1. Diabetes model
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  2. Regular (Natural Insulin)
    • unmodified, relatively rapid onset and short
    • duration, clear solution. Only form that can be administered IV* Administered
    • SC absorption is slightly delayed. Does not need to be refrigerated.

    Adm. 30-60 minutes before meals
  3. Lispro Insulin (Humalog)
    • rapid acting analog. Effects begin within
    • 15-30 minutes of SC inj. Last 3-6 hours.
    • Acts faster than Regular insulin.
    • Adm. Immediately before eating.
    • Use in combination with intermediate or long acting insulin preparations.
  4. Insulin Aspart (Novolog)
    • analog of human insulin with a rapid onset (10-20 minutes) and short duration (3-5 hours).
    • Inject immediately before meals.
    • Can be mixed with other preparations (NPH)
  5. Neutral Protamine Hagedorn (NPH)
    • Prepared by conjugating regular insulin with Protamine (a large molecule).
    • The presence of the large molecule retards absorption, resulting in delayed onset of action.
  6. Lente Insulin/Ultralente
    • Produced by complexing reg. insulin with Zinc, which changes the physical state , thereby reducing solubility.
    • Less allergenic than NPH
  7. Insulin Glargine ( Lantus)
    • Modified human insulin with a prolonged duration of action (atleast 24 hours). Indicated for once daily injections SC. Administer at bedtime.
    • Slowly absorbed, relatively steady levels over 24 hours.

    • Cannot be mixed with other insulins even
    • though it is clear !
  8. Oral Hypoglycemic Agents:
    Type II Diabetes


    Biguanides ( Metformin )

    Thiazolidinediones (Glitazones)

    Alpha Glucosidase Inhibitors
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  10. Name/ Duration/ Action/ Side Effects
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  11. orals cont...
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  12. Sulfonylureas
    Promote insulin release

    Derived from sulfonamide antibiotics

    Maybe used alone or in combination

    First & second generation ( 2nd. Generation more potent)

    • Tolbutamide
    • (Orinase)*

    Amaryl(Glimeperide), Diabeta(Glyburide)

    • Glucotrol XL(Glipizide)
    • Use in patients with Type II DM

    Stimulates release of insulin from pancreas

    Readily absorbed after oral administration

    Peak levels in 3-5 hours

    • Hepatic metabolism & renal excretion
    • monitor for renal impairment ( Cr.Cl)
  13. Meglitinides
    Indicated for Type II DM

    Stimulate release of insulin from pancreas

    Similar mechanism of action like sulfonylureas

    Blood levels peak within 1 hour

    Side effect is hypoglycemia

    • Repaglinide(Prandin), Nateglinide(
    • Starlix)
  14. Biguanides (Metformin
    • Metformin (Glucophage) lowers blood glucose 1° by decreasing production of glucose from
    • the liver. Suppresses gluconeogenesis. Enhances glucose uptake.
    • Does not cause hypoglycemia
    • Excreted renally; monitor renal function
    • Use alone or in combination
    • Side Effects: Decreased appetite, nausea and
    • diarrhea, decreased absorption of B12 and folic acid
    • Lactic Acidosis
    • Metformin and the Biguanides
    • inhibit mitochondrial oxidation of lactic acid and can cause lactic acidosis.
    • Avoid in patients with liver disease, ETOH XS., heart failure and shock
  15. Thiazolidinediones (Glitazones)
  16. Rosiglitazone (Avandia), Pioglitazone (Actos)
    • Reduce glucose by decreasing insulin
    • resistance.
    • Glitazones cause volume increase which can lead to heart failure and edema
    • Benefits take several weeks to develop
    • Mixed effects on plasma lipid levels: raises
    • LDL, and HDL, lowers triglycerides
  17. Alpha-Glucosidase Inhibitors
  18. Acarbose (Precose)
    • Act to delay the absorption of CHO
    • Use in Type II DM
    • Reduces the rise in glucose
    • Maybe used in combination with other drugs
    • Causes flatulence, cramps and abdominal
    • distention, borborygmus
    • and diarrhea
  19. TRMT for DKA
    • Insulin Replacement ¨Initial IV bolus (.1U/kg BW) followed by continuous infusion at.1U/kg/hr.
    • Bicarbonate for Acidosis¨Controversial (pH<6.9-7.1) treat empirically
    • Water and Sodium replacement ¨NS or I/2NS 8-10 liters for adults
    • Potassium replacement nNormalization of glucose levels
  20. Diabetes Diagnostics
    —FPG diagnostic at > 126mg/dl

    —2 hour OGTT > 200 mg/dl

    —Random glucose ( non-fasting) >200

    —Hgb AIC < 7.0%
  21. —Basal & bolus regimens (ideal) most closely mimics
    endogenous insulin production
    • —Lispro (Humalog) prior to meals
    • —Also consider Glargine (Lantus)with 24hr. coverage
  22. —Somogyi Effect
    • —Rebound effect in which an overdose of insulin induces
    • hypoglycemia, the counterregulatory system will cause an
    • increase glucose causing hyperglycemia and in some cases ketosis

