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Insulin & Oh Gs(10 13)


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Insulin & Oh Gs(10 13)

  2. 2. Insulin and Oral Hypoglycemics <ul><li>OBJECTIVES: </li></ul><ul><li>1. Understand the process of insulin synthesis and secretion </li></ul><ul><li>2. Understand the physiology of circulating insulin, C-peptide and proinsulin. </li></ul><ul><li>3. Identify factors influencing insulin secretion. </li></ul><ul><li>4. Describe the metabolic effects of insulin and the major metabolic aberrations of insulin resistance. </li></ul><ul><li>5. Identify therapeutic problems encountered in insulin therapy. </li></ul>DR.UMA K.
  3. 3. Insulin and Oral Hypoglycemics <ul><li>OBJECTIVES: </li></ul><ul><li>6.Explain the limitations of oral Hypoglycemics in management </li></ul><ul><li>7. Explain the differences among commercially available insulin preparations. </li></ul><ul><li>8. Understand the different mechanisms of action between the commonly used oral hypoglycemic agents. </li></ul>DR.UMA K.
  4. 4. Prototype Drugs: <ul><li>Insulin and analogs: </li></ul><ul><li>Insulin (Humulin) </li></ul><ul><li>LisPro (Humalog) </li></ul><ul><li>Glargine (Lantus) </li></ul><ul><li>Insulin aspart (NovoLog) </li></ul><ul><li>Inhaled Insulin (Exubera) </li></ul><ul><li>Somatostatin analogs: </li></ul><ul><li>Octreotide (Sandostatin) </li></ul><ul><li>Hyperglycemic Agent </li></ul><ul><li>Diazoxide (Proglycem) </li></ul><ul><li>Oral Hypoglycemic Agents: </li></ul><ul><li>Sulfonylureas: Glipizide </li></ul><ul><li>Tolbutamide </li></ul><ul><li>Meglitinides: Repaglinide </li></ul><ul><li>Biguanides: Metformin </li></ul><ul><li>Thiazolidinediones </li></ul><ul><li>Rosiglitazone, Pioglitazone </li></ul><ul><li>Synthetic Incretin: Exenatide </li></ul><ul><li>Alphaglucosidase inhibitors: Acarbose, Miglitol </li></ul><ul><li>Others : Gaurgum </li></ul>DR.UMA K.
  5. 5. Pancreas <ul><li>Endocrine </li></ul><ul><li>Exocrine </li></ul><ul><li>Islands of Langerhans secretes 3 hormones: </li></ul><ul><ul><li>Glucagon (alpha cells) </li></ul></ul><ul><ul><li>Insulin (beta cells) </li></ul></ul><ul><ul><li>Delta cells - somatostatin </li></ul></ul>DR.UMA K.
  6. 6. INSULIN: Polypeptide hormone secreted by the pancreatic Islets of Langerhans essential for the metabolism of carbohydrates and is used in the treatment and control of diabetes mellitus DR.UMA K.
  7. 7. DR.UMA K.
  8. 8. Insulin Biosynthesis and Secretion <ul><li>1. Insulin gene is on chromosome 11 </li></ul><ul><li>2. Synthesized by β cells of the Islets of </li></ul><ul><li>Langerhans of the endocrine pancreas as a 12,000 Dalton precursor (preproinsulin) which is processed to final secreted products (proinsulin, insulin, C-peptide). </li></ul><ul><li>3. Synthesis is regulated at the transcriptional and translational levels. </li></ul>DR.UMA K.
  9. 9. Three Biosynthetic Products: <ul><li>A. Proinsulin </li></ul><ul><li>- Released in small amounts (3-4%) </li></ul><ul><li>except in pathologic states* </li></ul><ul><li>- Constitutes 10-50% of circulating immunoreactive insulin content </li></ul><ul><li>- Reduced biological action ~ 2% activity of insulin </li></ul><ul><li>- Prolonged circulation time - T1/2 = 17 min. </li></ul><ul><li>* Insulinoma, familial hyperproinsulinemia </li></ul><ul><li>- Diagnostic = 80% </li></ul>DR.UMA K.
