Metabolic bone diseases Flashcards
Types of hyperparathyroidism
primary- cause unknown but thought to be by excessive secretion of PTH
secondary- usually due to disease state such as renal failure which causes decrease in ionized serum calcium levels
Excess secretion of PTH interrupts metabolism of calcium, phospahte, and bone
Results of primary and secondary hyperparathyroidism
primary- results in hypercalcemia
secondary- results in initial hypocalcemia followed by hypercalcemia
Clinical manifestations of hyperparathyroidism
bones- demineralization due to excessive osteoclast and osteocyte activity
kidneys- renal calculi, UTI
GI- anorexia, petic ulcers, constipation, hypergastrinemia
psychiatric issues
muscles weakness, myalgias
Clinical management of hyperparathyroidism
adequate hydration, increase urinary excretion of Ca++ with diuretics, drugs that decrease resorption of Ca++ by bone-biphospates, calcitonin
Surgery- parathyroidectomy
Hypoparathyroidism
decreased secretion of PTH
Patho:
hypocalcemia-decreased intestional Ca+ absorption
bones decreased mineralization and decreased bone resorption
metabolic alkalosis
parkinsons like symptoms
hypoparathyroidism clinical presentation
mental fatigue, abdominal pain, pt hx of alcoholism
physical exam- muscle spasm, tetany, excitability, increased deep tendon reflec, dry skin, hair loss, weak tooth enamel
hypoparathyroidism clinical management
acute-medial emergency
chronic- lifetime vit D therapy, calcium supplement, muscle relaxants
symptoms of hypercalcemia
stones
bones
moans
groans
osteoporosis
clinical syndrome caused by a decrease in bone mass
dec osteoblast and inc osteoclast
“porous bone”
osteoporosis clinical manifestations
early osteoporosis asymptomatic
fractures can occur with minimal trauma
vertebral compression fractures most common
end stage disease has marked dorsal kyphosis
causes of osteopenia
hypogonadism, cushing’s syndrome, hyperparathyroidism, hyperthyroidism, osteomalacia, multiple myeloma
osteoporosis treatment
PT (strengthening and fall prevention), cacium, and vit D
osteomalacia
adult’s rickets
rickets= decrease in calcium to provide hardness to bone. Uncalcified areas become soft and even in epiphyseal plates.
oseomalacia=soft bone
clinical syndromes that results from inadequate bone mineralization
Vit D deficiency or resistance and phosphate deficiency
osteomalacia clinical manifestations
bone pain and pathologic fractures
decreased bone density
pseudofractures
bowing of legs in children
paget’s disease of bone
common disorder of increased bone turnover
enlargement and deformity of multiple bones
etiology unknown
increased bone resorption with compensatory inc bone formation lead to thick, abnormal bones
