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Clin Med - MSK > Lecture 5 - Gout and Septic Arthritis > Flashcards

Lecture 5 - Gout and Septic Arthritis Flashcards

1
Q

Septic Arthritis

A

inflammation of the synovial membrane and joint space due to infection

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2
Q

How does bacteria gain access to the joint?

A

hematogenous (70%)
synovial vascularized and lacks a basement membrane

direct spread from adjacent local infection

direct inoculation (iatrogenic)

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3
Q

What are risk factors of septic arthritis?

A 
impaired host defense 
Rheumatoid arthritis 
IV drug use 
prosthetic joint
joint with pre-existing damage (RA, OA)
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4
Q

What happens if septic arthritis is left untreated?

A

this is an ortho emergency

loss of articular cartilage 
bone erosion 
bony ankylosis 
joint fibrosis 
joint deformity

this can happen over a course of days to weeks

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5
Q

How do pts with septic arthritis present?

A

monoarticular arthritis (80%) = septic arthritis until proven otherwise

abrupt, swelling, warmth, and pain of joint

restricted joint range of motion (d/t tenderness)

fever, chills

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6
Q

Which joints are most commonly involved in septic arthritis?

A

knee > hip > everything else

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7
Q

How do you dx septic arthritis?

A

arthrocentesis = gold standard

labs:
leukocytosis
elevated ESR/CRP
blood cultures may be positive

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8
Q

How long does it take for septic arthritis is present on xray?

A

2-3 weeks

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9
Q

What is the most common pathogen responsible for septic arthritis?

A

staph aureus

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10
Q

What is the DDx for septic arthritis?

A

crystalline arthritis (gout, CPPD)
inflammatory arthritis
Traumatic arthritis
hemarthrosis

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11
Q

What is the treatment for septic arthritis?

A 
surgical debridement and irrigation 
IV ABX (typically Vancomycin) for 7-10 days then transition to PO ABX for at least 2 weeks
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12
Q

Osteomyelitis

A

infection of bone
occurs via hematogenous spread of contiguous spread
Staph aureus

clinical exam: probe to bone
Labs: elevated ESR and CRP

tx: surgical debridment
6 weeks of directed ABX treatment

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13
Q

Epi of Gonococcal Arthritis

A

Women > male

most common cause of septic arthritis in adults <30 years old

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14
Q

What are the risk factors for gonococcal arthritis?

A

high risk sexual practices
congenital or acquired complement deficiency
asplenia or sickle cell anemia

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15
Q

What do you seen on arthrocentesis for septic arthritis?

A

opaque
cloudy yellow
WBC > 100K
PMNs >75%

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16
Q

What is the most common cause of septic arthritis in adults <30 yo?

A

gonococcal arthritis

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17
Q

What is the gonococcal arthritis triad?

A

tenosynovitis
dermatitis (pustules, hemorrhagic bullae on plams and soles)
polyarthralgia (migratory or additive)

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18
Q

Tenosynovitis

A

inflammation of a tendon
classic sign in gonococcal arthritis
MC wrist > fingers

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19
Q

Is gonococcal arthritis more commonly monoarthritis or polyarthtitis?

A

monoarthritis

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20
Q

How do you dx gonococcal arthritis?

A

NAAT of synovial fluid is preferred

GC is not readily isolated in synovial fluid

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21
Q

What is the treatment for gonococcal arthritis?

A

ceftriaxone 1 g IM daily until signs and sxs improve

+

1g azithromycin for Chlamydia (treat empirically)

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22
Q

What is the most common vector-borne illness in US?

A

lyme

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23
Q

For lyme disease, what is being transmitted to the human host?

A

Borellia

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24
Q

Early localized lyme disease presentation?

A

occurs few days after tick bite

erythema migrans (80%): target/bull’s eye rash

fatigue 
arthralgias 
myalgia
malaise
HA
regional lymphadenopahty
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25
Q

Early disseminated lyme clinical presentation

A

occurs weeks to months after tick bite

MSK involvement (60%): migratory arthralgias 
AV block 
facial palsy
meningitis
eye disease 
liver disease
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26
Q

Late Disseminated Lyme disease clinical presentation

A

occurs months to years after tick bite

lyme arthritis (60% of untreated pts)

  • monoarticular or oligoarticular arthritis
  • cold, large effusions
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27
Q

How do you dx lyme arthritis?

A

serum ELISA followed by Western Blot for confirmation

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28
Q

When do you expect to see Lyme IgM and IgG?

A

IgM: 1-2 weeks post exposure

IgG: 2-6 weeks post exposure

IgM can remain in serum for years after treatment of lyme

29
Q

What is the treatment for lyme arthritis?

A

doxycycline x 21-28 days

if pt is in early disseminated: IM ceftriaxone x 14 -28 days

30
Q

What is the most common viral arthritis?

A

Parvovirus B19 (fifths disease)

31
Q

What is the clinical presentation for parvovirus arthritis?

A

similar to RA but these pts should have a hx of being exposure to a child or someone with parvovirus
+/- skin rash: lasts 2-4 days
self limiting: resolves in 1 - 2 months
does NOT cause destructive arthritis

32
Q

What is the treatment for parvovirus arthritis?

A

NSAIDs

33
Q

Bursae

A

fluid filled sac lined by synovial membrane

provides cushion in areas of friction between bones and soft tissue

34
Q

How can you tell the difference between bursitis and septic arthritis?

