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Minerals Powered By Docstoc

   Dr Reed Berger
   Nutrition Course Director
   Visiting Clinical Professor
General Lecture Format
 -test questions will come from clinical
  correlations--these will be relevant in clinical
  training and practice
 -RDA’s and food sources—see Institute of
  Medicine website (food and nutrition, DRI—
  elements)—also on nutrition website
 -will not be tested on this! Contact me if you
  have problems with the website
 -items with *** and those with photos are
   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
 -most abundant mineral in the body
 -1.5 to 2% of body wt
 -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
 -available in non-exchangeable and
  exchangeable pools
 -non-exchangeable is for short term
 -exchangeable is used for increased needs
  (growth, pregnancy, lactation) and is
  accumulated when diet has adequate calcium
 -if there is no reserve, calcium is drawn from
  bone—leading to deficiency
Serum Calcium
 -levels: 8.8 to 10.8 mg/dl
 3 fractions
      1) free/ionized—50%
     2) complexed with phos, bicarb, citrate—5%

     3) protein bound with albumin or globulin—45%

    -***when albumin is low (malnutrition, liver dz),
       calcium is decreased in ratio of 0.8 mg of calcium
       to every 1 g of albumin (for each gram of albumin
       below 4, add 0.8 to calcium level)
 -factors such as pH and changes in plasma
  protein affect distribution
 -ionized calcium is increased in acidosis and
  decreased in alkalosis
 -total calcium changes with plasma protein
  but ionized remains the same
       ***-example: in resp alkalosis, total serum calcium
        is normal, but ionized is low—always check
        ionized level with acid/base disorders
 -building and maintaining bones and teeth
 -transport fxn 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
 -cofactor in conversion of prothrombin to
 -***absorbed mainly in the acidic part of the
 -absorption is decreased in the lower GI tract
  which is more alkaline
 20-30% of digested calcium is absorbed
 Absorption is thru 1,25 (OH)2D3 (vit D
  derivative)--stimulates production of calcium
  binding protein and alk phos
 -unabsorbed form is excreted in feces
Factors that increase calcium
 -***more efficiently absorbed when the body
  is deficient
 -best absorbed in acidic environment (upper
 -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
 -***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
 -physical/mental stress increases absorption
 -aging decreases absorption efficiency (to be
  discussed with vit D)
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
Maintenance of serum level
 ***-always need to correct low Mg level
  before treating a low calcium level
 -calcium may correct by itself
 -hypomagnesemia decreases tissue
  responsiveness to PTH
Causes of hypocalcemia
Decreased Intake or absorption
  -small bowel bypass, short bowel
  -vit D deficiency
Increased Loss
  -***chronic renal insufficiency
  -***diuretic therapy
Causes of hypocalcemia
Endocrine Disease
 -calcitonin secretion with medullary
 carcinoma of the thyroid
Causes of hypocalcemia
Physiologic Causes
 -***associated with low serum albumin
 (ionized calcium will be wnl)
 -decreased end organ response to vit D
 -***aminoglycosides, plicamycin, loop
 diuretics, foscarnet
Causes of hypercalcemia
Increased intake or absorption
  -milk-alkali syndrome
  -vit D or vit A excess
Endocrine Disorders
  -primary hyperparathyroidism
  -secondary hyperparathyroidism (renal insuff,
  -adrenal insufficiency
Causes of hypercalcemia
***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
Miscellaneous causes
  -***thiazide diuretic
  -paget’s disease of bone
  -familial hypocalciuric hypercalcemia
  -complications of renal transplant
 -normal  is 65-70% of ingested calcium
  to be excreted in the feces and urine
 -strenuous exercise increases loss (in
 -***immobility with bed rest and space
  travel increase calcium loss because of
  lack of bone tension
 -see   handout
 1)***bone—to be discussed in osteoporosis
 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
 -***polyuria,constipation, bone pain,
  azotemia, coma
 -”stones, bones(bone pain), groans,
  psychiatric overtones”
Vitamin D
 -to be discussed in the fat-soluble
  vitamin lectures in more detail
 -but, some key points that may be
  clinically relevant…..
