Osteoarthritis profoma Flashcards
What is Osteoarthritis?
Disorder of synovial joints characterised by articular surface damage, formation of new bone & secondary inflammation.
also called degenerative bone disease
A disorder of the synovial joints where the cartilage disintegrates
Epidemiology of OA
Prevalence increase w/ age
Common in women - 1.7 times higher than in men.
Classification of OA
Primary OA - just comes gradually w/ age.
Secondary OA caused by:
-Trauma
- infection
- Inflammation (RA)
- Perthes’ disease - disorder of the hip in young children (btw 4-10 yrs) occurs when the blood supply to the femoral head is temporarily disrupted & the bone begins to die. The blood supply is reinstated & the ball heals but it is no longer round.
- Slipped upper femoral epiphyses (SUFE)
Pathophysiology: what role do chondrocytes play in healthy joints & OA joints?
Chondrocytes maintain healthy cartilage by producing Type II collagen & extracellular matrix
They break down cartilage (via degrading enzymes) & make new cartilage (via synthetic enzymes).
Factors that make chondrocytes secrete more degradative enzymes than synthetic:
- Increased age
- Inflammation
- Joint injury
- Genetics
Chondrocytes start to die via apoptosis, so cartilage repair can’t occur - late stage.
Pathophysiology:
Subchondral cysts & Sclerosis:
- Chondrocytes start working faster as a result of repeated microtrauma & abnormal biomechanical forces.
- They release degradative enzymes in an attempt to repair & lay down new cartilage, but degradation exceeds synthesis.
- Sclerosis is caused by new bone formation due to microfracturing the articular surface.
Osteophytes - the unregulated process of synthesis & degradation causes disorganised bone formation at the joint margins.
Pathophysiology: what does the joint space narrow?
Joint Space narrowing - Inflammation occurs because the degraded cartilage exposes the bone surface, so the 2 bones rub against each other, & the synovial lining thickens.
Synovial lining - thickens & gets inflamed, producing excess synovial fluid (effusions).
Pathophysiology: role of genetics?
Mutation in genes that encode components of cartilage matrix can cause OA.
Strong association between obesity & hip OA - either because of biomechanical factors or because of cytokines being released from adipose tissue (cytokines break down cartilage).
Absence of oestrogen = flare of OA symptoms.
Pathophysiology: role of occupation?
Farmers are more likely to get hip OA
Miners are more likely to get knee OA
Athletes are more likely to get knee & ankle OA
NOTE- view diagram of early & late stage of OA
Presentation of OA: Clinical signs, joint pattern, pain presentation
Clinical signs:
- Restricted movement due to capsule thickening or osteophyte blocking- difficulty performing tests
- Crepitus due to rough articular surfaces
- Swelling around joint margins
- Jointline tenderness
- Synovitis- synovium swollen
- Deformity- Herberden’s (DIP)or Bouchards (PIP) node or virus or valves knee
Joint pattern:
- Hips
- knee
- DIP
- Thumb carpometacarpal
- 1st MCP
- 1st metotarsalphalangeal (toe)
- Neck
- Lumbar spine
- Can be mono- oligo- or poly- arthritis
- Assymetrical distribution!
Pain:
- Slow onset over months or years
- Aching or burning pain
- Relieved by rest
- Only brief morning stiffness (less than 15 mins)
- Worse in evenings
- Night pain due to secondary inflammation in more progressed disease.
- Usually only 1 or a few joints painful
- Hip OA pain can radiate to knee
Investigations for OA
X-rays- findings:
1. Asymmetric joint space narrowing
2. Sclerosis = whitening
3. Subchondral cyst formation= black holes in white sclerosis
4. Osteophytes= new bone formation usually at edges
Blood tests:
- to exclude septic or inflammatory arthritis
NOTE- view x-rays on notes!
Management of OA: conservative, pharmacological, surgical
Conservative:
- Physiotherapy - muscle strengthening
- Weight loss if overweight
- Exercise - aerobic fitness training (NOT during acute attack!)
- Supports, braces & assistive devices
- Heat
Pharmacological:
1st line:
- Paracetamol- first line
-Topical NSAIDs- should be considered ahead of oral NSAIDs. Look out for contra-indications for NSAIDs e.g. hypertension or GI issues & heart burn.
- PPI - co-prescribe a proton pump inhibitor e.g. Lansoprazole.
- NOTE: you can do paracetamol + NSAID
2nd line:
- Opioid analgesic - consider if paracetamol & topical NSAIDs aren’t working e.g. codeine, morphine, oxycodone & fentanyl methadone
- Intra-articular injections of corticosteroids
Surgical:
- Joint arthroplasty - replacement
- Arthrodesis - joint fusion e.g. foot or ankle
- Joint excision - removal of failing joint - uncommon
- Osteotomy - joint realignment
NOTE- view diagram on notes!
