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BPT 1 > Gout and crystal arthropathy > Flashcards

Gout and crystal arthropathy Flashcards

1
Q

Risk factors for gout

A
  1. Age 40-50 males and >60 females
  2. Higher in maori and pacific islanders
  3. Medical comorbidities: HTN, diabetes, CKD, obesity
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2
Q

Pathophysiology of gout

A

Metabollic end product. Purine -> xanthine -> urate by xanthine oxidase.

Urate concentration depends on
1. Urate production
2. Purine intake
3. Excretion: renal and GIT

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3
Q

Primary urate overproduction

A

Inborn errors of metabolism
1. Accelerated purine synthesis (PRPP synthase enzyme hyperactivity)

  1. Impaired purine salvage (HGPRT1 deficiency). X-linked recessive:
    i. Complete HGPRT1 deficiency - lesch-nyhan syndrome (gout, nephrolithiasis, mental retardation, movement disorder)
    ii. Partial HGPRT1 deficiency: kelley-seegmiller syndrome (gout with limited or no neurological symptoms)
  2. G6PD deficiency, frusctose-1-phosphate deficiency
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4
Q

Secondary urate overproduction

A

Increase cell turnover
- autoimmune/hemolytic anemia
- sickle cell anemia
- Polycythemia vera
- megaloblastic anemia/ thallessemia
- tumour lysis syndrome

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5
Q

Dietary factors for gout

A
  1. High purine diet: seafood (shellfish), red meat, fructose (sucrose in soft drinks metabolized and alters hepatic metabolism to increase purine)
  2. Alcohol, particularly beer high in purine
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6
Q

Food associated with low PU

A

Low-fat dairy products, cherries, high caffeine.

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7
Q

Underexcretion of urate (most common cause of hyperurecemia) - primary and secondary

A
  1. GIT (20-30%)
  2. Renal (proximal tube reabsorption 90-98% and proximal tube secretion 10%)

Primary - renal urate transporter mutations ABCG2 (reduce GI and renal excretion) and URAT1 (decrease reabsorption)

Secondary - CKD, medication (thiazide, loop, low dose aspirin, pyrazinamide, ciclosporin), lead

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8
Q

Presentation of gout

A
  1. asymptomatic hyperuricemia
  2. Gout flares - acute inflammatory arthritis
  3. subcutaneous tophi - a collection of subcut crystals
  4. Chronic gouty arthrtis - persistent synovitis

Usually monoarticular: MTP 1 most commonly involved (podagra). Pain worse in 4-12 hrs

Intercritical gout - asymptomatic period of gout

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9
Q

Differential dx of gout

A
  1. CPPD
  2. Septic arthritis
  3. Trauma
  4. Spondyloarthritis
  5. Sarcoidosis
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10
Q

Diagnostic tests gout

A
  1. Serum urate: May be reduced during gout flares
  2. Raised inflammatory markers
  3. Joint aspiration: polarized light microscopy shows intra-cellular needle shaped, negatively birefringement crystals.
  4. Plain film: evidence of cortical break +/- sclerotic margin
  5. USS: double contour sign , tophi, synovitis, erosion
  6. Dual energy CT (DECT): Erosions and MSU crystal deposition
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11
Q

Gout flare management

A
  1. NSAID, COX-2 inhibitor
  2. Prednisolone - high dose
  3. Colchicine: 1mg followed by 500microg in an hour, adjusted for renal inefficiency
  4. steroid inj
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12
Q

Management - Continuing management

A

Xanthine oxidase inhibitor - reduce urine production: allopurinol, fabuxostat

Uricosuric agent: promote uric acid excretion: probenecid

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13
Q

First line - allopurinol - half life, dose

A

Half life: 15 hrs after oxidation (increased in renal insufficiency)

Dose: 100mg (50mg if GFR<60). Dose increased by 100/50mg every 2-4 weeks until serum urate level reached (<0.36 in all pt and <30 in severe gout - increase flares, tophi, bone erosion)
Max dose 800-900mg

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14
Q

Allopurinol side effects, prevention and drug interation

A
  1. Hypersensitivity reaction - rare - happens within 2 months of start - desquamation, fever, eosinophilia, end-organ damage
    - If rash comes up: discontinue allopurinol
    - Han chinese and thai people are more prone: HLA B5801
    - Prevention: adjust the initial dose with renal function
  2. Increase in gout flares during the initiation or adjustment
  3. Drug interaction: other medications metabolized by xanthine oxidase: azathioprine, mercaptopurine, theophyline. Thiazide reduces renal excretion - reduces hypersensitivity risk
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15
Q

Febuxostat - MOA, dose, drug interaction, CARES trial

A

Alternative to allopurinol. Selective non-purine analogue XO inhibitor.

Dose: started at 40mg daily and then increased to 120mg daily

Drug interaction: with medication that gets metabolized by xanthine oxidase - as for allopurinol

CARES trial: Increase in CVD mortality compared to allopurinol

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16
Q

Uricosuric therapy: MOA, contraindication, Dosage of probenecid

A

MOA: Inhibit URAT1 and GLUT9 in proximal tubule - reduces reabsorption of urate.

Contraindicated in urolithiasis

Probenecid: 250mg BD -> 1g BD. Can be used as monotherapy or in combination with XO I

17
Q

Prevention of gout flares during initiation of tx

A
  1. Slow up-titration of allopurinol
  2. Limited evidence for low dose colchicine 500mcg - for 6 months since the start of tx (reduced/avoided in CKD/statin therapy)
  3. Low dose nsaid (naproxen250mg BD) if not contraindicated
  4. Rarely low-dose prednisolone
18
Q

CPDD - Calcium pyrophosphate deposition disease
Risk group

A
  1. Risk: >55yrs, strong >85, joint injury, osteoarthritis. Associated with metabolic disease: low mg, hyperparathyroidism, hypophosphatemia, hemochromatosis
19
Q

Factors enhancing nucleation of CPP crystals

A
  1. Increased Ca (hyperparathyroidism) and iron (hemochromatosis)
  2. Decreased Mg (Mg inhibits nucleation)
  3. Cartilage damage due to osteoarthritis
20
Q

Clinical presentation of CPDD - acute and chronic

A
  1. Monoarthritis - commonly the knee, other joints include wrist, shoulder, ankle, elbow
  2. Self-limiting - 1 to 3 weeks
  3. Chronic: Can mimic seronegative RA, polymyalgia rheumatica
  4. Osteoarthritis: in joints which are not usually involved (MCP, wrist, elbow)
21
Q

How to diagnose
What to do if pt <55yrs

A
  1. Joint aspirate: CP crystals - rhomboid or rod-shaped crystals, high neutrophils, weak positive befringement
  2. If <55yrs: evaluate for metabolic disorder - Ca, PO4, ALP, PTH, Mg, iron studies
  3. X-ray: shows chondrocalcinosis, prominent osteophyte formation, and hook osteophytes at the MCP joint (especially in hemochromatosis)
  4. USS: double contour sign + crystal deposition under hyaline articular cartilage
22
Q

Why CT of the spine in CPDD

A
  • For cervical stenosis and crowned dens syndrome (neck + shoulder girdle pain, possible meningism) - due to CPD
  • Intervertebral disc calcifications and sacroiliac joint involvement
23
Q

Management

A
  1. Acute: NSAID, COX2, high dose pred with tapering, steroid injection
  2. Prophylaxis: low dose colchicine 500mcg OD/BD
    - Low evidence for hydroxychloroquine and methotrexate

BPT 1 (2 decks)

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