GI - Small Intestine Flashcards
SI section length/time
2 - 4 hrs in total, 3/4 length GI
duodenum: 8 inches
jejunum: 8 ft
ileum: 12 ft
ways to increase SA in SI
circular folds (x3)
villi (x10)
microvilli (x20)
total = 250 sq m
crypts of lieberkuhn fxns
secrete water and electrolytes
nurseries - high mitotic activity makes cells that migrate up to replace old villi cells (100 million shed/min)
cells migrating from crypts to villi
[ ] of brush border enzymes goes up and absorptive capacity goes up as they get higher
segmentation description
circular contractions @ alternate sites
main mvmt in SI
segmental contraction rates by area
duodenum: 12/min
jejunum: 10 - 11/min
ileum: 8 - 9/min
peristalsis location
occur for only short length of intestine
types of SI motility
segmentation*
peristalsis
migrating motor complex
ileocecal juncture structure
valve-like folds of ileum protrude into cecum
SM of last few cm is thickened
ileocecal juncture regulation
neural and hormonal
ex: gastroileal reflex - gastrin stim extrinsic nerves relax sphincter
ileocecal juncture fxn
prevent contamination of SI by LI bacteria
makes for one way transit
places food can be digested
in GI secretions
on luminal surface of GI
inside epithelial cells
CHO digestion (main)
duodenum + jejunum
kinds of CHO we eat
amylopectin**
amylose*
cellulose
animal glycogen
amylopectin
plant starch
major source of CHO in most humans
glucose polymer
alpha-1,4 glycosidic bonds w. branch points at alpha-1,6
salivary amylase actions
catalyze the hydrolysis of internal alpha-1,4 bonds
not terminal alpha-1,4 or alpha-1,6
main products of starch digestion
maltose, maltotriose, branched oligosaccharides (alpha-dextrins?)
actions of maltase
cleaves terminal alpha-1,4 bonds
starch digestion
starch + salivary amylase –>
partially converted starch + pancreatic amylase –>
maltose, maltotriose, alpha-dextrins + maltase, maltase, isomaltase (brush border) –> GLUCOSE (in lumen)
how to absorb monosaccharides
Into epi from lumen: glucose: use SGLT1 w/ Na galactose: use SGLT1 w/ Na fructose: use GLUT5 out of epi into cap: all use GLUT2
lactose intolerance
low levels of lactase
lactose isnt broken down
lactose is osmotically active
brings water into lumen –> diarrhea
protein digestion location
stomach
upper GI
is all CHO absorbed in SI?
5 - 15% CHO goes to colon
CHO metabolized by bacteria to make SCFA (important fuel for colon epi cells)
protein digestion in stomach
max 15% protein digested by pepsin in stomach
not totally necessary
intestinal protein digestion
proteins + pancreatic –> oligopeptides + brush border peptidases –> AAs, dipeptides, tripeptides
pancreatic enzymes that digest protein
trypsin
chymotrypsin
carboxypeptidase (A/B)
elastase
brush border peptidases
amino-oligopeptidase
amino peptidase
dipeptidyl aminopeptidase
absorption of small peptides
single membrane transporter
high affinity for di and tri peptides
low affinity for larger peptides
absorption of AAs
7 diff AA transporters
some Na dependent, some independent
main locations of lipid digestion
duodenum
jejunum
digestion of fats
dietary fat + bile salts –> lipid emulsification + pancreatic lipase –> monoglyceride, FAs + bile salts –> micelles
where are bile salts reabsorbed
terminal ileum
absorption of fat
micelles absorbed passively
processing recycled bile salts
hepatocytes extract bile salts
unconjugated bile salts reconjugated in hepatocytes
secondary bile salts rehydroxylated
water in and out of GI system
GI absorb ~ 9 L /day
2 L water ingested
7 L GI secretions
only 100 ml of water in feces
chyme tonicity
hypertonic in stomach
isotonic in duodenum
Na absorption
*cotransport w/ glucose and AAs (D/J)
cotransport w/ bile salts (I)
NaCl secreting cell actions
Cl into lumen via CFTR (when open)
Na into lumen paracellularly
need Na in lumen for Na-nutrient reabsorption
(Na/K/Cl into cell from blood by cotransporter)
NaCl secreting cells and pathogens
cholera ups cAMP
opens CFTR
much Cl out
much water follows
oral rehydration therapy
give glucose and Na
actively pumped in together
changes dire`ction of Na mvmt
cholera and CF
CF patients dont get diarrhea from cholera – abnormal CFTR
carriers do – sufficiently normal
Ca absorption locations
all portions of intestines
esp. duodenum and jejunum
things that make you Ca deficient
Ca deficient diet
growth
pregnancy
lactation
Ca absorption based on Ca need
need for Ca up
up synth of vit D precursor
up Ca absorption
how vit D changes Ca absorption
- rapid open Ca channels
- increase calbindin synthesis (maintain Ca gradient so Ca can come in)
- increase # of Ca ATPase (gradient)
excessive iron
toxic (mammals don’t have excretion path)
iron absorption location (+cell)
proximal duodenum
enterocytes
iron adsorption and pH
need acidic environment
antacids/gastric acid secretion issues interfere w/ Fe absorption
iron absorption in enterocyte
leave enterocyte via ferroportin transporter
bind to ferritin and get sloughed off
how metals get into enterocytes
divalent metal transporter-1 (DMT-1)
zinc, lead, copper
iron absorption when iron stores full in liver
liver secretes hepcidin hepcidin binds to ferroportin ferroportin degraded all iron bind to ferritin instead limit iron intake
absorption in duodenum
CHO, PRT, FAT (high)
Ca, Fe, folate (moderate)
bile acids (very low)
absorption in jejnunum
CHO, PRT, FAT (moderate)
Ca, bile acids (low)
absorption in the ileum
CHO, PRT, FAT, Ca (low)
cobalamin (B12) (moderate)
bile acids (high)
results of intestinal inflammation
increase motility
move too fast for proper absorption
diarrhea, dehydration and pH imbalance
order of hormones during a meal
gastrin
secretin/CCK
motilin
colon fxns
absorption: Na, SCFAs, water
secretion: K, mucus
colon motility
mix: haustrations - like segmentation but less frequent
propulsion: mass mvmts - propel distances, gastrocolic reflex
