Minerals

Shajan xaviour

Minerals

A naturally occurring , homogeneous,

inorganic substance required by humans in

amts of 100 mg/day or more

-functions

-high and low serum levels

-absorption

-excretion

-deficiency

-toxicity

Minerals in a 60-kilogram (132-pound) Human Body

TRACE MINERALS

There are more than a dozen trace minerals,

although only six are shown here.

Amount (g)

MAJOR MINERALS

The major minerals are those present in amounts

larger than 5 g (a teaspoon). A pound is about

454 g; thus only calcium and phosphorus appear

in amounts larger than a pound.

calcium

Calcium

-most abundant mineral in the body

-99% of calcium is in the bones and teeth

-the remaining 1% is in the blood and ECF in

cells and soft tissues

Skeletal Calcium

-if there is no reserve, calcium is drawn from bone—leading to deficiency

Serum levels: 8.8 to 10.8 mg/dl

**when albumin is low (malnutrition,

liver dz), calcium is decreased

Ratio: for each gram albumin is

decreased below 4, add 0.8 to calcium

-ionized calcium is increased in acidosis and decreased in alkalosis (increased bicarb binds calcium)

***-example: in resp alkalosis, total serum calcium is normal, but ionized is low—always check ionized level with acid/base disorders

Functions

-building and maintaining bones and teeth

-transportation of cell membranes and membrane stabilizer

***-nerve transmission and regulation of heartbeat—use calcium gluconate IV to treat hyperkalemia (EKG—peaked T waves)

-ionized form initiates formation of the blood clot

-cofactor in conversion of prothrombin to thrombin

-required for muscle contraction

Regulate permeability of capillary walls

Regulate citric acid cycle

Absorption

-***absorbed mainly in the acidic part of the duodenum

-absorption is decreased in the lower GI tract which is more alkaline

20-30% of digested calcium is absorbed

Absorption is affected when Vit D is deficient

-unabsorbed form is excreted in feces

Factors that increase calcium

absorption

-***more efficiently absorbed when the body is deficient

-best absorbed in acidic environment (upper duodenum)

-HCL in stomach allows better absorption in the proximal duodenum

-taking calcium with food increases abs

-fat increases intestinal transit time and increases absorption

Factors that decrease

absorption

-***lack of vitamin D

-oxalic acid forms insoluble complex which decreases absorption (rhubarb, spinach, chard, beet greens)

-phytic acid found in outer husks of cereal grains also form insoluble complex

-alkaline medium decreases abs.(lower GI tract)

Aging decreases absorption

Maintenance of serum level

-parathormone (PTH) by the parathyroid gland and thyrocalcitonin secreted by the thyroid gland maintain serum levels

-***with decreased serum calcium levels, PTH increases and causes transfer of calcium from bone to blood to increase serum levels

-decreased levels also cause kidney to reabsorb calcium more efficiently (might normally be excreted in the urine) and to increase intestinal absorption

-when blood levels are increased, calcitonin acts by the opposite mechanisms as PTH to decrease serum levels

Maintenance of serum level

cont’d

***-always need to correct low Mg level

before treating a low calcium level

-hypomagnesemia decreases tissue

responsiveness to PTH

Causes of hypocalcemia

-***malabsorption

-small bowel bypass, short bowel

-vit D deficiency

-alcoholism

-***chronic renal insufficiency

-***diuretic therapy

Causes of hypocalcemia

cont’d

-hypoparathyroidism

-***hypomagnesemia

-sepsis

-pseudohypoparathyroidism

-calcitonin secretion with medullary

carcinoma of the thyroid

Causes of hypocalcemia

cont’d

-***associated with low serum albumin

(ionized calcium will be wnl)

-decreased end organ response to vit D

-hyperphosphatemia

-***aminoglycosides, plicamycin, loop

diuretics, foscarnet

Causes of hypercalcemia

-milk-alkali syndrome

-vit D or vit A excess

-primary hyperparathyroidism

-secondary hyperparathyroidism (renal insuff, malabsorption)

-acromegaly

-adrenal insufficiency

Causes of hypercalcemia

cont’d

***Neoplastic Disease

-tumors producing PTH-related proteins (ovary, kidney, lung)

