Gout and Pseudogout Flashcards by Paige Hamay

what substance level can you NOT use as a diagnostic measure during a acute attack

uric acid level

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an acute gout flare looks really similar to what? why?

very similar to septic gout because the body attacks MSU crystals the same way as it attacks bacteria

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three characteristics of crystal-induced arthritis

rapid onset, self-limited arthritis, and synovial fluid leukocytosis/phagocytosis of crystals

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what is found in the synovial fluid analysis for gout and pseudogout?

gout- MSU crystals

pseudogout- CPPD

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what two things is gout also called?

podagra- when in 1st MTP joint
OR
uric acid arthropathy

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4 components of gout syndrome

acute gouty arthritis
tophaceous gout- chronic
gouty nephropathy- chronic kidney diseases that produce high levels of uric acid
uric acid kidney stones

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what is primary vs secondary gout

primary- metabolic error or reduced excretion without renal disease
secondary- caused by acquired disease or use of certain drugs

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most people with ____________ DONT develop gout

hyperuricemia (10% have this but gout develops in less than 0.5% of that group)

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prevalence of gout in gender

primarily middle aged men, younger males > females

- women incidence increases until it surpasses males over 80 yrs old

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4 other factors associated with the prevalence of gout

elevated serum Cr levels, body weight, blood pressure, and alcohol intake

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__% of patients report a family member with a hx of gout

40%

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7 risk factors for gout

ethanol ingestion
family hx
meds: caffeine, cytotoxic drugs, diuretics
obesty
HTN
renal failure
hypothyroidism

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diuretic use accounts for 20% of what?

secondary gout

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uric acid is a product of? describe how it goes through the kidney

dietary purines (protein breakdown)
** all of these are filtered at the glomerulus and 80% are reabsorbed at proximal tubule

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hyperuricemia results from one of two things?

decreased renal excretion of uric acid or increased metabolic production

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80-90% of patients with primary gout have this problem

renal undersecretion (idiopathic)

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urate overproduction for primary gout accounts for __-__% of cases. what is this due to?

10-20%

due to HGPRT deficiency or PRPP synthetase overactivity

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what three disease states can cause uric acid undersecretion which leads to secondary gout?

renal insufficiency, polycystic kidney disease, lead nephropathy

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drugs that cause gout have an effect on what body system? what are some of these drugs? (7)

have their effects on renal mechanisms

diuretics, pyrazinamides, niacin, didanosine, salicylates, ethambutol, cyclosporine

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what type of drug can exacerbate an acute attack?

aspirin

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7 conditions that can cause secondary gout- uric acid overproduction

psoriasis
glycogen storage disease
lymphoproliferative disease
hemolytic anemias
polycythemia vera
myeloproliferative disease
other malignancies

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what are three other random things that can cause secondary gout?

obesity, ethanol consumption (beer), and hypoxemia/tissue hypoperfusion

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hyperuricemia is classified as levels over what?

serum urate over 2.5 SD above the mean

OR level above which urate concentration exceeds its saturation point in serum (>7.5-8 mg/dl)

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solubility for urate decreases with what?

temperature

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how does saturation impact which joints gout affects?

in extremely joints like feet, ankles, knees, hands elbows, saturation point is much less than 7.0 so impacts these joints first

tophi deposition also occurs in ____ areas. what two places does this usually develop?

cool areas: external ear and olecranon bursa

what factors can affect urate precipitation? (4)

1) . sudden rise or drop in serum urate level (trauma, chemo, radiation) 2) . low temp 3) . low pH 4) . reduced ability to bind to plasma protein (low protein)

at what concentrations does urate precipitate as MSU crystals?

greater than 6.5-7 mg/dl

how do MSU crystals look under microscope?

negatively birefringent needle shaped crystal under polarized light

how is acute gout formed?

