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MDTI > Infectious Arthritis > Flashcards

Infectious Arthritis Flashcards

1
Q

synovial intima

A

lining tissue of the synovium and all intracapsular structures, typically 1-3 cells deep

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2
Q

two types of synovial lining cells

A

intimal macrophages with increased cytoplasmic organelles and intimal fibroblasts that have decreased organelles and increased ER

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3
Q

what is the synovial intima lacking?

A

a lmiting basement membrane

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4
Q

what supports the synovial lining?

A

fenestrated microvessels in the interstitium of the subintima

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5
Q

subintima

A

contains collagen fibrils, proteoglycans, and VASCULAR SUPPLY (fenestrated blood vessels)

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6
Q

importance of fenestrations in subintima vascular supply

A

blood plasma can freely flow out into synovial lining

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7
Q

what is the most rapidly destructive form of joint and bone disease?

A

bacterial arthritis (a rheumatologic emergency!)

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8
Q

what are most cases of septic arthritis due to?

A

hematogenous spread (bacteremia) followed by direct innoculation

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9
Q

why is the joint susceptible to infection from hematogenous spread?

A

abundant vascular supply and lack of limiting membrane

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10
Q

entheses

A

ligamentous insertion into bone

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11
Q

two divisions of septic arthritis

A

gonococcal and nongonoccal

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12
Q

what is the most common nongonococcal bacteria causing septic arthritis?

A

staph aureus (gram positive clustering cocci)

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13
Q

risk factors for septic arthritis

A

age (>80), infection with bacteremia, joint disease/pre-existing damage (OA, RA), immunosuppressed state (diabetes, steroids), trauma, prosthetic joint, IV drugs, endocarditis

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14
Q

pathogenesis of septic arthritis

A

virulence factors of different bacteria sustain the infection and cause joint damage

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15
Q

virulence factors for s. aureus

A

MSCRAMMs and agr

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16
Q

MSCRAMMs

A

bind host matrix proteins to enable s aureus to anchor itself in the interstitium

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17
Q

agr

A

accessory gene regulator. regulates s aureus surface proteins and exotoxins

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18
Q

timeline of virulence factors in S. aureus septic arthritis

A

at low cell concentrations, agr up regulates cell surface proteins important for attachment. once cell growth enters stationary phase, age down regulates adhesion proteins and up regulates tissue destroying enzymes

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19
Q

virulence factors for N gonorrhea

A

pili enable attachment, outer membrane protein I inactivates complement and prevents neutrophil phagolysosomal fusion

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20
Q

3 ways septic arthritis leads to damage

A

direct effects from invading bacteria, host’s own immune response, mechanical effects from pressure of joint effusion

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21
Q

direct damage

A

the organism produces destructive toxins and enzymes which mediate joint damage. (hemolysins)

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22
Q

host inflammatory overreaction

A

activated inflammatory cells produce cytokines which help recruit more cells, cytokines activate MMPs, neutrophils/marophages engulf bacteria and release cytokines, which stimulate proteases and ROSs

23
Q

mechanical effects causing damage

A

ischemia due to excess purulent exudate accumulation causing intra-articular pressure increase and reduced blood flow

24
Q

clinical presentation of septic arthritis

A

fevers, chills, malaise, monoarticular involvement (due to cytokines)
dolor/calor/tumor/rubor (due to inflammation)

25
Q

clinical presentation of gonococcal arthritis

A

sexually active young adults, 1 or more joints affected, DGI

26
Q

DGI

A

disseminated gonorrheal infection: fevers, shaking chills, vesiculopustular rash, tenosynovitis, polyarthralgias

27
Q

normal joint effusion

A

clear, colorless, viscous. <200 leukocytes

28
Q

noninflammatory joint effusion (OA)

A

clear, yellow, viscous, leukocytes 200-2000

29
Q

inflammatory joint effusion

A

cloudy, yellow, decreased viscosity, leukocytes 2000-100,000

30
Q

septic joint effusion

A

purulent, markedly decreased viscosity, usually leukocytes >50,000 with mostly neutrophils

31
Q

bone infection

A

osteomyelitis

32
Q

organism causing lyme disease

A

borrelia burgdorferi via ixides tick

33
Q

three stages of lyme disease

A

early localized, early disseminated, late disease

34
Q

in which stage of lyme disease do you see inflammatory arthritis?

A

late disease

35
Q

early localized lyme disease

A

within days, bulls eye rash (erythema migrans), viral symptoms (fevers, lymphadenopathy, malaise, arthralgias, myalgias)

36
Q

early disseminated lyme disease

A

1-3 mos after bite, cardiac and neurological symptoms (myopericarditis, Bells palsy)

37
Q

late lyme disease

A

> 3mos, main clinical feature is inflammatory arthritis (2/3 of patients who reach this stage)

38
Q

which joint is typically affected in lyme arthritis

A

knee

39
Q

lyme arthritis pathophysiology

A

host inflammatory response, since borrelia doesn’t produce any proteases!

40
Q

what is the typical synovial leukocyte count for septic arthritis from lyme?

A

<50,000

41
Q

antibiotic resistant lyme arthritis

A

rare, can’t detect borrelia in fluid PCR, most likely due to molecular mimicry

42
Q

molceular mimicry

A

immune response driven by foreign stimuli that cross reacts with self elements.

43
Q

support for molecular mimicry in lyme arthritis

A

specific class 2 MHCs are predisposed, human LFA-1a has sequence homology to borrelia OspA and activates OspA reactive T cells, patients have high titers of Abs to OspA. becomes autoimmune

44
Q

problems with molecular mimicry hypothesis

A

LFA-1a is only a weak agonist to OspA, OspA T cells diminish in synovial fluid after antibiotic Rx in both regular and resistant lyme arthritis

45
Q

clinical appearance of viral associated arthritis

A

acute onset, symmetric, inflammatory, polyarticular (small joints), may have rash

46
Q

hep B arthritis

A

immune complex mediated, serum sickness

47
Q

parvovirus arthritis

A

antigenic persistence

48
Q

serum sickness

A

prodrome characterized by urticaria (hives), maculopapular rash, inflammatory arthritis of small joints

49
Q

presumed mechanism of hep B arthriits

A

hep b surface antibodies form soluble immune complexes that are deposited in synovium, which activates complement and neutrophils, enzymes released by neutrophils cause damage

50
Q

when does clinical disease begin in hep b arthritis?

A

once the circulating complexes start lowering serum complement

51
Q

what is the most common viral arthritis

A

parvovirus b19

52
Q

who is predominately affected by parvovirus b19 arthritis?

A

adults

53
Q

mechanism of parvovirus arthritis

A

parvovirus enters joint via interaction with Gb4 on synovium, antigenic persistence causes ongoing immune response

54
Q

antigenic persistence

A

various pieces of infectious agent remain in the absence of the whole organism and cause ongoing immune response

MDTI (42 decks)

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