Download MBBS Biochemistry PPT 77 Mineral Lecture Notes

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v Widely distributed in nature
v Present in foods of Plant and

Animal origin

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1

?Minerals in human body

have various structural and

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functional roles

?Hence it is essential to

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ingest Minerals through

diet.

2

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Human Body Ingests

Seven Food Nutrients

Dietary Fiber

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Minerals

Water

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Food Substances

Vitamins

Proteins

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Lipids

Carbohydrates

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3

?Minerals are classified

based on:

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vFunctional need to body
vIts daily requirement

4

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Two Broad Classes Of Minerals

? Macro elements
? Micro/trace elements-
? Ultra trace element (required

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in amounts <1 mg/d)

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?Macro/Principle/Chief

elements

? Body needs Macro elements

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relatively in large quantities

? present in body tissues at

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concentrations >50 mg/kg

? Requirement of these Minerals is

>100 mg/day

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6
Macro elements

1. Calcium (Ca)

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2. Phosphorus (P)
3. Sulfur (S)
4. Magnesium (Mg)
5. Sodium (Na)
6. Potassium (K)

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7. Chloride (Cl)

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? Micro Minerals /Trace Elements

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? Body needs Micro Minerals

relatively in less amount

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? Present in body tissues at

concentrations <50 mg/kg

? Requirement of these

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Minerals is 100 mg/day

8
Name Of 10 Essential

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Micro/Trace Elements

1. Iron (Fe)

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2. Copper (Cu)

3. Cobalt (Co)

4. Chromium (Cr) (120 ?g/d)

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5. Fluoride (F)

6. Iodine (I) (150 ?g/d)

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7. Manganese (Mn)

8. Molybdenum (Mo) (75 ?g/d)

9. Selenium (Se) (35 ?g/d)

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10.Zinc (Zn)

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Possibly Essential Elements

for Humans (functions not

known)

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Nickel(Ni), Silicon(Si), tin(Sn),

Vanadium(V)

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Toxic elements

Arsenic, Lead, Mercury

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Nutritional y Important Minerals (60Kg)

Macro Minerals

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Trace Elements

Element

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g/kg

Element

mg/kg

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Ca

15

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Fe

20-50

P

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10

Zn

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10-50

K

2

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Cu

1-5

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Na

1.6

Mo

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1-4

Cl

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1.1

Se

1-2

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S

1.5

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I

0.3-0.6

Mg

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0.4

Mn

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0.2-0.5

Co

0.02-0.1

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Distribution of Calcium,

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Phosphate and Magnesium in

the Body

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Tissue

Calcium

Phosphate

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Magnesium

Skeleton

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99%

85%

55%

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So t tissue

1%

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15%

45%

Extracel ular fluid

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<0.2%

<0.1%

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1%

Total

1000 g (25 mol)

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600 g (19.4 mol)

25 g (1.0 mol)

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Equilibria and determinations of calcium in serum.

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Physiochemical States of Calcium, Phosphate,

and Magnesium in Normal Plasma

State

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Calcium

Phosphate

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Magnesium

Free (ionized)

50

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55

55

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Protein-bound 40

10

30

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Complexed

10

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35

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Total (mg/dL)

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8.6-10.3

2.5-4.5

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1.7-2.4

(mmol/L)

2.15-2.57

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0.81-1.45

0.70-0.99

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Free calcium

4.6-5.3

(mg/dL)

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Functions of calcium

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Intracellular calcium

1.Muscle contraction

2.Hormone secretion

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3.Second Messenger

4.Glycogen metabolism

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5.Cell division

6.Enzyme activation

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Enzymes regulated by Ca++

Adenyl cyclase

Ca++ dependent protein kinases (PKC)

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Ca++ -Mg++ -ATPase

Glycerol-3-phosphate dehydrogenase

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Glycogen synthase

Myosin kinase

Phospholipase C

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Phosphorylase kinase

Pyruvate carboxylase

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Pyruvate dehydrogenase

Pyruvate kinase

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Functions of calcium

Extracellular calcium

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1.Bone mineralization

2.Blood coagulation

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Calcium Dietary Requirements

