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15 Cards in this Set

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Parathyroid derived from?
Pharyngeal Pouch
Location of parathyroid
Four poles if thyroid, or anywhere along embriological descent(tongue to mediastinum)
Two types of cells in parathyroid
Cheif:Granules of PTH, glycogen
Oxyphil Cells: Mitochondria and glycogen
Fat cells: 30% by age 25
Decreases PTH secretion
Increase in free ionized calcium
PTH Functions
Activates osteoclasts
increase renal tubular reabsorption of Calcium, Activates Vit D, increase PO4 3- excretion
increases serum calcium
Pathogenesis of Hypercalcemia due to malignancy
Osteolytic Mets: mets release RANK to activate bone resorpion
PTHrP: From squamous (bronchogenic or renal cell carcinoma)
Causes of Primary hyperparathyroidism
Primary Hyperplasia(10-15%)
Familial Primary Hyperparathyroidism
MEN-1: MEN-1 gene, tumor suppressor
MEN-2a: ret gene
Familial Hypocalciuric Hypercalcemia: AD CASR(calcium sensing receptor in PT and Kidney) gene mutation
3 types
Cause of sporadic Parathyroid Adenoma
PRAD(Parathyroid Adenoma), cyclin D1, MEN-1
Adenoma Morphology
Rim of compressed PT tissue, decrease adipose tissue, solitary lesion.
Can only tell carcinoma if invasion
Primary PT hyperplasia morphology
Four glands affected, decrease in fat cells
Skeletal changes in primary Hyperparathyroidism
Decrease bone matrix
Osteitis Fibrosa Cystica
Brown tumor: fibrous tissue associated with foci of hemorrhage
Renal and other changes in primary HyperParathyroidism
Urinary tract stones (renal calculi), nephro-calcinosis, Metestatic calcinosis: lungs, stomach, myocardium, bloodvessels
Labratory Findings in primary Hyperparathyroidism
Htpercalcemia, hypercalciuria, decreased serum phosphorus, Increase serum Alk Phos, Increase parathormone
Symptoms in primary Hypercalcemia
Bone pain(Ostioporosis, fractures), chronic renal insufficiency(renal calcula), abdominal groans(pancreatitis, gallstones, constipation, ulcers), psychic moans (depressionand seizures)