Osteoarthititis and crystal arthropathies Flashcards

1
Q

What is osteoarthiritis

A

Progressive, degenerative condition affecting joints due to gradual thinning of cartilage, loss of joint space and formation of bony spurs

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2
Q

What is the matrix of the cartilage formed by?

A

Chondrocytes which are embedded within it

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3
Q

What is the pathogenesis

A

Loss fo matrice, release of cytokines including IL-1,TNF and mixed metalloproteinases as well as prostaglandins by the chondrocytes

Formation of the cartilage surface and attempted repair with osteophyte formation then occurs

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4
Q

What are the classic symptoms?

A

Gradual onset ( moths-years)
Mechanical pain- i.e. pain worse on activity, worse end of the day, received by rest
Crepitus- grinding/cracking on movement
Stiffness (<30 mins),inactivity gelling
Bony swellings and deformities of joints
Can get effusions and soft tissue swelling (synovial thickening)
Can lead to loss of function and morbility

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5
Q

What is general varus

A

A cowboy leg appearance

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6
Q

What may be seen in the hands?

A

DIP,PIP and 1st CMC joints
Bony enlargements may be seen as DIPs (Heberdens nodes ) and PIPs (Bouchards nodes)
Squaring of the thumb

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7
Q

What can be seen in the knee?

A

osteophytes, effusion, crepitus and restrictions of movement
Genu varus and valgus deformities
Bakers cyst

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8
Q

What can be seen in the hip?

A

Restricted movement

the pain felt here may be radiating from the lower back

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9
Q

What can occur with osteophytes?

A

cervical-may impinge on nerve roots

lumbar-osteocytes can cause spinal stenosis if encroach on spinal canal

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10
Q

What are risk factors for OA

A

Age (40+)
Gender- F
Genes (e.g. nodal arthritis)
occupation 0 rep stain, heavy lifting
Previous injury/joint abnormality e.g. hypermobiility
Obesity
Other underlying conditions e.g. rheumatoid arthritis, gout, acromegaly

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11
Q

Why are history and examination so important

A

Exclude primary inflammatory arthiritis

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12
Q

What investigations are usually done?

A

Bloods- inflammatory markers usually normal

X-rays - typical changes inc joint narrowing, subchondral sclerosis, bony cysts and osteophytes

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13
Q

What are the primary joints affected in RA and OA

A

RA- MCP, PIP

OA-DIP, CMC

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14
Q

Heberden’s nodes are frequently present in RA T/F

A

F- they are absent . hebredens nodes are frequently present in OA

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15
Q

What are the joint characteristics of RA and OA

A

RA- sort, warm,tender

OA-Hard, bony

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16
Q

RA is worse after resting t/f

A

T

N.B. is present stiffness will be worse in OA after effort, may be described as evening stiffness

17
Q

Which arthritis has a positive rheumatoid factor, anti CCP antibody and elevated ESR and C reactive protein

A

RA

18
Q

What is the non-pharmacological management?

A
Education
Physiotherapy
WT loss
Footwear
Aids
19
Q

What is the pharmacological management?

A

Analgesia- paracetamol ect
NSAIDs
Pain modulators - amitriptyline ,gabapentin
Intraarticular steroids-only short term relief

20
Q

What could be done in terms of surgery?

A

Arthroscopic washout, loose body, soft tissue trimming

joint replacement

21
Q

What are the two main conditions of crystal arthopies

A

Gout

Pseudogout

22
Q

What is Gout?

A

Inflammatory arthiritis associated with Monosodium urate crystal deposition

most common inflammatory arthritis in men

23
Q

What is Pseudogout?

A

Calcium pyrophosphate sihydrate/CPPD

24
Q

What is hyperuricaemia?

A

serum uric acid >7mg/dL

The risk of developing gout is higher the higher the serum uric acid

25
Q

What is diagnosis of gout based on?

A

Diagnosis of gout is based on identification of crystals or classic radographical findings, not hyperuricemia alone

26
Q

When is the best time to check uric acid

A

2 weeks after the attack

27
Q

What is acute monoarticular gout

A
Rapid onset
red-hot joint
severe pain
Duration- up to 2 weeks
Site- 1st MTPJ>ankle>knee>upper limb joints>spine
28
Q

Ddx of gout

A

Septic arthritis
Trauma
Seronegative arthritis (e.g. psoriatic arthititis, Reiter’s- but need to ask regarding associated symptoms e.g. skin psoriasis, eye symptoms, urethritis

29
Q

Chronic polyarticular gout

A

Chronic joint inflammation
Usually after having recurrent acute attacks >10 years
often diuretic associated

30
Q

What is the gold standard for dignosing gout

A

joint aspirate
needle-shaped crystals
Negative birefringerence on polarised light microscopy

31
Q

Management of gout

A

NSAIDs if no contraindication or colchicine or corticosteroids (oral/IM/IA)

Other analgesia e.g. opiates, paracetamol

32
Q

What lifestyle modifications- can help with gout

A

Restrict red meat, offal, beans, shellfish
Reduce alcohol
lose weight
Fluids- 2L/day

33
Q

What could be included in prophylaxis of gout attacks?

A

Urate lowering therapy

  • Allopurinol/Febuxostat
  • start 2-4 weeks after acute attack
  • start low dose and titrate
  • aimf or target serum rate <0.30mmol/L
34
Q

What is Pseudogout and how is it diagnosed (also called CPPD)

A

using a microscope to see small calcium pyrophosphate crystals in joint fluid. They are rhomboid/envelope shaped and there is a weakly positive birefringence

35
Q

What is the treatment of pseudo gout?

A

NSAIDs
Colchicine
Steroids
Rehydration

36
Q

What is hydroxyapatite?

A

Hydroxyapatite crystal deposition in and around the joint. Females 50-60
Alizarin stain shows red clumps