Crystal Arthropathies Flashcards

(49 cards)

1
Q

what are the two main forms of crystal arthropathies

A

Gout and Pseudogout

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2
Q

what is gout

A

pathological reaction to the presence of urate crystals in and around synovial joints

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3
Q

what type of crystal causes gout

A

monosodium urate monohydrase

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4
Q

what joints are more specifically targeted in Gout

A

1st MCP swelling is almost pathomnemonic for gout

knee is also common, along with small joints of hands/feet

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5
Q

what is the time course for gout

A

takes months-years for crystals to grow to a detectable amount in the first place

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6
Q

what proportion of hyperuracaemic patients get gout

A

5%

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7
Q

what is the gender split with gout

A

10:1

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8
Q

what are risk factors for gout

A
male
increased serum uric acid 
increased age
metabolic syndromes (insulin resistance, dyslipidaemia, HTN) 
high alcohol intake - predominantly beer
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9
Q

what are features of secondary gout

A

primary
Chronic hyperuricaemia resulting from drug therapy or renal impairment
Mainly affects >65 and is the form usually seen in women
In diuretic induced gout, secondary OA is particularly an issue – thought to be due to a genetic definiciency in fighting crystal formation

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10
Q

what factors affect serum uric acid level

A

IN
1/3 is due to diet
2/3 due to endogenous purine metabolism regulated by xanthine oxidase

OUT
2/3 Kidney Elimination
1/3 gut elimination

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11
Q

what are some factors that predispose to chronic hyperuricaemia (not gout risk factors)

A

Diminished renal excretion
Renal impairment
Long term diuretics
Low dose aspirin

Increased production of uric acid
Uncommon

Increased purine turnover
Chronic myeloproliferative or lymphoproliferative disorders

Increased de novo synthesis
Most commonly an unidentified enzyme defect

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12
Q

what is the most common reason for gout

A

90% have an isolated inherited defect in the fractional uric acid excretion impairing the ability to excrete more

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13
Q

when should you suspect a rare specific defect of purine synthesis in a patient with gout

A

<25 years old
uric stones in urinary tract
strong Fhx of early gout

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14
Q

what is the cause of pseudogout

A

calcium pyrophosphate crystal deposition in hyaline and fibrocartilage of joints causing chondrocalcinosis

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15
Q

what is the incidence stratified by ages above 55 of pseudogout

A

rare <55
10-15% in 65-75
30-60% >85

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16
Q

what sites are most affected in pseudogout

A

knee

wrist

symphsis pubis

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17
Q

how does pseudogout present

A

acute self limiting synovitis or a chronic arthritis

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18
Q

what metabolic diseases predispose to CPP deposition

A
Haemachromatosis 
hyperparathyroidism
hypophosphatasia
hypomagnesaemia 
Wilson's disease
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19
Q

what is calcific periarthritis

A

deposition of hydroxyapatite (main constituent of bones/teeth) into soft tissues - usually periarticular tissues

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20
Q

what is the most common site for calcific periarthritis

A

supraspinatus tendon (rotator cuff)

21
Q

how does calcific periarthritis present

A

can be incidental

may cause severe acute inflammation of the subacromial bursa due to crystal shedding into and around the bursa

22
Q

what are risk factors for calficic periarthritis

A

renal failure
hyperparathyroidism
hypophosphatasia

23
Q

what marker is raised in calcific periarthritis

24
Q

how does gout present

A

rapid onset, monoarticular inflammation

10/10 pain

extreme tenderness

marked swelling

25
how does an acute attack of gout progress
usually self limiting over 5-14 days with no loss in function
26
what are the important differentials that need to be excluded when investigating a ?gout
septic arthritis Cellulitis
27
how does an acute attack of pseudogout progress
self limiting but takes longer than regular gout - 1-3 weeks until recovery
28
how does calcific periarthritis present
may be related to trauma shoulder pain/tenderness with associated swelling and redness systemic upset/fever common
29
how does calcific periarthritis progress
self resolves in 1-3 weeks
30
why may hypouricaemic treatment induce an acute crystal associated attack
Crystal formed in deep tissues like cartilage or tendon can lay dormant for years due to the avascular, aimmune nature of the areas they're embedded in, but when they're removed from their sites of origin (an action called crystal shedding) inflammation occurs acutely Shedding may occur due to local trauma, partial dissolution reducing crystal size (such as in hypouricaemic treatment) or occur as part of an acute phase of an unknown illness
31
what chronic feature of gout are seen on XR
``` Osteophyte formation Cyst formation Sclerosis Narowing of joint space (all similar to OA) ``` gouty erosions - well demarcated punched out defects with retained bone density around the joint space
32
what features of pseudogout are seen on XR
X-rays will show chondrocalcinosis in hyaline or fibrocartilage with or without the associated structural changes seen in OA However this is not always evident and its absence does not exclude pseudogout
33
how do you diagnose gout
crystal analysis of synovial fluid showing strongly negatively bifringent needle-shaped crystals
34
what gout fluid appear to look like
increased turbidity if acute chronic = white
35
how should you investigate a ?gout
aspirate the sample for a cell count, crystal examination and gram stain/culture Bloods(U+E, FBC, lipids, glucose, ESR) BP Urine dip
36
on crystal examination what should pseudogout crystals appear as
positively bifringent rod/rhomboid shaped crystals
37
what is the management for an acute gout attack
1. Fast acting NSAID (diclofenac/naproxen) 2. if not improving oral colchicine 3. corticosteroids, articular or PO
38
what are the side effects for colchicine
severe vomiting/diarrhoea
39
what is the management for an acute pseudogout attack
Aspiration quickly reduces pain and is usually sufficient Fluid reaccumulation is common however so an additional intraarticular corticosteroid injection is often also required Oral NSAIDS and colchinine are also useful but should be avoided in older people In older people early active mobilisation is the most useful
40
when is hypouricaemic treatment indicated for gout
``` chronic hyperuricaemic gout Recurrent attacks of acute gout Tophi Evidence of bone or joint damage Renal disease Gout with greatly elevated serum uric acid levels ```
41
what is the treatment for chronic hyperuricaemic gout
allopurinol
42
when starting someone on allopurinol, how often should they be reviewed + what monitoring is done
uric acid levels every 3-4 weeks and the dose of allopurinol should be increased in 100mg increments (starting dose 100-300mg) until the max dose 900mg is achieved or the levels are normal
43
why do you not give allopurinol in an acute attack of gout
may prolong it as it will promote shedding of alredy embedded crystals
44
what are the side effects of allopurinol
Acute attacks may be caused by the drug induction as it encourages crystal shedding due to reduction in the crystal size Patients should be counselled this and told to continue concurrent NSAID/colchicine in the first few weeks may mitigate this risk Extremely Small risk of TEN so if there is ANY risk of a rash patients should be counselled to stop the drug Interacts with azathioprine (causes myelosuppression) and potentiates warfarin
45
what is a lifethreatening interaction allopurinol has
azathioprine - causes myelosupression
46
what are second line options if allopurinol is insufficient + why arent they used more
Uricosuric drugs Probenecid Sulfinpyrazone As effective as allopurinol But they require several doses per day and the maintenance of a high urine flow (to avoid uric acid crystallisation In the renal tubules
47
what are second line options for chronic hyperuricaemic gout contraindicated in
Over-producers Renal impairment Urolithiasis
48
what is chronic tophaceous gout
deposition of nodular uric crystal masses
49
where are nodules formed in chronic tophaceous gout
``` Extensor sites of fingers Hands Forearms Elbows Achilles tendon Helix of ear ```