deck_636935 Flashcards
GI Functions
Digestion and absorptionEliminationProtection of epithelium
Myenteric plexus
Part of enteric nervous systemlocated b/w circular and longitudinal muscle layersRegulates motility, peristalic and segmental contractions
Submucosal Plexus
Part of enteric nervous systemlocated b/w submucosa and circular muscularisregulates: glandular, endocrine and epithelial cell secretion; also circular muscle layer
Parasymp on GI
synapse in enteric nervous ganglionsexcitatory and release of ACH–> increase ENS activityIncrease motilityvasodilation (indirect)Increase secretionDecrease sphincter tone
Sympathetic on GI
Inhibitory and release norepinephrine –> decrease ENS activityDecrease motilityvasoconstrict (direct)Decrease secretionincrease sphincter tone
Blood drainage through GI
Drains into hepatic portal vein –> liver –> general circulation
GALT roles
- Protection from pathogens2. immunogenic tolerance to food and “good” bacteria
Gastrin
Released by G cells of antral stomach Stim by: small peptides and aa’s distention of the stomach vagal stimulation by GRP Gastrin stimulates: parietal cells to secrete HCl ECL cells to secrete histamine –> stimulates acid secretion growth of mucosaAcid (low pH) in the stomach inhibits gastrin release.
CCK
Released by I cells in duodenumStim by: proteins, fat CCK stimulates: gallbladder contraction –> bile release secretion of pancreatic enzymes (lipase and proteases) inhibits gastric emptying increases secretin action growth of exocrine pancreas
Secretin
Released by S cells in duodenumStim by: H+ and FA’sSecretin Stimulates: HCO3 release from pancreas pancreatic secretion exocrine pancreas growth inhibits parietal cell H+ release
GIP
Released by: cells of the duodenum and jejunumStim by: oral glucose, FAs, AAsGIP stimulates: insulin release by pancreatic ß-cells (sensitizes beta cells) may inhibit gastric acid secretion
Motilin
Released by: duodenal mucosa during fastingincreases contraction and motility–> prepare GI for next meal
Ghrelin
Produced by stomachincreases b/w mealscauses: GH release, hunger, weight gain, fat massdecreases: fat utilization
Vasoactive Intestinal Peptide
relaxes GI SM (particularly around sphincters)stim’s local mesenteric blood flowstim’s pancreatic and intestinal fluid secretion
Somatostatin
GI paracrine that puts stops GI activityinhibits GI hormones and gastric acidinhibited by vagal parasympathetic
Interstitial Cells of Cajal
Pacemaker cells of SM in the GIDrives the frequency of slow waves –> determines rate of action potential and contraction
Hormones and Nerves effect on GI SM
set slow wave frequency by ICC not changed by hormone or nervesamplitude/contraction strength (via increased action potential frequency) can be modified Norepinephrine –> decrease contractile activityACH –> increases contractile activity both modulate Ca efflux and influx
GI SM excitatory agents
ACH, substance P, Opeoids, CCK, Bombesin, serotonin
GI SM inhibitory agents
VIP, glucagon, NO, somatostatin, norepinephrine
Bile functions
emulsify fat for digestion by lipasessolubilize FA’s into micellesvehicle for toxins and waste
describe flow of bile
bile salts and acids secreted from liver continuouslysecretion draws water and electrolytes into bileadditional fluid and electrolytes added by ductsclose sphincter of odi and hydrostatic pressure causes filling of gallbladdergallbladder concentrates bile CCK and ACh stimulate release of bilebile acts in small intestines -> reabsorbed in ileum to portal vein -> back to liver
Primary Bile acids
synthesized in hepatocytes from cholesterolcholic acidchendodeoxycholic acid
secondary bile acids
synthesized by gut bacteria from primary bile acids
bile salts
form by liver from conjugating bile acids with glycine or taurinedecreases pKa -> more soluble in intestinal pH
components of bile
bile acids and salts 50%cholesterol 4%lecithin (phospholipid) 30-40%bile pigment (bilirubin) 2%
bile and blood flow through liver
counter current flow ->allows exchange of bile and blood and minimizes concentration gradient b/w the bile and bloodbile caniculi carry bile peripherally while hepatic artery and portal artery carry blood centrallyCanicular fluid similar to plasma… ducts modify
blood and bile transport
bile acids: secondary active transport into hepatocyte from blood, facilitated diffusion into bilewater and electrolytes: paracellularlly down [] gradient
regulation of bile flow
Feedback regulation: B.A.’s in hepatic portal blood -> stim. bile acid secretion and inhibit bile acid synthesissecretin - stim. duct cell secretionCCK and ACh - stim gallbladder contraction
reabsorption of bile
95% reabsorbedIleum: active absorption of ionized conjugated bile salts (Na dependent)passive of unconjugated and unionized conjugated throughout entire SI and colon
total body bile pool
2-3 grams -> cycles through liver multiple times per day -> total liver bile output 15-30 g/day
colon cancer
associated with high fat dietsLithocholic Acid is also linked to colon cancerVitamin D is associated with less colon cancer
Formation of gallstones
organ substances of bile precipitate out of solutionCholesterol gallstone: increased cholesterol and decreased bile acids = gallstones Pigment stone: formed by precipitation of unconjugated bilirubin and Ca
risk factors for gallstones
ObesityGenderEthnicityAge Rapid weight lossFastingEstrogendiabetescholesterol lowering drugs
Carb digestion
begins in mouth with alpha amylasecontinues in duodenum w/ lumenal break down of polysaccharidescontact membrane digestion of disaccharides by brush border (alpha dextranase)absorption of monosaccharides
Carb absorption
Must be monosaccharideslumen -> enterocyte: SGLT1 (fructose via GLUT 5)enterocyte -> blood: GLUT 2
exocrine pancreas produces
enzymes to digest carbohydrates, fats, and proteins and HCO3 to neutralize gastric acid.
