Small Intestine Digestion and Absorption of Lipids and other nutrients Flashcards

1
Q

fat soluble vitamines

A

A, D, E, K

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2
Q

Triglyceride subunits

A

glycerol and fatty acids…

phospholipids have the same subunits

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3
Q

non polar side of bile salts

A

emulsify the fats

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4
Q

polar side of the bile salts

A

promotes water solubility of the fat droplets

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5
Q

bile salts and phospholipids do what

A

convert large fat globules into smaller pieces with polar surfaces that inhibit reaggregation

increases surface area

now the lipases can gain access to degrade the TGs to monoglycerides and FAs which enter the absorptive cells by simple diffusion or aggregate to form loosely held micelles which readily break down

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6
Q

lingual and gastric lipase

A

resistant to pepsin

inactivated by pancreatic lipases in the SI

15% of fat digestion

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7
Q

CCK

A

secretion is stimulated by the entrance of fat into the duodenum

stimulates the flow of bile into the intestine (sphincter of Oddi relaxes)

also stimulates secretion of pancreatic lipases

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8
Q

glycerol ester hydrolase (pancreatic lipase)

A

operates only at the oil water interface of the TG droplet

surface emulsifiers (phospholipids and proteins) present at the surface inhibit its action

bile salt micelles also inhibit it

TG –> 2-monoglyceride _ fFAs

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9
Q

colipase

A

amphipatic protein secreted by pancreas

reverses the inhibition mechanism for pancreatic lipase by anchoring it to the lipid droplet

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10
Q

cholesterol ester hydrolase

A

active against a wide range of esters (pancreatic)

cholesterol ester –> cholesterol

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11
Q

phospholipase A2 (PLA 2)

A

active against glycerophospholipids (lecithin) to make lysophospholipids (lysolechitin)

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12
Q

micelles

A

3-10nm in diameter

formed by bile acdis with the products of fat digestion
- especially 2MG, FAs, cholesterol, and lysolechitin

surface is mostly covered in bile acids

interior = hydrophobic materials like ADEK, FAs, cholesterol

DO NOT contain TGs

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13
Q

critical micelle concentration

A

minimal concentration of bile acids needed for micelles to form

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14
Q

mixed micelles of bile acids and lipid digestion products

absorption

A

diffuse through the unstirred layer and among the microvilli

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15
Q

as digestion products are absorbed from free solution

A

more digestion products partition out of the micelles while its in the unstirred layer

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16
Q

how much of the brush border surface is available for lipid absorption

A

the whole surface

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17
Q

lipid resynthesis after absorption

A

occurs in the SER of the intestinal epithelial cells

then accumulate into chylomicrons –> exocytosis

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18
Q

chylomicrons fate

A

enter lacteals, leave the intestine in the lymph,

enter the thoracic duct

enter circulation left subclavian vein

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19
Q

chylomicron components

A

2MG, fFAs, TGs, LysoPL, PL, Chol, CholE

fat vitamins

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20
Q

rate limiting step for lipid absorption

A

micelle diffusion through the unstirred layer

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21
Q

pH of fluid immediately in contact with the brush border…why important

A

1 pH unti lower than the luminal fluid

helps protonate the FAs -COO- end

makes them more lipid soluble to cross the membrane

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22
Q

FAs, 2MG, chol, and lysolechitin absorption

A

diffuse across the apical membrane

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23
Q

cholesterol esterase

A

bound to luminal membrane

promotes uptake of cholesterol across the membrane

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24
Q

microvillus membrane FA binding protein (MVM-FABP)

A

specific protein that uses Na+ gradient to transport long chain FAs into the cell

25
Q

how much of cholesterol absorbed is pumped back into the lumen?

how?

