Nutrition: Minerals and Electrolytes Flashcards
1
Q
What is the estimated average requirement for a vitamin?
A
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
So it won’t be enough for 50%
2
Q
What is the recommended daily allowance?
A
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
this is how much you should advice people to take
3
Q
What is the tolerable upper limit
A
This is the conservative limit for the highest amount you can take - risk of overdose in about 0.1% of the population
4
Q
What are the 6 major minerals in order of abundance in the body?
A
caclium phosphorus potassium sodium, chloride magnesium
5
Q
What are the 4 trace elements in the body?
A
iron
zinc
copper
manganese
6
Q
What are the 5 main functions of minerals in the body?
A
osmotic balance maintaining charge/cocnentration gradients enzyme cofactors structure taste
7
Q
What’ sthe major extracellular cation? Intracellular?
A
extracellular = Na Intracellular = K
8
Q
Again, what is the most abundant metal ion in the body?
A
calcium
9
Q
Where is most of the calcium in the body?
A
bone
10
Q
What are the dietary sources?
A
dairy, seafood, turnip, broccoli, kale, dietary suppleemtns
11
Q
What are the 4 main functions of calcium?
A
bone mineralization
blood clotting
muscle contraction
metabolism regulation
12
Q
How is calcium absorbed? Two ways….
A
- saturable carrier mediated transport with TRPv6 transporter on the luminal membrane, calbindin chapterone in the cell and Ca2+/ATPase across the basolaterla membrane
- paracellular transport around tight junctions - past claudin under vitamin D influence
13
Q
What molecule regulates the saturable carrier-mediated transport of Ca?
A
calcitriol
14
Q
What are some substances that will increase Ca2+ absorption?
A
vitamin D
sugars, sugar alcohols
protein
15
Q
What are some substances that decrease Ca2+ absorption?
A
fiber
phytic, oxalic acids
other divalent cations like Mg2+ and Zn2+
unabsorbed fatty acids
16
Q
What are the three general forms in which calcium ccan be found in the blood?
A
~40% of Ca2+ is bound to protein, e.g. albumin
~50% is free ionized Ca2+
~10% is complexed with sulfate, phosphate, citrate, etc
17
Q
Is calcium higher in the intracellular or extracellular compartments?
A
cytosolic conentration is very low - extracellular concentration is 100000x higher!!!
18
Q
Where in the cell is calcium sequetsered?
A
mitochodnria and endoplasmic reticulum
19
Q
What are the two ways Ca2+ can be exported from the cell?
A
Ca2+/3Na exchanger (low affinity, high capacity)
Ca2+/2H exchanger (high affinity, low capacity)
20
Q
What molecule basically mediates all the effects of calcium?
A
Calmodulin - acts as a clacium sensor
21
Q
What are the 4 general things activated calmodulin will do?
A
activate calcineurin to inhibit Ca2+ channels
myosin light chain kinase for muscle contraction
calcium/calmodulin kinase to inhibit glycogen synthase (shut off glycogen production)
Phosphorylase kinase to phosphorylate glycogen phosphorylase (use glycogen)
22
Q
What are two other metals that calcium will block the uptake of?
A
phosphorus (high doses of Ca are used to treat hyperphosphatemia)
iron
23
Q
What can high levels of caclium do to bile salts? What does this mean in terms of cholesterol?
A
It can trap them in soaps that aren’t digestable
this means the bile salts aren’t reccycled
this means cholesterol needs to be diverted to bile acid synhthesis so you get a decrease in LDL
24
Q
How is calcium excreted?
A
Mostly in the urine
some in feces and sweat
25
What are some things that increase urinary excretion of calcium?
caffeine and high sodium
26
What two groups of patients are at risk for calcium deficiency?
fat malabsorption disorders
| immobilized patients due to bone calcium store depletion
27
What three things does calcium deficiency cause?
rickets (in relation to vitamin D)
tetany (intermittant muscle contractions)
ostoporosis
28
What are three chronic diseases associated with calcium deficiency?
colorectal cancer
HTN
Type II diabetes
29
What happens in acute calcium toxicity? Chronic toxicity?
acute = contripation and bloating
chronic= calcification of soft tissue, hypercalciuria and kidney stones, maybe worsens cardiovascular disease
30
How do you assess calcium status?
serum levels of Ca2+ are so tightly regulated that measuring serum levels doesn't tell you much
need to do bone scans
31
What is the second most common metal in the body?
magnesium
32
Where in the body is most magnesium located?
50-60% is in bone
| 40-50% is in soft tissues and only 1% is in the extracellular fluid
33
What are some foods with high magnesium?
anything rich
nuts, legumes, whole grains, chloorphyll, chololate and hard water
34
What transporter takes up magnesium from the lumen? Sautrable or unsaturable?
TRPM6 saturable
there is also non-saturable paracellular diffusion
35
What is the basolateral transport for Mg?
2Na/Mg2+ antiporter
energy for which comes from Na/K ATPase
36
Of the Mg in bone, how much is associated with phorphorous and calcium in a crystal lattice? Where is the rest?
