Immunosuppressants Flashcards
Methotrexate:
- mechanism
- how to take
- se
- contraind
- monitering
Methotrexate:
- mechanism: inhibits t cell activity (and inc cancer cells stops dihydrofolate reductase)
- how to take: once a week, with folic acid on a different day
- se: teratogenic (no baby for 6 months after), cirrhosis, mucositis, pneumonitis, bm suppression, ulcers, hair thinning, pul fibrosis
- contraind: nsaids (thrombocytopenia), trimethoprim (pancytopenia), cotrimazole
- monitoring: fbc, u+es, lfts before then weekly until stable then every 2-3 months. Asked to report signs of bruising/sore throat/ulcers - blood disorders. If toxicity then folinic acid
Sulfasalazine:
- class + mech action
- SE
- contraind
Sulfasalazine:
- class + mech action: DMARD, prodrug for 5ASA which dec neutrophil chemotaxis, t cells and inflammatory cytokines
- SE: gi upset, rash, hepatitis, bm suppression, temporary azospermia, ILD, SJS, heinz body anaemia, stains contact lenses
- contraind: caution if aspirin allergy + g6pd def
Hydroxychloroquine:
- SE
- Monitering
- SE: gi, bulls eye retinopathy/corneal deposits
- monit: baseline ophthal ex and monitor acuity annually
Azathioprine:
- mechanism
- se
- contraind
- mech: is metabolised to mercaptopurine which inhibits purine synthesis which dec inflamm cytokine production. But need to test TPMYT levels otherwise prone to aza toxicity and bm suppression
- se: bm suppression, n+v, pancreatitis
- contra: caution if allopurinol
Cyclophosphamide:
- mech
- se
- contraind
- mech: crosslinks dna suppressing b/t cells
- se: haemorrhagic cystitis, myelosuppression, transitional cell carcinoma
- contraind : preg
Ciclosporin:
- mechanism
- se
- mech: calcineurin inhib dec t cells and prolif
- se: nephrotoxicity, htn, gingivitis, hepatotox, fluid retention, hyperkal, tremor, impaired glucose tolerance, hyperlipid, excessive hair growth
DMARDS:
- examples
- monitoring
- uses
- examples: azathio, methot, sulfas, hydroxyhlor
- monit: u+es, no live vaccines
- uses: ra, psa, sle, vasculitis
combination therapy more effective. can take 3 months to notice. slows disease progression
Biologics
- monoclonal ab
- anti tnf dec inflammatory cytokines cascade. like adalimumab, infliximab. tnfa essential for granuloma formation so screen for latent tb
- anticd20 on b cells causing apoptosis. rituximab.
- il17 antag: as, psa
- il12/23 - enteropathic arthritis
Mycophenolate mofetil:
- mechanism
- se
- mech: dec guanine synth hence b/t cell prolif
- se: n+v, myelosupp, mouth ulcers
Corticosteroids:
- mechanism
- SE
- mech: prevents production inflamm mediators from mO. Inducing remission (or mainstay treatment in gca/pmr). Pred/dexameth have mainly glucocorticoid activity whilst fludrocort and hydrocort have mainly mineralocorticoid activity
- se: weight gain, osteoporosis, avn femoral head, immunosuppression, cushingoid appearance, htn, cataracts, insomnia, mania, peptic ulcer, suppresses growth, neutrophilia (in mineralcorticoid more fluid retention + htn)
- important things: if on long term double dose during illness. Don’t withdraw abruptly
Bisphosphonates:
- def
- indic
- how to take
- se
- def: oral alendronic acid reduces osteoclast activity so dec bone resorption. iv zlendronate if hip fracture. denosumab is monoclonal ab if renal impairment
- indic: osteoporosis, hypercalc, pagets
- how to take: upright 30 mins post, empty stomach 30 mins post, big glass water
- se: oesophagitis, osteonecrosis jaw, hypoalc, atypical stress fractures, ulcers. fever/myalgia following dose administration
if gi SE bad switch to risedronate/etidronate
Oral antihistamines
- classifications
- se
- classsif: non sedative (cetirizine, loratidine), sedative (chlorpheniramine)
- se: sedation, antichol effects (dry mouth, blurred vision, urin retention, constip)
