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Bloc H - Movement > May30 M2-Osteoarthritis > Flashcards

May30 M2-Osteoarthritis Flashcards

1
Q

charact of mechanical joint pain

A
  • no pain when resting, lying or sitting
  • morning stiffness <30 min
  • pain with no swelling
  • no systemic symptoms fatigue, anorexia, fever
  • worse with use and mobility
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2
Q

OA typical history

A

pain that has been getting worse, no trauma, not clear when started, history very normal. old person

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3
Q

pathology of OA

A
  • damage to articular cartilage
  • osteophyte formation at joint margins
  • subchondral bone sclerosis
  • synovial joint and capsule thickening
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4
Q

consequence of OA pathology

A
  • joint degeneration
  • pain, stiffness and loss of function
  • loss of tissue homeostasis
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5
Q

steps of articular damage in OA

A
  • smooth to rough
  • clefts become cracks
  • cracks extend to middle
  • get holes with bone exposed
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6
Q

steps of subchondral sclerosis in OA

A

-happens bc of increased remodelling
-eburnation (ivory=like) of bone
-bone cysts
-bone marrow edema
+osteophytes

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7
Q

structures with homeostasis affected in OA joint

A
  • cartilage
  • bone
  • synovium
  • ligaments
  • muscle
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8
Q

changes in cartilage matrix in OA

A
  • type II becomes type 1 cartilage
  • less proteoglycans
  • shorter glycosaminoglycans
  • less water retention by ECM so changes in force distribution to subchondral bone
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9
Q

what causes cartilage damaged in OA

A
  • MMPs upregulated and chew ECM proteins (inbalance, more catabolism than anabolism)
  • ADAMTS (aggrecanases) cleave aggrecan (the major proteoglycan in cartilage)
  • upregulated bc cytokines released or bc of mechanical stress
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10
Q

anabolic developmental pathways activated in OA lead to what

A
  • TGF-beta (and Wnt and BMP) which have phgy role on cartilage
  • in aging and OA, this leads to cartilage hypertrophy, osteophyte formation, synovial fibrosis
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11
Q

synovitis and pro-inflammatory molecules components in OA

A
  • more synovial inflam. bc of cartilage breakdown
  • inflamed synovoum makes pro-inflam mediators (IL-1, TNF-a)
  • consequence is excess prod of proteolytic enzymes (back to MMPs and aggrecanases)
  • systemic mediators too (adipokines) IMPORTANT***
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12
Q

inflammation in OA vs in RA (why still said to be non-inflammatory)

A
  • local inflammation
  • same as a blister and accum of a bit of fluid, not more
  • inflammation is secondary, not primary
  • bit of irritation
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13
Q

most important systemic mediators in OA

A

adipokines (like adipokinesare). obese people may get OA in non weight-bearing joints

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14
Q

OA prevalence

A

90% women and 80% men above 70 so is normal

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15
Q

OA predisposing (non modifiable) factors

A

age, female gender, ethnicity, genetics, joint deformity, laxity, acute injury, occupational factors

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16
Q

best description of type of disease OA is

A

chronic degenerative disease

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17
Q

modifiable risk factors in OA

A
  • obesity

- muscle weakness

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18
Q

why obesity problem in OA

A
  • higher bone mass
  • more mechanical stress to weight bearing joints
  • higher levels of IGF1 and visfatin
  • hyperglycemia induces MMPs
  • hypercholesterolemia assoc with OA
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19
Q

why muscle weakness problem in OA

A

OA of knee = quadriceps weakness, altered muscle activation patterns and proprioceptive defects

20
Q

charact of hx in an inflammatory arthritis (not OA)

