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Core Conditions - Locomotor > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is osteoarthritis?

A

it is a degenerative disease of synovial joints

it is characterised by progressive loss of articular cartilage leading to pain, deformity and loss of function

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2
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A
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3
Q

What are the radiological features, pathological changes and clinical consequences associated with OA?

A
  • pathologically, there is an alteration in cartilage structure
  • radiologically, there are osteophytes and joint space narrowing
  • clinically, patients complain of pain and disability
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4
Q

What % of people over 60 have features of OA?

How many are symptomatic?

A

80% of people >60 have some radiographic features

only 25% of these are symptomatic

radiologic signs are more common than symptoms in OA

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5
Q

What gender is more commonly affected by OA?

What age range?

A

it more commonly affects women ( M : F of 1 : 3 )

it rarely presents below the age of 55

it is the leading cause of disability in those aged over 55

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6
Q

What is the gene implicated in familial OA?

How is it identified?

A

genes that encode collagen type II are likely to be involved in familial OA

this is most commonly disease with interphalangeal joint involvement (nodal OA) and primary generalised OA

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7
Q

In what populations is OA more common?

A

it is less common in African and Asian populations than in Caucasians

this suggests that genetic factors are involved

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8
Q

What other factors can increase the chance of someone developing OA?

A
  • previous trauma of a joint increases risk of OA in that joint
  • obesity
  • hypermobility of joints
  • occupations involving manual labour / sports
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9
Q

What is the common pathological feature in OA?

What is involved in the spectrum of OA?

A

the common pathological feature is focal destruction of articular cartilage

the spectrum of OA ranges from atrophic disease in which cartilage destruction occurs without any subchondral bone response

to hypertrophic disease in which there is massive new bone formation at the joint margins

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10
Q

What is the structure of cartilage like?

A
  • it is 75% water
  • the rest is mainly type II collagen
  • as well as some chondrocytes, fibroblasts and proteoglycans
  • chondrocytes and fibroblasts are the only cells found in cartilage and are found throughout
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11
Q

How is the structure and function of cartilage maintained in a healthy individual?

A

cartilage is smooth and can absorb impact

it is constantly damaged in normal use, but this is then repaired by chondrocytes

the damage and repair process is balanced in normal health

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12
Q

What are the 5 stages involved in the pathophysiology of OA?

A
  • influx of water into the cartilage leads to oedema
  • articular (hyaline) cartilage softens and becomes more susceptible to microtrauma
  • fissuring occurs - tears in the surface
  • fragmentation and collapse
  • subchondral bone exposure with sclerosis, cysts and compensatory osteophytes
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13
Q

How does cartilage get nutrients?

Why can it not be painful?

A

cartilage has NO blood supply and NO nervous supply

nutrients diffuse into the cartilage from the synovial fluid, and from the nearest blood supply in the bone marrow

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14
Q

How can OA be painful when cartilage has no nervous supply?

A

the pain is mainly due to irritation of the bone surface after the cartilage has been worn away

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15
Q

What gives cartilage its ability to absorb impact?

What happens to the structure involved as the day progresses?

A

the structure of collagen means that water molecules are held in place by electrostatic forces between sidechains of the collagen

this gives cartilage its ability to absorb impact

throughout the day, colalgen becomes dehydrated and we lose height due to intervertebral discs becoming thinner

the collagen rehydrates at night when we are laid flat

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16
Q

How is the balance between damage and repair of collagen lost in OA?

Is cartilage still formed initially?

A

there is chondrocyte proliferation and excess cartilage is produced, but it is oedematous

this leads to focal erosions forming

there is rapid destruction of cartilage, for which the chondrocytes cannot compensate for

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17
Q

Later on in the progression of OA what happens to chondrocytes?

What is the result of this on the surface of the cartilage?

A

the chondrocytes die through apoptosis

adjacent areas of cartilage try to take over the role of repair, but this is inadequate

eventually, the synthesis of new matrix stops completely and the surface of the cartilage becomes fistulated and fibrillated

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18
Q

What are fibrillations?

A

small ridges in the surface of the articular cartilage

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19
Q

How does osteoarthritis progress after the surface of the cartilage has become fistulated and fibrillated?

A

the bone has lost its protection so is exposed to extra stressors

the two bones of a joint may rub directly against each other

there may be microfractures in the surface or cyst formation

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20
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A
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21
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22
Q

How are osteophytes formed?

A

the damaged bone attempts to repair itself but it produces abnormal sclerotic subchondral bone

and overgrowths at the joint margins, which are osteophytes

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23
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A
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24
Q

What is meant by subchondral sclerosis?

