Diabetes mellitus


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Diabetes mellitus

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Diabetes mellitus

  2. 2. THE PANCREASbehind stomach (LUQ)6” longHorizontalBoth endocrine & exocrine functionsexocrine : secretes hormones & enzymes that help in the digestion of proteins, carbohydrates & fats
  3. 3. Endocrine: carried out by islets of Langerhans alpha cells – glucagons beta cells – insulin delta cells – somatostatin
  4. 4.  Endocrine:  alpha cells – glucagons:  blood glucose – hyperglycemia  beta cells – insulin:  blood glucose – hypoglycemia  delta cells – somatostatin:  secretion of glucagons, insulin, GH Insulin – facilitates transport of glucose across the cell membrane to be utilized by the cell.
  5. 5. INSULINPrimary function…  Stimulates the active transport of glucose  from the blood into muscle, liver and adipose tissue   __?__ blood glucose levels i
  6. 6. GLUCOSE CONTENT OF FOODWhat % of the carbohydrates consumed breaks down into glucose?  100%What % of the protein consumed breaks down into glucose?  58%What % of the fat consumed breaks down into glucose?  10%
  7. 7. SECRETION OF INSULINIs stimulated by: What change in homeostasis does the sensor identify and then stimulates the beta cells to secrete insulin? HyperglycemiaGlucose levels in the bloodstream regulate the rate of insulin secretion
  8. 8. THE MAJOR ACTION OF INSULINi blood glucose levelsh the permeability of target cell membrane to glucose Main target cells  Muscle  Liver  Adipose tissue
  9. 9. INSULIN INFOThe glucose is either metabolized or storedIn the absence of insulin, glucose is not able to get into the cells and it is excreted in the urineBrain cells are not dependent on insulin for glucose intake
  10. 10. INSULIN Eat the glucose  Muscle  energy Storage of glucose  Liver = freezer  Glycogen  Synthesis of Adipose tissue = 2nd freezer Give it away  Glycosuria
  11. 11. OTHER FUNCTIONS OF INSULINPromote the conversion of glucose  glycogen  GlycogenesisAlso inhibits the conversions of glycogen  glucose  GlycogenolysisGlycogen = the form in which glucose is stored in the liver
  12. 12. OTHER FUNCTIONS OF INSULINPromoting the conversion of fatty acids  fat  Adipose tissue
  13. 13. OTHER FUNCTIONS OF INSULINPreventing the breakdown of fat  ketone bodiesKetone bodies: the byproduct of fat metabolism
  14. 14. OTHER FUNCTIONS OF INSULINStimulating protein synthesisInhibiting the breakdown of protein  amino acids
  15. 15. INSULIN SUMMARYInsulin i blood glucose levelsPromotes the storage of glucosei energy production from other sources Glycogen, fat or protein metabolism
  16. 16. GLUCAGONProduced and secreted by the Alpha cells of the Islets of LangerhansGlucagon stimulates the release of Glucose by the liver
  17. 17. GLUCAGON STIMULATES THE RELEASE OFGLUCOSE BY THE LIVER• What “G” word means the release of glucose by the liver?A. GlycogenB. GlycogenesisC. GlycogenolysisD. GlucoseE. Gone-is-my-brain
  18. 18. The effect of glucagon h blood glucose level Hyperglycemia
  19. 19. GLUCAGONGlucagon is secreted is response to Hypoglycemia StressHypoglycemia may occur during Stress Exercise Fasting
  20. 20. SOMATOSTATINA hormone secreted by the delta cells of the Islets of LangerhansSecreted in response to HyperglycemiaAction Interferes with glucagon Interferes with growth hormone
  21. 21. SOMATOSTATINHas a hypoglycemic effect
  23. 23. PREVALENCE
  24. 24. DIABETES MELLITUS:6th leading cause of death in US3rd leading cause of death by diseaseAssoc. with many complicationHeart disease is the leading cause for a diabetic65% of diabetics have hypertension
  25. 25. DIABETES MELLITUS:Risk of heart attack or stroke 3 times great if you have DMDM leading cause of blindness in adultsDM leading cause of new cases of renal failure50% of all people with non-traumatic leg amputation have DM
  26. 26. DIABETES MELLITUS:DM shortens peoples life spanDM creates disabilitiesDM is an economic burden12% of all health care expenditures are for diabetic care/treatmentSeen in all age groups and races1/3 of diabetics are over the age of 60
  27. 27. International Diabetes Federation predicts that the number of people living with diabetes will to rise from 366 million in 2011 to 552 million by 2030.
