Diabetes mellitus

1. Diabetes mellitus Presented by Dr. Abeer Shatnawi Superviser by Dr maysoon Al Kylani Dr Mai Al Hadidi

2. What is diabetes? • Diabetes mellitus (DM) is a chronic diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both. • It is one of the five most common diagnoses in primary care • The effects of diabetes mellitus include long–term damage, dysfunction and failure of various organs.

4. 2. Classification and Diagnosis of Diabetes

5. Type 1 diabetes Autoimmune β-cell destruction,usually leading to absolute insulin deficiency Type 2 diabetes Progressive insulin secretory defect on the background of insulin resistance Gestational Diabetes Mellitus (GDM) Other specific types of diabetes due to other causes: Monogenic diabetes syndromes Diseases of the exocrine pancreas, e.g., cystic fibrosis Drug- or chemical-induced diabetes Classification of Diabetes

6. Criteria for the Diagnosis of Diabetes

7. To avoid misdiagnosis or missed diagnosis, the A1C test should be performed using a method that is certified by the NGSP and standardized to the Diabetes Control and Complications Trial (DCCT) assay. B Marked discordance between measured A1C and plasma glucose levels should raise the possibility of A1C assay interference due to hemoglobin variants (i.e., hemoglobinopathies) and consideration of using an assay without interference or plasma blood glucose criteria to diagnose diabetes. B In conditions associated with increased red blood cell turnover, such as sickle cell disease, pregnancy (second and third trimesters), hemodialysis, recent blood loss or transfusion, or erythropoietin therapy, only plasma blood glucose criteria should be used to diagnose diabetes. B A1C: New Recommendations

8. Prediabetes: Impaired glucose tolerance and impaired fasting glucose • Prediabetes is a term used to distinguish people who are at increased risk of developing diabetes. People with prediabetes have impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Some people may have both IFG and IGT. • IFG is a condition in which the fasting blood sugar level is elevated (100 to 125 milligrams per decilitre or mg/dL) after an overnight fast but is not high enough to be classified as diabetes. • IGT is a condition in which the blood sugar level is elevated (140 to 199 mg/dL after a 2-hour oral glucose tolerance test), but is not high enough to be classified as diabetes.

9. Prediabetes: Impaired glucose tolerance and impaired fasting glucose (cont.) • Progression to diabetes among those with prediabetes is not inevitable. Studies suggest that weight loss and increased physical activity among people with prediabetes prevent or delay diabetes and may return blood glucose levels to normal. • People with prediabetes are already at increased risk for other adverse health outcomes such as heart disease and stroke.

10. Categories of Increased Risk for Diabetes (Prediabetes)

11. Testing for Diabetes or Prediabetes in Asymptomatic Adults

12. Risk factors for Prediabetes and T2D

13. Risk-Based Screening in Asymptomatic Children and Adolescents

15. If tests are normal, repeat testing carried out at a minimum of 3-year intervals is reasonable. C To test for prediabetes, fasting plasma glucose, 2-h plasma glucose during 75-g oral glucose tolerance test, and A1C are equally appropriate. B In patients with prediabetes, identify and, if appropriate, treat other cardiovascular disease risk factors. B Prediabetes: Recommendations (2)

16. Type 1 diabetes • Was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes. • Type 1 diabetes develops when the body’s immune system destroys pancreatic beta cells, the only cells in the body that make the hormone insulin that regulates blood glucose. • This form of diabetes usually strikes children and young adults, although disease onset can occur at any age. • Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes. • Risk factors for type 1 diabetes may include autoimmune, genetic, and environmental factors.

17. Staging of Type 1 Diabetes

18. Presentation • Type 1 D.M.: • New onset Polyphagia ,Polyuria ,thirsty,weight loss Usually Diabetic Ketoacidosis(DKA). Triad of hyperglycemia,ketosis,acidosis Precipitating conditions :omission of previously prescribed insulin dose,pneumonia,urinary tract infection,alcohol abuse ,trauma,pulmonary embolus,myocardial infarction Symptoms rapid course <24h,nausea,vomiting,and abdominal pain signs rapid deep respirations(kussmaul breathing),fruity smell,signs of dehydration mental status changes It is a medical emergency characterized by hyperglycemia, wide anion gap metabolic acidosis and ketosis. It requires hospital admission and aggressive iv insulin therapy and fluid and electrolyte management.

