OA Flashcards

(26 cards)

1
Q

incidence and aetiology

A

Very common
> 55 years: 44 -70%
> 75 years: 85%

Associated with increase age / weight
Knee> Hip> Hand (DIPJ and CMC)
However, multisite pain is common (hips, knees, hands, feet): 60-80% reported

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2
Q

pathology

A

Biochemical changes
Articular cartilage = water +collagen +proteoglycans
Loss of proteoglycan relative to collagen
Decrease in water content and permeability
85% in younger people, 70% in older people
Reduction in collagen tensile stiffness and strength
Proteolytic enzymes-Matrix mettalloproteases (MMPs).
Pro-inflammatory cytokines; TNF, IL-1 (some inflammatory component)

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3
Q

metabolic changes

A

Most critical changes occur in hyaline cartilage

Fibrillation in superficial layers  deeper layers

Joint Space Narrowing

Bony sclerosis
Excessive shear at the joint space

 osteoblast activity as attempt to redistribute load
Osteophyte formation

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4
Q

risk factors

A
intrinsic - jt vulnerabilities 
previous damage 
bridging muscle weakness 
increasing bone density 
malalignment 
proprioceptive deficiencies

systemic factors: age female ethnicity
genetics
nutritional

use (loading on joints)
obesity
injuries
activities

unmodifiable- genetics ethnicity age early menopause diabetes local mechanical factors
genu varum/ valgum
increase medial knee loading
previous trauma

modifiable
- obesity
- occupational - squatting, kneeling and heavy liftin
excess PA - soccer

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5
Q

diagnosis

A
clinical - history of jt pain 
stiffness <30 mins am /prolonged rest 
\+/- crepitis on mvmt 
bony enlargement 
little/no swelling 
radiological - joint space narrowing 
\+/- osteophyte formation 
\+/- bony sclerosis
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6
Q

Classification of OA

A
primary: idiopathic 
spontaneous onset 
small joints hand hip and knee 
may affect >1 joint 
stront link with genetics 
secondary OA
specific to jt 
causes - several - trauma? - knee/ hip 
occupations 
post inflammatroy arthritis
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7
Q

diagnosis OA

A
clinical - Hx PE 
radiology - jt space narrowed 
osteophyte formation 
sclerosis subchondral bone 
altered alignment 
subchondral cyts
loose body 

lab - ESR CRP
differential from inflammatory arhtritis
other - acthroscopy
CT
MRI + US better at detecting early signs not detected by plain xray

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8
Q

differential diagnosis

A

inflammatory arthritis
other intra-articular jt disorders
hip - labral tear
knee - meniscal injury

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9
Q

Hand OA

A

most commonin PIP DIP and thumb CMC

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10
Q

co-morbidity

A

Having at least one co-morbidity significantly associated with worse, or greater deterioration, of symptoms of pain and physical function

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11
Q

pain

A

Activity-related pain initially -worse end of day / after rest
Eased by movement
As disease progresses, night pain and rest pain are present
Cartilage is aneural so what causes pain?

Peri-articular-capsule/ligaments
Periosteal
Muscular
Compensatory e.g LBP assoc with hip OA: why? 
Inflamed tissue
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12
Q

stiffness SE PE

A

SE
subjective
differentiate from inflammatory by duration of stiffness
PE
- can be physical sign tested on physio assessment
loss of PROM
end-feel

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13
Q

fatigue

A

Subjective sensation of generalized tiredness or exhaustion
Less commonly reported in OA than auto-immune related arthritis e.g. RA

Can be a barrier to physical activity

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14
Q

exam findings

A
Inflammation / effusion
(will be minor compared with inflamm arthritis) 
Heat
Erythema
Tenderness
Effusion
Discomfort
Pain
loss of ROM 
Pain, stiffness +/- effusion may limit ROM
Compare Active vs Passive ROM loss 
Capsular patterns
Lower limb
Upper limb
muscle weakness Muscle weakness/atrophy	(Hurley, 1997)
Pain inhibition 
Disuse Atrophy
Inhibition 2 effusion  
Reduced function (related back to S/E)
Specific to body region e.g. UL vs LL