  10. 10. B. C-peptide <ul><li>- Connecting peptide (joins A and B chains) </li></ul><ul><li>- Removed from proinsulin by proteases within secretory granules </li></ul><ul><li>- Released in equimolar amounts with insulin </li></ul><ul><li>- Not removed from the circulation by the liver - thus found in higher concentrations than insulin (4:1) </li></ul><ul><li>- Clinically important marker of insulin secretion </li></ul><ul><li>DIAGNOSTIC </li></ul>DR.UMA K.
  11. 11. C. Insulin <ul><li>Released from the beta cell in a rapid first phase and </li></ul><ul><li>slower second phase </li></ul><ul><li>- Represents release of insulin stored in granules and </li></ul><ul><li>newly synthesized insulin, respectively. </li></ul><ul><li>- Significant amount is removed during first pass </li></ul><ul><li>through the liver, therefore hepatic insulin levels exceed </li></ul><ul><li>peripheral level. </li></ul><ul><li>- T1/2 = 5-6 min </li></ul>DR.UMA K.
  12. 12. DR.UMA K. proinsulin
  13. 13. Insulin needs <ul><li>Normal daily pancreatic output 30-40U/day </li></ul><ul><li>Diabetics usually need 30-50U/day (best to start lower and build up) </li></ul><ul><li>Need continuous background level of insulin with larger amounts at the time of meals and snacks </li></ul>DR.UMA K.
  14. 14. Endogenous Insulin <ul><li>Protein Hormone </li></ul><ul><li>Secreted Beta Cells-Pancreas </li></ul><ul><li>1-2 Units per hour </li></ul><ul><li>4-6 Units per meal </li></ul><ul><ul><li>1 units x 24hrs + </li></ul></ul><ul><ul><li>4 units x 3 meals </li></ul></ul><ul><ul><ul><li>Total 36 Units per day </li></ul></ul></ul>DR.UMA K.
  15. 15. Normal Insulin Production <ul><li>Pancreas releases insulin into the bloodstream </li></ul><ul><li>Blood carries it to all cells in the body </li></ul>DR.UMA K.
  16. 16. Normal Insulin Profiles After a meal Just to function normally Basic Requirements What happens when you eat and a background level of insulin and extra insulin is needed the blood sugar rises the body needs a constant level of sugar in the blood
  17. 17. Normal Insulin Profiles Mealtime insulin Background insulin Blood sugar Daily Requirements Breakfast Lunch Evening Meal
  18. 18. Physiological Insulin Levels DR.UMA K. Breakfast Lunch Dinner Insulin Levels
  19. 19. Factors Affecting Insulin Secretion <ul><li>A. Stimulatory Factors: </li></ul><ul><li>Metabolic components </li></ul><ul><li>glucose* / amino acids / fatty acids / ketones </li></ul><ul><li>Hormonal components - cAMP - Ca2+ </li></ul><ul><li>Growth Hormone / ACTH / Glucagon </li></ul><ul><li>Cholinergic and β2-adrenergic stimulation (Propranolol ) </li></ul><ul><li>Intestinal nutrients via gastrin, secretin, enteroglucagon, CCK, Glucagon Like Peptide (GLP)-1 </li></ul><ul><li>- Oral vs. iv glucose yields a larger response </li></ul><ul><li>B. Inhibitory Factors : </li></ul><ul><li>Decrease cAMP Levels </li></ul><ul><li>Insulin / epinephrine / adrenergic stimulation / serotonin </li></ul>DR.UMA K.
  20. 20. DR.UMA K.
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  23. 23. DR.UMA K.
  24. 24. DR.UMA K.  subunit  subunit
  25. 25. DR.UMA K. insulin  
  26. 26. DR.UMA K.
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  34. 34. DR.UMA K.
  35. 35. DR.UMA K.
