Your SlideShare is downloading. ×
0
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Insulin & Oh Gs(10 13)
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Insulin & Oh Gs(10 13)

42,056

Published on

3 Comments
12 Likes
Statistics
Notes
No Downloads
Views
Total Views
42,056
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
0
Comments
3
Likes
12
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide
  • Transcript

    • 1. DR.UMA KADAM M.B.B.S. MD ASSOCIATE PROFESSOR PHARMACOLOGY SKNMC DR.UMA K.
    • 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. 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. 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. 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. 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. DR.UMA K.
    • 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. 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. 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. 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. DR.UMA K. proinsulin
    • 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. 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. 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. 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. Normal Insulin Profiles Mealtime insulin Background insulin Blood sugar Daily Requirements Breakfast Lunch Evening Meal
    • 18. Physiological Insulin Levels DR.UMA K. Breakfast Lunch Dinner Insulin Levels
    • 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. DR.UMA K.
    • 21. DR.UMA K.
    • 22. DR.UMA K.
    • 23. DR.UMA K.
    • 24. DR.UMA K.  subunit  subunit
    • 25. DR.UMA K. insulin  
    • 26. DR.UMA K.
    • 27. DR.UMA K.
    • 28. DR.UMA K.
    • 29. DR.UMA K.
    • 30. DR.UMA K.
    • 31. DR.UMA K.
    • 32. DR.UMA K.
    • 33. DR.UMA K.
    • 34. DR.UMA K.
    • 35. DR.UMA K.
    • 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. 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.
    • 38. DR.UMA K. NORMAL GLUCOSE UPTAKE INSULIN RESISTANCE
    • 39. Insulin is like the key that cannot get fit into the lock (cells)!!!! DR.UMA K.
    • 40. DR.UMA K.
    • 41. DR.UMA K.
    • 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. DR.UMA K.
    • 44. DR.UMA K.
    • 45. DR.UMA K.
    • 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. 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. 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. 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. 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. 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. DR.UMA K. (semilente)
    • 53. DR.UMA K.
    • 54. DR.UMA K.
    • 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. DR.UMA K.
    • 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. 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. 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. 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. 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. DR.UMA K.
    • 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. 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. DR.UMA K. Twice daily injections e.g. Humulin M3 Breakfast Lunch Dinner Insulin Levels Soluble insulin Long/intermediately acting insulin
    • 66. DR.UMA K. 3-4 daily injections - more physiological profile Breakfast Lunch Dinner Insulin Levels
    • 67. DR.UMA K.
    • 68. DR.UMA K.
    • 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. 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. 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. Who is a good candidate for an Insulin Pump? DR.UMA K.
    • 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. Adverse effects of insulin: DR.UMA K.
    • 75. DR.UMA K.
    • 76. DR.UMA K.
    • 77. DR.UMA K.
    • 78. DR.UMA K.
    • 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. DR.UMA K.
    • 81. DR.UMA K.
    • 82. DR.UMA K.
    • 83. DR.UMA K.
    • 84. DR.UMA K.
    • 85. DR.UMA K.
    • 86. DR.UMA K.
    • 87. DR.UMA K.
    • 88. DR.UMA K.
    • 89. DR.UMA K.
    • 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. DR.UMA K.
    • 92. DR.UMA K.
    • 93. DR.UMA K. /Miglitol Antihyperglycemic
    • 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. DR.UMA K.
    • 96. DR.UMA K.
    • 97. DR.UMA K.
    • 98. DR.UMA K.
    • 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. 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. 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. DR.UMA K.
    • 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. 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. 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. 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. 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. 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. 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. 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. Treatment of diabetes DR.UMA K.
    • 112. DR.UMA K. Diabetic Ketoacidosis/ ketotic coma Hyperosmolar/ Nonketotic coma Type-1(IDDM) Type-2 (NIDDM)
    • 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. <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. <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. 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. DR.UMA K.
    • 118. DR.UMA K.
    • 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. DR.UMA K.
    • 121. DR.UMA K.
    • 122. DR.UMA K.
    • 123. DR.UMA K.
    • 124. DR.UMA K.
    • 125. DR.UMA K.
    • 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. THE END!!!!

    ×