Monoarthritis: Gout & pseudogout Flashcards
Define gout [1]
Gout is a crystal arthropathy resulting from excess levels of uric acid leading to precipitation in joints and other tissue.
Describe the basic pathophysiology of gout [3]
Gout is the result of high uric acid levels leading to supersaturation in plasma, causing a precipitation of monosodium urate crystals (MSU) in soft tissue, joints and kidneys
Conditions that alterate local environment, such as OA or joint injury can facilitate tissue deposition.
MSU crystals in a joint drives an inflammatory response - specifically TNF-a and ROS: causes the classical symptoms of gout
Describe what tophi are / caused by? [1]
Tophi are nodules composed of MSU crystals surrounded by a chronic inflammatory reaction, and can develop in the soft tissues, cartilage, and bones.
Clinical presentation of gout? [2]
Monoarthritic joint pain - most commonly MTPJ (podagra) with very acute onset
Redness, swelling and tenderness of the affected joint.
Which patients are more likely to acute polyarticular gout? [2]
Acute polyarticular gout:
- It is more likely to occur in patients with longstanding hyperuricaemia or those with co-morbid conditions such as renal impairment or cardiovascular disease.
Describe different causes of gout
Due to hyperuricaemia:
Inherited causes
- Lesch-Nyhan syndrome
Acquired causes
- XS purine
- malignancy
- XS alcohol
Underexcretion:
- renal disease
- lead nephropathy
- hypothyroidism
Drugs:
- Thiazides
- Aspirin (low dose)
- Alcohol
- Ciclosporin
Describe how you dx gout [3]
Clinical features and Hx
Synovial fluid aspiration
- This is the gold standard investigation for the diagnosis of gout but is often not required if sure
- presence of needle-shaped monosodium urate crystals that are negatively birefringent under plane-polarised light
Serum uric acid
- Levels should be taken 4-6 weeks following an acute attack to confirm hyperuricemia
- Hyperuricaemia is NOT diagnostic of gout however, increased levels do correlate with increased risk of developing gout.
- Though suggestive, elevated levels are not themselves diagnostic of gout
NOTE: During an acute attack, plasma urate levels often fall.
Describe x-ray findings in gout [1]
X-rays are usually normal unless the disease is at an advanced stage.
In chronic gout, joint effusion is usually the earliest sign. Later, x-rays show punched out lytic lesions, sclerotic margins and outlines of tophi.
Rat bites
Both gout and pseudogout can manifest as acute-onset monoarticular arthritis. While gout frequently affects the [] joint, pseudogout more commonly targets [2]
Both gout and pseudogout can manifest as acute-onset monoarticular arthritis. While gout frequently affects the first metatarsophalangeal joint, pseudogout more commonly targets larger joints like the knee or wrist.
How do you differentiate gout and septic athritis? [1]
Synovial fluid in septic arthritis typically demonstrates a high leukocyte count with neutrophil predominance. Gram stain and culture can identify the causative organism.
Describe the general managment plan and first and second line tx for acute gout?
General advice:
- Advise rest, ice and elevation.
- Lifestyle measures such as weight loss, diet and alcohol consumption should be discussed.
First-line therapy:
- Offer NSAIDs (e.g. naproxen) OR oral colchicine.
- Co-prescribe a PPI for gastric protection if giving an NSAID. Aspirin is not indicated.
Second-line therapy:
- If NSAIDs or colchicine are ineffective or contraindicated - prednisolone 15mg/day can be used
NB: if the patient is already taking allopurinol it should be continued
What is urate-lowering therapy (ULT)? [1]
When is it indicated? [1]
(aka what is the long term management for gout)
Allopurinol is first-line
- indicated after first attack of gout
- xanthine-oxidase inhibitor that prevents the conversion of hypoxanthine to xanthine and xanthine to uric acid.
- cover with colchicine / NSAID
for 3 - 6 months
Febuxostat (xanthine oxidase inhibitor) is second line
- may be used if allopurinol is contraindicated.
