pharm endocrine condensed

  1. drugs that cause hypothyroidism
    • amiodarone interferes w/ conversion of T4 to T3
    • Li+ blocks release of thyroid hormones & I- incorporation to thyroglobulin
  2. More potent than levothroxine, but not recommended due to its multiple dosing schedule (up to 4x/daily)
    Higher potency not advised in Cardiovascular (CV) patients. Stimulates SANS
    May have some benefit for short term TSH suppression
  3. Medication should be taken on empty stomach
    Levothyroxine & biphosphonate
  4. Levothyroxine drug interactions
    • Reduction of T4 absorption
    • Induction of drug metabolism
    • Increase catabolism of vitamin K dependent clotting factors, enhancing effect of anticoagulants Increase insulin
    • increases digoxin clearance
  5. drugs whose actions are further induced by Levothyroxine
    Nifedipine, protease inhibitors, carbamazepine, glucocorticoids, phenytoin, phenobarbital, and rifampin
  6. Should give sugar to pts on Levothyroxine because...
    Levothyroxine incr insulin and raises metabolism
  7. inhibits thyroid-peroxidase catalyzed rxn --> inhibits T3, T4 synthesis.
    Block iodine organification
    Block iodotyrosine couplings
    Inhibit deiodination of T4 and T3
    Require 3-4 weeks to take effect
    Thiomides, Propylthiouracil (PTU), Methimazole
  8. Action of radiocontrast agents, beta blockers, amiodarone, proprylthiouracil, and methimazole
    blocks T4 --> T3 peripherally
  9. Rapid but incomplete absorption, large first pass effect
    T1/2 1.5hr, is preferred over methimazole due to its high protein binding --> doesnt cross placenta
    Inhibits T4 to T3 conversion –brings thyroid level down quicker than methimazole
    AE: rash, nausea, hepatitis
  10. Drugs in pregnancy
    • Category A: levothyroxine (safe)
    • Category B: amoxicillin and some types of insulin (safe)
    • Category C: sertraline (risk vs benefit)
    • Category D: chemotherapeutics, proprylthiouracil (risk vs benefit)
    • Category X: misoprostol, isotretinoin (contraindicated—NEVER used)
  11. Agranulocytosis
    rare side effect of antithyroids (PTU, methimazole, thiomides), risk in elderly & high dose pts.
  12. stimulate insulin release
    sulfonylureas and Meglitinides
  13. increase glucose uptake
  14. suppresses glucagon release
  15. binds to liver receptors to induce IGF production
    recombinant hGH
  16. Blocks GH receptors
  17. GHRH antagonists at Anterior Pituitary
    • Octreotide (analog of Somatostatin)
    • Bromocriptine (DA agonist)
  18. Recombinant human IGF-1 (rhIGF-1)
  19. side effects of mecasermin
    Hypoglycemia, Intracranial hypertension, joint and muscle pain, convulsions, tonsilar hypertrophy, snoring, apnea
  20. Octreotide
    somatostatin formulation. sc, 1/2 90 min
  21. Lanreotide
    somatostatin formulation. sc, 1/2 90 mins
  22. side effect of Pegvisomant
    Block of negative feedback may double GH levels. Opposes Pegvisomant action.
  23. Susceptible to proteolytic cleavage, only given parenterally (by injection). Short t1/2
    posterior pituitary hormones
  24. side effects of oxytocin
    Toxicities uncommon, but can cause hypertension, water retention (similar to ADH structurally), uterine rupture & fetal death.
  25. Releases von Willebrand Factor; Used for von Willebrand Disease & Hemophilia A
    Desmopressin. V2 agonist, not much activity at V1
  26. medication that replaces T3
  27. Lispro, Aspart, Glulisine
    rapid acting insulin for diabetes type 1. Onset for all three is 5-15 min and all claim an advantage over regular insulin of no delay (30 min)
  28. shorting acting insulin
    • exact structure as human insulin (hexamer). Advantage: cost effective and available IV for diabetic crisis situations.
    • Disadvantage: Slow, inconvenient onset and coverage (hyperglycemia early in meal) extended duration (hypoglycemia later)
  29. Neutral Protamine Hagedorn (NPH)
    intermediate acting insulin. complexing protamine with insulin to create stable, slowly degraded product. Onset 2-5 h, duration 4-12 h. Can cover the day w/ 2-4 injections/day. Used w/ rapid or regular insulin to cover day plus meals
  30. Glargine and Determir
    Long acting insulin. onset 1-2 h, duration 12-24 h, no peak. Rapid or regular insulin may be added at meals to stop spikes in sugar. These formulas result in less hypoglycemia
  31. Glargine action
    formulated to precipitate upon injection, forming a crystalline depot for slow and continuous release
  32. Determir action
    formulated to bind albumin. A slow dissociation from the protein results in a prolonged, constant rate of availability
  33. Sulfonylureas 1st generation
    • increase insulin release from pancreatic β cells; reduces glucagon levels long term
    • Tolbutamide (safest in avoiding hypoglycemia)
    • Chlorpropamide (t1/2 32 hrs, flush w/ alcohol)
    • Tolazemide (t1/2 7 hrs)
  34. Both are contraindicated in the elderly and in patients with renal or hepatic impairment
    Risk of hypoglycemia especially with drugs that inhibit metabolism
    Chlorpropamide and Tolazemide. 1st gen sulfonylureas. incr insulin release from beta cells
  35. 2nd generation sulfonylureas
    • Glyburide – daily, AM. Give lower dose in renal or hepatic impairmt
    • Glipizide – give 30 min or more before food. Lower dose in renal or hepatic impairmt Glimepiride – daily, AM. No concern in renal. Completely metabolized by liver****
    • High protein bound; may be displaced from albumin binding sites by NSAIDs --> temporary hypoglycemia
    • Watch DI (CYP2C9) with any drug that induces or inhibits its metabolism
  36. MOA is same as sulfonylureas. However, absence of sulfur in structure means they are an alternative to patients with drug sensitivity
    • Meglitinides: Repaglinide.
