Arthritides Flashcards
1
Q
Key manifestations of arthritis?
A
- pain, swelling and limited motion
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
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
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
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
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
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)
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
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
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
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
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
13
Q
What can you see on imaging of OA?
A
- jt space narrowing
- surface irregularity
- osteophytes
- subchondral sclerosis
- subchondral cysts
14
Q
Nonpharm rx for OA?
A
- moderate wt loss
- exercises
- PT/OT
- braces
- heat/cold
- rest
15
Q
Pharm Rx for OA?
A
- acetaminophen
- NSAIDs: naproxen/ibuprofen
- Tramadol
- opioids
- intraarticular injections
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
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
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
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
20
Q
Total knee replacement-pros, cons?
A
- relieves pain, corrects deformity, improves fxn
- reqrs sig post-op rehabilitation
21
Q
Total hip replacement - pros, cons?
A
- relieves pain, restores fxn, relatively quick recovery - out pt
- leg length inequality not uncommon
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
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
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
