DIABETES MELLITUS.pptxschoolofclinicalsc

Detailed explanation about Diabetes mellitus

1. DIABETES MELLITUS BY: DR.K.S.K JUSU DEPARTMENT OF INTERNAL MEDICINE MAKENI SCHOOL OF CLINICAL SCIENCES

2. ANATOMY The adult pancreas is entirely retroperitoneal organ that is 12 to 15cm long and grayish-pink in color. Has head, neck, body and tail. Located in epigastric and L hypochondrium and lies across the L1-L3 vertebrae. .

3. ANATOMY Has two ductal system-Duct of Wirsung, main duct and Duct of Santorini, minor duct. The are of considerable interest in the causation of pancreatic dzs. BLOOD SUPPLY; Neck, body and tail-chiefly from the splenic artery and head supply by S and I pancreatico-duodenal arteries. Numerous small veins drain into splenic vein and head via pancreatico-duodenal vein into SMV .

4. CONT… Lymphatic drainage; Head and R side of the body is into pancreatico-duodenal lymph nodes into sub-pyloric nodes. Tail and L side of the body drains into splenic hilar glands. Nerve supply; PS supply is from the coeliac branch of the P vagus and S supply from the 3 splenic nerves.

5. PHYSIOLOGY The pancreas is both an exocrine and endocrine organ and its hormone production is centered on the Islets of Langerhans. At least 4 different types of secretory cells have been identified in the Islets; Β eta cells 60-80% Islets cells hormonal contents-Insulin Alpha cells 15-20% “ “ “ “ -Glucagon Delta cells 5-10% “ “ “ “ -Somatostatin

6. EXOCRINE FXN Secretes pancreatic juice, colorless with a pH =8.0-8.8 that helps in digestion. Also secretes proteolytic enzymes as trypsinogen and chymotrypsinogen by intestinal enteropeptidase. The hydrolyze proteins to peptones and peptides. Pancreatic lipase hydrolyses fat producing glycerol and FAs aided by bile salts. Pancreatic amylase splits CHO into maltose and other disaccharides.

7. ENDOCRINE FXN Beta cells-insulin; Promotes transfer of glc across cell membranes Plays a major role in conversion of glc to glycogen in the liver Alpha cells-Glucagon- enhances liver glycogenolysis and thus produces systemic hyperglycemia. Delta cells-Somatostatin; Inhibits pancreatic exocrine and endocrine secretions and gastric secretion and motility Also inhibits secretions of VIP, secretin and motilin

8. PANCREATIC TUMORS Insulinoma-Beta cell tumor; Most common Tumor produce insulin Hypoglycemia, sweating, hunger, confusion, insulin coma Labs-elevated insulin and C-peptide TX-Glc Factitious hypoglycemia-Patients inject themselves with insulin either to lose wt or somebody trying to get out of work, most often nurses. Here there is decrease C-peptide.

9. CONT….

10. DEFINITION OF DM DM is a disorder of metabolism of CHO, protein, and fat due to absolute or relative deficiency of insulin secretion and with varying degrees of insulin resistance. The metabolic disorder results in long term dz specific microangiopathy( nephropathy, retinopathy, neuropathy) and aggravation of macroangiopathy.

11. DEFINITION A syndrome of chronic hyperglycaemia with other metabolic abnormalities together with micro and macro-vascular complications.

12. What is wrong with diabetes Insulin deficiency Insulin resistance Hyperglycaemia

13. TYPES OF DM . TYPES OF DM Type 1 DM Type 2 DM Gestational DM Impaired fasting glycaemia Impaired glc tolerance Secondary DM

14. Criteria of diagnosis FBS > 125. PP > 200 OGTT. normal: FBS <100 PP <140

15. T1DM Usually in young age Characterized by absolute insulin deficiency. Increased catabolism and liability to ketosis. Stormy presentation. must be treated with insulin.

16. Pathophysiology of T1DM Possible contributing factors: Autoimmune disease. HLA typing Viruses chemicals

17. Pathophysiology of T1DM Absence of insulin secretion Failure to use glucose as a fuel Hyperglycaemia & using fat Ketosis

18. T2DM Usually in older age. Relative insulin deficiency. Increased insulin resistance. Can be treated with OHA or insulin. Slow onset, less likely to develop ketosis. May present with complications.

19. Pathophysiology of T2DM Insulin resistance hyperinsulinaemia Relative hypoinsulinaemia Hyperglycaemia, dyslipidaemia, atherosclerosis, HTN

20. MODY A special type of diabetes similar to type 2 diabetes but develop in young age groups. Increased prevalence worldwide. Associated with increased childhood obesity. Maturity onset diabetes of the youth

21. GDM Diabetes discovered for the first time during pregnancy. Every pregnant lady should be screened. Usually disappears after labor. Increased risk to develop T2DM later in life. Gestational diabetes mellitus

22. Diagnosis How to diagnose diabetes: Signs and symptoms Blood glucose test OGTT HbA1c

23. Current Criteria for the Diagnosis of Diabetes Most people are diagnosed with diabetes when they are suspected to have symptoms of polyuria, polydypsia, fatigue, loss of weight. This is confirmed by fasting or PP blood glucose. In case of doubt OGTT may be done. Urine testing should not be used in diagnosis.

24. Diagnosis Peers and medical ‘advisors’ should be aware of the following: T1DM & T2DM are two distinct diseases. T1DM is stormy at presentation, delay in diagnosis can be disastrous. Among the presentations of T1DM could be some non-specific symptoms like vomiting, abdominal pain….

