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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

enzyme responsible for breaking down uric acid?

A

uricase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

pathognomonic sign of gout?

A

tophi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

causes of hyperuricemia? main cause?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how to definitively diagnose gout?

A

identification of monosodium urate crystals in synovial fluid or a tophus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what needs to be done on all synovial fluid aspirations?

A

culture!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

appearance of monosodium urate crystals under polarized light microscopy?

A

needle-like morphology and strong (=) birefringence pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

most important condition to differentiate possible gout from?

A

septic arthritis

gout can also look like pseudogout and rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

radiography appearance of gout?

A

“rat-bite” erosions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

overconsumption of what EtOH increases risk for gout?

A

beer - b/c it is high in purines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cause of pseudogout? where do you see it?

A

calcium pyrophosphate crystals in the joints

see ssxs in knee, wrist or ankle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

triggers of gout?

A
low temperatures
trauma
surgery
chemo
diuretics
stopping or starting allopurinol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what two HTN drugs have a decreased risk of gout?

A

CCBs and losartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
MOA of glucocorticoids?
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
delivery method of cortisone? SEs?
can give intra-articular injection, PO, IM, IV, spray and apply topically SEs: hyperglycemia, insulin resistance, DM, osteoporosis, anxiety, depression, amenorrhea, cataracts, glaucoma
27
primary anti-inflam mech of glucocorticoids?
lipocortin-1
28
action of lipocortin-1?
both suppresses phospholipase A2 (blocks eicosanoid production) and inhibits various leukocyte inflammatory events
29
potential SEs of IM or IA cortisone injections?
pain, infxn, skin pigment changes, loss of fatty tissue and tendon rupture
30
when utilizing cortisone topically what are the 5 medications typically used?
beclometasone, budesonide, fluticasone, mometasone, ciclesonide
31
category of colchicine? indications? MOA?
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
therapeutic index of colchicine?
relatively low
33
how to give colchicine? SEs? overdose sxs?
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
ssxs of colchicine poisoning
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
category of allopurinol? indications? MOA? how to deliver? SEs?
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
allopurinol is a structural isomer of what? what does it inhibit and why is this important in treating gout?
structural isomer of hypoxanthine inhibits enzyme xanthine oxidase which is responsible for successive oxidation of hypoxanthine and xanthine and ultimately uric acid production
37
what are uricosuric meds?
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
SE of uricosuric meds?
can lead to KD stones | so C/I in those who already have a high urine concentration of uric acid
39
category of probenecid/probalan? indications? MOA? how to give? SEs?
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
off-label use of probenecid?
extends the duration of action of penicillin
41
if pt experiences exacerbation of gout following probenecid/probalan therapy what to prescribe next?
can prescribe colchicine