The electrolytes

• There are 3 major electrolytes:

– sodium
– potassium
– chloride
 Sodium (Na)
• Sodium is the principal cation in
extracellular fluids
• functions include:
• osmotic equilibrium
• acid-base balance
• carbon dioxide transport
• cell membrane permeability
• muscle irritability
 Sodium (Na)
• food sources: table salt, salty foods
(potato chips etc.), baking soda, milk
• absorption and metabolism:
– readily absorbed
– excreted in the urine and sweat
– aldosterone increases reabsorption in renal
tubules
 Sodium (Na)
• RDA for adults: 1.1 to 3.3 gm/day
• sodium deficiency(hyponatreamia):
– Dehydration due to vomiting, diarrhea,
– -burns
– -addision s disease
– -renal tubular acidosis
– -chronic renal failure, nephrotic syndrome
– -congestive cardiac failure
– -hyperglycemia and keto acidosis
 Hypernatreamia
• - cushing syndrome
• -prolonged cortisone therapy
• -primary hyperaldosteronism
• -elderly with poor water intake
• -drugs like ampicillin, tetracycline,
anabolic steriods, oral contraceptives,
diuretics etc
 Sodium (Na)
• Sodium supplements:
– usually used to replace sodium and
chloride lost through perspiration
during high heat
• Pedialyte solution
• Normal level ; 136 – 145 mEq/l
• Serum concentration of sodium is
measured by ion selective electrodes
 Potassium (K)
• Potassium is the principal cation in
intracellular fluid
• functions:
– buffer constituent
– acid-base balance
– water balance
– membrane transport
– neuromuscular irritability
 Potassium
• Food sources: vegetables, fruit (bananas),
whole grains, meat, tender coconut
water, oranges, pineapple etc
• absorption and metabolism:
– readily absorbed (more so than sodium)
– intracellular
– secreted by kidney (also in sweat)
• RDA for adults: 1.5 - 4.5 gm/day
 Potassium
• Normal level; 3.5- 5.0 mEq/l
• deficiency (hypokalemia)
– causes:
• increased renal excretion
(diuretics)
• Cushing s syndrome
• Hyperaldosteronism
• Renal tubular acidosis
 Potassium(hypokalemia)
• Shift or redistribution of potassium
• Insulin therapy
• Alkalosis
• Gastrointestinal loss
• severe vomiting and diarrhea
• Malabsorption
• Pyloric obstruction
• cutaneous losses via perspiration
• Intravenous saline infusion in excess
• Drugs like insulin, osmotic diuretics,
corticosteroids, salbutamol etc.
 potassium
– symptoms:

. weakness of skeletal muscles

(paralysis and impaired respiration
• Hypotension, palpitation, cardiac
arrhythmias
weakness of smooth muscles
• cardiac anomalies: AV block,
cardiac arrest
 Potassium supplements
• Oral products:
– tablets: potassium chloride, potassium
gluconate, Slow-K
– effervescent tablets: K-Lyte, K-Lor,
– parenteral products: usually administered
by slow IV infusion (KCl and K acetate)
 Potassium
• Excess (hyperkalemia)
• decreased renal excretion of potassium
• Entry of potassium to extracellular space
• severe tissue trauma and burns
• acute and chronic acidosis
• Hyperkalemic periodic paralysis
• Improper blood collection- hemolysis
• Drugs like spiranolactone, ACE inhibitors
etc
 potassium
– symptoms:
• weakness and paralysis
• Bradycardia
• Ventricular arrhythmia and fibrillation
• cardiac anomalies (impaired conduction,
fibrillations, cardiac arrest)
 Treatment of hyperkalemia
• reverse cardiotoxic effects:
– calcium gluconate IV
• increase potassium uptake by cells:
– dextrose (IV)
– insulin (IV)
– sodium bicarbonate (IV)
• remove excess potassium from the body:
– sodium polystyrene sulfonate (Kayexalate)
 Chloride (Cl)
• an essential anion
• Chloride conc. in plasma; 96- 106 mEq/l
• closely connected with sodium in foods,
body tissues and fluids and excretions
• readily absorbed along with sodium
• excreted mainly in the kidneys (~ 2% in
feces and ~ 4-5% in perspiration )
 chloride

