Compare & contrast gout, osteo- & rheumatoid arthritis
Aetiology:
Pathogenesis:
Typical joints & population(s) at risk:
What is gout? Describe symptoms
Aetiology:
Common systemic metabolic disorder
Pathogenesis:
- Hyperuricaemia in vulnerable people (not everyone with hyperuricaemia gets gout)
- Monosodium urate crystals form in joints & soft tissues causing severe pain & inflammation
Typical joints & population(s) at risk:
- Often affects the big toe in men.
- Rare in women before menopause then tends to affect the hands
- Increased incidence in age but can be diagnosed at any stage of life.
- Particularly affects First Nations populations
What is osteoarthritis? Describe symptoms
Aetiology:
- Wear & tear resulting in loss of cartilage
Pathogenesis:
There is little inflammation compared
to other forms of arthritis but reactive
bone growth & swelling in surrounding soft tissues causes pain
Typical joints & population(s) at risk:
- Tends to affect weight bearing joints like the hips & knees.
- Because it’s caused by wear & tear it is most likely to occur in the elderly, overweight or people who have engaged in sports such as netball, AFL & running
What is rheumatoid arthritis? Describe symptoms
Aetiology:
- Systemic autoimmune disease causing destruction of synovial Joints
Pathogenesis:
- The joints are affected by chronic inflammation (type IV cell mediated
response); formation of pannus; bone erosion, cartilage & tendon
degradation leads to irreversible joint
deformation.
Typical joints & population(s) at risk:
- It affects multiple small joints like those of the hands & causes systemic
inflammation
- Affects women more than men.
- Can be diagnosed at any age but typically it is first diagnosed in middle
age
List the main types of fractures & how healing may be impaired.
Fracture types:
Greenstick, simple, compound (open), comminuted, spiral, transverse
Bone repair process:
Haematoma, soft callous, hard callous, remodelling
Compound - increase risk of infection, broke through skin
Comminuted - fragments need to be removed otherwise necrosis occurs
List the factors that contribute to attaining peak bone mass.
Peak bone mass is influenced by genetics, we have a height and weight range based upon genetic predisposition but we need adequate nutrition (calcium, vitamin D and protein) and weight-bearing activity while growing to attain our peak bone mass. While growing, growth hormone is very important for the development of both bone and muscle. Oestrogen is important for the maintenance of
osteoblasts and the maturation of the epiphyseal growth plates. Testosterone and other androgens can be converted into oestrogens in fat via aromatase enzyme. Androgens stimulate muscle development and skeletal muscle contraction is critical for bone maintenance
List the risk factors for the development of osteoporosis; the possible consequences of osteoporosis & how bone loss may be retarded/accelerated
Factors increasing the risk of developing osteoporosis include:
Ageing, sarcopenia, reduced weight-bearing physical activity, amenorrhea, loss of oestrogenic activity after
menopause, smoking and low initial bone mass, also endocrine disorders like Cushing’s and hyperthyroidism
Drugs like androgen and oestrogen blockers, NSAIDs, glucocorticoids, corticosteroids and thyroxine
increase the rate of bone loss.
List the tumours that occur in the skeletal system (reviewing what was covered in neoplasia week)
Osteosarcoma
Chondrosarcoma
Osteogenic sarcoma (osteosarcoma)
Ewing’s tumor
Why are the bones frequently affected by metastatic cancer?
Bone is very vascular, so arterial metastases are easily distributed to this site plus it’s a good site for tumor cells to become trapped.
What impact does renal failure have on the musculoskeletal system?
Chronic renal failure can cause renal osteodystrophy (under mineralization of bone & soft tissue calcification). In failure, the kidney may not be able to convert vitamin D into its active metabolite (activated by chemical changes in the kidney) and without active vitamin D the gut cannot absorb calcium from food, which results in low levels of serum/blood calcium.
The control of the plasma concentration of calcium is finely controlled, PTH is released in response to low serum calcium and promotes resorption of calcium from bones by osteoclasts and induces the kidney to
retain calcium in blood, excrete phosphate and activate more vitamin D. In renal failure, less vitamin D is
activated and calcium is lost in urine so serum levels decline resulting in increased PTH secretion. The result is liberation of calcium from bones which forms complexes with the high levels of phosphate in the blood which can be deposited in soft tissues including arterial walls and heart valves while any free calcium is destined to be lost in urine as the kidneys no longer respond to PTH.
