GI Physiology Flashcards
Meissner’s plexus
submucosal plexus, primarily conrtols the secretion and blood flow
Parasympathetics on the GI tract
usually excitatory, carried via vagus and pelvic nerves
Vagus nerve- GI organs
Esophagus, Stomach, Pancreas and upper large intestine
Pelvic Nerve - GI organs
lower large intestine, rectum and anus
Sympathetics on the GI tract
inhibitory
Auerbach’s plexus
Myenteric plexus, controls motility of GI smooth muscle
G cells
in antrum of stomach, secrete gastrin in response to a meal
Actions of gastrin
increases H+ from parietal cells
stimulates gastric mucosal growth
Most important stimuli for gastrin secretion
phenylalanine and tryptophan
others: distention of stomach, vagal stimulation mediated by GRP
gastrin inhibitors
H+ in stomach lumen (negative feedback)
somatostatin
gastrin is secreted by non-beta cell tumors of pancreas
Zollinger-Ellison Syndrome
Peptide that is homologous to gastrin
CCK
Actions of CCK
1) contract GB and relaxes sphincter of Oddi
2) pancreatic enzyme secretion
3) growth of exocrine pancreas
4) potentiates HCO3- from pancreas
5) inhibits gastric emptying
I cells of duodenal and jejunal mucosa
secrete CCK
Stimuli for CCK
small peptides, AA, FAs and monoglycerides
homologous to glucagon
secretin
Actions of secretin
stim panc HCO3- secretion and increase exocrine pancreatic growth
increase bile production
inhibits H+ from parietal cells
S cells
In duodenum, Secrete secretin in response to H+ and FAs in duodenum
Actions of GIP
Insulin release in response to ORAL glucose
inhibits H+ secretion
hormone secreted in response to carbs, fats and protien
GIP
Somatostatin
secreted by cells throughtout the GI tract in response to H+ in lumen
inhibits release of ALL GI hormones
inhibits gastric H+ secretion
Histamine
Secreted by mast cells of the gastric mucosa
increases gastric H+ secretion directly and potentiating gastrin and vagal stimulation
VIP
relaxes the lower esophageal sphincter
stimulates the pancreatic HCO3- secretion and inhibits gastric H+ secretion
secreted by pancreatic islet cell tumors
VIP
presumed to mediate pancreatic cholera
Bombesin
GRP, release from vagus nerves that innervate the G cells
stim gastrin release from G cells
Stimulate the contraction of GI smooth muscle, particularly the LES, pyloric and ileocecal sphincter
Inhibit intestinal secretion
Enkephalins
Opiate use in GI tract
Tx diarrhea
Tonic contractions
LES, orad stomach, ileocecal and internal anal sphincter
always closed unless stimulated to open
Phasic contraction
esophagus, stomach, gastric antrum, small intestine. contract and relax periodically
oscillating membrane potentials inherent to smooth muscle of GI tract
Slow waves
Pacemaker of GI tract
interstitial cells of Cajal
Mechanism of Slow Wave production
Cyclic calcium channels open (depolarization) which brings mem potential closer to threshold
followed by K channels opening (repolarization)
Slow wave frequency
lowest in stomach (3 slow waves/min)
highest in duodenum (12 slow waves/min)
Swallowing coordination
Medulla
Sequence of Events in Swallowing
Nasopharynx closes, breathing inhibited
Glottis is closed and larynx is elevated
peristalsis in pharynx and UES relaxes
Primary vs Secondary Peristaltic Contraction
1 - high pressure behind bolus to move it down
2 - clears esophagus of remaining food
Receptive relaxation
food in upper part of GI tract will relax GI tract further down to allow passage of food, Vagovagal reflex
Gastroesophageal Reflux
tone of LES is decreased and gastric content reflux into esophagus
Achalasia
LES does not relax during swallowing and food accumulates in esophagus
Contractions of GI tract during fasting
migrating myoelectric complex, occurs at 90 minute intervals
Mediated by Motilin
How fats inhibit gastric emptying
fat stimulates CCK release which inhibits gastric emptying
How H+ in duodenum inhibit gastric emptying
direct neural reflexes
Segmentation contractions
mix intestinal contents
back-and-forth movement
peristaltic contractions in small intesting
propel the chyme
contraction behind bolus and relaxation in front
coordinated by enteric nervous system
Gastroileal Reflex
mediated by extrinsic ANS and possibly gastrin
prescence of food in the stomach triggers increased peristalsis in the ileum and relaxation of ileocecal sphincter
Haustra
sac-like segments, contracts of large intestine
Frequency of Mass movements in large intestine
1-3x/day
cause colonic contents to move distally
Rectosphincteric reflex
rectum fills, it contracts and the internal anal sphincter relaxes
urge to defecate
when rectum is filled ~25%
Gastrocolic Reflex
food in stomach increases motility of the colon and increases the frequecy of mass movements
has a rapid PS component
Hirschsprung’s Disease
absence of the colonic enteric nervous system resulting in constriction of involved segment
reverse peristalsis beginning in small intesting
Vomiting
Vomiting center of medulla
stimulated by tickling bac kof throat, gastric distention and vestibular stimulation (motion sickness)
