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Stage 2: Ageing > Crystal Arthritis > Flashcards

Crystal Arthritis Flashcards

1
Q

What is crystal arthritis?

A

An acute inflammatory mono arthritis due to precipitation of crystals within the joint

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2
Q

What are the two types of crystal arthritis?

A

1) Gout (accumulation of uric acid)

2) Calcium pyrophosphate disease (pseudogout)

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3
Q

What crystals accumulate in pseudogout?

A

Calcium pyrophosphate crystals

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4
Q

What crystals accumulate in gout and where?

A

Uric acid (urate) crystals in synovial fluid

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5
Q

How does gout typically present?

A
  • Very acute onset of swelling in a joint e.g knee
  • Very painful
  • Typically are well the day/night before and then wake up in the early hours with pain in a joint (typically peripheral)
  • Developing no pain to maximum intensity pain in < 24h
  • Normal temperature
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6
Q

Which joint is most affected by gout (half of all first episodes of gout)?

A

MTP joint of big toe (many people self diagnose and so goes unpresented)

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7
Q

Describe the progression of pain in gout

A
  • Often wake up with discomfort
  • Pain then elevates to severe to the point that they don’t want to keep the bed sheets over it bc it is painful to touch
  • By the morning they can’t put weight on it and pain score is 10/10
  • If it is first attack, by 24h pain has already peaked and start to subside
  • If untreated, will settle over next 10 days
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8
Q

What is the other major differential of crystal arthritis and how would it present?

A

Septic arthritis

  • Prodrome of feeling systemically unwell with malaise, loss of appetite for maybe a week leading up to the symptoms
  • Joint pain presents rapidly but not usually over 12h, more like 2-3 days
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9
Q

Describe uric acid

A
  • Uric acid is the final product of purine metabolism so any cell turnover will result in the production of uric acid
  • Humans have inactive uricase gene (uric acid → allantoin + CO2) so can’t metabolise uric acid
  • Most of the time, uric acid is an important by product of metabolism which should cause no harm but in some people it can trigger an inflammatory response
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10
Q

What enzyme involved in the production of uric acid can be inhibited as a treatment for gout?

A

Xanthine oxidase

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11
Q

Describe inflammation in gout

A
  • Gout and pseudogout are driven by innate immunity (unlike RA and SLE - adaptive)
  • When the monosodium urate crystals are taken up by macrophages in the joint they can activate NLRP3 and the inflammasome
  • IL-1beta is the cytokine that is the driver of the inflammatory innate immune response (there are drugs against IL-1beta that suppress that pathway and are incredibly effective in gout but don’t actually use them v much bc have other treatments)
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12
Q

What is the link between hyperuricaemia and gout?

A
  • In order to get gout and the immune activation ned to have high levels of uric acid
  • Hyperuricaemia is more common than gout (5-8% prevalence)
  • Only about 5% of people with > 0.54 mmol/l urate level ever get an attack of gout
  • Therefore most people with hyperuricaemia don’t get gout
  • Need other risk factors as well as hyperuricaemia to get gout
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13
Q

What are hyperuricaemia levels in men and women?

A
  • Men = > 0.42 mmol/L

- Women = > 0.36 mmol/L

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14
Q

Explain the link between gender and gout

A
  • Women virtually never get gout esp. if pre-menopausal
  • Exceptions = younger women with kidney failure where they can’t clear uric acid
  • So for the most part gout is a disease of men or post-menopausal, older women
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15
Q

What are the risk factors for gout?

A

1) Hyperuricaemia
2) Persistent alcohol consumption
3) Diuretic use esp. furosemide, bendroflumethiazide reduce fractional clearance of urate
4) High BMI (type of diet)
5) Lipid disorders (type of diet)
6) Older age
7) Male
8) Genetics

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16
Q

Describe parts of a high urate diet that can cause gout

A

1) Shellfish esp. oysters
2) Marmite (high in purines)
3) Red meat
4) Beet (real ale contains hops which has purines)
5) Alcohol (reduces fractional clearance of urate)
6) Sugary drinks (fructose reduces fractional clearance of urate)

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17
Q

What is the main reason for the rising incidence and prevalence of gout in modern society?

A

Diet

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18
Q

What is a classic description of someone with gout?

