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GI > Minerals > Flashcards

Minerals Flashcards

1
Q

Major minerals

A
  • -Calcium
  • -Phosphorus
  • -Potassium
  • -Sodium
  • -Chloride
  • -Magnesium
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2
Q

Trace minerals (

A
  • -Iron
  • -Zinc
  • -Copper
  • -Manganese
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3
Q

Ultratrace minerals (

A
  • -Selenium
  • -Molybdenum
  • -Iodine
  • -Chromium
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4
Q

Functions of minerals

A
  • -Maintain osmotic balance
  • -Maintain charge/concentration gradients across membrane
  • -Enzyme cofactors
  • -Structure
  • -Taste
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5
Q

What is the major extracellular cation?

A

Sodium

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6
Q

What is the major intracellular cation?

A

Potassium

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7
Q

Dietary sources of calcium

A

Dairy, seafood, turnips, broccoli, kale, dietary supplements

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8
Q

Most abundant metal in the body?

A

Calcium. About 1.4 Kg in 70 kg man

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9
Q

Functions of calcium

A

–Bone mineralization
–Signaling molecule for muscle contraction
–Helps regulate
metabolism
Blood clotting

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10
Q

What regulates absorption of calcium?

A

Calcitriol (Vitamin D)

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11
Q

What chaperones calcium within the cell

A

Calbindin

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12
Q

What helps increase absorption of calcium?

A

Vitamin D, sugars, sugar alcohols, protein

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13
Q

What decreases absorption of calcium?

A

Fiber, phytic acid, oxalic acid, other divalent cations, unabsorbed fatty acids

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14
Q

What increases expression of calcium channel TRPV6 at brush border and alters tight junction permeability to calcium?

A

Activated VDR

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15
Q

[Ca++] in the blood

A

8.5-10 mg/dL
40% bound to protein
50% free ionized
10% complexed with sulfate, phosphate, citrate etc.

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16
Q

Cytosolic [Ca++] vs. extraceullular

A

Very low in cytosol (100nMol).

10,000x higher in extraceullular area (2.3 mmol)

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17
Q

Where is Ca++ stored in cells?

A

Intracellular compartments

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18
Q

Ca++/ 3Na+ transporter

A
  • -Helps export calcium from cells

- -Low affinity, high capacity

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19
Q

Ca++/2H+ transporter

A
  • -Helps export calcium from cells

- -High affinity, low capacity

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20
Q

Calmodulin

A

Mediated intracellular signalling by calcium. Protein whose association with other proteins is regulated by calcium binding

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21
Q

What happens when intracellular calcium increased?

A

Glycogen synthase inactivated and glycogen phosphorylase is activated

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22
Q

Calcium interactions with other dietary components

A
  • -Calcium blocks phosphorus uptake
  • -Calcium transiently blocks iron uptake
  • -Calcium can trap fatty acids, bile salts in “soaps” that are not digestible
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23
Q

Calcium excretion

A
  • -Urinary: 100-240 mg/day (controlled by calcitriol)
  • -Feces: 45-100 mg/day
  • -Sweat: 60 mg/day
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24
Q

People at risk of calcium deficiency

A
  • -Fat malabsorption disorders

- -Immobilized patients

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25
Q

Causes of calcium deficiency

A

Rickets
Tetany
Osteoporosis

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26
Q

Calcium deficiency associated with what?

A

Colorectal cancer
Hypertension
Type II diabetes

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27
Q

Calcium TUL

A

2,500 mg/day

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28
Q

Acute calcium toxicity

A

Constipation, bloating

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29
Q

Chronic calcium toxicity

A

Calcification of tissue, hypercalciuria, kidney stones, maybe CV disease

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30
Q

Best assessment of calcium status?

A

Bone density scan

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31
Q

Magnesium dietary sources

A

Nuts, legumes, whole grains, chlorophyll, chocolate, hard water

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32
Q

Magnesium functions

A
  • -Calcium metabolism
  • -Component of bone
  • -Muscle contraction
  • -Nerve impulse propagation
  • -Cofactor in ATPases
  • -Needed for kinases and polymerases that use nucleotide triphosphates
  • -Needed for activation of Vit D by 25-hydroxlase
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33
Q

Magnesium in body

A

25 grams

–50-60% in bone, 40-50% in soft tissues, 1% in extracellular fluid

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34
Q

What allows for saturable transport of magnesium across the brush border?

A

TRPM6

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35
Q

Basolateral transport of magnesium

A

2Na+/Mg++ antiporter, 2K+/3Na+ ATPase

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36
Q

Is paracellular diffusion of magnesium saturable?

