Ca, P, Mg, F

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emmayarewhy
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Ca, P, Mg, F
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2014-05-16 05:28:46
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  1. 1. How many minerals are essential for life? How many exist?

    2. What are macroelements? Name all 7

    3. What are microelements? (requirement)

    4. Define trace and name (5)

    5. Define ultratrace and name (6)
    1. 22, 90

    2. Macroelements (>100 mg/day) - calcium, phosphorus, magnesium, sodium, potassium, chloride, sulfur

    3. Microelements (<100 mg/day)

    4. Trace (1-100 mg/day) - Fe, Zn, Mn, Cu, F

    5. Ultratrace (<1 mg/day) - selenium, molybdenum, iodine, chromium, boron, cobalt
  2. 1. What are the main forms of phosphorus? (2)

    2. What is the breakdown of where its found in tissues? (3)

    3. What is the normal phosphate level in serum?

    4. Dietary sources? 

    5. RDA?

    6. UL? for pregnant women?
    1. Organic/inorganic phosphates

    2. Bone (85% with calcium as hydroxyapatite), 15% in extraskeletal tissues - phospholipids, phosphoproteins, nucleic acids), 0.1% in EC fluid 

    3. 2.5-4.5 mg/dL

    4. Protein rich food (Phosphorus= Protein)

    5. 700 mg/day

    6. 4g/day, 3.5 g/day for pregnant women
  3. 1. How is phosphate absorbed? Mech 

    2. How does vitamin D play into this?

    3. How does Pi travel in blood? What minerals can PI bind to? What are percentage breakdowns? What is the most common?
    • 1. (1) Organically bound phosphate is hydrolyzed into Pi via hydrolyzing enzymes (phospholipase, alkaline phosphatase)
    • (2) Inorganic phosphate enters cell via paracellular diffusion and active 2Na+ cotransporter - NPT2B (3) Pi leaves cell no transporter (4) Pi travels in blood

    2. Vitamin D activates transcription of NPT2b, increasing intestinal absorption of phosphorus

    3. (1) Pi complexes with other minerals (Ca, Na, Mg) - 5% (2) Pi complexes as organic phosphate (70%) (3) Free phosphate and HPO42- <--> H2PO4-) (25%)
  4. 1. What does phosphate do overall? (7)

    2. Where is major reservoir for calcium and phosphorus? what percentages are stored there?

    3. What % of bone is mineral? organic in the form of?
    1. Hydroxyapatite, DNA/RNA synthesis, phospholipid, ATP/creatine phosphate, traps cells, reverse covalent modification via kinases/phosphatases, acid-base balance regulation

    2/ Skeleton - 99% of calcium and 80-90% of phosphorus. 

    3. 60%, 40% (collagen)
  5. Draw how PTH, calcitonin, and vitamin D act in thyroid, kidney, bone, and intestine
    Look at real sheet of paper
  6. 1. Is phosphate deficiency rare?

    2. Who is at risk? (4) 

    3. For question above, what are the 2 types of genetic causes of phosphate deficiency?

    4. Symptoms of phosphate deficiency? (7)

    5. What body organs are affected by phosphate def? (8)
    1. yes

    2. Antacids (Mg2+, Al3+), premature infants, patients fed enterally/parentally w/o add'l phosphate --> refeeding syndrome, genetic causes

    3. X-linked hypophosphatemia and hypophosphatemic rickets (Dent's syndrome) and defects in P resorption in kidneys

    4. Anorexia, decrease in cardiac output, decreased contractility of diaphragm, myopathy/weakness, neurological problems, death

    5. Neurologic, endocrine, skeletal, cardiac, renal, muscular, respiratory, hematologic
  7. 1. What is the difference between hypophosphatemia and phosphate deficiency?

