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67 Cards in this Set

  • Front
  • Back
Divisions of the Extrinsic Nervous System
1) Parasympathetic 2) Sympathetic
GI and Parasympathetic Nervous System: Nerves
1) Vagus nerve 2) Pelvic nerve
Vagus Nerve Innervation
Innervates: 1) Esophagus 2) Stomach 3) Small intestine 4) Upper colon
Pelvic Nerve Innervation
Innervates: 1) Descending colon 2) Sigmoid colon 3) Rectum 4) Anal canal
Vagovagal Reflex
1) Information from receptors in mucosa and smooth muscle relayed to CNS via vagus nerve afferents 2) Triggers a response that is carried back to GI tract via vagus nerve efferents
GI and Sympathetic Nervous System: Innervation
1) Nerve fibers typically synapse outside GI tract in prevertebral ganglia 2) A few innervate blood vessels and secretory cells directly.
Enteric/Intrinsic Nervous System Function
1) Relay information to and from gut via extrinsic system 2) Stimulus in one part of GI tract can produce response in another part in absence
of extrinsic nervous system
Enteric/Intrinsic Nervous System Structure
Networks formed by myenteric and submucosal plexuses
Enteric/Intrinsic Nervous System Innervation
Innervate: 1) Blood vessels 2) Smooth muscle 3) Secretory cells 4) Endocrine cells
Overview of Neural Control of GI
1) Nutrients activate: A) Special senses B) Sensory nerve endings 2) Responses conveyed by A) ANS (vagus nerve) and B) ENS 3) Leads to changes in: A) Secretion and B) Motility.
Zollinger-Ellison Syndrome
Hypersecrete gastric acid due to continuous release of gastrin into blood from gastrinoma
G Cell Secretion
Parietal Cell Secretion
Gastric acid (HCl)
Excess fat in stools
1) Cholecystokinin 2) Secreted by I cells 3) Released in response to: A) Small peptides B) Amino acids C) Fatty acids D) Monoglycerides (containing 8 or more carbon atoms) 4) Stimulates: A) Gallbladder contraction B) Pancreatic enzyme secretion 5) Potentiates pancreatic bicarbonate secretion 6) Inhibits gastric emptying
I Cell Secretion
Reason Fatty Meals Empty More Slowly than Non-Fat Meals
CCK, released in response to fatty acids, inhibits gastric emptying
1) Released by S cells 2) Stimulates: a) Bicarbonate b) Water secretion in: i) pancreas ii) liver 3) Increases bile production 4) Inhibits gastric acid secretion 5) Released in response to acid
S Cells
1) Duodenum 2) Secretes secretin in response to acid
1) Glucose-dependent insulinotropic peptide 2) Secreted by K cells 3) Released in response to: A) Fat B) Protein C) Carbohydrate 4) Stimulates insulin release from pancreas
K Cells
1) Duodenum and jejunum) 2) Secretes GIP in response to: A) Fat B) Protein C) Carbohydrate
Why Is Oral Glucose Load More Effective than IV Glucose in Causing Insulin Release?
1) IV glucose circulates through the blood and therefore fails to stimulate the GIP secreting K cells of the small intestine which stimulate insulin release from pancreas 2) Oral glucose passes through the small intestine, stimulating GIP and insulin release
1) Released cyclically about every 90 minutes from upper small intestine (duodenum and jejunum) during fasting
2) Stimulates migrating myoelectric complex in: A) Stomach B) Small intestine 3) Release abolished by eating
Gastrointestinal Peptides: Types
1) Hormones 2) Paracrines 3) Neurocrines
Gastrointestinal Peptides: Hormones
1) Gastrin 2) CCK 3) Secretin 4) GIP 5) Motilin
Gastrointestinal Peptides: Paracrines
1) Somatostatin 2) Histamine
Gastrointestinal Peptides: Neurocrines
1) VIP 2) GRP 3) Enkephalins
1) Secreted by D cells 2) Inhibits: A) Gastric acid secretion B) Release of gastrin C) Release of all GI hormones
D Cells
1) Throughout GI tract 2) Release somatostatin in response to acid in lumen
1) Secreted by ECL cells 2) Increases gastric acid secretion: A) Directly B) Potentiating effects of: a) gastrin b) ACh 3) Releaser: gastrin
ECL Cells
1) Enterochromaffin-like cells 2) Located in acid secreting portion of stomach 3) Secrete histamine in response to acid
1) Vasoactive intestinal peptide 2) Released from nerves in: A) Mucosa B) Smooth muscle of GI tract 3) Relaxes smooth muscle of GI 4) Stimulates: A) Intestinal secretion B) Pancreatic secretion 5) Secreted from pancreatic islet cell tumor
What Is Thought to Mediate Pancreatic Cholera/Watery Diarrhea Syndrome?