• important for osmotic balance, acid-base

balance and in the formation of gastric
HCl
• Hyperchloremia is seen in dehydration,
cushing syndrome, renal tubular acidosis.
• The CFTR chloride conducting channel
is involved in cystic fibrosis
 Chloride (Cl)
• Deficiency of chloride:
– hypochloremic alkalosis
– -excessive sweating
– -addisons disease
 Sulphur
• Most sulfur in the diet comes in from protein
sources containing sulfur amino acids such as
cysteine, cystine and methionine
• Some enters as inorganic sulfur (sulfate,
sulfide, chondroitin sulfate and certain other
sulfate esters)
• Sulfur is also present in thiamine, biotin,
sulfolipids, conjugated bile acids and
coenzyme A
 Functions of Sulphur
• Sulphur containing amino acids are
important constituents of body proteins.
• Eg: insulin, immunoglobulins
• Chondroitin sulfate are seen in cartilage
and bones.
• Keratin is rich in sulphur and is present
in hair and nails.
 Functions of Sulphur
• Many enzymes and peptides contain –SH
group at active sites eg: glutathione
• Co-enzymes derived from thiamine,
biotin, pantothenic acid and lipoic acid
also contain sulphur.
• Sulphates are also important in
detoxification mechanism.
 Zinc
Biological roles
– Involved in many enzymes (over 20
metalloenzymes)
• Carbonic anhydrase
• Alkaline phosphatase
• Lactate dehydrogenase
• Alcohol dehydrogenase
• Glutamate dehydrogenase
• Superoxide dismutase
 Zinc
• Carboxypeptidase A
– Four types of proteases
» Serine
» Cysteine
» Aspartic acid
» Zinc
• ACE (angiotensin I convering enzyme)
• RNA and DNA polymerases
 Zinc
• zinc absorption appears to be dependent
on a transport protein, metallothionein
• deficiencies include poor growth, delayed
wound healing, impairment of sexual
development and decreased taste acuity
• zinc is present in gustin, a salivary
polypeptide that is necessary for the
development of taste buds
 Zinc
• severe zinc deficiency is seen primarily in
alcoholics (especially if they have developed
cirrhosis), patients with chronic renal
disease or severe malabsorption diseases
• Acrodermatitis enteropathica
• occasionally seen in patients on long term
total parenteral nutrition (TPN) –patient
develop a dermatitis
• zinc is occasionally used therapeutically to
promote wound healing and may be of some
use in treating gastric ulcers
Zinc supplements
 Iron (Fe)
• 2 types of body iron
– heme iron
• hemoglobin, myoglobin, catalases,
peroxidases, cytochromes (a, b
and c – involved in electron
transport), cytochrome P450
(involved in drug metabolism)
 Iron
– non-heme iron
• ferritin, hemosiderin, hemofuscin,
transferrin, ferroflavoproteins, aromatic
amino acid hydroxylases
• food iron is also classified as heme
and non-heme
 Food iron
heme iron non-heme iron
– vegetables
– meats
– fruits
– poultry
– legumes
– fish
– nuts
– breads and cereals
20-23% of heme-iron is
– -jaggery
absorbable
only ~ 3% on non heme
iron is absorbed
 Iron absorption
• occurs in upper part of small intestine
• about 10% of food iron is absorbed
• requires gastric HCl (releases ionic iron)
• also requires copper
• ferrous is better absorbed than ferric
form
• Ascorbic acid, cysteine and –SH groups
of proteins favour iron absorption
 Iron
• Iron absorption is decreased by phytic
acid and oxalic acid.
• Calcium, copper, lead and phosphates
will inhibit iron absorption.
• Adults;10 mg/dl
• Children; 20-30 mg/dl
• Pregnant,lactating women; 30-40 mg/dl
 Iron distribution and storage
• carried in blood stream via transferrin
• a b- globulin)
• stored in 2 forms:
• ferritin (a water soluble complex consisting
of a core of ferric hydroxide and a protein
shell (apoferritin)
• hemosiderin (a particulate substance
consisting of aggregates of ferric core
crystals)
• stored in liver, spleen, bone marrow, intestinal
mucosal cells and plasma
 FOOD IRON

