Crystalline Arthropathies Flashcards

1
Q

How common is gout?

A

Common, about 2% of the population is affected

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2
Q

Gout is one of a group of diseases characterized by ___ throughout the body

A

crystalline deposition

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3
Q

What must be elevated in the blood to predispose gout?

A

Uric acid

normal byproduct of purine metabolism

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4
Q

What type of patient is most likely to present with gout?
Why is this so?

A

Older (40-50s) males
Males produce more uric acid than females

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5
Q

What are the crystals composed of in gout?

A

Uric acid

sodium monourate

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6
Q

What are the etiologies of gout?

A
  • 85% idiopathic impairment of renal uric acid excretion
  • Genetic (purine metabolism)
  • Stress
  • Alcoholism
  • Diabetes (long term)
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7
Q

How might alcoholism lead to gout?

A
  • Beer and red wine increase purines, thus increasing uric acid
  • Can lead to renal disease, gout would be secondary to kidney issues
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8
Q

What is the pathogenesis of gout?

A
  • Overproduction of purine metabolic byproducts (uric acid)
  • Inability to dispose of/break down metabolic byproducts
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9
Q

A patient comes in for a routine urinalysis and has hyperuricemia, but does not report any related symptoms.
Do they have gout?

A

No gout

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10
Q

A patient reports that their great toe is big, red, and swollen. They noticed this, along with other acute arthritis symptoms, shortly after a bout of alcohol consumption. Upon urinalysis, the patient has hyperuricemia.
What is the diagnosis?

A

Gout

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11
Q

Primary gout is the case for ___ of patients with gout
What makes gout primary?

A

1/3
Etiology is metabolic overproduction of uric acid

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12
Q

Secondary gout is the case for ___ of patients with gout
What makes gout secondary?

A

2/3
Underlying pathological etiology is present

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13
Q

What are some underlying pathologies that can lead to secondary gout?

A
  • Multiple myeloma (protein in blood destroys kidneys)
  • Alcoholism
  • Diabetes (destroys kidneys)
  • Kidney disease
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14
Q

In the pathogenesis of gout, uric acid crystals deposit in the soft tissue of an extremity joint.
What sort of pain will result from this?

A

Uric acid crystals are not irritating; found in asymptomatic joints

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15
Q

gout

Urate crystals are phagocytized by ___

A

PMNs and macrophages

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16
Q

gout

PMNs and macrophages try to phagocytize urate crystals, which induces a release of leukotrienes, cytokines, and chemotactins that elicit an intense ___

A

inflammatory reaction

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17
Q

gout

PMNs and macrophages try to phagocytize urate crystals, which induces a release of ___, ___, and ___ that elicit an intense inflammatory reaction

A

leukotrienes, cytokines, and chemotactins

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18
Q

How does chronic gout lead to joint destruction?

A

Lysosomes and other enzymes released

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19
Q

If untreated, gout will generally resolve in about ___, but can recur ___ later

A

gout will generally resolve in about 1 week, but can recur months to years later

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20
Q

What is the differential diagnosis for what grossly appears to be gout?

A

Septic arthritis

big, red, swollen joint; occurs quickly

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21
Q

What is the differential diagnosis for septic arthritis presenting as a single swollen red joint in the lower extremity?

A

Gout

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22
Q

What test differentiates gout from septic arthritis?

A

Joint aspiration:

  • Septic arthritis reveals purulent exudate
  • Gout appears clear with crystals
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23
Q

90% of patients with gout have ___

A

acute arthritis

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24
Q

How often is gout chronic?
What makes gout chronic?

A

10-15% chronic
Demonstrates pannus production and destruction

pannus production and destruction also presents with rheumatoid arthritis

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25
Q

How many joints are usually affected by gout?

A

One or two

often intially podagra (great toe)

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26
Q

Besides the great toe, what are some common locations for gout?

A

Peripheral joints:

  • Instep
  • Heel
  • Ankle
  • Knee
  • Wrist

(not spine)

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27
Q

Which clinical manifestation is indicative of chronic gout?

A

Tophi (chalky deposit)

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28
Q

What are tophi?

A

A chalky deposit; monosodium urate (crystal) deposit in soft tissues

found in chronic gout

develop over 10-20 years time

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29
Q

What are the cardinal signs of gout?

A

Rubor, calor, dolor, tumor

(all of them)

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30
Q

What is the pattern of pain with gout?

A

Begins at night and builds rapidly over 24 hours

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31
Q

What are some clinical manifestations of gout?

