2023 Diabetes Mellitus.pptx

DM

1. DIABETES MELLITUS

2. S ession Objectives On completion of this session, students will be able to: Define Diabetes Mellitus Describe the Pathophysiology of Diabetes Mellitus Discuss the different types of Diabetes Mellitus Differentiate between type 1 and type 2 diabetes Identify the clinical manifestation of Diabetes Mellitus Describe the diagnostic approaches of DM Describe the relationship between diet, exercise, and medication ( ie , insulin or oral hypoglycemic agents) for people with diabetes Identify acute and chronic complications of DM.

3. Introduction Pancreas The pancreas functions: Exocrine function: produces and secretes digestive enzymes Endocrine Function: produces important hormones in Islets of Langerhans ; insulin, glucagon, and Somatostatin .

4. Pancreatic Hormones Insulin Produced by the beta cells (ß-cells) in the pancreas. stimulates the uptake of glucose by body cells decreasing blood levels of glucose Somatostatin Produced by the delta Cells (  -cells ) in the pancreas. Inhibits both glucagon and insulin.

5. Pancreatic Hormones Glucagon Produced by the alpha cells (  -cells) . Stimulates the breakdown of glycogen and the release of glucose from liver increasing blood levels of glucose. When liver glucose is not available, Lipolysis ( breakdown of fat) OR Proteolysis (breakdown of aas ) occurs Glucagon and insulin work together to regulate & maintain blood sugar levels

6. Insulin Pancreas secretes 40-50 units of insulin ( U-40 to 50 ) daily in two steps: Secreted at low levels during fasting ( basal insulin secretion) Increased levels after eating ( prandial insulin secretion) An early burst of insulin occurs within 10 minutes of eating Then proceeds with increasing release as long as hyperglycemia is present

7. Functions of insulin Enables glucose to be transported into cells for energy for the body Glucose is the preferred fuel of the body cells and the only fuel that the brain can use Facilitates conversion of: excess glucose  fat glucose  glycogen to be stored in muscles and the liver Prevents the breakdown of body protein for energy

8. How Food Becomes Glucose During digestion, food is broken down to sugar (glucose) Insulin lowers blood sugar by helping sugar move from blood into cells The body’s cells use sugar for energy Pancreas

9. Glucose Insulin Pancreas Muscle cells Glucose Bloodstream Glucose and Insulin Carbohydrate

10. What Is Diabetes Mellitus ? In people with diabetes… The pancreas does not make any insulin The pancreas does not make enough insulin (this gets worse with time) The body prevents the insulin that is being made from working correctly Blood sugar gets too high and can lead to many serious problems (complications) OR OR

11. Epidemiology of DM 3rd leading cause death, 10.5% of the adult population (20-79 years) has diabetes and half of them are unaware of it (IDF, 2021) In 2021 about 537 million adults are living with DM , and by 2045, IDF projects 1 in 8 adults (approximately 783 millions will be living with DM), i.e an increase of 46%. Ethiopia : 0.5% & 4.7% prevalent in the overall population and over 40 years of age

12. Types of Diabetes Type 1 DM /T1DM/ Type 2 DM /T2DM/ Gestational DM Other types: LADA (Latent Autoimmune Diabetes in Adults) MODY (maturity-onset diabetes of youth) Secondary Diabetes Mellitus

13. Type 1 diabetes Mellitus /T1DM/ Previously called IDDM or juvenile-onset DM. Characterized by an acute onset. Usually strikes children and young adults, although disease onset can occur at any age. May account for 5% to 10% of all diagnosed cases of diabetes.

14. T1DM Etiology: Most cases of T1D are due to destruction of the pancreatic ß-cells by T-cells (WBCs concerned with the immune system). Clinical symptoms of T1D occur when ~90% of ß-cells cells have been destroyed.

15. Pathophysiology of T1DM

16. Type 2 diabetes Mellitus Previously called NIDDM or adult-onset DM . May account for about 90% to 95% of all diagnosed cases of diabetes. Usually seen in older people. With the onset many people do not have dramatic symptoms compared to those with T1D.

17. T2DM Associated with older age, obesity, family history of DM, history of gestational diabetes, impaired glucose metabolism, physical inactivity, & race/ethnicity. In recent years, T2D has been increasingly found among children and adolescents; in association with increasing early obesity and in those who have a family history of T2D, or whose mothers had diabetes in pregnancy

18. T2DM Etiology: it results from either Insulin resistance, /IR/ (overweight people), is the decreased response of the liver and peripheral tissues (muscle, fat) to insulin, Inadequate insulin production (lean people), or combination of both .

