Drugs for Osteoporosis and Gout Flashcards
(21 cards)
Where are the following found:
Ergocalciferol
Cholecalciferol
Ergocalciferol: D2 - occurs in plants and used in fortified foods.
Cholecalciferol: D3 - produced in skin exposed to sunlight, or as a prescription drug.
What is the MOA of Calcitonin-salmon?
What is the indication?
What are the adverse-effects?
Similar to endogenous calcitonin, but has a longer half-life and greater potency. It decreases bone resorption.
Only used for the treatment of established osteoporosis, not in prevention.
Very few - considered to be safe.
What is the MOA of Bisphosphonates-alendronate?
What is the indication?
What are the adverse-effects? (3)
Structural analogs of pyrophosphate (normal bone constituent) and inhibits bone resorption.
1st choice for essentially every kind of osteoporosis.
Esophagitis
Osteonecrosis of jaw*
Atypical femoral fractures
Aside from Alendronate, what are the other bisphosponates? (4)
Risedronate (PO)
Ibandronate (PO, IV)
Tiludronate (PO)
Zolendronic acid (IV 1x/year) - avoids GI problems, but associated with osteonecrosis of jaw.
What is the MOA of Raloxifene?
What is the indication?
What are the adverse-effects? (3)
SERM that is an agonist at bone and an antagonist in the breast and uterus.
Primarily post-menopausal osteoporosis.
DVT, PE and stroke.
What is the MOA of Teriparatide?
What is the unique frequency that it is given?
What are the indications?
How is it administered?
What are the adverse-effects?
A variant of PTH that increases bone formation (only osteoporosis drug that can do this).
It’s given in a pulsatile fashion so that osteoblast responses dominate.
OP: Post-menopausal, men, GC-induced.
Once-daily admin, by using pre-filled injectors.
Well-tolerated, but may cause nausea, HA, myalgias and cramps. Possibly elevated Ca++, Mg++ and uric acid levels.
What is the MOA of Denosumab?
What are the indications? It should be taken with…
How often is it given?
What are the adverse-effects? (3)
mAb that is an inhibitor of RANKL. This decreases the formation and function of osteoclasts (reduced bone resorption).
Post-menopausal OP at high risk for fractures, bone metastases from solid tumors.
Should be taken with Vit. D to prevent hypoglycemia.
Injected subQ every 6 mo.
Delays in fracture healing, new fractures and osteonecrosis of the jaw.
What is a major risk of treating osteoporosis in men?
What is the drug of choice for men with osteoporosis?
Hypogonadism, so testosterone replacement is important.
Bisphosphonates (1st), Denosumab (2nd).
They tend to respond to similar drugs as women.
What is the MOA of Cinacalcet?
What are the indications?
What are the adverse-effects?
A “calcimimetic” drug that binds in the PT glands and increases its sensitivity to extracellular Ca++ and decreases PTH secretion.
Hypercalcemia:
- primary hyperparathyroidmism (parathyroid CA).
- secondary hyperparathyroidism due to CKD.
N/V/D.
What topical NSAID is useful in OA?
What can be given for pain-resistant therapy? (3)
1% diclofenac gel.
Duloxetine (SNRI)
Opioid analgesics
Intra-articular: hyaluranons, glucocorticoids, PRP injections.
What are the 4 major antibiotics used to treat Osteomyelitis?
How long is it treated?
Clindamycin
Rifampin
TMP/SMX
Fluoroquinolone
Approx. 4-6 wks.
What are the causes of Primary Hyperuricemia due to the following:
Uric acid underexcretion (90%)
Urate overproduction (10%)
Uric acid underexcretion (90%): lower fractional excretion of filtered urate.
Urate overproduction (10%): metabolic disorders, idiopathic.
What are the causes of Secondary Hyperuricemia due to the following:
Uric acid underexcretion (90%)
Urate overproduction (10%)
Uric acid underexcretion (90%): impaired renal function limiting urate excretion; drug-induced inhibition of urate excretion.
Urate overproduction (10%): excessive purine intake; tumor lysis syndrome.
What causes plasma [urate] to increase? (2)
Fractional excretion is less than normal.
GFR falls (i.e. kidney disease).
Treatment of Gout acutely:
Treatment of Gout if there are recurrences:
Acutely, anti-inflammatory drugs:
- NSAIDs
- Colchicine
- Glucocorticoids
If recurrences, must lower [urate]
- Lifestyle changes.
- Meds: allopurinol, febuxostat, probenecid, pegloticase, etc.
What is the MOA of Colchicine?
What is the indication?
Which patients are contraindicated?
What are the major adverse-effects?
It diffuses into cells to block tubulin and blocks formation of microtubules which leads to inhibition of WBC migration and phagocytosis.
NSAID intolerances/contraindations.
Advanced renal and hepatic impairment.
GI distress, N/V/D.
What is the MOA of Allopurinol?
What are the indications?
What are the major adverse-effects?
Competitive inhibition of xanthine oxidase, which inhibits the conversion of hypoxanthine and xanthine to uric acid.
Recurrent gout, cancer/chemo-induced hyperuricemia (tumor lysis syndrome).
*SJS, skin rash, N/V, elevated LFTs.
What is the MOA of Febuxostat?
What are the indications?
What are the major adverse-effects?
Inhibition of xanthine oxidase so that hypoxanthine and xanthine are excreted more easily.
Patients who can’t tolerate allopurinol.
Very few, but it is highly expensive.
What is the MOA of Pegloticase?
What are the major adverse-effects?
It is a recombinant mammalian uricase and is covalently attached to methoxyy-polyethelyene glycol. It converts uric acid to allantoin (more solluble).
Infusion reactions mainly.
What is the MOA of Rasburicase?
What is it used for?
Non-pegylated recombinant uricase.
Prevention of acute uric acid nephropathy due to tumor lysis syndrome in a patient with high-risk lymphoma or leukemia.
What is the MOA of Probenecid?
What is the major indication?
What are the major adverse-effects?
It is an organic acid that blocks urate resorption more than urate secretion. Thus, it increases fractional excretion of urate (decreases plasma concentration).
Underexcreters with GFR > 60 ml/min and NO stones.
- hyperuricemia
- frequent attacks
It is a sulfa-containing drug, so sulfa reactions are possible.
