MINERALS INORGANIC SUBSTANCES BIOLOGICAL IMPORTANCE COFACTORS or PROSTHETIC

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MINERALS INORGANIC SUBSTANCES BIOLOGICAL IMPORTANCE: COFACTORS or PROSTHETIC GROUPS ENZYMES CONSTITUENT OF MOLECULES CONSTITUENT

MINERALS INORGANIC SUBSTANCES BIOLOGICAL IMPORTANCE: COFACTORS or PROSTHETIC GROUPS ENZYMES CONSTITUENT OF MOLECULES CONSTITUENT OF STRUCTURES WATER & ELECTROLYTE BALANCE ELECTRICAL ACTIVITY

BIOMEDICAL IMPORTANCE FEW MINERALS ESENTIAL FOR GROWTH, DEVELOPMENT & MAINTAINANCE OF HEALTH. HENCE THEY

BIOMEDICAL IMPORTANCE FEW MINERALS ESENTIAL FOR GROWTH, DEVELOPMENT & MAINTAINANCE OF HEALTH. HENCE THEY MUST BE INCLUDED IN THE DIET WHEN INTAKE IS BELOW REQUIRED AMOUNT, DEFICIENCY SYMPTOMS APPEAR SOME MINERALS IN EXCESS MAY CAUSE TOXICITY

CLASSIFICATION MAJOR or MACROELEMENTS WHERE THE DIETARY REQUIREMENT IS MORE THAN 100 mg/ day

CLASSIFICATION MAJOR or MACROELEMENTS WHERE THE DIETARY REQUIREMENT IS MORE THAN 100 mg/ day AND TOTAL BODY CONTENT IS MORE THAN 5 gm Eg: Ca, Mg, P, Na, K, Cl, S TRACE ELEMENTS WHERE THE DIETARY REQUIREMENT IS LESS THAN 100 mg/ day AND TOTAL BODY CONTENT IS LESS THAN 5 gm

CALCIUM BODY DISTRIBUTION: MOST ABUNDANT BODY CONTENT 1 - 1. 5 Kg 99% SEEN

CALCIUM BODY DISTRIBUTION: MOST ABUNDANT BODY CONTENT 1 - 1. 5 Kg 99% SEEN IN BONES & TEETH 1% ECTRACELLULAR FLUID- PERFORMS WIDE VARIETY OF FUNCTIONS

FUNCTIONS 1. CONSTITUENT OF BONES & TEETH: PRESENT IN BONE AS CALCIUM HYDROXY APATITE

FUNCTIONS 1. CONSTITUENT OF BONES & TEETH: PRESENT IN BONE AS CALCIUM HYDROXY APATITE Ca 10(PO 4)6(OH)2 CALCIUM OCCURS AS CALCIUM PHOSPHATE IN BONE MATRIX AND THE ENAMEL, DENTIN & CEMENTUM OF TEETH AND RENDERS PHYSICAL STRENGTH BONES ACT AS RESERVIORS PF CA & P

FUNCTIONS 2. MUSCLE CONTRACTION: Ca INTERACTS WITH TROPONIN C TRIGGERING MUSCLE CONTARCTION ACTIVATES ENZYME

FUNCTIONS 2. MUSCLE CONTRACTION: Ca INTERACTS WITH TROPONIN C TRIGGERING MUSCLE CONTARCTION ACTIVATES ENZYME ATPase, INCREASES THE INTERACTION BETWEEN ACTIN & MYOSIN 3. BLOOD COAGULATION: FACTOR IV

FUNCTIONS 4. ACTIVATION OF ENZYMES: DIRECT ACTIVATION- LIPASE, ATPase, SDH THROUGH CALMODULIN – eg

FUNCTIONS 4. ACTIVATION OF ENZYMES: DIRECT ACTIVATION- LIPASE, ATPase, SDH THROUGH CALMODULIN – eg ? 5. NERVE IMPULSE TRANSMISSION: PRESYNAPTIC AND POSTSYNAPTIC REGION 6. NEUROMUSCULAR EXCITABILITY: Ca REDUCES MEMBRANE PERMEABILITY (See TETANY under clinical aspects)

FUNCTIONS 7. SECOND MESSENGER: FOR HORMONE MEDIATED ACTION eg: EPINEPHRINE ( THIRD MESSENGER ADH)

FUNCTIONS 7. SECOND MESSENGER: FOR HORMONE MEDIATED ACTION eg: EPINEPHRINE ( THIRD MESSENGER ADH) 8. REGULATES ENDOCYTOSIS, EXOCYTOSIS & CELL MOTILITY: MICROFILAMENT AND MICROTUBULE MEDIATED PROCESSESHORMONE SECRETION: RELEASE OF CERTAIN HORMONES INSULIN, PTH, CALCITONIN THROUGH EXOCYTOSIS 9. HEART: ACTS ON MYOCARDIUM AND PROLONGS SYSTOLE

