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
2
Q
A
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
18
Q
What are fibrillations?
A
small ridges in the surface of the articular cartilage
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
20
Q
A
21
Q
A
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
23
Q
A
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
25
What condition can reduce the risk of OA?
**_Osteoporosis_** reduces the risk of OA
26
When does disability occur as a result of OA?
disability results when the knee and hip joints are affected
27
What are the typical clinical features associated with OA?
* joint **pain and stiffness**
* joint **gelling**
* joint **instability**
* **loss of function** as a result of ^^^
* **synovitis** can also occur
28
What is the pain usually like in OA?
How does this change as disease progresses?
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_**
29
What is joint stiffness often like in OA?
How is this different to in RA?
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
30
What is joint gelling?
stiffness and pain of the joint after a period of immobility
31
What is synovitis?
**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**
32
What can synovitis in OA lead to in the bone?
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_**
33
34
What movement of the limb is lost in osteoarthritis?
there is loss of **_abduction_** and **_internal rotation_**
35
What are the 4 signs of OA?
* **_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_**
36
What are the clinical signs suggestive of OA?
* joint **tenderness**
* **limited range of movement** of the joint
* **crepitus** on movement
* **bony swelling**
* **joint effusion** with varying levels of inflammation
* **muscle wasting**
37
What nodes may be seen in OA?
**_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)
38
What is meant by "squaring of the hand"?
What causes it?
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"**
39
How can OA be categorised by cause?
**_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
40
What are the major known factors that can predispose to osteoarthritis?
(secondary OA)
* **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
41
Which joints are implicated in nodal OA?
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)
42
What is important to note about PIP-predominant nodal OA?
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_**
43
Around what time does nodal OA commonly present?
It has a higher incidence in **_women_**
It tends to develop around the time of the **_menopause_**
It also has a **familial component**
44
Are both hands usually affected by nodal OA?
yes
it is usually **_bilateral_** with a typical pattern of polyarticular involvement of the hand joints
45
What does the onset of nodal OA present like?
What clinical test will be abnormal?
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
Over time, how does the pain and symptoms of nodal OA change?
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
What features are present on an X-ray of nodal OA?
* joint space narrowing
* nodes - these are essentially large osteophytes
48
What often co-exists with nodal OA?
How does this affect hand function?
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
What is polyarticular hand OA?
What is it associated with?
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
What 3 features are common to all types of hand OA?
* symptoms are episodic and may settle over time
* it is rarely disabling
* family history
51
What are the 2 different types of hip OA?
What % of Caucasians are affected?
* ***superior pole OA***
* ***medial cartilage loss***
affects 7-25% of all Caucasians and is less common in black Africans
52
What radiological features are seen in superior pole OA?
Who tends to be affected?
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
Where is the pain usually felt in superior pole OA?
pain is usually felt in the **_groin_**, typically **_on exercise_**
it may radiate to the **buttocks**, **anterior thigh**, **knee** and **lower leg**
54
What is a typical presentation of superior pole OA?
How does pain in the knees change as disease progresses?
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
What is involved in medial cartilage loss hip OA?
medial cartilage loss is usually **bilateral** and is **rapidly disabling**
it is usually seen in **_women_** and is associated with **_hand involvement_**
56
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?
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
What are other clinical features associated with hip OA?
* **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
What % of people over 75 have knee OA?
Who is more likely to get it?
**40%** of people aged over 75 have knee OA
it is more common in **_women_**
it is strongly associated with **_obesity_**
59
Does knee OA tend to be unilateral or bilateral?
What is it strongly associated with?
is usually **_bilateral_**
it is strongly associated with **_polyarticular osteoarthritis of the hand_** in **elderly women**
60
What part of the knee is most commonly affected in knee OA?
What deformity does this lead to?
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
What are the risk factors for developing knee OA?
* previous trauma
* meniscal tears
* cruciate ligament tears
62
What are the typical symptoms associated with knee OA?
* knee pain
* **pain on walking** - particularly when going **upstairs**
* **difficulty getting out of chairs**
63
What are the signs of knee OA?
* **antalgic gait**
* joint **tenderness**
* joint line **bony swelling**
* **crepitus** in the joint
* wasting of the quadriceps muscles
* **varus deformity**
* **fixed flexion deformities**
64
What is meant by antalgic gait?
