Gout, pseudogout... Flashcards
etiology of gout
monosodium urate cystals precipitate within join and surrounding tissue space –> inflammatory needle like pain
patient presents with severe pain in great toe MTP. You notice redness and swelling. You predict this patient is suffering from gout..What is your next step
GOLD STANDARD: arthrocentesis (send fluid for culture and gram stain to r/o infection)
- for gout = negatively birefringent monosodium urate crystals
- 24 hour urinary uric acid secretion: overproducers >800 mg/dl, underexcreters ,700 mg/dl (not best for dx)
what would radiographic evidence of gout consist of
joint erotion, rat bite appearance, punched out erosions
List the stages of a gout attack
stage 1: asymptomatic hyperuricemia
stage 2: acute gouty arhritis triggered by acute change in uric acid
stage 3: intercritical gout/intermittent attacks
Stage 4: chronic tophaceous gout
Types of gout…
- Primary Hyperuricemia = idiopathic overproduction uric acid
- Secondary hyperuricemia: either
a) overproduction of uric acid due to enzyme defect, malignancy, obesity, psoriasis, drugs etc
b) under excretion of uric acid (90%) due to renal insufficiency, diuretics, lead nephropathy, acidosis (DM, EtOH)
treatment for stage 1 (acute stage) of gout attack
first line = NSAIDS specifically INDOMETHACIN (indomethacin also used for ankylosing spondylosis); may do intra articular steroid injection if r/o infection, oral steroids
*second line = COLCHICINE: back!, use at lower dose during acute attack, can be used for prevention as well to reduce inflammation and pain (not helpful for decreasing uric acid or bone damage)
tx for stage 2/3 (prophylaxis to prevent flares and lowering excess uric acid stores)
overproducers = ALLOPURINOL (watch hypersensitivity)
- under excretors: PROBENECID
- new med: FEBUXOSTATE (good for over producers if impaired renal function)
risks for gout
obesity, HTN, DM, family hx, alcohol/yeast, hospitalization, transplants, acidotic state, post menopause, high purine diet (organ meats, anchovies, mushrooms, spinach, asparagus, cauliflower, beans, seafood)
what lab result differentiates Pseudogout from gout
synovial fluid aspiration in PSEUDO reveals POSITIVELY birefringent crystal, gout reveals NEG birefringent crystals
*note: no specific serum study for pseudogout, dx based on fluid analysis and xray revealing chondrocalcinosis
what is the etiology of pseudogout
SYNOVITIS due to build up of calcium pyrophosphate dihydrate crustals (CPPD) –> chondrocalcinosis (cystal deposits into synovial tissue)
A patient has acute onset of erythema pain and swelling in LARGE joints (wrist, hips, shoulders, ankles, elbows). Primary Dx and why
Pseudogout bc in large joints (gout is more in a single smaller joint ie MCP)
**50% pseudogout cases affect Knees
What other diseases are associated with pseudogout
hyperparathyroidism, hypothyroidism, hypophosphatemia, hypomagnesemia, OA, joint trauma
xray reveals evidence of calcium deposition (see punctate and linear radiodensities in cartilage, ligaments, joints) and osteophytes. Pt has positively birefringent crystals in synovial fluid and an elevated WBW. Dx?
Dx: pseudogout
tx :treat underlying cause, reduce pain (joint aspiration), intra articular steroid, NSAIDS, colcincine, joint immobilization, ice pack
PROPHYLAXIS = colchicine
Pt has complaints of fever, fatigue, joint pain, head ache and rash. What studies might you order
ESR, ANA (subtypes: anti-dsDNA, anti-smith Ab) antiphopholipid Ab
OTher:
*checking for SLE
Lab results reveal +ANA. What diseases are consistent with this result
95% of SLE cases, 70% scleroderma, 30-40% RA, 60% sjogren