The Crystal Arthropathies II Flashcards

1
Q
A
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2
Q

Explain if presence of hyperuricemia is diagnostic? [1]

What level of uric acid found would indicate treatment is immediately needed? [1]

A

No: because 5-8% of population have elevated serum uric acid levels (>7mg/dL (0.07mg/ml))

If higher than 11mg/dL (0.11mg/ml) should be treated

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3
Q

What will a doppler ultrasound show in a gout patient? [5]

A

Doppler ultrasound
* soft tissue swelling
* increased blood flow
* vasodilation
* maintenance of joint space
* erosion outside the joint capsule

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4
Q

How would you treat acute gout / gout attack? [4]

A

NSAIDs:
* Start with highest dose for 2-3 days & taper down over 2 weeks

Colchicine:
* 2nd line (narrow therapeutic window and risk of toxicity)

Corticosteroids
* For those that can’t use NSAID or colchicine

IL1 biologicals
* Rilonacept, canakinumab, anakinra
* Reduces length of attack and reoccurrences
* Used for patients who have severe and frequent flares

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5
Q

How long should gout symptoms be absent for before stopping NSAID treatment for gout? [1]

A

2 days

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6
Q

Which IL1 biologicals can be used to treat acute gout? [3]

A

Rilonacept, canakinumab, anakinra

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7
Q

What type of diet is recommended for gout patients? [2]

A

Low purine diet AND diet high in vitamin C

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8
Q

Will doppler ultrasound imaging show damage in first gout attack? [1]

A

In the first attack however, you will not see any damage: Recurrent attacks is when damage starts to show

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9
Q

What x-ray findings are present in gout patients? [1]

A

Rat-bite erosions form on the main shaft of the bone where tendons are inserting/joint capsule is inserting

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10
Q

Describe a new technique for visualising gout [1]

A

Dual energy computed tomography (DECT): able to detect the uric acid crystals deposited in the joint & soft tissue

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11
Q

Describe the pathogenesis of rat-bite erosions

A

rat-bite erosions are due to osteoclasts eroding the bone in joints with gout

TNF-alpha, IL-1, etc will convert synovial macrophages to osteoclasts

The crystals tend to get lodged in the deeper folds of the joint capsule, meaning the osteoclasts will attack the shaft of the bone

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12
Q

Why are IL-1 biologicals not as useful for treating gout than RA? [1]

A

have to be used daily, yet with gout flares they are only used acutely for short periods of time. Only used if a patient has severe and frequent flare due to their extreme cost.

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13
Q

What is the treatment aim for chronic gout? [1]

A

A to lower the uric acid levels to get below the saturation point, preventing fluctuations in the serum

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14
Q

Describe how you treat chronic gout [5]

A

Allopurinol:
* Blocks xanthine oxidase, which is responsible from converting xanthine (which comes from purines in the diet) to urate

Febuxostat:
* non-purine selective inhibitor of xanthine oxidase

uricosuric:
* increases uric acid excretion

Probenecid:
* increases the secretion of uric acid
* fewer side effects than allopurinol.

Rasburicase:
* Catalyses conversion of uric acid to allantoin

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15
Q

Which ARB can be used to treat chronic gout? [1]

A

Losartan

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16
Q

Describe the pathogenesis of pseudogout [2]

A

Deposition of calcium pyrophosphate in and around joints onto the surface of the articular cartilage and the fibrocartilage:

  • Release of calcium pyrophosphate crystals into the joint space
  • followed by neutrophils, macrophages etc phagocytosing the crystals: cytokine release and inflammation.
  • The crystals are not as shiny or sharp/needle like, meaning they don’t cause NETosis and the attack is much milder, with a slower onset.
17
Q

Where is a common place for pseudogout to occur? [2]

Explain why [1]

A

Wrist and the elbow due to big amounts of fibrocartilage that can be deposited with CPP.

18
Q

Describe the diagnosis of pseudogout [3]

A

Diagnosis of pseudogout is based on synovial fluid analysis and plain film radiography:
* mild to moderate inflammation SF analysis
* the crystals are rhomboid shaped, weakly birefringent and not as sharp/shiny or big as the MSU crystals of gout.

Ultrasound:
* calcification within the soft tissue, and articular cartilage

19
Q

Which cell type is primarily involved in pseudogout CPP formation? [1]

A

Chondrocytes are the principle cell involved in the formation and deposition of CPP.

20
Q

Which cell type is primarily involved in pseudogout CPP formation? [1]

A

Chondrocytes are the principle cell involved in the formation and deposition of CPP.

21
Q

What would the shape, size and birefringence of pseudogout crystals be like? [3]

A

Shape
* rhomboid

Size:
* small (0.5 - 10 microns)

Birefringence:
* weakly positive on plane-polarised light

22
Q

Which is the most commonly affected joint by pseudogout? [1]

A

Knee is most commonly affected joint but can affect any joint

23
Q

Decribe the difference in gout and pseudogout:

  • Crystal structure & appearance
  • Symptoms
  • Joint most commonly affected
A

Crystals:
* MSU very shiny under polarised light & needle like
* CPP crystals are not as shiny and are rhomboid shaped

Symptoms
* gout: has very painful acute attacks that come on sudden
* pseudo gout: more slowly progressing

Joint:
* Gout: 1st MTP joint
* Pseudogou: knee or wrist

24
Q

Cholesterol crystals are sometimes seen in which MSK disease? [1]

A

RA

25
Q

How do cholesterol crystals present under magnification? [1]

A

Monohydrate cholesterol crystals are identified on the basis of their geometric plates with notched corners

Synovial fluid clearly shows the milky appearance.

26
Q

Describe how cholesterol crystals are made [1]

A

Defective drainage of synovial fliud back into the venous system due to synovitis, local destruction, increased permeability of synovial membrane to LDL and HDL & intraarticular bleeding

27
Q

Which joint in the hand is commonly affected by gout? [1]

A

carpometacarpal joints

28
Q

Describe the appearance of aspiration fluid of gout [4]

A

No bacterial growth
Needle shaped crystals
Negatively birefringent of polarised light
Monosodium urate crystals

29
Q

FYI about prophylaxis

A

Do not initiate allopurinol prophylaxis until after the acute attack is settled. Once treatment of allopurinol has been started then it can be continued during an acute attack.