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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

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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
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

SF4 Exam I (16 decks)

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