Crystalline Arthropathies Flashcards

1
Q

what is hyperuricemia?

A

serum urate values >6.8 mg/dl

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2
Q

what is gout?

A

inflammatory arthritis developing as a consequence of urate deposition in the joint

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3
Q

where does most acute gouty arthritis occur?

A

1st MTP (podagra)- (90% )

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4
Q

what is the order of freuqnecy of joints involved?

A
  1. 1st MTP
  2. mid-foot
  3. ankle
  4. heel
  5. knee
  6. wrist
    7;. finger
  7. elbow
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5
Q

what are the 4 stages of gout?

A
  1. asymptomatic hyperuricemia
  2. acute flares
  3. intercritical segments
  4. advanced gout
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6
Q

what is asymptomatic hyperuricemia?

A

elevated serum urate with no clinical manifestations of gout

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7
Q

what happens in acute flares stage of gout?

A

acute inflammation in the joint caused by urate crystallization

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8
Q

what happens in intercritical segments?

A

the intervals btwn acute flares

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9
Q

what happens in advanced gout?

A

long-term gouty complications of uncontroleld hyperuricemia

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10
Q

what are some pathognomonmic changes of gouty tophus on radiograph?

A

“overhanging edges” with periarticular erosions

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11
Q

why is gout on the rise?

A
  • increased longevity
  • aging population
  • increased comorbidity
  • low dose aspirin
  • thiazides
  • fructose intake
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12
Q

which degradation pathway produces uric acid?

A

purine degradation

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13
Q

which enzyme is targeted for treatment of gout because it catalyzes the final conversion to uric acid?

A

xanthine oxidase

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14
Q

at what level does urate crystallize?

A

at a level of 6.8 mg/dL

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15
Q

which medications are risk factors for development of gout?

A
  1. diuretics- lead to increased uric acid reabsorption
    2, low dose aspirin- increased serum urate and decreased uric acid clearance
  2. pyrazinamide, ethambutol, niacin- gout observed at higher incidence
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16
Q

which patient population is at risk for development of gout?

A

transplant patients

bc they are often on calcineurin inhibitors that put them at risk for hyperuricemia

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17
Q

which drug is a contrindication to allopurinol use?

A

azathioprine

*bc it needs xanthine oxidase, which allopurinol blocks

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18
Q

people who have gout often have what other disease?

A
obesity
metabolic syndrome
Diabetes mellitus
heart failure
hyperlipidemia
hypertension
19
Q

what is the gold standard for diagnosing gout?

A

synovial fluid analysis- visualizing MSU crystals

20
Q

how would you describe gout crystals?

A

negatively birefringent under polarized light

21
Q

what acute changes are seen in gout radiographs?

A

acutely, often only soft tissue swelling is seen

22
Q

what chronic changes are seen in gout radiographs?

A
  • “overhanging edges”
  • erosions w/ demarcated round deficits with sclerotic margins
  • very destructive
23
Q

how do you terminate acute flare?

A
  1. control crystal-induced inflammation and pain using NSAIDs, colchicine, steroids
24
Q

what are the critical considerations for terminating the acute flare?

A
  • rapid initiation of therapy

- appropriate duration of therapy

25
Q

which drug to treat gout-inflammation is contraindicated in dialysis patients?

A

colchicine

26
Q

which drug should not be given thru IV?

A

colchicine

27
Q

what is the first-line treatment for gout?

A

intraarticular corticosteroids

28
Q

what are 2 approved urate-lowering agents for gout?

A

uricosuric agents

xanthine oxidase inhibitor (allopurinol & febuxostat)

29
Q

what are the limitations of uricosuric agents like probenecid?

A
  • efficacy dependent on functioning kidneys (Crcl>50 mL/min)
  • 2x a day dosing
  • risk of UA crystallization, stone formation
30
Q

what are the advantages of xanthine oxidase inhibitors?

A
  • single daily dose
  • efficacious in patients w/ renal insufficiency
  • effective for both overproducers and underexcretors
31
Q

what is the #1 side effect of allopurinol?

A

ironically, it is gout flares.

lowering serum urate mobilizes deposited crystals

32
Q

what are the drug interactions with allopurinol?

A

azathioprine

6-mercaptopurine

33
Q

what is the 2nd most common side effect of allopurinol?

A

severe hypersensitivity syndrome (a rash that occurs early on in treatment)

34
Q

what are prophylactic treatments for gout flares?

A

NSAIDs, colchicine

*initiate agents prior to starting urate-lowering therapy

35
Q

what is the formation of CPPD crystals in articular hyaline and fibrocartilage called?

A

CPPD deposition disease

36
Q

what is the CPPD -crystals induced inflammation called?

A

pseudogout

37
Q

what is severe, atypically distributed structural joint damage called?

A

pyrophosphate arthropathy

38
Q

what is pathologically or radiologically evident cartilage calcification called?

A

chondrocalcinosis

39
Q

what age population gets pseudogouts?

A

elderly , 80-90 y/o

40
Q

which metabolic disease is associated with CPPD?

A

hemachromatosis

41
Q

what is the order of likelihood that psuedogout affects joints?

A

knees
wrists
shoulders
ankles

42
Q

describe the cryastals in pseudogout

A

blue (+) birefringent crystals

43
Q

describe treatment for CPPD.

A

no mechanis, to reduce CPPD crystal load so is more frustrating to treat