Joint Disease

Question 1

Processes at the joint

Answer 1

• synovial joint made out of connective tissue (collagen) - contains synoviocites which act as fibroblasts.
• synovial membrane produces fluid which lubricates the joint and provides nutrients to the cartilage, shock absorbance.
• overlying and underlying bone- give structure to the joint, structure for cartilage, weight bearing
• cartilage: gives joint near frictional surface, protection for the bone, shock absorbance. Contains an abundance of water, chondrocytes form collagen fibres (type 2, only sound in cartilage) and proteoglycans

Question 2

Osteoarthritis

Answer 2

Degeneration of cartilage in the synovial joint, causing pain, limited movement and therefore limited function. 
- majority in women, increases with age 
- idiopathic  
- increases with age 
- primary aetiology: 
Wear and tear from load bearing 
Genetics 
Congenital structure of the joint- lax joints, double jointed, more common in women due to oestrogen 
- secondary aetiology:
Injury

Question 3

Pathogenesis of OA

Answer 3

Possibility: repetitive impulse loading- more impact on underlying bone as bone takes up more shock absorbance. Causes micro fractures in underlying tubercular bone, resulting in healing/remodelling, followed by bone stiffening (sclerosis), causing increased stress on articulate cartilage, cartilage breakdown and then joint degeneration.

• fibrillation- splitting of cartilage. Increased number of chondrocytes- hyperplasia. Lose proteoglycans and gain water- more vulnerable to destruction.
• osteophyte (bony spur)- formation of cartilage and bone laterally from the joint due to trauma, load bearing. Synoviocites change into osteoblasts or chondrocytes forming mostly bone. Cartilage mah not have blood or nerve supply.
• not symmetrical
• no fusion of joints (ankylosis)

Question 4

Rheumatoid arthritis

Answer 4

A chronic progressive disease causing inflammation in the joints and resulting in painful deformity and immobility, especially in fingers, wrists, feet and ankles
- females
- autoimmune- HLA linkage
- ankylosis
- generally feel unwell
- pannus- thickened synovial membrane releases enzymes to destroy underlying cartilage and bone
- can have inflammation of blood vessels
(Phlebitis- veins, arteritis - arteries)
- presence of mycobacteria
- high prevalence of UTI in women than males

Question 5

Rheumatoid nodules

Answer 5

• elbow
• can occur anywhere with connective tissue
• painless
• knocking and bumping- ulceration and infection

Question 6

Pathogenesis of RA

Answer 6

• bacterial or viral infection
• cell mediated hypersensitivity- macrophages, cytotoxic T cells and NK cells
• present cells to the helper T cells, cause NK cells and macrophages to kill the cell
• antibody binds to antigen, activates compliment cascade,’causes cell death
• immune complexes; serum, joints and other tissues.
  Rheumatoid factors (RF): from antibodies against our own antibody- think it’s an antigen- IgM- IgG in serum
  Abs against cyclic citrullinated peptides (CCPs): citrullinated fibrinogen type 2 collagen and other - arginine being added to the peptides

Question 7

Gout

Answer 7

Abnormality in purine metabolism 
- high risk in men 
- genetic predisposition 
- alcoholics 
- food binge
Possible progression 
- hyperuricaemia
- acute arthritis, monosodium urate crystal deposition- dependent on temp- more readily at lower temp
- asymptomatic periods 
- chronic tophaceous gout (tophus lesions- lymphocytes, macrophages, scar tissue) 
- can lead to kidney stones

Question 8

Gout aetiology

Answer 8

Uric acid

• overproduction, normal excretion
• overproduction, increase excretion
• normal production decreased excretion

Types

• primary, idiopathic, genetic, environment
• secondary: overproduction