Bone Disorders Flashcards
heritary bone disorders
macrodacty- larger digit
polydacty- extra digit
syndacty- webbing
osteogenisis imperfecta
defective syntheisis of type 1 collagen fibres
collagen chains usually made in the Endoplasmi reticukum causing a tripple hekix made with glyceni-x-r
maturation and seretion occurs- enzymes cut the mature collagen into fibres
glyceine is replaced and causes the collagen to be delayed and stuck in EPR leads to faulty proteins
osteogenisis imperfecta symptoms
extreme skeletal fragility
thin poorly developed bones
short limbs
problems with connective tissue
suseptible to fractures easily
treatment of osteogenisis imperfecta
biophosphanates- increase cortical bone width and strength
physio -increase muscle strength
hydroptherapy
change positions regular
new ways of movement
osteochondrosis
interuption of blood supply to bone
scheurmans disease
irregular vertebrae growth= extreme kyphotic position
apex of curve is in thoracic region- stiff
tight hamstrings
legg-calve perthis disease
abnormal coagulation of the blood
the disruption in the blood flow causes nexrosis/ infarction of the proximal femoral epiphysis
then fragmentation occurs as body reabsorbs infarcted bone
reossification
remodelling takes 2-4 years
symptoms of legg-calve-pethis disease symptoms
short stature
hip nee groin pain
reduced ROM
atrophy in thigh
osgoood schlatersp
pain in the knee specifically tibial tuberosity
microfractures in tibial tuberosity due to infammed and thickened patella tendon
swelling of the tendon
osgood schlaters treatment
limitation of activity
anti inflam cryotherapy
release quad tension
scoliosis
lateral deviation of the spinal collumn in adults the facets are damaged
idiopathic/ congenital/ neuromuscular
scoliosis deformity
high shoulder/ prominant hip/ prohecting scap
osteomalacia
due to decrease vitamin D- causes hypoglycemia and hypophosphatanemia
this cause release of calcium and phosphate of bones
decrease bone mineralisation
bone pain
altered mobility
muscle weakness
fractures
rickets
due to decrease VD decrease calcium and phosphate in growth plate leads to hypertrophy to chondrocytes
widened growth plate
bone pain
altered mobility
muscle weakness
fractures
osteopenia
decrease bone mineral density
gradual decline in bone mass over time
genetic/ weight bearing issues/ calcium intake/ VD consumption
cause: due to uncoupling of osteoclast and blast activity
osteoporosis
low bone mass skeletal fragility hormone imballance
imballance of bone remodelling- bone reabsotption is greater then bone remodel
osteoarthritis
imballance between breakdown and repair of joint tissue
mechanical stress and inflammation
ageing- mitacondrial dysfuncton causes cartliage breakdown
gentics- predispostion with mutations to type 2 collagen
joint injury
obesity- joint load
inflammation- low grade inflammation increases production of degrading enzymes
hormone- osetrogen
damage of osteoarthritis
cartilage breakdown- collagen loosens/ chondrocytes hypertonic
bone changes
- bone spurs/ bone marrow lessions
synovial fluid- sell and pain
soft tissue- ligament meniscus degradation
pain stffness creptisu joint deformation
rhumatoid arthritis
chronic autoimmube synovial inflammation
gentic HLA-DRB 1 gene
swelling thickened synovial memebrane destruction of cartilage
stages of RA
early- inflammation/ joint still intake
moderate- joint damage with pain and stiffness
serve- permenant cartliage damage