  28. 28. top 10 countries in number of people with diabetes are currently India, China, the United States, Indonesia, Japan, Pakistan, Russia, Brazil, Italy, and Bangladesh.
  29. 29. In 2009, diabetes mellitus was the seventh leading cause of death in the United States
  30. 30. Approximately 1 in 5 health care dollars in the United States was spent caring for someone with diagnosed diabetes
  31. 31. DIABETES MELLITUSA chronic systemic disease characterized by disorder of carbohydrate, protein and fat metabolismcharacterized by hyperglycemia due to an absolute or relative lack of insulin or to a cellular resistance to insulin   or no production of insulin  Ineffective insulin or insulin resistance
  32. 32. TYPES OF DM
  33. 33. Type 1Type 2GDM
  34. 34. TYPE 1 DM
  35. 35. DIABETES TYPE 1Metabolic condition in which the beta cells of pancreas no longer produce insulin; characterized by hyperglycemia, breakdown of body fats and protein and development of ketosisAccounts for 5 – 10 % of cases of diabetes; most often occurs in childhood or adolescence
  36. 36. TYPE 1 – DIABETES MELLITUSOld names  Juvenile diabetes  Insulin dependent diabetes mellitus (IDDM)Destruction of the Beta cellsResult NO insulin production Insulin dependent
  37. 37. ETIOLOGY TYPE 1 DM#1: Auto-immune Autoimmune disease reaction in which the beta cells that#2: Idiopathic produce insulin areGenetic susceptibility destroyed Alpha cells produce excess glucagons causing hyperglycemia
  38. 38. TYPE 1genetic/hereditary  1. Genetic predisposition for increased susceptibility; HLA linkageEnvironmental triggers stimulate an autoimmune response  Viral infections (mumps, rubella, coxsackievirus B4)  viral infections: attacks islet cells of the pancreas  Chemical toxins autoimmune: islet cell antibodies
  39. 39.  Brittle DM Unstable DM Absolute insulin deficiency DKA prone Thin
  40. 40. Process of beta cell destruction occurs slowly;hyperglycemia occurs when 80 – 90% is destroyed;often trigger stressor event (e. g. illness)
  41. 41. S&S OF TYPE 1 DMHyperglycemia ↑ blood glucose levels No insulin  Glucose stays in the blood streamWhat effect does insulin have on glycogen? Inhibits the conversion of glycogen to glucose
  42. 42. S&S OF TYPE 1 DMGlycosuria  Glucose in the urine
  43. 43. S&S OF TYPE 1 DMPolyuria  Osmotic diuresisNocturia  Urinating during the nightNursing diagnosis  Fluid Volume Deficit
  44. 44. S&S OF TYPE 1 DMPolydipsia  Excessive thirst
  45. 45. S&S OF TYPE 1 DMPolyphagia  Excessive hunger
  46. 46. S&S OF TYPE 1 DMDehydration
  47. 47. S&S OF TYPE 1 DMKetonuria  No insulin  Burn fats  Byproduct  ketones  ↑ ketone in the blood  Metabolic Acidosis
  48. 48.  Liver can not excrete all of the ketones  spill into the urine  Ketonuria
  49. 49. SUMMARY OF PATHOPHYHyperglycemia leads to a. Polyuria (hyperglycemia acts as osmotic diuretic) b. Glycosuria (renal threshold for glucose: 180 mg/dL) c. Polydipsia (thirst from dehydration from polyuria) d. Polyphagia (hunger and eats more since cell cannot utilize glucose) e. Weight loss (body breaking down fat and protein to restore energy source f. Malaise and fatigue (from decrease in energy) g. Blurred vision (swelling of lenses from osmotic effects)
  50. 50. PATHOPHYSIOLOGY :TYPE 1 VIRAL INFECTION Inflammation of islets of the pancreas Beta cells produce antigen Antigen detected & destroyed by T cells Production of islet cell antibodies Autoimmune destruction of beta cells HYPERGLYCEMIA
  51. 51. PATHOPHYSIOLOGY: TYPE 2 Obesity  insulin resistance by tissues Compensatory increase of insulin production by islets  insulin resistance & defect in insulin receptors HYPERGLYCEMIA
