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35 Cards in this Set

  • Front
  • Back
Inflammatory joint disease is commonly termed ______.
arthritis
What's IJD characterized by?
inflammatory damage or destruction of synovial membrane, articulating cartilage AND by systemic signs of inflammation.
What's the 2nd most common form of arthritis?
How many people does this effect?
Rheumatoid arthritis
1.3 million Americans
Rheumatoid arthritis is a _____ _______ ______ ______ disease.
chronic systemic progessive autoimmune
Rheumotoid arthritis is a ___________ group of disorders in which inflammation of _________ joints is a major manifestation.
heterogenous
multiple
Many patients have _______ manifestations with the most common manifestation of ____ ________
systemic
joint involvement
In Rheumatoid arthritis, patients have _______ _______ of ________.
fibrinoid necrosis of
collagen
R.Arthritis is characterized by joint ________ and _________.
deformities
disabilities
R.Arthritis occurs most frequently in women (___:___ female:male) during _______ years.
2&1/2-3:1
childbearing years
Onset of R.Arthritis is _____ or may be _____.
insidious
acute
RA occasionally goes into ______ ________, indicating that one can restore some type of _________ with intervention.
remission spontaneously
balance with intervention
If shown a picture of a joint that's effected by RA, one would see what?
inflamed synovium, pannus, loss of cartilage, fibrous tissue (ankylosis) and pannus-filled erosion?
Etiology of RA includes no single agent that's responsible. It can be a combination of _______ and _________.
genetics and environment
What's the coding system called that tells if you're susceptible to RA?
HLA system
T/F? RA appears to be an immune response initiated by an antigen.
true
What are some possible sources of this antigen for RA?
==EBV (Epstein-Barr virus)
==Parvovirus infection (small DNA viruses)
==bacteria or microplasms
Eventually normal antibodies somehow become __________.
autoantibodies
These tranformed autoantibodies are termed ____________--antibodies against ____, ____, ____ and form _______________.
rheumatoid factors (RF's)
IgG, IgM, occas. IgA and form immune complexes.
T/F? Some of the immune complexes that form in the RA response include activation of T helper cells and the release of cytokines.
true
RA main be due to some _______ immune responses to an unidentified antigen in genetically susceptible individuals.
aberrant
T/F? The release of cytokines or T helper cells eventually gets antibody formed to react with fragments from what were normal antibodies?
true
____ bind with their target self antigens in blood and form complexes in blood and _ _________.
RF's
synovial membranes
What type of injury is this called?
This has ________ __________ of antigenic material to stimulate the immune response.
type III
continual production
_____ antibodies also have been demostrated in synovial fluid in patients with RA
Anti-collagen
Synovial inflammation is also termed ________.
synovitis
2 aspects of synovitis include:
synovial fluid
synovial membrane
Synovial fluid phase is comprised predominantly of _____.
PMN's
PMN's _____ immune complexes in RA and release ______.
phagocytize
mediators
_____ is in constant supply, unlike other microorganisms.
RF
In the synovial membrane of RA, there is ____a______ infiltration with ___b______ cells and a striking accumulation of new blood vessels (termed ____c_____)
a) perivascular
b) mononuclear
c) angiogenesis
Synovial membranes ultimately form into what? (a)

This tissue is rich in what? b

Can lead to what? c
a) forms a granulation tissue (pannus)

b)inflammatory cells that secrete enzymes and various mediators of inflam. to destroy cartilage and bone

c) eventually leads to join deformity and muscle atrophy
Monocytes/macrophages and fibroblasts release ______ and _______ to resorb bone and connective tissue.
proteases and chemotactic factors
What's the term that describes the loss of functional synovial membrane vascularity DECREASING as granulation tissue and fibrosis develops called?

What does this cause? What does this stimulate?
-hypoxemia from diminished blood flow.

-acidosis

-stimulates release of hydrolytic enzymes--gets even more damaged.
What plays a major role in the amplification of the immune response in RA?

What does this lead to?
What does this serve as?
-immune complexes (containing RF)

-proliverative synovitis

-chemotaxis force
What is another source of amplification of inflammatory condition?

What does this lead to?

What else is activated?
-PMN's

-leads to aggregation, degranulation, and superoxide anion generation

-other inflammatory pathways are activated (HF, kinins, complement)