Calcium deficiency in the human body which causes Hypocalcemia

Introduction of hypocalcemia

Important minerals that are useful for bone formation and various physiological processes
are calcium, these physiological processes such as transportation between cell membranes,
activation and inhibition of several enzymes, intracellular metabolic regulation, hormone
secretion and activation, blood clotting processes, muscle contractility and nervous system
conduction . Calcium in bones has a percentage of 90%, a few of which are found in intra and
extra cellular spaces. Homeostatic calcium is a complex process that requires various things,
including adequate supply, adequate absorption process in the intestine, as well as the help of
several hormones such as parathyroid, vitamin D and calcitonin. Serum calcium is one percent of
total body calcium, found in extracellular fluid and soft tissue. Serum calcium consists of ion
components (50%), is bound to protein (40%), especially albumin, and a small portion (8-10%)
is bound to organic acids and inorganic acids such as citrate, lactate, bicarbonate and sulfate.

Under normal circumstances, serum calcium levels are regulated by parathyroid hormone
(PTH) and calcitriol (1,25-dihydroxy vitamin D3; 1,25 [OH] 2D3) which function to reduce
serum calcium levels, and calcitonin to reduce serum calcium levels, especially glucocorticoids. ,
phenytoin, and phenobarbital. Hypocalcemia is defined by a variety of limitations, including
calcium calcium levels less than 8 mg/dL (2 mmol/L), 7.48 mg/dL (1.87 mmol/L) or 7 mg/dL
(1.75 mmol /L). A more precise definition is based on calcium ion levels, but at normal acid-base
and albumin levels, this value has linear correlation with serum calcium levels, so measurement
of serum calcium levels can be used as the first screening.

Hypocalcemia is a condition where the serum calcium concentration is less than 8.5
mg/dL. The inability to access bone calcium deposits due to dysfunction, suppression, or
transport of the parathyroid gland can lead to hypocalcaemia. In addition hypocalcemia can be
caused by vitamin D deficiency, which causes a decrease in calcium absorption in the diet.
Increased serum calcium protein bonds due to a decrease in H + can also cause hypocalcemia,
because kidney failure can cause phosphate levels to rise. (Corwin, Elizabeth J, 2009)

Hypocalcemia causes neurimuscular dysfunction, in the form of muscle spasm and

cramps, and numbness and tingling in the extremities. Hypotension and decreased cardiac output
are signs of the cardiovascular system. Bone pain, deformity and fracture can also appear.
Osteomalasia and rickets in childhood will occur treatment of acute hypocalcaemia in the form
of intravenous infusion.

Hypocalcemia can occur due to reduction in total body calcium or reduction in ionized
calcium percentage. Total calcium levels are likely to decrease due to increased calcium lost,
decreased input secondary to changes in intestinal absorption, or changes in regulation. Increased
phosphorus levels and decreased magnesium levels can trigger hypocalcemia. Calcium and
phosphorus have reciprocal relationships: when one increases, the other tends to decrease. This
hypomagnesia can cause hypocalcaemia caused by a decrease in the work of parathyroid
hormone. (Carpenito, 2000)

Hypocalcemia is a condition in which calcium levels decrease, the effect of a deflection

of calcium to sodium also decreases. As a result, cell depolarization that can be stimulated occurs
when sodium moves in. Therefore, if low calcium levels increase the excitability of the central
nervous system and muscle spasm occurs. Convulsions and tetanidan can occur. (Price, 2012).

Acute hypocalcaemia will cause tingling in the oral environment (circumcision), tetany,
especially in muscles innervated by long fibers, and convulsions (At Glance Medichine).
Hypocalcemia refers to lower than normal serum calcium concentrations, which occur in a
variety of clinical situations.

Hypocalcemia is a decrease in the decrease in serum calcium that can occur in a number
of circumstances, such as hypoparathyroidism, vitamin D deficiency, disturbance of vitamin D
metabolism, hypomagnesaemia and acute or chronic renal failure. By looking at PTH hormone
levels, hypocalcemia can be grouped into 2 parts, namely hypocalcemia with increased PTH
levels (secondary hyperparatiodism).

The description above is some explanation of hypocalcemia from several points of view,
but if it is drawn on the red thread hypocalcemia refers to a condition where the calcium in the
normal body is not in the amount (not in normal conditions, because normal calcium levels in the
body). Normally 90% of calcium is in the bone, a few of them are in the intra and extra cellular
spaces. If something is not in proportion then there will be instability, meaning that if calcium is
not in the amount in the body or in the bone, then there will be instability that will cause a
problem.

