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MSK Lectures > PHAR: Gout > Flashcards

PHAR: Gout Flashcards

1
Q

The breakdown of WHAT leads to uric acid biosynthesis?

A

Purines.

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2
Q

What is the most common gout presentation?

A

Extremely painful big toe.

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3
Q

Failing NSAIDs (eg if the patient has a bad reaction), what is most ideal for treatment of acute gout?

A

Colchicine.

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4
Q

Is having hyperuricemia synonymous with having gout?

A

No. About 10% of people with hyperuricemia develop gout at some point in their lifetimes.

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5
Q

What proportion of uric acid is derived from our diet?

A

About 1/3.

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6
Q
  • What is the mechanism of action for colchicine?
  • What does this effect? (3 things from lecture slides)
A
  • Inhibition of microtubule assembly by binding to tubulin.
  • Cell division.
  • Neutrophil motility.
  • Chemokine production (decreases).
  • NET ANTI-INFLAMMATORY EFFECT.
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7
Q

What problems are associated with colchicine?

A
  • Narrow therapeutic window (fine line between therapeutic and toxic).
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8
Q

What are the major adverse effects of colchicine? What are the rarer adverse effects of colchicine?

A

MAJOR - NVD (nausea, vomiting, diarrhoea). RARE - Muscle damage - Myelosuppression - Multiple organ failure

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9
Q

What is the drug of choice for long term treatment of chronic gout?

A

Allopurinol.

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10
Q

What is the mechanism of action of allopurinol.

A

Xanthine oxidase inhibitor. - Decreases uric acid synthesis.

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11
Q

Who are groups at risk to consider when prescribing allopurinol?

A
  • People with the HLA-B*5801 allele i.e. East Asians.
  • People currently being treated with mercaptopurine and azathioprine (purine analogues that act as cancer and autoimmune drugs).
    • Allopurinol increases the effects of these two drugs.
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12
Q

Purines are broken down into uric acid with the assistance of the xanthine oxidase enzyme. At what steps does xanthine oxidase act in this sequence?

A

USED IN BOTH STEPS Hypoxanthine –> Xanthine Xanthine –> Uric acid

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13
Q
  • What reaction does the enzyme urate oxidase/uricase catalyse? - Does it exist in the human body?
A
  • Oxidation of urate to allantoin. - No.
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14
Q

In what two locations is uric acid metabolised?

A
  • The kidney (renal, ~2/3) - The gut (enteric, ~1/3)
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15
Q

What are three risks groups associated with gout?

A
  • The obese (more tissue = more turnover = more purines)
  • People who consume excess sweet soft drink.
  • Ageing population.

ALSO

  • hypertension
  • men
  • metabolic syndromes
  • kidney failure
  • transplant patients
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16
Q
  • Failing NSAIDs and colchicine (oral treatment), what would be the next line of treatment for relieving the pain in acute gout?
  • When would this line of therapy be taken?
A
  • Intra-articular glucocorticoid injection.
  • If the joint wasn’t septic.
17
Q

Why does gout occur in the extremities e.g. in the big toe?

A
  • Uric acid has lower solubility in lower temperatures.
  • Large crystals of uric acid form here (tophi).
18
Q
  • Is it safe to begin treatment for chronic gout during an acute attack?
  • Why may it be prudent to do so?
A
  • Yes.
  • Ensures therapeutic adherence.
19
Q

Xanthine oxidase converts allopurinol to the metabolite form oxypurinol. Name two ways that it differs from allopurinol.

A
  • Oxypurinol has a longer half-life (18-30 hrs vs 2-3 hrs).
  • Oxypurinol non-competitively inhibits xanthine oxidase.
  • Note: The pharmacological action of allopurinol is largely due to oxypurinol.
20
Q

What are the three categories of treatment for chronic gout?

  • Describe their mechanism briefly.
  • Give an example of each.
A
  • Xanthine oxidase inhibitors.
    • Competitively inhibits XO to decrease uric acid synthesis.
    • Allopurinol.
  • Uricase agents.
    • Oxidises uric acid to allantoin.
      • Uricase is also called urate oxidase.
      • Uricase is absent in the human body.
    • Rasburicase.
  • Uricosuric agents.
    • Blocks urine reuptake in the proximal tubule, increasing uric acid excretion in urine.
    • Probenecid.
21
Q

What is thought to be the genetic component to Gout?

A

Genetic renal undersecretors.

As a small, unbound molecule 100% of the uric acid passes through the glomerulus, 99% is reabsorbed in proximal tubule, 6-10% is secreted in the distal tubule.

Undersecretion = too much uric acid -> Gout

MSK Lectures (22 decks)

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