Minerals

1
Minerals and its Metabolism
By
Akanksha Dubey

Introduction
• Minerals are inorganic elements required for
variety of functions.
• As per the human requirements minerals can be
grouped as Macrominerals (per day req. more
than 100 mg) and Microminerals (per day req.
less than 100 mg) and Microminerals)

Introduction
 Calcium is the most abundant mineral in the body.
 Adult human contain around 1 kg of calcium 99 % of which is
present in bone along with phosphorus as Hydroxyapatite and
remaining is present in soft tissues and ECF.

Important function of Calcium: Calcium(Ca) is required for the
following functions :
 Muscle contraction: Muscle contraction is initiated by binding
of calcium to Troponin.
 Nerve conduction: Influx of Calcium from ECF to neurons
causes release of Neurotransmitters.
 Hormone release: Release of certain hormones s/a parathyroid
hormone and calcitonin req. calcium ions.

• Blood coagulation: For conversion of inactive protein
prothrombin to active thrombin req. calcium which is Blood
Clotting Factor IV
• Regulation of Enzyme activity: Activation of several
enzymes require Ca as a cofactor s/a Glycogen Phosphorylase
and Salivary/Pancreatic Amylase.
• Second Messengers: It act as a Second Messenger for
Hormone Action s/a Epinephrine, Glucagon and Third
messenger for ADH

• Formation of Bones and Teeth: 99 % of calcium of body is
present in bones and teeth Hydroxyapatite crystals. The
hardness and rigidity of bones is due to Hydroxyapatite.

Sources of calcium
• Widely distributed in food substances such as
 Milk (Half litre of milk contains 1000
mg of calcium )
 Cheese
 Egg- yolk
 Fish
 Beans Lentils Nuts and Cabbage

Recommended Dietary Allowance
Per day req. of calcium:
 Adults: 800 mg/day
 Women's during pregnancy and Lactation and Teenagers:
1200 mg/day
 Infants: 300-350 mg/day

Calcium Absorption
The absorption of calcium occurs in intestine and depends on
several factors.
Factors favouring calcium absorption:
 An acidic pH: Calcium salts are more soluble in acidic pH , the
acidic foods and Organic acids s/a Citric Acid , lactic acid and
pyruvic acid promote calcium absorption.
 High protein diet- Lysine and Arginine cause maximal
absorption

 Vitamin D: stimulates calcium absorption by inducing
synthesis of Calcium binding protein.
 Ca : P ratio- A ratio of dietary Ca: P not more than 2:1 is
adequate for optimal absorption, ratio of less than 1:2 reduces
absorption
 State of health and intact mucosa- A healthy adult absorbs
about 40% of dietary calcium.
 PTH (Parathormone) stimulates the activation of vitamin
D, thus indirectly increases absorption of vitamin D

Factors inhibiting absorption of calcium
 Alkaline pH
 High fat diet- High amount of Fatty acids form calcium
soaps that can not be absorbed
 Presence of Phytates and oxalates- Insoluble calcium salts
are formed which can not be absorbed
 Dietary fiber in excess inhibits absorption
 Excess phosphates form Insoluble Calcium-Phosphate.

 Calcitonin reduces calcium absorption indirectly by
inhibiting the activation of vitamin D
 Advancing age and intestinal inflammatory disorders
inhibit absorption of calcium
Excretion
The excretion of Calcium occurs partially through kidney
and mostly by the way of Intestine through Feces

Distribution of Body calcium
 Of the total amount, 50% is free ionized calcium, 10% is
combined with various anions (including bicarbonate,
citrate, phosphate, lactate and sulphate) and the remaining
40% is bound to serum proteins mainly albumin.
 Free ionized calcium is the physiologically
important component of the total calcium.
 In plasma, the ionized calcium concentration is
normally maintained within a tight range (1.0-
1.25mmol/l).

