export_gi 2 Flashcards
gastric secretion inhibitors:
1) neural inputs from ENS and CNS
2) cholecystokinin (CCK)
3) secretin
CCK
stimulus?
- hormone released by I cells in upper part of SI
- FAs and AAs in duodenum
secretin
stimulus?
- hormone released by S cells in upper part of SI
- acidity (low pH) in the duodenum
Short vs. Long Neural Reflex
SHORT: occurs completely within the wall of the GI tract
- Enteric nervous system can act WITHOUT CNS
input/output
LONG: involves output to CNS and input from CNS
parts of SI (high to low)
duodenum
jejunum
ileum
secreted by intestinal epithelial cells to create osmosis
1) sodium
2) Cl-
3) bicorbonate
anatomy of crypt:
- invaginate into underlying lamina propria
- transit-amplyfying cells
- stem cells and Paneth cells
types of epithelial cells in SI and fxns
1) enterocyte- absorption and secretion
2) musuc (goblet)- secrete mucus
3) endocrine- CCK (I) and secretin (S)
4) paneth- anitmicrobial agents
5) stem- progenitor of epithelial cells
ever 3-5 days
SI epithelial surface replaces
what is brush border?
microvilli in intestinal lumen of absorptive cells (apical surface)
What is found inside the villi?
Blood vessels, lymph vessels, smooth muscle, nerve fibers
2 types of motor activity and characterizations
1) fasting- postabsorptive- migrating myoelectric complex (MMC)- peristalsis
2) postprandial (after meal)- absorptive- segmentation- stationary contractions and relaxations
What is MMC?
- short peristaltic waves
- lower stomach down intestine
-sweeps undigestible material and bacteria through intestine
regulation of MMC
- activated by motilin hormone via ENS and ANS
- inhibited by meal in stomach (changes to segmentation)
what is segmentation? and how is it regulated?
mixes chyme and brings into contact with intestinal epithelium
-regulated by pacemaker cells in smooth muscle layer (cells of Cajal), hormones, ENS, and ANS
- gastroileal reflex stim segmentation intensity
- parasymp- increases contraction force
- syp- relaxes
- after meal is absorbed it stops
fxn of pancreas during digestion
secrete digestive enzymes and bicarbonate into SI
-insulin, glucagon, other hormones
composition of pancreas:
exocrine and endocrine (islets ~1-2%)
2 types of pancreatic cells and fxns
1) exocrine (acinar)- panc enzymes digst carbs, fats, proteins, and NAs
2) duct cells- bicarbonate to neut HCl from stomach into SI
regulation of pancreatic secretions:
1) neural- vagus nerve inputs
2) hormones (predominant)-
- CCK- stim by fats and prots- affects acinar cells- release enzymes
- secretin- stim by acid- affects duct cells- bicarbonate release- further effects CCK
effects of CCK after meal
meal–>inc CCK secreation–>inc plasma CCK–>inc pancreas enzyme secrection–>ince flow of enzymes into SA–>in digestion in SI
effects of CCK on secretin and vice versa
increases power of secretion of the other
pancreatic stim by long reflexes?
luminal acid and FAs stim secretions (CCK and secretin) through afferent long reflexes
effects of secretin after meal
meal–>inc secretin in SI–>inc plasma secretin–>inc pancreatic bicarbonate secretion–>inc bicarbonate in SI–>neutralize intestinal acid
duct cells release __ into lumen via the ___.
HCO3, Cl/HCO3 exchanger
___ enters duct cells from blood through ___. while ___ is released into circulation
HCO3, Na/HCO3 cotransporter, H+ (Na/H exchanger)
what triggers HCO3 release in duct cells?
secretin
what innervates acinar cells?
vagus nerve
all nutrients except __ are first sent to the liver
fat
main fxn of liver
- metabolize/detox compound
- make bile
fxnal unit of liver
hepatic lobules
capillaries of liver
hepatic sinusoids
fxn of hepatic sinusoids?
bring bile back to liver for recycling
where is bile taken out of liver?
bile canalculi (form bile duct)
what is bile made of?
- phospholipids (lecithin)
- bicarbonate
- cholesterol
- bile pigments
- bile salts
what do hepatocytes synthesize?
bile salts (from cholesterol) and lechithin
where is bicarbonate released from?
duct cells
sphincter of oddi
where common bile duct enters duodenum
where is bile stored?
gallbladder
what stimulates release of CCK?
fatty acids
fxn of CCK
- stim gallbladder –> bile to duodenum
- relaxes sphincter of oddi to allow
what does secretin regulate? stimulated by?
- bicarbonate secretion
- acid
where (organs) is bicarbonate released from?
pancreas and bile duct
enterohepatic circulation
bile salts enter duodenum via oddi
-bile salts back into circulation from ileum
-returned to liver via hepatic portal vein
how is cholesterol excreted?
in bile
what role does fiber play in bile?
- binds to bile
- bile not able to be recycles
- inc bile in feces
- dec plasma cholesterol (liver needs to make more)
bilirubin
- bile pigment
- made from hemoglobin of digested RBC
how is bilirubin excreted?
urine or feces
jaundice
- inc bilirubin in tissues, mucus membranes, and eyes
- blocked common bile duct
gallstones
- crystallized cholesterol
- when chol is too high relative to bile salts
large intestines anatomy
1) cecum
2) colon
- ascending colon
- transverse colon
- descending colon
- sigmoid colon
3) rectum
large intestine fxn
store and concentrate fecal material
secretions of LI
mucus, bicarb, K+
what causes fluid absorption in LI?
transport of Na+ into blood
ileocecal sphincter
- regulated chyme into cecum
- keeps bact out of SI
- ileal contractions relax it
- LI distension contract it
motility of LI
slow segmentation (~1/30mins)
mass movement of LI
- coincides with gastroileal reflex
- smooth muscles remain contracted
segmental contractions regulated by
parasymp-inc
symp-dec
what triggers defecation
- feces in rectum
- parasymp reflexes
why is defecation voluntary?
internal (smooth) and external (skeletal) sphincters
diarrhea
- inc fluid secretion or dec absorption
- dietary intolerance, infections
meds for diarrhea
- relax intestine
- allow more time for absorption
-dec gastroileal reflex
cholera toxin
inc cAMP –> activate Cl- channels in SI –> Na and H2O follow osmosis
constipation
- dec motility of LI
- distension of rectum
laxatives
- fiber (inc stoll volume)
- lubs (soften stool)
- water retention
- stimulants (inc motility)
IBD
- immune and tissue-repair response not working
- strictures caused by inflammation
crohn’s disease
inflammation and thickening of GI wall
-leads to blockages
ulcerative colitis
- restricted colon
- disrupts mucosa (bleeding, edema, ulceration)
bacteroidetes vs firmicutes in lean/obese
lean: inc bact, dec firm
obese: dec bact, inc firms