19. IR– reduced response to circulating insulin Insulin resistance  Glucose output  Glucose uptake  Glucose uptake Hyperglycemia Liver Muscle Adipose tissue IR

20. Insulin resistance and  -cell dysfunction are core defects of type 2 diabetes Insulin resistance Genetic susceptibility, obesity, sedentary lifestyle Type 2 diabetes IR b -cell dysfunction  Rhodes CJ & White MF. Eur J Clin Invest 2002; 32 (Suppl. 3):3–13.

21. Pathophysiology of T2DM

22. Difference between T1DM and T2DM Characteristics Type 1 Diabetes Type 2 Diabetes Formerly known as IDDM or “Juvenile-onset” DM NIDDM or “adult-onset” DM Etiology Autoimmune Peripheral resistance % of diabetic pop/n 5-10% 90-95% Age of onset Usually < 30 yr + some adults Usually > 40 + some obese children Onset Rapid Gradual Pancreatic function Little or no insulin Insulin is: low, normal or high Family history Generally not strong Strong Obesity Rare (Normal or underweight) Common (80% are overweight ) Hx of ketoacidosis Often present Rare except in stress Clinical presentation moderate to severe symptoms: 3Ps, fatigue, wt loss and ketoacidosis Mild symptoms: Polyuria and fatigue. Diagnosed on routine PE Treatment Insulin, Diet, Exercise Diet , Exercise, Oral anti-diabetics , Insulin

23. Gestational D iabetes Mellitus/GDM/ Hyperglycemia diagnosed in some women during pregnancy . Ethiology: placental hormones, which causes insulin resistance. During pregnancy, GDM requires treatment to normalize maternal blood glucose levels to avoid complications in the infant.

24. GDM After pregnancy, 5% to 10% of women with gestational diabetes are found to have T2D. Women who have had gestational diabetes have a 20% to 50% chance of developing T2D in the next 5-10 years. Screening for diabetes during pregnancy is now being recommended between the 24th & 28th weeks of gestation.

25. GDM GDM occurs more frequently among : age 25 years or older; age 25 years or younger and obese; family Hx of diabetes in first-degree relatives; or Member of an ethnic/racial group with a high prevalence of diabetes ( eg , Hispanic American, Native American, Asian American, African American).

26. Secondary DM Secondary causes of DM include: Acromegaly, Cushing syndrome, Thyrotoxicosis , Chronic pancreatitis, Cancer Drugs

27. Risk factors of DM Risk factors that cannot be changed : Family history of diabetes High-risk ethnic population History of heart disease History of GDM or delivery of babies over 4kg (9 lbs) Age ≥ 45 years Risk factors that can be changed: Overweight (i.e., BMI ≥ 27 kg/m2) High blood pressure (≥140/90 mm Hg) Physical inactivity

28. Clinical manifestations of DM

29. CMs of DM Other symptoms include: sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infection, Impotence in men, The signs of ketoacidosis are: Nausea, Vomiting, Pain in the stomach, Rapid / Acidotic breathing, High pulse rate, Abnormal tendency to sleep

30. CMs of DM Some patients may be Asymptomatic mainly Type 2 and Gestational diabetes patients In the long term, T1D can severely hurt the blood vessels in vital organs. This can further cause damage to the heart, eyes, kidneys or other body organs. T2D can cause atherosclerosis with blood vessel narrowing, heart disease and stroke.

31. In the long term, Diabetes Can Cause Problems in Many Parts of the Body: Nerves: Unusual sensations: tingling, burning, numbness, or shooting pain Problems with digestion Sexual dysfunction Eyes: Blurred vision/ vision loss Heart: Chest pain Shortness of breath Fast heart beat Kidneys: Swelling in feet and legs Increase in blood pressure Blood Vessels: Slow healing of wounds

32. DIAGNOSIS OF DIABETES

33. Laboratory Tests 1. Blood Tests FBG test: two tests > 126 mg/ dL OGTT: > 200 mg/ dL at 2hrs. Glycosylated hemoglobin (HbA1c) test FSBS (finger stick blood sugar)

34. Laboratory Tests Hemoglobin A1c is: glycosylated hemoglobin . a good indicator of blood glucose control. gives a % that indicates control over the preceding 2-3 months . Performed 2 times a year. A hemoglobin of 6% indicates good control and level >8% indicates action is needed.

35. Checking Both A1C and Blood Sugar Is Important + A1C Reflects average blood sugar for past few months If at goal, check twice a year* Blood Sugar Provides instant feedback of current blood sugar level *If not at goal or if treatment changes, check more often ( eg , every 3 months). Checking both A1C and blood sugar helps assess diabetes control American Diabetes Association. Diabetes Care. 2010;33( suppl 1):S11-S61.

