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Minerals all

  1. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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.
  11. 11. 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
  12. 12.  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
  13. 13. 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.
  14. 14. 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
  15. 15. 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.
  16. 16.  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
  17. 17. 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
  18. 18.  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.
  19. 19. 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
  20. 20.  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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