Gout + PMR Flashcards
What type of disease is Gout and Pseudogou?t
Crystal deposition diseases
Gout - Sodium urate crystal deposition (NEEDLE SHAPED)
Pseudogout - Calcium pyrophosphate crystal deposition (BRICK SHAPED)
What is gout and which part of the body is mostly affected?
Hyperuricaemia- Abnormality in uric acid metabolism resulting in deposition of uric acid crystals, which can cause intermittent attacks of acute joint pain
Great toe (75% cases)
Can also result in tophi (white nodules) in skin and around joints (commonly ears, fingers, achilles tendon)
What are the risk factors for Gout?
Family history (33%) Obesity Excess alchohol High purine diet Diuretics Acute infection Ketosis Surgery
What are the causes of Hyperuricaemia?
- Impaired renal excretion - idiopathic primary gout
2. Increased production of uric acid
How do we diagnose Gout?
- Rapid response to NSAIDs
- Serum uric acid levels
- Joint aspirate
- Renal function test
- X-ray to visualise joint erosion
What is the treatment for an ACUTE attack of gout?
- NSAIDs e.g. Naproxen
- Colchicine if NSAIDs are contraindicated e.g. active peptic ulceration
- Corticosteroids: Intra-articular injection in monoarticular gout (unlicensed indication)
Intramuscular injection also can be effective in podagra
Why is the use of Colchicines limited in replacement of NSAIDs? But who is it good for?
As effective as NSAIDs, but use is limited by toxicity
Useful for heart failure patients - doe not induce fluid retention and can be used by those on anticoagulants
What dose of Naproxen is recommended for Gout?
by mouth, initial dose of 750mg initially, then 250mg every 8 hours until attack has passed m 100–200mg daily.
What are the counselling and cautionary advice for Naproxen?
Avoid if patient has history of hypersensitivity to aspirin and other NSAIDS
Avoid) in patients active GI ulceration or bleeding
Use with caution if patient has asthma
Use with caution with drugs that increase bleeding risk
Use with caution in elderly (i.e. use gastroprotective treatment)
Increases risk of thrombotic events
What is Colchicine and what is its mechanism of action?
An alkaloid extracted from autumn crocus
Prevents migration of neutrophils/phagocytes into gouty joints
Binds to tubulin resulting in depolymerisation of microtubules and reduced cell motility
Also prevents release of inflammatory products by these cells by preventing/limiting the phagocytosis of urate crystals
What dose of Colchicine is to be given?
Acute attack: 1mg, then 0.5mg no more frequently then every 4 hours until pain is relieved OR until vomiting or diarrheoa OR Max. dose of 6mg is reached.
Course not to be repeated within 3 days
What are some side effects of Colchicine ?
largely GI disturbance (nausea, diarrhoea, vomiting, abdominal pain).
How can we prevent gout?
Withdraw thiazides and salicylates
Lifestyle changes:
- Lose weight
- Reduce alcohol
- Dietary changes
- Reduce total calorie and cholesterol intake
- Avoid purine-rich foods (i.e. Offal, red meat, certain fish (such as anchovies, sardines), shellfish, pulses, such as lentils, peas and spinach)
When is preventative treatment for gout required?
- Frequent recurrent attacks (more than 2 per year)
- Tophi present
- Signs of chronic gout (joint erosion)
Prophylaxis of gout include?
Drugs that reduce serum uric acid levels are used to prevent gout attacks
Allopurinol inhibits uric acid synthesis
Uricosuric agents (probenecid and sulfinpyrazone) increase uric acid secretion
Initiation of treatment may precipitate an acute attack so colchicine or NSAIDs should be used as prophylaxis and continued for at least 1 month after normouricaemia is achieved
Gout treatment: Allopurinol
Drug class?
What is it and its Mechanism of action?
The drug of choice.
Drug class: Xanthine oxidase inhibitors
An analogue of hypoxanthine
reduces uric acid synthesis by competitive inhibition of xanthine oxidase
Alloxanthine (metabolite) also inhibits xanthine oxidase (non-competitive)
Reverses tophi and renal stone formation and can be used in patients with renal impairment
What side effects of Allopurinol?
