Flashcards in Arthritides Deck (58):
Key manifestations of arthritis?
- pain, swelling and limited motion
Diff types of jts?
- fibrous/bony: minimal to no motion
- cartilaginous: limited motion
compromised of 2 or more bones
may have a meniscus
What is osteoarthritis?
- degenerative arthritis or jt disease, osteoarthrosis
- more than simple aging, not all old people get arthritis, absence of clear cut etiology
- loss of articular cartilage: exposed bone - leads to pain, tenderness, stiffness, effusion, loss of motion, creaking
- can develop progressive deformity, muscular atrophy and ligamentous laxity
- MC form of arthritis: affects nearly 27 mill in US, leading cause of chronic disability
Predisposing factors for osteoarthritis?
- age, female sex, previous injury
- obesity: esp for knees
- heavy physical labor
- positive family hx
- sports activities
- running doesn't appear to increase the risk: monitor sxs
PP of OA?
- in most pts, trigger is damage to normal articular cartilage
- chondrocytes react by releasing degradative enzymes: can be caused by macro-trauma or repeated micro-trauma, leads to further cartilage damage
- bone reacts w/ subchondral sclerosis and osteophytes
- degradation of cartilage (trauma, aging), and bony rxn
- superficial erosions - complete loss of cartilage
- jt space narrowing and possible deformity
- hypertrophy/hyperplasia of osteocytes - leads to subchondral sclerosis - leads to osteophyte formation
What are the features of OA?
- jt pain, swelling, crepitation, tenderness, effusions
- hands, hips, knees, spine: beware radiating pain and bursitis
- tenderness on palpation and on passive motion are late signs
- multiple jt involvement in older pts
- hip and knee involvement seen in the middle aged
- single jt involvement in the young: trauma or congenital abnormality
Presentation of OA- hands?
- MC jt affected (70%)
- middle-aged and elderly women
- strong family hx
- DIP and PIP jts of fingers
- osteophytes and palpable***:
heberden's nodes (DIP)
Bouchard's nodes (PIP)
Presentation of OA-Shoulder?
- progressive anterior shoulder pain, worse w/ motion
- difficulty w/ overhead activities, sleeping, axillary hygiene
- often seen w/ rotator cuff disease/tears, AC jt arthritis: spurs and AC arthritis can cause impingement of rotator cuff
Presentation of OA-hip?
- 10% of pts: pain deep in groin:
pain on lateral side of hip, usually greater trochanteric bursitis, pain behind hip, usually from back
- starts w/ prolonged standing/walking can become intolerable
- difficulty putting on shoes/socks - pain and loss of motion
- pain w/ abduction
Presentation of OA-knee?
- 30% of pts: obesity is contributing factor
- osteophytes, effusions, crepitus, and limited motion
- difficulty: doing stairs, getting out of low chairs, off of toilets
- pain w/ kneeling/squatting - hard to get off the ground
- imaging: get standing views (AP and 45 degrees) and sunrise view
Presentation of OA-spine?
- can be seen in up to 60% of pts
- sxs from facet jt arthritis and DDD (degenerative disc disease)
- cervical: pain and stiffness, aching pain down the arm: can develop cervical cord compression
- lumbar: pain across low back/buttocks w/ LOM flex/ext: can develop spinal stenosis
How do you dx OA?
- clinical dx supported by H&P, lab and imaging
- no specific lab studies: r/o other arthritides (RF, ESR- rule out RA, tap the jt)
- Imaging: rarely need more than plain x-rays
What can you see on imaging of OA?
- jt space narrowing
- surface irregularity
- subchondral sclerosis
- subchondral cysts
Nonpharm rx for OA?
- moderate wt loss
Pharm Rx for OA?
- NSAIDs: naproxen/ibuprofen
- intraarticular injections
Diff types of OA intraarticular injections?
- both steroids and hyaluronans have been shown to be effective: can provide months of relief for many pts
glucocorticoids (triamcinolone, methylprednisolone):
-slow cartilage degradation, provide pain relief
- often used in knee and shoulder, less in other jts
- repeated injections have been proven safe
- adverse effects: post injection flare, feeling high, possible infection
hyaluronans (synvisc, hyalagen):
- macromolecules that absorb water and may protect cartilage
- have been used for knees and hips
- series of injections, can have a flare, possible infection
Process of knee injection/aspiration?
- thorough skin prep
- supero-lateral portal: not antero-medial
- pt supine
- sit w/ knee at eye level
- little pain when slow
- numbing skin: usually not needed
What non-surgical Rx for arthriti knee pain helps, what doesnt?
these have shown to help:
- intra-articular steroids and hyaluronans
- gentle exercises, swimming, ice
- wt loss
studies show those haven't helped:
- arthroscopic debridement
What are surgical tx for OA?
