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Locomotor year 2 > Crystal Arthopathy > Flashcards

Crystal Arthopathy Flashcards

1
Q

GOUT

  1. define
  2. cause
  3. disorder
  4. gender
A
  1. acute inflammatory arthritis
  2. uncoated monosodium urate crystals in soft tissue
  3. uric acid metabolism
  4. MEN - higher uric acid levels naturally
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2
Q

podagra

A

Gout involving the BIG TOE

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3
Q

Incidence in the population of gout

A

1% in population

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4
Q

Clinical features of gout

A
  • EXTREMELY PAIN (most painful disorder known to man)
  • red
  • HOT
  • swelling
  • 1st MTP foot =50% cases
  • monoarticular= 90% cases
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5
Q

Which joints are most commonly affected in gout

A

DISTAL + SMALL JOINTS

  • lowest temp = crystallisation occurs more easily
  • less synovial fluid = more concentrated uric acid
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6
Q

progression of gout (if untreated)

A
  • polyarticular
  • spread more proximal (to knees)
  • gout attacks increase in freq + intensity
  • affects bone - rat bites erosion +
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7
Q

Why are you unlikely to see gout under age 30

A

require >20years raised uric acid levels
men- onset = puberty
women- onset = menopause

(therefore gout seen in:
men 40-60s
women 60-70s)

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8
Q

TOPHI

  1. define
  2. sites
  3. time for tophi to develop in gout
  4. when tophi develops
A
  1. FORIEGN BODY-TYPE GIANT CELL REACTION to urate crystals deposition
  2. white smooth deposits -ears + hands + elbows + feet
  3. > 10years
  4. untreated gout (50% patients)
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9
Q

Histology of tophi

look at a slide

A

LAYERS

  1. core/centre uric acid
  2. macrophage + dendritics
  3. fibrotic material
  4. Calcification - wall off infection
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10
Q

pathophysiology of gout

A
  1. uncoated urate crystals (foreign material) - NEUTROPHILS - lysis (crystals=sharp)
  2. cytokine cascade - IL1 -triggers more neutrophils
  3. acid lysosomes- decrease pH - crystallation occurs more easily
  4. spiral of gout attacks
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11
Q

Is the presence of gout crystals in the synovial fluid enough to trigger a gout attack?

A

NO
-need to have UNCOATED crystals (stim. immune response
OR
-sudden large increase in uric acid

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12
Q

How does the body normally die with mono-sodium urate crystals

A

-serum proteins -apoB/E- COAT crystals - inert

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13
Q

what is the saturation point

  1. define
  2. define by uric acid
A
  1. point at which all the lipoprotiens are saturated- unable to coat any more crystals - therefore crystals precipitate into soft tissues - GOUT
  2. saturation point = 6.8mg/dl
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14
Q

Complications of untreated gout

A
  1. joint destruction
  2. renal damage - urate excess cannot be excreted - KIDNEY STONES
    (3. tophi)
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15
Q

4 Cause of gout

A

DISORDER OF URIC ACID METABOLISM

  1. overproduction of uric acid
  2. disorders involving high cell turnover (invovles purines)
  3. overconsumption purine rich foods
  4. impaired excretion of purines
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16
Q

what is uric acid the metabolite of?

A

purine

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17
Q

PURINE CYCLE
input
output

A

input =600mg/d =diet
=300-600mg/d= new purine synthesis in body

output=600mg/d -kidneys -urine
=200mg/d -intestines-faeces

use in body = purine nucleotide bases for DNA/RNA

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18
Q

Dietary sources of purine

A

beer, shellfish, porte, red wine, beef , lamb

19
Q

Use of purines in body

A

nucleotide bases

20
Q

Main method by which uric acid is excreted

A

renal excretion

21
Q

Main cause of hyperuricaemia

A

90% patients - impaired renal excretion - excess urate stores in the body

22
Q

2 genetic conditions linked to gout

A

CAUSE OVERPRODCUTION OF URIC ACID

  1. Lesch Nyhan syndrome
  2. von wilke’s disease (G6Pase deficiency)
23
Q

Enzyme involved in purine metabolism

A

XANTHIANE OXIDASE

  1. hypoxathine -xanthine
  2. xanthine -uric acid
24
Q

Use of this medication to treat hypertension if patient also suffers gout should be avoided

