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GI Week 1 - WLB > Fat Soluble Vitamins, Minerals & Electrolytes - Skildum > Flashcards

Fat Soluble Vitamins, Minerals & Electrolytes - Skildum Flashcards

1
Q

What cofactors are required by the pyruvate dehydrogenase complex?

A
  • TPP (Thiamine)
  • NAD+
  • CoASH
  • Lipoate
  • FAD
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2
Q

What are the four fat soluble vitamins that we need to know?

A
  • Vitamin A
  • Vitamin D
  • Vitamin E
  • Vitamin K
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3
Q

What are all the activation transfer cofactors that we need to know?

A
  • Ascorbic acid (Vitamin C)
  • Thiamine
  • Pyridoxine
  • Biotin
  • Pantothenic acid
  • Lipoate
  • Cobalamin
  • Folate
  • Tetrahydrobiopterin (Ring hydroxylations; PKU)
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4
Q

What is the RDA?

A
  • Recommended Daily Allowance.
    • The average daily dietary nutrient intake level sufficient to meet the nutritional requirements of nearly all (97-98%) healthy persons in a particular life stage and gender group.
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5
Q

What is the EAR?

A
  • Estimated Average Requirement.
    • The average daily nutrient intake level estimated to meet the requirements of half of the healthy members of a particular life stage and gender group.
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6
Q

What is the UL?

A
  • Tolerable Upper Limit.
    • Risk of ‘overdose’ is ~0.1% (risk of adverse effects)
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7
Q

What are the structural elements of Vitamin A?

A
  • b-ionone ring
  • branched polyunsaturated acyl chain alcohol

The biologically active form of Vitamin A is all-trans-retinol.

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8
Q

In the body, the alcohol of trans-retinol (Vitamin A) can be converted to what?

A

aldehyde carboxylic acid ester with fatty acid (e.g. palmitate)

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9
Q

What are the main dietary forms of Vitamin A?

A
  • retinyl-acyl esters and carotenes
  • They all can be converted to all-trans-retinol.
  • Found in: Red, yellow, orange fruits and vegetables.
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10
Q

What nutrient digestion parallels the digestion of Vitamin A?

A
  • Fats/lipids
    • bile salts help package free carotenoids into micelles that can be transported into the intestinal cells
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11
Q

What form of digested Vitamin A is soluble enought to be transported in the blood by being associated with albumin?

A

Retinoic acid

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12
Q

What part of the liver serves as a reservoir for Vitamin A storage?

A

Stellate cells

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13
Q

What role do hepatocytes play in the digestion/absorption/storage of Vitamin A in the body?

A
  • Hepatocytes mediate retinol homeostasis in the body.
    • Retinyl esters go in…
      • Sources: Dietary → Chylomicrons
      • Stored: Stellate cells
    • Retinyl esters go out to. . .
      • Stellate cells (storage) VLDL (to tissues)
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14
Q

Why is Vitamin A important in the body?

A
  • Retinol is important for vision, and vitamin A deficiency can manifest as night blindness.
  • Vitamin A toxicity can result in blurred vision.
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15
Q

What specific role does Vitamin A/Retinol play in vision?

A
  • cis-retinal bound to the protein opsin = photoreceptor rhodopsin
    • Light causes conversion to trans-retinal.
    • Rhodopsin bound to trans-retinal activates a heterotrimeric G protein, closure of a Na+ channel, hyperpolarization of the rod cell => signaling to the neuron.
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16
Q

What specific role does Vitamin A/Retinol play in transcription factor activation?

A
  • Retinoic acid acts as a ligand for the retinoic acid receptors (RAR)
  • retinoic X receptors (RXR) and some peroxisome proliferator activated receptor (PPARb and PPARd).
  • RAR, RXR, and PPAR act as ligand activated transcription factors.
    • Differentiation of goblet cells.
    • Prevention of keratinization of goblet cells
    • Apoptosis of cancer cells.
    • Maturation of dendritic cells.
    • Recruitment of antibody secreting cells to small intestine.
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17
Q

How does Vitamin A help in immune system function in the GI System?

A

Dietary Vitamin A => stores of retinyl esters => Retinoic Acid => Maturation of dendritic cells => Recruitment of antibody secreting cells (ASC) to small intestine

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18
Q

What happens if the Carotene by-products of Vitamin A digestion are not cut by monooxygenases to form molecules of retinal?

