Crystal Arthropathies Flashcards

1
Q

gout

A

inflammatory arthritis associated with monosodium urate crystal deposition in a joint

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2
Q

how does gout usually present

A

acute monoarthropathy with severe joint inflammation

50% cases in big toe

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3
Q

what is gout called when at MTP of big toe

A

podagra

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4
Q

gout epidemiology

A

men more common

prevalence increases with age

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5
Q

gout aetiology

A

high serum uric acid levels

may be due to renal underexcretion or excessive intake of foods high in protein (alcohol, red meat and seafood)

gout is the end product in protein metabolism

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6
Q

what is gout associated with

A

cardiovascular disease, hypertension, diabetes mellitus and chronic renal failure

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7
Q

what can exacerbate renal under excretion

A

diuretics or renal failure

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8
Q

what is the diagnosis of gout based on

A

identification of crystals and radio graphic findings (not hyperuricaemia alone)

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9
Q

how does the level of uric acid affect gout

A

level doesnt precipitate gout

rather acute changes in the level of uric acid

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10
Q

what can trigger uric acid precipitation in joints

A

dehydration, trauma or surgery

(uric acid is water soluble)

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11
Q

is there a genetic predisposition for gout

A

no evidence of

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12
Q

clinical presentation of gout

A

intensely painful red, hot swollen joint

rapid onset, lasts for up to 2 weeks if untreated

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13
Q

what may gout mimic

A

septic arthritis

  • inflammatory markers
  • felt unwell?
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14
Q

what joints are commonly affected in gout

A

50% podagra

also knee and ankle

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15
Q

DD of gout

A

exclude septic arthirits in any monoarthropathy

trauma

seronegative arthritis

CPPD

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16
Q

what are gout tophi

A

painless white accumulations of uric acid which can occur in soft tissues and occasionally erupt through the skin

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17
Q

chronic polyarticular gout

A

usually occurs after recurrent acute attacks for more than 10 years

diuretic associated often

tophi present

can resemble RA

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18
Q

what can chronic polyarticular gout result in

A

destructive erosive arthritis

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19
Q

gout - inflammatory markers

A

raised a lot

WCC may be raised

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20
Q

gout x ray

A
  • normal in acute attack
  • chronic/repeated - erosion, overhanging osteophyte, joint destruction
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21
Q

how can a definitive diagnosis of gout be made

A

analysing a sample of synovial fluid with polarised microscopy

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22
Q

what befringence do uric acid crystals display

A

negative

  • change from yellow to blue when lined across direction of depolarisation)
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23
Q

managment of acute attack of gout

A

NSAIDs (symptoms subside 3-5 days)

if cant tolerate - colchicine (slower to work)

corticosteroids

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24
Q

in whichb situations would NSAIDs be contraindicated

A

eg peptic ulcer

25
what can colchicine cause in excess quantities
diarrhoea
26
when are urate lowering therapies given
* recurrent acute attacks (\<2 in a 12 month period), joint destruction, renal stones or tophi
27
how should allopurinol etc be used
* after acute attack has settled down (2 weeks) so as not to cause a sudden change in uric acid levels * start at low dose and titrate up until serum urate level is achieved (\<360micromol/L)
28
what lifestyle modifications should people with gout do
restrict red meat shell fish and alcohol weight control drink lots of fluid
29
calcium pyrophosphate deposition (CPPD)
an umbrella term use to describe different patterns of disease including pseudogout and chondrocalcinosis
30
pseudogout
(acute CPP crystal arthritis) crystal arthropathy causing an acute atthritis by deposition of CPP crystals
31
where does pseudogout tend to occur
in the large joints of elderly people
32
course and aetiology of pseudogout
usually spontaenous and self limiting, but can be triggered by illness, trauma or sepsis
33
chondrocalcinosis
CPP depostion in cartilage in the absence of acute inflammation
34
where are CPPDs often found
knee wrist and ankle
35
what can chronic CPPD result in
osteoarthritic changes
36
what is the cause of CPPD
exact cause unknown can coexist with hyperPTH, hypothyroidism, renal osteodystrophy, haemachromatosis and wilsons disease
37
who is CPPD most common in
elderly
38
what shape are CPP crystals
rhomboid
39
what befringence do CPP crystals show
postitive - blue to yellow when aligned across direction of polarisation
40
treatment of CPPD
NSAIDs colchicine steroids rehydration
41
hydroxyapatite crystal deposition
is a calcium phospahte causes acute and rapid deterioration
42
hydroxyapatite deposition in the shoulder
milwaukee shoulder - destructive shoulder arthropathy
43
hydroxyapatite deposition epidemiology
females around 50/60
44
diagnosis of hydroxyapatite deposition
**alizarin** stain shows red clumps
45
side effects of allupurinol
rash - must discontinue drug
46
allopurinol mechanism
xanthine oxidase inhibitor
47
whaat is another xanthine oxidase inhibitor
Febuxostat
48
mechanism of uricosuric agents
* block active transport of organic acids leading to reduced reabsorption and secretion of urate - overall reduced net reabsorption * not suitable in renal impairment of history of renal stones
49
uricosuric agents
Probenecid, Sulfinpyrazone, Benzbromarone
50
which uricosuric agent can be used in mild renal impairement
Benzbromarone
51
what serious drug reaction can allopurinol cause
SJS
52
what must one ensure whilst taking allopurinol
adequate urine output
53
what may be a problem with uricosuric agents
* As crystallization of urate in the urine can occur with the uricosuric drugs, it is important to ensure an adequate urine output especially in the first few weeks of treatment * Patients must increase fluid intake to 2-3 litres daily
54
what is an additional precuation that may be advised in the first few weeks of uricosuric treatment
render urine alkaline
55
which drugs antagonise uricosuric drugs in the PT
aspirin and other salicylates
56
management of patient on allopurinol who develops an acute attack
treat acute attack separately
57
what ocular manifestation is gout associated with
scleritis
58
management of scleritis
oral NSAIDs, steroids and steroid sparing agents