PMNs phagocytose crystals and release inflammatory mediators. Mediators (toxic superoxide radicals, prostaglandins, leukotrienes) cause inflammation

most of the long term damage of gout is caused by?

inflammatory response

acute gout: sudden onset of what? affects how may joints? usually affects what joint?

sudeen onset of pain and swelling with exquisite tenderness - usually monoarticular (80-90%) - usually lower extremity: 1st MTP joint is most common, then ankle and knee

acute gout may also affect ________

bursa: olecranon or prepatellar

do you see acute gout on radiology?

no, usually not seen until 6-12 years after initial attack (AND only presents in 50% of patients)

what are some soft tissue findings in acute gout (4)

1) . calcific deposits in gouty tophi (50% of people) 2) . soft tissue masses near an affected joint 3) . bilateral olecranon bursitis 4) . aural calcification

acute gout: what happens to joint space initially? absence of? what is eroded? what kind of swelling?

joint space is preserved initially; absence of periarticular demineralization (bone that has had calcium removed and is damaged); joint margins are eroded and sclerosis present; periarticular swelling in acute monoarticular gout

what joint finding is present in late disease course (gout)

cartilage destruction

how long does it usually take to develop tophaceous gout?

average of 12 years

what three things are characteristic of tophaceous gout?

1) . wider distribution of joint involvement 2) . chronic joint destruction 3) . urate deposition in and around joints including tendon and other soft tissue

where can subcutaneous tophi be found?

- periarticular and bursal tissues at knees, elbows and along tendons - can also be found at non-articular sites (such as pinna, visceral locations- myocardium, pericardium, aortic valves, epidural spinal regions)

how does subcutaneous tophi feel?

firm and mobile

how is gout related to a fever?

acute gout attacks are not necessarily associated with a fever

what are three labs that support gout diagnosis?

elevated WBC with left shift elevated ESR hyperuricemia

can xray be used in acute gout diagnosis?

seldom used acutely - might be able to see "punched out" erosions in and around joints OR overhanging edge sign (periosteum, vascular layer, over growing erosions)

three objectives for gout treatment

1) . termination and prevention of acute attacks 2) . correction of hyperuricemia (inhibit further precipitation of MSU crystal and promote absorption of current crystals) 3) reduce joint inflammation and pain

when do we treat hyperuricemia for gout?

after an acute attack is relieved (uricosuric med) | ** drugs used to tx acute attack have no effect on serum urate level

what to use first for acute gout attack tx?

colchicine- 1.2 mg dose and then 0.6 mg one hour later (0.6 mg 1-2x per day each day after until flare resolves)

what acute gout agent is great for young healthy adults?

NSAIDs (be careful in renal or elderly pts)

what do you not use in acute gout attack tx?

aspirin- causes retention of uric acid

what is another agent, besides colchicine and NSAIDs, used for acute gout tx

steroids intraarticular for one joint oral for multiple affected joints

what are two drugs to treat chronic gout?

1) . probenecid- inhibits renal tubular urate reabsorption | 2) . allopurinol- inhibits conversion of xanthine to uric acid

5 prevention techniques for gout

1) . hydration 2) . moderate alcohol consumption 3) . avoid purine rich foods 4) . maintain ideal weight 5) . adherence of lifelong use of meds

pseudogout is also called what? what metabolic disorders is it often associated with? (5)

CPPD - hyperparathyroidism - hemochromatosis - hypothyroidism - hypomagnesemia - hypophosphatemia

what two places are CPPD crystals found?

joints and periarticular tissues

what is chondrocalcinosis?

calcification of articular cartilage, menisci, and synovium

what can pseudogout lead to?

acute, subacute, or chronic arthritis of wrists (most common), knees, elbows, shoulders, ankles

pseudogout articular damage is _________

progressive, although the disease is not severe in most people

pseudogout is dz of the _________

elderly >70 yr | no difference between male and female

how are crystals formed in pseudogout?

elevated levels of either calcium or pyrophosphate

how do you diagnose pseudogout? where are the crystals located?

synovial fluid analysis with weakly positive (bluish-white) birefringence (crystals are rhomboid or rod shaped) - crystals can be intra or extra cellular

what do xrays show you for pseudogout?

chondrocalcinosis of the articular cartilage (build up of calcium on the cartilage)

what do you use for acute treatment of pseudogout?

similar to gout** - NSAIDs (use with caution in elderly) - Steroids - Colchicine- use with caution in elderly, if at all used - don't really use allopurinol and related uricosuric meds