Week 2 - A - Osteoarthritis and Crystal Arthropathies (Gout and Pseudogout) Flashcards
What does the term arthopathy mean? What does the term arthalgia mean? What does the term arthritis mean?
Arthropathy means disease of the joint
Arthalgia means joint pain
Arthritis means inflammation of the joint
The two main categories of arthritis are * Non-inflammatory arthritis * Inflammatory arthrtitis What is non-inflammatory arthritis known as? How is inflammatory arthritis divided?
Non-inflammatory arthritis is known as Osteoarthritis
Inflammatory arthritis can be divided into
- * Seropositive arthritis
- * Seronegative arthritis
What is the difference between seropositive and seronegative inflammatory arthritis?
Seropositive arthritis includes the inflammatory arthritis conditions which result in auto-antibody production
Seronegative arthritis - also autoimmune however there are no auto-antibodies in the serum
Auto-antibodies are antibodies generated by the immune system against the body’s own proteins usually within cells Does this usually happen?
Usually the immune system recognizes and ignores its healthy proteins
Sometimes however, if the immune system loses its normal regulatory processes, it stops recognizing these healthy proteins as its own and forms auto-antibodies to target these proteins - as if they were a virus
These auto-antbodies then begin to attack various organs and tissues, causing inflammation and damage Some autoantbodies are organ specific eg autoimmune thyroid disease Is the loss of the immune systems normal regulatory processes thought to be due to * Genetic predisposition OR * Environmental insults OR * Both of the above
The loss of the immune systems normal regulatory processes is thought to be a multifactorial response - therefore both genetic predisposition and environmental insults
What is the most common form of arthritis?
Osteoarthritis is the most common form of arthritis
What does OA do to the cartilage and what does it cause growths of on bones?
OA thins the cartilage and causes the growth of bony spurs (osteophytes)
Is OA rapid onset or gradual? When is pain worse and how is it relieved?
OA is very gradual - typically symptoms slowly arise over months to years
Pain is typically worse on movement and relieved by rest
What is it known as when there is a creaking on movement due to OA? (NAN from carehome) What differs in the length of morning stiffness between OA and RA?
The creaking on movement due to OA is known as crepitus
In OA, morning stiffness typically lasts less than 30 minutes
In RA, there is prolonged stiffness lasting more than 30 minutes
In OA affecting the hands, bony enlargements (bony spurs) are often seen in the fingers. What are they known as when affecting the DIPs and PIPs? Which joints in the hand does rheumatoid tend to affect?
OA affecting:
* Distal interphalangeal joints - known as Heberdens nodes
* Proximal interphalangeal joints - Bouchard’s nodes
Rheumatoid arthritis tends to affect the MCP and PIP joints
What is the commoner name for genu valgus (Valgum) and genu varus (varum)?
Genu valgus - knock knees
Genu varus - bow leggedness
If osteophytes grow in the spine, what can this cause?
This can cause spinal stenosis - can lead to impinging on a spinal root/nerve
What are the different risk factors for osteoarthritis?
Age - greater than 40
Gender - more common in female
Weight - obesity
Occupation - heavy weight lifting - wear and tear of bone
What are the three recommended diagnosing factors for osteoarthritis without clinical investigation as recommended by NICE guidelines?
* Person aged >45 years AND
* Activity related joint pain AND
* No morning joint related stiffness or stiffness lasting less than 30 minutes
Distinguishing between rheumatoid and OA
* Are Heberden’s nodes present?
* How would you describe the joints?
* When is stiffness worse?
* What is the difference in laboratory investigations?
* Both can cause inflamed PIPs (Bouchard’s nodes) - only OA will cause inflammed DIPs
RA
- * Inflamed joints - soft, warm tender
- * Stiffness worse after rest or in the morning
- * Positive RF, positive anti-CCP (cyclic citrullinated peptide), raised ESR and CRP
OA
- * Hard and bony joints
- * Stiffness worst after exercise, (evening stiffness)
- * Negative autoantibodies and inflammatory markers
What are the typical radiograph findings in the diagnosis of osteoarthritis?
Loss of joint space
Osteophyte formation
Subchrondral sclerosis
Subchrondral cyst formation
What are the core non-pharmacological management options for OA? What can be used as an adjunct by healthcare professionals?
Core non-pharmacological management options - exercise and weight loss
Transcutaneous electrical nerve stimulation (TENS) can be used as an adjunct to treat OA
How does TENS work?
Transcutaneous electrical nerve stimulation works by:
Apply pads on or near the arthritis pain
TENS sends sooth pulses via electrodes through the skin and along the nerve fibres
The pulses suppress the arthritis pain signals to the brain
What analgesia is recommended for initial management of OA? If it does not work, what is recommended to be given in addition?
Paracetamol +/- topical NSAIDs are the preferred 1st line treatment for OA
If they fail to work or are not tolerated by the patient, Prescribe oral NSAIDs or opiod medication eg co-codamol
What is co-prescribed if an oral NSAID is prescribed? When may intra-articular steroid injections be given?
If oral NSAIDs are prescribed, a PPI must also be prescribed for gastroprotection
Intra-articular corticosteroid injections should be considered as an ajdunct to core treatments for the relief of moderate to severe pain in people with OA
Which patients should be considered for surgery in OA?
