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Flashcards in Gout Deck (36):
1

Natural history (4)

Natural history=
1. asympT hyperU
2. acute arthritis
3. intercritical gout
4. chronic tophaceous

2

Pathogenesis

+uric acid (from purine metabolism)-->
not all hyperuricemia= gout
Precipitation of monosodium urate into joint->+in periphery where -ve temperature
Urate crystals form-->incitng event
(trauma?) released in to synovium-
+inflammation
MacroP ingest-> +inflammasome->+neutrophils->+free radicals, leukotrienes, joint damage->neutrophils ingest, lyse and release lysosomal factors

3

Renal metabolism influencing gout (4)

-ve glomerular filtration
-ve excretion
+absorption
+post secretion reabsorption

4

Risk factors (7)

Hyperuricemia
Age >30, male
Heavy alcohol
Obesity
Drugs->diuretics/aspirin, cyclosporin
genetics

5

Complications (5)

Nephropathy
Chronic gouty tophy
Pyeloneprhitis
Nephrocalcinosis
Hypertension
Atherosclerosis

6

Association with CVD

+LDL, -ve HDL. Must do CVD risk assessment

7

Morphology in chronic

Chronic-->precipitation on
cartilage. Becomes fibrotic, thickened,
pannus forms. erosions,
fibrous ankylosis

8

Morphology of gouty tophy

+aggregates urate
crystal w/ surrounding
macroP, lymphocytes
In joint/cartilage surface
periarticular tissues-->
patellar bura, olecronon,
earlobe, achilles tendo and
elsewhere

9

Morphology of nephropathy

precipitate in interstitium,
tubules-->
uric acid stones, pyelonephritis

10

Morphology of acute

Acute--> neutrophilic
aggregates (w/ crystals inside),
edematous, congested. some
macroP, lymphocytes. when
crystals solubilised, attack abates

11

Where are tophy found

Extensor surfaces->elbows, knees, achilles, helix of ear

12

Diagnosis

Arthrocentesis:
WCC usually exceeds 2.0 x 10^9/L
PMN
Monosodium urate crystals, negative birefringent

Serum uric acid may be low, normal or high

Search for secondary causes->renal insufficiency, +cell turnover in malignancy

13

When is treatment for hyperuricemia indicated

Recurrent gout
Uric acid neprhopathy
Urolithiasis
Tophi
Comorbidities putting at +CVD risk

14

Management of acute

1. NSAID- indomethacin
2. Colchicine
3. Prenisilone

15

Why is colchicine less often use

Side effects-> GIT

16

Prevention

Low purine diet
Limit alcohol and fructose containing drinks
Avoid drugs that worsen
Lose weight, reduce CVD risk

Consider urate lowering therapy + colchicine+/- NSAID (to prevent acute attack)

17

Best time to commence urate lowering therapy

Intercritical gout

18

Urate lowering therapy

allopurinol 50 mg orally, daily for the first month, then increase the dose by 50 mg every 2 to 4 weeks depending on the patient's renal function and plasma urate levels

19

Management of chronic gout

Allopurinol
Colchicine
NSAID

20

Alternative if colchicine or NSAID CI/not tolerated

Prednisilone

21

How to prevent acute attack when starting on allopurinol

Wait 3 weeks from acute attack
Cover with NSAID/colchicine for 3 months.

22

Allopurinol SE

Rash, fever, -ve WCC
Caution in renal impairment

23

Acute pseudogout

Acute monoarthropathy
Large joints
Spontaneous and self limiting

24

Provoked pseudogout

Surgery
Illness
Trauma

25

Risk factors for pseudogout

Age +
OA
DM
Hypothyroidism
+PTH
Haemachromatosis
Wilsons
Low PO4,Mg

26

Microscopic findings for PPD

Weakly birefringent

27

What condition is PPD associated with

Chondrocalcinosis->soft tissue calcium deposition

28

Management of PPD

NSAId, analgesia

29

Advice to patients

Foods that have a high purine content (i.e., alcohol, seafood, and offal) are associated with higher risk of elevated uric acid and gout. [2]

Reducing intake of alcohol, especially beer, lowers the risk of gout. [31]

Reducing seafood and meat intake helps to a lesser degree.

Reducing the intake of vegetables high in purines (i.e., asparagus, spinach, and mushrooms) does not seem to affect uric acid levels.

Dairy products reduce the risk of gout.

30

Monitoring recommendations in gout

Recurrent attacks, tophy, radiographic changes
F/U uric acid levels 1-3 monthly, then 6 monthly
FBC, RFTs, LFTs every 3-6 months
When begin on allopurinol, monitor for hypersensitivity
Consider drug interactions

31

Crystals seen on polarising microscopy

Monosodium urate
Calcium pyrophosphate dehydrate
Calcium hydroxyappatite
Calcium oxalate

32

Appearance of CPPD

Rod
Rhomboid
Weakly birefringent

33

Appearance of calcium oxalate, and when do they occur

Bipyramidal
Strong +ve birefringent
End stage renal

34

What is the term for gout of first MTP joint

Podagra

35

When is monitoring uric acid levels useful

Monitoring in hypouricemic therapy

36

Radiographic appearance of gout

Cystic changes in joint surface
Punched out lesions
Soft tissue calcifications