CALCIUM HOMEOSTASIS & BONE

Protect vital organs Support muscles Reservoir of calcium

Excitable tissue / muscle / nerve Cell adhesion Structural integrity

ENDOCRINE CONTROL OF CALCIUM HOMEOSTASIS: 1. PARATHYROID HORMONE (PTH) 2. VIT AMIN D 3. CALCITONIN

CALCIUM HOMEOSTASIS IS IMPORTANT TO PREVENT HYPO/HYPER-CALCAEMIA Some exchanged with bone Some lost in urine Some is absorbed from kidney Some used by intestine

BONE: CONSISTS OF: a) Mineral (Calcium / Phosphate)

b) Collagen (connective tissue)

c) Bone cells OSTEOBLASTSMake osteoid which mineralizes to become bone

OSTEOCLASTS-

Responsible for bone resorption Found in lacunae attachment to bone important Produce acid to excavate pit around damaged mineral

OSTEOCYTES -

Embedded in bone matrix, have long processes which contact other bone cells

d) Bone resorption, or turnover Process by which osteoclasts break down bone and release minerals, resulting in a transfer of calcium from bone fluid to blood. Remodelling bone reduces its volume. Followed by replacement of bone by osteoblasts PURPOSE: o o o TYPES OF BONE: 1. CORTICAL / COMPACT (exterior): dense, hard 2. TRABECULAR / CANCELLOUS (interior): spongy to regulate calcium homeostasis repair micro-damage shape / sculpture skeleton during growth

N.B Metaphysis: portion of long bone between epiphysis and diaphysis (growth plate) RICKETS (child) / OSTEOMALACIA (adult): Deficiency of active vitamin D - bone is unduly soft due to lack of mineralization of collagen component of bone (osteoid) Failure to absorb sufficient calcium from GI tract SYMPTOMS: Osteoid at growth plate is weak (bow legs) Growth plate expands to compensate (swollen joints) TREATMENT: Vit D replacement (dietary, through sunlight) N.B. Harder to absorb vit D from sunlight with pigmented skin OSTEOPOROSIS: Loss of bone mass / density (i.e. normal bone but less of it), leading to increased risk of fractures (of wrist, spine, hip) 1. Senile: males & females show increases gradual decline in bone density 2. Post-menopausal: rapid decline in female bone density following decline in estrogen at menopause TREATMENT: Estrogen deficiency increases the rate of bone remodelling / resorption. Osteoclasts increase in number & activity: become more aggressive Excavate the tribeculae aggressively (may perforate completely in which case it is lost for good) Increased risk of micro-fracture

HRT Osteoclast poisons (bisphosphonates): aim to reduce bone remodelling by reducing number / activity of osteoclasts)

RENAL OSTEODYSTROPHY:

PTH: Regulates calcium & phosphate levels PTH: Essential to life calcium, phosphate

PTH increases serum calcium & decreases serum phosphate by; Increasing calcium resorption in renal distal tubule Increasing intestinal calcium resorption (via activation of vitamin D) Increasing calcium release from bone (stimulates osteoclast activity) Decreasing phosphate resorption PTH is inhibited with increased calcium and 1, 25D3
RESORPTION: Process by which osteoclasts break down bone and release minerals, resulting in a transfer of calcium from bone fluid to blood. Remodelling bone reduces its volume. Followed by replacement of bone by osteoblasts PURPOSE:

o o

to regulate calcium homeostasis repair micro-damage

VITAMIN D: SOURCES: sunlight on skin, dairy products Most active form: 1, 25dihydroxyvitamin D3 (1000x more active than the storage form, converted in kidney)

CALCITONIN: Produced by thyroid (parafollicular) cells Calcitonin released in hypercalcaemia: inhibits bone resorption (by direct effect on osteoclasts) NOT essential to life

HYPERCALCAEMIA: CAUSES decreased PTH (parathyroid glands), which has the following effects; Bone: bone resorption urinary phosphate, urinary calcium) phosphate absorption) bone resorption SERUM CALCIUM

Kidney:

Intestine: calcium absorption,

Calcitonin produced by the thyroid also o o o

Joint pain / increased risk of fractures due to calcium liberation from bone Leakage of Ca+ into kidneys kidney stones Lethargy / thirst

HYPOCALCAEMIA: CAUSES increased PTH (parathyroid glands), which has the following effects

 Bone: Kidney:

bone resorption urinary phosphate, urinary calcium) phosphate absorption)

SERUM CALCIUM

Intestine: calcium absorption,

N.B. HypERphosphataemia produces the same effects (

urinary phosphate

serum phosphate

HYPERPARATHYROIDISM: 10 HPT parathyroid tumour: causes hypERcalcaemia & low serum phosphate o o o Joint pain / increased risk of fractures due to calcium liberation from bone Leakage of Ca+ into kidneys kidney stones Lethargy / thirst

20 HPT renal disease: decreased activation of vitamin D 30 HPT longstanding HPT: leads to irreversible parathyroid hyperplasia