Osteoarthritis and Crystal Arthropathies Flashcards

1
Q

What is osteoarthritis?

A

Most common form of arthritis; it is a progressive, NON-INFLAMMATORY degenerative condition affecting joints due to gradual thinning of cartilage, loss of joint space and formation of bony spurs (osteophytes)

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2
Q

Pathogenesis of osteoarthritis?

A

Loss of cartilage matrix and release of cytokines (inc. IL-1, TNF and mixed metalloproteinases), as well as PG release by chondrocytes

There is fibrillation of the cartilage surface and attempted repair, which results in over-stimulation of bone and OSTEOPHYTE formation

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3
Q

Characteristic symptoms of osteoarthritis?

A
  • Gradual onset (months-years)
  • Mechanical pain, i.e: pain worse on activity, worse end of the day, relieved by rest
  • Crepitus (grinding/creaking) on movement
  • Stiffness (< 30 mins), inactivity gelling
  • Bony swellings (hard, unlike in RA) and deformity of joints
  • Can get effusions and soft tissue swelling (synovial thickening)
  • Can lead to loss of function and mobility
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4
Q

Which joints are affected by osteoarthritis?

A

Any joint but most often the neck, lower back, hips, base of thumb, ends of fingers, knees and base of the big toe

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5
Q

Hand signs in osteoarthritis?

A

DIP, PIP and the 1st CMC joints are affected (DIP joints spared in rheumatoid)

Bony enlargement may be seen:
• Heberden’s nodes (DIPs)
• Bouchard’s nodes (PIPs)

Squaring of the thumb

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6
Q

Knee signs in osteoarthritis?

A

Osteophytes, effusions, crepitus and restriction of movement

Genu varus (knees out, legs in) and valgus (knees in, legs out) deformities

Baker’s cyst (swelling behind knee)

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7
Q

Hip signs in osteoarthritis?

A

Restriction of hip movements

Pain may be felt in groin or radiating to knee

Pain felt in hip may be radiating from the lower back

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8
Q

Spine signs in osteoarthritis?

A

Cervical pain and restriction of movement

Lumbar – osteophytes can cause spinal stenosis if encroach on spinal canal

Osteophytes may impinge on nerve roots

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9
Q

Risk factors for osteoarthritis?

A

Age (typically mid-late 40s)

Gender (more common in women, esp. in hands and knees)

Genetic factors, e.g: nodal osteoarthritis

Occupation with heavy lifting or repetitive strain

Previous injury/joint abnormality, e.g: hypermobility

Obesity

Other underlying conditions, e.g: RA, gout, acromegaly (cause pre-damage)

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10
Q

Ix for osteoarthritis?

A

Blood tests - inflammatory markers usually normal

X-ray

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11
Q

4 X-ray signs of osteoarthritis?

A

Joint space narrowing

Subchondral sclerosis (denser area of bone just under the cartilage in your joint)

Sub-chondral cysts (cortical bone fractures and synovial fluid leaks down)

Osteophytes (bone attempts to remodel but does do in a disorganised manner)

LOSS = Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts

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12
Q

Differentiating osteoarthritis from RA?

A

PICTURE 5

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13
Q

Non-pharmacological management of osteoarthritis?

A

Physiotherapy for muscle strengthening (advise exercise)

Weight loss

Footwear

Aids, e.g: walking sticks, jar openers

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14
Q

Pharmacological management of osteoarthritis?

A

Analgesia - paracetamol, compound/topical analgesia

NSAIDs may provide additional relief; must look at risk:benefit ratio

Pain modulators - tricyclics, e.g: amitriptyline, anti-convulsants, e.g: gapapentin

Intra-articular steroids only provide short-term relief

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15
Q

Uses of surgery in osteoarthritis?

A

Arthroscopic washout

Loose body

Soft tissue trimming

Joint replacement

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16
Q

2 main conditions under crystal arthropathies and the crystals assoc. with each?

A
  1. Gout (monosodium urate)

2. Pseudogout (calcium pyrophosphate dihydrate/CPPD)

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17
Q

Define gout?

A

Inflammatory arthritis associated with monosodium urate crystal deposition

18
Q

Occurrence of gout?

A

Most common inflammatory arthritis in men

Prevalence increases with age

19
Q

Pathogenesis of gout?

A

There are 2 sources of uric acid:
Internal - uric acid is a product of purine breakdown (these are converted to xanthines and then to uric acid)
External - alcohol, diet, etc

20
Q

Define hyperuricaemia?

