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Clinical Nutrition 1 > Macrominerals > Flashcards

Macrominerals Flashcards

1
Q

name the macrominerals

A 
calcium
magnesium
phosphorous
potassium
sodium
chloride
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2
Q

is the most abundant mineral in the body

A

calcium

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3
Q

where is most of the calcium found in the body

A

99% in bones and teeth

the rest in blood and soft tissues

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4
Q

dietary sources of calcium

A
  • dairy: milk, yogurt, cheese
  • some seafood: salmon, sardines canned with bones, oysters
  • vegetables: turnip, spinach, broccoli, cauli, kale
  • legumes: soy beans, tofu
  • sesame seeds
  • figs
  • molasses
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5
Q

inhibitors of calcium absorption

A

oxalic acid

phytic acid

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6
Q

oxalic acid

A

aka oxylate
is the most potent inhibitor of calcium absorption
found in spinach, rhubarb
less in sweet potatoes, dried beans

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7
Q

phytic acid

A

a less potent inhibitor of calcium absorption
can still significantly reduce bioavailablility of calcium
found in wheat bran or dried beans

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8
Q

is calcium found in the form of soluble salts or insoluble salts in food and supplements

A

relatively insoluble salts

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9
Q

digestion of calcium

A

calcium can be solubized from most calcium salts in 1 hour at acidic pH
however, this doesn’t necessarily ensure calcium absorption because calcium can bind to other things like oxalic acid and phytic acid that then prevent absoprption

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10
Q

absorption of calcium

A

through 2 routes:

  1. duodenum and proximal jejenum (active)
  2. jejenum and ileum (passive)
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11
Q

active transport of calcium is stimulated by:

A

calcitriol and low calcium diets

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12
Q

passive transport of calcium is stimulated by:

A

high concentrations of calcium in intestinal lumen

FOS and inulin

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13
Q

is calcium absorbed in the large intestine?

A

yes, in small amounts

- bacteria release Calcium bound to fermentable fibers

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14
Q

factors the enhance calcium absorption

A 
growth, pregnancy, lactation
vitamin D
protein
simple sugars
food in general
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15
Q

factors that inhibit calcium absorption

A 
oxalate/oxalic acid
phytate/phytic acid
fiber
other divalent cations
undigested fat
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16
Q

transport of calcium

A
  • calbindin = CBP, transports calcium across cytoplasm

- calcium ATPase transports calcium from enterocyte into ECF and a Calcium/sodium antiporter is on the outside

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17
Q

transport of calcium into the blood

A

50% free/ionized in the blood
40% is bound to proteins like albumin
10% is complexed with sulfate, phosphate, or citrate

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18
Q

regulation of calcium levels done by

A

PTH
calcitriol
calcitonin

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19
Q

PTH and calcitriol in calcium regulation

A

low plasma calcium stimulates PTH secretion

calcitriol increases calcium absorption

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20
Q

calcitonin and calcium regulation

A

low plasma calcium levels inhibit calcitonin release

high plasma calcium levels stimulate calcitonin secretion which lower serum calcium inhibititing bone breakdown

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21
Q

functions of calcium in the body

A
  • bone mineralization
  • nerve conduction
  • muscle contraction
  • coagulation
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22
Q

calcium and coagulation

A

calcium is needed to stabilize proteins and enzymes which optimizes their acitivites
binding of calcium is required for activation of the 7 vitamin K-dependent blood clot-regulating factors in the coagulation cascade

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23
Q

calcium excretion

A
  • mostly filtered and reabsorbed by kidneys

- mostly excreted through urine and feces, some through perspiration

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24
Q

results of calcium deficiency

A
  • hypocalcemia

- osteoporosis

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25
Q

hypocalcemia

  • reasons/causes
  • symptoms
A

low blood calcium

  • suggests abnormal parathyroid function, rarely due to low dietary calcium intake
  • possible causes: chronic kidney failure, vit D deficiency, low blood magnesium (often occurring in alcohol abuse disorder)
  • symptoms: tetany, muscle spasms, paresthesias
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26
Q

Chvostek’s sign

A
  • a test for hypocalcemia

- involves testing for muscle spasms by tapping on facial nerve

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27
Q

Trousseau’s sign

A
  • a test for hypocalcemia

- looking at hand for muscle spasms

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28
Q

tests for hypocalcemia

A

Chvostek’s sign

Trousseau’s sign

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29
Q

osteoporosis

- cause?