  36. 36. Type 2 Diabetes Etiology <ul><li>There is abnormally high level of glucose </li></ul><ul><li>Pancreas does produce insulin </li></ul><ul><li>Body resists the insulin’s effects </li></ul>DR.UMA K.
  37. 37. As a result, the glucose circulating cannot enter the cells, so that the glucose cannot be used for energy!!!!!! Therefore, there is INSULIN RESISTANCE!!! DR.UMA K.
  39. 39. Insulin is like the key that cannot get fit into the lock (cells)!!!! DR.UMA K.
  40. 40. DR.UMA K.
  41. 41. DR.UMA K.
  42. 42. Insulin Resistance: Causes and Associated Conditions Medications Aging INSULIN RESISTANCE Atherosclerosis Genetics Obesity and inactivity Rare disorders PCOS Dyslipidemia Hypertension Type 2 diabetes
  43. 43. DR.UMA K.
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  45. 45. DR.UMA K.
  46. 46. Type 2 Diabetes Signs and Symptoms <ul><li>Hyperglycemia </li></ul><ul><li>Polyuria </li></ul><ul><li>Polydipsia </li></ul><ul><li>Blurred vision </li></ul><ul><li>Fatigue </li></ul><ul><li>Paresthesias </li></ul><ul><li>Skin infections </li></ul>DR.UMA K.
  47. 47. Type 2 Diabetes <ul><li>80% are obese </li></ul><ul><li>10% non-obese </li></ul><ul><li>10% unstable: may look more like a Type 1 Diabetic </li></ul>DR.UMA K.
  48. 48. Summary <ul><li>Diabetes mellitus is a complicated spectrum of conditions </li></ul><ul><li>Each patient requires tailored therapy depending on: </li></ul><ul><ul><li>Pathology of diabetes </li></ul></ul><ul><ul><li>Lifestyle </li></ul></ul><ul><ul><li>Special circumstances/ill health </li></ul></ul>DR.UMA K.
  49. 49. Summary 2 <ul><li>Drugs that lower blood sugar form only part of the treatment of diabetes </li></ul><ul><li>Attention must be paid to many other aspects including: </li></ul><ul><ul><li>lifestyle </li></ul></ul><ul><ul><li>diet/alcohol consumption </li></ul></ul><ul><ul><li>cardiovascular risk factors </li></ul></ul><ul><ul><li>foot care </li></ul></ul>DR.UMA K.
  50. 50. Insulin Treatment <ul><li>Insulin preparations </li></ul><ul><ul><li>Onset of action </li></ul></ul><ul><ul><li>Duration of action </li></ul></ul><ul><ul><li>Degree of purity </li></ul></ul><ul><ul><li>Source </li></ul></ul>DR.UMA K.
  51. 51. Insulin Preparations <ul><li>Short Acting </li></ul><ul><ul><li>Regular- Humulin R </li></ul></ul><ul><ul><li>ALWAYS USED FOR SLIDING SCALE COVERAGE!!!!!! </li></ul></ul><ul><ul><li>Semilente </li></ul></ul><ul><li>Intermediate Acting </li></ul><ul><ul><li>NPH-Humulin N </li></ul></ul><ul><li>Mixtures </li></ul><ul><ul><li>70/30= 70 Units NPH & 30 Units Regular </li></ul></ul><ul><li>Long Acting </li></ul><ul><ul><li>Lantus </li></ul></ul>DR.UMA K.
  52. 52. DR.UMA K. (semilente)
  53. 53. DR.UMA K.
  54. 54. DR.UMA K.
  55. 55. Flexible insulin <ul><li>Insulin Lispro </li></ul><ul><li>Change in 2 amino acids from physiological insulin </li></ul><ul><li>Molecules dissociate and are absorbed from injection sites more quickly </li></ul><ul><li>can be given immediately before eating rather than 30 minutes before food </li></ul><ul><li>Injection devices </li></ul><ul><li>Insulin pen devices </li></ul>DR.UMA K.
