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MINERALS
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Introduction
Minerals are inorganic elements required for a variety
of functions.
They are essential for normal growth and maintenanceof the body.
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Classification of Minerals
Minerals
MacroMinerals
Traceelements
Essential
Possiblyessential
Non -essential
ToxicMinerals
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Macro Minerals
Required in excess of 100 mg/day.Eg:
Calcium
Phosphorous Magnesium
Sodium
Potassium
Chloride &
Sulfur
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Trace Elements
Required in amounts less than 100 mg/day. Further classified into 3 sub categories.
A. Essential trace elements:
Iron, Iodine, Copper, Manganese, Zinc,Molybdenum, Selenium, Flouride.
B. Possibly essential trace elements:
Nickel, Vanadium, Chromium, Barium.
C. Non-essential trace elements:
Rubidium, Silver, Gold, Bismuth
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Toxic Minerals
These are toxic to the body & should beavoided.
Eg:
Aluminium Lead
Mercury
Arsenic Cadmium
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Functions of Minerals
Minerals
OsmoticPhenomenon
Nerve MuscleConduction
Structure
Physiologicallyimportant
Eg: Hb,thyroxine
Co-factors inenzymes
Regulation ofacid-basebalance
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CALCIUM
Most abundant mineral in the body.
Total calcium in the human body1 to 1.5kg.
99% of the bodys calcium is present in bonesas hydroxyapatite.
1% in the extra-cellular fluid.
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Sources of CalciumMedium SourcesGood Sources
Small amount
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Recommended Daily Allowance of
Calcium
Adults: 500 mg/ day.
Children: 1200 mg/day.
Pregnant and lactating women: 1500 mg/day. Old age & menopausal women:
1500 mg/ day of Calcium + 20 g/ day of Vitamin D.
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Functions1) Bone mineralization.
2) Blood coagulation - prothrombin to thrombin.
3) Muscle Contractionexcitation-contraction coupling.
4) Nerve conduction.
5) Release of hormonesinsulin, parathyroid hormone,vasopressin, calcitonin, etc.
6) Second messenger.
7) Regulation of enzyme activity.
8) Action on myocardiumprolongs systole.9) Vascular permeabilitydecreases passage of serum
through capillaries.
10) Cell division.
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Absorption of Calcium
Site: 1stand 2ndpart of duodenum.
Active transportrequires energy.
Carrier proteinCalbindin.
Excretion of Calcium
Partly through kidneys. Mostly by small intestine through faeces.
Small amount of calcium may be lost in sweat.
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Factors affecting Calcium absorption
Factors stimulating
Vitamin Dinduces synthesis of CALBINDIN ->
facilitates absorption of Ca.
Parathyroid hormone (PTH)
Acidityfavors absorption
Amino acidsLysine, Arginine.
Lactoseforms soluble complexes with Ca ions.
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Factors affecting Calcium absorption
Factors inhibiting
Phytic acids (Inositol Hexaphosphate)
Oxalates.
Malabsorption syndromeCeliac disease.
Phosphates
Obstruction of bile duct
Chronic renal failure.
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Plasma Calcium Levels
Normal levels : 911 mg/dL. Calcium is present in 3 forms
1. Free / ionized/ ionic CalciumBiologically active.
2. Bound Calcium3. Complexed Calcium
- bicarbonate
- Phosphate- Lactate
- Citrate
Ionized Calcium
Bound Calcium
Complexed Calcium
50%
40%
10%
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Regulation of Calcium
3 main organs
Bone,
Kidney &
Intestine.
3 main hormones
PTH,
Vitamin D &
Calcitonin.
Homeostasis of plasma calcium is dependent on thefunction of
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Regulation (cont.)
3 major processes are involved
1. Absorption of calcium from the intestine,
mainly through the action of Vitamin D.
2. Reabsorption of Calcium from the kidney,
mainly through the action of PTH & Vitamin D.
3. Demineralization of bone mainly through
action of PTH but facilitated by Vitamin D.
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Vitamin D1. Intestine
Increases synthesis of Calbindin
Increases absorption of calcium.
2. Bones
- Increased mobilization of calcium.
- Increase in number and activity of Osteoblasts.
3. Kidney- Increased reabsorption of Calcium.
Regulation of Calcium Homeostasis
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Regulation (cont..)
Parathyroid Hormone (PTH)1. Bone
1. Demineralization.
2. Increased Osteoclasts.2. Kidney
1. Loss of Phosphates.
2. Slight increased reabsorption of Calcium.
3. Intestine (indirect action)1. Increased absorption.
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Regulation (cont.)
