Serum Calcium and Inorganic Phosphate in Pregnancy
It is an accepted biological principle that when ever the supply of nutrient is decreased or the endogenous requirement is increased, the body will respond with measures of improved utilization and decreased excretion. To order the Complete Project Material, Pay thr Sum of N3,000 to: BANK NAME: FIRST BANK PLC ACCOUNT NAME: CHIBUZOR TOCHI ONYEMENAM ACCOUNT NUMBER: 3066880122 Then send the Project Topic, Your Email Address and Full Name to 07033378184.
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The maternal contribution approximates 32gm or 2 percent of the total maternal calcium (Ardsley et al, 1956). The major portion of this calcium is assimilated by the fetus during the last trimester (Albright & Reifenstein, 1948). Many previous calcium balance studies may be criticized for their short duration or rapid alteration of levels of dietary calcium intake. Employing experimental diets in well controlled studies of male prisoners, it was noted that a period of 1 – 3 months was required before balance could be evaluated (Malm et al, 1958).
The finding of a negative or positive balance in an individual is merely evidence that the experimental diet is not the usual diet of that person. In short term dietary experiments, a positive balance is noted if the experimental diet provides more calcium than the subjects usual diet. Like wise, a negative balance is observed when the experimental diet contains less calcium (Hegsted et al, 1952; Nichola and Nimalasurga, 1939). Calcium excretion during pregnancy totals approximately 30g, mostly in the fetal skeleton and is deposited during the last trimester studies in several pieces of animals on magnesium deficient diets which have adequately demonstrated that the animal organism conserves magnesium only to a limited extent.
The concentration of inorganic phosphate in the plasma is increased, often to between 6 and 9 mg per 100ml. There is little increase until the glomerular filtration rate falls below 25ml per min (Goldman & Bassett, 1954). It is often assumed that there is reciprocal relationship between the plasma calcium and phosphate, and that the low calcium of renal failure is a result of the high inorganic phosphate; these assumption are wrong (Mitchell 1930, Stanbury and Lumb, 1966). The high concentration of inorganic phosphate in the blood favours the precipitation of calcium and probably accounts for the metastatic deposition of calcium (Herbert et al, 1941).
Following experimental procedures (Elamme & Jowsey, 1972), phosphate loading has been found to precipitate extra skeletal calcification, and clinical experience indicates that this is also true during uraemia (Delvez and Slatopolsky; 1992; Gimez et al, 1987). Hypercalaemia became a limiting factor for treatment with calcium containing phosphate binders (Argiles et al, 1995).
Intake and Absorption of Calcium and Phosphorus:
At any intake level, calcium balance is achieved by regulation of intestinal absorption and renal excretion. Both function as complimentary physiologic mechanism preventing systemic depletion during periods of increased requirement or diminished intake. Renal conservation of calcium is an active tabular process. Changes in excretion may be utilized as indexes, provided that the diet is not grossly deficient in calcium and vitamin D. There are the endogenous and exogenous sources of calcium present in the digestive secretions and in the intestinal epithelia cells shed into the digestive tract. About 400mg per day are derived from this source (Raphael et al, 1983).
The exogenous sources are the calcium derived from diets such as milk, cheese, butter and hard water etc. in adults, the daily intake is about 25 mmol/L (0.lg), with a wide variation, and calcium balance can be maintained on a minimum intake of about 10 mmol/L (0.4g) (Baron et al, 1989). Only about 250mg is absorbed and the remaining 750mg is excreted in faeces. Calcium absorption takes place in the upper small intestine, is promoted by vitamin D. Absorption across the small intestine is brought about by an energy – dependent and carrier mediated active transport and by a process of passive diffusion across the distal small intestine. The rate by which calcium is absorbed from the gut is controlled by some factors:
(a) Dietary Intake:
In hypocalaemia, there is a reduced intake of dietary calcium and as such, the rate of absorption increases. This potentiates stimulus for the release of parathyroid hormone (PTH), which in turn promotes formation of active vitamin D3 (1,25 dhydroxy- cholecaciferol) in the kidney.
Many a worker have reported that the amount of calcium absorbed varies inversely with the age of the individual (Raphael et al, 1983).
(c) Chelating Agent:
Insoluble complexes are formed from calcium with substances such as phosphates, citrates, phytic acids, Oxalic acids and fatty acids. Their complexes inhibit the absorption of calcium from the gut. Calcium absorption is not affected by small amount of phosphate.
(d) Bile and Bile Salt:
The presence of these substances cause increased calcium salts solubility and the absorption is facilitated (Micelles, 2005)
(e) Increased Metabolic Requirement:
Greater metabolic requirements of calcium increases the absorption. For instance, in late pregnancy, in growing children and during lactation, women absorb an extra 300mg/day and thus a normal diet containing dairy products usually will provide this without extra supplements (Raphael et al, 1983).