A

Dietary factors, metabolic syndrome, CKD, male

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19
Q

What other thing causes gout other than high consumption of purines?

A

Reduced renal (fractional) clearance of urate e.g. diuretics, one kidney, CKD, alcohol, fructose

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20
Q

Describe joint involvement in gout

A

1) First attack always single joint mostly in foot (MTPJ > 50%) and never affects axial skeleton
2) Future attacks can occur in multiple joints anywhere in the body

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21
Q

What is polyarticular gout?

A
  • Multiple joint inflammation
  • Can incl. spinal inflammation (spinal abscesses) and ocular inflammation (uveitis = inflammation of middle layer of eye)
  • Gout can leave the articular system in people with extensive disease with v high urate burden
22
Q

Describe what a gout swelling might look like

A
  • White spot on red lump

- Slight yellowish appearance due to some urate crystals precipitating out

23
Q

What is tophaceous gout (gouty tophi)?

A
  • When urate crystals precipitate out (crystal deposits)
  • When this occurs, uric acid can remain even after the attacks and get crystals forming and depositing around joints and skin (tophi)
  • Can see these in multiple places, not just around the joints that have been inflamed
  • Bc gout is v acute in clinic might not have active gout but tophi may indicate that previous episodes of joint pain described are due to gout
24
Q

Where do you see gouty tophi in the body?

A

1) Auricle (pinna) of ear (common place) - always examine
2) Bursa e.g. olecranon bursa
3) Subcutaneously (uric acid precipitate within skin) e.g. under thumb (could be mistaken for infection with cellulitis) - just looks white
4) DIP joint
5) Extensor tendon surfaces

25
Q

What would you see/feel if you examine an olecranon bursa affected by gout?

A
  • Filled up with fluid and become chronically inflamed

- On palpation it feels v boggy and full of fluid with lumps in it which would be full of the needle shaped crystals

26
Q

Why is an X ray an important way to distinguish gout and pseudogout?

A

1) Gout - can see soft tissue swelling but cant see urate deposition bc it doesn’t show up on radiograph (radiolucent), bone looks normal and clear
2) Pseudogout - crystals are calcium containing and radio-opaque so show up (like bone)

27
Q

What does gout look like on an x-ray?

A
  • Soft tissue swelling
  • Looks like someone has hole punched through joint if look at area around joint
  • It is not the joint line but is periarticular
  • Hallmark of gout on x ray = periarticular punched out lesions
  • Distinct from RA which causes marginal erosions which aren’t periarticular, right on joint margin
  • Can look like ‘bite mark’ taken out of MTPJ bc crystals are radiolucent
28
Q

Describe spinal involvement in gout

A
  • Intervertebral disc disease at multiple disc levels e.g. lower lumbar and lower thoracic spine
  • Could not radiographically distinguish this from a septic discitis
29
Q

How do you diagnose gout?

A

Arthrocentesis

30
Q

Describe an arthrocentesis

A
  • Diagnosis to demonstrate crystals (negatively birefringent crystals)
  • Take a joint fluid aspirate from joint affected e.g. from knee using a needle into the joint fluid
  • Most aspirated without US
  • But can be aspirated using an US probe (US in parallel to probe)
  • Inside the joint, the black anechoic area is joint fluid
31
Q

How is dietary/drug restriction used to treat gout?

A
  • Dietary advice to diminish their exogenous purine intake and also reduce drugs that reduce renal clearance
  • e.g. minimise exposure to diuretics, reduce alcohol, sugary drinks
  • Stop eating oysters, red meat
32
Q

When would you prescribe someone a drug to diminish their purines?

A

If they have had more than one attack

33
Q

What are pharmacological treatments to use for (chronic) gout/to prevent gout?

A

1) Xanthine oxidase inhibitors - prevent formation of urate
2) Recombinant uricase - rarely use bc when stop it can cause rebound hyperuricaemia
3) Uricosuric agents - increase renal clearance through renal tubule system, however many people with gout have CKD and need kidneys to be working to use these drugs so often avoid these

34
Q

When are recombinant uricase drugs used?

A

To treat acute hyperuricaemia to prevent tumour lysis syndrome related to complications (not used for chronic gout)

35
Q

What are the two xanthine oxidase inhibitors used to treat gout?