FUNCTIONS MEMBRANE TRANSPORT AND STRUCTURE: Ca INFLUENCES TRANSPORT OF WATER AND SEVERAL IONS THUS

FUNCTIONS MEMBRANE TRANSPORT AND STRUCTURE: Ca INFLUENCES TRANSPORT OF WATER AND SEVERAL IONS THUS INFLUENCING MEMBRANE STRUCTURE

ABSORPTION OF CALCIUM MAINLY IN THE DUODENUM BY ENERGY DEPENDENT PROCESS VITAMIN D INDUCES

ABSORPTION OF CALCIUM MAINLY IN THE DUODENUM BY ENERGY DEPENDENT PROCESS VITAMIN D INDUCES SYNTHESIS OF CALBINDIN, INTESTINAL EPITHELIAL CELLS PARATHYROID HORMONE: ABSORPTION ACIDITY INCREASES BY FAVOURING IONIC FORM LYSINE & ARGININE FAVOUR IONIC FORM

INHIBITION OF CALCIUM PHYTATES IN PLANTS, OXALATES FORM INSOLUBLE SALTS HIGH DIETARY PHOSPHATES PRECIPITATE

INHIBITION OF CALCIUM PHYTATES IN PLANTS, OXALATES FORM INSOLUBLE SALTS HIGH DIETARY PHOSPHATES PRECIPITATE AS CALCIUM PHOSPHATES ALKALINE CONDITION HIGH DIETARY FIBRE CONTENT (ADSORBED) MALBSORPTION SYNDROMES- FORM INSOLUBLE CALCIUM SALTS OF FATTY ACIDS.

STORAGE & EXCRETION 99% STORED IN BONES AND TEETH EXCRETION: MAINLY IN FECES, PARTLY

STORAGE & EXCRETION 99% STORED IN BONES AND TEETH EXCRETION: MAINLY IN FECES, PARTLY IN URINE. RENAL THRESHOLD 10 mg/Dl VITAMIN D ENHANCES Ca REABSORPTION. IN VIT D DEFICIENCY URINARY EXCRETION OF Ca INCREASED BLOOD: SERUM 9 -11 mg/d. L

PHYSIOLOGICAL FORMS Ca EXISTS IN THREE FORMS: IONIZED (5 mg/d. L) COMPLEXED (1 mg/d.

PHYSIOLOGICAL FORMS Ca EXISTS IN THREE FORMS: IONIZED (5 mg/d. L) COMPLEXED (1 mg/d. L) PROTEIN BOUND – NON DIFFUSIBLE (ALBUMIN- 3 mg/Dl, GLOBULINS- 1 mg/d. L)

REGULATION OF CALCIUM HYPERCALCEMIC VITAMIN D PARATHYROID HORMONE HYPOCALCEMIC CALCITONIN PHOSPHATE LEVEL PO 42

REGULATION OF CALCIUM HYPERCALCEMIC VITAMIN D PARATHYROID HORMONE HYPOCALCEMIC CALCITONIN PHOSPHATE LEVEL PO 42 -

PHOSPHATE METABOLISM BODY DISTRIBUTION ABUNDANT NEXT TO CALCIUM ADULT BODY 1 Kg OF PHOSPHORUS

PHOSPHATE METABOLISM BODY DISTRIBUTION ABUNDANT NEXT TO CALCIUM ADULT BODY 1 Kg OF PHOSPHORUS AS PHOSPHATE SEEN IN EVERY CELL 80% OCCURS COBINATION WITH Ca 10% MUSCLES AND PROTEINS 10% VARIOUS CHEMICAL COMPOUNDS

FUNCTIONS OF PHOSPHATE CONSTITUTENT OF BONE AND TEETH PRODUCTION AND UTILISATION OF HIGH ENERGY

FUNCTIONS OF PHOSPHATE CONSTITUTENT OF BONE AND TEETH PRODUCTION AND UTILISATION OF HIGH ENERGY COMPOUNDS SYNTHESIS OF NUCLEOSIDE COENZYMES SYNTHESIS OF NUCLEIC ACIDS PHOSPHATE ESTERS REGULATION OF ENZYMES IN ACTIVATE/DEACTIVATION BUFFERING ACTION-Ph MAINTANANCE

ABSORPTION, STORAGE, EXCRETION ABSORPTION JEJUNUM, FACILITATED BY VIT D STORAGE BONES, TEETH & MUSCLES

ABSORPTION, STORAGE, EXCRETION ABSORPTION JEJUNUM, FACILITATED BY VIT D STORAGE BONES, TEETH & MUSCLES EXCRETION REGULATED AT EXCRETION LEVEL RENAL THRESHOLD 2 mg/Dl 1 g EXCRETED. 70% FILTERED REABSORBED PTH DECREASES RENAL TUBULAR REABSORPTION OF PHOSPHATE SMALL AMOUNT - FECES

