Digestion and Absorption of Lipids, Intestinal Secretion, Diarrhea Flashcards Preview

SF4 Exam I > Digestion and Absorption of Lipids, Intestinal Secretion, Diarrhea > Flashcards

Flashcards in Digestion and Absorption of Lipids, Intestinal Secretion, Diarrhea Deck (84):
1

what constitutes most of all dietary lipids

triglycerides

2

name all the sources of dietary lipids

triglycerides
phospholipids
cholesterol

3

before they can be absorbed what must be done to lipids?

be made water soluble

4

in the stomach lipids tend to separate into what?

oily phase
this is emptied later from stomach

5

mixing in the stomach does what to lipids and why?

breaks them into droplets
to increase total surface area available to digestive enzymes

6

what prevents complete emulsification of lipids

low pH of stomach

7

gastric lipase (what does it do)

hydrolyzes triglycerides to diglycerides and free fatty acids

8

what slows gastric emptying to allow for sufficient time for digestion and absorption in duodenum

CCK

9

in the small intestine fats are emulsified by what (and what property of them) and why

bile salts and lecithin
detergent action
increase total surface area

10

what type of environment does emulsification require?

neutral or slightly basic

11

pancreatic enzymes hydrolyze lipids into what?

fatty acids
monoglycerides
lysophospholipids
cholesterol

12

pancreatic lipase (what does it do, what is result)

cleaves fatty acids from 1 and 3 positions of triglycerides
results in 2 free fatty acids and a 2-monoglyceride

13

cholesterol ester hydrolase (what does it do, what is result)

cleaves fatty acid from cholesterol esters, leaving free cholesterol and fatty acid

14

phospholipase A2 (what does it do, what is result)

releases fatty acid from position 2 of phospholipids yielding lysophospholipids and free fatty acid

15

colipase (is secreted as what from where)

pancreas
inactive precursor

16

colipase (what type of protein is it, where is it activated, and by what)

non-enzymatic protein
intestinal lumen
trypsin

17

colipase (what type of protein is it, where is it activated, and by what)

non-enzymatic protein
intestinal lumen
trypsin

18

colipase prevents what and how?

inhibition of pancreatic lipase by bile salts (displace enzyme from surface of emulsion droplet)

19

emulsification products of lipolysis form what?

water-soluble mixed micelles with bile

20

what role to the micelles play in absorption of lipids?

bring products of lipid digestion through unstirred water layer into contact with microvilli on surface of enterocytes

21

how do monoglycerides, fatty acids, cholesterol, lysophospholipids, and fat-soluble vitamins get across luminal membrane

simple diffusion (highly lipid soluble)
some evidence of transporters

22

what lipid digestion products are water-soluble enough to diffuse into cell without aid of micelles

medium chained fatty acids

23

where are bile salts (freed of associated lipids) absorbed

terminal ileum

24

what lipid is hydrophilic and not contained in micelles

glycerol

25

what happens to products of lipid digestion in the enterocyte

reesterified to triglycerides and phospholipids

26

in the monoglyceride acylation pathway triglycerides are synthesized from what?

2-monoglycerides (product of pancreatic lipase) and CoA- activated fatty acids

27

in the monoglyceride acylation pathway where does reesterification take place

smooth ER

28

in the monoglyceride acylation pathway how do the long chain fatty acids get transported within the cell

fatty-acid binding proteins

29

what fatty acids are absorbed directly into blood stream without resynthesis into triglycerides

medium-chained fatty acids

30

what fatty acids are absorbed directly into blood stream without resynthesis into triglycerides

medium-chained fatty acids

31

phosphatidic acid is synthesized from what?

2 Acyl CoA and alpha-glycerophosphate

32

alpha-glycerophosphate is derived from where

hexose metabolism

33

in the phosphatidic acid pathway triglycerides are synthesized from what, and what is the byproduct?

phosphatidic acid and Acyl CoA
phosphate is also produced in reaction

34

what happens to absorbed lysophospholipid in the enterocyte

combined with fatty acid to form phospholipid

35

cholesterol is absorbed in what form

free form

36

what form(s) of cholesterol are transported in chylomicrons?

free and re-esterified

37

what happens to most free cholesterol once in the enterocyte

re-esterified with fatty acids

38

what forms chylomicrons?

resynthesizes triglycerides,
cholesterol,
cholesterol esters,
phospholipids

39

the core of the chylomicron contains what?

triglycerides
esterified cholesterol
fat-soluble vitamins

40

the surface of the chylomicron contains what?

phospholipids
apoprotein
free cholesterol

41

how are chylomicrons transported out of cell

exocytosis

42

what do chylomicrons enter as they leave enterocyte and how

lacteals (central lymphatic vessels in villi)
through gaps b/w endothelial cells lining lymphatics

43

how do chylomicrons reach bloodstream?

thoracic duct (too big to get into capillaries)

44

lipid malabsorption is defined as what?

excretion of more than 7 g fat/day in feces (steatorrhea)

45

what can cause lipid malabsorption

failure to digest fat
absence of bile salts
conditions that affect or decrease the number of absorbing cells
failure to synthesize apoproteins

46

what causes lipid malabsorption due to failure to digest fats?

pancreatic enzymes either not secreted into gut or inactivated by low pH

47

lipid malabsorption due to failure to digest fats occurs in what conditions?

pancreatitis
pancreatic carcinoma
cystic fibrosis

48

lipid malabsorption due to absence of bile salts occurs in what conditions?

liver disease (hepatitis)
obstruction of common bile ducts by gallstones
bacterial overgrowth of small intestine (leads to deconjugation of bile salts)
increased acidity in duodenum (bile salts less soluble)

49

lipid malabsorption due to absence of bile salts can be treated how?

feeding medium chain in place of long chain fatty acids

50

conditions that affect or decrease number of absorbing cells are?

tropical spruce
gluten enteropathy/ celiac spruce (allergic reation to glutten in wheat products causes los of villi in lining)

51

gluten enteropathy/ celiac spruce causes what other than lipid malabsorption

malabsorption of carbohydrates and proteins

52

gluten enteropathy/ celiac spruce can be treated how

gluten-free diet

53

lipid malabsorption due to failure to synthesize apoproteins is caused by what

ApoB (component of chylomicrons) not synthesized, thus chylomicrons do not form or cannot be transported and dietary fats, cholesterol, and fat-soluble vitamins no absorbed

54

abetalipoproteinemia

ApoB (component of chylomicrons) not synthesized

55

small and large intestines secrete water and electrolytes from where?

crypt cells

56

small and large intestines secrete mucus from where?

goblet cells

57

how does Cl- enter crypt cell

Na/Cl cotransport (against Cl gradient)

58

Cl- channels in apical membrane of crypt cell are activated by what?

increase in cAMP or Ca2+

59

how does Na+ enter intestinal lumen

paracellular transport passively following Cl-

60

water and electrolyte secretion in intestine is stimulated by what

GI hormones and neutrotransmitters

61

water and electrolyte secretion in intestine assists in what?

digestion and absorption by maintaining liquidity of chyme in small intestine

62

diarrhea is defined as what?

excretion of 200g or more of water in stools of adult during 24hr

63

osmotic diarrhea (what causes it and where)

accumulation within small intestine of nonreabsorbable solutes
this attracts water from intestinal wall in volumes that exceed absorptive capacity of gut

64

secretory diarrhea (what causes it and where)

excess stimulation of secretory cells in crypts of small intestine and colon
Cl- channel is always open (causes Na and water to follow)
inhibition of Na absorption by ileal enterocytes

65

secretory diarrhea (what causes it and where)

excess stimulation of secretory cells in crypts of small intestine and colon
Cl- channel is always open (causes Na and water to follow)
inhibition of Na absorption by ileal enterocytes (Na-glucose cotransport unaffected)

66

inflammatory/infection diarrhea (what causes it)

infection by bacteria and viruses
loss of enterocytes leads to inability to absorb

67

inflammatory/infection diarrhea (what causes it)

infection by bacteria (salmonella, campylobacter clostridium difficile)
and viruses (rotavirus, norovirus)

inflammation/ immune response leads to loss of enterocytes leads to inability to absorb

68

oral rehydration therapy (what type of diarrhea does is it used for and what is it?)

secretory diarrhea
oral adminstration of Na+ and glucose (and/or amino acids) can reduce fluid and electrolyte loss- NA still absorbed by Na-glucose cotransport and Cl and water follow

69

with age what happens to mouth?

lose taste buds
chewing muscles weaken
may lose teeth

70

with age what happens to esophagus?

swallowing becomes more difficult
LES function declines

71

with age what happens to stomach?

lose parietal cells
increase in ulcers b/c of increase use of NSAIDs

72

with age what happens to small intestine?

decrese in motility
increase in malabsorption

73

with age what happens to colon?

decrease in motility
increase in polyps

74

with age what happens to small intestine?

decrease in motility
increase in malabsorption

75

with age what happens to colon?

decrease in motility
increase in polyps

76

colonic flora (what is is)

numerous bacteria that reside in large intestine
remain stable unless perturbed

77

colonic flora (physiological functions)

digest carbohydrates that enter large intestine
forme secondary bile and deconjugate bile acids
generate short-chain fatty acids that are absorbed by colon
limit invasion and/or growth of pathogenic microorganisms

78

intestinal gas (sources)

swallowed hair (aerophagia)-
gas form by bacterial action in ileum and colon
diffusion of gas from bloodstream

79

gas in small intestine (usually from where, goes where)

swallowed air
passed on to colon

80

gas in large intestine comes from where?

colonic gas (flatus) produced in large volume

81

colonic gas (main components and their sources)

N2- swallowed air
H2 and CO2- bacterial fermentation of unabsorbed sugars
CO2- byproduct of chemical reaction with acid in stomach

82

what happens to large volume of flatus produced in colon

all but N2 diffuse easily through small intestine so volume expelled is much reduced

83

methane production in flatus (whats special about it)

found in 1/3 of adults
genetic factors are involved in the ability to produce it

84

odor of flatus (due to?)

minute amounts of volatile chemicals formed by bacterial metabolism of residual fats and proteins