Crystal ARTHROPATHIES Flashcards
what does monosodium urate cause?
Gout
what does calcium pyrophosphate dihydrate (CPPD) cause?
Pseudogout
what does basic calcium phosphate hydroxy-apatite (BCP) cause?
Calcific periarthritis/ tendonitis
explain purine metabolism and how it contributes to uric acid formation
Endogenous production of uric acid from degradation of purines usually contributes about two-thirds of the body urate pool, the remainder being dietary in origin. Of the uric acid produced daily, the majority (∼ 70%) is excreted via the kidney and the remainder is eliminated into the biliary tract and subsequently converted by colonic bacterial uricase to allantoin. In the vast majority of people with gout, hyperuricaemia results from reduced efficiency of renal urate clearance
what does hyperuraemia result from usually?
reduced efficiency of renal urate clearance.
Name things which cause overproduction of urate and uric acid
malignancy (lymphoproliferative - leukaemia), psoriasis, ethanool, cytotoxic drugs, HGPRT deficiency, increased purine turnover,
Name things which cause underexcretion of urate and uric acid
renal impairment, hypertension, hypothyroidism, alcohol, low dose asprin, diuretics, cyclosporin, exercise, starvation, dehydration, lead poisioning.
breifly outline Lesch nyan syndrome
HGPRTenzyme deficiency = overproduction of urate, X linked recessive, intellectual disability, aggressive impulsive behaviour, delf mutilation, Gout, renal disease
What is Gout?
Gout is an inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals depositing inside the joints. Hyperuriaemia and sodium urate deposition is also often asymptomatic.
epidemiology of gout
The disease is five times more common in men, occurs rarely before young adulthood (when it suggests a specific enzyme defect), and seldom occurs in pre-menopausal females. There is often a family history of gout.
explain the pathogenesis of Gout
Hyperuricaemia results from overproduction of uric acid or renal underexcretion. Urate is derived from the breakdown of purines (adenine and guanine in DNA and RNA), which are mainly synthesized in the body. Idiopathic (primary) gout is the most common form and most patients have impaired renal excretion of uric acid.
INCREASED PURINE TURNOVER - leukaemia, psoriasis. INCREASED PURINE SYNTHESIS - lesch-nyhan syndrome, alcohol excess, DRUGS - loop diuretics, low dose asprin, Toxins -lead.
how does gout present?
SUDDEN ONSET, SEVERE PAIN (6-12hrs), swelling and redness of the metatarsophalangeal joint of the big toe. The signs of inflammation may extend beyond the joint, giving the impression of cellulitis. The attack may be precipitated by dietary or alcoholic excess, by dehydration or by starting a diuretic. Acute attacks must be differentiated from other causes of monoarthritis, particularly septic arthritis. Presentation can also be with a polyarticular inflammatory arthritis, particularly in elderly women on long-term diuretics.
even soft touch is extremely painful.
Chronic MSK feature - gouty trophi - a joint deformity due to bony erosion and cartilage destruction.
Questions to ask in a consultation
previous experience of a pain like this? Weight bearing/ movement of joint? Hx of trauma? Painful to touch? Medication hx? Alcohol intake? Diet (shellfish)? Weight?
ddx for gout
cellulitis, septic arthritis
Ix
joint fluid aspiration - with needle shaped crystals seen. (serum uric acid is NOT used in diagnosis for gout). Usually diagnostic and a resopnse to NSAID’s.
random blood glucose, Bloods - crp, esr, hyperuricaemia, Xray.
(SERUM URIC ACID), XRAY, JOINT ASPIRATE.
Mx of gout
Acute - NSAIDs, Colchicine, Corticosteroids/steroids
Chronic - Allopurinol (if used in an acute phase it will precipitate an attack of gout).
lifestyle - lose weight, stop drinking alcohhol.
Hyperuricaemia - treat the first attck if its is a single attack of polyarticular gout, trophaceous gout, urate calculi, renal insufficiency. Treat 2nd attack if within a year. DO NOT treat asymptomatic hyperuricaemia.
Lowering uric acid - Xanthine oxidase inhibitor e.g. Allopurinol. Febuxostat. Uricosuric agents e.g. sulphinpyrazone, probenecid, benzbromarone. Canakinumab. cvs and lifestyle factors.
what are the rules for lowering uric acid levels?
Wait until the acute attack has settled before attempting to reduce the urate level
Use prophylactic NSAIDs or low dose colchicine/steroids until urate level normal
Adjust allopurinol dose according to renal function
NSAID, Colchicine and Allopurinol side effects
NSAID’s - Renal and gi upset, osteoporosis,
Colchicine - diarrhoea, nausea, vomiting, abdo pain, renal impairment, rash.
Allopurinol - worsens a gouty episode
Pseudogout outline…
Common in elderly females, erratic flareups, idiopathis, fhx, metabolic, triggers of trauma.
Romboid shaped calcium pyrophosphate crystals seen on aspiration
Deposition of calcium pyrophosphate dihydrate in articular cartilage and periarticular tissue produces the radiological appearance of chondrocalcinosis (linear calcification parallel to the articular surfaces) (knee).
Mx - NSAIDs, i/a steroids,
Polymyalgia Rheumatica outline…
PMR is an inflammatory condition of the elderly, close relationship with giant cell arteritis (most common systemic vasculitis – effects the large vessels). 20% of PMR patients have evidence of GCA, 50% of GCA patients have PMR.
GCA, RAISED ESR, Sudden onset of shoulder/pelvic girdle stiffness, Usually <50 y and > 70y, F:M = 1:2, ESR > 45.
Anaemia, malaise, weight loss, fever, depression, Arthralgia/synovitis, May have features of giant cell arteritis – scalp tenderness, headaches, blindness.
Tx - prednisolone 15mg per day 18-24month course, bone prophylaxis (bisphosphonates)
ddx - fibromyalgia, bilateral shoulder capsulitis, hypo/hyper thyroidism.