70% is in the lattice
| 30% is in the amorphous form on the surface which is available for exchange with the serum to maintain Mg homeostasis
37
What is the biggest use for magnesium intracellularly?
over 90% of it is associated with ATP - it's essential for any kinase or polymerase that use nucleotide trophosphates
basically it helps the ATP switch between the alpha-beta form to the beta-gamma form which is necessary for any kinase or polymerase reaction
38
Magnesium is required for the activation of what other vitamin?
vitamin D
it's a cofactor for 25-hydosylase in the liver
39
What is the interaction between Mg and Ca+?
| WHat's the interaction between Mg and phosphorous?
Mg2+ competes with Ca2+ for resorption in the kidney: hypermagnesemia causes hypocalcemia
Mg2_ inhibits phosphorous absorption by forming Mg3(PO4)2 precipitate which can't be absorbed thorugh the gut, so hypermagnesemia causes hypophosphatemia
40
How do you assess Mg status?
serum is such a minor store that it's not helpful
erythrocyte Mg is not turned over as rapidly so it's a better measure
you can also check renal Mg excretion before and after a loading dose - this is the best measure
41
Dietary deficiency of Mg isn't describe, but what happens in experiment models?
nausea, vomiting, headache, anorexia, seizures, ataxia, fibrillation
42
What autosomal recessive mutation can lead to hypomagnesemia?
Gitelman syndrome
43
Ok, now descrive Gitelman syndrome?
It's an autosomal recessive mutation of SLC12A3, which is a thiazide-sensitive Na/Cl transporter
characterized by hypoMg, hypoK, and hypoCa
44
When does Mg toxicity usually occur?
with use of epsom salts (MgSO4)
45
What are the symptoms of Mg toxicity?
diarrhea, dehydration, flushing, slurred speech, muscle weakness, loss of deep tendon reflex
at higher concentrations you get cardiac arrest
46
Chloride is next....
Is chloride more prevalent in the intracellular or extracellular compartments?
88% in extracellular fluid
| 12% intracellular
47
What are the two methods of Cl absorption?
paracellularly or through an Na/Cl electorneutral transporter
48
What does Cl win the prize for in terms of GI cells?
It's the only anion Secreted by gastrointestinal cells
49
What's hte main function of Cl in the RBC?
It's in the chloride/bicarbonate exchanger....
bicarbonate is ht emain pH buffer
when bicarb is pulled into the RBC, Cl leaves to balance the charge. When bicarb is spit out, Cl is pulled in to balance the charge.
50
What is the function of Cl in immune cells
hypochlorous acid (bleach) is secreted by neutrophils during phagocytosis to neutralize pathogens
51
What is the funciton of Cl in some gastric mucosal cells?
parietal cells use it to make gastric hydrochlorid acid
52
Next is potassium....
| what foods have it?
fruit
leafy green veggies
milk
53
What are the two ways K is absorbed?
paracellular
| K/H ATPase on the luminal membrane with a K channel on the basolateral membrane
54
What is the main purpose of K?
it's the major intracellular cation so it functions to generate and maintain the electrical potential across cell membranes
55
What is another major function of K?
muscle contractility in all types of muscle
56
How is K excretion regulated?
Uptake isn't really regulated, so excretion needs to be
Vasopressin and aldosteron will increase urinary potassium excretion (opposite of wha thtey do to sodium)
57
What effect will potassium have on calcium excretion?
it will decrease it
| same reason is decreases excretion of sodium
58
What can case hypokalemia?
fluid loss
thiazide or loop diuretics
refeeding syndrome
59
What are the symptoms of hypokalemia?
```
cardiac arrhythmias
musclar weakness
hypercalciuria
glucose intolerance
mental disorientation
```
60
Moderate hypocalemia is associated with what two chronic diseases?
elevated blood rpessure
| osteoporosis (due to an increase in urinary Ca2_ excretion that occurs without the inhibition form K)
61
What can cause hyperkalemia? What's the main issue with it?
renal fialure can cause it
the issue it is can cause cardiac arrrythmias and even arrest
62
Next is phosphorous....
Where in the body is phosphrous?
85% in bone
1% in fluids
14% in soft tissue, esp. muscle
63
How do we get phosphorous in the diet?
meat, poultry, fish, eggs, dairy, cola
64
What are the three kinds of phosphorous in the diet?
inorganic (phosphates)
organic (associated with protein, sugar, lipids, nucleic acids)
phytic acid
65
THe saturable carrier mediated active transport is used when phosphorous intake is low. What activate sit?
calcitriol
66
Where in the GI tract can diffusion of Phosphate occur? What form?
the proximal duodenum because the lightly acidic environment puts phosphate in the H2PO4- form
67
What three metals will inhibit phosphorous absorption? What is the clinical significant here?
magnesium, aluminum and calcium
these are all in antacids - so can be used to treat hyperphosphatemia from kidney failure or can put you at risk for hypophasphatemia
68
What is the main use for phosphorous in the body?
bone mineralization
69
What type of bones is phosphorous important for?
any high-energy bond like nucleotides, DNA, RNA, cofactors, etc.
70
Where in the body is phosphorous an important acid bugger?
the kidney
71
How is phosphorous related to the availability of oxygen?
