Minerals

Macrominerals Required in amount more than 100 mg/day As Ca, P, Mg, Na, K, Cl (Microminerals (Trace element Required in amount less than 100 mg/day ,As Chromium, Cobalt, Cuper , Fluoride, Iodine, Iron ,Manganese, Molybdenium Selenium, Zinc

Sources (Milk and its product (cheese- 1

Beans, egg yolk- 2 Both Ca and P are required for bone formation and other non-skeletal .functions

Factors affecting Ca absorption

Factor Ca absorption
1- Diet: A- High protein diet (A.A. form soluble Ca salt so easy absorbed) B- Lactate and citrate in lemon and orange C- Vitamin D3 2-Acidity 3- Parathyroid hormone

Factor Ca absorption
1- Diet: Phosphate (in fish) , oxalate (in tomato), Phytate (in cereal) which form insoluble Ca salt

2-Alkalinity 3- Impaired fat absorption: FA form insoluble Ca salts

Body Ca

of Ca present in bones and % 99 teeth in the form of hydroxyapatite (Ca10(PO4(6(OH(2 present in body fluid % 1

Blood Ca Blood Ca level 9- 11 mg/dl, No Ca in RBC Plasma Ca present in 2 form Ionized: 50% (diffusable( 5-6 mg- 1 It is active form if lead to tetany Non Ionized: 50% (bound( 4-5- 2 mg , bound to albumin if no tetany

Factors affecting blood Ca (Ca homeostasis(

Hormonal factor
( Parathyroid hormone (PTH- 1 blood Ca by Absorption of Ca from intestine- 1 Reabsorption of Ca from kidney- 2 Resorption (mobilization of Ca- 3 from bone to blood P excretion- 4

Calcitriol (1,25- 2 dihydroxycholecalciferol( active vitamin D3, Ca by Absorption of Ca from intestine-1 Reabsorption of Ca from kidney-2 Resorption (mobilization of Ca-3 from bone to blood

Vitamin D Metabolism
VitD3

25-hydroxycalciferol (25-HCC)

VitD2

ACTIVE 1,25-dihydroxycalciferol

INACTIVE 24,25-dihydroxycalciferol

Calcitonin secreted from C- 3 cell of thyroid gland Ca in blood by deposition in bones Estrogen- 4 Has role in Ca metabolism in ,bones as calcitonin
Ca in blood by deposition in bones

In menopause , oestomalachia occur due to estrogen

Other factors;z Solubility product- 1 Optimum absorption of Ca occur at ration 2: 1 or 1:1 with P pH- 2 Ca is soluble and ionized at normal pH 7.4, alkalosis Ca

Function of Ca (role of Ca in (metabolism Enter structure of bone and-1 teeth Contraction of muscle- 2 Transmission of nerve- 3 impulse

neuromuscular irritability - 4 so its deficiency lead to tetany that treated by Ca Blood and milk clotting- 5 casein in milk + Ca rennin + insoluble Ca paracasinate (milk (clot( (give sense of fullness Combine with calmodulin- 6 which act as second messenger for some hormone

5.Activates various enzymes (glycogen phosphorylase ,kinase(.

Lots of functions

Excretion Mainly in feces, small amount in urine Requirement , Adult 800 mg/day Pregnancy & lactation 800-1200 mg/day

Alteration in serum Ca Hypercalcemia Causes Primary hyperparathyrodism- 1 due to adenoma in gland Secondary hyperparathyrodism- 2 intake of vitamin D- 3 Cancer bones- 4 Drug- 5

Effect hypercalcemia Stone kidney, vomiting, abdominal cramp, constipation

Hypocalcemia Hypoparathyrodism (primary-1 (or surgical removal Alkalosis- 2 Kidney disease- 3 Due to formation of calcitriol

Calcium Deficiency in bone Rickets-1 .in growing Children .Osteomalacia in adults- 2

Phosphorus

Sources Milk and its product-1 ((cheese Fish, meat and liver- 2

Factor affect P absorption the same as affect Ca absorption Body phosphorus present in bones and teeth % 80 present in body fluid % 20 Blood P Normal level 3-5 mg/dl, P present in RBC in the form as ATP

