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

Digestion and Absorption of Lipids, Intestinal Secretion, Diarrhea Flashcards

1
Q

what constitutes most of all dietary lipids

A

triglycerides

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2
Q

name all the sources of dietary lipids

A

triglycerides
phospholipids
cholesterol

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3
Q

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

A

be made water soluble

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4
Q

in the stomach lipids tend to separate into what?

A

oily phase

this is emptied later from stomach

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5
Q

mixing in the stomach does what to lipids and why?

A

breaks them into droplets

to increase total surface area available to digestive enzymes

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6
Q

what prevents complete emulsification of lipids

A

low pH of stomach

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7
Q

gastric lipase (what does it do)

A

hydrolyzes triglycerides to diglycerides and free fatty acids

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8
Q

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

A

CCK

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9
Q

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

A

bile salts and lecithin
detergent action
increase total surface area

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10
Q

what type of environment does emulsification require?

A

neutral or slightly basic

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11
Q

pancreatic enzymes hydrolyze lipids into what?

A

fatty acids
monoglycerides
lysophospholipids
cholesterol

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12
Q

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

A

cleaves fatty acids from 1 and 3 positions of triglycerides

results in 2 free fatty acids and a 2-monoglyceride

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13
Q

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

A

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

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14
Q

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

A

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

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15
Q

colipase (is secreted as what from where)

A

pancreas

inactive precursor

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16
Q

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

A

non-enzymatic protein
intestinal lumen
trypsin

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17
Q

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

A

non-enzymatic protein
intestinal lumen
trypsin

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18
Q

colipase prevents what and how?

A

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

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19
Q

emulsification products of lipolysis form what?

A

water-soluble mixed micelles with bile

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20
Q

what role to the micelles play in absorption of lipids?

A

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

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21
Q

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

A 
simple diffusion (highly lipid soluble)
some evidence of transporters
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22
Q

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

A

medium chained fatty acids

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23
Q

where are bile salts (freed of associated lipids) absorbed

A

terminal ileum

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24
Q

what lipid is hydrophilic and not contained in micelles

A

glycerol

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25
Q

what happens to products of lipid digestion in the enterocyte

A

reesterified to triglycerides and phospholipids

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26
Q

in the monoglyceride acylation pathway triglycerides are synthesized from what?

A

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

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27
Q

in the monoglyceride acylation pathway where does reesterification take place

A

smooth ER

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28
Q

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

A

fatty-acid binding proteins

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29
Q

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

A

medium-chained fatty acids

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30
Q

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

A

medium-chained fatty acids

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31
Q

phosphatidic acid is synthesized from what?

A

2 Acyl CoA and alpha-glycerophosphate

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32
Q

alpha-glycerophosphate is derived from where

A

hexose metabolism

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33
Q

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

A

phosphatidic acid and Acyl CoA

phosphate is also produced in reaction

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34
Q

what happens to absorbed lysophospholipid in the enterocyte

A

combined with fatty acid to form phospholipid

35
Q

cholesterol is absorbed in what form

A

free form

36
Q

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

A

free and re-esterified

37
Q

what happens to most free cholesterol once in the enterocyte

A

re-esterified with fatty acids

38
Q

what forms chylomicrons?

A

resynthesizes triglycerides,
cholesterol,
cholesterol esters,
phospholipids

39
Q

the core of the chylomicron contains what?

A

triglycerides
esterified cholesterol
fat-soluble vitamins

40
Q

the surface of the chylomicron contains what?

A

phospholipids
apoprotein
free cholesterol

41
Q

how are chylomicrons transported out of cell

A

exocytosis

42
Q

what do chylomicrons enter as they leave enterocyte and how

A

lacteals (central lymphatic vessels in villi)

through gaps b/w endothelial cells lining lymphatics

43
Q

how do chylomicrons reach bloodstream?

A

thoracic duct (too big to get into capillaries)

44
Q

lipid malabsorption is defined as what?

A

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

45
Q

what can cause lipid malabsorption

A

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

46
Q

what causes lipid malabsorption due to failure to digest fats?

A

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

47
Q

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

A

pancreatitis
pancreatic carcinoma
cystic fibrosis

48
Q

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

A 
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
Q

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

A

feeding medium chain in place of long chain fatty acids

50
Q

conditions that affect or decrease number of absorbing cells are?

A

tropical spruce

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

51
Q

gluten enteropathy/ celiac spruce causes what other than lipid malabsorption

A

malabsorption of carbohydrates and proteins

52
Q

gluten enteropathy/ celiac spruce can be treated how

A

gluten-free diet

53
Q

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

A

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
Q

abetalipoproteinemia

A

ApoB (component of chylomicrons) not synthesized

55
Q

small and large intestines secrete water and electrolytes from where?

A

crypt cells

56
Q

small and large intestines secrete mucus from where?

A

goblet cells

57
Q

how does Cl- enter crypt cell

A

Na/Cl cotransport (against Cl gradient)

58
Q

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

A

increase in cAMP or Ca2+

59
Q

how does Na+ enter intestinal lumen

A

paracellular transport passively following Cl-

60
Q

water and electrolyte secretion in intestine is stimulated by what

A

GI hormones and neutrotransmitters

61
Q

water and electrolyte secretion in intestine assists in what?

A

digestion and absorption by maintaining liquidity of chyme in small intestine

62
Q

diarrhea is defined as what?

A

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

63
Q

osmotic diarrhea (what causes it and where)

A

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

64
Q

secretory diarrhea (what causes it and where)

A

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
Q

secretory diarrhea (what causes it and where)

A

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
Q

inflammatory/infection diarrhea (what causes it)

A

infection by bacteria and viruses

loss of enterocytes leads to inability to absorb

67
Q

inflammatory/infection diarrhea (what causes it)

A 
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
Q

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

A

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
Q

with age what happens to mouth?

A

lose taste buds
chewing muscles weaken
may lose teeth

70
Q

with age what happens to esophagus?

A

swallowing becomes more difficult

LES function declines

71
Q

with age what happens to stomach?

A

lose parietal cells

increase in ulcers b/c of increase use of NSAIDs

72
Q

with age what happens to small intestine?

A

decrese in motility

increase in malabsorption

73
Q

with age what happens to colon?

A

decrease in motility

increase in polyps

74
Q

with age what happens to small intestine?

A

decrease in motility

increase in malabsorption

75
Q

with age what happens to colon?

A

decrease in motility

increase in polyps

76
Q

colonic flora (what is is)

A

numerous bacteria that reside in large intestine

remain stable unless perturbed

77
Q

colonic flora (physiological functions)

A

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
Q

intestinal gas (sources)

A

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

79
Q

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

A

swallowed air

passed on to colon

80
Q

gas in large intestine comes from where?

A

colonic gas (flatus) produced in large volume

81
Q

colonic gas (main components and their sources)

A

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

82
Q

what happens to large volume of flatus produced in colon

A

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

83
Q

methane production in flatus (whats special about it)

A

found in 1/3 of adults

genetic factors are involved in the ability to produce it

84
Q

odor of flatus (due to?)

A

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

SF4 Exam I (16 decks)

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