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CP3 MDD > Crystal Associated Arthritis > Flashcards

Crystal Associated Arthritis Flashcards

1
Q

Define gout?

A

Gout can be defined as arthritis due to deposition of monosodium urate (MSU) crystals within joints causing acute inflammation and eventual tissue damage

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2
Q

What are the risk factors for the development of gout?

A
  • General: Male (oestrogen lowers uric acid as it encourages renal excretion), Age, FH
  • Lifestyle: Diet (High purine**: offal, shellfish, red meat) Alcohol (beers and spirits), obesity, dehydration
  • Co-existing conditions: Renal disease, high blood pressure, cancer, psoriasis, myeloproliferative disorders,
  • Medication: Diuretic use, chemo and radiotherapy
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3
Q

What is the pathogenesis of an acute attack of gout?

A

Acute attacks of gout occurs when small crystals are shed and recognised by the immune system which causes a large inflammatory response.

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4
Q

What are the common target sites of gout?

A

1st Metatarsophalangeal joint (big toe)

Other common sites: 
Ankle & midfoot
Knee
Small joints of hands & wrist
Elbow

Large proximal joints are rarely affected

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5
Q

A small number of patients with primary gout have an underlying inherited enzyme defect of purine synthesis; when should you be suspicious of this?

A
  • Early onset Gout before 25 years of age
  • Uric acid renal caliculi
  • Strong FH of early onset gout
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6
Q

What is the difference between primary and secondary gout?

A

1y: Underexcretion or overproduction of uric acid
- e.g. diet, alcohol, DM
2y: medications or conditions that cause hyperuricemia, such as the following : Myeloproliferative, diuretic, CKD, lead poisining

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7
Q

What are the classical symptoms of an acute crystal synovitis (gout/pseudogout)?

A

Extremely painful joint. (usually a single joint)

Pain is at its worse within 1st 6hours.

Extremely tender (can’t put on a sock) and often described as worse pain ever.

Marked swelling and redness.

Self limiting over 5-14 days. pain comes on quiclly

+/- fever, malaise

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8
Q

What are the main differentials of an acute crystal synovitis?

A

RED HOT JOINT=

  • Gout
  • Psuedogout (acute calcium pyrophosphate crystal arthritis)
  • Cellulitis (potentially more systemic signs, pain not as severe and will be worsening)
  • Septic arthritis (patient will be systemically very unwell, pain will be worsening and will not be at its worse immediately) have a low threshold as this disease carries a high mortality.
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9
Q

What is pseudogout?

A

Also known as Ca Pyrophosposphate crystal arthritis.

It is caused by CPPD crystal deposition in hyaline and fibrocartilage of joints = chondrocalcinosis.

It triggers acute attacks of self limiting crystal synovitis.

It is also strongly associated with OA.

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10
Q

In which joints is pseudo gout most likely to affect?

A

Knee (most common)
Wrist
Pelvis (symphysis pubis)

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11
Q

Describe what is seen in chronic tophaceous gout?

A

Large irregular firm nodules form these are known as tophi.

They usually occur in the:

  • hands (extensor surfaces of the fingers)
  • forearm
  • elbow
  • achiles tendon
  • helix of the ear

Secondary gout may present with painful, sometimes discharging tophi without preceding acute attacks.

This is particularly seen in older, mainly female patients with nodal OA who develop tophi in and around their osteoarthritic finger joints as a consequence of chronic (> 1-2 years) diuretic therapy.

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12
Q

How should you investigate ACUTE crystal synovitis?

What extra investigations might you do if the patient was suffering with chronic gout/ further attacks?

A

Acutely:

Clinical diagnosis if Podagra (single distal toe)
If unsure of diagnosis:
- Aspirate joint > MCS and light microscopy
- FBC, U+E, Serum uric acid, CRP

Note: In acute crystal synovitis likely to have a neutrophillia and a raised CRP due to the acute phase response.

Chronic:

  • Look for cause Assessment of: GFR, BP, Glucose, FBC, ESR, urine dip
  • X-ray to look for any chronic damage
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13
Q

How should you treat an attack of gout and pseudogout?