    2. What are the cutoffs for mild,moderate, and severe hypophosphatemia?

    3. What causes hypophosphatemia (4)
    1. Hypophosphatemia =  low levels of serum phosphate while phosphate deficiency = decrease in total body 

    2. mild = 2-2.5 mg/dL, 1-2 mg/dL, <1 mg/dL

    3. (1) IC shifting - infusion of glucose solutions (phosphate follows glucose), hyperalimentation, treatment of hyperkalemia with insulin/dextrose

    • (2) increased renal excretion
    • (3) Decreased phosphate intake
    • (4) decreased vitamin D production/intake
  8. 1. Why does Mg2+ have an essential role in physiology? 2

    2. What is the most abundant mineral IC? 2nd most?

    3. How does Mg2+ compare to Ca2+? (2)

    4. What does it bind poorly to? What does it mainly bind to?

    5. Dietary sources of Mg2+ (5)

    6. RDA?
    1. (1) abiilty to chelate anionic ligands (ATP) and (2) ability to compete with Ca2+ for binding sites

    2. K+, then Mg2+

    3. Less flexible, more hydrated

    4. To proteins, mainly binds to phosphorus-containing molecules

    5. Legumes, vegetables, nuts, chocolate, fish, cereals

    6. ~300-400 mg/day
  9. Mg2+

    1. Is it toxic?

    2. What is UL from non-food sources?

    3. What happens if you take excessive Mg2+ salts? Excessive IV admin? (2 each)

    4. Signs of toxicity? (4)
    1. No

    2. 350 mg/day from non-food sources

    3. Diarrhea/dehydration; cardiac/respiratory failure

    4. Nausea, flushing, double vision, muscle weakness.
  10. 1. Describe how Mg2+ is absorbed into enterocyte (2)

    2. What is the transporter?

    3. What influences paracellular diffusion? 2
     
    4. What pumps Mg2+ out of enterocyte cell? 

    5. How is blood transported and % 3
    • 1. (1) Free Mg2+ can be actively transported via TRPM6 or passively via paracellular diffusion
    • (2) Mg2+ is pumped out of cell across the BL membrane by a Na+dep ATPase 

    2. TRPM6

    3. Electrochemical gradient and solvent drag

    4. Na+-dep ATPase

    5. (1) Bound to proteins - albumin, globulins (35%), (2) Free Mg2+ (50-55%), (3) Non-protein complexed Mg-citrate, phosphate, sulfate (15%)
  11. 1. What is central organ in Mg2+ homeostasis?

    2. How much of Mg2+ is resorbed? How much can urinary excretion of Mg2+ be reduced to?

    3. What increases excretion? (4) 

    4. How does protein intake affect absorption of Mg2+? Excretion?

    5. What is bioavailability of Mg2+? What reduces bioavailability? (3)
    6. What does Mg2+ inhibit absorption of?
    1. Kidney

    2. 95%, 1%

    3. Alcohol, diuretics, caffeine, high protein intake

    4. Low protein (<30 g/day) inhibits absorption of Mg2+. High protein increases excretion

    5. 30-50% in normal dietary conditions. Fibers, phytates, fatty acids

    6. Phosphorus
  12. 1. Where in kidney is Mg2+ resorbed? What forms of transport? (2)

    2. What are the 2 main types of Mg2+ transporters? 

    3. Where are these transporters expressed?

    4. What does 6 transport? (6) What is it suppressed by? (2)

    5. Do PTH/vit D affect 6?

    6. What happens when there's a mutation of 6? Effective treatment?

    7. Which transporter plays essential role in cellular Mg2+ homeostasis?

    8. Which transporter is insensitive to fluctuations in Mg2+?

    9. Which has a mutant in Parkinson's
    1. Thick ascending loop (passive resorption via voltage gradient) and distal convoluted tubule (active resorption)

    2. TPRM6 and 7

    3. TRPM6 is found in epithelial intestine and kidney cells. TRPM7 is found in nearly all cells

    4. 6 transports divalent cations: Ca, Mg, Zn, Mn, Co, Ni

    5. No

    6. Hypomagnesia with secondary hypercalemia. Oral high Mg2+ supplements

    7. TRPM7

    8. TRPM7

    9. . TRPM7
  13. 1. How much Mg2+ does normal adult ahve? 