-***mets to bone

-lymphoproliferative disease including multiple myeloma

-secretion of prostaglandins and osteolytic factors

Causes of hypercalcemia

cont’d

-***thiazide diuretic

-sarcoidosis

-paget’s disease of bone

-***immobilization

-familial hypocalciuric hypercalcemia

-complications of renal transplant

-iatrogenic

Excretion

-normal is 65-70% of ingested calcium

to be excreted in the feces and urine

-strenuous exercise increases loss (in

sweat)

-***immobility with bed rest and space

travel increase calcium loss because of

lack of bone tension

RDA

-see handout

sources

Deficiency

1)***bone—to be discussed in osteoporosis lecture

2) tetany—decreased serum levels increase the irritability of nerve fibers resulting in muscle spasms, fatal laryngospasm ***-Chvostek’s sign: contraction of the facial m.

after tapping the facial n.

***-Trousseau’s sign: carpal spasm after occlusion of the brachial a. with blood pressure cuff for 3 min

3) HTN—controversial

4) prolonged QT--arrythmias

Toxicity

-***polyuria, constipation, bone pain,

azotemia, coma

-”stones, bones(bone pain), groans,

psychiatric overtones”

Phosphorus

Levels maintained by parathyroid gland

Functions -structure of teeth and bones

-essential component in cell

membranes, nucleic acids,

phospholipids

-phosphorylation of glucose

-buffer system in ICF and kidney

Major role in A/B balance

Essential for lipid metabolism &CHO

Cell division and protein synthesis

absorption

-best occurs when calcium and phos are

ingested in equal amts (milk)

-vit D also increases absorption

Sources

***dietary sources should be restricted in renal disease (usually see increased phos, decreased Ca)

-protein sources

-meat, poultry, fish, eggs, legumes, nuts, milk, cereals, grains

RDA

1-1.5 Mg/day

Causes of hypophosphatemia

-starvation

-TPN with inadequate phos content

-malabsorption, small bowel bypass

-vit D deficient and vit D resistant

osteomalacia

Causes of hypophosphatemia

cont’d

-phosphaturic drugs: theophylline, diuretics, bronchodilators, corticosteroids

-hyperparathyoidism (primary or secondary)

-hyperthyroidism

-renal tubular defects

-hypokalemic nephropathy

-inadequately controlled DM

-***alcoholism

Causes of hyperphosphatemia

-excessive growth hormone

(acromegaly)

-hypoparathyroidism assoc with low Ca

-pseudohypoparathyroidism assoc with

low Ca

-***chronic renal insufficiency

-acute renal failure

Deficiency

-fatal

-usually rare with food intake

-***respiratory muscle collapse

-heart failure

-muscle aches, bone pain, and fracture

Magnesium

Function

-bone, muscle contractility, nerve

excitability

-antagonistic to calcium

--in a muscle contraction, Mg relaxes, and

calcium contracts

--low Mg can cause pregnancy induced

HTN

Absorption / Excretion

-absorption varies

-similar to calcium (low pH, upper GI), however, no Vit D required-kidney conserves Mg when intake of Mg is low

-large losses with vomiting because of high levels of gastic juice

sources

Sources

-seeds, nuts, legumes, unmilled cereal

grains, dark greens

-fish, meat, milk, fruits

-lost during refining of flour, rice, vinegar

Causes of hypomagnesemia

-malabsorption, chronic diarrhea, laxative abuse

-prolonged GI suction

-small bowel bypass

-malnutrition

-***alcoholism

-refeeding

-TPN with inadequate Mg

Causes of hypomagnesemia

cont’d-DKA

-diuretics

-hyperaldosteronism, Barrter’s syndrome

-hypercalcuria

-renal Mg wasting

-hyperparathyroidism

-postparathyroidectomy

-vit D therapy

-aminoglycosides, ***cisplatin, ampho B

Causes of hypermagnesemia

Decreased renal fxn

***Increased intake—abuse of Mg

containing antacids (MOM) and

laxatives in renal insufficiency

Deficiency

-anorexia, growth failure, cardiac and

neuromuscular changes—weakness,

irritability, mental derangement

-tetany, muscle cramps

Toxicity

-respiratory—depression, apnea

-CV—hypotension, cardiac arrest, EKG (prolonged QRS and QT, heart block, peaked T waves)