Deformity - knee valgus/ varus
hand
joint instability - ligament laxity
compounded by muscle weakness

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15
Q

deformity

A
Hip - flexion / adduction contracture, loss of MR 
Knee – flexion, genu varum and valgum. 
Loss of extension>flexion 
Ankle -  inversion / supination
Foot - hallux valgus

Hands - Heberden’s (DIP) & Bouchard’s (PIP) nodes
Shoulder -  abduction / rotation

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16
Q

mgmt of OA

A

Combination of Non-Pharmacological and Pharmacological interventions
Numerous clinical guidelines available
Currently no ‘cure’ for OA
Aim
Manage symptoms
Reduce deterioration
Enhance functional ability and quality of life
Due to its chronicity emphasise self-management

17
Q

core recommended mgmt

A

exercise
education self mgmt
weight mgmt

18
Q

exercise

A
aerobic and strengthening exercise 
water-based exercise 
min 30 mins 5 days/week 
tailored to persons problems 
supervised 12 wks 
  • aerobic
  • muscle strengthening - bdy weight/ weights bands
  • balance and flexibility
19
Q

pharm mgmt

A

Oral NSAIDS – Difene, Aulin, Mobic
GI and CVS side-effects
May need Proton Pump Inhibitor (PPI) drug
Topical NSAIDS – Feldene, Voltarol
Strongly recommended for Knee OA patients with GI or CV comorbidities
Intra-articular steroid injections
Recurrent cortisone injections into the knee decrease cartilage volume (McAlindon et al, 2018)
DMOADS; Glucosamine and Chondroitin sulphate
No evidence of benefit vs placebo
Paracetamol (previously recommended) now shown to have no clinical benefit
High quality evidence from 10 RCTs in 2019 Cochrane Review
Topical or Oral opioids not recommended
Strong evidence for limited or no benefit on OA symptoms
Concerns re dependence and addition

20
Q

surgical mgmt

A
osteotomy 
arthroplasty 
THR 
TKR
athrodesis
21
Q

Subjective assessment

A
Problems arising 
Symptoms body chart
One joint or multiple joints ?
Pain behaviour (24 hour, aggs/eases, quality of pain)
Stiffness, Swelling? Crepitus, weakness etc
Functional difficulty
History of onset
General health- co-morbidities common due to age profile
Heart disease,  BP, Diabetes etc. 
Investigations 
Management to date 
Outcome measures: WOMAC, KOOS, AUSCAN
22
Q

physical assessment

A
Observation- gait, posture, functional difficulties 
ROM 
Strength
Palpation 
Special tests – consider pathology and outrule other pathologies 
Exercise tolerance- examples? 
QoL, psychological health 
Problem list &amp; Goals 
Treatment plan
23
Q

physio intervention

A

Education
Self-management NB
Cognitive Behavioural principles

Exercise therapy
Hydrotherapy
ROM
Strengthening 
Aerobic
Posture re-education
? Manual therapy 
Pain
Stiffness
Gait re-education/Mobility aids 
Joint protection 
Orthotics/Braces/Insoles
Assistive devices 
Hand splints 

Electrotherapy
Pain

Evaluate rx effectiveness with validated outcomes
e.g WOMAC, KOOS, HOOS, VAS, Aggregate physical performance tests

24
Q

exercise therapy

A
knee hip 
strengthening 
quads for knee OA - lots of evidence 
glute strengthening 
aerobic exercise 
hydrotherapy
25
self mgmt
Educate patient on coping skills and behavioural approaches to managing OA Important adjunct to physical activity Long standing programme Arthritis Self-Management programme (ASMP) (Lorig et al, 1985). Delivered by lay people or health professionals Arthritis Ireland –Living well with Arthritis
26
other treatment
Psychological interventions Incorporated into self-management programmes Cognitive-behavioural approaches (Pisters et al, 2010) Pain Coping Skills (Bennell et al, 2016) Often MDT driven Weight reduction Strong link between high BMI and OA Combined Weight and Exercise Intensive Diet and Exercise for Arthritis (IDEA) trial (Messier et al, 2013)