A

low calcium intake results in failure to attain peak bone mass

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30
Q

kidney stons and calcium

A
  • most kidney stones are composed of calcium oxalate but increased dietary calcium only slightly increases the urinary calcium levels
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31
Q

calcium toxicity conditions

- what is it called and when does it occur

A
  • hypercalcemia - not known to occur from food sources, only from excess intake of calcium supplements in combination with calcium-containing antacids
  • called milk alkalai syndrome
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32
Q

symptoms of hypercalcemia

A
  • mild: loss of appetite, vomiting, constipation, abdominal pain, dry mouth, thirst, frequent urination
  • severe: confusion, delirium, coma, even death if untreated
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33
Q

what increases risk for kidney stones?

A
  • supplemental calcium taken on an empty stomach because there is no longer a beneficial effect of decreasing intestinal oxalate absorption
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34
Q

calcium interactions with nutrients

A
  • high sodium intake can increase calcium excretion in the urine
  • high calcium intake may decrease absorption of non-heme iron and zinc
  • high calcium intake may decrease tissue levels of magnesium
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35
Q

where is most of the magnesium found in the body?

A

> 60% is in the bones
25% is in muscle tissue
< 1% is in ECF

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36
Q

sources of magnesium

A
  • nuts and seeds
  • legumes, whole grains (oats, barley, brown rice)
  • most vegetables - esp leafy greens, corn, carrots
  • seafood, dairy
  • coffee, tea, cocoa, chocolate
  • molasses
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37
Q

location of absorption of magnesium

A

in small intestine - jejunum and ileum

may be absorbed in colon, especially in diseases affecting the small intestine

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38
Q

pathways of magnesium absorption

A

2 pathways:

  1. saturable active transport when intake is low, stimulated by calitriol
  2. simple diffusion when intake is high
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39
Q

factors that enhance magnesium absorption

A
  • calcitriol

- simple sugars like lactose and fructose

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40
Q

factors that inhibit magnesium absorption

A
  • phytate
  • fiber
  • excessive unabsorbed fatty acids
  • other minerals (calcium, phosphorus)
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41
Q

methods of transport of magnesium through the body

A

50-55% in free ionized form
33% bound to protein (like albumin)
13% complexed with other ions

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42
Q

homeostasis regulation of magnesium

A

not well understood,

but with calcium, PTH increases plasma concentrations of magnesium

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43
Q

how does PTH increase plasma concentrations of magnesium?

A
  • increasing intestinal absorption by activating vit D
  • decreasing renal excretion of Mg++
  • enhancing its bone resorption
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44
Q

functions of magnesium in the body

A
  • energy production (cofactor)
  • structural role (bone crystal matrix)
  • ion transport across cell membranes
  • cell signalling
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45
Q

excretion of magnesium

A
  • primarily through the urine but lots of magnesium is reabsorbed by the kidney
  • also perspiration
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46
Q

conditions that increase risk of magnesium deficiency

A
  • renal disorders (diabetes and long term use of diuretics)
  • chronic alcohol abuse
  • elderly people (have lower intestinal Mg++ absorption)
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47
Q

signs and symptoms of magnesium deficiency

A
  • hypomagnesemia
  • over time can see chronic PTH resistance leading to hypocalcemia
  • retention of Na+ and hypokalemia
  • muscle tremor, spasms, cramps, tetany
  • SOB, tight chest
  • palpitations, cardiac arrhythmias
  • anxiety, depression, fatigue, insomnia
  • loss of appetite, N&V
48
Q

clinical indications for magnesium

A
  • hypertension (correlation between HTN and low Mg levels)