2,3-BPG
72
Excretion of phosphorous is promoted by what molecules/condtions?
elevated dietary phosphorous (duh)
PTH
acidosis
phosphotonins like FGF-23 from osteoblasts and osteoclasts
73
Excretion of phosphorous is inhibited by what?
```
low dieatyr phosphorous
calcitriol
alkalosis
estrogen
thyroid homrone
growth hormone
```
74
What are the three inherited disorders that can reuslt in phosphorous deficiency?
Dents disease
X-linked hypophatemic rickets
autosomal dominant hypophasphatemic rickets
75
What is Dent's disease a mutation in?
an x-linked mutation in a renal chloride channels
76
What are the hypophosphatemic rickets mutations in?
either the gene or modulation of FGF-23 (which promotes excretion)
77
What are the symptoms of phosphorous deficiency?
anorexia, reduced cardiac output (kills you), decreased diaphragmatic contractility, myopathy death
78
WHat foods have iron in it?
meat, fish, pultry (half heme-iron, half non-heme iron)
| nuts, fruits, vggies, grains (mostly non-heme)
79
What are the two charged forms of Fe in the body?
ferrous irons = Fe2+
| ferric iron = Fe3+
80
Does the gut lumen have more ferric or ferrous iron?
More ferric - Fe3+
this is an issue because Fe3+ can't be taken up by the epithelial cells
81
How does the gut convert Fe2+ to Fe3+ so it can be taken up? What transporter?
THere is a reductase at the brush border that will convert it to Fe2+w hich is then transported throuhg the divalent metal transporter 1 (DMT1)
82
What molecule holds Fe when it's in the cell?
ferritin
it ferrits it away
83
What transporter will transporter Fe from the cell to the blood?
ferroportin
84
To be carried in the blood, Fe needs to be in what form? What puts it that way?
Fe3+ - haphaestin or ceruloplasmin oxidizes it
85
Whatadditional metal is required by ceruloplasmin to oxidize Fe2+ to Fe3+ to be carried int he blood?
copper
86
After iron is in the Fe3+ form in the bloood, what's the carrier protein?
transferritin
87
What's the primary storage site for iron in the body?
the liver - as hemosiderin
88
Regulation of iron uptake is thorugh what molecule? From what?
hepcidin from the liver
when iron stores in the liver are high it will make hepsidin which will bind to ferroportin to cause it's degradation
this means the GI epithelialc ells won't be able to spit it out into the blood
89
What is the main use for iron?
heme synthesis
90
What vitamin will enhance abosprtion of iron and maintain it in the reduced state?
vitamin C
91
Iron will inhibit the abosprion of what other metal?
zinc
92
Iron deficiency is observed in wha tgroups of patients?
infants
adolescents
pregnant women
absorption disorders
93
What are the symptoms o firon deficiency?
microcytic hypochromic anemia, listelessness and fatige
94
What is the issue with iron toxicity?
it can form free radicals via the fenton reaction and increased oxidative stress
95
What disorder is caused by an inherited mutation in hepcidin such that you constantly absorb iron and store is in the liver and elsewhere?
hemochromatosis
96
Copper next....What foods have it?
meat, shellfish and nuts
97
How is coper uptake similar to Fe uptake in the gut?
a brush border reductase needs to reduce Cu2+ to Cu+ in order for it to be brought in by CTR1
98
Cu+ enters the blood through what basolateral transporter?
ATP7A
then circulates bound to albumin
99
What syndrome arises from a mutation of the ATP7A tasolateral transporter?
Menke's kinky hair syndrome - it's a copper deficiency
100
What are the symptoms of menke's kinky hair syndrome?
hypothermia, hypotonia, poor feeding, failure to thrive and seizures
the patients have normal hair at birth but it become sbrittle and sparse as they age because hair follicles require copper
101
What are the three main uses for copper in the body?
cofactor for ceruloplasmin for iron transport in the blood
cytochrome C oxidase
cofactor for lysyl oxidase for collagen synthesis (also requires vitamin C)
102
What antioxidant enzyme require copper as a cofactor?
superoxide dismutase
103
Why is copper necessary fot NT synthesis?
it's a cofactor for dopamine beta-hdyroxylase required for catecholamine synthesis
104
Who gets copper deficiency?
people who consume a lot of zinc (fight for absorption)
take a lot of proton pump inhibitors
105
WHat are the symptoms of copper deficiency?
anemia, leukopenia, hypopigmentation of skin and hair, altered cholesterol metabolism
106
What disease is caused by a mutation in the liver specific copper transporter ATP7B?
Wilson disease - you get copper toxicity
107
What symptoms are asociated with copper toxicity?
epigastric pain, nausea, vomiting, diarrhea, hematuria, liver damage, kidney damage,
108
What does ATP7B do normally?
transports excess copper into the bile for excretion
if it's defective, the copper will accumulate and leak out unbound to ceruloplasmin and ubild up
109
What are the treamtnes for wilson's disease?
avoid high copper foods and chelation
110
What happens in the eyes in wilson disease?
Kayser-Fleischer ring - a ring of copper around the iris