Etimilogy of Hypocalcemia

Transient hypocalcaemia can occur with coughing blood (such as in exchange

transfusions in newborns), because citrate can combine with calcium ionizing and temporarily
remove it from the circulation. (Brunner & Suddarth, 2002)

Inflammation of the pancreas causes rupture of protein and fat. It is suspected that
calcium ions combine with fatty acids released by hypolysis to form soap. As a result of this
process hypocalcemia occurs and is common in pancreatitis. It is also suspected in that
hypocalcemia may be related to excessive secretion of glucagon from the pancreas that is
inflamed, resulting in increased secretion of calcitosin (a hormone that lowers calcium ions).

Hypocalcaemia generally occurs in patients with kidney failure because patients often
experience elevated serum phosphate levels. Hyperphosphatemia usually causes a reciprocal
decrease in serum calcium levels. There are also other causes of hypocalcaemia such as
inadequate vitamin D consumption, magnesium deficiency, thyroid medullary carcinoma, low
serum albumin levels, and alkalosis. Medications that can predispose to hypocalcemia include
antacids containing aluminum, aminoglycosides, caffeine, sisplatin, corticosteroids, mitramicin,
phosphate, isoniasid, and loop diuretics.

The main symptom of hypocalcemia is an increase in neuromuscular irritability that can

tingle at the fingertips and around the mouth. There are other symptoms that will be felt, namely
muscle spasms that affect the waist, legs and feet. In severe circumstances can arise spontaneous
spopedpas (tetani), laryngospasm or bronchospasm, to general seizures.

Hypocalcaemia often occurs asymptomatic. Hypoparathyroidism is often assumed by

clinical manifestations (eg cataracts, basal ganglia calcification, chronic candidiasis in idiopathic
hypoparathyroidism).

Symptoms of hypocalcaemia are caused by violations of membrane potential, which

causes neuromuscular irritability. Cramps of the back and leg muscles are more common.
Gradually developing hypocalcemia can cause mild encephalopathy to spread, should be
suspected in patients with unexplained dementia, depression or psychosis. Sometimes there is
optic nerve edema, with prolonged hypocalcemia developing cataracts. Severe hypocalcaemia
with plasma calcium levels less than 7 mg/dL (<1.75 mmol/L) can cause tetany, laryngospasm,
general seizures.

Aetania develops with severe hypocalcemia, but can develop as a result of a decrease in
the calcium fraction of ionized calcium in the absence of significant hypocalcemia, which is
observed in severe alkalosis. Theta is characterized by sensory symptoms, including paresthesia
of the lips, tongue, fingers, feet; carpopedic spasm, which can be long and painful; Common
muscle pain, facial muscle spasms. Tans can be expressed with spontaneous or latent symptoms,
requiring provocative tests to be identified. Latent flow is more often observed at plasma calcium
levels 7-8 mg/dL (1.75-2.20 mmol/L).

Symptoms of Khvostek and Tissaur are easily done in the patient's bed to detect latent
teten. The tail symptoms are involuntary contractions of facial muscles in response to light
hammer blows in the facial nerve area in front of the outer ear canal. Positive in <10% of healthy
people and in most patients with acute hypocalcaemia, but often negative for chronic
hypocalcaemia. The Trusso symptom is the detection of spastic seizures with a decrease in blood
flow in the hand with the help of a tourniquet or cuff tonometer which is applied to the forearm
for 3 minutes with pumped air above the blood pressure of 20 mmHg. Art. Trusso symptoms are
also observed in alkalosis, hypomagnesemia, hypokalemia, hyperkalemia and about 6% of
people without electrolyte balance disorders.

In patients with severe hypocalcaemia, arrhythmias or heart blockages are sometimes

observed. When hypocalcemia on the ECG is usually observed an extension of QT and ST
itervalov. There are also changes in repolarization in the form of sharp teeth.With chronic
hypocalcaemia, many other disorders can occur, such as dryness and flaking of the skin, brittle
nails, hard hair. With hypocalcaemia, candidiasis is sometimes observed, but more often in
idiopathic hypoparathyroidism patients. Long-term hypocalcaemia causes the development of
cataracts.

Diagnostic hypocalcemiaHypocalcaemia is diagnosed based on the determination of

plasma calcium levels totaling <8.8 mg / dL (<2.20 mmol / L). However, given the fact that low
levels of plasma protein can reduce total calcium but are not ionized, the level of ionized calcium
must be determined by the level of albumin. If a low level of ionized calcium is suspected, direct
measurement is needed, regardless of the normal total calcium-calcium level. In patients with
hypocalcemia, kidney function, serum fofat levels, magnesium, alkaline phosphatase must be
evaluated.

If the cause of hypocalcaemia is unclear (eg calcosis, kidney failure, massive blood
transfusion), further research is needed. Because hypocalcaemia is the main stimulus of PTH
secretion in hypocalcemia it must be increased. At low or normal PTH levels,
hypoparathyroidism can be assumed. Hypoparathyroidism is characterized by low plasma
calcium, high plasma phosphate levels and normal alkalli phosphatase. Hypokalism with high
plasma phosphate levels indicates kidney failure.