  52. 52. HyperglycemiaIncreased osmolarity due Gluconeogenesis to glucose Wasting of Increased ketones lean body mass Metabolic acidosis Fatigue and Polyphagia weight loss Acetone breathPolyuria Polydypsia Sluggish blood Proliferation of Weight loss flow microbes Infections
  53. 53. Chronic elevations in blood glucose levels 1. Small vessel disease Nephropathy Neuropathy Retinopathy ESRD Loss of vision/blindnessSymmetrical Numbness and Wasting of Charcot’s Autonomic DM loss of tingling in the intrinsic muscles joints neuropathy foot sensation extremities and ulcer
  54. 54. Chronic elevations in blood glucose levels Accelerated atherosclerosis Impaired immune function Infection Delayed wound healingHypertension Coronary Stroke Increased low artery disease density lipoprotein
  55. 55. TYPE 2 DM
  56. 56. DIABETES TYPE 2condition of fasting hyperglycemia occurring despite availability of body’s own insulin
  57. 57. PATHOPHYSIOLOGYSufficient insulin production to prevent DKA; but insufficient to lower blood glucose through uptake of glucose by muscle and fat cellsCellular resistance to insulin increased by obesity, inactivity, illness, age, some medications
  58. 58. TYPE 2 DMHereditary HHNC proneAdult Onset  production of insulinStable DM by islets or  receptorKetosis resistant DM sites and insulin resistance
  59. 59. TYPE 2 DMEtiology  The pancreas cannot produce enough insulin for body’s needs  Impaired insulin secretion
  60. 60. TYPE 2 DMWeakened Beta cells Due to over use High glucose intake “Insulin Resistance”  The target cells have decreased sensitivity to insulin
  61. 61. INSULIN AND TYPE 2 DMDon’t all require insulin1/3 will at some time need to take insulinSeldom get Ketoacidosis (enough insulin to prevent high levels of fat metabolism)
  62. 62. Simplified scheme for the pathophysiology oftype 2 diabetes mellitus.
  63. 63. TYPE 1 VS. TYPE 2Etiology Etiology Auto-immune Overused/tired IdiopathicAge of onset Age of onset Usually < 30 Usually > 40Percent of Percent of diabetics diabetics 5-10% 85-90%
  64. 64. TYPE 1 VS. TYPE 2Onset Onset Rapid less than 1 yr Gradual – yearsBody wt at onset Body wt at onset Normal to thin 80% overweightInsulin production Insulin production None Not enoughInsulin injections Insulin injections Always Sometimes
  65. 65. TYPE 1 VS. TYPE 2Ketones Ketones Children/adolescence Unlikely problem Stress Pregnancy Management Diet (wt. Loss)Management Exercise Insulin Possibly oral Diet hypoglycemic meds Exercise Possibly insulin
  66. 66. CLASSIFICATIONS OF DM3. Gestational diabetes mellitus  DM first detected during pregnancy  Due to placental hormones
  67. 67. GESTATIONALOccurs during pregnancy2nd -3rd trimesterScreening 24-28 weeksExtra metabolic demands triggers onset
  68. 68. GDM• #1 complication  Macrosomia• Controlled with diet and insulin (no oral meds)• Generally glucose level return to normal after delivery• Predisposes to – type 2 diabetes
  69. 69. WHAT TYPE OF DIABETES DOESJONNY HAVE?Jonny is a 11 year old male child. He is a thin youth at 75 lbs and 4’6” tall. He suddenly became very ill and his mother brought him to the ER. He was complaining of weakness, nausea & vomiting and blurred vision. He reported having to urinate a lot. His vital signs were pulse:125; Respirations 28; BP: 80/40.  Type 1
  70. 70. NCLEX QUESTIONThe antepartum patient is being routinely screened for gestational diabetes by administering 50 mg of glucose and testing the woman’s blood sugar in an hour. The patient asks for the normal glucose values an hour after taking the glucose. The nurse replies:A. “It should be less than 140 or we do further testing.”B. “Anything under 105 is acceptable.”C. “We like to see a result between 130 and 165.”D. “It is different for each individual.”
