Diabetes ppts

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Diabetes ppts
2011-07-24 16:28:48

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  1. Insulin
    Regulates carbohydrate metabolism

    Metabolism of fats and protein

    • Lowers blood glucose levels by stimulating peripheral glucose uptake especially in the skeletal
    • muscles
  2. Types of Diabetes
    Type I--Absolute Insulin Deficiency

    Type II--Relative Insulin Deficiency



    • Diabetes Mellitus and Diabetes Insipidus (insufficient amount of Antidiuretic Hormone) are two different, distinct endocrine disorders!
    • Commonality: both disorders produce large volume of urine.
  3. Type 1
    Often manifests in childhood or puberty

    Abrupt failure of the pancreas

    Pathogenesis is unclear

    5-10% of all diabetics

    • Leading theory is born with predisposition and exposed to virus which pulls it out.
    • Type 1-used to be referred to as IDDM (insulin dependent DM).
  4. Type 2 Diabete
    Correlated with obesity

    • Usually seen in adults over the age of 30 but also
    • identified in young

    Insulin resistance

    Type 2 was referred to as NIDDM(non insulin dependednt DM).
  5. Insulin Resistance
    -insulin is still produced but cells arent as sensitive to it. Meds increase cell sensitivity
  6. Acute Complications (Diabetes Mellitus)


    Diabetic Ketoacidosis (DKA)/Hyperosmolar Glycemic State (HHS)
  7. Hypoglycemia-sugar below
    50. brain damage can ensue if if it is below 40
  8. Hyperglycemia-sugar above
  9. DKA-see it in
    Type 1 diabetes
  10. HHS see it in
    • Type 2
    • whats happening is the osmolality of the blood is
    • completely off bc sugar is so highly concentrated in blood. Lot of urine.
  11. Most severe manifestation of insulin deficiency



    –Electrolyte imbalance: Na+ and K+



  12. Ketoacidosis
    body starts to break apart fat and muscle to get glucose bc body doesn’t see all of the glucose that you have in your blood.

    • This is why a manifestation of type
    • 1 is weight loss. Your body thinks its starving itself of glucose when it really has an abundance.

    • Fat will yield fatty acids and protein/muscle yeilds ketones=ketoacidosis. Throws the body
    • into an acidic state. These people hyperventilate to blow off the acid. All of these things contribute to shock
  13. Macrovascular damage (diabetes Mellitus)

    –Myocardial Infarctions

    –Cerebral Vascular Accidents

  14. Microvascular damage (Diabetes Mellitus)
    –Erectile dysfunction

    –Blindness secondary to retinopathy

    –Amputation secondary to Infections such as gangrene

    –Renal damage

  15. Other drugs in in class (Insulin)
    • Short-rapid Lispro (Humalog, Novolog),
    • short-slow (Humulin–R, Novolon–R)
    • intermediate NPH (Humulin–N, Novolin–N),
    • long acting glargine (Lantus)
    • combination
    • (70/30)
  16. Pharmacological Class of Insulin
    Diabetic Agents
  17. Therapeutic Uses of Insulin
    Glycemic control of diabetes mellitus type I to prevent complications
  18. Physiologic action (Insulin)
    Necessary for carbohydrate, fat and protein metabolism

    Increases glucose transport across muscle and fat-cell membranes to reduce serum glucose levels.

    Promotes the conversion of glucose to its storage form: glycogen

    Triggers amino acid uptake and conversion of protein in muscle calls and inhibits protein degradation

    Stimulates triglyceride formation and inhibits release of free fatty acids from adipose tissue

    Converts lipoproteins to fatty acids
  19. Insulin Side Effects
    Metabolic: hypoglycemia, hyperglycemia, or Somogyi, or dawn phenomenon

    Local: lipoatropy, itching, swelling and redness
  20. Insulin Interactions
    Decrease hyperglycemic effect

    Increase hypoglycemic effect

    Beta adrenergic blocking agents
  21. Insulin Labs and Monitoring
    Blood sugar, HgA1c, Cholesterol
  22. Dawn phenomonen
    • they take insulin and in morning sugars may be high. Rebound hypoglycemia.
    • Body sees sugars go low so they start to use glycogen storage in the liver.
  23. Brittle diabetic
    tried to get control of sugars but are unable to do this
  24. Insulin is prepared in units
    per milliliter in concentrations of 100 or 500U/mL
  25. Insulin Must be given
    parenterally because it is destroyed in the GI tract
  26. When giving Insulin Sub-Q it
    provides slow steady absorption. Absorption is dependent on the site.
  27. Which Insulins are given in IV administration
    regular, aspart, lispro and glulisine can be given IV.

