Digestion 4: Digestion & Absorption Flashcards

1
Q

what are the nutrients we get from diet?

A
  • carbs
  • fat
  • protein
  • water, electrolytes, vitamins
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2
Q

what are the nutrients absorbed by the small intestines?

A
  • monosaccharides
  • fatty acids
  • monoglycerides
  • cholesterol
  • AA
  • water, vitamins, electrolytes
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3
Q

what type of transport is endocytosis or exocytosis?

A

transcytosis

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4
Q

function of sucrase

A

sucrose → glucose + fructose

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5
Q

function of maltase

A

maltose → glucose + glucose

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6
Q

function of lactase

A

lactose → glucose + galactose

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7
Q

function of amylase

A

starch, glycogen → disaccharides

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8
Q

2 ways in which shorter peptide chains can be formed

A
  1. endopeptidase → shorter peptide chains

2. exopeptidase (aminopeptidase & carboxypeptidase) → digest peptide chains from either end to release AA

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9
Q

what is needed when peptide chains are broken?

A

H2O (hydrolysis)

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10
Q

does body make more aminopeptidase or carboxypeptidase

A

carboxypeptidase

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11
Q

function of lipase

A

triglyceride → monoglyceride + FFA

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12
Q

what are the fats that we eat? What is the main one?

A
  • triglycerides (90%)
  • phospholipids
  • cholesterol
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13
Q

how does monosaccharides get through epithelial cells in small intestines?

A

enter: facilitated diffusion & co-transport
exit: facilitated diffusion

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14
Q

how does fat get through epithelial cells in small intestines?

A

enter: diffusion
exit: exocytosis as chylomicrons

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15
Q

how does AA and short peptides get through epithelial cells in small intestines?

A

enter: facilitated diffusion & co-transport
exit: facilitated diffusion & co-transport

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16
Q

brush-border enzyme for AA?

A

dipeptidases

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17
Q

which macronutrient is not digested in the stomach?

A

lipids

carbs get some digestion from leftover salivary amylase

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18
Q

digestion of carbs at the small intestines

A
  1. pancreatic a-amylase

2. lactase, maltase, sucrase

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19
Q

digestion of proteins at the small intestines

A
  1. trypsin, chymotrypsin, elastase, carboxypeptidase

2. dipeptidase

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20
Q

digestion of fat at the small intestines

A

bile acids;

pancreatic lipase

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21
Q

function of salivary amylase

A

starch → MALTOSE + maltotriose + dextrin

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22
Q

__% of starch digestion occurs in mouth, __% occur in stomach

A

5;

35

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23
Q

about ___ min after swallowing, salivary amylase becomes inactivated by low stomach pH

A

30-40

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24
Q

function of pancreatic amylase

A

starch → MALTOSE + maltotriose + dextrin

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25
Q

even though pancreatic amylase == salivary amylase, it is more potent because…

A
  • food is smaller at small intestines, so there is more SA for it to act on
  • food stays in intestines longer
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26
Q

___ is important for pancreatic amylase activity because…

A

bicarb;

need to neutralize acidic chyme so pancreatic amylase is at the optimal pH

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27
Q

how to explain the symptoms of lactose intolerance?

A

diarrhea: lactose in large intestines draw water into lumen
gas: bacteria in large intestines use lactose as food → gas is byproduct of fermentation
cramps: build up of CO2 → distention → peristalsis

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28
Q

what is used to absorb monosaccharides?

A

GLUT-5 & SGLT (sodium glucose linked transporter)

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29
Q

brush-border enzymes used to digest saccharides

A
  • maltase-glucoamylase
  • dextrinase
  • sucrase
  • lactase
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30
Q

where are brushborder enzymes located?

A

embedded in walls of small intestines

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31
Q

which transporters are used to absorb glucose, galactose, and fructuse?

A

SGLT: glucose & galactose (exit by facillitated diffusion or GLUT2)
GLUT5: fructose (exits the cell using GLUT2)

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32
Q

there is competition for absorption of the different monosaccharides. What is the order?

A

absorbed first → last:

galactose > glucose > fructose

33
Q

function of pepsin

A

protein → peptides + AA

  • endopeptidase
  • cleaves at aromatic AA (FYW)
34
Q

pancreas secretes ____ for protein digestion

A

zymogens

  • chymotrypsinogen
  • procarboxypeptidase
  • procolipase
  • prophospholipase
35
Q

function of enterokinase

A

activate trypsinogen → trypsin

36
Q

how are zymogens activated?

A
  1. enterokinases activate trypsinogen → trypsin

2. trypsin activates rest of zymogens

37
Q

activated pancreatic enzymes for protein digestion

A
  • chymotrypsin
  • carboxypeptidase
  • colipase
  • phospholipase
38
Q

Pancreatitis

A

if trypsinogen is activated too early → digestion of the pancreas

39
Q

how does the pancreas protect itself from being digested by protein-digesting enzymes?

A
  1. separate trypsinogen from lysozymes in cytoplasm
  2. trypsin can digest itself
  3. pancreas can make trypsin inhibitor (secreted if trypsin present in pancreas)
40
Q

___ and ___ are endopeptidases, while ___ removes AA from C-term

A

trypsin & chymotrypsin;

carboxypeptidase

41
Q

brushborder enzymes for proteins

A
  • aminopeptidase (cleave from N-term)

- dipeptidase (dipeptide → AA)

42
Q

where are aminopeptidase & dipeptidase located?

A

embedded in brushborder

43
Q

which forms of protein can be absorbed?

A
  1. di- & tripeptides
  2. AA
  3. small peptides
44
Q

absorption of di- & tripeptides

A

transporter: PepT1
- cotransport with H+ on both apical side
- exchange with H+ on basolateral side
- can be cleaved inside cell by peptidases → AA
- functionally linked to NHE to keep [H] inside the cell low

45
Q

absorption of AA

A
  • cotransport with Na+ on apical side
  • exchange with Na+ on basolateral side
  • Na/K-ATPase used to keep concentration of Na low inside cell
46
Q

absorption of small peptides

A

transcytosis

47
Q

gastric lipase is secreted by…

A

chief cells

48
Q

digestion of fat in stomach

A
  • gastric lipase

- agitation forms smaller fat droplets

49
Q

what is 1 instance in which gastric lipase > pancreatic lipase?

A

ZE syndrome:

very acidic chyme means gastric lipase is in optimal environment, but pancreatic isn’t

50
Q

why is 1 symptom of ZE syndrome malnutrition?

A

super acidic chyme makes all pancreatic enzymes (majority of digestion for all nutrients) less effective

51
Q

what emulsify fats?

A
  • bile salt (from liver)

- phospholipid lecithin (from liver)

52
Q

purpose of emulsion?

A

increase SA for further digestion by pancreatic lipase

53
Q

colipase

A
  • pancreatic lipase can’t attach on emulsified fat due to bile salts
  • colipase attaches bile salt on 1 end and lipase on other end → allows digestion to happen
54
Q

micelles

A
  • very small emulsified fat particles
  • hydrophilic shell
  • hydrophobic core (FFA, cholesterol, etc.)
  • small enough to be soluble
55
Q

absorption of fat

A
  1. FFA & monoglycerides diffuse into cell
  2. go to smooth ER → re-esterify back to triglycerides
  3. cholesterol enters cell via NPC1L1 (energy dependent transporter) → sER
  4. everything comes together at sER → packaged at Golgi → chylomicron
  5. leaves cell via exocytosis → lymphatic system → thoracic duct → subclavian vein
56
Q

ezetimibe

A

drug that lowers cholesterol levels by preventing absorption

- block NPC1L1 transporter

57
Q

function of lipoprotein lipase (LPL)

A

TG in chylomicrons → FFA + glycerol

58
Q

chylomicrons is made up of…

A
  • TG (most)
  • Cholesterol
  • PL
  • apoproteins
59
Q

LPL can be found most abundantly in…

A
  • capillaries associated with muscles
  • adipose tissues
  • capillaries associated w/ lactating boobs
60
Q

vit B12 sources

A
  • made by bacteria
  • seafood
  • meat
  • milk
61
Q

Pernicious anemia causes

A
  • lack of intrinsic factors being secreted by parietal cells
  • not enough dietary B12
  • too much bac’t in gut (eat up B12 before reaching ileum)
62
Q

B12 is required for…

A

maturation of RBC

63
Q

Pernicious anemia

A

condition where patients don’t have mature RBC because Vitamin B12 is required for the maturation of RBC

64
Q

calcium can be absorbed 2 ways…

A

1) paracellular

2) hormone dependent absorption

65
Q

hormone-dependent Ca absorption

A
  1. Ca enters cell through Ca-channel
  2. Ca bind to calbindin in cell (free Ca is very bad for cell
  3. when needed, Ca is released from calbindin and exits through Ca-ATPase
66
Q

calbindin is increased by…

A

vit D (calcitriol)

67
Q

how does 1,25(OH)2 vitD3 enhance Ca absorption?

A

1) increase Ca channels on apical membrane

2) increase amount of calbindin

68
Q

iron is absorbed in which forms?

A

1) heme (easily absorbed)

2) ferrous (Fe++)

69
Q

absorption of heme iron

A

transporter: HCP1 (heme carrier protein)

after getting into cell, dissociates → porphyrin + ferrous form

70
Q

absorption of ferrous iron

A

transporter: DMT-1 (divalent metal transporter)
- Fe and H cotransporter

  1. ferrous form + apoferritin → ferritin
  2. ferritin can be used to store lots of iron inside cell until needed
71
Q

what happens when we want to use iron bound in ferritin?

A
  • ferrous iron transported outside by ferroportin

- ferroportin levels regulated by hepcidin

72
Q

ferroportin regulation

A
  • hepcidin causes internalization of ferroportin
  • YES hepcidin = no ferroportin = no Fe leaving cells
  • NO hepcidin = yes ferroportin = yes Fe leaving cells
73
Q

hepcidin

A

hormone released by liver to regulate levels of ferroportin

74
Q

Na+ absorption

A

apical membrane transporters for Na+:

  • Na channel
  • Na/Cl-cotransporter
  • Na/H-exchanger
  • Na/organic solute cotransporter

basolateral membrane transporters for Na+:
Na/K-ATPase

75
Q

Cl- absorption

A

apical membrane transporters for Cl-:

  • Na/Cl-cotransporter
  • bicarb/Cl-exchanger

basolateral membrane transporter for Cl-:
- Cl channel

76
Q

how does water get absorbed?

A
  • paracellular pathway, following solute

- active transport with SGLT transporter

77
Q

how does K+ get absorbed?

A

paracellular pathway, along with water

78
Q

SGLT is only present on __ membrane

A

apical

79
Q

how is water transported with SGLT?

A
  • Na binds, then glucose/galactose
  • follows glucose/galactose when it binds
  • about 250 molecules moved every time