Flashcards in Rheumatoid Deck (62)
T/F: Acute Rheumatic diseases are often spontaneously initiated
They are typically onset from an outside force like infection, medications, or exposure
Are acute rheumatic diseases typically self-limiting?
Chronic rheumatic disease typically occurs as a result of what?
An autoimmune response
Once a disease establishes flares of chronic rheumatic disease, those flares become _________ (less frequent/more frequent)
What is this a result of?
Likely the result of immune system memory
How is the endothelium involved in the initiation of a rheumatic response?
What happens to neutrophils and monocytes during this time?
Regional Blood vessel endothelium is activation by pro-inflammatory cytokines
The endothelium expresses ligands (attachment sites) for inflamatory cell markers (integrins) which allow neutrophils and monocytes to preform diapedesis into the underlying tissues
Antibody-antigen complexes are _________ (activators/deactivators) of the complement cascade
When the complement cascade is activated......
It ________ (attracts/repels) additional imflammatory cells
It ________ (Increases/Decreases) cell permeability which ________ (Increases/Decreases) inflammation
Helper T1 cells activate _________ which increase __________
Helper T2 cells activate ________ which increases what?
Increases Antibody Production
Helper T-17 cells activate __________ and ________ ________
T/F: In some tissues, cells that ordinarily are unrelated to the immune response can alter their form and function to become part of a chronic inflammatory response.
What condition involves crystal induced inflammation in synovial joints?
What crystals are typically responsible for gout?
What joints does gout primarily effect?
What is the name for the collections of urate crystals that collect in joint spaces in gout?
What are TWO common ways people develop gout and hyperuricemia?
Under Excretion (90%)
Over Production (10%)
Only about ___% of people with hyperuricemia will develop gout
What increases your risk for developing gout?
How does a patient develop a gout 'flare'?
1. Uric acid crystals precipitate in a joint
2. IL-1 and TNF activate the endothelium and inflammatory mediator come into the joint
3. Complement gets activated leading to more inflammation
4. Inflammation builds even more with phagocytosis, degranulation, free radical release/damage, and protein destruction with proteinases
What medications can reduce joint inflammation in gout flares?
What are THREE 'lifestyle' changes that can prevent future gout attacks?
Decrease Protein in diet
Control Co-morbid conditions (HTN, BP, Met-S)
How does colchicine work in gout?
It is a microtubule poison, so WBC can not squeeze through the small endothelial spaces into joints and produce inflammation
Which rheumatic disease is characterized by joint inflammation, pain, and swelling, with a prevalence for joint destruction, a higher mortality, and an unknown trigger?
Women are more effected by this than men by a 3:1 ratio
What are the THREE most common joints effected by RA?
A _________ is a membrane of granulation tissue made of mesenchyme and bone-marrow derived cells that forms in the joints during chronic RA.
This stimulates the release of what?
This stimulates the release of cytokines (ex: IL-1, Prostagladins, Substance P) by macrophages leading to cartalige destruction and bone erosion
What is the most sensitive antibody test for RA?
Which antibody is present in about 50% of RA patients?
Rheumatoid Factor (RF)
Which gene is associated with Anti-CCP and RA?
What lifestyle habit is also associated with the above two things?
T/F: There is a foolproof blood test to diagnosis RA
There is not