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Lex Clin Pharm 3 > Gout and Hyperuricemia > Flashcards

Gout and Hyperuricemia Flashcards

1
Q

gout

A

inflammatory arthritis that develops in people who have increased uric acid in the blood

uric acid forms needle like cyrstals in joints and cause sudden and severe episodes of pain

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2
Q

clinical progression of gout

A

1 asymptomatic hyperuricemia

  1. acute gouty arthritis
  2. interval/intercritical gout
  3. chronic trophaceous gout
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3
Q

asymptomatic hyperuricemia

A

no dug therapy just monitor

Only 20% of pts with elevated uric acid develop gout

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4
Q

acute gouty arthritis

A

inflammatory response, treatment needed

b. Must be differentiated from:
i. Pseudogout – build up of calcium deposits
ii. Acute septic arthritis – joint aspiration

NSAID(indomethacin, naproxen, sulindac)
colchicine,
corticosteriods

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5
Q

interval/intercritical gout

A

time period in between attacks

Prophylactic or anthyperuricemic therapy

colchicine

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6
Q

chronic trophaceous gout

A

long term buildup of uric acid:

Solid urate in connective tissue
Very rare due to effective meds
If untreated 60% of pts will develop tophi

Risk factors: poor compliance with medication, chronic renal insufficiency

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7
Q

risk factors for acute gouty arthritis

A

trauma/surgery,
alcohol consumption,
dietary overindulgence,
drugs (diuretics, low dose ASA, Niacin, cyclosporin),
rapid lowering of uric acid (allopurinol)

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8
Q

GOAL of treatment

A

relieve pain and inflammation

do not start or stop hypouricemia drugs until 3 weeks after acute attack: immobilzation of uric acid and drugs will mobilize it

it will increase uric acid in blood = increase risk of acute attack

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9
Q

prophylactic therapy

A

severe attacks of gouty arthritis
complicated course of uric acid nephrolithasis
substantially increased serum uric acid (>10mg/dl)
24 hr urinary excretion of uric acid more than 1000mg

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10
Q

do not initiate anti-hyperuricemic agents unless:

A

pt has frequent acute attacks (1-2/yr)
clinical radiographic signs of acute gouty arthritis
presence of tophacous deposits
evidence of urate nephroliathasis

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11
Q

Tx options

A

NSAIDS
colchicine
corticosteriods

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12
Q

NSAIDS

A

indomethacin, naproxen, sulindac

MOA: inhibitng COX-2 metiated PGs and syntheisis at site of injury

USE: acute gout attack

dangerous in prophlyaxis

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13
Q

Cholchicline

A

reduced inflammatory response to depsoited crystals
diminished PMN phagocytosis of crystals
blocks cellular response to depsotied crystals
CYP450 3A4 involved in metabolism

USE: acute gout attack, prophylaxis

ADR: GI intolerance, heme/penias, hepatomeagly (inc LFT), myopathy

drug interactions: Strong 3A4 inhibitors, p-pg inhibitors,s tatins, fibrates, dogoxin

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14
Q

corticosteriods

A

prednisone

acute gouty attack when reistsent to toher therapy ot pt cannot tolerate NSAIDs

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15
Q

antihyperuricemic drugs

A

uricosuric agents (probenecaid)

xanthine oxidase inhibitors (allopurinol, febuxostat)

uric acid trabnsporter inhibitors (lesinurad, pegloticase, rasburicase)

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16
Q

uricosuric agents

A

probenecaid

USE: normal renal function, under excrete uric acid, negative hx of nephrolithias

MOA : antagonist of URAT1 transporter to block uric acid reabsorption -> increase uric acid secretion

ADR: precipiation of acute attack, nephroliathisis, GI intolerance, hypersenstivity reactions

NOT EFFECTIVE in over producers

17
Q

Xanthinine oxidase inhibitors

A

allopurinol (high risk first line) , febuxostat (intol to allo)

MOA: inhibits breakdown of xanthinine into uric acid

effective for over and under excreters

ADR: hypersensitivity reactions, allopurinol desensitization

drug interactions:
azathiopurine
mercaptopurine
ACEI
Warfarin
18
Q

uric acid transport inhibitor

A

lesinurad

pegloticase, rasburicase

19
Q

lesinurad

A

uric acid transport inhibitor

MOA: inhibit URAT1

used in combo with xanthinine oxidase inhibitors for hx of hyperuricemia

ADR: not monotherapy

20
Q

petloticase

A

indicated for adult pts who are refractory to conventional therapy

MOA: catalyzes oxidation of uric acid to readily eliminated metabolite

ADR: anaphylaxis, infusion reactions, G6PD deficency assoc with hemolysis, methmeglobinemia

21
Q

rasburicase

A

hyperuricemia due to malignancy in pts with risk of tumor lysis syndrome

MOA: catalyzes oxidation of uric acid to readily eliminated metabolite

ADR: anaphylaxis, infusion reactions, G6PD deficency assoc with hemolysis, methmeglobinemia

Lex Clin Pharm 3 (5 decks)

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