Chemoreceptor trigger zone
in 4th ventricle, activated by emetics, radiation and vestibular stimulation
Composition of Saliva
High K and HCO3-
Low Na Cl
hypotonic
alpha-amylase, lingual lipase, and kallikrein
Slow Flow rate for Saliva
lowest osmolarity, lowest Na, Cl and HCO3-
highest K conc
High Flow rate for Saliva
highest osmolarity, closest to that of plasma
Acinus for Saliva production
produces initial saliva, composition is similar to plasma
isotonic
Ducts for Saliva production
modifies initial saliva, reabsorbs NaCl, secretes K and HCO3-
Aldosterone acts on these
Saliva becomes hypotoniic
Parasympathetic Stimulation of Saliva
CN VII and IX
increases saliva production by causing vasodilation
Muscarinic - IP3/Ca
Sympathetic Stimulation of Saliva
beta-adrenergic receptors
cAMP
Parietal Cells
located in the body of stomach, secrete HCl and intrinsic factors
Stimulus is gastrin, Ach, Histamine
Chief Cells
located in body of stomach, secretes pepsinogen, stimulated by vagal stimulation
Mucous Cells
Antrum of Stomach, secretes mucus and pepsinogen
stimulus is ACh
Alkaline Tide
pH of blood increases around the stomach due to Cl/HCO3-exchange when making acid for the stomach
Cimetidine
H2 receptor blocker, inhibits H+ secretion
ECL cells
inhibits histamine
messenger for histamine
Gs/cAMP
messenger for somatostatin to inhibit H+
Gi thus decreasing cAMP
indirect pathway to inhibit H+ secreteion is inhibiting the release of gastrin and histamine
Protective factors for Peptic Ulcer Disease
mucus, HCO3, prostaglandins, mucosal blood flow, GFs
Gastric Ulcers
H+ secretion is decreased
Gastrin is increased
major cause = H. pylori
Duodenal Ulcer
H+ secretion is increased
gastrin in response to a meal is increased
major cause = H. pylori
3 Drugs that block gastric H+ secretion
Atropine, Cimetidine, Omeprazole
Low Flow Rates - Pancreas
isotonic fluid primarily of Na and Cl
High Flow Rates - Pancreas
isotonic fluid, primarily Na and HCO3-
Acinar cells - Pancreas
small volume, mainly Na and Cl
Ductal cells - Pancreas
secreting HCO3 and absorbing Cl through HCO3/Cl-exchange
Bile Salts
amphipathic
surround lipid droplets (emulsification) and aid in intestinal digestino and absorption of lipis into micells
Micelle
contains FFAs and monoglycerides
conjugates with bile acids to make bile salts
glycine or taurine
where are bile acids reabsorbed
terminal ileum, Na-Bile acid cotransporter
alpha-amylase
hydrolyze 1,4-glycosidic bonds in starch, yields maltose, ,altotriose and alpha-limit dextrans
maltase, alpha-dextrinase and sucrase
part of intestinal brush border which hydrolyze oligosaccharides into glucose
lactase
lactose to glucose and galactose
trehalase
trehalose to glucose
sucrase
sucrose into glucose and fructose
SGLT1
Na-dependent cotransport with glucose in lumen of intestine
sugar transported uphill, Na transported downhill
GLUT2
facilitated diffuse from inside enterocyte to blood
Fructose
transported by facilitated diffusion
Lactose intolerance
causes osmotic diarrhea
lack lactase in brush border
Endopeptidases
hydrolyze interior peptide bonds
Exopeptidases
hydrolyzes 1 AA at a time from C terminus
Pepsin
optimal pH 1-3
enterokinase
a brush border anzyme that makes trypsin from trypsinogen
Trypsin
converts chymotrypsinogen, proelastase and procarboxypeptidase A and B to their active forms
also makes more trypsin
Free AA
Na-dependent amino acid cotransport
then facilitated diffusion into blood
4 separate carrier for neutral, acidic, basic, and imino amino acids
Dipeptides and Tripeptides
absorbed faster than free AA
H+-dependent cotransport of dipeptides and tripeptides on luminal memrbane
cytoplasmic peptidases make them into AA
facilitated transport into blood
Chylomicrons
re-esterfied products of TGs, cholesterol ester, phospholipids with apoprotein attached so it can leave the intestinal cells
Lymph Vessels
Where chylomicrons are exocytosed into and travel in until thoracic duct (then goes to blood)
How dietary postassium is absorbed
small intestine by passive diffusion through the paracellular route
Potassium in the Colon
K is secreted in the colon, sitmulated by aldosterone
Diarrhea = hypokalemia
Primary ion secreted into the intestinal lumen
Chloride, regulated by cAMP
Cholera toxin (from vibrio cholerae)
catalyzes ADP ribosylation of alpha-s of Gs coupled to AC, permanently activating it
chloride is excreted
SECRETORY DIARRHEA
Fat Soluble Vitamins
A, D, E, K
incorporated into micelles
Water Soluble Vitamins
absorbed by Na-dependent cotransport mechanisms
Vit B12 absorption
Ileum, requires intrinsic factor
Gastrectomy
loss of parietal cells, the source of intrinsic factor, lead to loss of vit B12, causes pernicious anemia
Calcium
Need 1,25-dihydroxycholecalciferol from kidney to induce syn of calcium-binding protein calbindin D-28K
Apoferritin
Free Fe2+ binds this to be transported into the blood
Transferrin
Fe2+ bound protein in the blood taking Fe from intestine to liver or from liver to BM
Most common cause of anemia
Iron deficiency
Best channel to watch?
Disney channel