A

Without being cut, carotenes act as antioxidants.

Their double bonds can neutralize singlet oxygen and free radicals.

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19
Q

What are the consequences of Vitamin A deficiency?

A
  • anorexia
  • retarded growth
  • increased susceptibility to infections
  • alopecia
  • keratinization of epithelial cells eyes:
    • night blindness
    • xeropthalmia (dry eye due to keratinization)
    • Bitot’s spots
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20
Q

How do you diagnose Vitamin A deficiency?

A
  • The Relative Dose Response (RDR) Measure plasma retinol concentration.
    • Give an oral bolus of retinyl-palmitate.
    • Measure plasma retinol concentration again after 5 hours.
    • The higher the RDR, the more the body is relying on short term dietary Vitamin A, rather than liver and adipose stores.
    • RDRs > 20% indicate the liver is not maintaining serum Vitamin A.
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21
Q

What happens in Hypervitaminosis A?

A
  • The tolerable upper limit (TUL) for Vitamin A is 3,000 mg RAE / day.
  • Doses in vast excess of this can cause:
    • nausea
    • vomiting
    • blurred vision
    • headache
    • desquamation of skin
    • alopecia
    • ataxia
    • liver damage (from excess stellate cell growth and proliferation)
    • conjunctivitis
    • eye pain
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22
Q

What are the structural elements of Vitamin E?

A
  • tocopherols
    • with saturated 16 carbon acyl chains
  • tocotrienols
    • with polyunsaturated 16 carbon acyl chains
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23
Q

What are the dietary sources of Vitamin E?

A
  • Abundant in plant oils
    • e.g. palm oil, sunflower oil, canola oil, wheat germ
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24
Q

Vitamin E digestion and absorption parallels digestion and absorption of what other nutrient?

A

Fat/lipids

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25
Q

What is the general outline of Vitamin E digestion?

A
  • tocopherols, tocotrienol-acyl esters + pancreatic lipase => tocopherols, tocotrienols
  • uptake by intestinal epithelial cell
  • tocopherols, tocotrienols => packaged into chylomicrons
  • chylomicrons distribute to tissues
  • chylomicron remnants return to liver => taken up by VLDL (only RRR stereoisomers of vitamin E)
  • VLDL distributes remnants to tissues
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26
Q

What are the main functions (4) of Vitamin E?

A
  • Vitamin E functions in lipid bilayers in intracellular and plasma membranes.
  • The phenolic hydroxyl can distribute and stabilize singlet oxygen and free radicals as part of cellular oxidative stress defense => ANTIOXIDANT
  • Regenerate Vitamin C:
    • Vitamin E, when oxidized, can be regenerated by ascorbate (vitamin C).
  • Vitamin E inhibits Vitamin K absorption and metabolism.
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27
Q

What are the consequences of Vitamin E deficiency?

A
  • Deficiency is rare except in people with absorption problems
    • e.g. premature infants, Crohns, short bowel syndrome.
    • Also can occur with inherited lipoprotein disorders.
  • Symptoms:
    • myopathy
    • hemolytic anemia
    • peripheral neuropathy
    • ataxia
    • loss of vibratory sense
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28
Q

Tell me about Vitamin E toxicity?

A
  • Not very toxic.
  • TUL is 1,000 mg per day (high)
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29
Q

What are the dietary sources of Vitamin K?

A
  • *Phylloquinone is the main form of Vitamin K in the diet.
    • It is abundant in leafy green vegetables.
  • *Menaquinones have variable numbers of isoprenoid subunits on the acyl chain.
    • They are produced by fermentation. (In gut, in cheese.)
  • (Menadione is a synthetic Vitamin K used in animal feed.)
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30
Q

What is the main function of Vitamin K?

A

Carboxylation + Coagulation

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31
Q

Vitamin K digestion and absorption parallels digestion and absorption of what nutrient?

A

Fat/lipids

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32
Q

Where is Vitamin K stored in the body?

A
  • Vitamin K is stored in cellular membranes
    • especially the lung, kidney, bone marrow, and adrenal glands.
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33
Q

What is the general outline of Vitamin K digestion?

A
  • phylloquinone, menaquinone => taken up by intestinal epithelial cells
  • packaged into chylomicrons => distributed to tissues
  • remnants go back to liver => packaged into VLDL
  • VLDL distributes remnants to tissues
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34
Q

How does Vitamin K act to promote coagulation?

