Week 2 - A - Osteoarthritis and Crystal Arthropathies (Gout and Pseudogout)

Question 1

What does the term arthopathy mean? What does the term arthalgia mean? What does the term arthritis mean?

Answer 1

Arthropathy means disease of the joint

Arthalgia means joint pain

Arthritis means inflammation of the joint

Question 2

The two main categories of arthritis are * Non-inflammatory arthritis * Inflammatory arthrtitis What is non-inflammatory arthritis known as? How is inflammatory arthritis divided?

Answer 2

Non-inflammatory arthritis is known as Osteoarthritis

Inflammatory arthritis can be divided into

• * Seropositive arthritis
• * Seronegative arthritis

Question 3

What is the difference between seropositive and seronegative inflammatory arthritis?

Answer 3

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

Question 4

Auto-antibodies are antibodies generated by the immune system against the body’s own proteins usually within cells Does this usually happen?

Answer 4

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

Question 5

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

Answer 5

The loss of the immune systems normal regulatory processes is thought to be a multifactorial response - therefore both genetic predisposition and environmental insults

Question 6

What is the most common form of arthritis?

Answer 6

Osteoarthritis is the most common form of arthritis

Question 7

What does OA do to the cartilage and what does it cause growths of on bones?

Answer 7

OA thins the cartilage and causes the growth of bony spurs (osteophytes)

Question 8

Is OA rapid onset or gradual? When is pain worse and how is it relieved?

Answer 8

OA is very gradual - typically symptoms slowly arise over months to years

Pain is typically worse on movement and relieved by rest

Question 9

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?

Answer 9

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

Question 10

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?

Answer 10

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

Question 11

What is the commoner name for genu valgus (Valgum) and genu varus (varum)?

Answer 11

Genu valgus - knock knees

Genu varus - bow leggedness

Question 12

If osteophytes grow in the spine, what can this cause?

Answer 12

This can cause spinal stenosis - can lead to impinging on a spinal root/nerve

Question 13

What are the different risk factors for osteoarthritis?

Answer 13

Age - greater than 40

Gender - more common in female

Weight - obesity

Occupation - heavy weight lifting - wear and tear of bone

Question 14

What are the three recommended diagnosing factors for osteoarthritis without clinical investigation as recommended by NICE guidelines?

Answer 14

* Person aged >45 years AND

* Activity related joint pain AND

* No morning joint related stiffness or stiffness lasting less than 30 minutes

Question 15

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?

Answer 15

* 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

Question 16

What are the typical radiograph findings in the diagnosis of osteoarthritis?

Answer 16

Loss of joint space

Osteophyte formation

Subchrondral sclerosis

Subchrondral cyst formation

Question 17

What are the core non-pharmacological management options for OA? What can be used as an adjunct by healthcare professionals?

Answer 17

Core non-pharmacological management options - exercise and weight loss

Transcutaneous electrical nerve stimulation (TENS) can be used as an adjunct to treat OA

Question 18

How does TENS work?

Answer 18

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

Question 19

What analgesia is recommended for initial management of OA? If it does not work, what is recommended to be given in addition?

Answer 19

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

Question 20

What is co-prescribed if an oral NSAID is prescribed? When may intra-articular steroid injections be given?

Answer 20

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

Question 21

Which patients should be considered for surgery in OA?

Answer 21

Those whose OA has a substantial impact on quality of life should be considered for surgery

Question 22

What are the two main crystal arthropathy conditions?

Answer 22

Gout and pseudogout

Question 23

What type of crystal deposition is associated with gout? When is best to measure the serum uric acid levels if suspecting gout?

Answer 23

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

Question 24

Which purines are broken down in DNA metabolism to form uric acid?

Answer 24

Uric acid is the final compound in the breakdown of purines, adenosine and guanine in DNA metabolism

Question 25

Which percentage of the adult population is affected by gout? Which sex is it more common in? WHat is hyperuricaemia defined as?

Answer 25

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

Question 26

What are the different risk factors for gout?

Answer 26

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

Question 27

What are the symptoms of gout? What is important to rule out as the cause?

Answer 27

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

Question 28

What is the gold standard test for diagnosing gout?

Answer 28

Gold standard test is joint aspiration and synovial fluid microscopy under polarized light - diagnoses the gout and rules out septic arthritis

Question 29

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?

Answer 29

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

Question 30

What is the first line choice for the management of an acute attack of gout? What is second line? What is third line?

Answer 30

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

Question 31

How long are NSAIDs or colchicine given for in the treatment of acute gout?

Answer 31

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)

Question 32

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?

Answer 32

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

Question 33

Allopurinol is started at a low dose and titrated upwards (where tolerated) every 4 weeks until the serum uric acid level is below what?

Answer 33

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)

Question 34

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?

Answer 34

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

Question 35

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?

Answer 35

Colchicine should be continued for up to 6 months NSAIDs should be continued for up to 6 weeks

Question 36

After establishing the prophylaxis treatment, ff the patient has an acute gout attack, would you stop the treatment?

Answer 36

NO- do not stop the urate lower prophylactic treatment once established

Question 37

What is pseudogout also known as? What causes it? Who does it usually affect?

Answer 37

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

Question 38

What shape are the crystals and what about birefringence in pseudogout?

Answer 38

The crystals are rhombus shaped and are weakly positive birefringence (turn from yellow to Blue when under polarised light)

Question 39

What conditions are linked to the formation of pseudgout?

Answer 39

Risk factor conditions include \* Hyperparathyroidism \* Wilson's disease \* Haemochromatosis \* Hypothyroidism \* Renal osteodrystrophy

Question 40

What is the treatment of pseudogout? WHat can be given for prophylaxis of the condition?

Answer 40

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