REGULATION SERUM 2. 5 – 4. 5 mg/Dl (4 – 6) 40% FREE IONS

REGULATION SERUM 2. 5 – 4. 5 mg/Dl (4 – 6) 40% FREE IONS 50% COMPLEXED 10% PROTEIN BOUND HYPERPHOSPHATEMIC VITAMIN D – MOBILISES PHOSPHATE HYPOPHOSPHATEMIC PTH – DECREASES TUBULAR REABSORPTION

NUTRITIONAL ASPECTS SOURCES: RDA: 500 mg CLINICAL SIGNIFICANCE: HYPOPHOSPHATEMIA �RICKETS �HYPERPARATHYROIDISM �FANCONI SYNDROME HYPERPHOSPHATEMIA

NUTRITIONAL ASPECTS SOURCES: RDA: 500 mg CLINICAL SIGNIFICANCE: HYPOPHOSPHATEMIA �RICKETS �HYPERPARATHYROIDISM �FANCONI SYNDROME HYPERPHOSPHATEMIA HYPERVITAMINOSIS D HYPOPARATHYROIDISM RENAL FAILURE

MAGNESIUM MAINLY INTRACELLULAR ADULT BODY 20 g 75% FOUND IN BONES WITH Ca &

MAGNESIUM MAINLY INTRACELLULAR ADULT BODY 20 g 75% FOUND IN BONES WITH Ca & P 25% SOFT TISSUES AND BODY FLUIDS

FUNCTIONS FORMATION BONE AND TEETH ACTIVATION ENZYMES : ALP, HK, FK, PFK, AC, c.

FUNCTIONS FORMATION BONE AND TEETH ACTIVATION ENZYMES : ALP, HK, FK, PFK, AC, c. AMP DEPNDANT KINASES NEUROMUSCULAR FUNCTION : LOWERS NEUROMUSCULAR EXCIITABILITY INSULIN SENSITIVITY, GLUCOSE UPTAKE, GLUCOSE TOLERANCE

NUTRITIONAL ASPECTS ABSORPTION: SPECIFIC CARRIER MECHANISM INTESTINE LARGE Ca, P & ALCOHOL ABSORPTION PTH

NUTRITIONAL ASPECTS ABSORPTION: SPECIFIC CARRIER MECHANISM INTESTINE LARGE Ca, P & ALCOHOL ABSORPTION PTH INCREASES AS Ca SERUM Mg 2 -3 m. G/Dl 60% IONISED 10% COMPLEXED CITRATES, PHOSPHATES 30% PROTEIN BOUND

CLINICAL SIGNIFICANCE SOURCES: RDA 400 mg HYPOMAGNESEMIA (<1. 7) CHRONIC ALCOHOLISM LIVER CIRRHOSIS PROTEIN

CLINICAL SIGNIFICANCE SOURCES: RDA 400 mg HYPOMAGNESEMIA (<1. 7) CHRONIC ALCOHOLISM LIVER CIRRHOSIS PROTEIN CALORIE MALNUTRITION DURETIC THERAPY MANIFESTATIONS: IRRITABILITY, TRMORS, CARPOPEDAL SPASM, CARDIAC ARRYTHMIAS

MANGANESE TRACE ELEMENT TOTAL BODY 15 mg MAINLY FOUND LIVER AND KIDNEYS CONFINED TO

MANGANESE TRACE ELEMENT TOTAL BODY 15 mg MAINLY FOUND LIVER AND KIDNEYS CONFINED TO CELL NUCLEI WITH NUCLEIC ACIDS

FUNCTIONS COFACTOR OF SEVERAL ENZYMES: SYNTHESIS OF CHOLESTEROL, GLYCOPROTEINS, CHONDROITIN SULPHATE, RNA, Hb INHIBITS

FUNCTIONS COFACTOR OF SEVERAL ENZYMES: SYNTHESIS OF CHOLESTEROL, GLYCOPROTEINS, CHONDROITIN SULPHATE, RNA, Hb INHIBITS LIPID PEROXIDATION: MITOCHONDRIAL SOD

ABSORPTION, EXCRETION ABOUT 3 -4% DIETARY Mn IS ABSORBED IRON INHIBITS EXCRETION: BILE &

ABSORPTION, EXCRETION ABOUT 3 -4% DIETARY Mn IS ABSORBED IRON INHIBITS EXCRETION: BILE & PANCREATIC JUICE SERUM : 5 – 20 mg/Dl, BOUND TO A SPECIFIC CARRIER PROTEIN TRANSMANGANIN, BETA GLOBULIN

NUTRITIONAL ASPECTS SOURCES: TEA RICH SOURCE RDA 2 -5 mg CLINICAL SIGNIFICANCE: RARE IN

NUTRITIONAL ASPECTS SOURCES: TEA RICH SOURCE RDA 2 -5 mg CLINICAL SIGNIFICANCE: RARE IN HUMANS

IODINE TRACE ELEMENT ADULT 25 – 30 mg 80% STORED IN THYROID GLAND FUNCTIONS:

IODINE TRACE ELEMENT ADULT 25 – 30 mg 80% STORED IN THYROID GLAND FUNCTIONS: SYNTHESIS OF THYROID HORMONES ABSORPTION: INTESTINE 30% DIETARY IODINE ABSORBED, ALSO THROUGH SKIN AND LUNGS

STORAGE, EXCRETION STORAGE: 80% ORGANIC FORM IODOTHYROGLOBULIN EXCRETION: MAINLY THROUGH KIDNEYS, ALSO THROUGH SALIVA,

STORAGE, EXCRETION STORAGE: 80% ORGANIC FORM IODOTHYROGLOBULIN EXCRETION: MAINLY THROUGH KIDNEYS, ALSO THROUGH SALIVA, BILE, SKIN (MILK LACTATING) PLASMA IODINE: 4 -10µg/Dl MOST OF PROTEIN BOUND

NUTRITIONAL ASPECTS SOURCES: RDA 100 -200µg CLINICAL SIGNIFICANCE: SIMPLE ENDEMIC GOITER DEFICIENCY OF IODINE

NUTRITIONAL ASPECTS SOURCES: RDA 100 -200µg CLINICAL SIGNIFICANCE: SIMPLE ENDEMIC GOITER DEFICIENCY OF IODINE GEOGRAPHICAL LOCATIONS GOITEROGENS THIOCYANATE ADVISED IODISED SALT

IODINE TRACE ELEMENT ADULT BODY 25 -30 mg 80% STORED IN THYROID GLANDS FUNCTIONS:

IODINE TRACE ELEMENT ADULT BODY 25 -30 mg 80% STORED IN THYROID GLANDS FUNCTIONS: SYNTHESIS OF THYROID HORMONES T-3 & T-4

ABSORPTION STORAGE EXCRETION ABSORPTION IN THE INTESTINE 30% DIETARY IODINE IS ABSORBED ALSO THROUGH

ABSORPTION STORAGE EXCRETION ABSORPTION IN THE INTESTINE 30% DIETARY IODINE IS ABSORBED ALSO THROUGH SKIN & LUNGS STORAGE : 80% THYROID GLAND ORGANIC FORM IODOTHYROGLOBULIN EXCRETION MAINLY HROUGH KIDNEYS ALSO –SALIVA, BILE, SKIN, MILK & LACTATION

FLUORINE FLUORIDE- TRACE ELEMENT TEETH & BONES Ca HYDROXYFLUOROAPATITE KNOWN TO PREVENT CARIES NOT

FLUORINE FLUORIDE- TRACE ELEMENT TEETH & BONES Ca HYDROXYFLUOROAPATITE KNOWN TO PREVENT CARIES NOT CONSIDERED AS ESSENTIAL FUNCTIONS: PRODUCES A FLUOROAPATITE LAYER OVER TOOTH ENAMEL RESISTANT TO ACID

FLUORIDE BONE DEVELOPMENT: TRACES PRESENT IN BONE PROBABLY FORMING CALCIUM APATITE NUTRITIONAL ASPECTS SOURCE:

FLUORIDE BONE DEVELOPMENT: TRACES PRESENT IN BONE PROBABLY FORMING CALCIUM APATITE NUTRITIONAL ASPECTS SOURCE: WATER, FISH RDA: 1 ppm IN WATER (1 mg/1000 m. L) CLINICAL SIGNIFICANCE <0. 5 ppm ASSOCIATED WITH DENTAL CARIES FLUOROSIS- >2 ppm IN WATER

CLINICAL MANIFESTATIONS MOTTLING OF ENAMEL, DISCOLORATION IN CHILDREN TEETH BECOME WEAK >20 ppm TOXIC

CLINICAL MANIFESTATIONS MOTTLING OF ENAMEL, DISCOLORATION IN CHILDREN TEETH BECOME WEAK >20 ppm TOXIC – OSTEOPOROSIS AND OSTEOSCLEROSIS WITH BRITTLE BONES ADVANCED STAGES, ACCUMULATES IN BONES, CAUSING BREAKDOWN OF BONE MATRIX CAUSING STIFF JOINTS AND CRIPPLING

IRON BODY CONTENT 3 -5 gm 75% BLOOD, LIVER, BONE MARROW & MUSCLES HEME

IRON BODY CONTENT 3 -5 gm 75% BLOOD, LIVER, BONE MARROW & MUSCLES HEME PREDOMINANT IRON CONTAINING COMPOUND HEME IRON- Hb, Mb, CYTOCHROMES, CATALASE, PEROXODASE, TRY PYRROLASE NON HEME IRON- SDH, XO, ACONITASE, TRANSFERRIN, FERRITIN, Fe. S PROTEINS, MITO NADH DEHYDROGENASE

