Macrominerals Flashcards
1
Q
name the macrominerals
A
calcium magnesium phosphorous potassium sodium chloride
2
Q
is the most abundant mineral in the body
A
calcium
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
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
5
Q
inhibitors of calcium absorption
A
oxalic acid
phytic acid
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
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
8
Q
is calcium found in the form of soluble salts or insoluble salts in food and supplements
A
relatively insoluble salts
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
10
Q
absorption of calcium
A
through 2 routes:
- duodenum and proximal jejenum (active)
- jejenum and ileum (passive)
11
Q
active transport of calcium is stimulated by:
A
calcitriol and low calcium diets
12
Q
passive transport of calcium is stimulated by:
A
high concentrations of calcium in intestinal lumen
FOS and inulin
13
Q
is calcium absorbed in the large intestine?
A
yes, in small amounts
- bacteria release Calcium bound to fermentable fibers
14
Q
factors the enhance calcium absorption
A
growth, pregnancy, lactation vitamin D protein simple sugars food in general
15
Q
factors that inhibit calcium absorption
A
oxalate/oxalic acid phytate/phytic acid fiber other divalent cations undigested fat
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
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
18
Q
regulation of calcium levels done by
A
PTH
calcitriol
calcitonin
19
Q
PTH and calcitriol in calcium regulation
A
low plasma calcium stimulates PTH secretion
calcitriol increases calcium absorption
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
21
Q
functions of calcium in the body
A
- bone mineralization
- nerve conduction
- muscle contraction
- coagulation
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
23
Q
calcium excretion
A
- mostly filtered and reabsorbed by kidneys
- mostly excreted through urine and feces, some through perspiration
24
Q
results of calcium deficiency
A
- hypocalcemia
- osteoporosis
25
hypocalcemia
- reasons/causes
- symptoms
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
26
Chvostek's sign
- a test for hypocalcemia
| - involves testing for muscle spasms by tapping on facial nerve
27
Trousseau's sign
- a test for hypocalcemia
| - looking at hand for muscle spasms
28
tests for hypocalcemia
Chvostek's sign
| Trousseau's sign
29
osteoporosis
| - cause?
low calcium intake results in failure to attain peak bone mass
30
kidney stons and calcium
- most kidney stones are composed of calcium oxalate but increased dietary calcium only slightly increases the urinary calcium levels
31
calcium toxicity conditions
| - what is it called and when does it occur
- 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
32
symptoms of hypercalcemia
- mild: loss of appetite, vomiting, constipation, abdominal pain, dry mouth, thirst, frequent urination
- severe: confusion, delirium, coma, even death if untreated
33
what increases risk for kidney stones?
- supplemental calcium taken on an empty stomach because there is no longer a beneficial effect of decreasing intestinal oxalate absorption
34
calcium interactions with nutrients
- 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
35
where is most of the magnesium found in the body?
> 60% is in the bones
25% is in muscle tissue
< 1% is in ECF
36
sources of magnesium
- nuts and seeds
- legumes, whole grains (oats, barley, brown rice)
- most vegetables - esp leafy greens, corn, carrots
- seafood, dairy
- coffee, tea, cocoa, chocolate
- molasses
37
location of absorption of magnesium
in small intestine - jejunum and ileum
| may be absorbed in colon, especially in diseases affecting the small intestine
38
pathways of magnesium absorption
2 pathways:
1. saturable active transport when intake is low, stimulated by calitriol
2. simple diffusion when intake is high
39
factors that enhance magnesium absorption
- calcitriol
| - simple sugars like lactose and fructose
40
factors that inhibit magnesium absorption
- phytate
- fiber
- excessive unabsorbed fatty acids
- other minerals (calcium, phosphorus)
41
methods of transport of magnesium through the body
50-55% in free ionized form
33% bound to protein (like albumin)
13% complexed with other ions
42
homeostasis regulation of magnesium
not well understood,
| but with calcium, PTH increases plasma concentrations of magnesium
43
how does PTH increase plasma concentrations of magnesium?