A

PO NSAIDS 1st line (naproxen or diclofenac)

PO Colchicene if CI (use instead of NSAIDs in patients with renal, CCF, chemotherapy)

Steroids 3rd line if CI (PO, IM, intrarticular)

Rest, ice pack, early mobilisation +/- opiates

Address lifestyle risk factors: intense exercise, WL, smoking cessation, med review, drink less beer, avoid specific foods

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14
Q

Describe the role of rate lowering therapy in gout?

A

Urate crystals form when the rate level is above 360µmol.

Aim of therapy is to lower rate levels to below 200µmol as this will prevent crystal formation and dissolve crystals.

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15
Q

Which patients should be given rate lowering therapy?

A

Indications are:

  • Recurrent attacks of acute gout
  • Tophi
  • Evidence of bone or joint damage
  • Associated renal disease
  • Gout with greatly elevated serum uric acid levels
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16
Q

What are the two main urate lowering drug and what are the important prescribing points?

A

Allopurinol.

  • Titrate dose up (as can cause acute attack if too quick)
  • 100mg every 3-4 weeks
  • Check uric acid levels monthly
  • Starting dose 100-300mg max dose is 900mg.
  • Don’t prescribe during an acute attack. 4 weeks later
  • Colchicine/NSAIDs can also be prescribed concurrently to prevent acute attacks.

Other meds:

  • Probenecid
  • In patients that cannot take allopurinol (heart failure) an alternative is febuxostat.
17
Q

What is basic calcium phosphate deposition?

A

Ca phosphate crystals may deposit in tendons, cartilage and muscle.

Most commonly occurs in the supraspinatus tendon but can occur anywhere in the body other common sites are around the greater trochanter.

Causes calcific tendonitis

18
Q

Symptoms of basic calcium phosphate deposition?

A

Can often be asymptomatic but can cause pain and reduced range of motion.

Crystals may also break off and cause an inflammatory acromiol bursitis which is self limiting.

19
Q

What X-ray findings might you see in gout?

A

OA changes (loss of joint space, osteophytes, sclerosis and cysts)

Tophi

Gouty ‘erosions’ are a less common but more specific feature occurring as ‘punched-out’ defects with well-delineated borders and retained bone density.

20
Q

What X-ray findings might you see in CPPD?

A

Calcification of the cartilage (chondrocalcinosis)

Most commonly seen in the knee menisci. Rare in under 55’s.

21
Q

What X-ray findings might you see in basic calcium phosphate deposition?

A

Calcification of the effected tissue.

In acromiol bursitis associated with BCP may see a level of Ca crystals.

22
Q

What is the relationship between hyperuricaemia and gout?

A

The duration and magnitude of hyperuricaemia is directly correlated with the likelihood of developing gouty arthritis and developing uric acid kidney stones.

However, gout can occur in people with normal plasma urate levels and many people with hyperuricaemia never develop gout

23
Q

Describe some side effects of colchicine

A

Diarrhoea, rashes
Caution in the elderly or co-morbidities
Interacts with some medications

24
Q

How do these gout medications work:

  • Allopurinol
  • Probenecid
  • NSAIDs
A
  • Allopurinol prevents conversion of purines to uric acid (urecostatic)
  • Probenecid increases excretion of uric acid in the kidneys (uricosuric)
  • NSAIDS don’t help cure the attack just treat the symptoms
25
Q

What causes Calcium pyrophosphate crystal deposition?

A

Sporadic, Familial
Metabolic conditions:
- Hyperparthyroidism, hypophosphatasia, hypomagnesaemia, Wilsons disease, haematochromotosis

NB// more common in women!

26
Q

What can calcium pyrophosphate crystal deposition cause?

A 
Often asymptomatic
Causes chondrocalcinosis
Can cause acute self-limiting synovitis (pseudogout)
- hot, red tender joint
Can cause chronic arthritis (OA)
27
Q

How do you investigate and manage pseudogout

A

Joint aspirate > polarised light microscopy
(+vely biofringent rhomboid shaped crystals)

XR may show chondrocalcinosis

If present under 55 years then screen for genetic predisposition disorders

Treat the same as gout. responds well to joint aspiration

CP3 MDD (17 decks)

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