A
  • In target cells, Vitamin K acts as a cofactor for g-glutamyl carboxylase.
    • This enzyme carboxylates glutamic acid side chains on blood clotting proteins.
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35
Q

What clotting factors are dependent on Vitamin K dependent carboxylation?

A
  • Factor IX (Christmas factor)
  • Factor VIIa
  • Factor X (Stuart factor)
  • Prothrombin
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36
Q

What are the consequences of Vitamin K deficiency?

A
  • Rare; most people get adequate Vitamin K.
  • Can occur in infants (milk is low in Vitamin K), people with absorption disorders.
  • Severe deficiency manifests as coagulation disorder:
    • increased prothrombin time
    • increased bleeding
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37
Q

Tell me about Vitamin K toxicity?

A
  • Not described
  • no TUL for Vitamin K
  • Menadione causes liver toxicity at high doses
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38
Q

What are the sources of Vitamin D?

A
  • Vitamin D is found primarily in food of animal origin such as:
    • liver, eggs, fatty fish.
    • It is also present in shitake mushrooms, and is fortified in many dairy products.
  • Vitamin D can be synthesized de novo from cholesterol.
  • To make the active Vitamin D3, metabolism of skin, liver, and kidney is required.
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39
Q

What is the most important function of Vitamin D?

A
  • Vitamin D’s most important function is to regulate calcium homeostasis, but it may play other beneficial roles.
    • cancer prevention
40
Q

How is dietary form of Vitamin D digested?

A
  • The dietary form of Vitamin D, cholecalciferol, is absorbed through passive diffusion with fat into intestinal epithelial cells.
  • It is transported to tissue in chylomicrons, and taken up by the liver in chylomicron remnants.
41
Q

What is the main form circulating in the blood and the form measured to assess Vitamin D status?

A

25-hydroxycholecalciferol (25-OH D3)

42
Q

What is the key enzyme regulating Vitamin D digestion?

A

1-alpha-hydroxylase

43
Q

What important hormone regulates 1-alpha-hydroxylase and the digestion of Vitamin D?

A
  • 1-alpha-hydroxylase expression is regulated by parathyroid hormone in the kidney
    • this helps maintain calcium homeostasis
    • The hydroxylation to make the biologically active 1,25-dihydrocholecalciferol (1,25-OH D3) occurs in the kidney in response to parathyroid hormone (PTH).
    • PTH is produced by the parathyroid in response to low calcium concentrations.
44
Q

What does the Vitamin D receptor in the gut act as?

A
  • The vitamin D receptor (VDR) acts as a ligand activated transcription factor.
    • regulates transcription of Calcium transport proteins: calbindin, TRPV6, PMCA1b
    • Activated VDR increases expression of:
      • the calcium channel TRPV6 at the brush border
      • calbindin in the cytoplasm
      • calcium ATPase pumps at the basolateral membrane
45
Q

What are the consequences of Vitamin D deficiency?

A
  • Rickets
    • characterized by seizures, growth retardation, failure of bone mineralization (osteomalacia).
  • Vitamin D deficiency can be dietary, genetic, or secondary to an absorption problem such as Crohns.
46
Q

What are the effects of Vitamin D toxicity?

A
  • Vitamin D is the most likely vitamin to have toxic effects.
  • The TUL is 4,000 IU for age 9+
  • Toxic effects begin when serum 25-OHD3 > 500 ng/mL
    • calcification of soft tissues (kidneys, heart, lungs, blood vessels)
    • hyperphosphatemia
    • hypertension
47
Q

What are the redox cofactors that are water soluble vitamins?

A
  • Niacin
  • Riboflavin
  • Ascorbic acid (Vitamin C)
48
Q

What are the water soluble vitmans that we need to know?

A
  • Redox cofactors:
    • Niacin
    • Riboflavin
    • Ascorbic acid (Vitamin C)
  • Activation transfer cofactors:
    • Ascorbic acid (Vitamin C)
    • Thiamine
    • Pyridoxine
    • Biotin
    • Pantothenic acid
    • Lipoate
    • Cobalamin
    • Folate
    • Tetrahydrobiopterin (Ring hydroxylations; PKU)
49
Q

What is the most toxic vitamin?

A

Vitamin D

50
Q

How does Vitamin D prevent colorectal cancer?

A
  • The Vitamin D receptor physically interacts with b-catenin
    • preventing its transactivation of genes that promote cellular proliferation.
51
Q

What are the 5 major minerals in order of abundance in the body?