A

Allopurinol (best) and febuxostat

36
Q

What drugs are used to treat acute gout?

A

Drugs to treat PAIN

1) NSAIDs (naproxen)
2) Colchicine
3) Prednisolone

37
Q

How would you treat gout with NSAIDs?

A
  • Young patient with risk factors but otherwise fit and well then short course of NSAID (500mg bd 5 days) is v effective
  • Most commonly used treatment
  • However contra-indicated in people with renal, cardiac or liver disease (many people with gout have these)
  • DO NOT USE NSAIDs in CKD (serious complications)
38
Q

How do you treat gout with colchicine?

A
  • 1mg dose immediately followed by 0.5mg 2-3x a day usually for 5-7 days
  • Usually v well tolerate but in some people can cause terrible diarrhoea
  • Some drug interactions to be cautious about
  • Can be used in people for who NSAIDs are contra-indicated
39
Q

How do you treat gout with prednisolone?

A
  • Can give as daily treatment (20-30mg for a week od)
  • Need to be cautious in diabetes (steroids make it worse) or congestive heart failure
  • If gout is only affecting one joint can give intra-articular injections of steroid which are v effective
40
Q

How do you manage acute therapy with preventative therapy?

A
  • If already on preventative therapy e.g. allopurinol don’t stop
  • Don’t delay initiation of preventative therapy
41
Q

How do you treat gout with allopurinol?

A
  • Most commonly used, usually v well tolerated
  • Give it at low dose (100mg) and gradually titrate up (max 800mg) bc there is a risk of drug reaction causing a potentially severe systemic syndrome incl. skin rash and eosinophilia which can occur if don’t titrate up cautiously (rare)
  • In first few months might have more frequent episodes of gout - as start to lower uric acid will cause more attacks in short term, need to bear with it
42
Q

What drug can you not give with allopurinol and why?

A

Azathioprine

  • The active metabolite of azathioprine (6-mercaptopurine) is metabolised by xanthine oxidase
  • So if on allopurinol or febuxostat, can’t metabolise azathioprine as would lead to build up of drug and life-threatening complications
43
Q

What causes pseudogout?

A
  • Calcium pyrophosphate is part of bone mineral so it is the bone mineral itself that is getting into the joint
  • So key process is that as you lose the cartilage layer over the joint and exposure the joint surface/bone inside the joint, start to develop some calcium pyrophosphate crystals within the joint
44
Q

What are the risk factors for pseudogout?

A

1) Advancing age
2) Prior joint trauma e.g. meniscectomy
3) Familial chondrocalcinosis (calcium in joint) - some genetic causes
4) Haemochromatosis
5) Some endocrine disturbances e.g. hyperparathyroidism, hypomagnesaemia and hypophosphatasia incl. Gitelman’s syndrome

45
Q

What are the clinical features of pseudogout?

A
  • Rapid onset severe joint pain
  • Peak intensity within 6-24h
  • Fever (50-60%) - contrast to gout where 10% have fever and are usually unaware of it
  • Overlying erythema and desquamation
  • Resolution in 3-4 days
46
Q

Describe joint involvement in pseudogout

A
  • Mono or oligoarticular disease seen in 89% of cases
  • First onset is almost always monoarticular
  • In some people it can be oligoarticular but even in people who have it recurrently it usually remains a monoarticular disease
47
Q

What might you see on an x ray of a joint with pseudogout?

A
  • e.g. in triangular fibrocartilage region of the joint between ulnar and carpal bones (ulnar compartment of joint in wrist) may see calcification within it
  • Extensive intra-articular calcification (chondrocalcinosis) between the femoral condyle and tibial plateau
48
Q

Describe the crystals in pseudogout

A
  • Crystals are positively birefringent, small, rhomboid heaped
  • Tend to be sparser in number then what you see in uric acid inflammation so can be easily missed
  • In contrast to urge crystals which are v strongly birefringent, these are weakly birefringent
49
Q

What is the acute treatment for pseudogout?

A

Same as gout (NSAIDs, colchicine or prednisolone)

50
Q

What is long term treatment for pseudogout?

A
  • No evidence based drug treatment or anything that prevents recurrence of pseudogout
  • If it is a single joint that is the problem can do a joint replacement if there is significant osteoarthritis

Stage 2: Ageing (10 decks)

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