen (|stored form of sugar in the body) GLUCONEOGENSIS = FROM PROTEIN IN THE LIVER. OR Synthesis Of Glucose From Another Fundamental Unit(aminoacids) INSULIN EFFECTS

11. TYPE-I DIABETES ABSOLUTE INSULIN DEFICIENCY DUE TO INABILITY OF BETSA CELLS TO RELEASE INSULIN

12. TYPE-II DIABETES RELATIVE INSULIN DEFICIENCY NUMBER OF INSULIN RECEPTORS COMPLEX IS TOO LOW

13. INSULIN RECEPTOR GLUCOSE MEMBRANE EFFECTS RECEPTOR SECOND MESSENGER ENZYME EFFECTS LYSOSOME INSULIN

14. DIAGNOSIS FASTING BLOOD SUGAR POST PRANDIAL GLUCOSE LEVEL GLUCOSE TOLERANCE TEST GLYCOSYLATED HEMOGLOBIN LEVELS URINE GLUCOSE LEVELS

15. REFERENCE VALUES CONDITION FBS RBS LEVEL AT 120 mg NORMAL BELOW 115 BELOW 200 BELOW 140 IMPAIRED 115-139 ABOVE 200 140-199 DM ABOVE 140 ABOVE 200 ABOVE 200

16. HbA1c The HbA1c is a blood test that measures your average blood sugar over two to three months. The term ‘HbA1c’ refers to changes in the haemoglobin molecule. Glucose can attach itself to the haemoglobin molecule. The difference is that once the glucose is attached, it remains there until the red cell dies. Red cells live for about three months. As blood glucose levels rise, more and more glucose becomes attached to the haemoglobin molecule. The HbA1c test measures how much glucose has become attached and therefore provides an indication of your average blood glucose for the past 6 weeks or so

17. HbA1c

18. COMPLICATIONS DUE TO INCREASE BLOOD GLUCOSE LEVELS RETINOPATHY NEUROPATHY NEPHEROPATHY MICRO ANGIOPATHY MACROANGIOPATHY

19. PILLARS FOR THE DIABETIC TREATMENT DIABETIC THERAPY PHYSICAL ACTIVITY DIET EUGLUCON MEDICAL TREAMENT DIABETIC INSTRUCTION + SELF-MONITORING

20. Diabetes is on of the most common metabolic diseases The prevalence of Diabetes is increasing all around the world especially in developing countries .

21. Management of Diabetes DIET EXERCISE OHA INSULIN

22. Oral anti-hyperglycemic agents Sulfonylureas: FIRST GENERATION Chlorpropamide-Glyburide-Acetohexamide-Tolbutamide-Tolazamide- SECOND GENERATION Glibenclamide-Glipizide-Glibornurid- Glimepride GLICLAZIDE * Biguanides: Phenformin Metformin * a-glycosidase inhibitors: Acarbose - Miglitol * Thiazolidendiones: Troglitazone Ciglitazone Pioglitazon englitazone * Meglitinide: Repaglinide

23. Biguanides (Metformin) Trade names: Glucophage, NEOPHAGE, NEODIPAR. Mode of action: reduces hepatic glucose production decreased intestinal absorption of glucose increases peripheral utilization of glucose in muscle & fat tissue decreased insulin requirements for glucose disposal

24. Biguanides (Metformin) Precautions: chronic renal or cardiac failure hepatic impairment elderly excessive alcohol intake Side effects: gastrointestinal disturbances metallic taste malabsorption of B12 Administer: with or after meals

25. Sulphonylurea Generic : Trade : Administer : Glipizide Minidiab before meals Gliclazide Diamicron with meals Glibenclamide Euglucon Before meals Tolbutamide Rastinon with meals

26. Sulphonylureas Mode of action: increase pancreatic insulin secretion may improve insulin sensitivity in peripheral tissue and decrease hepatic glucose output

27. Sulphonylureas Contra-indications : pregnancy, surgery, severe renal failure, type 1, hypersensitivity Precautions: renal impairment, hepatic impairment, elderly Side effects: hypoglycemia weight gain

28. Alpha Glucosidase Inhibitor (Acarbose) Trade name: Glucobay Mode of action: delays breakdown of CHO such as starch & sucrose Contra-indications: pregnancy renal impairment gastrointestinal disorders

29. Alpha Glucosidase Inhibitor (Acarbose) Precautions: high sucrose diet Side effects: gastrointestinal rash erythema Important considerations: take directly before or with the first few spoons of the meal

30. Repaglinide Trade Name: NovoNorm Mode of action: short acting oral hypoglycaemic agent stimulates pancreatic insulin release

31. Repaglinide Contra-indications: type 1 diabetes, pregnancy, lactation, children < 12 years Precautions: impaired renal or hepatic function Side effects: hypoglycaemia, gastrointestinal upset, raised Left's, blurred vision

32. Thiazolidinedione (Rezulin) Trade name: Rosiglitazone, Poiglitizone Mode of action: improves sensitivity to insulin in skeletal muscle and adipose tissue inhibits glucose release from the liver

33. Thiazolidinedione Contra-indications heart failure, moderate to severe hepatic impairment. Precautions oedema or heart failure anovulatory premenopausal women with insulin resistance as ovulation may resume (consider contraception.