?Adult : 800 mg/day
?Pregnancy, lactation and post-menopause:

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1500mg/day

?Growing Children: (1-18 yrs): 1200 mg/day
?Infants: (< 1 year): 300-500 mg /day

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Dietary Calcium sources

? Rich Calcium Sources

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- Milk and Milk Products
- Mil et (Ragi)
- Wheat-Soy flour
- Black strap molasses

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? Calcium Good sources

- Yoghurt, sour cream, ice cream

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- Tofu

- Guava ,Figs

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- Cereals

- Egg yolk

- Legumes

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- Green leafy vegetables as collard,

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kale , Broccolli, Cabbage and raw

turnip

- Small Fish as trout, salmon and

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sardines with bones

- Meat

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- Almonds, brazil nuts, dried figs,

hazel nuts

- Also soybean flour and cottonseed

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flour

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?Absorption of Calcium

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occurs in the Duodenum

and proximal Jejunum

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?Mediated by Calbindin

(synthesized by mucosal cel s)

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Factors Promoting Calcium Absorption

v Parathyroid Hormone (PTH) indirectly enhances

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Ca absorption through the increased activation of Calcitriol

vCalcitriol /activated Vitamin D induces the synthesis

of Ca binding protein Calbindin

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vAcidity Increases the solubility of calcium salts

vAmino acids Lysine and Arginine form soluble complexes

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with Calcium

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Factors Inhibiting Calcium Absorption

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Phytates and Oxalates present in plant origin diet form insoluble salts

The high content of dietary Phosphates forms insoluble Ca phosphate

Dietary ratio of Ca : P ---1:1 / 2:1 is ideal for Ca absorption

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The Free Fatty acids forms insoluble Ca soaps

Alkaline condition

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Low Estrogen levels Estrogen increases Calcitriol levels

High content of Dietary fiber, Caffeine, Sodium

Excess Magnesium in diet inhibits Calcium absorption

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(Magnesium competes with Calcium for absorption)

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Factors Regulating Blood Calcium

Levels

?Parathyroid Hormone (PTH)

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?Vitamin D- Calcitriol
?Calcitonin

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Organs involved for action of PTH

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Intestine

Bone

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Kidney

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PTH Action on the Bone

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Stimulating osteoclastic bone resorption-
Indirect effect through local mediators
(RANK ligand, tissue growth factor )
blood Ca level

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This Inhibits osteoblast function- Directly by

interacting with their PTH receptors

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Action Of PTH on the Kidney and Intestine

Parathyroid hormone acts on distal tubule through a cAMP dependent

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mechanism and Increases renal re absorption of Calcium

PTH increases phosphate excretion at the proximal tubule

by lowering the renal phosphate threshold.

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Action on the Intestine: indirect

PTH is a trophic factor for renal 25(OH)D1 hydoxilase.

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Increases conversion of 25(OH)D to the active metabolite 1,25(OH)2D

increases the intestinal absorption of Ca by promoting the

synthesis of Calcitriol.

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Effect of vitamin D

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vIncrease calcium binding protein synthesis

vIncrease calcium absorption

vIncrease phosphate absorption

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Causes of Hypocalcemia

Hypoalbuminemia

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Chronic renal failure

Magnesium deficiency

Hypoparathyroidism

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Pseudohypoparathyroidism

Osteomalacia and rickets due to vitamin D def. or resis.

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Acute hemorrhagic and edematous pancreatitis

Healing phase of bone disease of treated hyperpara

and hematological malignancies (hungry bone synd.)

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Causes of Hypercalcemia

Primary hyperparathyroidism

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Parathyroid adenoma, hyperplasia,

carcinoma

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Malignancy

Skeletal metastases

Humoral hypercalcemia

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PTH-rP

Hematological malignancy

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Cytokines (interleukin-1, tumor

necrosis factor, etc.)

