arthritis joints

7/29/2019 Arthritis Joints

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Insidious over several weeks usu.

Usu. Not symmetric at the beginning

Must have an inflammatory synovitis

If deformity is in a non-wt bearing jnt, you canassume its due to synovitis

85% have serum RF

May start sero-(-) but become sero(+) w/ progression

ESR is typically helpful to follow the inflammatoryactivity


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Prolonged morning stiffness is universal

Active phase: warm, swollen jnts Structural damage

Bone on bone crepitusTry injected corticosteroids for anti-inflammation

C/sneck stiffness w/ possible loss of motion

C1 transverse lig tenosynovitis and possible z-jntsynovitis

Pain doesnt always accompany instability even in

significant myelopathy


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Immobilization due to pain is the kiss of death to

joint mobilizations. The result is contractures and

deformity

You need to keep pts ROM esp. in non-wt bearing jnts

like shoulder and hand

Once cartilage is completely gone, bones may fuse ifimmobilized10% remit usu in first two yrs of dz

90% of jnts that are affected are involved during the

1

st

yrSevere dz= 10-15yr decr in life expectancy due to

infection, pulmonary or renal dz, lymphoproliferative

disorders, GI bleeds and cardiovascular


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RA criteria below:

Morning stiffness3+jnts

Arthritis of hand

Symmetric arthritis

Rheumatoid nodules

RF

X-ray changes

Need 4 of the 7

1-4 must occur for at least 6

wks


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Stage I Earlyno destruction

Stage II Moderateno jnt deformity,

osteoporosis w/ or w/out some bone andcartilage destruction

Stage III Severecartilage and bone

destruction with osteoporosis, jnt deformity

Stage IV Terminalfibrous or bony

ankylosis


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GOUT


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GOUT

Monosodium urate deposition - hyperuricemia

Tophi accumulation of crystal in articular, osseous,ST, and cartilage

Recurrent attacks of inflammation

Uric acid calculi in GU; renal fxn impairment calledgouty nephropathy

M/c 5th decade men African-Americans

Serum urate levels rise over time in men but dont in womenuntil after menopause due to estrogen

Gout in women is often due to thiazide diuretic use and renal failure

Blacks due to more HTN, not genetic


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Crystals have decr solubility in low temps thatswhy it likes toes and ears

Likes areas of minor trauma like 1st MTP

Hemiplegiatophi wont form on paralyzed side-> something to do w/ CT structure and turnover

Tophi is inflammatory cells around crystal w/erosion of surrounding cartilage and bone.Fibrous capsule around tophi

Crystals are needle-shaped and formed radially


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Three stages: asymptomatic hyperuricemia,cute intermittent gout, Chronic tophaceous gout.

Initially rubor, tubor, dolor and pain of jnt. Pain

cr. Over hours. Pt. May not be able to walk.ay get fever, chills, malaise. May last up to 2

eeks. Attacks become more frequent w/ time

involve 1st MTP as monoarticular site and 90% ofpts overall


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CHRONIC TOPHACEOUS GOUT

About 10yrs after initial dx usu.

No pain free period but not as severe as acute

Factors for tophi development: early onset, longactive phases, 4+attacks/yr, UE or polyarticular

episodes

Tophi can also be in heart valves and sclera

Supcutaneous gouty tophy are usu in fingers

heberdens nodes


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Early onset gout


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10% die of renal failure; 25% have renal

stones

25-50% have HTN ->due to reduced renal

blood flow from urate

Hyperlipidemia/obesity contraversial

Xray ST swelling -> asymmetric in

peripheral jnts erosions slightly removed from

jnt (unique) (overhanging edge)

No osteopenia, and maintained jnt space until late


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Osteoarthritis


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OA

Garrod in 1907 differentiated RA from OA10% of OApatients had reduced work hours and 13.7% retired early.

Arthritis is the main reason for decr. Activities in the elderly

arthritis joints

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