 -the two main sources of Vit D production are
  the vit D made in our skin from UV light and
  that taken up in the diet
 -as little as 20 minutes of UV exposure 3x/wk
  is good even without dietary intake
 -liver and the kidney are both needed for
  synthesis of the active form
 -***disease of either organ can lead to low Vit
  D levels and problems with calcium regulation
 -***elderly are especially at risk because of
  lack of sunlight and renal insufficiency with
 -northern climates that have less sun
  exposure, get the vitamin from diet (fatty fish
  such as salmon)
 -osteoporosis and osteomalacia
 -***think of Vit D deficiency in pts with
  abnormal calcium levels, osteopenia or
  osteoporosis, malabsorption, and/or
  kidney/liver disease
 -2nd to calcium in abundance
 -80% is calcium phos crystals in bones
  and teeth
 -remainder is in every cell and ECF
 -levels maintained by the parathyroid
 -structure of teeth and bones
 -essential component in cell
  membranes, nucleic acids,
 -phosphorylation of glucose
 -buffer system in ICF and kidney
-best occurs when calcium and phos are
  ingested in equal amts (milk)
-vit D also increases absorption
 -see   table (and for all RDA’s)
 **see  handout for sources and RDA
 ***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
Renal Disease
 -need to monitor phos levels to prevent renal
  osteodystrophy (osteitis fibrosa and
  osteomalacia seen in renal dz)
 -***used to use phos binders in renal dz, but
  caused aluminum toxicity—irreversible CNS
  and bone dz
 -***now use Ca Carbonate supplements tid
  as phos binders
 -don’t supplement vit D until phos is
  controlled because vit D increased calcium
  and phos absorption
Causes of hypophosphatemia
Diminished supply or absorption
  -TPN with inadequate phos content
  -malabsorption, small bowel bypass
  -absorption blocked by oral aluminum
  hydroxide or bicarb (to be discussed)
  -vit D deficient and vit D resistant
Causes of hypophosphatemia
Increased loss
  -phosphaturic drugs: theophylline, diuretics,
  bronchodilators, corticosteroids
  -hyperparathyoidism (primary or secondary)
  -renal tubular defects
  -hypokalemic nephropathy
  -inadequately controlled DM
Causes of hypophosphatemia
Intracellular shift of phosphorus
  -administration of glucose
  -anabolic steroids, estrogen, OCP
  -respiratory alkalosis
  -salicylate poisoning
Electrolyte abnormalities
  -metabolic alkalosis
Causes of hypophosphatemia
Abnormal losses followed by inadequate
  -***DM with acidosis—with aggressive therapy
  -***recovery from starvation or prolonged catabolic
     state—refeeding syndrome
  -***chronic alcoholism, especially with nutritional
     repletion, assoc with hypomagnesemia—”
  -recovery from severe burns
Causes of hyperphosphatemia
Endocrine disease
  -excessive growth hormone (acromegaly)
  -hypoparathyroidism assoc with low Ca
  -pseudohypoparathyroidism assoc with low
Decreased excretion
  -***chronic renal insufficiency
  -acute renal failure
Causes of hyperphosphatemia
Catabolic states, tissue destruction
  -stress or injury, rhabdomyolysis (esp with
  renal insufficiency)
  -chemotherapy of malignant disease,
  particularly lymphoproliferative disease
Excessive intake or absorption
  -laxatives or enemas containing phosphate
  -hypervitaminosis D
 -fatal
 -usually rare with food intake
 -***respiratory muscle collapse
 -hemolytic anemia
 -increased infection
 -platelet dysfxn w/ petechiae
 -encephalopathy
 -heart failure
 -muscle aches, bone pain, and fracture
 -symptoms   of the primary disorder
 -ranks   second to calcium as intracellular
 -60% in bone, 26% in muscle,
  remainder in soft tissues, body fluids
 -1/2 is free, 1/3 is bound to albumin,
  remainer is in bone and not
-bone, muscle contractility, nerve excitability
-antagonistic to calcium
-excess Mg inhibits bone calcification
-in a muscle contraction, Mg relaxes, and
   calcium contracts
-excessive calcium induces signs of typical Mg
-low Mg can cause pregnancy induced HTN
Absorption / Excretion
 -absorption varies
 -similar to calcium (low pH, upper GI),
  however, no Vit D required
 -as dietary calcium decreases, Mg absorption
  is increased
  -kidney conserves Mg when intake of Mg is
 -large losses with vomiting because of high
  levels of gastic juice
 -seeds,  nuts, legumes, unmilled cereal
  grains, dark greens
 -fish, meat, milk, fruits
 -lost during refining of flour, rice, vinegar
Causes of hypomagnesemia
Diminished absorption or intake
  -malabsorption, chronic diarrhea, laxative
  -prolonged GI suction
  -small bowel bypass
  -TPN with inadequate Mg
 Causes of hypomagnesemia
Increased loss
  -hyperaldosteronism, Barrter’s syndrome
  renal Mg wasting
  -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
 -anorexia,    growth failure, cardiac and
  neuromuscular changes—weakness,