A

hardening of the bone just below the cartilage surface

this occurs as the hard bone is less likely to fracture

this is identified on X-rays by very white edges to the bone

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25
Q

What condition can reduce the risk of OA?

A

Osteoporosis reduces the risk of OA

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26
Q

When does disability occur as a result of OA?

A

disability results when the knee and hip joints are affected

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27
Q

What are the typical clinical features associated with OA?

A
  • joint pain and stiffness
  • joint gelling
  • joint instability
  • loss of function as a result of ^^^
  • synovitis can also occur
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28
Q

What is the pain usually like in OA?

How does this change as disease progresses?

A

initially, the pain is intermittent and often described as an ache

pain is usually provoked by movement of the affected joint and relieved by resting the joint

in later disease, there may also be pain at rest

pain can be severe enough to wake the patient at night

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29
Q

What is joint stiffness often like in OA?

How is this different to in RA?

A

stiffness is worse after long periods of inactivity - e.g. first thing in the morning

stiffness typically only lasts for a few minutes, opposed to in RA where there are long periods of morning stiffness

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30
Q

What is joint gelling?

A

stiffness and pain of the joint after a period of immobility

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31
Q

What is synovitis?

A

inflammation of the synovial membrane

this is the membrane that forms the border of the joint capsule

as the volume of synovial fluid increases, it can cause joint swelling

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32
Q

What can synovitis in OA lead to in the bone?

A

if synovitis occurs due to inflammation, synovial fluid may not be able to escape the joint capsule so may enter the bone and cause a cyst

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33
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A
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34
Q

What movement of the limb is lost in osteoarthritis?

A

there is loss of abduction and internal rotation

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35
Q

What are the 4 signs of OA?

A
  • loss of joint space
    • this is due to loss of cartilage, which is not visible on X-ray
  • osteophyte formation
  • cysts in the bone
    • ​as a result of synovitis
  • subchondral sclerosis
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36
Q

What are the clinical signs suggestive of OA?

A
  • joint tenderness
  • limited range of movement of the joint
  • crepitus on movement
  • bony swelling
  • joint effusion with varying levels of inflammation
  • muscle wasting
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37
Q

What nodes may be seen in OA?

A

Heberden’s nodes:

  • seen at the distal interphalangeal joints of the hands (DIP)
  • remember as “outer hebrides”

Bouchard’s nodes:

  • seen at the proximal interphalangeal joints (PIP)
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38
Q

What is meant by “squaring of the hand”?

What causes it?

A

a deformity of the carpometacarpal joint of the thumb, leading to fixed adduction of the thumb

the CMC joint appears more prominent and makes the base of the hand look “squared”

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39
Q

How can OA be categorised by cause?

A

PRIMARY OSTEOARTHRITIS:

  • idiopathic with no underlying cause / predisposing factor
  • genetic factors likely to be involved

SECONDARY OSTEOARTHRITIS:

  • likely to be the result of another underlying disease process or event
    • e.g. trauma
    • acromegaly
    • gout
    • occupation / sports
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40
Q

What are the major known factors that can predispose to osteoarthritis?

(secondary OA)

A
  • obesity
  • hypermobility
    • increased range of joint motion & instability leads to OA
  • trauma
    • a fracture through any joint can predispose to OA
  • congenital joint dysplasia
    • alters joint biomechanics and can lead to OA
  • joint congruity
    • congenital dislocation of the hip or osteonecrosis of the femoral head in children leads to early onset OA
  • occupation
    • e.g. farmers develop OA of the hip, knee and shoulder
  • sports
    • repetitive use and injury in some sports causes high incidence of lower limb OA
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41
Q

Which joints are implicated in nodal OA?

A

this invoves the joints of the hands

they are usually affected one at a time over several years

the distal interphalangeal joints (DIPs) are affected more often than the proximal interphalangeal joints (PIPs)

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42
Q

What is important to note about PIP-predominant nodal OA?

A

if the PIPs are affected, it may mimic early rheumatoid arthritis

The patient may even be weakly positive for rheumatoid factor, but this is NOT diagnostic and is of no significance

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43
Q

Around what time does nodal OA commonly present?

A

It has a higher incidence in women

It tends to develop around the time of the menopause

It also has a familial component

44
Q

Are both hands usually affected by nodal OA?

A

yes

it is usually bilateral with a typical pattern of polyarticular involvement of the hand joints

45
Q

What does the onset of nodal OA present like?

What clinical test will be abnormal?

A

the onset is often painful

it is associated with tenderness, swelling, inflammation and impairment of hand function

despite there being inflammation, CRP and ESR are usually normal !!!