FUNCTIONS TRANSPORT OF O 2 - Hb, Mb ETC & OXIDATIVE PHOSPHORYLATION PEROXIDASE ANTIOXIDANT

FUNCTIONS TRANSPORT OF O 2 - Hb, Mb ETC & OXIDATIVE PHOSPHORYLATION PEROXIDASE ANTIOXIDANT ABSORPTION & TRANSPORT: 10% FROM DIET IS ABSORBED 1 -2 mg ABSORBED FROM DIET UPPER PART OF DUODENUM

FUNCTIONS IRON IS AVAILABLE AS HEME & NON HEME MEAT HEME IRON TAKEN UP

FUNCTIONS IRON IS AVAILABLE AS HEME & NON HEME MEAT HEME IRON TAKEN UP INTACT VEGETABLES NON HEME IRON TAKEN UP AS IONIC OR HEME IRON ABSORPTION OF HEME IRON- INTESTINE HEME IS SPLIT FROM GLOBIN ENTEROCYTE AS HEME OR FREED INTO ENTROCYTE POOL OR ABSORBED INTACT NON HEME IRON ABSORBED AS Fe 2+

FACTORS INFLUENCING ABSORPTION GASTRIC SECRETION- PEPSIN & HCl PHYTATES, OALATES, CARBONATES, FIBRES, PHOSPHATES, ALKALIES

FACTORS INFLUENCING ABSORPTION GASTRIC SECRETION- PEPSIN & HCl PHYTATES, OALATES, CARBONATES, FIBRES, PHOSPHATES, ALKALIES Ca, Cu, Pb, INHIBIT

BODY IRON

BODY IRON

BODY IRON STATUS CONTROLLED IRON ABSORPTION DIETARY IRON, EXCESS NOT ABSORBED OR STORED IN

BODY IRON STATUS CONTROLLED IRON ABSORPTION DIETARY IRON, EXCESS NOT ABSORBED OR STORED IN ENTEROCYTE AND SHED INTO THE GUT Dcyt. B, REDUCES Fe 3+ TO Fe 2+ REDUCING SUBSTANCES VITC, GLUTATHIONE, CYSTEINE, SH GROUPS PROTEINS FACILITATE ABSORPTION Fe 2+ CROSSES MEMBRANE, DMT-1 BINDS TO IRON INTO THE MUCOSAL CELL

BODY IRON STATUS IN THE MUCOSAL CELL, Fe 2+ TO Fe 3+ BY A

BODY IRON STATUS IN THE MUCOSAL CELL, Fe 2+ TO Fe 3+ BY A FERROXIDASE CONJUGATES WITH APOFERRITIN TEMPORARY STORAGE IN MUCOSAL CELLS Fe 3+ RELEASED FROM FERRITIN BY FERROREDUCTASE DEPENDING ON IRON STATUS, IRON IS EITHER ABSORBED OR LOST DESQUAMATISED

INTESTINAL IRON UPTAKE FERROPORTIN- TRANSPORTS Fe++ TO BLOOD HEPHAESTIN OXIDISES Fe++ TO Fe+++ IRON

INTESTINAL IRON UPTAKE FERROPORTIN- TRANSPORTS Fe++ TO BLOOD HEPHAESTIN OXIDISES Fe++ TO Fe+++ IRON IS TRANSPORTED BY TRANSFERRIN MUCOSAL BLOCK THEORY- REGULTION OF IRON ABSORPTION AT THE INTESTINAL MUCOSAL CELLS.

IRON UPTAKE AND STORAGE

IRON UPTAKE AND STORAGE

REGULATION OF ABSORPTION MUCOSAL REGULATION: BODY IRON STORES: ERYTHROPOIETIC : ERYTHROPOIETEIN TRANSPORT IN BLOOD

REGULATION OF ABSORPTION MUCOSAL REGULATION: BODY IRON STORES: ERYTHROPOIETIC : ERYTHROPOIETEIN TRANSPORT IN BLOOD & CELL UPTAKE RED CELLS AS HEMOGLOBIN PLASMA TRANSPORT TRANSFERRIN (Fe+++) CARRIES IRON BETWEEN BODY LOCATIONS AND UPTAKE BY TANSFERRIN RECEPTORS INTO CELLS

APOTRANSFERRIN (Fe 3+) SYNTHESISED IN THE LIVER REF RANGE 200 – 36 - mg/Dl

APOTRANSFERRIN (Fe 3+) SYNTHESISED IN THE LIVER REF RANGE 200 – 36 - mg/Dl EACH MOLECULE CAN BIND TWO Fe 3+ CONTAINS 95% OF IRON OVERLOAD PRODUCTION DECREASED IRON DEFICIENCY INCREASED USED AS A MARKER IRON STATUS

