Crystal Arthritis (gout and pseudogout) Flashcards Preview

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Flashcards in Crystal Arthritis (gout and pseudogout) Deck (29):
1

enzymatic pathway for production of uric acid

Hypoxanthine --> xanthine --> uric acid
via xanthene oxidase

2

allopurinol, febuxostat target

xanthene oxidase

3

describe normal uric acid handleing in the kidney

Filtered at glomerulus (100%)
reabs by: URAT-1 → GLUT9 → circulation (98%)
secreted by OAT → urine (5-10%)

4

What is uricase

enzyme that normally breaks down urate

5

epidemiology of gout

purine rich diet (red meat, seafood)
alcohol (beer) abuse
Men > women
older people

6

In general how do you get hyperuricemia?

make too much uric acid or don't get rid of enough
**the later is the cause of hyperuricemia in 90% of cases

7

congenital causes of hyperuricemia?

1. HGPRT deficiency (Lesch-Nyhan syndrome)--> surplus substrate (PRPP)
2. G6PD deficiency (interferes with renal excretion)
3. Fructose-1-phosphae adolase deficiency
4. Phyosphoribosyl-pyrophosphate synthase overactivity

8

secondary causes of increased uric acid production

increased cell turnover
• leukemia/lymphoma
• tumor lysis syndrome
• treating psoriasis
• sickle cell disease, etc

9

What drugs cause decreased secretion of uric acid

o Thiazide and loop diuretics
o Low dose aspirin/salicylates: blocks secretion
o Ethanol
o Cyclosporine

also, Nicotinic acid, Pyrazinamide and Ethambutol

10

how does DM lead to hyperuricemia

enhances uric acid reabs

11

pathophys of gout

hyperuricemia --> uric acid ppt and forms crystals
--> Urate crystals are recognized as a foreign substance by macrophages, fibroblasts, and mast cells and activate NLRP3 inflammasome → release of IL-1Beta → neutrophils influx into joint and are activated → IL-8, TNF released + neutrophil cell lysis → INFLAMMATION

12

Presentation of gout

Sudden onset of agonizing pain, swelling ad redness of first MTP joint
Raised serum uric acid levels (>6.8 mg/dL)
Trophi (more with chronic)
Leuckocytosis

13

Gout can occur at any time but is often precipitated by

• too much food or alcohol (beer in particular)
• dehydration
• starting a diuretic
• illness or stress

14

in skin and around joints = Smooth white deposits

trophi

15

Elicits a granulomatous reaction = macrophages

chronic gout
--> erosive arthritis

16

What other clinical conditions are seen with gout?

1. nephrolithiasis
2. lead poisoning (produces interstitial nephritis which interferes with uric acid secretion )
3. HTN and CAD

17

What conditions are necessary for uric acid nephrolithiasis to form

inc uric acid excretion
decreased urine volume
low urine pH

18

risk factors for gout

age
obesity
metabolic syndrome
alcoholism
chronic diuretic or low dose aspirin use

19

Where do the CPP deposit in CPDD dz?

cartilage >>> tendons, ligaments, bursa

20

pathophys of CPDD dz

CPP crystals recognized as foreign substance → activate NLRP3 inflammasome → IL-1B released → neutrophils move into joint and are activated → INFLAMMATION

21

Familial CPPD linked to mutation in ...

ANHK gene
**seen in pts <55 yo

22

What joints does CPDD effect?

KNEE
(rarelt affects MTP)

chronic CPDD: wrists, elbows, hip
= joints less likely affected by OA

23

Assc diseases to consider when pt presents with CPDD

younger: hemachromatosis
polder: hyperparathyroidism

24

How is the diagnosis of CPDD made?

detecting rhomboidal, WEAKLY birefringent, intracellular crystals in joint fluid

25

What is seen on XR in CPDD?

chondrocalcinosis

26

What is due to HA crystal deposition

Basic Calcium Phosphate Crystal Dz (BCP)

27

Who typically gets basic calcium phosphate crystal dz

dialysis pts

28

What joints does BCP dz involve

axial skeleton

29

is uric acid more or less soluble as an anion

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