Arthropathies Flashcards

1
Q

What is OA?

A

degenerative disorder of joints

imbalance between wear and repair of cartilage

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2
Q

What predisposes you to developing OA?

A

obesity
age
mechanical injury
high impact sport

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3
Q

How does OA present?

A

joint pain

short lived morning stiffness

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4
Q

What joints does OA effect?

A

DIP, PIP, hip, knee

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5
Q

What is found on examination in OA?

A

effusion, tender joint, crepitations, bony enlargement
Baker’s cyst - behind knee
Heberden’s nodes - bony enlargement of DIP joints

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6
Q

What is seen on xray in OA?

A
LOSS
loss of joint space 
osteophytes 
sclerosis 
subchondral cysts
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7
Q

How is OA managed?

A

weight loss
physio
analgesia:
- paracetamol, topical NSAIDs (hands, knee)
- oral NSAIDs or COX2 inhibitors, opioids, capsaicin cream, IA steroids
- duloxetine
?joint replacement

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8
Q

What is RA?

A

autoimmune inflammatory symmetrical polyarthropathy

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9
Q

What predisposes you to developing RA?

A

female
smoker
genetics (HLA DR1/4)

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10
Q

How does RA present?

A

joint pain and swelling
morning stiffness
deformity

extra articular manifestations:
lungs - pulmonary fibrosis
eyes - keratoconjunctivitis sittica, episcleritis, uveitis
anaemia

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11
Q

What joints does RA effect?

A

small joints of hands and feet
cervical spine

DIP not affected

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12
Q

What can cervical spine RA cause?

A

cord compression - atlantoaxial subluxation

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13
Q

What is found on examination in RA?

A

synovitis
deformity
swelling
tenderness

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14
Q

How is RA diagnosed?

A

raised CRP
xray - osteopenia, soft tissue swelling
USS - synovitis
autoantibodies - anti CCP, rheumatoid factor

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15
Q

How is RA managed?

A

simple analgesia, NSAIDs, steroids used in combination
aim to start DMARDS within 3 months of symptoms
- methotrexate (first line)
- sulfasalazine
- hydroxychloroquine
- leflunomide

flares - steroids

if inadequate response to at least 2 DMARDs (including methotrexate)
- anti TNF (etanercept, infliximab)

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16
Q

What are the side effects of methotrexate?

A

pneumonitis
liver cirrhosis/ LF derangement
myelosuppression

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17
Q

What can happen with anti TNF use?

A

reactivation of TB

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18
Q

What is ankylosing spondylitis?

A

chronic inflammatory disease of the spine and the sacro-iliac joints

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19
Q

What can ank spon lead to?

A

fusion of the IV and SI joints

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20
Q

What is associated with ank spon?

A

HLA B27

21
Q

How does ank spon present?

A

spinal pain
morning stiffness
worse at night, improves with exercise
loss of spinal movement over time

22
Q

What extra articular manifestations of ank spon are there?

A

anterior uveitis
pulmonary fibrosis
aortitis
amyloidosis

23
Q

What is a question mark spine in ank spon?

A

loss of lumbar lordosis

24
Q

How is ank spon diagnosed?

A
Schober's test <5cm (lumbar spine flexion) 
increased inflammatory markers 
HLA B27 positive 
xray 
MRI
25
Q

What is seen on xray and MRI in ank spon?

A

xray - sclerosis, fusion, sacroiliitis, bamboo spine

MRI - early features (e.g. bone marrow oedema)

26
Q

How is ank spon managed?

A

physio
exercise
NSAIDs e.g. naproxen (prescribe PPI alongside)
Anti-TNF - for aggressive disease

27
Q

What kind of arthritis do you get with psoriasis?

A

psoriatic

asymmetrical oligoarthritis

28
Q

What nail changes do you get in psoriatic arthritis?

A

pitting

onchylysis

29
Q

What do you see on xray in psoriatic arthritis?

A

pencil in cup

erosive changes

30
Q

What do you get in psoriatic arthritis that you don’t in RA?

A

dactylitis (swelling of entire digit)

31
Q

How is psoriatic arthritis managed?

A

like RA

32
Q

What antibodies are positive in RA?

A

anti CCP

33
Q

What is enteropathic arthritis?

A

affects peripheral joints and spine in people with IBD

34
Q

How does enteropathic arthritis present?

A

symptoms of IBD, history of IBD

large joint arthritis

35
Q

What organisms can cause reactive arthritis?

A

salmonella, campylobacter

chlamydia, neisseria gon.

36
Q

What is Reiter’s syndrome?

A

urethritis
uveitis
arthritis

37
Q

What causes gout?

A

deposition of urate crystals within a joint - usually due to increased serum uric acid levels

38
Q

What is uric acid?

A

final product of purine breakdown (DNA metabolism)

39
Q

What can trigger gout?

A

trauma
surgery
dehydration

40
Q

What causes hyperuricaemia?

A

renal underexcretion (precipitated by diuretics)

high red meat, alcohol, seafood diet

41
Q

How does gout present?

A

intensely painful, hot, swollen joint
unilateral
1st MTPj, ankle, knee
gouty tophi

42
Q

What are gouty tophi?

A

painless white accumulations of uric acid in chronic gout

43
Q

How is gout diagnosed?

A

increased inflammatory markers
joint aspirate
- polarised microscopy - needle shaped crystals, negative birefringence

44
Q

How is gout managed?

A

acute: NSAIDS, colchicine (when NSAIDs are contraindicated)
chronic: allopurinol (what until acute flare is over as can precipitate), lifestyle changes

45
Q

What is pseudogout?

A

calcium pyrophosphate crystals deposited in joint

46
Q

How is pseudogout diagnosed?

A

joint aspiration - polarised microscopy

  • weakly positive birefringence
  • rhomboid shaped crystals
47
Q

How is pseudogout treated?

A

NSAIDs, corticosteroids

48
Q

What are the side effects of hydroxychloroquine and what should you monitor?

A

monitor visual acuity

can cause retinopathy and corneal deposits

49
Q

What helps to distinguish gout from pseudogout?

A

pseudogout - chondrocalcinosis