Pdf Diabetes for nurses

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Diabetes for nurses

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Pdf Diabetes for nurses

  1. 1. DIABETES MELLITUS IN RENAL COMPLICATIONS นพ.กมล โฆษิตรังสิกุล อายุรแพทย์โรคไต โรงพยาบาลมหาราชนครศรีธรรมราช
  2. 2. WHAT IS DIABETES ? A chronic metabolic disorder causing elevation of blood glucose and specific & nonspecific complications
  3. 3. INTRODUCTION Between 1985 and 2010, the worldwide prevalence of DM has risen almost 10-fold, from 30 million to 285 million cases. In the United States, DM prevalence in 2010 is estimated at 26 million, or 8.4% of the population. A significant portion of persons with DM are undiagnosed.
  4. 4. THE BURDEN OF DM IN THAILAND Prevalence of DM in Thai adults (age > 35 years) was 9.6% 4.8% Known DM, 4.8% newly Dx DM 2.4 million people have diabetes Fair access to diabetes medications Diabetes Care 2003; 26: 2758-63
  5. 5. INCIDENT COUNTS & ADJUSTED RATES OF ESRD 2012 USRDS annual Data Report
  6. 6. CAUSE OF CKD IN THAI RRT 2003 DM, 1348, 34% HT, 1043, 26% CGN, 558, 14% Other, 448, 11% Unknown, 613, 15%
  7. 7. DIAGNOSIS OF DM Criteria for the diagnosis of DM include one of the following:" Hemoglobin A1c >6.5% Fasting plasma glucose ≥7.0 mmol/L (≥126 mg/dL) Symptoms of diabetes plus a random blood glucose concentration ≥11.1 mmol/L (≥200 mg/dL) 2-h plasma glucose ≥11.1 mmol/L (≥200 mg/dL) during a 75-g oral glucose tolerance test. ADA 2010
  8. 8. DIAGNOSIS Categories of increased risk for DM" Impaired fasting glucose (IFG) for a fasting plasma glucose level of 5.6–6.9 mmol/L (100–125 mg/dL) Impaired glucose tolerance (IGT) for plasma glucose levels of 7.8–11.1 mmol/L (140–199 mg/dL) 2 h after a 75-g oral glucose load HbA1C 5.7-6.4%
  9. 9. การแปลผล FPG Normal FG IFG Provisional DM 100 126 mg/dL
  10. 10. OGTT การทดสอบความทนกลูโคส เป็นวิธีทดสอบการทํางานของβ-cell ของตับอ่อน ในการหลั่ง insulin หลังกินกลูโคสในปริมาณสูง (75 g) คนปกติสามารถลดระดับนํ้าตาลลงมาได้ภายใน เวลา 2 ชั่วโมง ผู้ที่มีการหลั่งinsulin บกพร่องหรือเป็นโรค เบาหวาน จะต้องใช้ เวลาในการลดระดับนํ้าตาลนานกว่า 2 ชั่วโมง
  11. 11. 75 gm glucose
  12. 12. ข้อบ่งชี้ การส่งตรวจ OGTT 1. เพื่อตรวจยืนยันการวินิจฉัยโรคเบาหวานในกรณีที่การตรวจ FPG ให้ ผลไม่ชัดเจน(IFG) 2. FPG ให้ผลปกติแต่มีความสงสัยว่าจะเป็นโรคเช่น 2.1 มีอาการทางคลินิกของโรคเบาหวาน เช่น retinopathy, neuropathy, peripheral arterial disease 2.2 กลุ่มที่มีแนวโน้มอาจจะเป็นโรคเบาหวานได้ มากกว่าผู้อื่น (high risk group)
  13. 13. การแปลผล OGTT Normal GT Provisional DM 140 200 mg/dL 75 gm glucose then 2 hour plasma glucose Impaired GT (DIABETES CARE 2007; 30)
  14. 14. ! SCREENING Screening with a fasting plasma glucose level is recommended every 3 years for individuals over the age of 45, as well as for younger individuals who are overweight (body mass index ≥25 kg/m2) and have one or more additional risk factors.
