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49 Cards in this Set

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What are the 5 official GI H's?
Gastrin, CCK, secretin, Gastric inhibitory peptide, and motilin
-produced where
-stim by
-inhib by
- prod: I cells of duod and jej, a peptide H
-function: stim pancreatic enz, hepatic bile, gallbladder contraction and sphincter of oddi relaxation
-stim by: fat in duod
-inhib by: ?
-produced where
-stim by
-inhib by
-produced where: S cells of duod and jej, a peptide H
-function:stim bicarb secretion from pancreas, liver and brunners glands
-stim by: low pH in duod
-inhib by: ?
Gastric Inhib peptide:
-produced where
-stim by
-inhib by
-produced where: K cells of duod and jej,
-function: an incretin, induces insulin
-stim by:
-inhib by
-produced where
-stim by
-inhib by
-produced where: Mo cells of duod and jej
-function: increases migrating myoelectric complex
-stim by
-inhib by
Where produced
stim by
inhib by
-prod: G cells of antrum, a peptide H
-Function: increase HCL
-Stim: vagal stim, stomach distension, aa's in stomach, Ca
-Inhib: low pH, SS (somatostatin)
GI paracrines
SS and histamine
GI neurons
Ach - excitatory NT
Vasoactive intestinal peptide - released by inhibitory motor neurons of myenteric plexus and submucosal
GRP - excitatory NT
Enkephalins - contract sphincters
Food intake regulators
CCK(decrease) and Ghrelin(increase)
GI paracrines
SS and histamine
GI neurons
Ach - excitatory NT
Vasoactive intestinal peptide - released by inhibitory motor neurons of myenteric plexus and submucosal
GRP - excitatory NT
Enkephalins - contract sphincters
Food intake regulators
CCK(decrease) and Ghrelin(increase)
parasymp: preganglionic and cholinergic

symp: postganglionic and adrenergic, terminate on intremural plexuses
Enteric NS plexuses and NT's
Myenteric plexus: mostly motor, excitatory Ach onto muscarinic R, inhib VIP and NO, interneurons release AcH onto Nicotinic R

Submucosal: mostly glands and endocrine, secretomotor nn release Ach and VIP, sensory nn respond to chem and mechanical stim, interneurons release Ach
are smooth muscle slow waves more or less frequent in the stomach compared to the duodenum
stomach is 3/min
duod is 11-13/min
what initiates slow waves?
intertitial cells of cajal
list the three phases of swallowing
oral phase: tongue
Pharyngeal phase: nasopharynx closes, vocal cords and larynx move up and close the epiglottis while opening the UES, only phase you cant breath
Esophageal phase: primary peristaltic wave begins below ues and travels esoph in less than 10 min, secondary waves come after, caused by refelx cranial and vagal nn's
failure of les to relax causing dysphagia(difficulty swallowing)
Diffuse esophageal spasm
simultaneous contractions
metabolism and blood flow of salivary glands
more blood = higher rate of saliva formation,
parasympathetic increases blood flow via vasodilation Ach(stim NO) and VIP
composition of saliva(ions) changes ith blood flow
Low flow
High flow

hyper/hypotonicity, pH, K+, Na Cl, bicarb
Low flow: HYPOTONIC but close to isotonic, acidic, high K+ with respect to plasma, low NA CL with respect to plasma, low bicarb with respect to plasma

High flow: HYPOTONIC, but approaches isotonicity with respect to plasma, basic, high K+ w/Respect to plasma but it has decreased and plateau'd, low Na Cl w/RTP but concentrations have increased, high bicarb with respect to plasma
Two stage model of salivary secretion
primary secretion that is nearly isotonic containing amylase is secreted by acinar cells

excetory and striated ducts modify primary secretion by secreting K and bicarb, and taking up nacl
innervation of the salivary glands
parasymp and symp and hormonal
parasymp: primary control! is cut will cause atrophy, increases synthesis of salivary amylase, transport, blood flow, myoepithelial cells and gland growth

Sympathetic: if cut will not cause atrophy, from cervical ganglion, contracts myoepithelial cells and thats it, constricts blood,
No Hormonal control
Controll of salivary secretion, NT's and their R's
Ach, Substance P and NE use a G prot R to mediate IP3 Ca++ release
NE also increases cAMP through a different R

