Gout & crystal arthropathies

Question 1

Gout

Answer 1

A group of conditions characterised by hyperuricaemia and uric acid (monosodium urate) crystal formation. Clinically this can cause acute gout, Tophaceous Gout, uric acid nephrolithiasis & Gouty nephropathy

Question 2

Calcium pyrophosphate deposition disease (CPPD) (3)

Answer 2

2nd commonest form of crystal arthropathy diagnosed by rhomboid calcium pyrophosphate dihydrate crystals - weakly positively birefringent
Can cause pseudogout, destructive arthropathy or asymptomatic chondrocalcinosis

Question 3

Basic calcium phosphate associated conditions (3,1,3)

Answer 3

hydroxyapatite, octacalcium phosphate or tricalcium crystal deposition
Include milwaukee shoulder (destructive arthropathy) , acute arthritis, acute calcific periarthritis and calcific tendonitis/bursitis

Question 4

Calcium Oxalate arthritis

Answer 4

An unusual arthritis with bipyramidal crystals, treat with NSAIDs & colchicine as with CPPD – can present acutely or subacutely
Associated with ESRD, short bowel syndrome and thiamine or pyridoxine deficiency

Question 5

Epidemiology of Gout (4)

Answer 5

4:1 male to female ratio - men 45yrs, women 60yrs
approx 1% of people will suffer from some gout
Incidence increases with age

Question 6

Clinical Features of Gout arthritis (3)

Answer 6

Intially asymptomatic, then acute, self-limiting (3-10days) inflammatory monoarthritis in a small joint
70-80% have a 2nd attack within 2 years. –
Attacks become polyarticular with shorter remissions (may mimic RA)

Question 7

Treatment for Gout Arthritis

Answer 7

Acute: high dose NSAIDs w/or w/out colchicine

>1 attack/year: allopurinol. May trigger an attack

Question 8

Tophaceous Gout (4)

Answer 8

Occurs when tophi of uric acid crystals are deposited within a matrix of lipid subcutaneously, or in organs.
Mainly occur in long term, severe hyperuriaemia
Presents with large, whitish/chalky subcut nodules
Commonest on extensor surfaces or trauma sites

Question 9

Gout associated kidney damage (3)

Answer 9

Urate nephropathy - minor damage due to inflammation directly due to urate crystals
Uric acid nephropathy - occurs in ill, dehydrated pts, often taking cytotoxic drugs
Acute obstructive uropathy due to uric acid stones can also occur

Question 10

General risk Factors for Gout (8)

Answer 10

General–> male, >40yo, obese, FH, HTN, alcohol/purine rich food, kidney disease, hyperlipidaemia

Question 11

Investigation for Gout – Synovial fluid

Answer 11

most useful and will show needle shaped crystals (negatively birefringent) - yellow when parallel, blue when perpendicular

Question 12

Treatment of Hyperuricaemia - decrease production (2,4)

Answer 12

Allopurinol –> a xanthine oxidase inhibitor,
Risk of fatal hypersensitivity reaction (particularly if second exposure or interaction with azathioprine) and can trigger acute attacks
Use if: frequent, erosive disease, nephropathy, tophi

Question 13

Other conditions which can include Calcium pyrophosphate deposition (4,3,4)

Answer 13

Low Mg or phosphate, haemochromatosis, wilson’s disease, hyperparathyroidism, haemosiderosis, hypothyroidism, Gout, amyloidosis, trauma, familial hypocalciuric hypercalcaemia (FHC)

Question 14

How common is uric acid nephropathy/nephrolithasis?

Answer 14

10-25% of gout sufferers

Question 15

Hyperuricaemia

Answer 15

A blood urate level above 7mg/dl in men and 6mg/dl in women

Question 16

Causes of urate overproduction (5)

Answer 16

Cell lysis (necrosis, haemolysis, tumours)
Drugs (cytotoxics, warfarin),
type I glycogen storage disease or Psoriasis
Dietary purines or Alcohol
Lympho- or myelo-proliferation

Question 17

Causes of urate under-secretion (5)

Answer 17

Drugs (alcohol, diuretics, laxatives)
Lead toxicity & inherited conditions
Lactic, respiratory or keto-acidosis
Hypothyroidism
Renal failure

Question 18

Drugs which can cause gout (AACDEN)

Answer 18

Thiazides or Frusemide Alcohol
Low dose aspirin Ethambutol
Cyclosporin Nicotinic acid

Question 19

Alcohol and gout

Answer 19

Commonest cause – increases ATP turnover (increased urate production)
Lactic acidosis (under secretion)
Beer has lots of purines

Question 20

What causes an acute attack?

Answer 20

A sudden change in serum urate – either sudden formation or shedding from synovial membrane
Urate is normal in 20% if cases during an attack

Question 21

Treatment of Hyperuricaemia - increase secretion

Answer 21

Sulphinpyrazone, benzbromarone & Probenicid - uricosuric agents but sulphinpyrazone is contraindicated in renal insufficiency
Aim to keep serum urate <6mg/dl

Question 22

Podagra

Answer 22

Gout of the big toe – most common (50% of first attacks and 90% will have it effected at some point)

Question 23

Investigation for Gout – Serum uric acid

Answer 23

May be normal during an acute attack but are useful to monitor hyperuricaemia (not universal)

Question 24

Investigation for Gout – Radiographs (6)

Answer 24

Only be useful to exclude other causes in early disease but later may show tophi, swelling, Periarticular joint erosions and new periosteal bone
‘Punched out lesions’ without sclerosis or osteoporosis

Question 25

Stages of Gout

Answer 25

Asymptomatic hyperuricaemia
Acute gout (85% monoarthritis, 15% polyarthritis)
Intercritical gout
Chronic trophaceous gout

Question 26

Features of Acute gout

Answer 26

Mimics septic arthritis – warm, red and tender/painful
Neutrophilia
Can affect bursas as well
Resolves in 3-10days

Question 27

Chronic trophaceous gout (4)

Answer 27

Urate crystal deposits surrounded by macrophages
Commonly - ears, olecranon, achillies, periarticular
High incidence of renal impairment
Develop 10yrs after first attack

Question 28

Allopurinol (5)

Answer 28

a xanthine oxidase inhibitor - Risk of fatal hypersensitivity reaction - particularly if second exposure or interaction with azathioprine
Can trigger acute attacks
Careful to use in elderly with poor kidney function
Always give NSAIDs as well to begin with

Question 29

Pseudogout

Answer 29

Due to CPPD
large joint monoarthritis with endocrine/electrolyte disturbances
Responds to same treatment a gout but underlying cause should be investigated

Question 30

Risk factors for Pseudogout

Answer 30

Hyperparathyroidism or hypothryoidism
Haemochromatosis or wilson’s disease
Acromegaly
Low magnesium or phosphate

Question 31

Features of pseudogout

Answer 31

Knee, wrist and shoulders most commonly effected.
Will have weakly-positively bifringent rhomboid shaped crystals
X-ray will show chondrocalcinosis

Question 32

Management of Pseudogout

Answer 32

Aspirate joint fluid to exclude septic arthritis

NSAIDs, RICE, intra-articular steroids

Question 33

When to begin allopurinol treatment

Answer 33

2 weeks after the end of an acute attack but always give NSAID cover (Diclofenac or other) for the start incase an acute attack is triggered. If attack occur when already started keep going with allopurinol.