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MS/Rheum > Crystal Arthritis (gout and pseudogout) > Flashcards

Crystal Arthritis (gout and pseudogout) Flashcards

1
Q

enzymatic pathway for production of uric acid

A

Hypoxanthine –> xanthine –> uric acid

via xanthene oxidase

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2
Q

allopurinol, febuxostat target

A

xanthene oxidase

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3
Q

describe normal uric acid handleing in the kidney

A

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

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4
Q

What is uricase

A

enzyme that normally breaks down urate

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5
Q

epidemiology of gout

A

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

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6
Q

In general how do you get hyperuricemia?

A

make too much uric acid or don’t get rid of enough

**the later is the cause of hyperuricemia in 90% of cases

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7
Q

congenital causes of hyperuricemia?

A
  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
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8
Q

secondary causes of increased uric acid production

A 
increased cell turnover
•	leukemia/lymphoma
•	tumor lysis syndrome
•	treating psoriasis
•	sickle cell disease, etc
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9
Q

What drugs cause decreased secretion of uric acid

A

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

also, Nicotinic acid, Pyrazinamide and Ethambutol

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10
Q

how does DM lead to hyperuricemia

A

enhances uric acid reabs

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11
Q

pathophys of gout

A

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

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12
Q

Presentation of gout

A

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

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13
Q

Gout can occur at any time but is often precipitated by

A
  • too much food or alcohol (beer in particular)
  • dehydration
  • starting a diuretic
  • illness or stress
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14
Q

in skin and around joints = Smooth white deposits

A

trophi

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15
Q

Elicits a granulomatous reaction = macrophages

A

chronic gout

–> erosive arthritis

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16
Q

What other clinical conditions are seen with gout?

A
  1. nephrolithiasis
  2. lead poisoning (produces interstitial nephritis which interferes with uric acid secretion )
  3. HTN and CAD
17
Q

What conditions are necessary for uric acid nephrolithiasis to form

A

inc uric acid excretion
decreased urine volume
low urine pH

18
Q

risk factors for gout

A 
age
obesity 
metabolic syndrome 
alcoholism 
chronic diuretic or low dose aspirin use
19
Q

Where do the CPP deposit in CPDD dz?

A

cartilage&raquo_space;> tendons, ligaments, bursa

20
Q

pathophys of CPDD dz

A

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

21
Q

Familial CPPD linked to mutation in …

A

ANHK gene

**seen in pts <55 yo

22
Q

What joints does CPDD effect?

A

KNEE
(rarelt affects MTP)

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

23
Q

Assc diseases to consider when pt presents with CPDD

A

younger: hemachromatosis
polder: hyperparathyroidism

24
Q

How is the diagnosis of CPDD made?

A

detecting rhomboidal, WEAKLY birefringent, intracellular crystals in joint fluid

25
Q

What is seen on XR in CPDD?

A

chondrocalcinosis

26
Q

What is due to HA crystal deposition

A

Basic Calcium Phosphate Crystal Dz (BCP)

27
Q

Who typically gets basic calcium phosphate crystal dz

A

dialysis pts

28
Q

What joints does BCP dz involve

A

axial skeleton

29
Q

is uric acid more or less soluble as an anion

A

more

MS/Rheum (23 decks)

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