A

DIURETICS (esp thiazide) - reduces urine output - reduce renal excretion of uric acid

25
Q

Diagnosis for definitive gout

A

Urate crystals present during acute attack

26
Q

Investigations to confirm gout diagnosis

A
  1. synovial fluid analysis (+ under polarizing light)
  2. serum uric acid analysis
  3. x-ray
  4. ultrasound
27
Q

Synovial fluid analysis in gout

A
  • white + cloudy = infiltration of immune cells - esp neutrophils
  • sharp + shiny + highly negative + birefringent under polarizing light
28
Q

Appearance of neutrophils in gout

A 
POLYMORPHONUCLEAR neutrophils (PMNs)
-granules -release lytic enzymes under infection
29
Q

Serum uric acid levels

A

treat if >11mg/dL

NB - hyperuricaemia - NOT diagnostic - 5% pop have elevated uric acid levels and do not suffer from gout

30
Q

Radiological features of gout

A
  1. soft tissue swelling
  2. ‘rat bites’ (erosion with overhanging edges)
  3. erosion OUTSIDE joint capsule
  4. erosion with maintains of joint space

problem- changes are only seen after MULTIPLE GOUT ATTACKS
solution - ultrasound - detect uric acid + soft tissue damage

31
Q

Treatment for acute attack

  1. aim
  2. options
A

1.reduce pain
2.NSAIDs = 1st line treatment
colchichine =2nd line
corticosteroids=3rd line
IL 1 blockers

32
Q

NSAIDs use for acute gout attacks

A
  • high dose
  • 2 weeks
  • only stop once asymptomatic for 2 days
33
Q

2 Biological DMARDs which could be used for gout

+why are they not currently used

A
  • Rilonacept
  • Anakinra
  • both IL1 blockers -IL1 is released during neutrophil lysis by urate crystals
  • reduce length + reoccurrence of attacks
  • currently not FDA approved due to £££££
34
Q

Colchichine

  1. MOA
  2. S.E
A

1.prevents microtubule formation - prevents mitosis
.prevents neutrophil motility + activity
(effect = anti-inflammatory in gout)

  1. apalstic anaemia + alopecia + neutopenia
35
Q

Treatment of chronic gout

  1. aim
  2. 4 options
A
  1. lowering uric acid levels - reduce gout attacks
  2. diet + allupinrol + rasburicase + probenecid

probenecid -preferential - fewest SE

36
Q

Allopurinol

  1. MOA
  2. S.E
A
  1. blocks xanthine oxidase- reduces generation uric acid

2. sever skin rashes

37
Q

Rasburicase

  1. MOA
  2. S.E
A

1.catalytic enzyme for conversion: xanthiane-urate-allantoin
ALLANTOIN -more sol than urate - passes into urine
2.anaphylaxis

38
Q

Probenecid

1.MOA

A

1.URICOSURIC - increase uric acid renal excretion -decrease serum uric acid

39
Q

PSEUDOGOUT

  1. type of crystals
  2. ass with which joint disorder
  3. clinical presentation
  4. incidence >85year olds
A
  1. calcium pyrophosphate
  2. OA
  3. most cases are ASYMPTOMATIC
  4. 50% of people >85years (esp women)
40
Q

Synvoial fluid analysis in pseudogout

A
  • rhomboid + dull + weakly birefringement crystals

- white + mildly cloudy

41
Q

Imaging investigations in Pseudogout

A

X-ray or Ultrasound to observe CHONDROCALCINOSIS

calcium deposits on cartilage

42
Q

Joints in psuedogout vs gout

A 
pseudogout = knees, wrists, ankles
gout = 1st MTP joint, knees, wrists, fingers, olecranon bursae
43
Q

Treatment for pseudogout

A

NSAIDs + intra-articular corticosteroids

Locomotor year 2 (11 decks)

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