• The plasma Calcium concentration of Normal Individual is
9-11 mg/dl
Regulation of calcium homeostasis
Three principal hormones are involved in calcium homeostasis
• Vitamin D
• Parathormone and
• Calcitonin

Which act on three target organs:
• Intestine,
• Bone and
• Kidneys

The four major processes are:
 Absorption of calcium from Intestine through Vitamin D
 Reabsorption of Calcium from Kidney through Vitamin D
and PTH
 Demineralization of Bones mainly through the action of
PTH and supported by Vitamin D
 Mineralization of bone through Calcitonin.

Role of vitamin D in calcium
homeostasis
The actions of Vitamin D(Calcitriol) are as follows:
The main role of Vitamin D is to increase Serum Calcium by
following Mechanism:
 Enhances calcium absorption from the intestine
 Facilitates calcium re-absorption from the kidney
 Mobilizes calcium and phosphate from
Bones(Demineralization)

Role of Parathyroid hormone (PTH)
• Parathyroid hormone is releases in response to Low Blood
calcium level which is a linear polypeptide containing 84
amino acid residues.
• It is secreted by the chief cells in the four parathyroid
glands.
• It mainly acts on two main Target organs i.e. Bones and
Kidney and indirectly on Intestine by activation of
Vitamin D.

Action on Bones: PTH stimulates bone
demineralization by moving calcium and phosphates
from bones to plasma.
Hence increases Osteoclastic activity.
It also decreases uptake of Calcium and Phosphates from
bones.

Action on Kidney: PTH stimulates renal reabsorption
and decreases excretion of calcium to maintain blood calcium
level. It also increases excretion of Phosphates.
Action on Intestine: action of PTH on Intestine is
indirect via Vitamin D

Role of Calcitonin
 Calcitonin is a 32 amino acid polypeptide secreted by the
parafollicular cells in the thyroid gland .
 It tends to decrease serum calcium concentration and, in
general, has effects opposite to those of PTH.

The actions of calcitonin are as follows:
 Inhibits bone resorption
 Increases renal calcium excretion
The exact physiological role of calcitonin in calcium
homeostasis is uncertain.
The effects of calcitonin on bone metabolism are much
weaker than those of either PTH or vitamin D.

Hypocalcaemia
Hypocalcemia is Total Serum Ca concentration < 8.8 mg/dL (<
2.20 mmol/L) or a serum ionized Ca concentration < 4.7 mg/dL (<
1.17 mmol/L).
 Causes Include: Hypoparathyroidism(Surgical Removal of
Gland or d/t Mg Deficiency), Vitamin D deficiency(Dietary
Insufficiency, Malabsorption or low exposure to sunlight), and
Renal disease(Failure to synthesize Calcitriol)

 Acute hypocalcaemia can also occur in the immediate
post-operative period, following removal of the thyroid or
parathyroid glands.
 Hypocalcaemia can occur following rapid administration of
citrated blood or large volumes of albumin.
 Drugs including anticonvulsants (e.g., phenytoin ,
phenobarbital and rifampcin which alter vitamin D
metabolism)

Clinical manifestations of Hypocalcaemia
 Hypocalcemia is frequently asymptomatic. Major clinical
manifestations of hypocalcemia are due to disturbances in
cellular membrane potential, resulting in neuromuscular
irritability.
 Clinical signs include: tetany, carpopedal spasm and
Sensory symptoms consisting of paresthesias of the lips,
tongue, fingers, and feet
 Generalized muscle aching and spasm of facial
musculature are also there

Clinical manifestations of Hypocalcaemia
• Hypocalcaemia may lead to Cardiac Dysrhythmias
• Decreased cardiac contractility
• Neuromascular Irritibality
• Neurological features s/a Tingling, Tetany Numbness(Finger and
Toes)
• Mascular Cramps
• Chronic hypocalcemia, such as dry and scaly skin, brittle
nails, and coarse hair.

Diagnosis of Hypocalcaemia
 Estimation of ionized Ca
 Biochemical Analysis of Phosphorus Vitamin D and Magnesium
 Electrocardiographic changes

Treatment of Hypocalcaemia
• IV Ca Gluconate for tetany
• Oral Ca for postoperative hypoparathyroidism
• Oral Ca and vitamin D
• In patients without renal failure, vitamin D is
given as a standard oral supplement (e.g.,
Cholecalciferol 800 IU once/day).

