MSK/Rheumatology - Gout - Exam 3 Flashcards

1
Q

How does gout develop?

A
  1. Uric acid precipitates into monosodium urate (MSU) crystals
  2. Deposits in and around joints, bones, and soft tissues
  3. Pain and inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What types of food can trigger a gout flare and why?

A

High purine diet (red meat and seafood)

Uric acid is the breakdown product of purine metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the hallmark clinical feature of gout and how is it classified?

A

Hyperuricemia

Uric acid level exceeding 6.8 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are possible causes of hyperuricemia overproducers?

A

Inherited enzyme defects
High cell turnover
Increased purine consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are possible causes of hyperuricemia underexcretors?

A
90% of all hyperuricemia cases
Renal insufficiency
Diuretics
Volume depletion
Lead nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What population is gout most prevalent in?

A

Males age 30-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are some modifiable risk factors for gout?

A

Obesity, HTN, hyperlipidemia, CKD, diabetes, diet, ETOH, medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the four stages of gouty arthritis?

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis
  3. Intercritical gout (asymptomatic interval between gout attacks)
  4. Chronic gouty arthritis (chronic swelling and tophi)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are white chalky material consisting of dense concentration of MSU crystals that are indicative of the duration of severity of hyperuricemia?

A

Tophi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are complications of gout?

A

Uric acid nephrolithiasis

Urate nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the clinical presentation of an acute gout flare?

A
Monoarticular 
1st MTP joint "Podagra"
Rapid onset, often at night
Severe pain
Erythema
Warmth
Edema
Recurrent
Self limiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can trigger an acute gout flare?

A

Acute increase OR decrease in uric acid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What medications can trigger an acute gout flare?

A

Thiazide or loop diuretics

Urate-lowering medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What will appear on imaging of established gout disease?

A

“punched out” with sclerotic margin, overhanging edges (rat bite erosions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is gout diagnosed with an ultrasound?

A

Double contour sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What test provides a definitive diagnosis of gout?

A

Arthrocentesis/synovial fluid analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What technique is used to test the arthrocentesis/synovial fluid analysis and what would be a positive test for gout?

A

Polarized Light Microscopy
Needle shaped
Negatively birefringent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What test can be helpful to monitor effect of urate-lowering therapy?

A

Serum Uric Acid (sUA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What test can be used to determine if a patient is a candidate for uricosuric therapy?

A

24h urinary uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the first line treatment for an acute gout flare?

A

NSAIDs- Indomethacin or Naproxen

Glucocorticoids (must exclude infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If a patient is already on ULT, and comes in with an acute gout flare, should you continue or discontinue the medication?

A

Continue without interruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What can be used for treatment for an acute gout flare if patients have a contraindication to NSAIDs and glucocorticoids?

A

Colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does urate-lower therapy (ULT) work to lower serum uric acid levels?

How long is the course of tx?

A
  1. Decreases urate synthesis (XOIs)
  2. Enhances renal excretion of uric acid (uricosuric agents)

Continued indefinitely

24
Q

What are the two types of Xanthine Oxidate Inhibitors (XOIs) used to treat gout?
How do they work?
Who are they indicated for?

A

Allopurinol 100mg/day
Febuxostat 40mg/day
MOA: Decreases Urate Synthesis
Indicated for overproducers and underexcretors

25
Q

What is the uricosuric agent used to treat gout?
How does it work?
Who is it indicated for?

A

Probenecid 250mg bid
MOA: Enhances renal excretion of uric acid
Indicated for underexcretors

26
Q

What is the first line XOI tx for gout? What is its main side effect?

A

Allopurinol

Severe cutaneous adverse reactions

27
Q

What is the FDA warning for Febuxostat?

A

Mortality risk for patients at high cardiovascular risk

28
Q

Why should ULTs not be used to treat an acute gout flare? When is it safe to initiate tx?

A

Initiation may precipitate an acute flare

2 weeks after flare has resolved

29
Q

During initiation of ULT, what can be used to reduce the risk of flares?

A

NSAIDs or colchicine can be used for ~6mo to reduce the risk of flares

30
Q

What is the treat-to-target goal of long term gout tx?

A

Achieve target serum urate levels
sUA of 6.0mg/dL or less
sUA of 5.0mg/dL or less for tophaceous gout

31
Q

What is another name for calcium pyrophosphate crystal deposition disease (CPPD)?