19. DX. OF DKA • GLU.>250mg/dl • PH<7.30 • BIC.<18Mm • High AG Positive serum ketones

20. MANAGEMENT AND COMPLICATIONS OF DKA • Underlying cause • Hypovolemia • Insulin therapy • Pottasium,Ph.,Mg. • Bicarbonate. • Shock • Infection • Thrombosis • Respiratory Distress • Arrythmias • Cerebral edema • Acute gastric dilatation or erosive gastritis

21. Plasma blood glucose rather than A1C should be used to diagnose type 1 diabetes in individuals with symptoms of hyperglycemia.E Screening for type 1 diabetes with a panel of autoantibodies is currently recommended only in the setting of a research trial study or in first-degree family members of a proband with type 1 diabetes. B Persistence of two or more autoantibodies predicts clinical diabetes and may serve as an indication for intervention in the setting of a clinical trial. B Type 1 Diabetes: Recommendations

22. Type 2 diabetes • Was previously called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. • Type 2 diabetes may account for about 90% to 95% of all diagnosed cases of diabetes. • It usually begins as insulin resistance, a disorder in which the cells do not use insulin properly. As the need for insulin rises, the pancreas gradually loses its ability to produce insulin. • Type 2 diabetes is associated with older age, obesity, family history of diabetes, history of gestational diabetes, impaired glucose metabolism, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, American Indians, and some Asian Americans • Type 2 diabetes is increasingly being diagnosed in children and adolescents.

23. Presentation • Type 2 D.M.: • fatigue,weight loss Polyuria, polydipsia,polyphagia blurred vision, recurrent candidiasis or balanitis,periodontal infections,slow healing wounds,neurological syndromes(focal limb neuropathies,paresthesias,burning ,tingling in the extremities • HHS coma( A medical emergency). • Accidental discovery. • Presentation with any of the diabetic complications.

24. HHS • Present with more extreme levels of hyperglycemia >1000mg/dl than dka without ketosis or acidosis • INSULIN ENOUGH TO PREVENT KETOSIS BUT NOT HYPERGLYCEMIA • Typical presntation: insidious onset over day to weeks,with increasing thirst polydipsia polyuria weight loss and mental status changes obtundation, DEHYDRATION Leads to hyperosmolality,seizures • MILD ACIDOSIS • More common in older adults

25. HHNKC-MANAGEMENT • PRECIPITANTS: SIMILAR TO DKA. • AGGRESSIVE FLUID MANAGEMENT. • ALWAYS START WITH N.S.>REPLETE INTRAVASCULAR VOLUME. • THEN SHIFT TO ½ NS OR 5%DW. • AVERAGE LOSS IS 8-10 L. • INSULIN THERAPY:ELECTROLYTE REPLETION.

26. Features to Distinguish Type 1 from Type 2 1 vs 2 Mode of onset acute insidious Insulin resistance absent present DKA present usually absent Insulin reserve absent present Autoantibodies present absent Features which help distinguish between type 1 and type 2 diabetes include abruptness of onset, acanthosis nigricans, diabetic ketoacidosis, insulin reserve, and the presence of autoantibodies.

27. Other types of DM • Other specific types of diabetes result from specific genetic conditions (such as maturity-onset diabetes of youth), surgery, drugs, malnutrition, infections, and other illnesses. • Such types of diabetes may account for 1% to 5% of all diagnosed cases of diabetes.

28. Monogenic Diabetes Syndromes: Recommendations • All children diagnosed with diabetes in the first 6 months of life should have immediate genetic testing for neonatal diabetes. A • Children and adults, diagnosed in early adulthood, who have diabetes not characteristic of T1DM or T2DM that occurs in successive generations (suggestive of an autosomal dominant pattern of inheritance) should have genetic testing for MODY. A • In both instances, consultation with a center specializing in diabetes genetics is recommended to understand the significance of these mutations and how best to approach further evaluation, treatment, and genetic counseling. E

29. LADA • Latent Autoimmune Diabetes in Adults (LADA) is a form of autoimmune (type 1 diabetes) which is diagnosed in individuals who are older than the usual age of onset of type 1 diabetes. • Alternate terms that have been used for "LADA" include Late-onset Autoimmune Diabetes of Adulthood, "Slow Onset Type 1" diabetes, and sometimes also "Type 1.5 • Often, patients with LADA are mistakenly thought to have type 2 diabetes, based on their age at the time of diagnosis.

30. MODY • MODY – Maturity Onset Diabetes of the Young • MODY is a monogenic form of diabetes with an autosomal dominant mode of inheritance: • Mutations in any one of several transcription factors or in the enzyme glucokinase lead to insufficient insulin release from pancreatic ß-cells, causing MODY. • Different subtypes of MODY are identified based on the mutated gene. • Originally, diagnosis of MODY was based on presence of non-ketotichyperglycemia in adolescents or young adults in conjunction with a family history of diabetes. • However, genetic testing has shown that MODY can occur at any age and that a family history of diabetes is not always obvious.