Why does it develop?
gait that develops as a way to **_avoid pain whilst walking_**
the **stance phase is abnormally shortened** when compared to the swing phase
65
What is primary generalised OA often seen with?
What joints are affected?
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
Who tends to develop nodal generalised OA (NGOA)?
What could potentially cause it?
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
What is erosive OA?
Which joints tend to be affected?
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
How is the outcome of erosive OA different to nodal RA?
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
What is a key radiological feature of erosive OA?
there are marked **_subchondral cysts_** present on X-ray
70
What 2 deformities are looked for on X-ray in order to diagnose erosive OA?
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
72
What usually causes crystal associated OA?
What are alternative names?
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
Who is usually affected by chondrocalcinosis?
What are the usual symptoms?
chondrocalcinosis is usually **_asymptomatic_**
the frequency increases with **age**
it usually affects the **_knees_** and the **_wrists_**
74
How can chondrocalcinosis be seen on X-ray?
it produces **_patchy linear calcification_** on X-ray
75
What more severe condition can crystal-associated OA / chondrocalcinosis lead to?
it can cause a **_chronic arthropathy_** (pseudo-OA)
this usually occurs in ***elderly women*** with ***severe chondrocalcinosis***
arthropathy = chronic joint pain
76
What does pseudo-OA look like on X-ray?
* 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
What joints tend to be affected in pseudo-OA?
* predominantly affects the **_knees_**
* then the **_wrists_** and **_shoulders_**
* also the **elbows**, **ankles** and **hips**
78
What other type of arthritis is chondrocalcinosis associated with?
it is associated with **_pseudo-gout_**
this is an acute crystal-induced arthritis
79
What causes pseudo-gout?
**_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
Which joints / people are more commonly affected by pseudo-gout?
it is more common in **_elderly women_**
it usually affects the **_knee and wrists_**
81
What type of arthritis occurs if there are **_calcium apatite crystals_** in the joints?
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
What is the course of the disease like in OA?
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
What type of X-ray is usually used to investigate OA?
How does it correlate with symptoms?
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
What type of X-ray is needed to assess joint space narrowing?
Why is a good history from the patient needed?
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
What are typical signs to look for on an X-ray for OA?
* joint space narrowing
* subchondral cyst formation
* cortical thickening / sclerotic changes
* osteophyte formation
* trabeculations of bone
86
What blood tests are used to investigate OA?
Why might they be useful?
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
What is MRI used for in OA?
it is not widely used for investigating OA
it shows **_early_** **cartilage** and **subchondral bone changes**
88
When may arthroscopy be used to investigate OA?
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
What is the underlying principle for treating OA?
What should be focussed on?
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
What are the physical measures that can be taken to improve symptoms of OA?
* 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
What types of medications can be prescribed for symptomatic relief in OA?
**_analgesia_**
* patients should be prescribed **short courses** of **simple analgesics** before NSAIDs
* NSAIDs can be used intermittently
92
Why should caution be taken before giving NSAIDs to patients with OA?
What precautions are in place?
* 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
According to NICE guidelines, what are the non-surgical treatments for OA?
* 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
What treatments should NOT be given for OA?
* glucosamine
* chondroitin
* rubefacients
* acupuncture
* hyaluronic injections
95
What are the 3 different types of surgical treatments for OA?
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
When is joint replacement performed?
What are the benefits of this?
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
What are the contraindications for joint replacement?
* ongoing sepsis / leg ulcer
* peripheral vascular disease
98
What is involved in a total and partial hip replacement (arthroplasty)?
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
How long does it take to recover from a hip replacement?
What advice / treatment is given to the patient?
* 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
What are the 4 risks associated with hip replacement surgery?
* DVT
* infection
* altered leg length (although patient still has better function and less pain than before surgery)
* dislocation (risk of 2%)
101
What is done during hip replacement to avoid DVT?
What should the patient be told prior to surgery?
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
What is done to reduce the risk of infection prior to hip replacement surgery?
**_PROPHYLACTIC ANTIBIOTICS_**
the ones most commonly used are **cephalosporins**
e.g. cefazolin or cefuroxime
103
What is involved in a tibial osteotomy?
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
When is tibial osteotomy particularly useful?
What is the main drawback?
it is useful when there is a varus or valgus deformity
the recovery process is often longer and more difficult than knee replacement
105
What are the benefits and drawbacks of knee replacement?
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
