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GI- Week 3 > Skildum: Electrolytes > Flashcards

Skildum: Electrolytes Flashcards

1
Q

What is EAR?

A

Estimated Average Requirement. 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.

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2
Q

What is RDA?

A

Recommended Daily Allowance. 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

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3
Q

What are the major minerals in the body?

A 
Ca
phosphorus
K
Na, Cl
Mg
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4
Q

What are the major trace elements in the body?

A

Iron
Zinc
Copper
Manganese

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5
Q

What are the ultratrace elements in the body?

A

Selenium
Molybdenum
Iodine
Chromium

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6
Q

Molybdenum

A

four human enzymes require it sulfite oxidase, xanthine oxidoreductase, aldehyde oxidase, and mitochondrial amidoxime reductase

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7
Q

Chromium

A

Role in insulin sensitivity, binds chromodulin, an insulin receptor binding protein

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8
Q

Selenium

A

Role in antioxidant proteins; de-iodinases in the thyroid: Selenocysteine

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9
Q

Iodine

A

thyroid hormone

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10
Q

What is the major extracellular cation?

A

Na

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11
Q

What is the major intracellular cation?

A

K

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12
Q

What is hte most abundant metal ion in the body?

A

Ca (mostly in bone)

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13
Q

What are the dietary sources of Ca?

A 
dairy
seafood
turnip
broccoli
kale
supplements
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14
Q

What are the fxns of Ca?

A

bone mineralization
blood clotting
muscle contraction
metabolism regulator

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15
Q

How is Ca absorbed?

A
  1. Saturable carrier mediated transport (TRPV6 transports Ca across the brush border membrane> calbindin chaperones Ca in the cell> Ca/ATPase transports Ca across the basolateral membrane)
  2. Pericellular transport around tight jxns (claudin)
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16
Q

What regulates Ca absorption?

A

calcitrol

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17
Q

What increases Ca absorption?

A

Vit D
sugars; sugar alcohols
protein

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18
Q

what decreases Ca absorption?

A

fiber
phytic, oxalic acids
divalent cations (Mg, Zn)
unabsorbed fatty acids

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19
Q

How much Ca is in the blood?

A

8.5-10 mg/dL

40% bound to protein (albumin)
50% free ionized Ca
10% complexed w/ sulfate, phosphate, citrate

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20
Q

What is the cytosolic conc of Ca in cells?

A

LOW 100nmol

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21
Q

How does the extracellular conc of Ca differ from the intracellular?

A

10,000x higher (2.3 mmol)

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22
Q

Where is Ca stored?

A

intracellular compartments (mitochondria, ER)

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23
Q

How is Ca exported from cells?

A

Ca/2Na exchanger- low affinity, high capacity transporter

Ca/2H exchanger is a high affinity, low capacity transporter

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24
Q

What is is the affect of the Ca -calmodulin complex?

A

Stimulates:

  1. Calcineurin> inhibits Ca channels
  2. MLCK> muscle contraction
  3. Ca/calmodulin kinase> inhibits glycogen synthase
  4. phosphorylase kinase> phosphorylase
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25
Q

What happens to glycogen synthase and glycogen phosphorylase when intracelluar Ca increases?

A

Glycogen synthase> inactivated

glycogen phosphorylase> activated

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26
Q

How does Ca affect phosphorus uptake?

A

blocks it

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27
Q

How do you treat hyperphosphatemia secondary to kidney failure?

A

high doses of Ca

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28
Q

How does Ca affect Fe uptake?

A

transiently blocks it

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29
Q

Ca can trap fatty acids and bile salts in soaps that are not digestable. This can cause…

A
  1. bile salts not recycled
  2. cholesterol diverted to bile acid synthesis
  3. LDL decreases
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30
Q

What does hydroxylation at the #12 carbon do when Ca is present?

A

Re-uptake tag

Chenodeoxycholate in bile decreaes and the ratio of deoxycholate to lithocholate in feces decreases

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31
Q

What much Ca is excreted daily?

A

100-240 mg/day urinary

45-100 feces

60 sweat

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32
Q

What controls resorption of Ca in the proximal tubule?

A

calcitrol

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33
Q

How does caffeine affect urinary excretion of Ca?

A

increases it

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34
Q

How does a high Na content affect Ca?

A

inhibits Ca reuptake and increases excretion

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35
Q

How is at risk for Ca deficiency?

A

fat malabsorption disorders

imobilized patients

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36
Q

What causes Ca def?

A

rickets
tetany
osteoporosis

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37
Q

What is Ca def associated wtih?

A

colorectal cancer
HTN
Type II diabetes

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38
Q

What is the TUL for Ca?

A

2,500 mg/day

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39
Q

What are clinical signs of acute Ca toxicity?

A

constipation and bloating

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40
Q

What are clinical signs of chronic Ca toxicity?

A

hypercalcemia that can cause calcification of soft tissue that can lead to hypercalciuria and kidney stones

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41
Q

How do you assess Ca status?

