Gout Flashcards

1
Q

what is gout considered?

A

a crystal induced arthropathy

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2
Q

what type of crystals cause gout

A

monosodium urate monohydrate crystals

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3
Q

where can the crystals deposit?

A

joint, bursae, tendon

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4
Q

are males or females more affected? age?

A

males

30-60

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5
Q

when tissues become supersaturated, the urate salts precipitate, in the form of needle-like crystals called….

A

NEGATIVE BIFRINGENT CRYSTALS

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6
Q

what is the role of the WBCs

A

they attack the negative bifringent crystals and cause an acute attack

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7
Q

uric acid is an end-stage by-product of what?

A

purine metabolism

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8
Q

how do humans normally remove uric acid

A

renal metabolism

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9
Q

when might hyperuricemia develop

A

when the saturation level of uric acid drops below 6.8mg/dL in the urine. then it’’ deposit in the soft tissues

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10
Q

what are the two reasons for accumulation of urate?

A
over producers (10%)
underexcreters (90%)
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11
Q

what are the RFs for over producers

A
overconsumption of purines (seafood, meat, fructose, soft drinks, wine) OR production of excessive amts of uric acid endogenously
ETOH
myeloproliferative d/o
psoriasis
hemolytic anemia
cell lysis-chemotherapy
excessive exercise
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12
Q

what are the reasons for someone to be an underexcreter?

A
inability to excrete uric acid in the urine
medications
kidney dz
starvation
dehydration
chronic ETOH use
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13
Q

what causes an acute flare?

A

an acute increase or decrease in urate levels that may lead to the production, exposure of shedding of crystals

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14
Q

what can cause changes in levels of urate?

A

acute alcohol ingestion
acute overindulgence in high purine foods
rapid weight loss
dehydration

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15
Q

can gout be genetic?

A

yes! 3 genes thought to be involved

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16
Q

what is the MC presentation?
when does it reach max intensity?
when does it improve?

A

commonly starts as monoarticular
1st MTP - “Podagra”
12-24 hrs
improvement of sx within days to weeks

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17
Q

what might you see on a severe attack (hint: it might look similar to a septic arthritis)

A

severe pain, redness, warmth, swelling
+/- fever
you may have arthritis at other sites (finger joints, instep, ankle, knee)

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18
Q

what can happen to attacks over time?

A

they become more severe and polyarticular over time

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19
Q

what if attacks are left untreated?

A

they become more frequent and abate more slowly with time

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20
Q

what is the stage of gout when they “get out of their attack”

A

intercritical gout

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21
Q

20 years of untreated urate deposition can lead to

A

chronic tophaceous gout

22
Q

what are tophi

A

urate crystal masses surrounded my inflammatory cells and fibrosis

23
Q

what are the characteristics of the tophi

A

firm, movable, yellowish. they ulcerate with chalky material

24
Q

where are some common places to have tophi

A
pinna of the ear
over involved joints
extensor surfaces of the forearm
olecranona
infrapatellar
Achilles tendon
25
diagnosis of acute attack
arthrocentesis - urate crystals in joint fluid are diagnostic (neg biferengent - bright yellow) plain radiographs - erosions with overhanging edges
26
why must you get the sample from the athrocentesis to the lab right away?
over time, the crystals dissolve
27
what is the WBC count in the synovial fluid?
high! | >15,000 but usually
28
what is out goal in an acute attack?
relieve pain and inflammation | *note: symptoms do resolve on their own in weeks, but treating with meds improve sx more quickly
29
1st line 2nd line 3rd line for acute attacks of gout
NSAIDS (Indomethacin or Naproxen) Colchicine Glucocorticoids (oral or intra-articular)
30
what are the contraindications to NSAID use?
CKD with Cr clearance
31
when should tx with NSAIDs be stopped?
1-2 days after clinical symptoms resolve
32
when is Colchicine used and what is its MOA?
for pt with NSAID intolerance or with an absolute indication to NSAID use Inhibits neutophil chemotaxis and inflammatory mediator release only used for gout (still gonna have to give em something for pain)
33
what are the two options for glucocorticoids?
prednisone (oral), triamcinolone (intraarticular)
34
should you use the intraarticular triamcinolone if you have more than 1 or 2 joints involved?
no
35
what helps with gout risk reduction?
weight loss reduce ETOH intake stop diuretic stop ASA
36
what do diuretics and ASAs do?
increase serum urate levels
37
when should you start prophylaxis (urate lowering therapy)?
2 weeks after acute flare has resolved
38
what are the 3 options for intercritical period treatment (prophylaxis)
Probenecid Allopurinol Febuxostat (Uloric)
39
what is the MOA of probenecid and what are the contraindications
promotes renal clearance of uric acid by inhibiting urate anion exchangers in the proximal tubule that mediates urate reabsorption. CANNOT use in pts with nephrolithiasis or impaired renal function. mult doses/day
40
MOA of Allopurinol and Febuxostat (Uloric)
xanthane oxidase inhibitor (xanthane oxidase produces uric acid)
41
what are the SE's of Allopurinol
mild rash may disappear if stop then restart diarrhea and GI distress can cause hypersensitivity syndrome of eosinophilia, fever, hepatitis, poor renal funx, erythematous desquamative rash.. stop if it develops bc it could lead to SJS, TEN
42
allopurinol + what antibiotic causes rash in 20%
ampicillin
43
what is more effective for hyperuricemia than allopurinol but more expensive
Febuxostat (Uloric)
44
does Uloric have a hypersensitivity reaction like allopurinol?
nope
45
what is CPPD
calcium pyrophosphate deposition disease
46
what type of crystals are seen in CPPD
calcium pyrophosphate crystals
47
what do the calcium crystals in CPPD cause
chondrocalcinosis (deposits on cartilage)
48
is CPPD mono or poly articular?
can be both
49
what is the initial location for CPPD
knee
50
whats the onset of CPPD compared to gout
slower
51
what does joint fluid show for CPPD
rhomboid crystals
52
what is the tx for CPPD
joint aspiration and NSAIDS