Diabetes Mellitus

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Diabetes Mellitus Management

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Diabetes Mellitus

  1. 1. Diabetes Mellitus
  2. 2. Glucose metabolism • Normal level: 3.5–8.0 mmol/L (63–144 mg/dL) • Liver absorbs/stores glucose in the postabsorptive state and releases it into the circulation between meals to match the rate of glucose utilization by peripheral tissues. • Liver combines 3-carbon molecules derived from breakdown of fat, muscle glycogen (lactate) and protein into the 6-carbon glucose molecule by the process of gluconeogenesis. • Insulin is involved in storage of glycogen in liver and muscle, and triglyceride in fat. • During meal: insulin is released from pancreas into the portal vein and facilitates glucose uptake by fat and muscle and suppresses glucose production by the liver. • Fasting state: insulin are low and modulates glucose production from the liver • Counter-regulatory hormones: glucagon, adrenaline, cortisol and GH: opposes insulin and cause production of glucose from the liver and less utilization of glucose in fat and muscle for a given plasma level of insulin.
  3. 3. Cause Type 1 diabetes mellitus: • due to an autoimmune destruction of the pancreatic β cells. • occurs in genetically susceptible individuals and is triggered by environmental antigens • Autoantibodies against insulin and islet cell antigens (e.g. glutamic acid decarboxylase) predate the onset of clinical disease by several years. • It is an association with other organ-specific autoimmune diseases (autoimmune thyroid disease, Addison’s disease and pernicious anaemia)
  4. 4. Cause Type 2 DM • genetic causes of type 2 DM include: >mutations of the insulin receptor > structural alterations of the insulin molecule • Environmental factors: central obesity: trigger DM in susceptible individuals • β-cell mass is reduced to 50% at time of DX • Hyperglycemia: result of reduced insulin secretion and peripheral insulin resistance
  5. 5. Clinical features Acute presentation: • Young pt: 2– 6week hx: thirst, polyuria and wt loss • Polyuria is due to osmotic diuresis, blood glucose exceed renal tubular reabsorptive capacity • Fluid and electrolyte losses stimulate thirst. • Wt loss is due to fluid depletion and breakdown of fat and muscle secondary to insulin deficiency. • Ketoacidosis: if early sx are not recognized and treated. Subacute presentation: • Older patients may present with the same symptoms, although less marked and extending over several months. • may also complain of lack of energy, visual problems and pruritus vulvae or balanitis due to Candida infection.
  6. 6. Diagnosis if any one of the following is present: • Casual plasma glucose ≥11.1 mmol/l • Fasting plasma glucose ≥7.0 mmol/l • 2-hour postprandial plasma glucose ≥11.1 mmol/l
  7. 7. Treatment Biguanide • Metformin is a biguanide • it reduces glucose production by the liver and sensitizes target tissues to insulin. • It is the first line treatment in patients who have not achieved optimal glucose control with diet alone, in overweight patients • It reduces cardiovascular risk in diabetics.
  8. 8. • Metformin: can be used in combination tx when single agent has failed to control DM Side-effects: • anorexia and diarrhoea • Lactic acidosis in pts with severe heart failure, liver disease or renal disease (serum creatinine > 150 μmol/L), in whom its use is contraindicated.
  9. 9. Sulphonylureas: promote insulin secretion. • Glibenclamide is best avoided in elderly people and in those with renal failure because of its relatively long duration of action (12–20 hours) and renal excretion. • Tolbutamide, which is shorter acting and metabolized by the liver, is a better choice in older pts • The most common side-effect of sulphonylureas is hypoglycaemia, which may be prolonged. • Meglitinides, e.g. repaglinide and nateglinide, are also insulin secretagogues. • They have a rapid onset of action and short duration of action and are administered shortly before each main meal.
  10. 10. Acarbose: inhibits intestinal α-glucosidases and impairs carbohydrate digestion and slows glucose absorption. • Postprandial glucose peaks are reduced. • Gastrointestinal side-effects, e.g. flatulence, bloating and diarrhoea, are common and limit the dose and acceptability of this treatment.
  11. 11. • Weight loss is associated with improved diabetic control and even remission of diabetes. • Orlistat is an intestinal lipase inhibitor and reduces the absorption of fat from the diet. • It promotes weight loss in patients under careful dietary supervision on a low fat diet. • Gastric banding and gastric bypass surgery should be offered to those with marked obesity unresponsive to 6 months intensive attempts at dieting and graded exercise.
  12. 12. main types of insulin: 1. Short-acting (soluble) insulins: • start working within 30–60 minutes andlast for 4–6 hours. • They are given 15–30 minutes before meals in patients on multiple dose regimens 2. Short-acting insulin analogues • human insulin analogues (insulin aspart, insulin lispro, insulin glulisine) have a faster onset and shorter duration of action than soluble insulin but overall do not improve diabetic control. • They have a reduced carry-over effect compared to soluble insulin and are used with the evening meal in patients who are prone to nocturnal hypoglycaemia.
  13. 13. 3. Longer-acting insulins. • Insulins premixed with retarding agents (either protamine or zinc) precipitate crystals of varying size according to the conditions employed • These insulins are intermediate (12–24 hours) or long acting (more than 24 hours). • The protamine insulins are also known as isophane or NPH insulins • zinc insulins as lente insulins • Insulin glargine is a structurally modified insulin that precipitates in tissues and is then slowly released from the injection site.
  14. 14. • Thank you google… • Harrisons • WHO guideline http://crisbertcualteros.page.tl

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