Gout Meds Flashcards

1
Q

gout is a disorder of metabolism of what? what is depositing and where?

A

purine metabolism

uric acid crystallizes in form of monosodium urate and precipitates in joints, on tendons and in surround tissues

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2
Q

enzyme responsible for breaking down uric acid?

A

uricase

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3
Q

pathognomonic sign of gout?

A

tophi

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4
Q

causes of hyperuricemia? main cause?

A

diet
genetic predisposition
under-excretion of urate
main cause is renal under-excretion of uric acid

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5
Q

how to definitively diagnose gout?

A

identification of monosodium urate crystals in synovial fluid or a tophus

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6
Q

what needs to be done on all synovial fluid aspirations?

A

culture!

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7
Q

appearance of monosodium urate crystals under polarized light microscopy?

A

needle-like morphology and strong (=) birefringence pattern

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8
Q

most important condition to differentiate possible gout from?

A

septic arthritis

gout can also look like pseudogout and rheumatoid arthritis

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9
Q

radiography appearance of gout?

A

“rat-bite” erosions

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10
Q

overconsumption of what EtOH increases risk for gout?

A

beer - b/c it is high in purines

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11
Q

cause of pseudogout? where do you see it?

A

calcium pyrophosphate crystals in the joints

see ssxs in knee, wrist or ankle

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12
Q

what pharmaceutical agent increases the risk of gout attacks? what drug within it’s category does not increase the risk? what two other drugs increase the risk of gout?

A

diuretics have been assoc w/gout attacks
hydrochlorothiazide however does not seem to increase the risk
niacin and aspirin increase the risk

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13
Q

triggers of gout?

A
low temperatures
trauma
surgery
chemo
diuretics
stopping or starting allopurinol
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14
Q

what two HTN drugs have a decreased risk of gout?

A

CCBs and losartan

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15
Q

MC spot for a gout attack?

A

big toe joint
can also appear in heels, knees, wrists and fingers
usu pn begins over 204 hrs and during the night

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16
Q

first line tx of gout? CCIs to gout?

A

NSAIDs (indomethacin) are usu first line tx

not recommended in those w/certain health problems such as GI bleed, renal failure, heart failure

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17
Q

what 2 drugs can be used to protect the stomach from NSAID use? which one will speed up damage to the stomach w/NSAID use?

A

protective: PPIs and misoprostol

speed up damage: H2 blockers

18
Q

3 txs for an acute gouty attack?

A

NSAIDs
steroids
colchicine

19
Q

3 prophylactic tx options?

A

colchicine
allopurinol
probenecid

20
Q

category of indomethacin/indocin? indications? MOA? how to deliver?

A

category: NSAID
indications: gout, arthritis, bursitis, migraines, hemicrania, pain and swelling
MOA: COX I and COX 2 inhibitor
generally given PO

21
Q

sampter’s triad?

A

allergy to aspirin or other NSAIDs
nasal polyps
asthma

22
Q

C/Is of indomethacin/indocin? use in caution with what pts?

A

C/Is: allergy to, nasal polyps, children less than 2 yo, severe pre-existing renal and liver damage
caution: hx of ulcers, bleeding tendencies, Parkinson’s, epilepsy, psychotic d/os, concurrent use of potassium sparing diuretics, significant HTN

23
Q

SEs of indometacin/indocin?

A

SEs: bleeding, gastritis, PUD, may exacerbate HTN or CHF

24
Q

category of cortisone? indications? MOA?

A

category: steroid
indications: short-term pn relief and reduced swelling from inflammation of a jt, tendon or bursa as well as for marked allergic rxn or post-EPI tx of anaphylaxis
MOA: decreases inflammation by inhibiting pro-inflammatory proteins

25
Q

MOA of glucocorticoids?

A

bind to glucocorticoid receptor, actives it which in turn up-regulates the expression of anti-inflammatory proteins in the nucleus and represses pro-inflam proteins by preventing the translocation of other transcription facts from the cytosol into the nucleus

26
Q

delivery method of cortisone? SEs?

A

can give intra-articular injection, PO, IM, IV, spray and apply topically
SEs: hyperglycemia, insulin resistance, DM, osteoporosis, anxiety, depression, amenorrhea, cataracts, glaucoma

27
Q

primary anti-inflam mech of glucocorticoids?

A

lipocortin-1

28
Q

action of lipocortin-1?

A

both suppresses phospholipase A2 (blocks eicosanoid production) and inhibits various leukocyte inflammatory events

29
Q

potential SEs of IM or IA cortisone injections?

A

pain, infxn, skin pigment changes, loss of fatty tissue and tendon rupture

30
Q

when utilizing cortisone topically what are the 5 medications typically used?

A

beclometasone, budesonide, fluticasone, mometasone, ciclesonide

31
Q

category of colchicine? indications? MOA?

A

category: mitotic inhibitor
indications: gout (flares and prophylaxis)
MOA: inhibits microtubule polymerization by binding tubulin; availability of tubulin is essential to mitosis therefore inhibited; also inhibits neutrophil motility and neutrophil activity so anti-inflammatory as well

32
Q

therapeutic index of colchicine?

A

relatively low

33
Q

how to give colchicine? SEs? overdose sxs?

A

given PO
SEs: GI upset, anemia, neutropenia, hair loss, peripheral neuropathy, neutropenia, thrombocytopenia
overdose sxs: vomiting, diarrhea, acute renal failure and possible hypovolemic shock, no specific antidotes are known

34
Q

ssxs of colchicine poisoning

A

burning in mouth, throat, fever, vomiting, diarrhea, abd pn, KD failure, hypovolemic shock dt extreme vascular damage and fluid loss through the GI tract, KD damage resulting in low urine output, bloody urine, low WBC count, anemia, muscular weakness, respiratory failure

35
Q

category of allopurinol? indications? MOA? how to deliver? SEs?

A

category: purine analog
indications: hyperuricemia, gout, prophylaxis against tumor lysis syndrome
MOA: xanthine oxidase inhibitor
deliver PO
SEs: N/V, skin rash, Stevens-Johnson Syndrome, toxic epidermal necrolysis, hypersensitivity syndrome: fever, skin rash, eosinophilia, hepatitis, decreased renal fxn

36
Q

allopurinol is a structural isomer of what? what does it inhibit and why is this important in treating gout?

A

structural isomer of hypoxanthine
inhibits enzyme xanthine oxidase which is responsible for successive oxidation of hypoxanthine and xanthine and ultimately uric acid production

37
Q

what are uricosuric meds?

A

substances that increase the excretion of uric acid in the urine thus reducing the concentration of uric acid in blood plasma
by decreasing plasma uric acid levels, uricourics help to dissolve these crystals while limiting the formation of new ones

38
Q

SE of uricosuric meds?

A

can lead to KD stones

so C/I in those who already have a high urine concentration of uric acid

39
Q

category of probenecid/probalan? indications? MOA? how to give? SEs?

A

category: uricosuric
indications: hyperuricemia, gout
MOA: probenecid works by interfering w/the KDs organic anion transporter, which reclaims uric acid from the urine and returns it to the plasma thus reabsorption of uric acid is decreased
give PO
SEs: N/V, skin rash, SJS, hypersensitivity syndrome: fever, skin rash, eosinophilia, hepatitis, decreased renal fxn, gastritis, possible drug induced hepatitis, dizziness, may cause KD stones

40
Q

off-label use of probenecid?

A

extends the duration of action of penicillin

41
Q

if pt experiences exacerbation of gout following probenecid/probalan therapy what to prescribe next?

A

can prescribe colchicine