Pathophysiology of Hypercalcemia

serum Ca Pre-disposing Factors:

resorption of Ca in the bones

Destruction of bone tissue

Ca is released in extracellular fluids

Ca absorption in Excess Ca in Cell membrane Disturb cardiac muscle function

the intestines the kidney threshold becomes and electrical conduction through
the heart
more positive

Release of HCl, Retention of Ca by

S/Sx:
gastrin and the kidney HR
pancreatic enzymes Neuromuscular BP
excitability Bounding, full
peripheral pulses
Ca precipitates tend
Slows bowel to form ureteral or
transit time Causes osmotic Neurologic depression
diuresis kidney stones
Risk for thrombus formation

Constipation Lethargy
Urinary blockage
Bradycardia
Polyuria
S/Sx: Impairs glomerular
motility blood flow Depressed sensorium
Confusion Cardiac arrest
hypoactive bowel
sounds Muscle weakness
abdominal distention Decrease deep tendon
S/Sx: reflex
Urinary output Renal failure
Thirst
S/Sx:
Polyuria
Polydipsia
Nocturia
 Fluid deficit

Tx: Dehydration
Diuretics – enhance
excretion of Ca
Calcium chelators –
lowering the serum Ca Coma
level
Fluid Volume Therapy –
restore normal Ca levels Death