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Musculoskeletal

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Submitted By oj1993
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Musculoskeletal Pathophysiology Bones

Bone remodeling
Minerals have to be deposited into the bones and to be remodeled
Osteoblasts = builds the bone
Osteoclasts = corroding the bone, originate from stem cell * Big cells, a number of nuclei * Ruffled edges to increase surface area * Mineral resorption (dissolves crystals and releases minerals into the blood) * Acid dissolves the bone minerals
Things can do wrong * Preventing bones from generating in other parts of the body * Inhibitors include hydroxyapatite crystal deposition and thus not calcify * Calcification of arteries
SMC (Smooth muscle cells) in calcification
Media
Contractile phenotype
Low proliferation, low synthesis, expression of SMC markers

Intima
Synthetic phenotype
Proliferative, migratory, secretory
Osteoblast-like phenotype Mineralising, expression of osteoblast markers

It is more common to have hypocalcemia than hypercalcemia

Common cause of hypercalcemia is thyroid tumour
Calcium homeostasis * Controlled by 3 hormones: calcitriol, calcitonin and PTH (parathyroid hormone)

Calcium is not strong/high enough weak bones
Calcium into blood from our bones (99% Ca stored) * Two hormones to tell osteoclast to reabsorb Ca out of the bones and back into the blood (PRH and Calcitriol) or redeposited into the bones via osteoblast * Adults have low levels of calcitonin (children have higher levels since their bones are still forming, stronger effect in children)

Calcitriol (Activated Vit D)
Precursor steroid in our skin exposed to UV Converted to Vit D3 Cholecalciferol Calcidiol Calcitriol (Vit D) Bone resorption

Vitamin D deficiency (chronic) in children * Abnormal softness of bone (rickets) and osteomalacia (in adults)
Osteomalacia
* Little deposition of Ca crystals
Vitamin D:
Calcium in blood in the gut and bone resorption

PTH * Released by tiny parathyroid gland on the posterior aspect of thyroid gland in the neck * Release PTH when blood Ca is low * 1% drop in Ca double PTH release
Hypoparathyroidism
* Rapid decline in blood Ca

Hyperparathyroidism * Too much PTH * Results from parathyroid tumour * Bones are soft, deformed
Calcitonin
* Secreted by C cell of thyroid gland when Ca increases * Act when too much Ca in the body
Osteoporosis
* Common disease * Porous bones, due to loss of bone density, osteoclast activity takes over osteoblast activity * Fractures can occur * Fractures in vertebra (kypnosis)
Estrogen and Osteoporosis * Estrogen maintains bone density by preventing osteoclast activity * Estradiol dampening osteoclast * Menopause ovaries stop secreting estrogen and osteoclast activity rises and takes over osteoblast * ERT
Other risks of osteoporosis * ~ 20% men (low estrogen) * Low body fat (usually in females) – not making estrogen enough to make osteoclast to dampen * DMellitus * Smoking
DEXA (measure good bone density)

Prevention of osteoporosis * Adequate Ca in diet * Fluoridated water (Fl is a –ve ion, Ca is a +ve ion, ionic balance) * Decrease HCO3 weak aci (carbonated water) dissolves bone

Paget’s Diseases * Less common * Excessive remodeling, osteoclast activity out of control * Primarily affects spine, pelvis * Increasingly deformed (patients who have this disease) * Affect Caucasians – maybe a genetic disposition? * Rarely occurs before 40yrs * Prevention: Estrogen, PTH inhibitors
Osteomyelitis
* Affects children * Bacterial infection of bones * Occurs in lone bones * Antibiotic therapy * Chronic surgery
Sciatica
* Affects the sciatic nerve * Compression of vertebral column (due to dismovement) or bone irregularity can impact on spinal cord and act on sciatic nerve leading to intense pain * Can often occur during pregnancy

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