  56. 56. DR.UMA K.
  57. 57. Short-Acting Insulin <ul><li>Soluble </li></ul><ul><li>Clear </li></ul><ul><li>Onset 30 minutes </li></ul><ul><li>Peak 1 - 3 hours </li></ul><ul><li>Duration up to 8 hours </li></ul>
  58. 58. Intermediate Acting Insulin <ul><li>Crystals in suspension (need re-suspending) </li></ul><ul><li>Cloudy </li></ul><ul><li>NPH or Isophane (NPH = Neutral Protamine Hagedorn) </li></ul><ul><li>Onset 1 1 / 2 hours </li></ul><ul><li>Peak 4 - 12 hours </li></ul><ul><li>Duration up to 24 hours </li></ul>
  59. 59. Pre-mixed Insulin <ul><li>Pre-mixed combinations of short and intermediate acting Insulins (biphasic) </li></ul><ul><li>Cloudy (needs re-suspending) </li></ul><ul><li>5 different combinations (10, 20, 30, 40, 50) </li></ul><ul><ul><li>e.g. 30/70 Mixture = 30% fast acting </li></ul></ul><ul><ul><li>+ 70% intermediate acting </li></ul></ul><ul><li>Onset 30 minutes </li></ul><ul><li>Peak 2 - 8 hours </li></ul><ul><li>Duration up to 24 hours </li></ul>
  60. 60. Long-Acting Insulin Glargine (Lantus) <ul><li>Synthetic Human Insulin </li></ul><ul><ul><li>Do not mix with any other insulin </li></ul></ul><ul><ul><li>Long Acting Up to 24 hours </li></ul></ul><ul><ul><li>NO PEAK </li></ul></ul><ul><ul><li>Given at BEDTIME </li></ul></ul>DR.UMA K.
  61. 61. DR.UMA K. Lispro Lente Insulin Regular Insulin NPH Insulin Ultralente Insulin 70/30 (human isophane sus./NPH& human insulin-DNA origin) 50/50 (human isophane sus.& human insulin-DNA origin)
  62. 62. DR.UMA K.
  63. 63. Species of Insulin <ul><li>Human - Genetically engineered using either yeast (pyr) or e.coli (prb) </li></ul><ul><li>Animal </li></ul><ul><ul><li>Beef - Increased incidence of allergic problems </li></ul></ul><ul><ul><li>Pork - Less antigenic than beef (Kurtz et al. 1980) </li></ul></ul><ul><ul><ul><li>- Available as purified insulin </li></ul></ul></ul>
  64. 64. Insulin regimes <ul><li>Soluble insulin at the time of meals </li></ul><ul><li>Intermediate or long acting insulin to provide background cover </li></ul><ul><li>Minimise number of injections </li></ul><ul><li>Questions </li></ul><ul><li>How do soluble, intermediate and long acting insulin differ? </li></ul>DR.UMA K.
  65. 65. DR.UMA K. Twice daily injections e.g. Humulin M3 Breakfast Lunch Dinner Insulin Levels Soluble insulin Long/intermediately acting insulin
  66. 66. DR.UMA K. 3-4 daily injections - more physiological profile Breakfast Lunch Dinner Insulin Levels
  67. 67. DR.UMA K.
  68. 68. DR.UMA K.
  69. 69. Storage of Insulin <ul><li>Before use Store in fridge </li></ul><ul><li>In-use vials Store in fridge (3 months) </li></ul><ul><li>Out of fridge at max 25 C </li></ul><ul><li>(4-6 weeks) </li></ul><ul><li>In-use pens Out of fridge at max 25 C (4 weeks) </li></ul>
  70. 70. Insulin Delivery <ul><li>Insulin devices (pens) </li></ul><ul><ul><li>Durable (replace insulin cartridge) </li></ul></ul><ul><ul><li>Disposable (no need to replace cartridge) </li></ul></ul><ul><li>Insulin vials and syringes </li></ul>DR.UMA K.
