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105 Cards in this Set
- Front
- Back
RA is characterized by...
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symmetrical arthritis
joint deformity/erosions |
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extra articular effects of RA
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pericarditis
pleurisy episcleritis and scleritis |
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__ % of the population is affected by RA
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1
|
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RA is __ times more prevalent in women than men until...
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3X
after 5th decade it becomes 1:1 |
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t/f about half of pts w/ advanced RA will have shortened lifespans by as much as 18 years
|
T
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structural damage occurs w/in the ______ years w/ RA
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first 2-3
|
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poor prognosis indicators for RA
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fxnl limitation
extra-art. dz + RF + CCP bony erosions on x-ray |
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t/f autoimmunity and genetics are established etiologies of RA
|
t
|
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what plays a suspected role in the etiology of RA
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infectious dz
-HTLV-1 -rubella -viral illnesses -mycobacteria |
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t/f RA tx is based on trying to reverse changes
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F, changes can't be reversed
just try to stop from progressing |
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non-pharm tx of RA includes...
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rest
exercise diet/weight control physical therapy |
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t/f analgesic and anti-inflamm drugs do not modify the dz progression
|
T
|
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____ effect of NSAIDs is quick but the ____ effect may take ___ weeks
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analgesic
anti-inflamm 4-6 |
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role of corticosteroids in RA tx
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-initial, while waiting for DMARDs to work
-combo w/ NSAIDs when DMARDs aren't adequate -for acute flares, dec. inflamm |
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____ dose of corticosteroids should be used to avoid
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lowest effective
ADRs |
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long term prednisone use can lead to...
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bone loss
|
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which roid is preferred to use for RA
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prednisone
|
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toxicities of long-term steroid use
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bone loss (50% of pts)
cataracts atherosclerosis |
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t/f long term low-dose glucocorticoids may be effective for many years
|
F
dec. in anti-inflamm effect after 1st year |
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t/f cytokines are produced in large amounts and work systemically
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F
|
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what cytokine plays a role in the destructive proces in bone
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IL-1
|
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TNF stimulates...
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-growth of rheumatoid synovial tissue
-neutrophils, fibroblasts and chondrocytes -induces macrophage production of other pro-inflamm cytokines |
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t/f tx w/ anti-TNF prevents joint destruction and returns the joint to a more normal state
|
T
|
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t/f MTX alone is as effective as MTX + steroid w/ taper and TNF inhibitor
|
F
the combo resulted in earlier fxnl improvement and less radiographic damage after 1 year |
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advantages of dmards
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-reduce signs and symptoms of RA
-reduce fxnl disability -retard radiographic progression |
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what is the most commonly used non-biologic dmard and the most common choice for initial monotherapy
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mtx
|
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name the recommended nonbio. dmards
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mtx
leflunomide hydroxychloroquine sulfasalazine minocycline |
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what is the DOC for moderate to severe dz/aggressive dz
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mtx
|
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MOA of mtx
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dec. TNF-alpha
inc. IL-10 *acts by inhibiting AIRCR *can affect chemotaxis *folate antagonist (enters cell w/ reduced folate carrier) |
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ADRs of mtx
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-GI upset
-hepatofibrosis and cirrhosis -myelosuppression -interstitial pneumonitis -stomatitis (responds to folic acid) -alopecia |
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what ADR of mtx gets better when given folic acid
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stomatitis
but may dec. anti-rheumatoid effect |
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what do you need to monitor w/ mtx
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CBC q 4 mos.
LFTs q 8-12 mos. |
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what's in sulfasalazine
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sulfapyradine and ASA
|
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MOA of sulfasal.
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-antimicrobial portion (sulfa) is activated in small intestine
-suppresses TNF-a, IL1 -inhibits chemotaxis and neutrophil migration -enhances adenosine release (dec. inflamm) |
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t/f sulfasal. has ADRs but they are not severe
|
F
25% of pts d/c therapy due to ADRs |
|
ADRs of sulfasal
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-GI distress (enteric coating dec. it)
-rash -hepatitis -blood dyscrasias (rare) |
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t/f you need to check CBCs and LFTs on sulfasal
|
T
check q 2-4 weeks for first 3 mos then q 3 mos. after |
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sulfasal may be combo'd w/....
