Osteoarthritis and Crystal Arthropathies Flashcards

1
Q

how common is osteoarthritis (OA)?

A

1/3 of people over 45
1/2 people over 70
8 million people in UK

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2
Q

what does OA do?

A

destruction of articular cartilage

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3
Q

how does OA appear on X ray?

A

decrease in joint space

usually a space is sees as cartilage doesn’t appear, when cartilage lost, bone are tight together

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4
Q

what causes OA?

A

wear and tear in the joints

partly a consequence of ageing but many other risk factors

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5
Q

OA risk factors?

A
age
female
obesity
previous injury (occupation, sports)
muscle weakness
proprioceptive deficits
genetic elements
acromegaly
joint inflammation
crystal deposition
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6
Q

4 components of cartilage?

A

water
chondrocytes
proteoglycan
collagen filaments

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7
Q

what can cause a solid, bony swelling in OA?

A

formation of osteophytes

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8
Q

what can cause secondary OA?

A

injury
calcium crystal deposition (pseudogout)
RA
etc

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9
Q

what jobs give increased OA risk/earlier presentation?

A

manual jobs (e.g farmers)

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10
Q

what joints does OA affect?

A

weight bearing joints

most commonly used joints (neck, thumb base)

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11
Q

does OA affect MCP joint?

A

generally no

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12
Q

OA vs RA sites?

A

RA can only affect C1 and C2

OA can affect whole spine

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13
Q

describe the clinical presentation of OA?

A

pain worse on activity and relieved by rest - can progress to become painful with little/no activity
morning stiffness lasting less than 30 mins
slow progression (years)

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14
Q

OA examination features?

A

crepitus (friction of bones)
joint swellings (osteophytes)
sometimes tenderness and effusion

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15
Q

clinical hand features of OA?

A

affects DIPs and CMC joint
not MCP
bony enlargements
squaring of hand

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16
Q

what are heberdens nodes?

A

bony enlargements at DIPs

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17
Q

what are bouchard’s nodes?

A

bony enlargements at PIPs

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18
Q

clinical knee features of OA?

A
osteophytes
effusions
crepitus
restricted movement
Genu varus/vlgus deformities
bakers cyst (in popliteal fossa)
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19
Q

clinical hip features of OA?

A

pain may be felt in groin or radiating to knee

restricted hip movement

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20
Q

clinical spine features of OA?

A
cervical = pain and restriction of movement
lumbar = pain on walking or standing
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21
Q

what causes spinal symptoms in OA?

A

destruction of IV discs

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22
Q

what is a possible complication of OA in the spine?

A

osteophytes can cause spinal stenosis if they encroach on spinal canal or pinch nerve root

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23
Q

how is OA diagnosed?

A

radiological - loss of joint space, subchondral sclerosis and cysts, osteophytes
clinical - mechanical pain, sites of pain, history etc

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24
Q

how is OA graded?

A

Kellgren-Lawrence
0 = no radiological findings
1 = minute osteophytes
2 = definite osteophytes with unimpaired joint space
3 = definite osteophytes with moderate joint space narrowing
4 = definite osteophytes with sever joint space narrowing and subchondral sclerosis

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25
Q

hands vs knees vs hips progression?

A

hands - pain often improves over 2 years
knees - 1/3 improves, 1/3 stays same, 1/3 gets worse
hip - 10% symptoms improve

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26
Q

non-pharmacological management of OA?

A

explanation - keep moving
physiotherapy
common sense - weight loss etc

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27
Q

pharmacological management of OA?

A

analgesia
NSAIDs - mainly gels
Pain modulators - anti-convulsants, tricyclics (amitriptyline)
Intra-articular - steroids (occasionally hyaluronic acid helps)

28
Q

definitive OA treatment?

A

surgical
joint replacement
washout and soft tissue trimming can also help

29
Q

what is gout?

A

inflammation in the joint triggered by uric acid crystals

30
Q

normal uric acid level?

A

0.42 mmol/l

above 0.42 it becomes insoluble and precipitates out (hyperuricaemia)

31
Q

common sites of gout?

A

big toe

fingers

32
Q

what can cause increased uric acid production?