The daily normal intake of phosphorus (in all forms) in adults is 1.5–3.0g, while 1.0-1. 5g is the recommended minimum. Phosphorus is never deficient in any satisfactory diet. About two thirds of phosphorus is usually absorbed and this is more than that of calcium absorption; even in the phylate forms of phosphorus. This is because they are hydrolyzed during cooking or in digestion. Inorganic phosphate is absorbed as a phosphate ion. The mechanism of absorption involves both active and passive processes. Adequate amount of vitamin D are required for the absorption of normal amount, and both excess calcium and aluminum hydroxide (ALCOh3) reduce gastro intestinal absorption (Gray and Howorth, 1979).
Calcium and Phosphorus in Blood:
The normal rang of total calcium in serum is 8.9 – 10. 3mg/dl (2.2 – 2.6mmol/l) (Landenson et al, 1980). The serum calcium is regulated within a closely defined limits. Calcium exists in serum in 3 physicochemical states:
Protein bound (-45%); complex with small difusable Liquids such as lactate, citrate, phosphate and biocarbonate (-10%), and ionized (-45%). The concentration of total calcium in human phasm (or serum) is 2.5 mmol/L (10mg/dL), and that of the ionized is 1.125mm ol/L (4. 5mg/dL) under normal conditions. 80% of the protein bound fraction is bound to albumin, 20% to globulins. The ionized fraction (Ca++i) is the physiologically active form. This form is in dynamic equilibrium with other forms, it’s magnitude depending largely upon PH and the concentration of plasma proteins. Acidosis favours dissociation and raises the proportion existing as Cai, while alkalosis has an opposite effect (Tietz, 1986).
The normal range of serum inorganic phosphate in adult is 2.5 – 4. 8mg/dL (0.81-1.5 mmol/L). The level is 25 – 50% higher in growing children. Serum phosphate level varies with time of the day, diet (Nelson, 1964) and activity of the subject. The phosphorus content of the enythrocyte is high, and phosphate estimations should always be performed fasting (there is a daily variation of + 0.3 mmol/L because of meals), and on unhaemolysed phasma or serum, either freshly separated or preserved with fluride because erythrocyte organic phosphate are easily hydrolysed. About 85% extracellular phosphate occurs in inorganic form as hydroxyapatite. Phosphate in serum exist as both the monovalent and divalent phosphate anions. The ratio of H2P04:HPO4 varies from approximately one in acidosis to1: 4 at PH 7. 4 and 1: 9 in alkalosis. Approximately 10% of the phosphate in serum is protein bound; 35% is complex with sodium, calcium and magnesium; and the remainder, or 55% is free. Although both inorganic and organic are present in blood, only inorganic phosphate is measured.
The Excretion of Calcium and Phosphorus.
The excretion of calcium is very small during the night and it is maximal during the first part of the day (Chapal et al 1962, Carruthers et al, 1964, Louitit, 1965). Calcium excretion varies from person to person especially among children.
The calcium in the faces consist of both unabsorbed calcium and also of calcium which has passed from the plasma into the intestine. Of a daily intake of 25mmol(lg) of calcium, 2.5 mmol (0.1-0.3g) is excreted in the urine, normally almost all of the filtered calcium is reabsorbed. Calcium behaves as a threshold substance, and when the plasma calcium level falls below 1. 8mmol/L, its excretion in the urine ceases.
The phosphorus in the faces consist of both phosphorus from the diet, and also of phosphorus which has passed the plasma into intestine. About one – third of the intake of phosphorus is excreted in the faces and two third in the urine. There is a diurate rhythm of phosphate excretion. The kidney excretes what the gut absorbs, the rate being higher during the night (Kleiman, 1925, fourman, et al, 1952). Approximately 70 – 80% of the filtered phosphate is actively reabsorbed in the proximal tubules and in the distal tubules.
The Physiological Functions of Calcium and Phosphorus
The physiological state of pregnancy is associated with significant placental transfer of calcium (Ca) and phosphorus (P) and necessary for mineralization of the fetal skeleton. This increased demand on maternal body stores of these mineral was first proposed Albright and Reinfenstein, 1948 as a cause of maternal hyperparathyroidism. This hypothesis was confirmed subsequently by direct measurement of parathyroid hormone (PTH) by lequim, et al, 1970 who found elevated parathyroid hormone concentration in 7 of 10 women in labour. cusjard, et al, 1972; evaluated PTH secretion in greater detail in pregnancy and observed a significant rise in PTH during the third trimester. However, in the later study, no correlation between total serum calcium and PTH was observed. Further more, the free calcium ion (Ca++) which is the primary determinant of parathyroid hormone secretion was not determined.
