week 4: rheumatoid arthritis

Question 1

what is rheumatoid arthitis (inflammatory arthitis)

Answer 1

• auto immune disorder
• systemic (usually have other issues)
• unknown atiology
• periods of exaberation and remission
• progressive
• it is symmetric arthritis in synovial joints

Question 2

what is the differnce between RA and OA and OP?

Answer 2

osteoarthritis:
general wear and tear on joints

rheumatoid arthitis:
casued by an autoimmune disease

osteoporosis:
condidtion where the bones become weak and brittle

Question 3

atiology

Answer 3

cause:
- unknown
- could be a predisposition initiating trigger
- somehow the body launches an immune reaction against its own tissues
- producing antibodies that react with immunoglobin
- causes inflammation due to infiltration of T cells into synovial fluid

Question 4

what is rheumatoid factor (RhF)?

Answer 4

it is an “anti” antibody that attacks cells
- however it is not unique to people with RA
- 80% of ppl with RA have RhF + ve
- abnormal production of B cells (cells that make the RhF)
- triggered by? virus, bacteria etc. unkown..

antigen/antibody complex is formed, and deposited in joint and other tissues/ organs
- therfore amplifies RA inflammation but is not a primary cause

Question 5

what are the 3 phases of RA

Answer 5

1. inflammatory response
2. synovitis
3. prolifereative response
4. continued inflammation

Question 6

describe the inflammatory phase

Answer 6

• invasion of antigen into synovium
• triggers anti-body antigen reaction complex
• T cell infiltration (destroy antigen)

Question 7

describe the synovitis phase

Answer 7

• synovial blood vessels proliferate, dilate and conjest the synovial lining
• go into joint
• the excessive collection of blood vessels in the synovial lining causes synovitis

Question 8

describe the proliferative response

Answer 8

• proliferation of cells in the synovium, joint, tendon and sheaths of synovium
• hypertrophy of synovium
• fibrin and collagen deposition on synovial membrane and articular cartiliage
  – cytokines and MMPs degrade cartiliage

Question 9

describe the continued inflammation phase?

Answer 9

• outgrowth of synovial tissue and granulation
• pannus formation happens
• pannus fills joint space and releases cytokines and enzymes that damage cartiliage, subchondral bone etc.
• it becomes organised like a scar tissue that bridges the joint and lead to loss of ROM and joint function
• this is because sytokines influence osteoclasts, osteoblasts leading to bony ankylosis

Question 10

what does RA lead to

Answer 10

• tendon/liogament laxity/destruction
• altered biomechanics
• deformities
• loss of ROM

Question 11

clinical features of RA

Answer 11

• pain
• tendeness
• swelling
• fatigue
• warmth/heat
• stiffness (early morning)
• decrease ROM
• decreased muscle strength
• loss of function

Question 12

extra-articular features (not directly related to RA)

Answer 12

• subcutaneous features
• vascular lesions

heart:
- pericardisis

lung:
- pulmonary nodules, intertertestial fibrolosis

kidney

Question 13

pharmacology of RA

Answer 13

aims:
- - provide symptom release
- maintain function
- stop progressive joint destruction
- reduce long term joint disability

treatment:
- corticosteroids
- anti-rhumatic drugs (cytokine modulation)
- disease modifying anti-rhumetic drugs

Question 14

what is spondyloarthritis?

Answer 14

spondylos: vertebrae
arthors: joint
itis: inflammation

• it is inflammatory back pain
• peripheral and asymetic dyoarthritis
• not just joints
• can be in enthesis (insertional sites: achellis)

Question 15

what is seronegative spondyloarthritis?

Answer 15

• no rhumatoid factor

Question 16

what do we see with SpA… symptoms?

Answer 16

• helper and killer T cell infiltration
• prolonged inflammation = damage and destruction

leads to:
- inflammatory degradation of SI joints
- ankylosis
- bone formation around annulus fibrosis
- osteoblast stimmulation
- bridges vertebrae