Gout

Question 1

Natural history (4)

Answer 1

Natural history=

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

Question 2

Pathogenesis

Answer 2

+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

Question 3

Renal metabolism influencing gout (4)

Answer 3

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

Question 4

Risk factors (7)

Answer 4

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

Question 5

Complications (5)

Answer 5

Nephropathy
Chronic gouty tophy
Pyeloneprhitis
Nephrocalcinosis
Hypertension
Atherosclerosis

Question 6

Association with CVD

Answer 6

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

Question 7

Morphology in chronic

Answer 7

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

Question 8

Morphology of gouty tophy

Answer 8

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

Question 9

Morphology of nephropathy

Answer 9

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

Question 10

Morphology of acute

Answer 10

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

Question 11

Where are tophy found

Answer 11

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

Question 12

Diagnosis

Answer 12

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

Question 13

When is treatment for hyperuricemia indicated

Answer 13

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

Question 14

Management of acute

Answer 14

1. NSAID- indomethacin
2. Colchicine
3. Prenisilone

Question 15

Why is colchicine less often use

Answer 15

Side effects-> GIT

Question 16

Prevention

Answer 16

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)

Question 17

Best time to commence urate lowering therapy

Answer 17

Intercritical gout

Question 18

Urate lowering therapy

Answer 18

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

Question 19

Management of chronic gout

Answer 19

Allopurinol
Colchicine
NSAID

Question 20

Alternative if colchicine or NSAID CI/not tolerated

Answer 20

Prednisilone

Question 21

How to prevent acute attack when starting on allopurinol

Answer 21

Wait 3 weeks from acute attack

Cover with NSAID/colchicine for 3 months.

Question 22

Allopurinol SE

Answer 22

Rash, fever, -ve WCC

Caution in renal impairment

Question 23

Acute pseudogout

Answer 23

Acute monoarthropathy
Large joints
Spontaneous and self limiting

Question 24

Provoked pseudogout

Answer 24

Surgery
Illness
Trauma

Question 25

Risk factors for pseudogout

Answer 25

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

Question 26

Microscopic findings for PPD

Answer 26

Weakly birefringent

Question 27

What condition is PPD associated with

Answer 27

Chondrocalcinosis->soft tissue calcium deposition

Question 28

Management of PPD

Answer 28

NSAId, analgesia

Question 29

Advice to patients

Answer 29

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.

Question 30

Monitoring recommendations in gout

Answer 30

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

Question 31

Crystals seen on polarising microscopy

Answer 31

Monosodium urate Calcium pyrophosphate dehydrate Calcium hydroxyappatite Calcium oxalate

Question 32

Appearance of CPPD

Answer 32

Rod Rhomboid Weakly birefringent

Question 33

Appearance of calcium oxalate, and when do they occur

Answer 33

Bipyramidal Strong +ve birefringent End stage renal

Question 34

What is the term for gout of first MTP joint

Answer 34

Podagra

Question 35

When is monitoring uric acid levels useful

Answer 35

Monitoring in hypouricemic therapy

Question 36

Radiographic appearance of gout

Answer 36

Cystic changes in joint surface Punched out lesions Soft tissue calcifications