gastric HCl, ascorbic acid

Fe++
unabsorbed Fe
(fecal excretion)

mucosal cell
(upper small Fe+++
intestine)
APOFERRITIN

FERRITIN

intestinal
apotransferin secretion
1-2 mg/day
plasma
Fe+++ - transferrin

Fe++ - hemoproteins Fe+++ - ferritin

(hemoglobin, myoglobin

Fe+++ - hemosiderin
bone marrow
liver
muscle
 Iron elimination
• there is no mechanism for excretion of iron
• iron is normally lost by exfoliation of
intestinal mucosal cells into the stools
• trace amounts are lost in bile, and sweat
(no more than 1 mg per day)
• bleeding (vaginal, intestinal) is a more
serious mechanism of elimination
• Mucosal block theory
 IRON DEFICIENCY
Initial symptoms are vague and ill-defined
• easy fatigability
• lack of appetite
• headache
• dizziness
• palpitations

then: hypochromic-microcytic anemia

• microcytosis (small RBCs)
• hypochromia (poor fill of hemoglobin)
• poikilocytosis (bizarre shapes)
• anisocytosis (variable sizes)
 IRON DEFICIENCY
Causes:
– excessive blood loss (parasitic, accidental,
menstrual): is most common cause
– rapid growth in children with limited intake
of iron
– malabsorption
• gastric resection
• sprue
– increased metabolic requirement
• pregnancy, lactation or neoplasia
 Diagnosis of iron deficiency
• hematology (microcytic hypochromic cells)
• low serum iron
• low serum ferritin( indicates low body stores)
• low hemosiderin
• high total iron binding capacity (TIBC)
 Treatment of iron deficiency
• give 200 - 400 mg of iron per day
• up to 25% of the iron preparation may
be absorbed
• 50 - 100 mg of iron may be utilized in
case of deficiency
• give on an empty stomach
 Treatment of iron deficiency