- arthroscopic procedures:
no studies that show pts do anay better, may aggravate the underlying arthritis
- total jt replacement:
gold std for severe knee, hip, or shoulder jt arthritis, unincompartmental replacement and resurfacing more controversial, not as clear cut for ankle, wrist, elbow
- chondrocyte grafting: for small, isolated defects, no long term studies
Total knee replacement-pros, cons?
- relieves pain, corrects deformity, improves fxn
- reqrs sig post-op rehabilitation
Total hip replacement - pros, cons?
- relieves pain, restores fxn, relatively quick recovery - out pt
- leg length inequality not uncommon
What are the long term issues of replacements?
more susceptible due to implant - dental procedures, colonoscopy, use heart assoc guidelines for prophylaxis, sudden pain, look for infection
- loosening: may be due to bone resorption or macrophage response, follow up xrays
- periprosthetic fractures:
metal creates stress risers, difficult to tx, avoid contact sports
What is RA? Who does it commonly affect?
- one of the MC inflammatory arthritis: 1# of the pop, women to men 3:1
- autoimmune disease that primarily involves jts:
mult jts, often symmetrical, progresses from peripheral to proximal jts
- breakdown of immune tolerance to synovial inflammation: complex interaction of genetic and enviro factors
PP of RA?
- prominent immunologic abnormalities
- plasma cells produce ABs
- macrophages migrate to diseased synovium
- macrophages and lymphocytes produce pro-inflammatory cytokines and chemokines in synovium
- over time synovium thickens: synovial cells produce collagenase and stromelysin (contributes to destruction and fibrosis of jts)
- hyperplastic synovial tissue (pannus) releases inflammatory mediators
Clinical presentation of RA?
- wide variability of sxs
- gradual, insidious onset
- sxs wax and wane
- usually involves mutliple jts: more w/ time, characteristically symmetric
- can cause significant disability in 10-20 yrs
- may not respond to tx in 10-20% of cases
Systemic and jt sxs of RA?
early morning stiffness of affected jts, generalized afternoon fatigue and malaise, anorexia
pain, swelling, stiffness, erythema
Imaging for RA?
- xray hands and feet: as part of intital W-U
- plain xrays show:
jt space narrowing
soft tissue swelling
osteopenia about jt
laxity leads to deformity
- MRI, US:
show more damage, not clinically useful
Presentation of RA in the hand?
- swollen painful MP, PIP jts: tender, limited motion
- reduced grip strenght
- tendon ruptures, triggering
- jt deformities: ulnar deviation at MP jts, swan neck, boutonniere
- up to 5% have carpal tunnel syndrome (from synovitis pressing on median nerve)
Presentation of RA in the upper extremity?
- wrist: MC -
loss of extension
- elbow: nodules -
loss of extension
- shoulder: late -
rotator cuff disease
Presentation of RA in the lower extremity?
- foot: similar to hand - MP jt involvement, toe deformities, heel, ankle pain
- knee: often - synovitis and effusion, baker's cyst, loss of flexion
- hips: late - groin pain, loss of rotation
Extra-articular RA manifestations?
- skin and pulmonary nodules
Lab findings in RA?
- synovial fluid:
inflammatory effusion w/ elevated WBCs
- xrays: of affected jt
Dx of RA? DDX?
clinical dx can be made when:
- inflammatory arthritis in 3 or more its for more than 6 wks
- positive RF and ACCP testing
- elevated CRP and ESR
- have excluded gout, CPDD, viral arthritis, SLE, psoriatic arthritis
lab tests may be normal in seronegative or inactive RA
- acute viral poly arthritis
-systemic rheumatoid diseases
- crystalline and infectious arthritides
- many others
Criteria for RA dx?
- jt involvement:
2-10 large jts: 1 pt
over 10 jst: 5 pts
low + RF or low + ACPA: 2
high + RF or high + ACPA: 3
- acute phase reactants:
abnorm CRP or abnorm ESR: 1 pt
- duration of sxs:
6 or more weeks: 1 pt
General tx for RA?
- early dx and Rx by rheumatologist
- management of acute flares: NSAIDs and glucocorticoids (relieve discomfort, don't stop progression)
- use DMARDs early - disease modifying anti-rheumatic drugs:
- surgery for soft tissues and jts
- helping the pt manage:
PT, OT, bracing
nonpharm tx for RA?
- orthotics and splints
- therapeutic exercise
Tx for acute pain in RA?
- when first seen or during a flare
pain relief- OTCs
aspirin, ibuprofen, naproxen
(GI and CV side effects)
usually systemic (mult jts):
- part of feedback of immune system, turns activity down, also have metabolic effects, can also effect arousal and cognition
hyperglycemia, skin fragility, osteoporosis, wet gain, adrenal insufficiency, muscle breakdown, euphoria, glaucoma
DMARDs used in RA?
