Download MBBS Biochemistry PPT 54 Minerals Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st year (First Year) Biochemistry ppt lectures Topic 54 Minerals Notes. - biochemistry notes pdf, biochemistry mbbs 1st year notes pdf, biochemistry mbbs notes pdf, biochemistry lecture notes, paramedical biochemistry notes, medical biochemistry pdf, biochemistry lecture notes 2022 ppt, biochemistry pdf.


Mineral Metabolism

Introduction


What are Minerals?

Minerals

v Minerals are Inorganic elements
v Not biosynthesized in human

body

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

Animal origin
Minerals In Human body

?Minerals in human body

serve for various structural

and functional roles

?Hence it is essential to

ingest Minerals through

diet.
Human Body Ingests

Seven Food Nutrients

Dietary Fiber

Minerals

Water

Food Substances

Vitamins

Proteins

Lipids

Carbohydrates

Minerals In Human body

v Minerals are Nutrient Of

Human Food

v Essential Nutrient
v Micro Nutrient
v Non Calorific Nutrient
Characteristics Of Minerals

Minerals ? Natural in Occurrence

? Solid in nature
? Inorganic
? Definite chemical

composition

? Crystal structure due

to internal

arrangement of atoms


v Minerals ingested are not

changed in the body.

v Minerals are not destroyed by

heat, light, acid or mixing

Classification Of Minerals
Body Minerals

q30 Chemical elements are

identified as Minerals.

qImportant for human

growth, development and

regulation of vital functions

?Minerals are classified

based on:

vFunctional need to body
vIts daily requirement
Two Broad Classes Of Minerals

? Macro Minerals ? 60-80 %
? Micro Minerals- 20%

?Macro/Principle/Chief

Minerals

? Body needs Macro Minerals

relatively in large quantities

? Minerals present in body tissues at

concentrations >50 mg/kg

? Requirement of these Minerals is

>100 mg/day
7 Names Of Macro/Chief Minerals

1. Calcium (Ca)
2. Phosphorus (P)
3. Sulfur (S)
4. Magnesium (Mg)
5. Sodium (Na)
6. Potassium (K)
7. Chloride (Cl)

? Micro Minerals /Trace Elements

? Body needs Micro Minerals

relatively in less amount

? Present in body tissues at

concentrations <50 mg/kg

? Requirement of these

Minerals is 100 mg/day
Subclasses Of Micro/Trace Minerals

? Essential Trace Elements
? Possibly Essential Trace

Elements

? Non Essential Trace Elements

Name Of 10 Essential

Micro/Trace Elements

1. Iron (Fe)

2. Copper (Cu)

3. Cobalt (Co)

4. Chromium (Cr)

5. Fluoride (F)

6. Iodine (I)

7. Manganese (Mn)

8. Molybdenum (Mo)

9. Selenium (Se)

10.Zinc (Zn)
Possibly Essential Elements

for Humans

Ni, Si, Sn, V, Ba, Li

Non Essential

Trace Elements

Of Humans

Pb, Hg, Al, Ag, Bo
Body Minerals

C

H

N

O

S

P

Na

K

Ca

Mg

Cl

Biological forms of minerals in living

systems

Fe

Zn

Cu

Mn

Se

Co

V

Si

As

Mo

I

Br

F

Nutritional y Important Minerals

Macro Minerals

Trace Elements

Element

g/kg

Element

mg/kg

Ca

15

Fe

20-50

P

10

Zn

10-50

K

2

Cu

1-5

Na

1.6

Mo

1-4

Cl

1.1

Se

1-2

S

1.5

I

0.3-0.6

Mg

0.4

Mn

0.2-0.5

Co

0.02-0.1
Minerals in the Body

General Characteristic Features

Of

Human Body Minerals
Sources Of Minerals

To Human Body

?A mixed diet of varied

foods

?Is the best source of

Minerals
Minerals in Foods

? Minerals are found in al food

groups.

? More reliably found in

?Fresh Fruits

?Vegetables

?Animal products

Factors Affecting Mineral Requirements

? Form of Mineral fed - Inorganic

vs Organic forms

? Interactions with other minerals
? Tissue storage
? Physiological State
Site for Mineral Absorption

?Small intestine
?Large intestine

Variable Bioavailability of Minerals
Bioavailability Of Minerals

? Bioavailability (absorption capacity) of

Minerals is influenced by :

?Genetics
? Aging
? Nutritional Status
?Other food compounds

Nutrient Interactions

vSome food components bind with

Minerals reducing their bioavailability

vMineral interactions can affect another

minerals absorption, and excretion


? Often other substances in

foods decrease absorption

(bioavailability) of Minerals:

?Oxalate, found in spinach,

prevents absorption of most

Calcium in spinach.

?Phytate, in most plants

makes minerals poorly

available

Oxalate

Phytate


Factors Affecting Requirements

? Interactions with other Minerals

? Phosphorous binds with

Magnesium in the small

intestine.

? So Magnesium absorption is

limited when Phosphorous

intakes are high
Uptake And Transportation

Of Minerals

v Some Minerals require no carriers

to transport into intestinal wall.

v Some Minerals require carriers to

enter into intestinal wall.
? Excretion and Regulation

Site Of Minerals.

?Smal intestine
?Kidneys

General Functions of Minerals
? Minerals with structural functions:

Ca, P ,Mg in bones; S in Keratin.

? Minerals serve as Inorganic Cofactors:

participate with Enzymes in metabolic

processes .

? Role of Minerals in Acid-Base and Water

balance: Na+, K+ and Cl-

? Minerals have role in Nerve & Muscle

Function : Ca, Na, K, Mg

? Minerals are components of certain

biomolecules:

?Fe- Heme,

?Co- Vitamin B12

?I2-Thyroid hormones.
Mineral Deficiencies and Excesses

Mineral Balance

Minerals Inn=Minerals Out
? Most Minerals have an optimal

range in blood/body.

?Minerals below range leads to

deficiency symptoms

?Minerals above range leads to

toxicity symptoms

? Deficiency and excess of

Minerals in human body

? Affect the normal health

and vitality of human body

? Which may lead to suffer

from various manifestations.
Note

?Mineral content of

soils

?Dictates Mineral

status of plants.

? Mineral deficiencies usual y are rare

? As they are widely distributed and

essentially taken through food.

? However there are many deficiency

cases noted of

? Iron , Iodine and Calcium

deficiencies.
? It may take many months to

develop Mineral toxicity.

?The time taken to develop

is impacted by body

stores.

Study Of Specific Minerals
Study Of Macrominerals

Calcium Metabolism
? Symbol : Ca+2
? Divalent Cation
? Atomic Weight : 40 g/mol
? Atomic Number: 20
? Nature :Soft Grey Alkaline

Earth Metal

? Calcium is the most

essential abundant

Macromineral of human

body.

? Fifth most abundant

element in Earth?s crust
Calcium Occurrence In

Nature

? Natural y Calcium does not

exist freely

? Calcium occurs in form of Salts

?Limestone (CaCO3)

?Gypsum (CaSO4*2H2O)

?Fluorite (CaF2)

Calcium In the Human Body

vCalcium is the most

abundant Macro

Mineral

vAverage adult body

contains approx. 1.5 kg

of Calcium.
? 99% of the body Calcium is

associated to skeleton (Bones

and Teeth).


? 1% Calcium is present in other

tissues and body fluids.

vCalcium in bones is in dynamic

state

vCalcium of bones may serve as

large reservoirs storing excess

Calcium

vBones releases Calcium when

extracel ular fluid Calcium

concentration decreases.
RDA

Recommended

Daily Amount

Of Calcium

Calcium Dietary Requirements

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

1500mg/day/1.5 g/day

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

Age/ sex

Ca (mg)

1-3

350

4-6

450

7-10

550

11-18 M

1000

11-18 F

800

19 +

700

Dietary Sources Of Calcium


Dietary Calcium sources

? Rich Calcium Sources

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

Ragi/Red Millet/Finger Millet
? Calcium Good sources

- Yoghurt, sour cream, ice cream

- Tofu

- Gauva ,Figs

- Cereals

- Egg yolk

- Legumes

- Green leafy vegetables as collard,

kale , Broccolli, Cabbage and raw

turnip

- Small Fish as trout, salmon and

sardines with bones

- Meat

- Almonds, brazil nuts, dried figs,

hazel nuts

- Also soybean flour and cottonseed

flour
Ca ? Dietary Sources

? Milk ? 100 ml =120mg

? Cheese ? 15gm = 110mg

? Yoghurt pot ? 80gm = 160mg

Absorption Of Calcium
?Absorption of Calcium

occurs in the smal

intestine

?In Duodenum and first

half Jejunum

?Calcium must be in a

soluble and ionized

form for its absorption.

?Calcium salts are

unabsorbable forms.
Calcium Absorption

?Absorption depends on

need of Calcium to body:

?Particularly high during

growth, pregnancy and

lactation

Calcium

Transport Mechanism

Across Intestinal Mucosal

Membrane
Ca Absorption Simple diffusion/Passive

Mechanism

An active transport involving Ca pump

Calcium Passive Transport

? Is a non saturable,

paracellular

? It is less efficient process

? Is not affected by calcium

status or parathyroid

hormone
?Active Absorption of Calcium:

? Against electrical and

concentration gradient, by an

energy dependent active

process.

Calcium Active Transportation

?Regulated by the active form of

Vitamin D/Calcitriol.

?Which involves Calbindin

(Calcium-Binding Protein) ?
Factors Promoting

Calcium Absorption

Parathyroid Hormone

(PTH) indirectly
enhances Ca absorption
through the increased
activation of Calcitriol.
Calcitriol

vCalcitriol /activated Vitamin D ,

induces the synthesis of Ca binding

protein Calbindin

vCalbindin in the intestinal

epithelial cel s then promotes Ca

absorption.

Acidity (low pH)

vAcidity is more favorable for Ca

absorption.

qCalcium salts are soluble in acid

solutions

qSo acidity increases the absorption

of Calcium.
vLactose , Citric acid

promotes Calcium
uptake by intestinal cell.

? Amount of Proteins in Diet:

? Amino acids Lysine and

Arginine form soluble

complexes with Calcium

? Hence high protein diet

favors the absorption of

Calcium.
? Concentration of

Calcium in diet:

? Higher the concentration

of Calcium

? More is the absorption of

Calcium.

Factors Inhibiting

Calcium Absorption
? Phytates and Oxalates

present in plant origin diet

form insoluble salts and

interfere with Ca

absorption.

? The high content of dietary

Phosphates results in the

formation of insoluble Ca

phosphate and prevent Ca uptake.

? Dietary ratio of Ca : P ---1:1 / 2:1
? is ideal for Ca absorption.
?The Free Fatty acids

react with Ca to form

insoluble Ca soaps.

?The Alkaline condition

(high pH) is

unfavorable for Ca

absorption.
?Low Estrogen levels in

postmenopausal

women lowers Calcium

absorption.

?Since Estrogen increases

Calcitriol levels

?High content of Dietary

fiber,Caffeine,Sodium

interferes with Ca

absorption.
? Amount of Magnesium in diet:

Excess Magnesium in diet

inhibits Calcium absorption.

? As Magnesium competes with

Calcium for absorption.

Calcium

Absorption and Excretion at

GIT
?Usual Ca intake is1000

mg/day.

?About 35 % is absorbed

(350 mg/day) by the

intestine.

? Remaining Calcium in the

intestine is excreted in the

feces

? 250 mg/day enters

intestine via secreted

gastrointestinal juices and

sloughed mucosal cells
90 % (900 mg/day) of the

daily intake is excreted in

the feces

10 % (100 mg/day) of the

ingested calcium is

excreted in the urine.

Body Distribution Of

Calcium


?Total content of Calcium in

an Adult body is 1-1.5 Kg.

?Calcium constitutes 2% of

total body weight.

BODY CALCIUM

?99% of Calcium is in Bones
?0.8% of Calcium is in soft

tissues (ICF)

?0.1% in Blood ( ECF)


PLASMA CALCIUM

Three Forms of Circulating Ca2+
Diffusible Calcium

? 50% Ca2+ Ionized/Physiological y

active form.


? 10% combined with anions (Citrate,

Phosphate) ?Non-dissociated/Non

ionizable form.

Non diffusible Calcium

? 40% combined with plasma

proteins

? Combination with proteins

depends on pH 0.2 mmol/l ,Ca2+ on

each pH unit
Blood Calcium Levels

?The normal serum

total calcium is:

? 9-11 mg/dL

? 2 -3 mmol/L

? Normal levels of the

ionized/free/diffusible/physiological

form of Calcium is

?4.5-5.6 mg/dL

?1.1-1.4 mmol/L
?Protein bound Calcium

(Mostly bound to

Albumin)/Non

diffusible/Bound form of

Calcium: 4 mg%.

?Calcium Salts /Bound

form/Inorganic

Salts/Diffusible:

? Calcium Phosphate and

Calcium Citrate=1mg%
Erythrocytes

Almost Contain

No Calcium

Calcium In Alkalosis

? Alkalosis favors binding of

more Calcium with

Proteins.

? This consequently lowers

ionized Calcium.
Acidosis Favors Ionization of Calcium

Multiple Biological

Functions of Calcium
?Calcium is widely

distributed in the body

? Involved with many

functions to keep the

body vital and active.

1. Structural Role Of Calcium

?Calcium is a major

structural element in

the vertebrate skeleton

forms bones and teeth.
? Calcium along with

Phosphorous, Magnesium

forms the inorganic matrix of

the bone as Hydroxyapatite

crystals

? Which gives the tensile

strength to the bones and

teeth.

? In the form of Calcium

Phosphate(Ca10(PO4)6(OH)2

known as Hydroxyapatite
?Osteoblasts are

responsible for bone

formation


?While Osteoclasts are for

bone resorption.

?Bones undergo

mineralization during

osteoblastic activity

? Demineralization during

osteoclastic activity.
Bone Act As Major Reservoir Of

Calcium


? Osteoclasts secrete acid,

causing the release of calcium

and phosphate into the

bloodstream.