A
  • pain acute or subacute
  • wake up in 2nd half of night
  • > 30 min morning stiffness
  • better with mvmt
  • fatigue
  • all joints can be involved
21
Q

charact of hx of mechanical joint problem like OA

A
  • pain is chronic
  • no night awakening
  • <15 min stiffness in morning
  • worse with mobility
  • no fatigue and constitutional symptoms
  • PIP, DIP, AC, spine, hip, knee, 1st MTP, CMC
22
Q

joints NOT involved in OA

A
  • ankles, wrists, shoulders, elbows

- no toes should be affected except 1st MTP

23
Q

inspection in RA vs OA

A
  • RA: redness (in acute arthritis) and swelling with synovitis
  • OA: bony swelling but not joint swelling
24
Q

palpation RA vs OA

A
  • RA: pain, warmth, swelling

- OA: minor pain, minimal warmth, may palpate osteophytes, maybe joint swlling but no synovitis

25
Q

passive ROM RA vs OA

A
  • RA: pain throughout the movement worse with joint stress

- OA: pain at extremes of movement

26
Q

things to asses on OA exam including SEADS mnemonic

A
  • swelling, erythema, atrophy, deformity, symmetry
  • temp, crepitus (cracking noise), joint line pain, assoc structures
  • ROM (passive and active)
  • NO JOINT SYNOVITIS
27
Q

differences in joints involved in OA and RA

A
  • OA: MCPs not involved and DIP involved

- RA: MCPs involved and DIP not involved

28
Q

antalgic gait meaning

A

painful gait, limp

29
Q

fluid aspiration in small OA effusion: what do yo uget

A

clear fluid as in fluid of a blister, with no white cells

30
Q

what’s secondary OA

A

OA that is secondary to a known cause (another disease)

31
Q

ddx of primary OA (what are the causes of secondary OA)

A
  • metabolic (crystal as in gout, CPPD, hydroxyapetite. acromegaly. hemochromatosis. Wilson’s
  • anatomic (hypermobility, LLD, Legg-Perth, slipped femoral epiphysis)
  • traumatic (fracture, osteonecrosis=avascular necrosis, joint surgery)
  • inflammatory
  • septic
32
Q

what’s CPPD crystal

A

calcium deposition disease (pseudogout)

33
Q

imaging for OA that may be needed to make dx

A

XR

  • smaller joint space
  • asymmetric narrowing of joint space
  • osteophyte
  • subchondral sclerosis
  • BUT YOU DON’T GET MORE SPECIFICITY AND SENSITIVITY WITH XR*
34
Q

main clinical criteria for OA dx

A

knee pain with some of

  • age > 50
  • crepitus
  • bony tenderness
  • bony enlargement
  • osteophytes
  • morning stiffness <30 min (so the whole non-inflam hx)
  • no warmth
35
Q

most important tx step in OA

A

education

  • strengthening exercises
  • stay active
  • aerobic fitness training
  • weight loss if overweight or obese
36
Q

after education, what else can you do for OA tx

A
  • paracetamol (acetaminophen)

- topical NSAID (voltaren emulgel very good)

37
Q

if NSAIDs and acetaminophens fail in OA, what can you do

A
  • oral NSAIDs
  • opioids
  • intraarticular CS injection
  • heat and cold
  • assistive devices
  • joint arthroplasty
  • manual therapy
  • TENS
  • shock-absorbing shoes or insoles
  • supports and braces
  • topical capsaicin
38
Q

good exercise for people with weight bearing problem with OA

A

aquafit

39
Q

which is better NSAIDs or acetaminophens in OA

A

both equal FOR PAIN (and big placebo effect 20-25% so tell the pts it will work)
note NSAIDs SE renal, CV, GI

40
Q

2 safest NSAIDs in studies

A
  • naproxen

- celebrex

41
Q

most important thing to remember in using NSAIDs in OA patients

A

use for the shortest amount of time in very select patient population

42
Q

can you use the RA meds in OA (anti IL1, anti-TNFa, DMARDs)

A

no don’t work

43
Q

(imp) best prevention method for OA

A

exercising

44
Q

most important pathology charact in OA

A

loss of homeostasis between anabolic and catabolic factors

45
Q

normal vs damaged joint P

A
  • normal joint = negative pressure

- damaged joint = broken seal = pressure change

Bloc H - Movement (48 decks)

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