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MOD 2 Quiz 1 > Medications for Gout > Flashcards

Medications for Gout Flashcards

1
Q

Urate/ uric acid?

A

end product of purine metabolism

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2
Q

Hyperuricemia cause?

A

underexcretion, overproduction

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3
Q

Gout?

A

deposition of monosodium urate crystals in tissues (joints and tendons)
cause inflammatory response/ mediator release

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4
Q

what happens when synoviocytes phagocytose urate crystals?

A

secrete inflammatory mediators, attract polymorphonuclear leukocytes (PMN) and mononuclear phagocytes (MNP) (macrophages)

drugs active in gout inhibit crystal phagocytosis and polymorphonuclear r lecukocyte and macrophage release on inflammatory mediators

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5
Q

Acute treatment of gout goal?

A

relieve pain, not stop the cause

dampen immune response, otherwise cause eroision and permanent damage

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6
Q

Chronic treatment of gout goal?

A

lower and prevent recurrent uric acid

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7
Q

Characteristics of gout?

A 
exquistely painful
typically single joint 
-podagra(big toe), first MTP joint
result of an imbalance btw uric acid production and renal excretion
-hyperuricemia
Asymptomatic hyperuricemia
-does not always cause gout
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8
Q

Characteristics of gouty arthritis?

A 
sudden onset
intense inflammation
distal joints
severe pain
middle aged males
recurrent episodes
influenced by diet and comorbidities
bony eroisions on xray
hyperuricemia
-durgs may exacerbate, thaizedes, loops, salicylates
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9
Q

Acute gouty arthritis?

A

precipitation of monosodium urate crystals

acute inflammatory response

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10
Q

Chronic?

A 
chronic arthritis
joint destruction
tophi
renal calculi and damage
-nephrlithiasis and neuropathy
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11
Q

First attack?

A

short duration
-resolves within a few days to several weeks (if untreated)
typically involves one joint
subsequent attacks may last weeks and involve many joints

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12
Q

Without prophylaxis?

A

asymptomatic periods become shorter
more frequent attacks
chronic joint symptoms cause permanent erosive joint deformity

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13
Q

Manage asymptomatic hyperuricemia?

A

lifestyle mod and risk reduction
-diet, alcohol
Comorbid disease management
-hypertension, obesity, diabets, alcoholism, hyperlipidemia

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14
Q

Treatment aims for Gout?

A
  1. prompt relief of acute attacks
  2. prevention of recurrent attacks
    prevent/ reverse crystal depositis in
    -joints, urinary tract, renal intersitium, tissue and paranchymal organs (tophi)
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15
Q

Acute treatment?

A

inhibit immune response

-nasaids, corticosteroids, colchicine

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16
Q

Prevention?

A

inhibit uric acid synthesis
-allopurinol
increase uric acid elimination
-probenecid

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17
Q

NSAIDs?

A

first line therapy for most patients
fast-acting (hrs)
decrease inflammtory response

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18
Q

MOA Nsaids?

A

mainly inhibit prostaglandin synthesis

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19
Q

General properties of NSAIDS?

A

analgesic
antipyretic
anti-inflammatory

20
Q

Indomethacin?

A

drug of choice for acute attacks
significant GI and CN side effects

prostaglandin synthase inhibitor

21
Q

Other nsaids?

A

ibuprofen, naproxen

22
Q

Avoid aspirin with gout?

A

low dose- cause renal retention of uric acid

high dose- uricosuric action increases risk of renal calculi

23
Q

Colchicine?

A 
treat acute attacks
slower onset than NSAIDS
GI side effects (narrow therapeutic index)
Antiinflammtory- blocks cellular response to crystals
not an analgesic
not uricosuric
-not effect uric acid serum levels
-not stop destructive aspects of gout
24
Q

Colchicine MOA?

A

binds to tubulin
cause antimitotic effect, interferes with microtubules and spindle formation, neutrophils and GI epithelium
inhibits luekocyte migrattion, phagocytosis, and leukotriene B4 formation
can’t activate immune cells, cant cause inflammatory response

25
Q

High dose of colchicine?

