Difference between revisions of "Rheumatoid Arthritis"

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m (Text replace - "Type IV Hypersensitivity - WikiBlood" to "Type IV Hypersensitivity")
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* Macrophages phagocytose self antigens and can present peptides on their MHC Class II molecules. The autoreactive TH-1 cells release IFN-gamma which activates macrophages to release prostaglandins, MMP enzymes and TNF-alpha (pro-inflammatory mediator), see diagram. These cytokines cause inflammation and tissue destruction.
 
* Macrophages phagocytose self antigens and can present peptides on their MHC Class II molecules. The autoreactive TH-1 cells release IFN-gamma which activates macrophages to release prostaglandins, MMP enzymes and TNF-alpha (pro-inflammatory mediator), see diagram. These cytokines cause inflammation and tissue destruction.
  
 
+
[[Category:Cell Mediated Autoimmune Diseases]][[Category:To Do - James]]
 
 
*Occurs in the dog, mainly smaller breeds
 
*Uncommon
 
*Progressive erosive polyarthritis
 
*Mostly involves elbows, stifles, carpal and tarsal joints
 
*Grossly:
 
**Marked villus hypertrophy of synovial membrane
 
**Cartilage erosion
 
**[[Musculoskeletal Terminology - Pathology|Pannus and periarticular osteophyte]] formation
 
**In severe cases ankylosis
 
*Histologically:
 
**Hyperplasia of lining cells
 
**Proliferative synovitis
 
**Synovial membrane has fibrin deposits
 
**Lymphoid and plasma cell infiltration
 
**Surrounding haemorrhagic areas
 
**Macrophages containing [[Pigmentation - Pathology#Haemosiderin|haemosiderin]]
 
**Connective tissue may contain foci of necrosis
 
**Areas of erosion of peripheral articular cartilage and underlying subchondral bone
 
*Pathogenesis:
 
**May involve deposition of immune complexes within joints
 
**Substances degrading cartilage are released by synovial cells and macrophages involved in pannus formation
 
 
 
 
 
 
 
 
 
 
 
[[Category:Cell Mediated Autoimmune Diseases]][[Category:To Do - Clinical]][[Category:To Do - Blood]]
 

Revision as of 13:22, 18 August 2010

Rheumatoid Arthritis-Brian Catchpole RVC 2008

Pathogenesis:

  • Type IV hypersensitivity: CD4 Th-1 cell mediated.
  • Macrophages phagocytose self antigens and can present peptides on their MHC Class II molecules. The autoreactive TH-1 cells release IFN-gamma which activates macrophages to release prostaglandins, MMP enzymes and TNF-alpha (pro-inflammatory mediator), see diagram. These cytokines cause inflammation and tissue destruction.