  71. 71. Insulin Devices <ul><li>Advantages </li></ul><ul><li>Improved dose accuracy </li></ul><ul><li>More convenient </li></ul><ul><ul><li>Easy to use </li></ul></ul><ul><ul><li>Portable </li></ul></ul><ul><ul><li>Quick and discreet </li></ul></ul><ul><li>May improve client self-management/compliance </li></ul><ul><li>Preferred by patients </li></ul><ul><li>Disadvantages </li></ul><ul><li>Cannot mix insulin in a free-mixing regimen </li></ul>DR.UMA K.
  72. 72. Who is a good candidate for an Insulin Pump? DR.UMA K.
  73. 73. Insulin Pumps <ul><li>Continuous subcutaneous insulin infusion (CSII) </li></ul><ul><li>Battery operated </li></ul><ul><li>Programmable computer </li></ul><ul><li>Basal insulin throughout day </li></ul><ul><li>Bolus insulin before meals </li></ul><ul><li>Needles/catheters changed </li></ul><ul><li>every 2-3 days </li></ul>
  74. 74. Adverse effects of insulin: DR.UMA K.
  75. 75. DR.UMA K.
  76. 76. DR.UMA K.
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  78. 78. DR.UMA K.
  79. 79. Drug interactions and diabetes <ul><li>Increase risk of hypoglycaemia </li></ul><ul><ul><li>beta blockers, alcohol, sulphonamides, monoamine oxidase inhibitors </li></ul></ul><ul><li>Decrease awareness of hypoglycaemia </li></ul><ul><ul><li>beta blockers </li></ul></ul><ul><li>Raise blood glucose </li></ul><ul><ul><li>corticosteroids, oral contraceptive, thiazides, loop diuretics, diazoxide </li></ul></ul>DR.UMA K.
  80. 80. DR.UMA K.
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  90. 90. Nateglinide: <ul><li>Nonsulfonylurea principally stimulates first phase insulin release resulting in rapid onset & short duration of hypoglycemic action than repaglitanide </li></ul><ul><li>Ingested 10-30 minutes before meal, limits pp hyperglycemia in NIDDM patients. </li></ul><ul><li>Does not produce late phase hypoglycemia & little effect on fasting BSL </li></ul><ul><li>EPISODES OF HYPOGLYCEMIA ARE LESS FREQUENT COMPARED TO SULFONYLUREAS </li></ul>DR.UMA K.
  91. 91. DR.UMA K.
  92. 92. DR.UMA K.
  93. 93. DR.UMA K. /Miglitol Antihyperglycemic
  94. 94. OTHER ANTIHYPERGLYCEMICS: <ul><li>GAURGUM: </li></ul><ul><li>Dietary fiber obtained from Indian cluster beans (Gaur) </li></ul><ul><li>Forms viscous gel after coming with contact with water </li></ul><ul><li>If mixed with food or taken before meal it slows gastric emptying & GI transit time hence decrease carbohydrate absorption; prevents pp hyperglycemia </li></ul><ul><li>Used as an adjuvant with sulphonylureas; it lowers dose of it. </li></ul><ul><li>GI discomfort, flatulence, diarrhea are common ADRs </li></ul>DR.UMA K.
  95. 95. DR.UMA K.
  96. 96. DR.UMA K.
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  98. 98. DR.UMA K.
  99. 99. Nursing Assessment for All Diabetic Clients <ul><li>What time will the insulin/oral agent act? </li></ul><ul><li>What carbohydrates are available? </li></ul><ul><li>Observe for Therapeutic Effects </li></ul><ul><li>What are the Adverse Effects? </li></ul>DR.UMA K.
  100. 100. Lab Assessment for All Diabetic Clients <ul><li>Blood tests </li></ul><ul><li>1. Fasting Blood Glucose </li></ul><ul><li>Test (Cavenaugh pg. 105) </li></ul><ul><li>2. Blood Glucose </li></ul><ul><li>Monitor Systems </li></ul><ul><li>2. Oral Glucose </li></ul><ul><li>Tolerance Test </li></ul><ul><li>3. Glycosylated Hemoglobin </li></ul><ul><li>Assays </li></ul><ul><li>4. Glycosylated Serum Proteins and Albumin </li></ul>DR.UMA K.