TIBC TOTAL IRON BINDING CAPACITY TRANSFERRIN ( 250 – 450 μg/Dl) USED ROUTINE TEST

TIBC TOTAL IRON BINDING CAPACITY TRANSFERRIN ( 250 – 450 μg/Dl) USED ROUTINE TEST FOR IRON STATUS HIGH LEVELS- LOW IRON STORES LOW LEVELS – HIGH IRON STORES

IRON STORAGE & FERRITIN LIVER & BONE MARROW (SPLEEN) STORAGE VARIES WITH GENDER, AGE,

IRON STORAGE & FERRITIN LIVER & BONE MARROW (SPLEEN) STORAGE VARIES WITH GENDER, AGE, DIET, DISEASE STORED AS FERRITIN SMALL FRACTION FOUND IN BLOOD 30 -400 ng/ml M & 15 -200 ng/Ml F LOW LEVELS – IRON DEFICIENCY HIGH LEVELS – IRON OVERLOAD

HEMOSIDERIN IRON STORAGE COMPLEX, FERRITIN, DENATURED FERRITIN & OTHER MATERIAL IRON WITH HEMOSIDERIN IS

HEMOSIDERIN IRON STORAGE COMPLEX, FERRITIN, DENATURED FERRITIN & OTHER MATERIAL IRON WITH HEMOSIDERIN IS VERY POORLY AVAILABLE IRON REUSED- RBC’s BROKEN DOWN Hb TANSPORTED TP LIVER & OTHER SITES FREE Hb – HAPTOGLOBINS TAKENUP BY THE LIVER FREE HEME- HEMOPEXIN TAKEN BY LIVER KIDNEYS REABSORBED

EXCRETION / IRON LOSS VERY LITTLE EXCRETED BLOOD LOSS, GIT (DESQUAMATION) MENSTRUAL BLOOD LOSS

EXCRETION / IRON LOSS VERY LITTLE EXCRETED BLOOD LOSS, GIT (DESQUAMATION) MENSTRUAL BLOOD LOSS URINARY (PATHOLOGICAL) BLEEDING – GUT, MENORRHAGIA, SURGERY, HEMATURIA

NUTRITIONAL ASPECTS SOURCES: RICH, GOOD, POOR LOW ECONOMY GROUPS COOKING IN IRON VESSELS RDA:

NUTRITIONAL ASPECTS SOURCES: RICH, GOOD, POOR LOW ECONOMY GROUPS COOKING IN IRON VESSELS RDA: M-10 mg, F- 20 mg, P&L – 40 mg

IRON DEFICIENCY ANEMIA <12 g/Dl , SEVERE < 10 g/Dl, CHARACTERISED BY MICROCYTIC, HYPOCHROMIC

IRON DEFICIENCY ANEMIA <12 g/Dl , SEVERE < 10 g/Dl, CHARACTERISED BY MICROCYTIC, HYPOCHROMIC ANEMIA COMMON- CHILDREN, ADOLESCENT GIRLS, PREGNANTS, LACTATING WOMEN. IDA- MOST COMMON NUTRITIONAL DISORDER IN INDIA OCCURANCE: 30% WORLDWIDE. INDIA 70% IRREVERSIBLE IMPAIRED LEARNING ABILITY DUE TO DIET CONTAING IRON ABSORPTION INHIBITORS

IRON DEFICIENCY ANEMIA SYMPTOMS: DULL, INACTIVE, SLUGGISH METABOLIC ACTIVITIES, RETARDED GROWTH, LOSS OF APETITE

IRON DEFICIENCY ANEMIA SYMPTOMS: DULL, INACTIVE, SLUGGISH METABOLIC ACTIVITIES, RETARDED GROWTH, LOSS OF APETITE MATERNAL ANEMIA PRENATAL MORTALITY PROLONGED DEFICIENCY- ATROPY OF GASTRIC EPITHELIUM- ACHLOROHYDRIA, DECREASED IRON ABSORPTION, AGGRAVATING ANEMIA

CAUSES FOR IDA INCREASED DEMAND- PREG / HYPOXIA NUTRITIONAL DEFICIENCY IRON LOSS- HOOKWORM (RURAL)

CAUSES FOR IDA INCREASED DEMAND- PREG / HYPOXIA NUTRITIONAL DEFICIENCY IRON LOSS- HOOKWORM (RURAL) CHRONIC BLOOD LOSS- BLEEDING, NEPHROSIS, GASTRECTOMY- ABSORPTION LEAD TOXICITY TREATMENT: IRON SUPPLEMENTATION

ANEMIA- LAB DIAGNOSIS LOW IRON – POOR SPECIFICITYINFECTIONS LOW FERRITIN- SPECIFIC <12µg/d. L INCREASED

ANEMIA- LAB DIAGNOSIS LOW IRON – POOR SPECIFICITYINFECTIONS LOW FERRITIN- SPECIFIC <12µg/d. L INCREASED TRANSFERRIN (TIBC) >450µg/d. L Hb- <13 g/d. L M <12 g/d. L F

