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CNSLF Med - Osteoarthritis (i) (Intro (commonest form of arthritis,…
CNSLF Med - Osteoarthritis (i)
Intro
commonest form of arthritis
present in most people over 60 to some extent
wear + tear - degenerative joint disease
not confined to humans
loss of cart
narrowing of joint space
low grade synovial inflamm
thickening of subchondral bone + developing of bony outgrowths - osteophytes
abnormal loading of normal tissues or normal loading of abnormal tissues gives progressive OA
ability of tissues to adapt + respond to injury + insult (repair potential) fives stabilisation or repair
NB determine site + severity
damage cart @ arthroscopy - frayed + thinned
Aetiology
age
systemic factors - genetic + environmental
local biomechanical factors (e.g. previous injuries)
Risk factors
systemic
age
older cart repairs less well
reduced muscle strength + bulk
reduced joint proprioception
time for wear + tear
obesity
counsel patients about weight loss
major risk
a/w 40% increased risk
weightloss of 5kg reduces risk
obesity potentates other risks
BMI 30-35 = x4 increased risk of knee OA
hereditary/genetics
twin studies: 65% concordance genetic
multiple genes involved - complex
sex
women have more knee (mechanical) + hand (hormonal) OA
metabolic risk factors
local
joint shape
trauma/injury
repetitive use
muscle weakness
joint laxity
occupational factors
Secondary OA
metabolic
onchronosis (accumulation of homogentisic acid in connective tissues)
HFE
acromegaly
CPPD (ca pyrophosphate dehydrate crystal deposition disease) aka pseudo gout
all affect cart repair
anatomic
slipped epiphysis
avasc necrosis (AVN)
congenital diaphragmatic hernia (CDH)
any condition (congenital or acquired) that alters joint mechanics
trauma
major joint trauma
facture
meniscectomy (surgical removal of meniscus esp @ knee)
occupational/repetitive injury or stress
prior septic of inflamm arthritis (e.g. RA)
Cart metabolism
chondrocytes in early OA are v metabolically active + seem to engaged in repair
progression: CKs, TNFalpha, IL1, IL6, collagensases, metalloproteinsases, aggregecanses released - degradation
chondrocyto apoptosis, loss of proteoglycans, collagen fibre damage
some factors protective: IL4, TIMP, TGF-beta, IGF1
Symptoms
pain + stiffness
gel phenomenon, stiffness after mobility
worse with prolonged use (unlike RA which is first in morning + improves with use)
poor correlation with radiography (x-rays can't predict symptom severity)
patients perceives pain differently
multiple dicots influence pain perception incl cognition, emotion, stress, sleep
Patterns
hands + feet
Heberden's nodes @ DIPs (often spared in RA)
Bouchard's nodes @ PIPs
guttering of hand (wasting of small muscles)
spine
large weight-bearing joints
genu varus (bow/bandy legs - outward bending)
generalised or just a few joints
most joints can be affected
usually asymmetry (RA symm)
Dx
mostly clinical - often hx + exam enough - typical pattern of symptoms + joints
blood tests normal unlike RA
x-rays late to show joint space narrowing, osteophytes, sclerosis
Goals of tx
relieve pain
maintain/restore function with rehab + exercise
delay progression of possible
Pain control
paracetamol should be tried 1st - many will respond
NSAIDs + coxibs should be tried next - many but not all will respond better
Ibuprofen
naproxen
diclofenac
meloxican
celecoxib
etoricoxib
anti-inflamm + analgesic
inhibit PG production
somewhat more effect that analgesia
symptom relief
SEs: GI bleeds, gastritis, IHD worsens, AKI, can aggravate renal impairment + HTN
coxibs are definitely GI safer but have more cardiac risk
mild opiates
co-proxamol
codeine (SE = constipation)
tramadol (SEs = euphoria, neurocognitive effects)
start with simplest + use as needed only
Psychological aspects
depression common - may need to tx
+ve attitude, learn about disease, prepare for MDT management do best (self-efficacy)
depends on personality (+ resilience)