1. MINERALS
Classification:
 Bulk elements/ macroelements
o Required in >100 mg/day in the diet
 Calcium
 Potassium
 Magnesium
 Sodium
 Potassium
 Chloride
 Sulfur
 Trace elements
o Required in <100mg/day in diet
 Iron
 Iodine
 Copper
 Manganese
 Zinc
 Molybdenum
 Selenium
 Fluoride
 Cobalt
 chromium
 Possibly essential trace elements
o Considered to be essential, though actual function is not yet known
 Nickel

2.  Tin bromine
 Lithium
 barium
 Unessential but found in diet
 Rubidium
 Silver
 Gold
 Bismuth
 Toxic minerals
o Found in food but toxic
 Lead
 Aluminium
 Mercury
 Arsenic
 cadmium
CALCIUM
Sources:
 Milk and milk products
 Egg, fish and meat
 Vegetables, cereals, pulses, nuts
Recommended dietary allowance (RDA):
 ADULT: 500 mg/day
 Children: 1200 mg/day
 Pregnant and lactating: 1500 mg/day
 Aged : 1500mg/day; vit D - 20µg/day to facilitate Calcium absorption

3. Functions:
 All functions are by the ionic form- Ca 2+
 Constituent of bones and teeth
o Present as calcium hydroxy apatite crystals
o Provides strength and hardness
o Storehouse of calcium (i.e., if serum calcium level decreases, it can be
supplied by the bones)
 Blood coagulation
o Factor IV
o Activation of other clotting factors- VIII, IX, X and prothrombin.
 Enzyme action
o Activates enzymes via calmodulin
Eg: adenylate cyclase, phosphorylase kinase, pyruvate carboxylase, pyruvate
dehydrogenase, glycogen synthase etc.
 Role in muscle contraction
 Role in nerve conduction
 Neuromuscular excitability
o Decreases neuromuscular excitability
o Counteracts the excitatory effects of Na+ and K+
o Decreases serum Ca2+ - spasms – hypocalcemic tetany
 In myocardium, it prolongs systole; if calcium level is very high, cardiac arrest
is caused in systole.
 Release of stored hormones- insulin, PTH, calcitonin, ADH
 Second messenger in hormonal action
o G proteins & inositol triphosphate
 Secreted in milk
Absorption:

4.  In first and second part of duodenum
 Active process- against concentration gradient
Factors favouring absorption:
 Vit D- active form- calcitriol- i.e., 1, 25-dihydroxy cholecalciferol
o Increases synthesis of carrier protein CALBINDIN
o Action of Vit D is similar to that of steroid hormones; hence it itself is
considered as a hormone.
 Parathormone (PTH)
o Increases calcium absorption by activating Vit D through 1αhydroxylase
 Acidity if increased in intestine favours calcium absorption
 The amino acids lysine and arginine also favour absorption.
Factors decreasing absorption:
 Phytates like inositol hexaphosphate
 Oxalates precipitate calcium as calcium oxalate
 Malabsorption syndromes
 The change in Ca : P ratio from the normal range of (2:1 to 1:2) decreases
absorption
Serum calcium:
 Normal : 9-11 mg/dL
 Torniquet should not be tied while testing Ca2+ levels as it will give wrong higher
values.
 Calcium exists in three forms in serum
o Ionic calcium (Ca2+) – 50%
o Anions (phosphate/ citrate/ oxalate/ complexes) < 1 mg
o Bound to albumin (protein bound calcium)- 4mg/dL
o First two are called diffusible calcium
Regulation:

5. 1. Effect of Vit D
 On intestine: increase synthesis of calbindin thus increasing calcium
absorption
 On bone: calcification (deposition of calcium & phosphate in bone
mineralisation) and also increase osteoblast activity thus decreasing serum
calcium level
 On kidney: decreases excretion/ increases reabsorption of calcium thus
increasing serum calcium levels.
 Overall : hypercalcemic effect
2. Effect of PTH
 On bone: causes resorption/ demineralisation by stimulating osteoclasts
 On kidney: increases reabsorption of calcium; excretion of phosphorus
(phosphaturic effect)
 On intestine: increases absorption of calcium
 Overall: hypercalcemic effect
3. Effect of calcitonin
 Secreted by parafollicular cells of thyroid
 32 amino acids
 On bone: deposition of calcium & phosphorus (mineralisation)
 On intestine: decreases absorption but not prominent
 On kidney: not much action, probably increases excretion of calcium
 Overall: hypocalcemic effect
 In medullary carcinoma of thyroid, calcitonin concentration increases; hence is
used as tumour marker.
4. Phosphorus level inversely affects calcium level.
i.e,. Ca × P = 40, a constant (higher in children)
5. Serum protein levels
 1 g decrease in serum albumin leads to 0.8 mg decrease in serum calcium

6. 6. pH of plasma
 Alkalosis – makes ionic Ca bind with protein – ionic Ca decreases – causes
tetany
7. In children, serum Ca level is closer to the upper limit
8. Renal threshold – 10 mg/dL
Hypercalcemia:
Effects:
 Deposition in kidneys along with phosphorus – tubular damage and renal
calculi
 Deposition in extra osseous tissues
 Decrease in neuromuscular excitability characterised by constipation,
abdominal pain, muscular hypotonia
 In heart if the level goes beyond 15 mg/dL, cardiac arrest is caused.
Causes:
 Hyperparathyroidism
 Excess intake/ increased absorption of Vit D/ calcium/ both.
 Sarcoidosis – increased sensitivity to Vit D – increased Ca absorption
 Secondary malignancies (carcinoma) in bone
 Leukemias
 Paget’s disease
 Osteoporosis
 Thyrotoxicosis
 Drugs like thiazides (diuretic)
Hypocalcemia:
Effects:
 Tetany (only when IONIC calcium decreases) – tested using CHVOSTEK’S SIGN
& TROUSSEAU SIGN

7.  Usually asymptomatic
 Carpopedal spasm (affects hands, feet, face & larynx)
Causes:
 Chronic renal failure
 Defecient intake/ dietary defeciency/ decreased absorption of Ca and Vit D
 Diseases of pancreas, biliary tract and intestine
 Hypoparathyroidism – acquired/ idiopathic
 Neonatal hypocalcemia due to maternal hyperparathyroidism
 Hypoproteinemia
 Acute pancreatitis
 Renal tubular defects
PHOSPHORUS
Sources: milk, meat, fish, eggs, vegetables
RDA: 500 mg/day in adults; >1 g in children
Absorption: in mid jejunum as inorganic phosphorus (mechanism not clearly
understood)
Factors affecting absorption:
 Ca : P ratio of 2:1 to 1:2 has best absorption
 Vit D increases phosphorus absorption
 PTH increases P absorption
 Calcitonin decreases P absorption
 Iron and phytic acid decrease absorption by binding with P and forming
complexes
Functions:
 Component of bones and teeth
 Totally, 1 kg of phosphorus is found in body,

8. o 80% in bones and teeth
o 10% in muscles
o 10% in cells
 As components of high energy compounds like ATP, GTP, CTP, carbamoyl
phosphate, creatine phosphate, PEP etc.
 Intermediates in carbohydrate metabolism are phosphate derivatives.
 In lipid metabolism,
o Intermediates of TAG synthesis are phosphate derivatives
o As components of membranes (phospholipids)
 Phosphoproteins
 In the nucleotides and nucleic acids, backbone has phosphate
 In acid base balance, as phosphate buffer system
 Component of coenzymes like TPP, PLP, NAD+, NADP+, FMN, FAD, CoA etc.
 Regulation of enzyme activity by phosphorylation and dephosphorylation. eg.,
glycogen synthase and glycogen phosphorylase
Serum phosphorus:
 Normal: 2.5 – 4.5 mg/dL in adults; 4 – 6 mg/dL in children
 To estimate serum P level, hemolysis of collected blood must be avoided.
Regulation of serum P level:
PTH
 In intestine: increases absorption
 In bone: bone resorption
These increase serum P level
 In kidneys: phosphaturic effect
This decreases serum P level, which is more pronounced. Therefore, overall
effect if decrease in serum P level
Calcitonin

