minerals1 add
TRANSCRIPT
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Minerals
Shajan xaviour
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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
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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.
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calcium
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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
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Skeletal Calcium
-if there is no reserve, calcium is drawn from bone—leading to deficiency
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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
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-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
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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
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-required for muscle contraction
Regulate permeability of capillary walls
Regulate citric acid cycle
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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
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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
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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
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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
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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
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Causes of hypocalcemia
-***malabsorption
-small bowel bypass, short bowel
-vit D deficiency
-alcoholism
-***chronic renal insufficiency
-***diuretic therapy
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Causes of hypocalcemia
cont’d
-hypoparathyroidism
-***hypomagnesemia
-sepsis
-pseudohypoparathyroidism
-calcitonin secretion with medullary
carcinoma of the thyroid
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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
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Causes of hypercalcemia
-milk-alkali syndrome
-vit D or vit A excess
-primary hyperparathyroidism
-secondary hyperparathyroidism (renal insuff, malabsorption)
-acromegaly
-adrenal insufficiency
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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
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Causes of hypercalcemia
cont’d
-***thiazide diuretic
-sarcoidosis
-paget’s disease of bone
-***immobilization
-familial hypocalciuric hypercalcemia
-complications of renal transplant
-iatrogenic
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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
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RDA
-see handout
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sources
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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
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Toxicity
-***polyuria, constipation, bone pain,
azotemia, coma
-”stones, bones(bone pain), groans,
psychiatric overtones”
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Phosphorus
Levels maintained by parathyroid gland
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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
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absorption
-best occurs when calcium and phos are
ingested in equal amts (milk)
-vit D also increases absorption
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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
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RDA
1-1.5 Mg/day
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Causes of hypophosphatemia
-starvation
-TPN with inadequate phos content
-malabsorption, small bowel bypass
-vit D deficient and vit D resistant
osteomalacia
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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
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Causes of hyperphosphatemia
-excessive growth hormone
(acromegaly)
-hypoparathyroidism assoc with low Ca
-pseudohypoparathyroidism assoc with
low Ca
-***chronic renal insufficiency
-acute renal failure
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Deficiency
-fatal
-usually rare with food intake
-***respiratory muscle collapse
-heart failure
-muscle aches, bone pain, and fracture
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Magnesium
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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
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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
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sources
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Sources
-seeds, nuts, legumes, unmilled cereal
grains, dark greens
-fish, meat, milk, fruits
-lost during refining of flour, rice, vinegar
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Causes of hypomagnesemia
-malabsorption, chronic diarrhea, laxative abuse
-prolonged GI suction
-small bowel bypass
-malnutrition
-***alcoholism
-refeeding
-TPN with inadequate Mg
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Causes of hypomagnesemia
cont’d-DKA
-diuretics
-hyperaldosteronism, Barrter’s syndrome
-hypercalcuria
-renal Mg wasting
-hyperparathyroidism
-postparathyroidectomy
-vit D therapy
-aminoglycosides, ***cisplatin, ampho B
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Causes of hypermagnesemia
Decreased renal fxn
***Increased intake—abuse of Mg
containing antacids (MOM) and
laxatives in renal insufficiency
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Deficiency
-anorexia, growth failure, cardiac and
neuromuscular changes—weakness,
irritability, mental derangement
-tetany, muscle cramps
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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
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Iron
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Function
-respiratory transport of O2 and CO2
-immune system
-cognitive performance
-found in Hgb (in RBC’s) and myoglobin
(in muscles)
-cytochrome p450 system
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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
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2 types
Heme proteins-
Hgb,Mb,Cytochromes,Catalases,Perioxi
dase
Non Heme Proteins
Ferritin,Hemosiderin,Transferrin,Iron
sulphur proteins,Aconitase
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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
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-phytate and tannins decrease abs
-Fatty acids
-increased intestinal motility decreases
absorption because it decreases
contact time for absorption
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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
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Excretion
-lost thru bleeding, feces, sweat,
exfoliation of hair and skin
-none in urine
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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
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RDA
Man and post.mp-10-30 mg/day
PMp-20-40
Children 15-50 mg
Preg &lactation-18-36
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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
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COPPER
Total body Cu is 100 mg
Sources
Liver,fish,meat ,nuts but milk is a poor
source
RDA
2-3 mg/day
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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
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Deficiency
Microcytic anaemia(types of anemia
characterized by small red blood cells
(called microcytes)
Over consumption can leads to V/D
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Clinical significance
Wisons disease or hepato lenticular
degeneartion
Excess deposition of Cu in liver, brain
leads to kayserFleisure ring
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Menkes Disease
Its due to defect in absorption of copper
Symptoms:
Copper in urine and Plasma, anaemia
and depigmentation of skin and hair
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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
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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)
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Inhibiting Factors
-fiber, phytate
-high doses of copper
-Fe competes with zinc for absorption
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Enhancing Factors
-glucose, lactose, and soy protein
-red wine
-human milk
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Excretion
-feces—almost entirely
-***in urine with starvation, nephrosis,
DM, alcoholism, hepatic cirrhosis (zinc
supplementation in encephalopathy),
porphyria
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Sources and Intakes
-meat, fish, poultry, milk
-oysters, shellfish, meat, liver, cheese,
whole grains, dry beans, nuts
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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
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-immunologic deficits—lymphopenia,
thymic atrophy
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***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
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***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.
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Acrodermatitis
Enteropathica
Autosomal recessive disease
associated with a defect causing a
reduction in zinc absorption
Can be treated by pharmacologic
doses of oral zinc
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Acrodermatitis
Enteropathica
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Toxicity
->100-300 mg/d
-rare
-interferes with copper absorption
-decrease in HDL
-GI irritation, vomiting
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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
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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
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Mottled teeth in fluorosis
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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.
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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.
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Dental F Skeletal F
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Maganese
-found in many enzymes
-connective and bony tissue formation
-growth and reproduction
-CHO and lipid metabolism
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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
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Sources and Intakes
-whole grains, legumes, nuts, teas, fruit,
veggies, instant coffee, and tea
RDA- 5-6mg/day
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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
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Mn is required for formation of Bones,
Skeletal development, Proper
reproduction, blood clotting and noramal
nervous functioning
Mn required for Hb synthesis
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Deficiency
-wt loss, ataxia, dermatitis, N/V,
decreased hair growth, impaired
reproductive activity, decreased
pancreatic function and CHO
metabolism
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Toxicity
-accumulates in liver and CNS—
parkinsonian sx