34. Glucose Regulation Glucose Sources: Endogenous (liver) Diet GLUCOSE REGULATION IN BODY: LIVER PANCREAS KIDNEY ADIPOSE TISSUE GI TRACT

35. MODE OF ACTION OF EUGLUCON ATP dependent K+ channels VDCC Ca++ CHANNEL Ca++ ACTIVATED CHANNEL Ca++ RESTING CELL K+

36. MODE OF ACTION OF EUGLUCON ATP dependent K+ channels VDCC Ca++ CHANNEL Ca++ ACTIVATED CHANNEL Ca++ DEPOLARIZATION K+ INSULIN SECRETION CA++

37. MODE OF ACTION OF EUGLUCON ATP dependent K+ channels VDCC Ca++ CHANNEL Ca++ ACTIVATED CHANNEL Ca++ REPOLARIZATION K+ - +

38. EUGLUCON EUGLUCON IS AVAILBLE AS WHITE,OBLONG, SCORED, CONTAINING 5mg GLIBENCLAMIDE

39. EUGLUCON STIMULATE BETA-CELLS OF PANCREAS TO RELEASE INSULIN INCREASE SENSITIVITY OF THE PERIPHERAL TISSUE TO INSULIN MILD DIURESIS

40. EUGLUCON RAPIDLY ABSORBED MAX.BLOOD LEVEL WITHIN 1-4 HOURS BIOAVAILIBILITY 90-100 % PROTEIN BINDING 90 % VOLUME OF DISTRIBUTION 155ml/kg ELIMINATION HALF-LIFE BIPHASIC 2.1 HOURS & 10 HOURS

41. EUGLUCON EXECRETION 50% KIDNEY 50% FECES HIGHEST TISSUE CONCENTRATION IN LIVER NO TERTOGENEIC EFFECTS CONTERA INDICATIONS TYPE-1 DIABETES DIABETIC COMA KETO-ACIDOSIS SDVERE RENAL IMSUFFICENCY PREGANACY HYPERSENSITIVITY TO GLIBENCLAMIDE

42. EUGLUCON GLIBECLAMIDE EXCRETION THROUGH BILE RENAL FUNCTION 53% 47% NORMAL FUNCTION 79% 21% MODERATE IMPAIRMENT 94% 6% SEVERE IMPAIRMENT DEPENDING UPON THE DEGREE OF RENAL EXCRETION DISORDER,AN INCREASE EXCRETION IN THE BILE AND FECES OCCURS AS COMPENSATORY EFFECT

43. EUGLUCON ADVERSE REACTION NAUSEA AND EPIGASTRIC BLOATING ALLERGY SKIN REACTION ALLERGY CROSSS REACTION SULPHONAMIDES EFFECTS HAEMATOPOIETIC SYSTEM HAEMOLYTIC ANAMEIA CHOLESATITIC JAUNDICE HEPATITIS INDICATIONS NIDDM “(TYPE-II) MATURITY ONSET DIABETES, WNENEVER TREATMENT BY DIET ALONE PROVES INADIQUATE

44. EUGLUCON Dosage Administration Administration scheme Daily Dose To Be Taken ½ - 1 - 2 - 2 1

45. EUGLUCON INSULIN SECRETION IN RHYTHM WITH MEALS NO RISK OF ACCUMLATION DUE TO DUAL ROUTE OF EXCRETION. NORMALIZE TISSUE RESPONSE TO ENDDOGENOUS INSULIN. IMPROVES DISTURBED LIPID PROFILE. BETTER PATIENT COMPLIANCE. LOW INCIDENCE OF ADVERSE RECATIONS. RELIABLE LONG-THERAPY.

46. EUGLUCON POWERFUL MOBLIZATION OF THE DELAYED INSULIN SECRETION. PARTICULARLY GREAT SYNERGISTIC WITH GLUCOSE. RELEASE OF INSULIN WHEN NEEDED: AFTER EVERY MEAL. SMOOTH DAILY BLOOD SUGAR PROFILE. MOSTLY SINGLE DOSGE ADMINISTRATION. BREAKING THROUGH OF PERIPHERAL INSULIN RESISTANCE. REDUCTION OF PLATELET AGGREGATION. BETTER STABILIZATION. MORE DIABETICS CAN BE OPTIMALLY CONTROLLED. EXCELLENT TOLERANCE.

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