A
  • Tophi
  • Cardinal signs
  • Pain at night, gets worse over a day
  • Hyperuricemia
  • Renal impairment in chronic cases
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32
Q

What are the 4 stages of gout?

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis
  3. Polyarticular gouty arthritis
  4. Chronic tophaceous gout
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33
Q

How does chronic tophaceous gout characteristically appear?

A

Tophi presenting as lumpy bumpy joints

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34
Q

A patient presents with a red, swollen bump at their first metatarsophalangeal joint.
What is your differential diagnosis?

A
  • Septic arthritis (infection)
  • Gout
  • Rheumatoid arthritis

infection can also be cellulitis, osteomyelitis, etc.

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35
Q

Does gout have to be in joints?

A

No, it is a soft tissue disease

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36
Q

What are three radiographic characteristics of gout?

A
  • Marginal erosions
  • Periarticular erosions
  • Intraosseous erosions

subchondral white line maintained

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37
Q

gout

What is a corticated erosion?

A

Marginal erosion: has an overhanging margin due to a longer remission period that allowed for some regrowth/repair

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38
Q

gout

What is a periarticular erosion?

A

Deposits from periarticular soft tissues erode the bone

39
Q

gout

What is an intraosseous erosion?

A

Deposits within the bone (intraosseous tophus with or without calcification)

40
Q

A patient’s radiograph of their great toe reveals corticated marginal erosions, periarticular erosions, and intraosseous erosions around the metatarsophalangeal joint.
What is your differential diagnosis?

A

Gout

erosion followed by remission

rheumatoid arthritis and psoriatic arthritis have non-corticated margins

41
Q

A patient’s radiograph of their swollen elbow displays what looks like gouty crystals in the olecranon bursa.
What is your differential diagnosis?

A
  • Gout
  • Olecranon septic bursitis
42
Q

Gout should first be treated with a low purine, high water intake diet and a referral to a rheumatologist.
What are some drug therapies they might be prescribed?

A
  • NSAIDs (early, short-term)
  • Corticosteroids (acute, short-term)
  • Colchicine
  • Allopurinol
  • Uloric

avoid corticosteroids for recurring gout

43
Q

A patient comes in and reports that they take colchicine.
Why might they be taking this medication?

A

Used for recurrent attacks of gout or acute CPPD

44
Q

A patient comes in and reports that they take allopurinol.
Why might they be taking this medication?

A

Inhibits xanthine oxidase, treats gout

45
Q

Joint destruction due to gout is radiographically visible after ___.

46
Q

A patient reports that they had a big, red, swollen heel that went away on its own in about a week without treatment.
Was this more likely a case of gout or septic arthritis?

A

Gout

infection takes longer to heal

47
Q

What is the defining pattern of gout recurrence?

A

Exacerbation and remission

exacerbation will get longer and remission shorter

48
Q

Both gout and septic arthritis will have increased white blood cells.
What additional information about white blood cells differentiates the two?

A

Infectious disease (septic arthritis) has increased white blood cells with a left shit

gout has no wbc shift

uric acid will also be normal in septic arthritis

49
Q

What is the full name of CPPD?

A

Calcium Pyrophosphate Dihydrate Crystal Deposition Disease

50
Q

CPPD deposition disease is also called ___

A

pseudogout

51
Q

CPPD looks like ___ because it is a big, red, swollen joint with exacerbation and remission

A

gout and septic arthritis

52
Q

CPPD entails ___ crystals in ___ leading to inflammation

A

calcium pyrophosphate crystals in hyaline and fibro-cartilage

53
Q

Onset of CPPD occurs at ___ years of age and peaks at age ___

A

onset at 30
peak at 60

54
Q

CPPD is experienced by ___ of those over age 85

55
Q

What are four other joint pathologies that CPPD may simulate?

A
  • Gout
  • Rheumatoid arthritis
  • Degenerative joint disease
  • Neuropathic arthropathy
56
Q

Generally, gout precipitates in ___,
CPPD precipitates in ___

A

soft tissue
cartilage

57
Q

What is a key difference between CPPD and rheumatoid arthritis?

A

Rheumatoid arthritis can be bilateral and symmetrical, CPPD cannot

58
Q

What is a key difference between CPPD and DJD?

A

DJD is associated with deep, dull, achy pain
CPPD is usually asymptomatic (at least early on)

59
Q

What is a key difference between CPPD and neuropathic arthropathy?

A

NA has a slower destruction than CPPD

60
Q

What are some etiologies of CPPD deposition disease?