    2. What tissues is it found? (3) main one?

    3. Where is Mg2+ found in cells? (3)
    1. 25 g (1000 mmol)

    2. Bone (50-60%), 1% in EC fluids, rest in soft tissues

    3. Mitochondria, sarcoplasmic/endoplasmic reticulum, nucleus
  14. What are functions of magnesium? (4 main ones)

    1-2 (2 examples), 2-3, 3-2, 4-2

    How does magnesium functionally block calcium? (3)
    1. Cellular energy metabolism - macronutrient metabolism requires Mg2+ in form of (1)ATP/ (2) stabilization of enzymes - (ex. enolase and pyruvate kinase)

    2. DNA, RNA, Protein Synthesis - DNA/RNA pol, formation of aminoacyl tRNA

    3. Secondary messenger pathways (ATP/GTP utilizing pathways, phosphatidylinositol cycle - phospholipidS)

    4. Regulation of ion channels: (1) Mg2+ regulates Na+-K+-ATPase pump and (2) functional blocker of calcium


    ---

    • 1. mimics/displaces Ca2+ from its binding sites
    • 2. inhibits release of Ca2+ from organelles
    • 3. activates ca2+ ATPase pump, which decreases IC Ca2+ concentration
  15. 1. How is Mg status assessed? (3)

    2. What is Mg deficiency caused by? 7

    3. What are symptoms of Mg depletion?
    1. Plasma levels - low sensitivity/specificity; RBC levels - better for long-term; URinary excretion - ~80% of Mg2+ load is normally excreted. Low excretion could indicate low status

    2. (1) secondary to another disease therapeutic/agent (2) GI disorders - diarrhea, malabsorption syndromes, bowel resection, pancreatitis) (3) Renal loss - hypercalcemia, osmotic diuresis, chronic parental fluid therapy (4) Drugs - diuretics/immunosuppressors (5) Alcohol (6) Metabolic acidosis (7) Endocrine disorder - hyperthyroidism, hyperaldosteronism

    3. Biochemical (hypokalemia - excess renal excretion and decreased IC K+ and hypocalcemia - reduced PTH secretion, increased resistance to PTH and vit D), Neuromuscular - spasms, seizures, muscular weakness. Cardiovascular - tachycardia, fibrillations
  16. 1. What does fluoride have high affinity for? 

    2. What metals is it often found in combo with? (3)

    3. Where is majority of fluoride found/stored? How much

    4. Is it essential?

    5. What are sources of F?

    6. RDA?
    1. Divalent and trivalent cations

    2. Ca2+, Mg2+, Al3+

    3. Skeleton/teeth - 99%

    4. No, but its beneficial

    5. F-water, dental products, seafood, tea, legumes/grains/cereals, root vegetables, fruits

    6. ~3-4 mg/day
  17. 1. How much of F is bioavailable? %

    2. How much is bioavailable in presence of high Ca2+?

    3. What % is absorbed from stomach? From upper intestine?

    4. Half-time absorption of F?

    5. How much of F goes to calcified tissue? Where does rest go? How is it excreted? (2)
  18. 1. How does pH affect F resoption? 

    2. What conditions affect F resorption? (4)

    3. What is it called when OH is replaced by F in hydroxyapatite? What does it do (2)

    4. Where is rapidlye xchangeable F pool located?

    5. What are main minerals in tooth enamel and dentin? (2)
  19. 1. How are dental caries produced? 

    2. HOw does F- prevent dental caries? 3 By how much?
    1/. By acid degradation of calcium salts 

    • 2. (1) Increasing resistance of enamel to acid degrdation (2) promoting remineralization of lesions (3) inhibition of acid production by bacteria
    • %
    • by 40-60%

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