Lecture 18 - SI absorption (Freeman) Flashcards Preview

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Flashcards in Lecture 18 - SI absorption (Freeman) Deck (39)
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sites of absorption

proximal small intestine - Ca, Fe, sugars, a.a., fats
distal small intestine - sugars, a.a., fats, bile salts (passively)
ileum - bile salts (atively) vitamin B12, water, electrolytes
cecum and colon - bacterial fermentation, absorption of water, electrolytes, VFAs


anatomy of mucosa: SI and LI

includes crypts and villi
- SI have microvillie and villi
- colon has microvillie BUT NOOOO VILLI!! (therefore less absorption capabilities)
- both have crypts!
- 3 zones: zone of proliferation, zone of migration/differentiation, zone of exfoliation


specialization in epithelial cells

crypts migrate up toward the tips of villi as they mature and gain digestive and absorptive functions

shortened villi: crypts cant travel far enough to mature and normal mucosal function is lost

cells have a short life span (<96 hours) and are lost to intestinal lumen


epithelial transport mechanisms: gotta know 5 things

1. differences btwn epithelial and nonepithelial cells
2. improtance of Na transport mechanisms in teh transport of other substances like water and water soluble nutrients
3. driving forces for absorption
4. interactions between transport systems
5. concepts of concentrations in salt sol'ns


differences between epithelial and nonepithelial cells

specialization in apical (faces lumen) and basement cell membranes (faces capillaries)

tight junctions between epithelial cells



concentation of ions expressed as millimoles/kg of water



concentration of ions expressed as millimoles/liter of solution



refers to the concentrations inside and outside the cells


transcellular transport (primary transport)

entry of Na: Na into lumen > Na in cell
this is favorable electrochemical gradient: no energy needed!

exit of Na: out of lumen into blood REQUIRES ENERGY
provided by Na-K/ATPase located on the basolateral membrane of cell - this keeps the intracellular concentrations of Na low (to favor Na entry from lumen)


paracellular transport

after Na is pumped into the lumen on the capillary side, Na builds up and can "leak" back into the lumen between the cells (Cl and water will follow!) through tight junctions


ion gradient hypothesis (secondary active transport)

energy necessary to drive flow into a cell against a concentration gradient is derived from coupling between transport of that solute with the transport of an ion (Na) down the concentration gradient

ex: Cl moves against EC gradient to "piggyback" with Na into cell. the Na pump on basolateral side drives this.


things that are transported via secondary active transport

glucose, amino acids, B vitamins, Cl-, glucose, bile salts


counter transport

involves exchange of one item for a similar item

like a cation for a cation (Na for H)


charactersitics of isotonic fluid

NaCl is pumped in, creates high osmotic pressure, causes water to flow in, creates high hydrostatic pressure, this causes water ions to flow into blood


which is more permeable jejnum or colon?

jejunum is more permeable than colon


how do tight junctions control back leak?

thru the paracellular pathway (which is permeable to low molecular weight substrates and water)


colon: tight or loose epithelium?

tight = water absorber


small intestine: tight or loose epithelium?

loose !
- ineffective in absorbing water and ions (back leaK)
- ineffecitve at maintaining a minute buildup of Na across epithelium
- lower transepithelial potential difference
- easier for Na pump to transport Na out of cell causes transcellular movement of Na to decrease along with a.a., sugars, and other nutrients that enter the cell thru a coupled Na-dependent system at the apical membrane


solvent drag

a mechainsm by which water flow from lumen to blood thru the paracellular pathway draws low molecular weight substrates with it


what weak electrolytes are absorbed from the colon?

VFAs: acetate, butytrate, propionate

negatively charged drugs


normal ammonia absorption

ammonia is brought to liver from colon --> liver detoxifies ammonia via urea cycle --> converts ammonia to urea


if ammonia absorption fails

happens in liver disease

ammonia accumulates in blood causes hyperammonia, can cause hepatic encephalopathy

can be managed by reducing colonic absorption of ammonia (give a synthetic disaccharaide which bacteria will break down and make H+ to combine with ammonia)

converts ammonia to ammonium


ferrous iron (Fe++)

= absorbed


ferric iron (Fe+++)

not absorbed


where is iron mainly abosrbed



normal iron absorption

cells that absorb iron (ferritin), form iron-binding proteins that complex with ferrous iron entering the cell through an energy dependent brush border


what happens when iron stores are low

little enters crypt cells from the blood --> migration to top of villi is low in iron binding protein --> Fe is absorbed from lumen at top


what happens when iron stores are high

more enters crypt cells --> induces synthesis of Fe binding protein --> migration up villi --> iron is stored at tip and is eventually sloughed and excreted


carbohydrate (CHO) absorption

starch digsted --> brush border --> starch digestion by amylase --> disaccharides --> monosaccharides --> absorbed



absorbed with GLUT5 (not Na dependent)


glucose and galactose

absorbed with SGLT1


which are released with GLUT2 transporter?


glucose and galactose


protein and a.a. absorption - peptides

absorbed as small di and tri peptides and mainly a.a.

a.a. are Na dependent

dipeptides and tripeptides are H dependent

glutamine a.a. - most important fuel source for SI epithelium


fat absorption

micelar solubilization
consists of: bile salts, carbs, triglycerides
micelles diffuse thru unstirred layer
micelles are no absorbed they break apart and components are absorbed at brush border

absorption of fatty acids and monoglycerides

reesterification and fromation of cylomicrons


where do chylomicrons go



where do fat and carbs go?



calcium absorption

highest in duodenum

regulated by form of Vit D (1,25 dihydroxycholecaliferol) - stimulates syntehsis of Ca binding protein in duodenal enterocytes

Ca absorption involves: Diet (Vit D) --> liver --> kidney --> duodenal enterocyte


viral diseases:

TCE coronoavirus - severe villi atrophy
rotavirus - villi damage to tips
parvovirus - attacks crypt cells --> collapse of villi


adhesion of organisms to cells:

cryptosporidium - damages cell, causing villi blunting
E.coli - DOES NOT DAMAGE CELL or alter length - enterotoxin does!
salmonella - affects large intestine (produce enterotoxin --> diarrhea)

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