Pharm Block 1(Diabetes& Cortical Steroids)

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Pharm Block 1(Diabetes& Cortical Steroids)
2010-11-06 11:57:55
Pharm Block Diabetes Cortical Steroids

Pharm Block 1(Diabetes& Cortical Steroids)
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  1. Type One Diabetes
    • Due to no or very litle insulin
    • Seen more in children
  2. Type Two diabetes
    • Tissue is resistant to insulin
    • Seen in adults and the obese
  3. Type 4 diabetes
    Gestational Diabetes
  4. Where are insulin recepters found?
    • Liver
    • Adipose tissue and skeletal muscle
  5. What are the regulators of Insuline secretion?
    Chemical--- Glucose Concentration and AAs

    Hormonal--- GH, Corticosteroids, adrenaline and glucagon
  6. What are the Effects of Insulin?
    -on K
    • Promotes Potassium Uptake
    • Enhances Glucose uptake and Storage (glycogen)
    • Increases triglycerides and VLDL production
    • Decreases breakdown of Proteins
  7. insulin actions on:
    • enhances Glucose uptake
    • decreases the breakdown of proteins for energy and enhances their synthesis

    Enhaces lipogenesis and glucose uptake
  8. What is added to Insulins to increase the stability, duration of action and shelf life?

    Where is insulin metabolized?
    Zinc and Protamine

    In the Liver and Kindney
  9. What is the Function of Long or intermediate acting Insulins?

    What is the function of Short Acting insulins
    - To maintain the background or basal level of insulin

    - to control postprandial hyperglycemia
  10. Ultra-rapid onset of action and very short
    acting Insulins are? They dont LAG
    • Insulin lispro,
    • Insulin aspart,
    • Insulin glulisine
  11. What are the Therapeutic uses of insulin?
    • -All Type 1 DM patients
    • -Only the type II patients that fail to maintain blood glucose
    • Gestational DM
    • Postpancreatectomy
    • Diabetic Ketoacidosis ( regular insulin)
  12. Rapid onset - Short acting Insulin
    • Crystalline Zinc insulin (Regular type)
    • -Only insulin given in ketoacidosis !!!
    • -Leads to early postprandial hyperglycemia and late postprandial hypoglycemia
  13. Intermediate Onset ?
    NPH insulin
  14. Slow Onset & Long Acting insulins (takes to GD long)
    Insulin Glargine and Insulin Detemir

    Prevents hyperglycemia between the doses.
  15. Ultra-rapid onset and regular insulin types control?
    • postprandial hyperglycemia &
    • administered just before meal
  16. Intermediate onset and Slow onset control what?
    maintain basal insulin levels and control blood glucose between meals
  17. know
  18. When will you see Hyperosmolar, hyperglycemic syndrome (nonketotic coma)?
    occurs in elderly patients with type II DM

    Have hyperglycemia and dehydration

    Treat: Faster fluid replacement and low dose insulin
  19. What are the Main Clinical Symptoms of Diabetic ketoacidosis?
    • Dehydration (due to deep slow respirations)
    • and Tachycardia

    • See elevated Ketones in the urine
    • Low blood pH
  20. What do you do to treat diabetic Ketoacidosis?
    • -Insulin (Regular) by IV
    • -IV fluids (normal saline or with glucose)
    • - Monitor Potassium levels (because it would be peeed out when trying to concentrat the urine)
  21. What is Hyperosmotic Hyperglycemic syndrome?
    • Seen in elderly patients with Type II
    • See Hyperglycemia and dehydration
    • decline in mental status and convulsions (see NO acidosis)

    • - Faster replacement of fluids
    • - prophylatic heparin
  22. What are the signs and symptoms of Hypoglycemia?

    Sweating, anxiety, palpation, tremor, diziness and weakness.

    Sever--> Seizures and Coma

    • Mild- Sugar tablet
    • Sever-- 50% Glucose IV, Glucagon
  23. What is the Effect of Betablockers on Insulin?
    Prolongs Hypoglycemia by:

    • Decreasing warning signs
    • Inhibit Glycogneolysis
  24. What are the Effect of Thiazides, Furosemie and Vifedipine on insulin?

    Corticosteroids act by?
    They inhibit insulin secretion.

    increaseing the Blood sugar and decreasing the effectivness of insulin
    (OHA), what are they?
    • 1. Insulin secretagogues-- increase insulin production
    • 2. Biguanides-- decreaseglucose production by the liver
    • 3. Thiozolidinediones-- Increase uptake of sugar my muscle
    • 4. Alpha- glucosidase inhibitors-- slow suger absorption in the gut
    • 5. Incretin based therapy
  26. 1. Insulin secretagogues, what are they?
    Name the different ones
    how do they work?
    what are the newer ones?
    What are they used for?