46
Q

Over time, how does the pain and symptoms of nodal OA change?

A

the inflammatory phase settles over some months or years, leaving stiffness and deformity

deformity is usually in the form of painless bony nodules (Bouchard’s and Heberden’s nodes) as a result of osteophyte formation

functionally, patients do not tend to have any problems, but there may be reduced grip strength if there is severe involvement of the DIPs

47
Q

What features are present on an X-ray of nodal OA?

A
  • joint space narrowing
  • nodes - these are essentially large osteophytes
48
Q

What often co-exists with nodal OA?

How does this affect hand function?

A

OA of the carpometocarpal and metocarpalphalangeal joints co-exists with nodal OA

it is often painful at first, but pain declines over time as the joint stiffens

may cause a “squared hand” due to fixed adduction of the thumb

49
Q

What is polyarticular hand OA?

What is it associated with?

A

polyarticular OA is joint pain / arthritis that affects 5 or more joints simultaneously

polyarticular hand OA is associated with an increased risk of OA at other sites

(mainly the knee, hip and spine)

50
Q

What 3 features are common to all types of hand OA?

A
  • symptoms are episodic and may settle over time
  • it is rarely disabling
  • family history
51
Q

What are the 2 different types of hip OA?

What % of Caucasians are affected?

A
  • superior pole OA
  • medial cartilage loss

affects 7-25% of all Caucasians and is less common in black Africans

52
Q

What radiological features are seen in superior pole OA?

Who tends to be affected?

A

there is joint space narrowing and sclerosis that is predominantly affecting the weight-bearing upper surface of the femoral head and adjacent acetabulum

it is more common in men and tends to be unilateral at presentation

it can spread to become bilateral as the disease is progressive

53
Q

Where is the pain usually felt in superior pole OA?

A

pain is usually felt in the groin, typically on exercise

it may radiate to the buttocks, anterior thigh, knee and lower leg

54
Q

What is a typical presentation of superior pole OA?

How does pain in the knees change as disease progresses?

A

the patient is unable to reach down to tie their shoelaces / put on their socks

pain in the knee becomes more common as the disease progresses

pain can also disturb sleep in later disease

55
Q

What is involved in medial cartilage loss hip OA?

A

medial cartilage loss is usually bilateral and is rapidly disabling

it is usually seen in women and is associated with hand involvement

56
Q

How does pain change with disease progression in hip OA?

What feature is rare in this form of OA that is often seen in other forms?

A

in early disease, there is pain on internal rotation

in late disease, there is pain on external rotation

TENDERNESS is rare in hip OA

57
Q

What are other clinical features associated with hip OA?

A
  • limb shortening
  • quadriceps and gluteal wasting and weakness
  • reduced range of movement in all directions
    • rotation movements are usually the most painful
  • fixed flexion deformity
58
Q

What % of people over 75 have knee OA?

Who is more likely to get it?

A

40% of people aged over 75 have knee OA

it is more common in women

it is strongly associated with obesity

59
Q

Does knee OA tend to be unilateral or bilateral?

What is it strongly associated with?

A

is usually bilateral

it is strongly associated with polyarticular osteoarthritis of the hand in elderly women

60
Q

What part of the knee is most commonly affected in knee OA?

What deformity does this lead to?

A

the medial compartment is most commonly affected

this leads to a varus deformity

this is excessive inward angulation of the distal part of a bone or joint

in the case of the knee, it produces a bow-legged appearance

61
Q

What are the risk factors for developing knee OA?

A
  • previous trauma
  • meniscal tears
  • cruciate ligament tears
62
Q

What are the typical symptoms associated with knee OA?

A
  • knee pain
  • pain on walking - particularly when going upstairs
  • difficulty getting out of chairs
63
Q

What are the signs of knee OA?

A
  • antalgic gait
  • joint tenderness
  • joint line bony swelling
  • crepitus in the joint
  • wasting of the quadriceps muscles
  • varus deformity
  • fixed flexion deformities
64
Q

What is meant by antalgic gait?

Why does it develop?

A

gait that develops as a way to avoid pain whilst walking

the stance phase is abnormally shortened when compared to the swing phase

65
Q

What is primary generalised OA often seen with?

What joints are affected?

A

it is less common than nodal OA but is usually seen in combination

sometimes called “nodal generalised OA”

the other joints affected are:

  • first MTP
  • hip
  • knee
  • intervertebral joints (spondylosis)
66
Q

Who tends to develop nodal generalised OA (NGOA)?

What could potentially cause it?