? There is constant exchange of

calcium between bone and

blood.




Cross section through

trebecular and cortical

bone revealing the

internal architecture

surrounded by marrow

tissue.

Cortical bone with

Halversion system (a

series of channels

supplying nutrients).

Black dots are

osteocytes

Leg bone of a horse

showing the trebecular

(spongy) bone and the

Trebecular bone of

cortical (solid) bone. This

the lower spine.

bone is able to withstand

Changes with aging.

forces generated by this

1,500 lb animal

Demineralized bone: Shown is the organic

matrix consisting mostly of collagen upon

which the bone crystals are laid.


Hydroxyapatite (crystal structure)

Ca10(PO4)6 OH2

Ca

P

O

H

Remember/Note

? During growth , pregnancy and lactation

phase

? To give strength for building bones and teeth.

? One should take adequate amounts of

dietary Calcium and Phosphorous
2. Calcium Role in Muscle Contraction

? The ionized free form of

Calcium interacts with

? Muscle Protein Troponin C to

trigger muscle contraction.

? Calcium also activates Ca-ATP ase

and increases the interaction

between Actin and Myosin during

muscle contraction.

? Thus Calcium has role in excitation

and contraction of muscle fibers.
3. Role Of Calcium In Nerve Impulse

Conduction

?Ionized Calcium transmits

nerve impulses

?From pre-synaptic to post-

synaptic region.

4. Role of Calcium in Hormonal

Actions

? Calcium serves as second and

third messenger for certain

hormonal activities.

? Calcium ?Calmodulin

complex mediates the

hormonal action.
? Calmodulin is a Calcium binding

regulatory Protein which binds

with 4 Calcium ions.

? Calmodulin serve as messenger

during hormonal action by

stimulating Protein Kinases.

? Epinephrine require

Calcium as second

messenger at the time of its

action.

? ADH require Calcium as

third messenger during its

action.
5. List Of Enzymes Activated By

Calcium and Mediated By Calmodulin

? Adenyl Cyclase
? Glycerol-3-PO4 Dehydrogenase
? Glycogen Synthase
? Pyruvate Carboxylase
? Pyruvate Dehydrogenase
? Pyruvate Kinase

6. Calcium as Chelating Agent In Blood

Clotting Mechanism.

? Calcium as Clotting factor IV

serves as a cofactor for several

reactions in the Cascade of blood

clotting process.

? Calcium serves as chelating agent

during Thrombin formation.
7.Calcium act as a Cofactor of

Enzymes

? Calcium serve as an inorganic

cofactor of: (Direct action)

?Pancreatic Lipase
?ATPase
?Succinate Dehydrogenase

8.Calcium Role in Secretion of

Hormones

? Calcium stimulates to release

of fol owing Hormones:

?PTH
?Insulin
?Calcitonin
?Vasopressin/ADH
9.Calcium Transport Across The

Biomembranes

? The cel membrane is general y

impermeable to Calcium ions.

? Calcium influx into cel s is via

Calcium channels by Na /Ca

exchange mechanism.

?There are different

Calcium Channels

located in the

membranes of various

cell organelles.
10. Calcium Prolongs Systole

?Calcium acts on Heart

and prolongs Systole.

?Hypercalcemia may lead

to Cardiac arrest in

Systole.

Remember

?When Calcium is

administered intra venously

?It should be infused very

slowly to avoid the cardiac

arrest.
11.Calpains ? Calcium Dependent

Cysteine Proteases

? Calpains are involved in:

?Cel mobility
?Cel cycle progression
?Cel membrane fusion

events

?Cell fusion in Myoblasts
?Neural vesicle Exocytosis
?Platelet aggregation
?Increased concentration

of Calcium in cells.

?Increases Calpain

activation.

? Increased Calpains causes

unregulated proteolysis .

? Hyperactivity of Calpains

consequent leads to

irreversible tissue damage.
? Calcium is a key component

in the maintenance of the

cel structure

? Membrane rigidity,

permeability and viscosity

are partly dependent on local

calcium concentrations

?11. Calcium promotes

? Transportation of water and

ions across the membranes.

? Excitability of cell membranes.
?Calcium regulates

cellular secretory

process such as :

?Endocytosis
?Exocytosis
?Cell motility

? Calcium has role in:

?Cel to Cel contact
?Cel to cel communication
?Cel adhesion in tissues
?Calcium is added to

mothers milk during

lactation phase of

women.

Calcium Active Role:

- In the relaxation and constriction

of muscles

- In nerve impulse transmission

- As an intracel ular signal

- In cel aggregation and movement

- In secretion of hormones

- In cel division
Calcium Passive Role:



- As a cofactor for many

enzymes (e.g. Lipase) and

proteins

- As component in the

blood clotting cascade
Homeostasis Of Blood

Calcium

OR

Regulation of Blood Calcium

? The normal levels of total

serum Calcium is 9-11 mg%.

? It is very essential to maintain

the constant range of Calcium.

? For normal health and

survivallence of human body.
? Most important is the ionized or

physiological form of Calcium

present in blood


? This plays an important roles in

various physiological and

metabolic functions of human

body.

? Maintenance of calcium

homeostasis.

?Regulation in dietary absorption

?Storage

?Excretion of Ca
Factors Regulating Blood Calcium

Levels

?Parathyroid Hormone (PTH)
?Vitamin D- Calcitriol
?Calcitonin

? The PTH , Calcitriol and

Calcitonin cooperatively

works

? To regulate the transiently

increased and decreased

levels of serum Calcium .


Parathyroid hormone

(PTH)

q PTH is secreted by two pairs

of parathyroid glands.

v PTH is initially synthesized as a

precursor, preProPTH.

v Two proteolytic cleavages

produce the ProPTH and the

secreted form of PTH (84 aa).
?The secretion of PTH

are promoted
?By low Ca2+

concentration in blood.

Regulation of PTH Secretion and

Biosynthesis

? Extracel ular Ca 2+ regulates secretion of

PTH

?Low Ca 2+ increases PTH levels
?High Ca 2+ decreases PTH levels
Mechanism of action of PTH

? PTH is the most important

endocrine regulator of Ca and

Phosphorous concentration.

? Function:

?Elevate serum Ca level.

?PTH has 3 independent

tissues to exert its action.

?Intestine (Indirectly)
?Bone (Directly)
?Kidney (Directly)
? PTH Regulates through

3 Main Effects:

-Stimulating activation of

vitamin D intestinal

Ca absorption

-Stimulating bone

resorption

-Increasing renal tubular

calcium reabsorption

Actions of Parathyroid Hormone

On Bone
?Parathyroid hormone

acts directly on bone to

stimulate resorption

?This releases Ca2+ into

the extracellular space

and fluids (slowly)

PTH Action on the Bone

? Decalcification or Demineralization

of bone, carried out by osteoclasts.

? blood Ca level
? Note: this is being done at the

expense of loss of Ca from bone,

particularly in dietary Ca deficiency.


? Gs protein-coupled receptors in

osteoblasts increase cAMP and

activate Protein Kinase Activity

(PKA)

? This Inhibits osteoblast

function

? This occurs when PTH is

secreted continuously.


Circulating Forms of PTH

Action Of PTH

on the Kidney and Intestine

?Action on the Kidney: increase

the Ca reabsorption.

?Action on the Intestine:

indirect, increase the intestine

absorption of Ca by promoting

the synthesis of Calcitriol.
? PTH Effects in Kidney

?Parathyroid hormone

acts directly on kidney

?To increase calcium

reabsorption and

phosphate excretion

(rapid)

? Gs protein-coupled receptors

? Parathyroid hormone acts on

distal tubule

? Increases renal reabsorption

of Calcium.

? Adds Calcium to blood

regulating its levels.


Role Of Calcitriol/ Activated

Vitamin D

- Calcitriol several effects on the

intestine and kidneys that

increase absorption of calcium

and phosphate into the

extracellular fluid

- Important effects on bone

deposition and bone absorption
PTH and Calcitriol By their Activity

Increases Blood Calcium Levels

? Calcium levels below

subnormal levels

? Stimulates the secretion of

PTH

? PTH then stimulates the

Vitamin D activation to

Calcitriol.


Calcitriol (1,25-dihydroxy-

cholecalciferol, 1,25 DHCC)
Activation of Vitamin D3

- Cholecalciferol formed in the skin

by sun

- Converted in liver and Kidney to



- 1,25 DHCC Control ed by PTH

- Plasma calcium concentration

inversely regulates 1,25 DHCC

?PTH and Calcitriol then

acts on three target

organs

?They try to increase the

blood Calcium levels by

their Hypercalcemic

action.
Action On Intestinal Mucosal cel s

? Calcitriol enters intestinal mucosal cells.
? Acts like Steroidal hormone
? Stimulate the biosynthesis of Calbindin

a Calcium binding Protein by gene

expression.

? Calbindin binds with dietary Calcium in

GIT, promotes it absorption and diffuse

in blood.
Calcitriol Action On Renal Tubules

? Calcitriol acts on renal tubules and

increases tubular renal absorption of

Calcium from plasma ultra filtrate

there by decreasing excretion of

Calcium.

? The reabsorbed Calcium by renal

tubules add Calcium to blood these by

increasing blood Calcium levels.

Action On Bones

? PTH hormone directly acts on bones

causing decalcification of bones

? To release bound form of Calcium into

free form, catalyzed by increased

activity of ALP

? Which increases the levels blood

Calcium to blood there by increasing

blood Calcium levels to attain a normal

level of 9-11 mg%
Remember

? The low intake of dietary Calcium may

increase the bone resorption by PTH to

regulate blood Calcium levels.

? This may decrease the blood Calcium

content of bones

? Leading to weakness in bones

manifesting bone pain and recurrent

bone fractures.

Calcitonin

? Calcitonin a peptide hormone

(32 aa) secreted by the

parafol icular cel s of Thyroid

gland

- Calcitonin tends to decrease

plasma Calcium

concentration
Role Of Calcitonin In Decreasing The

Blood Calcium Views

? When ever the blood Calcium

goes above 11 mg%

? The Calcitonin by its

Hypocalcemic action

? Tries to lower the increased the

blood Calcium levels.

? Calcitonin promotes the

bone mineralization or

Calcification of bones.

? The blood Calcium is taken

up by bones and reserved.
? Thus Calcitonin increases

Osteoblasts activity

? Enhances bone mineralization.
? Promotes bone growth
? Reduces increased blood

Calcium levels to attain 9-11

mg%.

-Calcitonin adds

Calcium to bones

and increases bone

mineralization.
Role Of Calcitonin (CT)

?CT has the ability to decrease blood Ca and P
levels and its major target cells also in bone,
kidney and intestine.

1. Bone: Stimulate Osteogenesis.
2. Intestine: Inhibit absorption of Ca.
3. Kidney: enhance of Ca excretion from

urine.

?PTH and Calcitonin are

antagonistic in actions.

?OR

?Action of Calcitonin is

opposite to that of PTH.
Hormonal Regulators

? Calcitonin (CT)

?Lowers Ca++ in the blood

?Stimulates Osteoblasts

?Inhibits Osteoclasts

?Parathormone (PTH)

?Increases Ca++ in the

blood

?Stimulates Osteoclasts


? Calcitriol

?Increases Ca++ in the

blood

?Increase Ca++ uptake

from the gut

?Stimulates osteoclasts

(+)


Regulation of Calcium Homeostasis

Calcium Turnover


Calcium Balance

? Calcium Intake = Calcium output

? Negative calcium balance: Output >

intake

?Negative Ca2+ balance leads to

osteoporosis

? Positive calcium balance: Intake >

output

?Positive Ca balance occurs during

growth

Calcium Balance


Exercise and Calcium

? Normal bone function

requires weight-bearing

exercise

? Total bed-rest causes bone

loss and negative calcium

balance.

Calcium Homeostasis


Calcium and the Cel

? Translocation across the plasma membrane

? Translocation across the ER and mitochondrion;

Ca2+ ATPase in ER and plasma membrane


Regulation of

Calcium

Homeostasis

Calcium Homeostasis

kidney

bone

calcium deposition

Blood

Ca++

calcium resorption

1000 g Ca++

stored in bone

Ca++ absorbed

Ca++

into blood

lost in urine

Calcium in

the diet

calcium lost in feces

smal intestine




Calcium Homeostasis

storage

kidney

bone

calcium deposition

Blood

Ca++

calcium resorption

1000 g Ca++

stored in bone

intake

Ca++ absorbed

Ca++

into blood

excretion

lost in urine

Calcium in

the diet

calcium lost in feces

smal intestine

Calcium Homeostasis

kidney

bone

calcium deposition

Blood

Ca++

calcium resorption

Ca++ absorbed

Ca++

into blood

lost in urine

Calcium in

the diet

calcium lost in feces

smal intestine




Calcium Homeostasis

kidney

bone

1,25 Vit. D3 (+)

Parathormone (+)

Calcitonin (-)

Blood

resorption

Ca++

deposition

PTH

Ca++

Ca++

1,25 Vit D3

Ca++

Ca++

smal intestine

1,25 Vitamin D3

UV

Cholesterol precursor 7-dehydrocholesterol

Vitamin D3

25 Vitamin D3

1,25 Vitamin D3

Low plasma Ca++ increase kidney enzymes
Excretion Of Calcium

Excretion of Ca

? Mostly through the intestine.
? Partly through the kidney.
Calcium Excretion

qIn feces: 80%
qIn urine: 20%

?Unabsorbed dietary

Calcium is mostly

excreted out through

feces.
?Excretion of Ca into the

feces is a continuous

process

?This is increased in

vitamin D deficiency

When Wil Calcium Excreted In Urine?
? The renal threshold for

Calcium is 10 mg%.

? When blood Calcium crosses

more than 10 mg% it is

excreted in Urine.

Excretion of Calcium

under influence of PTH.
?The excretion of Calcium

and Phosphorous is

reciprocal y regulated.

?If Phosphorous excretion

is increased Calcium

excretion is decreased.

