Diabetes mellitus
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Diabetes mellitus

Diabetes mellitus

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Diabetes mellitus Presentation Transcript

  • 1. DIABETESMELLITUS
  • 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. Endocrine: carried out by islets of Langerhans alpha cells – glucagons beta cells – insulin delta cells – somatostatin
  • 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. INSULINPrimary function…  Stimulates the active transport of glucose  from the blood into muscle, liver and adipose tissue   __?__ blood glucose levels i
  • 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. 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. 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. 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. INSULIN Eat the glucose  Muscle  energy Storage of glucose  Liver = freezer  Glycogen  Synthesis of Adipose tissue = 2nd freezer Give it away  Glycosuria
  • 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. OTHER FUNCTIONS OF INSULINPromoting the conversion of fatty acids  fat  Adipose tissue
  • 13. OTHER FUNCTIONS OF INSULINPreventing the breakdown of fat  ketone bodiesKetone bodies: the byproduct of fat metabolism
  • 14. OTHER FUNCTIONS OF INSULINStimulating protein synthesisInhibiting the breakdown of protein  amino acids
  • 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. GLUCAGONProduced and secreted by the Alpha cells of the Islets of LangerhansGlucagon stimulates the release of Glucose by the liver
  • 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. The effect of glucagon h blood glucose level Hyperglycemia
  • 19. GLUCAGONGlucagon is secreted is response to Hypoglycemia StressHypoglycemia may occur during Stress Exercise Fasting
  • 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. SOMATOSTATINHas a hypoglycemic effect
  • 22. DIABETESMELLITUS
  • 23. PREVALENCE
  • 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. 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. 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. 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. 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. In 2009, diabetes mellitus was the seventh leading cause of death in the United States
  • 30. Approximately 1 in 5 health care dollars in the United States was spent caring for someone with diagnosed diabetes
  • 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. TYPES OF DM
  • 33. Type 1Type 2GDM
  • 34. TYPE 1 DM
  • 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. 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. 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. 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.  Brittle DM Unstable DM Absolute insulin deficiency DKA prone Thin
  • 40. Process of beta cell destruction occurs slowly;hyperglycemia occurs when 80 – 90% is destroyed;often trigger stressor event (e. g. illness)
  • 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. S&S OF TYPE 1 DMGlycosuria  Glucose in the urine
  • 43. S&S OF TYPE 1 DMPolyuria  Osmotic diuresisNocturia  Urinating during the nightNursing diagnosis  Fluid Volume Deficit
  • 44. S&S OF TYPE 1 DMPolydipsia  Excessive thirst
  • 45. S&S OF TYPE 1 DMPolyphagia  Excessive hunger
  • 46. S&S OF TYPE 1 DMDehydration
  • 47. S&S OF TYPE 1 DMKetonuria  No insulin  Burn fats  Byproduct  ketones  ↑ ketone in the blood  Metabolic Acidosis
  • 48.  Liver can not excrete all of the ketones  spill into the urine  Ketonuria
  • 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. 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. PATHOPHYSIOLOGY: TYPE 2 Obesity  insulin resistance by tissues Compensatory increase of insulin production by islets  insulin resistance & defect in insulin receptors HYPERGLYCEMIA
  • 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. 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. Chronic elevations in blood glucose levels Accelerated atherosclerosis Impaired immune function Infection Delayed wound healingHypertension Coronary Stroke Increased low artery disease density lipoprotein
  • 55. TYPE 2 DM
  • 56. DIABETES TYPE 2condition of fasting hyperglycemia occurring despite availability of body’s own insulin
  • 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. 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. TYPE 2 DMEtiology  The pancreas cannot produce enough insulin for body’s needs  Impaired insulin secretion
  • 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. 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. Simplified scheme for the pathophysiology oftype 2 diabetes mellitus.
  • 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. 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. 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. CLASSIFICATIONS OF DM3. Gestational diabetes mellitus  DM first detected during pregnancy  Due to placental hormones
  • 67. GESTATIONALOccurs during pregnancy2nd -3rd trimesterScreening 24-28 weeksExtra metabolic demands triggers onset
  • 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. 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. 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. 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. 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. RISK FACTORS
  • 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. 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. 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. 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. 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
  • 79. CLINICAL MANIFESTATIONS
  • 80. S&S OF DIABETES MELLITUSDefinition:  A group of disorders characterized by chronic Hyperglycemia3 P’s Polydipsia Polyuria Polyphagia
  • 81. S&S OF HYPERGLYCEMIANeuro Fatigue C/O headache Dull senses Stupor Drowsy Loss of Consciousness Blurred Vision
  • 82. S&S OF HYPERGLYCEMIACardiovascular Tachycardia Decreased BP (Dehydration)Respirations Kussmauls respirations Sweet and fruity breath Acetone breath
  • 83. S&S OF HYPERGLYCEMIAGastro-intestinal Polyphagia (Decreased hunger in late stages) N/V Abd. Pain Polydipsia Dehydration
  • 84. S&S OF HYPERGLYCEMIAGenital-urinary Polyuria Nocturia GlycosuriaSkeletal-muscular Weak
  • 85. S&S OF HYPERGLYCEMIAIntegumentary Dry skin Flushed face Hypothermia
  • 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. DX EXAMS
  • 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. DIAGNOSTICS FBS2-hr PPGOGTTGlycosylated hemoglobinUrine ketone levels
  • 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. DIAGNOSIS OF DMFBS: ≥126mg/dlOGTT: 2-hour plasma glucose ≥ 200mg/dlSymptoms of DM plus RBS ≥ 200mg/dl
  • 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. FASTING BLOOD GLUCOSENURSING RESPONSIBILITYFast 6-8 hoursWater OKNo insulin or anti-diabetic medsExercise will effect resultsMeds that interfere
  • 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. 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. 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. 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. 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. 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. HGB A1C Provides an average blood glucose levels Past 2-3 months Can be taken any time
  • 101. Normal levels (non-diabetic) 4-6%Diabetic level (goal) <8%
  • 102. HBA1c(%) Mean blood sugar (mg/dl)6 1357 1708 2059 24010 27511 31012 345
  • 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. 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. 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. MONOFILAMENT
  • 107. DIABETICS & SURGERY
  • 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. Management Check BS before surgery No sub-Q IV
  • 110. HOSPITALIZED DIABETIC
  • 111. HOSPITALIZED DIABETICIndependenceSliding scaleDiets  NPO  Still need insulin  Clear liquids  Most simple carbs  Low sugar if possible
  • 112. PREVENTION
  • 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