Pharm- RA Flashcards
What is the analgesic of choice for rheumatoid arthritis and why?
What are examples of them and how they work?
NSAIDs are drug of choice for RA b/c of their fast acting anti-inflammatory and pain relief effects
1st gen- inhibit COX1 and 2- aspirin and naproxen
2nd gen- inhibit COX2- celecoxib
Glucocorticoids Examples and the two classes MOA Actions Uses AE and why you cant stop taking abruptly
Glucocorticoids
Prednisone (prodrug), methylpredisolone, fluorinated (beta and dexamethasone- inc half life and potency)
MOA- GR binds GRE and alters transcription; GR complexing w/ NFKB or AP1 have indirect immunosuppression
Actions- suppress eicosinoids, immune system, cytoknes, and inflammatory cells
Uses- relieve pain/inflammation of RA while waiting for DMARD effects
AE- cushings; fatal if stop abruptly
What are the 4 examples of non-biological/traditional DMARDs (disease modifying antirheumatoid drugs)?
MTX
Hydroxychloroquine
Sulfasalazone
Leflunomide
How do you monitor non-bio traditional DMARDs once you start taking them?
you have to monitor CBC, aminotransferase, and Cr for all except hydrochloroquine
MTX MOA Kinetics Uses AE for low and high dose
MTX
MOA- undergoes polyglutamation which accumulates and blocks AICAR which accumulates causing adenosine efflux which binds GPCR and has anti-inflammatory effects
Kinetics- effects w/in 6 weeks; take once a week (oral or inject)
Uses- 1st choice RA
AE- low dose- well tolerated but take folate weekly; high dose suppresses BM, liver fibrosis, ulcers, pneumonitis, fetal death
Hydroxychloroquine MOA Kinetics Uses AE
Hydroxychloroquine
MOA- accumulates in lysosomes inc pH preventing peptide interaction w/ MCHII
Kinetis- effects w/in 6 months
Uses- RA if prego, mild RA, or triple therapy for severe RA
AE- retinal damage
Sulfasalazone MOA Kinetics Uses AE
Sulfasalazone MOA- metabolized into sulfapyridine Kinetics- onset w/in a month Uses- RA; combo or alone; ok to use if prego AE- GI and sulfa hypersensitivity
Leflunomide MOA Kinetics Uses AE
Leflunomide
MOA- inhibit mito dihydrooratate DH which dec rUMP which inhibit T cell prolif
Kinetics- needs loading dose
Uses- 2nd choice for RA after MTX; combo w/ another traditional
AE- diarrhea, resp infection, alopecia, rash
Biological DMARDs
Explain how they can be combo treatments
General info comparing them to traditional
Bio DMARDs
Can combo w/ traditional but CANNOT combo w/ another bio
Fast acting and very effective but have inc risk of severe AE
TNF antagonists Drugs and how they are taken MOA Uses AE
TNF antagonists
Etanercept- subQ x2 week; Infliximab- IV every 6 mon; Adalimumab- subQ every 2 weeks
MOA- neutralize TNF
Uses- very effective at reducing symptoms and progress in mod to severe RA after traditional has failed; combo w/ MTX
AE- serious infection (TB) and allergic rxn
Rituximab
MOA
Uses (when is it most effective?)
AE
Rituximab
MOA- target and deplete CD20 b cells (no effect on plasma cells so Ig levels are nml)
Uses- combo w/ MTX if pt where TNF antag failed; best if pt is + for rheumatoid factor and CCP
AE- IV hypersensitivity rxn
Abatacept
MOA
Uses
AE
Abatacept
MOA- inhibit CD28 from binding CD80/86 and prevents T cell activation
Uses- mod-severe RA where TNF antag failed; combo w/ traditional
AE- serious infection but generally very well tolerated
Tocilizumab
MOA
Uses
AE
Tocilizumab
MOA- IL-6R antag limits acute phase response and prevents activation of B/T cells, macrophages, and osteoclasts
Uses- mod severe RA if other DMARDs fail; use w/ or w/o MTX
AE- URI and serious infection
Tofacitinib
MOA
Uses
AE
Tofacitinib
MOA- inhibit JAK3 and suppress IL17 and INF-r and inhibit prolif of CD4 T Cells
Uses- mod severe RA; use w/ or w/o MTX
AE- opportunistic infection and inc risk of malignancy; expensive
Anakinra
MOA
Uses
AE
Anakinra
MOA- IL-1R antagonist
Uses- mod severe RA when traditional fails; last choice- not effective
AE- serious infection and hypersensitivity
