Brainscape's Knowledge GenomeTM

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


See full index

MDD > Crystal Arthropathies > Flashcards

Crystal Arthropathies Flashcards

1
Q

what are the two main forms of crystal arthropathies

A

Gout and Pseudogout

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

what is gout

A

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

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

what type of crystal causes gout

A

monosodium urate monohydrase

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

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

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

what proportion of hyperuracaemic patients get gout

A

5%

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

what is the gender split with gout

A

10:1

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the cause of pseudogout

A

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

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

what is the incidence stratified by ages above 55 of pseudogout

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what sites are most affected in pseudogout

A

knee

wrist

symphsis pubis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how does pseudogout present

A

acute self limiting synovitis or a chronic arthritis

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

what metabolic diseases predispose to CPP deposition

A 
Haemachromatosis 
hyperparathyroidism
hypophosphatasia
hypomagnesaemia 
Wilson's disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is calcific periarthritis

A

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

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

A

CRP

24
Q

how does gout present

A

rapid onset, monoarticular inflammation

10/10 pain

extreme tenderness

marked swelling

25
Q

how does an acute attack of gout progress

A

usually self limiting over 5-14 days with no loss in function

26
Q

what are the important differentials that need to be excluded when investigating a ?gout

A

septic arthritis

Cellulitis

27
Q

how does an acute attack of pseudogout progress

A

self limiting but takes longer than regular gout - 1-3 weeks until recovery

28
Q

how does calcific periarthritis present

A

may be related to trauma
shoulder pain/tenderness with associated swelling and redness
systemic upset/fever common

29
Q

how does calcific periarthritis progress

A

self resolves in 1-3 weeks

30
Q

why may hypouricaemic treatment induce an acute crystal associated attack

A

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
Q

what chronic feature of gout are seen on XR

A 
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
Q

what features of pseudogout are seen on XR

A

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
Q

how do you diagnose gout

A

crystal analysis of synovial fluid showing strongly negatively bifringent needle-shaped crystals

34
Q

what gout fluid appear to look like

A

increased turbidity if acute

chronic = white

35
Q

how should you investigate a ?gout

A

aspirate the sample for a cell count, crystal examination and gram stain/culture

Bloods(U+E, FBC, lipids, glucose, ESR)

BP

Urine dip

36
Q

on crystal examination what should pseudogout crystals appear as

A

positively bifringent rod/rhomboid shaped crystals

37
Q

what is the management for an acute gout attack

A
  1. Fast acting NSAID (diclofenac/naproxen)
  2. if not improving oral colchicine
  3. corticosteroids, articular or PO
38
Q

what are the side effects for colchicine

A

severe vomiting/diarrhoea

39
Q

what is the management for an acute pseudogout attack

A

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
Q

when is hypouricaemic treatment indicated for gout

A 
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
Q

what is the treatment for chronic hyperuricaemic gout

A

allopurinol

42
Q

when starting someone on allopurinol, how often should they be reviewed + what monitoring is done

A

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
Q

why do you not give allopurinol in an acute attack of gout

A

may prolong it as it will promote shedding of alredy embedded crystals

44
Q

what are the side effects of allopurinol

A

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
Q

what is a lifethreatening interaction allopurinol has

A

azathioprine - causes myelosupression

46
Q

what are second line options if allopurinol is insufficient + why arent they used more

A

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
Q

what are second line options for chronic hyperuricaemic gout contraindicated in

A

Over-producers
Renal impairment
Urolithiasis

48
Q

what is chronic tophaceous gout

A

deposition of nodular uric crystal masses

49
Q

where are nodules formed in chronic tophaceous gout

A 
Extensor sites of fingers  
Hands  
Forearms  
Elbows 
Achilles tendon 
Helix of ear

MDD (22 decks)

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