A

treat gouty arthritis, can do even with narrow TI, because only short use, acute

26
Q

Low does colchicine?

A

prevent recurrent attacks, particularly in early stages of antithyperuricemic therapy, better tolerated

27
Q

Colchicine toxicity?

A 
GI (primary)
-drug use for acute attacks 
-diarrhea (can be severe), nausea, vomit, ab pain
Hematological
-bone marrow suppression
myopathy (chronic use)
28
Q

Corticosterioids?

A

for acute attacks
antiinflammatory steroids
intra-articular injections (one or 2 joints)
PO/parenteral (systemic) use
-can’t take nsaids or colchicine
-pts not candidates for intra-artiuclar injections
toxicity limits chronic use (last resort)

29
Q

Xanthine oxidase?

A

prevent uric acid formation by inhibiting it

30
Q

Hypoxanthine and xanthine?

A

they will accumulate because of inhibited xanthine oxidase but is water soluble

31
Q

Indications for uric acid lowering drug therapy?

A 
frequent/diabling attacks
clin/radiographic signs of joint disease
tophaceous deposits
gout with renal insufficiency
recurrent uric acid stones
not recommend for asymptomatic
no role in managing acute attacks
32
Q

Allupurinol clin use?

A 
chronic treatment of gout (1st choice)
prevent stone formation
protect kidneys
eliminate tophi
cancer chemo
33
Q

Allupurinol effectiveness?

A

in both underexcetors/ overproducers
ease of use (once daily)
effective in renal insufficiency (elderlu, dose adj)

34
Q

Hypoxanthine analog?

A

competitive inhibitor of xanthine oxidase

inhibits uric acid production

35
Q

Allupurinol inhibits metabolism of? (caution with these other drugs)

A

6-mercaptopurine (anticancer agent)
Azathioprine (immunosuppressive agent)
Both metabolized by xanthine oxidase

reduce doses of these drugs

36
Q

Allopurinol adverse effects?

A

generally well tolerated
most common issue is hypersentivity
can cause acute gouty attacks

37
Q

hypersensitivity?

A

mostly rashes but can be more serious
may occur after months or years
desentization possible in 50% pts

38
Q

acute gouty attacks? prevent them?

A

mobilizes tissue stores of uric acid

use NSAIDs or colchcine (low dose) when starting therapy

39
Q

Febuxostat?

A 
xanthine oxidase inhibitor 
may be better for pts with mild to moderate chronic kidney disease
-no dose adjust
-allupurinol- watch GFR and adjust dose
may have increased CV risk
high cost
40
Q

Uricsuric agents?

A

second line
patients that are underexcretors
acoid use where nephrolithiasis or neprhropathy might occur, likely ineffective in pts with renal impairment, less effective in elderly pts
requires bid or tid dosing (less compliant)

for patients resistant to or intolerant of allopurinol(hypersensitivity)

41
Q

Uricosuric agents?

A

urate excretion
reabsorption redominates, trasnporter mediated

these drugs are weak organic acids
inhibit urate-anion exchangers in proximal tubule
decrease uric acid reabsorption

42
Q

Probenecid?

A

decrease serum uric acid level
block tubular reabsorption or uric acid
enhance urine uric acid excretion (increase uric acid level in urine, increase risk of nephrolothiasis) not used in pts with renal disease
frequent but mild, side effects

43
Q

Contraindications Probenecid?

A

history of nephrolithiasis
existing renal disease
avoid use in pts that excrete a large amount of UA already, renal calculi is a risk (DONT USE IF URINARY URATES ARE TOO HIGH)

urine flow is low/history or renal calculi

less effective in elderly
2-3 times a day dosing (compliance)

44
Q

Drug Drug interactions Probenecid?

A

can interfere with renal excretion of other drugs
-penicillin, cephalosprins, quinolones, loops, NSAIDs

aspirin can diminish probenecid’s effect

45
Q

Adverse effects Probenecid?

A

generally well tolerated (some GI, hypersentivity, uric acid stone formation)

May cause acute attack of gout
- until theurpeutic levels are reached, may happen
give nsaids/ colchicine before to reduce risk

MOD 2 Quiz 1 (9 decks)

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