Function
High energy phosphate- 1 (compounds (ATP, GTP Nucleic acids: Nucleoproteins,-2 .cAMP .Phospholipids-3 .Phosphoproteins- 4 (.Coenzymes (NAD, NADP- 5

Factors affecting blood P

(Parathyroid hormone (PTH-1 P by P excretion

(,Calcitriol (active vitamin D3- 2 P by Absorption of P from intestine- 1 Reabsorption of P from kidney- 2 Resorption (mobilization of P from- 3 (bone to blood The power of PTH in excretion more than vitamin D in reabsorption from kidney

Requirement
Adults: 1000 mg/day- 1 Pregnancy and lactation: 1200- 2 mg/day Sources as (sodium phosphate( .are highly digestible . P absorbed in the small intestine

Magnesium
Sources: Green leafy vegetables Body Magnesium present in bones and teeth % 70 present in body fluid % 30 Blood Mg: Plasma Mg 2-3 mg/dl

Function Enter formation of bone and teeth- 1 Mg helps to prevent the dental caries by enabling the calcium adhere to the teeth. Activation of many enzyme as- 2 .kinase , Phosphatases .Pyrophosphatases .Others as pyruvate dehydrogenase Active transport of some cation- 3 , As Ca, Na, K has role in muscle contraction decrease neuromuscular irritability so deficiency lead to tetany

Alteration in serum Mg Hypermagnesemia Cause: Intake of laxative Effect: Hypotension , loss of tendon reflex Hypomagnesemia Cause: Chronic alcoholism Effect: tetany

Sodium

Sources : Table salts Body Na of Na present in body fluid , 2/3 main extracellular cation Na in skeleton 1/3 Plasma Na (mmol/L (330 mg/dl 137-143

Function Maintain osmotic pressure- 1 Transmission of nerve- 2 impulse Contraction of muscle- 3 Regulate acid base- 4 balance

Alteration in serum Na Hyponatremia Addison disease- 1 Due to aldosterone (Na reabsorption and K excretion ( Renal faliure- 2 Dehydration due to vomiting &- 3 diarrhea Diuretic block reabsorption of Na- 4

Hypernatremia Causes Cushing syndrome due to- 1 (excess cortisone (Na reabsorption Conns syndrome due to excess- 2 aldosterone Diabetes insibidus (excessive- 3 ( water loss

Effect of hypernatremia Dehydration in brain cell lead to convulsion , coma and death

Potassium Sources : Fruits & nuts Body K of K present in body fluid , 2/3 main intracellular cation K in skeleton 1/3 Plasma K (mmol/L (20 mg/dl 3.5-5

Function Maintain osmotic pressure-1 Transmission of nerve-2 impulse Contraction of muscle-3 Regulate acid base balance-4

Alteration in serum K Hyperkalemia Causes Addison disease- 1 Acidosis- 2 ECF ICF K K H H

Due to shift of K from intracellular to extracellular in exchange with H

Chronic renal failure- 3 D.M- 4 insulin help of shift K from blood ( (to cell :Effect Neuromuscular irritability- 1 Arrhythmia and cardiac arrest-2

Hypokalemia Cause Alkalosis ECF K H ICF K H

Due to H in plasma lead to shift H from ICF to ECF with reverse shift of K from plasma into cell

Cushing sundrome- 2 Cortisone cause K excretion Hyperaldosteronism- 3 Diuretic & excess steroid-4 intake Effect Weakness, Hyporeflexia Cardiac arrhythmia

Neuromuscular irritability (tetany( proportional to this ratio Na + K Ca +Mg

Chloride
Sources : Table salts mmol/L : 106- 961 Plasma Cl Function Its main extracellular anion Essential for formation of HCL- 1 Activate pancreatic amylase- 2

Microminerals (Trace (element

Iron

Sources Liver , heart, kidney-1 Molasses, Dates- 2 Spinach is a poor sources- 3 of iron Absorption : in duodenum and stomach

