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LOCO > 17 - Crystal Arthropathies > Flashcards

17 - Crystal Arthropathies Flashcards

(52 cards)

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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

22
Q

What do you see on a histology of tophi

Study These Flashcards
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

Study These Flashcards
A

Purine metabolism

24
Q

Where does purine intake come from

Study These Flashcards
A

Diet

Meat - high protein food

25
How is uric acid removed
Renal excretion | Faeces
26
What is hyperuricemia
Serum urate above 6.8ml/dL
27
What can cause hyperuricemia
Insufficient excretion of uric acid
28
Risk factors for gout
``` Male Obesity Age Ethnicity - pacific islanders Kidney disease ```
29
Diagnosis of gout
Mainly via history
30
What would you see in synovial fluid in gout
WBC - >2000uL Polymorphonuclear neutrophils Urate crystals
31
What conc does urate crystallise
6.8mg/dL
32
Why does elevated serum uric acid not equal gout diagnosis
presence of serum proteins to coat the crystals
33
Over what level should you treat someone for gout due to high serum uric acid
Higher than 11mg/dL
34
Features of X-ray in gout
Soft tissue swelling/increased blood flow Erosion outside joint capsule Rat bites Maintenance of joint space
35
What is DECT
Dual Energy Computed Tomography | Able to detect uric acid crystal deposits
36
Clinical benefit of DECT
Able to predict gout flare | measure MSU volume
37
What causes joint damage in gout
Cytokines stimulate osteoclasts via RANKL
38
How do you treat an acute attack of gout
``` 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
What is MoA of colchicine
Microtubule inhibitor
40
IL1 biologicals
Rilonacept Canakinumab Anakinra
41
Lifestyle factors for gout
Low purine diet Avoid meat, yeast, beer Eat vegetables, coffee etc
42
Treatment for chronic gout
Aim to reduce uric acid levels Allopurinol Probenecid Rasburicase
43
MoA for Allopurinol
Blocks xanthine oxidase (used in production of purines to urate) Reduces generation of uric acid
44
MoA of Probenecid
Increases Uric Acid excretion | fewer adverse effects than allopurinol
45
MoA of Rasburicase
Catalyses conversion of uric acid to allantonin | Increases excretion of a less toxic substance
46
What is pseudogout
Deposition of calcium pyrophosphate in joints with soft tissue
47
Where is pseudogout most common
the knee
48
pathophysiology of pseudogout
Same as gout lol
49
What triggers an acute attack of psuedogout
Trauma | Rapid reduction of serum calcium concentration
50
What is in the synovial fluid of pseudogout
Mild to moderate inflammation 10,000 - 50,000 | Rhomboid shaped weakly birefringement crystals
51
What would you see in pseudogout
Calcification in soft tissue calcification in articular cartilage Chondrocalcinosis of articular disk
52
Treatment of pseudogout
Intra articular corticosteroids | NSAID

LOCO (25 decks)

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