Hypercalcaemia
Hypercalcemia is total serum Ca concentration > 10.4 mg/dL
(> 2.60 mmol/L) or ionized serum Ca > 5.2 mg/dL (> 1.30
mmol/L).
Principal Causes of Hypercalcemia:
Hypercalcemia usually results from excessive bone
resorption. There are many causes of hypercalcemia
 Any Malignancy related to Bones
 Hyperparathyroidism

Clinical manifestations of Hypercalcaemia
In mild hypercalcemia, many patients are asymptomatic.Clinical
manifestations of hypercalcemia include
 GI problems s/a constipation, anorexia, nausea and vomiting,
abdominal pain
 Renal features s/a polyuria, nocturia, and polydipsia.
 Muscle Weakness
 Neurological Symptoms s/a Depression confusion and lack of
concentration

 Elevation of serum Ca > 12 mg/dL (> 3.00 mmol/L) can
cause emotional lability, confusion, delirium, psychosis, and
coma.
 Hypercalciuria with nephrolithiasis is common(Renal Calculi)
 Hypercalcemia > 18 mg/dL (> 4.50 mmol/L) may cause shock,
renal failure, and death.

Diagnosis of Hypercalcaemia
 Total serum Ca concentration
 ionized Ca, PO4, alkaline phosphatase
 Measurement of PTH

Treatment of Hypercalcaemia
There are 4 main strategies for lowering serum Ca:
 Decrease intestinal Ca absorption
 Increase urinary Ca excretion
 Decrease bone resorption
 Remove excess Ca through dialysis

 Ca is required for the proper functioning of muscle
contraction, nerve conduction, hormone release, blood
coagulation and for various other metabolic processes.
 Maintenance of body Ca stores depends on Dietary
Ca intake
 The regulation of both Ca and PO4balance is greatly
influenced by concentrations of circulating PTH, vitamin D,
and, to a lesser extent, Calcitonin.

 Hypocalcemia is total serum Ca concentration < 8.8 mg/dL (<
2.20 mmol/L) or a serum ionized Ca concentration < 4.7 mg/dL
(< 1.17 mmol/L).
 Causes include hypoparathyroidism, vitamin D
deficiency, and renal disease.
 Manifestations include paresthesias, tetany, and, when severe,
seizures and heart failure.
 Diagnosis involves measurement of serum Ca
 Treatment is administration of Ca, sometimes with
vitamin D.

• Hypercalcemia is total serum Ca concentration > 10.4 mg/dL
(> 2.60 mmol/L) or ionized serum Ca > 5.2 mg/dL (> 1.30
mmol/L).
 Principal causes include hyperparathyroidism, vitamin D
toxicity, and cancer.
 Clinical features include polyuria, constipation, muscle
weakness, confusion, and coma.
 Diagnosis is by serum ionized Ca and parathyroid
hormone concentrations.

 Phosphorous isa widely distributed in thebody
 Thehuman body contains about 1kg of phosphorous out of which
about 80%of phosphorous isfound in bones &teeth in combination
with calcium
 About 10 % of phosphorous ispresent in Muscles and Blood
Circulation in the form of component of phospholipids,
phosphoproteins, nucleic acids & nucleoproteins.
 Remaining 10 % is occurs as a Chemical Compounds.

Requirement and Sources
 Thefood rich in calciumarealso rich in phosphorous, i.e. milk,
cheese,beans, eggs, cereals, fish and meat
 Milk isgood source of phosphorous, which contains about100
mg/dl of phosphorous
 Thedaily requirement of phosphorous isabout 800mg/day
 During pregnancy and lactation 1200mg/day is required

Biochemical Function of Phosphorus
 Phosphorous isessential for formation of bones &teeth.
Inorganic phosphate isconstituent of hydroxyapatite in bone
 It provides structural support
 The formation and utilization of high energy
phosphate compounds like ATP, ADP, GTP, Creatine
phosphate, etc. contains phosphorous
 Essentialfor the formation of phospholipids, phosphoproteins,
nucleicacids,nucleotides (NAD, NADP, cAMP, c-GMP)