    NPH, Detemir and glargine insulin cannot be given IV
  28. What are the fastest sites of absorption when giving Insulint
    • Stomach is most rapid absorption,
    • followed by arm or thigh.
    • Most people stick with one site and then rotate places in the site.
    • You can give rapid and regular acting IV.
    • You cannot give slow acting IV.
  29. Short Acting Insulin (onset, peak, duration)
    -Regular Insulin (Humulin R, Novolin R)

    Onset: 0.5-1hr

    Peak: 1-5 hr

    Duration: 6-10 hr
  30. Isophane insulin suspension (NPH)

    (Intermediate Insulin)(Onset,peak,duration)
    (Humulin N, Novolin N)

    Onset: 1-2 hr

    Peak: 6-14 hr

    Duration:16-24 hr
  31. Insulin Detemir

    (Intermediate Insulin) (Onset,peak,duration)

    Onset: 6-8 hr

    Peak: 12-24 hr
  32. Long Acting Insulin
    Insulin Glargine (Lantus)

    Onset: 70 minutes

    Peak: none

    Duration: 24 hr

    Shouldn’t be mixed with other insulins. One drawback is basal control. Need to give something else before meals.
  33. Combination Insulin (onset,peak,duration)
    Isophane Insulin Suspension (NPH) and regular insulin (Novolin 70/30, Novolin 50/50)

    Onset: 30 min

    • Peak 70/30: 2-12 hr
    • Peak 50/50: 2-5.5 hr

    Duration: 24 hr
  34. Short Acting (Inhalation)
    Exubera inhalation system withdrawn from the market in 2007 due to poor sales.

    Side effects: cough, bitter taste, hypoglycemia

    Higher cost than injectables

    Concern about allergic reactions, pulmonary irritation and lung cancer
  35. Six chemical classes (Oral)


    Glinides (Meglitinides)


    Alpha-glucosidase Inhibitors

  36. Biguanides
    Metformin (Glucophage)
  37. Biguanides Therapeutic Uses
    Initial choice of treatment for most Type II DM patients Glycemic control of diabetes mellitus type II to prevent complications

    Prevention of Type II DM

    Used in treatment of polycystic ovary disease

    Gestational diabetes
  38. Biguanides: Metformin (Glucophage) Physiological Actions
    Produces its antidiabetic effects only in the presence of insulin

    Decreases glucose production in liver

    Facilitates insulin’s action on the peripheral receptor sites

    Lowers triglycerides to promote weight loss

    Peak: 2 hours
  39. Biguanides: Metformin (Glucophage) Side Effects
    • Most Common: GI: nausea, vomiting, diarrhea,
    • metallic taste, abdominal discomfort, flatulence, decreased appetite

    Metabolic: lactic acidosis

    Hematologic: symptomatic B12 deficiency or megoblastic anemia
  40. Biguanides: Metformin (Glucophage) Interactions
    Alcohol, Cimetidine, contrast dye for radiographic studies
  41. Biguanides: Metformin (Glucophage) Labs and Monitoring
    Blood sugar, HgA1c, cholesterol
  42. Sulfonylureas
    glipizide (Glucotrol)
  43. Sulfonylureas: glipizide (Glucotrol) Other drugs in class
    1st generation: tolbutamide ( Orinase), chlorpropamide (Diabinase)

    2nd generation: glyburide (Diabeta, Micronase), glimepiride (Amaryl)

    beats pancreas into shape
  44. Sulfonylureas: glipizide (Glucotrol) Therapeutic Uses
    Glycemic control of diabetes mellitus type II to prevent complications
  45. Sulfonylureas: glipizide (Glucotrol) Physiologic Actions
    • Lowers blood glucose level by stimulating insulinrelease from functioning beta cells in the pancreas
    • Inhibits hepatic glyconeogenesis
    • Increase number of insulin receptors in peripheral tissue increasing insulin sensitivity
  46. Sulfonylureas: glipizide (Glucotrol) side effects
    Hypoglycemia, pallor, muscle weakness, blurred vision, agitation, irritability, mental confusion, tachycardia, alterations in consciousness

    GI: nausea, anorexia, heartburn, metallic taste

    Dermatologic: maculopapular rash, uticaria, pruritus and erythema

    CV: ? Sudden cardiac death?
  47. Sulfonylureas: glipizide (Glucotrol) Interactions
    Alcohol-disulfiram reaction

    Low BS: Alcohol, NSAIDS, sulfonamide antibiotics, cimetidine

    Beta Blockers
  48. Sulfonylureas: glipizide (Glucotrol) Labs and Monitoring
    Blood glucose, HgA1c, cholesterol
  49. Sulfonylureas: glipizide (Glucotrol) Onset, Peak,Duration
    Onset: 2 hr

    Peak: 2- 4 hr

    Duration: 24 hr

    Pregnancy Cat C

    Renal or hepatic alterations will increase drug levels
  50. Meglitinides
    Repaglinide (Prandin)
  51. Meglitinides: Repaglinide (Prandin) Other drugs in class
    nateglinide (Starlix)
  52. Meglitinides: Repaglinide (Prandin) Therapeutic Uses
    Glycemic control of diabetes mellitus type II to prevent complications
  53. Meglitinides: Repaglinide (Prandin) Physiologic Actions
    similar to sulfonylurea