31. Secondary DM Secondary causes of Diabetes mellitus include: Cystic fibrosis • Acromegaly, • Cushing syndrome, • Thyrotoxicosis, • Pheochromocytoma • Chronic pancreatitis, • Cancer • Drug induced hyperglycemia: • Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin resistance. • Beta-blockers - Inhibit insulin secretion. • Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium release. • Corticosteroids - Cause peripheral insulin resistance and gluconeogensis. • Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels. • Naicin - They cause increased insulin resistance due to increased free fatty acid mobilization. • Phenothiazines - Inhibit insulin secretion. • Protease Inhibitors - Inhibit the conversion of proinsulin to insulin. • Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased insulin resistance due to increased free fatty acid mobilization.

32. 3. Comprehensive Medical Evaluation and Assessment of Comorbidities

33. Components of the Comprehensive Diabetes Evaluation

34. Components of the Comprehensive Diabetes Evaluation

35. Components of the Comprehensive Diabetes Evaluation * ≥65 years

36. Components of the Comprehensive Diabetes Evaluation

37. Components of the Comprehensive Diabetes Evaluation † May be needed more frequently in patients with known chronic kidney disease or with changes in medications that affect kidney function and serum potassium. # May also need to be checked after initiation or dose changes of medications that affect these laboratory values (i.e., diabetes medications, blood pressure medications, cholesterol medications, or thyroid medications),. ˄ In people without dyslipidemia and not on cholesterol-lowering therapy, testing may be less frequent.

38. Components of the Comprehensive Diabetes Evaluation † May be needed more frequently in patients with known chronic kidney disease or with changes in medications that affect kidney function and serum potassium.

39. Immunization: Recommendations • Provide routinely recommended vaccinations for children and adults with diabetes by age. C • Annual vaccination against influenza is recommended for all people ≥6 months of age, including those with diabetes. C • Administer 3-dose series of hepatitis B vaccine to unvaccinated adults with diabetes aged 19-59 years. C • Consider administering 3-dose hepatitis B vaccine to unvaccinated adults with diabetes ages ≥ 60 years. C

40. Immunization: Recommendations (2) • Vaccination against pneumococcal disease, including pneumococcal pneumonia, with 13-valent pneumococcal conjugate vaccine (PCV13) is recommended for children before age 2 years. People with diabetes ages 2-64 years should also receive 23-valent pneumococcal polysaccharide vaccine (PPSV23). Ag age ≥65 years, regardless of vaccination history, additional PPSV23 vaccination is necessary. C

41. Common Comorbidities • Autoimmune Diseases (T1D) • Cancer • Cognitive Impairment/ Dementia • Fatty Liver Disease • Pancreatitis • Fractures • Hearing Impairment • HIV • Low Testosterone (Men) • Obstructive Sleep Apnea • Periodontal Disease • Psychosocial/Emotional Disorders

42. Human Immunodeficiency Virus (HIV): Recommendation • Patients with HIV should be screened for diabetes and prediabetes with a fasting glucose level every 6–12 months before starting antiretroviral therapy and 3 months after starting or changing antiretroviral therapy. If initial screening results are normal, checking fasting glucose every year is advised. E

43. Low Testosterone in Men: Recommendation • In men with diabetes who have symptoms or signs of hypogonadism such as decreased sexual desire (libido) or activity, or erectile dysfunction, consider screening with a morning serum testosterone level. B

44. Depression: Recommendations • Beginning at diagnosis of complications or when there are significant changes in medical status, consider assessment for depression. B

45. Complications • Acute complications: • DKA in type 1 D.M. • HHS in type 2 D.M. • Hypoglycemia

46. Glycemic Recommendations

47. Classification of Hypoglycemia

49. Management of hypoglycemia • Identification of cause. • Urgent treatment: oral vs. parenteral; glucagon use. • Definitive treatment. • In case of coma….always presume hypoglycemia.

50. Hypoglycemia: Recommendations • Individuals at risk for hypoglycemia should be asked about symptomatic and asymptomatic hypoglycemia at each encounter. C • Glucose (15–20 g) is the preferred treatment for the conscious individual with blood glucose <70 mg/dL, although any form of carbohydrate that contains glucose may be used. Fifteen minutes after treatment, if SMBG shows continued hypoglycemia, the treatment should be repeated. Once SMBG returns to normal, the individual should consume a meal or snack to prevent recurrence of hypoglycemia. E