36. Laboratory Tests 2. Urine Test: Urine Test If blood glucose test strips are not available Ketone Renal function Glucose

37. Diagnostic Criteria of Diabetes American Diabetes Association. Diabetes Care. 2004;27( suppl 1):S5-S10 FPG 2-h PPG (OGTT) 126 60 80 100 120 140 160 180 200 Plasma glucose (mg/ dL ) Normal Diabetes Mellitus 240 220 Diabetes Mellitus Normal IGT IGT Normal Diabetes Mellitus C/RPG ‘Casual’ -that measured at any time of day . OR Symptoms of DM OR

38. Diagnosis of Pre-diabetes and Diabetes Category ADA & AACE Recommendations ADA Recommendations FPG (blood sugar in the morning, before eating) 2-h PPG (OGTT) (blood sugar after meals)* A1C † No Diabetes <100 mg/ dL <140 mg/ dL <5.7% Prediabetes 100-125 mg/ dL 140-199 mg/ dL 5.7%-6.4% Diabetes ≥126 mg/ dL ≥200 mg/ dL ≥6.5% ADA=American Diabetes Association; AACE=American Association of Clinical Endocrinologists; FPG=fasting plasma glucose; PPG=postprandial glucose. *2-h plasma glucose on the 75-g oral glucose tolerance test. †ADA only. 1. American Diabetes Association. Diabetes Care . 2010;33( suppl 1):S11-S61. 2. Rodbard HW, et al. Endocr Pract . 2007;13( suppl 1):3-68. ** O n 2 separate occasions A1C ~ average blood sugar for past few months

39. Pre-Diabetes Pre-diabetes refers to a state between “normal” and “diabetes”. FBG100 -125mg/ dL (higher than normal but not high enough for diagnosis of diabetes) Affects about 41 million people in USA Previously referred to as either IFG or IGT

40. Pre-Diabetes Impaired Fasting Glucose (IFG) Defined as a FBG >= to 100 but < 126 Impaired Glucose Tolerance (IGT) Defined as a plasma blood glucose of >/= to 140 but < 200 after a 2 hr 75gm glucose tolerance test 8-10% of US population have this problem with a 25 % risk of developing T2DM

41. Values of Diagnosis of DM & Other Hyperglycemias Category Venous Plasma*Glucose concentration, Mmol l -1 (mg dl -1 ) Diabetes mellites Fasting or 2-h post glucose load ≥7.0 (≥126) ≥11.1 (≥200) Impaired Glucose Tolerance (IGT) 2-h post glucose load (≥140 – < 200) Impaired Fasting Glycaemia (IFG) Fasting (≥ 100 - <126 )

42. Screening for DM All persons > 45 years; repeat Q 3 years Additional risk factors: screen at younger age and more frequently Women with a history of GDM: lifelong screening for diabetes or at least Q3 yrs for prediabetes (up to 7x higher risk than non-GDM) GDM test values Overnight fast, 75g OGTT Fasting > 92 mg/dl 1 h > 180 mg/dl 2 h > 153 mg/dl

43. A complete medical evaluation should be performed to Classify the diabetes Detect presence of diabetes complications Review previous treatment, glycemic control in patients with established diabetes Assist in formulating a management plan Provide a basis for continuing care Perform laboratory tests necessary to evaluate each patient’s medical condition Diabetes Care: Initial Evaluation

44. Medical history Age and characteristics of onset of diabetes (e.g., DKA, asymptomatic laboratory finding) Eating patterns, physical activity habits, nutritional status, and weight history; growth and development in children and adolescents Diabetes education history Review of previous treatment regimens and response to therapy (A1C records) Comprehensive Diabetes Evaluation (1)

45. Current treatment of diabetes, including medications, meal plan, physical activity patterns, and results of glucose monitoring and patient’s use of data (1) DKA frequency, severity, and cause Hypoglycemic episodes Hypoglycemia awareness Any severe hypoglycemia: frequency and cause Comprehensive Diabetes Evaluation (2) ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

46. Current treatment of diabetes, including medications, meal plan, physical activity patterns, and results of glucose monitoring and patient’s use of data (2) History of diabetes-related complications Microvascular: retinopathy, nephropathy, neuropathy Sensory neuropathy, including history of foot lesions Autonomic neuropathy, including sexual dysfunction and gastroparesis Macrovascular: CHD, cerebrovascular disease,... Other: psychosocial problems*, dental disease* Comprehensive Diabetes Evaluation (3) ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

