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Gastrointestinal System > Digestion and Absorption - Jacinto 2/25/16 > Flashcards

Digestion and Absorption - Jacinto 2/25/16 Flashcards

1
Q

overview of digestion and absorption in intestine

A

digestion: occurs in lumen and on membrane surface

  • enzymes and transporters in brush border are often heaviily glycosylated so they wont be digested by luminal digestive enzymes

absorption: from lumen into blood and lymph

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2
Q

surface area amplification

A

levels on levels of folds in intestinal lumen (villi made of epithelial cells with microvilli)

  • length of sm int ~ .33 m2
    • fold of Kerkring, 3x
    • villi, 10x
    • microvilli, 20x
  • total SAn~ 175 m2
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3
Q

intestinal villi structure

A

intestinal cells

  • born in crypts
  • mature/migrate to apical portion of microvilli
  • total lifespan: 4-5 days
    • superproliferative

villi interior: lacteals and capillaries

  • capillaries for nutrient abs and oxygen delivery
  • lacteals for lymph
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4
Q

transport of nutrients across enterocyte

types of transporters

A

enterocyte = int epithelial cell

1. passive: no energy, down conc gradient

2. primary active: ATP-ase, establishes concentration gradient for other transport

3. secondary active: symporters or antiporters that take multiple things across membrane, driven by an existing conc gradient

also as a means of transport to leave the cell

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5
Q

carbs in the diet

A
  • plant starch: amylopectin, amylose
  • dietary fiber: cellulose
  • animal starch: glycogen
  • disaccharides: sucrose, lactose
  • monosaccharides: glucose, fructose
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6
Q

carb breakdown: amylases

A

starch/glycogen digested via breakdown of 1:4 linkages (linear) and 1:6 linkages (perpendicular) by amylases

  • mouth: salivary amylase
    • partially degrade carbs → generate disacchs, trisacchs, alpha-limit dextrin with 1:6 link
    • once you get to stomach, amylase is deactivated
  • intestine: duodenum/jejunum: pancreatic amylases go to work, break down into monosacchs
    • most absorption happens in upper sm int
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7
Q

carb breakdown

luminal vs membrane digestion

A

luminal digestion

  • salivary amylase, pancreatic amylase
  • can digest polysacchs into disacchs (lactose, dextrins, maltotriose, maltose, trehalose, sucrose)

membrane digestion

  • lots of disaccharidases which take dissachs and break down into glucose/galactose/fructose
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8
Q

abs of dietary carbs

A

lumen into enterocyte (apical side)

  • fructose via GLUT5
  • glucose/galactose via SGLT1

enterocyte into circulation (baslateral side)

  • fructose/glucose/galactose via GLUT5

gradient for SGLT1 action maintained by Na/K ATPase

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9
Q

carb maldigestion

[lactose intolerance]

A

lactose intolerance: inability to break down dairy products (occurs on a spectrum)

  • after infancy, enzyme needed to digest them (lactase) drops in production
    • NOT AN INABILITY TO ABSORB; it’s an inability to digest the products in the first place

what happens to the lactose?

  • in colon, bacteria use it as a source of nutrients, break it down and make H2 gas (pt feels bloated, gassy)
  • bacterial fermentation produces short chain FAs
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10
Q

bacterial fermentation in lactose intolerance

why is it a good thing?

A

bacterial fermentation of lactose that makes it to the colon produces H2 gas as well as short chain FAs

  1. salvages calories from lactose that cant otherwise be gotten
  2. reduces water loss in feces
  3. combats int inflammation: FAs can support regulatory T cells in gut immune system
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11
Q

carb dig/abs abnormalities

A

1. genetic

  • lactose intolerance
  • glucose/galactose malabsorption : SGLT1 error

2. pancreatic insufficiency : issues with panc amylase

3. secondary cause (non-genetic)

  • decreased abs surface area = reduction # of membrane enzymes
  • parasitic infection
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12
Q

proteins in diet

A
  • animals and plant sources
  • endogenous proteins: recycling of proteins from digestive enzymes, dead epithelial cells
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13
Q

digestion of proteins

A
  • no digestion in mouth
  • digestion begins in stomach via pepsin → polypeptides + a.a.s
  • pancreatic proteases [trypsin, chymotrypsin, elastase, carboxy-peptidase] → oligopeptides + a.a.s
  • intestinal proteases [amino peptidases, di- and tripeptidases] → a.a.s
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14
Q

protein digestion

luminal vs membrane digestion

A

luminal digestion

  • pepsin, pancreatic proteases

membrane digestion

  • peptidases in brush border to break down large peptides
  • carrier proteins that can move di/tripeptides in
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15
Q

