Skeleton and Osteoporosis Flashcards
Osteoporosis
the surface level of the bones may be worn away , exposing the tissue beneath.
Open (Compound) Fracture
The broken end penetrates skin
Comminuted
Bone splits into three or more pieces at fracture site.
Compression
Bone is crushed due to force example: veterbral bodies
Spiral
Ragged break due to twisting force; breaks in many layers deep.
Epiphyseal
Epiphysis detaches from the diaphysis at epiphyseal plate. Occurs when cartilage cells are dying and calcification of matrix occurs.
Depresssion
Broken due to bone pressed inwards (skull)
Greenstick
Bone breaks incompletely, one side breaks and other bends. Common in children who have more organ flexible matrix.
Colle’s and Pott Fracture
Colles: due to fall, small hand bones of scaphoid or lunate can break.
Potts: fracture affecting one or both malleoli, inversion of ankle can break
Fracture Repair 4 Steps:
- Hematoma Forms: broken blood vessels surrounding fracture leads to mass of clotted blood at site:
- Lack of circulation –> bone cells die, swelling
- macrophages remove debris, bacteria, pathogens. while osteoclasts absorb dead cells and make the jagged site around the bone smooth for repair.
- Activate mast cells for inflammatory response: ( histamine makes blood vessels leaky and swells up.) - Fibrocartiliagous Callus Forms: fibroblasts from the periosteum invade fracture site and produce collagen fibers.
- Mesenchymal cells from periosteum develop into chondroblast and produce fibrocartilage.
- Callus is mass of repair tissue containing fibers and bridges fracture gap. - Boney Callus Formation 3-4 months: In areas of healthy bone , osteogenic cells develop into osteoblasts and start producing spongey bone trabeculae.
- Osteoblasts secrete ostoid, becomes calcified forming trabeculae (spongey bone)
- The trabeculae helps to join the living and dead fragments and the fibrocartilage is converted to spongey bone. - Bone Remodelling: Dead portions of fragments are reabsorbed via osteoclasts and compact bone replaces spongey bone around the periphery of fracture.
Pathological Conditions of Bone
Rickets: low calcium absorption
Anchondroplastic Dwarfisum: epiphyseal plate changed and long bones do not develop
Pitutitary Dwarifusm: pituttary tumor, not enough hgH.
Giantism: hyper hgH secretion
Avascular necrosis: tearing of blood vessel to head of bone
Osteosacoma: bone caner in children
Osteomyelits: bone inflammation
Osteoporosis ( describe, pathology, risk factors and injuries, possible treatments)
Two main mechanisms by which osteoporosis develops involve decrease in bone mass denisty. Due to excessive bone resorption and inadequate bone formation.
Loss of Bone mass and density, lack of bone deposition
Osteoporosis = osteoclastic activity (Bone Reabsorption) > Osteoblastic (Bone Deposition)
- Reasons behind Osteoporosis
- Lack of estrogen (menopause) inhibits bone remodelling: increases bone resorption as well as decreases deposition of new bone. Inhibits bone remodelling by promoting osteoclastic activity, inhibiting osteoblastic, and maintaining osteocyte activity.
- Calcium metabolism: calcium definacy ( low Ca stimulates PTH which promotes osteoclastic to deposit ca from bone to blood. )
- Effects of Osteoporosis
- Fractures in lower spine resulting from decrease in strength of vertebral bodies (pain) , occur without trauma, deformities in spine ( lower height) due to collapsed veterbrae.
- Fractures in wrist from fall, hips etc
- Risks of Osteoporosis
- Female
- Older age
- Senditary lifestyle
- Thin body
- Low Ca diet
- Vit D Low
- Menipause
- Smoking