Question

In your own opinion what is the pathophysiology of rheumatoid arthritis involving multiple site?

Answer 1

Ans) Rheumatoid arthritis(RA) is a chronic systemic autoimmune disorder.

Etiology:

- Autoimmune and genetic factor

Predisposing factors:
- Familial predisposition and usually in females.

Joints involved:
- Symmetrical involvement (small joints of
hands/feet, writs/ankles, TMJ)

Pathophysiology Of RA:
synovitis = pannus formation, which causes
cartilage erosion and fibrosis
ankylosis = muscle atrophy; development of
malalignment, contractures, and deformities

Sign & Symptoms:
- Aching/stiffness, impaired mobility, deformities/
funcitonal losses.

Systemic effects:
Rheumatoid factor in blood, elevated ESR, low-
grade fever, malaise, fatigue, subQ nodules,
pleura, heart valves, eyes.

Treatment:
physiotherapy: ambulatory aids
OC THx; assistive devices
NSAIDs, COX -2 inhibitors, Glucocorticoids,
Immunosuppressants, Gold salts, arthroplasty,
joint replacement.Type A synoviocyte interacts with Type B synoviocyte, c/o IL-6, TNF (from macrophages); IL-1; IL-17 and IL-23.
Pathogenesis: is
Type B synoviocytes proliferate and release:
- TNF
- IL17
- PGE2
- TGF-B
- M-CSF (macrophage colony stimulating factor)
- RANKL

So Type A syn's are recruited; and eat away at cartilage.

Type B syn's proliferate, causing bone resorption via RANK-L.

Both Type A&B produce
a) MMP-ases that eat away at cartilage.
b) VEGF >> vascular proliferation
c) chemokines causing influx of Th1, Th17 and B cells

IL-17 causes increased chemokine production in various tissues to recruit monocytes and neutrophils to the site of inflammation, similar to IFN-gamma. IL-17 is produced by T-helper cells and is induced by IL-23 which results in destructive tissue damage in delayed-type reactions.