47. Physical examination Height, weight, BMI Blood pressure determination Fundoscopic examination* Thyroid palpation Comprehensive foot examination Inspection, Palpation of dorsalis pedis and posterior tibial pulses Determination of proprioception , vibration, and sensation Comprehensive Diabetes Evaluation (4) ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

48. Referrals Eye exam Family planning for women of reproductive age Dietitian Diabetes self-management education Dental examination Mental health professional, if needed Comprehensive Diabetes Evaluation (7) ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

49. Recommendations for Screening of Diabetes Complications in Stable Patients Neuropathy Visual foot inspection and sensation testing each year Retinopathy Dilated and complete eye exam — document each year Cardiovascular Disease Nephropathy Check urine albumin and serum creatinine level each year Peripheral Vascular Disease Foot exam that includes checking pedal pulses each year American Diabetes Association. Diabetes Care. 2010;33(suppl 1):S11-S61. Check blood pressure at each visit and lipids (cholesterol) each year

50. Management of DM

51. Type One: Insulin + Diet + Exercise Type Two : Diet + exercise then Diet + exercise + OHG tablets then Diet + exercise + OHG tablets + insulin

52. Treatment Goals INDEX GOAL Glycemic control A1C Preprandial plasma glucose Peak post prandial plasma glucose FBS or RBS <7% 90-130 mg/dl <180 mg/dl <130 or <200 Blood pressure <130/80 Lipids LDL HDL Triglycerides <100mg/dl >40mg/dl <150mg/dl American Diabetes Association Standards of medical care in diabetes. Diabetes Care 30:S4-S36, 2007

53. Healthcare Team Members of the team include Primary care provider Endocrinologist/ Diabetologist Certified diabetes educator Nutritionist Sub specialists

54. A. Non pharmacologic Therapy Patient or Diabetes Education Healthy eating/Diet Exercise Weight reduction Self-monitoring of blood glucose (SMBG)

55. 1. Diabetes education Diabetes educator is healthcare professional (nurse, dietician or pharmacist)

56. Education topics include: Benefit of weight reduction, diet and regular exercise Self monitoring of blood and urine glucose Insulin administration Management of hypoglycemia Foot & skin care Diabetes mgmt. before, during & after exercise Risk factor & Complications of diabetes

57. 2. Exercise Positive benefits Reduces cardiovascular risks, BP, body fat, weight Maintenance of muscle mass Lowers blood glucose Increases insulin sensitivity in T2D Time 150 min per week ( 3 days) In type 2 DM, resistance training

58. Exercise Problems either hypo/ hyperglycemia Guidelines to avoid these problems Monitor blood glucose before, during & after exercise Delay exercise if: Blood Glucose > 250 mg/dl and Ketone bodies are present If blood Glucose < 100 mg/ dl, ingest carbohydrate before exercise

59. Exercise General Precautions for Exercise in Diabetics Use proper footwear and, if appropriate, other protective equipment. Avoid exercise in extreme heat or cold. Inspect feet daily after exercise. Avoid exercise during periods of poor metabolic control.

60. 3. Weight reduction Maintain normal BMI of 20 and 25. Weight loss: increase sensitivity to insulin and may lead to decrease in the demand of exogenous insulin or the dose of Oral hypoglycemic agents.

61. Weight reduction Benefits of a 10kg weight loss Fall of 50% in fasting glucose Fall of 10% total cholesterol Fall of 15% LDL Fall of 30% triglycerides Rise of 8% HDL Fall of 10 mmHg systolic, 20 mmHg diastolic SIGN guidelines

62. 4. Diet ADA Food groups: CHO- 60% Fats - 30% Protein - 12-20%

63. Diet Dietary Guidelines: Eat a diet low in saturated and total fat. Eat a diet moderate in sodium and sugar. Eat 5 or more fruits and vegetables a day. Choose a diet rich in whole grains. Moderate use of alcohol Eat at the same time every day. Eat about the same amount of carbohydrate with each meal. Avoid simple sugars

64. 5. Self-monitoring of blood glucose (SMBG) Frequent SMBG enables people with diabetes: to adjust the treatment regimen to obtain optimal blood glucose control for detection and prevention of hypoglycemia and hyperglycemia To normalizing blood glucose levels To reduce the risk of long-term diabetic complications.

