Arthropathies and Septic arthritis Flashcards

1
Q

What are the s/sx of septic arthritis?

A

Hot, edematous joint that is painful and TTP

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2
Q

What is the ddx for acute onset monoarthropathy?

A
  • Hemarthrosis
  • Septic arthritis
  • Infectious
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3
Q

What is Pigmented villonodular synovitis? Presentation? Prognosis?

A

Idiopathic inflammation and overgrowth of the synovium in a joint that usually presents as an acute onset of focal joint pain and swelling. Usually recurs.

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4
Q

Over what age is a risk factor for septic arthritis?

A

80

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5
Q

What are the systemic diseases that predispose a patient to septic arthritis?

A

DM

RA

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6
Q

What are some shx bits that predispose patients to septic arthritis?

A

Alcoholism

IV drug abuse

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7
Q

What is the bacteria that more commonly causes septic arthritis in IV drug users? Which joint in particular?

A

Pseudomonas

Sternoclavicular joint

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8
Q

What is the most common cause of a septic joint (how do bacteria get there)?

A

Hematogenous spread from drug abuse or catheters

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9
Q

What is the most common joint that is affected with septic arthritis?

A

Knee

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10
Q

What bacteria that, if found in a joint, should raise suspicion for endocarditis?

A

Staph Aureus

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11
Q

What is the WBC level in a joint aspirate that is suggestive of a septic joint?

A

50,000-150,000

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12
Q

What is the classic triad for gonococcal septic arthritis?

A
  • Tenosynovitis
  • Vesiculopustular skin lesions
  • Polyarthralgias
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13
Q

What is the auger that is used to culture Neisseria?

A

Chocolate auger

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14
Q

Where does sporotrichosis septic arthritis usually show up?

A

Finger joints

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15
Q

What are the chances of causing a joint infection with steroid injections using proper technique?

A

Very low

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16
Q

What is the most common joint infected with Lyme disease?

A

Knee

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17
Q

What is the drug of choice for gram + cocci septic arthritis?

A

Vancomycin

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18
Q

What is the drug of choice for gram - bacteria caused septic arthritis?

A

Third generation cephalosporin

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19
Q

What are the three forms of joint drainage that can be done with septic arthritis?

A
  • Aspiration
  • Arthroscopy
  • Open drainage
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20
Q

What are the non-diet precipitating factors of gout? (4)

A
  • Trauma
  • Surgery
  • Meds
  • cold exposure
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21
Q

What are the dietary factors that can precipitate gout? (4)

A
  • EtOH
  • Fatty diet
  • Starvation
  • Dehydration
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22
Q

What is the effect of ASA on gout?

A

Low dose increases uric acid, but high dose decreases

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23
Q

What diuretic in particular increases uric acid levels?

A

HTZ

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24
Q

What are the skin findings of the area over a gouty inflammation?

A

Cracked from the swelling

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25
Q

What is the usual onset and duration (relative) for gouty attacks?

A

Fast onset, and quickly resolves

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26
Q

What is the role of estrogen/progesterone in gout?

A

Decreases uric acid levels

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27
Q

What is the effect of prolonged, untreated gout?

A

Increases frequency of attacks, and number of joints affected

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28
Q

What are tophi?

A

a deposit of crystalline uric acid and other substances at the surface of joints or in skin or cartilage, typically as a feature of gout.

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29
Q

When is synovial fluid analysis warranted with suspected gout attacks?

A

If first time to r/o septic joint

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30
Q

What is the birefringence findings with uric acid crystals?

A

If yellow in parallel plane of polarized light = uric acid (“ye-ll-ow in para-ll-el light”)

If perpendicular, then blue

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31
Q

What is the sensitivity of uric acid levels in gout flares?

A

Not that great

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32
Q

True or false: urate crystals always cause pain

A

False–only if cell is affected. This causes cytokine release.

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33
Q

What are the plain radiograph findings with an acute, new gouty attack?