1,25-Dihydroxyvitamin D (lymphoma)

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Familial hypocalciuric hypercalcemia

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Causes of Hypercalcemia contd

Idiopathic hypercalcemia of infancy

Vitamin overdose, vitamin D

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Granulomatous diseases (e.g., sarcoidosis, tuberculosis)

Renal failure

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Chronic, acute (diuretic phase) or after transplant

Chlorothiazide diuretics

Lithium therapy

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Milk-alkali syndrome

Immobilization

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Increased serum proteins

Hemoconcentration,

Paraprotein

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Factors altering the distribution of calcium

Factors altering protein binding of calcium

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Altered concentration of albumin or globulin

Heparin

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pH

Free fatty acids

Bilirubin

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Drugs

Temperature

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Factors altering complex formation

Citrate

Bicarbonate

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Lactate

Phosphate , Sulphate

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Anion gap

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Preanalytical Factors in Measurement of

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Serum Total or Free Calcium

In Vivo

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Tourniquet use and venous occlusion (protein bound ca

Incrd)

Changes in posture: increase of total calcium on standing

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Decrease of total ca on recumbency

Exercise (free ca)

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Hyperventilation (free ca)

Fist clenching

Alimentary status

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Alterations in protein binding

Alterations in complex formation

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Prolonged bed rest (both total and free ca increased)

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Preanalytical Factors in Measurement of

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Serum Total or Free Calcium contd

In Vitro

Inappropriate anticoagulants

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Dilution with liquid heparin

Interfering concentrations of

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heparin

Contamination with calcium

Corks, glassware, tubes

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Specimen handling

Alterations in pH ( free calcium)

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Adsorption or precipitation of calcium

Spectrophotometric interference

Hemolysis, icterus, lipemia

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Causes of Hypophosphatemia

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v

Shift of phosphate from extracel ular to intracel ular space

Glucose

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Insulin

Respiratory alkalosis-accelerates glycolisis

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v

Renal phosphate wasting

Lowered renal phosphate threshold

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Primary or secondary hyperparathyroidism

Renal tubular defects

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Familial hypophosphatemia

Fanconi syndrome

v Decreased net intestinal absorption

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Increased Loss---Vomiting, Diarrhoea, antacids

Decreased absorption

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Malabsorption

Vitamin D deficiency

v Intracel ular phosphate loss

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Acidosis Ketoacidosis, Lactic acidosis

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Clinical manifestation of serum phosphate depletion

depend on length and degree of deficiency

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Plasma conc <1.5 mg/dL----produce clinical manifestation

Glycolysis impaired

Muscle weakness

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Acute respiratory failure

Decreased cardiac output

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Very low serum phosphate (<1 mg/dL)

Rhabdomyolysis

Tissue hypoxia

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Mental confusion, Coma

Serum phosphate concentration <0.5 mg/dL

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Hemolysis of red blood cells

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Causes of Hyperphosphatemia

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Decreased renal phosphate excretion

Decreased glomerular filtration rate

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Renal failure

Increased tubular reabsorption (increased threshold)

Hypoparathyroidism

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Pseudo hypoparathoidism

Acromegaly

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Increased phosphate intake

Oral or intravenous administration

Phosphate containing enema

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Increased extracellular phosphate load

Transcellular shift

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Lactic acidosis, Resp acidosis, DKA

Cell lysisRhabdomyolysis

Intravascular hemolysis

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Magnesium

Fourth most abundant cation in the body

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RBC content of Mg= 3 times of serum

Absorbed from distal small bowel

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Excreted mainly through kidney

Daily requirement: 300-350 mg/d (male)

Reference interval 1.7-2.4 mg/dL

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Mg is important in neuromuscular excitability

Activator of large number of enzymes:

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Alkaline phosphatase, hexokinase, Adenylyl cyclase,

cAMP dependent kinase, Squalene synthase,

Glutamine synthase

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Required for many cellular transport processes:

insulin dependent glucose uptake.

