• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/105

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

105 Cards in this Set

  • Front
  • Back
RA is characterized by...
symmetrical arthritis
joint deformity/erosions
extra articular effects of RA
pericarditis
pleurisy
episcleritis and scleritis
__ % of the population is affected by RA
1
RA is __ times more prevalent in women than men until...
3X
after 5th decade it becomes 1:1
t/f about half of pts w/ advanced RA will have shortened lifespans by as much as 18 years
T
structural damage occurs w/in the ______ years w/ RA
first 2-3
poor prognosis indicators for RA
fxnl limitation
extra-art. dz
+ RF
+ CCP
bony erosions on x-ray
t/f autoimmunity and genetics are established etiologies of RA
t
what plays a suspected role in the etiology of RA
infectious dz
-HTLV-1
-rubella
-viral illnesses
-mycobacteria
t/f RA tx is based on trying to reverse changes
F, changes can't be reversed
just try to stop from progressing
non-pharm tx of RA includes...
rest
exercise
diet/weight control
physical therapy
t/f analgesic and anti-inflamm drugs do not modify the dz progression
T
____ effect of NSAIDs is quick but the ____ effect may take ___ weeks
analgesic
anti-inflamm
4-6
role of corticosteroids in RA tx
-initial, while waiting for DMARDs to work
-combo w/ NSAIDs when DMARDs aren't adequate
-for acute flares, dec. inflamm
____ dose of corticosteroids should be used to avoid
lowest effective
ADRs
long term prednisone use can lead to...
bone loss
which roid is preferred to use for RA
prednisone
toxicities of long-term steroid use
bone loss (50% of pts)
cataracts
atherosclerosis
t/f long term low-dose glucocorticoids may be effective for many years
F
dec. in anti-inflamm effect after 1st year
t/f cytokines are produced in large amounts and work systemically
F
what cytokine plays a role in the destructive proces in bone
IL-1
TNF stimulates...
-growth of rheumatoid synovial tissue
-neutrophils, fibroblasts and chondrocytes
-induces macrophage production of other pro-inflamm cytokines
t/f tx w/ anti-TNF prevents joint destruction and returns the joint to a more normal state
T
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
advantages of dmards
-reduce signs and symptoms of RA
-reduce fxnl disability
-retard radiographic progression
what is the most commonly used non-biologic dmard and the most common choice for initial monotherapy
mtx
name the recommended nonbio. dmards
mtx
leflunomide
hydroxychloroquine
sulfasalazine
minocycline
what is the DOC for moderate to severe dz/aggressive dz
mtx
MOA of mtx
dec. TNF-alpha
inc. IL-10
*acts by inhibiting AIRCR
*can affect chemotaxis
*folate antagonist (enters cell w/ reduced folate carrier)
ADRs of mtx
-GI upset
-hepatofibrosis and cirrhosis
-myelosuppression
-interstitial pneumonitis
-stomatitis (responds to folic acid)
-alopecia
what ADR of mtx gets better when given folic acid
stomatitis
but may dec. anti-rheumatoid effect
what do you need to monitor w/ mtx
CBC q 4 mos.
LFTs q 8-12 mos.
what's in sulfasalazine
sulfapyradine and ASA
MOA of sulfasal.
-antimicrobial portion (sulfa) is activated in small intestine
-suppresses TNF-a, IL1
-inhibits chemotaxis and neutrophil migration
-enhances adenosine release (dec. inflamm)
t/f sulfasal. has ADRs but they are not severe
F
25% of pts d/c therapy due to ADRs
ADRs of sulfasal
-GI distress (enteric coating dec. it)
-rash
-hepatitis
-blood dyscrasias (rare)
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
sulfasal may be combo'd w/....
mtx
hydrochloroquine
t/f sulfasal works better than gold
T
MOA of leflunomide
prevents CD4 T cells prolif. in early RA
alter IL-2 and growth factor conc.
inhibits leukocyte adhesion
who is leflunomide good for and why
pts who can't tolerate mtx
it's $$$$
how long can benefit from leflunomide be sustained
at least 2 yrs
what nonbio. dmard requires a loading dose
leflunomide
which nonbio dmard was designed to target T-cells, making it more selective
leflunomide
metab, half-life and onset of leflunomide
-rapid conversion in intestine and plasma and then extensive metab in liver
-2 week half life
-rapid onset (faster than mtx)*
ADRs of leflunomide
rash
diarrhea
alopecia
inc. LFTs
CIs of leflunomide
preggos
lactating*
childbearing age w/o contraception
MOA of hydroxychloroquine
supress lysosomal enzymes
inhibit B and T cells
inhibit IL release
hydroxychloroquine is indicated for...
mild dz
ADRs of hydroxychloroquine
BM suppression
in eye disorders can cause irreversible retinopathy--screen q 6 mos.
time to response for hydroxychloroquine
can take up to 4 mos
if no response in 6 mos then d/c
who is azathioprine good for?
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)
efficacy of azathioprine
similar to parenteral gold and penicillamine BUT inc. toxicity
inferior to mtx
DDI of azathioprine w/ steroids
steroid sparing
can even dec. steroid dose
ADRs of azathioprine
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
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
MOA of penicillamine
inhibits T cell fxn and chemotaxis of phagocytes
dec. RF
comparable in efficacy to gold
*metabolite of pcn
ADRs of penicillamine
bone marrow suppression
proteinuria
autoimmune (SLE, polymyositis, etc.)
taste disturbance
*more toxic than mtx
time to onset and DDI of penicillamine
3-4 weeks
6 months to determine efficacy
-impedes absorption of other drugs
what is the most commonly used ABX used in RA
minocycline
*used early in dz
*add-on for refractory pt
what drug is a chimeric monoclonal Ab and what does chimeric mean?
infliximab
part mouse part human
MOA of infliximab
binds to TNFa w/ high affinity and specificity
indications and half life of infliximab
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
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
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
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
dosing and onset of adalimumab
subQ dosing q 2 weeks
onset w/in 3 mos
DDI of adalimumab
anakinra
inc. hypersens.
hematologic probs
MOA of anakinra
directly blocks IL-1
what drugs can be combo'd w/ anakinra
other dmards EXCEPT TNF blocking agents
ADRS of anakinra
injxn site rxn
CI of anakinra
-infxn that requires abx
-allergy to proteins made from e. coli or any ingredient in kineret
-concurrent TNF inhibitor
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
MOA of abatacept
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
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