BRS Physiology Flashcards
layers of the GI tract
epithelial cell Lamina propria muscularis mucosae submucosal plexus circular muscle myenteric plexus longitudinal muscle serosa
ELMS CMLS
vagus nerve innervates
stomach, upper large intestine, pancreas, esophagus
pelvic nerve innervates the
lower large intestine, rectum, anus
myenteric plexus (auerbach plexus)
motility of GI smooth muscle
submucosal (meissner plexus)
controls secretion and blood flow
actions of gastrin
stimulates H+ release by parietal cells
stimulates growth of gastric mucosa
gastrin secreted by what cells
G cells of the gastric antrum
stimuli for gastrin secretion
small peptides and amino acids in lumen of stomach
distension of stomach
vagal stimulation, mediated by GRP
inhibition of gastrin secretion
H+ in the lumen of the stomach: negative feedback
somatostatin: Gi
Actions of CCK
1) HCO3- release from pancreas potentiation with secretin
2) growth of Exocrine pancreas
3) pancreatic enzyme secretion
4) inhibits gastric emptying
5) contraction of the gallbladder and relaxation of sphincter of Oddi
HEPIC
cells that release CCK
released from I cells of duodenal and jejunal muscosa
stimuli for release of CCK
small peptides and amino acids
fatty acids and monoglycerides
(no triglycerides)
Secretin is homologous to ____
glucagon
actions of secretin
coordinate to reduce amount of H+ in the lumen of SI
1) stimulates pancreatic HCO3- secretion and increases growth of exocrine pancreas
2) stimulates HC)3- and H20 secretion by liver and increases bile production
3) inhibits H+ secretion by gastric parietal cells
secretin from what cells
S cells of duodenum
stimuli for secretin release
H+ in duodenum
Fatty acids in lumen of duodenum
GIP is homologous to
secretin and glucagon
actions of GIP
1) stimulates insulin release
2) inhibits H+ secretion by gastric parietal cells
Stimuli for release of GIP and where secreted
secreted by duodenum and jejunum
fat, protein, carbs,
FA,AA,oral glucose
GLP-1 action
binds pancreatic B-cells and stimulates insulin secretion
somatostatin inhibits what
is inhibited by?
1) inhibits release of all GI hormones, inhibits gastric H+ secretion
2) inhibited by vagal stimulation
histamine action
increases H+ secretion directly
potentions effects of gastrin and vagal stimulation
VIP homologous to?
secretin
VIP action
relaxation of GI smooth muscle including lower esophageal sphincter
stimulates pancreatic HCO3- section, inhibits gastric H+ secretion
GRP (bombesin) action and released from
released from vagus nerves that innervate G cells
stimulates gastrin release from G cells
Enkephalins secreted from
secreted from nerves in mucosa and SM of GI tract
enkephalins action
stimulate contraction of GI smooth muscle
inhibit intestinal secretion of fluid and electrolytes
Satiety center location
ventromedial nucleus of hypothalamus
feeding center
lateral hypothalamic area
anorexigenic neurons release
POMC and decrease appetite
orexigenic neurons release
neuropeptide Y and stimulate appetite
leptin
secreted by fat cells, decrease appetite
ghrelin
secreted by gastric cells, increase appetite
location of highest freq slow wave contraction and low
high is in duodenum
low is in stomach
achalasia
lower esophageal sphincter does not relax during swallowing and food accumulates in the esophagus
orad region of stomach
fundus and proximal body
contains oxyntic glands and responsible for receiveing ingested meal
caudad region of stomach
distal body and antrum
responsible for contactions that mix food and propel it into the duodenum
what is the regulator of contractions every 90 mintues even under fasting conditions
motilin
when is the rate of gastric emptying the fastes
when the stomach contents are isotonic
fat ___ gastric emptying by stimulating the release of ___
inhibits, CCK
H+ in the duodenum ___ gastric emptying
inhibits
segmetation contractions
mix intestinal contents with back and forth motion of chyme
when food in the intestinal lumen is sensed by __ they release ___ which bind to __ and initiate the peristaltic relex
enterochromaffin cells, 5-HT, intrinsic primary afferent neurons (IPAN)
gastroileal relex
mediated by extrinsic ANS and possibly gastrin
triggered by food in stomach
where in the colon is most water absorbed
proximal colon
initial starch digestion is done by what in saliva
a-amylase (ptyalin)
initial triglyceride digestion is done by what in saliva
lingual lipase
composition of saliva
high volume high K+ and CO3- low Na and Cl hypotonic a-amylase, lingual lipase, kalikrein
at the lowest flow rate
lowest osmolarity, lowest Na+ and Cl- and HCO3-
highest K+ concentration
at highest flow rate
composition of saliva is closest to that of plasma
saliva is formed by 3 glands
parotid, submandibular, sublingual
STRUCTURE OF GLAND:
Acinus
branching duct system
myoepithelial cells
acinus, secrete initial saliva
BDS, lined with columnar epithelial cells, modify saliva
myoepithelial cells, line acinua and initial ducts, contract and eject saliva into mouth
ducts modify initial isotonic saliva
reabsorb
secrete
reabsorb Na+ and Cl-
secrete K+ and HCO3-
aldosterone working on ducts
reabsorb Na+ and secrete K+
why does saliva become hypotonic
ducts are relatively impermeable to water
parasympathetic stimulation of saliva production
NT and receptor and second messenger
Ach binds muscarinic receptors on acinus and ductal cells
second messenger is IP3 and increased Ca2+
what is an anticholinergic drug that inhibits production of saliva and causes dry mouth
atropine
sympathetic stimulation of saliva production
NT and receptor and second messenger
NE binds B adrenergic receptors on acinar and cutal cells and the second messenger is cAMP
what increases saliva production
food in mouth
smells
conditioned relex
nausea
what decreases saliva production
sleep
dehydration
fear, anticholinergic drugs
parietal cells secrete __ and _
where and resbsorb __
HCL and intrinsic factor
into lumen of stomach, absorb HCO3- into bloodstream
in parietal cells how is H+ transported into the lumen of the stomach?
through the H+/K+ ATPase
Cl- is also transported into the lumen as well = HCl
what drug inhibits the H+/K+ ATPase
omeprazole (proton pump inhibitor)
what is the HCO3- that is reabsorbed in parietal cells exchanged for?
