exam 1 lecture 9 and 10 GI Flashcards
sphincter of oddi
controls flow of bile and pancreatic enzymes to duodenum
paracrine vs endocrine
paracrine= peptide hormone control locally
endocrine= hormonal control globally via the blood stream
The lining of the GI tract can be subdivided into 3 layers: ___
-the mucosal, submucosal, and muscle layers.
There are three major interlinked control mechanisms of the GI system are:
hormonal (endocrine)
paracrine
neural
innervation of the GI tract is by ___
extrinsic (ANS)
Intrinsic (enteric NS)
most CNS influence on the GI occurs indirectly via the ENS and GI endocrine system
the extrinsic innervation of the GI is by the ___
ANS
parasympathetic and sympathetic
Both have an important sensory (afferent) component.
the two plexuses of the ENS are ___
submucosal (Meissner) plexus
myenteric (Auerbach) plexus
When a meal is in different regions of the tract, ____ mechanisms detect the presence of the nutrients and mount appropriate physiological responses in that region of the tract, as well as in more distal regions. These responses are mediated by endocrine, paracrine, and neural pathways.
sensory
•The major function of the GI tract is ___
absorption.
•GI control systems operate to provide an ____ for absorption.
optimal environment
regulated processes of the GI are GI motility and ___
GI secretions
three types of chemical control of the GI tract
- endocrine secretions- all over control
- paracrine secretions- peptide hormones acting locally
- neurocrine secretions
___ is GI muscle contraction via interstitial cells of Cajal
myogenic control
what part of the ANS stimulates the GI tract with preganglionic fibers?
parasympathetic
rest and digest
stimulatory(excitatory)
triggers the GI directly does not need to go through ganglion
what part of the ANS stimulates the GI tract with post ganglionic fibers?
sympathetic
(fight or flight)
inhibitory
goes through prevertebral ganglion to get to GI
the ___ system uses cholinergic: use Ach. Also, substance P, and others to trigger the GI tract
parasympathetic
the ___ system uses peptide neurocrines including somatostatin, PACAP, but also NO to stimulate the GI tract
sympathetic (fight or flight)
The preganglionic ___ fibers to the GI tract synapse on postganglionic neurons in the prevertebral ganglia. The postganglionic sympathetic fibers either synapse in the ENS or directly innervate effector cells.
sympathetic
parasympathetic innervation of the ENS is ___. while sympathetic innervation of the ENS is ____
preganglionic
postganglionic
explain parasympathetic innervation of the GI tract
Parasympathetic innervation of the GI tract from the pharynx to the distal colon is through the vagus nerve; the distal third of the colon receives its parasympathetic innervation from the pelvic nerves. The preganglionic fibers of the parasympathetic nerves use acetylcholine as their neurotransmitter and synapse on some neurons of the ENS. These ENS neurons are thus postganglionic parasympathetic fibers, and their cell bodies are, in a sense, the parasympathetic ganglion. These postganglionic parasympathetic fibers use mainly ACh as their neurotransmitter
why does the myenteric plexus need extensive interneuronal connections
controls the muscle along the GI tract, needs to be able to sense what is happening in one part of the tract to tell the other parts what to do
___ is the ENS ganglia between the circular and longitudinal muscle
myenteric plexus
___ is the ganglia in the submucosal layer of the GI tract
submucosal plexus
__ places where nerves branch and rejoin
plexuses
___ bunch of nerve cell bodies (soma)
ganglia
how is motor neuron innervation of GI muscle different from skeletal muscle
skeletal: neuromuscular junction
GI: no direct synaptic junction, neurons terminate in varicosities in vicinity of target cells. Varicosities release neurocrines to effect muscle contraction/glandular secretions.
most ANS signal has to go through the ENS to stimulate GI, some times fibers of the ___ with bypass the ENS and go directly to the GI
sympathetic (fight or flight)
____ of the GI are postganglionic when they reach the GI because they passed through the mesenteric ganglia prior to terminating at target muscle, secretory cells, or ENS neurons.
Sympathetic nerves
____ nerves are preganglionic when they reach the GI because they do not pass through such ganglia prior to interfacing w/ the GI tract and neurons of the ENS.
Parasympathetic
ENS axons end in ___ that release ___ affecting nearby muscle and glandular cells
varicosities
neurocrine
ENS neurocrines that are stimulatory:
cholinergic-acetylcholine, substance P
ENS neurocrines that are stimulatory:
cholinergic-acetylcholine, substance P
ENS neurocrines that are inhibitory:
somatostatin, PACAP, nitric oxide, ATP, etc…
enteroendocrine cells
found in the GI
secrete hormones basally into the interstitial fluid to stimulate local/paracrine function
gastrin is produced where and its function, release stimulus are ___
primary function: stimulates acid secretion from stomach glands
secondary function: stimulates gastric motility, growth of stomach epithelium
release stimulus: proteins in stomach, high gastric pH, vagal stimulation (physical distention)
production: distal stomach
secretin is produced where and its function, release stimulus are ___
primary function: stimulates bicarbonate secretion from pancreas
secondary function: stimulates biliary bicarbonate secretion
release stimulus: acid in duodenum
production: duodenum
CCK is produced where and its function, release stimulus are ___
primary function: stimulates enzyme secretion from the pancreas
secondary function: inhibits gastric emptying
release stimulus: proteins and fats in small intestine
production: duodenum to ileum,
what cells produce HCl in the stomach?