enzymes involved in protein digestion

A
  • stomach chief cells release pepsinogen (zymogen)
    • pepsinogen activated → pepsin by stomach acidity
    • pepsin isn’t particularly efficient at hydrolyzing polypeps - mostly recognizes a.a.s
  • sm intestine enteropepsidase activates trypsinogen → trypsin
    • trypsin then activates a bunch of proenzymes → [trypsin, chymotrypsin, elastase, carboxypeptidase A, carboxypeptidase B]
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16
Q

di- and tripeptides

A

once in cells, di- and tripeptides are further digested by cytoplasmic peptidases → a.a.s, which move into bloodstream

17
Q

protein absorption

A
  1. passive transport
  2. [majority] Na-a.a. cotransport
    * NHE can drive absorption by setting up gradient

absorption is efficient, but not as efficient as carbs

18
Q

protein dig/abs abnormalities

A
  1. genetic
  • enteropeptidase deletion (can’t activate trypsin)
    • not the worst; autohydrolysis of trypsinogen is possible; survivable defect
  • trypsinogen deletion
  • amino aciduria (cystinuria, prolinuria)
  • Hartnup’s disease: Trp transporter
  1. pancreatic insufficiency
  2. other
  • decreased surface area
  • surgery
  • parasitic infection
19
Q

nucleoprotein dig/abs

A

digestion

  • pancreatic DNase, RNase
  • polynt hydrolysis via brush border phosphodiesterases and nucleotidases

absorption

  • nucleoside transporters
  • uric acid excreted in urine
  • sugar reabsorbed into circ
20
Q

dig/abs of vitamins

A
  • in most cases, protein to which the vitamin is bound is digested
    • vitamin is released and absorbed by specific transporters in int (most in upper part of sm int)
  • exception: B12/cobalamin
    • deficiency or malabs can lead to pernicious anemia
21
Q

absorption of B12/cobalamin

A

B12/cobalamin-IntrinsicFactor binds to cubulin receptor in the ileum → endocytosis

  • deficiency can be due to strict veg diet
  • def can also be due to issues with dig/abs
    • lack of IF
    • pancreatic insufficiency
    • intestinal disorders

the process

in stomach,

  • food-bound B12 interacts with stomach acid, becomes unbound
  • R protein/haptocorrin [formerly known as transcobalamine] binds to B12 to protect it from acidity of stomach
  • IF produced

in sm intestine

  • R protein gets digested, B12 on its own again
  • IF binds newly single B12

in ileum

  • you find IF-Cbl receptors on enterocytes
22
Q

ways B12 abs could be compromised

A
  • lose ileum
  • not secreting IF
  • defects in R protein [if you cant get your pancreatic enzymes to get R protein off]
23
Q

Roux en Y surgery

A

gastric bypass [obesity, diabetes]

  • stomach stapled (cuts down on ingestion - can only tolerate small portions)
    • mid sm intestine connected to mini-stomach
    • proximal sm intestine connected to mid sm int
  • no IF produced
    • pts need to receive IV B12
24
Q

lipids in diet

A
  • triacylglycerol
  • phospholipids
  • lycolipids
  • sterols
  • lipid-soluble vits : A, D, E, K
25
Q

lipid digestion enzymes

A
  • cholesterol esterase aka nonspecific lipase
    • digest CE → C
    • can also digest diff lipids
  • lipases
    • ​digest PL
  • pancreatic lipases
    • ​digest TAGs
    • need to be activated, bind with a colipase (bc you dont want them to be active without food and go and digest membrane PLs)

*short- and med-chain FAs that are generated are easily absorbed, long-chain FAs are more difficult

**we have some gastric lipases but they are v inefficient, so the int handles the vast majority of load

26
Q

lipid dig/abs

A
  • emulsification
    • hydrolysis by gastric lipases
    • more hydrolysis by pancreatic lipases
    • emulsification/solubilization by bile salt micelles
  • uptake of lipids
    • resynth of lipids in ER (chylomicrons)
    • exocytosis into lymph
27
Q

emulsification overview

A
  • stomach mixes and churns
  • duodenum is site of bile salt release
    • CCK slows down gastric emptying, stimulates gallbladder contraction/bile release
    • secretin stimulates release of bile and pancreatic bicarb
28
Q

track: lipases from duodenum [action of panc lipases] into “circulation”

A
  • pancreatic lipase doesnt bind super-well to TAGs (has to compete with bile salts for purchase)
    • colipase allows pancreatic lipase to bind even in presence of bile salts : can bind and digest TAG down to micelles
  • micelles break up into constituents (incl FAs) as they get closer to the slightly acidic environment around the villi
    • FAs can be absorbed through transporters

how does absorption actually happen?