Phosphate has several divers actions in cells. It has a critical role, a high energy phosphate bound in adenosine triphosphate (ATP) and other high energy compounds. These energy sources maintain physiological functions such as muscle contractility, neurological function and electrolyte transport phosphate is a constituent of cyclic adenine and guanine nucleotides as well as nicotinamide adenine dineucleotide phosphate (NADP), which are important in many enzymes systems. Phosphate is also an essential element in phospholipids cell membranes, nucleic acids, and phosphoproteins. Intracellular phosphate is therefore involved in the regulation of intermediary metabolism of proteins, fats and carbohydrate, as well as in gene transcription and cell growth. Phosphate is critical for important enzyme systems: adenylate cyclase and 1,2,5–hydroxyvitamine –D- hydroxylase. This is intracellular.
Extracellular phosphate maintains the critical intracellular concentration and provides substrate for bone mineralization. An actual decline in the serum phosphate concentration may result in rapid complication such as rhabdomyolysis and altered red blood cell function. Inorganic phosphate is a major component of hydroxyapatite, thereby playing an important part in structural support of the body. The cellular demands for metabolic function in bone cells are similar to those in other cells. The skeleton also serves as a store house for phosphate.
Calcium ions are essential for the conversion of prothrombin to thrombin. Calcium ion act at the plasma membrane, affecting neuromuscular conduction, within cells, their functions are manifold. Calcium is the prime inorganic messenger for regulation of cell functions. The largest part of the calcium in the body is concerned with the metabolism of bone.
Factors Altering Normal Calcium and Phosphorus Metabolism:
The serum calcium and phosphate metabolism can be altered by a variety of factors and such factors may predispose to either hypocalaemia or hypercalaemia or by hyperphosphataemia in the phosphorus metabolism.
A low ionized calcium activity causes hyper – excitability of the nervous system, which may present clinically as convulsions, and tingling and numbness leading to tetany. Tetany is likely to appear if the (Ca++) falls below 4.3mg/100ml of plasma water (Fanconi – & Rose, 1958). Other effects of long standing hypocalaemia are cataracts, calcification of the basal ganglion, a long coagulation time and mental depression.
The association of hypoproteinaemia with hypocalaemia in a normal ionized calcium concentration and ionized calcium activity could be as a result of the following:
(a) Anticovulsant therapy, hypomanganesaemia and acute pancreatitis.
(b) Deficient dietary intake related to physiological need.
(c) High level of loss: through the intestine (usually associated with b above).
(d) Through the kidneys tubular disorders.
(e) Deficient intestinal absorption: Vitamin D deficiency, the malabsorption syndrom, phytate excess or improper high phosphate infant feeding.
Deficiency in ionized calcium may be due to:
(a) Binding of calcium to other ions especially intravenous
EDTA or citrate. Massive blood transfusion such as in cardiac surgery or liver transport may result in citrate toxicity.
Extreme thirst, gastrointestinal symptoms, giddiness and muscular weakness result from an increased ionized calcium activity. Hypercalaemia leads to hypercalciuria and often to renal damage and then to renal calculi especially when there is also hyperphosphataemia. Increased total and ionized calcium may be due to:
(a) Decreased renal excretion: from thiazide diuretics
(b) High intestinal absorption: hyper – vitaminosis D and the mil – alkali syndrome.
(d) Hyperparathyroidism, (thyrotoxicosis and immobilization.
Hypercalaemia does not result from increased or excessive dietary intake alone.
This is a state of deficiency in the phosphate levels of the body and a direct effect on bone causes osteomalasia and also rickets. This condition cause cardiac and skeletal muscular weakness, depletion of ATP, and central and peripheral neurological disorders.
Deficient plasma (or serum) phosphate concentration may result from:
a. Low intestinal absorption such from phosphate binding agents as aluminium hydroxide. High ionic level: In severe diarrhea; through the intestines, in hyperparathyroidism, through renal tubules or in specific disease with failure of reabsorption. C. Low intake: from imperfect intravenous fluid replacement or in general malabsorption.
Higher plasma phosphate concentrations are found in children than in adults which are normal. Hyperphosphataemia effects bone through alteration of calcium distribution and it has no direct metabolic effect. Hyperphosphataemia may result from:
(a) High intestinal absorption; in hyper – vitaminosis D.
(b) Excessive intake: from enemas or from dietary Laxatives.
(c). Low renal excretion; in glomerular failure or in hypoparatharoidism.
(d). Redistribution from cells to ECF: from somatic cell breakdown; for instance, chemotheraphy of lymphoma.
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This article was extracted from a Project Research Work/Material Topic “SERUM CALCIUM AND INORGANIC PHOSPHATE IN PREGNANCY”
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