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42 Cards in this Set

  • Front
  • Back
What are the four actions of the non selective COX inhibitors?
anit-inflammatory, Anti-platelet, Anti-pyretic, and analgesic
Acetaminophen exhibits which two properties?
anti-pyretic and analgesic
MOA of the non selective COX inhibitors
blocks cyclooxygenase COX pathway, limiting prostaglandin synthesis
Difference between aspirin and other non selective COX inhibitors
aspirin is irreversable
Name the three oral, reversible non selective COX inhibitors
Ibuprofin, Indomethacin, and naproxen
Which NSAID is available in a parenternal formulation and is mainly used for its analgesic properties.
Ketorlac use is restricted to 72 hours due to which side effects?
GI and renal damage
Which non selective, oral, COX inhibitor has the highest anti-inflammatory property, and is a 1st line treatment of a gouty attack?
Indomethacin (reduces prostaglandin, and crystal phagocytosis by macrophages)
Toxicity of Aspirin
tinnitis, vertigo, GI bleeding, and increased bleeding time, risk of reyes syndrome in kids with viruses.
Common side effects of all NSAIDS
risk of renal damage, especially in preexisting renal disease, and GI upset.
What is acetaminophen, what is it used for?
is an OTC antipyretic/analgesic, used in patients with renal disease. metabolized by liver
Toxicity of acetaminophen
hepatic failure in cases of overdose due to toxic metabolite by phase II reactions. Alcohol predisposes to this toxicity
Antidote for Acetaminophen poisoning
N-acetylcysteine. used to regenerate glutathione, and continue degredation of toxic metabolite
What are the COX 2 inhibitors, and why were they developed?
Celecoxib, refecoxib, valdecoxib. developed to limit GI effects of non selective NSAIDs
Toxicities of COX 2 selective inhibitors
renal toxicity, as well as increased risk of myocardial infarction and stroke. this is due to the increased inhibition of prostacyclin (PGI2), than over TXA2. causes platelet aggregation and vasoconstriction
What are DMARDS, and what is their clinical use?
slow active disease modifying drugs, may take 6 weeks to 6 months to have effect. Limit or even reverse progression of Rheumatic disease
What class of drugs have an intermediate effect on rheumatic disease, but are too toxic for long term, chronic use?
corticosteroids, reduce inflammation, and other immune responses in rheumatic disease.
Which cytotoxic drug acts by limiting the number of immune cells available to carry out inflammatory response?
methotrexate, also used to treat cancer, inhibits dihydrofolate reductase (thereby stopping DNA synthesis)
Toxicity of methotrexate
nausea, mucosal ulcers, hematotoxicity, hepatotoxicity, teratogenicity
Antidote used for methotrexate overdose
DMARD drugs used that interfere with activity of T lymphocytes
sulfasalazine, cyclosporin, hydroxychloroquine.
Toxicity of T lymphocyte altering DMARDS
hepatotoxicity, GI disturbance, rash, headache, leukopenia
DMARD drugs that act by limiting activity of B lymphocytes and macrophages
Rituximab for B lymphocytes Gold compounds for macrophages
Other use for Rituximab and toxicities
also used for Non-Hodgkins lymphoma, causes infusion reaction, rash, infection, and cardiac toxicity
Other use for Hydroxychloroquine
anti malarial
Other use for Sulfasalazine
Ulcerative colitis
Other use for methotrexate
cancer treatment
Other use for cyclosporine
tissue transplant
What immunoglobulin based biologic agents work by inhibiting Tumor necrosis factor A, and have shown success in treating RA?
Infliximimab, adalimumab, and entarecept.
What is another major use for the tumor necrosis factor A drugs?
Crohn's disease
Which DMARD for RA works as an interleukin 1 receptor antagonist
Anakinra, causes infection, worsening of COPD, and hypersensitivity reactions
DMARDS have also shown to be of use in what other autoimmune diseases?
SLE, sjogrens arthritis, JRA, and ankylosing Spondylitis,
What are the 3 treatment strategies associated with gout?
1) reduce inflammation during acute attacks 2) accelerating renal excretion of uric acid 3) reducing conversion of purines to uric acid
Which treatment of acute gout works by inhibiting microtubule assembly, reducing leukocyte migration, and phagocytosis? also works with familial mediterranean fever
colchicine. is a general mitotic poison, and is being phased out due to severe liver and kidney damage
What is the standard 1st line treatment for acute gouty attacks, and is used in conjunction with other treatments to reduce risk of acute attack?
indomethacin. (NSAID) anti-inflammatory. reduces protsaglandin formation, and phagocytosis of crystals by macrophages
What are the uricosuric agents, and how do they work
probenecid and sulfinpyrazone. these are weak acids that compete for reabsorption in in the proximal tubules. at low doses can compete for secretion (bad)
When should these be used, and why should they be combined initially with indomethacin?
they can precipitate an acute attack during early use, should not be used for treatment of initial attack. Indomethacin reduces chance of precipitating an attack
What are the Xanthine Oxidase inhibitors? what are they used for?
Allipurinol and febuxostat. these are used to reduce formation of uric acid in the body, by inhibit xanthane oxidase, which breaks down hypoxanthine and xanthine into uric acid. Allopurinol is a suicide inhibitor, and febuxostat is a non purine inhibitor, and is more selective
When should these be used, and why are they combined with indomethacin?
not for 1-2 weeks after acute attack. combined with indomethacin because they can induce an acute attack
What other clinical use is there for Allopurinol?
used as adjunct to cancer therapy to slow the formation of uric acid from purines released by the death of large numbers of neoplastic cells
Toxicities of allopurinol
GI upset, rash, peripheral neuritis, vasculitis, aplastic anemia. Also inhibits metabolism of mercaptopurine and azathioprine, drugs which need xanthine oxidase for metabolization
Toxicities of Febuxostat
liver function abnormalities, headaches, and GI upset