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LSS Alimentary System > ions, vitamins and minerals lecture > Flashcards

ions, vitamins and minerals lecture Flashcards

1
Q

sequential molar concentrations (factor 10^-3)

A

molar, millimolar, micromolar, nanomolar, picomolar, femtomolar

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2
Q

define diffusion

A

process where atoms or molecules intermingle due to random thermal motion; fast over microscopic distances, slow over macroscopic differences

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3
Q

purpose of circulatory system in multicellular organisms

A

bring individual cells within diffusion range

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4
Q

function of cell membrane

A

act as diffusion barrier so cells can have different cytoplasmic concentrations vs. EC

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5
Q

water potential from low to high

A

hypotonic (swell), isotonic, hypertonic (shrink)

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6
Q

how do molecules cross epithelium to enter bloodstream

A

paracellular transport through tight junctions and lateral intercellular spaces; transcellular transport
through epithelial cells in apical membrane

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7
Q

2 types of transport proteins involved in faciliated diffusion or active transport

A

channel proteins (form aqueous pores - fast), carrier proteins (bind to solute and undergo conformational change - slow)

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8
Q

4 types of gated channel-mediated transport

A

voltage-gated, EC ligand-gated, IC ligand-gated, mechanically gated

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9
Q

3 types of carrier-mediated transport

A

uniport, symport (same direction), antiport (opposite direction - equalise charge); secondary active transport

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10
Q

define primary active transport

A

linked directly to cellular metabolism, using ATP to power transport

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11
Q

define secondary active transport

A

derives energy from concentration gradient of another substance that is actively transported

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12
Q

effect of facilitated diffusion on rate of substance flowing down concentration gradient

A

enhances, but tends to equilibrate substance across membrane

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13
Q

how is absorption of glucose and galactose achieved

A

secondary active transport, with SGLT-1 carrier protein on apical membrane, which can transport glucose against concentration gradient

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14
Q

how is absoprtion of fructose achieved

A

facilitated diffusion using GLUT-5 carrier protein on apical membrane, which is effective at low concentrations of fructose in lumen as tissue and plasma levels low

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15
Q

how does glucose exit basolateral membrane

A

facilitated diffusion through GLUT-2 carrier protein (high-capacity, low-affinity); glucose between plasma and enterocyte generally equilibrated as glucose moves out to blood

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16
Q

what requires specific absorption

A

water and ions, calcium, iron, vitamins (B12)

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17
Q

where is most water absorbed

A

jejunum in small intestine (small intestine: 8L, colon: 1.4L)

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18
Q

how are most ions slowly absorbed

A

passive diffusion

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19
Q

source of water

A

ingest, saliva, gastric secretions, bile, pancreas, intestinal

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20
Q

what drives standing gradient osmosis

A

Na+ (transported from lumen into enterocyte, which becomes more efficient down intestine)

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21
Q

Na+ absorption in proximal bowel

A

counter-transport in exchange for H+ (equilibrating charge)

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22
Q

Na+ absorption in jejunum

A

co-transport with amino acids and monosaccharides

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23
Q

Na+ absorption in ileum

A

co-transport with Cl- (equilibrating charge)

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24
Q

Na+ absorption in colon

A

restricted movement through ion channels

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25
Q

2 types of secondary active transport of Cl-

A

co-transported with Na+ in ileum or exchanged with HCO3- in colon (both equilibrate charge)

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26
Q

how is K+ absorbed

A

passive diffusion via paracellular pathways into small intestine, and leaks out between cells in colon

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27
Q

fate of IC Na+

A

active transport into lateral IC spaces by Na+K+-ATPase in lateral plasma membrane, changing electrochemical gradient

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28
Q

why are Cl- and HCO3- transported into IC space

A

electrical potential created by Na+ transport

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29
Q

effect of high ion concentration in IC spaces

A

fluid around cells becomes hypertonic (high water potential)

30
Q

effect of water on IC channels

A

distends, causing increase in hydrostatic pressure in cell; water also dragged into lateral intercellular spaces

31
Q

fate of ions and water

A

move across basement membrane of epithelium and carried away by capillaries

32
Q

where is Ca2+ absorbed

A

duodenum, ileum

33
Q

effect of Ca2+ deficient diet on gut’s ability to absorb

A

increases

34
Q

what stimulate absorption of Ca2+

A

vitamin D, parathyroid hormone

35
Q

Ca2+ concentration gradient

A

low IC (100nM), high EC (1-3mM), allowing passive movement

36
Q

how is Ca2+ carried across apical membrane

A

intestinal Ca2+-binding protein (IMcal) by facilitated diffusion, ion channel

37
Q

purpose of Ca2+ and implications

A

IC signalling molecule, so must transport it in while maintaining low IC concentrations (prevent signalling cascade)

