Gout

Question 1

what is gout?

Answer 1

• uric acid crystals deposit in joints

- crystal induced (uric-acid) Joint damage

Question 2

there are 2 types of gout

Answer 2

-primary & secondary

Question 3

uric acid is a by product of what?

Answer 3

purine metabolism, but is usually excreted by kidneys

Question 4

what are purines & what are pyrimidines

Answer 4

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

Question 5

primary gout accounts for _____% of gout

Answer 5

90%

Question 6

Primary gout

Answer 6

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

Question 7

Secondary gout

Answer 7

• 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)

Question 8

what is the patho of gout

Answer 8

• 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)

Question 9

what are the stages of gout

Answer 9

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

Question 10

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

Answer 10

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)

Question 11

what does the recurrent acute attacks of gout cause?

Answer 11

formation of Tophi (plural) or Tophus (singular)

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

Question 12

diagnosing gout

Answer 12

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

Question 13

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

Answer 13

• 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)

Question 14

treatment of gout

Answer 14

• 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

Question 15

treatment of gout

Answer 15

• 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)