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83 Cards in this Set

  • Front
  • Back
in which part of the SI does a large amt of digestion occur?
duodenum, jejunum
what are fold of kerckring?
longitudinal folds of SI; villi project from the folds with microvilli on each intestinal cell
allows for massive incr in absorptive SA
what are cypts?
projection down into the surface at the base of the villi (3 per villi)
what are the 3 cells of the SI?
enterocytes, goblet cells, crypt cells
replaced every 3-6 days
enterocytes of SI
columnar epithelial cells that make up the villi
have microvilli from apical border
digest, absorb, secrete
which enterocytes on a villi are best able to absorb and digest?
the ones near the tip of the villi
goblet cells and crypt cells of SI
goblet-mucus
crypt-at base of villus; proliferative cells of intestine; form both enterocytes and goblet cells; secrete fluid, electrolytes
fxn of SI: (5)
mix chyme with digestive juice, bile
reduce size of chyme particles to incr solubility
bring chyme into contact with absorptive surface
propel chyme into colon
2-4hrs to go length of SI
what are the 3 types of contractions in the SI?
segmentation, peristaltic, migrating motility complex
describe segmentation
most common
contraction of one segment of circular smooth mm moves chyme in both directions-> mixes
net movement towards colon b/c more contractions in proximal SI
fxn of peristalsis
propel chyme
only covers short distances
describe the migrating motility complex (MMC)
every 90 min
clears remaining chyme in SI
(~ migrating myoelectric complex in stomach)
what must occur for contraction in SI?
spike potentials must be present on top of slow waves (vs. stomach)
what det the strength of the contraction?
proportional to freq of spike potentials generated by amplitude of the slow wave

(grter amplitude of slow wave-> more spike potentials-> greater strength of contraction)
how does the freq of contractions change along the length of the SI?
freq decr distally
is SI motility affected by nervous system?
yes
what is the peristaltic reflex/rush?
moves intestinal contents along SI
initiated by chyme that distends or irritates mucosa
can also be caused by infectious diarrhea
what is the intestinointestinal reflex?
overdistention of one segment of SI prevents contraction in rest of SI
prevents movement of material into already distended bowel
what is the gastroileal reflex?
gastric empyting incr peristalsis in ileum and relaxes ileocecal sphincter to allow movement into colon
what are the 2 types of cells of the pancreas rel to GI physio?
acinar cells and ductal cells
fxn of acinar cells of pancreas
prod enzymes for digestion: peptidases, lipases, amylases
fxn of ductule cells of pancreas
rel pancreatic juice with high bicarb
neutralize acidic pH to allow max digestion by enzymes
what is the aqueous component of pancreatic secretion?
isotonic with plasma at ALL rates of secretion
composed primarily of Na and Cl at slow rates; contains Na and HCO3 at high rates
HCO3 higher than plasma but Cl lower than plasma;
Na, K stay the same at all flow rates
initial pancreatic juice
Na and Cl from acinus
modified by ductule and centroacinar cells which secrete HCO3 and absord Cl
transport across ductal cells of pancreas
Na/H antiporter on basolateral surface (Na into cell, H into blood)
H in blood combines with HCO3 to form more CO2 that diffuses back into cell-> forms more HCO3 in the cell that is secreted into duct lumen in exchange for Cl
Na/K ATPase on BL mbr keeps intracell Na low for Na/H exchange
how does venous blood from an actively secreting pancreas differ from nonactive?
with active pancreas, more H is being transported into blood-> more acidic venous blood
what det the rate of secretion of HCO3 into the duct lumen?
the presence of Cl in the duct lumen; the presence Cl in the duct lumen dep on a fxning Cl channel in the apical mbr that moves Cl from cell into lumen (CF channel)
what follows HCO3 into pancreatic lumen to keep neutral?
Na
how does water flow across ductule cell of pancreas?
permeable to water; osmosis
what comprises the enzymatic component of pancreatic secretion?
active lipase and amylase
inactive proteases: typisin and chymotrypsin (activated in SI)
trypsin inhibitor to prevent autodigestion
regulation of pancreatic secretion: cephalic and gastric phases
ACh acts on acinar and ductule cells
vasovagal reflex stim by stomach distention-> secretion
when does most pancreatic secretion take place?
intestinal phase (70%)
stim by acid, fat and protein in duodenum
how does acid in the duodenum activate pancreatic secretion?
acid rel secretin from S cells of duodenum
Secretin acts on ductule cells to incr HCO3 secretion
how do fat and protein contribute to pancreatic secretion?
stim rel of CCK from I cells of duodenum
CCK stim acinar cells to rel enzymes
describe the potentiation of pancreatic secretions?
