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GI (Elaina) > Minerals and Electrolytes > Flashcards

Minerals and Electrolytes Flashcards

1
Q

Major minerals in order of abundance in the body

A 
Calcium
Phosphorous
Potassium
Sodium, Chloride
Magnesium
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2
Q

Trace elements (require < 100 mg/day)

A

Iron
Zinc
Copper
Manganese

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3
Q

Ultratrace elements (require < 1 mg/day)

A

Selenium
Molybdenum
Iodine
Chromium

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4
Q

Functions of minerals in the body

A 
Osmotic balance
Maintaining charge / concentration gradients across membranes
Enzyme cofactors
Structure
Taste
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5
Q

Major extracellular cation

A

sodium

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6
Q

major intracellular cation

A

potassium

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7
Q

Most abundant metal ion in body

A

Calcium

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8
Q

Dietary sources calcium

A

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

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9
Q

major functions calcium

A

Bone mineralization
Blood clotting
Muscle contraction
Metabolism regulator

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10
Q

Calcium absorption

A

Saturable carrier mediated transport

paracellular transport around tight junctions (claudins)

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11
Q

saturable carrier mediated transport of calcium

A

TRPv6 transports Ca2+ across the brush border membrane
Calbindin chaperones Ca2+ within the cell
Ca2+ /ATPase transports Ca2+ across the basolateral membrane

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12
Q

ca absorption regulated by

A

calcitriol (vitamin D)

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13
Q

what increases Ca absorption

A

Vitamin D
sugars, sugar alcohols
protein

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14
Q

what decreases ca absorption

A

Fiber
Phytic, oxalic acids
Other divalent cations, e.g. Mg2+ & Zn2+
Unabsorbed fatty acids

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15
Q

what inhibits PTH

A

calcitonin (peptide hormone made by thyroid)

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16
Q

what form is calcium in blood

A

40% bound to protein
50% free
10% w/ sulfate, phosphate, citrate, etc

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17
Q

where is calcium in 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

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18
Q

export of ca from cells

A

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

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19
Q

Intracellular signaling by calcium is mediated by

A

Intracellular signaling by calcium is mediated by calmodulin, a protein whose association with other proteins is regulated by calcium binding.

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20
Q

ca/calmodulin w/ calcineurin

A

inhibit ca channels

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21
Q

ca/calmodulin w/ MLCK

A

muscle contraction

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22
Q

ca/calmodulin w/ ca/calmodulin kinase

A

inhibit glycogen synthase

When intracellular calcium increases, glycogen synthase is inactivated and glycogen phosphorylase is activated.

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23
Q

ca/calmodulin w/ phosphorylase kinase

A

phosphorylase

When intracellular calcium increases, glycogen synthase is inactivated and glycogen phosphorylase is activated.

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24
Q

calcium interactions with other dietary components

A

Calcium blocks phosphorous uptake

Calcium transiently blocks iron uptake

Calcium can trap fatty acids and bile salts in ‘soaps’ that are not digestable. (LDL decreases)

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25
Q

calcium excretion

A

Urinary 100-240 mg/day

Feces 45 – 100 mg/day

Sweat 60 mg/day

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26
Q

urinary excetion calcium impacted by

A

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.

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27
Q

those at risk of calcium deficiency

A 
fat malabsorption disorders
immobilized patients (bone calcium stores depleted)
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28
Q

calcium deficiency causes

A

Rickets
Tetany (intermittant muscle contractions)
Osteoporosis

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29
Q

calcium deficiency associated with

A

Colorectal cancer
Hypertension
Type II diabetes

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30
Q

calcium toxicity TUL

A

2500 mg/day

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31
Q

calcium toxicity acute and chronic

A

Acute toxicity:
constipation, bloating

Chronic toxicity:
hypercalcemia can cause calcification of soft tissue
may lead to hypercalciuria and kidney stones
cardiovascular disease (?)

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32
Q

assessment of calcium status

A

Serum levels of Ca2+ are tightly regulated; measuring serum levels doesn’t tell much.

Bone density scan is more clinically useful.

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33
Q

magnesium in the body

A

25 grams
50-60% in bone
40-50% in soft tissues
1% in extracellular fluid

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34
Q

RDA magnesium

A

400 mg

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35
Q

magnesium foods

A

nuts, legumes, whole grains, chlorophyll, chocolate, and ‘hard’ water.

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36
Q

transport of magnesium

A

Saturable transport across brush border: TRPM6

Basolateral transport:
2Na+/Mg2+ antiporter
2K+/3Na+/ATPase

Non-saturable paracellular diffusion.

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37
Q

mg in the blood

A

50% free Mg2+
13% salts
37% bound to protein

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38
Q

functions of magnesium on bone

A

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

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39
Q

actions of mg intracellularly

A

Intracellularly, >90% of magenesium is associated with ATP.

