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30 Cards in this Set
- Front
- Back
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What is osteoarthritis?
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A clinical syndrome of joint pain, accompanied by functional limitation and reduced quality of life
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What are the constitutional risk factors for developing OA?
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- Ageing
- Hereditory - Gender - Hormonal - Osteoporosis - Smoking |
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What are the local risk factors for developing OA?
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- Trauma
KNEE - Obesity - Quadriceps weakening - Joint laxity/malalignment HIP - Developmental dysplasia - Occupation |
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Is OA just wear and tear or articular cartilage?
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NO
It is a metabolically active, dynamic repair process and effects all type of joint tissue |
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What is characteristic about a joint of someone suffering from OA?
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- Pseudo cysts
- Osteophytes (bony projections) - Subchondral sclerosis - Capsular fibrosis |
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What are the consequences of joint trauma?
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Trauma causes a metabolically active repair process involving all tissue however
- It can be slow but efficient resulting in a structurally altered joint but no symptoms OR - The repair process can not compensate reulting in symptomatic OA and 'joint failure' |
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How have attitudes and beliefs changed about OA?
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Previously
- Only old people get it - Its a static process - Its degenerative - Caused by wear and tear Currently - Its a reparitive process - Caused by wear and repair - Its a dynamic process |
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What is the prognosis for OA?
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OA does not inevitably lead to decline and eventual joint replacement. Outcome is variable, progressive decline is not inevitable however radiographic imporement is rare. Symptoms are episodic rather than persistant and it varies due to site
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What is the rule of thirds?
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With improvement of pain and function knees;
One third of patients improve One third of patients stay same One third of patients get worse |
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What are the main clinical features of OA?
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- Joint pain worse with activity
- Morning stiffness less than 30 mins - Funtional limitation - Reduced QoL - Bony swellings - Heberden's nodes (DIP) - Bouchard's nodes (PIP) - Muscle wasting - Deformity - Palpable crepitus on movement |
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What are the NICE guidelines on diagnosing OA?
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- Persistent joint pain with use
- 45 years or older - Morning stiffness less than 30 - No X-ray required (are often normal) |
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What are the radiographic features of a joint with OA?
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- Joint narrowing
- Osteophytes (bony protrusions) - Subchondral sclerosis (hardening) - Subchondral cysts |
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Is there any use in X-ray?
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Yes
For ruling out other diagnosis like - RA - Gout - Infection - Osteoporosis |
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What is at the core of OA treatment?
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EDUCATION
- Dispelling myths - Access to information - Strengthening and aerobic excercise - Weight loss - OA is not inevitable consequence of ageing - It is not just wear and tear - It involves the whole joint - Decline and joint replacement is not inevitable |
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What are the first pain relievers to be had with OA?
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- Paracetamol
- Topical NSAIDS |
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What are the more potent drugs used in OA treatment?
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- Capsaicin
- Cox-inhibitors - Oral NSAIDS - Opiods - Intra-articular corticosteroid injections |
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Other than drugs, how can OA be treated/managed?
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- Supports and braces
- Hot and cold treatment - Assistive devices - Manual therapy (manipulation and stretch) - TENS transcutaneous electrical nerve stimulation - Shock absorbing shoes/insoles |
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Is exercise damaging in OA?
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NO
- Disuse leads to atrophy - Physiological loading increases health - Extreme loading leads to tissue damage |
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What would you advise a patient regarding exercise?
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It is healthy to do a bit of exercise but do not exert yourself.
Aerobic exercise such as swimming and walking helps. Quadriceps strengthening is best delivered by a physio. Exercise improves pain, physical function, QoL and balance |
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Why is adherence to exercise an issue?
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It can be painful and effects arent seen immediately
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When would you offer joint arthroplasty?
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When symptoms have significant impact on quality of life eg limiting AoDL or pain at rest or at night
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Briefly describe purine metabolism.
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Purine nucleotides
| Hypoxanthine | Xanthine | Uric acid Xanthine oxidase catalyses the reaction of hypoxanthine to uric acid |
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What happens to the uric acid produced by purine metabolism?
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1. 90% excreted by the kidney
2. Passes into guy 3. Excess uric acid forms urate crystals |
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What are the main risk factors for gout?
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Being male
Family history High blood pressure Obesity/metabolic syndrome Cardiovascular disease Purine-rich diet Alcohol (beer) Taking diuretic medication Renal failure Osteoarthritis |
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What drugs cause high uric acid levels?
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Ciclosporin
Alcohol Nicotinic acid Thiazide diuretics Loop diuretics Ethambuatamol Asprin Pyrazinamide |
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Describe acute gout.
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Rapid onset
Severe pain Redness, swelling and tenderness Likely to be 1st metatarsal phalangeal joint May have systemic resolution Complete resolution |
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What investigations should be made before diagnosing gout?
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Aspiration of joint (painful)
Compensated polarised light microscopy Strongly negative birefringent, needly shaped crystals Allows sepsis to be included Serum urate may be normal during acute attack FBC - inflammatory markers |
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What drugs are used to manage acute gout?
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- NSAID's
- Colchicine - Intra articular steroids - Application of ice-pack |
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What drugs are used to manage long term gout?
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- Xanthine oxidase inhibitors (allopurinol)
- Uricosurics which increase excretion of uric acid in kidney (sulpinpyrazone, probenecid, benzbromarone) |
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What life style advice would you give to someone suffering from gout attacks?
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- Stop diuretics if possible
- Loose weight (diet and excercise) - Reduce intake of purine rich foods - Reduce alcohol consumption (beer) |