    • —Treatment typically consists of small protein snacks
    • before bedtime
  23. —Dawn Phenomenon
    • —Characterized by hyperglycemia on awakening due to Counterregulatory secretion of GH
    • & cortisol. Most severe during
    • adolescence and young adulthood

    —Adjustment in insulin dosing and timing is needed
  24. Diabetic Ketoacidosis
    • —Worldwide, infection
    • is the cause of DKA in about 30-50% of cases, with pneumonia, and UTI being the
    • most common etiologies

    • —Once DKA becomes
    • apparent patient will exhibit Kussmaul’s respirations as a result of metabolic acidosis,
    • abdominal pain and vomiting

  25. HHS
    • Less common than DKA but more serious is HHS which is a hyperosmolar state 2° to hyperglycemia
    • but with little or no ketosis

    • —***Insulin therapy to correct hyperglycemia is always
    • secondary to aggressive fluid infusion in HHS
  26. DKA
    • 12-24 hours prior to the development of DKA the patientmay experience progressive weakness, blurred vision, polyuria and polydipsia—
    • The patient becomes extremely volume depleted
    • —His temperature may range from hypothermic to febrile ifinfection precipitated event.
  27. DKA cont..
    • Profound deficiency of insulin characterized by
    • hyperglycemia (>250 mg/dl), ketosis, acidosis, glucosuria and dehydration

    —May have marked left shift if underlying infection

    • —Most often seen in TYPE1, may occur in TYPE 2 to a
    • lesser degree

    —When circulating supply of insulin is not sufficient , glucose cannot be properly used for energy

    —Body breaks down fat stores as a 2nd. Source of fuel

    —Ketones are acid by-products that build up

    —Ketosis alters ph= metabolic acidosis

    —Ketonuria occurs along with depletion of electrolytes while attempting maintain electrical neutrality
  28. Goals of Treatment
    Restoring perfusion

    —Arrest ongoing ketoneogensis

    —Correct electrolyte losses

    —Avoid hypokalemia

    —Avoid hypoglycemia
  29. Treatment for DKA
    • Initial goal is to establish fluid & electrolyte
    • replacement, improve volume status

    • —IV NS (open) titrate for urine output 30-60ml/hr…this
    • will correct Na, K, HCO3.

    • —Replace 50% of the deficit in first 8 hours and
    • remaining deficit within next 16 hours

    • —Early K replacement is essential (insulin deficiency may
    • cause K to move extracellularly, total body deficit
    • of K)

    • —Understand that initially K can be alarmingly high but
    • will drop with treatment

    —IV insulin therapy ( bolus of .1-.15U/kg)
  30. Hyperosmolar Hyperglycemic Non-Ketotic
    Syndrome (HHNS)
    • —Typically seen in
    • Type 2 patients, they can make a certain amount of insulin so they ward off

    • —Have severe
    • hyperglycemia

    —Osmotic diuresis resulting in osmolarity over 300 mosm/kg

    • —Extracellular fluid
    • depletion

    • —Typically an have
    • glucose in XS 900-1000mg/dl. Before manifestations
  31. Management of HHNS
    —Similar to DKA

    —Fluid hydration .9% NS (greater than in DKA)

    —Regular Insulin IV

    —May require some Dextrose to prevent hypoglycemia
  32. Dyslipidemia
    —Type II & metabolic syndrome

    • —Presence of insulin* increases lipolysis and breakdown of TG
    • in adipocytes this results in
    • increase in Free Fatty Acids…increase VLDL

    • —VLDL leads to increase in LDL and circulating
    • cholesterol
  33. Pancreas Transplantation
    —Treatment option for patients with type 1 DM

    —K-P performed together in most instances

    —Rare to perform only pancreas txpl.

    —Only partially successful in reversing long term microangiopathies and neuropathies.

    • —Pancreatic Islet transplant another potential treatment
    • measure
  34. Glucagon for Insulin Overdose
    Produced by the alpha cells

    • ¨Increase plasma glucose
    • levels and relaxes smooth muscle
    • of the GI tract

    • ¨Glucagon causes glucose levels to
    • rise

    • ¨For sever hypoglycemia IV glucose
    • is preferred

    ¨May be administered parenterally IV, IM, SC (0.5-1mg)
  35. Sulfonylurea drugs are contraindicated for
    use in patients with an allergy to:
    (Choices given, answers not given)



  36. The effects of metformin (Glucophage) include:
    (Choices given, answers not given)
    • suppression of hepatic glucose
    • production

    lowering of triglyceride levels

    enhanced insulin sensitivity

    all of the above
  37. Which of the following adverse effects is
    SPECIFIC to metformin (Glucophage)?
    (Choices given, answers not given)

    ¨GI distress

    ¨lactic acidosis

  38. Acarbose (Precose) works by:
    Choices given, Answer not given
    ¨sensitizing insulin receptors

    • ¨decreasing carbohydrate
    • absorption

    ¨increasing insulin secretion

    • ¨decreasing hepatic glucose
    • production

  39. Thiazolidinedione antiglycemics
    like rosiglitazone (Avandia) work by:
    Choices given, Answer not given
    ¨enhancing insulin production

    ¨sensitizing insulin receptors

    • ¨decreasing hepatic glucose
    • production

    ¨inhibiting CHO absorption
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