10. Treatments for OA (Robson) Flashcards
What are the symptoms of OA?
Joint pain when in use Morning stiffness - lasting less than 30 minutes Joint instability or joint buckling Loss of function of the joint Crepitus on motion of the joint
What are the signs of OA?
Bony enlargement at the affected joints - osteophyte formation Limited range of movement at the joint Crepitus on motion Malalignment and/or joint deformity Muscle atrophy/weakness
What is the core treatment in the management of OA and why?
Exercise and change in diet:
Allows for local muscle strengthening to increase the stability of the joint
Allows for weight loss - decreased weight being placed on the joints
What is TENS in the treatment of OA?
Transcutaneous electrical nerve stimulation - used as an adjunct for pain relief
What non-pharmacological methods can be used to treat OA?
Exercise and diet change
TENS
Acupuncture
Aids and devices e.g. walking stick, orthopedic insoles
What are neutriceuticals?
Give three neutriceuticals recommended for treatment of OA
Foods that can help to increase health
Omega-3 in diet
Chondroitin sulphate supplements
Glucosamine supplements
Why should you increase omega-3 in the diet of someone with OA?
Omega-3 - releases natural pain-relieving chemicals
How can doctors ensure that they are offering patient centred care?
Offer personalised plan
Carefully and explicitly outline to patients reasons for their medication prescribed
Should offer accurate verbal and written communication
What is the first line pharmacological management for OA?
Oral analgesics - paracetamol and/or topical NSAIDs
What oral analgesic can be prescribed to a patient if paracetamol/topical NSAID is ineffective and why?
Cox-2 inhibitor - should not cause the same side effects as cox 1 e.g. gastric ulcers
(cox-1 present all the time and cox-2 specific to inflammation)
Why might paracetamol/topical NSAID not be effective for some patients with OA?
Cox 1 inhibitor - may result in comorbidities or adverse side effects
Cox - inhibitors should not be used in certain patients e.g. with gastric ulcers
Why are topical NSAIDs particularly useful in relieving joint pain?
These target the specific joint and have very specific effects
These are absorbed through the skin directly into the synovial fluid - therefore the NSAID will be concentrated in and around the actual joint - does not pass first past metabolism
What are the two main benefits of topical NSAIDs?
Increased concentration - does not pass first pass metabolism
Does not result in gastric ulcers forming
What is the last line pharmacological management for OA?
Intra-articular injections - corticosteroids
Why are corticosteroids the last line treatment for OA and how should they be used?
Can further aggregate the OA - should be used sparingly only as an adjunct to get them through a particularly bad moment
When might a patient with OA be referred for surgery?
When pain stiffness and reduced function have a substantial impact on the quality of life of the patient e.g. waking up at night