9.  In bone: decreases resorption
 In intestine: decreases absorption
 In kidneys: increases phosphaturia
Overall effect is decrease in serum P level
Calcitriol/ vit D
 In intestine: increases absorption
 In kidneys: increases reabsorption
These increase serum P level
 In bones: increases mineralization
This decreases serum P level. Overall effect is increase in serum P level.
Hyperphosphatemia: no definite symptoms seen
Causes:
 Excess Vit D
 Renal failure
 Hypoparathyroidism and pseudohypoparathyroidism
 Diabetic ketosis
 Healing fractures
 Acromegaly
Hypophosphatemia: anorexia, bone pain, muscular weakness, dizziness
Causes:
 Hyperparathyroidism
 Rickets and osteomalacia
 Hyperinsulinism
 Steatorrhea – decreases fat absorption – decreases Vit D absorption
 Fanconis syndrome

10. IRON
Sources: green leafy vegetables, cereals, pulses, jaggery, fish, meat, liver. Milk is a
very poor source.
RDA: males: 20 mg, females: 30 mg, pregnant: 40 mg per day.
Functions: totally, 3 to 5 g of iron is found in body.
 Part of proteins. They are of two types:
o Heme proteins
 Hb, Mb
 Enzymes like cytochromes, tryptophan pyrrolase, catalase,
peroxidase
o Non heme iron proteins
 Fe-S centres
 Aconitase – activated by iron
 Ferritin
 Transferrin
o 75% in Hb; 5% in Mb; 20% in other proteins.
Absorption: only 10% of iron intake is absorbed from upper duodenum
Factors affecting absorption:
 Gastric HCl liberates Fe3+ from food, favouring absorption
 G-SH, Vit C, ferrireductase, -SH of cysteine help to convert Fe3+ to Fe2+
 Vit C and amino acids form soluble chelates (iron ascorbate and iron
aminoacid) favouring absorption.

12. Transport:
 In blood, through transferrin
 Each transferrin has 2 binding sites for iron
 300 mg of transferrin present in 100 mL of blood can bind with 400 μg of Fe3+
(range 250 to 400 μg) – Total Iron Binding Capacity (TIBC)
 But, only one third of the sites are used in normal individual. Therefore, total
serum iron is 100 to 150 μg/dL
 In liver diseases, TIBC decreases
 In iron deficiency anemia, TIBC increases.
Uptake of iron:
 By reticulocytes in bone marrow
 By receptor mediated process in reticulocyte membrane.
Receptor + transferrin
Receptor-transferrin complex
Internalized
Iron liberated
Receptor-apotransferrin complex
Goes back to its membrane site
Receptor remains; apotransferrin returns to blood
Storage : in ferritin
 Has 24 subunits

13.  Can bind to 4000 atoms of Fe3+, but in normal, only 2000 Fe3+ are bound
to one ferritin molecule.
 20% of iron is in this form.
Hemosiderin:
 Insoluble, amorphous form of iron
 37% of iron is in this form
 Ferritin in centre, with aggregates of iron on it
 Formed only during iron overload.
Excretion:
 1 to 1.5 mg/day through faeces
 Unabsorbed iron and iron from the desquamated mucosal cells.
Disorders:
Iron deficiency anemia
 Most common nutritional deficiency disorder
 30% of world’s population is anemic
 In India, it is 70%; in pregnants, 80% are anemic
 Microcytic, hypochromic type.
Causes:
 Lack of nutrition
o The food may not contain iron
o Phytates and oxalates in food bind to iron and prevent its absorption
 Hookworm infection (one worm – 0.3 mL blood/day)
 Repeated pregnancies (1 g iron lost per pregnancy)
 Chronic blood loss
o Haemorrhoids/piles
o Peptic ulcers

