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MPH322 Musculoskeletal - RA > 4. Gout > Flashcards

4. Gout Flashcards

1
Q

Define: Gout

A

Heterogenous disorder that results in deposition of uric acid salts and crystals in and found joints and crystallisation of uric acid in urinary joint

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2
Q

Describe the two different types of Gout

A
  • Uric acid is the normal end product for the degradation of purine compounds
  • Humans cannot break down uric acid into more soluble for Allantoin
  • Hyperuricaemia - metabolic disorder
    • Defined as 2SD above 7.0mg/dL - conc is limit of solubility for MSU in plasma - at high levels, MSU precipitates in tissues
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3
Q

What is the name of the enzyme that cannot break down uric acid?

A

Enzyme Uricase

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4
Q

When is peak incidence most probable with Gout?

A

5th decade - but it can occur in any age
Males
however incidence in women increase after menopause

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5
Q

What is gout?

A

excess production or reduced excretion of uric acid leading to deposition of uric acid crystals

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6
Q

What is the root cause of Gout?

What is it commonly associated with?

A

Hyperuricaemia

commonly associated with obesity, diabetes, hypertension, CHD, renal insufficiency and inc triglycerides

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7
Q

The formation of urate crystals leads too..

A

formation of tophaceous deposits

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8
Q

What is the most painful manifestation of Gout?

A

Gouty arthritis - caused berate crystals interact with neutrophils triggering an inflammatory response

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9
Q

What are the two types of hypereuricaemia?

A

Uric acid overproduction
- Genetic disorders: under regulation of purine nucleotide synthesis
- Hypoxanthine-guanine phosphoribzosyltransferase
Uric acid under-excretion
- Accounts for over 90% of hyperuricaemia
- Diminished tubular secretory rate, inc tubular reabsorption , diminished uric acid filtration

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10
Q

Name 5 of 6 drug groups that can cause gout

Why do they cause it?

A
  • ACE inhibitors - Reduced rate renal clearance
  • Cytotoxic chemo - Cisplatin - Rapid cell lysis - breakdown of cells causes more purines
  • Ciclosporin - Dec grate clearance, defc GFR
  • Diuretics - inc uric acid retention
  • Ethanol - Inc uric acid production due to adenine nucleotide turnover
  • Levodopa - Inhibition urate secretion
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11
Q

How is inflammation caused in joints?

A

Urate crystals are phagocytised by synovicytes

  • Release PGs, lysosomal enzymes and IL-1
  • These attract and activates polymorphonuclear leukocytes and mononuclear phagocytes
  • PMN and MNPs migrate to joint space and amplify inflammation
  • In the later phases of an attack, macrophages digest rate crystals and release more inflammatory mediators
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12
Q

4 stages of gout

A
  • asymptomatic hyperuricaemia - leading to progressive urate crystal deposition
  • acute gouty arthritis
  • intercritical gout - the period between gouty attacks
  • Chronic tophaceous gout
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13
Q

What can precipitate gouty attacks?

A
  • Trauma
  • Surgery
  • Excessive alcohol consumption
  • drugs
  • purine rich food
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14
Q

How do we investigate gout?

A
  • Serum Urea and Creatinine - renal impairment

- Joint fluid microscopy - long needle shaped crystals that are negatively birefringement (glow) in polarised light

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15
Q

Name some purine rich foods?

A
  • All meats - gravy, anchovies, sardines, herring
  • Mushrooms, lentil, kidney beans and asparagus
  • Beer
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16
Q

What is acute gout?

A
  • Associated with big toe
  • Pain and inflammation b y uric acid crystal deposition
  • More common in men, obesity, HPT
  • Sudden symptoms - appear overnight
  • Red and painful
17
Q

How do we aim treat the different kinds of gout?

A
  • Acute - Pain and inflammation
  • Chronic - Attack prevention
  • Lifestyle advice
18
Q

What caution should we take with long term drugs

A

DO NOT give during acute attack

It exacerbates the pain and inflammation

19
Q

How do we do lifestyle management?

A

Weight loss

Dietary modification

20
Q

First line treatment for acute gout

A
  • First line - NSAIDs
  • Diclofenac - 100mg start, then 50mg tds for 2 days then 50mg bds for 8 days
  • Indometacin - 75-100mg bds then reduce dose after 5 days
  • Naproxen - 750mg start then 250mg ads
  • Piroxicam 40mg daily then 10-20mg daily
  • Etoricoxib - only COX2 - 120mg daily
21
Q

Second Line treatment for acute gout

Dose?

A

Colchicine

  • administer ASAP
  • 1mg initially followed by by 0.5mg every 2-3 hours until pain, GI symptoms
  • 6mg max dose

Corticosteroids - IA injections. Oral prednisolone 30mg/day for 7 days

22
Q

Chronic treatment for gout - 1st line

A

Xanthine oxidase inhibitors

  • Allopurinol and febuxostat
  • 100mg daily and inc 3-4 weeks
  • Maintenance dose 100-600mg daily
  • Febuxostat is given 40-80mg daily
23
Q

Chronic treatment of gout - 2nd

A

Uricosuric drugs
- Probenecid - 500mg-1g twice daily
- Sulphinpyrazone - - 100mg tds-qds
Not useful in patients over-producing uric acid or with poor renal functions

24
Q

How do uricosuric drugs work?

A
  • They act on URAT1 to prevent re-uptake or uric acid and thus increase its renal excretion
25
Q

What is Lesinurad?

A
  • Selective uric acid reabsorption inhibitor (SURI) that inhibits the URAT1 transporter
26
Q

How does Lesinurad work?

A
  • Inhibit URAT1, lesinurad increases uric acid excretion and thereby lowers serum uric acid (sUA)
  • It also inhibits OAT4, a uric acid transporter involved in diuretic-induced hyperuricaemia
27
Q

What do we monitor with Lesinurad?

A

Renal function

28
Q

What drug can be given during chemo?

A
  • Rasburicase
29
Q

What is the enzyme responsible for converting uric acid to allantoin?

A
  • Uricase
30
Q

What are the common side effects of Rasburicase and Uricase?

A
  • Fever
31
Q

Why can we not use pegloticase?

A
  • Side effects - anaphylactic reactions with the production of antibodies that neutralise uricase enzyme activity
  • cost effectiveness
32
Q

What is canakinumab? why don’t we use it?

A

anti IL-1 therapy

- far too expensive

MPH322 Musculoskeletal - RA (5 decks)

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