 Phosphate present in nucleotides, some of which function as
coenzymes, PLP,TPP,NADP and flavincoenzymes
 Several enzymes and proteins are activated by
phosphorylation (Phosphorylation & Dephosphorylation)
 Mixture of HPO4
-- and H2PO4
-constitutes the phosphate
buffer which plays a role in maintaining the pH of body
fluid
 Formation of phosphate esters, suchasglucose-6-phosphatase

Absorptionand regulation
About 90%of dietary phosphorous isabsorbed
 Phosphorous isabsorbed from small intestine
 Theabsorption isstimulated by both PTHandcalcitriol
 TheCa:Pratio in diet affects the absorption &excretion of
phosphorous
 Regulation of Ca &Pisunder the similar control mechanisms
by kidney with respect to PTHandcalcitriol

 PTHincreases calcium &phosphate release from the bone
& decreases lossof calcium&increases lossof phosphate in
urine
Excretion
 500mg of phosphate isexcreted through urine per day
 Phosphate excretion isinfluenced by many factors
including musclemass,renal function &age
 Phosphates are mainly excreted by kidneys as NaH2PO4
through the urine

 About 90%of the phosphate filtered at the
glomeruli is reabsorbed by the tubules
 PTHdecreases the reabsorption of phosphorous from the
proximal as well as distal convoluted tubules &cause increased
excretion of phosphorous in urine
 Only small amounts are excreted infaeces

Normal Range
 Plasma phosphorous is3 - 4mg/dl inadults
 In children’s it isabout 5.0mg/dl - 6.0mg/dl

Hypophosphataemia
• Serum inorganic phosphate concentration < 2.5mg/dl iscalled as
Hypophosphataemia
• Commonly seen in conditionslike:
 Hyperparathyroidism: High PTHincreases phosphate excretion by the
kidney &this leads to low serum concentration of phosphate
 In the treatment of Diabetes the effect of insulin in causing the
shift of glucose into cellsalso enhances the transport of phosphate
into cells,which may result into hypophosphataemia

 Renal rickets isassociateswith low phosphate &increased ALP
concentration
 Congenital defect of tubular phosphate reabsorption.
Symptoms
 Cellular function is impaired
 Muscle pain, weakness with respiratory failure and
decreased myocardial output
 Ricketsin children’s &Osteomalacia in adults may develop

Hyperphosphataemia
Increase in serum inorganic phosphate levels than the normal
levels iscalled as hyerphosphataemia
• Seen in conditionslike:
Renalfailure: In renal failure, excretion of phosphorous is
impaired, leads to increased serum phosphate levels
Hypoparathyroidism: Low PTHdecreases phosphate excretion
by the kidney and leads to high serum concentration

Symptoms:
 Increased serum phosphate levels causesdecrease in serum
calciumconcentration; therefore tetany & seizures may be the
presenting symptoms

• Questions:
A 10 year old boy appears with Muscle
pain, stiffness cramps and spasm in both
hands and feet. He was a strict vegetarian
and did not even consume milk and milk
products. On examination no signs of
rickets were found and he had positive
Trosseau’s and Chcostek’s sign. Serum
calcium level were as low as 4 mg/dl. How
will you investigate the case and what is
your probable diagnosis?
Overuse of Anta-acids leads to hypo-
phosphatemia why??

 Sodium is the principal cation of ECF. Total body content of
sodium is about 70 gm. About 50 % of which occurs in bones
and 40% in ECF and remaining 10 % in soft organs.
 Dietary sources: common salt (Nacl) used in cooking medium
is the major source of sodium. Whole grains, nuts, eggs, leafy
vegetables, milk and bread are good source of Na
 Absorption: sodium is readily absorbed from GIT and very
little is excreted.

 RDA: mostly sodium is ingested as common salt. The RDA for
sodium is 5-10 gm/day. This should be low in cases of persons
with family history of hypertension (5 gm/day) and 1 gm/day is
recommended for patients of HTN
 10 gm of NACL contain 4 gm of Na

 Sodium in ECF: the normal concentration of sodium in
plasma/serum is 135-145 mEq/L.
 Sodium metabolism is largely monitored by Aldosterone
 Excretion: kidney is the major route for the excretion of sodium
from the body. Sweating also causes considerable amount of
sodium loss from the body.