14. o Menorrhagia
 Nephrosis
o Loss of haptoglobin (binds Hb), haemopexin (binds heme) and transferrin
 Lead poisoning (it inhibits ALA dehydratase – decreased Hb synthesis)
 Lack of absorption after gastrectomy
 Hypoclorrhydria
Clinical manifestations:
 Person becomes uninterested – apathetic – due to decreased O2
 Decreased ATP synthesis as iron is a component of cytochromes
 Atrophy of gastric epithelium
 Dysphagia – Plummer Wilson syndrome – precancerous condition
 Impaired attention, irritability, poor memory – decreased scholastic performance
 Person becomes less efficient.
Lab findings:
 Hb < 12 g/dL
 Serum iron < 100 μg/dL
 Increased TIBC
Treatment:
 Treating the underlying cause than the symptoms.
 Iron and folic acid - 100 mg & 500 μg in pregnants; 20 mg & 100 μg in
children
Iron toxicity:
Hemosiderosis:
 Golden brown granules of hemosiderin accumulate in liver and spleen
 Seen in patients receiving repeated blood transfusion as in thalassemia,
hemophilia etc.

15. Hemochromatosis/Bronze diabetes:
 Total body iron > 30 g (normal 4 to 5 g)
 Hemosiderin in large quantity, in liver – liver cirrhosis; in pancreas – diabetes;
in skin – brown appearance
Bantu siderosis:
 Found in African Bantu tribe
 Due to cooking in iron vessels
MAGNESIUM
Sources: all green vegetables (chlorophyll has Mg)
RDA: 350 mg/day
Total body Mg content: 25 g
Functions:
 60% of body’s Mg is found in bones and teeth
 Cofactor for enzymes utilizing ATP, like kinases (PFK, alkaline phosphatase,
hexokinase, cAMP dependent kinases.
In body, Mg-ATP complex is found.
 Mg-ATP is substrate for adenylate cyclase
to form cAMP
 Activation of myosin ATPase
 Nucleic acid and protein biosynthesis need Mg as cofactor – polymerases,
aminoacyl tRNA synthetase
 Reduces neuromuscular excitability
Mg deficiency – hypomagnesemic tetany
Serum levels: 1.8 to 2.2 mg/dL

16. Hypomagnesemia:
Causes:
 Severe, prolonged diarrhea
 Malabsorption
 Protein Calorie Malnutrition (PCM)
 Alcoholism and malnutrition
Hypermagnesemia:
 CNS depression
 Lousiness, lethargia
Causes:
 Increased use of Mg containing laxatives and antacids
 Renal failure
COPPER
RDA: 2 – 3 mg/day
Total body copper content: 100 mg
Serum concentration: 70 to 140 μg/dL
Transport: bound to albumin
Functions:
 Role in iron metabolism (component of ceroluplasmin/ferroxidase)
Deficient ceruloplasmin – iron deficiency anemia – CANNOT be treated by oral
iron therapy (normal blood concentration of ceruloplasmin (an acute phase
protein) is 25 to 50 mg/dL
 Component of the enzyme superoxide dismutase. This enzyme is of two types:
o Cytosolic – has 2 Zn2+ and 2 Cu2+ per molecule
o Mitochondrial – has 2 Zn2+ and 2 Mn2+ per molecule
 For cross linking of collagen, enzyme lysyl oxidase has Cu.

17.  Tyrosinase needs copper.
 Other enzymes requiring copper are cytochrome oxidase, tryptophan pyrrolase,
dopamine β hydroxylase, monoamine oxidase, δ ALA synthase.
 Copper increases HDL concentration.
Disorders:
Wilson’s disease (hepato-lenticular degeneration):
 Decrease in plasma ceruloplasmin
 Due to defect in gene coding for Cu containing ATPase
 Liver cirrhosis due to Cu deposition
 In lentiform nucleus of brain, Cu is deposited, leading to Parkinson’s disease
like symptoms
 Damage to kidney tubules – aminoaciduria
 Deposition in pancreas – diabetes
 Deposition in edges of cornea – in Descemet’s membrane, forming golden
brown/blue/green ring (Kayser-Fleischer ring)
 Penicillamine – chelating agent
Menke’s kinky/steely hair disease:
 Deficient Cu binding ATPase.
ZINC
RDA: 10 to 15 mg/day
Total body zinc content: 2 to 3 g
Functions:
 Component of enzymes
o More than 300 enzymes need Zn2+ as cofactor.
o Eg., superoxide dismutase, carbonic anhydrase, alcohol dehydrogenase,
LDH, glutamate dehydrogenase, retinine reductase, RNA polymerase.
 Vit A metabolism