A

bursitis is much more superficial than septic arthritis

35
Q

Which bursa are most commonly infected?

A

adults: olecranon bursitis
children: prepatellar

36
Q

How do pts get septic bursitis?

A

hematogenous
local adjacent tissue
direct inoculation

37
Q

How do you dx septic brusitis?

A

aspiration and culture (be careful not to pass the needle all through the bursa to the joint–risk of spreading infection)

WBC not as elevated as septic joints
Staph aureus = 80%

38
Q

How do you tx septic bursitis?

A

IV ABX

Surgical debridement of bursa

39
Q

Gout

A

Hyperuricemia + spectrum of clinical and pathologic features of uric acid deposition (1 of the follow sxs):

  • inflammatory arthritis
  • tophi
  • urate nephrolithiasis
  • urate nephropathy
40
Q

Who is more likely to get gout?

A

Men > Women

genetic component

41
Q

What do human lack that can lead to gout?

A

uricase

42
Q

What is the underlying path of gout?

A

hyperuricemia

overproduction 
exogenous (diet) or endogenous

and under excretion (90%)

43
Q

What can cause under excretion of uric acid, as seen in 90% of gout pts?

A

genetic
CKD
medications (diuretics, cyclosporine)
metabolic syndrome

44
Q

Lesch - Nyhan Syndrome

A

an endogenous reason for hyperuricemia

complete HGPRT deficicency

inherited X link disorder

45
Q

What are different endogenous reasons of overproducition of uric acid?

A

tumor lysis syndrome
psoriasis
lesch nyhan syndrome

46
Q

Acute Gout pathogenesis

A

monosodium urate crystals activates innate immune system

infiltration of neutrophils for pathogocytosis of MSU crystals

rapid profound inflammatory arthritis

47
Q

Podagra

A

the most common location for acute gout

1st MTP

48
Q

Clinical presentation of acute gout?

A

1st MTP MC

onset night or early morning 
rapid onset (few hours) 
pain, warmth, redness, swelling 
tenosynovial or bursal involvement 
fever, leukocytosis (must r/o septic arthritis) 
natural hx: self -limiting

“i can’t tolerate the bedsheet touching my toe”

49
Q

How do you dx gout?

A

arthrocentesis = gold standard
inflammatory synovial fluid cell count

“strongly negatively birefringent needle shaped crystals on polarizing microscopy”

negative gram culture

50
Q

Double contour lines

A

seen on US for gout pts

uric acid line sitting on top of bone

51
Q

What is the treatment for acute gout?

A

Anti-inflammatories:

Colchicine
NSAIDs
Steroids

remember that during an acute attack you should not start or stop allopurinol

52
Q

Colchicine

A

an anti-inflammatory used for acute gout

inhibits polymerization of microtubules inhibiting neutrophil chemotaxis

drug interactions: CYP3A4
no analgesic effects

53
Q

What dosage of steroids is used to treat acute gout?

A

prednisone 0.5mg/kg daily for 5-10 days

54
Q

What is the first line treatment for chronic gout?

A

weight loss –reduce uric acid level

regular exercise - also decreases uric acid levels

55
Q

Which foods should a pt with gout avoid d/t their high purine foods?

A 
shellfish 
organ meats (Liver) 
red meat 
alcohol (BEER) 
fructose (soft drinks, sweet breads, ketchup)
56
Q

Which foods are protective against gout?

A

uricosuric effects

cherries
dairy (milk, yogurt)
coffee
vitamin C

57
Q

Which medications effect uricosuria?

A

negative: thiazide or loop diuretics
Niacin

positive effect:
losartan
CCB (amoldiopine)
Statins

58
Q

Who with chronic gout gets treated?

A 
frequent attacks (>/=2 per year) 
tophus 
erosive arthritis 
chronic kidney disease stage 
past urolithiasis
59
Q

Which drugs are used as first line for urate lowering agents in chronic gout?

A

Allopurinol

remember that you MUST start them on an anti-inflammatory prophylaxis such as Colchicine to prevent gout flare

60
Q

Allopurinol

A

purine analog, competitive inhibitor of xanthine oxidase
most commonly prescribed drug for chronic gout
metabolized to oxypurinol
decreases serum and urinary uric acid level
contraindicated with azathioprine use

61
Q

What is a major risk of allopurinol?

A

SJS, TENs

test for HLA-B*5801 Allele

62
Q

How long are chronic gout pts on prophylaxis anti-inflammatories?

A

until they reach the goal uric acid level <6mg/dL

monitor levels every 6 months to make sure they are still at their goal level

63
Q

Which drug is used for refractory gout?

A

Pegloticase (Krystexxa)

infusions every 2 weeks

64
Q

CPPD

A

pseudogout

calcium pyrophosphate dihydrate crystal deposition disease

age: >70 yo
M = W

most commonly affects knees, hips, shoulders, wrists
self limiting

65
Q

How do you tell the difference between gout and pseudo gout?

A

CPPD has weakly positively birefringent rhomboid shaped crystals on polarizing microscopy

66
Q

Chondrocalcinosis

A

cartilage calcifications

67
Q

What is the treatment for CPPD?

A

anti-inflammatories

Colchicine
NSAIDs
Steroids

no medication for chronic management

68
Q

Basic Calcium Phosphate

A

hydoxyapatitie crystals

alazarin red staining to identify crystals

“Milwuakee shoulder”

70-90yo, Women&raquo_space; men

Clin Med - MSK (10 decks)

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