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PCM IV Test 2 > gout and pseudogout > Flashcards

gout and pseudogout Flashcards

1
Q

what leads to production of uric acid

A

degradation of purines

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2
Q

what is the pathway of endogenous and dietary purines

A

inosine->hypoxanthine->xanthine->uric acid

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3
Q

what enzyme helps catalase breakdown of purines

A

xanthine oxidase

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4
Q

what are sources of purine in humans

A
  • diet

- nucleotide synthesis and metabolism

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5
Q

in what organs does excretion of uric acid occur?

A

1) kidneys (70%)

2) gut (30%)

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6
Q

definition of gout

A

-Gout is characterized by intermittent painful, inflammatory joint attacks, in response to uric
acid crystals as a consequence of hyperuricemia

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7
Q

what % of adults in US does gout affect

A

4%

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8
Q

what are risk factors for gout

A

1) male sex (estrogen increases excretion)
2) age (older)
3) obesity
4) HTN
5) hyperlipidemia
6) CV disease
7) CKD
8) medications (thiazides)
9) diet
10) lead exposure

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9
Q

gouty tophi

A

-deposition of uric acid in body tissues

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10
Q

what does hyperurcemia result from

A

1) overproduction

2) underexcretion (MAIN CAUSE)

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11
Q

clinical presentation of gout

A

-Acute gouty flares present with acute onset joint pain usually with maximal pain within the first
24 hours
-Acute gouty flares are often begin overnight
-The affected joint is typically swollen, erythematous, warm, and exquisitely painful
-fever can also be seen

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12
Q

what joints does gout most commonly affect

A
  • 1st MTP joint (called Podagra when affected)
  • Knee joints
  • Ankle joints
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13
Q

what are provoking factors for gout

A
  • ETOH consumption
  • Trauma
  • Inflammatory states (infection, surgery, myocardial infarction, etc…)
  • Dehydration, etc…
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14
Q

what is the definitive test for gout

A

arthrocentesis of affected joint’s synovial fluid

-send for cell count, culture, gram stain

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15
Q

what do crystals look like under polarized light

A

monosodium urate crystals, which are

needle shaped, negatively birefringent crystals

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16
Q

what other tests should be ordered for gout

A

-Serum uric acid level (higher levels make diagnosis of gout more likely)
-CBC with differential (if considering septic arthritis, look for left shift)
-X-ray is not helpful in acute gouty flares
-However, in chronic gout patients, x-ray may reveal bony erosions (i.e. “punched out
Lesions” or “overhanging edge”)

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17
Q

synovial fluid non-inflammatory arthritis < 2,000 WBCs/ʅ>

A

-Typically from mechanical or degenerative disorder (i.e. osteoarthritis)

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18
Q

synovial fluid inflammatory arthritis > 2,000 WBCs/ʅ>

A

-Typically from autoimmune conditions but can be from infection or crystal-induced
-Autoimmune conditions include Rheumatoid arthritis (RA) or spondyloarthritis (i.e. ankylosing spondylitis,
psoriatic arthritis, etc…)

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19
Q

synovial fluid (septic) arthritis

A

typically with > 20,000 to 50,000 WBCs/ʅ> but could have less WBCs present
-Gram stain and fluid culture will be positive and will help differentiate this etiology from others

20
Q
  • Crystal-induced fluid
A
  • typically 10,000-50,000 WBCS

- Typically Gout or Pseudogout

21
Q

tx of acute gouty flare

A

-Untreated gout will resolve within days to weeks (but it will be a very painful period)
-NSAIDS (Indomethacin, Naproxen, etc…), use with caution in CKD patients
-Colchicine – inhibits cytoskeletal function of neutrophils preventing activation and
migration of neutrophils
-Glucocorticoids
-Oral Prednisone or intra-articular/intramuscular steroid injection
-May be preferred treatment option in patients with CKD

22
Q

tx for chronic gout

A

-Xanthine oxidase inhibitors (cannot initiate during acute flares as it can precipitate a

gouty flare, typically wait 2 weeks after flare to initiate)

