gout and pseudogout Flashcards
(45 cards)
what leads to production of uric acid
degradation of purines
what is the pathway of endogenous and dietary purines
inosine->hypoxanthine->xanthine->uric acid
what enzyme helps catalase breakdown of purines
xanthine oxidase
what are sources of purine in humans
- diet
- nucleotide synthesis and metabolism
in what organs does excretion of uric acid occur?
1) kidneys (70%)
2) gut (30%)
definition of gout
-Gout is characterized by intermittent painful, inflammatory joint attacks, in response to uric
acid crystals as a consequence of hyperuricemia
what % of adults in US does gout affect
4%
what are risk factors for gout
1) male sex (estrogen increases excretion)
2) age (older)
3) obesity
4) HTN
5) hyperlipidemia
6) CV disease
7) CKD
8) medications (thiazides)
9) diet
10) lead exposure
gouty tophi
-deposition of uric acid in body tissues
what does hyperurcemia result from
1) overproduction
2) underexcretion (MAIN CAUSE)
clinical presentation of gout
-Acute gouty flares present with acute onset joint pain usually with maximal pain within the first
24 hours
-Acute gouty flares are often begin overnight
-The affected joint is typically swollen, erythematous, warm, and exquisitely painful
-fever can also be seen
what joints does gout most commonly affect
- 1st MTP joint (called Podagra when affected)
- Knee joints
- Ankle joints
what are provoking factors for gout
- ETOH consumption
- Trauma
- Inflammatory states (infection, surgery, myocardial infarction, etc…)
- Dehydration, etc…
what is the definitive test for gout
arthrocentesis of affected joint’s synovial fluid
-send for cell count, culture, gram stain
what do crystals look like under polarized light
monosodium urate crystals, which are
needle shaped, negatively birefringent crystals
what other tests should be ordered for gout
-Serum uric acid level (higher levels make diagnosis of gout more likely)
-CBC with differential (if considering septic arthritis, look for left shift)
-X-ray is not helpful in acute gouty flares
-However, in chronic gout patients, x-ray may reveal bony erosions (i.e. “punched out
Lesions” or “overhanging edge”)
synovial fluid non-inflammatory arthritis < 2,000 WBCs/ʅ>
-Typically from mechanical or degenerative disorder (i.e. osteoarthritis)
synovial fluid inflammatory arthritis > 2,000 WBCs/ʅ>
-Typically from autoimmune conditions but can be from infection or crystal-induced
-Autoimmune conditions include Rheumatoid arthritis (RA) or spondyloarthritis (i.e. ankylosing spondylitis,
psoriatic arthritis, etc…)
synovial fluid (septic) arthritis
typically with > 20,000 to 50,000 WBCs/ʅ> but could have less WBCs present
-Gram stain and fluid culture will be positive and will help differentiate this etiology from others
- Crystal-induced fluid
- typically 10,000-50,000 WBCS
- Typically Gout or Pseudogout
tx of acute gouty flare
-Untreated gout will resolve within days to weeks (but it will be a very painful period)
-NSAIDS (Indomethacin, Naproxen, etc…), use with caution in CKD patients
-Colchicine – inhibits cytoskeletal function of neutrophils preventing activation and
migration of neutrophils
-Glucocorticoids
-Oral Prednisone or intra-articular/intramuscular steroid injection
-May be preferred treatment option in patients with CKD
tx for chronic gout
-Xanthine oxidase inhibitors (cannot initiate during acute flares as it can precipitate a
gouty flare, typically wait 2 weeks after flare to initiate)
- Ex: Allopurinol and Febuxostat
- Goal serum uric acid level:
- < 6.0 mg/dL in patients without tophi
- < 5.0 mg/dL in patients with tophi
-Uricosuric agents – Inhibit reabsorption of uric acid in proximal convoluted tubule
-Probenecid
-Lesinurad
-Uricase
- Humans lack the enzyme uricase, which converts uric acid into the highly
soluble allantoin
-Ex: Pegloticase is used in severe gout when other treatments have failed
what tx should you use if pt has gout and CKD
- be cautious with NSAIDS and colchicine
- intraarticular or oral steroids are preferred
what drug used to tx HTN also has some uricosuric effects
losartan