38
Q

how is Ca2+ action as intracellular signal prevented

A

binds to calbindin in cytosol; dissociates when going to be pumped out

39
Q

how is Ca2+ pumped across basolateral membrane into blood (higher concentration gradient)

A

primary active transport: Ca2+ATPase (PMCA) - high affinity - don’t need much Ca2+, low capacity - slow, maintaining very low concentrations of Ca2+ IC; secondary active transport: Na+/Ca2+ exchanger - low affinity, high capacity, requiring large Ca2+ concentrations

40
Q

what is required for Ca2+ absorption

A

vitamin D (1,25-dihydroxy D3)

41
Q

deficiency of vitamin D

A

rickets, osteoporosis

42
Q

why is vitamin D taken up by enterocytes (3)

A

enhances Ca2+ transport through cytosol, increases calbindin levels, increases rate of extrusion across basolateral membrane by increasing level of Ca2+ATPase

43
Q

functions of iron

A

electron donor and acceptor, used in oxygen transport and oxidative phosphorylation

44
Q

iron toxicity

A

toxic in excess but no mechanism to actively excrete iron, so must be able to absorb quickly but able to limit absorption

45
Q

how is iron present in diet

A

inorganic (Fe3+ - ferric/Fe2+ - ferrous), part of haem group (Hb, Mb, cytochromes)

46
Q

what iron can be absorbed

A

Fe2+

47
Q

why can’t Fe3+ be absorbed

A

forms insoluble salts with OH-, PO4 3-, HCO3-

48
Q

what reduces Fe3+ to Fe2+

A

vitamin C

49
Q

features of haem absorption

A

more readily absorbed, so dietary haem highly bioavailable; absorbed intact into enterocyte, via heme carrier protein 1 (HCP-1 via receptor-mediated endocytosis), Fe2+ liberated by Heme oxygenase

50
Q

what catalyses reduction of Fe3+ to Fe2+ in duodenum

A

liberated by Heme oxygenase using duodenal cytochrome B

51
Q

how is Fe2+ transported into cytosol

A

via divalent metal transporter 1 (DMT-1) - H+ coupled co-transporter

52
Q

how does Fe2+ enter blood

A

binds to factors, carried to basolateral membrane, moves via ferroportin ion channel into blood

53
Q

what converts Fe2+ to Fe3+ for transport around body

A

hephaestin (copper-dependent ferroxidase)

54
Q

how does Fe3+ travel in blood

A

binds to apotransferrin and travels as transferrin

55
Q

effect of hecidin on ferroportin function

A

suppresses so decreases iron absoprtion as can’t pump out into blood

56
Q

how else does Fe3+ travel in blood

A

binds to apoferritin in cytosol to form ferritin micelle (Fe2+ oxidised and crystalises in protein shell) to trap Fe3+ in cell and make biologically inert

57
Q

number of iron ions in single ferritin molecule

A

<4000

58
Q

what happens in excess dietary iron consumption

A

produce more ferritin in cytosol to prevent it entering blood - stored as Fe3+

59
Q

fate of ferritin in enterocytes if too much iron

A

irreversibly binds to iron in epithelial cells, so both unavaliable for transport into plasma, so are lost in intestinal lumen and excreted in faeces when enterocytes sloughed off

60
Q

what are vitamins

A

organic compounds that cannot be manufactured by body but vital to metabolism

61
Q

how are fat soluble vitamins (A,D,E,K) transported to brush border

A

micelles, except K+ which is actively taken up

62
Q

what vitamins are there specific transport mechanisms for

A

vitamin C, folic acid, vitamin B1, vitamin B12

63
Q

how are other vitamins taken up

A

passive diffusion

64
Q

where is vitamin B12 stored

A

liver

65
Q

effect of impaired B12 absoprtion

A

folate deficiency causing retarded maturation of red blood cells, causing pernicious anaemia

66
Q

how is most B12 found in food

A

bound to proteins

67
Q

how is denaturation of B12 by HCl in stomach avoided

A

binds to R protein (haptocorrin) released in saliva and parietal cells (R protein digested in duodenum)

68
Q

what protein binds to vitamin B12 to prevent digestion in duodenum

A

binds to intrinsic factor (if no IF, no absorption of B12)

69
Q

fate of B12/IF complex

A

binds to cubilin receptor, taken up in distal ileum by receptor-mediated endocytosis

70
Q

where is B12/IF complex broken

A

mitochondria

71
Q

fate of B12 in enterocyte, bloodstream and liver

A

binds to protein transcobalamin II (TCII), crosses basolateral membrane, travels to liver, uptaken by binding to TCII receptors, undergo proteolysis to break down TCII

LSS Alimentary System (40 decks)

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