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LOCO > 17 - Crystal Arthropathies > Flashcards

17 - Crystal Arthropathies Flashcards

1
Q

Population with gout

A

1%

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2
Q

What age do people usually get gout

A

Men - 40-60

Women - 60-80

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3
Q

How long does uric acid levels rise before onset of gout

A

20 years

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4
Q

When do men uric acid levels start to rise

A

Puberty

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5
Q

When do women uric acid levels start to rise

A

During menopause

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6
Q

What is gout

A

Disorder of uric acid metabolism whereby negatively charged monosodium urate crystals are deposited in soft tissues causing an acute inflammatory process

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7
Q

What are 2 complications of gout

A

Joint destruction

Renal damage

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8
Q

Why does high levels of urate crystals in the synovial fluid not mean gout

A

The crystals are coated by serum proteins which are inert

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9
Q

What triggers a gout attack

A

Uncoated crystals

Sudden large change in concentration of crystals so there is not enough time to coat the proteins

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10
Q

In what conditions do monosodium urate crystals precipitate best

A

Colder conditions

Therefore flares usually early morning + in distal joints

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11
Q

What are the steps of a gout attack

A

1) Crystals embed in the synovium
2) This causes an immune response
3) Neutrophils phagocytose the crystals
4) Crystals are sharp and pop the neutrophil
5) Nutrophil releases it’s contents - lysosomes, free radicals, cytokine
6) Cytokines(mainly IL1) cause more white blood cells into the joint
7) Causes inflammation and pain
8) Proteins lower pH making it possible for more crystals to form quickly
THIS IS THE GOUT ATTACK!!!

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12
Q

What percent of cases are monoarticular in gout

A

90%

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13
Q

Which joints are more commonly affected by gout

A

Small, lower extremity joints e.g 1st MTP

Can spread to other joints e.g foot and ankle

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14
Q

What is podagra and what percent of cases does it appear in?

A

Inflammation of the 1st MTP joint

50% of cases

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15
Q

How does gout first present

A

Waking up with intense pain

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16
Q

How long before gout attack reaches maximum intensity

A

8-12 hours

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17
Q

What are the joint symptoms of gout

A

Red
Hot
Tender

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18
Q

What can untreated gout lead to over time

A 
Attacks more frequent and last longer
Polyarticular 
More proximal and upper extremity involvement
Damage to the joint
Rat bites
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19
Q

What are rat bites

A

Erosions to the shaft of the bone

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20
Q

What is a Tophi

A

Monosodium urate in soft tissue e.g cartilage or tendons in ear, kidney, bursae

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21
Q

How long before tophi develop

A

10 years

22
Q

What do you see on a histology of tophi

A

Histocytes in the tissue which form an outer barrier - lymphocytes outside of them
This walls off the crystals from healthy tissue
Causes the lumps on the ski

23
Q

What metabolism causes the end stage byproduct to be uric acid

A

Purine metabolism

24
Q

Where does purine intake come from

A

Diet

Meat - high protein food

25
Q

How is uric acid removed

A

Renal excretion

Faeces

26
Q

What is hyperuricemia

A

Serum urate above 6.8ml/dL

27
Q

What can cause hyperuricemia

A

Insufficient excretion of uric acid

28
Q

Risk factors for gout

A 
Male 
Obesity 
Age
Ethnicity - pacific islanders
Kidney disease
29
Q

Diagnosis of gout

A

Mainly via history

30
Q

What would you see in synovial fluid in gout

A

WBC - >2000uL
Polymorphonuclear neutrophils
Urate crystals

31
Q

What conc does urate crystallise

A

6.8mg/dL

32
Q

Why does elevated serum uric acid not equal gout diagnosis

A

presence of serum proteins to coat the crystals

33
Q

Over what level should you treat someone for gout due to high serum uric acid

A

Higher than 11mg/dL

34
Q

Features of X-ray in gout

A

Soft tissue swelling/increased blood flow
Erosion outside joint capsule
Rat bites
Maintenance of joint space

35
Q

What is DECT

A

Dual Energy Computed Tomography

Able to detect uric acid crystal deposits

36
Q

Clinical benefit of DECT

A

Able to predict gout flare

measure MSU volume

37
Q

What causes joint damage in gout

A

Cytokines stimulate osteoclasts via RANKL

38
Q

How do you treat an acute attack of gout

A 
1) NSAIDs - high dose and taper down
(symptoms should be absent for 2 days before u stop)
2) Colchicine 
3) Corticosteroids
4) IL1 biologicals
39
Q

What is MoA of colchicine

A

Microtubule inhibitor

40
Q

IL1 biologicals

A

Rilonacept
Canakinumab
Anakinra

41
Q

Lifestyle factors for gout

A

Low purine diet
Avoid meat, yeast, beer
Eat vegetables, coffee etc

42
Q

Treatment for chronic gout

A

Aim to reduce uric acid levels
Allopurinol
Probenecid
Rasburicase

43
Q

MoA for Allopurinol

A

Blocks xanthine oxidase (used in production of purines to urate)
Reduces generation of uric acid

44
Q

MoA of Probenecid

A

Increases Uric Acid excretion

fewer adverse effects than allopurinol

45
Q

MoA of Rasburicase

A

Catalyses conversion of uric acid to allantonin

Increases excretion of a less toxic substance

46
Q

What is pseudogout

A

Deposition of calcium pyrophosphate in joints with soft tissue

47
Q

Where is pseudogout most common

A

the knee

48
Q

pathophysiology of pseudogout

A

Same as gout lol

49
Q

What triggers an acute attack of psuedogout

A

Trauma

Rapid reduction of serum calcium concentration

50
Q

What is in the synovial fluid of pseudogout

A

Mild to moderate inflammation 10,000 - 50,000

Rhomboid shaped weakly birefringement crystals

51
Q

What would you see in pseudogout

A

Calcification in soft tissue
calcification in articular cartilage
Chondrocalcinosis of articular disk

52
Q

Treatment of pseudogout

A

Intra articular corticosteroids

NSAID

LOCO (25 decks)

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