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Diabetes Mellitus - Medicine - ATOT
- 1. Diabetes Mellitus Dr. SalmanAhmad Ansari(MBBS) Kanachur Institute of Medical Sciences
- 2. Contents ● Definition ofDM ● Types of DM ● Causes ● Clinical features ● Diagnosis ● Treatment ● Complications
- 3. Diabetes Mellitus ● Definition:Metabolic disease in which there is hyperglycemia due to insulin deficiency or insulin resistance or both ● Most common endocrine disease ● Becoming more common due to sedentary lifestyle ● India and China: highest prevalence of diabetes
- 4. Normal fasting glucose levels <100mg/dl Pre-diabetes(impaired) fasting glucose levels 100-125 mg/dl Diabetes glucose levels: >125 mg/dl
- 5. Types of DM Type1 DM Type 2 DM
- 6. Other types ofdiabetes ● Gestational diabetes mellitus(GDM): in pregnancy ● Maturity-onset diabetes of the young(MODY) ● Latent autoimmune diabetes in adults(LADA)
- 7. Etiology and pathogenesisof Type 1 DM(T1DM) - 5-10% of all cases - Most common in childhood(<20 years of age) Etiology: - Autoimmune destruction of beta cells of pancreas - Absolute deficiency of insulin
- 8. Pathogenesis of Type1 DM - Autoimmune disease - Genetic risk factors: human leukocyte antigen HLA-DR3. HLA-DR4 - Environmental risk factors: viral infection - Phases of development: 1. Phase of normal glucose tolerance 2. Phase of impaired glucose tolerance 3. Phase of frank diabetes
- 9. Etiology and pathogenesisof T2DM Multiple factors 4 major factors: 1. Increasing age 2. Obesity 3. Ethnicity 4. Family history
- 10. Environmental risk factors: -Sedentary lifestyle - Dietary habits and associated obesity: over-eating, obesity and less exercise Genetic risk factors: more chances if parents are diabetic
- 12. Insulin resistance - Decreasedresponse of target tissues to stimulation by insulin - Due to genetic susceptibility and obesity
- 14. Clinical features ofDiabetes Mellitus Type 1 DM: - Age: usually before 30 years of age - Weight is normal to lean(wasted) - Classical triad of diabetes: sudden onset of - Polyuria(increased urination) - Polydipsia(increased thirst) - polyphagia(increased hunger) - Severe cases: diabetic ketoacidosis - Low plasma insulin level
- 15. Type 2 DM: -Age: usually above 40 years of age - Weight: obese - Sedentary lifestyle - Gradual onset of polyuria, polydipsia, weight loss - Lack of energy, blurring of vision - Severe cases: diabetic ketoacidosis - Insulin levels: normal to high
- 16. Investigations - RBS - FBS -PPBS - OGTT - HbA1C - Others: RFT, Fundoscopy
- 17. Diagnosis of DM Symptomsof diabetes plus RBS>200 mg/dL or FBS ≥125 mg/dl on 2 occasions or 2-hour plasma glucose ≥200 mg/dl during an oral glucose tolerance test (OGTT) or Glycated haemoglobin (HbA1c): ≥6.5%
- 18. Oral glucose tolerancetest(OGTT) Indication: not done routinely Done when: - Fasting glucose is in the impaired range(100-125 mg/dl) - Diagnosis of gestational DM - Uncertainty about diagnosis of diabetes
- 19. Preparation: - Patient shouldtake carbohydrates without restriction for 3 days or more before the test - OGTT is performed in the morning after patient has fasted overnight(at least 8 hours) - Patient should rest for half an hour before the test
- 20. Test: A fastingvenous sample of blood is taken to measure glucose level - Patient is given 75 g of anhydrous glucose dissolved in 300 ml of water over orally over 5 minutes - Venous sample of blood is taken 2 hours after giving glucose and glucose level is measured Result: Plasma glucose between 140 and 200 mg/dl 2 hours after oral glucose load is called Impaired Glucose Tolerance
- 21. Management of diabetesmellitus Diet and lifestyle(‘Medical Nutrition Therapy’) Medical therapy
- 22. Diet and lifestyle -Aim is to achieve good glycemic control, reduce hyperglycemia and avoid hypoglycemia, and reduce risk of diabetic complications - Dietary management is also called ‘Medical Nutrition Therapy’(MNT) - Regular pattern of meals and snacks - Aim for BMI of 22