A

Tightly regulated–bone density scan is most useful

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42
Q

Where is most Mg in the body stored?

A

bone

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43
Q

What food are rich in Mg?

A

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

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44
Q

How is Mg transported across the brush border?

A
  1. Saturable transport (TRPM6)>

basolateral transport (2Na/Mg antiporter and 2K/3Na/ATPase)

  1. Non-saturable paracellular diffusion through tight junctions
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45
Q

In the bone, where is Mg located?

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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46
Q

Intracellularly, what percent of Mg is associated w/ ATP?

A

> 90%

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47
Q

What is Mg essential for?

A

kinases and polymerases that use NTPs

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48
Q

Activation of vitamin D requires what cofactor?

A

25-hydroxylase requires Mg to make circulating vitamin D

49
Q

What are the three things that Mg can interact with?

A
  1. Vitamin D
  2. Compete w/ Ca for resorption in the kidney
  3. Inhibit phosphorus absorption by forming a Mg (PO4) precipitate
50
Q

How do you assess Mg levels?

A
  1. Renal Mg excretion before and after a loading dose is best!
  2. Erythrocyte Mg
51
Q

Mg def rarely occurs but can be experimentally induced. What are the sxs of Mg def?

A

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

52
Q

Chronic Mg def is associated with what conditions?

A

Type II diabetes

HTN

53
Q

What is Gitelman syndrome?

A

Autosomal recessive

Mut in SLC12A3–> thiazide sensitivie Na/Cl transporter

54
Q

What is gitelman syndrome characterized by?

A

hypomagnesemia
hypokalemia
hypocalciuria

55
Q

Mg toxicity is usually associated with…

A

epsom salts

56
Q

What are the sxs of Mg toxicity?

A

diarrhea, dehydration, flushing, slurred speech, muscle weakness, loss of deep tendon reflex.

High concentrations can cause CARDIAC ARREST

57
Q

Is most Cl intracellular or extracellular?

A

extracellular

58
Q

How is Cl absorbed?

A

paracellularly or through a Na/Cl electroneutral transporter

59
Q

What is teh only anion secreted by GI cells?

A

Cl

60
Q

What is the fxn of Cl when cells deliver O2 to tissues?

A

Cl ENTERS RBC in exchange for bicarb

61
Q

What is the fxn of Cl when cells take oxygen from the lugns?

A

Cl LEAVES RBC in exchange for bicarb

62
Q

How do neutrophils use Cl?

A

Neutrophils combine Cl w/ ROS to make hypochlorous acid that is secreted during phagocytosis to neutralize pathogens.

63
Q

Parietal sells secrete…

A

hydrochloric acid

64
Q

Where does K come from in the diet?

A

fruit, leafy green veggies, milk

65
Q

How is K absorbed?

A

paracellular diffusion
K/H ATPase

basolateral K channel

66
Q

What is the major intracellular cation?

A

K (maintains electrical potential across cell membranes)

67
Q

How is K accumulated w/in cells?

A

Na/K ATPase consumes energy to accumulate K which is then released through channels resulting in a positive charge.

68
Q

What is the major fxn of K?

A

muscle contractility (smth, skieletal, cardiac)

69
Q

What increases urinary K excretion?

A

vasopressin and aldosterone

70
Q

What does K do to Ca excretion?

A

Decreases it

Na INCREASES Ca excretion

71
Q

What causes hypokalemia?

A

fluid loss, thiazide or loop diuretics, refeeding syndrome

72
Q

What are the sxs of K def?

A

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

73
Q

Moderate K def is associated with…

A

elevated blood pressure

decreased bone density (increased urinary Ca++ excretion)

74
Q

Hyperkalemia caused by renal failure can cause…

A

cardiac arrythmia/arrest

75
Q

Where is most phosphorus in the body stored?

A

bone

76
Q

Where do we get phosphorus in the diet?

A 
meat
poultry
fish
eggs
dairy
cola
77
Q

How does phosphorus cross the brush border?

A
  1. Saturable carrier mediated active transport when phosphate intake is LOW. Activated by calcitrol.
  2. Diffusion in the proximal duodenum (slightly acidic)
78
Q

What inhibits phosphorus absorption?

A

Mg
Aluminum
Ca

79
Q

What is used to treat hyperphosphatemia?

A

antacids (mg, Al, Ca)

80
Q

What are the functions of phosphorus?

A
  1. bone mineralization–amorphous and crystalline
  2. molecules w/ high E bonds–nucleotides, RNA, DNA, proteins, phospholipids, vitamins
  3. Acid base balance–impt buffer in the kidney
  4. Availability of O2–helps Hb deliver O2 under low O2 conc
81
Q

What is hte difference between calcitonin and calcitrol?

A

calcitonin–phosphorus deposition in bone

calcitriol–phosphorus desorption in bone

82
Q

How is phosphorus regulated?

A

through renal clearance

83
Q

What promotes the excretion of phosphorus?