? Conditions Increasing

Excretion Calcium

- Low Parathyroid hormone

(PTH)

- High extracellular fluid volume

- High blood pressure

- Low plasma Phosphate

- Metabolic Alkalosis
? Excretion Of Calcium Is

decreased by:

- High Parathyroid hormone

- Low extracellular fluid volume

- Low blood pressure

- High plasma phosphate

- Metabolic acidosis

- Low Vitamin D3

Clinical Significance Of Calcium
Disorders Associated

To

Calcium Metabolism

Defect In Fol owing Factors

Leads to Calcium Related Disorders

? Dietary Intake Of Calcium
? Role of PTH , Calcitriol and

Calcitonin

? Status of Parathyroid , Thyroid

, Liver and Kidney
Investigations To Diagnose

Calcium Related Disorders

? Serum Ca and Pi levels
? PTH
? Vit D ( 1,25 Dihydroxy levels)
? Mg
? Urinary Ca/ Cr ratio

Disorders Of Calcium

Metabolism

Hypercalcemia

And

Hypocalcaemia
Hypercalcemia

?Hypercalcemia is the

condition where there is

?Persistent high levels of

blood Calcium above 11

mg%.

Conditions Leading To Hypercalcemia

? Excessive intake of Calcium
? Hyperparathyroidism-

Increased PTH

? Parathyroid Adenoma
? Hypervitaminosis D
? Pagets Disease
(Increased Release From Bones)
? Addisons Disease
(Decreased Excretion Of Calcium)
? Bone Tumors
(Leak of Calcium From Bones)
? Multiple Myeloma-Leukemia ,

Polycythemia

? Milk Alkali Syndrome( Calcium+Alkali)

?Excessive use of

antacids with phosphate

-binding

?Prolonged immobility

?Thiazide diuretics

?Thyrotoxicosis
Hypercalcemia Signs and Symptoms

?Muscle weakness
?Personality changes
?Nausea and Vomiting
?Polyuria
?Extreme thirst

? Anorexia
? Constipation
? Pathological fractures
? Calcifications in the skin and

Cornea

? Cardiac arrest(prolonged Systole)




Clinical manifestations of Hypercalciemia

Osteodystrophy (Recklinhauzen disease)

Cystosis swel ing in the distal

ends of both fibula bones

Mechanism

Hyperparatireosis ? increasing of in blood ? waste of from bones by

resorbtion ? osteoporosis ? overgrowth of connective tissue (but isn't

deposited) - osteofibrosis

Hypocalcemia

? Hypocalcemia is the condition

where there is persistent low levels

of blood Calcium below 9 mg %.

? Hypocalcemia is more dangerous

and life threatening if not

corrected and managed timely.
Conditions Causing Hypocalcemia

? Malnutrition and

Malabsorption

? Diarrhea
? Acute Pancreatitis
? Hypoparathyroidism
? Hypovitaminosis D

? Rickets
? Osteomalacia
? Renal Rickets (Deficiency of 1

Hydroxylase)

? Fanconis Syndrome
? Hypoalbuminemia( Decreases

Protein bound Calcium)
? Chronic kidney failure
? Low blood magnesium level

(in cases with severe

alcoholism)

? Diet high in Phytate

Hypocalcaemia ? Clinical Features

? Neuromuscular excitability

? Paraesthesia (tingling

sensation) around mouth,

fingers and toes

? Tetany

? Muscle cramps, Carpopedal

spasms

? Seizures ? focal or generalised

? Laryngospasm, Stridor and

apneas (neonates)

? Cardiac Rhythm disturbances

(prolonged QT interval)

? Chvostek's and Trousseau's

signs ? latent hypocalcemia

Calcium Deficiency Manifestations


Calcium Deficiencies

? Tetany
? Rickets

?In growing children's

? Osteomalacia (Osteoporosis)

?In adult animals

Tetany

? Tetany is the manifestations

caused due to hypocalcemia.

? Serum Calcium below 7 mg %

causes Tetany.
? Tetany is a life threatening

condition.

? Tetany may be suffered in

persons whom

?Parathyroid gland is surgical y

removed

?Parathyroid dysfunction due to

auto immune disorder.

? Low Calcium levels directly

affects neuromuscular

activity.

? Leads to increased

neuromuscular irritability

of muscles.
?Twitching and spasm

of muscles of

face,hand,feet neck

?Carpopedal and

Laryngeal and Stridor

Spasm.

Clinical Sign Of Tetany
? Chvostek's Sign (Tapping over

facial nerve causes facial

contraction)

? Trousseaus Sign (Inflation of

BP Cuff for 3 minutes causes

Carpopedal spasm).

ECG Changes In Tetany

?Increased Q-T interval

in ECG.
? Low blood Calcium
? Increased Phosphate in

blood

? Low urine Calcium and

Phosphorous

Treatment Of Tetany

?Intravenous

infusions of Calcium

salts.






Clinical manifestations of Hypocalcaemia

Tetany

The process of tetany potentiation

at the motor neurons and interneuron of spinal cord violate

Conduction of impulses at reflex arch become easier

Activate a reflex muscles contraction on mechanical and other stimuli

Spasm of larynx, bronchus

Coronarospasm (cardiotetanus)

Cramps



asphyxia



angina

death

Stop of heart

Calcium Deficiencies -Rickets

?weakness and deformity of the bones that occurs from
vitamin D deficiency or dietary deficiency of Ca and P in
a growing person or animal.






Clinical manif

e st

a

ti

o

n s

of

Hy

pocalcaemia

Ricket

Calcium and Osteoporosis

? Around age 40,

bone breakdown

exceeds

formation.

? By age 65, some

women have

lost 50% of bone

mass.


Calcium Deficiencies -Osteoporosis

?progressive loss of bone density, thinning of bone tissue
and increased vulnerability to fractures in the elderly
people of both sexes.


Calcium and Osteoporosis

? Bone growth is greatest during "linear growth"

? Peaks out at around age 30

How does Osteoporosis Look?
Effect Of pH On

Extracellular Calcium

? Binding of Calcium to Albumin
is pH dependent

? Acute alkalosis increases

calcium binding to protein and

decreases ionized calcium

? Patients who develop Acute

Respiratory Alkalosis

? Have increased neural excitability

and are prone to seizures

? This is due to:

? Low ionized calcium in the

extracel ular fluid

?Increased permeability to Sodium

ions
Prevention is the Key

? Maintain adequate Calcium

and Vitamin D intake--

? Perform weight-bearing

exercise

? Take Estrogen supplements?

Treatment of Hypocalcaemia

Severe Symptomatic:

?IV 10% Calcium Gluconate @ 0.11 mmol/kg

(0.5 mls/kg ? max 20 mls) over 10 minutes

?Continuous IV infusion of Calcium Gluconate

@ 0.1 mmol/kg (Max 8.8 mmols) over 24

hours

Severe Asymptomatic:

Oral Calcium Supplements @ 0.2 mmol/kg

(Max 10 mmols or 400 mg Ca) 4 x a day
Calcium Toxicity

? Calcium deposition in soft tissue

? Impaired kidney function

? Interference of other nutrient

absorption

?Iron & zinc

? Toxicity ? Hypercalcemia

(normal y does not to

occur)

? Hyperparathyroidism,

vitamin D intoxication,

cancer are few causes.


Toxicity Of Calcium

? MAS (Milk Alkali Syndrome)
- Rare and potentially life threatening

condition in individuals consuming large

quantities of calcium and alkali

- Characterized by renal impairment,

alkalosis and Hypercalcemia: cause

progressive depression of the nervous

system

Metabolic calcinosis ( )

Pathogenesis unknown

Limestone deposits in skin, tendons, fascias, muscles, along nerves and vessels






Dystrophic static calcinosis (petrification)

It arises in necrotic and dystrophic tissues - tuberculosis center , infarctions,

dead fetus, chronic focus of inflamations (lungs and heart like an armor ),

focuses of atherosclerosis, scar tissue

Mechanism: alkalinity conditions ? increased absorption from blood ?

The increased activity of phosphatases, which prodused from necrotic cel s ? formation of

insoluble salts of

Metastasic calcinosis

Calcinosis of aortic valve
Phosphorous

Metabolism

Phosphorous

? Phosphorous is a

Macromineral /Chief/Principle

Element of human body.

? It is a second most abundant

Mineral of human body.
Daily Requirement/RDA of

Phosphorous

? The dietary Ca:P ratio ideal y

should be 1:1 for optimal

absorption and functions.

? Thus the requirement of

dietary Phosphorous is more

or less same as that of

Calcium.

?Adults= 800 mg/day
?Growing Children=1000

mg/day
Dietary Sources Of Phosphorous

? Milk and Milk Products
? Cereals
? Egg
? Meat
? Green Leafy Vegetables ,

Cabbage , Cauliflower

Absorption Of Dietary Phosphorous

? Absorption of Phosphorous is

along with Calcium.

? Hence factors promoting and

inhibiting Calcium absorption

are likely with Phosphorous.
? The Calcium and Phosphorous

ratio in diet affects absorption

and excretion of Phosphorous.

? If any one of this is excess in

diet the excretion of the other

is increased.

Body Distribution Of Phosphorous

? Total content of

Phosphorous in an adult

body is 1 Kg.

? Phosphorous is present in

each and every cell of

body cell.
? 80 % of Phosphorous is present in

bones and teeth along with

Calcium as Hydroxyapatite

crystals.

? 10% of Phosphorous is present in

Muscles and blood associated to

Proteins, Lipids and Carbohydrate

moieties.

?10 % of Phosphorous is

component of various

Phosphorylated

biomolecules.
Phosphorous In Blood

? In blood Phosphorous is

present in following forms:

? Free/Ionized Phosphorous:

40%

?H2PO4-
?HPO4- -

? Bound/Complex forms of

Phosphorous:

? Phosphorous bound and present

as organic forms- Non diffusible

form.

? Phosphorous bound to other

Cations /Inorganic salt : Calcium

Phosphate
? Total Phosphorous levels in

Whole blood= 40 mg%

? Serum Inorganic

Phosphorous

? Adults= 2-4 mg%
? Children's= 4- 6 mg%

? Fasting levels of serum inorganic

Phosphorous are higher than post

prandial values.

? Since after meals the inorganic

Phosphorous from blood are drawn into

cells

? Where it is utilized for phosphorylation

of Glucose , Fructose and Galactose

during metabolism.
? After a rich Carbohydrate diet

there decreases serum inorganic

Phosphorous levels.

? In Diabetes mel itus the levels of

serum inorganic Phosphorous get

increased due to low utilization

within cells.



Functions Of Phosphorous

? Phosphorous along with Calcium has

important role in bone mineralization

and bone development.

? Phosphorous and Calcium are

components of Hydroxyapatite crystals

of bone inorganic matrix.
? Phosphorous is important

component during biosynthesis of

certain Phosphorylated

biomolecules viz:

?Phospholipids
?Nucleotides- Components of DNA

and RNA

?Phosphoproteins

? Phosphorylation reactions of

metabolism and forming Esters ex

Glucose-6-PO4,Fru-6-PO4 etc

? High energy phosphorylated

compounds.

?Creatine Phosphate ATP,GTP ,CTP

,UTP.

? Nucleotide Coenzymes

:NAD+,NADP,FAD,PLP
? Phosphorous is a component of

Phosphate Buffer system which

participate in Acid Base Balance.

?KH2PO4/K2HPO4

? Phosphorous is involved in

phosphorylation of certain

enzymes and bringing covalent

modification.

Excretion Of Phosphorous

? About 500 mg of

Phosphorous is excreted

through urine per day.

? Renal threshold for

Phosphorous is 2 mg%.
? PTH hormone stimulates

the excretion of

Phosphorous

? By inhibiting tubular renal

reabsorption of

Phosphorous.

? Thus there is inverse relationship

of PTH activity and serum

Phosphorous levels.

? Hyperparathyroidism decreases

serum inorganic Phosphorous

levels.
? Excretion of Phosphorous

and Calcium is reciprocal y

regulated.

? When Phosphorous is

excreted Calcium is retained

and vice a versa.

Disorders Associated To Phosphorous
Hyperphosphatemia

?Hyperphosphatemia is

abnormal y persistent

high levels

?Of serum Inorganic

Phosphorous above the

normal range.

Conditions Causing

Hyperphosphatemia

? Increased dietary intake of Phosphorous
? Hypoparathyroidism
(Decreased PTH decreased excretion)
? Hypervitaminosis D
(Increased Calcitriol increased absorption)
? Bone Tumors
(More turn over of Phosphorous)
? Diabetes mel itus
(Decreased utilization)
? Renal Failure
? Chronic Nephritis
? Intake of Steroids
(Decreased excretion)

Hypophosphatemia

?Hypophosphatemia is

abnormal y persistent low

levels

?Of serum Inorganic

Phosphorous below the

normal range.
Conditions Of Hypophosphatemia

? Starvation and Malabsorption Syndrome
? Hyperparathyroidism
? Hypovitaminosis D
? Rickets
? Osteomalacia
? Rich Carbohydrate diet
? Intake of antacids, contraceptives and

Diuretics

Sulfur Metabolism
Sulfur

?Sulfur is an essential

Macromineral.

?Third most abundant

Mineral of human

body.

RDA of Dietary Sulfur

?No specific dietary

requirement for Sulfur.

?Sulfur as free element

cannot be utilized.
? Sulfur is mainly associated to Sulfur

containing compounds viz:

?Sulfated Amino acids and Proteins
?Sulfolipids
?Mucopolysaccharides (Sulfated)
?Sulfated Vitamin B complex

members: Thiamine, Pantothenic

acid, Biotin and Lipoic acids

? Proteins contains about 1%

Sulfur by weight.

? The ingestion of dietary

Proteins rich in Sulfur

containing amino acids is

sufficient source of Sulfur.
Dietary Sources Of Sulfur

? Dietary sources of Sulfated Proteins:

? Egg

? Fish

? Meat

? Liver

? Legumes

? Cereals

Dietary Absorption

?The sulfated Amino

acids are absorbed

from intestine

?Through active

transport mechanism.
Body Distribution Of Sulfur

? The total content of Sulfur in an

adult body is 150-200 gm.