- 23. - Calorie recommendation:36 kcal/kg for male and 34 for females - Protein requirement: at least 0.9 g/kg of body weight per day and it should be 15% of total calorie intake - Fat: 30% or less of total calories - it should be - Carbohydrates: 55% of total calorie intake
- 25. - Carbs withhigher fiber content(brown rice, oats) - Alcohol: best to avoid - 4 meals: breakfast, lunch, evening snack, dinner - Lunch and dinner should be heaviest
- 27. - Exercise: 30-60minutes of aerobic activity 3-4 times a week - Brisk walking, swimming, cycling
- 28. Medical therapy - Whenlifestyle and dietary measures fail to control blood glucose - Use of oral anti-diabetic drugs(hypoglycemic agents) and insulin
- 29. Oral antidiabetic drugs(previously called hypoglycaemic drugs): • Sulphonylureas • Biguanides • Meglitinide • Thiazolidinediones • ⍺-glucosidase inhibitors • Incretin-based therapy • Other drugs:
- 30. Sulfonylureas Mechanism of action:insulin secretagogues - they increase insulin secretion Example: - Glimepiride - glyburide Side-effects: ● Hypoglycemia ● Weight gain
- 31. Glinides Mechanism of action:act on ATP-sensitive potassium channel to increase insulin secretion. Examples: ● Nateglinide ● Repaglinide Side-effects: ● Hypoglycemia ● Weight gain
- 32. Biguanide Example: Metformin Mechanism ofaction: reduces hepatic glucose productio. Avoid in renal failure Side effects: ● Nausea, vomiting ● Diarrhoea initially ● weight loss ● Risk of lactic acidosis
- 33. Thiazolidinediones Mechanism of action:binds to PPAR-Ɣ receptor and reduces insulin resistance Example: ● Pioglitazone ● Rosiglitazone Side effects: ● Weight gain ● Fluid retention(edema)
- 34. ⍺-glucosidase inhibitors Mechanism ofaction: decreases absorption of carbohydrates in intestine Example: ● Acarbose ● Voglibose Side-effects: ● Abdominal cramps ● Bloating ● flatulence ● diarrhoea
- 35. Sodium-glucose cotransporter 2(SGLT2)inhibitors Mechanism of action: inhibit glucose absorption from renal tubules Examples: ● Canagliflozin ● Dapagliflozin Side effects: ● Thirst ● Urination ● Increased risk of UTI
- 36. Dipeptidyl peptidase 4(DPP4)inhibitors Mechanism of action: block action of DPP4 which acts on incretin and increase effects of incretin(it potentiates insulin effects) Examples: ● vildagliptin ● sitagliptin Weight neutral Side effects: ● Nausea, diarrhoea ● Headache ● Risk of pancreatitis
- 37. Treatment guidelines Lifestyle modification(exercise,diet, weight loss) ↓Follow up in 3 months - check HbA1C level If not controlled, start metformin ↓Follow up in 3 months - check HbA1C level If not controlled, add a 2nd anti-diabetic drug(e.g: sulfonylurea)(dual therapy) ↓Follow up in 3 months - check HbA1C level If not controlled, add 3rd drug to regimen(triple therapy) ↓Follow up in 3 months - check HbA1C level Start insulin
- 38. Insulin therapy Indications tostart insulin: - If oral antidiabetic therapy has not worked - If patient has HbA1C>9% Types of insulin(check next slide) Guidelines: - Start long acting insulin, 0.1 unit/kg - Check morning sugar, adjust dose accordingly - If not controlled, add a rapid acting insulin to the biggest meal of
- 39. Insulin(...continued) Types of insulin -Ultra short-acting(lispro, aspart, glulisine) - short-acting(regular, semi-lente) - intermediate-acting(NPH, lente) - Long-acting(detemir, glargine, degludec) Side-effects: ● Hypoglycemia ● lipodystrophy(changes in skin due to repeated s.c injections)
- 40. Complications of diabetes Acutecomplications Long-term complications
- 41. Acute complications ● Diabeticketoacidosis(DKA) ● Hyperosmolar hyperglycemic state ● Lactic acidosis ● Hypoglycemia
- 42. Long-term complications Vascular Non-vascular: infections,skin changes Microvascular: Diabetic retinopathy, cataract Diabetic nephropathy Diabetic neuropathy Diabetic foot Macrovascular: stroke, HTN
- 43. References: ● Archith Boloor,Ramadas Nayak - Prep Manual for Undergraduates ● K. George Mathews - Prep Manual Questions: [email protected] For notes, click here Or scan: For PPT, scan: