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SF4 Exam I > Digestion and Absorption of Carbohydrates and Proteins > Flashcards

Digestion and Absorption of Carbohydrates and Proteins Flashcards

1
Q

carbohydrates must be what before being absorbed

A

digested into monosaccharides

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2
Q

starches are converted by what into what

A

salivary and pancreatic alpha-amylases

to maltose, maltotriose, and alpha-limit dextrins

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3
Q

the oligosaccharides produced by amylases are hydrolyzed into glucose by what and where

A

glucoamylase, isomaltase, and maltase

brush border of membrane

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4
Q

sucrose is cleaved by what into what?

A

sucrase

fructose and glucose

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5
Q

lactose is cleaved by what into what

A

lactase

glucose and galactose

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6
Q

trehalose is what (what cleaves it)

A

glucose dimer

trehalase

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7
Q

what is not digested by human enzymes

A

cellulose

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8
Q

glucose and galactose are absorbed into enterocytes how?

A

Na+ cotransport

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9
Q

fructose is absorbed how?

A

facilitated diffusion (GLUT 5)

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10
Q

glucose, galactose, and fructose are transferred from cell to blood how

A

facilitated diffusion (GLUT 2)

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11
Q

lactose intolerance is caused by a deficiency in?

A

lactase

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12
Q

lactose intolerance (what happens to lactose)

A

remains in GI as unabsorbed solute (decreasing water absorption of intestine and leading to diarrhea)
undigested lactose metabolized by colonic bacteria

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13
Q

symptoms of lactose intolerance

A

intestinal distension, borborygmi (gurgling noises in intestines), gas, diarrhea

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14
Q

sucrase-isomaltase deficiency is what kind of disorder and what happens

A

inherited

cannot digest sucrose and isomaltase

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15
Q

glucose/galactose malabsorption is caused by what?

A

genetic defect in glucose/galactose transporter (SGLT1)

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16
Q

what are the GI tacts two sources of proteins

A

endogenous- secretory proteins and cells shed into GI tract lumen
exogenous- dietary proteins

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17
Q

proteins are absorbed as what

A

amino acids, dipeptides, and tripeptides

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18
Q

essentially all ingested protein is what

A

assimilated

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19
Q

almost all glucose and galactose in intestine are what

A

absorbed

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20
Q

endopeptidases (what do they do and what types are there

A

hydrolyze interior peptide bonds
gastric pepsin
pancreatic enzymes

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21
Q

gastric pepsin (what does it do)

A

digests small amount of ingested protein

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22
Q

pancreatic enzymes are secreted as what

A

inactive precursors

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23
Q

trypsinogen is converted to trypsin by what?

A

enterokinase

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24
Q

enterokinase is secreted where

A

brush border in small intestine

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25
Q

trypsin autocatalysis the conversion of what

A

trypsinogen to trypsin
chymotrypsinogen to chymotrypsin
proeleastase to elastase
procarboxypeptidases A and B to carboxypeptidases A and B

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26
Q

exopeptidases (what do they do and name them)

A

hydrolyze one amino acid at a time fro C terminal end of proteins and peptides
carboxypeptisades A and B

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27
Q

carboxypeptidases A and B are secreted from where and converted by what

A

secreted from pancreas as proenzymes

converted to active enzymes by trypsin

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28
Q

what is the role of peptidases in brush border

A

cleave peptides produces by pancreatic proteases to oligopeptides and amino acids

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29
Q

how are most amino acids absorbed into enterocytes

A

Na+ cotransport

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30
Q

how are di and tripeptides absorbed into enterocytes (compared to amino acids and the transport mechanism)

A

faster and more efficiently than amino acids

H+ cotransport (PEPT1)

31
Q

majority of proteins is absorbed as what

A

di and tri peptides (then hydrolyzed to amino acids as peptidases in enterocytes)

32
Q

protein in stool is normally from what

A

bacteria and cellular debris

33
Q

protein in stool is normally from what

A

bacteria and cellular debris

34
Q

whole proteins can be absorbed but what is their significance

A

not nutritionally but immunological

can lead to food allergies

35
Q

trypsin deficiency is cased by what

A

congenital lack of trypsin and pancreatic disease

36
Q

cystinuria (what is it)

A

congenital defect that affects uptake of basic amino acids

37
Q

Hartnup disease

A

congenital defect that affects uptake of neutral amino acids

38
Q

familial iminoglycinuria

A

congenital defect that affects uptake of proline and hydroxyproline

39
Q

what amount of iron ingested each day is absorbed

A 
small fraction (about 10%)
amount absorbed about equal to amount lost
40
Q

iron is absorbed in what forms

A

heme or free iron

41
Q

what is the most easily absorbed form of iron

42
Q

who is heme iron absorbed

A

receptor mediated endocytosis or transporter protein (HCP1)

43
Q

what form of free iron is more readily absorbed

44
Q

gastric acid does what to iron which permits what

A

dissolves iron

allows it to form complex with ascorbic and citric acid (reduces ferric iron to ferrous)

45
Q

Duodenal cytochrome B (Dcytb)

what does it do

A

reduces ferric to ferrous iron

46
Q

how if ferrous iron transferred into enterocyte

A

ferrous iron transporter (DMT1)

47
Q

in cell iron binds to what and forming what

A

apoferritin

forming ferritin for storage

48
Q

iron is transported out of cell by what?

A

ferroportin

49
Q

ferroportin and ferroxidase hephaestin doe what

A

convert ferrous to ferric iron

50
Q

transferrin (where is it, what binds it, what does it do)

A

transferrin is in plasma and binds to ferric iron to transport it to other tissues

51
Q

what mechanism is there for removing excess iron

A

no mechanism

52
Q

most of iron regulation is orchestrated by what?

53
Q

hepcidin (what does it regulate)

A

entry of iron into plasma by binding directly to ferroportin

54
Q

binding fo hepcidin to ferroportin leads to what

A

internalization and degradation of ferroportin (blocks cellular iron export and recedes plasma iron)

55
Q

when iron levels are low what are hepcidin levels like

A

low- leads to increase iron absorption and elevated iron release fro enterocytes

56
Q

what is the most prevalent nutrient deficient

57
Q

most common cause of anemia in the world

A

iron deficiency

58
Q

hemochromatosis (what is it)

A

chronic absorption of too much iron

59
Q

most common genetic disorder in US

A

hereditary hemochromatosis

60
Q

hemochromatosis (defect in)

A

HFE gene which causes hepcidin levels to drop

61
Q

hemochromatosis (leads to)

A

excess iron collects in liver which can lead to cirrhosis and eventually liver cancer

62
Q

hemochromatosis (issues other than with liver

A

damage pancreas- leading to diabetes

contribute to coronary disease

63
Q

hemochromatosis (treatment)

A

periodically removing blood

64
Q

electrolytes and water cross intestinal epithelial cells by what mechanisms

A

transcellular

paracellular

65
Q

small intestines absorbs water and electrolytes from where

A

diet

salivary, gastric, biliary, and pancreatic secretions

66
Q

failure of small intestines to absorb water and electrolytes leads to what

A

rapid dehydration, electrolyte imbalance and eventually circulatory collapse

67
Q

failure of small intestines to absorb water and electrolytes leads to what

A

rapid dehydration, electrolyte imbalance and eventually circulatory collapse

68
Q

Na is moved from lumen of small intestine across apical membranes of enterocytes how?

A

Na/glucose or Na/amino cotransport
Na/Cl cotransport
Na/H exchange

69
Q

in duodenum and jejunum Na is absorbed by what mechanism(s)?

A

Na/glucose or Na/amino acid cotransport and Na/H exchange

70
Q

in ileum Na is absorbed by what mechanism(s)?

A

Na/glucose or Na/amino acid cotransport and Na/H exchange

cotransport with Cl

71
Q

in colon Na is absorbed by what mechanism(s)?

A

Na channels

72
Q

Cl transport into enterocytes from lumen of intestine is mediated by what?

A 
passive diffusion (paracellularly)
cotransport with Na and K
exchange with HCO3-
73
Q

Cl transport into enterocytes is mediated by what?

A 
passive diffusion (paracellularly)
cotransport with Na and K
exchange with HCO3-

SF4 Exam I (16 decks)

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