  • FFAs can diffuse
  • everything else needs a transporter [2MG, lysoPL, chol]
  • once inside, lipids must be reassembled in the ER before exocytosed!!!
    • packaged with betalipoproteins (which make them soluble) into lacteal lympatics
29
Q

dig/abs of fat soluble vitamins

A

ADEK

  • digestion: hydrolysis by pancreatic lipase releases vitamins
  • absorption: dependent on absorption of dietary lipids
30
Q

bile acid reabs

A

in distal ileum

  • conjugated bile acids cotransported with Na
  • unconjugated bile acids (more lipophilic) diffuse

from there, both get into enterohepatic circ and head back to liver

31
Q

sites of absorption: fat and bile acid

A
  • fat: passive reabs in prox sm intestine
  • bile acid: active reabs in distal ileum
    • also some passive reabs in prox int, colon
32
Q

effect of bile acid conc on lipid abs

A

if bile acid conc is above critical micelle concentration

  • fat abs heavy in prox sm intestine

if bile acid conc is below critical micelle concentration

  • fat abs light throughout sm intestine
33
Q

causes of lipid malabs

A
  1. genetic
    * CM metabolism defects
  2. bile deficiency (block in release)
  3. pancreatic insufficiency (block in release of enzymes)
  4. other (secondary)
  • tropical sprue
  • Crohn’s disease/ulcerative colitis
  • Zollinger Ellison - too much gastrin, too much acidity in stomach - gets into sm int, inactivates a lot of pancreatic enzymes!
  • Celiac disease

**some of these knock out reabs SA

34
Q

dig/abs of minerals

A
  • digestion: release of protein-bound mineral
  • absorption: low efficiency! tightly controlled to prevent tox!
    • other substances in lumen affect bioavailability
35
Q

duodenal Fe abs

A

absorption (lumen into enterocyte)

  • iron reductase takes Fe+3 and makes it Fe+2
  • Fe+2 contransported with H via DCT1
  • heme transported via heme transporter
    • inside cell, heme oxidase breaks heme down into Fe+2

in epithelial cell, Fe+2 → Fe+3 via ferroxidase

  • storage pathway: Fe+3 stored in ferritin
    • if unused, ferritin excreted when epithelial cells die/slough off
  • usage pathway: Fe+3 packaged with Fe binding protein
    • move into blood via IREG1, binds with transferrin
36
Q

Ca dig/abs

A
  • Ca can move from lumen…
    • into cell via transporters
    • to plasma via paracellular transport

pathway for abs through cell

  • low Ca triggers PTH release
    • PTH circulates to kidney, activates catalyst for activation of vitamin D3/calcitriol
    • activated calcitriol enhances transcription of Ca binding protein → aids in getting Ca over to basolateral Ca ATPase → pumping Ca out into plasma
37
Q

GI tract receives/dumps in approx 9L of fluid daily, but only excretes 100mL in feces

A

intercellular aqueous channel = “shunt” pathway

  • proximal to distal, the alimentary canal goes from leaky to tighter
38
Q

ion transport throughout sm intestine

A

water will move with solute

duodenum

  • osmotically active particles: glucose, a.a.s
    • lots of SGLT1 pulling in Na/glucose → water follows through aquaporins and paracellular jx
  • what if there’s no food present?
    • ions like Na can still pull water in

jejunum

  • SGLT1 still in action
  • Na/H exchanger working in conjunction with HCO3/Cl exchanger to move ions when there’s no food available

ileum

  • tight jx are tighter (abs is more efficient)
  • not much left to absorb, but still have electrolytes
    • Na pulled in, water comes along
  • when youre losing sodium: conservation!
    • aldosterone secretion occurs, gets more Na back via enhanced colon EnAC transporters

in crypt cells

  • driving force is CFTR secreting chloride

how does water get reabsorbed?

  • aquaporins
  • paracellular transport
39
Q

water imbalance

diarrhea vs. steatorrhea

A

syndromes that enhance secretion

  • mineral laxatives are osmotically active, draw out water - too much, can get diarrhea
  • bile acids and lipids can irritate colon if theyre poorly reabsorbed so can cause increased secretion and diarrhea
  • dumping syndrome : dumping too much chyme into sm intestine (more than can be digested) - too much solute pulls water out and causes diarrhea

Gastrointestinal System (35 decks)

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