Arthritis Flashcards

(53 cards)

1
Q

what is primary OA

A

idiopathic

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2
Q

what is secondary OA

A

post - traumatic
underlying cause or event or congenital malformation

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3
Q

prevalance of OA

A

302 mil world wide
1 in 4 people in US

leading cause of disability in older adults

spands decades of life

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4
Q

most commonly affects joints

A

hips
knees
hands

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5
Q

clinical features of OA

A

loss of articular cartilage

synovitis

boney changes

ligamentous changes

meniscal changes

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6
Q

patient impct of OA

A

Pain- -secondary affects contribute to the pain such as synovitis not necessarily loss of cartilage

Swelling – occur w synovitis

Stiffness – walking/moving on it less

Loss of Function

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7
Q

OA pathophysiology

A

degenerative process of the whole joint with different phenotypes emerging

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8
Q

risk factors for primary OA

A

age
obesity/metabolic disease
sex (60% female(

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9
Q

major components of normal cartilage

A

water
extracellular matrix (ECM) and proteoglycans
chondrocytes (responsible for both catabolism and anabolism)

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10
Q

function of cartilage

A

Withstand highly repetitive compressive and shear loads, maintain a near frictionless joint surface environment, allow force transmission between articulating bones

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11
Q

physiology and biomechanics of normal cartilage

A

Uses hydrodynamics- water flows out in response to compression

Proteoglycans are hydrophilic, attract water to flow back into cartilage following water loss

Combination of hydrodynamics and ECM structure allow compressive forces to be converted to shear at the calcified cartilage/bone interface

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12
Q

cartilage regeneration of normal cartilage

A

Chondrocytes repair ECM (very slow process) (Otero 2012, Eyre 2006) -> poor healing potential (Buckwalter 1998)

Chondrocytes are mechanosensitive, regenerative process is stimulated in response to loading (Gilbert 2018)

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13
Q

impairment of cartilage regeneration of OA

A

Regeneration is too slow to keep up with damage repair AND/OR regeneration pathway is altered
- Presence of inflammation impacts chondrocyte function
–Produce more pro-inflammatory markers and matrix degrading enzymes
–Early chondrocyte senescence (Liu-Bryan 2015) = death

Proteoglycan loss occurs first, followed by eventual ECM breakdown
-Loses ability to handle loads via hydrodynamics (less water), placing more stress on ECM

Articular Cartilage Breakdown
–This process is going on for YEARS/DECADES before we can see cartilage breakdown
–Translation: By the time we start to see cartilage breakdown its far too late

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14
Q

secondary OA due to an associated event could be

A

joint injury: PTOA
- knee injury 6x risk increases

abnormal alignment or geometry
- malalignment of the knee is on independent risk of OA progression

The normal joint structure and biomechanics are impacted resulting in both inflammatory environment and changes to loading environment
Slow cartilage metabolism does not adapt quickly enough to joint changes

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15
Q

PTOA

A

The major issue:
250k ACLR yearly (mostly impacting people under 25)
~50% will have radiographic OA within 10-20 yrs

Translation:
- Huge cohort of young individuals with old knees
–Lots of years left in the medical system
—Downstream healthcare impacts of physical inactivity and/or disability
–Joint arthroplasty only lasts~ 20 yrs
—These people may need multiple arthroplasties in their lifetime = $$$$$

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16
Q

summary of OA?

A

Much more complex than originally thought (not just wear and tear)
Cartilage regeneration is unable to keep up with microdamage
Impacted by biomechanics and/or inflammatory environment
Impacts the whole joint (not just articular cartilage)
We don’t fully understand what causes symptoms
Worse radiographic OA more likely to have symptoms
Primary OA: Intersection between aging, genetics, metabolic syndrome/obesity, lifestyle choices
Secondary OA: Intersection between joint biomechanics and inflammation

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16
Q

common imaging features

A

Loss of joint space width
Osteophyte formation
Sclerosis of subchondral bone

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17
Q

imaging modalities

A

radiographs (gold standard)
MRI
CT

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18
Q

grade 1 OA

A

possible osteophites
doubtful JSN
doubtful OA

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19
Q

grade 2

A

definite osteophites
possible JSN
mild OA

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20
Q

grade 3 OA

A

moderate osteophites
definite JSN
moderate OA

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21
Q

grade 4 OA

A

large osteophites
great JSN
severe OA

22
Q

grade 0 OA

A

no OA
no osteophites
no jsn

23
Q

OA imaging

A

Advanced Imaging Techniques

New promising imaging sequences that allow us to assess cartilage physiology before cartilage damage is evident