acinar cells and stimuli
produce enzymesstimuli: CCK, ACh
ductal cells and stimuli
produce HCO3- (aqueous secretion)stimuli: secretin (CCK and ACh potentiate)
secretin 2ndary messenger
cAMP
CCK and ACh 2ndary messenger
increased [Ca] via IP3
Most Carb abnormality
deficiency in digestion increased osmotic pressure in lumen -> osmotic diarrhea ex) lactose intolerance
acinar cells and stimuli
produce enzymesstimuli: CCK, ACh
ductal cells and stimuli
produce HCO3- (aqueous secretion)stimuli: secretin (CCK and ACh potentiate)
secretin 2ndary messenger
cAMP
CCK and ACh 2ndary messenger
increased [Ca] via IP3
Most Carb abnormality
deficiency in digestion increased osmotic pressure in lumen -> osmotic diarrhea ex) lactose intolerance
Protein digestion
All proteins assimilatedbegins in stomach with pepsinThen proteases in SI take over and cleave proteins into AA’s, di, and tri peptides
Pancreatic proteases
trypsin, elastase, chymotrypsin, carboxypeptidase A and BTrypsin is activated by enterokinase, then activates all the restDigest themselves after
Protein absorption
Absorbed across 7 different AA specific channelsAA absorption is Na coupledPeptide absorption is proton coupleddi and tri peptides absorb faster (70% of absorbed protein)
Lipid digestion:
begins in mouth and stomach via lingual and gastric amylases -> release FA’smajority digested in SI: bile eulsifies fats -> increased exposure of fats to amylases -> TG’s -> FA’s and MonoglyceridesPL’S -> lysolecithin, FA’s, monolipidsCHO -> free cholesterol, FA’s, Glycerol
Lipid absorption
bile salts aid in micelle formation of lypolitic products -> transports to acid microclimate outside of enterocytes -> lipids are protonated by acid aid in solubility and diffusion into enterocytes with help of FA binding proteinsglycerol = soluble -> free diffusion short and medium chain -> free diffusionCholesterol absorbed slowest
Chylomicron structure
core: FA’s and cholesterolsurface: phospholipids and apoproteins
Chylomicron synthesis
Lipids are converted back to TG’s, PL’s and cholesterols are re-esterified in SERchylomicron form by GolgiChylomicron is exocytized and enters lacteal -> enters blood at thoracic duct
3 types of lipid absorption abnormalities
- decreased bile salts ex) resected ileum2. increased acid in duodenum -> from hypersecretion in stomach ex) zollinger-elison syndrome3. Pancreatic insufficiency -> decreased enzymes ex) cystic fibrosis, pancreatitislipid absorption abnormalities are more common than carb and protein
ß-lipoproteinemia
Failure of enterocytes to synthesize apoprotein B results in the inability to export chylomicrons
Fat soluble vitamins
D. E. A. K
Ca absorption
- passive paracellular2. active transcellular - vit. D stim taken up in Ca channel extruded by Na-Ca pump
Iron reabsorption
reabsorbed as Fe2+enters: DCT1 channel or binds transferrin
B12 reabsorption
binds heptacurrin in mouthbinds IF in duodenumtaken up in ileum by IF receptor mediated transport
pernicious anemia
autoimmune destruction of Parietal cells in stomach -> decrease IF -> decreased B12 reabsorption
fluid in intestines and how much aborbed
9L in (2 ingested, 7 secreted)8.8 absorbed (majority in SI)
Small intestines absorption
leaky epithelium -> isotonic absorption
Colon aborption
tight epithelium -> hyperosmotic absorption
How is feces alkalinized
by the colon Cl-HCO3 exchangernet secretion of H2CO3 and absorption of NaCl in these cells
K+ in intestines
absorbed in small intestines -> passively paracellularlysecreted actively by K+ channels (aldosterone stimulated) and passively paracellularly
Intestines reabsorption site
villi
intestines secretion site and substance
cryptsCl is main secretion (through CFTR regulated by cAMP)Na (paracellularly) and water follows
4 causes of diarrhea
- secretory - increased Cl secretion (cAMP mediated)2. Osmotic diarrhea3. mucosal destruction - leaky epithelium and decreased absorption and increased secretion4. increased motility - decrease absorption time
GI secretegogues
Mucosa: serotonin, neurotensin, guanylinLamin propria: prostaglandins, NO, histamineEnteric nerves: ACh, VIP
Stress Activation (LES)
pressure on LES –> contracts
Active relaxation (LES)