A

Serum uric acid > 7mg/dL (0.42 mmol/L)

Risk of developing gout is related to the degreeof hyperuricaemia

21
Q

When does over-production of uric acid occur?

A

Genetic conditions, like Lesch-Nyhan and Von Gierke’s

High cell turnover as in:
• Cancer and chemotherapy
• Psoriasis
• Haemolytic pernicious anaemia
• Obesity 
• Sepsis
• Excessive exercise

Also, due to over-consumption of foods rick in purines, e.g: red meat, offal, shellfish, sardines, dried peas, legumes

22
Q

When does under-excretion of uric acid occur?

A

Renal insufficiency

Starvation and dehydration

Hypothyroidism

Hyperparathyrodism

Drugs (DIURETICS, levodopa, cyclosporin A, pyrazinamide)

Alcohol abuse

23
Q

Why does hyperuricaemia alone not confirm a diagnosis of gout?

A

Level of uric acid does not actually precipitate gout; rather, ACUTE CHANGES in the level of uric acid do (sometimes, serum urate is normal in an acute attack)

24
Q

When is the best time to measure serum urate?

A

2 weeks following an acute attack

25
Q

What is a gout diagnosis based on?

A

Identification of crystals or classic radiographic findings

26
Q

Describe the clinical presentation of acute monoarticular gout

A

Rapid onset (often overnight) of severe pain with a red, hot joint

It lasts only 1-2 WEEKS and then DISAPPEARS (if this does not happen, suspect something else)

Tends to affect:
1st MTP > ankle > knee > upper limb joints > spine

27
Q

Differential diagnosis of gout?

A

Septic arthritis

Trauma

Seronegative arthritis, e.g: psoriatic, Reiter’s), but these would have assoc. symptoms, like rash, eye symptoms and urethritis

28
Q

Presentation of chronic polyarticular gout?

A

Chronic joint inflammation, usually after having recurrent acute attacks for > 10 years; they may still have acute attacks

They develop TOPHI (swelling where uric acid crystals have been deposited)

It is often DIURETIC assoc. and there is a high serum uric acid

29
Q

Ix for gout?

A

Raised inflammatory markers

WCC MAY be raised

X-ray is NORMAL in an ACUTE attack; with CHRONIC/repeated attacks, it may show erosions, over-hanging osteophytes and joint destruction

30
Q

Gold standard Ix for gout?

A

JOINT ASPIRATE shows needle-shaped crystals with -ve birefringence on polarised light microscopy

31
Q

Management of gout?

A

NSAIDs, if there is no contraindication; otherwise, Colchine or corticosteroids (oral/injection/IM)

Other analgesia, e.g: opiates, paracetamol

32
Q

Lifestyle modification with gout?

A

Restrict red meat, offal, beans, shellfish

Reduce alcohol (3 alcohol free days/week and keep in limits)

Lose weight

Fluids

33
Q

What are the indications that prophylaxis of gout is required?

A

> 2 attacks, tophi, erosions on xray, renal stones

34
Q

Guidelines for gout prophylaxis?

A

Urate lowering therapy:
• Allopurinol/Febuxostat (start 2-4 weeks after an acute attack; start low and increase slowly while aiming for a target serum urate of <0.30 mmol/L)

35
Q

Occurrence of pseudogout?

A

More common in elderly and assoc. with osteoarthritis

36
Q

Locations affected by Pseuodgout?

A

Affects FIBROCARTILAGE, e.g: knees, wrists, ankles

37
Q

Diagnosis of pseudogout?

A

Rhomboid/envelope shaped crystals with weakly positive birefringence

38
Q

Assoc. with calcium pyrophosphate disease?

A

Ageing

Hyperparathyroidism

Familial hypocalciuric hypercalcaemia

Haemochromatosis

Hypomagnesaemia

Hypothyroidism

Neuropathic joints

Trauma

Amyloidosis

Gout

39
Q

Treatment of pseudogout?

A

NSAIDs

Colchine

Steroids

Rehydration

40
Q

What is hydroxyapatite?

A

Another type of crystal arthropathy, AKA Milwaukee shoulder; rare but tends to be females who are 50-60 years

Hydroxyapatite crystal deposition in/around the joint assoc. with rapid deterioration

41
Q

Diagnosis of hydroapatite?

A

Alizarin stain shows red clumps

Crystals are NOT detected under light/polarised microscopy