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mtx
hydrochloroquine |
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t/f sulfasal works better than gold
|
T
|
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MOA of leflunomide
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prevents CD4 T cells prolif. in early RA
alter IL-2 and growth factor conc. inhibits leukocyte adhesion |
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who is leflunomide good for and why
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pts who can't tolerate mtx
it's $$$$ |
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how long can benefit from leflunomide be sustained
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at least 2 yrs
|
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what nonbio. dmard requires a loading dose
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leflunomide
|
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which nonbio dmard was designed to target T-cells, making it more selective
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leflunomide
|
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metab, half-life and onset of leflunomide
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-rapid conversion in intestine and plasma and then extensive metab in liver
-2 week half life -rapid onset (faster than mtx)* |
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ADRs of leflunomide
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rash
diarrhea alopecia inc. LFTs |
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CIs of leflunomide
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preggos
lactating* childbearing age w/o contraception |
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MOA of hydroxychloroquine
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supress lysosomal enzymes
inhibit B and T cells inhibit IL release |
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hydroxychloroquine is indicated for...
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mild dz
|
|
ADRs of hydroxychloroquine
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BM suppression
in eye disorders can cause irreversible retinopathy--screen q 6 mos. |
|
time to response for hydroxychloroquine
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can take up to 4 mos
if no response in 6 mos then d/c |
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who is azathioprine good for?
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pts w/ severe, active, erosive dz that is NOT responsive to other agents
-*also good for pt's who are steroid dependent (can even dec. roid dose) |
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efficacy of azathioprine
|
similar to parenteral gold and penicillamine BUT inc. toxicity
inferior to mtx |
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DDI of azathioprine w/ steroids
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steroid sparing
can even dec. steroid dose |
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ADRs of azathioprine
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bone marrow suppression (aplastic anemia, thrombocytopenia)
hepatic inflamm lymphoprolif. cancer |
|
do you need to monitor azathioprine
|
yep
LFTs and CBCs q 2-4 weeks |
|
onset of action w/ azathioprine
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1-3 months
if no response w/in 3 mos. -->d/c |
|
t/f the bone marrow ADRs are the same at all doses of azathioprine
|
F
dec. in ADRs w/ a dec. in dose |
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MOA of penicillamine
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inhibits T cell fxn and chemotaxis of phagocytes
dec. RF comparable in efficacy to gold *metabolite of pcn |
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ADRs of penicillamine
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bone marrow suppression
proteinuria autoimmune (SLE, polymyositis, etc.) taste disturbance *more toxic than mtx |
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time to onset and DDI of penicillamine
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3-4 weeks
6 months to determine efficacy -impedes absorption of other drugs |
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what is the most commonly used ABX used in RA
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minocycline
*used early in dz *add-on for refractory pt |
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what drug is a chimeric monoclonal Ab and what does chimeric mean?
