Gout Flashcards
Natural history (4)
Natural history=
- asympT hyperU
- acute arthritis
- intercritical gout
- chronic tophaceous
Pathogenesis
+uric acid (from purine metabolism)–>
not all hyperuricemia= gout
Precipitation of monosodium urate into joint->+in periphery where -ve temperature
Urate crystals form–>incitng event
(trauma?) released in to synovium-
+inflammation
MacroP ingest-> +inflammasome->+neutrophils->+free radicals, leukotrienes, joint damage->neutrophils ingest, lyse and release lysosomal factors
Renal metabolism influencing gout (4)
-ve glomerular filtration
-ve excretion
+absorption
+post secretion reabsorption
Risk factors (7)
Hyperuricemia Age >30, male Heavy alcohol Obesity Drugs->diuretics/aspirin, cyclosporin genetics
Complications (5)
Nephropathy Chronic gouty tophy Pyeloneprhitis Nephrocalcinosis Hypertension Atherosclerosis
Association with CVD
+LDL, -ve HDL. Must do CVD risk assessment
Morphology in chronic
Chronic–>precipitation on
cartilage. Becomes fibrotic, thickened,
pannus forms. erosions,
fibrous ankylosis
Morphology of gouty tophy
\+aggregates urate crystal w/ surrounding macroP, lymphocytes In joint/cartilage surface periarticular tissues--> patellar bura, olecronon, earlobe, achilles tendo and elsewhere
Morphology of nephropathy
precipitate in interstitium,
tubules–>
uric acid stones, pyelonephritis
Morphology of acute
Acute--> neutrophilic aggregates (w/ crystals inside), edematous, congested. some macroP, lymphocytes. when crystals solubilised, attack abates
Where are tophy found
Extensor surfaces->elbows, knees, achilles, helix of ear
Diagnosis
Arthrocentesis:
WCC usually exceeds 2.0 x 10^9/L
PMN
Monosodium urate crystals, negative birefringent
Serum uric acid may be low, normal or high
Search for secondary causes->renal insufficiency, +cell turnover in malignancy
When is treatment for hyperuricemia indicated
Recurrent gout Uric acid neprhopathy Urolithiasis Tophi Comorbidities putting at +CVD risk
Management of acute
- NSAID- indomethacin
- Colchicine
- Prenisilone
Why is colchicine less often use
Side effects-> GIT
Prevention
Low purine diet
Limit alcohol and fructose containing drinks
Avoid drugs that worsen
Lose weight, reduce CVD risk
Consider urate lowering therapy + colchicine+/- NSAID (to prevent acute attack)
Best time to commence urate lowering therapy
Intercritical gout
Urate lowering therapy
allopurinol 50 mg orally, daily for the first month, then increase the dose by 50 mg every 2 to 4 weeks depending on the patient’s renal function and plasma urate levels
Management of chronic gout
Allopurinol
Colchicine
NSAID
Alternative if colchicine or NSAID CI/not tolerated
Prednisilone
How to prevent acute attack when starting on allopurinol
Wait 3 weeks from acute attack
Cover with NSAID/colchicine for 3 months.
Allopurinol SE
Rash, fever, -ve WCC
Caution in renal impairment
Acute pseudogout
Acute monoarthropathy
Large joints
Spontaneous and self limiting
Provoked pseudogout
Surgery
Illness
Trauma
Risk factors for pseudogout
Age + OA DM Hypothyroidism \+PTH Haemachromatosis Wilsons Low PO4,Mg
Microscopic findings for PPD
Weakly birefringent
What condition is PPD associated with
Chondrocalcinosis->soft tissue calcium deposition
Management of PPD
NSAId, analgesia
Advice to patients
Foods that have a high purine content (i.e., alcohol, seafood, and offal) are associated with higher risk of elevated uric acid and gout. [2]
Reducing intake of alcohol, especially beer, lowers the risk of gout. [31]
Reducing seafood and meat intake helps to a lesser degree.
Reducing the intake of vegetables high in purines (i.e., asparagus, spinach, and mushrooms) does not seem to affect uric acid levels.
Dairy products reduce the risk of gout.
Monitoring recommendations in gout
Recurrent attacks, tophy, radiographic changes
F/U uric acid levels 1-3 monthly, then 6 monthly
FBC, RFTs, LFTs every 3-6 months
When begin on allopurinol, monitor for hypersensitivity
Consider drug interactions
Crystals seen on polarising microscopy
Monosodium urate
Calcium pyrophosphate dehydrate
Calcium hydroxyappatite
Calcium oxalate
Appearance of CPPD
Rod
Rhomboid
Weakly birefringent
Appearance of calcium oxalate, and when do they occur
Bipyramidal
Strong +ve birefringent
End stage renal
What is the term for gout of first MTP joint
Podagra
When is monitoring uric acid levels useful
Monitoring in hypouricemic therapy
Radiographic appearance of gout
Cystic changes in joint surface
Punched out lesions
Soft tissue calcifications
