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WEEK 24:
Bone 2:
| Question | Answer |
|---|---|
| types of bone development in embryo (2) | intramembranous and endochondral - both involve replacing a CT template |
| intramembranous bone development in embryo | sheets of mesenchymal cells, differentiation of osteoblasts in centres of ossification which merge to form trabecular bone (eg skull, maxilla) that is remodelled + remaining mesenchyme makes bone marrow + periosteum |
| endochondral bone development in embryo | cartilage template, with blood supply to shaft of bone causing osteoblast differentiation (primary centre of ossification) and cartilage growth plate remains to allow bone to lengthen eg long bones + base of skull |
| endochondral bone development at birth | at birth blood supply to epiphyses instigate secondary centres of ossification |
| bone growth in epiphyseal end | proliferate |
| bone growth in diaphyseal end | chondrocytes mature + die then are replaced by bone |
| long bone growth | grows in length via epiphyseal growth plate and fuses in adulthood |
| how do other bones grow | by coordinated appositional growth at periosteum and resorption at inner surface |
| humerus ossification | |
| femur ossification | |
| ossification of carpal bones | predictable sequence starting with capsule and ending with pisiform |
| ossification of carpal bones at birth | no calcification although there is a great individual variability |
| capitate + hamate ossification time | 4 months |
| triquetral ossification time | 3 years |
| lunate ossification time | 4 years |
| scaphoid, trapezium and trapezoid ossification time | 6 years |
| pisiform ossification time | 11 years |
| achondroplasia (impaired bone elongation)- dwarfism | congenital bone disease caused by mutation of fibroblast growth factor receptor 3: activation. Activation of FGFR3 inhibits chondrocyte proliferation affecting growth plates- disorganised + hypoplastic and long bone growth stunted |
| signs and symptoms of achondroplasia | Lordosis (back), bowed legs and stunted extremities (especially proximal) |
| bone contributes to calcium homeostasis under influence of (3) | PTH (parathyroid hormone), calcitonin , and vitamin D |
| calcium homeostasis** | |
| calcitonin | thyroid C cells - decreases blood calcium |
| vitamin D metabolism mechanism of action** | |
| bone fracture repair | occurs when periosteum is breached, haematoma (injury to blood vessels) or blood clot forms |
| bone fracture repair involves replacement with | affected parts is replaced by vascular collagenous tissue (granulation tissue) which becomes increasingly fibrous (fibrous granulation tissue) or replaced by hyaline cartilage (form flexible provisional callus) |
| bone fracture repair to fill gap involves | osteoprogenitor cells from periosteum and endosteum differentiate into osteoblasts and lay down new woven bone (bony callus) and site completely bridged by bone (bony union)- slowly remodelled to form oriented lamellar bone |
| metabolic bone disease examples (4) | osteoporosis, rickets + osteomalacia, paget's disease, and hyperparathyroidism |
| osteoporosis | increased bone erosion due to imbalance of osteoblasts + osteoclasts causing loss of bone mass leading to thinner trabeculae initially and then thinned cortical bone however bone tissue is normal but fracture risk increased |
| osteomalacia | lack of vitamin D leading to inadequate mineralisation of bone - weak and soft - where osteoid is normal and bowing of bones and bone pain occurs |
| pagets disease | Overactive osteoclasts. These destroy bone and result in osteoblasts responding by laying down bone rapidly-immature woven bone. Therefore bone mass is increased but it is weak. Metabolic consequences due to energy demands of the disease. |
| hyperparathyroidism | Increased osteoclast activity as a result of increased levels of PTH due to renal disease or tumour. Destruction of cortical and trabecular bone. Inadequate compensation by osteoblasts leads to loss of bone mass. Fracture risk. |
| osteoporosis pt2 - s21 + s22 | |
| osteoporosis diagnosis | Asymptomatic pre fracture, Serum ALP, Ca and Pi levels are unreliable, 30-40% reduction in bone mass needed to be seen radiologically. No marked numbers of osteoclasts on histology: Need sensitive DEXA |
| osteoporosis clinical outcomes (3) | Pathological fractures due to falls in the elderly Back pain and kyphosis due to compression fractures Hip replacements-fractured neck of femur |
| osteoporosis treatment | prevention (diet and exercise), Bisphosphonates, oestrogen receptor agonists, PTH |
| osteomalacia + rickets s23 treatment diagnosis etc** | |
| hyperparathyroidism types | Primary: Tumour. Elevated serum calcium Secondary: low serum calcium caused by renal disease (excessive loss via abnormal kidneys) causes hyperplasia of parathyroid glands. |
| pagets disease ** s25 |
Created by:
kablooey
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