Arthritides Flashcards

1
Q

Key manifestations of arthritis?

A
  • pain, swelling and limited motion
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2
Q

Diff types of jts?

A
  • fibrous/bony: minimal to no motion
  • cartilaginous: limited motion
  • synovial:
    freely mobile
    compromised of 2 or more bones
    may have a meniscus
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3
Q

What is osteoarthritis?

A
  • 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
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4
Q

Predisposing factors for osteoarthritis?

A
  • 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
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5
Q

PP of OA?

A
  • 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
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6
Q

What are the features of OA?

A
  • 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
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7
Q

Presentation of OA- hands?

A
  • 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)
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8
Q

Presentation of OA-Shoulder?

A
  • 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
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9
Q

Presentation of OA-hip?

A
  • 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
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10
Q

Presentation of OA-knee?

A
  • 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
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11
Q

Presentation of OA-spine?

A
  • 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
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12
Q

How do you dx OA?

A
  • 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
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13
Q

What can you see on imaging of OA?

A
  • jt space narrowing
  • surface irregularity
  • osteophytes
  • subchondral sclerosis
  • subchondral cysts
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14
Q

Nonpharm rx for OA?

A
  • moderate wt loss
  • exercises
  • PT/OT
  • braces
  • heat/cold
  • rest
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15
Q

Pharm Rx for OA?

A
  • acetaminophen
  • NSAIDs: naproxen/ibuprofen
  • Tramadol
  • opioids
  • intraarticular injections
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16
Q

Diff types of OA intraarticular injections?

A
  • 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
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17
Q

Process of knee injection/aspiration?

A
  • 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
  • aspiration/injection
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18
Q

What non-surgical Rx for arthriti knee pain helps, what doesnt?

A

these have shown to help:

  • intra-articular steroids and hyaluronans
  • gentle exercises, swimming, ice
  • wt loss

studies show those haven’t helped:

  • orthotics
  • taping
  • acupuncture
  • glucosamine
  • chondroitin
  • arthroscopic debridement
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19
Q

What are surgical tx for OA?

A
  • 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
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20
Q

Total knee replacement-pros, cons?

A
  • relieves pain, corrects deformity, improves fxn

- reqrs sig post-op rehabilitation

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21
Q

Total hip replacement - pros, cons?

A
  • relieves pain, restores fxn, relatively quick recovery - out pt
  • leg length inequality not uncommon
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22
Q

What are the long term issues of replacements?

A
  • infections:
    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
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23
Q

What is RA? Who does it commonly affect?

A
  • 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
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24
Q

PP of RA?

A
  • 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
25
Q

Clinical presentation of RA?

A
  • 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
26
Q

Systemic and jt sxs of RA?

A
  • systemic:
    early morning stiffness of affected jts, generalized afternoon fatigue and malaise, anorexia
  • jt:
    pain, swelling, stiffness, erythema
27
Q

Imaging for RA?

A
  • xray hands and feet: as part of intital W-U
  • plain xrays show:
    jt space narrowing
    soft tissue swelling
    bony erosions
    osteopenia about jt
    laxity leads to deformity
    destruction/fusion late
  • MRI, US:
    show more damage, not clinically useful
28
Q

Presentation of RA in the hand?

A
  • 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)
29
Q

Presentation of RA in the upper extremity?

A
- wrist: MC -
loss of extension
carpal drift
tendon rupture
- elbow: nodules -
loss of extension
olecranon bursitis
ulnar neuritis
- shoulder: late -
adhesive capsulitis
rotator cuff disease
jt destruction
30
Q

Presentation of RA in the lower extremity?

A
  • 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
31
Q

Extra-articular RA manifestations?

A
  • skin and pulmonary nodules
  • pericarditis
  • splenomegaly
  • neuropathy
  • vasculitis
  • episcleritis
  • lymphadenopathy
32
Q

Lab findings in RA?

A
- labs:
RF
Anti-CCP
ESR
CRP
- synovial fluid:
inflammatory effusion w/ elevated WBCs 
- xrays: of affected jt
33
Q

Dx of RA? DDX?

A

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

DDx:

  • acute viral poly arthritis
  • systemic rheumatoid diseases
  • crystalline and infectious arthritides
  • osteoarthritis
  • many others
34
Q

Criteria for RA dx?