? Very smal amount of inorganic

Sulphate occurs in tissues and body

fluids.

? Sulfur levels in blood=0.1-1 mg%

Functions Of Sulfur
? Sulfur in the body is present in organic

form as various biomolecules carrying

following functions:

? Sulfated Proteins ,Enzymes containing

Sulfur containing amino acids possess ?

SH groups serves as functional parts.

? The SH groups are responsible for

forming S-S bonds in the structures.

Sulfated Compounds Of Human Body

? Immunoglobulins
? Keratin of Nail and Hair
? Glutathione Peroxidase
? FAS Complex
? Coenzymes-TPP , Biotin ,CoA
PAPS

?Phospho Adenosine

Phospho Sulfate(PAPS) is

an active Sulfate

?PAPS is a conjugating

agent involved in:

? Detoxification process
? In Conjugation reaction
? By Sulfuration
? Substances like Phenol , Indole , Skatole

and Steroids are detoxified by

Sulfuration Conjugation reaction

? To form Organic Sulfates like Etheral

Sulfates: Indoxyl Sulfate, Skatoxyl

Sulfate to get excreted in urine.

? PAPS is also used during

biosynthesis of

Glycosaminoglycans/MPS:

?Heparin

?Chondritin Sulfate

?Dermatan Sulfate

? Keratan Sulfate
? SAM activated Methionine a

Sulfated Amino acid

? Is an active donor of Methyl

groups

? SAM is actively involved in

Transmethylation reactions.

? Iron Sulfur Proteins are

components of ETC

(Respiratory Chain).
Excretion Of Sulfur

?The Sulfur from different

sulfated compounds is

oxidized in Liver and

excreted through Urine.

?Urine excretes both

inorganic and organic

forms of Sulfur.

?In the form of

Thiocynates and Sulfur

containing amino acid.
Forms Of Sulfur Excreted

? Inorganic Sulfate = 80%.
? Organic Sulfate/Etheral

Sulfate-10 %

? Unoxidized Sulfur =10%

Magnesium Metabolism
Magnesium

? Magnesium (Mg) is a

Macromineral of human body

? It is the fourth most abundant

mineral and important Cation

of human body.

Daily Requirement/RDA of Magnesium

?Adults = 300-400 mg/day

?High doses of Mg above

600mg/day oral y causes

diarrhea.
Dietary Sources Of Magnesium

? Cereals
? Nuts, Beans , Almonds
? Meat, Milk
? Green Leafy Vegetables (Chlorophyll-

Mg)

? Cabbage, Cauliflower
? Fruits

Absorption of Mg

? About 50-80 % of dietary

Magnesium is absorbed by

intestinal mucosal cel s.

? Through a specific carrier

system.
Factors affecting Mg Absorption

Factors promoting Mg absorption:

?PTH
?Calcitriol
Factors inhibiting Mg absorption:

?High Calcium and

Phosphorous in diet

?Phytates
?Fatty acids
?Alcohol consumption

Body Distribution Of Magnesium

? The content of Mg in an adult

body is 20 gm.

? 70 % of Mg is in bones along

with Ca and P

? 30 % of Mg is in soft tissues

and body fluids.
Blood Magnesium Levels

?Free/Ionized form of Mg

-60%

?Mg bound to Proteins-

30%

?Salts of Mg-10%

Normal range of

Serum Magnesium-2

-3 mg%
Functions Of Magnesium

? Magnesium along with

Calcium and Phosphorous.

? Is a component of inorganic

matrix of Bones and Enamel

of teeth

?Ionized form of

Magnesium has role

in neuro muscular

function.
? Mg++ is inorganic cofactor of

Enzyme Kinases:

?Hexokinase

?PFK

?PK

?Glucokinase

?Mg has role in

sensitizing Insulin

?Which Promotes

Glucose uptake by

cel s.
? Mg is a component of

Chlorophyl pigments of

plants.

? Hence green leafy

vegetables are good

sources of Mg.

Disorders Associated To Magnesium
Hypomagnesemia

? Hypomagnesemia low levels of

Mg(< 2mg%) leads to :

? Neuromuscular irritability
? The manifestations are managed

by oral dosage of Mg +2

Hypomagnesemia Conditions

? Starvation and Malnutrition

? Malabsorption

? Chronic Alcoholism

? Liver Cirrhosis

? Uncontrolled Diabetes mellitus(Osmotic

diuresis)

? Hyperthyroididsm

? Rickets
Hypermagnesemia

? Hypermagnesemia is

increased levels of serum Mg.

? Hypermagnesemia depresses

nerve conduction.

Hypermagnesemia Conditions

?Hypothyroidism
?Advanced Renal

Failure (Less

excretion)
Sodium Metabolism

Sodium

? Sodium is an essential

Macromineral

? Sodium serves as a body

Electrolyte.

? Sodium (Na +) is the chief

Cation of ECF.
RDA Of Sodium

? Sodium is taken through diet in

the form of NaCl.

? 5-10 gm of NaCl per day

provide the required amount

of Na.

? 10 gm of NaCl contains 4 gm

of Na.

Remember

? Hypertensive patients

/Patients having history of

Hypertension should limit

their intake of NaCl.

? For them RDA is 1 gm

NaCl/day.
Dietary Sources of Na

? Common Salt (NaCl)
? Bread
? Whole grains
? Nuts
? Eggs
? Milk
? Green Leafy Vegetables

Absorption Of Sodium

? Sodium is readily absorbed from

GIT.

? Less than 2 % is normal y

excreted through feces.

? However in diarrhea large

quantities of Na is lost through

feces.
Body Distribution Of Sodium

? 50% of Sodium is in bones
? 40 % of Sodium is in ECF
? 10% of Na is in Soft tissues.

?Na + is estimated by

Electrolyte Analyzers

?Normally in Serum Na + -

136-146 mEq/L.

?Na + in ICF is 35 mEq/L
Biomedical Functions Of Na

?Na+ along with other

electrolytes in ECF

exerts osmotic pressure

and maintains fluid

balance.

?Na+ has role in

neuromuscular

function.
?Na is a component of

ECF buffer system

plays role in acid base

balance.

? Na+ is involved in Sodium

dependent active transport

mechanism

? For Glucose , Galactose and

Amino acids absorption from GIT

lumen into the intestinal mucosal

cells.
? Sodium has role in

maintenance of cel

permeability.

? Sodium initiates and maintains

heart beat .

? Hence high Sodium content in

hypertensives aggravate the

condition of BP.

Excretion Of Sodium

? Sodium absorbed from GIT after its

functional role it is excreted out

through Urine.

? Sodium metabolism is influenced by

Aldosterone a Mineralocorticoids.
?Aldosterone act to:

?Increase renal

reabsorption of Na from

ultrafiltrate.

?Retain blood Sodium.

?Decrease Na excretion.

? In Adrenocortical

insufficiency there is

decreased Aldosterone


? Which decreases renal

reabsorption of Na leading

to Hyponatremia.
?Na is alternatively

excreted out through

Skin sweating.

Disorders Of Sodium Metabolism
Hypernatremia

?Sodium levels

above 150 mEq/L in

ECF is termed as

Hypernatremia.

Conditions Causing Hypernatremia

? Parenteral Therapy (IV infusion) with

Saline Solution.

? High intake of Salt without

corresponding in take of Water

? Hyperaldosteronism (Increased renal

reabsorption of Na)
? Cushing's Syndrome (Hyper

Adrenal Cortex Activity)

? Osmotic diuresis
? Decreased ADH secretion

(Causes Hemoconcentration)

Hyponatremia

? Hyponatremia is decreased

levels of blood Na .

? Low Sodium levels is an

emergency critical condition

which has to be managed at

earliest.
Conditions Causing Hyponatremia

? Diarrhea
? Excessive Sweating
? Nephrotic Syndrome
? Addison's Disease (Decreased

Na+ renal reabsorption)

? Malnutrition

Potassium Metabolism
Potassium

?Potassium (K) is a

Macromineral and a body

Electrolyte.

?K+ is a chief cation of ICF.

RDA and Dietary Sources Of

Potassium

? 3-4 gm/day is the RDA for Potassium.
Dietary Rich Sources Of K+

? Fruits: Banana ,Oranges

,Pineapple

? Tender Coconut water
? Potatoes
? Beans
? Chicken,Liver

Absorption Of Potassium

? 90% of K is efficiently

absorbed from GIT and very

little is lost through feces.

? During diarrhea there is

significant loss of K+ ions out

from the body.
Blood Levels Of Potassium

? Whole blood contains K+ level

upto = 50 mEq/L

? K+ is the chief Cation of ICF
? The serum /plasma K+ is 3.5-

5.0mEq/L

Biochemical Functions Of Potassium

? Potassium along with other

blood Electrolytes

? Exerts Osmotic pressure and

maintains fluid balance in

E.C.F and I.C.F.
?K+ has role in

neuromuscular function.

?K+ of E.C.F influences

Cardiac muscle activity.

?K+ is component of

I.C.F buffer system

?Plays important role

in acid base balance.
?K+ is cofactor for

Enzyme Pyruvate

Kinase of Glycolysis.

? K+ of I.C.F is necessary for

proper Protein biosynthesis

by Ribosomes.
Excretion Of Potassium

Excretion of Na+ and K+ are

reciprocal y regulated.

? If Na+ is excreted K+ is

retained vice a versa.

?Aldosterone increases K+

excretion .

?Aldosterone inhibits

tubular renal reabsorption

of K+ and promotes its

excretion.
? Thus in Adrenal Cortex

insufficiency decreased

Aldosterone levels .

? Decreased K+ excretion and

leads to Hyperkalemia.

Disorders Of K + Metabolism
Hyperkalemia

?Hyperkalemia is

increased K+ levels

more than 5 mEq/L .

Hyperkalemia Conditions

? Dehydration Conditions
? Violent Muscular Activity
? Intravascular Hemolysis
? Addisons Disease (Adrenal Cortex

Insufficiency)

? Acidosis
? Renal Failure (Decreased Excretion)
Hypokalemia

?Hypokalemia is

decreased K+ levels

more than 3 mEq/L .

Hypokalemia Conditions

? Starvation

? Insulin Therapy

? Cushing's Syndrome

(Increased Adrenal Cortex Activity)

? Alkalosis
Chloride Metabolism

? Chloride is a Macromineral

and an Electrolyte of

human body.

? Chloride is negatively

charged anion liberated

from NaCl.
The metabolism

of Na+ and Cl-

goes paral el

RDA OF Chloride

?The daily requirement

of Chloride is in the

form of NaCl is 5-10

gm/day.
Dietary Sources

? Common Salt (NaCl)
? Whole grains
? Green Leafy Vegetables.
? Eggs
? Milk
? Chlorinated Water

Absorption Of Chloride

?Dietary Chloride is

almost total y absorbed

from the GIT.
Blood And CSF Chloride

? Serum Chloride Levels= 95-105 mEq/L
? CSF Chloride Levels= 125- 130 mEq/L

? C.S.F Chloride is higher than serum

Chloride

? Since in CSF the concentration of

Proteins is very low as compared to

Serum Protein Levels.

? The higher CSF Chloride maintains

the osmotic pressure and Donan

Membrane Equilibrium.
Functions Of Chlorides

? Chloride is an anion, serves as

an electrolyte of body

? It maintains osmotic pressure

along with other Electrolyte and

regulate water balance.

?Chloride has role in

Acid Base Balance

by Chloride Shift

related to RBC's.
?Cl- is essential for

production of gastric

HCl for digestion

process.

?Enzyme Amylase

requires Chloride as

cofactor.
Excretion Of Chloride

?The excretion of Cl- and

Na+ is paral el.

?The renal threshold for

Cl- is about 110 mEq/L

?The retention of Na+ wil

retain Cl- in the body.

?Aldosterone has

influence on Na +

retention which retains

Cl-
Disorders Of Chloride Metabolism

? The Chloride and Sodium ions goes

simultaneously.

? Conditions increasing Sodium also

increases Chloride and vice versa.

? Chloride and Sodium has direct

relationship.

? The Chloride(Cl-) and Bicarbonate

(HCO3-) ions have inverse

relationship.

? In Acidosis there is decreased

HCO3- and increased Cl-

? In Alkalosis there is increased

HCO3- and decreased Cl-
Hyperchloremia

? Hyperchloremia is increased

Chlorides in serum.

? Excess intake of salt with

insufficient of water.

? Parenteral infusion of Saline (I.V

infusion)

? Dehydration without loss of

Salts.

? Cushings Syndrome( Retention

of Na+ and Cl-)

? Acidosis increases Cl-
? Nephritis (Decreased excretion

of Cl- by kidneys
Hypochloremia

? Hypochloremia is decreased

Chlorides in serum

? Less Intake of Salt
? Severe vomiting and

Diarrhoea (Loss of Salt)

?Congestive Cardiac Failure

(Sweating looses Salt)

?Addisons Disease
(Decreased Renal

Reabsorption)
?Alkalosis (Increases HCO3-

Decreases Cl-)

?Kidney Dysfunction where

there is no renal

reabsorption of Cl-

Study Of

Trace Elements
Iron Metabolism

Iron

? Iron is an essential trace

element of human body.

? It is an important component

of many essential vital

biomolecules vital for human

body.


RDA of Dietary Iron

?Adult Man =10 mg/day
?Menstruating Women =

18mg/day

?Pregnant and Lactating

Women= 40 mg/day

Dietary Type Of Iron
Two Types of Iron in Food

vHeme Iron

v Derived from the Hemoproteins

viz Hemoglobin and Myoglobin

vPresent in Animal Foods

vMeat ,Liver tissue

vPlant foods do not contain any

Heme Iron .


vNon-Heme Iron

v Derived mainly from Plant

foods

vCereals ,Legumes, Nuts, Dates

Fruits and vegetables.

vThe Iron in Meat is

approximately

v 40% Heme Iron
v 60% Non-Heme Iron
Dietary Sources Of Iron

? Rich Sources Of Iron-

? Organ Meat Like Liver ,Heart Kidney

and Jaggery.

