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pharmacology 3 > drugs for crystal arthropathies > Flashcards

drugs for crystal arthropathies Flashcards

1
Q

facts about gout

A

an inflammatory arthritis
common in men
associated with an incease in cardiovascular mortality

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2
Q

normal upper range of uric acid

A

in men - 0.42mmol/L (saturation point)

in women - 0.36 mmol/L

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3
Q

hyperuricaemia

A

levels > 0.42 mmol/L

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4
Q

when uric acid is above saturation point

A

monosoodium urate crystals deposit into joint and peri articualr tissues throughout the body

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5
Q

hyperuricaemia will cause gout

A

false
not everyone with increased uric acid get gout
uric acid may not be increased in acute gout
however, 80-90% of patients with gout are hyperuicaemic

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6
Q

uric acid/uate is derived from

A

diet (1/3)
endogenoous liver biosynthesis (2/3)
- final product of purine metabolism (in humans)

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7
Q

uric acid/urate is eliminated by

A

gut (1/3)

kidneys (2/3)

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8
Q

uric acid solubility

A

is a weak organic acid - poorly soluble in acidic pH (urine) and low temperatures (why peripheraal joints are more severely effected)

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9
Q

uric acid biosynthesis

A

derived from purine metabolism in the liver

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10
Q

uric acid excretion

A

100% uric acid is filtered through the glomerulus
99% is reabsorbed in proximal tubule
6-10% secreted in the distal proximal tubule

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11
Q

genetic component of gout

A

90% of hyperuraemics under excrete uric acid

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12
Q

what is gout

A

inflammatory arthritis
chronic asymptomatic hyperuricaemia leads to supersaturation of body tissues with urate crystals
uric acid - decreased solubility in acidic and cold conditions
crystals depsit around joints, especially extremities
crystals shed into joint

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13
Q

definitive diagnosis of gout

A

urate crystals in synovial fluid

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14
Q

causes of gout

A

exact cause uncertain in most cases
polygenic but mostly due to decreased renal excretion of uric acid
men 3x more than women

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15
Q

dietary triggers

A

obesity
increased purine intake
increased fructose
meta, seafoood, sugary drinks, beer, spirits,

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16
Q

good foods for diet

A

coffee
dairy products
vit C

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17
Q

other risk factors for gout

A 
urate transporter mutations 
hyperrtension 
metabolic syndrome 
chronic renal failure 
drugs 
transplantation - kidney and heart
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18
Q

drugs triggering gout

A

thiazide and loop diuretics (for hypertension)
low dose aspirin (causes problems with renal excretion)
cyclosporin (used to prevent transplant rejection)

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19
Q

main cause of gout

A

decreased renal excretion in distal proximal tubule
increased purines in diet (alcohol, meat, seafood)
increased purine turnover (alcohol, fructose, obesty, tumour lysis)

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20
Q

monosodium urate crystals building up into the tissues

A

get shed into the joints
set up inflammatory response
kinin, complement and plasmin systems
neutrophilc infiltration - engulf crystals
release of toxic oxygen metabolites
tissues lysis and release of proteolytic enzymes

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21
Q

preclinical gout

A

asymptomatic hyperuricaemia

crystall deposits increase in tissues fro years then finally crystals may shed into the joint

22
Q

two clinical phases of gout

A

intermittent acute gout - s symptoms of gout or signs of tophi between attacks
chronic tophaceous gout - if raised uric acid not adequately treated

23
Q

acute gout

A

intermittanet pauci-articular inflammatory arthritis
sudden onset
red and intensely painful
extensive swelling
50% first attacks occur in 1st metatarsophalangeal joint (podagra)

24
Q

acute gout is assciated with

A

fever
can be poly articular (especially in eldery and women)
self limiting

25
Q

chronic gout

A

recurrent attacks + inadequate urate lowering treatment leads to chronic toophaceous gout
erosion of neighbouring joints - deformity and restricted movement