• Biochemical Functions:
 Sodium regulate Acid-base balance of body along with chloride
and bicarbonate. It is involved in forming bicarbonate buffer
system and phosphate buffer system.
 Plays important role in maintaining osmotic pressure and fluid
balance
 Sodium is important for muscle excitability and necessary for
initiating and maintenance of heart beat.
 Important role in cellular permeability

 Absorption of glucose galactose and amino acids are done by
sodium
 Major inorganic component of saliva, gastric juice, pancreatic
and intestinal juices
 Na-K pump maintains electrical neutrality
 Involved in formation of bile salts

Clinical Importance:
Hyponatremia: low sodium than normal range is k/a hyponatremia.
The major causes are:
• Vomiting and Diarrhoea
• Burns
• Addison’s disease
• Renal tubular acidosis
• Severe sweating
Symptoms include: muscle cramps, headache, nausea,
• Chronic hyponatremia leads to low BP and cardiac failure

Hypernatremia: this condition is marked by elevation in plasma
sodium level. Less common than hyponatremia and occurs in
low body water content.
The major causes are:
• Cushing syndrome
• Prolonged cortisol therapy
• Pregnancy(steroid hormones causes sodium retention)
• Dehydration
Symptoms include : increase in blood volume and blood pressure

 Potassium is the major intracellular cation.
 Total body potassium is about 3500 mEq (150 grams) out of
which 75 % is in skeletal muscle and remaining 25 % is
distributed in all over body.
 Sources: Banana, orange, pine-apple, potato, beans, meat, are
good sources of Potassium. Coconut water is best source of
potassium.
 RDA: 3-4 gm/day.

 Absorption : Potassium is readily absorbed by passive diffusion
from gastrointestinal tract. Almost 90 % of potassium is absorbed
and very little is lost.
 The amount of potassium in the body depends on the balance
between potassium intake and output.

Excretion
 Potassium output occurs through three primary routes, the
gastrointestinal tract, the skin and the urine.
 Under the normal conditions loss of potassium through
gastrointestinal tract and skin is very small.
 The major means of potassium excretion is by the kidney
through Urine.
 Aldosterone increases excretion of potassium.

Biochemical Functions:
Many functions of potassium and sodium are carried out in
coordination with each other and are common.
1. Potassium influences the muscular activity.
2. Involved in acid-base balance and water balance in cells.
3. It has an important role in cardiac function.
4. Certain enzymes such as pyruvate kinase require K+ as cofactor.
5. Involved in neuromuscular irritability and nerve conduction
process.
6. Potassium is required for proper biosynthesis of proteins by
ribosomes.

7. Potassium maintains osmotic pressure: movement of water
across the biological membrane is dependent on osmotic
pressure differences between ICF and ECF . In healthy state
the osmotic pressure of ECF (mainly due to sodium) is equal to
osmotic pressure of ICF(due to potassium)

 Normal Serum/Plasma Potassium concentration is 3.5 to 5.0
mEq/L.
Clinical Importance
Hypokalemia:
 Plasma potassium level below 3 mEq/L is considered as
Hypokalemia
 It is clinical condition associated with low plasma potassium
concentration than the normal level. Low serum K results from
depletion of total body K. Nearly all food contains K in sufficient
amount hence dietary deficiency is uncommon.

Common causes of K loss are mentioned below:
 Gastrointestinal losses: both prolonged vomiting and severe
diarrhoea
 Excessive loss of Fluids
 Habitual users of Laxatives eventually develop potassium loss
 Loss in Urine: many diuretics leads to potassium depletion along
with sodium loss.
 Conn’s Tumour also causes loss of K in urine

 Cushing syndrome also leads to hypokalemia
 Loss of Extracellular potassium into Intracellular spaces: in
Diabetic Ketoacidosis and Alkalosis(Redistribution of potassium
occurs in exchange of Hydrogen ions)
 In renal tubular acidosis low serum potassium is seen.