- increasing intestinal absorption by activating vit D
- decreasing renal excretion of Mg++
- enhancing its bone resorption
44
functions of magnesium in the body
- energy production (cofactor)
- structural role (bone crystal matrix)
- ion transport across cell membranes
- cell signalling
45
excretion of magnesium
- primarily through the urine but lots of magnesium is reabsorbed by the kidney
- also perspiration
46
conditions that increase risk of magnesium deficiency
- renal disorders (diabetes and long term use of diuretics)
- chronic alcohol abuse
- elderly people (have lower intestinal Mg++ absorption)
47
signs and symptoms of magnesium deficiency
- 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
clinical indications for magnesium
- hypertension (correlation between HTN and low Mg levels)
| - migraine headaches
49
what is different about magnesium sulfate
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
magnesium toxicity
- 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
hypermagnesemia
results in hypotension and later effects of magnesium toxicity: lethargy, confusion, cardiac arrhythmia, kidney dysfunction, all related to severe drop in BP
52
contraindications to magnesium supplementation
- 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
nutrient interactions of magnesium and why
- 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
where is phosphorous found in the body
as phosphates (PO4)
85% found in bone
14% in soft tissue
1% in blood and body fluids
55
sources of phosphorous
- dairy, meat, poultry, fish, eggs
- nuts, legumes, grains
- coffee, tea, soft drinks
56
bioavailability of phosphorous
- 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
is phosphorous absorbed in its organic or inorganic form
inorganic form
58
where is phosphorous absorbed in the body
small intestines, primarily duodenum and jejenum
59
processes of phosphorous absorption?
2 processes:
1. facilitated diffusion - primary route
2. saturable Na-dependent, carrier mediated transport stimulated by calcitriol and low phosphorous intake
60
factors that enhance phosphorous absorption
vitamin D
61
factors than inhibit phosphorous absorption
```
phytates
other minerals (Ca, Mg, Aluminum)
```
62
what form of phosphorous is transported in the body
most as organic but can be transported as inorganic form as well
- organic form found in phospholipids and lipoproteins
63
storage of phosphorous
in all cells but mostly bone and muscle tissue
64
functions of phosphorous in the body
- 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
excretion of phosphorous
- where?
- as organic form or inorganic form?
in its inorganic form, in the urine
66
phosphorous deficiency - is it common?
hypophosphatemia
| - not common because is easy to obtain from diet, seen in near-starvation
67
signs and symptoms of hypophosphatemia
- anemia
- muscle weakness
- bone pain and softening of bones (rickets and osteomalacia)
- peripheral neuropathy
- severe hypophosphatemia may result in death
68
who is at risk of hypophosphatemia? why?
- 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
what phosphorous toxicity called?
| symptoms?
hyperphosphatemia
| - can see calcification of non-skeletal tissues, commonly the kidneys
70
who is affected by hyperphosphatemia?
end-stage renal disease
| hypoparathyroidism
71
who has increased risk of osteoporosis
- 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
distribution of potassium in the body
potassium is the primary intracellular cation
73
sources of dietary potassium
richest sources are fruits and vegetables
74
absorption of potassium
2 pathways:
1. active transport via K+/H+ ATPase pump
2. passive diffusion
75
transport of potassium
Na+/K+ pumps maintain high intracellular potassium concentrations - pump out 3 sodium for 2 potassium
76
potassium homeostasis and excretion
primarily excreted by the kidneys under control of aldosterone which is secreted in response to increased serum potassium
77
functions of potassium in the body
maintain membrane potential
| intracellular fluid balance
78
what is potassium deficiency called
hypokalemia
79
symptoms associated with hypokalemia
- increased risk of developing hypertension and kidney stones
- fatigue, muscle weakness, muscle cramps, muscle paralysis, cardiac arrtythmias
80
who has increased risk of hypokalemia?
