Rheumatology Flashcards
What are the 6 A’s of AKS?
- Apical lung fibrosis
- Anterior uveitis
- Aortic regurgitation
- Achilles tendonitis
- AV node block- atrial conduction defects
- Amyloidosis
Why does gout form where it does?
○ Gout tends to attack joints in the extremities because temperatures in the feet and hands can be low enough to precipitate urate from plasma
Thus tophi typically form in the helix of the ear, fingertips, olecranon bursae, and other cool anatomical sites.
How should you investigate gout?
History + examination- No initial investigation is needed when managing people with typical gout like symptoms if NO SUSPICION OF OTHER CONDITIONS E.G SEPTIC ***
But when indiciated:
- Serum urate- remember that 40% are normal usually do after 4-6 weeks, not that typically form and deposit when >380micromol/L, hyperuricaemia may occur without gout and presence does not equal gout and most do not have gout. Normal does not mean not gout, often normal in acute flare
- Synovial fluid analysis → see increased WBC (neutrophils especially), + monosodium urate cystrals need to gram stain and culture
- Negatively bifridgent- yellow under parallel light and blue under peripendicular light
- ALSO DO IMAGING- x ray or CT
What do the the gout crystals do under polarized light? What shape are they?
Negative bifringent-yellow under parallel light and blue under peripendicular light
Rod shape!
What is coclhicine, what are some SE?
• (anti-inflammatory- inhibits leukocyte micro-tubular formation and migration-inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity
• Must be given early in gout until good pain relief or G.I side effects (nausea, vomiting , diarrhoea, abdo pain) t1/2= 30hrs clearance reduced in renal impairment.
• Colchicine makes you run before you can walk” - diarrhoea side effect
Azathioprine and allopurinol have a severe interaction causing bone marrow suppression!!1 therefore lower doses
What is the acute treatment of gout?
• NSAIDs orcolchicine(this is used if NSAIDS are CI e.g from peptic ulcer) are first-line
• the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled. Gastroprotection (e.g. a proton pump inhibitor) may also be indicated
• colchicine* has a slower onset of action. The main side-effect isdiarrhoea
• oral steroidsmay be considered if NSAIDs and colchicine are contraindicated. A dose of prednisolone 15mg/day is usually used
• another option is intra-articular steroid injection
• if the patient is already taking allopurinol it should be continued
Self care: keep joint cool and rest, elevate, avoid trauma, keep exposed
What are some indications for urate lowering therapy?
• the British Society of Rheumatology Guidelines now advocate offeringurate-lowering therapy to all patients after theirfirst attack of gout • ULT isparticularlyrecommended if: ○ → >= 2 attacks in 12 months ○ → tophi or joint damage ○ → renal disease ○ → uric acid renal stones ○ → prophylaxis if on cytotoxics or diuretics → younger age of onset
What is urate lowering therapy?
Prophylaxis against tophaceous gout, erosions, stones, nephropathy
Includes as first line allopurinol (xanthine oxidase inhibitor) then febuxostat (also a xanthine oxidase inhibitor-especially for renal impairment patients!)
Uricosuric acid (probenicid, benzbromarone)
Phenfibrate
Typically started 2 weeks after flare
But 25% of people flare therefore there has been suggested that you should cover with NSAIDS and colchicine
Initial dose is 100mg od then dose is titrated upwards to get a uric acid <0.35 if no tophi or 0.3 if tophi present- lower with reduced eGFR
There are others which are cytokine inhibitors
What lifestyle modifications should be made?
• reduce alcohol intake and avoid during an acute attack
• lose weight if obese
avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
- consideration should be given to stopping precipitating drugs (such asthiazides)
- losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
- increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
What is the prognosis with gout?
· Gout is an independent risk factor for chronic kidney disease, myocardial infarction and cardiovascular disease mortality
· Acute attacks of gout usually completely subside in 1-2 weeks without treatment. However, attacks may recur.
· Chronic gout occurs with repeated acute attack→ arthritis and tissue destruction and tophi, increased risk of kidney stones, urate nephropathy
· Tophi occur in 50% of untreated gout after 10 years
Tophi may create problems with activities of daily living, become inflamed, exude tophaceous material, or develop secondary infection, and adversely impact on quality of life
What is the definition of gout vs. pseudogout?
Gout is a form of inflammatory arthritis.-Acute inflammatory monoarthritic due to precipitation of monosodium urate crystals in the joints synovium→ red, hot, tender, swollen
It is caused by chronic hyperuricaemia (uric acid > 450 µmol/l)
Pseudogout: form of monocrystal synovitis- calcium pyrophosphate deposition disease within the joint space synovium
What is the clinical presentation of pseudogout?
Most commonly in the knee or wrist but also shoulders, elbow, wrist
Pain and swelling with acute inflammation and/orchronic degeneration (pseudo-osteoarthritis)
Indistinguish from acute gout
TYPICALLY >1 JOINT
What do you see on imaging in pseudogout?
x-ray:chondrocalcinosis in joint cartilade calsification
What is the management of pseudogout?
- NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
Acute treatment: NSAIDS, colchicine, glucocorticoids
Prophylaxis: colchicine
NO hypouricaemic equivalents to improve long term control of acute attacks or reverse CPPD
Investigate the underlying cause
What are the etiological causes of gout? primary, inheritary, secretory (with overproduction, under secretion, lead poisoning)
Primary: overproduction 10% and undersecretion 90%
Inheritary forms:
Young males, overproducers, associated with hyperuricaemia neph, HGPRT deficiency- lesch nyhan syndrome (neurological and behavioural abnormalities and the overproduction of uric acid in the body)
Secretary forms:
• Overproduction
○ Haematological disease, psoriasis, trauma, alcohol, cytotoxics, warfarin
• Under secretation
○ Renal failure, alcohol, aspirin, diuretics, laxatives, L dopa
• Lead poisoning (Sauturnine gout)
○Moon shine, paint, pipes