A
enzyme defects
increased cell turnover disorders (leukaemia, lymphoma, psoriasis etc)
haemolytic disorders
alcohol link
high purine diet (red meat, seafood)
33
Q

causes of reduced urate excretion?

A
chronic renal impairment
volume depletion (heart failure)
hypothyroidism
diuretics
cytotoxics (cyclosporin)
34
Q

who is gout more common in?

A

men

doesn’t really occur in women before the menopause

35
Q

is gout mono, orli or poly arthropathic?

A

usually mono (one joint)

36
Q

how does gout arise and resolve?

A

arises overnight often

settles in 10 days without treatment or 3 days with treatment

37
Q

what does gout look like?

A

very sudden red swelling over a joint

38
Q

how does uric acid change during an acute attack?

A

can be normal

39
Q

chronic tophaceous gout?

A
chronic joint inflammation
often diuretic associated
high serum uric acid
tophi involved
may get acute attacks
40
Q

how is gout investigated?

A
blood test
- raised inflammatory markers
- serum uric acid raised (or normal if acute)
synovial fluid microscopy
renal impairment
X ray
41
Q

how is acute gout treated?

A

NSAIDs
colchicine
steroids

42
Q

how is chronic gout treated via prophylaxis?

A

allopurinol (must be with NSAIDs etc)

Febuxostat

43
Q

when is gout prophylaxis started?

A

2-4 weeks after acute attack

44
Q

what is deposited in pseudogout?

A

calcium pyrophosphate

45
Q

what happens in pseudogout?

A

fibrocartilage in knees, ankles and wrists affected

chondrocalcinosis

46
Q

what are the 2 types of calcium crystal deposition?

A
calcium pyrophosphate (CPP) crystals (pseudogout)
calcium hydroxyapatite crystals
47
Q

what age group is pseudogout common in?

A

elderly

48
Q

what do CPP crystals look like?

A

envelope shaped

49
Q

how is CPP treated?

A

NSAIDs
cochicine
steroids
rehydration

50
Q

what is hydroxyapatite?

A

“Milwaukee shoulder”
deposition of hydroxyapatite crystals
usually in 50-60 y/o females

51
Q

what happens in hydroxyapatite?

A

release of collagenases, serine proteases and IL1

acute and rapid deterioration

52
Q

how is hydroxyapatite treated?

A

NSAIDs
intra-articular steroid injection
physiotherapy
partial or total arhtroplasty

53
Q

what is soft tissue rheumatism?

A

General term to describe pain caused by inflammation to muscle, tendon, ligament, nerve etc near a joint rather than the joint itself

54
Q

how does pain appear in soft tissue rheumatism?

A

usually localised to a specific site

55
Q

what is a more generalised soft tissue pain suggestive of?

A

fibromyalgia

56
Q

what is the most common area for soft tissue pain?

A

shoulder

57
Q

what can cause soft tissue pain in the shoulder?

A
adhesive
capsulitis
rotator cuff tendinosis
calcific tendonitis
impingement
partial rotator cuff tears
full rotator cuff tears
58
Q

where else does soft tissue pain commonly occur?

A

elbow
wrist
pelvis
foot

59
Q

name some causes for soft tissue pain

A

carpal tunnel
bursitis
plantar fascitis

60
Q

how is soft tissue rheumatism treated?

A
pain control
rest
ice compress
PT
steroid injections
surgery
61
Q

how is soft tissue rheumatism investigated?

A

usually not needed

x ray can show calcific tendonitis

62
Q

how does joint hypermobility syndrome present?

A
arthralgia
premature osteoarthritis
normal investigations
can be general or local
more common in females and usually presents in childhood or 3rd decade
63
Q

what can cause joint hypermobility?

A

genetic syndromes

  • marfans
  • ehlers danlos syndrome
64
Q

how is joint hypermobility treated?

A

physiotherapy

explanation to the patient

65
Q

what is modified beighton score?

A

classification of hypermobility

if >4 of the 9 features = hypermobility

66
Q

what are the features of the modified beighton score?

A
  • > 10 degree hyperextension of the elbow
  • passively touch the forearm with the thumb
  • passive extension of the fingers or a 90 degree+ extension of the fifth finger
  • hyperextension of the knees >10 degrees
  • touching the floor with the palms of the hands without bending the knees