? Good Sources of Iron-

? Dates, Nuts, Green Leafy Vegetables,

Pulses, Cereals, Apples and Spinach.

? Poor Sources

? -Milk , Wheat and Polished Rice.

IRON IN VEGETABLES

VEGETABLES

IRON IN /mg

Mushroom, pleurote

1.74

Potatoes

0.76

Cabbage, Collards

0.19

Cabbage, Green

0.59

Roasted Pumpkin and Squash Seeds

15

Spinach

2.71

Sesame Butter(Tahim) and Seeds

14.8

Sundried Tomatoes

9.1

Dried Apricot

2.2

Lentils

6.20
IRON IN FRUITS

FRUITS

IRON IN/mg

Apples, without skin

0.07

Blackberries

0.57

Dates

1.15

Pears, without skin

0.25

Pineapple

0.37

Raspberries

0.57

IRON IN GRAINS

GRAINS

SERVING

IRON IN /mg

Wheat Flour, White Cake,

1 cup

10.03

Enriched
Wheat, Soft White

1 cup

9.02

Wheat, Hard White

1 cup

8.76

Sorghum

1 cup

8.45

Corn flour, Masa, Enriched 1 cup

8.22

White
Corn flour, Masa, Enriched 1 cup

8.22

Yellow
Millet

1 cup

6.02

Oats

1 cup

7.36

Quinoa

1 cup

2.36

Rice Bran, crude

1 cup

21.88
HEME IRON RICH FOODS

Meat

IRON IN/mg

Beef Lean Chuck

2.9mg

Turkey Meat(Dark)

2.3mg

Chicken Leg(Roasted)

1.3mg

Tuna(Bluefin)

1.3mg

Halibut

1.3mg

Pork Chops(Loin)

1mg

White Tuna

0.9mg

Shrimp(Prawns/Camarones)

1mg

Liver

30.5mg

Clams, Oysters and Mussels

28mg

Absorption Of Dietary Iron

?Only 10% of Dietary Iron is

absorbed (1-2 mg/day).
? The site of absorption is:
? Duodenum and Jejunum

of GIT by active transport

process.

The Absorption of Iron is

Regulated at GIT level
? The absorption of Iron is

proportionately increased

where Iron stores are depleted.

?In growing Children's
?In Iron Deficiency Anemia

HEME IRON Absorption



v Heme Iron is well absorbed and relatively

unaffected by other factors .

v It is influenced to some extent by the

body's Iron stores.

vThe average absorption of Heme Iron in

meat is about 25%.
NON-HEME IRON Absorption

v Non Heme Iron is not so well

absorbed as Heme Iron

vIt is affected by both the Iron

status of an individual

v Components in foods eaten at

the same time.

v Absorption of non-Heme Iron can vary :
v1% in an individual with replete stores
v20% in an individual with depleted Iron

stores .

v Generally Non-Heme Iron absorption

is less than 5%.
? Dietary Iron is mostly found in

Ferric form associated with

food Proteins and organic

acids.

? Gastric HCl releases Ferric form

of Iron in the GIT lumen.

? Ferric form of Iron (Fe+3) is

unabsorbable form of Iron.

? Ferric form is transformed to Ferrous

form of Iron at GIT in presence of

Vitamin C (Ascorbic acid).

Fe+3 Fe+2

Vitamin C

Glutathione-SH
?Thus Ascorbic acid

transform non absorbable

Ferric form of Iron to

absorbable Ferrous form

?Vitamin C is the most potent

enhancer Iron absorption.

Factors Affecting Iron Absorption
Iron Absorption Promoting Factor

? Gastric acidity- HCl facilitates in

releasing the dietary bound form

of Iron to free form.

? Vitamin C, Glutathione ?Cys ?SH

help in reduction of Ferric to

Ferrous in GIT and make it

absorbable.

? Gastroferrin a Glycoprotein

of gastric juice facilitates

the uptake of Fe+2 Iron from

Duodenum and Jejunum.
?Dietary items promotes

and facilitates Iron

absorption.

?Smal peptides
?Amino acids and
?Low phosphate

Factors Inhibiting Iron Absorption

? Alkalinity
? Phytates and Oxalates
? Long free Fatty acids (In Steatorrhoea)
? Dietary fibers

? High concentration of dietary

Calcium and Phosphorous inhibits

Iron absorption.

? Low Copper and high lead in body

affects Iron metabolism.

Mineral Interactions

Zn

(

Cu

-)

(+)

Fe

(-)

Mn
? Tea and Eggs decrease Iron

absorption to some extent.

? Iron absorption is severely

impaired in patients who has

undergone partial or total

surgical removal of Stomach

/Intestine.
? Absorption of Non-Heme iron (plant sources) increased

by:

? Vitamin C

? Meat in diet (MFP factor)

? Citric acid and lactic acid from foods

? HCl in the stomach

? Sugars

? Absorption is decreased by:

? Phytates and fibers (grain products)

? Polyphenols (tea, coffee)

? Oxalates

? Calcium and phosphorus in milk

? Tannic acid

? Other minerals (calcium, zinc)

Uniqueness Of Iron

? Iron is one way element

? Iron once absorbed and enter in

body not excreted out through

Urine.

? Iron is not excessively absorbed

and then get excreted in urine

? Hence Iron is little absorbed and

little/no loss.
Regulation Of Iron Metabolism In GIT

Remembering

?Iron is not excessively

absorbed from GIT

?Iron is not excreted out

through Urine.
? Regulation of Iron

metabolism takes place at

GIT level

? By Intestinal Mucosal block

/Mucosal block theory of

Iron absorption.

Mucosal Block Theory

Of

Iron Absorption
? For Iron absorption at GIT

level Garnick Proposed

Mucosal block theory

?Mucosal block theory

explains the regulation

of the bodies Iron

content within normal

state
?Ferrous (Fe+2) form of Iron

from the intestinal lumen

is absorbed

?Made its entry into

intestinal mucosal cells

through receptor mediated

uptake.

?Inside the cytosol of

Intestinal mucosal cel s,

Intestinal Iron Carrier

(I.I.C) bind with

absorbed Fe+2 form of

Iron.
? Fe+2 form of Iron in intestinal

mucosal cel s is then oxidized

to Fe+3 by Ferroxidase I

activity .

? This Ferric form of Iron is

temporarily stored as Ferritin

form, in intestinal mucosal

cel s.

? The Iron absorption from

GIT lumen is regulated by:

?The saturation of I C (Carrier

Iron Pool) and

?Adequate mucosal Ferritin

content.
? As per the bodies requirement

the temporarily stored Iron as

Ferritin is released in Ferrous

form by Ferroreductase

activity.

? The Ferrous form of Iron from

intestinal mucosal cel s is then

diffused in blood.

? Ferrous form Fe+2 form of Iron

diffused in blood circulation is

transformed to Ferric Fe+3 form

in blood circulation

? By Ferroxidase II activity of

Ceruloplasmin (A Copper containing

Protein) .



Effect of Iron Status on Iron Absorption

HEME IRON UPTAKE

HEME IRON

HEME IRON

TRANSPORT

ENDOCYTOSIS

FERROUS IRON

LIBERATED WITH IN ENDOSOME
NON-HEME IRON UPTAKE

FERRIC IRON

REDUCED BY

ASCORBIC

ACID

INCLUDE

DUODENAL

FERROUS IRON

CYTOCHROME

B

TRANSFERRIN

FERROPORTIN

HEPHAESTIN

VITAMIN C IMPROVE

NON-HAEM IRON

ABSORPTION


IRON ABSORPTION IN HUMAN BODY
Iron Absorption

Transport Of Iron In Blood
Transport Of Iron

? Transport of Iron through

blood is accomplished

? With the help of a specific

Iron Transport Protein

Transferrin.

? Transferrin is chemically a

Glycoprotein with mol.weight

90,000 daltons.

Transferrin is a beta Globulin

plasma Protein.


Iron Transported By Transferrin

? Apo transferrin is a Protein, not

bound with Iron.

? Apo transferrin binds with two

atoms of Fe+3 form of Iron and get

transformed to

Transferrin/Siderophil in .

Transferrin

? Transports Iron in the blood

? Contains only 2 atoms of Iron in Ferric state

? Transferrin is the only source of Iron for

Hemoglobin

? Transferrin saturation is clinical y useful

for Iron metabolism studies
Total Iron Binding

Capacity

(TIBC)

? The plasma Transferrin

concentration is 250 mg%

? Transferrin can bind 400 g

of Iron/dl of plasma.

? This is known as Total Iron

Binding Capacity Of Iron

(TIBC).


? Transferrin Saturation:

? Normal about 30-50 %

? Transferrin saturation under 15 %=

Iron deficiency
?TIBC is reduced in

patients suffering from

Iron Deficiency Anemia

and Liver Diseases.

?High concentration

of TIBC is noted in

Iron toxicity.
Iron Uptake By Cel s

? The Cells of various tissues

have specific receptors for

Transferrin.

? An Iron Transferrin Receptor

Complex is formed and Iron is

internalized within the cel s.

?Transferrin receptors

are richly present on:

?Liver

?Spleen

?Bone Marrow

? Pancreas


Iron Circulation, Uptake Into Cel s, &

Storage

? Transferrin

?Delivers Iron to body cells through
?Transferrin Receptors
Storage Of Iron As Ferritin

? Iron is normal y stored in Liver,

Spleen and Bone marrow

? Iron is temporarily stored in the

form of Ferritin til it get

utilized.

? Apoferritin is a Glycoprotein of

500,000 daltons mol.wt

? Apoferritin is not bound to Iron.



?An Apoferritin can bind

with 4,000 atoms of

Ferric form of Iron and

form Ferritin.

? Ferritin protein consists of

24 subunits

? Ferritin stores are approx.

25% of Iron on weight

basis.


? Inside the Ferritin shel , Iron

ions form crystal ites

together with phosphate and

hydroxide ions.

Ferritin:

Iron Storage protein

In men, Ferritin contains up to

1 gram of Iron
? Ferritin levels reflects the amount of

BODY IRON STORES

? Men: 20-275 g/litre

? Women: 15-200 g/litre

? 15 g/ litre and less: insufficient Iron

stores

Hemosiderin

? Hemosiderin is Iron complex

Proteins

? Found in tissues in Iron toxic

conditions.

? Hemosiderin is Ferritin with

partial y stripped shel .
? Hemosiderin contains Ferric form

of Iron stored around 35% on

weight basis.

? Hemosiderin is rather insoluble

form and mobilization of Iron is

much slower from Hemosiderin

than Ferritin.

Body Distribution Of Iron
Body Distribution Of Iron

? Total Iron content of an

adult body varies and

ranges from 2-5 grams.

? About 70% of Iron is present in

RBC's associated to Hemoglobin

? 5% of Iron is present in Muscles

associated to Myoglobin.

? Remaining 25 % in other cel s

associated to Heme and non

Heme compounds.
Role Of Iron In Human Body

Functions Of Iron

?Iron is an essential trace

element

?Iron is utilized for the

biosynthesis of various

Iron containing functional

biomolecules.
? Iron is a component of Prosthetic group

Heme which in turn forms various

Hemoproteins:

?Hemoglobin
?Myoglobin
?Cytochromes
?Glutathione Peroxidase
?Catalase
?Xanthine Oxidase
?Tryptophan Pyrrolase

?Iron Involved In

Oxygen Transport &

Storage:

?Hemoglobin

?Myoglobin
?Iron Involved In Electron

Transport & Energy

Metabolism(ATP)

?Cytochromes

?Fe-S proteins

?Iron In Drug Detoxification:

?Cytochrome P450
? Substrate Oxidation & Reduction

? Iron dependent Enzyme-

?Ribonucleotide reductase

?Amino acid Oxidases

?Fatty acid Desaturases

?Nitric oxide Synthetase

?Peroxidases

? Iron serve as an inorganic cofactor

for fol owing Enzymes:

?NADH Dehydrogenase-FeS Proteins
?Succinate Dehydrogenase-Iron

Sulfur Proteins

?Aconitase
?Cytochrome Oxidase
?Acyl-CoA Dehydrogenase
?NADH Reductase
Iron Content in Hemoproteins

? Hemoglobin: more than one half of total body iron

(2.5 grams)

? Myoglobin: about 0.3 grams Fe, muscle oxygen

storage protein

? Cytochromes of the mitochondrial respiratory chain

(100 mg of iron)

? Cytochrome P450: most abundant Hemoprotein of

the liver (about 1 mg) detoxifies foreign compounds



Function

Flavoproteins

Heme

2Fe-2S

Other Nzms

Flavoproteins

4Fe-4S

Nzms

Transferrin

Fe-sulfur

Iron

&

Nzms

Activated

Others

Nzms

Other Fe

Fe-Containing

Other Fe

Proteins

Proteins

Nzms

Ferritin

&

Other Nzms

Hemosiderin

Hemeproteins

Hemoglobin

Myoglobin

Cytochromes

Other Nzms
Non - Heme Iron Proteins Of

Body

? Ferritin - Iron storage

protein

? Transferrin: Iron transport

protein

Excretion Of Iron
Conservation Of Iron In Human Body

OR

Iron Is One Way Element

? Iron is a rare element
? It is produced and present in

deep core of Earth surface .

? Since it contains comparatively

little Iron, hence Iron is

considered as very precious

element for biological system.
? The dietary Iron has to face

many interferences in GIT

with many factors.

? Only 1-2 % of dietary Iron

succeed to get absorbed

inside the intestinal mucosal

cells.

Note

?Iron absorption and

release in blood stream

is regulated by Hepcidin

to maintain the body

Iron stores.
?Iron is conserved

recycled and

reutilized within the

body cel s.

