Arthritis Flashcards
arthritis is defined as
swelling and pain of a joint
ddx of acute monoarthritis
trauma
infection
crystals
what is the most common form of arthritis?
osteoarthritis
what is the most prominent symptom of OA
pain
definition of OA
progressive destruction of the cartilage in the joint, which is accompanied by new bone formation
3 things to consider when making the diagnosis of RA
clinical picture (classical joints)
radiographic
normal laboratory tests (ESR, serologies, uric acid)
classical joints of OA
knees
hip
hands
spine
3 radiographic features of OA
joint space narrowing
osteophyte formation
bone sclerosis
which node is associated with OA on the DIP joint?
Heberden’s nodes
which node is associated with OA on the PIP joint
Bouchard’s nodes
what happens to the first CMC joint in OA
squared due to the osteophytes at that joint
swan neck deformity is associated with
RA
is RA symmetric or asymmetric?
symmetric
sausage toes are prominent in
psoriatic arthritis
onchodystrophy is associated with
psoriatic arthritis
what’s the greatest risk factor for OA progression
age > 60
bow-legged
varus
knock-kneed
valgus
treatment for mild-to-moderate pain OA
simple analgesics, topical creams
treatment for moderate-to-severe pain OA
COX2 selective inhibitors
NSAIDs + gastroprotection
increased risk of OA conferred by
obesity, prior injury, family history
how is obesity related to OA
may exacerbate OA via chronic inflammatory state
two sources of uric acid
dietary
cellular nucleotides and nucleoproteins
how much uric acid is excreted through the gut
⅓- not adjustable
how much uric acid is excreted through the kidneys
⅔- adjustable
what food increases the risk of gout
meat
fructose
what food decreases the risk of gout
dairy
what converts ribose-5-P to purines
PRPP synthase, which is inhibited by excess purines (ATP, ADP, AMP)
what converts xanthine to uric acid
xanthine oxidase
purine salvage enzyme
HGPR transferase
what converts uric acid to allantoic acid (that humans don’t have)
uricase
mechanisms of abnormal purine metabolism
increased production- PRPP synthase up
decreased salvage- HGPRT down
increased cell (and purine) turnover conditions
myelo- and lymphoproliferative malignancies
hemolytic anemias
chemotherapy with tumor lysis
how much of urate is filtered in the glomerulus
100%
dysfunction of urate secreting transporters promotes
hyperuricemia
dysfunction of urate transporters (or inhibitors of them) promotes
urate excretion
how much of urate is excreted
90% of filtered loads
important urate transporters
URAT1
ABCG2
2 conditions promoting uric acid retention
lactic acid and ketoacidosis
drugs
drugs causing hyperuricemia
alcohol diuretics ethambutol pyrazinamide nicotinic acid salicylates
serum urate concentration for a gouty attack
> 8.9 mg/dL
how to crystals initiate inflammation
activation of complement and other serum factors
activation of synovial macrophages
activation of synovial macrophages produces
IL1, TNF-alpha, IL8
chemoattractants activate
integrins
ICAMs upregulated and activated by
cytokines
phagocytosis of crystals results in
degranulation, O2- generation
what happens to ESR in gout
elevated
what happens to WBC in gout
elevated
what happens to uric acid levels in gout
may be elevated. but maybe not
short, squat, positively birefringent crystal is likely to be
calcium pyrophosphate
release of PPi from the chondrocyte
Ank transporter- releases PPi, binds with extracellular Ca++
colchicine action
diminishes stimulated endothelial adhesiveness for leukocytes
anakinra
IL1 receptor antagonist
rilonacept
IL1 trap
canakinumab
anti-IL1 Ig
drugs that block urate production
allopurinol, febuxostat
drugs that promote urate excretion
probenecid, lesinurad
drugs that prevent gout attacks
colchicine, NSAIDs, low-dose steroids
allopurinol, febuxostat block
xanthine oxidase
probenecid and lesinurad inhibit
URAT1
**only works if renal filtration is adequate
pegloticase is used for treating
chronic tophaceous gout- reducing tophi
chondrocalcinosis results from
calcium pyrophosphate deposition in cartilage
peak age of RA onset
40-60 years
MCP involvement in OA or RA
RA
presentation of advanced RA
ulnar deviation
volar subluxation
interosseous wasting
marginal erosions of the bone present in
RA
RA effects on the eyes
scleritis
keratoconjunctivitis
RA effects on the lungs
fibrosis, nodules, pleuritis, pleural effusions
cardiovascular manifestations of RA
atherosclerosis
vasculitis
increased MI risk 2-3X
1 cause of death in RA
CV related
RA increases which hematologic malignancy
B-cell non-hodgkin’s lymphoma increased 2-3X
increased systemic inflammation
RA susceptibility to which MHC gene
MHC II DRb1
characteristic lab abnormalities of RA
RF anti-citrullinated protein antibody (ACPA, CCP) elevated ESR elevated CRP anemia of chronic disease
which RF’s do we usually test for
IgM-RF
3 Ddx for RF
SLE
Hepatitis B, C
malignancies: lymphoma, plasma cell dyscriasis
what accomplishes citrullination
PADI’s
higher specificity for RA
associated with progression and worse prognosis
3 cytokines promoting damage to RA joints
TNF-alpha
IL1
IL6
tofacitinib
selective inhibitor of janus kinases- modulates cytokines important in pathogenesis of RA
HLA_B27 contributes to susceptibility to what
ankylosing spondylitis
sacroiliitis is a hallmark of
ankylosing spondylitis
chief complaint of AS
low back pain and morning stiffness
acute anterior uveitis is a systemic feature of
AS
IBD is a feature of
AS
lung involvement in AS
pulmonary fibrosis
costovertebral joint fusion–> restrictive lung disease
cardiac involvement in AS
valvular insufficiency and variable degrees of AV block in ~5% of patients
what is used to treat spine symptoms in AS
TNF antagonists (etanercept)
nail changes seen in
psoriatic arthritis
achilles tendonitis seen in
psoriatic arthritis
