Gout, Migraine Flashcards
Rheumatoid arthritis
- disease
- treatment
- auto-immune disease = + immune cells active = + cytokines needed to communicate with them
- count number of inflamed joints before and after treatment to see if it was effective
- treatment: act on immune cells directly
- Traditional DMARs - monotherapy (leflunomide) or combination therapy
- Glucocorticoids combined with DMARDs
Anti-rheumatic drugs
- NSAIDs
- Non-biologic disease modifying anti-rheumatic drugs (DMARDs) – methotrexate, leflunomide, sulfasalazine, gold salts
- Biologic disease modifying anti-rheumatic drugs (DMARDs) - abatacept, rituximab, tocilizumab, anakinra, adalimumab, etanercept, infliximab
Methotrexate
-mechanism of action (4)
- inhibits enzymes involved in the purine metabolism, leading to accumulation of Adenosine, which is a inhibitor of inflammation
- DNA and RNA synthesis is inhibited
- Anti-folic agents –> use folic acid to decrease side effects
- inhibit dihydrofolate reductase = affect lymphocytes and macrophages function
Methotrexate
- pharmacokinetics (4)
- indications (6)
- adverse effects (3)
- Non-biologic disease modifying anti-rheumatic drug
- 70% is absorbed after oral administration
- 1/2 life is 6-9 hours
- Excreted principally in the urine
-rheumatoid arthritis, psoriasis, Wegener’s granulomatosis, giant cell arteritis, lupus, vasculitis
- nausea, mucosal ulcers
- leukopenia, anemia, stomatitis, GI ulcerations, alopecia
- contraindicated in pregnancy
TNF inhibitors
- names (3)
- adverse effects
-adalimumab, etanercept, infliximab
- injection site reactions (adalimumab, etanercept)
- infusion reactions (infliximab)
- infectious complications (tuberculosis)
- development of blocking antibodies
- other –> lymphomas, vasculitis, congestive heart failure
Gout
- disease
- treatment
-too much uric acid = some drugs decrease uric acid production and some increase uric acid elimination
- acute gout attacks - NSAID, corticosteroids, Colchine
- Prevent episodes - allopurinol, febuxostat
- urate lithiasis - probenecid, pegloticase
Colchine
-mechanism of action
- used to treat acute between gout attacks
- relieves the pain and inflammation in 12-24h without other analgesic effects
- bind to intracellular protein tubulin
- prevents its polymerization into microtubules
- leads to inhibition of leukocyte migration and phagocytosis
-it also inhibits the formation of some leukotrienes
Colchine
-adverse effects (4)
- diarrhea, nausea, vomiting, abdominal pain
- hepatic necrosis
- acute renal failure
- hair loss, bone marrow depression, peripheral neuritis
Allopurinol
- pharmacokinetics
- mechanism of action
- used between gout attacks
- 80% absorbed (oral)
- long duration of action - given only once a day
-uric acid is produced from xanthine –> allopuriol inhibits xanthine oxidase = decrease uric acid production
Allopurinol
- indications (2)
- adverse effects (5)
- chronic gout in period between attacks
- when starting, colchine or NSAID should be used until steady state of uric acid is normalized and they should be co-administered for 6 months or longer
- GI intolerance
- bone marrow depression
- aplastic anemia
- hepato-toxicitiy
- cataracts
Febuxostat
we dont need to know
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Uricosuric drugs
- name
- mechanism of action
- contraindication
- Probenecid
- inhibit active transport site for re-absorption and secretion in proximal renal tubule = net reabsorption of uric acid in the proximal tubule is decreased = high amount will be eliminated in the urine
- patients with renal failure
Why shouldn’t aspirin be used for the analgesia of gout?
Because it causes the net retention of uric acid by inhibiting the secretory transporter
Uricosuric drugs
- name
- indications
- adverse effects
- Probenecid
- in gouty patients with under excretion of uric acid when other drugs are contraindicated. Should not be started until 2-3 weeks after an acute attack
- GI irritation, rash, nephrotic syndrome, aplastic anemia
Pathogenesis of migraine
- initiating event may be abnormal neuronal discharge
- Localized spreading depression - aura
- Sensitization of central pain pathways
- aura = constriction of blood vessels - partial ischemia
- acute migraine attack
- vessels are dilated (by serotonin), Trigeminal nerve endings are activated