Magnesium is essential for kinases and polymerases that use nucleotide triphosphates.

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40
Q

activation of ______ requires magnesium

A

vitamin D

25-hydroxylase in liver

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41
Q

mg interactions in diet

A

Vitamin D

Mg2+ may mimic Ca2+ and compete for resorption in the kidney.

Mg2+ inhibits phosphorous absorption by forming Mg3(PO4)2 precipitate

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42
Q

Mg assessment

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.

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43
Q

Mg deficiency

A

Not described. Experimentally induced, chronic or gitelman syndrome.

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44
Q

Mg deficiency symptoms, chronic

A

Symptoms include nausea, vomiting, headache, anorexia; progresses to seizures, ataxia, fibrilation.

Chronic magnesium deficiency is associated with hypertension and type II diabetes.

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45
Q

Gitelman syndrome

A

is an autosomal recessive mutation of SLC12A3, a thiazide sensitive Na/Cl transporter characterized by hypomagnesemia, hypokalemia, hypocalciuria.

46
Q

Magnesium toxicity

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.

47
Q

Chloride locations in body

A

88% ec

12% intracellular

48
Q

chloride absorption

A

Chloride is absorbed paracellularly, or through a Na+/Cl- electroneutral transporter.

49
Q

chloride secretion

A

GI cells

50
Q

chloride functions (bicarb)

A

cl/bicard exchanger

Chloride enters red blood cells in exchange for bicarbonate when cells deliver oxygen to tissues.
Chloride leaves red blood cells in exchange for bicarbonate when cells take in oxygen from lungs.

51
Q

chloride functions (immune system)

A

Hypochlorous acid (~ bleach) is secreted by neutrophils during phagocytosis to neutralize pathogens.

52
Q

chloride functions (stomach)

A

Gastric hydrochloric acid secretion by parietal cells.

53
Q

Potassium in the diet

A

fruit, leafy green vegetables, milk

54
Q

potassium absorption

A

Paracellular diffusion

K+/H+ ATPase
Basolateral: K+ channel

55
Q

K function

A

It functions to generate and maintain electrical potential across cell membranes.

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.

Muscle contractility

56
Q

K regulation

A

Vasopresin and aldosterone increase urinary potassium excretion.
Opposite of sodium.

57
Q

K interactions

A

decreases calcium excretion (opposite of sodium)

58
Q

normal K levels

A

3.5-5 mEq/L

59
Q

K deficiency

A

< 3.5 mEq/L = hypokalemia

60
Q

causes hypokalemia

A

Caused by fluid loss, thiazide or loop diuretics, or refeeding syndrome

61
Q

symtpoms hypokalemia

A

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

Moderate deficiency associated with:
elevated blood pressure
decreased bone density (increased urinary Ca++ excretion)

62
Q

toxicity potassium

A

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

63
Q

phosphorus locations

A

85% in bone
1% in fluids
14% in soft tissue, esp. muscle

64
Q

diet phosphorus

A

widely distributed in the diet: Meat, poultry, fish, eggs, dairy, cola (phosporic acid).

65
Q

kinds of phosphates

A

Inorganic (phosphates)
Organic: associated with protein, sugar, lipids, nucleic acids
Phytic acid: limited bioavailability

66
Q

absorption phosphorus

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).

67
Q

phosphorus absorption inhibited by

A

Magnesium ( Mg3(PO4)2 is un-absorbable.)

Aluminum

Calcium

68
Q

Functions of phosphorus

A

bone mineralization
molecules with high energy bonds
acid base balance
availability of oxygne

69
Q

phos and bone mineralization

A

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

70
Q

phos and high energy bonds

A 
Nucleotides
Nucleic acids:  DNA, RNA
Proteins:  Serine, Threonine, Tyrosine
Phospholipids
Vitamins  cofactors
thiamin  thiamine pyrophosphate (TPP)
pryidoxine  pyridoxal phosphate (PLP)
71
Q

phos and acid-base balance

A

Na2HPO4 + H+  NaH2PO4 + Na+

Phosphorous is an important buffer in the kidney.