A

No

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37
Q

How much of the magnesium intracellularly is associated with ATP?

A

Greater than 90%

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38
Q

Interactions of magnesium with other things in the diet?

A
  • -Can mimic Ca++ and compete for absorption in the kidney

- -Inhibits phosphorus absorption

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39
Q

Best measurement of magnesium status?

A

Rena Mg++ excretion before and after a loading dose

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40
Q

Magnesium deficiency

A
  • -Dietary deficiency not described (can be induced though)
  • -Nausea, vomiting , HA, anorexia. Progresses to seizures, ataxia, fibrillation
  • -Chronic deficiency associated w/HTN and DMII
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41
Q

Gitelman syndrome

A
  • -Autosomal recessive mutation of SLC12A3 (thiazide sensitive Na/Cl transporter)
  • -Characterized by hypomagnesemia, hypokalemia, hypocalciuria
42
Q

Magnesium TUL

A

350 mg/day

43
Q

Magnesium toxicity

A
  • -Associated with epsom salt use
  • -Diarrhea, dehydration, flushing, slurred speech, muscle weakness, loss of deep tendon reflex
  • -If higher that 15 mg/dL, can cause cardiac arrest
44
Q

Chloride dietary sources

A

Primarily table salt

45
Q

Chloride absorption

A

Paracellular or through Na+/Cl- electroneutral transporter

46
Q

Chloride distribution

A

Neutrophils and parietal cells

47
Q

Chloride functions

A
  • -Cl-/HCO3- exchangers–> enters RBCs in exchange for HCO3- when cells deliver oxygen to tissues and leaves RBCs in exchange for HCO3- when cells take in oxygen from the lungs
  • -Hypochlorous acid is secreted by neutrophils during phagocytosis to neutralize pathogens
  • -Gastric hydrochloric acid secretion by parietal cells
48
Q

Potassium function

A

Major intracellular cation, muscle contractility

49
Q

Potassium regulation

A

Vasopressin and aldosterone increase urinary K+ excretion (opposite of Na+)

50
Q

Potassium interactions

A

Decreases calcium excretion (opposite of Na+)

51
Q

Hypokalemia causes

A

Fluid loss, thiazide or loop diuretics, refeeding syndrome

52
Q

Hypokalemia symptoms

A

Cardiac arrhythmias, muscular weakness, hypercalciuria, glucose intolerance, mental disorientation

53
Q

Moderate K+ deficiency is associated with?

A

Elevated BP, decreased bone density

54
Q

Hyperkalemia causes and possible effects

A

Renal failure and can lead to cardiac arrhythmia/arrest

55
Q

Phosphorus amount in body and distribution

A
  • -850 g
  • -85% in bone
  • -1% in fluids
  • -14% in soft tissue, esp. muscle
56
Q

Phosphorus sources

A

Meat, poultry, fish, eggs, dairy, cola (phosphoric acid)

57
Q

When is saturable carrier mediated active transport used for phosphorus absorption? How is it activated?

A

When phosphate intake is low. Activated by calcitriol

58
Q

Where does diffusion of phosphorus occur?

A

In the proximal duodenum (slightly acidic)

59
Q

What inhibits phosphorus absorption?

A

Magnesium, albumin, calcium. All found in antacids and used to treat hyperphosphatemia from kidney failure

60
Q

Phosphorus functions

A
  • -Bone mineralization
  • -Component of DNA and RNA
  • -Component of phosphorylated vitamins
  • -Traps monsaccharides in cells
  • -Activates protein kinase and deactivates glycogen synthase
  • -Helps maintain pH
61
Q

What promotes excretion of phosphorus?

A
  • -Elevated dietary phosphorus
  • -PTH
  • -Acidosis
  • -Phosphotonins
62
Q

Excretion of phosphorus is inhibited by?

A
  • -Low dietary phosphorus
  • -Calcitriol
  • -Alkalosis
  • -Estrogen
  • -Thyroid hormone
  • -Growth hormone
63
Q

Dents disease

A

X-linked

  • -Mutation in renal chloride channel
  • -Can lead to phosphate deficiency
64
Q

Phosphorus deficiency causes

A
  • -Extreme use of antacids
  • -Malnourishment
  • -Refeeding syndrome
  • -Inherited disorders
65
Q

Phosphorous deficiency symptoms

A

Anorexia, reduced CO, decreased diaphragmatic contractility, myopathy, death

66
Q

X-linked hypophosphatemic rickets

A
  • -Mutation in PHEX gene–>elevated FGF-23

- -Can cause phosphorus deficiency

67
Q

Autosomal dominant hypophosphatemic rickets

A
  • -Mutation in gene encoding FGF-23–> prevents it’s degradation
  • -Can cause phosphorus deficiency
68
Q

Iron dietary sources

A

Meat, fish, poultry, nuts, fruits, vegetables, grains

69
Q

How much iron usually in a 70 kg man?