  71. 71. CLASSIFICATIONS OF DM4. Impaired fasting glucose  FBS levels of >100mg/dl but < 126mg/dl5. Impaired glucose tolerance  Glucose levels >140mg/dl but < 200mg/dl
  72. 72. OTHER SPECIFIC TYPES OF DIABETESMELLITUSBeta-cell genetic defectEndocrinopathiesPancreatitisCystic FibrosisSecondary diabetes :  Drug or chemical induces diabetes (steroids - glucocorticoids  conditions that antagonize the actions of insulin (eg, Cushing syndrome, acromegaly, pheochromocytoma).
  73. 73. RISK FACTORS
  74. 74. RISK FACTORS FOR TYPE 2 DM Family history Age Obesity Gestational diabetes or large baby Hypertension High fat diet Lack of exercise High carb. Diet
  75. 75. MAJOR RISK FACTORS TYPE 2 DMAge : 45 and older Race or ethnicity: (note: occurring with Hispanic, Native increasing frequency American, African in young individuals) American, AsianFamily history of American, or Pacific type 2 diabetes in a Islander descent first-degree relative (eg, parent or sibling)
  76. 76. MAJOR RISK FACTORS TYPE 2 DM History of previous  History of gestational impaired glucose diabetes mellitus or of tolerance (IGT) or delivering a baby with a impaired fasting glucose birth weight of over 9 lb (IFG)  Polycystic ovarian Hypertension (>140/90 syndrome (which mm Hg) results in insulin Dyslipidemia (HDL resistance) cholesterol level < 40  Depression mg/dL or triglyceride level >150 mg/dL)
  77. 77. RISK FACTORS Overweight: weight greater than 120% of desirable body weight sedentary lifestyle Smoking diet high in red meat, processed meat, high- fat dairy products, and sweets
  78. 78. RISK FACTORS FOR WOMENgiven birth to a baby > 9 lbshistory of polycystic ovary syndrome: cause insulin resistance (+) family history obesity above 40 y/o
  80. 80. S&S OF DIABETES MELLITUSDefinition:  A group of disorders characterized by chronic Hyperglycemia3 P’s Polydipsia Polyuria Polyphagia
  81. 81. S&S OF HYPERGLYCEMIANeuro Fatigue C/O headache Dull senses Stupor Drowsy Loss of Consciousness Blurred Vision
  82. 82. S&S OF HYPERGLYCEMIACardiovascular Tachycardia Decreased BP (Dehydration)Respirations Kussmauls respirations Sweet and fruity breath Acetone breath
  83. 83. S&S OF HYPERGLYCEMIAGastro-intestinal Polyphagia (Decreased hunger in late stages) N/V Abd. Pain Polydipsia Dehydration
  84. 84. S&S OF HYPERGLYCEMIAGenital-urinary Polyuria Nocturia GlycosuriaSkeletal-muscular Weak
  85. 85. S&S OF HYPERGLYCEMIAIntegumentary Dry skin Flushed face Hypothermia
  86. 86. MANIFESTATIONS TYPE 21. Client usually unaware of diabetes aDiscovers diabetes when seeking health care for another concern Usually does not experience weight loss2. Possible symptoms or concerns Hyperglycemia (not as severe as with Type 1) Polyuria Polydipsia Blurred vision Fatigue Paresthesias (numbness in extremities) Skin Infections
  87. 87. DX EXAMS
  88. 88. To diagnose Diabetes Mellitus, one of the three following tests must be positive and must be confirmed on another day with one of the three tests
  89. 89. DIAGNOSTICS FBS2-hr PPGOGTTGlycosylated hemoglobinUrine ketone levels
  90. 90. AMERICAN DIABETES ASSOCIATION (ADA)CRITERIA FOR DIAGNOSIS OF DIABETES HbA1c level of 6.5% or higher Or fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or higher Or a 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during a 75-g oral glucose tolerance test (OGTT) Or a random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a patient with classic symptoms of hyperglycemia (ie, polyuria, polydipsia, polyphagia, weight loss) or hyperglycemic crisis
