Brainscape's Knowledge GenomeTM

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


See full index

2nd year > Gout > Flashcards

Gout Flashcards

1
Q

what is gout?

A

purine metabolism disorder

crystal arthropathy from excess levels of uric acid leading to precipitation in joints and other tissue

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

epidemiology of gout

A

most common inflammatory arthritis across the world
prevalence is increasing
more common in elderly
males more at risk

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

what are the risk factors?

A 
high uric acid levels/ hyperuricaemia 
alcohol
obesity
male
age 
renal disease
dyslipidaemia
chemotherapy
diabetes mellitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is uric acid?

A

breakdown product of purines

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

excretion of uric acid

A

predominantly renally excreted and the rest excreted via GI tract
imbalance between production and excretion of uric acid it may crystallise and deposit in soft tissue and joints

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

what are the main mechanisms for gout development

A

purine overproduction
increased purine intake
decreased uric acid secretion

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

purine overproduction

A

when there is increased cell turnover or lysis of cells leading to release of purines and breakdown to uric acid. Causes include myelo- or lymphoproliferative disorders, psoriasis and use of chemotherapy agents

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

increase purine intake

A

several foods and beverages that are rich in purines and increase the risk of developing gout. includes seafood, red meat, alcohol and fructose-rich beverages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

decreased uric acid secretion

A

uric acid is predominantly renally excreted so anything that affects the kidneys can increase the risk of developing gout. Causes include diuretics, acute kidney injury, CKD, ACE inhibitors and diabetes mellitus

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

crystal formation

A

high uric acid levels leads to supersaturation and precipitation of monosodium urate crystals in soft tissue, joints and kidneys. Monosodium urate crystals precipitate in peripheral joints because they are less soluble at low temperatures

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

shape of urate crystals

A

forms needle-like crystals that can be detected on plane-polarised light. Characteristically monosodium urate crystals are negatively birefringent

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

symptoms caused by crystal formation

A

deposition of crystals can occur asymptomatically, such as in chronic gout
acute attacks = crystals trigger an acute inflammatory reaction leading to acutely painful swollen joints

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

classical presentation of gout

A

acutely painful and swollen joint coming on abruptly

intensity reached within 12 hours and lasts less than 2 weeks if untreated

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

joints affected

A

typically affects first metatarsalphalangeal joint
other common joints:
- knees
- ankles
- wrists
- finger joints
can affect more than 1 joint at a time = polyarticular gout, this is rarer

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

untreated hyperuricaemia

A

chronic tophaeous gout
development of multiple tophi - collections of urate crystals in soft tissue
classically located on helix of ear, fingers, toes, prepatellar bursa and olecranon

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

recurrent flares of acute gout

A

can lead to chronic polyarticular arthritis

17
Q

types of gout

A

acute monoarticular gout
acute polyarticular gout
chronic tophaeous gout

18
Q

presentation of acute monoarticular gout

A

joint pain
joint swelling
erythema
most commonly 1st metatarsophalangeal joint

19
Q

presentation of acute polyarticular gout

A

joint pain
joint swelling
erythema
fingers, toes, wrists, ankles and knees

20
Q

presentation of chronic tophaeous gout

A

tophi

degenerative arthropathy

21
Q

diagnosis

A 
clinical diagnosis
joint aspiration
serum uric acid
plain radiographs 
screening for cardiovascular and renal disease
22
Q

serum uric acid

A

levels should be taken 4-6 weeks following acute attack
elevated levels are not diagnostic of gout and normal serum uric acid doesn’t exclude gout
during an acute attack, plasma urate levels often fall

23
Q

joint aspiration

A

gold standard investigation
often not required
should be completed if there is concern about septic arthritis or where diagnosis is in doubt
send joint fluid for crystal microscopy, microscopy, culture and sensitivities

24
Q

how is gout diagnosed from microscopy of joint fluid?

A

presence of needle-shaped monosodium urate crystals that are negatively birefringent under plane-polarised light

25
Q

plain radiographs

A

typically normal in acute gout episodes
may show subcorticol cysts or bone erosion
can be used to exclude differentials

26
Q

management of gout

A

acute management and long-term prevention

27
Q

acute management of gout

A

general advice
first line therapy
second line therapy

28
Q

general advice for gout

A

advise rest, ice and elevation of joint
weight loss
diet discussion
alcohol consumption discussed

29
Q

first-line therapy

A

NSAIDs - naproxen or oral colchicine
co-prescribe a PPI for gastric protection if giving NSAID
no aspirin!

30
Q

second-line therapy

A

if NSAIDs or colchicine are ineffective or contraindicated then give short course of oral steroids or intra-articular injection of steroids

31
Q

prevention

A

urate-lowering drugs should be discussed with all patients diagnosed with gout
these drugs should be initiated once an acute attack has resolved

32
Q

which patient groups should be advised to commence urate-lowering drugs?

A 
2 or more attacks within 12 months
tophi
chronic gouty arthritis 
arthropathy
renal impairment 
renal calculi
young age onset
diuretic use
33
Q

prevention: first-line therapy

A

allopurinol

monitor uric acid levels every 4 weeks and dose can be uptitrated in relation to levels

34
Q

aim for uric acid levels

A

under 300 micromol/L

35
Q

cautions for allopurinol

A

renal impairment

can cause severe, potentially life-threatening hypersensitivity syndrome

36
Q

allopurinol

A

xanthine-oxidase inhibitor that prevents conversion of hypoxanthine to xanthine and xanthine to uric acid

37
Q

prevention: second-line therapy

A

febuxostate if allopurinol contraindicated
LFTs need to be done prior to and after commencing febuxostat as it can cause acute liver injury
uric acid levels should be monitored every 4 weeks and dose uptitrated in relation to these levels

38
Q

cautions in febuxostat

A

renal impairment

hypersensitivity to allopurinol and renal impairment may indicate hypersensitivity to febuxostat

39
Q

prevention of acute attacks

A

consider colchicine cover when starting or increasing urate lowering therapies such as allopurinol or febuxostat to prevent acute attacks. This may continue for 6 months
don’t stop urate lowering therapies during acute attacks

2nd year (48 decks)

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