parietal
what cells produce pepsinogen in the stomach?
chief cells
G cells in the ___ part of the stomach produce ___ to stimulate ___
pyloric region
gastrin
parietal cells that create HCl in the gastric and fundic part of the stomach,
HCl then decreases the amount of gastrin produced(negative feedback)
explain how H is released from parietal cell
H2O +CO2→(carbonic anhydrase)→ carbonic acid(H2CO3) which changes into H + HCO3-(bicarbonate)
H/K ATPase antipump pushes H out and K in
bicarbonate is then exchanged for a Cl- (HCO3/Cl antiporter) Cl and K bind together and leave the parietal cell and into the stomach lumen
what enzyme breaks H2O and CO2 into a usable H to leave the parietal cell?
carbonic anhydrase
H+ ions for secretion from parietal cells are generated from the dissociation of carbonic acid (H2CO3), leaving behind one bicarbonate ion (HCO3-) per H+. The carbonic acid utilized in H+ generation is a product of carbonic anhydrase, which combines H2O and CO2. This enzyme exists at high concentrations in the gastric mucosa.
how does H/K ATPase pump work in parietal cell
H+ is secreted by parietal cells through the H+, K+,-ATPase pump (aka Proton Pump) at the luminal surface. The proton pump expels one H+ from the cell for each K+ taken into the cell. This process uses energy by hydrolyzing ATP to ADP. Intracellular K+ couples with Cl- and is then pumped out of the cell. The net result is H+ and Cl- secretion with little net change in K+ .
How does Cl get into parietal cell
Intracellular biocarbonate (HCO3-) is then exchanged for Cl- ions on the cell’s nonluminal (basal) surface where it enters the bloodstream. This exchange is catalyzed by the HCO3-/Cl- antiporter and results in a transient alkalization of the blood during digestion in what is termed the “alkaline tide”. This alkaline tide is subsequently resolved via consumption of bicarbonate during intestinal neutralization of gastric acids. Therefore stomach acidification has little net effect on blood pH.
explain HCl secretion by parietal cell
H+ is secreted by parietal cells through the H+, K+,-ATPase pump (aka Proton Pump) at the luminal surface. The proton pump expels one H+ from the cell for each K+ taken into the cell. This process uses energy by hydrolyzing ATP to ADP. Intracellular K+ couples with Cl- and is then pumped out of the cell. The net result is H+ and Cl- secretion with little net change in K+ .
H+ ions for secretion from parietal cells are generated from the dissociation of carbonic acid (H2CO3), leaving behind one bicarbonate ion (HCO3-) per H+.The carbonic acid utilized in H+ generation is a product ofcarbonic anhydrase, which combines H2O and CO2. This enzyme exists at high concentrations in the gastric mucosa.
Intracellular biocarbonate (HCO3-) is then exchanged for Cl- ions on the cell’s nonluminal (basal) surface where it enters the bloodstream. This exchange is catalyzed by the HCO3-/Cl- antiporter and results in a transient alkalization of the blood during digestion in what is termed the “alkaline tide”. This alkaline tide is subsequently resolved via consumption of bicarbonate during intestinal neutralization of gastric acids. Therefore stomach acidification has little net effect on blood pH.
In disease states where gastric secretions are not able to enter the intestine, or are lost via vomiting, blood pH can ___ to dangerous levels**.
raise
basic bicarbonate not released into blood stream
how does gastrin work on parietal cell
stimulates release of HCl
more specifically- stimulates activationof the H/K ATPase pump that pushes H out and pulls K into the parietal cell
explain
see and chew food
brain stimulates release of ACh from the vagus nerve: stimulates parietal cell to produce HCl, stimulates G cell to produce gastrin, stimulates ECL cell to produce histamine
all of these then also stimulate parietal cell to produce more gastrin
paracrine- ECL cell (local hormonal control by histamine)
endocrine- G cell produces gastrin into blood stream back into GI into parietal cell
neurocrines- ACh directly on parietal cell
explain what happens during cephalic phase of digestion
During the cephalic phase of digestion (anticipation-prior to food entry into stomach), vagal cholinergic nerves (Parasympathetic, stimulatory, Ach) stimulate parietal cells and induce release of histamine from ECL cells, which also stimulate parietal cells. Vagal fibers also release gastrin-releasing peptide (GRP) in the antrum to induce gastrin secretion, which is carried in the bloodstream to induce release of histamine and stimulate parietal cells. During the gastric phase of digestion, food in the stomach triggers vagovagal reflexes and also stimulates gastrin secretion. Acidification of the gastric antrum stimulates the release of somatostatin (from Delta cell), which inhibits gastrin release and thus acid secretion; vagal ACh inhibits somatostatin release.