    • Fast acting, 1 h peak, 5-8 h duration. Take with meals. Hypoglycemia if doesn't eat.
  37. same MOA as Repaglinide but is Phenylalanine derivative (also a Meglitinide)
    Nateglinide. Hypoglycemia (Safest of all oral diabetic agents). shorter duration than Repaglinide
  38. Biguanides
    Phenformin (discontinued due to fatal lactic acidosis) and Metformin (1st line for diabetics)
  39. risk for lactic acidosis, decr B12 levels.
    Other treatments: polycystic ovary syndrome (reduces insulin resistance in these patients)
    Lowers LDL/TG
  40. Thiazolidinediones (TZD)
    • Pioglitazone, Rosiglitazone. agonist at PPAR-γ (Peroxisome Proliferator-Activated Receptor-Gamma)
    • incr glucose uptake into adipose tissues
    • decr insulin resistance, improved TG/HDL values
  41. TZD w/ incr risk of cardiovascular dz
  42. side effects of TZDs (pioglitazone and rosiglitazone)
    • Edema, weight gain, mild anemia, fractures in women, CI in pregnancy, CHF, hepatotoxicity
    • CV risks w/ rosiglitazone
  43. induces metabolism of oral contraceptives
  44. Suppresses glucagon release, delays gastric emptying, and produces appetite suppression due to CNS effect. Synthetic amylin analog (amylin released like insulin from β cells)
  45. Synthetic amylin analog (amylin released like insulin from β cells)Injected sq before each meal; never mix with insulin. Peak in 20 min. Duration 150 min.
    For type I and II diabetics
  46. Side effects of pramlintide
    GI upset and possible hypoglycemia
  47. Incretin based drugs
    • exenatide: GLP-1 analog, binds to GLP- receptors, incr beta cell mass
    • sitagliptin, and saxagliptin: DPP-4 inhibitor, blocks GLP-1 degradation, raises GLP-1 levels
  48. Injected 60 min before meal. Dosed twice daily. Weight loss potential makes it attractive
    AE: GI upset, hypoglycemia possible
    Fatal: necrotizing, hemorrhagic pancreatitis
  49. Glucagon-like peptide-1 (GLP-1) receptor agonist; antagonist to glucagon release. Helps pancreas make insulin after meals. New drug of 2010
  50. behaves like beta agonists, incr cAMP --> gluconeogenesis
    glucagon injection. for hypoglycemic pts who are unconscious
  51. Reversible and drug-related causes of osteoporosis
    • Glucocorticoids, long-term therapy
    • Post-menopausal estrogen deficiency
    • Thyrotoxicosis
    • Hyperparathyroidism
    • Alcoholism
    • Cigarette smoking
  52. MOA of biphosphonates
    inhibition of osteoclast bone resorption
  53. Action of prednisone in Ca balance
    • rapid reduction of hypercalcemia
    • may enhance PTH mediated bone resorption
  54. Imitates Parathyroid Hormone. low dose PTH or intermittent PTH causes bone formation as the osteoblastic/osteoclastic ratio has not reached a bone resorption outcome
  55. admin routes for salmon calcitonin
    subcapsular, intramuscular, and nasal inhalation
  56. SERM (Selective Estrogen Receptor Modulator). less potent than estrogen on bone density, offers less breast and endometrial cancer, and improves outcome against vertebral fractures. Has same risk of thrombophlebitis as estrogen
  57. Agonist at the Calcium Sensing Receptor (CaR)
    Blocks release of PTH by the Parathyroid Gland
  58. Managemt of hypercalcemia of malignancy.
    Inhibits bone resorption.
    Possible nephrotoxicity.
    Gallium nitrate
  59. Cortisol withdrawal
    • Acute adrenal insufficiency. Fever, myalgia, arthralgia, and malaise
    • Rarely pseudo tumor cerebri
  60. Inhibits 11β-hydroxylation
    Interferes w/ cortisol and corticosterone synthesis
    Treatment of Cushings
    Testing the integrity of the feedback loop
  61. Inhibits 3β dehydrogenase. Treatment of Cushings
Card Set
pharm endocrine condensed
pharm endocrine condensed