A

Pseudogout

32
Q

What are some disease association of CPPD/pseudogout?

A

Hemochromatosis

Hyperparathyroidism

33
Q

What is the clinical presentation of CPPD/pseudogout?

A

Severe acute inflammation

Knee is most commonly affected

34
Q

What may you find on radiograph of CPPD/pseudogout?

A

Chrondrocalcinosis “cartilage calcification”

35
Q

What test provides a definitive diagnosis of CPPD/pseudogout?

A

Arthrocentesis/synovial fluid analysis

36
Q

What technique is used to test the arthrocentesis/synovial fluid analysis and what would be a positive test for pseudogout?

A

Polarized Light Microscopy
Rhomboid shaped
Positively birefringent

37
Q

What is the acute treatment of CPPD/pseudogout?

A

NSAIDs or Colchicine

Intraarticular glucocorticoid injection (rule out infection)

38
Q

When is prophylactic treatment of CPPD/pseudogout recommended? What is the prophylatic tx?

A

3 or more attacks/yr

Colchicine

39
Q

What is spondyloarthritis (SpA)?

A

Family of inflammatory rheumatic diseases that cause arthritis

40
Q

What are shared clinical features of SpA?

A
Inflammatory back pain
Peripheral arthritis
Dactylitis
Enthesitis
Uveitis
HLA-B27 association
Seronegative
41
Q

How does inflammatory back pain caused by SpA present?

A
Age of onset < 40 years
Improvement with exercise
No improvement with rest
Pain at night
Often have morning stiffness
42
Q

How does peripheral arthritis caused by SpA present?

A

Predominantly involves the lower extremities, frequently asymmetrical and often affects only 1-3 joints (oligoarthritis)

43
Q

How does enthesitis caused by SpA present?

A

Inflammation around the entheses—site of insertion of ligaments, tendons, joint capsule, or fascia
Most commonly on the achilles tendon or the plantar fascia at the calcaneus

44
Q

What is the triad saying for reactive arthritis (ReA)?

A

Can’t see: Conjunctivitis/uveitis
Can’t pee: Urethritis
Can’t climb a tree: peripheral arthritis, enthesitis, dactylitis, inflammatory low back pain

45
Q

What is reactive arthritis?

A

An acute aseptic inflammatory arthritis triggered by a preceding GI or GU infection

46
Q

What is the clinical presentation of reactive arthritis?

A

Acute onset
Typically present with an asymmetrical oligoarthritis
Occurs usually 1-4 weeks following the inciting infection

47
Q

How is reactive arthritis diagnosed?

A

Antecedent or concomitant infection

Positive HLA-B27 antigen

48
Q

What is the 1st line management of reactive arthritis?

A

Refer to rheumatology

1st line- NSAIDs

49
Q

What can use to treat reactive arthritis if the patient has an inadequate response to NSAIDs?

A

Glucocorticoids

50
Q

What can use to treat reactive arthritis if the patient is resistant to NSAIDs and glucocorticoids?

A

Disease-modifying antirheumatic drugs (DMARDs)

51
Q

What is ankylosing spondylitis (AS)?

A

Chronic inflammatory disease of the axial skeleton, particularly the sacroiliac (SI) joints and spine

52
Q

What is the clinical presentation of ankylosing spondylitis?

A
Inflammatory back pain and progressive stiffness of the spine
Enthesitis
Peripheral arthritis
Sx worse in the morning or with activity
Good response to NSAIDs
53
Q

What is the disease pathology of ankylosing spondylitis?

A
  1. Enthesitis with chronic inflammation
  2. Structural damage
  3. New bone formation (ossification)
  4. Anklosis (fusion)
54
Q

What may imaging of ankylosing spondylitis show?

A

Fusion of the spine
“bamboo spine”
Sacroiliitis

55
Q

What may physical findings of ankylosing spondylitis show?

A

Limited spinal mobility (and chest expansion)
Hyperkyphosis
Loss of lumbar lordosis

56
Q

What is the physical diagnostic test for ankylosing spondylitis and what would be an abnormal finding?

A

Modified Schober

On forward flexion, distance <5 cm is abnormal

57
Q

When should you refer to rheumatology?

A

In patients with ≥ 3 months back pain and age at onset < 45 years