? Iron is said to be one way element

since

?The dietary absorbed Iron at GIT

level(approx 10%) once entered in

the body

?Iron is stored and functionally

reutilized.

?Almost no Iron is excreted out

through urine.
? The Hemoglobin (Hb) and Heme (Iron

containing compounds)released from

lysed RBC's get bound to

?Haptoglobin (Hp)
?Hemopexin respectively.

? Which prevent Iron excretion

through Urine.

? Hb-Hp complex and Heme-

Hemopexin complex prevents

the excretion of Iron through

Urine and conserve the Iron

within body.

? Iron is restored as Ferritin and

reutilized.
?To prevent Iron overload

and toxicity in the body.

?Only 10 % absorbed Iron at

GIT is recycled, reutilized

and conserved

Remember

? Iron absorption is regulated at GIT

level depending upon:

? Bodies demand and requirement

of body cel s

? Since Iron is not excreted through

Urine

? There is no excess absorption of

Iron at GIT level
?Generally Body Iron

stores are greater in

men than in women

Routes Of Iron Loss

? Physiologically during

Menstruation Iron is lost

(1mg/day).
? During Parturition Iron loss is

1gm/pregnancy

? Loss of Iron in males is less than

0.5 mg/day.


Only 1 mg of Iron is lost daily from the body

(about 0.025% of total body iron)

Nonspecific pathways

(sloughing of dead cells, iron excretion in bile)

In women, additional 30 mg of iron is lost monthly

by menstruation

(about 1% of total body iron)

Loss of Iron is more from a Women's body than

Men's body.

? Feces contains unabsorbed Iron and

Iron lost due to desquamation of

intestinal cells (about 30%).

? The upper layers of skin cel s

contain Iron which are being lost and

becomes another source of Iron loss.
Pathological Loss Of Iron

? Excess of blood loss in cases

of Hemorrhage due to

accidents

? Hemorrhoids is another

major source of Iron loss.


Iron Recycling

Copyright 2005 Wadsworth Group, a division of Thomson Learning

Disorders Of Iron Metabolism
Disorders Due To Iron Deficiency

Iron Deficiency Anemia (IDA)

?Iron Deficiency Anemia is

most common

?Nutritional deficiency

disease of world

population.
Prevalence Of IDA

? 30 % of World population is anemic due

to IDA

? 70% of Indian population is suffering

from IDA.

? 85% of pregnant women suffer from

IDA.

? 15% of maternal deaths are attributed

due to IDA.

Six Causes Of IDA

1. Malabsorption Syndrome:

? Gastrectomy
? Achlorhydria
? Vitamin C deficiency

2. Nutritional deficiency of Iron:

?Poverty
?Ignorance
?Faulty food habits
3. Chronic loss of blood

?Hook worm Infections (0.3 ml/day/hookworm)
?Bleeding Hemorrhoids (Piles)
?Peptic Ulcers
?Uterine Hemorrhage

4. Repeated Pregnancies ( 1gm/delivery)

5. Nephrosis -Kidney dysfunction

leads to loss of Haptoglobin,

Hemopexin ,Transferrin loss through

Urine.
6. Copper and Ceruloplasmin

deficiency: Affects Iron transport and

Heme biosynthesis .
Consequences and Manifestations Of

IDA

?Iron deficiency Anemia is

characterized by:

?Microcytic Hypochromic

Anemia

?Hb less than 10 gm%
? Low Iron content in human body Lowers:

?Hb levels which in turn

? Decreases low Oxygen supply to tissues and

cells.

?Cytochrome function in ETC
?ATP production
?Cel activity

Manifestations Of IDA

? Apathy (Uninterested in Surroundings)
? Sluggishness ,Fatigue
? Impaired attention
? Irritability
? Poor Memory
? Palpitation
Diagnosis Of IDA

?Hb Concentration
?Peripheral Smear (PS) of

blood

?Serum Iron Levels
?TIBC Levels

Other Parameters: Measuring Iron Status

? Serum Ferritin

? Hematocrit

? Ceruloplasmin levels

? Vitamin C
Treatment Of IDA

? Dietary Sources Containing Rich

Concentration Of Iron

? Vitamin C Supplementation

? Oral Iron Supplementation

Iron Toxicity Disorders
Hemosiderosis Iron Toxic Condition

Hemosiderosis

? Hemosiderosis is Iron overload

condition

? Where there is increased Iron

Stores as Hemosiderin

? In Liver, Spleen, Bone marrow

etc without associated tissue

injury and cel ular dysfunction.
? Hemosiderosis is an initial

Stage of Iron overload.

? Hemosiderin are golden

brown granules

Causes of Hemosiderosis

? Prolonged Parenteral Iron

supplements

? Repeated Blood

Transfusions
? Hemosiderosis occurs during treatment

of Hemophilia and Beta Thalassemia

? Since these patients receive repeated

blood transfusions.

? GIT level of regulation is bypassed in

the parenteral infusion of blood.

Types Of Hemosiderosis
Primary Hemosiderosis

? Genetic cause due to presence of

abnormal gene on short arm of 6th

Chromosome.

? In these cases Iron absorption is

increased at GIT level and

? Transferrin levels in serum are

elevated.

Acquired Hemosiderosis/

Nutritional Siderosis /

Bantus Siderosis
? Bantus are tribal people of

Africa.

? Who cooked their food in Iron

pots.

? Staple food of them contained

low Phosphate and High Iron

content.

?The Iron absorption is

high in the Bantus

?Gradually leading to

Hemosiderosis termed

as Nutritional/Bantus

Siderosis
Hemochromatosis

What Is Hemochromatosis?

?Hemochromatosis is much

more severe condition of

Iron overload.
? Deposition of large concentrations of

Hemosiderin

? In functional stores of organs causing

dysfunction and injury to these

organs.

? In Hemochromatosis

Hemosiderin is spil ed out of

tissues and found in blood

circulation.

? Thus there is Hemosiderin,

also deposited under skin.
Consequences And Clinical

Manifestations Of Hemochromatosis

Iron Poisoning

? Acute or over dosage of Iron may lead to Iron

poisoning this manifests with:

? Vomiting

? Nausea

? Diarrhea

? Hematemesis (Blood Vomits)

? Liver Damage

? Organ Dysfunctions

? Coma
? Liver Cirrhosis
? Pancreatic Damage-Diabetes mel itus
? Skin Pigmentation-Bronze Diabetes
? Hypothyroidism
? Arthritis
? Arrhythmia
? Heart failure

? Severe Hemochromatosis leading

to organ dysfunctions lead to

death.

? 90% of affected individuals are

Males.
Organ systems susceptible to

Iron overload

Clinical sequelae of Iron overload

Pituitary Impaired growth, infertility
Thyroid

Hypothyroidism

Heart Cardiomyopathy, cardiac
Liver Hepatic cirrhosis
Pancreas Diabetes mellitus
Gonads Hypogonadism

?Liver is the principal site for

iron storage and has the

largest capacity for excess

Iron storage.

?When the Liver capacity is

exceeded, Iron is deposited in

other organs.
?In patients with -Thalassemia,

Iron loading of the anterior

pituitary

?Is primarily responsible for

disrupted sexual maturation.

? Hemochromatosis also

leads to Growth failure

due to :

?Growth hormone

deficiency

?Defective synthesis of

Insulin-like growth factor
Hepcidin And Its Role

Discovery of HEPCIDIN (2000)

Hepcidin: "Iron Regulatory Hormone"
What Is Hepcidin?

?Hepcidin is a natural protein

hormone of human body

?Encoded by the HAMP gene.

vHepcidin is 25 amino-acid peptide

hormone.

vHepcidin is synthesized by

Hepatocytes.

vIt is then transported in the blood

stream for its function.

vHepcidin regulates Iron absorption in

blood.


Hepcidin blocks Iron Export from:

MACROPHAGES

And

ENTEROCYTES IN THE SMALL INTESTINE

? Hepcidin is the principal

regulator of systemic/blood

Iron homeostasis
? Hepcidin blocks Iron

export from Macrophages

and Enterocytes into

blood circulation.

? Hepcidin Reduces



? Dietary Iron absorption by reducing Iron

transport across the gut mucosa

(enterocytes)

? Iron exit from Macrophages the main site of

Iron storage

? Iron exit from the Liver
Specific Action Of Hepcidin

? Hepcidin inhibits iron transport by binding

to the Iron export channel Ferroportin

? Which is located on the basolateral surface

of

?Gut Enterocytes
?Plasma membrane of Reticuloendothelial cells

Macrophages

? Hepcidin controls Blood Iron

concentration

? Tissue distribution of Iron by:

?Inhibiting intestinal Iron

absorption

?Iron recycling by macrophages

?Iron mobilization from hepatic

stores.
HEPCIDIN In Inflammation

? In states of inflammation

the Hepcidin level is abnormal y high.

? In inflammation serum Iron fal s down
? Due to Iron trapping within

Macrophages and Liver cel s

? Decreased Gut iron absorption.

? Hepcidin elevated during infections and

inflammation,

? Causing a decrease in serum Iron levels
? Contribute to the development of

anemia of inflammation

? Probably as a host defense mechanism

to limit the availability of Iron to

invading microorganisms.
Regulation Of Hepcidin Synthesis

Hepcidin is released from the Liver

according to body Iron status:

? Iron overload increases

Hepcidin expression


? Iron deficiency decreases

Hepcidin expression

? Due to mutations in the Hepcidin

gene itself or due to mutations in

the regulators of Hepcidin

synthesis.

? Hepcidin defects appears to be the

ultimate cause of most forms of

Hemochromatosis.



Iodine Metabolism

Iodine

? Iodine is an essential trace

element

? Iodine is very vital for

normal health , growth and

reproduction of human

body.
RDA For Iodine

? For Adults ? 100- 150 g/day

? Pregnant Women-200 g/day

Dietary Sources

? Iodized Salt
? Sea Foods
? Fruits Vegetables grown on sea

beds

? Onions
? Drinking Water
Absorption Of Iodine

? Absorption of Iodine is

mainly from smal intestine.

? Smal amounts of Iodine

are absorbed through Skin

and Lungs.

Body Distribution Of Iodine

? Total body content of Iodine= 25-30

mg.

? 80 % of Iodine is taken up by

Thyroid gland.

? Skin and Skeleton contains small

amount of Iodine.

? Blood levels of Iodine- 5-10g%
Functions Of Iodine

? Iodine is mainly taken up

by Thyroid gland.

? Iodine is utilized for the

biosynthesis of Thyroid

Hormones .

? The Iodine is activated and

added to Tyrosine residues of

Thyroglobulin Protein

? To form MIT and DIT which in

turn forms T3 and T4.
? Iodine metabolism requires

Selenium.

? T4 is transformed to T3 in

presence of Se containing

Enzyme DeIodinase.

Functions Of Thyroid Hormones

? Thyroid Hormones Regulate

Basal Metabolism

? Thus Iodine regulate

Carbohydrates, Lipids and

Protein Metabolism
? Iodine develops Brain

? Regulate Body Temperature

Excretion Of Iodine

? Nearly 70-80% of Iodine is excreted

through Urine.

? Small amount of Iodine may get

excreted through Bile ,Skin and

Saliva.

? Milk of lactating women contains

some Iodine.
Disorders Of Iodine Deficiency

?Iodine is general y scarce in

soil of Mountanious

regions.

?Upper regions of

mountains contain less

Iodine such areas are called

as Goiterous belt.
? Deficiency of Iodine to an

adult human body causes

Goiter.

? Deficiency of Iodine in

Children leads to Cretinism,

? Severe Iodine deficiency in

pregnant mothers leads to

?Intrauterine hypothyroidism

resulting in Cretinism.

? The condition is characterized

by mental retardation ,slow

body development-Dwarfism,

Characteristic facial Structure.


Endemic Goitre

? Severe Iodine deficiency in

adults leads to Endemic Goitre.

? Goitre is a condition of enlarged

Thyroid gland

? With decreased Thyroid

hormone production due to

Iodine deficiency.
? In Goitre enlargement of

Thyroid gland

? Due to proliferation of Thyroid

epithelial cells.

? Enlarged Thyroid gland in Iodine

deficient state is significant

? To extract Iodine from blood

more efficiently.

Types of Goitre

?Simple Goitre
?Toxic Goitre
? A simple goiter can occur without a

known reason.

? In this person thyroid gland is not able

to make enough thyroid hormone to

meet the body's needs.

? This can be due to a lack of iodine in a

person's diet.

? To make up for the shortage of thyroid

hormone, the thyroid gland grows

larger.

?Simple goiters

may occur in people

?Who live in

areas where the soil

and water do not have

enough Iodine.
? Toxic Nodular Goiter is an

enlarged thyroid gland that has

a small, rounded growth or

many growths cal ed nodules.

? One or more of these nodules

produce too much thyroid

hormone.

Goitrogens

? These are compounds

present in food stuffs

? Which prevent utilization of

Iodine

? Goitrogens leads to Iodine

deficient disorder Goiter.
?Cabbage and Tapioca

contain Thiocyanate

?This inhibits uptake of

Iodine by Thyroid

gland.

? Mustard seed contain

Thiourea

? Which inhibit Iodination of

Thyroglobulin during T3

and T4 hormone synthesis.
Copper Metabolism

Copper

? Copper is an essential trace

element

? Required for varied

functions of human body

keeping it vital and active.
RDA Of Copper

?Adults 2-3 mg/day
?Infants and Childrens-

0.5-2 mg/day

Dietary Sources Of Copper

? Organ Meat
? Liver
? Kidney
? Eggs
? Cereals
? Nuts
? Green Leafy Vegetables.
Absorption Of Copper

? About 10% of dietary Copper is

absorbed mainly by Duodenum.

? Metal othionein facilitates

Copper absorption by mucosal

cel s.

?Phytate ,Zinc,

Molybdenum (Mo+2)

decreases Copper

uptake into intestinal

mucosal cells.
Body Distribution Of Copper

? Total body content of Copper

is 100 mg distributed in

different organs.

? The Copper concentration of

Plasma=100-200g%.