A

50%

ABC transport protein (ATP binding cassette) present in the intestinal cell

26
Q

I-FABP & L-FABP

SCP1 & SCP2

A

fatty acid and sterol binding proteins within the cytosol

important to prevent formation of oil droplets in the cytosol and transport these products to the SER

27
Q

phospholipid resynthesis in cytosol

A

lysophospholipid + FA

in SER

28
Q

lipid droplets in the SER after resynthesis of lipids and some new synthesis of lipids

A

prechylomicrons

surface covered with phospholipids (polar groups out)

they are now transported to the Golgi

29
Q

chylomicron processing

A

in the golgi

60-750 nm

30
Q

where are bile salts reabsorbed

A

terminal ileum

cross via secondary active transport (co transported with Na+) and by simple diffusion

31
Q

water soluble vitamins absorbtion

A

diffusion or mediated transport

exception = B12 (very large charged molecule)

32
Q

vitamin C (ascorbic acid)

A

Ileum

active cotransport with Na+

essential for oxidation reactions

33
Q

folic acid

A

jejunum

facilitated diffusion

nucleic acid synthesis, promotes growth and maturation of RBCs

34
Q

vitamin B6 (pyridoxine)

A

jejunum

simple diffusion

acts as coenzyme in reactions of amino acid and protein metabolism

35
Q

vitamin B2 (riboflavin)

A

jejunum

facilitated diffusion

constituent of flavin nucleotide coenzymes

36
Q

vitamin B1 (thiamine)

A

jejunum

co transport with Na+

metabolism of carbs and some amino acids

37
Q

vitamin B12 (cobalamine)

A

ileum

receptor mediated endocytosis

essential for DNA synthesis; promotes growth and maturation of RBCs

38
Q

Niacin (nicotinamide)

A

jejunum

active transport

coenzyme in oxidation reactions

39
Q

any vitamin absorption in duodenum?

A

NO

40
Q

intrinsic factor

A

glycoprotein secreted by parietal cells in stomach

41
Q

vitamin B12 metabolsim

A
  1. released from ingested proteins by pepsin and acid
  2. rapidly bound by a gastric vitamin B12 binding protein (haptocorrin) –> higher affinity for B12 at acidic pH than intrinsic factor
  3. in SI, pancreatic proteases digest the binding proteins….then IF binds to it
  4. receptors in ileal mucosa for IF –> absorption
42
Q

Ca2+ absorption steps

A
  1. cross apical border via Ca2+ channel
  2. in cytosol –> binds to calbindin (CaBP)
  3. intracellular vesicles take up Ca2+ and transport it through the cytosol
  4. released across basolateral by exocytosis
    or. …
  5. Ca2+ bound to Calbindin diffusion out via Ca2+ ATPase or Na+/Ca2+ exchanger

**this is limited to the duodenum….everywhere else its paracellular diffusion

43
Q

vitamin D and Ca2+ absorption

A

facilitates active Ca2+ absorption

promotes formation of calbindin

also enhances all 3 pathways of Ca2+ pathways

44
Q

Ca2+ absorption in stomach

A

acidic environment solubulizes Ca2+ and its diffused into cells

45
Q

Ca2+ in duodunem (pH)

A

vitamin C (ascorbic acid) increases acidity of intestine –> enhances absorption

46
Q

calcium citrate (citric acid)

A

most effective absorption form of Ca2+

47
Q

conditions where iron complexes are most soluble

A

low pH

presence of vitamin C

48
Q

how heme form of iron crosses apical membrane

A

facilitated diffusion

then in cytosol….heme oxidase (heme –> Fe2+)

49
Q

how non heme Fe3+ crosses apical membrane

A

apical membrane iron reductase Fe3+ –> Fe2+ in lumen then…

co transported with H+ by a divalent cation transporter (DCT1) in the brush border membrane

50
Q

fate of Fe2+ in the cytosol

A

oxidized to Fe3+ and binds to ferritin

51
Q

how Fe3+ (bound to ferritin) crosses the basolateral membrane

A

IREG1 and hephaestin

52
Q

in the blood….Fe3+ binds to what

A

transferrin….cells that take up iron have receptors for transferrin

53
Q

iron bound to ferritin in lumen of intestine

A

cannot be absorbed and lost in feces

54
Q

iron basolateral receptors in crypt cells

A

receptors for transferrin-iron complex

55
Q

when blood levels are high Fe3+ binds

A

iron regulatory protein (IRP)

56
Q

when iron is deficient (anemia)

A

IRP increase the translation of mRNA encoding the iron transport proteins DCT1 and IREG1

57
Q

relative absorption sites for carbs, lipids, and proteins

A

most –> least

duodenum –> jejunum –> ileum

58
Q

relative absorption sites for Ca2+, iron, and folate

A

all three = duodenum

Ca2+ then has some in jejunum and ileum as well

59
Q

relative absorption sites for bile acids

A

little in duodenum

moderate in terminal jejunum

high in ileum

moderate in ascending colon