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CALCIUM

- Essential for myocardial contraction

REGULATION:
- Hormones that regulates the calcium
- Parathyroid hormones
- Vitamin D
- Calcitonin

PTH
- Secretion of PTH that is stimulated by a decreased in ionized Ca (thus, PTH
secretion is stopped by increase ionized Ca)
- PTH exerts 3 major effects on both BONE and KIDNEY
- In Bones:
o PTH activates a process known as BONE RESORPTION
o Activated osteoclasts break down bone and subsequently release Calcium
into the ECF.
- In Kidneys:
o PTH conserves calcium by increasing tubular reabsorption of calcium
ions. PTH also stimulates renal production of vitamin D.

Vitamin D
- It is a cholecalciferol
- Obtained from diet or exposure of skin to sunlight
- Vitamin D3  converted in the liver to 25-hydroxycholecalciferol (inactive form of
vit D)  in the kidney, 25-OH-D3 is hydroxylated to form 1,25-
hydroxycholecalciferol (the biologically active form)
- Active form of vit D increases the calcium absorption in the intestine and
enhances the effect of PTH on bone resorption.

Calcitonin
- Originates in the medullary cells of the thyroid gland.
- Secreted when the concentration of calcium in blood increases.
- Inhibits the actions of both PTH and Vit D.
- It is secreted in response to hypercalcemic stimulus.

DISTRIBUTION
- 99% of Calcium is part of the bones
- 1%  blood and ECF
- Ionized calcium in blood is greater than in the cytosol of cardiac or smooth
muscle cells  in order to maintain rapid inward flux of calcium.
- In blood:
o 45% circulates as free calcium
o 40% is bound to protein (albumin)
o 15% is bound to anions

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HYPOCALCEMIA

- Absence of PTH calcium will not be properly regulated (such as

hypoparathryoidism)
- The bone will “hang-on” to its stored calcium, while the kidney increases the
excretion of calcium.
- Lack of PTH can also lead to lack of vitamin D because in the metabolism of Vit
D, PTH is required.
- PRIMARY HYPOPARATHYROIDISM  glandular aplasia, destruction, removal.
- Hypomagnesemia = Hypocalcemia
o 3 mechanism
 It inhibits the glandular secretion of PTH across the parathyroid
gland membrane
 It impairs PTH action at its receptor site on the bone
 It causes vitamin D resistance
- Hypermagnesemia  inhibits PTH release  target tissue response
hypocalcemia and hypercalciuria.
- Hypocalcemia based on total Ca++ hypoalbuminemia
o Often associated with chronic liver disease, nephrotic syndrome,
malnutrition.
o 1 g/dL decrease in serum albumin = 0.2 mmol/L decrease in total calcium
- Acute pancreatitis
o Hypocalcemia (due to increased intestinal binding of calcium as increase
lipase activity occurs)
- Vitamin D deficiency and Malabsorption
o Decreased absorption  increased PTH production
- Renal disease (glomerular failure)
o Altered concentration of calcium
- Renal disease (chronic)
o Secondary hyperparathyroidism develops
o Compensate for hypocalcemia caused by either hyperphosphatemia or
altered vitamin D metabolism.
- PSEUDOHYPOPARATHYROIDISM
o Rare hereditary disorder
 Parathyroid hormone target tissue response is decreased.
- SURGERY AND INTENSIVE CARE
o Calcium levels must be monitored during surgery
 Calcium promotes cardiac output and maintain adequate blood
pressure
o Hypocalcemia common among critically ill patients (sepsis, thermal burns,
renal failure or cardiopulmonary insufficiency
 Abnormal acid-base balance and losses of protein and albumin
 Best suited to monitoring calcium status by ionized calcium
measurements.
- NEONATAL MONITORING

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o Blood ionized calcium concentration in neontates are high at birth and

then rapidly decline by 10-20% after 1-3 days, after about 1 week, ionized
calcium concentration in the neonates stabilized at levels slightly higher
than in adults.

I. Signs and Symptoms

a. Neuromuscular irritability
a. Paraesthesia
b. Muscle cramps
c. Tetany
b. Cardiac irregularities
a. Arrhythmias
b. Heart bock
c. Occurs with severe hypocalcemia
i. Calcium levels below 1.88 mmol/L

II. Treatment
a. Oral or parenteral calcium therapy
b. Administration of vitamin D
c. If hypomagnesemia is concurrent
a. Magnesium therapy should also be provided

Hypercalcemia

- Primary hyperparathyroidism
o Main cause of hypercalcemia
- Hyperparathyroidism
o Excess secretion of PTH
o Common among older woman
- Malignancies
o Second leading of cause of hypercalcemia
o May releases PTH-relate peptide
 Which binds to normal PTH receptors and causes increased
calcium levels
- Hyperthyroidism may sometimes cause hyperparathyroidism
- Familial hypicalciuria
- Thaizied diuretics
o Increase calcium reabsorptions
 Hypercalcemia

I. Signs and Symptoms

a. Mild hypercalcemia (2.62-3.00 mmol/L) = ASYMPTOMATIC
b. Moderate to severe hypercalemia
c. Neurologic
i. Drowsiness

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ii. Weakness
iii. Depression
iv. Lethargy
v. Coma
d. GI
i. Constipation
ii. Nausea
iii. Vomiting
iv. Anorexia
v. Peptic ulcer
e. Renal symptoms due to renal nephrolithiasis and nephrocalcinosis
f. Hypercalciuria can result in nephrogenic diabetis insipidus
i. Polyuria
ii. Hypovolemia
iii. Aggravates the hypercalcemia
g. Symptoms of digitalis toxicity

II. Treatment
a. Estrogen replacement for hypercalcemia among older woman
b. Parathyroidectomy among hyperparathyroidism
c. Salt and water intake to increase calcium excretion

DETERMINATION

Specimen
- Serum or lithium heparin plasma
- Samples must be collected anaerobically (loss of CO2 will increase the pH)
- Times urine concentration + 6 mol/L HCl  1 mL per 100 mL of urine

Methods
- 2 common methods
o Ortho-cresolphthalein complexone (CPC)
 Arseno III dye to for a complex with calcium
 Calcium is released from its protein carrier
 Complexes by acidification of the sample
o ISEs

REFERENCE VALUES

Serum/Plasma
- Child < 12 years 2.20 – 2.70 mmol/L (8.8-10.8 mg/dL)
- Adult 2.15 - 2.50 mmol/L (8.6 – 10 mg/dL)

Ionized Calcium (serum)

- Child 1.20 – 1.38 mmol/L (4.8-5.5 mg/dL)

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- Adult 1.16-1.32 mmol/L (4.6 – 5.3 mg/dL)

Ionized Calcium (plasma)

- Adult 1.03-1.23 mmol/L (4.1-4.9 mg/dL)

Ionized Calcium (whole blood)

- Adult 1.15-1.27 mmol/L (4.6 – 5.1 mg/dL)

Total calcium (urine-24 hour)

2.50-7.50 mmol/day (100-300 mg/day)

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