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MDTI > Gout > Flashcards

Gout Flashcards

1
Q

what type of an arthritis is gout?

A

a crystal arthritis

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2
Q

clinical syndrome of gout

A

monosodium urate (MSU) crystal deposition

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3
Q

physiologic syndrome of gout

A

hyperuricemia

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4
Q

hyperuricemia

A

excess urate in the plasma that may or may not result in precipitation of uric acid crystals. >6.8 mg/dl

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5
Q

most common form of inflammatory arthritis?

A

gout

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6
Q

who does gout mostly affect?

A

middle aged men

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7
Q

why doesn’t gout affect pre-menopasual women?

A

estrogen promotes renal uric acid excretion

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8
Q

risk factors for gout

A

obesity, metabolic syndrome, hypertension, insulin resistance, purine rich diet, alcohol

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9
Q

role of PRPP synthase

A

conversion of ribose 5P to PRPP

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10
Q

role of PRPP in gout

A

increased activity leads to increased PRPP (X linked mutation) that leads to increased uric acid (hyperuricemia)

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11
Q

HGPRT role

A

catalyzes single step salvage reaction for guanine and hypoxanthine.

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12
Q

HGPRT in gout

A

enzyme deficiency leads to higher levels of guanine and hypoxanthine –> hyperuricemia

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13
Q

uricase

A

enzyme not present in humans, catalyzes the conversion of uric acid to soluble allantion, leading to lower levels of uric acid

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14
Q

recombinant uricase used for gout treatment

A

pegloticase

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15
Q

xanthine oxidase role

A

catalyzes oxidation of hypothanxine to xanthine and xanthine to uric acid

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16
Q

xanthine oxidase in gout

A

inhibition decreases uric acid level

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17
Q

drugs targeting XO

A

allopurinol & febuxostat

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18
Q

circulating uric acid

A

urate anion

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19
Q

limit of solubility for serum urate anions

A

6.8mg/dL

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20
Q

where is uric acid produced?

A

liver (from degradation of purine compounds)

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21
Q

sources of urate production

A 
not direct (always from liver metabolism of purine compounds). 
dietary intake, tissue nucleic acids, endogenous purine synthesis
22
Q

urate excretion

A

GI (1/3) and renal (2/3)

23
Q

URAT1 (urate/organic anion exchanger)

A

highly urate specific anion exchanger (organic anions) that is responsible for the reabsorption of filtered urate

24
Q

where is URAT1?

A

on the luminal membrane of proximal renal tubular epithelial cells.

25
Q

stimulation of URAT1

A

increased irate absorption and hyperuricemia

26
Q

inhibition of URAT1

A

decreased irate absorption, hypouricemia

27
Q

drug that inhibits URAT1 and causes more uric acid secretion in urine (uricosuria)

A

probenecid

28
Q

is hyperuricemia more likely due to overproduction or under excretion?

A

90% underexcretion

29
Q

causes of irate overproduction

A

primary and secondary hyperuricemia

30
Q

primary hyperuricemia

A

inherited defects in regulation of purine nucleotide synthesis (HGPRT deficiency and PRPP synthetase super activity)

31
Q

secondary hyperuricemia

A

dietary consumption, increased nucleic acid turnover (MPNs), accelerated ATP degradation

32
Q

causes of irate underexcretion

A

kidney disease , medications, stimulation of URAT1

33
Q

how does alcohol affect homeostasis of urate pool?

A

overproduction: increases plasma concentration of purines due to liver metabolism
underexcretion: stimulates URAT1 via increased lactic acid fro fermentation, dehydration inhibits excretion

34
Q

pathogenesis of gout-basic version

A

uric acid crystals are mobilized and shed into synovial fluid, which causes a very strong inflammatory response

35
Q

pathogenesis of gout- detailed version

A

crystal phagocytosis by synovial cells leads to the activation of the NALP3 inflammasome, which releases IL-1B, which binds to IL1 in synovial cells, which activates NF-kB which in turn increases secretion of cytokines that cause neutrophil activation and acute inflammation

36
Q

IL-1B

A

inflammatory cytokine produced and released by NALP3 inflammasome complex

37
Q

MSU crystals and complement

A

crystals can directly activate the C5b-9 complex that leads to mediator production involved in systemic symptoms like fever, high white count, etc

38
Q

how does gout spontaneously resolve?

A

mediators either undergo death/deactivation/differentiation and lose inflammatory function, or up regulation of anti-inflammatory cytokines, or increased vascular permeability leads to urate transport out/increased entry of anti-inflammatory molecules

39
Q

asymptomatic hyperuricemia

A

elevation of serum urate concentration in absence of signs of gout. 2/3s of hyperurimic patients

40
Q

acute gout

A

acute onset, maximal severity within 12-24 hrs. severe pain, redness, swelling, disability. monoarticular

41
Q

which joints are most commonly affected in acute gout?

A

hallux and knee

42
Q

hallux involvement in gout

A

podagra

43
Q

pseudogout

A

crystals of calcium pyrophosphate

44
Q

chronic tophaceous gout

A

chronic hyperuricemia with recurrent acute flares. persistence of synovial fluid crystals with low grade inflammation. presence of tophi and erosions

45
Q

tophi

A

deposits of MSU crystals. nests of crystals enveloped by granuloma like chronic inflammatory response with macrophages and multi nucleated giant cells, encased by dense connective tissue

46
Q

urolithiasis

A

uric acid kidney stones. precipitation of crystals in the collecting ducts and ureters

47
Q

acute uric acid nephropathy

A

uric acid precipitation within the renal tubules or interstititum. causes acute renal failure

48
Q

synovial fluid aspirate diagnostic of gout

A

needle shaped, negatively birefringent (yellow=parallel, blue=perpendicular)

49
Q

treatment for acute gout

A

control acute inflammation with non steroidal anti-inflammatory meds, colchicine, glucocorticoids

50
Q

colchicine

A

blocks activation of NALP3 inflammasome, inhibits neutrophil activation in response to crystals

51
Q

treatment from chronic gout

A

decrease uric acid levels with XO inhibitors (allopurinol), uricase (pegloticase), and URAT1 agents (probencid) or via lifestyle modification (decreased purine intake)

MDTI (42 decks)

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