Digestions of Lipids and Vitamins Flashcards

1
Q

small intestine

A

villi absorptive

crypts secretory

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2
Q

large intestine

A

surface epithelium absorptive
colonic crypts secretory
columnar epithelium cells

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3
Q

progentior cells

A

in small and large intestine
-high turnover

decreased when starving
increased when eating

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4
Q

secretion

A

within crypts

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5
Q

absorption

A

tops of villi

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6
Q

dietary lipid distribution

A

TAGs 90%
phospholipids 5% (cell membranes)
unesterified cholesterol 0.5%

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7
Q

phosphatidylcholine

A

lecithin

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8
Q

bile

A

secreted lipid

-unesterified cholesterol and lecithin

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9
Q

secreted lipids

A

bile and sloughed membrane lipids

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10
Q

emulsification

A

formation of oil droplets in aqueous solution

chewing, churning, peristalsis, etc. all decrease droplet size and increase overall surface area

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11
Q

droplet organization

A

surface - secreted sources

-center - dietary lipids (TAGs, DAGs, cholesterol)

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12
Q

gastric lipase

A

stable pH 4
pepsin resistant
inactivated by pancreatic protease in bile salts

pancreatic deficiency - gastric lipase activity

cleaves fatty acid from TAG
-one FFA and one DAG** (center of droplet)

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13
Q

medium and short chain FA

A

can move through enterocyte membrane

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14
Q

pancreatic lipase

A

major enzyme

  • dependent on colipase, Ca, bile salts
  • active at alkaline pH

liberates 2 FFAs and one MAG**

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15
Q

alli (orlistat)

xenical

A

inhibits pancreatic lipase

-prevents TAGs from being digested

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16
Q

phospholipase A2

A
from pancreas
requires bile salts
active at alkaline pH
cleaves FFA from glycerophosholipids (SN2)
leaves MAG
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17
Q

carboxyl ester hydrolase

A

not substrate specific
hydrolyzes ester linkage

release free cholesterol and glycerol

same action as - bile salt stimulated milk lipase
-infant no pancreatic lipase - in human milk

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18
Q

CCK

A

released with free FAs in duodenum

-stimulates bile flow and pancreatic secretion

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19
Q

sudan III testing

A

chemical test for fat in stool

lipid rarely found in stool (bacterial digestion colon)

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20
Q

in case of malabsorption

A

use short and medium chain FAs orally

-bc they can pass enterocyte cell membrane

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21
Q

multilamellar

A

multiple lipid bilayers

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22
Q

unilamellar

A

one lipid bilayer

23
Q

micelle

A

lipid monolayer with tails facing hydrophobic core

24
Q

micelle structure

A

surface - cholesterol, MAGs, lecithins
bile salts on surface with pancreatic lipase

core - DAG, TAG, esterified cholesterol

25
Q

digestion at micelle

A

MAG digested on surface

DAG and TAG move to surface and are digested

26
Q

bulk water phase

A

micelle formation and hydrolysis of lipids

27
Q

mucous gel layer

A

lines epithelial surface
-created by mucin

barrier to diffusion

28
Q

unstirred water layer

A

next to cell membrane
-protonated environment (Na/H pump)

diffusion of short and medium chain FAs
-large FA back to micelles

29
Q

enterocyte apical membrane

A

micelle doesn’t diffuse

-long chain FAs - fatty acid translocase

30
Q

fatty acid translocase

A

for long chain fatty acid at enterocyte membrane

31
Q

lipid inside enterocyte

A

re-esterification at smooth ER

apolipoprotein from rough ER shuttled to SER or golgi

chylomicrons (dietary) VLDL (endogenous) form from apolipoproteins and lipids

32
Q

VLDL and chylomicrons from SER

A

to golgi cis face
-associate with apolipoprotein A1 (in golgi**)

vesicles carry from trans face to basolateral membrane

33
Q

secreted VLDL and chylomicrons

A

too large to pass through fenestrae

through lymph capillaries to cisterna chyli

34
Q

glycerol, short chain, and medium chain FAs?

A

pass through enterocyte and enter blood capillary

long chain - cannot pass through

35
Q

fat soluble vitamins

A

rely on lipid absorption
-to SER, to lymph

A, D, E, K

36
Q

malabsorption of lipids

A

fat soluble vitamin deficiency

bariatric surgery, drugs

treatment - water-miscible emulsion

37
Q

folate deficiency

A

neural tube defects
-spina bifida and anencephaly

natal vitamins with folic acid

38
Q

THF

A

bio active folate

  • functions of cofactor
  • important in DNA synthesis (thymine and purine)
39
Q

megaloblastic amenia

A

folate deficiency
-RBCs don’t divide, but become large

treatment PteGlu1

40
Q

food form of folate

A

poly glutamate - PteGlu7

converted to PteGlu1 and transported into enterocytes

41
Q

folate conjugase

A

PteGlu7 > PteGlu1

42
Q

liver and folate

A

PteGlu1 > THF

43
Q

Vit B12

A

cobalamin

  • synthesized by microbes
  • vegetarians at risk

coenzyme for homocysteine > methionine

44
Q

methionine

A

essental AA

needs Vitamin B12

45
Q

methionine deficiency

A

uses folate

-causes folate deficiency (megaloblastic amenia)

46
Q

absorption of Vitamin B12

A

released from protein in stomach
-binds haptocorrin

bicarbonate releases haptocorrin in small intestine
-Vit B12 then binds intrinsic factor

in enterocyte - Vit B12 IF disocciate and bind transcoblamin II

taken to liver (excess secreted in bile - can be taken up again)

47
Q

intrinsic factor

A

secreted in stomach

48
Q

transcobalamin II

A

binds Vit B12 in enterocyte

49
Q

pernicious anemia

A

lack of parietal cells - no IF secretion
-no B12 absorption

swollen tongue, and neuropathy

Ab-mediated immune response or H. pylori infection may cause this to occur

50
Q

Vit B12 deficiency

A

ileal resection

crohns disease

51
Q

water soluble vitamins

A

folate and B12

52
Q

Tx of pernicious anemia

A

IM injection of hydroxycobalamin

53
Q

shilling test

A

for IF deficiency

  • labeled B12 in urine - normal test
  • in feces - abnormal

1 - oral radioactive B12 and IM injection non-labeled B12 to block liver storage

2 - both repeated with oral IF

3 - both repeated with antibiotic to rule out GI bacteria

4 - both repeated with pancreatic enzymes to rule out pancreatitis