65. Pharmacotherapy :Type 1 DM The choice of therapy is simple All patients need Insulin

66. Types of Insulin Source Animal sources Recombinant DNA = human insulin Strength The number of units/ml e.g. U-100 , U-20, U-10, U-500, U-40

67. Who should have insulin therapy? Newly Diagnosed Type 1 The Type 2 diabetic on maximum tablets The Type 2 diabetic with contraindications to OHA e.g. renal failure, poor tolerance Pregnancy Post acute MI Acute illness/ infection Control of blood glucose level essential to minimise long term complications

68. Types of Insulin Rapid-acting in sulin e.g. Insulin lispro and insulin aspart Short-acting insulin e.g. Regular insulin Intermediate-acting insulin e.g. NPH and Lente insulin Long-acting insulin e.g. Insulin Glargine Mixture of insulin can provide glycemic control over extended period of time e.g. Humalin 70/30 (NPH + Regular) 71

69. Types of Insulin Preparation Onset (hr) Peak (hr) Eff.duration(hr) Clinical use and rout of administration Rapid-acting Lispro Aspart <0.25 “ 0.5- 1.5 “ 3-4 “ Used in ketoacidosis for rapid control of high sugar & acidosis. It can be administered IV, IM or SC Short acting-inhaled Regular <0.25 0.5-1.5 4-6 Intermediate-acting insulin ( NPH or Lente ) 2–4 h 6–12 h 16–20 h Used for ambulatory long term control of sugar level Given not more than twice a day Rout of administration is limited to SC Long acting Detemir Glargine “ “ Dual peak Dual peak 12-20 24 Not available for use in our country

70. Insulin Combinations 75 / 25 - Protamine lispro + Lispro 50 / 50 - “ + “ 70 / 30 - Protamine aspart + Aspart 70 / 30 - NPH + Reg. Insulin 50 / 50 - “ + “

71. Guidelines For Mixing of Insulin Mix the different insulin formulations in the syringe immediately before injection & inject within 2 min after mixing Do not store insulin as mixture Regulate the response Do not mix insulin glargine or detemir with other insulins

72. Insulin Regimens 75 Example: 1- Morning dose (before breakfast): Regular + NPH or Lente 2- Before evening meal: Regular + NPH or Lente Require strict adherence to the timing of meal and injections

73. INSULIN REGIMENS

74. Insulin administration sites A. Abdomen; B. Lateral and Anterior Aspects of Upper Arm and Thigh; C. Scapular Area on Back; and D. Upper Ventrodorsal Gluteal Area.

75. Rotation Rotation between different sites (e.g. abdomen to arm) no longer recommended Choose one site to maintain day to day consistent absorption Rotation within site must occur to prevent lipoatrophy Inject at appropriate angle (45-90) depending on depth of subcutaneous tissue

76. Stepwise Management of T2DM Insulin ± oral agents Oral combination Oral monotherapy Diet & exercise

77. Oral Hypoglycaemic Agents The use of oral medications with diet & exercise can manage the problem But oral hypoglycaemics are NOT insulin & therefore cannot replace insulin Hypoglycaemics help the body to utilise or make insulin Beta cells must make enough insulin to work, otherwise combination with insulin is necessary.

78. Classes of Oral Hypoglycaemic Agents Target insulin secretion Sulphonylureas ( glibenclamide ) Meglitinides ( repaglinide ) Target insulin resistance Biguanides ( metformin ) ( Thiazolidinediones ) ( rosiglitazone ) Target glucose absorption from intestine Alpha glucosidase inhibitors ( ascarbase )

79. Sites of action of oral antidiabetic agents  Glucose output  Insulin resistance Biguanides  Insulin secretion Sulfonylureas/ meglitinides  Carbohydrate breakdown/ absorption  -glucosidase inhibitors  Insulin resistance Thiazolidinediones Kobayashi M. Diabetes Obes Metab 1999; 1 (Suppl. 1):S32–S40. Nattrass M & Bailey CJ. Baillieres Best Pract Res Clin Endocrinol Metab 1999; 13:309–329.

80. drugs advantages Disadvantages biguanides Weight loss Lactic acidosis, GI dysfunctions Alpha glucosidase inhibitor Reduce postprandial glycaemia Liver & GI dysfunctions DPP4 inhibitors No hypoglcaemia --- sulfonylureas Lowers fasting blood glucose Weight gain, hypoglyacemia Nonsulfonylureas thiazolidinediones Shorter onset of action Lowers postprandial glycaemia Lower an insulin requirements Hypoglycaemia CHF, weight gain, fractures

81. Disease Progression Insulin initiation Insulin intensification As Type 2 Diabetes Progresses, Insulin Therapy is Needed Oral therapy initiation Hypothetical Model

