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Clinical Medicine > Gout And Pseudogout > Flashcards

Gout And Pseudogout Flashcards

1
Q

What increases the risk of gout?

A

Hyperuricemia increases risk of gout

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2
Q

Is hyperuricemia always indicative of gout?

A

No, it is not diagnostic for gout

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3
Q

What is a feature of estrogen as it relates to gout?

A

Estrogen is uricosuric
-Promotes excretion of uric acid in the urine

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4
Q

What are the properties of mono sodium urate crystals

A

Needle-shaped, negatively birfringent

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5
Q

What are the properties of calcium pyrophosphate crystals?

A

Rhomboid, positively birefringent

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6
Q

Is it okay to give a patient allopurinol if they are actively having a gouty flare up?

A

No!
- Allopurinal should never be used as treatment for acute gouty arthritis
-Allopurinal should never be given to someone who is also taking azathiprine

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7
Q

What is the definition of gout?

A

A disease characterized by hyperuricemia and mono sodium urate deposition in the body

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8
Q

What is the definition of gouty arthritis?

A

Joint inflammation caused by mono sodium urate crystals in the synovial fluid and or joint tissues

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9
Q

In what populations is gout most common in?

A

Women: occurs more often after menopause
Also common in Pacific Islanders (Filipino and Samoan)

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10
Q

What demographic of patients are at a high risk of developing gout?

A
  1. Obese
  2. Hypertensive
  3. Family h/o gout
  4. Alcoholics, alcohol ingestion (beer)
  5. Hospitalized patients
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11
Q

What effect does alcohol have on the urate production?

A

Alcohol increases urate production and decreases renal excretion
- So there would be more urate overall in the system

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12
Q

Why do hospitalized patients have a higher risk of developing gout?

A

because there will be changes in the person diet, fluid intake, and medication
- Can cause rapid reductions/ increases in serum urate level

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13
Q

What are primary reasons of hyperuricemia?

A
  1. Increased production of purine
  2. Idiopathic
  3. Specific enzyme defects
  4. Decreased renal clearance of uric acid (idiopathic)
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14
Q

What are some causes of secondary hyperuricemia

A

(The hyperuricemia is caused by something else)
*there are lots of reasons

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15
Q

What are the mechanisms of urate production?

A

MC: Cellular nucleoproteins/nucleotides (made in the body)
Diet

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16
Q

What are the mechanisms of urate excretion?

A
  1. Kidney (66%)
  2. Gut (33%)
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17
Q

How does the renal system work to excrete uric acid

A
  1. uric acid is completely filtered by the glomerulus
  2. Then completely reabsorbed at the proximal tubule
  3. Next, 50% is secreted back into the tubule
  4. 80% ( of the 50%) is reabsorbed in the ascending loop
  5. Finally the net excretion is 10% of filtered load
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18
Q

What is the relationship between diet and gout?

A
  1. High levels of meat and seafood increased the risk
  2. High levels of diary decreased the risk
  3. Moderate intake of purine-rich vegetable or protein not associated with increase risk of gout
    *Diet can cause acute gouty flares
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19
Q

if a patient has hyperuricemia is that enough information to make a diagnosis for gout?

A

No
*only a subset of people with hyperuricemia will develop gout

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20
Q

What can increase the probability of having gout?

A

Patients with a higher uric acid levels

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21
Q

Why would the uric acid levels be normal during an acute attack?

A

The uric acid is now taken out of the blood and now in the joint and tissue

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22
Q

Does a patient need medical treatment for hyperuricemia?

A

No

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23
Q

What are conditions that are associated with hyperuricemia?

A
  1. Lymphomas
  2. Myeloproliferative disorders
  3. Diabetes
  4. Psoriasis
  5. Sarcoid
  6. Meds (diuretics, low-dose ASA)
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24
Q

Why are diuretics associated with secondary hyperuricemia

A

The medication will raise the serum uric acid level by an increase of uric acid reabsorption and/or decrease in uric acid secretion

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25
Q

What are some clinical manifestations of gout?

A
  1. Acute gouty arthritis
  2. Podagra (MTP joint of great toe MC affected)
  3. Inter critical gout (period between acute attacks)
  4. Chronic tophaceous gout
  5. Gouty nephropathy (gout develops around nerves)
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26
Q

What are the clinical features of Acute Gouty Arthritis?

A
  1. Acute onset (hours) of severe arthritis
  2. Usually mono articular (inflammation of one joint that could potentially develop to other joints)
  3. Swollen, very tender, skin is tense, arm, dusky red (joints)
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27
Q

What are some associated findings with Acute Gouty Arthritis?