Symptoms of Hypokalemia: The symptoms includes
 anorexia,
 nausea,
 vomiting,
 muscle cramps, or tender ness,
 electrocardiographic changes,
 polyuria, polydipsia, lethargy and confusion

Hyperkalaemia: Plasma level above 5.5 mEq/L is considered as
hyperkalaemia.
 The mechanism of excretion of potassium is so effective in normal
person that it is difficult to produce Hyperkalaemia by just high
oral intake. In clinical practice hyperkalaemia may be d/t Kidney
failure with decreased excretion or Sudden release of potassium
from ICF
 Anuria: complete shut down of kidney function(Renal Failure)

 Tissue Damage: Sudden Trauma/Muscle Injury /Massive
haemolysis leads to movement of potassium into ECF
 Vigorous muscle exercise leads to temporary hyperkalaemia due
to movement of potassium into ECF.
 Addison’s Disease: In absence of Aldosterone exchange of
Sodium and Potassium is disturbed hence Increased excretion of
sodium occurs and retention of potassium occurs.

 Diabetes Mellitus: in ketoacidosis there is substantial loss of
Intracellular K in ECF. This is due to overactivity of Na-K
ATPase which is d/t impairment in Glucose metabolism. If
ketoacidosis persist for long time then major depletion of body K
occurs.
 Symptoms: in hyperkalaemia there is increased membrane
excitability occurs which leads to ventricular arrhythmia and
ventricular fibrillation, bradycardia and may lead to cardiac
arrest.

 Pseudohyperkalemia: it is seen in haemolysis, thrombocytosis,
leucocytosis, and polycythaemias. In these cases while sample
collection potassium leaks into plasma which give false result of
potassium level increased.

Chloride
Chlorine is a constituent of sodium chloride hence metabolism of
sodium and chlorine are closely related.
RDA: 5-10 g/day
Sources: common salt, leafy vegetables, eggs and milk.
Absorption: chloride is totally absorbed from GIT
Plasma chloride: 95-105 mEq/L
CSF Chloride: 125 mEq/L
Renal threshold for chloride is 110 mEq/L

Biochemical Functions:
Chloride is involved in regulation of acid base equilibrium, fluid
balance and osmotic pressure. These functions are carried out by
interaction of chloride with Na and K
Chloride is necessary for the formation of HCL in gastric juice.
Chloride shift involves participation of chloride.
The enzyme salivary amylase is activated by Chloride

Hypochloremia: Reduction in serum chloride occurs may be d/t
Vomiting removes hydrochloric acid from the stomach. Frequent
vomiting can cause a chloride deficiency.
Addison’s disease
Excessive sweating
Hyperchloremia: Increased concentration of chloride is may be d/t
Dehydration,
Respiratory Acidosis And
Cushing’s Syndrome

MAGNESIUM (Mg++)
 Magnesium is the fourth most abundant cation in the body and
second most prevalent intracellular cation.
 Magnesium is mainly seen in intracellular fluid. Total body
magnesium is about 25 g, 60% of which is complexed with
calcium in bone.
 One-third of skeletal magnesium is exchangeable with serum.
Magnesium orally produces diarrhea; but intravenously it
produces CNS depression.

Requirement:
 The requirement is about 400 mg/day for men and 300 mg/day
for women.
 Doses above 600 mg may cause diarrhea.
Major sources are cereals, beans, leafy vegetables and fish.
 Normal Serum Level of Magnesium Normal serum level Mg++ is
1.8-2.2 mg/dl. Inside the RBC, the magnesium content is 5
mEq/L. In muscle tissue Mg++ is 20 mEq/L.

 About 70% of magnesium exists in free state and remaining
30% is protein-bound (25% to albumin and 5% to globulin).
 Homeostasis is maintained by intestinal absorption as well as
by excretion by kidney.
 Magnesium is reabsorbed from loop of Henle and not from
proximal tubules.