  • Ex: Allopurinol and Febuxostat
  • Goal serum uric acid level:
  • < 6.0 mg/dL in patients without tophi
  • < 5.0 mg/dL in patients with tophi

-Uricosuric agents – Inhibit reabsorption of uric acid in proximal convoluted tubule
-Probenecid
-Lesinurad
-Uricase
- Humans lack the enzyme uricase, which converts uric acid into the highly
soluble allantoin
-Ex: Pegloticase is used in severe gout when other treatments have failed

23
Q

what tx should you use if pt has gout and CKD

A
  • be cautious with NSAIDS and colchicine

- intraarticular or oral steroids are preferred

24
Q

what drug used to tx HTN also has some uricosuric effects

A

losartan

25
Q

how do you prevent gout

A
  • Avoidance of factors that contribute to hyperuricemia:

- ex: Red meat, seafood, alcohol, high-fructose corn syrup beverages, etc…

26
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

27
Q

what are risk factors for pseudogout

A
  • Age > 60
  • Primarily affects the elderly
  • Osteoarthritis
  • Metabolic diseases:
  • Hyperparathyroidism
  • Hemochromatosis
  • Hypophosphatasia (rare genetic disease)
  • Hypomagnesemia
28
Q

what is the pathophys of pseudogout

A

-Pyrophosphate produced by chondrocytes likely precipitates with calcium forming CPP crystals
which then activate inflammatory pathways leading to an acute arthritic attack

29
Q

what is the clinical presentation of pseudogout

A
  • Ranges from asymptomatic to symptomatic
  • Typically presents as monoarticular or oligoarticular arthritis
  • The affected joint is typically swollen, erythematous, warm, and painful
  • fever can also be seen
30
Q

what joints does pseudogout effect

A
  • Knee joints
  • Wrist joints
  • Rarely the 1st MTP joint
31
Q

how long can acute attacks of CPPD lasts

A

-wks to months

32
Q

what are provoking factors for pseudogout

A

-surgery or acute illness

33
Q

what is difinitive way to dx pseudogout

A

-arthrocentesis

34
Q

what do CPP crystals look like under polarized light

A

Rhomboid shaped and positively birefringent under polarized light

35
Q

what would xrays show in pseudogout

A

-Chondrocalcinosis – cartilage calcification (not specific to CPPD)

36
Q

how do you tx pseudogout

A
  • NSAIDS
  • Colchicine
  • Intra-articular glucocorticoid injection or oral prednisone
  • Treat underlying metabolic disease if present (i.e. Hyperparathyroidism, hemochromatosis,
    etc. ..)
37
Q

differential dx for gout

A
  • CPPD
  • septic arthritis
  • cellulits
  • RA
  • osteoarthritis
  • psoriatic arthritis
  • sarcoidosis
38
Q

autonomic innervation of kidney

A

Sympathetics T10-T11, Parasympathetics Vagus Nerve (OA, AA)

39
Q

autonomic innervation UE

A

Sympathetics T2-T7

40
Q

autonomic innervation LE

A

Sympathetics T11-L2

41
Q

5 models of care biomechanical

A

OMT for SD

42
Q

5 models of care resp/circulatory

A

lymphatic OMT tx

43
Q

5 models of care neuro

A

-OMT to normalize sympathetics and parasympathetics

44
Q

5 models of care metabolic, energetic,immune

A

-Consider arthrocentesis for acute gout flare to confirm diagnosis
-Assess uric acid levels
-Assess renal function and renal dose medications as needed (i.e. NSAIDs,
Colchicine, and allopurinol)
-Caution with systemic steroid use in diabetics (may need to check glucose more
frequently or give insulin temporarily)
-Consider stopping Thiazide if recurrent gout (Thiazides raise uric acid levels)

45
Q

5 models of care behavioral

A

Dietary changes (avoid red meat and seafood) and avoid alcohol

PCM IV Test 2 (11 decks)

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