Osteoarthritis and Crystal Arthropathies Flashcards

(41 cards)

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
What is a gout diagnosis based on?
Identification of crystals or classic radiographic findings
26
Describe the clinical presentation of acute monoarticular gout
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
Differential diagnosis of gout?
Septic arthritis Trauma Seronegative arthritis, e.g: psoriatic, Reiter's), but these would have assoc. symptoms, like rash, eye symptoms and urethritis
28
Presentation of chronic polyarticular gout?
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
Ix for gout?
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
Gold standard Ix for gout?
JOINT ASPIRATE shows needle-shaped crystals with -ve birefringence on polarised light microscopy
31
Management of gout?
NSAIDs, if there is no contraindication; otherwise, Colchine or corticosteroids (oral/injection/IM) Other analgesia, e.g: opiates, paracetamol
32
Lifestyle modification with gout?
Restrict red meat, offal, beans, shellfish Reduce alcohol (3 alcohol free days/week and keep in limits) Lose weight Fluids
33
What are the indications that prophylaxis of gout is required?
>2 attacks, tophi, erosions on xray, renal stones
34
Guidelines for gout prophylaxis?
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
Occurrence of pseudogout?
More common in elderly and assoc. with osteoarthritis
36
Locations affected by Pseuodgout?
Affects FIBROCARTILAGE, e.g: knees, wrists, ankles
37
Diagnosis of pseudogout?
Rhomboid/envelope shaped crystals with weakly positive birefringence
38
Assoc. with calcium pyrophosphate disease?
Ageing Hyperparathyroidism Familial hypocalciuric hypercalcaemia Haemochromatosis Hypomagnesaemia Hypothyroidism Neuropathic joints Trauma Amyloidosis Gout
39
Treatment of pseudogout?
NSAIDs Colchine Steroids Rehydration
40
What is hydroxyapatite?
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
Diagnosis of hydroapatite?
Alizarin stain shows red clumps Crystals are NOT detected under light/polarised microscopy