  irritability, mental derangement
 -tetany, muscle cramps
 -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
 -30-40%  is in the storage form
 -90% is reused by the body
 -respiratory transport of O2 and CO2
 -immune system
 -cognitive performance
 -found in Hgb (in RBC’s) and myoglobin (in
 -ATP production in mitochondria involves
  both heme and non-heme enzymes
 -cytochrome p450 system
  -***plays a role in immunity because
  neutrophils work better when not iron
Absorption and Transport
 -transferrin—transports  Fe in blood to
  erythroblasts for use in heme synthesis
 -dietary Fe deficiency is reflected first by
  decreased Tf levels
 -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
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,
 -gastric acidity enhances absorption (antacids
 -pregnancy, increased growth, Fe defic all
  increase deficiency
 -phytate and tannins decrease abs
 -Fe used for enrichment are less
  absorbed than elemental Fe
 -increased intestinal motility decreases
  absorption because it decreases
  contact time for absorption
 -stored as ferritin and hemosiderin
 -30% is in the liver, 30% in the bone marrow,
  rest in spleen and muscles
 -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
 -lostthru bleeding, feces, sweat,
  exfoliation of hair and skin
 -none in urine
 -amts to about 1mg in the adult male
  and less in nonmenstruating females
 -loss of Fe with menstruation is
Sources and Intakes
 -best source is liver
 -oysters, shellfish, kidney, lean meat, poultry,
 -dried beans, veggies, dark molasses
 -egg yolks, dried fruit, enriched breads,
 -requirements are highest in infancy and
 -females stay high because of menstruation
 -decrease with menopause and increased
  with pregnancy
 -most common deficiency
 -most at risk: <2 yrs old, teens, pregnancy,
 -***anemia (hypochromic, microcytic)
 -tx: diets high in absorbable Fe and/or Fe
  supplements (ferrous sulfate, ferrous
 -can be caused by injury, hemorrhage,
  illness, poor diet
 -involved in synthesis or degradation of CHO,
  proteins, lipids, nucleic acids
 -metallothionein is the most abundant zinc
  containing protein
 -abundant in the nucleus where it stabilizes
  RNA and DNA and in chromatin proteins
  involved in transcription and replication
 -present in bone and is needed for bone
  enzymes and osteoblastic activity
 -balance  maintained by absorption and
  excretion from intestine
 -zinc levels are dose-responsive post-
 -protein-rich meal promotes zinc
  absorption by forming more absorbable
  zinc—AA complexes
 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
 -redwine
 -human milk
 -feces—almost    entirely
 -***in urine with starvation, nephrosis,
  DM, alcoholism, hepatic cirrhosis (zinc
  supplementation in encephalopathy),
Sources and Intakes
 -meat, fish, poultry, milk
 -oysters, shellfish, meat, liver, cheese,
  whole grains, dry beans, nuts
 -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
 -immunologicdeficits—lymphopenia,
 thymic atrophy
           ***Causes of
   Decreased intake
        Anorexia Nervosa
        TPN without zinc (diarrhea, small bowel fistulas)
   Decreased absorption
        High intake of phytate, tannins, binding drugs (EDTA), oxalate
        High iron intake
        Malabsorption syndromes
        Acrodermatitis enteropathica
   Increased loss
        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.
 Autosomal   recessive disease
  associated with a defect causing a
  reduction in zinc absorption
 Can be treated by pharmacologic
  doses of oral zinc
 ->100-300     mg/d
 -rare
 -interferes  with copper absorption
 -decrease in HDL
 -GI irritation, vomiting
 -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
  Abundant  in nature with varying
   amounts naturally found in water
  Epidemiologic studies have
   demonstrated inverse relationship
   between fluoride intake during tooth
   development and dental carries
Prevention of dental caries
 Numerous interventions have demonstrated
  that an intake of ~1.0 ppm of fluoride
  reduces dental caries by as much as 70%
 Possible beneficial effect on prevention of
 ***Incidence of dental fluorosis (mottled
  teeth) occurs with increased intake above 1-
  2 ppm.
Mottled teeth in fluorosis
 -10 to 20 mg in body
 -mainly in mitochondria
 -found in many enzymes
 -connective and bony tissue formation
 -growth and reproduction
 -CHO and lipid metabolism
Absorption and Excretion
 -carried by transmagnin
 -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
 -wholegrains, legumes, nuts, teas, fruit,
 veggies, instant coffee, and tea
    loss, ataxia, dermatitis, N/V,
 -wt
 decreased hair growth, impaired
 reproductive activity, decreased
 pancreatic function and CHO
 -accumulates in liver and CNS—
 parkinsonian sx

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