ICM - Rheum 1 Flashcards
uric acid level for hyperuricemia (doesn’t always lead to gout…most asymptomatic)
>6.8 mg/dL
uric acid is end product of this process
purine metabolism
these dietary excesses increase risk for gout
meat, seafood, alcohol
cytokine that is important in pathogenesis of acute gout flare (after crystals released into joint/bursae)
IL-1
normal urine uric acid excretion amount in 24 hours
250-75 mg
these can cause primary overproduction of uric acid
deficient HGPRT (salvage pathway), overactive PRPP, G6PD deficiency, F1P aldolase deficiency
normal amount of filtered load of uric acid that is excreted
10%
primary causes of renal underexcretion
deficiency in urate exporter, medullary cystic kidney disease (kids)
normal time it takes for acute gouty arthritis to resolve
3-10 days
80% of initial acute gouty arthritis attacks will be this
monoarticular
crystal in gout joint aspiration
monosodium urate monohydrate
crystal in pseudogout joint aspiration
calcium pyrophosphate dihydrate
perdiod after 1st gout attack…additional acute attacks (usually within 2 years), shorter asymptomatic periods, sever, prolonged polyarticular flares
intercritical gout
solid urate deposits in chronic gout
tophi
to prevent gout progression, want to lower serum urate to below this level (deplete total body urate pool)
6 mg/dL
typical drug of choice to treat gout
NSAIDs
alternative to NSAID treatment for gout, but has more side effects (*diarrhea*)
colchicine
typical length of corticosteroid treatment for gout
5-7 days
allopurinol inhibits this enzyme in purine metabolism (to reduce uric acid levels)
xanthine oxidase
this is overproduced in CPPD
cartilage pyrophosphate
where cartilage pyrophosphate crystals deposit
joint articular cartilage (hyaline), fibrocartilage, ligaments
x-ray showing calcification of cartilage and fibrocartilage
chondrocalcinosis
where are gout crystals mostly located?
synovium (versus CPPD in cartilage)
recessive renal tubular disorder –> older child/adult with hypokalemia, metabolic alklaosis, hypomagnesium, hypocalcuria, leg/arm cramps, weakness, polyuria, nocturia, chondrocalciosis
Gitelman syndrome
acute CPP crystal arthritis –> lasts 1-3 weeks, flares after parathyroidectomy, mono or oligo-articular arthritis
pseudogout
where CPP crystal arthritis most commonly affects
knee (50%), wrist, shoulder, ankle
chronic CPP crystal inflammatory arthritis –> CPPD crystals demonstrable in joint fluid of RA clinical joints, radiographic changes like OA
pseduo-RA
possible treatments for BCP crystal deposition arthropathy
NSAIDs, COX-2 inhibitors, steroid injection, irrigation (ultrasound to degrade and lowering serum phosphate also)
stain for calcium oxalate crystal test (appear bipyramidal)
alizarin red
where are calcium oxalate depositions found? (crystals can break off, causing acute synovitis stimulating synovial cell proliferation and enzyme release–> articular destruction)
bone, articular cartilage, synovium, periarticular tissue
bone that is lost in osteoporosis
trabecular (cortical also in type II)
common fractures in type I osteoporosis (postmenopausal women mostly, lost of trabecular bone)
compression fractures and Colles fracture
most common fractures in type II osteoporosis
femoral neck, proximal humerus, pelvis
risk factors for osteoporosis
female, estrogen depletion, Ca/VitD deficiency, low peak bone mass, decreased physical activity, hypogonadism, hyperthyroidism, smoking, corticosteroids
most common clinical finding of osteoporosis
vertebral body compression factors
gold standard for diagnosis of osteoporosis (measures bone density and compares to young adult)
DEXA
DEXA score in this range is osteopenia
1-2.5 below
DEXA score in this range is osteoporosis
less than 2.5
who should get DEXA screening?
women>65, postmenopausal50 with fracture
first line pharmacologic treatment for osteoporosis; how do these work?
bisphosphonates; inhibit osteoclast function
osteoporosis therapy that helps build bone –> must limit treatment for 2 years due to increased risk of osteosarcoma
PTH
possible treatment for osteoporosis….can decrease pain of vertebral fractures (not used as much anymore)
calcitonin
formation of new bone at joint surfaces
eburnation
formation of new bone in periarticular tissues
osteophyte formation
greatest modifiable risk factor for OA
obesity
gene that may be mutated to increase risk of OA
COL2A1
radiographic evidence of OA
joint space narrowing, osteophytes, subchondral cysts and sclerosis
nodal generalized OA has predisposition to affect these joints
knee, hip and spine
first line pharmacological treatment for OA; what is just as effective but has possible GI side effect?
acetaminophen; NSAIDs
DDX for OA
Ca pyrophosphate deposition disease, RA, infectious monoarticular disease, psoriatic arthritis
chronic inflammatory arthritis that affects the *synovium*
RA
how do joints feel in RA?
soft and squishy (warm, boggy)
cardiac manifestations of RA
pericarditis, myocarditis, CVD
pulmonary manifestations of RA
pleural effusion (low glucose and low complement), interstitial fibrosis
ocular manifestations of RA
Sjogrens, corneal inflammation, scleritis
these are pathognomonic for RA
rheumatoid nodules
seropositive RA, neutropenia, splenomegaly, occasional leg ulcers (hematological manifesation of RA)
Felty’s syndrome
these titer levels are good for prognosis of RA (higher=more severe)
RF
very specific test for RA (96%) –> helpful in diagnosis and prognosis
ACCP
anemia seen in RA
normocytic normochromic
diagnostic criteria for RA (from step up)
inflammatory arthritis more than 3 joints, >6 weeks, elevated CRP/ESR, + RF/ACPA, radiographic changes
drug of choice for pain control in RA
NSAIDs
best initial DMARD for RA
methotrexate
first line agent DMARDS for RA
methotrexate, leflunomide, hydroxychloroquine, sulfasalazine
