Intro to joint disease mono and polyarthritis Flashcards
patterns of arthritis (2 categories; 4 kinds)
inflammatory vs noninflammatory; monoarthritis vs polyarthritis
causes of inflammatory monoarthritis (3)
trauma
crystals: monosodium urate (gout) vs calcium pyrophosphate (pseudogout)
septic joint
Clinical presentation of joint inflammation (5)
morning stiffness;
erythema and warmth (in crystals and septic joints) may not be prominent in others
synovitis: thickening of synovium around joints/TTP
Joint inflammation
diagnostic tools-4 lab tests and 1 imaging technique
-lab tests for inflammation:
ESR
CRP
-peripheral blood leukocytosis (septic arthritis)
-joint fluid analysis
-xrayWBC and PMN values for synovial fluid analysis for:
noninflammatory
Inflammatory
Septic
noninflammatory: WBC 2,000 PMN2,000; PMN 50-90%
septic: WBC > 50,000; PMN >90%
Gout
Definition
cause (general)
metabolic disorder resulting in elevated uric acid levels (hyperuricemia) beyond saturation.
Could be due to underexcretion (90%) or overproduction (10%)
Gout
Patient population
Estrogen’s effect on urate excretion?
one increasing risk factor in the US
elderly men more than women, but increased incidence in women post menopause (because estrogen promotes urate renal excretion)
Obesity is a risk factor
Input sources of nucleoproteins and nucleotides? where do we get it from?
1/3 nucleoproteins and nucleotides come from diet and 2/3 comes from our own cells.
What happens to the nucleoproteins and nucleotides we consume?
converted to adenine and guanine nucleotides
metabolized adenine and guanine become what? about how much is that? in mg
uric acid (about 1,000 mg)
How is uric acid excreted? in what proportions? in mgs?
1/3 gut excretion (bacterial degradation) about 200mg/day
2/3 renal excretion (10% of filtered load (AKA 80%) reabsorbed) 600mg/day
Hyperuricemia
causes of overproduction (4)
causes of underexcretion (4)
Overproduction (10%):
enzymatic abnormalities, increased cell turnover, diet, ETOH
Underexcretion (90%):
metabolic syndrome, renal disease, drugs (diuretics, cyclosporine), ETOH
Physical findings of Gout
(2 sx; 1 microscopic finding)
potential presentation in more serious gout disease (2)
- joint/extremity pain
- swelling, warmth (Podagra-joint swelling)
- MSU crystals upon microscopy; often phagocytosed by PMNs
- potentially polyarticular
- potentially tophaceous gout (nodules on ears; “punched out” lesions and over hanging edges upon x-ray)
Precipitation of gout attack (3)
- elevation of uric acid
- reduction of uric acid–because stored crystals start mobilizing
- release of crystals from preformed deposits
Kidney filtration of uric acid: What percent is filtered at each of the following parts?
proximal tubule
descending limb
ascending limb
collecting duct
Proximal tubule 99% reabsorbed
Descending limb loop of henle 50% is secreted
Ascending loop of henle 80% is reabsorbed
collecting duct 10% is excreted
Onset of Gout is closely correlated to what?
At what value will 90% of men experience gout?
Gout is correlated to uric acid levels… at 9 or above 90% of men will have gout
Gout vs. CPPD
Crystal name
clinical description upon lab examination
color
Gout:
- monosodium urate crystals;
- negative bifrengent when indicator is PARALLEL
- YeLLOW when parallel
Pseudogout:
- calcium pyrophosphate
- positive bifrengent when indicator is parallel
- blue when parallel
What is polyarticular gout?
Gout involving multiple joints
What is Tophaceous gout? Clinical presentation (4)
presence of crystal accumulation. presentation include nodules on ears, large abscesses of calcium pockets, overhaning joint edges, and punched out bone
Inflammation cascade induced by MSU crystals. What does it end it? What are the steps? (5)
ends in recruitment of neutrophils.
Phagocytosis of crystals by monocyte–>activation of inflammation signals within inflammasome–> IL1B is produced–> IL1B triggers endothelial cells to produce inflammatory cytokines–>recruitment of neutrophils
Calcium pyrophosphate dihydrate Depositing disease.
etiology of majority cases?
patient population?
- mostly due to overproduction of inorganic pyrophosphate
- patient population is 12% of elderly. 5% at 60 years rise to 30% in 90 year olds
How do calcium pyrophosphate crystals form?
pyrophosphate crystals exit cell via the “ank” channel and bind to calcium to form calcium phyrophosphate
Common causes of CPPD (4) and the labs to test for CPPD?
- Hemochromatosis-Fe, Total Iron binding capacity (TIBC)
- Hypophosphatasia- alkaline phosphatatase function
- Hypomagnesemia-Mg level
- Hyperparathyroidism-Ca and PTH level
Psuedogout target joints
similar to gout but LARGER joints such as
Knee, wrist, shoulders
How to diagnose CPPD?
What is an indication for CPPD?
indication is “chondrocalcinosis” upon x-ray; this is not always seen.
Dx: positive bifringent crystals upon joint fluid analysis
Clinical Presentation of CPPD (pseudogout) (3) and the most common presentation of pseudogout
- asymptomatic-most common
- pseudogout
- Osteoarthritis–often widespread including shoulder/wrist…then you should be suspicious of pseudogout
- RA-like (MCP joint enlargement)
What is chondrocalcinosis?
deposition of calcium pyrophosphate crystals in hyaline cartilage
Therapeutic goals of treating Gout (4)
- increase urate excretion
- decrease urate synthesis
- inhibit inflammation
- symptomatic relief