-GI—N/V

-neuromuscular—paresthesias, somnolence, confusion, coma, hyporeflexia, paralysis, apnea

Iron

Function

-respiratory transport of O2 and CO2

-immune system

-cognitive performance

-found in Hgb (in RBC’s) and myoglobin

(in muscles)

-cytochrome p450 system

Absorption and transport

-dietary iron exists in heme (Hgb and myoglobin) and non-heme

-***heme Fe is absorbed better

-non-heme Fe has to be present in the duodenum or upper jejunum in soluble form if it is to be absorbed

-in Fe deficiency, 50% can be absorbed

-***2-10% of Fe from veggies is absorbed and 10-30% is absorbed from animal protein

2 types

Heme proteins-

Hgb,Mb,Cytochromes,Catalases,Perioxi

dase

Non Heme Proteins

Ferritin,Hemosiderin,Transferrin,Iron

sulphur proteins,Aconitase

Factors affecting absorption

-***ascorbic acid is the most potent enhancer

-animal proteins (beef, pork, veal, lamb, liver, fish, chicken) enhance

-but, proteins from cow’s milk, cheese, eggs, don’t

-gastric acidity enhances absorption (antacids interfere)

-pregnancy, increased growth, Fe defic all increase deficiency

-phytate and tannins decrease abs

-Fatty acids

-increased intestinal motility decreases

absorption because it decreases

contact time for absorption

Storage

-stored as ferritin and hemosiderin

-long term high Fe ingestion or frequent blood transfusions can lead to accumulation of Fe in the liver

-***hemosiderosis develops in individuals who consume a lot of Fe or have a genetic defect resulting in increased Fe absorption

-in associated with tissue damage, it is called hemochromatosis

Excretion

-lost thru bleeding, feces, sweat,

exfoliation of hair and skin

-none in urine

Sources and Intakes

-best source is liver

-oysters, shellfish, kidney, lean meat, poultry, fish

-dried beans, veggies, dark molasses

-egg yolks, dried fruit, enriched breads,

-requirements are highest in infancy and adolescence

-females stay high because of menstruation

-decrease with menopause and increased with pregnancy

RDA

Man and post.mp-10-30 mg/day

PMp-20-40

Children 15-50 mg

Preg &lactation-18-36

Deficiency

-most common deficiency

-most at risk: <2 yrs old, teens, pregnancy, elderly

-***anemia (hypochromic, microcytic)

-tx: diets high in absorbable Fe and/or Fe supplements (ferrous sulfate, ferrous gluconate)

-can be caused by injury, hemorrhage, illness, poor diet

COPPER

Total body Cu is 100 mg

Sources

Liver,fish,meat ,nuts but milk is a poor

source

RDA

2-3 mg/day

Functions of Cu

Mobilization of iron ie fe2+ to Fe 3+

Formation of enzymes like Dopamine

oxidase,MAO,Serum Ferroxidase,

Cytochrome Oxidase,etc

Hb,Elastin(Elastin is a protein in connective tissue that is

elastic and allows many tissues in the body to resume their

shape after stretching or

contracting),Melanin,Catacholamine etc

Deficiency

Microcytic anaemia(types of anemia

characterized by small red blood cells

(called microcytes)

Over consumption can leads to V/D

Clinical significance

Wisons disease or hepato lenticular

degeneartion

Excess deposition of Cu in liver, brain

leads to kayserFleisure ring

Menkes Disease

Its due to defect in absorption of copper

Symptoms:

Copper in urine and Plasma, anaemia

and depigmentation of skin and hair

Zinc

-involved in synthesis or degradation of CHO, proteins, lipids, nucleic acids

-stabilizes RNA and DNA

involved in transcription and replication

-needed for bone enzymes and osteoblastic activity

absorption

Impaired absorption in Crohn’s or

pancreatic insufficiency

-plasma zinc levels act as acute phase

reactants and fall by 50% with injury

(like platelets)