Those whose OA has a substantial impact on quality of life should be considered for surgery
What are the two main crystal arthropathy conditions?
Gout and pseudogout
What type of crystal deposition is associated with gout? When is best to measure the serum uric acid levels if suspecting gout?
Gout is a crystal arthropathy caused by monosodium urate crystal deposition (usually due to high serum uric acid levels - hyperuricaemia)
Best time to measure the serum uric acid levels is 2 weeks after the attack resolves - it may be falsely low or normal during the attack
Which purines are broken down in DNA metabolism to form uric acid?
Uric acid is the final compound in the breakdown of purines, adenosine and guanine in DNA metabolism
Which percentage of the adult population is affected by gout? Which sex is it more common in? WHat is hyperuricaemia defined as?
1-2% of the adult population is affected by gout It is more common in males than in females
Hyperuricaemia is defined as a serum uric acid level >0.42mmol/l
What are the different risk factors for gout?
Reduced urate exretion - exacerbated by diuretics, or renal impairment or aspirin
Excess urate production - dietary causes such as alcohol, seafood, red meat are high in purines
What are the symptoms of gout? What is important to rule out as the cause?
Gout typically presents with acute monoarthropathy with severe joint inflammation (>50% occur at the MTP joint of the big toe) - severe attacks of pain, swelling, redness and tenderness in the joints
It is very important to rule out septic arthritis
What is the gold standard test for diagnosing gout?
Gold standard test is joint aspiration and synovial fluid microscopy under polarized light - diagnoses the gout and rules out septic arthritis
What shape are the monosodium urate crystals in gout and are they positive or negative birefingence? * How can you tell if they are positive or negative?
Monosdium urate crystals are needle shaped & display negative birefringence
Positive birefringence is when there is a change from yellow to blue when lined acros the direction of polarised light
Uric acid crystals remain yeLLow when paraLLel to the polarizer -> negative
What is the first line choice for the management of an acute attack of gout? What is second line? What is third line?
Maximum dose NSAIDs are 1st line choice for an acute attack of gout - usually diclofenac or naproxen If CI or not tolerate, oral colchicine can be prescribed
* A single intramsucular corticosteroid injection (for mono-articular gout) or a short course of oral cortiocsteroids or can be considered in people who cannot tolerate NSAIDs or colchicine
How long are NSAIDs or colchicine given for in the treatment of acute gout?
NSAIDs are given at a maximum dose as early as possible and continued until 1-2 days after the attack has resolved
Colchicine is slower to work than NSAIDs and max 6mg per course is recommended (do not repeat course within 3 days of reaching max)
For sufferers of recurrent attacks or those with join destruction or tophi, what drug can be given 1st line as prophylaxis against gout? * What indicates its use? * How does it work? * How long after the attack should you wait before starting urate lowering drugs?
Allopurinol is the recommended first line urate-lowering agent.
* It should be started if two or more attacks in 12 months, tophi or renal stones
* It works by inhibiting xanthine oxidase and therefore decreasing uric acid production
Start urate lowering drugs 2-3 weeks after the attacks has settled as they can potentiate a further flare
Allopurinol is started at a low dose and titrated upwards (where tolerated) every 4 weeks until the serum uric acid level is below what?
Allopurinol is started at a low dose and is titrated upwards every four weeks until the serum uric acid level is blow 0.36mmol/l (360micromol/l)
What is considered as an alternative second-line therapy if allopurinol is not tolerate or contraindicated? What serum uric acid level do you aim for?
Febuxstat (another xanthine oxidase inhibitor) is considered 2nd line as prophylaxis against gout if allopurinol is not tolerate or is contraindicated
Titrate up aiming for serum uric acid level <0.36mmol/l
Consider prescribing colchicine when initiating or increasing the dose of urate lowering treatments such as prophylaxic against attacks If colchicine cannot be tolerate, consider a low dose NSAID with gastroprotection How long would colchicine or NSAID be continued for when initiating or increasing the dose of urate lowering treatment?
Colchicine should be continued for up to 6 months NSAIDs should be continued for up to 6 weeks
After establishing the prophylaxis treatment, ff the patient has an acute gout attack, would you stop the treatment?
NO- do not stop the urate lower prophylactic treatment once established
What is pseudogout also known as? What causes it? Who does it usually affect?
Pseudogout aka Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, is a rheumatologic disease which is thought to be secondary to abnormal accumulation of calcium pyrophosphate dihydrate crystals within joint soft tissues.
It typically affects the large joints (most commonly knee) of the elderly
What shape are the crystals and what about birefringence in pseudogout?
The crystals are rhombus shaped and are weakly positive birefringence (turn from yellow to Blue when under polarised light)
What conditions are linked to the formation of pseudgout?
Risk factor conditions include
* Hyperparathyroidism
* Wilson’s disease
* Haemochromatosis
* Hypothyroidism
* Renal osteodrystrophy
What is the treatment of pseudogout? WHat can be given for prophylaxis of the condition?
Treatment of acute attacks includes NSAIDs, corticosteroids (systemic and intra‐articular) and occasionally colchicine
No medications are used for prophylaxis of pseudogout to prevent recurrence