A
  1. Calcium
  2. Phosphorous
  3. Potassium
  4. Sodium, Chloride
  5. Magnesium
52
Q

What are the four trace elements that the body requires < 100 mg/day?

A
  • Iron
  • Zinc
  • Copper
  • Manganese
53
Q

What are the functions of the minerals in the body?

A
  • Osmotic balance
  • Maintaining charge / concentration gradients across membranes
  • Enzyme cofactors
  • Structure
  • Taste
54
Q

What is the most abundant metal ion in the body?

A

CALCIUM

A 70 kg man has ~1.4 kg of calcium, mostly in bone.

55
Q

What are the dietary sources of Calcium?

A

Dairy, seafood, turnip, broccoli, kale, dietary supplements

56
Q

What are the major function of calcium?

A
  • Bone mineralization
  • Blood clotting
  • Muscle contraction
  • Metabolism regulator
57
Q

How does calcium absorption happen in the body?

A
  • Saturable carrier mediated transport: TRPV6 transports Ca2+ across the brush border membrane
  • Calbindin chaperones Ca2+ within the cell Ca2+ /ATPase transports Ca2+ across the basolateral membrane
  • Pericellular transport around tight junctions:
    • Claudin
58
Q

What increases calcium absorption?

A
  • Vitamin D sugars;
  • sugar
  • alcohols
  • protein
59
Q

What decreases calcium absorption?

A
  • Fiber
  • Phytic, oxalic acids
  • Other divalent cations
    • e.g. Mg2+ and Zn2+
  • Unabsorbed fatty acids
60
Q

What is the composition of calcium in the blood?

A
  • [Ca2+] = 8.5 – 10 mg/dL
  • ~40% of Ca2+ is bound to protein
    • e.g. albumin
  • ~50% is free ionized Ca2+
  • ~10% is complexed with sulfate, phosphate, citrate, etc
61
Q

What is the composition of calicum in the cells?

A
  • The cytosolic concentration of Ca2+ is very low (100 nmol).
  • The extracellular concentration of Ca2+ is 10,000x higher (2.3 mmol).
  • Ca2+ is stored in intracellular compartments
    • e.g. mitchondria, ER
62
Q

How is calcium exported from the cells?

A
  • Ca2+/3Na+ exchanger is a low affinity, high capacity transporter
  • Ca2+/2H+ exchanger is a high affinity, low capacity transporter
63
Q

What is calcium’s main function inside the cell?

A
  • Secondary messenger!
    • Intracellular signaling by calcium is mediated by calmodulin, a protein whose association with other proteins is regulated by calcium binding.
64
Q

What protein activated by Calmodulin-Calcium Complex blocks calcium uptake into the cell?

A

Calcineurin

65
Q

What are the downstream effects of increased intracellular calcium?

A
  • glycogen synthase is inactivated (via calcium/calmodulin kinase activated by Calmodulin-Calcium Complex )
  • glycogen phosphorylase is activated (via phosphorylase kinase activated by Calmodulin-Calcium Complex )
66
Q

What three additional dietary interactions does calcium effect?

A
  • Calcium blocks phosphorous uptake
  • High doses of Ca2+ used to treat hyperphosphatemia secondary to kidney failure.
  • Calcium transiently blocks iron uptake
  • Calcium can trap fatty acids and bile salts in ‘soaps’ that are not digestable.
    • Bile salts are not recycycled
    • Cholesterol is diverted to bile acid synthesis decreased chenodeoxycholate in bile LDL decreases
67
Q

How is calcium excreted?

A
  • Excretion: Urinary 100-240 mg/day
  • Resorption in the proximal tubule is controlled by calcitriol.
    • Caffeine increases urinary excretion of calcium.
  • Sodium and calcium share common resorption mechanism in the proximal tubule.
    • Very high sodium inhibits calcium reuptake and increases excretion.
  • Feces 45 – 100 mg/day
  • Sweat 60 mg/day
68
Q

Who is at risk for calcium deficiency?

A
  • People with fat malabsorption disorders
  • Immobilized patients
    • (bone calcium stores depleted)
69
Q

What are the consequences of calcium deficiency?

A
  • Calcium deficiency causes:
    • Rickets
    • Tetany (intermittant muscle contractions)
    • Osteoporosis
  • Calcium deficiency is associated with:
    • Colorectal cancer
    • Hypertension
    • Type II diabetes
70
Q

What happens in calcium toxicity?

