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Musculoskeletal Physiopathology > Crystalline Arthropathies > Flashcards

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 must be elevated (a normal byproduct of purine metabolism)

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4
Q

What type of patient is most likely to present with gout and why?

A

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

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5
Q

What are the crystals composed of in gout?

A

Uric acid

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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. History reveals 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 of patients have primary gout
This is due to 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 of patients have secondary gout
Underlying pathology 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
  • Kidney disease
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14
Q

In the pathogenesis of gout, where are uric acid crystal found?

A

Asymptomatic joints; uric acid crystals are not irritating

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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 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 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

gout

What leads to joint destruction in chronic gout?

A

Lysosomal 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 gout?

A

Septic arthritis, it’s also one big, red, swollen joint that occurs quickly

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21
Q

What is the differential diagnosis for septic arthritis?

A

Gout, it’s also one big, red, swollen joint that occurs quickly

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22
Q

What differentiates gout from septic arthritis?

A

Joint aspiration reveals that septic arthritis presents with pus, while gout presents clear with crystals

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23
Q

90% of patients with gout present with ___

A

acute arthritis

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24
Q

How often is gout chronic?
What makes gout chronic?

A

10-15% patients have chronic gout
Chronic arthritis demonstrating pannus production and destruction (like rheumatoid arthritis)

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25
Q

How many joints are usually affected by gout?

A

One or two, often initially 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

Found in chronic gout: a chalky deposit; monosodium urate (crystal) deposit in soft tissues; this takes 10-20 years to develop

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29
Q

What are the cardinal signs of gout?

A

All of them (non-specific)

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30
Q

What is the pattern of pain of 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

Chronic tophaceous gout is characterized by what clinical features?

A

Tophi presenting as lumpy bumpy joints

34
Q

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

A
  • Septic arthritis/cellulitis/osteomyelitis
  • Rheumatoid arthritis
  • Gout
35
Q

Does gout have to be in joints?

A

No, it is a soft tissue disease

36
Q

What are three radiographic characteristics of gout?

A
  • Marginal erosions
  • Periarticular erosions
  • Intraosseous erosions
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

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 marginal erosions, periarticular erosion, and intraosseous erosions around the metatarsophalangeal joint.
What is your differential diagnosis?

A
  • Gout
  • Rheumatoid arthritis
  • Psoriatic arthritis

(all involve erosion and remission)

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 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 (short-term)
  • Corticosteroids (short-term)
  • Colchicine
  • Allopurinol
  • Uloric
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

What is the long form of CPPD?

A

Calcium Pyrophosphate Dihydrate Crystal Deposition Disease

46
Q

CPPD deposition disease is also called ___

A

pseudogout

47
Q

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

A

gout and septic arthritis

48
Q

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

A

onset at 30
peak at 60

49
Q

What are four other joint pathologies that CPPD may simulate?

A
  • Gout
  • Rheumatoid arthritis
  • Degenerative joint disease
  • Neuropathic arthropathy
50
Q

What is a key difference between CPPD and gout?

A

Gout precipitates in soft tissue
CPPD precipitates in cartilage

51
Q

What is a key difference between CPPD and rheumatoid arthritis?

A

Rheumatoid arthritis can be bilateral and symmetrical, CPPD cannot

52
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)

53
Q

What is a key difference between CPPD and neuropathic arthropathy?

A

NA has a slower destruction than CPPD

54
Q

What are some etiologies of CPPD deposition disease?

A
  • Idiopathic
  • Hereditary (rare)
  • Trauma
  • Metabolic disorders
55
Q

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

A

synovial fluid and neutrophils

56
Q

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

A

inflammatory mediators

57
Q

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

A

initially monoarticular, but become polyarticular

58
Q

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

A

Gout

59
Q

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

A

Severe attack involving peripheral and axial joints resolve slowly over weeks

60
Q

CPPD crystal may accumulate in the:

A
  • Synovial membranes (pseudogout)
  • Articular cartilage (chondrocalcinosis) (hyaline and fibrocartilage)
  • Tendons and ligaments
61
Q

What are some clinical manifestations of CPPD deposition?

A
  • Chronic progressive joint pain
  • Reduced ROM
  • Crepitus
62
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

63
Q

What are some radiographic characteristics of CPPD deposition disease?

A
  • Cartilage, synovium, tendons, and/or ligaments involved
  • Crystal deposition in peripheral joints (knees, wrists, hands)
  • Chondrocalcinosis (in hyaline and fibrocartilage)
64
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)

65
Q

CPPD responds to:

A
  • Rest
  • Joint protection
  • NSAIDs (DMARDs don’t work)
  • Colchicine (in acute attacks)
  • Corticosteroids (only during exacerbation)
66
Q

What is the long term for HADD?

A

(Calcium) Hydroxyapatite Deposition Disease

67
Q

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

A

CPPD

68
Q

What differentiates CPPD from HADD?

A

CPPD occurs in cartilage
HADD occurs in bursa, ligaments, and tendons (BLT)

69
Q

Calcium hydroxyapatite deposition disease is also known as…

A

calcific tendinosis (most common deposit), calcific bursitis

70
Q

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

A

hydroxyapatite

71
Q

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

A

leukocytes and mononuclear cells

72
Q

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

A

Within tendon, bursa, capsule, or ligament

73
Q

What is the nature (typical etiologies) of HADD?

A

Post-traumatic / degenerative nature

74
Q

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

A

Shoulder (most common), hip, cervical spine

75
Q

How might HADD in the shoulder present?

A

Presents as supraspinatus tendinosis (rotator cuff symptoms)

76
Q

How might HADD in the cervical spine present?

A

Presents in longus coli tendon for around 2 weeks; low grade symptom maintenance

77
Q

HADD may be asymptomatic at first
What symptoms follow?

A

Painful attacks lasting days to months

78
Q

HADD has been shown to respond well to…

A

ultrasound (or shock wave) to break up calcium

79
Q

What age group is most commonly affected by HADD?

A

Patients over 40-years-old

80
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)

81
Q

Is gout inflammatory?

A

Yes

82
Q

Is HADD inflammatory?

A

Yes

Musculoskeletal Physiopathology (31 decks)

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