  91. 91. DIAGNOSIS OF DMFBS: ≥126mg/dlOGTT: 2-hour plasma glucose ≥ 200mg/dlSymptoms of DM plus RBS ≥ 200mg/dl
  92. 92. BLOOD GLUCOSEFASTING BLOOD GLUCOSEMeasures blood glucose levels after fastingResults  Normal – 70-115 mg/dL  Diabetic level > 126 mg/dL  Critical > 400 mg/dL  Critical < 50 mg/dL
  93. 93. FASTING BLOOD GLUCOSENURSING RESPONSIBILITYFast 6-8 hoursWater OKNo insulin or anti-diabetic medsExercise will effect resultsMeds that interfere
  94. 94. 2-HOUR POST-PRANDIAL GLUCOSEMeasure blood glucose 2 hours after a mealNormal 70-140 mg/dLDiabetic level > 140 mg/dL
  95. 95. 2-HOUR POST-PRANDIAL GLUCOSENURSING RESPONSIBILITYEat entire mealDon’t eat anything more until blood drawWater  OKNotify lab when meal is finishedExercise with effect results
  96. 96. GLUCOSE TOLERANCE TESTNURSING RESPONSIBILITYEvaluates blood glucose and urine glucose 30 minutes before 1 hour after 2 hours after 3 hours after 4 hours afterA glucose load
  97. 97. GLUCOSE TOLERANCE TESTNormal Blood glucose < 140mg/dL at 2 hours Urine negative for glucose (all times)Diabetic level Blood glucose > 140 mg/dL at 2 hours Glucose in urine
  98. 98. GLUCOSE TOLERANCE TESTNURSING RESPONSIBILITYFasting 6-8 hours before testHold meds that interfereAdminister glucose loadWater  encouragedCollect urine hourlyAdminister meal and meds afterwards
  99. 99. GLYCOSYLATED HEMOGLOBIN ASSAYS(HGB A1C)Percentage of glycosylated hemoglobin RBC lifecycle  @ 120 days (4 months) Glucose slowly binds with Hgb  glycosylated  h serum glucose level  h glycosylated Hgb levels
  100. 100. HGB A1C Provides an average blood glucose levels Past 2-3 months Can be taken any time
  101. 101. Normal levels (non-diabetic) 4-6%Diabetic level (goal) <8%
  102. 102. HBA1c(%) Mean blood sugar (mg/dl)6 1357 1708 2059 24010 27511 31012 345
  103. 103. DIAGNOSTIC TESTS TO MONITOR DMFasting Blood Glucose (normal: 70 – 110 mg/dL)Glycosylated hemoglobin (c) (Hemoglobin A1C)  Considered elevated if values above 7 – 9 %  Blood test analyzes glucose attached to hemoglobin. Since rbc lives about 120 days gives an average of the blood glucose over previous 2 to 3 months
  104. 104. Urine glucose and ketone levels (part of routine urinalysis)  Glucose in urine indicates hyperglycemia (renal threshold is usually 180 mg/dL)  Presence of ketones indicates fat breakdown, indicator of DKA; ketones may be present if person not eatingUrine albumin (part of routine urinalysis)  If albumin present, indicates need for workup for nephropathy  Typical order is creatinine clearance testing
  105. 105. Cholesterol and Triglyceride levelsRecommendationsLDL < 100 mg/dlHDL > 45 mg/dLTriglycerides < 150 mg/dLMonitor risk for atherosclerosis and cardiovascular complications
  106. 106. MONOFILAMENT
  108. 108.  Risk of _________ if give shot of NPH and then NO surgery or surgery delayed  HypoglycemiaBS levels _____ during stress, surgery & illness  hIf not controlled (BG)  osmotic diuresis  dehydration
  109. 109. Management Check BS before surgery No sub-Q IV
  111. 111. HOSPITALIZED DIABETICIndependenceSliding scaleDiets  NPO  Still need insulin  Clear liquids  Most simple carbs  Low sugar if possible
  112. 112. PREVENTION
  113. 113. PREVENTION OF TYPE 2 DIABETESMELLITUSGuidelines from the American College of Clinical Endocrinologists  Weight reduction  Proper nutrition  Regular physical activity  Cardiovascular risk factor reduction  Aggressive treatment of hypertension and dyslipidemiaBlood glucose screening at 3 year intervals starting at age 45 for persons in high risk groups