A

elevated dietary phosphorous
parathyroid hormone (PTH) (calcitonin acts in oppos. To this)
acidosis
phosphotonins (e.g. FGF-23; secreted by osteoblasts and osteocytes)

84
Q

What inhibits the excretion of phosphorus?

A 
low dietary phosphorous
calcitriol
alkalosis
estrogen
thyroid hormone
growth hormone
85
Q

What can cause phosphorus def?

A
  1. extereme use of antacids
  2. malnourishment
  3. refeeding syndrome
  4. inherited disorders
86
Q

What inherited disorders are associated w/ phosphorus def?

A

dents
x-linked hypophosphatemic rickets
autosomal dominant hypophosphatemic rickets

87
Q

What is dents disease?

A

X-linked, mutation in renal chloride channel (interferes w/ P clearance in the kidney)

88
Q

What is X linked hyphosphatemic rickets?

A

Mutation in PHEX gene causes elevated FGF-23

89
Q

What is autosomal dominant hypophosphatemic rickets?

A

Mutation in the gene encoding FGF-23, prevents its degradation. (FRF-23 is a phosphatonin that promotes phosphorous excretion)

90
Q

What are sxs of phosphorus def?

A

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

91
Q

How do we get Fe in the diet?

A

half heme, half non heme–meat, fish, poultry

non heme–nuts, fruits, vegetables, grains

92
Q

How is Fe absorbed?

A

at the brush border of an enterocyte, REDUCTASE reduces ferric iron to ferrous iron>
ferrous iron is transported through DMT1>
Fe is stored as FERRITIN>
Ferrous iron is then transported out of the cell through FPN>
HEPHAESTIN uses COPPER to oxidize ferrous iron to ferric iron>
Ferric iron binds TRANSFERRITIN for transport to tissues

93
Q

Where is Fe primarily stored?

A

in the liver as hemosiderin that can be liberated when Fe is low.

94
Q

What regulates Fe upatake?

A

When Fe stores in the liver are high (increased hemosiderin)>
liver produces HEPCIDIN>
binds ferroportin (FPN)>
causes its degradation

95
Q

What are the fxns of Fe?

A
  1. heme synthesis
  2. Iron-sulfur clusters (electron transfer groups)
  3. Non-heme iron (dioxygenase)
96
Q

How does Vit C affect Fe?

A

Vit C maintains Fe in the REDUCED state

97
Q

What is required for export of Fe from enterocytes?

A

Cu

98
Q

What inhibits Zinc absorption?

A

Fe

99
Q

Fe def is commonly observed in what populations?

A

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

100
Q

What are sxs of Fe def?

A

Microcytic hypochromic anemia, listlessness, fatigue

101
Q

What happens if Fe intake exceeds the livers ferritin storage capacity?

A

it can accumulate in tissues and act as free radical causing oxidative damage

102
Q

What is chronic hemochromotosis?

A

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

103
Q

Where is Cu found in the diet?

A

meat
shellfish
nuts

104
Q

How is Cu absorbed in the enterocyte at the brush border?

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

105
Q

What causes Menkes Kinky hair syndrome?

A

Mut in ATP7A

106
Q

Hypothermia, hypotonia, poor feeding, FTT and seizures is characteristic of…

A

menkes kinky hair syndrome

*pts have normal hair at birth but it becomes brittle and sparse as they age b/c Cu requiring enzymes in hair follicles

107
Q

What are the functions of Cu?

A
  1. Cofactor for Ceruloplasmin
  2. Cytochrome C oxidase
  3. Cofactor for lysyl oxidase (collagen synthesis)
108
Q

How does Cu fxn in antioxidant defense?

A

Cofactor for superoxide dismutase (an antioxidant enzyme)

109
Q

How does Cu fxn in NT synthesis?

A

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

110
Q

What are the fxns of Fe?

A
  1. Heme for Hb and ETC complexes

2. Fe-S centers for ETC complexes

111
Q

What are the functions of Cu?

A 
Superoxide dismutase
Cytochrome C oxidase
Ceruloplasmin (a.k.a. hephaestin)
Oxidizes iron for transport in blood
Dopamine b-hydroxylase
112
Q

Cu def commonly occurs in…

A

people who consume a lot of zinc or take PPI

113
Q

A pt presents w/ anemia, leukopenia, hypopigmentation of skin & hair, altered cholesterol metabolism. What do they have?

A

Cu def

114
Q

What sxs are associated with actue Cu toxicity?

A

epigastric pain, N/V, diarrhea

115
Q

What sxs are associated with chronic Cu toxicity?

A

hematuria, liver damage, kidney damage

116
Q

What causes Wilson disease?

A

mut in the liver specific Cu transporter ATP7B–> accumulation of Cu in the liver–> toxic

117
Q

What is the role of ATP7B and what happens when its defective?

A

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

118
Q

How do you tx Wilson disease?

A

avoid high CU foods, chelation therapy

119
Q

What might be seen on physical exam of a pt with wilson disease?

A

kayser fleisher ring

GI- Week 3 (15 decks)

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