Flashcards in rheumatic drugs Deck (86)
how would you define arthritis? if uncontrolled what two things does it lead to?
Described as a chronic, inflammatory, progressive condition that attacks synovial tissue lining joints
If uncontrolled leads to:
Joint destruction due to erosion or cartilage and bone
arthritis Progresses from_____ to more ______ joints
periphery to more proximal joints
RA or OA? Autoimmune disease that causes INFLAMMATORY SYNOVITIS
RA or OA? Degenerative disease that causes articular CARTILAGE LOSS & joint space narrowing
RA vs OA: morning symptoms, symmetry + locations, and systemic or local symptoms?
RA: Morning symptoms > 1 hr (stiffness)
Symmetrical : Affects wrists, hands, feet
OA: Morning symptoms < 1 hr (stiffness)
RA vs OA: which is more predominant in females? which in old people?
old people: OA
lab findings in RA?
RA: Positive rheumatoid factor, anti-CCP antibody, and elevated ESR & CRP
**OA: normal lab findings
what is the onset for RA vs OA?
RA: rapid (weeks-months)
OA: progressive, longterm (years)
4 lab tests used to Dx RA vs OA?
Rheumatoid Factor (RF)
Erythrocyte Sedimentation Rate (ESR)
C-Reactive Protein (CRP)
of the classification criteria for RA, what score does on need to get dx? what is it based on?
(based on joint involvement, serology, acute phase reactants(CRP + ESR) and duration of symptoms)
goal of txt for RA? (3 things to include)
Goal of therapy is to control the inflammatory process so that disease remission occurs
This should lead to pain relief; maintenance of function; and improved quality of life
5 markers of txt for RA
1. Reduction in number of affected joints and in joint tenderness and swelling
2. Improvement in pain
3. Decreased amount of morning stiffness
4. Reduction in serologic markers such as RF (Rheumatoid Factor)
5. Improved quality of life
3 groups of drugs used to txt RA
1. anti-inflammatory : NSAIDs
2. anti-inflammatory/possible immunomodulatory: glucosteroids
what does DMARDS stand for? what 3 drug groups are included in this?
(disease modifying antirheumatic drugs)
do NSAIDs help modify the disease?
no, little effect on progression of bone/cartilage destruction, can preserve function
how long does it take for NSAIDs to work? analgesic vs anti-inflammatory effects
analgesic w/in hours
Anti-inflammatory effect occurs within 1-2 weeks of daily dosing
ADRs of NSAIDs
GI and cardiovascular
general MOA of glucocorticoids? (maybe weeds)
alter gene transcriptions - target downregulate COX and upregulate annexin 1 (pro-anti-inflammatory mediator)
glucocorticoids low dose vs high dose effects
Suppress inflammation at low doses and suppress immune system at high
Low dose <20mg prednisone/day
High dose> or= 40mg/day
what are glucocorticoids mostly used for regarding RA?
Often used as bridge therapy to provide anti-inflammatory effect while waiting for the DMARDs to take effect
4 general ADRs of steroids? (maybe weeds)
ADR: immune suppression, weight gain, insomnia, cushing
what do DMARDS work to do for RA?
Slow down the destruction from underlying disease, don’t stop it altogether
how long does it take DMARDS to work?
3 months of use before an effect is seen
*If no improvement by 3 months or target is not reached by 6 months-treatment needs to be modified
what kind of biologic agents may be used for RA? why?
inhibit tumor necrosis factor (TNF) & interleukin receptor antagonist
used in patients who don’t respond to first-line agents (methotrexate). Theyre better and more targetted BUT very expensive.
two main subgroups of DMARDS
1. conventional synthetic DMARDS(immunomodulating + immunosuppressing)
2. biologic DMARDS
what are the two immunomodulating csDMARDs?
what are the 3 immunosuppressive csDMARDs?
Azathioprine (Imuran) - not as commonly used
what are the TNFalpha biologic DMARDS?
all "-umab" and Etanerecept
"other biologic DMARDs" (kinda weeds)