  101. 101. Checking Blood Glucose <ul><li>CBGs </li></ul><ul><li>AccuChecks </li></ul><ul><li>Glucometer </li></ul><ul><li>Glucoscan </li></ul>DR.UMA K.
  102. 102. DR.UMA K.
  103. 103. Hemoglobin A 1c <ul><li>A blood test that shows glucose levels for the past 3 months </li></ul><ul><li>No preparation needed i.e. fasting, etc. </li></ul>DR.UMA K. Hb A1c
  104. 104. Values for HbA 1c <ul><li>Non-diabetic <6 % </li></ul><ul><li>Diabetic with good control <7 % </li></ul><ul><li>Diabetic out of control >8 % </li></ul>DR.UMA K.
  105. 105. ADA Treatment Goals <ul><li>Hgb A1C maintained at 7% or below </li></ul><ul><li>Premeal blood glucose level 70 to 110mg/dl </li></ul><ul><li>Blood glucose at bedtime 100-140mg/dl </li></ul>DR.UMA K.
  106. 106. HbA 1c Predicts CHD in Type 2 CHD mortality Incidence (%) in 3.5 years All CHD events Incidence (%) in 3.5 years HbA 1c HbA 1c Low <6% Middle 6-7.9% High >7.9% Low <6% Middle 6-7.9% High >7.9% 0 5 10 15 20 25 0 5 10 15 20 25
  107. 107. Effects of EXERCISE on Blood Glucose <ul><li>By increasing the uptake of glucose by body muscles, exercise does what to Blood Glucose? </li></ul><ul><ul><li>Lowers it by </li></ul></ul><ul><ul><li>increasing the </li></ul></ul><ul><ul><li>number of insulin </li></ul></ul><ul><ul><li>receptors!!!! </li></ul></ul>DR.UMA K.
  108. 108. Effects of ILLNESS on Blood Glucose <ul><li>Fever </li></ul><ul><li>Flu </li></ul><ul><li>Infections </li></ul><ul><li>N & V </li></ul><ul><li>Surgery </li></ul><ul><li>Sunburn </li></ul>DR.UMA K.
  109. 109. Being sick usually makes blood sugar HIGH! <ul><li>Stress increases Blood Glucose </li></ul><ul><li>Never OMIT normally ordered insulin!!! </li></ul>DR.UMA K.
  110. 110. Interventions for ILLNESS <ul><li>Check Blood Glucose q4 hr >240? Check for ketones!!! </li></ul><ul><li>Ketones: call MD!!!! </li></ul><ul><li>Sick Day Guidelines… </li></ul>DR.UMA K.
  111. 111. Treatment of diabetes DR.UMA K.