Secretion of VIP from pancreatic islet cell tumor
1) Secreted by G cells 2) Released in response to: A) Peptides B) Amino acids C) Distension of stomach D) Vagal stimulation 3) Stimulates HCl secretion 4) Increased in Zollinger-Ellison syndrome
1) Tumor in the pancreas or duodenum that secretes excess of gastrin 2) Implicated in Zollinger-Ellison syndrome
1) Gastrin-releasing peptide or bombesin 2) Released from nerves in gastric mucosa in response to vagal stimulation 3) Stimulates gastrin release
Gastric Mucosa
1) Contains nerves that release GRP 2) Responds to vagal stimulation
1) Secreted from: A) Nerves of mucosa and smooth muscle of GI tract 2) Stimulate GI smooth muscle contraction: A) lower esophageal B) Pyloric C) Ileocecal sphincters 3) Inhibit intestinal secretion of: A) Fluid B) Electrolytes
Why Are Opiates Useful in Treating Diarrhea?
Opiates mimic enkephalins, an endogenous opioid peptide, which inhibit intestinal secretion of fluid and electrolytes
Slow Wave Contraction Couplet
Slow waves without contractions, but not contractions without slow waves
Slow Waves
1) Smooth muscle cell potential rhythmically depolarizes and polarizes 2) Also called Basic Electrical Rhythm (BER) 3) Not action potentials
Cells of Cajal
1) Generate slow waves 2) Interstitial
Slow Wave Dispensation
1) Begin in cells of Cajal 2) Spread to other cells via gap junctions
Slow Wave Generation: Depolarization Phase
Ca++ influx
Slow Wave Generation: Plateau Phase
Ca++ influx
Slow Wave Generation: Repolarization Phase
K+ efflux
Slow Waves: Requirement for Contraction
Plateau phase must exceed threshold
Slow Waves: Plateau Exceeds Threshold
1) Voltage-gated Ca++ channels open 2) Ca++ enters 3) AP initiated
Slow Waves: Function of Action Potential
1) Increase strength and duration of contraction 2) Required for contraction everywhere except stomach
Slow Waves: Stomach Contractions and Action Potential
1) May occur in absence of AP 2) AP almost always present
Slow Waves: Affect of Neural and Hormonal Input on Frequency
Little affect on frequency of slow waves
Smooth Muscle Action Potentials: Neural and Hormonal Input
Influence variations in membrane potentials: 1) Produce AP, thus contractions 2) Inhibit AP 3) Determine strength of contractions
Slow Waves: Frequency
Sets maximum frequency for contraction of given part of GI tract
G Cell Location
Parietal Cell Location
Gastrinoma Location in Zollinger-Ellison Syndrome
1) Small Intestine 2) Pancreas
Zollinger-Ellison Syndrome Symptoms
1) Duodenal ulcers 2) Diarrhea 3) Steatorrhea
Signals for CCK Release
1) Small peptides 2) Amino acids 3) Fatty acids 4) Monoglycerides (containing 8 or more carbon atoms)
CCK Stimulates
1) Gallbladder contraction 2) Pancreatic enzyme secretion
CCK Releasing Cell
I cell
CCK Inhibits
Gastric emptying
CCK Potentiates
Pancreatic bicarbonate secretion
I Cell Location
Proximal small intestine: duodenum and jejunum
Secretin Stimulates
Bicarbonate and water secretion in liver and pancreas
Secretin Increases
Bile production
Secretin Inhibits
Gastric acid secretion by parietal cells
Signals for Secretin Release