Calcitonin
Opposite action to PTHDecrease Calcium
levels.
Decreases reabsorption of calcium from urine.
Decreases calcium uptake of intestines.
Increased deposition of calcium in bones.
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Regulation of Calcium
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Regulation (cont..)
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Disease states
Hypercalcemia.
Hypocalcemia.
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Hypercalcemia
Increase in Serum Calcium >11g/dL.
Causes
Hyperparathyroidism
Multiple myeloma
Malignant diseases.
Prolonged immobilization.
Increased loss of phosphates in urine
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Clinical features of hypercalcemia:-
Neurological symptomsdepression, confusion,inability to concentrate.
Generalized muscle weakness.
GI problemsanorexia, abdominal pain, nausea,
vomiting and constipation.
Renalpolyuria, polydypsia, renal calculi.
Cardiac arrhthymiasshortened QT interval on ECG.
Susceptibility to fractures.
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Hypocalcemia
More serious and life threatening condition.
Serum calcium levels < 9mg/ dL.
Causes:
Hypoproteinemia. Hypoparathyroidism.
Vitamin D deficiency.
Renal tubular defects.
Pseudohypoparathyroidism.
Malnutrition.
Malabsorption.
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Clinical features of hypocalcemia:-
Enhanced neuromuscular irritability.
Neurological featurestingling, tetany, numbness.
Muscle cramps.
Cardiac arrhthymiasprolonged QT interval.
Cataracts.
Trousseaus sign & Chovstekssign.
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Phosphorus
Adult body contains about 1kg of phosphate(400 -700g).
80% found in combination with Calcium as
hydroxyapatite. Present in bone and teeth.
Present in two forms-
Organic: soft tissues; as component ofphospholipids, nucleic acids.
Inorganic: Extracellular fluid.
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Functions Constituent of bone and teeth.
Acid-base regulationmaintains the pH of bodyfluids.
Energy storage and transfereg: creatine
phosphate and ATP. Essential constituent of phospholipid of cell
membrane, nucelic acids, nucelotides.
Enzyme actionas coenzymes eg: PLP, thiaminepyrophosphate(TPP), NADP
Regulation of enzyme activityphosphorylationand dephosphorylation reactions.
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Dietary sources
Foods rich in calcium are also rich in
phosphorus.
Milk, milk products.
Egg yolk
Fish
Meat
Cereals
Leafy vegetables.
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RDA of Phosphorus
Children: 1.0 g/ day.
Adults: 800 mg/ day.
Pregnant and lactating women: 1200mg/ day.
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Metabolism of Phosphorus
Absorption:
Site: Jejunum.
About 70% of phosphate present in the diet is
absorbed.
Organic phosphates are converted into inorganic
phosphates before absorption.
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Factors affecting absorption
Factors increasing
Bile salts.
Acidity.
Parathyroid hormone 1, 25 dihydroxy
cholecalciferol.
Calcium.
Factors decreasing
High Calcium: Phosphate
ratio. (optimum1:2)
Phytates.
Alkalinity.
Magnesium
Aluminium
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Excretion of Phosphorus
Mainly by kidneys.
Urine0.6 g/ day.
90% filtered at glomerulus is reabsorbed bytubules.
Increased by parathyroid hormone.
Decreased by 1, 25 dihydroxy Vitamin D3.
Growth hormone. Cortisol.
Small amount excreted in feces (0.20.5 g/ day)
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Serum Phosphorus
Normal levels
Adults: 2.54.5 mg/dL.
Children: 46 mg/dL.
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Regulation
1, 25 dihydroxy cholecalciferol
Increases plasma phosphorus.
Increases absorption from intestine.
Increases the renal reabsorption.
Increases the mobilization from bone (at high
doses).
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Parathyroid hormone
Decreases serum phorphorus.
Decreases the renal reabsorption.
Calcitonin
Decreases serum phosphorus.
Inhibits bone resorption.
Decreases the renal reabsorption.
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Disorders
Hypophosphatemia:
Serum inorganic phosphate
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Hyperphosphatemia:
Serum phosphate >4.5mg/dL.
Causeshypoparathyroidism,
pseudohypoparathyroidism, renal failure,
rhabdomyolysis, chemotherapy Clinical features:
Tetany & seizures.
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IRON
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IRON
Normal Iron levels: 35 g/dl. Hemoproteins hemoglobin, myoglobin,
cytochromes, xanthine oxidase, catalase,tryptophan pyrrolase, peroxidase.
Non-heme Irontransferrin, ferritin,hemosiderin.
70% is seen in RBCs as constituent of
Hemoglobin. 5% of body iron is present in myoglobin.
