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Flashcards in Infectious Arthritis Deck (54):
1

synovial intima

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

2

two types of synovial lining cells

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

3

what is the synovial intima lacking?

a lmiting basement membrane

4

what supports the synovial lining?

fenestrated microvessels in the interstitium of the subintima

5

subintima

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

6

importance of fenestrations in subintima vascular supply

blood plasma can freely flow out into synovial lining

7

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

bacterial arthritis (a rheumatologic emergency!)

8

what are most cases of septic arthritis due to?

hematogenous spread (bacteremia) followed by direct innoculation

9

why is the joint susceptible to infection from hematogenous spread?

abundant vascular supply and lack of limiting membrane

10

entheses

ligamentous insertion into bone

11

two divisions of septic arthritis

gonococcal and nongonoccal

12

what is the most common nongonococcal bacteria causing septic arthritis?

staph aureus (gram positive clustering cocci)

13

risk factors for septic arthritis

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

14

pathogenesis of septic arthritis

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

15

virulence factors for s. aureus

MSCRAMMs and agr

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MSCRAMMs

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

17

agr

accessory gene regulator. regulates s aureus surface proteins and exotoxins

18

timeline of virulence factors in S. aureus septic arthritis

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

19

virulence factors for N gonorrhea

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

20

3 ways septic arthritis leads to damage

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

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direct damage

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

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host inflammatory overreaction

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

mechanical effects causing damage

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

24

clinical presentation of septic arthritis

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

25

clinical presentation of gonococcal arthritis

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

26

DGI

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

27

normal joint effusion

clear, colorless, viscous. <200 leukocytes

28

noninflammatory joint effusion (OA)

clear, yellow, viscous, leukocytes 200-2000

29

inflammatory joint effusion

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

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septic joint effusion

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

31

bone infection

osteomyelitis

32

organism causing lyme disease

borrelia burgdorferi via ixides tick

33

three stages of lyme disease

early localized, early disseminated, late disease

34

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

late disease

35

early localized lyme disease

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

36

early disseminated lyme disease

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

37

late lyme disease

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

38

which joint is typically affected in lyme arthritis

knee

39

lyme arthritis pathophysiology

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

40

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

<50,000

41

antibiotic resistant lyme arthritis

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

42

molceular mimicry

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

43

support for molecular mimicry in lyme arthritis

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

problems with molecular mimicry hypothesis

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

clinical appearance of viral associated arthritis

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

46

hep B arthritis

immune complex mediated, serum sickness

47

parvovirus arthritis

antigenic persistence

48

serum sickness

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

49

presumed mechanism of hep B arthriits

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

when does clinical disease begin in hep b arthritis?

once the circulating complexes start lowering serum complement

51

what is the most common viral arthritis

parvovirus b19

52

who is predominately affected by parvovirus b19 arthritis?

adults

53

mechanism of parvovirus arthritis

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

54

antigenic persistence

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