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Pathology > C - Uric Acid Metabolism (E) > Flashcards

C - Uric Acid Metabolism (E) Flashcards

1
Q

name 3 purines

A

adenosine
guanosine
inosine

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2
Q

describe purine catabolism (4 steps with enzymes)

A

purines
–>
hypo-xanthine
–> (xanthine oxidase)
xanthine
–> (xanthine oxidase)
urate

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3
Q

why don’t animals get gout

A

they have a uricase enzyme that breaks down gout

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4
Q

plasma conc of urate in men / women

A

men 0.12 - 0.42
women 0.12 - 0.36

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5
Q

how is uric acid handled in the kidney

A

reabsorbed in PCT then resecreted later down the tubule
around 90% reabsorbed

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6
Q

2 types of purine synthesis

A

de novo pathway (from scratch)
salvage pathway (using other molecules)

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7
Q

when does the de novo pathway predominate

A

BM - making so much DNA that it needs de novo
everywhere else its salvage as its less energy

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8
Q

what is the rate limiting step of purine synthesis

A

PAT enzyme step

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9
Q

why is the PAT enzyme step rate limiting

A

has negative feedback from other steps

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10
Q

another key enzyme in purine metabolism

A

HPRT (sometimes called HGRT)

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11
Q

why is HPRT important

A

main enzyme of salvage pathway

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12
Q

what is complete HPRT deficiency called

A

Lesch Nyhan syndrome

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13
Q

PC of Lesch Nyhan syndrome at birth

A

normal at birth

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14
Q

PC of Lesch Nyhan syndrome at 6 months

A

developmental delay

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15
Q

PC of Lesch Nyhan syndrome at 1 year

A

choreiform movements

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16
Q

PC of Lesch Nyhan syndrome after 1 year

A

spasticity
mental retardation
self mutilation (85%) - bite lips / digits

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17
Q

key metabolic disturbance in Lesch Nyhan syndrome

A

hyperuricaemia (gout)

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18
Q

why do you get hyperuricaemia in Lesch Nyhan syndrome

A

no HPRT –> no negative feedback on PAT –> increased de novo pathway action –> increased synthetic pathway action –> lots of urate production

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19
Q

how can disorders of hyperuricaemia be classified

A

increased urate production
- primary / secondary
decreased urate excretion
- primary / secondary

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20
Q

primary causes of increased urate production

A

lesch nyhan syndrome
partial HPRT deficiency
glycogen storage disorders
fructose intolerance
PRPP synthetase over activity

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21
Q

secondary causes of increased urate production

A

myeloproliferative disorders
lymphoproliferative disorders
carcinomatosis
chronic HA
Gaucher’s disease
severe psoriasis

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22
Q

primary causes of decreased urate excretion

A

FJHN
- familial juvenille hyperuricaemic nephropathy

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23
Q

secondary causes of decreased urate excretion

A

CKD
Bartter’s syndrome
Down’s
lead poisoning
thiazide diuretics
aspirin

24
Q

T or F
de novo pathway predominates over salvage pathway in most tissues

A

F

25
Q

T or F
xanthine oxidase oxidises xanthine to uric acid

A

T

26
Q

T or F
HPRT is deficient in Lesh Nyhan syndrome

A

T

27
Q

T or F
PAT is the rate limiting enzyme

A

T

28
Q

what crystals are present ingout

A

monosodium urate crystals
needle shaped

29
Q

what is acute gout called

A

podagra

30
Q

what is chronic gout called q

A

tophaceous

31
Q

prevalence of gout in M or F

A

M 3%
F 0.6%

32
Q

which M / F get gout

A

post menopausal F or post pubertal M

33
Q

what does tophaceous gout look like

A

creamy cottage cheese looking lumps

34
Q

what are the exceptions to the rule that only post pubertal men get gout

A

Lesch Nyhan syndrome
familial juvenille hyperuricaemic nephropathy

35
Q

what does gout look like

A

red, shiny skin over a lump
+++ painful

36
Q

PC of acute gout

A

rapid build up of pain
affected joint is red, hot, swollen

37
Q

what % of first site joints is the MTP

A

50%

38
Q

in how many cases is the MTP joint involved either as first or later joint

A

90%

39
Q

2 aims of Tx of gout

A

reducing inflammation
managing the hyperuricaemia

40
Q

Tx of acute gout

A

1st NSAIDs
2nd colchicine
3rd glucocorticoids (pred)

41
Q

what should you NOT try to Tx in acute gout

A

the plasma urate conc - can worsen precipitations of gout crystals

42
Q

how do you treat the hyperuricaemia after the acute attack of gout

A

drink plenty of water
reverse any factors increasing the urate
allopurinol (reduce synthesis of urate)
probenecid (uricosuric - increases renal excretion)

43
Q

how does allopurinol reduce synthesis of urate

A

xanthine oxidase inhibitor

44
Q

which drug can you NOT co prescribe with allopurinol

A

azothioprine

45
Q

why is allopurinol CI if pt is taking azothioprine

A

increases bone marrow toxicity

46
Q

T or F
allopurinol should be used acutely

A

F

47
Q

T or F
NSAIDS are 1st line in acute attacks

A

T

48
Q

T or F
colchicine lowers urate levels

A

F

49
Q

T or F
allopurinol lowers urate levels by inhibiting HPRT

A

F

50
Q

T or F
allopurinol lowers urate levels by inhibiting xanthine oxidase

A

T

51
Q

how is gout Dx if any clinical uncertainty

A

tap effusion
view under polarised light
use red filters

52
Q

how does gout look under polarised light

A

negatively birefringent needle shaped crystals

53
Q

how does pseudogout look under polarised light

A

positively birefringent rhomboid shaped crystals

54
Q

what compound are the crystals in pseudogout

A

calcium pyrophosphate dihydrate

55
Q

who gets pseudogout

A

osteoarthritis pts

56
Q

prognosis of pseudogout

A

self limiting in 1-3 weeks

Pathology (87 decks)

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