Crystal-induced arthropathies Flashcards
1
Q
Crystal-induced arthropathies
A
- Crystalline deposition in articular and periarticular tissues that may have both acute and chronic progression
- Accompanied by inflammatory responses
2
Q
Crystal species in associated d/o
A
- Monosodium urate: gout (yellow when parallel, negative birefringence)
- Calcium pyrophosphate: pseudogout (yellow when perpendicular, positive birefringence)
- Hydroxyapatitie: calcific periarthritis
- Uric acid does not occur in synovial fluid (only in urine/blood), monosodium urate occurs in synovial fluid
3
Q
Crystal inflammation
A
- Stimulates release of inflammatory mediators: arachidonic acid (ACA) metabolites, ILs (IL1, IL6, IL8), TNF
- Promotes granulocyte influx
4
Q
Clinical presentation of gout
A
- Intermittent attacks
- First MTP joint (big toe) frequently first
- Recurrent attacks, tophaceous deposits over time
- Tophaceous gout: usually after 10 yrs of gout, no longer pain free btwn attacks
- There is subQ deposits of monosodium urate (tophi), can be in unusual places but often unilateral
- W/o Rx 50% will get them
5
Q
Conditions associated w/ urate overproduction
A
- HGPRT deficiency: salvage pathway for purines (HGPRT prevents catabolism of purines into uric acid)
- PRPP synthetase super activity: nz responsible for de novo purine synthesis
- Myeloproliferative disease
- Hemolysis
- Psoriasis
- Glycogen storage disease
- Etoh
6
Q
Gout lab findings
A
- Most pts w/ hyperuricemia do not have gout, but most gout pts have elevated uric acid
- Visual confirmation of crystals in joint fluid, w/ inflammation in synovial fluid
- Radiographic features: X-rays negative in early gout, erosions apparent w/ atrophy/hypertrophy of certain areas
- Results in overhanging edge appearance
7
Q
Excretion of uric acid in gout
A
- Normally uric acid is excreted mostly by kidneys (small amount from intestines)
- Most cases of gout are not over production of uric acid, but underexcretion of it
- These pts have normal purine metabolism but faulty renal excretion
- Some pts will have overproduction of purines, and will have large (normal) excretion of urinary uric acid
- Solubility of purine metabolites important for excretion
8
Q
Rx of gout
A
- For acute attacks use Colchicine: inhibits release of chemotactic protein to prevent inflammation (effective early in attacks and to prevent future attacks)
- NSAIDs (indomethacin), GCCs, uricosurates
- For Rx of hyperuricemia: asymptomatic pts do not need Rx usually, otherwise use xanthine oxidase inhibitor allopurinol
9
Q
Allopurinol
A
- Xanthine oxidase inhibitor (XO is nz in common pathway for purine degradation)
- Indications: urate overproducer, tophus formation, nephrolithiasis, excessive cell turnover
10
Q
Pseudogout
A
- Calcium pyrophosphate dihydrate crystal deposition disease (CPPD)
- Crystals present in cartilage: chondrocalcinosis
- Acute onset of self-limited attacks that may last 2 weeks
- First in knee joints for 50% of pts, all joints can be affected
- Asymptomatic btwn attacks, can have fever w/ attacks
- Chronic Sx in some pts
- Associated w/ hyperparathyroidism and hemochromatosis
11
Q
Pathogenesis of pseudogout (CPPD)
A
- Associated w/ hyperparathyroidism and hemochromatosis
- Normal plasma and urinary excretion of inorganic pyrophosphate, but synovial fluid pyrophosphate elevated
- Crystals form in joint fluid and elicit cytokine response
12
Q
Rx of CPPD
A
- NSAIDs, colchicine, GCCs can pharmacologically help
- Aspiration of joint capsule and steroid injections
13
Q
Calcium phosphate disease
A
- Generally more periarticular Sx, may also cause local inflammation
- High percentage of OA pts have CaPO in joint fluid
- Both acute and chronic forms
- Large joint (shoulder, hips, ect) destruction arthritis
- Calcinosis cutis: accumulation in soft tissues, mostly in pts w/ scleroderma
- Clinical Sx generally tendonitis, X-rays reveal soft tissue calcification
- Rx: NSADs, local GCCs, physical therapy to prevent contracture
