Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
27 Cards in this Set
- Front
- Back
|
What is the synovial intima?
|
The 1-3 cells deep lining tissue that surfaces the intracapsular structures
|
|
|
Does the synovial intima have a basement membrane?
|
NO NO NO
|
|
|
Is the synovium highly vascularized?
|
YES
|
|
|
What is the MOST RAPIDLY destructive form of joint and bone disease?
|
Septic (bacterial) arthritis
|
|
|
How are most cases of septic arthritis spread?
|
Hematogenous spread
|
|
|
What are the 2 characteristics of the joint which make it susceptible to infection from hematogenous spread?
|
1. Abundant vascular supply
2. No limiting basement membrane |
|
|
What are 3 major risk factors for bacterial arthritis?
|
1. Rheumatoid arthritis
2. Osteoarthritis 3. Diabetes mellitus |
|
|
What are virulence factors?
|
Mechanisms which infectious organisms have evolved to enhance their ability to evade the immune system and sustain an infection
|
|
|
What are the 2 main virulence factors of S. aureus?
|
1. MSCRAMMs - microbial surface components reconizing adhesive matrix molecules
- bind host matrix proteins 2. Agr (accessory gene regulator) - regulates S. aureus cell surface proteins and regulates S. aureus exotoxins |
|
|
At low concentrations of staph agr facilitates production of what?
At high concentrations of staph? |
Low concentrations: production of cell-surface proteins which facilitate attachment to tissue
High concentrations: represses cell surface proteins and expresses exotoxins to KILL |
|
|
What are the 3 ways that bacteria can actually cause joint damage?
|
1. Direct effects/attacks
2. Host's own immune system response 3. Mechanical effects from pressure of joint effusion |
|
|
How (pathophysiologically) can a host immune response cause joint damage?
|
- cytokine production IL-1B/IL-6 can activate metalloproteinases which can attack cartilage
- neutrophils/macrophages release additional cytokines which lead to production of proteases and ROS that can damage joints |
|
|
How can joint damage be caused by mechanical effects?
|
Ischemia plays a role as purulent exudate accumulates, pressure increases, which can prevent blood flow to avascular cartilage
|
|
|
How long does it take to get irreversible joint damage?
|
LESS THAN 48 HOURS!
|
|
|
What is the description and leukocyte count for the following joint effusions?
1. Normal 2. Noninflammatory 3. Inflammatory 4. Septic |
1. Normal: Clear, colorless, viscous. <200.
2. Noninflammatory: Clear, yellow, viscous. 200-2000 3. Inflammatory: Cloudy, yellow, low viscosity. 2000-100,000 4. Septic: Purulent, very low viscosity. >50000 (95% PMNs) |
|
|
What other organism/disease can cause infectious arthritis?
|
LYME DISEASE (borelia burgdorferi)
|
|
|
At what stage of the disease does Lyme disease cause inflammatory arthritis?
|
Late stage
|
|
|
What is the mechanism of how lyme disease causes arthritis?
|
Inflammatory response produce proteases which attack joint
|
|
|
What is the hypothesis for how lyme disease induces autoimmunity?
|
Molecular Mimicry
- T cell stimulated by foreign peptide that looks like self antigen. Becomes autoreactive and mediates a self-directed response |
|
|
What are 3 observations supporting the molecular mimicry hypothesis for antibiotic resistance lyme arthritis?
|
1. Certain MHC II types predisposed to antibiotic restance lyme arthritis
2. Presence of Ab's specific to Borrelia antigens in affected pt's 3. Identification of canditate autoantigen with sequence homology to Borrelia outer surface protein AND can activate T cells |
|
|
What HLA protein is linked to both antibiotic resistant lyme arthritis and Rheumatoid Arthritis?
|
HLA DRB1 *0401
MHC II |
|
|
What is the human autoantigen thought to be responsible for molecular mimicry?
What's the corresponding borrelia antigen? |
Human: LFA-1a
Borrela: OspA THESE CROSSSTIMULATE T CELLS |
|
|
What is one data that argues against the molecular mimicry hypotheses?
|
LFA-1a only acts as a partial, weak agonist to OspA reactive T cells
|
|
|
What symptoms suggest viral associated arthritis?
|
1. Acute onset
2. Symmetric inflammatory polyarthritis |
|
|
What is the most common viral arthritis in the US?
|
Parvovirus B19 (Hep B also seen as well)
|
|
|
What is thought to be the mechanism of Heb B arthritis?
|
Formation of immune complexes which get deposited in the joints
|
|
|
What is one prominent hypothesis as to how Parvovirus B19 causes arthritis?
|
Antigen persistence - when various pieces of an infectious agent remain in the absence of whole organism and can cause ongoing immune response
|