GI disturbances and allergic reactions (skin rashes +fever)
Fatal skin diseases e.g. toxic epidermal necrolysis
What is the prophylaxis dose of Allopurinol for gout?
initial dose of 100mg daily, preferably after food, then adjusted according to plasma or urinary uric acid concentration (maintenance doses range from 100–200mg daily (mild conditions) to 700–900mg daily (severe conditions)
What are Uricosuric agents and who can and can’t use them?
They increase uric acid secretion by direct action on renal tubule
useful in patients who fail to respond to Allopuinol
Contraindicated in patients with renal stones
Ineffective in those with renal insufficiency
What is Pseudogout and who does it mostly affect?
Acute attacks that resemble osteoarthritis.
Pyrophospahte crystals deposited in articular cartilage and periarticular tissues.
Elderly women. Knees, shoulders and wrists mostly affected.
Diagnosis of pseudogout?
Diagnosed through presence of small brick-shaped pyrophosphate crystals in synovium
Blood tests may show raised WBC count and normal serum calcium
X-ray may show calcification of articular cartilage (chrondrocalcinosis)
Treatment of Pseudogout?
Treatment is with rest, joint aspiration and NSAIDs
Local corticosteroid injections can sometimes be useful
Treatment options for Juvenile idiopathic arthritis?
NSAIDs
Many children don’t require DMARDs - methotrexate is effective
Corticosteroids may be required for systemic disease
Biologics - consideration based on age and treatment history
what is PMR?
Polymyalgia Rheumatica
What % of patients have PMR when they have GCA? and the other way around
GCA = Giant cell arthritis
50% patients with GCA have PMR
15% patients with PMR have GCA
What symptoms is PMR associated with?
PMR associated with abrupt onset of stiffness and pain in proximal muscles of shoulder and/or pelvic girdle, stiffness worse after rest, malaise, fever, weight loss, anorexia
What symptoms is GCA associated with?
GCA associated with localised headache, scalp tenderness, facial pain, visual symptoms (i.e. double vision or sudden loss of vision)
What investigations are carried out for PMR & GCA?
Blood tests - increased ESR (>30mm/hr) and normocytic anaemia
Temporal artery biopsy (esp. if GCA is suspected)
Before or within a week of starting treatment
Exclude other diagnoses
Malignancy, arthritis, referred pain etc
Treatment options for PMR/GCA?
Always treated with systemic corticosteroids and response is rapid
Prednisolone
PMR 10-15mg daily
GCA 40-60mg daily
Treatment continued until remission of disease activity before gradually decreasing dose
Reduced by weekly decrements of 5mg until 10mg is reached; then 2-4 weekly decreases of 1mg to dose of 5mg
Symptoms and ESR rate should be monitored as dose is decreased
Patients require osteoporosis prophylaxis and must carry STEROID card
What class does Prednisolone belong to? And what it its mechanism of action?
Systemic corticosteroid
Binds irreversibly to glucocorticoid receptors, preventing them from binding to steroid response elements and modifying gene expression. Modification of gene expression leads to systemic suppression of inflammation.
What is the maintence dose of prednisolone for PMR?
7.5-10mg daily
What are the counselling and cautions for prednisolone? (3)
Adrenal suppression can occur with long term use, leading to inability of body to produce natural corticosteroids (i.e. cortisol). Treatment should not be abruptly stopped!
Increase risk of osteoporosis; consider prophylaxis
Relapse is common if stop treatment for PMR prematurely (i.e. <2 years)
What are the issues with long term use of steroids?
Associated increased risk of osteoporosis/fracture, muscle wasting, mood changes (euphoria, depression, insomnia), growth suppression, infection (i.e. severe chicken pox), suppression of clinical symptoms of disease, diabetes, Cushing’s syndrome and adrenal atrophy, sodium and water retention, increased blood pressure
Why is gradual withdrawal of steroid use required? and in what instance?
Due to suppression of the adrenal axis (reduced adrenal function)
if patient has received treatment for >3 weeks, had repeated courses, has other causes of adrenal suppression, received dose >40mg od, taken short course within 1 yr of long-term therapy, given repeat doses in evening
In what cases can steroid withdrawal be abrupt?
if disease is unlikely to relapse and treatment duration is less than 3 weeks and situations described below don’t apply