- profound fluid losses (severe vomiting or diarrhea)
- use of certain medications (loop and thiazide diuretics and corticosteriods) and licorice the herb
- magnesium depletion
81
clinical indications of potassium
hypertension - K+ helps to lower blood pressure
82
cases where potassium toxicity is more likely
- 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
symptoms of hyperkalemia
- peripheral neuropathy, muscle weakness, temporary paralysis
- serious: cardiac arrhythmias
84
nutrient interactions of potassium
- 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
distribution of sodium in the body
70% in the extracellular fluid (ECF)
| 30% on the surface of bone crystals
86
dietary sources of sodium
- 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
what does the sodium/salt free label claim mean
<5mg of sodium per serving
88
what does the low in sodium/salt label claim mean
<141mg of sodium per serving
89
what does the reduced or lower in sodium label claim mean
at least 25% less sodium per serving
90
what does the lightly salted label claim mean
at least 50% less added sodium that the sodium added to a similar food
91
how is dietary sodium absorbed
3 pathways:
1. Na/glucose co-transport system
2. coupled Na/Cl system
3. electrogenic Na absorption mechanism
92
what is involved in the Na/glucose co-transport system
SGLT-1: sodium glucose linked transporter 1
| carrier mediated active throughout the small intestine
93
what happens in coupled Na/Cl system
exchanges Na/Cl for H/HCO3 because is electroneutral
| active in small intestine and proximal colon
94
what happens in the electrogenic Na absorption mechanism
concentration dependent sodium channel that operates principally in the colon
95
transport of sodium in the body
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
importance of the sodium/potassium ATPase pump
it maintains the sodium gradient required for the functioning of all 3 absorption mechanisms for sodium
97
functions of sodium in the body
- maintenance of membrane potential
| - maintenance of blood volume and blood pressure
98
how are sodium levels regulated in the body?
through:
- the renin-angiotensin-aldosterone system
- ADH/vasopressin
- atrial natriuretic hormone (ANP)
99
how does the renin-antiogensin-aldosterone system work?
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
3. aldosterone acts on kidneys to increase reabsorption of sodium and the excretion of potassium
100
how does ADH work?
significant decrease in BP or BV causes ADH to be secreted and it acts on the kidneys to increase reabsorption of water
101
how does ANP work?
ANP is secreted by heart muscle in response to high BV
| it increases GFR to allow increased excretion of sodium and water
102
what mainly controls excretion of excess sodium?
aldosterone - released in response to low sodium and promotes sodium retention
103
hyponatremia
results in sodium deficiency
104
causes of hyponatremia
- inappropriate ADH secretion
- severe vomiting or diarrhea
- excessive prolonged sweating
- use of some diuretics and certain kidney diseases
105
symptoms of hyponatremia
```
headache
N & V
muscle cramps
fatigue, weakness, and syncope
complications: cerebral edema, seizures, coma, acutely may be fatal
```
106
clinical indications of sodium supplementation
electrolyte replenishment
107
sodium toxicity
not really a thing, excessive intake leads to increased ECF volume but as long as water needs are met the person is okay
108
is there a connection between sodium intake and hypertension?
yes, Na is thought to be causally connected to HTN
109
sodium and nutrient interactions
- potassium - high K increases urinary Na excretion and protects against hypertensive effects of Na
- calcium - high sodium intake can increase urinary calcium excretion
110
chloride distribution in the body
is most abundant in ECF
111
sources of chloride
salt
| some in eggs, fresh meat, seafood
112
where is chloride absorbed?
almost completely in the small intestine and closely follows Na to maintain electrical neutrality
113
methods of chloride absorption
3 pathways:
- Na/glucose co-transport system using SGLT1
- coupled Na/Cl system
- electrogenic Na absorption mechanism
114
functions of chloride in the body
- gastric HCl production from parietal cells of the stomach
| - exchange anion for HCO3- in RBCs (chloride shift)
115
excretion of chloride in the body
- where
- how is it regulated?
- primarily through kidneys
- also excreted through skin in perspiration
- regulated indirectly through Na regulation
116
when does chloride deficiency occur?
does not happen under normal conditions but may happen from severe fluid loss (prolonged diarrhea or vomiting)