Mucosal block theory

Lumen
10-20 mg ingestion

Mucosa

Blood
Carried by transferrin Fe+++

Fe+++

Vit. C HCL Fe++

Fe++
Ferrioxidase

Fe+++ + Apoferritin Ferritin Fe++

ceruoloplasmin Fe++

(Cu binding protein )

Recent theory of iron absorption Iron binds to its receptors in the mucosal-1 . cells It is transported by specific carrier to-2 .inside of cells Inside the cells it is transported through- 3 the cells to portal circulation or enter in .ferritin formation

Factor affect iron absorption

Factor iron absorption Cooking of food and gastric HCL-1 Reducing substance as vitamin C and SH-2 as cysteine help reduction of Fe+++ ++to Fe Body need-3 Absorption occur more in case of iron deficiency anemia and during erythrobioesis

Factor iron absorption High dietary phosphate,-1 phytate, oxalate Impaired fat absorption-2 Alkali and tea- 3 Toast with milk- 4

Total body iron 3-5 gm 1% plasma in RBC as Hb % 66 in tissues % 33

%( Tissues iron (33 Available form Ferritin Its main storage form of iron, stored in liver, spleen, Bone marrow, skin Hemosidrein Present when the iron increase than capacity of apoferritin Present in the form of granules

Non Available form ((Hemoprotein Myoglobin-1 Respiratory cytochromes-2 Catalase & perioxidase- 3 Tryptophan oxygenaes- 4 Cytochromes P450- 5

Plasma iron 1% ,ug/dl( in male 60-160 ( ug/dl( in female 40-140 ( Transferrin Iron transferred in plasma in Fe+++ by transferrin Transferrin may carry up to 180-450 ug/dl this called total iron binding (capacity (TIBC

Function of iron O2 carry by Hb- 1 O2 storage by Mb- 2 O2 utilization by respiratory chain-3

Transport Iron enter blood in ferrous state +++Fe++ ceruloplasmin Fe Excretion In feces-1 In female due to menstruation-2 ((30 gm / month

Iron deficiency anemia Causes intake 2- absorption - 1 3- Excess loss as menstruation, bilharzia Biochemical change Plasma iron 2- Ferritin- 1 Treatment Addition of ferrous salts to diet

Bronze diabetes (hemochromatosis or (hemosiderosis :Cause I.V. intake of iron- 1 Abnormal increase iron absorption-2 Symptoms Iron deposited on Liver Cirrhosis- 1 Pancreas Skin skin Diabetes mellitus- 2 Bronze discolouration in- 3

Biochemical change Plasma iron- 1 Ferritin- 2 Treatment Periodic removal of large amount- 1 of blood Addition of iron chelator as- 2 desferrioxamine excretion of iron

Copper

Sources: Liver , kidney , nuts Blood copper In plasma 90 ug/dl-1 Ceruloplasmin (copper binding-2 ( protein +++Fe++ ceruloplasmin Fe In red cell present in some- 3 enzyme as super oxide dismutase

Function Hb synthesis- 1 Bone formation- 2 Copper essential for many- 3 enzyme as super oxide dismutase and cytochrome oxidase Copper activate many enzyme as- 4 tyrosinase, uricase

(Wilson disease (Hypocupremia

Accumulation of large amount of copper in tissues (defect in Cu P type dependant ATPase( which cause efflux Cu from cell

Symptoms Liver Cirrhosis- 1 Lenticular nucleus of brain -2 parkinosnism Cornea green discolouration in- 3 (corneal margin (Kayser Fleishre ring Kidney excretion of A.A- 4 ( (aminoaciduria

Treatment Diet low in copper- 1 D. penicellamine which chelate- 2 copper then excretion

Menke's disease

X-linked recessive trait. Defect in copper binding protein P-type ATPase enzyme which This disease involves a decrease in copper levels in the blood, liver, and brain and an increase in the gut cells, kidneys, and connective tissues as it is not mobilized normally from cells. The disorder causes severe cerebral degeneration and arterial changes, resulting in death in infancy.