MRI T1rho: Associated proteoglycan content/concentration

MRI T2*: Associated with ECM orientation and free vs bound water

24
OA treatment
We currently have zero treatments that have been proven effective at reversing OA or stopping its progression The treatments we do have: Treat the symptoms (reduce pain) Promote function Prevent OA from happening in the first place Injury prevention (Secondary OA) Lifestyle (Primary OA) Moderate Activity Weight Management
25
OA medical management treatment for NSAIDS
Effective at reducing pain and targeting synovitis Cheap Cons: Some with comorbidities unable to use Some have topical versions available Con: Treats symptoms, no impact on disease
26
common NSAIDS OA treatment
Ibuprofen Naproxen Diclofenac
27
pharm interventions for OA
NSAIDs Corticosteroids Hyaluronic Acid Biologics
28
surgery interventions for OA
Debridement Cartilage Repair Joint Replacement
29
corticosteroids treatment
common: cortisone injections (kenalog) tx: Effective at reducing short-term pain and inflammation Intended to be an adjunct More localized treatment Cons: Some with comorbidities unable to use Con: Treats symptoms, no impact on disease Con: Limited dosage schedule, infection risk
30
hyaluronic acid for OA
common: Viscosupplementation) Synvisc Hyalgen Euflexxa treatment: Can improve symptoms and function in mild/moderate OA (high bias evidence) “lubricates” the joint Cons: Expensive (limited insurance coverage) Con: Treats symptoms, no impact on disease Con: Limited dosage schedule
31
biologics for OA tx
Common: Stem Cell Therapy Platelet Rich Plasma (PRP) Treatment: Promising basic science results Some mixed results but mostly poor findings of effectiveness in vivo No Standardization Cons: Expensive (not covered by insurance) Cons: Travel to special clinic
32
summary of medical management for OA
DMOADs do not exist yet Corticosteroids have short-term symptomatic benefits and should be adjuncts Placebo effect from injections (Bannuru 2015, Ayhan 2014) Viscosupplementation studies that show benefit have high risk of bias Recommendation: try it if the patient had little to no effect from steroid or can’t have steroid Surgery: Joint replacement is highly effective but still considered a salvage procedure Reduces pain, reduces disability, improves QOL
33
rehab interventions: weight management
9-76% reduction in pain following gastric bypass (McGoey 1990) Pain scores reduced, functional scores improve (Abu-Abeid 2005) Improved joint space associated with weight loss (Abu-Abeid 2005) Con: Poor adherence to interventions Dose response exists (More weight loss more symptomatic improvement) Messier 2018
34
rehab interventions: exercise
Maintain and/or improve functional capacity Supplement diet for weight loss `No specific recommendations: Moderate activity (ACSM) No evidence to support a hierarchy of types of exercise Whatever the patient likes to do will improve adherence
35
rehab program for exercise OA management
Decrease pain, improve function, improve QOL Quad strength/power = Function PT had better outcomes through 1 year follow up vs corticosteroid injection
36
bracing for management
Unloader braces have some symptomatic benefit Other braces: Likely placebo/tactile Braces are generally bulky, uncomfortable, and/or not aesthetically pleasing
37
the debate
dont unnecessarily load vs dont change activity pendulum
38
current opinoin
Not all OA is the same: Primary vs secondary with phenotypes of each It is unlikely there will be one blanket recommendation, each subset will need its own specific recommendations that is also adjusted to the individual patient The most basic principle of treatment is the risk reward benefit to the patient Primary OA: Should we promote physical activity (including that with high joint loading) despite the risk of promoting articular cartilage degeneration Secondary OA: Does the risk reward benefit change given the different pathophysiology?
39
treattment principples summary
Promote physical activity for weight management, joint health maintenance, pain/mental health Weigh the risk reward for whether higher loading activity is appropriate Use irritability as a guide Quad strength and power to maintain function Combination of open and closed chain depending on joint irritability and compensations Assistive device use for significant gait deviations Self-management focus Booster visits currently being explored, watch for evidence
39
the future
Harness mechanosensitivity of chondrocytes to promote regeneration Can we identify specific loading inputs to optimize cartilage health after injury and surgery Likely in combination with pharm Use of biologics to regenerate damaged cartilage Our current post-injury and post-op treatments are focused on short term goals of return to sport and function and have little focus on long-term joint health
40
inflammatory arthritis history
UNEXPLAINED joint pain with associated swelling (No MOI but inflammation). Joint(s) can look acutely injured or infected (warm, red, swollen, painful) Frequently have relapsing remitting presentation Joints can become damaged over time leading to changes similar to OA (chronic joint degradation) Make sure you do a high quality systems review as many of these conditions have systemic effects impacting things other than MSK
41
rheumatoid arthritis
Fairly common: 0.3 – 1% in US (Alamanos 2006) Chronic Systemic autoimmune disease that attacks the joints Hands, wrists, shoulders, elbows, knees, ankles feet General fatigue How many joints and any structural deformity Increased cardiovascular risk Promote physical activity
42
psoriatic arthritis
Autoimmune disease in people with psoriasis that can impact joints Nail and skin changes 1/3 of people with psoriasis DIPs, wrists, ankles, knees Can also impact enthesis (usually heel)
43
lupus
Arthritis/arthralgia is present in 95% of patients with SLE -Mimics RA in 5-15%
44
lymes disease
Tends to occur in late stage infection After systemic symptoms have resolved Can have intermittent or persistent joint attacks Lyme bacteria enters joint and can remain Common in knee Can have swelling without pain
45
gout
Inflamed joints due to urate crystal formation in synovial fluid. 3.9% in US
46
boutonniere
PIP flexed and DIP ext
47
swan neck
PIP extended, DIP flexed, MCP flexed
48
hitchhikers thumb
MCP flexion, IP extension
49
claw toe
MTP ext, PIP/DIP flexion
50
IA medical management - disease modifying antirheumatic drugs (DMARDS)
Many different DMARD protocols, used in virtually all inflammatory arthritis conditions Typically have a maintenance dose that is then increased during flares Trial and error to get maintenance and flare doses right (as little as gets the job done) Can be combined with corticosteroids to minimize inflammation during flares Common Pharm Methotrexate Leflunomide Hydroxycholoroquine Sulfasalazine Because they inhibit immune response, increased risk of infection
51
IA PT Management
Identify when joints are “Hot”: Red, swollen, painful/irritable During Flare: Reduce pain and inflammation, promote ROM and maintain strength Avoid high impact activity During Remission: Promote physical activity to limit systemic impacts Promote moderate intensity exercise and maintenance of strength and ROM to avoid deformity and/or dysfunction Always use your irritability principles to guide your treatment Splinting for deformity (covered in Rehab Tech)