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Causes of Magnesium deficiency

GI disorder

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Prolonged nasogastric suction

Malabsorption syndrome

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Acute and chronic diarrhoea

Protein calori malnutrition

Renal loss

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Chronic parenteral fluid therapy

Osmotic diuresis

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Glucose (DM)

Mannitol

Metabolic acidosis

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Urea

Starvation,

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Hypercalcemia

ketoacidosis

Alcohol

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Alcoholism

Drugs Diuretics

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Aminoglycoside

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Causes of hypermagnesemia

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Excessive intake

Orally (usually in the presence of CRF)

Antacid

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Cathartic

Rectally Purgation

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ParentallyTreatment of pregnancy induced HT

Treatment of magnesium deficiency

Renal failure

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Chronic usually with administration of magnesium

Antacid

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Cathartic

Enema

Infusion

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Acute Rhabdomyolysis

Lithium ingestion

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Distribution of Iron in a 70-kg Adult Male

Transferrin

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3-4 mg

Hemoglobin in red blood cel s 2500 mg
In myoglobin and various

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300 mg

enzymes
In stores (ferritin)

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1000 mg

Absorption

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1 mg/d

Losses

1 mg/d

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In an adult female of similar weight, the amount in stores would general y be less

(100-400 mg) and the losses would be greater (1.5-2 mg/d).

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Nonheme iron transport in enterocytes

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Absorption of iron

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The transferrin cycle

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Recycling of iron in macrophages

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Schematic representation of the reciprocal relationship between

synthesis of ferritin and the transferrin receptor (TfR1).

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Role of hepcidin in systemic iron regulation

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Regulation of hepcidin gene expression

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Changes in Various Laboratory Tests Used to Assess Iron-Deficiency Anemia

Parameter

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Normal

Negative Iron

Iron-Deficient

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Iron-Deficiency

Balance

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Erythropoiesis

Anemia

Serum ferritin 50-200

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Decreased <20

Decreased <15

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Decreased <15

(g/dL)
(TIBC) (g/dL)

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300-360

Slightly increased Increased >380

Increased >400

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>360

Serum iron

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50-150

Normal

Decreased <50

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Decreased <30

(g/dL)
Transferrin

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30-50

Normal

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Decreased <20

Decreased <10

saturation (%)

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RBC

30-50

Normal

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Increase

Increase

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protoporphyrin

(g/dL)
Soluble

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4-9

Increase

Increase

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Increase

transferrin

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receptor (g/L)
RBC

Normal

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Normal

Normal

Microcytic

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morphology

Hypochromic 52
Diagnosis of Microcytic Anemia

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Tests

Iron

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Inflammation Thalassemia

Sideroblastic

Deficiency

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Anemia

Smear

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Micro/hypo

Normal

Micro/hypo

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Variable

micro/hypo

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with targeting

SI (g/dL)

<30

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<50

Normal to

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Normal to

high

high

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TIBC (g/dL)

>360

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<300

Normal

Normal

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Percent

<10

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10?20

30?80

30?80

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saturation

Ferritin (?g/L) <15

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30?200

50?300

50?300

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Hemoglobin

Normal

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Normal

Abnormal

Normal

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pattern

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Zinc

Second most abundant trace element in the body

The most available dietary sources of zinc : red meat and fish,

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Germ and whole bran

Dietary reference intake

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Male: 11 mg/d Female: 8 mg/d

Infants and young children= need small amount

Strict vegetarians= 50% more zinc /d

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Zinc in human breast milk is efficiently absorbed because of

presence of picolinate and citrate.

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Zinc metabolism

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Examples of Zinc containing enzymes

Cabonic anhydrase

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Alkaline phosphatase

RNA and DNA polymerase

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Thymidine kinase and carboxy peptidase

Alcohol dehydranase

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Reference interval of zinc

A guidance reference interval: 80-120 ?g/dL

Plasma samples are preferred to serum

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Serum concentration is 5% higher than that of plasma

Concentration decreased after food

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Concentration is higher in the morning

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Clinical deficiency of zinc

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Signs and symptoms :

Depressed growth with stunting---cereal based diet

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Increased incidence of infection
Diarrhoea
Skin lesions
Alopecia

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Acrodermatitits enteropathica

Autosomal recessive inborn error

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Mutation on SLC (solute linked carrier)39a4 gene

on chromosome 8 q24.3

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Affects zinc absorption from intestinal mucosa