70
Q

What form of iron is the reduced form?

A

Ferrous iron (Fe++)

71
Q

What form of iron is the oxidized form?

A

Ferric iron (Fe+++)

72
Q
  1. What promotes conversion of ferrous iron to ferric iron? 2. What about ferric to ferrous?
A
  1. Ceruloplasmin

2. Low pH

73
Q

What reduces ferric iron at the brush border

74
Q

Transport of ferrous iron in cell through what?

A

Divalent metal transporter-1 (DMT-1)

75
Q

What is iron stored to in a cell?

76
Q

What is required for iron transport into the blood

A

Oxidation to Fe+++ by hephaestin (ceruloplasmin). It’s a copper requiring enzyme

77
Q

What does Fe+++ bind to for transport to tissues?

A

Transferritin

78
Q

Main iron reservior

A

Located in liver. Hemosiderin and ferritin

79
Q

What is responsible for regulation of iron uptake?

A

Hepcidin. When iron stores high, hepcidin is produced.

80
Q

Hepcidin

A

Binds ferroportin and causes its degradation when iron stores in liver are high

81
Q

Iron functions

A
  1. Heme synthesis used in hemoglobin, myoglobin, monooxygenases, cytochrome B and C
  2. Iron-sulfur cluster involved in electron transfer groups
  3. Non heme iron is a dioxygenase
82
Q

Iron interactions

A
  • -Vit C enhances iron absorption and maintains iron in reduced state
  • -Copper needed for iron export from enterocytes
  • -Iron inhibits zinc absorption
83
Q

Iron deficiency observed in?

A
  • -Infants
  • -Adolescents (rapid growth)
  • -Pregnant women
  • -Absorption disorders
84
Q

Iron deficiency symptoms

A
  • -Microcytic hypochromic anemia
  • -Listlessness
  • -Fatigue
85
Q

Iron toxicity TUL and chemistry behind it?

A
  • -45 mg/day
  • -Can accumulate in tissues if intake exceeds ferritin storage capacity and can act as a free radical causing oxidative damage
86
Q

Chronic hemochromotosis

A
  • -Inherited mutations in hepcidin (or other iron metabolism genes)
  • -Causes organ failure from iron accumulation
87
Q

Copper dietary sources

A

Meat, shellfish, nuts

88
Q

Normal amount of copper in 70 kg man?

89
Q

What reduces Cu++ to Cu+

A

Brush border reductase

90
Q

What is responsible for Cu+ transport into cell?

91
Q

What allows for copper to enter the blood?

A

ATP7A (basolateral transporter)

92
Q

Menkes kinky hair syndrome

A
  • -Mutations in ATP7A.
  • -Hypothermia, hypotonia, poor feeding, FTT
  • -Normal hair at birth that becomes brittle and sparse with aging
93
Q

Functions of copper

A
  • -Cofactor for ceruloplasmin
  • -Cytochrome C oxidase needs copper
  • -Cofactor for lysyl oxidase (collagen synthesis, requires ascorbate)
  • -Cofactor for superoxide dismutase (antioxidant enzyme)
  • -Cofactor for dopamine beta-hydroxylase (needed for catecholamine synthesis)
94
Q

Copper deficiency causes

A

–Can occur in people who consume a lot of zinc or a lot of PPI

95
Q

Copper deficiency symptoms

A

Anemia, leukopenia, hypopigmentation of skin and hair, altered cholesterol metabolism

96
Q

Copper toxicity (TUL)

97
Q

Acute copper toxicity symptoms

A

Epigastric pain, N and V, diarrhea

98
Q

Chronic copper deficiency

A

Hematuria, liver damage, kidney damage

99
Q

Wilson disease

A
  • -Mutation in ATP7B (liver specific copper transporter)
  • -Treatment: avoid high copper foods, chelation therapy
  • -Kayser-Fleischer ring
100
Q

ATP7B

A

–Normally transports excess copper into bile for excretion

101
Q

What happens when ATP7B is defective?

A

Copper accumulates and “leaks out” unbound to ceruloplasmin

GI (12 decks)

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