- migraine headaches

49
Q

what is different about magnesium sulfate

A

aka epsom salts
it acts as a non-reabsorbable anion in the kidney and may also interfere with renal K+ absorption
is most likely form to cause diarrhea and is sometimes used as a laxative

50
Q

magnesium toxicity

A
  • diarrhea is a common dose related side effect of magnesium supplementation
  • individuals with renal impairment are more at risk of averse effects from excess supplemental Mg intake
51
Q

hypermagnesemia

A

results in hypotension and later effects of magnesium toxicity: lethargy, confusion, cardiac arrhythmia, kidney dysfunction, all related to severe drop in BP

52
Q

contraindications to magnesium supplementation

A
  • end-stage renal disease
  • myasthenia gravis
  • urinary tract infection with elevated urinary phosphates (may promote formation of Mg-ammonium-phosphate kidney stones)
  • caution in hyperparathyroidism
53
Q

nutrient interactions of magnesium and why

A
  • calcium - high Ca intake may decrease tissue levels of Mg
  • potassium - Mg is essential for uptake of K and so if someone is deficient in both, K supplementation won’t corrent Mg def
  • zinc - high doses of zinc (140mg) interfere with Mg absorption
  • thiamine - large doses increase need for Mg
  • vitamin B6 - increases Mg uptake and vise versa
54
Q

where is phosphorous found in the body

A

as phosphates (PO4)
85% found in bone
14% in soft tissue
1% in blood and body fluids

55
Q

sources of phosphorous

A
  • dairy, meat, poultry, fish, eggs
  • nuts, legumes, grains
  • coffee, tea, soft drinks
56
Q

bioavailability of phosphorous

A
  • phosphourous in all plant seeds is present in a storage form, phytate/phytic acid where only 50% of the phosphorous is available to humans
  • yeasts possess phytases (enzymes) and so this is why whole grains are incorporated into leavened breads to make phosphorous more bioavailable
57
Q

is phosphorous absorbed in its organic or inorganic form

A

inorganic form

58
Q

where is phosphorous absorbed in the body

A

small intestines, primarily duodenum and jejenum

59
Q

processes of phosphorous absorption?

A

2 processes:

  1. facilitated diffusion - primary route
  2. saturable Na-dependent, carrier mediated transport stimulated by calcitriol and low phosphorous intake
60
Q

factors that enhance phosphorous absorption

A

vitamin D

61
Q

factors than inhibit phosphorous absorption

A 
phytates
other minerals (Ca, Mg, Aluminum)
62
Q

what form of phosphorous is transported in the body

A

most as organic but can be transported as inorganic form as well
- organic form found in phospholipids and lipoproteins

63
Q

storage of phosphorous

A

in all cells but mostly bone and muscle tissue

64
Q

functions of phosphorous in the body

A
  • structural role in bone, cell membranes, DNA, RNA
  • energy production and storage (ATP)
  • cell signalling and enzyme activity regulation (phosphorylation)
  • pH buffering
  • oxygen availablility (2,3-DPG binds to Hb and liberates oxygen for use in tissues)
65
Q

excretion of phosphorous

  • where?
  • as organic form or inorganic form?
A

in its inorganic form, in the urine

66
Q

phosphorous deficiency - is it common?

A

hypophosphatemia

- not common because is easy to obtain from diet, seen in near-starvation

67
Q

signs and symptoms of hypophosphatemia

A
  • anemia
  • muscle weakness
  • bone pain and softening of bones (rickets and osteomalacia)
  • peripheral neuropathy
  • severe hypophosphatemia may result in death
68
Q

who is at risk of hypophosphatemia? why?

