Pharm Block 2 (Osteoporosis)

  1. What are Anion inhibitors?
    How do they work?
    Why dont we used them?
    What are they effective in?
    They are Anti-thyroid Drugs, They are Monovalent ions.

    They Competitively block the uptake of Iodine

    They are not used because they are highlly TOXIC and can cause Aplastic Anemia

    They are effective in iodine induced hyperthyroidism.
  2. Name some other Anti-thyroid drugs.

    What are they used for?
    • Propranolol- manage cardic sympoms of Thyrotoxicosis
    • Lithium- Inhibit the sythesis and release of thyroid hormones
    • Amiodarone- result in Hypothyroidism
  3. What is Myxedema coma?
    What do you do to treat it?

    What do you use to monitor this?
    It is an untreated from of hypothyroidism

    • Treat with Intravenous T4 (sometimes T3)
    • Monitor with plasma TSH levels
  4. Facts about Levothroxine (T4)
    • Stable
    • Long half life (7 days)
    • T4 is converted to T3 so both hormones are produced and available
  5. Facts about Liothyronine (T3)
    • Short half life (not used for replacement theropy)
    • Greater risk of cariotoxicity (avoid its used in patients with cardiac issues)
    • Used for short term suppression of TSH.
  6. What is Thyroid Strom (Thyrotoxic crisis)?
    What do you do to treat it?
    It is an acute life threatening stated caused by too much Thyroid hormone release

    • - Propronolol (decreases Cardiac sympoms)
    • - Propylthiouracil high does (inhibits T4 conversion to T3)
    • - potassium Iodide (blocks the release of thyroid hormones)
  7. What are PTH general effects?

    In the Kindney? Bone? GIT?
    -increases plasma Ca levels amd decreases plasma phosphate concentration

    • Kidney: increased reabsorption of Ca, Decreased of Phosphate.
    • Bone: Increases bone reabsorption by stimulating Osteoclasts.HIGH DOSE (low dose it increases bone formation)
    • GIT: Increases Ca and Phosphate Absorption by activating Vitamin D (Cacitriol)
  8. What is Terioaratide?
    It is a recombinant form of PTH that is used for the treatment of osteoporosis in patients that cannot tolerate Bisphosphonates.
  9. What is Vitamin D?
    Where is Vitamin D3 produced? What is it?
    Vitamin D is a prohormone

    • Vitamin D3 is produced in the Skin from 7 dehydrochlesterol under Ultraviolit light.
    • Vitamin D3 is an inactive precursure to the active Calcitriol
  10. What is Vitamin D's net effect?
    Where does activation (hydroxylation) of Vitamin D3 occur?
    What else is needed to get Calcitriol?
    To increase the plasma Ca AND phosphate concentrations.

    It occures in the Liver at eh 25th position.yeilding 25, hydroxyvitamin D3

    This PTH stimulates this to be activated in the KIDNEY at position 1 --> Calcitriol.
  11. Vitamin D effects in:
    on PTH?
    Immune System?
    • -increase absorption of Both Ca and Phosphate
    • -Increase bone formation
    • - decrease excretion of both Ca and Phosphate
    • - inhibits PTH secretion
    • -Increases Phagocytosis, anti-tumor activity and Immunomodulary functions
  12. What is Vitamin D used for Clinically?
    Treats Osteoporosis, Rickets and Osteomalacia

    Used it renal Failure (use Calcitriol because body cannot make its own with the kidney OOC)
  13. What is Calcipotiol or Calcipotriene?
    What are they used for?
    these are topical synthetic derivatives of Calcitriol that re used to treat Psoriasis

    Note: recall that in treating Psoriasis there is a step wise pattern. Topical>>Photo>>Systemic
  14. Name the different Bisphosphonates.
    • Alendronate (Fosamax)
    • Risedronate (Actonel)
    • Ibandronate (Boniva)
    • Pamidronate (Aredia)
    • Zoledronate (Zometa)
  15. What is special about Bisphosphonates>

    What does they inhibit and what is this effect?
    • These compounds have P-C-P which is nonhydrolyzable compared to Pyrophosphate P-O-P found in bone hydroxyapatite. Thus they decrease bone loss.
    • ______________________________________
    • They inhibit FPP synthase --> prevents Mevalonate from becomeing Farnesyl PPi which is needed for osteoclasts--> thus decreases Osteoclast activity and decreasing bone reabsorption.
  16. When are bisphosphates used Clinically?

    What are some adverse effects?
    • Osteoporosis
    • Pagets disease
    • Hypercalcemia of malignancy
    • ___________________________
    • Esophagitis and GIT distress (note: once taken you cannot lie down and need to drink alot of water)
  17. What are some other agents that can be used to treat osteoporosis?
    Estrogens ( inhibiting IL-1 and TNF, thus decrease osteoclasts differentiation)

    Raloxifene-selective estrogen receptor modulator
  18. Calcitonin. Where is it released from?
    How is it administered?
    What is Miacalcin?
    released from the Parafollicular cells in the thyroid fland due to increase of Ca levels

    Given via tablet or nasally

    Salmon calcitonin (Miacalcin) is 100 times more potent than human calcitonin.
  19. What are the Principle effects of Calcitonin?
    • Principal effects are to lower serum calcium and phosphate
    • --inhibits osteoclast activity
    • --inhibit the reabsorption of calcium and phosphate from the renal tubules
  20. What are some clinical uses for Salmon Calcitonin?
    • Calcitonin (Miacalcin):
    • Used in Paget’s disease of bone.
    • Postmenopausal osteoporosis.
    • Hypercalcemia.
  21. What is Fluorides effect?
    Stimulates new bone formation and renders it more resistnat to reabsorption.

    also used in dental caries
  22. name some drugs that treat Osteoporosis?

    1st line
    2ed line
    -Bisophosphonates, and Raloxifene

    -Teriparatide, and Calcitonin
Card Set
Pharm Block 2 (Osteoporosis)
Pharm Block 2 (Osteoporosis)