? 95% of Copper in blood is

tightly bound to a Copper

containing Protein

Ceruloplasmin.

? 1 molecule of

Ceruloplasmin contains 8

atoms of Copper.
Functional Role Of Copper

Enzymes and Proteins Containing Cu

?Copper is an essential

constituent of several

Enzyme and Proteins.
Cu- Containing Enzymes

?Cytochrome Oxidase

(In E.T.C)

?Catalase (H2O2

Detoxification)

? Tyrosinase (Melanin Biosynthesis)
? Super oxide Dismutase ( SOD) an

Antioxidant.

? ALA Synthase (Heme Biosynthesis)
? Ascorbic acid Oxidase
? Monoamine Oxidase
? Phenol Oxidase
? Lysyl Oxidase( Col agen Synthesis)
? Since Cu containing Lysyl

Oxidase Enzyme is involved

cross linking of Col agen Fibers

of bone

? Copper has indirect role bone

development.

Copper Containing Proteins

? Ceruloplasmin (Ferroxidase I Activity)
? Storage form of Copper
(Liver RBCs and Brain Cel s)

?Hepatocuperin
?Hemocuperin
?Cerebrocuperin
Role Of Copper In Iron Metabolism

Ceruloplasmin

? Ceruloplasmin is a Copper containing

Glycoprotein.

? Ceruloplasmin is blue colored.

? Ceruloplasmin contains both Cuprous

and Cupric forms of Copper in its

structure.
Remember

?Ceruloplasmin is not

Copper transport

Protein.

? Normal Concentration of

Ceruloplasmin -25-50mg%.

? 5% of Copper in blood is

loosely bound to Protein

Albumin.
? Function of Ceruloplasmin in

blood is Ferroxidase I activity.

? Ceruloplasmin converts Ferrous

to Ferric in blood and added to

Apotransferin for its transport.

? Thus Copper has role in Iron

metabolism.

? Copper deficiency affects the function

of Ceruloplasmin
? Low Ceruloplasmin levels affects

Iron Metabolism:

?Transport of Iron
?Storage of Iron
?Utilization of Iron
?Heme Biosynthesis

? Copper helps in

maintaining Myelin

Sheaths of Nerve Fibers

? Role in development of

Nervous system
? Recently found out Copper

helps to protect the Heart

? By increasing HDL activity

(Scavenging Action-Reverse

Transport Of Cholesterol)

? Reduces risk of

Atherosclerosis.

?Copper is necessary for

the biosynthesis of:

?Phospholipids
?Melanin ?Skin and hair

pigment
Excretion Of Copper

? Normal y 85-99 % of

ingested Copper is excreted

through feces via bile

? Remaining 1-15% may get

excreted through Urine.

Disorders Associated To Copper

Metabolism
Deficiency Of Copper

?Deficiency of Copper

consequently lowers:

?Saturation of Transferrin

?Ferritin Levels

?Hb concentration

?Oxygen supply to tissues

?ATP production in body
Deficiency Of Copper

? Deficiency of Copper in body directly and

indirectly affects:

?Iron Metabolism

?Heme Biosynthesis

?Leads to Iron deficiency Anemia

?Melanin Biosynthesis

?Collagen Biosynthesis

Copper Deficiency Manifestations

?Bone disorders

?Thin Cortices
?Deficient Trabeculae
?Wide Epiphyses
?Weakness ,Weight Loss
?Atropy of Myocardium
?Demyelination
?Non Coordinated

movements

Menkes Disease

Kinky /Steel Hair Syndrome

A Copper Deficiency Disorder
?Menkes Disease is

associated to Copper

Metabolism.

?It is inherited X linked

disorder affects male

only.

Biochemical Defects

? Defects in intestinal

Copper absorption.

? Leads to Copper deficiency

in human body.
? Due to absence of Copper

binding ATPase

? Defective Transport of Copper

across the Serosa of mucosal

cel membrane.

?In Menkes Disease

the serum and Urine

Copper levels are

markedly decreased.
? Copper deficiency affects the

Melanin biosynthesis.

? Causes hypopigmentation of Skin

and hair

? Leads to greying of hair
? Flag type of hair growth (alternate

grey and white patches on hair)

Clinical Manifestations Of Cu

Deficiency

? Iron Deficiency Anemia
? Depigmentation of hair
? Mental Retardation
? Abnormal Bone formation
? Susceptible to Infections.
Copper Toxicity Disorder



Wilsons Disease

Hepatolenticular Degeneration

Wilsons Disease

?Wilsons Disease is an

inherited disorder

associated to Copper

metabolism.
Inheritance

?Wilsons Disease is

inherited as

Autosomal Recessive.

Incidence

?Incidence of

Wilsons Disease is

1 in 50,000 of live

births.
Biochemical Defect

? Gene present on Chromosome 13

? Encoding for Copper binding ATPase

/ATP 7B Gene in cel s is defective

? Which affects the normal excretion of

Copper, through bile out from Liver

cel s.

? Copper is not excreted through bile.

? In Wilson disease, the Copper

builds up in toxic levels in Liver,

? Liver releases the copper directly

into blood stream.
?In Wilsons disease due to

high toxic levels of Copper

in Liver

?There occurs defect in

incorporation of Copper

into Apoceruloplasmin to

form Ceruloplasmin.

? Thus in Wilsons disease the Copper

atoms are underutilized

? Not incorporated into

Apoceruloplasmin to form

Ceruloplasmin.

? Wilsons disease has low Ceruloplasmin

levels in blood which affects its

Ferroxidase activity.
? In Wisons disease due to low

Ferroxidase activity of

Ceruloplasmin


? The Iron transport and Storage is

indirectly affected.

? In Wilsons disease the unutilized

Copper liberated out from

damaged hepatocytes

? Copper is markedly excreted out

through Urine.
Clinical Manifestations

? Due to retention of Copper in

functional organs like Liver

,Brain ,Kidneys and Eyes.

? In Wilsons disease following

manifestations are noted.

? Accumulation of toxic levels of

Copper in hepatocytes

? Leads to hepatocel ular

degeneration and Liver Cirrhosis.
? In Wilsons disease Copper is also

deposited in brain basal ganglia

? Leads to lenticular degeneration

and neurological symptoms.

? Copper deposits in Kidneys
? Leads to defect in renal tubular

reabsorption leading to

Aminoaciduria.


? Copper deposition in

Descemets membrane of the

eyes ,around cornea.

? Causes a golden brown ,yellow

or green ring round the Cornea

termed as Kayser Fleischer

Ring.
Wilsons Disease Treatment

? Penicil amine injection

Chelates the Copper

? Remove the Copper

deposited in tissues and

excreted out.

? Sometimes Zinc is used

therapeutical y in Wilsons

disease

? As Zn decreases Copper

absorption.
Copper Toxicity Manifestations

? Diarrhea
? Blue-Green Discoloration of Saliva
? Hemolysis
? Hemoglobinuria
? Renal Failure
? Proteinuria

Zinc Metabolism
Zinc

?Zinc is an important trace

element of human body.

?Zinc is mainly intracellular

element.

RDA of Zinc

?Adults= 10-15 mg/day

?Pregnant and Lactating

Women=25 mg/day
Dietary Sources Of Zinc

? Meat
? Fish
? Eggs
? Milk
? Legumes
? Pulses
? Spinach
? Lettuce
? Yeast Cells
? Beans
? Nuts

Absorption Of Zinc

? Only smal percentage of

dietary Zinc is absorbed

? From duodenal and ileal

part of smal intestine.
? Zn absorption is facilitated

by

? A low molecular weight Zinc

binding factor produced and

secreted by Pancreas.

?Zn absorption is

interfered with

?High amounts of dietary

Ca, P and Phytates.
Body Distribution Of Zinc

? The total content of Zinc in adult human

body is 1.5 -2 gm.

? high concentrations of Zinc in Prostate

and Skin (80-100 mg/100 gm).

? Bones and teeth contains moderate

amounts of Zinc.

? Very low content in Brain and Lungs.

Zinc In Blood

?Blood Zinc Levels 120-

140 g/100ml

?Zinc is associated with

Albumin in blood.
Biochemical Functions Of Zinc

? Zinc serves as inorganic

cofactor for certain Enzymes


? Zinc containing Enzymes:

?Alcohol Dehydrogenase
?Alkaline Phosphatase
?ALA Dehydratase
? Carbonic Anhydrase
? Carboxy Peptidase
? Super Oxide Dismutase-Zn
? LDH
? DNA and RNA Polymerase

?Zinc is required for the

storage and secretion of

Insulin hormone

?From the Beta cells of

Islets of Langerhans of

Pancreas.
?Zinc has role in wound

healing by promoting

epithelialization.

?The Salivary taste Protein

"Gustin " contains Zn.

? Zinc has role in growth and

reproduction of human beings.

? Zinc binds to regulatory Proteins

of DNA and

? Involve in the control of

Transcription (Zinc Finger Motif).



? Zinc helps in biosynthesis of

Retinol binding Protein.

? Thus Zinc is necessary to

maintain normal levels of

Retinol(Vitamin A) in blood.

Excretion Of Zinc

? A normal healthy body looses 9

mg of Zinc through Feces and 0.5

mg through Urine.

? Trace amount of Zn is lost in

sweat.

? 0.5 mg of Zn is retained in the

body.
Disorders And Manifestations Of Zinc

Zinc Deficiency Manifestations

?Poor Wound Healing
?Lesions of Skin
?Hyperkeratosis
?Dermatitis
? Alopecia
? Impaired Spermatogenesis
? Impaired Macrophage

Function

? Depression ,Dementia and

Other Neuropsychiatric

Complications.

Achrodermatitis Enteropathica

?This is a rare inherited

disorder of Zn

metabolism.

?It is a autosomal

recessive disorder.
Biochemical Defect

?Defect In Zinc

absorption from GIT

?Leads to Zinc

deficiency in human

body.

Clinical Manifestations

? Achrodermatitis-

Inflammation around mouth

,nose, fingers

(Dermatological Disorder)

? GIT disturbances-Diarrhea
? Neuropsychiatric features
?Ophthalmological

dysfunctions

?Growth Retardation.
?Hypogonadism
?Alopecia

Secondary Causes Of Zinc Deficiency

?Chronic Alcoholism
?Uncontrolled Diabetes

mellitus.
Zinc Toxicity

?Zinc Toxicity is manifested
?When dosage of Zn is more

than 1000 mg/day.

Causes Of Zinc Toxicity

? Zinc toxicity is commonly noted

in Welders who may inhale

fumes of Zinc Oxide.

? Many Rat poisons contain Zn

compounds ,ingestion of it leads

to Zn toxicity.
Manifestations Of Zn Toxicity

? Chronic toxicity of Zn produces

Gastric Ulcer

? Pancreatitis
? Nausea ,Vomiting
? Pulmonary Fibrosis

Acute Zinc Manifestations

? Fever
? Excessive Salivation
? Headache
? Anemia
? Leukocytosis
Therapeutic Value Of Zinc

? Recent evidences has proved Zinc

therapy may reduces

Atherosclerosis.

? Administration of 3.4 mg of

elemental Zn /day has

Significantly reduced serum LDL

Cholesterol.

? Prevents Aortic wal

Cholesterol deposition

? Prevent Platelet adhesion
? Increased Fibrinolytic

activity.
?Acute fal in Zinc is noted

on 3rd or 4th day of

Myocardial Infarction.

Fluorine Metabolism
Fluorine

?Fluorine is a trace

element

?important in preventing

tooth caries and decay.

RDA Of Fluorine

? Safe limit of Fluorine is

1ppm/day

? 1ppm= 1mg/10,000 ml
Dietary Sources Of Fluoride

? Drinking Water is the main

source

? Fluoride Tooth paste
? Tea
? Fishes
? Jawar

Absorption Of Fluoride

?The dietary soluble

forms of Fluorides are

absorbed by

?Simple diffusion from

intestine.
Body Distribution OF Fluoride

? Fluoride in body is mainly

present in bones and teeth.

? The blood contains ionized

form of Fluoride=10-20 g%.

Biochemical Functions Of Fluoride

? Fluorine in trace amounts help

in teeth development and

prevent dental caries

? By hardening of dental enamel

and maintaining Fluoroapetite

(Calcium Fluoride).
? Fluoroapetite makes:

?Tooth surface strong
?More resistant to plaque
?No bacterial attack
?Prevention of tooth decay

?Fluorine has role in

bone development

?Which Prevent old age

Osteoporosis.
? Fluoride is an inhibitor of

Enzyme Enolase of Glycolysis

(Antiglycolytic agent)

? Sodium Fluoride is content of

sugar bulb/grey vacutainer

? Used for blood col ection for

Glucose estimation.

Excretion Of Fluoride

?Fluorides are

mainly excreted

through Urine.

?

u
Disorders Of Fluorine Metabolism

Deficiency Of Fluorine

? Intake of Fluorine less than 0.5

ppm in Children

? May lead to Fluorine deficiency
? Fluorine deficiency directly

affects the health of teeth and

bones.
? In Fluorine deficient persons.

the Fluorapatite is not formed

and maintained on the enamel

of teeth

? These teeth are susceptible to

acid produced by bacterial

action on foods.

? In cases of low Fluoroapatite

?Enamel is removed by acid
?Dentine pulp is exposed
?Leads to plaque formation
?Inflammation , tooth

ache/decay
Toxicity Of Fluorine/ Fluorosis

?Intake of Fluorine

more than 5ppm/day

causes Fluorosis.

?The manifestations

of Fluorosis are

more severe than

Fluorine deficiency.
Causes Of Fluorine Toxicity

? Drinking Fluoridinated

Water

? Excessive use of Fluoride

Tooth paste

? Eating Jawar

Clinical Manifestations Of Fluorosis

? Fluorosis cause GIT upset

?Gastroenteritis
?Loss of Appetite
?Loss of Weight


? Dental Fluorosis leads to:

?Mottling of Teeth Enamel
?Stratification and

Discoloration of Teeth

(Brown/Yel ow Patches on Teeth).


