HYHO Gout and Pseudogout Flashcards

1
Q

What gets broken down to form uric acid? How is uric acid excreted?

A

purines

sources: diet, nucleotide synthesis and metabolism

excretion: 70% kidneys, 30% gut

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2
Q

What are the risk factors for gout?

A

male sex

age

obesity

HTN

hyperlipidemia

CVD

meds

diet

lead exposure

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3
Q

What are the two routes of hyperuricemia?

A

overproduction - hepatic metabolism, cell turnover

underexcretion - kidneys > gut; main cause in most pts

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4
Q

When is maximal pain felt for acute gouty flares?

A

within first 24 hrs

acute flares: often begin overnight, most commonly affects 1st MTP, knee, or ankle joints

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5
Q

What factors provoke a gout flare?

A

ETOH

trauma

inflammatory states (infection, surgery, MI…)

dehydration

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6
Q

___ is a definitive test for gout.

A

arthrocentesis of the affected joint’s synovial fluid

samples should be sent for cell count, culture, gram stain

needle shaped, negatively birefrigent crystals

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7
Q

What tests can support a gout dx?

A

serum uric acid level increase

CBC with diff (r/o septic arthritis)

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8
Q

When is an X-ray useful in gout dx?

A

chronic gout pts only –> may reveal bony erosions

“punched out lesions”

“overhanging edge”

X-ray is NOT helpful in acute gouty flaires

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9
Q

How do you treat acute vs. chronic gout?

A

acute: NSAIDs, colchicine, glucocorticoids
chronic: allopurinol, febuxostat, probenecid, lesinurad, uricase

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10
Q

In a pt with CKD, what treatment for gout may be preferred?

A

acute - glucocorticoids

NSAIDs and colchicine use should be used with caution

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11
Q

What medication used to treat HTN has some uricosuric effects?

A

Losartan

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12
Q

What is pseudogout?

A
  • deposition of calcium pyrophosphate (CPP) crystals in and on cartilaginous surfaces
  • can provoke an acute inflammatory arthritis clinically similar to gout

pathophys isn’t know, but pyrophosphate produced by chondrocytes likely precipitates with calcium forming CPP crystals which then activate inflammatory pathways leading to an acute arthritic attack

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13
Q

Risk factors for pseudogout include…

A

Age > 60

OA

hyperparathyroidism

hemochromatosis

hypophosphatasia

hypomagnesemia

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14
Q

Clinically, what is a difference between gout and pseudogout?

A

pseudogout acute attacks can last weeks to months

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15
Q

What is the definitive test for pseudogout?

A

arthrocentesis of affected joint’s synovial fluid

CPP cyrstals: rhomboid shaped, positively birefringent under polarized light

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16
Q

What is the treatment for pseudogout?

A

NSAIDs

Colchicine

Intra-articular glucocorticoid injection or oral prednisone

Treat underlying disease

17
Q

What are the autonomic innervation levels of the kidneys, UE, and LE?

A

Kidneys: SNS T10-11, PNS Vagus

UE: SNS T2-7

LE: SNS T11-L2

18
Q

What is the 5 model approach to gout?

A

biomechanical: OMT for SD

resp/circ: lymphatic OMT

neuro: OMT to normalize SNS/PNS

met/en/immune: arthrocentesis, uric acid levels, renal function/med doses, caution with systemic steroids in DM pts, consider stopping thiazides

behavior: diet changes, avoid alc