Osteroarthritis (OA) Flashcards

1
Q

Define osteoarthritis in simple terms.

A

Often described as “wear and tear” in the joints.

= NON-INFLAMMATORY DEGENERATIVE ARTHRITIS!

It is not an inflammatory condition like rheumatoid arthritis.
The –itis ending is misleading.

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2
Q

Is osteoarthritis an inflammatory condition?

A

NO!

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3
Q

Define osteoarthritis.

A

A non-inflammatory degenerative disorder of moveable joints characterised by the deterioration of articular cartilage and the formation of new bone.

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4
Q

Describe the epidemiology of OA.

A
  1. Most common type of arthritis
  2. Most common cause of disability in the Western world in older adults
  3. Prevalence increases with age - uncommon before the age of 50
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5
Q

Describe the usual onset of OA.

A

> 50yrs, slow and gradual

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6
Q

Give the key points in the pathophysiology of OA.

A

General wear and tear -> a chronic degenerative disease.

Loss of articular cartilage - exposed bone becomes sclerotic.

Attempts at repair produces osteophytes (nodules).

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7
Q

Describe the disease process behind OA in detail (pathophysiology).

A
  1. Normal physiology - there is a dynamic balance between cartilage degradation by wear and its production by
    chondrocytes.
  2. In OA: initial imbalance in cartilage homeostasis
  3. Leads to cartilage degradation, remodelling of the bone + associated inflammation of the joint
  4. Over time, continuous ‘wear’/trauma to the joint
    = local inflammation
    = stimulates chondrocytes
    = they release degradative enzymes
    = enzymes break down collagen + proteoglycan
    = lead to the destruction of the articular cartilage
  5. Over time, cartilage thins a lot:
    = exposes the underlying subchondral bone
    = causes subchondral sclerosis
    = continuous remodelling of subchondral bone
    = this forms subchondral cysts and osteophytes.
    = this eventually leads to a progressive loss of joint space.
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8
Q

What are the most important cells responsible for OA?

A

Chrondrocytes.

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9
Q

What are the 2 key pathological features of OA?

A

Main pathological features:
* Loss of cartilage
* Disordered bone repair

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10
Q

Which tissues gets most affected in OA?

A

Articular cartilage

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11
Q

What disease lowers your risk of developing osteoarthritis?

A

Osteoporosis

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12
Q

Give 5 risk factors for developing OA.

A
  1. Genetic predisposition.
  2. Local Trauma.
  3. Abnormal biomechanics e.g. joint hypermobility.
  4. Occupation e.g. manual labour.
  5. Obesity; pro-inflammatory state.
  6. Increasing age.
  7. Being female.
  8. Inflammatory arthritis e.g. RA.
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13
Q

OA risk factor: Occupation - what joints can manual labour be associated with?

A

The small joints of the hand

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14
Q

OA risk factor: Occupation - what joints can being a farmer be associated with?

A

OA of the hips

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15
Q

OA risk factor: Occupation - what joints can being a footballer be associated with?

A

OA of the knees

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16
Q

Why does the prevalence of OA increase with age?

A

Due to the cumulative effect of trauma and a decrease in neuromuscular function.

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17
Q

What joints might be affected in osteoarthritis? Give 5.

A

BASICALLY - Those that are used a lot!

Weight-bearing joints:
- Hips
- Knees
- Sacro-iliac joints in the cervical spine
- Veterbra

  • Distal-interphalangeal joints in the hands (DIPs - Heberden’s nodes)
  • The 1st carpometacarpal joints at the base of the thumb of the hands
  • Wrist
18
Q

Which surface of the knee is most commonly affected by OA?

A

The medial surface.

19
Q

Name 3 joints of the hand that are commonly affected in osteoarthritis.

A
  1. Distal interphalangeal joint (DIP).
  2. Proximal interphalangeal joint (PIP).
  3. Carpal metacarpal joint (CMC).
20
Q

Nodal osteoarthritis can affect the DIP and PIP joints. What are the two terms used for nodes on these joints?

A
  1. PIP - Bouchard’s nodes.
  2. DIP - Herbeden’s nodes.

Remember: since B is before H, so Bouchard’s are more proximal than Heberden’s.

21
Q

What are Herbeden’s and Bouchard’s nodes?

A

Soft tissue swellings on the fingers
Seen in the early stages of OA

Herbedens = DIP
Bouchards = PIP
(HD AND BP)

22
Q

Give 5 symptoms of OA.