A
  1. Fever
  2. Increased WBC (due to a inflammatory response)
  3. Increased Erythrocyte Sedimentation Rate (ESR) (Will measure the inflammation)
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28
Q

When does Acute Gouty Arthritis typically resolve?

A

Over days or weeks , regardless of treatment

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29
Q

What happens during the recovery phase of Acute Gouty Arthritis?

A
  1. Local desquamation (skin peeling)
  2. Pruritis
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30
Q

What are precipitating factors of Acute Gouty Arthritis?

A
  1. Surgery
  2. Alcohol
  3. Fluctuation of uric acid level
    *diuretics
    *aspirin (low ASA will raise uric acid levels, high ASA lower uric acid levels)
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31
Q

What is the only way to diagnose Acute Gouty Arthritis?

A
  1. Observation of mono sodium urate crystals in synovial fluid (also used to rule of a septic joint)
32
Q

What color would the mono sodium urate crystals be when a patient has Acute Gouty Arthritis?

A
  1. Yellow when parallel with the light
  2. Blue when perpendicular
    (Crystals are needle-shaped, negatively birefringent)
33
Q

If your patient has hyperuricemia does that mean they definitely have gout?

A

No
*Only 20% of patients with high uric acid levels have gout

34
Q

What is a common cause of high Uric Acid levels

A

Psoriatic arthritis

35
Q

How many measurements of serum uric acid should you take to determine if a patient has hyperuricemia?

A

There should be multiple measurements
*hyperuricemia is >7.4mg/dl

*A single measurement is normal about 25% of the time (will not exclude gout)

36
Q

What could be other reasons for developing podagra?

A
  1. Reiter’s syndrome
  2. Rheumatoid arthritis (RA)
37
Q

What will happen to the WBC during acute attacks of gout?

A

The WBC is frequently elevated

38
Q

What is shown on the radiographs during early and later stages of gout?

A

Early: normal
Later: Punched-out erosions with overhanging rim of cortical bone “rat bites”

39
Q

What are the treatment options for Acute Gouty Arthritis?

A
  1. NSAID’s
  2. Colchicine
  3. Steroids
  4. Joint aspiration
  5. Analgesics
  6. Observation
40
Q

When should steroids be used in treatment of acute gouty arthritis?

A

Only if there is no infection present, perform aspiration and gram stain first
*Intra-articular steroid (administered in the joint)

41
Q

What is inter critical gout?

A
  1. Symptom-free period between attacks (months or years)
    *second attack usually occurs within 6-24 hours
42
Q

What happens if intercritical gout is left untreated?

A

Then episodes of acute gouty arthritis become more frequent, last longer, and often involve more joints (poly articular)

43
Q

What are the treatment options of intercritical gout?

A
  1. Prevention
  2. Low purine diet, decrease alcohol consumption
  3. Avoid Thiazide and loop diuretics, Niacin, ASA
  4. Colchicine
  5. Allopurinol 1st line, or Probenecid, or uricase (IV only)
44
Q

What does allopurinol and Probenecid do?

A

A: decrease the production of uric acid
P: increase the secretion of uric acid

45
Q

What is Chronic Tophaceous gout?

A

Tophi are deposits of urate crystals in soft tissues

46
Q

What are common sites of chronic tophaceous gout?

A
  1. Synovium
    2.Subchondral bone
  2. Olecranon bursae
  3. Infrapatellar
  4. Achilles’ tendon
47
Q

What are the clinical features of Chronic tophaceous Gout

A
  1. Frequent attacks of acute gouty arthritis
  2. Bone destruction and degenerative arthritis are common in advanced cases
  3. “Rate bite” lesions on radiographs
  4. white appearance
48
Q

What are the treatment options of tophaceous gout?

A

Control and vent acute gouty arthritis
1. NSAIDs
2. Colchicine
3. Steroids
4. Analgesics
5. Surgical excision of tophi (last resort)
Reduce serum uric acid levels for ALL patients with tophi

49
Q

How can you reduce the serum uric acid levels?

A
  1. Decrease uric acid production (inhibit xanthine)
  2. Increase uric acid excretion (Uricosuric drugs)
  3. Uricase if refractory to allopurinol/probenecid
50
Q

What two medication create a Xanthine Oxidase inhibition?

A

Allopurinol and Feboxustat

51
Q

What is the MOA of Allopurinol and feboxustat?

A
  1. Blocks the conversion of hypoxanthine to xanthine, and xanthine to uric acid
  2. There will be an accumulation of hypoxanthine which inhibits de novo purine biosynthesis (negative feedback)
52
Q

When should you not use allopurinol?