Difference between Menkes and wilson disease

Menkes
1-Defect 2-Onset 3- Clinically Intestinal absorption At birth Silky hair Cerebral degeneration Death Decrease serum Cu Decrease liver Cu No TTT TTT

Wilson
Biliary excretion During child hood Liver disease

Lab. Finding

Decrease serum Cu Increase liver Cu D. Penicellamine

Iodine
Sources Salt water fish Total amount 20- 50 mg Plasma iodine Organic iodine : 4-8 ug Inorganic iodine: 1-2 ug

Iodine metabolism Concentration of iodide in thyroid gland Oxidation of iodide Inorganic iodide H2O2 thyroperoxidaes

oxidised iodide

Iodination of tyrosine Oxidised iodide + tyrosine Monoiodotyrosine (MIT( and (diiodotyrosine (DIT Coupling of tyrosine Coupling of DIT T4 coupling MIT + DIT T3

Excretion in urine % 70 Deficiency Result in goiter

Zinc
Sources : Liver, sea food, milk Body zinc in skin 20% in bone and teeth 80%

Function Essential for growth &-1 reproduction Essential for insulin synthesis-2 Essential for activation of-3 superoxide dismutase Deficiency Hypogonadism-1 Poor healing of wound- 2

(Selenium (Antioxidant Essential for glutathione-1 (perioxidaes enzyme (GSH-PX 2GSH + H2O2 (GSH-PX( 2GS + 2 H2O protective mechanism against oxidation of FA and formation of peroxide Protect RBC from hemolysis Deficiency : hemolytic anemia

Manganese
Sources It is found in grains (cereal), fruits, and vegetables in good quantities. Meats, fish, are poor sources. Adults should take between 2.5 to 5 mg/day.

Functions
1- Activator of several different enzymes: Phosphoglucomutase, isocitric dehydrogenase. Intestinal peptidase. Carboxylases, ATPases. Arginase. Mitochondrial superoxide dismutase 2- Essential for normal bone structure, reproduction and function of CNS.

.Manganese deficiency is rare Manganese deficiency causes poor growth, weight loss, skeletal abnormalities such as short leg .bones

Cobalt Enter formation of vitamin B12 Activate many enzyme

Chromium Important for glucose utilization Molybdenum Important for xanthine oxidase activity

Xanthine oxidase

OH N N N N HO

OH N N HO

OH N OH

N H

N xanthine

N H

N H

hypoxanthine

uric acid

xanthine oxidase

Xanthine oxidase is a flavoprotein which also contains Fe and Mo

Fluoride Sources: Water Function: Prevent dental caries by Formation of fluoroapatiete which resist bacterial growth Prevent enolase enzyme of glycolysis so prevent bacterial glycolysis that give energy

Flurosis Excessive intake of fluoride lead to Increase bone density Calcification of bone at point of insertion of muscle Inhibit enolase, aconitase enzyme

Sulfur metabolism Sulfur present in Sources Most sulfur in the diet comes from- 1 protein sources containing sulfur amino acids such as cysteine, cystine and .methionine Sulfur vitamin as B1- 2 Sulfur contain coenzyme as TPP- 3 Bile salts

Function Sulfate is a component of major :structural molecules of the body Carbohydrate: All GAGs except- 1 hyaluronic acid, for example: Chondroitin sulfate is a constituent .of cartilage

Lipids: Sulfolipids, conjugated bile- 3 .acids as taurocholic acid Proteins: Component of amino- 4 acids: cystine, cysteine, and methionine for bioactive and .structural proteins: insulin, keratin Active sulphate: 3 phospho- 5 adenosine- 5 phospho sulfate : .PAPS

.Vitamins: Thiamine, biotin and coenzyme A Etherial compounds formed by detoxification of phenolic compounds as .skatoxyl, indoxyl Major component of mucus: gastric mucus is a glycoprotein containing about 500 chains of carbohydrate, with sulfate .groups attached .Deficiency is related to protein deficiency