Type I Pseudo-hypoparathyroidism can be distinguished from the presence of

hypocalcaemia, regardless of the normal or high circulating PTH levels. Despite the high
circulating levels of PTH, cAMP and phosphate are not present in the urine. A provocative test
with an injection of parathyroid gland extract or recombinant human PTH does not cause an
increase in cAMP levels in plasma or urine. In patients with a type of hypoparathyroidism,
skeletal anomalies are often observed, including low growth, the first, fourth and fifth metacarpal
bone approaches. In patients with type IB, there are renal manifestations without skeletal anomal.

In type II pseudohipoparathyroidism, exogenous PTH raises the level of cAMP in the

urine, but does not cause phosphatization or increases in plasma plasma concentration. Before
the diagnosis of type II pseudohipoparathyroidism, vitamin D deficiency must be eliminated.

If osteomalacia or rickets on radiography, distinct changes in the skeleton are seen.

Plasma phosphate levels often decrease slightly, alkaline phosphatase levels increase, which
reflects increased calcium mobilization from bone. Determining the level of vitamin D in the
active and inactive form in plasma can help differentiate vitamin D deficiency from vitamin-
dependent conditions. Hypophosohatemic family rickets are identified by associated kidney
phosphate loss.

Treatment of hypocalcaemia

In tetany, 10 ml of 10% calcium gluconate solution is given intravenously. The answer

can be complete, but only lasts a few hours. Repeated infusions of 20-30 ml of 10% calcium
gluconate solution in 1 L of 5% dextrose solution or the addition of permanent infusion may be
needed in the next 12-24 hours. Harmful calcium infusion in patients receiving digoxin, and must
be treated slowly with constant ECG monitoring. If you are associated with hypomagnesemia, a
temporary response to calcium or potassium can occur, but complete recovery can only occur if
magnesium deficiency is compensated.

With transient hypoparathyroidism after partial thyroidectomy and parathyroidectomy,

oral administration of calcium may be sufficient. However, hypocalcemia can be very severe and
prolonged after subtotal parathyroidectomy in patients with chronic kidney failure or the last
stage of kidney disease. After surgery, long-term parenteral calcium administration may be
needed; For 5-10 days, it may be necessary to give 1 g of calcium per day. Increasing alkaline
phosphatase in such conditions can be evidence of rapid calcium uptake by bone tissue. The need
for large amounts of parenteral calcium is usually maintained until the level of alkaline
phosphatase decreases.

With chronic hypocalcaemia, calcium intake and sometimes vitamin D inside is usually
sufficient. Calcium can be taken in the form of calcium gluconate (90 g elemental calcium / 1 g)
or calcium carbonate (400 mg calcium element / 1 g) to give one to two grams of elemental
calcium per day. Although it is possible to use various forms of vitamin D, analogs of the active
form of vitamins have the best effects: 1 hydroxylation compound, as well as synthetic calcitriol
[1,25 (OH) 2D] and pseudohydroxylate analog (dihydrotachysterol). This drug has a more active
effect and is quickly eliminated from the body. Calcitriol is very useful in kidney failure, because
it does not require metabolic changes. In patients with hypoparathyroidism, the response usually
develops in doses of 0.5-2 μg / day orally. With pseudohipoparathyroidism, only calcium intake
can sometimes be used. The effect of calcitriol is achieved when consuming 1-3 μg / day.

Vitamin D intake is not effective without adequate calcium intake (1-2 grams of calcium
per day) and phosphate. Vitamin D toxicity with severe symptomatic hypercalcaemia can be a
serious complication of vitamin D analogue treatment. After stabilizing calcium levels, plasma
calcium concentrations must be monitored daily during the first month and then at 1-3 month
intervals. The treatment dose for calcitriol or dihydrotachysterol usually decreases over time.

In rickets caused by vitamin D deficiency, a dose of 400 IU per day of vitamin D (in the
form of vitamin D2 or D3) is usually used; in the presence of osteomalacia within 6-12 weeks, a
dose of 5000 IU per day of vitamin D is prescribed, and then drops to 400 IU per day. In the
early stages of treatment, an additional 2 g of calcium per day is expected. In patients with
rickets or osteomalacies caused by inadequate sun exposure, sun exposure or the use of
ultraviolet lights may be sufficient.

With type 1 rickets that contain vitamin D, calcitriol is 0.25-1.0 μg per day effective. In
patients with type II rickets who are dependent on vitamin D, the use of vitamin D for treatment
is ineffective [a more easily understood term is suggested - resistance to 1,25 (OH) 2D
derivatives]

Treated hypocalcaemia depends on the severity of bone tissue damage. In severe cases, it
is necessary to administer up to 6 μg / kg body weight or 30-60 µg / day calcitriol plus 3 g of
elemental calcium per day. When treating vitamin D, calcium levels in the plasma need to be
controlled; Hypercalcemia, which sometimes develops, usually reacts quickly to changes in the
dose of vitamin D.