82. Insulin Therapy in Type 2 Diabetes Reasons for use of insulin Progression of T2D over time People uncontrolled with maximal doses of OHA therapy (who are insulin resistant ) Pregnancy (oral therapy contraindicated) Patients with organ failure for whom oral therapy is contraindicated Acute illness/surgery in T2D

83. New technologies in treatment of diabetes Islet cell transplantation Gene therapy Foot ulcer- dermograft Artificial pancreas

84. Complications of DM

85. Acute Complications Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) Hypoglycemia

86. 1. Hypoglycaemia (Insulin Reactions) Is abnormally low blood glucose level occurs when the blood glucose falls to < 50 to 60 mg/ dL . Blood glucose values 45mg/dl are too low for normal neurological (brain) function. Even people without diabetes may develop symptoms of hypoglycemia when the blood glucose level is <65 mg/dl.

87. Causes too much insulin/tablets delayed or missed meal not enough carbohydrate in a meal more exercise than usual Alcohol ( especially if not taken with food ) illness

88. Hypoglycaemia Signs and Symptoms Initially occur as a result of adrenalin (autonomic activation) and include: Trembling Rapid heart rate Pounding heart (palpitations) Sweating Pallor Hunger and/or nausea

89. Hypoglycaemia symptoms of neuroglycopenia Difficulty in concentrating Irritability Blurred or double vision Difficulty hearing Slurred speech Poor judgment and confusion Dizziness and unsteady gait Tiredness Nightmares Loss of consciousness Seizures Death

90. Grading the seriousness of hypoglycemia 1. Mild hypoglycemia Occurs when the patient recognizes hypoglycemia and is able to self-treat without the assistance of others. Blood glucose values are around <70 mg/dl.

91. Grading the seriousness of hypoglycemia 2. Moderate hypoglycemia Occurs when the patient is aware of, responds to, and treats the hypoglycemia, but needs someone else to assist. Blood glucose values are again around <70 mg/dl

92. Grading the seriousness of hypoglycemia 3. Severe hypoglycemia It is defined when the patient: Either loses consciousness or has a convulsion (fit) associated with low blood glucose

93. Management of hypoglycaemia Immediate treatment. If the pt is having severe symptoms, give either: IV glucose ( eg 10% glucose drip or 1ml/ kg of 25% dextrose) OR IV, IM or SC glucagon (1 mg for adults). After an injection of glucagon, the blood glucose would be expected to rise within 10 -15 mins.

94. Management of hypoglycaemia If neither glucagon nor IV glucose is available, the usual recommendation is 15 g of a fast-acting concentrated source of CHO such as the following, given orally: 3 or 4 commercially prepared glucose tabs 4 to 6 oz of fruit juice 6 to 10 Life Savers or other hard candies 2 to 3 teaspoons of sugar or honey

95. If no improvement within 5 – 10 minutes, repeat the high GI food/drink Once improvement has occurred (feeling better, BGL rising if testing is available) then follow with a low GI snack eg glass of milk yoghurt sandwich piece of fruit meal if it is due

96. Preventing hypoglycemia 1: Teach the patient often about: The symptoms of hypoglycemia to recognize it. Those foods high in both fats and sugar (for example chocolate, fat-containing milk, peanut butter) 2: Remind them about what might cause hypoglycaemia .

97. 2. Diabetic Ketoacidosis Definition: DKA is an acute metabolic crisis in pts with DM. Pathophysiology DKA is caused by an absence or markedly inadequate amount of insulin. This deficit in insulin results in disorders in the metabolism of CHO, protein, and fat.

98. The three main clinical features of DKA are: Hyperglycemia Dehydration and electrolyte loss Acidosis

99. DKA Precipitating Factors Failure to take insulin Failure to increase insulin Illness/Infection Pneumonia MI Stroke Acute stress Trauma Emotional Medical Stress Counter regulatory hormones Oppose insulin Stimulate glucagon release Hypovolmemia Increases glucagon and catecholamines Decreased renal blood flow Decreases glucagon degradation by the kidney

100. Signs and symptoms Pathophysiologic effect Clinical features Elevated blood glucose Elevated blood glucose and urine glucose Dehydration Sunken eyes, dry mouth, decreased skin turgour, decreased perfusion Altered electrolytes Irritability, change in level of consciousness Metabolic acidosis (ketosis) Acidotic breathing, nausea, vomiting, abdominal pain, altered LOC

101. Lab Findings RBS: Hyperglycemia Anion gap acidosis Serum K+ level Serum Na+ level Urine and serum ketones Hyperosmolarity ABG analysis: can diagnose metabolic acidosis Bicarbonate <15 mEq /L pH <7.3