CCK and ACh potentiate actions of secretin on ductal cells
how does pancreatic secretion resp to a meal?
what is digested det what is secreted
how does a high protein, low carb diet affect pancreas secretion?
incr proteases, decr amylases
CCK incr expression of protease genes
secretin and GIP in expression of lipase genes
pancreatitis: causes and forms
due to gallstones or chronic alcoholism
acute and chronic forms
sx of acute pancreatitis
severe abdominal pain
nausea and vomiting, diarrhea
fever
what enzymes are elevated in pancreatitis?
serum amylase and lipase
chronic pancreatitis usually due to:
recurring acute pancreatitis due to chronic alcholism
CF:
red secretion of aqueous and enzymatic components of pancreatic secretion: less aqueous-> concentrated pancreatic juice-> blocks secretion of enzymatic
sx: malabsorption and steatorrhea
what is bile req for?
digestion and absorption of fats
excretion of water insoluble cholesterol and bilirubin
where is bile prod, stored, and what triggers its rel?
prod cont by hepatocytes
stored in gallbladder
rel when chyme triggers CCK rel which stim contraction of gallbladder and relaxation of sphincter of oddi
composition of bile
bile acids
phospholipids
cholesterol
bile pigments
electrolytes
where are bile acids prod? what do they eventually form?
primary bile acids prod in liver from cholesterol
conjugated w/ glycine/taurine and Na in liver to form bile salts that are more water soluble
what is the fxn of bile salts?
form micelles in which FFA,MAG, cholesterol and fat-soluble vitamins can be transported
bile salts amphipathic
what are the main phospholipids of bile? what is their fxn?
lecithin
solubiized by bile salt micelles
micelles able to solubilize other lipids better when they contain phospholipids
how is cholesterol incorporated into bile?
solubilized by micelles and excreted in bile
bile is main excretory path for cholesterol via bile acids
what happens if more cholesterol is in diet than can be solubilized?
crystal forms in bile and may seed gallstone formation
what is the main component of bile pigments?
bilirubin- breakdown prod of hemoglobin
how is bilirubin made soluble? how is it excreted?
conjugated to glucuronic acid in liver
excreted as soluble salt bilirubin glucuronide
NOT part of micelles
what is the electrolyte composition of bile?
Na, Cl, HCO3 (similar to pancreatic juice)
what is enterohepatic circulation?
circulation of bile salts at least 2X per meal (gallbladder, SI, portal circ, liver)
involved in bile secretion
what happens to bile salts when they are rel into the duodenum?
most are ACTIVELY reabsorbed in terminal ileum
transported in portal circulation bound to plasma proteins
how are the bile acids-Na reabsorbed in the liver? electrolytes and water?
bile acids reabsorbed via 2ndary active transport linked to Na reabsorption
req Na/K ATPase to keep intracell Na low
electrolytes and water move along osmotic gradient to be added to bile in liver
what det the rate of bile sale syn in the liver?
det by rate of return to liver
bile salts lost in feces replaced by syn in liver
what is the bile independent fraction of biliary secretion?
dep on vol of water and electrolytes secretion due to presence of secretin
what is the bile dependent fraction of biliary secretion?
dep on amt of bile salts secreted by liver
amt secreted proportional to amt reabsorbed by liver
what is choleretics?
bile salts and bile acids are potent stim of bile secretion
(they also inhibit new bile acid syn)
what are the 2 fxns of the gallbladder?
store bile in interdigestive periods
concentrates bile by actively reabsorbing Na, Cl and HCO3; water follows
what are the 2 stim for gallbladder contraction?
CCK and vagal activity
when is CCK rel and what are its actions on the gallbladder?
rel due to fatty acid and peptides in duodenum
stim gallbladder contraction and relaxation of sphincter of oddi
what are the 2 types of gallstones?
cholesterol and pigment stones
cholesterol 70-80% in W. societies
how do cholesterol stones form?
XS cholesterol cant be solubilized -> crystallizes
seed stone formation
how do pigment stones form?
composed of Ca-bilirubinate
unconjugated blirubin formed in gallbladder; not soluble in bile
precipitates with Ca-> seeds stone formation
how are gallstones treated?
cholecystectomy- remove gallbladder
normal digestion and absorption unaffected; should avoid high fat foods
bile empties slowly but continuously in SI
haustra of LI
present when colon empty
sac-like
ileocecal sphincter
relaxes when ileum distended
contracts when colon distended
segmentation contractions of LI
majority of contractions in prox colon and distal colon
mix contents
contribute to appearance of haustra
peristaltic contractions of LI
moves chyme slowly down length of colon
mass movements of LI
peristaltic wave 1-3 times/day
moves contents long distances
propels contents into rectum
contents of rectum
usually empty
freq of segmental contractions greater in rectum than sigmoid colon-> moves material into sigmoid colon (allows for absorption of suppositories)
what is the rectosphincteric reflex?
when fecal material moves into rectum, rectum contracts and internal anal sphincter relaxes
when is the urge to defecate produced?
when rectum filled 25%
what prevents defecation?
external anal sphincter (skeletal mm.)
what happens if defecation doesnt occur after urge is produced?
internal anal sphincter contracts and rectum relaxes to move feces back into rectum and urge to defecate subsides
contents of feces
inorganic material
undigested plant fibers
bacteria and water
contents rel unaffected by diet b/c lg amt of feces of nondietary origin
ex: even if starving will defecate
hirschsprungs disease
megacolon
absent enteric NS from segment of colon (normally inhibitory/regulates contractions)
loss-> tonic contraction and contents accumulate proximal to segment
severe constipation
tx by removing segment
constipation
MORE segmentation contractions
incr time through colon
what are some things that can lead to constipation?
ignoring urge to defecate
lack of exercise
meds-narcotics, antidepressants
old age
longterm use of laxatives
divertilulosis/ diverticulitis
small finger-shaped pouches through weak colon wall
can be inflamed
local pain
can perforate wall
may be due to longterm lack of fiber in diet
many are asx
crohns disease
breakdown of wall/transmural inflammation (primarily in SI)
tx with removal