    Increase the release of insulin from the pancreas
  54. Meglitinides: Repaglinide (Prandin) Side Effects
  55. Meglitinides: Repaglinide (Prandin) Interactions
    Gemfibrozil (Lopid)
  56. Meglitinides: Repaglinide (Prandin) Labs and Monitoring
    Blood sugar, HgA1c, Cholesterol
  57. Lopid
    drug that increases triglycerides. Affect the metabolism.
  58. Meglitinides: Repaglinide (Prandin) Onset,Peak,Duration
    Pregnancy Cat C

    Onset: rapid

    Peak: within 1 hour

    Duration: unknown
  59. Thiazolidinedione
    Rosiglitazone (Avandia)
  60. Thiazolidinedione: Rosiglitazone (Avandia) Therpeutic Uses
    Glycemic control of diabetes mellitus type II to prevent complications
  61. Thiazolidinedione: Rosiglitazone (Avandia) Physiologic Actions
    Enhance the activity of endogenous insulin by improving target cell response

    Decrease insulin resistance

    Recent FDA warning regarding increased risk cardiovascular events!
  62. Thiazolidinedione: Rosiglitazone (Avandia) Other drugs in class
    pioglitazone (Actos)
  63. Thiazolidinedione: Rosiglitazone (Avandia) Side Effects
    Most common: respiratory tract infections,

    Sinusitis, headache, myalgias, sore throat, fluid retention, edema, fatigue, diarrhea, increased LDLs

    Most serious: ? hepatotoxicity
  64. Thiazolidinedione: Rosiglitazone (Avandia) Labs and Monitoring
    Weight, LFTs, Cholesterol, Blood sugars, HgA1c
  65. Thiazolidinedione: Rosiglitazone (Avandia) Interactions
    Gemfibrozil (Lopid), Insulin
  66. Alpha Glucosidase Inhibitors
    Acarbose (Precose)
  67. Alpha Glucosidase Inhibitors: Acarbose (Precose) Other drugs in class
    miglitol (Glyset)
  68. Alpha Glucosidase Inhibitors: Acarbose (Precose) Therapeutic Uses
    Glycemic control of diabetes mellitus type II to prevent complications
  69. Alpha Glucosidase Inhibitors: Acarbose (Precose) Physiologic Actions
    Inhibit alpha-glucosidase inhibitors in the small intestine which delays absorption of dietary carbohydrates; this reduces the rise in BS after a meal.

    Does not depend on the presence of insulin
  70. Alpha Glucosidase Inhibitors: Acarbose (Precose) Side Effects
    Mostly GI: flatulence, diarrhea, abdominal distention, borborygimus

    Liver: elevated serum aminotransferases, especially ALT, AST

    Hypoglycemia, anemia
  71. Alpha Glucosidase Inhibitors: Acarbose (Precose) Interactions
    Sulfonylureas, Insulin, Metformin
  72. Alpha Glucosidase Inhibitors: Acarbose (Precose) Labs and Monitoring
    CBC, iron, blood sugars, HgA1c, LFT
  73. Alpha Glucosidase Inhibitors: Acarbose (Precose) Onset,Peak,Duration
    Onset: less than 30 minutes

    Duration: 4-6 hours

    Metabolized mainly in the GI tract

    Contraindicated in patients with GI disorders

    Pregnancy Cat B

    Cant give orange juice or table sugar
  74. Gliptins
    Sitagliptin (Januvia)
  75. Gliptins: Sitagliptin (Januvia) Other drugs in class
  76. Gliptins: Sitagliptin (Januvia) Therapeutic Uses
    • Glycemic control of diabetes mellitus type II
    • to prevent complications, used alone or in combination
  77. Gliptins: Sitagliptin (Januvia) Physiologic Actions
    Enhances the action of incretin hormones, endogenous compounds that stimulate insulin release and suppress postprandial release of glucagon
  78. Gliptins: Sitagliptin (Januvia) Interactions
    None known
  79. Gliptins: Sitagliptin (Januvia) Side Effects
    Most common: upper respiratory infection, headache, nasal passage inflammation
  80. Gliptins: Sitagliptin (Januvia) Labs and Monitoring
    blood sugars, HgA1c
  81. Gliptins: Sitagliptin (Januvia) Can be used During
  82. Pramlintide (Symlin)
    • Injectable drug
    • –Amylin mimetic

    –Peak: 20 minutes Duration: 2 hr

    –Adverse Effect: hypoglycemia, nausea
  83. Exenatide (Byetta)
    Injectable drug

    –Incretin mimetic

    –Peak: 2 hr Duration 5 hr

    –Adverse Effect: hypoglycemia, GI effects, development of anti-exenatide antibodies
  84. Amylin is a hormone that
    decreases gastric emptying and decreases glucagon secretion.
  85. Incretin stimulates
    Insulin release

    More insulin production. Worry about pancreatitis. Sign is abdominal and back pain.
  86. Glucose Elevating Agents
  87. Glucagon
    -A hyperglycemic polypeptide

    -Used in the unconscious diabetic patient to reverse hypoglycemia

    -Usually given IV and onset is within 1 minute

    Cannot give orange juice to someone who is fading in and out of consciousness. They could aspirate and they could have a lot of other problems. Cant give it orally.