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Clin Med- P > Gout and Pseudogout > Flashcards

Gout and Pseudogout Flashcards

1
Q

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

A

uric acid level

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2
Q

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

A

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

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3
Q

three characteristics of crystal-induced arthritis

A

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

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4
Q

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

A

gout- MSU crystals

pseudogout- CPPD

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5
Q

what two things is gout also called?

A

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

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6
Q

4 components of gout syndrome

A

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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7
Q

what is primary vs secondary gout

A

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

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8
Q

most people with ____________ DONT develop gout

A

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

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9
Q

prevalence of gout in gender

A
  • primarily middle aged men, younger males > females

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

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10
Q

4 other factors associated with the prevalence of gout

A

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

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11
Q

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

A

40%

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12
Q

7 risk factors for gout

A 
ethanol ingestion
family hx
meds: caffeine, cytotoxic drugs, diuretics
obesty
HTN
renal failure
hypothyroidism
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13
Q

diuretic use accounts for 20% of what?

A

secondary gout

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14
Q

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

A 
dietary purines (protein breakdown)
** all of these are filtered at the glomerulus and 80% are reabsorbed at proximal tubule
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15
Q

hyperuricemia results from one of two things?

A

decreased renal excretion of uric acid or increased metabolic production

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16
Q

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

A

renal undersecretion (idiopathic)

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17
Q

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

A

10-20%

due to HGPRT deficiency or PRPP synthetase overactivity

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18
Q

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

A

renal insufficiency, polycystic kidney disease, lead nephropathy

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19
Q

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

A

have their effects on renal mechanisms

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

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20
Q

what type of drug can exacerbate an acute attack?

A

aspirin

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21
Q

7 conditions that can cause secondary gout- uric acid overproduction

A 
psoriasis
glycogen storage disease
lymphoproliferative disease
hemolytic anemias
polycythemia vera
myeloproliferative disease
other malignancies
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22
Q

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

A

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

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23
Q

hyperuricemia is classified as levels over what?

A

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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24
Q

solubility for urate decreases with what?

A

temperature

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25
Q

how does saturation impact which joints gout affects?

A

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

26
Q

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

A

cool areas: external ear and olecranon bursa

27
Q

what factors can affect urate precipitation? (4)

A

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)

28
Q

at what concentrations does urate precipitate as MSU crystals?

A

greater than 6.5-7 mg/dl

29
Q

how do MSU crystals look under microscope?

A

negatively birefringent needle shaped crystal under polarized light

30
Q

how is acute gout formed?

A

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

31
Q

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

A

inflammatory response

32
Q

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

A

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
33
Q

acute gout may also affect ________

A

bursa: olecranon or prepatellar

34
Q

do you see acute gout on radiology?

A

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

35
Q

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

A

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

36
Q

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

A

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

37
Q

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

A

cartilage destruction

38
Q

how long does it usually take to develop tophaceous gout?

A

average of 12 years

39
Q

what three things are characteristic of tophaceous gout?

A

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

40
Q

where can subcutaneous tophi be found?

A
  • 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)
41
Q

how does subcutaneous tophi feel?

A

firm and mobile

42
Q

how is gout related to a fever?

A

acute gout attacks are not necessarily associated with a fever

43
Q

what are three labs that support gout diagnosis?

A

elevated WBC with left shift
elevated ESR
hyperuricemia

44
Q

can xray be used in acute gout diagnosis?

A

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)

45
Q

three objectives for gout treatment

A

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

46
Q

when do we treat hyperuricemia for gout?

A

after an acute attack is relieved (uricosuric med)

** drugs used to tx acute attack have no effect on serum urate level

47
Q

what to use first for acute gout attack tx?

A

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)

48
Q

what acute gout agent is great for young healthy adults?

A

NSAIDs (be careful in renal or elderly pts)

49
Q

what do you not use in acute gout attack tx?

A

aspirin- causes retention of uric acid

50
Q

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

A

steroids
intraarticular for one joint
oral for multiple affected joints

51
Q

what are two drugs to treat chronic gout?

A

1) . probenecid- inhibits renal tubular urate reabsorption

2) . allopurinol- inhibits conversion of xanthine to uric acid

52
Q

5 prevention techniques for gout

A

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

53
Q

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

A

CPPD

  • hyperparathyroidism
  • hemochromatosis
  • hypothyroidism
  • hypomagnesemia
  • hypophosphatemia
54
Q

what two places are CPPD crystals found?

A

joints and periarticular tissues

55
Q

what is chondrocalcinosis?

A

calcification of articular cartilage, menisci, and synovium

56
Q

what can pseudogout lead to?

A

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

57
Q

pseudogout articular damage is _________

A

progressive, although the disease is not severe in most people

58
Q

pseudogout is dz of the _________

A

elderly >70 yr

no difference between male and female

59
Q

how are crystals formed in pseudogout?

A

elevated levels of either calcium or pyrophosphate

60
Q

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

A

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

61
Q

what do xrays show you for pseudogout?

A

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

62
Q

what do you use for acute treatment of pseudogout?

A

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

Clin Med- P (124 decks)

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