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29 Cards in this Set

  • Front
  • Back
Who do you give De penicillamine to? (patient population)
rheumatoid arthritic patients, reduces rheumatoid factor. **chelates heavy metals and treats heavy metal poisioning (more common)
What is the MOA of methotrexate?
folic acid antagonist, inhibits DHFR
(treats rheumatoid arthritis, low doses and cancer at high doses)
What are the side effects of methotrexate?
cytopenia, esp leukopenia and megaloblastic anemia, mucousal ulceration, nausea
What are the anti-TNF agents?
thalidomide, pentoxyfillin, infliximab, and etancercept
What are the anti-inflamm drugs?
NSAIDS, steroids, methotrexate, anti-TNF (extreme inflammation)
What is the MOA of thalidomide?
inhibits the production and secretion of TNF
Who do you give thalidomide to?
patients--leprosy, HIV associated skin lesions, multiple myeloma
What is the MOA of pentoxyfilline?
phosphodiesterase inhibitor, causes TNF secretion inhibition
What does pentoxyfilline treat?
acute alcoholic hepatitis
What is the MOA of infliximab?
monoclonal antibody against TNF
What does infliximab treat?
rheumatoid arthritis, ankylosing spondylitis, psoriatric arthritis, moderate-->severe ulcerative colitis, crohns dz
What is the MOA of etancercept?
recombinant TNF receptor, binds to TNF in the bloodstream
What are the side effects of infliximab, etanercept, and adalimumab?
increased chances of MS, optic neuritis, and myelitis
What are the side effects of infliximab and etancercept?
increased chances of MS, optic neuritis, and myelitis

life threatening sepsis (acute onset)
secondary cancer
serum sickness (antibodies against injected protein)

others: headache, dyspnea, abdominal pain
What are the side effects of adalimumab?
increased chances of MS, optic neuritis, and myelitis

aplastic anemia
worsen heart failure
What is the MOA of adalimumab?
monoclonal antibody against TNF (mouse human chimera)
What do steroids inhibit?
phospholipase A2
What can cause chronic gout?
kidney dz or malignancy
What is the DOC for acute attacks of gout and its MOA?
colchicine, binds to tubilin, mitotic inhibitor (like vincristine)

*decreases number of future attacks
What do you normally give for acute attacks of gout?
NSAIDS (not aspirin)
What patient population is colchicine contraindicated in?
preggers, hepatic and CV dz
What is the MOA of allopurinol?
inhibits xanthine oxidase
What syndrome is due to deficient HGPRT (essential for purine salvage)?
Lesch-Nyhan syndrome, x linked recessive
What are the S/S of Lesch-Nyhan syndrome?
hyperuricemia, mental retardation, compulsive biting of lips and fingers, self mutilating activities.
What happens to the EXCESS uric acid and how is it related to gout?
uric acid-->phagocytosed by neutrophils-->leukotrienes + other mediators of inflammation. Lysosomes are ruptured-->phagocyte dies-->hydrolytic enzymes (phagocytosed urate released from dying cells)

*inflamm cells try to get rid of EXCESS uric acid but can't break down-->acute inflammation (attack)
What is the DOC for chronic gout?
probenecid, blocks tubular reabsorption of uric acid
Is probenecid a p450 inhibitor or inducer?
Probenecid is a p450 inducer
Do we give low or high doses of probenecid?
High doses because it will compete with uric acid at the renal transporters (therapeutic)
Why do we avoid aspirin in gout patients?
bc uses renal transporters like uric acid