Drugs Flashcards
Ibuprofen
NSAID: reversibly inhibits COX-1 and COX-2; blocks prostaglandin synthesis
Toxicity: renal damage, fluid retention, aplastic anemia, GI distress, ulcers
Naproxen
aka Alleve
NSAID
can use in acute gout treatment
NSAIDs
ibuprofen, naproxen, indomethacin, ketrolac
Mechanism: reversibly inhibit COX-1 and COX-2; block prostaglanding synthesis
Use: antipyretic, analgesic, anti-inflammatory. Can use NSAIDs in acute gout treatment.
EtToxicity: renal damage, fluid retention, aplastic anemia, GI distress, ulcers
Indomethacin
NSAID
can be used to close a PDA
Celecoxib
COX-2 inhibitor; reversibly inhibits COX-2, but spares COX-1 (so maintains gastric mucosa)
Use: rheumatoid and osteoarthritis; patients with gastritis or ulcers
Toxicity: increased risk of thrombosis; Sulfa allergy; less toxicity to GI mucosa than NSAIDs
Acetaminophen
Mechanism: reversibly inhibits COX, mostly in the CNS; is inactivated peripherally
Toxicity: overdose leads to hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in the liver
antidote to acetaminophen?
N-acetylcysteine (regenerates glutathione, which is depleted by acetaminophen metabolite)
Bisphosphonates:
- Mechanism?
- Use?
- Toxicity?
Etidronate, Pamidronate, Alendronate, Risedronate, Zoledronate (IV)
Mechanism: inhibit osteoclastic activity, reduces formation and resorption of hydroxyapatite
Use: malginancy-associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis
Toxicity: corrosive esophagitis (not zoledronate though), nausea, diarrhea, osteonecrosis of the jaw
Etidronate
a bisphosphonate
Mechanism: inhibit osteoclastic activity, reduces formation and resorption of hydroxyapatite
Use: malginancy-associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis
Toxicity: corrosive esophagitis (not zoledronate though), nausea, diarrhea, osteonecrosis of the jaw
pamidronate
a bisphosphonate:
Mechanism: inhibit osteoclastic activity, reduces formation and resorption of hydroxyapatite
Use: malginancy-associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis
Toxicity: corrosive esophagitis (not zoledronate though), nausea, diarrhea, osteonecrosis of the jaw
alendronate
a bisphosphonate:
Mechanism: inhibit osteoclastic activity, reduces formation and resorption of hydroxyapatite
Use: malginancy-associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis
Toxicity: corrosive esophagitis (not zoledronate though), nausea, diarrhea, osteonecrosis of the jaw
Risedronate
a bisphosphonate:
Mechanism: inhibit osteoclastic activity, reduces formation and resorption of hydroxyapatite
Use: malginancy-associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis
Toxicity: corrosive esophagitis (not zoledronate though), nausea, diarrhea, osteonecrosis of the jaw
Zoledronate
a bisphosphonate (IV):
Mechanism: inhibit osteoclastic activity, reduces formation and resorption of hydroxyapatite
Use: malginancy-associated hypercalcemia, Paget’s disease of bone, postmenopausal osteoporosis
Toxicity: corrosive esophagitis (not zoledronate though), nausea, diarrhea, osteonecrosis of the jaw
Probenecid
treatment for chronic gout; lowers urate levels by inhibiting reabsorption of uric acid in PCT; (also, inhibits secretion of penicillin)
Allopurinol
drug for chronic gout treatment; lowers urate by inhibiting xanthane oxidase, so decreases conversion of xanthine to uric acid.
Also, used in lymphoma and leukemia to prevent tumor lysis-associated urate nephropathy.
Get increased concentrations of azathioprine and 6-MP, which are both normally metabolized by xanthine oxidase
Febuxostat
drug for chronic gout treatment; inhibits xanthine oxidase
Colchicine
acute gout drug;
binds and stabilized tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation; GI side effects (diarrhea…) if given orally
Etanercept
TNF-alpha inhibitor;
Mechanism: recombinant fornm of human TNF receptor that binds TNF (etanerCEPT is a TNF decoy reCEPTor)
Clinical use: rheumatoid arthritis, psoriasis, ankylosing spondalitis
Infliximab
TNF-alpha inhibitor
Mechanism: anti-TNF antibody
Use: Crohn’s disease, rheumatoid arthritis, ankylosing spondilitis
(“INFLIXimab INFLIX pain on TNF” :))
Adalimumab
TNF-alpha inhibitor
Mechanism: anti-TNF antibody
Clinical use: rheumatoid arthritis, psoriasis, ankylosing spondylitis
What do TNF-alpha inhibitors predispose to?
All TNF-alpha inhibitors (ie etanercept, infliximab, adalimumab) predispose to infection including reactivation of latent TB, because TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes
Leuprolide
GnRH analogue:
-acts like an agonist if used in a pulsatile fashion
-acts as an antagonist when used in continuous fashion (so downregulates GnRH receptor in pituitary so decreased FSH/LH)
Use: infertility (if given pulsatile), prostate cancer (if given continuous, along with flutamide), uterine fibroids
Toxicity: anti-androgen, nausea, vomiting
Finasteride
anti-androgen
5-alpha-reductase inhibitor (so blocks Testosterone –> DHT);
Use: BPH; promotes hair growth (so can treat male-pattern balndess) (soooo encourages female breast growth, and prevents male hair loss!)
Flutamide
anti-androgen
nonsteroidal competitive inhibitor of androgens at the testosterone receptor
Use: prostate carcinoma
