gout and pseudogout Flashcards
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
how do you prevent gout
- Avoidance of factors that contribute to hyperuricemia:
- ex: Red meat, seafood, alcohol, high-fructose corn syrup beverages, etc…
what is pseudogout
-Deposition of calcium pyrophosphate (CPP) crystals in and on cartilaginous surfaces can
provoke an acute inflammatory arthritis clinically similar to gout
what are risk factors for pseudogout
- Age > 60
- Primarily affects the elderly
- Osteoarthritis
- Metabolic diseases:
- Hyperparathyroidism
- Hemochromatosis
- Hypophosphatasia (rare genetic disease)
- Hypomagnesemia
what is the pathophys of pseudogout
-Pyrophosphate produced by chondrocytes likely precipitates with calcium forming CPP crystals
which then activate inflammatory pathways leading to an acute arthritic attack
what is the clinical presentation of pseudogout
- Ranges from asymptomatic to symptomatic
- Typically presents as monoarticular or oligoarticular arthritis
- The affected joint is typically swollen, erythematous, warm, and painful
- fever can also be seen
what joints does pseudogout effect
- Knee joints
- Wrist joints
- Rarely the 1st MTP joint
how long can acute attacks of CPPD lasts
-wks to months
what are provoking factors for pseudogout
-surgery or acute illness
what is difinitive way to dx pseudogout
-arthrocentesis
what do CPP crystals look like under polarized light
Rhomboid shaped and positively birefringent under polarized light
what would xrays show in pseudogout
-Chondrocalcinosis – cartilage calcification (not specific to CPPD)
how do you tx pseudogout
- NSAIDS
- Colchicine
- Intra-articular glucocorticoid injection or oral prednisone
- Treat underlying metabolic disease if present (i.e. Hyperparathyroidism, hemochromatosis,
etc. ..)
differential dx for gout
- CPPD
- septic arthritis
- cellulits
- RA
- osteoarthritis
- psoriatic arthritis
- sarcoidosis
autonomic innervation of kidney
Sympathetics T10-T11, Parasympathetics Vagus Nerve (OA, AA)
autonomic innervation UE
Sympathetics T2-T7
autonomic innervation LE
Sympathetics T11-L2
5 models of care biomechanical
OMT for SD
5 models of care resp/circulatory
lymphatic OMT tx
5 models of care neuro
-OMT to normalize sympathetics and parasympathetics
5 models of care metabolic, energetic,immune
-Consider arthrocentesis for acute gout flare to confirm diagnosis
-Assess uric acid levels
-Assess renal function and renal dose medications as needed (i.e. NSAIDs,
Colchicine, and allopurinol)
-Caution with systemic steroid use in diabetics (may need to check glucose more
frequently or give insulin temporarily)
-Consider stopping Thiazide if recurrent gout (Thiazides raise uric acid levels)
5 models of care behavioral
Dietary changes (avoid red meat and seafood) and avoid alcohol