A
  • TUL = 2,500 mg/day
  • Acute toxicity:
    • constipation
    • bloating
  • Chronic toxicity:
    • hypercalcemia can cause calcification of soft tissue
    • may lead to hypercalciuria and kidney stones
    • cardiovascular disease (?)
71
Q

How do you assess magnesium in a patient?

A
  • Normal serum [Mg2+] ~ 1.7 mg/dL
  • Assessment: Serum is a minor store of magnesium, so concentrations are not reliable.
  • Erythrocyte magensium is not turned over as rapidly, and can be a better measure.
  • Renal Mg2+ excretion before and after a loading dose is the best measure of magnesium status.
72
Q

What are the consequences of magnesium deficiency?

A
  • Dietary deficiency is not described, but can be experimentally induced.
  • Symptoms include:
    • nausea, vomiting, headache, anorexia; progresses to seizures, ataxia, fibrilation.
  • Chronic magnesium deficiency is associated with hypertension and type II diabetes.
  • Gitelman syndrome is an autosomal recessive mutation of SLC12A3, a thiazide sensitive Na/Cl transporter characterized by hypomagnesemia, hypokalemia, hypocalciuria.
73
Q

What causes magnesium toxicity? What are the symptoms?

A
  • TUL = 350 mg/day
  • Toxicity associated with use of epsom salts (MgSO4).
  • Symptoms are:
    • diarrhea, dehydration, flushing, slurred speech, muscle weakness, loss of deep tendon reflex.
  • At concentrations higher than 15 mg/dL, can cause cardiac arrest.
74
Q

Where does magnesium reside in the body?

A
  • Magnesium in the body: 25 grams
    • 50-60% in bone
    • 40-50% in soft tissues
    • 1% in extracellular fluid
75
Q

What are the dietary sources of magnesium?

A
  • Magnesium rich foods include:
    • nuts
    • legumes
    • whole grains
    • chlorophyll
    • chocolate
    • ‘hard’ water
76
Q

Where does chloride reside in the body?

A
  • Chloride accounts for ~105 grams in a 70 kg man.
    • 88% in extracellular fluid
    • 12% intracellular
77
Q

How is chloride absorbed/secreted in the body?

A
  • Chloride is absorbed paracellularly, or through a Na+/Cl- electroneutral transporter.
  • Chloride is the only anion secreted by gastrointestinal cells.
78
Q

What are the functions of chloride?

A
  • Chloride / bicarbonate exchanger:
    • Chloride enters red blood cells in exchange for bicarbonate when cells deliver oxygen to tissues
    • when bicarbonate goes out, chloride goes in to balance charge
  • Hypochlorous acid (~ bleach) is secreted by neutrophils during phagocytosis to neutralize pathogens.
  • Gastric hydrochloric acid secretion by parietal cells.
79
Q

How is magnesium absorbed in the gut?

A
  • Saturable transport across brush border: TRPM6
  • Basolateral transport:
    • 2Na+/Mg2+ antiporter
    • 2K+/3Na+/ATPase
    • Non-saturable paracellular diffusion.
80
Q

What are the functions of magnesium?

A
  • Bone:
    • 70% of bone magnesium is associated with phosphorous and calcium in crystal lattice.
    • 30% of bone magnesium is in amorphous form on the surface; this is available for exchange with serum to maintain magnesium homeostasis.
  • Intracellularly:
    • >90% of magenesium is associated with ATP.
    • Magnesium is essential for kinases and polymerases that use nucleotide triphosphates.
  • Activation of vitamin D requires magnesium.
    • 25-hydroxylase requires magnesium to convert Cholecalciferol => 25-Hydroxycholcalciferol
81
Q

What are the dietary sources of potassium?

A
  • In the diet: Fruit, leafy green vegetables, milk
  • In a 70 kg man, there are ~245 grams of potassium.
82
Q

How is potassium absorbed in the gut?

A
  • Absorption:
    • Paracellular diffusion
    • K+/H+ ATPase
  • Basolateral: K+ channel
83
Q

What are the functions of potassium?

A
  • Potassium functions as the major intracellular cation.
    • generates and maintains electrical potential across cell membranes
    • muscle contractility (smooth, skeletal, cardiac)
    • Na+/K+ ATPases consume energy to accumulate potassium within cells
    • Channels then allow potassium to flow out of the cell, resulting in a loss of positive charge
84
Q

How is potassium regulated in the body?

