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Pathophysiology of Hypercalcemia

Pathophysiology of Hypercalcemia

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Published by joys11

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Published by: joys11 on Feb 22, 2010
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Pathophysiology of Hypercalcemia
Pre-disposing Factors:serum Caresorption of Ca in the bonesDestruction of bone tissueCa is released in extracellular fluidsCa absorption inthe intestines
Release of HCl,gastrin and pancreatic enzymesSlows boweltransit timeConstipationS/Sx:motilityhypoactive bowelsoundsabdominal distention
Excess Ca inthe kidneyRetention of Ca bythe kidneyCauses osmoticdiuresisCa precipitates tendto form ureteral or kidney stonesPolyuriaS/Sx:Urinary outputThirst
Urinary blockageImpairs glomerular  blood flowRenal failure
S/Sx:PolyuriaPolydipsia Nocturia
Cell membranethreshold becomesmore positive Neuromuscular excitability Neurologic depressionLethargyDepressed sensoriumConfusionMuscle weaknessDecrease deep tendonreflex
Disturb cardiac muscle functionand electrical conduction throughthe heartS/Sx:HR BPBounding, full peripheral pulses
Risk for thrombus formationBradycardiaCardiac arrest
Fluid deficitDehydrationComaDeath
Tx:Diuretics – enhanceexcretion of CaCalcium chelators – lowering the serum CalevelFluid Volume Therapy – restore normal Ca levels

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