  15. 15. ADDITIONAL RISK FACTORS Physical inactivity First-degree relatives with diabetes Members of high-risk ethnic population(eg. African American, Latino, Native American, Asian American, Pacific Islander) Women who delivered a body weighing 9 Ib (4 kg) or were diagnosed with GDM Hypertension (140/90 mHg or on therapy for hypertension)
  16. 16. ADDITIONAL RISK FACTORS HDL < 35 mg/dL and/or a triglyceride level > 250 mg/dL Women with polycystic ovary syndrome A1C 5.7 %, IGT, IFG on previous testing Other clinical conditions associated with insulin resistance (eg. severe obesity, acanthuses nigricans) History of CVD
  17. 17. ADA CLASSIFICATION OF DIABETES Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Other specific types Gestational Diabetes Mellitus
  18. 18. DIABETES MELLITUS Type 1 Diabetes (5-10%) Juvenile Onset, IDDM, type I Auto-immune disease Pancrease is unable to produce insulin (Beta cell destruction) Required insulin for survival Generally diagnosed from birth to age 30, highest incidence age 12-18
  19. 19. DIABETES MELLITUS Type 2 Diabetes (90-95%) Adult onset, NIDDM, type II Variable degree of insulin deficiency coupled with insulin resistance Disorder associated with obesity and the ageing process Generally diagnosed after age 40
  20. 20. DIABETES MELLITUS Gestational Diabetes Mellitus (GDM) Hyperglycemia first diagnosed in pregnancy Diagnosis made by OGTT
  21. 21. DIABETES MELLITUS Other specific types Maturity-Onset Diabetes of the Young (MODY)(<1%) Pancreatic disease Drug etc.
  22. 22. ETIOLOGY OF DIABETES
  23. 23. Adapted from DeFronzo RA.Diabets 1988;37:667-87
  24. 24. COMPLICATION OF DIABETES Acute complication: Hyperglycemic crisis Diabetic Keto-Acidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Long term complications Microvascular Macrovascular
  25. 25. ACUTE COMPLICATION Type I DM DKA Rapid deep breathing Abdominal pain Nuasea/Vomiting Fruity odor of ketone Type 2 DM HHS Weight loss Seizure Polyuria Polydipsia Drowsy Coma
  26. 26. ACUTE COMPLICATION DKA HHS DM Type1 Type2 Glucose(mg/dl) >250 >600 pH <7.3 >7.3 Serum HCO3(mEq/L) <15 >20 BUN (mg/dl) <25 >30 S. Osmolality <320 >320 Ketones > 3+ - / small
  27. 27. CHRONIC COMPLICATIONS OF DM Ophthalmologic: nonproliferative or proliferative diabetic retinopathy, macular edema, rubeosis of iris, glaucoma, cataracts Neurologic: distal symmetric polyneuropathy, polyradiculopathy, mono-neuropathy, autonomic neuropathy
  28. 28. CHRONIC COMPLICATIONS OF DM Gastrointestinal: gastroparesis, diarrhea, constipation Genitourinary: cystopathy, erectile dysfunction, female sexual dysfunction, vaginal candidiasis
  29. 29. CHRONIC COMPLICATIONS OF DM Cardiovascular: coronary artery disease, congestive heart failure, peripheral vascular disease, stroke Lower extremity: foot deformity (hammer toe, claw toe, Charcot foot), ulceration, amputation Dental: Periodontal disease
  30. 30. CHRONIC COMPLICATIONS OF DM Dermatologic: Infections (folliculitis, furunculosis, cellulitis), necrobiosis, poor healing, ulcers, gangrene
  31. 31. CHRONIC COMPLICATIONS OF DM Renal: proteinuria, end-stage renal disease (ESRD), type IV renal tubular acidosis
  32. 32. CHRONIC COMPLICATIONS cataract retinopathy ! ! proteinuria ! ! neuropathy ! ! ! Arthero sclerosis ! Blindness! !! Kidney failure! ! Amputation! ! MI! ! Stroke!
