Osteoarthritis Flashcards

1
Q

What is it?

A

A non-inflammatory disorder of movable joints characterised by deterioration or articular cartilage and the formation of new bone at the joint surfaces and margins.

New definition:
Age-related, dynamic reaction pattern of a joint in response to insult or injury. All tissues of the joint are involved. Articular cartilage is the most damaged but there is also damage to the underlying bone.

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2
Q

Is the condition inflammatory or non-inflammatory?

A

Non-inflammatory

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3
Q

What is another name for osteoarthritis?

A

‘wear and tear arthritis’

degenerative joint disease

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4
Q

Prevalence?

A

Most common disease affecting synovial joint
Prevalence increases with age
By 40, 90% have OA in weight bearing joints

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5
Q

What is the relationship to sex?

A

<45 yrs more common in males

>55 yrs more common in females

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6
Q

What cytokines are involved?

A

IL-1
TNF-a
NO
(Little inflammation, driven by mechanical forces)

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7
Q

What are the main pathological features?

A

Loss of cartilage and disordered bone repair

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8
Q

Define primary and secondary OA?

A

Primary/idiopathic - No identifiable predisposing cause

Secondary - underlying cause is implicated

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9
Q

Risk factors for OA?

A
Increased age
Family history - genetic component
Female post-menopausal
Caucasian
Obesity
Occupation - manual labour, sports
Local trauma
Inflammatory arthritis
Neuropathic conditions
Deformities - e.g. congenital, SUFE.
Increased bone density
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10
Q

Symptoms and signs of OA?

A
Pain - worse on exertion
Stiffness - worst after rest
Swelling - bony and soft tissue (effusion/intermittent or continuous from capsular thickening)
Functional impairment
(typically after middle age)
Morning stiffness
Alteration in gait
Bony enlargement
Synovitis
Limited ROM
Crepitus
Tenderness
Deformity
Muscle wasting
Joint instability - late onset
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11
Q

Key radiological features of OA? (5)

A
Joint space narrowing
Osteophyte formation
Subchondral scleosis
Subchondral cysts
Abnormalities of bone contour
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12
Q

What is the pathogenesis?

A

Articular cartilage failure
Chondrocytes are the most important cells responsible for osteoarthritis

Some involvement of proteases, cytokines, anabolic cytokines and inflammation.

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13
Q

What is one key difference between OA and inflammatory joint disease?

A

Not associated with systemic manifestations.

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14
Q

What joints are most commonly affected?

A
Knee
Hip
DIPJ + PIPJ (two end joints)
1st CMC
Spine
1st MTPJ
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15
Q

Describe the nature of the pain experienced in OA?

A

Insidious onset - months to years
Aggravated by activity
Relieved by rest
May be referred pain

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16
Q

What is the origin of the pain experienced in OA?

A

Articular cartilage and synovium has no nerve supply. Pain due to capsular stretching and vascular congestion of bone.

17
Q

What is the name of the stigmata present in the hands which are the palpable osteophytes in the joints?

A

Heberden’s nodes - DIPJ

Bouchard’s nodes - PIPJ

18
Q

What are the differential diagnosis of OA?

A

Rheumatoid arthritis
Gout
Osteonecrosis
Neuropathic joint

19
Q

What signs are characteristic?

A

Pain worse at night/ on use
Morning stiffness <30 mins, degenerative. >1hr, inflammatory
Herberden’s and Bouchard’s nodes

20
Q

What investigations would you do in OA?

A

X-ray (Asymmetric loss of joint space, sclerosis, cysts, osteophytes)
Majority of cases
Rheumatoid factor and anti-CCP negative

CT (for joints not clearly visible on x-ray)
MRI (rarely used)
Isotope bone scan (‘hot’ due to increased vascularity and new bone formation)
Laboratory tests (blood and synovial fluid - would expect to be normal)
Diagnostic injection
Arthroscopy (can help to isolate affected joint)

21
Q

What is the management option selected dependent on?

A
Joint involved
Stage of disorder
Severity of symptoms
Age of patient
Functional needs
22
Q

What are the management options for OA?

A

Conservative / Non-surgical
Injection
Surgical

23
Q

What might conservative management of OA include?

A
Decrease load on joint (weight loss and exercise)
Analgesia (topical products, capsaicin or NSAIDS, paracetamol, NSAIDs, Cox-2 inhibitors (w/o GI side effects of NSAIDS)
Promote movement (physiotherapy)
Mobility aids (waking sticks, heel raises)
24
Q

Do any exercises increase the risk of OA?

A

Neuroanatomically normal (NAN) joints are at increased risk of developing OA in the absence of adequate exercise.

NAN joints are not at increased risk upon exposure to repetitive, low-impact, exercise.

NA abnormal joints are at increased risk upon exposure to repetitive, low impact, exercise.

NAN joints are at increased risk upon exposure to repetitive, high-impact exercise.

So basically, running would be risky as high impact and could affect normal joint.
Something low impact like walking would only be bad if neuroanatomically abnormal joint.

25
Q

What substance might be injected as management of OA?

A
Steroid injections (definite short-term benefit)
Hyaluronic acid
26
Q

What surgical management options are there for OA?

What are the goals?

A

Remove pain
Improve function
Correct deformity

Debridement of joint
Realignment of osteotomies
Joint excision
Joint fusion
Joint replacement (arhroplasty) - metal joint
27
Q

What are some of the indications for arthroplasty?

A
Uncontrolled pain (esp. night)
Significant limitation of function
Fitness for surgery
(Note, age is a consideration due to limited lifespan of prosthetic joints (10-15 years))