?Fluoride levels more than

20 ppm is very toxic

?Leads to advanced

skeletal Fluorosis /Genu

valgum.
? Characteristic features of Skeletal

Fluorosis are:

?Alternate areas of

Osteoporosis and

Osteosclerosis with brittle

bones.

?Bone density is

increased due to

? Fluoride deposition in

bones of limbs ,pelvis

and spine.


?Individuals are crippled

and has stiff joints

?They are unable to

perform their daily

routines.


Prevention Of Fluorosis

? By checking the Fluoride levels

of drinking water of deep bore

wel s

? Reducing drinking water

containing excess levels of

Fluoride.
? Avoid use of tooth paste which

are excessively fluoridinated.

? Restricting intake of excess

Jawar.

? Supplementation of Vitamin C.

Metabolism Of

Manganese

(Mn)
Manganese

? Manganese (Mn) is a trace

element

? Mainly found in the Nucleus

? In association with Nucleic

acids.

RDA For Mn

?Adults- 2- 9 mg/day
Dietary Sources Of Mn

? Tea is a rich source of Mn.
? Other sources are

Cereals,Nuts,Leafy Vegetables

and Fruits.

? Liver an Kidney are animal

food sources of Mn.

.

? About 3-4% of dietary Mn is

normal y absorbed in Intestine.

? Dietary Calcium , Phosphorous

and Iron may inhibit Mn

absorption.
Body Distribution Of Mn

? The total body content of Mn is

about 15 mg

? Liver and Kidney are rich in Mn.
? The blood Mn levels 4-20 g%.

?Transmagnin a Beta 1

Globulin protein.

?Transports Mn in blood
Biochemical Functions Of Mn

? Mn is associated with

enzyme RNA Polymerase in

nucleus and helps in

transcription process.
? Mn serves as cofactor for

fol owing Enzymes:

?Arginase (Urea Cycle)
?Pyruvate Carboxylase (Pyr to OAA)
?IDH (TCA Cycle)

?SOD-Mn (Mitochondrial)
?Peptidase
?Succinate

Dehydrogenase
? Mn is associated with SOD

Antioxidant activity

? Thus Mn has an antioxidant

function and prevent Lipid

peroxidation

? Mn plays important role in

Glycoprotein and Mucoprotein

biosynthesis.

? Mn is necessary for Cholesterol

and Hemoglobin biosynthesis.
? Mn is also required for the

Bone formation and normal

function of nervous system.

Excretion Of Mn

?Mn is excreted through

bile and Pancreatic

juice.
Deficiency Of Mn

? Growth retardation
? Skeletal Deformities (Defective

Chondritin SO4)

? Increased ALP levels
? Functional activity of Beta cells to

produce Insulin diminished

? Severe deficiency may lead to sterility.

Manifestations Of Mn Toxicity

? Mn toxicity leads to

Psychotic and Parkinsonism

like symptoms.
Molybdenum

Metabolism

Molybdenum

? Molybdenum Trace

element

? Dietary requirement of Mo

in Adults is 0.5 mg/day

? For Children 0.3 mg/day
Dietary Sources OF Mo

?Cereals and Legumes

are rich sources of Mo.

?Liver is also rich in Mo.

Absorption Of Mo

? Mo is absorbed from the intestine.

? Higher levels of Mo in food wil

impair the absorption of Copper.
Body Distribution Of Mo

? The content of Mo in human

body is very little .

? It is mainly present in bones to

smal er extent in Liver and

Kidneys.

Biochemical Functions

? Mo is constituent of the Enzymes.

?Xanthine Oxidase
(Purine Catabolism)
?Sulfite Oxidase
?Aldehyde Oxidase
?Mo in Enzymatic reactions

participates

?Internal electron transfer

during oxido reduction.

Excretion Of Mo

? Mo is mainly excreted through

urine to smal extent through

feces via bile.
Disorders Of Mo

? Deficiency of Mo causes

decreased Xanthine oxidase

activity

? Which increases Xanthinuric

acid and decreases Uric acid

excretion

? Molybdenosis is a rare

disorder caused by excessive

intake of Mo.

? It manifests as impairment in

growth, diarrhea and

Anemia

? Excess Mo affects intestinal

Copper absorption.
Selenium Metabolism

Selenium

? Selenium is a trace element

associated to antioxidant

activity.

? RDA of Selenium in adults is

50-200g/day
Dietary Sources Of Selenium

? Rich sources of Selenium are organ

meat like Liver and Kidney.

? Sea Foods
? Food crops grown in Selenium rich

soil

? Soil of Punjab and Haryana is rich

in Selenium content.

Absorption Of Selenium

? Selenium is mainly absorbed

from Duodenum.

? Selenium is transported

bound to Plasma Proteins.
Body Distribution Of Selenium

? Selenium is widely distributed

in all tissues .

? Highest concentrations of

Selenium are found in Kidney

,Liver and Finger nails.

? Low concentration of Se is

found in Muscles , Bones

,Blood and Adipose tissues.

? Blood levels of Selenium are

0.05 to 0.34 g/ml
Biological Forms Of Selenium

? The termination codon UGA is

responsible for the direct insertion

of Seleno-Cystine

? In Selenium containing Enzymes

during Protein biosynthesis.

? Thus Seleno-Cysteine may be

considered as the 21 st amino acid.

? Biological forms of Selenium

are analogues of S containing

amino acids viz

?Selenomethionine
?Selenocysteine
?SelenoCystine
Biochemical Functions Of

Selenium (Se)

? Selenium along with vitamin E

has potent antioxidant function.

? Selenium has sparing effect on

Vitamin E

? Selenium reduces Vitamin E

requirement in the body.
?Selenium as

Selenocysteine is an

essential component of

enzyme Glutathione

Peroxidase

? Se containing Glutathione

Peroxidase detoxifies toxic free

radical H2O2 within cells.

? Thus this detoxification of H2O2

protects the cel s against the

damage caused by H2O2.
? Selenium also interacts with free

radicals including Superoxide

radicals.

? Se protects the cel s from Lipid

peroxidation of biological

membranes

? This maintains structural integrity

of the biomembranes

?Selenium prevents :

?Intracel ular

hemolysis

?Hepatic necrosis and

muscular dystrophy.
? Selenium has anticancer role

? Since it protects the body from

the action of chemical

Carcinogens on DNA and

prevent from mutations.

? 5'-Deiodinase enzyme is another Se

containing enzyme which has its role

in T3 Hormone biosynthesis.

( T4 to T3 transformation).

? Selenium is necessary for normal

development of Spermatozoa.
?Selenium has affinity for

Hg+2 and Cd ions

?It interacts with them and
?protect the body from

toxic action of heavy

metals atoms.

Excretion Of Selenium

? Main route of Selenium

excretion is through Urine

? Very smal amount of Se

excreted through feces and

expired air.
Disorders Associated

To

Selenium Metabolism

Selenium Deficiency Disorders
Keshans Disease/ Cardiomyopathy

? This Selenium deficiency disorder

was first reported in ?Keshan a

country of North Eastern China.

? Mostly Childrens and Womens were

affected due to low dietary intake of

Selenium.

Clinical Manifestations

? Acute or Chronic Cardiac

enlargement

? Arrhythmia

? E.C.G Changes

? Cardiomyopathy ( Multifocal

Myocardial Necrosis)
Treatment

? Supplementation of Sodium

Selenite

? Is highly effective in

Prophylaxis /prevention and

treatment of Keshans

disease.

Kashin Beck Disease (Osteoarthritis)

?Selenium Deficiency

affects mostly children's

of age between 5 to 13

years.
Clinical manifestations

? Severe enlargement and

dysfunctions of the joints.

? Shortens fingers and long

bones.

? Growth retardation
? Degenerative Osteoarthritis

Treatment

?Supplementing 20

to 120 g/day of

Selenium.
Selenium Toxicity Disorders

Selenosis

?Toxic doses (900

g/day) of Selenium

may lead to Selenosis .

? Early hal mark of Selenium

toxicity is garlicky odor in

breath.

? Due to exhalation of

Dimethyl Selenide.
Causes of Selenosis

?Workers working in

electronic ,glass and

paint industries suffer

from Selenosis.

Manifestations Of Selenosis

? Chronic Dermatitis
? Loss of hair
? Brittle nails
? Diarrhea
? Weight loss
Cobalt Metabolism

Cobalt

? Cobalt is the metal atom

an essential trace element.

? Cobalt forms an integral

parts of Vitamin B12.


?Cobalt is a component of

Corrin ring system.

?Corrin Ring is an internal

component of

Cyanocobalamin/Vitamin

B12
RDA Of Cobalt

? The daily requirement of

Cobalt is 5 to 8 g/day.

Dietary Sources Of Cobalt

? Cobalt is mainly present in

animal food sources

? Co not present in vegetables.
Absorption Of Cobalt

?70-80% of the dietary

Cobalt is readily absorbed

from the intestine.

Body Distribution Of Cobalt

? Cobalt is mainly stored in

Liver cells.

? Trace amount is present in

other tissues.
Biochemical Functions

? Cobalt is the component of Corrin

Ring System of Vitamin B 12/

Cyanocobalamin.

? In human body Cyanocobalamin is

transformed to Adenosyl

Cobalamin which has Coenzyme

role.
? Vitamin B 12 is used in

DNA multiplication.

? Cyanocobalamin has role in

normal functioning of

the Brain and Nervous

system.

? Cobalt is required to maintain

normal bone marrow

function. Blood formation

? Help in maturation of RBC's

by synthesis of Erythropoietin

hormone.
? Cobalt serve as cofactor for

enzyme Glycyl-Glycine

Dipeptidase of intestinal

juice.

Excretion Of Cobalt

?65% of ingested

Cobalt is excreted

almost through Urine.
Disorders Of Cobalt Metabolism

? Cobalt deficiency in humans is a

rare deficiency of Vitamin B12 leads

to Macrocytic Anemia.


? Cobalt toxicity results in

overproduction of R.B.Cs causing

Polycythemia.

Chromium Metabolism
?Traces of Chromium

plays important role in

Carbohydrate ,Lipid and

Protein Metabolism.

RDA Of Chromium

?10 -100 g/day is RDA

of Chromium for an

Adult body.
Dietary Sources Of Cr

? Yeast
? Cheese
? Grains
? Cereals
? Meat
? Food cooked in Steel vessels

increases Chromium contents of

food .

Absorption

?Chromium is mainly

absorbed from smal

intestine.

?It is transported through

Transferrin.
Body Distribution Of Chromium

? Human body contains about 6mg

of Chromium mainly resides in

Mitochondria, Microsomes and

Cytosol of Liver cells.

? Blood levels of Chromium 20 g %

Biochemical Functions Of Chromium

? Role of Cr in Carbohydrate

Metabolism:

? Trivalent Cr is known as Glucose

Tolerance Factor

? Since Cr along with Insulin promotes

the uptake and utilization of Glucose

by cel s (Cr alone is ineffective).

? Thus Cr is true promoter of Insulin.
? Role of Cr In Lipid

Metabolism:

? Chromium lowers the Serum

Cholesterol levels

? Decreases and prevents

atheromatous plaque

formation in aorta.

?Role of Cr in Protein

metabolism:

?Cr participates in the

transport of amino acids

into the cells of Liver

and Heart.
Chromium Related Disorders

? Deficiency of Cr causes

disturbances in

Carbohydrates ,Lipid and

Protein metabolism

? Causes impaired Glucose

tolerance.

Chromium Toxicity:

? Hexavalent Cr is more

toxic than Trivalent Cr.

? Cr toxicity increases lung

cancer ,Liver and Kidney

damage.
List Of Minerals With

Antioxidant Activity

?Selenium
?Copper
?Zinc
?Manganese

List Of Minerals

With Neuro Muscular Activity

? Calcium
? Sodium
? Potassium
? Chloride
List OF Minerals

With Bone Involvement

? Calcium

? Phosphorous

? Magnesium

? Copper

? Fluorine

Elements of Human Body


Questions
Long Essays

? Q.1.Enumerate the Principle

elements of our body? Describe the

calcium metabolism with respect to

dietary rich sources, RDA, factors

affecting its absorption, distribution,

functional role, excretion & disorders

associated with it.

? Q.2.Describe the Phosphorous

metabolism in details with

respect to dietary sources,

RDA, absorption, functions &

disorders associated with it.
? Q.3.Enumerate the body

electrolytes. Describe the role

of Na, K & Cl in the body.

? Q.4.Name the trace elements

in the body. Describe in details

of Iron metabolism.

? Q.5.Describe the role of trace

elements in the body with

respect to Cu, I2, Fl, Mn, Se,

Zn & Mo.
? Q.6.Describe the Magnesium

metabolism in details.


? Short Notes

?Factors affecting calcium absorption.

?Homeostasis of calcium/Regulation of

serum calcium.

?Condition of Hypercalcemia &

Hypocalcemia.

?Role of Calcitriol in calcium

metabolism.

?Tetany.

?Transferrin & Ferritin/Transport &

storage of Iron.

?Mucosal Block Theory/Absorption

of Iron.

?Differences between Ferritin and

Hemosiderin.

?Nutritional Hemosiderosis/Bantu's

Siderosis.
?Hemochromatosis/Bronz

e Diabetes.

?Iron deficiency Anemia-

cause & clinical

manifestations.

?Wilson's disease

?Menke's disease.

?Goiter

?Flurosis/Genu Valgum

?Selenosis/Selenium Toxicity

?Deficiency of Zinc

?Conditions of Hypernatremia &

Hyponatremia.

?Causes of Hyperkalemia &

Hypokalemia


?Clinical significance of Phosphorous.
?Give the list of Zn, Mg, Cu, Se, Cl, Mo

requiring enzymes of human body.

?Role of Ceruloplasmin.
?Keshan's disease
?Justify Iron is one-way element.
?How serum electrolytes are estimated?

What are its normal values present in

blood.

Thank you

This post was last modified on 05 April 2022