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
pt has +ANA, what other lab results would help dx this patient with SLE
+anti-dsDNA and +anti-smith (subtypes of ANA), +antiphospolipid Ab (thrombocytopenia)
- urinalysis with microscopy revealing pro/cell casts bc glomeruli damage,
- depressed complement levels (due to SLE immune complexes)
Name the eleven dx guidelines for SLE. How many will confirm dx?
- need 4/11
1. Malar (butterfly) rash)
2. +ANA
3. +anti-sm, anti-dsDNA, antiphospholipid Ab
4. discoid rash
5. photosensitivity rash
6. mucosal ulcers
7. polyarthritis
8. serositis
9. renal disorders
10. neuro disorders/HA/seizures
11. Hematologic disorders
tx for SLE
NSAIDS antimalarials (hydroxycloroquine (plaquenil)) corticosteroids (topical, intradermal) decrease sun exposure immunosuppressive meds (methotrexate)
Tx for Lupus nephritis
cyclphosphamide, methylprednisolone
tx for CNS involvement SLE
antipsychotics, anticonvulsants
tx thrombocytopenia SLE
corticosteroids, danazol
tx if +antiphospholipid Ab
warfarin, heparin
other extra manifestations of SLE
non specific fever, fatigue, wt. loss, anemia, visual changes (retinal vasculitis), raynauds phenom, recurrent miscarriages, hair loss, edema, effusions
Prognosis SLE
dep on severity (worse with Renal and CNS)
*infectious disease responsible for 29% death
10 yr survival in more than 90%
etiology of SLE
autoantibodies to nuclear and cytoplasmic antigens destroy cells resulting in tissue damage
*antibody, antigen complexes deposited in tissue, small vessel walls, and basement membrane resulting in inflammation
Pt has positive anti-histone antibodies but is negative for anti-dsDNA and anti-Sm. They complain of arthralgia, myalgia, malaise, and a rash. They take procainamide x 2 mth. Dx and tx?
drug induced SLE
tx: d/c drug, administer steroids
Pt indicates dry mouth and decreased tears in addition to fingers that freq turn white, myalgia, joint pain and hx of chrons. Primary dx? what labs would confirm dx?
Dx: sjogerns
Labs: +Rf, +ANA, CBC anemia of chronic disease
you determine pt has Sjogrens based off sx and labs indicating +Rf, +ANA, CBC anemia of chronic disease. How would you differentiate bw primary sjogren and sjogren related to SLE/RA
of the +ANA, anti SSA or SSB would indicate PRIMARY
anti SSC would indigate sjogren related to SLE/RA