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Sources of Iron
Rich sources: meat, liver, heart, kidney.
Good sources: Leafy vegetables, pulses,
cereals, fish, molasses.
Poor source: Milk, wheat, polished rice.
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RDA of Iron
Adult man10 mg/ day.
Menstruating woman18 mg/ day.
Pregnant & lactating woman40 mg/day.
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Functions of Iron
Iron is required for synthesis of
Hemoproteins: hemoglobin, myoglobin,
cytochromes, catalase, peroxidase, etc.
Non-Heme Iron compounds: Iron-sulfur protein offlavoproteins, Succinate dehydrogenase, NADH
dehydrogenase.
Iron helps mainly in transport, storage andutilization of oxygen.
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Absorption of Iron
Iron is mainly absorbed in the duodenum.
Normal intake of iron is 10 to 20 mg/day.
About 5 to 10 % of dietary iron is absorbed by
active transport.
Iron is mostly found in the ferric form (Fe3+) in
the foods.
Iron in the ferrous form (Fe2+) is soluble and
readily absorbed.
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Factors affecting absorption
Promoting
Acidity, Vitamin C, cysteine.
Small peptides & amino
acids. Diet with low phosphate
content.
Decreasing/ interfering
Phytates present in cereals.
Oxalates in leafy vegetables.
Diet with High phosphatecontent.
malabsorption syndrome
steatorrhea.
Patients with partial or totalgastrectomy.
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Storage of Iron
Iron is stored in liver, spleen and bone marrow
in the form of FERRITIN.
In the mucosal cells, ferritin is the temporary
storage form of iron.
A molecule of apoferritin (mol. wt 500,000)
can combine with 4000 atoms of iron.
Maximum iron content of ferritin on weight
basis is around 25 %.
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Iron Transport & Uptake
Transport form of ironTRANSFERRIN Synthesized in the liver.
Normal Plasma level200-300mg/dl.
In Iron deficiency, the level is increased.
TOTAL IRON BINDING CAPACITY (TIBC)
Normal TIBC300 - 360g/dl.
One-third is saturated with iron.
The protein bound iron in serum120mg/dl.
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Iron metabolism
IRON IS A ONE - WAY SUBSTANCE. Iron metabolism is unique as it operates in a
closed system.
It is very efficiently utilized and reutilized bythe body.
Iron is not excreted into urine.
Iron entry into the body is controlled at the
absorption level, depending on the bodyneeds.
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Mucosal Block Theory
When iron stores in the body are depleted,
absorption is enhanced. When adequate
quantity of iron is stored, absorption is
decreased.
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Iron deficiency anemia
Most common nutritional deficiency anemia. Causes: Nutritional deficiency.
Hookworm infestation.
Repeated pregnancies.
Lack of absorptionhypochlorhydria, subtotalgastrectomy.
Chronic blood losshemorrhoids, peptic ulcer,
menorrhagia. Lead poisoning.
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Iron deficiency anemia Clinical features:
Patient becomes uninterested in thesurroundingsapathy.
Prolonged iron deficiency of iron leads to
achlorhydria. Angular stomatitis, atrophy of the papilla of the
tongue.
Dysphagia- PlummerVinson syndrome
Impaired attention, irritability, lowered memory& poor performance.
Koilonychiaspoon shaped nails
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Lab findings
Hemoglobin: < 12g/dl
Serum Iron levels: Decreased 360g/dL)
Percent saturation:
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Treatment
Oral Iron is the treatment of choice.
200 mg of ferrous sulfate thrice daily for aperiod of 2 months, later continued for 3 to 6months.
Pregnant women: 100mg of Iron + 500microgram of folic acid.
Children: 20 mg of iron + 100 microgram of
folic acid. Severe anemia: Blood transfusion may be
required.
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Iron Toxicity Hemosiderosis
Microscopically visible form is hemosiderosis
Iron overload without tissue injury
Observed in patients receiving repeated blood
transfusions for eg: patients with hemolyticanemia, hemophilia.
Hemosiderosis is observed among the Bantu tribe
in South Africa. This is attributed to high intake ofiron from their staple diet corn and their habit of
cooking in iron pots.
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Hemochromatosis.
Macroscopically visible form
Iron is directly deposited in liver, spleen, pancreas
& skin.
Iron overload with tissue injury
Bronze diabetes
Bronze pigmentation of skin and tissues Cirrhosis of liver and pancreatic fibrosis.
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Koilonychia
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Menkeskinky hair Syndrome
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KayserFleischer Ring
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Cretinism
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Goitre
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Dermatitis Herpetiformis
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Dental Caries
Skeletal Fluorosis