Rheumatoid Arthritis Flashcards
• Chronic systemic inflammatory dse with unknown etiology
RHEUMATOID ARTHRITIS
RA Hallmark feature
Persistent symmetric inflammatory peripheral polyarthritis (SYNOVITIS)
Cigarette Smoking, Infection, and Trauma are the external triggers of RA
(CIT)
TRUE
Goals of RA Treatment
• Decrease joint inflammation
• Arrest dse progression
Important short-term option for controlling pain and inflammation
Rarely used w/o concomitant DMARD use
Should be tapered as soon as possible
NSAIDS
Prevent prostaglandin production by INHIBITING COX ENZYME
Aspirin and other NSAIDs
Inhibit SPECIFIC FORM OF COX-2
COX-2 Inhibitors
• Control pain and inflammation during EARLIER STAGES of RA
• Facilitate REMISSION during ACUTE FLARE-UPS and DECREASE DISABILITY
• Early use = DECREASE EROSION AND DAMAGE
“BRIDGE”
Glucocorticoids
• Inhibits proinflammatory substances
• Inhibits transcription factors that initiates synthesis of proinflammatory cytokines, enzymes, and receptor proteins
• increase production of annexins (lipocortins)
Glucocorticoids
• inhibits T cell function
• irreversible retinal damage
• eye examination
CHLOROQUINE
Inhibit toll-like receptors
6-6.5 mg/kg
HYDROXYCHLOROQUINE
• imidazolyl derivative of 6-mercaptopurine
• inhibit many aspects of B and T cell function
• Neutropenia
• Relatively high toxicity
• Used cautiously for those debilitated or with renal dse
AZATHIOPRINE
• inhibit mononuclear phagocytes
• bind strongly to specific proteins
• increases expression of anti-inflammatory proteins
• reduced synthesis of prostaglandin E2 and other inflammatory mediators
GOLD COMPOUNDS
• Intramuscular
• effects occur faster than oral gold
• long delay of 4 mos
GOLD SODIUM THIOMALATE
• inhibits dihydroorotate dehydrogenase (mitochondrial enzyme in de novo pyramidine synthesis)
• antiproliferative activity and anti-inflammatory effexts
• decrease joint erosion/destrcution with relatively few side effects
• long term side effects TBD
LEFLUNOMIDE
• inhibits DNA synthesis
• anything w/ folate
• assoc w pulmo probs
• PRIMARY DRUG when treating RA, yet other agents can be added
METHOTREXATE
• sequester harmful chemicals (reactive aldehydes)
• influence T CELL ACTIVITY AND IMMUNE FUNCTION
• aplastic anemia
• pemphigus
• MYASTHENIA GRAVIS
• relatively high incidence of toxicity
PENICILLAMINE
• inhibition of ARACHIDONIC ACID CASCADE (sulfing the sea)
• modulate LEUKOTRIENES
• may produce serious hypersensitivity reactions and blood dyscrasias
SULFASALAZINE
Adalimumab (Human IgG1 mAb)
Certolizumab (PEGylated Fab mAb fragment)
Etanercept (TNFR2 Fc fusion protein)
Golimumab (Human IgG1K mAb)
Infliximab (Chimeric mAb)
Tumor Necrosis Factor Inhibitors (TNFIs)
• suppresses T cell activation
ABATACEPT
• blocks interleukin-1 (IL-1) receptor to protect against autoinflammatory events
• should not be used with TNFIs
ANAKINRA
• Recombinant humanized interleukin-6 (IL-6) receptor monoclonal antibody
• IgG1K subclass
• Often combined witt methotrexate if other DMARDs not effective
TOCILIZUMAB
• GENETICALLY-ENGINEERED CHIMERIC MURINE/human monoclonal IgG
RITUXIMAB
