GI Structure and Function Flashcards
In the GI tract the vagus nerve innervates what structures?
esophagus
stomach
small intestine
upper colon
In the GI tract the pelvic nerve innervates what structures?
descending colon
sigmoid colon
rectum
anal canal
GI parasympathetic fibers synapse with what?
cells in enteric/intrinsic nervous system
GI sympathetics synapse where and what is the exception
outside the GI tract in pre-vertebral ganglia
some blood vessels and secretory cells are innervated directly
The enteric (intrinsic) nervous systemis made up of what types of neurons?
motor neurons
sensory neurons
interneurons
Vagovagal reflex (where is the information coming from and going to and through what nerves)
vagus nerve afferents relay info from mucosa and smooth muscle to CNS
vagus nerve efferents carry response back to GI tract
What are the two networks of the enteric nervous system
myenteric plexus
submucosal plexus
The enteric nervous system innervates what?
blood vessels
smooth muscle
secretory cells
endocrine cells
The enteric nervous system maintains what?
integrity of barrier between gut lumen and cells within gut wall
How does the enteric nervous system relay information to and from the gut (via what pathway)
extrinsic system
myenteric plexus (where is it found and what does it do)
found throughout GI tract
mostly controls motility
submucosal plexus (what does it do and where is it found)
found predominantly in intestines
mostly controls secretion
True/False: Stimulus in one part of GI tract can produce response in another part in absence
of extrinsic nervous system
True
Extrinsic Nervous System dominates control in what area
esophagus
stomach
defecation
Enteric Nervous System dominates control in what areas
small intestine
large intestine
What are the types of gastrointestinal peptides
hormones
paracrines
neurocrines
What are the GI hormones (name them all)
Gastrin Cholecystokinin (CCK) Secretin Glucose-dependent Insulinotropic Peptide (GIP) Motilin
Zollinger-Ellison Syndrome (what is it and what are the symptoms)
hypersecretion of gastric acid due to continuous release of gastrin into blood from gastrinoma in small intestine or pancreas
develop duodenal ulcers, diarrhea, and steatorrhea (excess fat in stool)
Gastrin (where is it secreted, in response to what, and what does it stimulate)
secreted from G cells in stomach (antrum)
released in response to peptides and amino acids from protein digestion, distention of stomach, vagal stimulation
stimulates HCl secretion by parietal cells
Vagal Stimulation of Gastrin is mediated by what
Gastrin Releasing Peptide (GRP)
Cholecystokinin (CCK) (where is it secreted, in response to what, and what does it do)
secreted from I cells of proximal small intestine (duodenum and jejunum)
released in response to small peptides, amino acids, fatty acids, and monoglycerides (w/ 8 or more Cs)
stimulates gallbaldder contraction and pancreatic enzyme secretion
potentiates pancreatic bicarbonate secretion stimulated by secretin
inhibits gastric emptying
signal for satiety
What is the reason fatty meals empty more slowly than non-fatty meals
because cholecystokinin (CCK) is secreted and inhibits gastric emptying
The signal for satiety is controlled by what hormone
cholecystokinin (CCK)
Secretin (where is it secreted, in response to what, and what does it do)
release by S cells of proximal small intestine (duodenum)
released in response to acid
stimulates bicarbonate and water secretion in pancreas and liver
increase bile production
inhibits gastric acid section by parietal cells
Glucose-Dependent Insulinotropic Peptide (GIP) (where is it secreted, in response to what, and what does it do)
secreted by K cells in proximal small intestine (duodenum and jejunum)
released in response to fatty acids, glucose, and amino acids (to a lesser extent)
stimulates insulin release from pancreas
Why is oral glucose load more effective than intravenous glucose in causing insulin release
because of glucose-dependent insulinotropic peptide (GIP) stimulating insulin release from pancreas in response to glucose
Motilin (where is it secreted, in response to what, and what does it do)
released cyclically every 90 minutes from upper small intestine during fasting (duodenum and jejunum)
stimulates migrating myoelectric complex in stomach and small intestine
release abolished by eating
Name the GI Paracrines
somatostatin
histamine
Somatostatin (where is it secreted, in response to what, and what does it do)
secreted by D cells throughout the GI tract (mucosa)
released in response to acid
inhibits gastric acid secretion and release of gastrin
inhibits release of all GI hormones
Histamine (where is it secreted, in response to what, and what does it do)
secreted by enterochromaffin-like (ECL) cells
increases gastric acid secretion both directly and by potentiating effects of gastrin and ACh
where are enterochromaffin-like (ECL) cells found in high concentrations
around the acid-secreting portion of stomach
What are the GI Neurocrines
vasoactive intestinal peptide (VIP)
gastrin-releasing peptide (GRP or bombesin)
enkephalins
Vasoactive Intestinal Peptide (VIP)
released from nerves in mucosa and smooth muscle of GI tract
predominant action- relaxation of GI smooth muscle
stimulates intestinal and pancreatic secretion
secreted from pancreatic islet cell tumor
what is thought to mediate pancreatic cholera/ watery diarrhea syndrome
Vasoactive Intestinal Peptide (VIP)
Gastrin-Releasing Peptide (GRP)
released from nerves in gastric mucosa by vagal stimulation
stimulates gastrin release
Enkephalins
secreted from nerves in mucosa and smooth muscle of GI tract
stimulate contraction of GI smooth muscle (particularly the lower esophageal, pyloric, and ileocecal sphincters)
inhibit intestinal secretion of fluid and electrolytes
Why are opiates useful in treating diarrhea
enkephalins (from the opiates) inhibit intestinal secretion of fluid and electrolytes
Slow waves are initiated by?
interstitial cells of Cajal
Slow waves are spread from interstitial cells of Cajal to other cells how?
via gap junctions
what are slow waves of GI smooth muscle
period changes in resting membrane potential of smooth muscle
potential rhythmically depolarizes and repolarizes
also called basic electrical rhythm (BER)
What are the phases of slow waves
depolarization phase
plateau phase
repolarization phase
depolarization phase of slow waves is caused by what?
Ca2+ influx
plateau phase of slow waves is caused by what?
Ca2+ influx
repolarization phase of slow waves is caused by what?
K+ efflux
for slow wave contraction to occur what most happen (in regards to plateau phase)
plateau phase must exceed threshold
action potentials being initiated in the GI tract do what?
increase strength and duration of contraction
action potentials in stomach contractions (required/not required and present/not present)
not required
almost always present
Action potentials in GI tract (requried/not required and where) for contraction
required everywhere except for stomach for contraction to occur
neural or hormonal input on slow waves and action potentials of GI tract
very little influence on slow waves
greatly influence action potentials
neural or hormonal input can influence variations in membranes how?
produce action potentials and thus contractions
can inhibit action potentials
determine strength of contractions
frequency of slow waves does what?
sets maximum frequency for contraction of given part of GI tract
Pancreatic Cholera/Watery Diarrhea Syndrome are mediated by what?
vasoactive intestinal peptide (VIP) b/c it stimulates intestinal and pancreatic secretion
Gastrinoma
small tumor in the small intestine (duodenum) or pancreas that produces high levels of gastrin
Steatorrhea
fat in feces