A
  • Vasopressin and aldosterone increase urinary potassium excretion.
  • Opposite of sodium.
85
Q

What are the consequences of potassium deficiency?

A
  • Normal [K+] ~ 3.5 – 5.0 mEq/L
  • Deficiency: < 3.5 mEq/L is Hypokalemia
    • Caused by fluid loss, thiazide or loop diuretics, or refeeding syndrome.
    • Symptoms:
      • Cardiac arrythmias, muscular weakness, hypercalciuria, glucose intolerance, mental disorientation
    • Moderate deficiency associated with:
      • elevated blood pressure
      • decreased bone density (increased urinary Ca++ excretion)
86
Q

What happens in potassium toxicity?

A

Hyperkalemia can be caused by renal failure and can cause cardiac arrythmia / arrest.

87
Q

Where does phosphorus reside in the body?

A
  • A 70 kg man has 560 – 850 grams of phosphorous.
    • 85% in bone
    • 1% in fluids
    • 14% in soft tissue
      • esp. muscle
88
Q

What are the dietary sources of phosphorus?

A
  • Phosphorous is widely distributed in the diet:
    • Meat
    • poultry
    • fish
    • eggs
    • dairy
    • cola (phosporic acid)
89
Q

How is phosphorus absorbed in the gut?

A
  • Saturable carrier mediated active transport is used when phosphate intake is low.
    • It is activated by calcitriol.
  • Diffusion occurs in the proximal duodenum (slightly acidic and phosphate is in the H2PO4- form).
90
Q

Phosphorous absorption is inhibited by what?

A
  • Magnesium (Mg3(PO4)2 is un-absorbable.)
  • Aluminum
  • Calcium

***All abundant in TUMS! Can use to treat phosphorus toxicity.

91
Q

What are the functions of phosphorus?

A
  • Bone mineralization:
    • amorphous: Ca3(PO4)2, CaHPO4-2H2O, Ca3(PO4)2-3H2O
    • crystalline: hydroxyapatite: Ca10(PO4)6(OH)2
    • calcitonin => phosphorous deposition in bone
    • calcitriol => phosphorous desorption from bone
  • Molecules with high energy bonds:
    • Nucleotides
    • Nucleic acids: DNA, RNA
    • Proteins: Serine, Threonine, Tyrosine
    • Phospholipids
    • Vitamins => cofactors
      • e.g. thiamin => thiamine pyrophosphate (TPP)
      • pryidoxine => pyridoxal phosphate (PLP)
  • Acid base balance: Na2HPO4 + H+ => NaH2PO4 + Na+
    • Phosphorous is an important buffer in the kidney.
  • Availability of oxygen: 2,3-bisphosphoglycerate
92
Q

How is phosphorus regulated in the body?

A
  • Regulation of phosphorous is at the level of renal clearance.
    • Excretion of phosphorous is promoted by:
      • elevated dietary phosphorous
      • parathyroid hormone (PTH)
      • acidosis
      • phosphotonins (e.g. FGF-23; secreted by osteoblasts and osteocytes)
    • Excretion of phosphorous if inhibited by:
      • low dietary phosphorous
      • calcitriol
      • alkalosis
      • estrogen
      • thyroid hormone
      • growth hormone
93
Q

Even though phosphorus deficiency is rare, what situations may cause a deficiency in phosphorus?

A
  • Extreme use of antacids containing magnesium, calcium, aluminum
  • Malnourishment Refeeding syndrome Inherited disorders:
    • Dents disease: X-linked, mutation in renal chloride channel
    • X-linked hyphosphatemic Rickets: Mutation in PHEX gene causes elevated FGF-23
    • Autosomal dominant hypophosphatemic Rickets: Mutation in the gene encoding FGF-23, prevents its degradation.
94
Q

What are the symptoms of phosphorus deficiency?

A
  • anorexia
  • reduced cardiac output
  • decreased diaphragmatic contractility
  • myopathy
  • death
95
Q

What dietary components does magnesium interact with?

A
  • Vitamin D Mg2+ may mimic Ca2+ and compete for resorption in the kidney.
  • Mg2+ inhibits phosphorous absorption by forming Mg3(PO4)2 precipitate.

GI Week 1 - WLB (11 decks)

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