swallow causes vagal relaxation of LES (VIF action potentials) and Orad stomach –> remains relaxed till peristalsis ends
swallowing phases
oral: voluntarily initated, becomes involuntarypharyngeal: pressure drops -> food passes -> pressure increases againesophageal: slower peristalsis
Gastric SM function
1) relax -> accomodate food (fundus)2) contraction -> mix and digest food3) peristalsis -> propel into duodenum (body and antrum)
Receptive relaxation
relaxation of orad region of stomach as food enters -> allows for increased digestion (particularly by alpha amylase) mediated by vagus (vagovagal) VIP important in relaxationCCK, secretin, GIP increase orad distensibility too
Gastric emptying stimulators
filling of stomach -> local enteric -> antral contractionproteins in stomach -> gastrin -> antral contraction
gastric emptying inhibitors
acid in duodenum -> secretin -> slows antral contraction, + pyloric contractionfats in duodenum -> CCK -> antral and pyloric contractionpeptides and AA’s in duodenumhyperosmolarity in duodenum
Migratory Motor Complex
sweeps undigestible, cell debris, mucus etc into colonduring fasting state3 phases: no spike potential -> irreg spike potentials -> regular spike potentialsMotilin stimulates
slow waves in stomach vs SI
stomach: slow waves trigger contractions, even if smallSI: only slow waves reaching threshold and causing AP’s or SP’s cause contraction
SI muscle contraction stimulators
Opiates, Parasympathetic, serotonin, opiates, gastrin, cck, insulin
SI muscle contraction inhibitors
Sympathetics, VIP, Glucagon, NO
Law of intestines
distension -> contraction above and relaxation below
Vomiting
ANS -> controled by vomiting center in medullaprotective (prolonged -> dehydration, alkalosis, hypokalemia)reverse peristalsis in distal SILES relaxesinspiration and abdominal contractionstrong abdominal contraction moves material through UES
motility of cecum and prox colon
high tone and enteric inhibits to relax -> mixing contractions -> 1-3 mass movements per day
saliva osmotic state
ALWAYS hypotonic to plasmaleaving acini it is isotonic to plasm -> ducts remove NaCl
rate of secretion and saliva
increased secretion rate -> less ductal modificationdecreased secretion rate -> more hypotonic
Salivary gland secretion stim
parasymp (ACh) and symp (norepinephrine)parasymp = stronger - increases ion transport, increases myoepithelial cell contraction, direct, metabolic and kallikrein stimulated vasodilation
components of gastric juice
HCl -> parietal cellsPepsinogen -> chief cellsMucin -> surface epithelial and mucous neck cellsIF -> parietal cells (essential)ALWAYS isotonic to plasma
Parietal HCl secretion mechanism
H2CO3 -> H+ to lumen via H-K exchange and HCO3 to blood via HCO3-Cl exchangeCl- to lumen via Cl channel
stimulators of gastric HCl secretion
AChGastrinHistamineTogether they potentiate each others response
Cephalic Phase
MOUTH: parasympathetic -> saliva secretionSTOMACH: vegas -> gastrin -> parietal cells and ECL cells -> HCl and histamine -> parietal cells -> HCl- vegas -> pepsinogenINTESTINE: vegas -> pancreatic enzyme secretion (acini)
Gastric phase
MOUTH: noneSTOMACH: - vegas -> gastrin -> parietal and ECL -> HCl and Histamine- distention -> parietal -> HCl- vegas -> parietal -> HCl- vegas -> chief cells -> pepsinogen- AA’s and fat -> gastrin -> parietal -> HCl- H+ -> chief -> pepsinogen and parietal -> decrease HClINTESTINE: vegas -> Pancreatic acinar -> enzymes
intestinal phase
MOUTH: nothingSTOMACH: CCK -> decreased gastric emptying and decreased HCl production- Secretin -> decreased HClINTESTINES: - AA’s, Fat, CHO -> CCK -> gallbladder contraction and Oddi relax and acinar secretion- H+ -> Secretin -> HCO3- Vegas -> ACh -> gallbladder contraction and acinar secretion- CHO -> GIP -> B-cell sensitization
inhibition of Gastric acid
secretin, CCK, GIP and Hypertonicity
Pepsinogen secretion stim
Vegas stim, Gastrin, Acid, Secretin, CCK
Pancreatic Acinar cells
secrete digestive enzymesACh and CCK mediated
Pancreatic Duct cells
secrete aqueous secretion -> HCO3 and fluidSecretin (potentiated by CCK and ACh)
pancreatic secretion
parasympathetic stimulatesSympathetic inhibits at all rates secretion is IsotonicCl and HCO3 are reciprocal