26
Q

tophi are

A

large crystal deposits oon the extensor surfaces (fingers/hands, elbows, tendons, ear)

27
Q

chronic gout can lead to

A

nephrolithiasis and renal tissue depsits - chronic renall faillure
contributes to cardioovascular disease and stroke

28
Q

podagra

A

sudden onset gout in the first metatarsophalangeal joint

29
Q

treatment approach for chronic gout

A

much earlier use of urate-lwering therapies to treat underlying disease

30
Q

treatment of acute gout - pain relief

A

pain relief

  • NSAIDs
  • colchicine
  • glucocorticoids - oral and intra-articular (not if septic arthritis)
31
Q

treatment of acute gout - urate lowering therapy

A

maintain ULT if previously diagnosed gout

start urate lowering therapy if new diagnosis - lowest dose and increase dose very slowly

32
Q

colchicine

A

alkaloid product of autumn crocus - ancient remedy
mechanism of action not fully understood but binds tubulin - stops microtubule assembly to reduce
- cell division
- neutrophil motility
- chemokine production
inflammatory cell recruitment stops

33
Q

colchicine is absorbed

A

rapidly orally

34
Q

why isnt colchicine given as a first line therapy

A

vomiting and diarrhoea - very common first sign of toxicity

muscle damage, myelosuppression, multple organ failure and there is no antidote

35
Q

do not prescribe colchicine if

A

kidney or liver function is poor

watch for DDIs

36
Q

how long does acute gout last

A

two week

37
Q

aim of treating chronic gout

A

long term decrease in uric acid

lifestyle - diet, alcohol, and weight loss

38
Q

3 main drug group for chroonic gout

A

xanthine oxidase inhibitors
uricosuric agents
uricase agents

start during acute attack - better capture and compliance

39
Q

main xanthine oxidase inhibitor

A

allopurinol

40
Q

allopurinol

A

xanthine oxidase inhibitor
hypoxanthine analogue
competitively inhibits XO to decrease uric acid production
XO also converts allopurinol to alloxanthine/oxypurinol
alloxanthine non competitively inhibits XO
pharmacological action is largely alloxanthine

41
Q

drug of choice for long term treatment of gout

A

allopurinol

42
Q

prescribing allopurinol

A

well absorbed orally
single daily dose
renally excreted
decrease dose and titrate more slowly in RF

43
Q

why start low, go slow

A

dose esclaltion strategy

decreases risk of acute flare

44
Q

aims of long term urate lowering therapy

A

decrease urc acid concentration to <0.36 mmol/L
disolve tophi, calculi and urate crystals in other tissues
maintain dose when SUA reaches 0.36

45
Q

preventing of acute gout flare treatment during SUA

A

prophylactic NSAIDs or cochicine

46
Q

adverse effects of allopurinol

A

mostly GI

allopurinol hypersensitivity syndrome - drug reaction, rash with eosinophilia and systemic symptoms

47
Q

alloopurinol hypersensitivity syndrome

A

if rash i severe - stevens-johnson syndrome - rare but potentially fatall
risk increased if starting dose is high
east asian patients at higher risk
consider testing patients (PCR)

48
Q

dangerous drug interactions with allopurinol

A

mercaptopurne and azathioprine
purine analogues metabolised by XO
allopurinol increases their effects by blocking XO
affects fast replicating tissues, myelosuppression, diarrhoea, life threateneing

49
Q

feboxostat

A 
non purine selective inhibitor of XO 
not a purine analogue 
metabolised mainly in theliver 
useful in pateints with renal failure or those who cannot tolerate allopurinol 
much more expensive than allopurinol
50
Q

uricosuric agents

A

blocks urate re uptake in proximal tubule

useful for under excreters

51
Q

uricase agents

A

rasburicase and pegloticase
dervides from aspergillus fluvus
catalyses conversion of uric acid to allantion
rapidly decreases serum uric acid levels
IV only
short half life
single use in tumour lysis syndromes

pharmacology 3 (8 decks)

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