  33. 33. CAUSES OF MORTALITY IN DIABETES 32! Heart Disease Cerebrovascular Disease Other Pneumonia/ InfluenzaMalignant Neoplasms Diabetes Geiss LS, et al. In: Diabetes in America. 2nd ed. NIH Publication No. 95-1468. 1995:233-257. Causes of Mortality in Patients With Diabetes 10% 13% 13% 4% 5% 55% Geiss LS, et al :Diabetes in America 2 nd ed, NIH publication No.95-1468. 1995:233-257
  34. 34. CLINICAL PROGRESSION Stage Onset Designation Kidney change 1 เมื่อวินิจฉัย Hyperfunction GFR ↑ 2 2-3 ปี Silent stage GFR ↑ ,Thick GBM 3 >5 ปี Incipient stage GRF ↑ or Microalbuminuria 4 >10 ปี Overt DN GFR or ↓ Clinical proteinuria 5 >15 ปี ESRD GFR  < 10 ml/min
  35. 35. DEFINITION IN ALBUMIN EXCRETION . Random** 24 hr Urine Timed (microgram/min) Normal <30 mg/g <30 mg/24h <20 Microalbuminuria 30-300 mg/g 30-300 mg/24h 20-200 Macroalbuminuria >300 mg/g >300 mg/24h >200 Diabetes Care 28, Supple 1, Jan 1998
  36. 36. No nephropathy Microalbuminuria Macroalbuminuria Rising Cr, RRT 0.3% 2.8% 0.1% 0.1% 1.4%/ years 2.3% 3.0% 19.2% 2.0% / years 4.6% DEATH UKPDS 64: Kidney Int 2003; 63:225-232
  37. 37. GLYCEMIC GOAL IN ADULT
  38. 38. GLYCEMIC GOAL IN ADULT DIABETES(CARE,(VOLUME(35,(SUPPLEMENT(1,(JANUARY(2012!
  39. 39. Monotherapy Insulin therapy Combination oral therapy Lifestyle modification Expected HbA1c (time allotted) 1% (3 months) 1 to 2% (1 3 months) 1 to 2% fall per additional OHA (1 3 months) Unlimited T2DM treatment strategies Adapted from Bergenstal RM. In: De Fronzo RA, et al (eds). International Textbook of Diabetes Mellitus. 3rd ed. Chichester, New York: John Wiley & Sons; 2004:995 1015.
  40. 40. PRIMARY SITE OF ACTION 48! Glucose Adipose tissue Gut Stomach Liver Sulphonylureas and glinides TZDs Biguanides Muscle Pancreas Insulin Adapted from Kobayashi M. Diabetes Obes Metab 1999; 1 (Suppl 1): S32–40; Nattrass M et al. Baillieres Best Pract Res Clin Endocrinol Metab 1999; 13: 309–29. α-glucosidase inhibitors Primary sites of action of oral antidiabetic agents incretin
  41. 41. METFORMIN Decrease hepatic glucose production Mechanism: Unclear, Activating the AMP-activated protein kinase (AMPK)
  42. 42. METFORMIN J. Clin. Invest. 2001;108(8): 1167-74.