72
Q

phos and oxygen availability

A

2,3-bisphosphoglycerate

73
Q

regulation of phos is at the level of

A

renal clearance

74
Q

excretion of phos promoted by

A

elevated dietary phosphorous
parathyroid hormone (PTH)
acidosis
phosphotonins (e.g. FGF-23; secreted by osteoblasts and osteocytes)

75
Q

excretion of phos inhibited by

A 
low dietary phosphorous
calcitriol
alkalosis
estrogen
thyroid hormone
growth hormone
76
Q

phos deficiency is rare but can occur in

A

Extreme use of antacids containing magnesium, calcium, aluminum
Malnourishment
Refeeding syndrome
Inherited disorders

77
Q

Inherited disorders with phos def

A

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. (FGF-23 is a phosphatonin; promotes phosphorous excretion)

78
Q

phos def symptoms

A

anorexia, reduced cardiac output, decreased diaphragmatic contractility, myopathy, death

79
Q

Iron in diet

A

meat, fish, poultry (half heme iron, half non-heme)

nuts, fruits, vegetables, grains (mostly non-heme; conjugated with phenols)

80
Q

ferrous iron

A

Fe 2+ (reduced)

81
Q

Ferric iron

A

fe 3+ (oxidized)

82
Q

low pH prefers ___ iron

A

ferrous iron (Fe2)

83
Q

ceruloplasmin prefers ___ iron

A

ferric iron (Fe3)

84
Q

Iron absorption into enterocytes

A

brush border: reductase makes ferric –> ferrous

Fe2+ transported through DMT-1

85
Q

iron in enterocyte

A

iron bound to ferritin

86
Q

iron transport in blood requires

A

oxidation to Fe 3+ by hephaestin (HP; ceruloplasmin), this enzyme also requires copper

87
Q

Fe 3+ binds ____ for transport to tissues

A

transferritin

88
Q

regulation of iron uptake through

A

hepcidin

When iron stores in the liver are high, hepcidin is produced. It binds ferroportin (FPN) and causes its degradation

89
Q

protein for export from enterocyte

A

ferroportin

90
Q

funtion of iron

A

heme synthesis
iron-sulfur clusters
non-heme iron

91
Q

iron and heme synthesis

A 
Glycine + succinyl CoA + Iron  heme
Heme is used in: 
cytochrome B, cytochrome C
hemoglobin, myoglobin
monooxygenases, e.g. phenylalanine dehdrogenase
92
Q

iron-sulfur clusters

A

Electron transfer groups in, e.g. NADH dehydrogenase

93
Q

non-heme iron

A

Dioxygenase, e.g. homogentisate dioxygenase

94
Q

iron interactions

A

Vitamin C enhances absorption and maintains iron in the reduced state.
Copper is required for export from enterocytes.
Iron inhibits zinc absorption.

95
Q

iron deficiency observed in

A

infants (low iron in diets)
adolescents (rapid growth rate)
pregnant women (rapid growth rate, blood loss at delivery)
absorption disorders

96
Q

iron def sxs

A

Microcytic hypochromic anemia, listlessness, fatigue

97
Q

iron toxicity, TUL

A

45 mg/day

98
Q

iron toxicity pathology

A

If intake exceeds the livers ferritin storage capacity, it can accumulate in tissues and act as a free radical, causing oxidative damage.

99
Q

chronic hemochromatosis

A

caused by inherited mutations in hepcidin (or other iron metabolism genes). It causes organ failure due to iron accumulation.

100
Q

copper diet

A

meat. shellfish, nuts

101
Q

copper absorbtion

A

A brush border reductase reduces Cu2+ to Cu+.

Cu+ then is transported through CTR1.

Cu+ can then enter the blood through ATP7A, a basolateral transporter, and circulate bound to proteins e.g. albumin.

102
Q

Menkes kinky hair syndrome

A

caused by mutations in ATP7A. It is characterized by hypothermia, hypotonia, poor feeding, failure to thrive, and seizures.

Patients have normal hair at birth, but it becomes brittle and sparse as they age.

103
Q

function of copper

A

Cofactor for ceruloplasmin; see iron.

Cytochrome C oxidase has 3 Cu+ per enzyme

Cofactor for lysyl oxidase (collagen synthesis; also requires ascorbate)

Copper is a cofactor for superoxide dismutase, an antioxidant enzyme.

Copper is a cofactor for dopamine b-hydroxylase, required for catecholamine synthesis.

104
Q

copper deficiency

A

May occur in people who consume a lot of zinc, or a lot of proton pump inhibitors.
Symptoms: anemia, leukopenia, hypopigmentation of skin & hair, altered cholesterol metabolism.

105
Q

copper TUL

A

10 mg/day

106
Q

copper toxicity acute, chronic, cong. disease

A

acute: epigastric pain, nausea, vomiting, diarrhea
chronic: hematuria, liver damage, kidney damage
Wilson disease

107
Q

wilson disease

A

is caused by mutation in the liver specific copper transporter ATP7B.

108
Q

normal ATP7B

A

ATP7B normally transports excess copper into the bile for excretion. When it is defective, copper accumulates and ‘leaks out’ unbound to ceruloplasmin.

109
Q

tx wilson diease

A

Treatment is to avoid high copper foods, and chelation therapy.

110
Q

sx wilson disease (hallmark)

A

Kayser-Fleischer ring

GI (Elaina) (7 decks)

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