Crystal-induced arthropathies Flashcards

1
Q

How do organic anions + thiazides promote hyperuricemia?

A

They act at the URAT1 exchanger in the kidney- they go out into the lumen while urate is reabsorbed. Thus, if there are higher concentrations of organic acids/ thiazides, then they are excreted more while urate is reabsorbed more.

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2
Q

Presentation of gout attack

A

Abrupt, rapid onset of monoarticular pain, swelling, erythema

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3
Q

Complication of chronic gout

A

Renal failure- due to urate crystal deposition in kidney (urate nephropathy)

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4
Q

Primary vs. secondary gout

A

Primary gout- etiology of hyperuricemia is not exactly known (most common form)

Secondary gout- etiology is known

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5
Q

Pattern of joint involvement in gout attack

A

Monoarticular involvement; MTP joint most commonly affected (podagra), other joints include ankle, heel, knee, and wrist

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6
Q

Where does crystals deposit in gout vs. CPPD

A

In CPPD, crystals deposit exclusively in articular cartilage. In gout, crystals deposit in synovial space + soft tissue

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7
Q

What is chronic gout characterized by?

A

Development of tophi- white chalky aggregates of uric acid crystals w/ fibrosis

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8
Q

Why alcohol can cuase hyperuriecmiea

A

Competes for same excretion site as uric acid

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9
Q

Factors that promote hyperuricemia

A

Alcohol, meat/seafood consumption (high purines), organic acidosis, obesity, diuretics, rneal disease

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10
Q

First step in diagnosing gout

A

Always aspirate the joint in order to rule out septic arthritis. Then identify crystals

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11
Q

Characteristic of monosodium urate crystals

A

Strongly negative birefringent- yellow when parallel + blue when perpendicular

Crystals are fine needle shaped

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12
Q

Pathophysiology of urate crystal formation

A

Urate crystals precipitate in joints –> neutrophils + macrophages phagocytize –> IL-1 and other cytokines released –> infalmmatoryt reaction –> tissue/joint injury

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13
Q

Characteristic of calcium pyrophosphate crystals

A

Weakly berefringent udner polarized light (blue when parallel to light)

Rhomboid shape

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14
Q

Imaging finding for calcium pyrophosphate deposition

A

Chondrocalcinosis- cartilage calcification

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15
Q

Common causes of secondary gout

A
  • High cell-turnover rates (e.g. myeloproliferative disorders, psoriasis, lymphoma) + tumor lysis w/ chemo
  • Genetic disorders (e.g. Leisch Nyhan syndrome)
  • Renal failure (decreased excretion of urate)
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