Gout Flashcards

1
Q

Gout?

A

Crystal deposits of uric acid in the joints

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2
Q

Is gout autoimmune?

A

NO

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3
Q

What is the crystal-induced joint damaged caused by?

A

the inflammation that follows NOT d/t the deposits

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4
Q

uric acid?

A

nitrogenous waste product usually produced in the liver and excreted by the kidney

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5
Q

Primary form?

A
  • 95% in men

- D/t a metabolic problem (altered metabolism leading to elevated levels of uric acid as a byproduct)

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6
Q

Secondary form?

A
  • renal disorders [where uric acid is not excreted and is retained]
  • any condition leading to excessive cell turnover (cellular destruction and formation)
  • alcohol (beer elevates purine content In the body which is a source of uric acid)
  • chemotherapy
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7
Q

Name the nitrogenous bases and what they are joined by?

A
  • Purines and pyrimidines joined by hydrogen bonds
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8
Q

Purines?

A

Adenine and guanine

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9
Q

Pyrimidine?

A

cytosine & thymine & uracil

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10
Q

Patho?

A

Altered purine metabolism -> results in asymptomatic hyperuricemia -> uric acid deposits as crystals within synovial joints -> an attempt to remove the abnormal accumulation by leukocytes causes damage (leukocytes migrate into joints) -> Polymorphonuclear (PMN) leukocytes -> “many shaped nuclei” -> follow the uric acid crystals into the joint and attempt to remove them. complement activation d/t WBC influx. -> PMN leukocytes engulf debris and foreign material in an attempt to remove the crystals, however, they are toxic to the PMN leukocytes and induce necrosis -> cells die and release their contents -> Lysosomal enzymes released from the WBC’s (from lysosomes within the cells) -> causes enzymatic damage to cartilage -> exposes subchondral bone -> bone-to-bone contact -> erosion of bone. -> inflammation causes non-specific damage -> Tophi

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11
Q

Hyperuricemia?

A

high levels of uric acid in the blood

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12
Q

Tophi?

A

hard; solid, space-occupying lesions formed within the joint upon recurrent acute attacks

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13
Q

List the stages of Gout

A
  1. Hyperuricemia -> (ASYMPTOMATIC) -> no obvious manifestations
  2. Acute inflammation in 1 joint
  3. Acute inflammation subsides within a week
  4. pt is asymptomatic for months - years
  5. frequent recurrent attacks -> gradually more and more joints become affected which results in permanent damage
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14
Q

Which joint is most commonly affected?

A

swollen, painful big tow joint in the late night/early morning (most commonly at this joint, but it may occur in others.

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15
Q

What are some precipitating events that may cause acute inflammation in 1 joint?

A
  1. Hearty meal d/t protein breakdown releasing amino acids and uric acid as a byproduct
  2. strenuous activity d/t diminished glucose stores and utilization of protein for energy
  3. alcohol binge esp. beer d/t increase purine metabolism and more uric acid as a byproduct
  4. drugs
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16
Q

When in the day does gout typically affect an individual?

A

At night/early morning because at with decreased activity, blood is flowing more slowly with less pressure to the periphery. with less in the blood stream, the uric acid is able to diffuse more easily into the joint cavity. The temperature in the distal joints is about 1 to 1.5 degrees lower than in proximal joints, so the uric acid crystallizes faster

17
Q

Is solubility greater in blood or uric acid and what does this mean?

A

greater solubility in blood than in synovial fluid so the uric acid crystallizes when it moves into the synovium

18
Q

Dx?

A
  • measure uric acid (serum and urine)

- xray

19
Q

Treatment?

A
ACUTE ATTACK: 
- NSAIDs 
- Steroids
-Colchicine 
LONG TERM TX: 
- Increasing uric acid excretion (URICOSURIC) 
- Decrease hyperuricemia (ALLOPURINOL) 
- Lifestyle modifications: low protein diet; alcohol cessation
20
Q

What disrupts the protein in Colchicine?

A

Tubulin