A

Nothing

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34
Q

What are the plain radiograph findings with chronic gout?

A
  • Subcortical bone cysts

- Bone erosions with overhanging edges

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35
Q

What are the US findings of chronic gout?

A

Hyperechoic linear density overlying the surface of joint cartilage

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36
Q

What if the definition of hyperuricemia?

A

Above 7%

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37
Q

What are the two major (very general) pathophysiological mechanism for gout?

A

Overproducer or underexcreter

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38
Q

What is the solubility or uric acid? What happens with decreased temperature?

A

7 mg/dL

Decreased solubility with decreased temperature

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39
Q

What is the treatment for acute gout attacks? (4)

A

NSAIDs
Glucocorticoids
Colchicine
TNF-alpha inhibitors

40
Q

What is the MOA of colchicine?

A

Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation

41
Q

What should alway be checked for prior to administering TNF-alpha inhibitors? Why?

A
  • Latent TB

- TNF-alpha needed to maintain granulomas

42
Q

What are the three major TNF-alpha inhibitors?

A

INfliximab
Etanercept
Adalimumab

43
Q

What is the MOA of infliximab? Use?

A
  • Anti-TNF-alpha monoclonal ab

- IBD, RA, psoriasis, ankylosing spondylitis

44
Q

What is the MOA of etanercept? Use?

A
  • receptor for TNF-alpha + IgG1 Fc

- RA, psoriasis, ankylosing spondylitis

45
Q

What is the MOA of adalimumab? Use?

A
  • Anti-TNF-alpha monoclonal ab

- IBD, RA, psoriasis, ankylosing spondylitis

46
Q

What is the MOA of allopurinol?

A

Inhibits xanthine oxidase to decrease the conversion of xanthine to uric acid

47
Q

What is the MOA of febuxostat?

A

Xanthine oxidase inhibitor

48
Q

What is the MOA of probenecid?

A

Inhibits reabsorption of uric acid in PCT (also inhibits the secretion of PCN)

49
Q

What is the MOA of rasburicase?

A

a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin, which is much more water soluble

50
Q

What are the drugs that predispose patients to gout?

A
  • ASA
  • Diuretics
  • ACEIs
51
Q

What are the drugs to prevent recurrent attacks of gout? (3)

A
  • Allopurinol
  • Febuxostat
  • Probenecid
52
Q

What is the role of EtOH in gout?

A

Predisposes

53
Q

What is the role of cherries in gout?

A

Preventative

54
Q

What is the role of vitamin C in gout?

A

Preventative

55
Q

What is the uric acid goal for preventing gout?

A

Below 6 mg/dL

56
Q

What organ is involved in the clearance of febuxostat?

A

Hepatic

57
Q

What are the ethnicities in which allopurinol is more toxic?

A

Korean
Thai
Han chinese

58
Q

How is allopurinol excreted?

A

Renally

59
Q

When are uricosuric agents contraindicated? Why?

A

If CrCl is less than 50 (will not work if not excreting enough)

60
Q

What diuretic has uricosuric activity?

A

Losartan

61
Q

What is uricase? Use?

A

Same MOA as rasburicase, but can be extremely toxic, so only use if severe cases

62
Q

What are the NSAIDs of choice for gout?

A

Naproxen

Indomethacin

63
Q

What is the steroid of choice for gout? High or low dose?

A

Low dose prednisone

64
Q

What color are uric acid crystals in parallel light? Calcium pyrophosphate crystals?

A

Uric acid = yellow

Ca = blue

65
Q

Who usually gets calcium pyrophosphate crystal deposits (pseudogout)?

A

Older people

66
Q

What are three major diseases that are associated with pseudogout?

A
  • Hemochromatosis
  • Hyper/hypoparathyroidism
  • Thyroid disease
67
Q

What is the treatment for pseudogout?

A

NSAIDs
Colchicine
Steroids

68
Q

Which gender is more affected by acute attacks of pseudogout?

A

Men

69
Q

Which gender is more affected by osteoarthritis with chondrocalcinosis of pseudogout?

