1804259
| Question | Answer |
| Intracellular [Ca2+]? | approx. 1micromol/l |
| Extracellular [Ca]? | approx. 1mmol/l |
| Reason for low [Ca]? | Increase allows cascade of events to occur. |
| Reason for high extracellular [Ca]? | Bone mineralisation Normal function of excitable tissue |
| Bone morphology? | Trabecular bone inside, spongy. Cortical bone outside, rigid. |
| Describe the change in Ca balance throughout life. | Growth, pregnancy = +ve balance Adulthood = neutral balance Aging = slow -ve balance loss in bone density |
| Bone function? | Body support Organ protection Ca reservoir/mineral homeostasis Endocrine function - osteocalcin, fibroblast GFactor 23 Haematopoiesis Reverage for movement |
| Bone = ? % BW | 17% |
| Order of 3 bone cells from outside in. | Osteoblasts - Makes bone matrix Osteocytes - Most abundant bone cell. May sense pressure during growth Osteoclasts - Resorbs/degrades bone - bone turnover, releases minerals for collagenous protein breakdown |
| Which bone cell is related to macrophages? | Osteoclasts |
| Osteogenic cells | Undifferentiated bone cells, gives rise to osteoblasts and osteocytes. |
| Are osteogenic cells responsible for formation of osteoclasts? | No - Osteoclasts formed from monocytes and macrophages. |
| What is an osteoid | uncalcified bone matrix |
| What is the mineral component of bone matrix? | hydroxyapatite Ca10(PO4)6(OH)2 |
| Role of hydroxyapatite? | Provides rigidity and resistance to bone compression |
| Osteoid mineralisation is dependant on? | Vitamine D3 (1,25-(OH)2D3) |
| What happens in Vit D3 deficiency for children? for adults? | Rickets in children Osteomalacia in adults |
| Osteomalacia | Softening of bone from failing mineralization i.e. low Ca and Phosphate Also occurs as a result of hyperparathyroidism which increases Calcium resorption from bones |
| Where is Alkaline Phospatase expressed? | On osteoblast surface |
| What are Alk Phos biomarkers of? | Osteoblast activity i.e. bone formation |
| Action of Alk Phos? | Formation of inorganic phosphate ions by hydrolysing pyrophosphate (P2O7) -> 2 (PO4 3-) Thus increasing local phosphate concentration |
| Why does pyrophosphate hydrolysis lead to bone formation? | Pyrophosphate = bone mineralisation inhibitor |
| Osteoclast formation occurs by? | Fusion of monocytes and macrophages |
| Characteristic of activated osteoclasts? | Ruffled border formation |
| How do osteoclasts resorb bone? | Contains high levels of Carbonic Anhydrase for H+ formation from CO2 and H2O plus enzymes e.g. Cathepsin K (protease) which breaks down collagen matrix |
| How do Osteoclast precursors become activated to become mature osteoclasts? | RANK-RANKL interaction which forms NFkB NFkB induces new gene transcription *RANK = Receptor Activated Nucleate Kappa (Ligand) |
| Osteopetrosis | Increased bone mass/density due to abnormal osteoclasts = impaired resorption Inheritedd condition 4 possible mutations - in CA, H+ pump, Cl channel or in Cathepsin K |
| 4 steps of bone remodelling cycle | Quiescence Resorption - 10 days Reversal Formation - 3 months total 4-6 months |
| How often are skeleton renewed? | 7 yrs |
| Where are calcitonin produced? | C-cells of thyroidal folliclces Lowers Ca level - reduce osteoclast activity? No clear role in Ca homeostasis |
| Role of PTH (Ca absorption) | Increased calcitriol formation by gut Ca absorption (indirect) Increased distal tubule Ca absorption (direct) |
| Role of PTH | Promotes loss of phosphate and bicarbonate |
| Why does PTH induce loss of phosphate? | PTH secretion = low Ca Phosphate reacts naturally with calcium to form hydroxyapatite so phosphate loss = release of Ca |
| Why does PTH induce loss of bicarbonate? | Loss of bicarbonate = increased H+ production = competes with Ca on Albumin = release of bound Ca |
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