Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RB Y2 MSK 02 - Rheumatology > Crystal Arthropathies > Flashcards

Crystal Arthropathies Flashcards

1
Q

gout

A

inflammatory arthritis associated with monosodium urate crystal deposition in a joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how does gout usually present

A

acute monoarthropathy with severe joint inflammation

50% cases in big toe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is gout called when at MTP of big toe

A

podagra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

gout epidemiology

A

men more common

prevalence increases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is gout associated with

A

cardiovascular disease, hypertension, diabetes mellitus and chronic renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what can exacerbate renal under excretion

A

diuretics or renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the diagnosis of gout based on

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what can trigger uric acid precipitation in joints

A

dehydration, trauma or surgery

(uric acid is water soluble)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

is there a genetic predisposition for gout

A

no evidence of

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

clinical presentation of gout

A

intensely painful red, hot swollen joint

rapid onset, lasts for up to 2 weeks if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what may gout mimic

A

septic arthritis

  • inflammatory markers
  • felt unwell?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what joints are commonly affected in gout

A

50% podagra

also knee and ankle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DD of gout

A

exclude septic arthirits in any monoarthropathy

trauma

seronegative arthritis

CPPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what can chronic polyarticular gout result in

A

destructive erosive arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

gout - inflammatory markers

A

raised a lot

WCC may be raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

gout x ray

A
  • normal in acute attack
  • chronic/repeated - erosion, overhanging osteophyte, joint destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how can a definitive diagnosis of gout be made

A

analysing a sample of synovial fluid with polarised microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what befringence do uric acid crystals display

A

negative

  • change from yellow to blue when lined across direction of depolarisation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

managment of acute attack of gout

A

NSAIDs (symptoms subside 3-5 days)

if cant tolerate - colchicine (slower to work)

corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

in whichb situations would NSAIDs be contraindicated

A

eg peptic ulcer

25
Q

what can colchicine cause in excess quantities

A

diarrhoea

26
Q

when are urate lowering therapies given

A
  • recurrent acute attacks (<2 in a 12 month period), joint destruction, renal stones or tophi
27
Q

how should allopurinol etc be used

A
  • 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
Q

what lifestyle modifications should people with gout do

A

restrict red meat shell fish and alcohol

weight control

drink lots of fluid

29
Q

calcium pyrophosphate deposition (CPPD)

A

an umbrella term use to describe different patterns of disease including pseudogout and chondrocalcinosis

30
Q

pseudogout

A

(acute CPP crystal arthritis)

crystal arthropathy causing an acute atthritis by deposition of CPP crystals

31
Q

where does pseudogout tend to occur

A

in the large joints of elderly people

32
Q

course and aetiology of pseudogout

A

usually spontaenous and self limiting, but can be triggered by illness, trauma or sepsis

33
Q

chondrocalcinosis

A

CPP depostion in cartilage in the absence of acute inflammation

34
Q

where are CPPDs often found

A

knee wrist and ankle

35
Q

what can chronic CPPD result in

A

osteoarthritic changes

36
Q

what is the cause of CPPD

A

exact cause unknown

can coexist with hyperPTH, hypothyroidism, renal osteodystrophy, haemachromatosis and wilsons disease

37
Q

who is CPPD most common in

A

elderly

38
Q

what shape are CPP crystals

A

rhomboid

39
Q

what befringence do CPP crystals show

A

postitive - blue to yellow when aligned across direction of polarisation

40
Q

treatment of CPPD

A

NSAIDs

colchicine

steroids

rehydration

41
Q

hydroxyapatite crystal deposition

A

is a calcium phospahte

causes acute and rapid deterioration

42
Q

hydroxyapatite deposition in the shoulder

A

milwaukee shoulder - destructive shoulder arthropathy

43
Q

hydroxyapatite deposition epidemiology

A

females

around 50/60

44
Q

diagnosis of hydroxyapatite deposition

A

alizarin stain shows red clumps

45
Q

side effects of allupurinol

A

rash - must discontinue drug

46
Q

allopurinol mechanism

A

xanthine oxidase inhibitor

47
Q

whaat is another xanthine oxidase inhibitor

A

Febuxostat

48
Q

mechanism of uricosuric agents

A
  • 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
Q

uricosuric agents

A

Probenecid, Sulfinpyrazone, Benzbromarone

50
Q

which uricosuric agent can be used in mild renal impairement

A

Benzbromarone

51
Q

what serious drug reaction can allopurinol cause

A

SJS

52
Q

what must one ensure whilst taking allopurinol

A

adequate urine output

53
Q

what may be a problem with uricosuric agents

A
  • 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
Q

what is an additional precuation that may be advised in the first few weeks of uricosuric treatment

A

render urine alkaline

55
Q

which drugs antagonise uricosuric drugs in the PT

A

aspirin and other salicylates

56
Q

management of patient on allopurinol who develops an acute attack

A

treat acute attack separately

57
Q

what ocular manifestation is gout associated with

A

scleritis

58
Q

management of scleritis

A

oral NSAIDs, steroids and steroid sparing agents

RB Y2 MSK 02 - Rheumatology (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions