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GI II > HECKdigestion of lipids and vitamins > Flashcards

HECKdigestion of lipids and vitamins Flashcards

1
Q

absorptive cells are generally found where? what bout secretory

A

absorptive on surface on villi

secretive in crypts

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2
Q

what type of cells are in the colonic crypts

A

gland cells

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3
Q

majority of dietary lipids are what

A

triacylglycerols TAGs

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4
Q

what is the rest of the dietary lipids

A

phosphlipids from cell membranes and cholesterol (unesterified)

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5
Q

where is esterified cholesterol found

A

liver and blood foods

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6
Q

What lipids are found in bile

A

phsopholipids (lecithin) and unesterified cholesterol

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7
Q

what is the first process of digesting dietary lipids

A

emulsification (chewing, gastric churning, peristalsis, movement between pylorus and duodenum)
forming oil droplets in aqueous solution

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8
Q

As we emulsify food how does SA change

A

SA on the droplets increase as they get smaller

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9
Q

describe structure of oil droplets

A

monolayer at interface formed by dietary and secreted lipids. core of triglycerides, diacylglycerol

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10
Q

What is the process of digestion

A

lypolysis

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11
Q

what enzymes are part of lypolysis

A

lipases to hydrolyze lipids

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12
Q

describe gastric lipase

A

active at pH 4
resistant to Pepsin
inactivated by pancreatic proteases in bile salts in the SI

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13
Q

What happens to gastric lipase in someone with an pancreatic deficiency

A

extended activity of gastric lipase in duodenum

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14
Q

What is the action of gastric lipase

A

cleaves FA from TAGs

leaves one protanated FFA and one diacylglycerol

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15
Q

Describe pancreatic lipase

A

major lypolytic enzyme from pancreas

secreted into duodenum in huge excess

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16
Q

what is the secretion of pancreatic lipase dependent on

A 
Colipase
alkaline pH of SI
Ca
bile salts
Fatty acid substrate
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17
Q

What is the action of pancreatic lipase

A

at oil-water interface colipase is necessary to reduce inhibition from phospholipids or proteins on micelle surface
hydrolyze all TAGs resulting in 2 FFA and 1 monoacylglyerol

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18
Q

most dietary lipids are digested as what

A

triglycerides

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19
Q

What must triglycerides be degraded into before taken up

A

FFA and Monoacylglycerides

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20
Q

Why did Alli drug cause oily stool

A

inhibits pancreatic lipase, prevents breakdown into FFA and MAGs from TAGs

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21
Q

What is Phospholipase A2

A

pancreatic enzyme

needs bile salts and alkaline pH in SI

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22
Q

What is the action of phospholipase A2

A

cleaves FFA from glycerophospholipid (at SN2 position)

leaves lysophospholipd, no middle fatty acid

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23
Q

Where is phsopholipase A2 found

A

SI and large intestine from all bacteria

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24
Q

Describe Carboxylester hydrolase

A

not substrate specific, hydrolyzes all esters, releases free cholesterol and glycerol

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25
Q

What is the action of carboxyl ester hydrolase

A

equivalent to bile-salt stimulated milk lipase

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26
Q

what is the role of bile salt stimulated milk lipase

A

lipase in the milk that aids in digestion since pancreas is not yet functioning.
Not activated until reaches duodenum with basic pH

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27
Q

What is the action of bile salt stim milk lipase and carboxyl ester hydrolase

A

hydrolyzes DAGs, MAGs, TAGs

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28
Q

What stimulates CCK

A

release of FFA in duodenum

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29
Q

What is the action of CCK

A

stimulates bile flow in duodenum and secretion of pancreatic enzymes (lipase and esterase)

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30
Q

What does it mean with there are lipids in stools

A

intact acylglycerols rarely found even in severe malabsorption

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31
Q

What is the test for stool fat

A

Sudan III staining, a dye that shows presence of oil droplets

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32
Q

Why is there no fat generally found in stool

A

bacteria like to digest in colon

33
Q

Where are med chain FA absorbed

A

independent of micells or bile salts

can diffuse towards enterocytes- directly transferred to blood

34
Q

What can be used as FA subsititue for patients with malabsoprtion

A

medium chain fatty acids

35
Q

The larger acylglycerides are in what part of emulsion droplet

A

core

smaller on outside

36
Q

Describe an emulsion droplet with multi layers

A

multilamellar at the begining but during digestion the layers decrease until it is a micelle

37
Q

What is a micelle

A

lipid monolaryer with tails facing hydrophobic core

bigger SA with shorter distance for substrates to cross

38
Q

What is a unilamellar droplet

A

one lipid bilayer around droplet

39
Q

What are the surface components of a micelle

A

cholesterol, MAGs, lecithin’s(phosphotidylcholine), pancreatic lipases, bile salts, liquid crystalline layer of bile salts and surface components and Ca rich FA soaps

40
Q

What are in the core of micelles

A

DAGs, TAGs and cholesterol esters

41
Q

What happens when MAGs are hydrolyzed on surface by lipases

A

FFA released

42
Q

What replace the MAGs when hydrolyzed by lipases

A

replaced by DAGs and TAGs (originate from core

43
Q

Increased deposition of liquid crystalline layer of micelle causes what

A

budding of multilamellar vesicles from emulsion droplet

44
Q

Bile salts convert multilamellar vesicle to what

A

unilamellar

45
Q

do bile salts hinder or assit micelle formation

A

assist

46
Q

micelles have to cross what area to enter

A

the mucous layer

47
Q

What are the microclimates of the intestine that micelles cross

A

bulk water area(hydrolysis and micelle formation)
mucus gel layer (barrier for bacteria)
unstirred water layer (juxtaposed to cell membranes)

48
Q

What does the unstirred water layer allow

A

diffusion of short and medium chain FA monomers into enterocytes
larger chains must be formed into micelles

49
Q

What liberates the FA from micelles into enterocytes

A

protonated environment

50
Q

Do micelles diffuse across lipid membranes

A

no, the lipids leave and cross

51
Q

What maintains the H [ ] in the unstirred water layer

A

Na/H exchanger

52
Q

What allow lipids to cross lipid bilayer

A

diffusion

FA translocases and FA binding proteins to enhance translocation

53
Q

What happens to lipids in the enterocyte

A

re-esterification
long chain FA are assembled back into TAGs and phopholipids in the sER
rER to package into lipoprotein particles (apolipoproteins trafficked to sER and golgi)

54
Q

What occurs in the sER of enterocytes

A 
apolipoprpteins meat TAGs, phospholipids and choesterol esters
form chylomicrons (covered in lecithin and phospholipids)
and form VLDLs (carry endogenous lipids during both fed and fasting states)
55
Q

Where are lipoprotein particles trafficked

A

to golgi from sER
apolipoprotein A1 associates and glycoslyation occurs, vesicles carry chylomicrons and VLDLs from golgi trans to the basolaterl membrane and fuse to release contents

56
Q

Why do chylomicrons and VLDLs have to enetr lymph and not blood

A

too big to enter fenestrated capillaries, have to go thru cisterna chyli and thoracic duct to enter circualtion via subclavian v

57
Q

Where are water soluble vit absorbed and desribe characteristics

A

absorbed in SI
have specific carriers and or brush border and luminal enzymes for deconjugatoin and phosphorylation
many Na dependent
many utilize GPCR and cAMP

58
Q

Describe Fat soluble Vit

A

chemical structure is hydrophobic(dissolved in fat deposits not aquesous environment)
rely on lipid absorption because chemical structure

59
Q

What hapens to fat soluble Vit in enterocyte

A

diffuse to sER (specific carriers (retinol binding is for Vit A))
associate with lipid to form chylomicrons and VLDLs (same path then)

60
Q

What can cause fat soluble vit deficiency from malabsorption

A 
bariatric surgery
drugs that impair lipid hydrolysis
drugs that impair bile acids
impaired hepatobiliary system
unabsorbed fat substrates
61
Q

What is the Tx for fat soluble vit deficiencies

A

make a water-miscible form (can be absorbed by aqueous environment)

62
Q

What can a folate deficiency cause

A

neural tube defect in developing fetus

causes spina bifida and anencephaly

63
Q

What is the biochemical active form of folate and function

A

tetrahydrafolate

important in DNA synthesis because needed for thymine and purines

64
Q

What can result from tetrahydafolate or folate deficiency

A

megaloblastic anemia (RBC are large because uninhibited protein and RNA synthesis)

65
Q

What is the tx for a folate deficiency

A

medicinal form of pteroylmonoglutamate (PteGlu1)

66
Q

What is the food form of folate

A

polyglutamate (PteGlu7)

67
Q

What is on the surface of entercyte membrane for folate digestion

A

folate conjugase that removes glutamate one by one

68
Q

Where is folate transported into enterocyres

A

PteGlu1 carrier in SI

69
Q

Where is folate activated to THf

A

in the liver

70
Q

Where is Vit B12 synthesized (cobalamin)

A

microbes (in animal products so need to be supplemented in vegetarians)

71
Q

What is Vit b12 a coenzyme for

A

transfers methyl group to homocystein to make methionine

72
Q

What is methionine essential for

A

without it body uses intracellular stores of folate so can also then lead to megaloblastic anemia

73
Q

Describe absorption of vit B12

A

starts in stomach because released via pepsin and low pH, bound to haptocorrin in stomach
interacts with IF in SI, the HCO3 release stimulates release of haptocorrin and vit B12 so that IF can bind it

74
Q

How are Vit B12 absorbed into enterocytes

A

enterocyte has apical cobalamin-IF Receptor

75
Q

Once in the enterocyte what happens to Vit B12-IF

A

dissociate and then Vit B12 binds transcobalamin II to exit basolateral surface

76
Q

Hpw is Vit B12 taken to liver

A

hepatic ciruclation

77
Q

What happens to excess vit B12 once in liver

A

excreted in bile

78
Q

What can cause a vit B12 deficiency

A 
can occur from not eating meat
can occur from pernicious anemia which happen due to lack of parietal cells
bacteria can metabolize it
crohn disease
ileal reaction
79
Q

what can lead to lack of parietal cells

A

atrophy or Ab-mediated immune response agasint parietal cells or IF
no IF secretion
no absorption without IF

GI II (12 decks)

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