    • 1st Generation – Tolbutamide, Chlorpropamide, Tolazamide
    • 2nd generation – Glyburide, Glipizide, Glimepiride

    -close the ATP sensitive K+ channels-->insulin released

    • - Newer drugs - Repaglinide & Nateglinide
    • - post prandial hyperglycemia in type II patients
  27. 2. Biguanides

    Name one
    What is its mechanism?
    Adverse reactions?

    -Inhibiting gluconeogenesis and Enhance tissue glucose uptake & utilization

    - Lactic acidosis
  28. 3. Thiazolidinediones / glitazones

    name them.
    Adverse effect?
    Pioglitazone & Rosiglitazone

    binding to Peroxisome proliferator activated receptor –gamma (PPAR-γ)-->Increase tissue glucose uptake

    Fluid retention
  29. 4. Alpha-glucosidase inhibitors

    Name them.
    • Acarbose & Miglitol
    • -Decrease digestion & absorption of
    • carbohydrates

    Adverse effects: Flatulence
  30. Newer drugs used to control postprandial glucose?
    • 1. Pramlintide
    • by inhibiting glucagon release
    • 2. Exenatide
    • Increase insulin release
    • 3. Sitaglipin
    • Prolongs effect of GLP-1
  31. What are the Glucocorticoid drugs?
    which are short acting and which are long acting?
    • -Short acting - Hydrocortisone
    • (cortisol), cortisone

    -Intermediate acting - Prednisone , Prednisolone, Methylprednisolone, Triamcinolone,

    -Long acting - Betamethasone, Dexamethasone
  32. What are the mineral corticoid drugs?
  33. Glucocorticoids – pharmacological actions?
    1. Anti-inflammatory & immunosuppressive effects

    • -Predominantly act on peripheral leukocytes (IL-2), decreasing their production by Inhibiting activation of phospholipase A2 (PLA2)
    • -Inhibits macrophages and APC
  34. Glucocorticoids – pharmacological actions 2?
    Effects on metabolism of carbohydrates,
    proteins & fats.

    Prolonged use leads to?
    • Stimulate gluconeogenesis, Increase serum glucose
    • Breaks muscle proteins, Induce lipolysis & redistribution of fat.

    adrenal atrophy
  35. When is glucocorticoids used for replacement theropy?
    1. Acute adrenal insufficiency (Addison’s crisis):

    2. Chronic adrenal insufficiency / Addison’s disease

    3. Congenital adrenal hyperplasia
  36. What are some Non-endocrine uses of Glucocorticoids?

    Should you use it for HSV?
    • (a) Allergic diseases
    • (b) Bronchial asthma
    • (c) Collagen vascular disorders
    • (d) Autoimmune diseases
    • (e) Ocular diseases
    • f) Skin diseases
    • (h) Gastrointestinal diseases
    • (i)To reduce cerebral edema
    • (j) Malignancies
    • (k) To prevent organ transplant rejection
    • (l) In preterm labor

    NO!!! it is Contraindicated
  37. Adverse effects of Glucocorticoids
    • -Sudden withdrawal
    • leads to Acute adrenal insufficiency
    • -Iatrogenic Cushing’s
    • syndrome: redistribution of fat -moon
    • face, thin extremities, buffalo hump
    • -Thin skin (fragile)
    • with purple striae and easy bruising
    • -Hypertension &
    • edema
    • -Hyperglycemia
    • -Myopathy & muscle wasting
    • -Susceptible for
    • infection: TB, candidiasis etc
    • -Peptic ulcer
    • -Osteoporosis
    • -Hypomania, acute psychosis & depression
    • -Posterior subcapsular Cataract
    • & glaucoma
    • -Delays wound healing
    • -Growth retardation in children
  38. Contraindications / cautiously used
    • -Osteoporosis
    • -Psychosis
    • -Epilepsy
    • -Peptic ulcer
    • -Glaucoma
    • -Diabetes Mellitus
    • -Hypertension & congestive heart failure
    • -Varicella & tuberculosis infections
    • -Pregnancy (esp 2nd trimester)
  39. Mineralocorticoids: Aldosterone

    What is the Drug?used in? what is a AE?

    replacement therapy in hypoadrenalism

    Edema due to Na retention
  40. What are some Adrenalcorticoal Antagonists?
    • Inhibitors of glucocorticoids synthesis
    • Metyrapone
    • Mifepristone
    • Mitotane

    • Aldosterone receptor blockers
    • Spironolactone & eplerenone