  43. 43. CLINICAL ADVANTAGES OF METFORMIN 1.Does not cause weight gain 2.Does not cause hypoglycaemia 3.Improve lipid profile Decrease plasma triglyceride 10-20% Decrease plasma cholesterol 5-10% Small increases in HDL-C Levels 4.Decrease plasma insulin levels
  44. 44. ADVERSE EFFECTS OF METFORMIN 1.Gastrointestinal 10-30% diarrhea, nausea, abdominal discomfort anorexia, metalic taste 2.Impaired absorption of Vit B12 and folate 3.Lactic acidosis
  45. 45. CONTRAINDICATION & CAUTION FOR THE USE OF METFORMIN Renal impairment : Cr > 1.5 mg/dL ; men Cr >1.4 mg/dL ; women Cardiac or respiratory insuffiency History of lactic acidosis Severe infection Liver disease Alcohol abuse Use of intravenous radio contrast agents
  46. 46. METFORMIN USE BASED ON GFR DIABETES CARE, VOLUME 34, JUNE 2011
  47. 47. SULFONYL UREA Pancreatic action Stimulation of insulin secretion by closing ATP- dependent potassium channels causing calcium influx
  48. 48. INSULIN SECRETAGOGUES Drug ! Dose !T 1/2 !Metabolites !Excretion" ! ! !(mg/d) ! (h)" Chlorpropamide 100 - 500 36 Active or Kidney unchanged Glipizide 2.5 - 30 2-4 Inactive Kidney 80% Bile 20 % Gliburide 1.25 - 20 10 Inactive & Kidney 50% weakly active Bile 50 % Glimepiride 1 - 8 9 Inactive & Kidney 60% weakly active Bile 40 % Repaglinide 1.5 - 6 1 Inactive Bile
  49. 49. CONTRAINDICATION TO SULFONYL UREA 1. IDDM 2. post-pancreatectomy 3.During acute diabetic complication 4.During stress, infection or major operation 5.Renal impairment 6.During gestation? 7.Adverse drug reaction
  50. 50. HYPOGLYCAEMIA FROM SULFONYLUREAS Risk factors 1.Age > 70 yr 2.Poor nutrition 3.Alcohol intake 4.Impaired renal function 5.Drug interactions
  51. 51. THIAZOLIDINE DIONE Ligand for PPAR ɣ , a nuclear receptor transcription factor regulates many gene expression involved in CHO and lipid metabolism Specific mechanism: unclear ⬆️ insulin-mediated glucose uptake by skeleton muscle ⬇️ lipolysis and enhance adipocyte differentiation indirect effect mediated through adipokines
  52. 52. ADVERSE EVENT OF TZD 1.Edema: generally dose related, more commonly observed when combination with SU, Insulin 2.Weight gain: up to 8 kg 3.Anemia: Hct drop around 3% 4.Congestive heart failure 5.Macular edema 6.Bone fractures 7.Exacerbate Grave’s opthalmopathy
  53. 53. INSULIN Types Examples Bolus (Meal) Insulin Rapid-acting lispro, aspart, glulisine Short-acting Regular Basal (Background) Insulin Intermediate-acting NPH, Lente Long-acting Glargine Pre-Mixed Insulin NPH/Regular 70/30, 50/50 NPL/Lispro Mix 75/25 NPA/Aspart Mix 70/30
  54. 54. INSULIN ACTION 76! Insulin Action: Comparison of New Insulin Analogs 0 20 40 60 80 100 120 140 0 2 4 6 8 10 12 14 16 Regular Rapid (Lispro, Aspart) InsulinLevel(µU/ml) Hours Intermediate (NPH) Long ( Detemir,Glargine)
  55. 55. INSULIN ACTION Comparison of Human insulins and insulin analogues Insulin Onset of Duration of Preparations Action Peak Action Action Lispro/Aspart 5-15 min 1-2 hr 4-6 hr Human Regular 30-60 min 2-4 hr 6-10 hr Human NPH/Lente 1-2 hr 4-8 hr 10-20 hr Glargine/Detrimir 1-2 hr Flat ~24 hr Endocrinol Metab Clin North Am 2001;30:944
  56. 56. Dyslipidemia
  57. 57. DM#Type#II#&#CVD,#CKD,# CVD#with#age#>#40#yr## with#TOD# #or#>#1#risk## # # LDL>C#goal#<#70#mg/dl ! Non#HDL>C#<100#mg/dl## #Apo#B#<#80#mg/dl# ! ! ! All!DM!type!II!!patients! ! LDL0C<100!mg/dl! Non!HDL0C!<130!mg/dl!! !Apo!B!<!100!mg/dl! ! European)Heart)Journal)(2011))32,)1769–1818)
  58. 58. ! Mod!to!severe!CKD! LDL.C!target!70!mg/dl! ! Expert!:!Sta;n!may!slow! rate!of!kidney!func;on!loss! ! CKD$=$CAD$Risk$equivalent$ $ LDL4C$lowering$is$useful$ $ European)Heart)Journal)(2011))32,)1769–1818)
  59. 59. FOLLOW UP AFTER START ACEI/ARB

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