Crystal-induced arthropathies Flashcards
How do organic anions + thiazides promote hyperuricemia?
They act at the URAT1 exchanger in the kidney- they go out into the lumen while urate is reabsorbed. Thus, if there are higher concentrations of organic acids/ thiazides, then they are excreted more while urate is reabsorbed more.
Presentation of gout attack
Abrupt, rapid onset of monoarticular pain, swelling, erythema
Complication of chronic gout
Renal failure- due to urate crystal deposition in kidney (urate nephropathy)
Primary vs. secondary gout
Primary gout- etiology of hyperuricemia is not exactly known (most common form)
Secondary gout- etiology is known
Pattern of joint involvement in gout attack
Monoarticular involvement; MTP joint most commonly affected (podagra), other joints include ankle, heel, knee, and wrist
Where does crystals deposit in gout vs. CPPD
In CPPD, crystals deposit exclusively in articular cartilage. In gout, crystals deposit in synovial space + soft tissue
What is chronic gout characterized by?
Development of tophi- white chalky aggregates of uric acid crystals w/ fibrosis
Why alcohol can cuase hyperuriecmiea
Competes for same excretion site as uric acid
Factors that promote hyperuricemia
Alcohol, meat/seafood consumption (high purines), organic acidosis, obesity, diuretics, rneal disease
First step in diagnosing gout
Always aspirate the joint in order to rule out septic arthritis. Then identify crystals
Characteristic of monosodium urate crystals
Strongly negative birefringent- yellow when parallel + blue when perpendicular
Crystals are fine needle shaped
Pathophysiology of urate crystal formation
Urate crystals precipitate in joints –> neutrophils + macrophages phagocytize –> IL-1 and other cytokines released –> infalmmatoryt reaction –> tissue/joint injury
Characteristic of calcium pyrophosphate crystals
Weakly berefringent udner polarized light (blue when parallel to light)
Rhomboid shape
Imaging finding for calcium pyrophosphate deposition
Chondrocalcinosis- cartilage calcification
Common causes of secondary gout
- High cell-turnover rates (e.g. myeloproliferative disorders, psoriasis, lymphoma) + tumor lysis w/ chemo
- Genetic disorders (e.g. Leisch Nyhan syndrome)
- Renal failure (decreased excretion of urate)