explain coupled sodium chloride absorption
CO2 +H20→(carbonic anhydrase) → H2CO3 which changes into HCO3 and H
H gets pumped back into lumen in exhange for Na+
HCO3(bicarbonate) gets pumped back into the lumen in exchange for Cl-
H and HCO3 in the lumen turn back into CO2 and H20
Na+ and Cl- are back into the blood stream (sodium is transported across the basolateral membrane to the lateral space via the Na+/K+-ATPase pump. Cl- remains in the cell until concentrations build up sufficiently to promote diffusion through chloride channels at the basolateral membrane.)
where do couples sodium chloride absorption take place
ileum and colon
transfers HCO3 and H into lumen
Na+ and Cl- into blood
3 ways Cl- is absorbed back into the blood stream
coupled sodium-chloride absorption
paracellular chloride absorption
chloride-bicarbonate exchange
explain paracellular chloride absorption
+ charge from Na+ leaving into the blood, causes electrochemical gradient that pulls Cl- through tight junctions into the blood to try to balance the charges
paracellular chloride absorption in association with sodium co-transport of glucose and amino acids. This is due to an electrical gradient. Na+ movement into the cell results in a positive electric charge across the apical membrane (since glucose and most amino acids are not charged). As sodium is subsequently transported to the basolateral space, the differential charge drives chloride into the basolateral spaces directly through tight junctions (not so tight since they are permeable to small anions) in an effort to reach electrical neutrality.
explain chloride-bicarbonate exchange
(HCO3-)bicarbonate is pushed into lumen, Cl- is pulled into the blood
chloride-bicarbonate exchange where bicarbonate secretion into the intestinal lumen is important (ie, colon of large herbivores in which fermentation acids require buffering)
how is bicarbonate recovered from the lumen?
CO2 + H20 (carbonic anhydrase) → H2CO3 → HCO3- and H+
the H+ leaves in exchange for Na+, this H+ will bind with luminal HCO3- → CO2 and H20
intracellular HCO3- and Na+ balance each others charge, Na+ gets pulled into the blood, then negative HCO3- will follow
Bicarbonate (HCO3-) is used in the neutralization of gastric HCl from the stomach where sodium bicarbonate reacts w/ HCl, yielding H2O, CO2, and NaCl in the intestine. However, significant bicarbonate remains in the intestine post-neutralization and must be reabsorbed. This occurs in the ileum and colon via ion exchange.
Bicarbonate is usually electrically balanced in the intestine with sodium (sodium bicarbonate). In the absorptive process, H+ and HCO3- are generated inside enterocytes from water and CO2. H+-Na+ exchange then occurs, and intracellular Na+ is electrically balanced w/ HCO3-, while luminal HCO3- is neutralized by exiting H+ ions.
The net result is: luminal sodium is transferred through the membrane and luminal bicarbonate is converted to H2O and CO2 in the lumen, and bicarbonate is regenerated intracellularly. The net effect if absorption of sodium bicarbonate.
Potassium is absorbed by simple ___. Water absorption in the upper intestine results in increased K+ in the lower intestine, generating a diffusion gradient.
diffusion paracellularly
chloride bicarbonate exchange happens where?
ileum and colon
bicarbonate and potassium absorption back into the blood occurs where?
ileum and colon
why does intestinal crypt have opposite secretory function from the villi?
wants to keep stem cells happy, in osmotic solution
In the crypt, Na and Cl are pumped into the cell from basolateral space. Na is quickly pumped out again, so Cl accumulates in the cell. Upon stimulation, Cl channels in apical membrane open, Cl moves luminally along a concentration gradient, which then attracts Na which follows the Cl through the paracellular route. Water then follows the NaCl osmotically, the net result being NaCl and H20 moving luminally from the crypt
Since water follows osmotic gradients, the net result is NaCl secretion into the crypt lumen
This mechanism functions to maintain proper hydration and ionic environment in the lumen for digestion and absorption
how does ACh effect ICC cell contraction
raises baseline so ICC signal and ACh reach threshold to release Calcium and start contraction
In the presence norepinephrine the slow wave baseline is ___, thus raising the threshold requisite for action potential
lowered
norepinephrine= fight or flight = GI inhibited
In the presence of ___ the slow wave baseline is raised, enabling the crest to reach the critical point of depolarization, near 0 mV
acetylcholine (rest and digest)
enterogastric reflex
food has to wait its turn to be digested
- Involves CNS and ENS, endo/paracrine signals
- Afferent fibers of the Vagus nerve receive stimuli in duodenum (pH, fat, osmolarity). These stimuli block Vagus-induced stomach emptying.
- CCK and secretin are though to be released by duodenum into the bloodstream (CCK in response to fat, secretin in response to low pH), suppressing gastric emptying. Other hormones likely tied in as well.