A

it is much more common in women and has a strong familial association

it is associated with immune complex deposition, so may have an autoimmune cause

onset is sudden and severe

67
Q

What is erosive OA?

Which joints tend to be affected?

A

erosive OA is rare and affects the distal interphalangeal joints (DIPs) and proximal interphalangeal joints (PIPs)

the DIPs and PIPs are inflamed and are equally affected

it is an inflammatory form of OA that is associated with abrupt onset of pain

68
Q

How is the outcome of erosive OA different to nodal RA?

A

unlike nodal OA, the functional outcome of erosive OA is poor

it can develop into RA, so may not be a true subset of OA

69
Q

What is a key radiological feature of erosive OA?

A

there are marked subchondral cysts present on X-ray

70
Q

What 2 deformities are looked for on X-ray in order to diagnose erosive OA?

A

erosive OA is defined as the presence of central erosions (gull wing or saw tooth) in at least 2 interphalangeal joints (1 must be a DIP)

these central erosions can either be gull wing deformity or a saw tooth appearance

71
Q
A
72
Q

What usually causes crystal associated OA?

What are alternative names?

A

also known as crystal arthropathy or crystal arthritis

it is usually the result of calcium pyrophosphate deposition in the cartilage

this is known as chondrocalcinosis

the deposits cause irritation that leads to inflammation and cartilage damage

73
Q

Who is usually affected by chondrocalcinosis?

What are the usual symptoms?

A

chondrocalcinosis is usually asymptomatic

the frequency increases with age

it usually affects the knees and the wrists

74
Q

How can chondrocalcinosis be seen on X-ray?

A

it produces patchy linear calcification on X-ray

75
Q

What more severe condition can crystal-associated OA / chondrocalcinosis lead to?

A

it can cause a chronic arthropathy (pseudo-OA)

this usually occurs in elderly women with severe chondrocalcinosis

arthropathy = chronic joint pain

76
Q

What does pseudo-OA look like on X-ray?

A
  • there is a florid inflammatory component
  • marked cyst formation on X-ray
  • marked osteophyte formation on X-ray
  • calcification of the cartilage is visible
77
Q

What joints tend to be affected in pseudo-OA?

A
  • predominantly affects the knees
  • then the wrists and shoulders
  • also the elbows, ankles and hips
78
Q

What other type of arthritis is chondrocalcinosis associated with?

A

it is associated with pseudo-gout

this is an acute crystal-induced arthritis

79
Q

What causes pseudo-gout?

A

calcium pyrophosphate deposits in hyaline and fibrocartilage produce the radiological appearance of chondrocalcinosis

shedding of crystals into a joint precipitates acute synovitis, which resembles gout

there is inflammation and pain in the joint

80
Q

Which joints / people are more commonly affected by pseudo-gout?

A

it is more common in elderly women

it usually affects the knee and wrists

81
Q

What type of arthritis occurs if there are calcium apatite crystals in the joints?

A

a rare and rapidly destructive arthritis in elderly women

it affects the shoulders, hips and knees

it is associated with finding calcium apatite crystals in a bloody joint effusion

82
Q

What is the course of the disease like in OA?

A

it begins with joint pain and stiffness, which progresses to joint destruction and then the need for joint replacement

it typically progresses slowly

even with early intervention, up to 65% of patients will show deterioration 15 years after diagnosis

83
Q

What type of X-ray is usually used to investigate OA?

How does it correlate with symptoms?

A

X-rays are usually AP

signs are often visible on X-ray before the symptoms of pain and stiffness develop

correlation between radiographic features and symptoms is usually poor

84
Q

What type of X-ray is needed to assess joint space narrowing?

Why is a good history from the patient needed?

A

a weight-bearing X-ray is needed to assess joint space narrowing

X-rays are not very useful to distinguish between different types of arthritis if the history is inconclusive

85
Q

What are typical signs to look for on an X-ray for OA?

A
  • joint space narrowing
  • subchondral cyst formation
  • cortical thickening / sclerotic changes
  • osteophyte formation
  • trabeculations of bone
86
Q

What blood tests are used to investigate OA?

Why might they be useful?

A

there aren’t any useful blood tests in OA

!!! ESR and CRP will be NEGATIVE !!!

rheumatoid factor & antinuclear antibodies are usually also negative

(if they are positive, this is unhelpful)

87
Q

What is MRI used for in OA?

A

it is not widely used for investigating OA

it shows early cartilage and subchondral bone changes

88
Q

When may arthroscopy be used to investigate OA?