A

Women

70
Q

What is the classic shape of pseudogout crystals?

A

Rhomboid

71
Q

What is crowned dens syndrome?

A

n inflammatory condition resulting from crystal deposition in cruciform and alar ligaments surrounding the dens, appearing as a radiopaque ‘crown’ surrounding the top of the dens. It typically presents with pain and increased inflammatory markers.

72
Q

What are some of the different presentations of CPPD? (4)

A
  • Acute
  • Asymptomatic
  • Pseudo RA
  • Pseudo OA
73
Q

What are the plain film findings of CPPD?

A

Chondrocalcinosis / degenerative changes in the wrist, knee, pubic symphysis

74
Q

What are spondyloarthropathies?

A

Inflammation of the axial joints, asymmetrical oligoarthritis,

75
Q

What are the four diseases associated with HLA-B27?

A
  • Psoriasis
  • Ankylosing spondylitis
  • IBD
  • Reactive arthritis
76
Q

What are the s/sx of spondyloarthropathies?

A

-Low back pain present when lying still for long periods, but resolves with movement

77
Q

What is enthesopathy?

A

a disorder involving the attachment of a tendon or ligament to a bone

78
Q

What is dactylitis?

A

Dactylitis or sausage digit is inflammation of an entire digit

79
Q

What will an x-ray show with ankylosing spondylitis?

A

Fusion of the vertebrae (“bamboo spine”)

80
Q

What are the three major nonpharmacologic treatments for spondyloarthropathies?

A
  • Smoking cessation
  • Exercise
  • Education
81
Q

What are the three major pharmacotherapies for spondyloarthropathies?

A

NSAIDs
Analgesics
DMARDs

82
Q

What are the 5 major NSAIDs, besides ASA?

A
  • IBU
  • naproxen
  • indomethacin
  • ketorolac
  • diclofenac
83
Q

What is the MOA and use of celecoxib?

A
  • Reversibly inhibits COX-2 (spares good COX-1).

- RA, OA

84
Q

Why does celecoxib spare platelet function?

A

No effect of TXA2

85
Q

What is the metabolite that causes the toxicity associated with acetaminophen? Treatment and MOA?

A

NAPQI

N-acetylcysteine is antidote regenerates glutathione

86
Q

What is the MOA of bisphosphonates?

A

Pyrophosphate analog; binds hydroxyapatite in bone, to inhibit osteoclast activity

87
Q

What is the MOA of alendronate?

A

bisphosphonate

88
Q

What is the suffix common to bisphosphonate drugs?

A

“-dronate”

89
Q

What is the classic toxicity associated with bisphosphonates?

A

Corrosive esophagitis

90
Q

Which TNF-alpha inhibitor does not affect the uveitis common to ankylosing spondylitis?

A

Etanercept

91
Q

What are the five different patterns of involvement for arthritis?

A
  • Distal oligoarthritis
  • Asymmetric polyarthritis
  • Symmetric polyarthritis
  • Arthritis mutilans
  • Spondyloarthritis
92
Q

What is Arthritis mutilans?

A

Arthritis mutilans, is a rare arthropathy originally described as affecting the hands, feet, fingers, and/or toes, but refers in general to severe derangement of any joint

(“mortar in a pestle”)

93
Q

What are the post enteric causative pathogens of reactive arthritis?

A

Campylobacter
Salmonella
Shigella
Yersinia

94
Q

What are the s/sx of reactive arthritis, besides the classic triad?

A

LBP
Dactylitis
Enthesitis

95
Q

What is the classic skin manifestation of reactive arthritis?

A
  • Keratoderma Blennorrhagicum

- rash on the soles of the feet

96
Q

Where is the associated arthritis found with IBD?

A

Sacro Iliac, spine, or peripheral joints

97
Q

What is the difference between type I and type II IBD arthritis?

A

Type I = peripheral, self limiting

Type II = polyarticular, peripheral, frequent recurrences