25. Diagnosis T2DM may present with late symptoms, like numbness, disturbed vision, generalized oedema. Patients with hypertension, dyslipidaemia, MI and family history of diabetes are very likely to develop T2DM.

26. WHO criteria for the diagnosis of diabetes Symptoms of diabetes plus casual venous plasma glucose 11·1 mmol/l. Casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss

27. WHO criteria for the diagnosis of diabetes Fasting plasma glucose 7·0 mmol /l or whole blood 6·1 mmol /l. Fasting is defined as no calorie intake for at least 8 hours 2 hour plasma glucose 11·1 mmol /l during oral glucose tolerance test using 75 g glucose load

28. Testing for Pre-Diabetes and Diabetes in Asymptomatic Patients All individuals at age 45 years or above. At younger age or more frequently in whom: ■ Are Obese ■ Have a first degree relative with diabetes ■ Are Hypertensive ≥ 140/90 ■ Have been diagnosed with GDM ■ Have Dyslipidaemia ■ Had IGT or IFG

29. TREATMENT In the treatment of diabetes mellitus, changes in lifestyle play a major role, in addition to treatment with insulin or oral glucose-lowering drugs. For most patients with type 2 diabetes, the changes in lifestyle (concerning diet and exercise) are the cornerstone of treatment whereas the pharmacologic intervention represents a supplementary treatment for those patients who do not respond adequately to lifestyle changes.

30. PHARMACOLOGIC MANAGEMENT It is now recommended that the management regimens of patients with type 2 diabetes be tailored to the individual patient, aiming for glycemic targets as close to normal as possible and, in most people, as early as possible. Multiple therapies may be required to achieve optimal glycemic control in type 2 diabetes. The choice of antihyperglycemic agent(s) should be based on the individual patient. Target A1C should be attainable within 6 to 12 months.

31. A combination of oral agents and insulin often effectively control glucose levels in people with type 2 diabetes. Insulin therapy, without concomitant use of oral agents, is generally used when other modalities have failed or are contraindicated. However, insulin may be used as initial therapy, especially in he presence of marked hyperglycemia (A1C  9%). There is no evidence that exogenous insulin accelerates the risk of macrovascular complications of diabetes and its appropriate use should be encouraged. It is important to prevent, recognize and treat hypoglycemic episodes secondary to the use of insulin or insulin secretagogues .

32. LIFESTYLE Clinical assessment and initiation of nutrition therapy and physical activity Mild to moderate hyperglycemia (A1C < 9%) Marked hyperglycemia (A1C > 9%) - continued on next slide - MANAGEMENT OF HYPERGLYCEMIA IN TYPE 2 DIABETES

33. MANAGEMENT OF HYPERGLYCEMIA IN TYPE 2 DIABETES - cont’d LIFESTYLE Mild to moderate hyperglycemia (A1C < 9%) Overweight (BMI  25) Non-overweight (BMI < 25) Metformin alone or in combination with one of: - insulin sensitizer (TZD) - insulin secretagogue - insulin - acarbose One or two agents from different classes: - metformin - insulin sensitizer (TZD) - insulin secretagogue - insulin - acarbose If not at target If not at target Add a drug from a different class OR use insulin alone or in combination with: - metformin - insulin secretagogue - insulin sensitizer - acarbose

34. MANAGEMENT OF HYPERGLYCEMIA IN TYPE 2 DIABETES - cont’d LIFESTYLE Marked hyperglycemia (A1C  9%) 2 agents from different classes: - metformin - insulin sensitizer (TZD) - insulin secretatogue - insulin - acarbose Basal and/or preprandial insulin If not at target If not at target Add an oral agent from a different class or insulin Intensify insulin regimen or add: - metformin - insulin secretagogue - insulin sensitizer (TZD) - acarbose

35. Obese patients: Diet and Exercise should be offered for all patients for 2 months. METFORMIN is the drug of choice Start with 500 mg PO three times a day up to 850 mg or 1 gm PO TDS. ■ If not controlled add Sulphonylurea or Glitazones

36. Non-Obese patients: Diet and Exercise Metformin Add Sulphonylurea (e.g. Glibenclamide or Gliclazide) In secondary failure, consider shifting to Insulin

37. TREATMENT REGIMENS OF TYPE 1 DM Conventional Insulin Therapy Two injections of NPH and Regular Insulin Mixed Insulin Two injections of 70/30 or 60/40 Multiple Insulin Injections ► 1 or 2 injections of NPH plus 3 injections of Regular or Lispro Insulin ► One injection of Glargine or Detemir plus 3 injections of Regular or Lispro Insulin

38. Hypertension/Blood Pressure Control Goals ● Patients with diabetes should be treated to a systolic blood pressure < 130 mmHg and a diastolic blood pressure < 80 mmHg.

39. COMPLICATIONS OF DIABETES MELLITUS 1.Acute Complications 2.Chronic Complications

40. 1.Acute complications of DM Diabetic Ketoacidosis Hyperosmolar non- ketotic state Lactic acidosis Hypoglycemia Coma Respiratory Infections

41. 2. Chronic Complications Of DM Vascular Complications Microvascular Complications Macrovascular ComPlications

42. Microvascular Complications Diabetic Retinopathy Diabetic Nephropathy Diabetic Neuropathy Diabetic Cardiomyopathy

43. Microvascular complications Atheroscerosis Hypertension

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