Lecture 18 - SI absorption (Freeman) Flashcards
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
- differences btwn epithelial and nonepithelial cells
- improtance of Na transport mechanisms in teh transport of other substances like water and water soluble nutrients
- driving forces for absorption
- interactions between transport systems
- 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
osmolality
concentation of ions expressed as millimoles/kg of water
osmolarity
concentration of ions expressed as millimoles/liter of solution
tonicity
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 !
consequences:
- 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
duodenum
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
fructose
absorbed with GLUT5 (not Na dependent)
glucose and galactose
absorbed with SGLT1
which are released with GLUT2 transporter?
fructose
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
lymphatics
where do fat and carbs go?
blood!!
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)