|
infliximab
part mouse part human |
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MOA of infliximab
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binds to TNFa w/ high affinity and specificity
|
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indications and half life of infliximab
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RA (w/ mtx)
crohn's/UC psoriatic arth. plaque psoriasis ankylosing sponylitis half life is 8-10 days injxns q month/6 weeks |
|
ADRs of infliximab
|
infusion rxns in 20% (1% severe - hypotension)
resp: upper resp. tract infxn -sinusitis -cough -pharyngitis development of ANAs infxn develop Abs to ds-DNA |
|
t/f if a pt develops and Ab to biologic dmards then the drug becomes ineffective
|
T
|
|
DDI of anakinra
|
anti-TNF agents inc. risk of serious infxn when combo'd w/ anakinra
-also seen w/ etanercept |
|
DDI of infliximab
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dead org. vaccine - inflix. dec. the effect of vax
|
|
t/f immunosuppresants may enhance the adverse/toxic effects of dead org. vaccines
|
F
live vaccines |
|
MOA of etanercept
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soluble TNFa receptor human Ig complex -->binds TNF and lymphotoxin
|
|
what kind of protein is etanercept
|
recombinant fusion protein
less immunogenic |
|
onset, dosing and other combos of other drugs w/ etanercept
|
onset in 14-90 days
dosing is subQ so pt can inject at home* can combo w/ mtx |
|
ADRs/CIs of etanercept
|
CIs/precautions
-allergic rxns -*avoid live vaccines* -immunosuppression ADRs -injxn site rxn -infxn |
|
MOA of adalimumab
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TNFa antagonist Mab
|
|
t/f adalimumab is fully human
|
T
|
|
t/f adalimumab inhibits progression of RA and dec. structural damage
|
T
|
|
t/f adalimumab must be given as monotherapy
|
F
may be combo w/ mtx or other dmards |
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dosing and onset of adalimumab
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subQ dosing q 2 weeks
onset w/in 3 mos |
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DDI of adalimumab
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anakinra
inc. hypersens. hematologic probs |
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MOA of anakinra
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directly blocks IL-1
|
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what drugs can be combo'd w/ anakinra
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other dmards EXCEPT TNF blocking agents
|
|
ADRS of anakinra
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injxn site rxn
|
|
CI of anakinra
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-infxn that requires abx
-allergy to proteins made from e. coli or any ingredient in kineret -concurrent TNF inhibitor |
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t/f anakinra is safe for preggos
|
T
(you can let your anaconda loose if she's already preggo) |
|
t/f 80% of anakinra is excreted in urine in 1 day
|
T
|
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MOA of abatacept
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soluble CTLA-4 Ig (cytotoxic T-lymphocyte associated Ag 4)
-dec. cytokine release -dec. b-cell activation --> dec. Ab production |
|
what drug may enhance toxicity of abatacept
|
infliximab
inc. risk of serious infxn |
|
MOA of rituximab
|
anti CD20 Chimeric Mab
-depletes B cells that have CD 20 on surface -used in B cell lymphoma -give w/ mtx and roids on days 1 & 15 |
|
ADRs of rituximab
|
hypersens. rxn*
-can be dec. w/ roids |
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what are the benefits of an ideal combo therapy for RA
|
-no inc. in toxicity
-long-term outcome more favorable -superior efficacy to single dmard |
|
arthritis affects __ americans and costs an average $___/ month
|
58 million (18% of pop)
$200/month |
|
risk factors for OA
|
obesity- esp. hip
repetitive use genetic (2x risk if dz in mom) osteoporosis |
|
what is the most prevalent rheumatoid dz in pop. over 60
|
OA
|
|
OA is more commen in men or women
|
women are 2x more likely to have OA
|
|
3 sites of pain in OA
|
synovium
ST around joints bone |
|
t/f nsaids are popular therapy for OA
|
T*
use caution in elderly due to kidney ADRs |
|
drug therapy of OA is directed at...
|
relief of symptomatic pain and inflamm
|
|
MOA of sodium hyaluronate
|
polysaccharide compound - forms viscoelastic sol'n in water
-fxns as tissue/joint lube |
|
CI of Na hyaluronate
|
egg/feather allergy*
|
|
route of Na hyaluronate
|
intra-articular injxn for pts who fail other OA tx
given q 6-8 months ***do not inject into area of active inflamm or infxn |
|
where shouldn't you inject sodium hyaluronate
|
into area of active inflamm or infxn
|
|
dietary supplements for OA
|
omega 3 fatty acids - dec. inflamm
capsaicin - topical/temp. SAM - as effective as nsaids, can inc. serotonin levels *all have slow onset |
|
MOA of glucosamine sulfate
|
building block necessary for making new cart
-may not be effective* -slow onset* |
|
ADRs of glucosamine sulfate
|
inc. in blood glucose in DM
GI drowsiness HA -limited info on ADRs |