Cl-
HCO3- is secreted in pancreatic secretions to neutralize H+ ions in SI
effect of vomiting
if vomiting occurs H+ never in SI and no HCO3- secretion causes metabolic alkalosis
vagal stimulation of gastric H+ secretion:
Direct and indirect
Direct: vagus nerve innervates parietal cells with Ach binding M3 receptor and IP3 and increased Ca2+ cause release H+
indirect: vagus n innervates G cells of antrum with GRP which secrete gastrin, bind to CCKb receptor and stimulate release of H+ from parietal cells
- IP3 and ca2+
atropine effect
anticholernergic drug blocks direct pathway of H+ secretion only
gastrin stmiulates which cells
parietal–H+
enterochromaffin-like cells (ECL)—> histamine secretion—> H+ secretion
Histamine action
released from ECL cells and binds H2 receptor on parietal cells, coupled to Gs protein, cAMP
H2 receptor blocking drug
cimetidine
inhibition of gastric H+ secretion
low pH of less than 3.0
somatostatin
somatostatin direct and indirect pathways
direct: binds to receptor on parietal cell coupled to Gi, inhibits adenylyl cyclase and cAMP
- antogonist of histamine
Indirect: inhibits release of gastrin and histamine
prostaglandins action
inhibit H+ secretion by Gi protein, inhibit adenylyl cyclase and decrease cAMP
Peptic ulcer disease and damaging factors
ulcerative lesion of gastric or duodenal mucosa
H+, pepsin, H. pylori, NSAIDs, smoking, stress, alcohol
gastric ulcer
H+ secretion decreased bc secreted H+ leaks back through damaged gastric mucosa–> more gastrin levels increase
-cause is H. Pylori
converts urea to NH3 with urease so less acidic and can live here
test for H. pylori
give person 13C-urea which is converted to 13CO2 by urease and measeured in expired air
H. Pylori have urease
zollinger-ellison syndrome
gastrin secreting tumor of the pancreas causes increased H+ secretion, no negative feedback
pancreatic secretion contains high concentration of what
HCO3-, also enzymes for digestion of protein, carbs, and fat
pancreatic juice is characterized by
1) high volume
2) about same Na+ and K+ as plasma
3) higher HCO3- than plasma
4) lower Cl- concentration than plasma
5) isotonicity
6) pancreatic lipase, amylase, and proteases
flow rate pancreas juice comp:
high = Na+ and HCO3- mainly, isotonic low= Na+ and Cl- mainly, isotonic
formation of pancreatic secretion
acinar cells secrete initial Na+ and Cl-
ductal cells reabsorb Cl- and secrete HCO3-
secretin and pancreas and second messenger
acts on pancreatic ductal cells to increase HCO3- secretion
happens when H+ goes from stomach to duodenum
-cAMP is second messenger
CCK and pancreas
acts on pancreatic acinar cells to increase enzyme secretion (amylase, lipase, proteases)
-potentiates effect of secretin on ductal cells to stimulate HCO3- secretion
second messengers are IP3 and increased CA2+
Ach and pancreas
released in response to H+, small peptides, aa, FA in duod lumen
stimulates enzyme secretion by acinar cells
potentiates effect of secretin on HCO3- secretion
a-amylases
hydroloze 1,4 glycosidic bonds in starch, yield maltose, maltotriose, and a-limit dextrins
maltase, a-dectrinase, sucrase
in intestinal brush border hydrolyze oligosaccharides to glucose
lactase degrades
lactose to glucose and galactose
trehalase degrades
trehalose to glucose
sucrase degrades
sucrose to glucose and fructose
glucose and galactose from lumen to cells then cells to blood
1) SGLT 1 with Na+ down gradient and glucose uphill
2) GLUT2 from cell to blood
fructose transport
exclusively by facilitated diffusion, cannot be absorbed against concentration gradient
lactose intolerance
absence of brush border lactase so lactose cannot be converted to glucose and galactose for absorption
noabsorbed lactose and H2O remain in lumen and cause osmotic diarrhea
endopeptidases
degrade proteins by hydrolyzing interior peptide bonds
exopeptidases
hydrolyze one amino acid at a time from C terminus proteins and peptides
pepsin
activated from pepsinogen by H+
optimal at pH between 1 and 3
if above 5 pepsin is denatured
trypsinogen to trypsin by what enzyme
enterokinase
what does trypsin work on
chymotrpsinogen, proelastase, and procarboxypeptidase A and B and also trypsinogen to make more trypsin
free amino acid absorbtion
cotransported from lumen to intestinal cell with Na+, then aa to blood via facilitated diffusion
dipeptide and tripeptide absorbtion
cotransported with H+ from lumen to cell
cyctoplasmic peptidases hydrolyze them to aas and then aas to blood via facilitated diffusion
