Gout Flashcards

1
Q

what is the definition of gout?

A

Gout is a syndrome characterised by: hyperuricaemia and deposition of urate crystals causing attacks of acute inflammatory arthritis; tophi around the joints and possible joint destruction; renal glomerular, tubular, and interstitial disease; and uric acid urolithiasis.

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2
Q

what is the epidemiology of gout?

A

6x more common in men

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3
Q

what is the aetiology of gout?

A

There is a causal relationship between hyperuricaemia (high urate level) and gout.
Urate is a metabolite of purines and the ionised form of uric acid (a weak acid at a physiological pH); hence, uric acid exists mostly as urate.

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4
Q

what are the risk factors for gout?

A
Older age
Male sex
Menopausal status
Consumption of meats seafood and alcohol 
Use of diuretics
Use of ciclosporin or tacrolimus
Use of pyrazinamide
Use of aspirin 
Genetic susceptibility 
High cell turnover rate
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5
Q

what is the pathophysiology of gout?

A

Big toe affected first
Big joints in core of body not be affected
Too much uric acid in blood
Urate crystals in the joint interact with undifferentiated phagocytes and trigger an acute inflammatory response by inducing tumour necrosis factor (TNF)-alpha and activating signal pathways and endothelial cells. TNF-alpha, interleukin (IL)-8, and other chemokines lead to neutrophil adhesion to endothelium, influx, and amplification, resulting in neutrophilic synovitis.
Colchicine works by intercepting the neutrophil-endothelial interaction. IL-8 accounts for 90% of the chemotactic activity of neutrophils in response to uric acid crystals; hence, inhibiting IL-8 may have therapeutic implications.
In addition there is evidence that urate crystals activate NALP3 inflammasome (a key regulator of IL-1beta secretion), which plays a role in the gout inflammatory reaction.
Urate crystals can induce chondrocytes to produce metalloproteinase and nitric oxide, and chronic inflammation, leading to synovitis, cartilage loss, bone damage by inhibiting osteoblasts, and bone erosions.

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6
Q

what are the key presentations of gout?

A
Presence of risk factors 
Rapid onset severe pain 
Joint stiffness
Foot joint disturbance 
Few joints affected 
Swelling of joints 
Tenderness 
Tophi
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7
Q

what are the signs of gout?

A
Presence of risk factors 
Rapid onset severe pain 
Joint stiffness
Foot joint disturbance 
Few joints affected 
Swelling of joints 
Tenderness 
Tophi
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8
Q

what are the symptoms of gout?

A
Erythema and warmth 
Tenderness 
Rapid onset severe pain 
Joint stiffness
Foot joint disturbance 
Few joints affected
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9
Q

what are the first line and gold standard investigations for gout?

A

Arthrocentesis with synovial fluid analysis - WBC count >2.0 x 10⁹/L (2000/mm³ or 2000/microlitre; mean, 20,000/mm³ or 20,000/microlitre); strongly negative birefringent needle-shaped crystals under polarised light

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10
Q

what are the differential diagnoses for gout?

A

Pseudogout
Septic arthritis
Trauma
RA

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11
Q

how is gout managed?

A

Acute:
NSAIDs, corticosteroids, colchicine, IL-1 inhibitor
Chronic:
Allopurinol, suppressive therapy, febuxostat, suppressive therapy, probenecid or sulfinpyrazone, pegloticase

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12
Q

how is gout monitored?

A

Patients should be monitored for recurrent attacks, the development of tophi, and radiographic changes.
In patients taking uric acid-lowering agents, follow up uric acid levels every 1 to 3 months initially, then every 6 to 12 months (target level <360 micromol/L [<6 mg/dL]).

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13
Q

what are the complications of gout?

A

Acute uric acid nephropathy

Nephrolithiasis

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14
Q

what is the prognosis of gout?

A

Gout attacks are painful and debilitating, but self-limiting. In patients who have not been treated with uric acid-lowering drugs, the risk of recurrence after the first attack is 62%, 78%, and 84% during the first, second, and third year, respectively

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