102. Treatment of DKA Managing DKA involves the following steps: 1: Correction of shock 2: Correction of dehydration 3: Correction of deficits in electrolytes 4: Correction of hyperglycaemia 5: Correction of acidosis 6: Treatment of infection 7: Treatment of complications (cerebral oedema )

103. Treatment of DKA Initial hospital management Replace fluid and electrolytes IV Insulin therapy Glucose administration Watch for complications Disconnect insulin pump Once resolved Convert to home insulin regimen Prevent recurrence

104. Treatment of DKA Fluids & Electrolytes Fluid replacement Restores perfusion of the tissues Lowers counter regulatory hormones Average fluid deficit 3-5 liters Initial resuscitation 1-2 liters of NS over the first 2 hours Slower rates of 500cc/hr x 4 hrs or 250 cc/hr x 4 hours When fluid overload is a concern If hypernatremia develops ½ NS can be used

105. Treatment of DKA Fluids & Electrolytes Hyperkalemia initially present Resolves quickly with insulin drip Once urine output is present and K<5.0, add 20-40 meq KCL per liter. Phosphate deficit May want to use Kphos Bicarbonate not given unless pH <7 or bicarbonate <5 mmol /L

106. Treatment of DKA Insulin Therapy IV bolus of 0.1-0.2 units/kg ( ~ 10 units) regular insulin Follow with hourly regular insulin infusion Glucose levels Decrease 75-100 mg/dl hour Minimize rapid fluid shifts Continue IV insulin until urine is free of ketones

107. Treatment of DKA Glucose Adm. Supplemental glucose Hypoglycemia occurs Insulin has restored glucose uptake Suppressed glucagon Prevents rapid decline in plasma osmolality Rapid decrease in insulin could lead to cerebral edema Glucose decreases before ketone levels decrease Start glucose when plasma glucose <300 mg/dl

108. Insulin-Glucose Infusion for DKA Blood glucose Insulin Infusion D5W Infusion <70 0.5 units/hr 150 cc/hr 70-100 1.0 125 101-150 2.0 100 151-200 3.0 100 201-250 4.0 75 251-300 6.0 50 301-350 8.0 351-400 10.0 401-450 12.0 451-500 15.0 >500 20.0

109. Complications of DKA Infection Precipitates DKA Fever Leukocytosis can be secondary to acidosis Shock If not improving with fluids r/o MI Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days after DKA Cerebral Edema First 24 hours Mental status changes Tx : Mannitol May require intubation with hyperventilation Pulmonary Edema Result of aggressive fluid resuscitation

110. Once DKA Resolved; ... Most patients require 0.5-0.6 units/kg/day Pubertal or highly insulin resistant patients 0.8-1.0 units/kg/day Long acting insulin 1/2-2/3 daily requirement NPH, Lente , Ultralente or Lantus Short acting insulin 1/3-1/2 given at meals Regular, Humalog , Novolog Give insulin at least 2 hours prior to weaning insulin infusion.

111. Prevention of DKA Never omit insulin Cut long acting in half Prevent dehydration and hypoglycemia Monitor blood sugars frequently Monitor for ketosis Provide supplemental fast acting insulin Treat underlying triggers Maintain contact with medical team

112. 3. Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia & dehydration Unable to excrete glucose as quickly as it enters the extracellular space When sum of glucose excretion plus metabolism is << the rate which glucose enters extracellular space.

113. Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and hyperosmolarity High mortality (12-46%) At risk Older patients with intercurrent illness Impaired ability to ingest fluids Urine volume falls Decreased glucose excretion Elevated glucose causes CNS dysfunction and fluid intake impaired No ketones Some insulin may be present Extreme hyperglycemia inhibits lipolysis

114. HHNS Presentation Extreme dehydration Supine or orthostatic hypotension Confusion coma Neurological findings Seizures Hemiparesis Hyperreflexia

115. HHNS Presentation Glucose > 600 mg/dl Sodium Normal, elevated or low Potassium Normal or elevated Bicarbonate >15 mEq /L Osmolality > 320 mOsm /L

116. HHNS Treatment Fluid repletion NS 2-3 liters rapidly Total deficit = 10 liters Replete ½ in first 6 hours Insulin Make sure perfusion is adequate Insulin drip 0.1U/kg/hr Treat underlying precipitating illness

117. Clinical Errors Fluid shift and shock Giving insulin without sufficient fluids Using hypertonic glucose solutions Hyperkalemia Premature potassium administration before insulin has begun to act Hypokalemia Failure to administer potassium once levels falling Recurrent ketoacidosis Premature discontinuation of insulin and fluids when ketones still present Hypoglycemia Insufficient glucose administration