- early use = better results
- no common MOA:
interfere w/ immune response, serious SEs
- nonbiologic agents:
methotrexate, sulfasalzine, leflunomide
hydroxychloroquine, cyclosporine, gold salts, azathioprine
- biologic agents: macromolecules, genetic engineering:
TNF inhibitors, entanercept (Enbrel), infliximab (Remicade), Adalimumab (Humira)
MOA of methotrexate? Adverse effects? CIs?
- antimetabolite that inhibits purine biosynthesis: essential to rapidly proliferating cells
- MC used DMARD: also used for cancer tx, terminating pregnancies
- Adverse effects:
ulcerative stomatitis, leukopenia, predisposition to infection, nausea, abdominal pain, fatigue, fever, dizziness, pneumonia, pulmonary fibrosis
renal dysfxn, pregnancy or possible pregnancy
Surgery for RA?
- soft tissue procedures:
synovectomy, tendon repairs, removal of nodules
- jt procedures:
total jt replacements, fusions
What is Gout?
- characterized by painful jt inflammation in the first metatarsophalangeal jt
- dx criteria from ACR
- one of the MC arthropathy: affects more than 8 mill Americans
PP of Gout?
- precipitation of monosodium urate crystals in jt space
- overtime jt space is damaged
- tophi may also form in the jt space (pathognomonic for gout)
- first metatarsophalangeal jt MC affected - podagra
- decreased excretion
- increased production
- increased purine intake
RFs for gout?
- increass w/ age
- female sex hormone increases urinary excretion of uric acid (protective factor)
- alcohol (beer)
Clinical presentation of gout?
- severe pain
- onset more at night
- overlying skin becomes tense
- clinical criteria
- synovial fluid analysis: needle shaped negative birefringent urate crystals
- elevated serum urate level
Tx for acute gout?
- resolve in a few days to weeks
- NSAIDs usually 1st choice: early use of naproxem or indomethacin can be helpful, beware of GI and CV effects
- colchine: main Rx for yrs -
derived from plants, known in antiquity, inhibits mitosis, low dose regimens effective w/ fewer SE. GI upset, neutropenia, peripheral neuropathy, don't use IV, serious even fatal SEs
intraarticular: injections often quickly resolve sxs
oral: mult jts and can't use NSAIDs or colchicine
Tx for hyperurecemia?
- reduced intake of purines (diet)
- xanthine oxidase inhibitors: allopurinol:
decreases purine synthesis, thus lowers monosodium urate, 1st choice of drug to lower serum urate levels, gouty attacks and skin lesions in up to 5% of pts, arthralgias, diarrhea, rash
- uricosuric drugs: probenecid - decreased uric excretion - up to 90% of hyperurecemia
this will increase urinary excretion, SEs: gouty attack, GI upset, stone formation
How can recurrent attacks of gout be prevented?
- lifestyle changes:
decreased alcohol intake
decreasing meat and fish
increasing dairy products
- lowering serum uric acid:
uricosuric agents, xanthine oxidase inhibitors
What is pseudogout? Etiologies?
- calcium pyrophosphate dehydrate (CPPD) crystal deposition disease: chondrocalcinosis
- equally affects men and women
presentation and dx of pseudogout?
similar to gout but less severe, usually occur in knee or other large peripheral jts
rhomboid or rod shaped crystals, positive birefringent crystals**
- X-rays: chondrocalcinosis
- acute attack of crystalline arthritis in pt w/ CPPD: most pts don't have acute attacks - chondrocalcinosis
- single jt involved: aspirate and inject w/ steroids, immobilize and apply ice or cool pack
- mult jts involved:
NSAIDs, colchicine, or systemic steroids
- prevention: after 3 or more attacks, daily colchicine
- tx of damaged jts same as for OA (replacements, injections)
Major features of osteoarthritis?
- degeneration of cartilage leads to jt damage
- slowly hampers activities of daily living
- disease limited to the jt (one or several, more w/ age)
- can see osteophyte formation, creaking w/ motion
Major features of RA?
- autoimmune disease that attacks synovium and soft tissue, see swelling and damage/destruction of multiple jts
- generalized disease that results in multiple, swollen, painful jts
- usually starts in hands and feet and progresses proximally
Major features of gout and pseudogout?
- deposition of crystals lead to jt inflammation and damage
- recurrent attacks, often the big toe in gout
- red, hot swollen jt/skin sensitivity, can have mult episodes that resolve over time
imaging diff in osteoarthritis, RA, and gouty arthritis?
jt space narrowing
jt space narrowing
soft tissue swelling
osteopenia about gout
- gouty arthritis:
can see erosions and jt destruction late
Diff OA and RA in the hand?
swelling - hard, bony
stiffness - worse after use (PM)
fingers: DIP/PIP + nodes (Heberdens and Bouchards)
soft, warm, tender
worse after resting - AM
MP and PIP + deformity
Diff in lab work for OA
- OA: usually normal
- RA: can have elevated ESR, CRP,
RF and ACCP (both + probably RA)
- gouty arthritis:
may have elevated uric acid, crystals in jt fluid (negative vs positive)