Inhibiting Factors

-fiber, phytate

-high doses of copper

-Fe competes with zinc for absorption

Enhancing Factors

-glucose, lactose, and soy protein

-red wine

-human milk

Excretion

-feces—almost entirely

-***in urine with starvation, nephrosis,

DM, alcoholism, hepatic cirrhosis (zinc

supplementation in encephalopathy),

porphyria

Sources and Intakes

-meat, fish, poultry, milk

-oysters, shellfish, meat, liver, cheese,

whole grains, dry beans, nuts

Deficiency

-short stature, hypogonadism, anemia

-with diets high in unrefined cereal and

unleavened bread

-delayed wound healing, alopecia

***-acrodermatitis enteropathica=AR dz with

zinc malabsorption

-eczematoid skin lesions, alopecia, diarrhea,

bacterial and yeast infections, death

-immunologic deficits—lymphopenia,

thymic atrophy

***Causes of

deficiency Anorexia Nervosa

TPN without zinc (diarrhea, small bowel fistulas)

High intake of phytate, tannins, binding drugs (EDTA), oxalate

High iron intake

Malabsorption syndromes

Acrodermatitis enteropathica

Diarrhea

Pancreatico-cutaneous fistula

Proximal entero-cutaneous fistulas

Hemolytic anemias (sickle cell anemia)

Renal failure patients on dialysis

***Zinc Deficiency

42 yo female with chronic uremia on dialysis. Recently started

on iron supplement for anemia. Presents with rash,

hypogeusia, hyposmia and poor dark adaptation.

Acrodermatitis

Enteropathica

Autosomal recessive disease

associated with a defect causing a

reduction in zinc absorption

Can be treated by pharmacologic

doses of oral zinc

Acrodermatitis

Enteropathica

Toxicity

->100-300 mg/d

-rare

-interferes with copper absorption

-decrease in HDL

-GI irritation, vomiting

Fluoride

-tooth enamel

-resistance to dental caries

-fluoridation of h20 has decreased

caries by half

-found in drinking h20, teflon pots and

pans (cooked in these)

-toxicity at doses >0.1 mg/kg/d

Intervention studies have demonstrated water supplementation reduces prevalence of caries

***Incidence of dental fluorosis (mottled

teeth) occurs with increased intake

above 1-2 ppm.

Functions

-Prevention of Dental caries /tooth

decay(fluoride helps to form fluroapatite of enamel and

dentine this is more resistant against acids ,plaques etc)

-Bone development

Mottled teeth in fluorosis

Deficiency

If the consumtipn less than 0.5 ppm can

leads to dental caries and also

osteoporosis

Note:- topical application of fluoride will

result in the formation of fluroapatite

layer on the enamel which prevent

decay of tooth.

excess

If Excess amount can leads to Flurosis

Dental flurosis and Skeletal flurosis

Dental flurosis- If intake is above 2ppm

Discoloration of teeth, teeth become

rough and yellow patches on surface

Skeletal flurosis:-If intake is above 20

ppm will leads to Hyper calcification,

increase density of bones of limb, pelvis

and spine.

Dental F Skeletal F

Maganese

-found in many enzymes

-connective and bony tissue formation

-growth and reproduction

-CHO and lipid metabolism

Absorption and Excretion

-after absorption, it appears rapidly in

the bile and is excreted in the feces

-concentrated in liver and increases with

liver disease

Sources and Intakes

-whole grains, legumes, nuts, teas, fruit,

veggies, instant coffee, and tea

RDA- 5-6mg/day

functions

Manganese is an integral part of glycosyl

transferase responsible for synthesis of

glyco proteins and chondrotin sulphate

Mn has a role in cholestrol synthesis

Mn needed for RNA polymerase(RNA

polymerase (RNAP or RNApol) is an

enzyme that produces RNA) activity

Mn is required for formation of Bones,

Skeletal development, Proper

reproduction, blood clotting and noramal

nervous functioning

Mn required for Hb synthesis

Deficiency

-wt loss, ataxia, dermatitis, N/V,

decreased hair growth, impaired

reproductive activity, decreased

pancreatic function and CHO

metabolism

Toxicity

-accumulates in liver and CNS—

parkinsonian sx