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22 Cards in this Set
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Gout- biochem
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due to elevated concentration of uric acid (UA) in blood and tissues due to overproduction or undersecretion- problems in the purine catabolism (AG)
Important enzymes- Adenine deaminase, guanine deaminase, and xanthine oxidase |
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Gout- pathophys
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elevated UA levels cause the formation of sodium urate crystals (tophi)- joints become inflamed, painful, and arthritic
(can be deposited in kidney tubules and lead to a damaged kidney and decreased excretion of UA) |
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NSAIDs- for Gout
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Acute Gout (esp Indomethacin)
relieve acute inflammation *Indomethacin has severe CNS side effects Aspirin is contraidicated at low dose |
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Colchicine
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Acute Gout
block the mobilization of the granulocytes leading to inhibition of inflammation- disrupts cellular microtubules *used prophylactically when initiating therapy with probenecid or allopurinol Side effects (due to microtuble effect)- GI distress, bone marrow depression, and alopecia |
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Allopurinol
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Chronic Gout
Xanthine oxidase inhibitor- allopurinol and its metabolite alloxanthine are able to inhibit xanthine oxidase- blocks overproduction of UA Side Effects: Initiation of therapy can increase frequency and severity of acute attacks |
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Probenecid
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Chronic Gout
uricosuric agent- targets the anion exchanger needed for UA reabsorption- promotes excretion of UA based on blocking reabsorption Side Effects:increase in frequency and severity of acute attacks or kidney stones |
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Non-Pharmacological Tx in Gout
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Avoid purine-rich foods (liver)
Avoid excessive alcohol Increase fluid intake Alkalinize urine |
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Rheumatoid Arthritis (RA)
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systemic inflammatory disorder- autoimmune mechanism that results in joint inflammation and bone destruction
symptoms: pain, stiffness, and swelling of peripheral joints |
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NSAIDS- in RA
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for analgesic and anti-inflammatory effects
block PG production by blocking cyclooxygenase (COX) * no effect on the disease process |
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Selective COX-2 inhibitors
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Celecoxib and Rofecoxib
Not constituatively on like COX1- COX2 expression is inducible in response to inflammation Side effects: dyspepsia, diarrhea, nausea, vomiting, skin reactions, CNS, etc. |
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DMARDs
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Disease-modifying antirheumatic drugs-
1. Immunosuppressant agents: Methotrexate (MTX), Leflunomide, Azathioprine 2. Gold compound such as auranofin 3. Other secondary agents such as Hydroxychloroquine 4. Glucocorticoids such as prednisone 5. Cytokine antagonists: etanercept, infliximab, anakinra |
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Methotrexate (MTX)
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most widely used DMARD for RA
MTX inhibits dihydrofolate reductase, lymphocyte proliferation and cytokine production, and interferes with migration of leukocytes *anchor agent in combination therapies. -rapid onset of action (2-3 wks) |
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Leflunomide
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DMARD for RA patients- immuno-suppressant- alternative to MTX
Inhibits dihydroorotate dehydrogenase in pyrimidine synthesis, thus preventing DNA replication and the synthesis of RNA and proteins in immune cells |
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Auranofin
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DMARD for RA- Gold compounds
aren’t used much anymore mechanism is unclear high incidence of adverse reactions |
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Hydroxychloroquine
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DMARD for RA- Other secondary agents
anti-malarial drug with anti-RA activity often used with an NSAID for mild RA. Side Effects: retinopathy (blurred vision and night blindness) |
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Prednisone
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DMARD for RA- Glucocorticoids
use is infrequent because of side effects |
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Cytokine antagonists
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DMARD for RA- newest generation ($$$)
TNF antagonists: etanercept, infliximab, adalimumab IL-1 antagonists: anakinra *The 2 major cytokines in RA are TNF ( inflammatory reaction) and IL-1 (cartilage destruction) |
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Etanercept (Enbrel)
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DMARD for RA- cytokine antagonist
soluble TNF-alpha receptor fused with the Fc portion of an antibody- binds to and clears TNF-_ to prevent its action with endogenous receptors. *used in combination with MTX- injected subcutaneously twice a week |
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Infliximab (Remicad)
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DMARD for RA- cytokine antagonist
a chimeric humanized anti-TNF-_ monoclonal antibody that binds to and clears TNF-_ |
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Adalimumab (Humira)
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DMARD for RA- cytokine antagonist
HUMAN IgG1 monoclonal antibody against TNF-_ |
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Anakinra (Kineret)
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DMARD for RA- cytokine antagonist
recombinant IL-1 receptor antagonist (IL-1Ra) which competitively inhibits the binding of IL-1 to IL-1R1 subcutaneously injection, and a response is seen within 4-13 wks |
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Combination therapy for RA
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MTX is the anchor drug:
MTX + etanercept MTX + infliximab MTX + leflunomide MTX + sulfasalazine and hydroxychloroquine |