1.Periorificial dermatitis

2.Alopecia

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3.diarrhoea

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Role of zinc on immune function

Increase in the activity of serum thymulin--

the thymus specific hormone involved in T cell function

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Maintain balance develops between Th1 and Th2 helper cells

Increase the lytic activity of natural killer cells

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Improve cell mediated immunity

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Dietary sources of copper

Organ meats , liver, kidney

Shell fish

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Whole grain cereals

Cocoa containing products

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Absorption

The extent of absorption: 20-50%

Absorption reduced by: Zinc, molybdate, iron

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Absorption increased by aminoacids

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Metabolism of copper

62
Functions of Copper

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In cellular respiration: cytochrome c oxidase-located on

mitochondrial membrane

Formation and maintenance of myelin : cytochrome c oxidase

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Iron homeostasis: ceruloplasmin

Melanin formation: tyrosinase

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Neuro transmitter production : Dopamine -hydroxylase catalyzes

the conversion of dopamine to the neurotransmitter norepinephrine

MAO- catalyzes the metabolism of seroronin

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Synthesis of connective tissue: lysyl oxidase- stabilization of

extracellular matrix- enzymatic cross linking of collagen and elastin

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Protection against oxidants: Superoxide dismutase- protects against

free radical damage

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Menkes disease

Kinky or steely hair disease

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X linked , affects only male infants

Mutations in the gene ATP7A gene for a

copper binding P type ATP ase: Responsible for directing the

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efflux of copper from cells

Copper is not mobilized from the intestine--accumulates

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Activities of enzymes are decreased--because of defect of its

incorporation into the apoenzyme

Absence of hepatic involvement

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Wilson disease

Mutation in a gene encoding a copper binding P type ATPase

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Copper fails to be excreted in the bile and accumulates

in liver, brain, kidney and RBC

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Inhibit the coupling of copper to apoceruloplasmin and

leads to low level of ceruloplasmin in plasma

Hemolytic anemia, chronic liver disease, neurologic syndrome

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Kayser-Fleisher ring

Liver biopsy should be performed

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Treatment:



65

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Major Laboratory tests used in the

investigation of diseases of copper metabolism

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Test

Normal adult range

Serum copper

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10-22?mol/L (70-

140?g/dL)

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Ceruloplasmin

200-600 mg/L

Urinary copper

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<1 ?mol (60?g)/24h

Liver copper

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20-50 ?g/g dry weight

66
Major Laboratory tests used in the

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investigation of diseases of copper metabolism

Test

Wilson disease

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Serum copper

<8 ?mol/L

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Ceruloplasmin

<200 mg/L

Urinary copper

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>3 ?mol/24h

Liver copper

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>250 ?g/g dry weight

67

Copper and Anaemia

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Interfering iron transport

Part of ALA synthase

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Microcytic hypochromic

Iron resistant

68

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Selenium

Selenium is an essential element for humans

Constituent of the enzyme glutathione peroxidse

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The most biologically active compounds contain

Selenocysteine: Selenium is substituted for sulphur

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in cysteine;

incorporated into protein by specific codon.....

Ingested selenium compounds include

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selenate, selenite , selenocysteine,

Selenomethionine

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RDA= 55?g/d

69

Dietary sources and metabolism of Selenium

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Mainly as selenomethionine from plants

Selenium from Inorganic salts are more

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rapidly incorporated than organic sources

50-60% of total plasma selenium- selenoprotein P

30%-- GSHPX-3

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Rest- into albumin as selenomethionine

Major route of excretion: Urine ( 20-1000?g/L) 70

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Metabolic pathways of selenium

71

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Functions of Selenium

Glutathione Peroxidase

Remove an oxygen atom from H2O2 and lipid hydroperoxide

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1. GSHPx-1 in red cell s, 2. GSHPx-2 in gastrointestina mucosa,

3. blood plasma GSHPx-3,

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4. the cell membrane? located GSHPx-4.

Iodothyronine Deiodinase

T4 T3

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Thioredoxin Reductases

Selenoprotein P-transport protein and has antioxidant function

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72
Severe Deficiency

Keshan Disease.

