Gout Flashcards
WHat are three characteristics of gout?
- Elevated serum uric acid (hyperuricemia)
Uric acid > 6 mg/dL - Tissue deposition of monosodium urate (MSU) crystals
- Gouty Arthritis: tender, hot, swollen joint caused by MSU crystals in joints and/or soft tissues
what are exogenous causes of increase in purines?
meat
seafood
beer
exogenous causes of purines?
fructose
genes
what decreases uric acid excretion?
genes
renal impairment
alcohol
diuretics
why does gout cause pain?
hyperuricemia –> precipitation of urate crystals in joints –> activates complement–> neutrophils phagocytosis of crystals –> lysis of neutrophils –> release of enzymes
plus -> phagocytosis of monocytes –> release of ILs and TNF in synovium –> release of proteases –> tissue injury and inflammation
“non-modifiable” risk factors
Assigned male at birth (or high testosterone? unknown)
Advanced age
Family History
Modifiable risk factors
High purine diet (seafood, red meat) High alcohol intake, esp. beer Medications (e.g. diuretics, cyclosporine) Obesity Hypertension Cardiovascular disease Chronic kidney disease
what are dietary restrictions and foods to encourage in a person with gout?
Limit:
Organ meats, herring, anchovies, mackerel, red meat, fatty fish and seafood
Alcohol – especially beer
High-fructose corn syrup (sodas and juice drinks)
Saturated fat (lowers ability to eliminate uric acid)
Good to eat:
Low-fat dairy
Fruits and vegetables
Complex carbs
what are precipitating factors for acute gout?
Surgery
Alcohol
Diet
Fluctuation of uric acid level
initiation of therapy to lower uric acid level
diuretics
When left untreated, what happens with gout?
Get worse, less reduction in symptoms, more frequent exacerbation,
eventually –> chronic tophaceous gout ie urate crystal deposits in tissue
Gout DDx
Septic Arthritis
Calcium Pyrophosphate Deposition Disease (Pseudogout)
Gonococcal Arthritis
Rheumatoid Arthritis
Psoriatic Arthritis
Reactive Arthritis
important factors for diagnosing gout
Evaluate for typical clinical manifestations of gout
Serum urate level may be normal at time of flare
Uric acid gets consumed by crystal formation
And people with high uric acid levels may never get gout
Gold standard: Synovial Fluid Analysis
MSU crystals are
Needle-shaped
Negatively birefringent
MSU = Yellow = Parallel = Negative
Differentiate between gout and pseudogout
gout:
- uric acid crystals
- tophi
- most common is first MTP joint
- negatively bifringent
- needle shaped
pseudogout
- usually affects larger joints such as knee
- chondocalcinosis on radiograph (visible on XR)
- calcium pyrophosphate dihydrate (CPPD) crystals (rhomboid)
- positively bifringent
treatment of acute gout flares
Non-steroidal anti-inflammatory drugs (NSAIDs)
Colchicine
Glucocorticoids
Intra-articular
Oral / systemic
Analgesics/Ice
Observation (no therapy)
How do you administer cochicine?
1.2 mg (2 tablets), followed by 0.6 mg 1 hour later, then 0.6mg one to two times daily until resolution of symptoms
Works best if used early (within hours) and in monoarticular attacks
Give to patients to have at home when attack starts
Side effects:
Diarrhea
Bone marrow suppression at high doses
Dose adjustments for renal impairment
How do you administer glucocorticoids in acute gout flare?
Typical starting dose is prednisone 30-40 mg daily
Taper over 9-12 days
ie, decrease by 10 mg every 3 days
Side effects = hyperglycemia, poor sleep, agitation, and others with long term use
Caution with diabetic patients
What are the goals of treating chronic gout?
Reduce serum uric acid levels (< 6.0 mg/dL)
decrease uric acid production (inhibit xanthine oxidase)
increase uric acid excretion (uricosuric drugs)
What is allopurinol and how do you administer?
Blocks xanthine oxidase, decreasing the generation of uric acid
Dose starts at 100mg (50mg with renal insufficiency)
Titrate up monthly until uric acid level of 6 mg/dL or less is achieved (many require > 300mg/day)
side effects of allopurinol
Rash
GI intolerance (diarrhea, nausea)
Increase in LFTs
Steven Johnson Syndrome – rare but life threatening
Risk elevated in renal impairment but low if dose titrated up slowly
Renal toxicity NOT a side effect!
What is febuxostat?
Also inhibits xanthine oxidase
Dose 40 mg or 80 mg daily
Metabolized mainly in the liver: no dose adjustment needed in renal insufficiency
Adverse reactions: LFT elevation, nausea, arthralgia, and rash
What are keys to urate-lowering therapy?
Titrate medications:
Monitor uric acid levels every 2-4 weeks and titrate dose until goal < 6.0 mg/dL is reached
Prevent gout flares:
Lowering uric acid often increases the rate of gout flares intially
Prophylactic therapy: NSAIDs, colchicine
During a gout flare, do not start new uric acid lowering therapy or stop therapy someone is on
What are gout take-home points?
Gout is common
Elevated uric acid leads to deposition of MSU crystals, causing episodes of debilitating joint inflammation
Definitive diagnosis is based on presence of MSU crystals in aspirated synovial fluid
Treat the inflammation of acute gout attacks
Then lower uric acid to prevent future attacks