IRON OVERLOAD HEMOSIDEROSIS – WITHOUT TISSUE DAMAGE HEMOCHROMATOSIS- TISSUE INJURY CELLULAR DEGENERATION & FIBROSIS

IRON OVERLOAD HEMOSIDEROSIS – WITHOUT TISSUE DAMAGE HEMOCHROMATOSIS- TISSUE INJURY CELLULAR DEGENERATION & FIBROSIS LIVER, SKIN, PANCREAS, HEART> CIRRHOSIS, DM, SKIN PIGMENTATION, CARDIAC PROBLEMS, JOINT PAIN SKIN PIGMENT & DM BRONZE DIABETES

IRON OVERLOAD

IRON OVERLOAD

IRON OVERLOAD GENETIC- INCREASED ABSORPTION CONDITIONS REQUIRING BLOOD TRANSFUSION DIETARY OVERLOAD- COOKING IN IRON

IRON OVERLOAD GENETIC- INCREASED ABSORPTION CONDITIONS REQUIRING BLOOD TRANSFUSION DIETARY OVERLOAD- COOKING IN IRON VESSELS TREATMENT: REPEATED PHLEBOTOMY DRUG- DESFERROXAMIN

COPPER (Cu) ADULT BODY 100 mg MUSCLES, LIVER, BONE MARROW, BRAIN, KIDNEY, HEART &

COPPER (Cu) ADULT BODY 100 mg MUSCLES, LIVER, BONE MARROW, BRAIN, KIDNEY, HEART & HAIR FUNCTIONS: ENZYMES- FERROCHELATASE, CO, SOD, ALA SYNTHASE, CERULOPLASMIN, TYROSINASE, LYSYL OXIDASE, MAO

ABSORPTION, STORAGE, EXCRETION 10% DIETARY Cu IS ABSORBED IN THE DUODENUM STORAGE: LIVER &

ABSORPTION, STORAGE, EXCRETION 10% DIETARY Cu IS ABSORBED IN THE DUODENUM STORAGE: LIVER & BONE MARROW EXCRETION: BILE. URINE DOES NOT CONTAIN COPPER PLASMA – 100 – 200 µg/Dl MAJOR- CERULOPLASMIN (25 -50 mg/Dl) ALBUMIN BOUND

NUTRITIONAL ASPECTS SOURCES: RDA: 2 -3 mg CLINICAL SIGNIFICANCE: Cu > ALA SYNTHASE> ANEMIA

NUTRITIONAL ASPECTS SOURCES: RDA: 2 -3 mg CLINICAL SIGNIFICANCE: Cu > ALA SYNTHASE> ANEMIA Cu>LYSYL OXIDASE> ELASTIN> WEAK BLOOD VESSELS>CVD Cu>TYROSINASE> MELANIN> HYPOPIGMENTATION

NUTRITIONAL ASPECTS MENKE’S KINKY HAIR SYNDROME: DEFECT IN INTRACELLULAR Cu BINDING ATPase X-LINKED DISORDER

NUTRITIONAL ASPECTS MENKE’S KINKY HAIR SYNDROME: DEFECT IN INTRACELLULAR Cu BINDING ATPase X-LINKED DISORDER MALE INFANTS NERVOUS SYSTEM, CONNECTIVE TISSUE & VASCULATURE AFFECTED KINKY- BRITTLE, TWISTED, STEEL LIKE HAIR

WILSON’S DISEASE HEPATOLENTICULAR DEGENERATION OCCURS LATE CHILDHOOD DEFECTIVE ATPase-Cu BINDING NORMAL EXCRETION OF Cu

WILSON’S DISEASE HEPATOLENTICULAR DEGENERATION OCCURS LATE CHILDHOOD DEFECTIVE ATPase-Cu BINDING NORMAL EXCRETION OF Cu LIVER CELLS LIVER, BRAIN, KIDNEY, RBC’s Cu DEPOSITION CIRRHOSIS NECROSIS LENTICULAR NUCLEUS BRAIN NEUROLOGICAL SYMPTOMS

WILSON’S DISEASE HIGH LIVER Cu FAILURE OF CERULOPLASMIN KAYSER FLEISCHER RING- DEPOSITION DESCEMETS MEMBRANE,

WILSON’S DISEASE HIGH LIVER Cu FAILURE OF CERULOPLASMIN KAYSER FLEISCHER RING- DEPOSITION DESCEMETS MEMBRANE, GREEN OR GOLDEN PIGMENT AROUND CORNEA TREATMENT - LOW Cu DIET