A
  1. Morning stiffness (<30 minutes).
  2. Pain - aggravated by activity.
  3. Tenderness (tender to palpation).
  4. Walking and ADLs affected (activities of daily living).
  5. Joint effusion (too much fluid builds up around a joint) and bony enlargement.
  6. Deformities.
  7. Crepitus (a popping, clicking or crackling sound in a joint).
23
Q

Describe the character of the pain from OA.

A

Increases with movement, worse at the end of the day.

24
Q

How is the pain different in osteroarthritis vs inflammatory arthritis?

A

Osteoarthritis:
- Morning stiffness only lasting up to 15 mins, generally worsens throughout day

Inflammatory arthritis:
- Stiff for 30+ mins, better with use

25
Q

Describe the pattern of joint involvement of OA.

A

Asymmetrical:
- Arthritis that occurs in just 1 joint or a joint on only 1 side of your body.

Finger joints, thumbs + weight bearing joints (hip/knee/big toe)

26
Q

What systemic features are present in osteoarthritis?

A

NONE

27
Q

A patient complains of ‘locking’, what is the most likely cause of this?

A

This is probably due to a loose body e.g. a bone or cartilage fragment.

28
Q

Investigations: What would the lab findings be in OA?

A
  1. Rheumatoid factor = RhF -ve
  2. Antinuclear antibodies = ANA -ve
  3. Normal ESR/CRP typically normal
29
Q

What is the primary investigation used to make a diagnosis of OA?

A

X-ray.

30
Q

Investigations: What would be the radiological findings in osteoarthritis?

A

X-ray - LOSS:
Loss of joint space.
Osteophytes.
Subchondral cysts.
Subchondral Sclerosis.

31
Q

What is an osteophyte?

A

An area of bone which has been reactively laid down in the wrong place.

32
Q

What is sclerosis in relation to arthritis?

A

Thickening and widening of the bone at the joint.

33
Q

How do you end up with bony changes in OA?

A
  1. Mechanical forces –> cartilege lost.
  2. Cartilage loss = cytokines - TNFa, IL-1, NO.
  3. Cytokines = cartilage cannot repair properly.
  4. Loss of cartilage = bone rubbing on bone.
  5. Reactive changes in bone, it is not designed to rub on bone.
34
Q

Describe features of the non-medical management for OA.

A
  • Education.
  • Exercise.
  • Weight loss.
  • Physiotherapy.
  • Occupational therapy.
  • Walking aids.
35
Q

Describe the pharmacological management for OA.

A

Step-wise use of analgesia to control symptoms:

1st line: topical NSAIDs

2nd line: oral paracetamol + topical NSAIDs
(consider adding a PPI to protect their stomach)

3rd line: short-term NSAIDs (+PPI) + paracetamol + topical capsaicin

4th line: weak opioid (e.g. dihydrocodeine), NSAIDs (+PPI) + paracetamol + topical capsaicin

  • Intra-articular corticosteroid injections
  • DMARDs if there is an inflammatory component
36
Q

Describe the surgical management for OA.

A
  1. Arthroscopy for loose bodies.
    - Scope inserted into joint to assess damage + remove loose
    bodies
  2. Osteotomy (cut bone to change bone length/shape).
  3. Arthroplasty (joint replacement - knee or hip).
  4. Arthrodesis - Fusion (usually ankle and foot - to prevent painful grinding of the bones).
37
Q

What is the indication for arthroscopy in OA?

A

Loose bodies e.g. bone or cartilage fragment that cause ‘knee lock’

38
Q

Give 3 indications for surgery - joint replacement in OA.

A
  1. Significant limitation of function.
  2. Uncontrolled pain (particularly at night).
  3. Waking at night from pain.
39
Q

What is the disadvantage of having a joint replacement and getting a prosthetic joint?

A

Prosthetic joint has lifespan of 10-15 years and will need
replacement.
In a young person, this could be as much as 3 times.

40
Q

What is the treatment for loose bodies?

A

Arthroscopy.

41
Q

What main features would you use to differentiate between rheumatoid arthritis and osteoarthritis
(inflammatory VS degenerative)?

A
  1. Pattern + distribution of joint involvement.
  2. Absence of systemic features of OA.
  3. RA has marked early morning stiffness lasting >60mins.