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Kashin-Beck Disease

Marginal Deficiencies

Thyroid Function

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Immune Function? both cell mediated and B cell function are impaired
Reproductive Disorders--necessary for testostereone synthesis

and maintenance of sperm viability
Mood Disorders-anxiety, confusion, hostility

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Inflammatory Conditions- arthritis, pancreatitis
Viral Virulence--Coxackie virus

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Cancer Chemoprevention

Toxicity of Selenium

Garlic odor

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Hair loss

Nail damage

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Reference interval: 63-160 ?g/L

Selenium depletion: <40?g/L

Tolerable upper limit 400 ?g/d

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Laboratory assessment: CFAAS (Carbon furnace AAS)

ICP(inductively coupled plasma)-MS

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74


Vitamin E sparing effect of Selenium

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75

Fluoride

Most widely used pharmacologically beneficial trace

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elements

Supplementation:

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Water

Salt

Sugar

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Milk

76
Function of fluoride

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The fluoride is exchanged for hydroxil in the

crystal structure of apatite, a main component of

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skeletal bone and teeth.

Stabilizes the regenerating tooth surface.

To reduce decay of the erupting teeth as well as

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Topical effect on adult teeth.

Pharmacological doses of fluoride may reduce the

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incidence of bone fracture in patients with

osteoporosis.

77

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Absorption, transport, metabolism

and excretion of Fluoride

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Absorbed from the stomach and the small intestine

Peak increase in blood plasma occurs within 1 hour

Ions are rapidly cleared from plasma into tissues

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In exchange with anion e,g. hydoxil, citrate, carbonate

96% of the 2.6 g of total body fluoride is located

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in bones and teeth

90% of excess fluoride is excreted in urine

78

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Toxicity of Fluoride

Dental fluorosis: The mottling of enamel in the

erupting teeth of children

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A disfiguring condiition

Caused by ingestion of fluoride containing toothpaste

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Skeletal fluorosis: Occupational exposure to

inhaled fluoride dust among Cryolite workers

during aluminium refining: Bone abnormalities

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79

Laboratory assessment of status of Fluoride

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Analysis of drinking water

Determination of fluoride in urine

Direct determination using fluoride specific electrode

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Reference interval of Fluoride

Concentration in body fluids and tissue vary widely

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For urine: a guideline interval is: 0.2 ? 3.2 mg/L

80

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Dental fluorosis

81

Common sources of dietary iodine

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naturally in soil and seawater

Iodized table salt

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Cheese

Cows milk

Eggs

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Frozen Yogurt

Ice Cream

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Iodine-containing multivitamins

Saltwater fish

Seaweed (including kelp, dulse, nori)

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Shellfish

Soy milk, Soy sauce

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Yogurt

82

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Synthesis o thyroid hormones

83

Deficiency of iodine

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Hypothyroidism

PREGNANCY-RELATED PROBLEMS:

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miscarriages, stillbirth, preterm delivery,

congenital abnormalities in their babies

Children of mothers with severe iodine deficiency

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during pregnancy

mental retardation (preventable cause)

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problems with growth, hearing, and speech

Cretinism ( permanent brain damage, mental retardation,

deaf mutism, spasticity,)

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84
The recommended average daily intake of iodine

Adult: 150 ?g/d

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children: 90?120 ?g/d

pregnant women: 200 ?g/d

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Urinary iodine is >10 ?g/dL in iodine-sufficient

populations

85

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MEDIAN POPULATION URINARY IODINE VALUES

AND IODINE NUTRITION

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MEDIAN URINARY IODINE

CORRESPONDING IODINE

IODINE NUTRITION

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CONCENTRATION (g/L)

INTAKE (g/day)

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<20

<30

SEVERE DEFICIENCY

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20-49

30-74

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MODERATE DEFICIENCY

50-99

75-149

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MILD DEFICIENCY

100-199

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150-299

OPTIMAL

200-299

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300-449

MORE THAN ADEQUATE

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>299

>449

POSSIBLE EXCESS

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86