Functions of Magnesium
1. Mg++ is the activator of many enzymes requiring ATP. Alkaline
phosphatase, hexokinase, fructokinase, phosphofructokinase,
adenyl cyclase, cAMP dependent kinases, etc. need magnesium.
2. Neuromuscular irritability is lowered by magnesium.
3. Insulin-dependent uptake of glucose is reduced in magnesium
deficiency. Magnesium supplementation improves glucose
tolerance.

Hypomagnesemia
 It is commonly seen in hospital patients.
 Conditions which require magnesium estimation are mentioned
below:
1. Increased urinary loss (Tubular necrosis)
2. Hyperaldosteronism, volume expansion
3. Familial hypomagnesemia
4. Increased intestinal loss Diarrhea, laxatives, ulcerative colitis
Nasogastric suction, vomiting

5. Liver cirrhosis
6. Malabsorption
7. Protein calorie malnutrition
8. Hypoparathyroidism
9. Toxemia of pregnancy
10. Drugs:Thiazide diuretics Aminoglycosides Cisplatin
Amphotericin Cyclosporin Haloperidol Alcohol

Hypomagnesemia
 When serum magnesium level falls below 1.7 mg/dl, it is called
hypomagnesemia.
 Vomiting, nasogastric suction, diarrhea, liver cirrhosis, protein-
calorie malnutrition and diuretic therapy are the common causes
 Serum magnesium levels need not always reflect body content.
 Measurement of urinary magnesium excretion will distinguish
between renal and gastrointestinal losses.

 Deficiency of magnesium leads to neuromuscular
hyperirritability and cardiac arrhythmias. The magnesium
deficiency symptoms are similar to those of calcium deficiency;
but symptoms will be relieved only when magnesium is given.
Oral therapy may lead to diarrhea, hence intravenous
magnesium sulfate is given.

 Hypermagnesemia It is uncommon and always due to excessive
intake either orally (antacids), rectally (enema) or parenterally.
 Causes of hypermagnesemia are listed below:
1. Excess intake orally or parenterally
2. Renal failure
3. Hyperparathyroidism
4. Oxalate poisoning
5. Rickets
6. Multiple myeloma
7. Dehydration
8. Drugs: Aminoglycosides Antacids Calcitriol Tacrolimus

 Magnesium intoxication causes depression of neuromuscular
system, causing lethargy, hypotension, respiratory depression,
bradycardia and weak tendon reflexes
 In severe conditions, acute rhabdomyolysis results.
Hypermagnesemia induces decrease in serum calcium by
inhibiting PTH secretion, which in turn will have deleterious
effects.

SULFUR
 Source of sulfates is mainly amino acids
cysteine and methionine. Proteins contain
about 1% sulfur by weight.
Inorganic sulfates of Na+, K+ and Mg++,
though available in food, are not utilized.

Functions of Sulfur
 Sulfur containing amino acids are important constituents of
body proteins. The disulfide bridges keep polypeptide units
together, e.g. insulin, immunoglobulins.
 Chondroitin sulfates are seen in cartilage and bone.
 Keratin is rich in sulfur, and is present in hair and nail.
 Many enzymes and peptides contain -SH group at the active
site, e.g. glutathione.
 Co-enzymes derived from thiamine, biotin, pantothenic acid
and lipoic acid also contain sulfur.

 If sulfate is to be introduced in glycosaminoglycans or in
phenols for detoxification, it can be done only by
phosphoadenosine phosphosulfate (PAPS).
 Sulfates are also important in detoxification mechanisms,
e.g. production of indoxyl sulphate.

Excretion
 All the sulfur groups are ultimately oxidized in liver to sulfate
(SO4) group and excreted in urine.
 The total quantity of sulfur in urine is about 1 gm/day. This
contains 3 categories. i. Inorganic sulfates: It is about 80% of the
total excretion. This is proportional to the protein intakeii. Organic
sulfate or ethereal sulfate: It is also called conjugated sulfate. It
constitutes 10% of urinary sulfates. This part is also proportional
to protein intake.

iii. Neutral sulfur or unoxidized sulfur: This fraction constitutes
10% of total sulfates. Sulfur containing organic compounds
such as amino acids, thiocyanates and urochrome constitute
this fraction. This will not vary with diet.

Minerals

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