GYHOJ

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ALTERATIONS OF
CALCIUM
METABOLISM
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018
ALTERATIONS OF CALCIUM METABOLISM

2. HYPERCALCEMIA
Definition.- The serum concentration of total calcium in the normal limits of 8.5
to 10.5 mg / dL. In patients with higher figures, pseudohypercalcemia should first
be ruled out, in which the elevations of total serum calcium are due to an increase
in the concentration of calcium transport proteins (albumin or a paraprotein).
Etiology.- The most important sources of calcium intake are the intestine and
bone, and it is useful to classify hypercalcemias according to these two origins.
More than 90% of cases of hypercalcemia are due to neoplasms or primary
hyperparathyroidism
a) Hypercalcemia due to increased bone resorption: It occurs in primary
hyperparathyroidism where 80% -85% of cases are due to a single
adenoma of the parathyroids, in 15% to diffuse hyperplasia and in 1% -3
% of patients with parathyroid carcinoma, likewise in secondary
hyperparathyroidism that appears in chronic renal failure. In the most
severe cases, a nodular hyperplasia of the parathyroid glands develops,
with monoclonality; that usually produces hypercalcemia and finally is
observed in the hypercalcemia associated with neoplasms. 10% -20% of
patients with neoplasia develop hypercalcemia, usually in the late stages of
the disease, and the diagnosis is usually evident. The neoplasms that most
commonly produce hypercalcemia are breast cancer, lung cancer and
multiple myeloma. In the context of a neoplasia, hypercalcemia can occur
by three distinct mechanisms: osteolytic metastases with local release of
cytokines such as IL-1, and TNF-a, release into the circulation by the
tumor of the PTH-related protein (PTHrP) , and production of calcitriol by
the tumor. Hypercalcemia is the most common cause of non-metastatic
solid tumors, malignant humoral hypercalcemia, caused by the release of
PTHrP.
b) Hypercalcemia due to increased intestinal calcium absorption:
association with lower renal calcium excretion, vitamin D poisoning,
sarcoidosis and other granulomatosis.

3. Clinical Table.- Anorexia and constipation are usually the first digestive
manifestations, followed by nausea and vomiting. In hypercalcemic individuals,
and particularly in primary hyperparathyroidism, there is an increased incidence
of peptic ulcer and pancreatitis, may be associated with high blood pressure with
high plasma renin. The shortening of the QT interval is the most characteristic
electrocardiographic sign of hypercalcemia. Serious cases add drowsiness,
confusion and coma.
Treatment.- They are dehydrated as a consequence of a decrease in urinary
concentration capacity and losses of another origin (vomiting and others).
This conditions a decrease in the filtrate that decreases the excretion of calcium,
with which the hypercalcemia is perpetuated. Therefore, the expansion of
extracellular volume through the infusion of isotonic saline should be the first step
in the treatment of hypercalcemia. It usually begins with 200-500 mL / h if the
cardiac reserve of the patient allows it, to maintain a diuresis of 100-150 mL / h.
The use of loop diuretics (furosemide 20-40 mg / 4-6 h) produces an increase in
the renal excretion of sodium and calcium; thiazides should not be used, since
they increase distal calcium reabsorption.
General measures such as withdrawing calcium and drugs that elevate calcemia,
maintain good oral hydration, promote mobility, and avoid the use of sedatives
and analgesics that worsen mental confusion, are mandatory.
HYPOCALCEMIA
It is defined as a decrease in calcium concentrations below 8.5 mg / dl (2.1 mmol /
L) in the absence of hypoalbuminemia. Whenever they persist, the determination
of ionic calcium concentrations should be used; a figure lower than 4.2 mg / dL
(1.05 mmol / L) indicates hypocalcemia.
Etiology.- It can be by:
a) Calcium exit from the blood compartment or intravascular ligament:
In hyperphosphatemia, phosphocalcic complexes are formed and deposited
in soft tissues, leading to hypocalcemia. The most common clinical

4. situations are renal failure, administration of phosphate (i.v. or enemas),
rhabdomyolysis and tumor lysis syndrome, it also appears during the acute
phase of pancreatitis although it has not yet been fully clarified.
Exceptionally, osteoblastic metastases, hungry bone syndrome and
administration of calcium chelators (EDTA, citrates, lactate, foscarnet).
b) Decrease in the flow of calcium from the intestine or bone to the
plasma: It may be due to hypoparathyroidism after surgery of the
parathyroid or neck and by irradiation or infiltration of the parathyroids.
Idiopathic hypoparathyroidism can occur in the context of a familial
autoimmune poly glandular syndrome type 1. Also in severe
hypomagnesemia and marked hypermagnesemia, in sepsis, large burns, in
pseudohypoparathyroidism and patients with primary or tertiary
hyperparathyroidism treated with calcimetics also they can develop
hypocalcemia; or another cause may be for hypovitaminosis D.
Vitamin D deficiency causes hypocalcemia and secondary hyperpathoidism,
through a decrease in intestinal calcium absorption, insufficient insolation in the
context of a deficit diet, malabsorptive syndromes, surgical intervention of the
upper digestive tract, hepatobiliary disease, renal failure and consumption of
anticonvulsants (difelhydantoin and barbiturates).
Clinical picture: Tetany is observed, produced by an increase in neuromuscular
irritability. It begins with circumoral and acrosal paresthesias to continue with
muscular spasms that end with carpedal spasm, Chevostek sign and Trosseau sign.
Acute intense hypocalcemia when it can cause seizures, papilledema, mental
retardation and dementia. A variety of extrapyramidal disorders, ectodermal
alterations, cataracts and lengthening of the QT interval on the ECG can occur.
Diagnosis: Once the presence of true hypocalcemia is established, the clinical
history itself will determine its cause in most cases. The determination of
creatinine, phosphorus and hypomagnesemia concentrations all cause
hypocalcemia. When in this context the diagnosis is not reached, it is necessary to
resort to the determination of PTH concentrations and the percentage of tubular
reabsorption of phosphorus (% RTP).

5. Treatment: In acute hypocalcemia, symptomatic or with calcemia figures lower
than 7 mg / dl, calcium will be administered i.v. If the situation is emergency,
initially use 10 ampoules of 10 mL of 10% calcium gluconate diluted in 100-250
mL of glucose solution at 5% for a period of at least 10-15 min and if the situation
does not is emergency, is infused 1-2 m / kg of weight and hour of calcium
element. If there is hyperphosphoremia, the calcium calcium oral calcium intake
of choice is calcium carbonate. When a hypoglycemia is suspected, a blood
sample should be taken for confirmation, and magnesium sulfate infused until the
results are available. In chronic hypocalcemia, an attempt should be made to
elevate calcemia to concentrations that are in the limit under normal conditions to
prevent an increase in the filtered calcium load that only produces hypercalciuria,
and in the long term, nephrolithiasis and nephrocalcinosis. The treatment is based
on the supply of calcium supplements orally and vitamin D. Calcium will be
administered in the form of lactate, gluconate or calcium carbonate, at a dose of 1-
2 g. of calcium element per day.
BIBLIOGRAPHIC REFERENCE:
A, Torres Ramírez "Alterations of calcium, phosphorus and magnesium
metabolism" In: Farreras Valenti - C. Rozman. Internal Medicine XVIII. Elsevier
Edition Spain (Barcelona) 2012 p. 787-796