Net result = increase K and HCO3 secondary secretion
what are the smooth muscle layers of the stomach?
outer longitudinal, middle circular, inner oblique, these layers get thicker as you approach the pylorus
receptive relaxation of the stomach
fundus and body of the stomach relax when a bolus of food passes down the esophagus, then returns to near pre-swallow pressures
a VAGAL reflex(VIP and NO)
gastric contractions and retropulsion
originate in body and increase in strength as it travels down, major mixing occurs in the antrum where retropulsed chyme mixes
Migrating myoelectric complex
fasted stomach state: quiescent for 75 to 90 minutes followed by vigorous 5-10 minute contractions in the antrum. sweeps from the stomach to the terminal ileum
mediated by motilin
purpose is to sweep undigested contents into the colon
Gastric slow waves
what initiates it
what does the wave look like
what increases the force of contraction
ICC initiates them,
it is triphasic and looks like a cardiac muscle AP EXCEPT it lasts 10 times longer and does not hyperpolarize(overshoot)

the longer the gastric muscle is depol'd the greater the force of contraction (Ach and gastrin increase contractility), AP's tend to occur during the plateau phase of slow waves
which part of the GI contracts irregularly

gall bladder
fundus of the stomach
what hormones promote constriction of the pylorus?
CCK, gastrin, GIP, and secretin, thus slowing gastric emptying
note: the rate at which chyme enters the small intestine does not exceed the rate at which the small intestine can process the material
does hyper or hypotonic solution slow gasric emptying
hypertonic, the hormone involved is unknown
Secretin and gastric emptyin
released in response to low pH in duodenum, inhibits antral contraction and constricts pyloric sphincter
gastrin and gastric emptying
AA's and peptides in cause gastrin release, it increases antral contraction strength AND pyloric sphincter so net effect is decreased gastric emptying

not GIP and CCK also is stim by aa's and inhib emptying
GIP and CCK in gastric emptying
fat and monoglycerides injejunum slow gastric emptying
which empties faster
carbs fats protein
carbs if fastest then protein then fat
gastric contents are forced into the esophagus but not the pharynx because the UES remains closed
major secretions of the stomach
HCL, pepsinogen, IF(essential glycoprotein that binds B12 and facilitates abs)and bicarb/mucus

parietal cells secrete hcl and IF
what are the primary secretions of the oxyntic region of the stomach? the pyloric?
oxyntic: acid
pyloric: mucus and gastrin
rates of secretion and gastric juice composition

hyper/hypotonic, na cl, pH K
low rates: hypotonic w/RTP(respect to plasma), primarily NACL and low pH(about 2)

high rates: approaches isotonicity, Cl increases, na drops a lot, pH decreases even more

K is always higher w/RTP
Two-component model of gastric secretion
non-parietal cells: secrete a soln that is primarily NaCl with K and bicarb at plasma levels, secreted at constant and low vol

parietal cells: KCL and HCL

as rate of secretion increases parietal component increases, non-parietal remains unchanged

therefore as rate increases cell approached pure Parietal !! (so all you have to do is mem what parietal secretes)
describe acid production in parietal cell
carbonic anhydrase makes H and bicarb,
h is pumped out to lumen in a H/K atpase
bicarb pumped out in Cl/bicarb exchanger
Cl:concentrated in cytoplams now and is pumped out via Cl channel and K channels on both sides pump out K to hyperpolarize cell and increase driving force for cl into lumen against a huge concentration grad
alkaline tide
huge bicarb secretion in exchange for Cl during times of high acid secretion, drop in pH of portal blood
hormones that increase acid secretion and the R they work on
AcH, Histamine and gastrin

Ach - M3 muscarinic R causing increased Ca

Histamine - paracrine released from nearby ECL cells, H2 R increasing cAMP

Gastrin - binds CCK-B R incresing Ca

all three potentiate eachother and cause secretion
hormones that decrease acid secretion and their R
SS PGE PGI and epidermal growth factor EGF

all inhib adenyl cyclase and decrease cAMP
stimulation of acid secretion
the three phases
cephalic: feel though smell, vagal efferents, but low gastric ph inhibits acid secretion and since ph drops rapidly b/c stomach is empty very little actual acid secretion occurs

gastric: distention, most acid is secreted during this phase, vagovagal and local reflex use Ach

intestinal: chyme in duodenum, vagovagal reflex and aa's stim Gcells, fats, SS CCK GIP and acid inhibit acid secretion via vagovagal
secreted in response to vagal reflex, Acid, CCK and secretin
soluble vs insoluble mucus secretion in stomach
soluble: mucus neck cells
Insoluble: surface mucus cells, trap dead cells and bicarb to form a protective coat, protecting the stomach lining