A

DO NOT USE with azathioprine (will inhibit the immune system with organ transplants, Crohn’s, UC), or 6-mercaptopurine

53
Q

When would it be appropriate to inhibit Xanthine Oxidase?

A
  1. Uric acid overproducers
  2. Tophaceous gout
  3. Unresponsive to uricosuric regimen
  4. Uric acid renal calculi
54
Q

What are the uricosuric agents used for gout?

A

Probenecid and sulfinpyrazone

55
Q

What is the MOA of probenecid and sulfinpyrazone?

A
  1. Block renal tubular reabsorption of uric acid (will stay in the urine)
    *used for under excretors
56
Q

When is Probenecid and sulfinpyrazone used?

A
  1. When gouty attacks increase in frequency or severity
  2. Most effective when urine pH basic and flow relatively high
  3. Used less frequently than allopurinol
57
Q

When would Probenecid specifically be used?

A
  1. Used with patients that fail with xanthine oxidase inhibitors
    *Can lead to uric acid stones (increase fluid intake if used)
    *dont use with a history of kidney stones
58
Q

What is uricase?

A

An enzyme that metabolizes urate to allantoin (More soluble)
*exists in non primate mammals
*last resort medication
*risk of anaphylaxis

59
Q

When is colchicine used?

A
  1. For prevention of future attacks
    *may be used when uricosuric drugs or allopurinol are initiated (suppresses attacks caused by uric acid level changes)
60
Q

What is the dosage for colchicine?

A

0.6mg QD (daily) or BID (2x a day)

61
Q

What is the dosage of Allopurinol? (For the reduction of serum uric acid)

A

300mg QD (max of 800mg/day)
*start at 100mg increase by increments of 100mg to achieve uric acid level below 5-6.0mg/dL
*use Probenecid if allopurinol is not tolerated or effective

62
Q

What should you do to the dosage if Allopurinol and Probenecid are taken together?

A
  1. Decrease the dose of probenecid
  2. Increase the dose of allopurinol
63
Q

What is the dosage of uricase?

A

8mg IV Q 2 weeks
*only administer in healthcare setting

64
Q

What is another name for Psuedogout?

A

Calcium Pyrophosphate Deposition Disease (CPPD)

65
Q

What causes pseudo gout?

A

Calcium pyrophosphate dihydrate crystals (CPPD)
*Chondrocalcinosis

66
Q

What is chondrocalcinosis?

A

Calcium-containing salts deposited in the cartilage

67
Q

What patient demographic is most likely to get pseudo gout?

A

> 60 YOA
Equal in men and women

68
Q

What is the clinical presentation of pseudogout?

A
  1. Frequent attacks after surgery (24-48 hrs after)
  2. Knee most commonly involved
  3. Almost always accompanied by chondrocalcinosis of affected joints
  4. Recurrent, rarely chronic
69
Q

What joints are commonly affected in pseudo-gout

A
  1. Knees (mc)
  2. Wrists/elbows
  3. MCP
  4. Hips
  5. Shoulders
    *acute, red, swollen, warm, large joints
70
Q

What are some diagnostic features of pseudogout?

A
  1. Normal uric acid levels (need serial tests)
  2. Observation of calcium pyrophosphate dihydrate crystals in synovial fluid
71
Q

What is the presentation of CPPD crystals?

A
  1. Rhomboid
  2. Positively birefringent
    *Blue when parallel and yellow when perpendicular (opposite of gout)
72
Q

What are common radiographic features of pseudogout

A

Chondrocalcinosis (calcification of cartilage)

73
Q

What are the treatment options of CPPD?

A

No definitive therapy for prevention
1. Joint aspiration
2. NSAIDs
3. Colchicine
4. Steroids (oral, intra-articular)
5. Analgesics
6. Surgery if necessary to preserve function

74
Q

For Asymptomatic Hyperuricemia when can you use uric-acid lowering drugs?

A

Until there is
1. Arthritis
2. Renal calculi
3. Tophi

75
Q

What are the treatment options for Acute Gout?

A
  1. NSAIDs (naproxen, indomethacin)
  2. Colchicine (if duration has been <36 hours)
  3. Corticosteroids (IV, oral)
    *Need gram stain and culture of synovial fluid
  4. Interleukin-1 inhibitors *Anakinra, Canakinumab, rilonacept
76
Q

What are the treatment options for Chronic, intercritical/Tophaceous gout?

A
  1. Uricosurics (Probenecid0
  2. Xanthine Oxidase inhibitors (Allopurinol)
  3. Colchicine (anti inflammatory) prophylaxis
  4. Cyclooxygenase (COX) 2 inhibitors
  5. Dietary restrictions (no organ meats)
  6. Increase urine output

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