  112. 112. DR.UMA K. Diabetic Ketoacidosis/ ketotic coma Hyperosmolar/ Nonketotic coma Type-1(IDDM) Type-2 (NIDDM)
  113. 113. <ul><li>More frequent in IDDM; infrequent in NIDDM </li></ul><ul><li>Common precipitating cause is infection; others are pancreatitis, trauma, stroke, stress & inadequate insulin doses </li></ul><ul><li>A medical emergency treatment as follows….. </li></ul><ul><li>Regular insulin to correct metabolic abn0rmalities, bolus dose of 0.1 – 0.2 U/kg iv followed by 0.1U/kg/hr infusion; rate can be doubled if no significant fall in BSL in 2 hrs.* </li></ul><ul><li>After 4-6 hrs when BSL becomes 300mg/dl rate of infusion can be made 2-3 U/hr & maintained till patient become conscious.(later insulin can be given sc) </li></ul><ul><li>Massive therapy with 1U/kg iv + 1U/kg sc followed by 1U/kg sc every 2 hrs is the must </li></ul>Treatment for Diabetic Ketoacidosis DR.UMA K. Osmotic diuresis Hyperglycemia Glycosuria Hyperventilation Impairment of consciousness Hypotension Shock Tachycardia Vomitting Dehydration
  114. 114. <ul><li>Correct fluid volume and electrolyte deficit </li></ul><ul><ul><li>1 liter of isotonic saline (NS)over 1 hour followed by gradual reduction to 0.5L/4hr </li></ul></ul><ul><ul><li>1 liter of hypotonic saline (1/2NS)over 6 to 8 hrs once BP/PR/Renal perfusion become normal </li></ul></ul><ul><ul><li>When BSL becomes 300mg/dl 1/2NS + 5%D: </li></ul></ul><ul><ul><li>Since BSL falls before ketones are fully cleared from circulation </li></ul></ul><ul><ul><li>Glucose required to restore exhausted hepatic glycogen stores </li></ul></ul><ul><ul><li>Once ketosis subsides K + driven intracellularly may cause dangerous hypokalemia to overcome this KCL 10-20mEq /hr should be added into infusion after 4 hrs. </li></ul></ul>Treatment for Diabetic Ketoacidosis DR.UMA K.
  115. 115. <ul><li>50 mEq sodium bicarbonate added into infusion fluid for correcting acidosis </li></ul><ul><li>5-10 m mol /hr of sod. / pot. Phosphate infusion </li></ul><ul><li>Antibiotics </li></ul>Treatment for Diabetic Ketoacidosis DR.UMA K.
  116. 116. Hyperosmolar (Nonketotic /hyperglycemic) coma <ul><li>More common in elderly with type-2 (NIDDM) </li></ul><ul><li>Precipitating factors same as DKA </li></ul><ul><li>Uncontrolled glycosuria produce diuresis resulting in dehydration & haemoconcentration over several days </li></ul><ul><li>Finally urine output is reduced & glucose gets accumulated in blood: >800mg/dl leading to coma & death (despite intensive therapy mortality rate is high) </li></ul><ul><li>Treatment line remain same except: </li></ul><ul><li>Rapid fluid replacement </li></ul><ul><li>Inj. Heparin to avoid thrombosis </li></ul><ul><li>Alkali not needed </li></ul>DR.UMA K.
  117. 117. DR.UMA K.
  118. 118. DR.UMA K.
  119. 119. Management of Hypoglycemia <ul><li>Hypoglycemic protocol </li></ul><ul><ul><li>Mild hypoglycemia (BG < 60 and symptomatic) </li></ul></ul><ul><ul><li>- 10 to 15g of carbohydrate </li></ul></ul><ul><ul><li>- Recheck BG in 15minutes </li></ul></ul><ul><ul><li>Moderate (BG < 40 and symptomatic) </li></ul></ul><ul><ul><li>-15 to 30g of rapidly absorbed CHO </li></ul></ul><ul><ul><li>Severe (BG < 20 and unable to swallow) </li></ul></ul><ul><ul><li>- 1mg of glucagon IM/SQ or amp of D50 IVP </li></ul></ul>DR.UMA K.
  120. 120. DR.UMA K.
  121. 121. DR.UMA K.
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  123. 123. DR.UMA K.
  124. 124. DR.UMA K.
  125. 125. DR.UMA K.
  126. 126. DR.UMA K. Complex internalised Drugs used to treat diabetes mellitus Gut Food Absorption Glucose Insulin Pancreas Insulin stored in  -islet cells Liver <ul><li>Reduced gluconeogenesis </li></ul><ul><li>Glycogenesis </li></ul><ul><li>Reduced lipolysis </li></ul>Receptor (tyrosine kinase) Muscle/fat cell Stimulates glucose uptake Adipose cell Insulin receptor Peroxisome proliferator-activated receptor Insulin Sulfonyl- ureas Metformin Acarbose Glitazones
  127. 127. THE END!!!!