18. o Stimulates Vit A from liver
o Increases plasma Vit A level and its utilization in Rhodopsin cycle
 Role in taste
o Protein gusten in saliva needs Zn
 For growth and reproduction
 Role in insulin action
o For storage and release of insulin
 Promotes wound healing, mechanism not known
Defeciency manifestations:
 Loss of appetite, poor growth, dermatitis, impaired wound healing, decreased
taste sensation (hypogeusia), loss of hair (alopesia), fetal malformations.
Disorder: Acrodermatitis enteropathica
 Disorder of Zn absorption
 Characterized by acrodermatitis
 Skin lesion around mouth, teeth, fingers
 Diarrhea
IODINE
Source: commercial salt
RDA: 150 to 200 μg/day
Total body iodine content: 25 to 30 mg; 80% of it is in thyroid gland
Function: component of thyroxin hormones – T3 and T4
Deficiency:
 Second major micronutrient deficiency in India (first place for iron, third place
for Vit A)
Goitre
 Goitrous belt – areas rich in goitre patients; along the Himalayas

19.  Goitrogens
o Present in food
o Decrease iodine utilization
o Present in cassava tubers, bamboo, sweet potato
o Cabbage and tapioca have thiocyanate which inhibits iodine uptake by
thyroid gland
o Mustard seeds have thiourea inhibits iodination of tyrosine in
thyroglobulin.
FLUORINE
Source:
 Drinking water is the main source
 Other sources are sea fish, tea, cheese, jowar, toothpaste
RDA: 2 to 4 mg/day
Functions:
 Present as fluoride ion.
 In places where water has fluoride >1 ppm (0.1 mg/dL), people are resistant to
dental caries
o Mode of action: fluoride gets incorporated to enamel of teeth and makes
it resistant to organic acids of bacteria
 Makes bone resistant to osteoporosis
 Inhibits enolase, thus stops glycolysis.
Fluorosis:
 Excess of fluoride (>3 to 5 ppm, also goes as high as 20 ppm) in drinking water
 Mottling of teeth
 Chalky appearance of teeth, brown pigmentation
 Pitting of teeth – pieces of teeth may be lost
 Alternate areas of osteosclerosis and osteoporosis.

20. MANGANESE
 Component of enzymes
o Superoxide dismutase – mitochondrial component
o Arginase
o Isocitrate dehydrogenase
o Cholinesterase
o Enolase
 Many kinases, hydrolases, decarboxylases need Mn
 Activation of glycosyl transferases, to synthesize oligosaccharides,
proteoglycans and glycoproteins
 In animals, for normal reproduction and bone formation.
SELENIUM
Functions:
 Component of glutathione peroxidase, hence acts as antioxidant
 It has sparing effect on Vit E and vice versa
 Part of 5-deiodinase needed to convert T4 to T3
 Component of thioredoxin reductase
 Amino acid selenocysteine (SeCys/SeC) is the 21st amino acid
o It has –SeH group instead of –SH group
o It is incorporated into proteins; coded by stop codon UGA
Deficiency:
 Liver necrosis and cirrhosis
 Cardiomyopathy, muscular dystrophy
Keschan cardiomyopathy:
 Seen in Keschan province in China
 Soil contains less Se causing deficiency

21.  Cardiac necrosis, arrhythmia
MOLYBDENUM
 Component of molybdoflavo enzymes xanthine oxidase and aldehyde oxidase
 Also found in sulfite oxidase and nitrite reductase
COBALT
 Component of cobalamin
 Stimulates formation of erythropoietin
 Activates glycyl glycine dipeptidase
CHROMIUM
 Role in glucose metabolism – increases glucose tolerance of an individual.
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