A

this involves an endoscope that is inserted into the joint through a small incision

this reveals early changes in the cartilage, such as fissuring and surface erosion

89
Q

What is the underlying principle for treating OA?

What should be focussed on?

A

treat the symptoms and disability, not the radiological findings

depression and poor quadriceps strength are better predictors of pain than radiological severity

educating the patient about disease mechanisms and prognosis can improve treatment compliance and reduce pain / distress

90
Q

What are the physical measures that can be taken to improve symptoms of OA?

A
  • weight loss
  • physiotherapy exercises to improve strength and stability
    • e.g. improving quadriceps strength helps knee stability
  • hydrotherapy is useful in lower limb OA
  • local heat or ice packs and massages can help
91
Q

What types of medications can be prescribed for symptomatic relief in OA?

A

analgesia

  • patients should be prescribed short courses of simple analgesics before NSAIDs
  • NSAIDs can be used intermittently
92
Q

Why should caution be taken before giving NSAIDs to patients with OA?

What precautions are in place?

A
  • NSAIDs have been associated with avascular necrosis & destructive arthropathy
  • to reduce the risk of gastritis, they should be prescribed along with some sort of gastro protection, such as Omeprazole
  • or a selective COX2 NSAID should be used
  • be wary of NSAIDs in patients with cardiovascular risk factors (a lot of patients in this age range)
93
Q

According to NICE guidelines, what are the non-surgical treatments for OA?

A
  • start with education, physical activity & weight loss
  • add adjuncts such as local heat, cold, manipulation, stretching & TENS machine
  • consider braces, orthotics and assisted devices (e.g. walking sticks)
  • add analgesia - first paracetamol, then topical NSAID, then oral NSAID
  • topical capsaicin for hand and knee OA
  • consider intra-articular corticosteroids
94
Q

What treatments should NOT be given for OA?

A
  • glucosamine
  • chondroitin
  • rubefacients
  • acupuncture
  • hyaluronic injections
95
Q

What are the 3 different types of surgical treatments for OA?

A

for OA of every joint…

Arthroscopy:

  • minimally invasive procedure where an arthroscope is inserted into the joint through a small incision

Arthrodesis:

  • artificial induction of joint ossification (“joint fusion surgery”)
  • it welds together the 2 bones that make up the aching joint, so it becomes one solid bone, which lessens the pain

Arthroplasty:

  • surgical procedure involving joint replacement
96
Q

When is joint replacement performed?

What are the benefits of this?

A

it is used to replace hip and knee joints

the risk of complications for both is 1%

for the vast majority of patients pain is greatly reduced and function is greatly increased

97
Q

What are the contraindications for joint replacement?

A
  • ongoing sepsis / leg ulcer
  • peripheral vascular disease
98
Q

What is involved in a total and partial hip replacement (arthroplasty)?

A

it is usually a metal “ball” in a plastic “socket” to reduce the friction coefficient

partial hip replacement means that the acetabulum is left in place and only the head of the femur is removed

99
Q

How long does it take to recover from a hip replacement?

What advice / treatment is given to the patient?

A
  • average recovery time is 6 to 7 months
  • the patient should be mobilised ASAP as that prevents long-term stiffness and aids a full range of movement
  • recovery can be painful, but this can be controlled with medication
  • there should be little pain after recovery
100
Q

What are the 4 risks associated with hip replacement surgery?

A
  • DVT
  • infection
  • altered leg length (although patient still has better function and less pain than before surgery)
  • dislocation (risk of 2%)
101
Q

What is done during hip replacement to avoid DVT?

What should the patient be told prior to surgery?

A

risk of DVT minimised with stockings & pumps to aid blood flow

the patient must be informed that there is a risk of death

this should be balanced by describing what will be done to reduce this risk

total risk of death is 1% and risk of death from DVT is < 0.1%

102
Q

What is done to reduce the risk of infection prior to hip replacement surgery?

A

PROPHYLACTIC ANTIBIOTICS

the ones most commonly used are cephalosporins

e.g. cefazolin or cefuroxime

103
Q

What is involved in a tibial osteotomy?

A

an alternative to knee replacement in younger and more physically active patients

the bones are cut, shaped and re-aligned to improve function of the joint

this can prolong the need for knee replacement by up to 10 years

104
Q

When is tibial osteotomy particularly useful?

What is the main drawback?

A

it is useful when there is a varus or valgus deformity

the recovery process is often longer and more difficult than knee replacement

105
Q

What are the benefits and drawbacks of knee replacement?

A

full recovery is usually seen in about 4 months

there is lots of pain relief, however the range of movement may not be improved

106
Q
A

Core Conditions - Locomotor (5 decks)

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