Which medication should you consider to prescribe when start ULTs? [1]
Clinicians should consider prescribing colchicine cover when starting (or increasing) urate lowering therapies such as allopurinol or febuxostat to prevent acute attacks. This may continue for six months.
Which medications can trigger gout? [2]
furosemide / loop diuretics
thiazide diuretics
Describe why purine production might occur (and cause gout) [3]
Purine overproduction:
- This occurs when there is increased cell turnover or lysis of cells leading to release of purines and breakdown to uric acid
- Causes include myelo- or lymphoproliferative disorders, psoriasis and use of chemotherapy agents.
Why might gout cause disrupted U&Es? [2]
Kidney stones may occur due to deposits of MSU crystals in the urinary tract as a result of hyperuricaemia
gout can cause kidney disease - passage of MSU crystals through kidneys causing scarring. This scarring then reduces functionality of the kidneys.
Describe bone complications of gout [2]
Repeated attacks of gout and the presence of tophi all contribute to bone erosion and weakening of joints resulting in degenerative arthritis. In the most serious of cases, surgery will be required to rectify this damage.
A 2018 population-based study found that gout conferred a 20% increased risk of osteoporosis.
Define pseudogout [1]
Describe the pathophysiology [1]
Pseudogout is a crystal arthropathy, which may cause an acute inflammatory arthritis from deposition of calcium pyrophosphate.
* Chondrocytes are the principle cell involved in the formation and deposition of CPP.
* Chondrocytes are the only cell type found in articular cartilage - essential for generating cartilage
* In pseudogout, excess pyrophosphate production causes local CPP supersaturation, crystal formation and deposition.
* CPP crystals stimulate a proinflammatory response leading to activation of phagocytes and neutrophils.
* The inflammatory response is usually self-limited due to the modification of CPP crystals (e.g. addition of lipoproteins), which reduces the inflammation.
5Suffering from which other patholigies may increase the liklihood of suffering from pseudogout? [4]
- haemochromatosis
- hyperparathyroidism
- acromegaly
- low magnesium, low phosphate
- Wilson’s disease
Clinical features of pseudogout? [4]
knee, wrist and shoulders most commonly affected
joint aspiration:
- weakly-positively birefringent rhomboid-shaped crystals
x-ray:
- chondrocalcinosis
in the knee this can be seen as linear calcifications of the meniscus and articular cartilage
Which disease is associated with pseudogout? [1]
Haemochromatosis
Dx of pseudogout? [2]
Based on synovial fluid analysis and plain film radiography:
- A definitive diagnosis of pseudogout (i.e. acute CPPD disease) requires evidence of BOTH CPP crystals on synovial fluid analysis and classical radiographic changes.
Radiograph findings include:
- cartilage calcification (CC) (will appear as a thin opaque line)
Describe the treatment plan for pseudogout?
The majority of acute flares of pseudogout will resolve within 7-14 days
Joint injection:
- useful if symptoms limited to ≤2 joints.
- Medication choice is corticosteroid in combination with lidocain
Medications:
- NSAIDs or
- Colchicine
- A short course of corticosteroids can be used in patients who don’t respond to first line treatments
https://app.pulsenotes.com/medicine/rheumatology/notes/pseudogout
Describe what is meant by palindromic rheumatism
Recurrent attacks of painful joint swellign
Pseudogout
inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity
A boy with a history of learning difficulties and self-mutilation presents with recurrent episodes of gout is a stereotypical history of which disease? [1]
Lesch-Nyhan syndrome
Describe what is meant by palindromic rheumatism [1]
Tx? [1]
RF for which disease? [1]
Rare type of inflammatory arthritis
- causes attacks of joint pain and swelling, the symptoms disappear, and the affected joints go back to normal with no lasting damage
Half of the people who have palindromic rheumatism eventually develop rheumatoid arthritis (RA)
Tx:
- NSAIDS
- Colchicine
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