A
  • alcohol abuse disorder
  • diabetics recovering from diabetic ketoacidosis (P required to buffer acids)
  • taking high amounts of antacids (calcium, magnesium and aluminum are the most common antacids and they bind P which prevents its absoprtion)
69
Q

what phosphorous toxicity called?

symptoms?

A

hyperphosphatemia

- can see calcification of non-skeletal tissues, commonly the kidneys

70
Q

who is affected by hyperphosphatemia?

A

end-stage renal disease

hypoparathyroidism

71
Q

who has increased risk of osteoporosis

A
  • the elderly
  • using certain medications: glucocorticoids, excess thyroid hormones, antiepileptics, aromatase inhibitors increase risk
  • decreased exposure to estrogen
  • sedentary lifestyle
  • high sodium intake
  • caffeine intake
  • chronic alcohol consumption
  • smoking
72
Q

distribution of potassium in the body

A

potassium is the primary intracellular cation

73
Q

sources of dietary potassium

A

richest sources are fruits and vegetables

74
Q

absorption of potassium

A

2 pathways:

  1. active transport via K+/H+ ATPase pump
  2. passive diffusion
75
Q

transport of potassium

A

Na+/K+ pumps maintain high intracellular potassium concentrations - pump out 3 sodium for 2 potassium

76
Q

potassium homeostasis and excretion

A

primarily excreted by the kidneys under control of aldosterone which is secreted in response to increased serum potassium

77
Q

functions of potassium in the body

A

maintain membrane potential

intracellular fluid balance

78
Q

what is potassium deficiency called

A

hypokalemia

79
Q

symptoms associated with hypokalemia

A
  • increased risk of developing hypertension and kidney stones
  • fatigue, muscle weakness, muscle cramps, muscle paralysis, cardiac arrtythmias
80
Q

who has increased risk of hypokalemia?

A
  • profound fluid losses (severe vomiting or diarrhea)
  • use of certain medications (loop and thiazide diuretics and corticosteriods) and licorice the herb
  • magnesium depletion
81
Q

clinical indications of potassium

A

hypertension - K+ helps to lower blood pressure

82
Q

cases where potassium toxicity is more likely

A
  • renal insufficiency, end stage renal disease
  • hypoaldosteronism
  • medications that cause potassium retention
  • a shift of intracellular potassium into circulation which may occur with the rupture of blood cells or tissue damage
83
Q

symptoms of hyperkalemia

A
  • peripheral neuropathy, muscle weakness, temporary paralysis
  • serious: cardiac arrhythmias
84
Q

nutrient interactions of potassium

A
  • calcium - potassium intake decreases with the excretion of calcium
  • magnesium - magnesium is a cofactor of the Na/K ATPase needed for uptake of K from ECF
  • sodium - high K intake increases Na excretion and prevents hypertensive effects of excess sodium
85
Q

distribution of sodium in the body

A

70% in the extracellular fluid (ECF)

30% on the surface of bone crystals

86
Q

dietary sources of sodium

A
  • primary source: added salt in the form NaCl
  • 75% from processed foods
  • 15% from added salt during preparation
  • 10% from water and vegetables, milk, eggs, and other naturally occurring sources
87
Q

what does the sodium/salt free label claim mean

A

<5mg of sodium per serving

88
Q

what does the low in sodium/salt label claim mean

A

<141mg of sodium per serving

89
Q

what does the reduced or lower in sodium label claim mean

A

at least 25% less sodium per serving

90
Q

what does the lightly salted label claim mean

A

at least 50% less added sodium that the sodium added to a similar food

91
Q

how is dietary sodium absorbed

A

3 pathways:

  1. Na/glucose co-transport system
  2. coupled Na/Cl system
  3. electrogenic Na absorption mechanism
92
Q

what is involved in the Na/glucose co-transport system

A

SGLT-1: sodium glucose linked transporter 1

carrier mediated active throughout the small intestine

93
Q

what happens in coupled Na/Cl system

A

exchanges Na/Cl for H/HCO3 because is electroneutral

active in small intestine and proximal colon

94
Q

what happens in the electrogenic Na absorption mechanism

A

concentration dependent sodium channel that operates principally in the colon

95
Q

transport of sodium in the body

A

Na+/K+ ATPase pump

  • pumps sodium out of the enterocytes across the basolateral membrane into the bloodstream
  • 3 sodium out for every 2 potassium in

once absorbed, Na+ is transported freely in the blood

96
Q

importance of the sodium/potassium ATPase pump

A

it maintains the sodium gradient required for the functioning of all 3 absorption mechanisms for sodium

97
Q

functions of sodium in the body

A
  • maintenance of membrane potential

- maintenance of blood volume and blood pressure

98
Q

how are sodium levels regulated in the body?

A

through:

  • the renin-angiotensin-aldosterone system
  • ADH/vasopressin
  • atrial natriuretic hormone (ANP)
99
Q

how does the renin-antiogensin-aldosterone system work?

A
  1. in response to a significant decrease in BP or BV, kidneys release renin into circulation which converts angiotensinogen -> angiotensin 1.
  2. ACE converts 1 into angiotensin 2 which stimulates arterioles to constrict resultin in increase BP
  3. angiotensin 2 stimulates aldosterone synthesis in adrenal glands
  4. aldosterone acts on kidneys to increase reabsorption of sodium and the excretion of potassium
100
Q

how does ADH work?

A

significant decrease in BP or BV causes ADH to be secreted and it acts on the kidneys to increase reabsorption of water

101
Q

how does ANP work?

A

ANP is secreted by heart muscle in response to high BV

it increases GFR to allow increased excretion of sodium and water

102
Q

what mainly controls excretion of excess sodium?

A

aldosterone - released in response to low sodium and promotes sodium retention

103
Q

hyponatremia

A

results in sodium deficiency

104
Q

causes of hyponatremia

A
  • inappropriate ADH secretion
  • severe vomiting or diarrhea
  • excessive prolonged sweating
  • use of some diuretics and certain kidney diseases
105
Q

symptoms of hyponatremia

A 
headache
N & V
muscle cramps
fatigue, weakness, and syncope
complications: cerebral edema, seizures, coma, acutely may be fatal
106
Q

clinical indications of sodium supplementation

A

electrolyte replenishment

107
Q

sodium toxicity

A

not really a thing, excessive intake leads to increased ECF volume but as long as water needs are met the person is okay

108
Q

is there a connection between sodium intake and hypertension?

A

yes, Na is thought to be causally connected to HTN

109
Q

sodium and nutrient interactions

A
  • potassium - high K increases urinary Na excretion and protects against hypertensive effects of Na
  • calcium - high sodium intake can increase urinary calcium excretion
110
Q

chloride distribution in the body

A

is most abundant in ECF

111
Q

sources of chloride

A

salt

some in eggs, fresh meat, seafood

112
Q

where is chloride absorbed?

A

almost completely in the small intestine and closely follows Na to maintain electrical neutrality

113
Q

methods of chloride absorption

A

3 pathways:

  • Na/glucose co-transport system using SGLT1
  • coupled Na/Cl system
  • electrogenic Na absorption mechanism
114
Q

functions of chloride in the body

A
  • gastric HCl production from parietal cells of the stomach

- exchange anion for HCO3- in RBCs (chloride shift)

115
Q

excretion of chloride in the body

  • where
  • how is it regulated?
A
  • primarily through kidneys
  • also excreted through skin in perspiration
  • regulated indirectly through Na regulation
116
Q

when does chloride deficiency occur?

A

does not happen under normal conditions but may happen from severe fluid loss (prolonged diarrhea or vomiting)

Clinical Nutrition 1 (2 decks)

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