118. Long-Term Complications of DM Macrovascular complications Cardiovascular disease (heart attack) Cerebrovascular disease (strokes) Microvascular complications Blindness (retinal proliferation, macular degeneration) Amputations Diabetic neuropathy (diffuse, generalized, or focal) Erectile dysfunction

119. Risk factors and complications Microvascular disease Eyes Kidneys Nerves Macrovascular disease Ischaemic heart disease Strokes Peripheral vascular disease Feet Hypertension Hyperglycaemia Dyslipidaemia Coagulopathy Smoking

120. Biology of Macrovascular Injury Metabolic injury to large vessels Heart Brain Extremities CAD – MI – CHF Cerebrovascular disease Peripheral vascular disease – Ulceration – Gangrene – Amputation

121. Biology of Microvascular Injury Hyperglycemia Neuropathy Peripheral Autonomic Kidney Nerves Retinopathy - Cataract - Glaucoma Nephropathy Microalbuminuria Gross albuminuria Blindness Kidney failure Amputation Death and/or disability Eye

122. Microvascular Complications of Diabetes 1. Retinopathy: Damage to blood vessels in and around the retina. It could occur with varying degrees of severity. Classification of Diabetic retinopathy Background retinopathy: early changes which is often asymptomatic Maculopathy : which manifests with central vision loss Proliferative retinopathy: asymptomatic unless complicated by hemorrhage

123. Microvascular Complications of Diabetes 4. Advanced diabetic disease : may cause severe vision loss to the extent of complete blindness Retinal detachment Vitreous hemorrhage Normal -------------  Small hemorrhages ---------  Large hemorrhage

124. Microvascular Complications of Diabetes Management Laser therapy ASA 100 mg /day may prevents further occlusion of small capillaries Surgery: Viterotomy removes blood clots and fibrosis that obstruct vision

125. Microvascular Complications of Diabetes 2. Nephropathy: Glomeruli are damaged in the kidneys. Results in loss of protein May lead to kidney failure Clincal features Periorbital edema, pedal edema Anemia, Uremia

126. Microvascular Complications of Diabetes Management Tight blood pressure control ACE- inhibitors: decreases progression of renal diseases Renal transplantation or Dialysis in End stage renal diseases

127. Microvascular Complications of Diabetes 3. Neuropathy Nerve fibers degenerate Blood vessels supplying the nerves are ‘grossly diseased’ Symptoms: include Burning sensation, numbness Diarrhea Impotence Foot ulcer

128. Microvascular Complications of Diabetes Neuropathy management Symptomatic treatment: Pain control Diarrhea control Treatment of impotence Avoidance of neurotoxins -> alcohol, smoking Vit . supp(B12, folate ) Symptomatic treatment Should check their feet daily & take precaution

129. Microvascular Complications of Diabetes 4. Diabetic Foot Ulcer Underlying mechanism for diabetic foot ulcers Neuropathy Loss of pain sensation exposes to injury Loss of sweating results dry skin that is susceptible to injury Vascular: poor blood supply to the foot causes decreased healing of wound poor recovery from secondary infections. Abnormal Pressure loading : due to neuropathy or anatomical deformity of the feet. Since the foot is not in a normal anatomic position it is exposed to abnormal load and pressure sores develop.

130. Microvascular Complications of Diabetes Foot care: should be essential part of diabetes care Put on comfortable shoe Check for stones in shoe Examine the foot daily to detect problems earlier Wash dry and oil the feet Take caution during nail cutting Treat athletes’ foot or any other foot infection as early as possible Remove hard skin Do not use hot water to wash the feet

131. Common nursing diagnoses Imbalanced nutrition related to imbalances in insulin, food, and physical activity Risk for impaired skin integrity related to immobility and lack of sensation (caused by neuropathy) Deficient knowledge about diabetes self-care skills and for disease process Risk for injury related to sensory alterations Risk for delayed surgical recovery Body image disturbance RT disease process

132. Nursing intervention Educate the patient about: The disease and the importance of maintaining normal glucose levels. Blood glucose monitoring. Diet and food choices, including portion sizes. Urge smoking cessation. Self-care. Acute management. Prevention of complications, such as hyperglycemia and hypoglycemia.

133. Common Nursing intervention Educate the patient about: Exercise. Self-injection of insulin (Type I). Importance of daily medications. Hypoglycemia signs and symptoms and interventions. Signs and symptoms and the management of hypoglycemia. The management of hyperglycemia. Glucagon injection for hypoglycemic events.

134. Reading Assignment Methods of insulin administration? How to calculate the dose of insulin needed?