Gout Flashcards

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1
Q

what is gout?

A
  • uric acid crystals deposit in joints

- crystal induced (uric-acid) Joint damage

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2
Q

there are 2 types of gout

A

-primary & secondary

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3
Q

uric acid is a by product of what?

A

purine metabolism, but is usually excreted by kidneys

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4
Q

what are purines & what are pyrimidines

A

purines: adenine & guanine (nitrogenous bases in DNA, metabolism then causes uric acid formation
pyrimidines: T&C (nitrogenous bases in DNA)

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5
Q

primary gout accounts for _____% of gout

A

90%

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6
Q

Primary gout

A
  • approx 95% in men
  • metabolic disease(metabolic issue with purines) (producing more uric acid then should)
  • familial (if in family has higher chance)
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7
Q

Secondary gout

A
  • far less prevalent
  • producing normal amount of uric acid then cannot excrete (problem with excretion)
  • renal (is leading cause of problem) (renal not excreting uric acid)
  • cell destruction(second leading cause) (will lead to excess uric acid ex. leukemia excessive cell turnover)
  • others (chemotherapy, excessive alcohol-alcohol inhibits excretion of uric acid causing a build-up in circulation-particularity beer has high purine content)
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8
Q

what is the patho of gout

A
  • alternate purine metabolism causing asymptomatic hyperuricemia (elevated uric acid in blood)
  • then crystals deposit in synovial joints (solubility of uric acid is higher in blood, less so in synovial fluid) that is why it crystallizes
  • WBC influx & complement activation (POLUMORPHONUCLEAR LEUKOCYTES -move in & remove crystals) Inflammation & damage, cell releases contents, lysosomal enzyme release
  • WBC phagocytize crystals which cause WBC necrosis then enzyme is released (lysosomal enzymes) causing inflammation & joint damage
  • recurrent acute attacks -formation of tophi (space occupying lesion in joint-hard nodules inside joint)
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9
Q

what are the stages of gout

A
  1. hyperuricemia (asymptomatic) (early onest, 30-40 yrs of age)
  2. acute inflm in 1 joint (usually large toe joint)
    triggers acute onset of inflm:
    -food
    -alcohol
    -drugs
    -strenuous exercise
  3. subsides in approx 1 wk (swelling & inflm)
  4. asymptomatic (months-years)
  5. Frequent, recurrent attack causing permanent damage
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10
Q

why does uric acid crystallize in synovial joints but not in blood?

A

uric acid is easily soluble in blood (high solubility), synovial fluid (low solubility uric acid crystallizes in there, temps is higher at core & blood more soluble at higher temp (toe lower temp and less prefused)

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11
Q

what does the recurrent acute attacks of gout cause?

A

formation of Tophi (plural) or Tophus (singular)

which is a space occupying lesion in joint (with hard nodules inside)

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12
Q

diagnosing gout

A
  • hyperurecemia (uric acid) in serum & urine(is not diagnostic)
  • crystals in joints (confirmed by x-ray)
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13
Q

what are some of the triggers for acute onset of inflammation with gout?

A
  • food (protein breakdown generates nitrogenous waste products makes nitrogenous waste products hyperurcemia)
  • drugs (may have metabolic side effects that affect hyperurcemia
  • alcohol (high purine content, ingest lots, metabolize purines, have hyperurcemia & advance)
  • strenuous exercise (strenuous activity, increases demand for energy once carbohydrates exhausted break down proteins & nitrogenous waste products)
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14
Q

treatment of gout

A
  • acute attack will have pain & inflammation :
    - NSAIDS
    - Steroids (anti-inflammatory)
    - colchicine (primary property is inhibiits migration of poleymorphonuclear leukocytes, also an anti-inflammatory also an anitmitoitic
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15
Q

treatment of gout

A
  • acute attack will have pain & inflammation :
    - NSAIDS
    - Steroids (anti-inflammatory)
    - colchicine (primary property is inhibiits migration of poleymorphonuclear leukocytes, also an anti-inflammatory also an anitmitotic-this property becomes a side effect because not trying to affect mitosis would likely not be a problem because using short term)

long term:

  • decrease hyperurcemia (with drugs)
  • Increase uric acid excretion (drugs)
  • simple increase fluid intake, excrete more urine, excrete more uric acid (not able to only do this)
  • decrease protein in diet (breakdown protein cause increase in uric acid, debatable/controversial contribution of protein breakdown limited)
  • no alcohol (particularly beer)
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