A
  • Idiopathic
  • Hereditary (rare)
  • Trauma
  • Metabolic disorders
61
Q

Phagocytosis of CPPD crystals by ___ leads to release of inflammatory mediators

A

synovial fluid and neutrophils

62
Q

Phagocytosis of CPPD crystal by synovial fluid and neutrophils leads to release of ___

A

inflammatory mediators

63
Q

In the pathogenesis of CPPD deposition disease, attacks are initially ___, but become ___

A

monoarticular, but become polyarticular

64
Q

Acute CPPD deposition disease attacks may be self-limiting lasting a day to several days.
What is this similar to?

65
Q

An acute CPPD deposition disease attack may be self-limiting.
How might a severe attack resolve?

A

Involving peripheral and axial joints, resolves slowly over weeks

66
Q

CPPD crystals may accumulate in which tissues?

A
  • Synovial membranes (pseudogout)
  • Articular cartilage (chondrocalcinosis) (hyaline and fibrocartilage)
  • Tendons and ligaments
67
Q

What are some clinical manifestations of CPPD deposition?

A
  • Chronic progressive joint pain
  • Reduced ROM with stiffness
  • Crepitus
68
Q

Joint destruction from CPPD will be seen radiographically within ___ years
For gout, destruction will be seen after about ___ years

A

CPPD = 2 years
Gout = 7 years

69
Q

What are some radiographic characteristics of CPPD deposition disease?

A
  • Cartilage, synovium, tendons, and/or ligament involvement
  • Crystal deposition in peripheral joints (knees, wrists, hands)
70
Q

How does chondrocalcinosis appear radiographically?

A

Cartilage (hyaline or fibro-) is visible

71
Q

CPPD

A patient’s radiographs show bright cartilage in the knee.
You think it’s chondrocalcinosis, but you should rule out ___.

A

joint degeneration

72
Q

A patient’s radiographs show bright cartilage in the knee.
What information would help you narrow your differential diagnosis?

A
  • History: symptoms
  • Joint aspiration

labs aren’t very helpful

DDx: chondrocalcinosis/CPPD, joint degeneration

73
Q

A patient’s radiographs present calcification in the meniscus of the knee (fibrocartilage), the hyaline cartilage, and the synovial membrane.
What is the likely diagnosis?

A

CPPD deposition disease

pyrophosphate arthropathy

74
Q

What are five treatments that CPPD responds to?

A
  • Rest
  • Joint protection
  • NSAIDs
  • Colchicine (in acute attacks)
  • Corticosteroids (only during exacerbation)
75
Q

Would CPPD respond to DMARDs?

76
Q

What is the long term for HADD?

A

(Calcium) Hydroxyapatite Deposition Disease

77
Q

What is another condition that may be in the differential diagnosis of HADD?

78
Q

CPPD occurs in cartilage.
Which tissues will HADD occur in?

A

Bursa, ligaments, and tendons

HADD a BLT

79
Q

Calcium hydroxyapatite deposition disease is also known as ___

A

calcific tendinosis (most common deposit), calcific bursitis

80
Q

HADD involves ___ deposition in leukocytes and mononuclear cells in joints and synovial fluid

A

hydroxyapatite

81
Q

HADD involves hydroxyapatite deposition in ___ and ___ in joints and synovial fluid

A

leukocytes and mononuclear cells

82
Q

Where in the joint might calcification occur if a patient has HADD?

A

Within tendon, bursa, capsule, or ligament

83
Q

What are the typical etiologies of HADD?

A

Post-traumatic / degenerative nature

84
Q

Where in the body might calcification occur if a patient has HADD?

A
  • Most commonly shoulder (rotator cuff)
  • Hip
  • Cervical spine
85
Q

How might HADD in the shoulder present?

A

Presents as supraspinatus tendinosis

rotator cuff symptoms

86
Q

How might HADD in the cervical spine present?

A

Presents in longus coli tendon for around 2 weeks

presents like torticollis

cannot treat, refer for pain management

87
Q

HADD may be asymptomatic at first
What symptoms follow?

A

Painful attacks lasting days to months

88
Q

HADD has been shown to respond well to ___

A

ultrasound (or shock wave) to break up calcium

89
Q

What age group is most commonly affected by HADD?

A

Patients over 40-years-old

90
Q

If a patient’s radiographs present with calcifications in the bursa and capsule of their shoulder, what is the likely diagnosis?

A

HADD (calcium hydroxyapatite deposition disease)

91
Q

Is gout inflammatory?

92
Q

Is HADD inflammatory?

93
Q

Is CPPD inflammatory?