• oral iron causes black stools,

constipation, cramping
• do not administer with antacids or metal
chelators (tetracyclines)
 Iron toxicity
Hemosiderosis: Occurs in persons
receiving repeated blood transfusions.
Primary hemosiderosis : abnormal gene
located on short arm of chromosome no.6
 Copper
component of several enzymes:
• ceruloplasmin (an oxidase)
• tyrosinase (production of melanin)
• amine oxidase (metabolism of
catecholamines)
• cytochrome C oxidase
• dopamine beta hydroxylase
• copper/zinc superoxide dismutase
 Functions of Copper
• It is necessary for iron absorption and
incorporation of iron into hemoglobin.
• Co-factor for vitamin C requiring
hydroxylations.
• It increases HDL and so protects the
heart.
• It is required for tyrosinase activity.
 Copper (Cu)
• Deficiency
– decreased iron absorption
– neutropenia and leukopenia
– bone demineralization
– failure of erythropoiesis
• sources
• liver, shellfish, whole grains, cherries, legumes,
nuts
 Abnormal metabolism of
copper
• 1. Wilsons disease: ceruloplasmin level is
drastically reduced in wilsons
hepatolenticular degeneration.
• Defect in the gene encoding a copper
binding ATPase in cells.
• This is required for normal excreation of
copper from the cells.
 Abnormal metabolism of
copper
2. Aceruloplasminemia
3. Copper deficiency anemia
4. cardiovascular diseases
5. Menke’s Kinky hair syndrome
• X- linked defect
• It is a condition in which dietary copper
is absorbed from GI tract, but cannot be
 Abnormal metabolism of
copper
• transported to blood due to absence of an
intracellular copper binding ATPase.
• Copper is not available for metabolism
resulting in defective cross linking of
connective tissue.
• Vascular and connective tissue are
affected, and child usually dies in
infancy.
 Fluorine
• Considered essential because of its beneficial
effect on tooth enamel
• Benefits include: less dental caries, stronger
bones, reduction in osteoporosis and
calcification of the aorta
• In large quantities it is deleterious to teeth;
dental fluorosis: pitting, chalky, dull white
patches and mottling of teeth
• 1 to 2 parts per million is adequate for
drinking water
 Fluorine
• Main sources include drinking water and
plants (spinach, lettuce, onions)
• Average daily intake: 1.5 – 4.0 mg/day
• Fluoride supplementation is available in
both oral and topical forms:
• Oral: mainly sodium fluoride
(Pediaflor Drops)
 Fluoride
• Level more than 5 ppm causes mottling of
enamel, stratification and discolouration of teeth.
• Level more than 20 ppm is toxic , leading to
alternate areas of osteoporosis and osteosclerosis
with brittle bones.this is called skeletal fluorosis.
Genu valgum is the characteristic feature.
• Prevention of fluorosis is to provide fluoride free
water, restriction of intake of jowar,
supplementation of vit. C and regulation of
fluoride containing toothpastes.
 Iodine
• iodine is necessary for the formation of thyroid
hormones (T-4 and T-3)
• deficiency of iodine is manifested by a goiter
(enlargement of the thyroid gland)
• salt water fish and seaweeds are a good source
of iodine
• to prevent the development of endemic goiter,
tablet salt has been spiked with sodium iodide
• Daily requirement is 150-200 micrograms.
 Manganese
• Manganese is an activator of several
different enzymes:
• Phosphoglucomutase
• Isocitric dehydrogenase
• Cholinesterase
• Intestinal peptidase
• Carboxylases
• ATPases
 Manganese
• Essential for sulfomucopolysaccharide
biosynthesis
• Deficiency leads to:
• Weight loss
• Transient dermatitis
• Nausea and vomiting
• Changes in hair color
• Sources: blueberries, wheat bran, beet greens,
lettuce, legumes, fruit
• RDA: 2.5 – 5.0 mg
 Chromium
• Cr may act as a cofactor for insulin, enhancing
glucose utilization.

• deficiency leads to impaired glucose tolerance

(glucose tolerance factor)

• sources: corn oil, whole-grain cereals, clams,

drinking water (variable)
 Chromium
• forms a coordination complex with micotinic
acid and the amino acids glycine, glutamate
and cysteine
• chromium may have a role in type 2 diabetes
• RDA: 0.05 – 0.2 mg
• frequently available in pharmacies as
chromium picolinate
 Chromium
• Radioactive Cr is widely used to tag
RBC.
• Chromium toxicity is an occupational
hazard in workers of tanning industry.
• Liver and kidney damage are seen.
 Selenium
Selenium intake depends on the nature of
soil in which food is grown.

Requirement 50-100 micrograms/day.

Selenium concentration in testis is the

highest in adult tissue.
It is required for normal development of
spermatozoa.
 Selenium
• appears to function in the metalloenzyme
glutathione peroxidase, which destroys
peroxides in the cytosol

• no deficiencies have been seen in humans

• has antioxidant activity (may have relationship

with vitamin E - sparing action)
 selenium
• Keshan disease is characterised by
multifocal myocardial necrosis, cardiac
arrhythmias, and cardiac enlargement.
• Selenium toxicity is called selenosis.
Selenium is present in metal polishes and
anti-rust compounds.
• Causes hair loss, diarrhea, weight loss
and garlicky odour in breath.
 Cobalt
• essentiality exists in some animals for
ionic cobalt (sheep and cattle)
• in rats administration of cobalt produces
a polycythemia
• cobalt in necessary in humans in the
form of vitamin B12
• animals and plants cannot synthesize B12
• daily intake: 0.3 mg
 Molybdenum
• Widely found in commonly used foods
(cereals, vegetables
• Mo is part of flavoproteins, xanthine
oxidase, aldehyde oxidase