A
- jt involvement: 
2-10 large jts: 1 pt
over 10 jst: 5 pts
- serology: 
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
35
Q

General tx for RA?

A
  • 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:
    nonbiologics
    biologics
  • surgery for soft tissues and jts
  • helping the pt manage:
    PT, OT, bracing
    support groups
36
Q

nonpharm tx for RA?

A
  • heat/cold
  • orthotics and splints
  • therapeutic exercise
  • PT/OT
37
Q

Tx for acute pain in RA?

A
  • when first seen or during a flare
  • NSAIDs:
    pain relief- OTCs
    aspirin, ibuprofen, naproxen
    (GI and CV side effects)
  • glucocorticoids:
    usually systemic (mult jts):
  • part of feedback of immune system, turns activity down, also have metabolic effects, can also effect arousal and cognition
    Adverse effects:
    hyperglycemia, skin fragility, osteoporosis, wet gain, adrenal insufficiency, muscle breakdown, euphoria, glaucoma
38
Q

DMARDs used in RA?

A
  • 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)
39
Q

MOA of methotrexate? Adverse effects? CIs?

A
  • 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
  • CIs:
    renal dysfxn, pregnancy or possible pregnancy
40
Q

Surgery for RA?

A
  • soft tissue procedures:
    synovectomy, tendon repairs, removal of nodules
  • jt procedures:
    total jt replacements, fusions
41
Q

What is Gout?

A
  • 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
42
Q

PP of Gout?

A
  • 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
43
Q

RFs for gout?

A
  • increass w/ age
  • female sex hormone increases urinary excretion of uric acid (protective factor)
  • alcohol (beer)
  • meat
  • seafood
44
Q

Clinical presentation of gout?

A
  • severe pain
  • redness/warmth
  • swelling/disability
  • onset more at night
  • overlying skin becomes tense
45
Q

Dx gout?

A
  • clinical criteria
  • synovial fluid analysis: needle shaped negative birefringent urate crystals
  • elevated serum urate level
  • x-rays
46
Q

Tx for acute gout?

A
  • 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
  • glucocorticoids:
    intraarticular: injections often quickly resolve sxs
    oral: mult jts and can’t use NSAIDs or colchicine
47
Q

Tx for hyperurecemia?

A
  • 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
48
Q

How can recurrent attacks of gout be prevented?

A
- lifestyle changes:
wt loss
decreased alcohol intake
- diet:
decreasing meat and fish
increasing dairy products
- lowering serum uric acid:
uricosuric agents, xanthine oxidase inhibitors
49
Q

What is pseudogout? Etiologies?

A
  • calcium pyrophosphate dehydrate (CPPD) crystal deposition disease: chondrocalcinosis
  • equally affects men and women
  • etiology:
    trauma
    hypomagnesemia
    hyperparathyroidism
50
Q

presentation and dx of pseudogout?

A
  • presentation:
    similar to gout but less severe, usually occur in knee or other large peripheral jts
  • dx:
    synovial fluid:
    rhomboid or rod shaped crystals, positive birefringent crystals**
  • X-rays: chondrocalcinosis
51
Q

Tx pseudogout?

A
  • 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)
52
Q

Major features of osteoarthritis?

A
  • 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
53
Q

Major features of RA?

A
  • 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
54
Q

Major features of gout and pseudogout?

A
  • 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
55
Q

imaging diff in osteoarthritis, RA, and gouty arthritis?

A
- OA:
jt space narrowing
subchondral sclerosis
osteophytes
subchondral cysts
- RA:
jt space narrowing
soft tissue swelling
bony erosions
osteopenia about gout 
- gouty arthritis:
can see erosions and jt destruction late
56
Q

Diff OA and RA in the hand?

A
  • OA:
    swelling - hard, bony
    stiffness - worse after use (PM)
    fingers: DIP/PIP + nodes (Heberdens and Bouchards)
  • RA:
    soft, warm, tender
    worse after resting - AM
    MP and PIP + deformity
57
Q

Diff in lab work for OA

A
  • 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)
58
Q

DIff in synovial fluid anaylsis b/t OA, RA, and crystalline arthritis?

A
  • OA:
    clear synovial fluid, negative for crystals
  • RA:
    slightly to moderately turbid
  • crystalline arthritis:
    turbid - monosodium urate or calcium pyrophosphate dehydrate