Limbs and Back: Week Six Flashcards
What is Osteoarthritis?
Progressive disorder of the joint caused by gradual loss of cartilage and resulting in development of bony spurs and cysts at margins
What is the difference between primary and secondary Osteoarthritis?
Primary: this is degenerative
Secondary: this is caused by trauma
What are some of the risk factors of Osteoarthritis?
Systemic: genetics, gender (men more likely under 50
-and women more likely over 50), low vitamin C and low vitamin D
Joint biomechanics: joint trauma, obesity, occupation,
What are some symptoms of Osteoarthritis?
- morning stiffness (< one hour)
- pain at the end of the day
- pain is sharp and burning
- pain with load-bearing
- difficultly moving
- decreased walking
- Trendelenburg sign
- pain worse during exercise
- abnormal alignment
- tenderness of palpation
- weakness and muscle wasting
- joints appear larger
What are the four signs shown on an x-ray with a patient with Osteoarthritis?
- Loss of joint space
- Osteophytes
- Subchondral sclerosis
- Subchondral cysts
What is involved in the non-operative treatment of Osteoarthritis?
- Medication: paracetamol, NSAIDs, alternative
- Physio: motion, weight loss, strengthening, aerobic conditioning
- Walking aids
- Joint injections
What is involved in the operative treatment of Osteoarthritis?
- Arthroscopy
- Cartilage transplant
- Joint replacement
In Osteoarthritis, tissue macrophages become activated due to trauma and the risk factors. What do they secrete and what is the cause of this?
- TNF, IL-1B, IL-6
- VEGF
VEGF will cause stimulate of E-selectin and this will increase blood supply and attract ore immune cells.
These molecules and cells will stimulate synoviocytes to produce proteases and this causes cartilage breakdown.
Cytokines will also stimulate osteoblasts to attempt to repair bone and this will result in the formation of Subchondral sclerosis.
Which cytokines are pain stimulators?
Prostaglandins and bradykinin
What molecules contribute to the elasticity and high tensile strength of the synovial fluid?
Type two collagen
Proteoglycans: hyaluronic acid, chondroitin sulphate and keratin sulphate
When there is cartilage damage, there is an increase in proteoglycans and an increase in collagen II synthesis. Chondrocytes will then eventually switch to another collagen. What type of collagen is this and what is the effect?
Chondrocytes switch to type one collagen. This collagen does not have the same interaction with proteoglycans and hence the elasticity decreases.
What will all decrease in osteoarthritis?
- water content (initial increase)
- proteoglycan synthesis
- collagen-x linking
- size of Aggrecan, hyaluronic acid and GAG
During osteoarthritis, osteophytes will form. This will cause enlarged joints in the fingers. what is the name for the swellings in the distal and proximal joints?
Distal: Heberden node
Proximal: Bouchard node
What is the difference in morning stiffness between rheumatoid arthritis and osteoarthritis?
Osteoarthritis stiffness lasts less than one hour whereas rheumatoid arthritis lasts more than one hour.
What is the main blood supply to the hip joint?
Lateral and medial circumflex arteries
What does an intracapsular fracture have a risk of?
Avascular necrosis
Explain the garden classification of hip fractures.
Type One: incomplete, undisplaced
Type Two: complete, undisplaced
Type Three: complete, partially displaced
Type Four: complete, fully displaced
What is the treatment for hip fractures, using the garden classification?
“One two pop in a screw, Three Four head to the floor”
What are treatments for hip fracture?
- Dynamic hip screw
- Cannulated hip screw
- Hemi-arthroplasty (only head replaced)
- Total hip arthroplasty (acetabulum and head replaced)
Name the roles and members of the multi-disciplinary team involved in hip surgery
- Physio: weight bearing exercises
- OTs: hand rails, walking aids, long-handled devices
- Social workers
- Orthopaedic surgeon
- Geriatrician
- Liaison nurse
- Dietarian
What is the percentage of annular bone turnover cortical bone and trabecular bone?
- 4% for cortical
- 25% for trabeculae
Give some examples of molecules that stimulate RANKL
PGE2, PTH, Glucocorticoids, vitamin D, IL-11, IL-1, PTH, TNF-alpha
How much bone loss occurs after menopause?
2-3%
What affect does glucocorticoids have on bone?
- increase RANKL production (there is a glucocorticoids receptor on osteoblasts)
- increased expression of RANK receptor ( glucocorticoids on osteoclasts)
- suppress OPG
- increase calcium excretion in urine
- decreased calcium absorption in GI tract