ZINC 2 g ADULT BODY 60% SKELETAL MUSCLES, 30% BONES FUNCTIONS ENZYMES-CA, ALP, LDH,

ZINC 2 g ADULT BODY 60% SKELETAL MUSCLES, 30% BONES FUNCTIONS ENZYMES-CA, ALP, LDH, EDH, Gl. DH, CARBOXYPEPTIDASE, ALA DEHYDRATSE, RNA POLYMERASE CYTOSOLIC SOD (Cu & Zn) INSULIN BETA CELLS STABILISES THE MOLECULE GUSTEN SALIVA TASTE SENSATION SYNTHESIS RBP-RODOPSIN WOUND HEALING, REPRODUCTION, DIARRHEA

ABSORPTION, STORAGE, EXCRETION MAINLY FROM DUODENUM Cu, Cd, PHYTATES, Fe INTERFERE Zn & Cu

ABSORPTION, STORAGE, EXCRETION MAINLY FROM DUODENUM Cu, Cd, PHYTATES, Fe INTERFERE Zn & Cu COMPETITIVELY INHIBIT STORAGE: LIVER EXCRETION: PANCREATIC JUICE, SWEAT PLASMA: 100µg/d. L

NUTRITIONAL ASPECTS SOURCES: RDA- 10 15 mg CLINICAL SIGNIFICANCE: DEFICIENCY- POOR WOUND HEALING, GROWTH

NUTRITIONAL ASPECTS SOURCES: RDA- 10 15 mg CLINICAL SIGNIFICANCE: DEFICIENCY- POOR WOUND HEALING, GROWTH RETARDATION, SKIN LEASIONS, IMPAIRED SPERMATOGENESIS MENTAL DISORDERS, DEPRESSION, DEMENTIA PSYCHIATRIC DISORDERS

NUTRITIONAL ASPECTS ACRODERMATITIS ENTEROPATHICA DFECTIVE ABSORPTION INFLAMMATION MOUTH, NOSE, FINGERS etc DIARRHEA, ALOPECIA, OPHTHALMOPLEGIA

NUTRITIONAL ASPECTS ACRODERMATITIS ENTEROPATHICA DFECTIVE ABSORPTION INFLAMMATION MOUTH, NOSE, FINGERS etc DIARRHEA, ALOPECIA, OPHTHALMOPLEGIA & HYPOGONADISM ZINC TOXICITY WELDERS- INHALE Zn OXIDE FUMES RAT POISON NAUSEA, GASTRIC ULCER, PANCREATITIS, ANEMIA & EXCESS SALIVATION

SELENIUM SELENOCYSTEINE DIRECTLY INCORPORATED DURING TRANSLATION CONSIDERED 21 St AMINO ACID ANTIOXIDANT- GLUTATHIONE PEROXIDASE

SELENIUM SELENOCYSTEINE DIRECTLY INCORPORATED DURING TRANSLATION CONSIDERED 21 St AMINO ACID ANTIOXIDANT- GLUTATHIONE PEROXIDASE VITAMIN E SPARING ACTION 5’ DEIODINASE CONVERTS T 4 TO T 3

SELENIUM ABSORBED FROM DUODENUM PLASMA – 50 – 100µg/Dl SOURCES: ORGAN MEATS, SEAFOODS RDA:

SELENIUM ABSORBED FROM DUODENUM PLASMA – 50 – 100µg/Dl SOURCES: ORGAN MEATS, SEAFOODS RDA: 50 – 100 µg, INTAKE DEPENDS NATURE OF SOIL CROPS ARE GROWN

CLINICAL SIGNIFICANCE DEFICIENCY- KESHAN DISEASES SOIL DEFICIENT MULTIFOCAL MYOCARDIAL NECROSIS CARDIAC ARRYTHMIA, ENLARGEMENT ISOLATED

CLINICAL SIGNIFICANCE DEFICIENCY- KESHAN DISEASES SOIL DEFICIENT MULTIFOCAL MYOCARDIAL NECROSIS CARDIAC ARRYTHMIA, ENLARGEMENT ISOLATED DEFICIENCY CAUSES LIVER NECROSIS, CIRRHOSIS, CARDIAC MYOPATHY, MUSCULAR DYSTROPHY

CLINICAL SIGNIFICANCE SELENIUM TOXICITY- 900µg METAL POLISH / ANTIRUST COATING MANIFESTATIONS- WEIGHT LOSS, EMOTIONAL

CLINICAL SIGNIFICANCE SELENIUM TOXICITY- 900µg METAL POLISH / ANTIRUST COATING MANIFESTATIONS- WEIGHT LOSS, EMOTIONAL DISTURBANCE, DIARRHEA, HAIR LOSS, GARLIC ODOUR OF BREATH TREATMENT- HALOGENATED AROMATIC HYDROCARBONS

MOLYBDENUM XANTHINE OXIDASE SULFITE OXIDASE RDA- 200µg DEFICIENCY VERY RARE

MOLYBDENUM XANTHINE OXIDASE SULFITE OXIDASE RDA- 200µg DEFICIENCY VERY RARE