GI (pt 1/5) Basic Overview Flashcards
The esophagus is ___ cm long, and connects the mouth to the stomach.
25 cm
Where is the cricopharyngeus muscle located?
At the level of the aortic arch and mainstem bronchus.
At the level of the esophageal hiatus of the diaphragm.
-Food bolus here and foreign body impaction
What marks the transition of pharynx to esophagus?
UES
What marks the distal end of the esophagus, where it meets the stomach?
LES
What is the function of the LES?
Smooth muscle- function is to prevent reflux of gastric contents from stomach to esophagus.
-Impaired contraction or reduced tone of LES = reflux
-Increased tone or increased pressure of LES = impaired relaxation dysphagia
Which system dominates innervation of the GI tract?
Parasympathetic NS dominates - normal parts of digestion we don’t have to think about.
What is the effect of SNS stimulation of the GI tract?
Inhibit gastric secretion.
-However, in extreme stress SNS overpowers with increased catecholamines– diarrhea, vomiting. “Gut Brain”
What is the Enteric Nervous System (intrinsic)?
Mesh like system that governs the GI tract.
-large system that is part of the peripheral nervous system that functions independently of Central Nervous System (brain, spinal cord)
What are the 3 layers of the stomach?
1) Mucous Layer
2) Submucosal
3) Muscle
Describe the Mucous Layer of the stomach.
Thick; 95% water, phospholipids, mucin proteins, and HCO3.
Describe the Submucosal Layer of the stomach.
Veins and arteries are present.
-If mucous layer erodes into this layer you can have GI bleeding, ulcers.
Describe the Muscle Layer of the stomach.
If damaged- abdominal pain, rupture.
What is the main function of the Parietal Cells?
Main function is to secrete H+ via the H+/K+/ATPase pump, as well as the release of intrinsic factor.
What is intrinsic Factor?
A glycoprotein that helps you absorb B12.
-The only gastric secretion necessary for life.
-Binds to B12 and gets absorbed in the ileal epithelium.
-B12 is needed for the metabolism of every cell, DNA synthesis, and in the nervous system.
-Severe dysfunction/destruction that leads to IF deficiency will need B12 injections
What are the 3 Main Receptors of Parietal Cells?
1) Gastrin Receptor (CCK-B)
2) Acetylcholine Receptor (M3 Receptor)
3) Histamine Receptor (H2)
What is the Gastrin Receptor (CCK-B)?
Cholecystinkinen receptor
-Involves Gastrin
What is Gastrin?
A hormone secreted by G-cells into blood vessels in response to food/proteins.
-Released by vagal stimulation
Vagal stimulation of enteric neurons releases gastrin via ________.
Gastrin releasing peptide
How does the Vagus nerve also indirectly promote gastrin release?
Vagus nerve also indirectly promotes gastrin release by inhibiting Somatostatin (acts as shut off)
Describe the effects of the Acetylcholine Receptor (M3).
Vagal stimulation of post ganglionic neurons of enteric nervous system releases ACH.
Describe the effects of the Histamine Receptor (H2)?
Enterochromaffin cells (ECL) secrete histamine when they are stimulated by gastrin or ACH.
What are the effects of the PGE2 receptor?
-Decrease activity of proton pump on parietal cells and decrease histamine release on ECL cells
-Responsible for mucous-neutralizing acids via cox 2-(arachidonic acid)
-Cox 2 inhibitors- NSAIDS, Celebrex, ASA
-When we inhibit COX2, have decreased ability to neutralize acids.
Destruction of Parietal Cells from chronic gastritis causes what?
-Decreased pH (less acidic), so can end up with bacterial overgrowth
-Also have decreased Intrinsic Factor, so have decreased B12 absorption.
What are Enterochromaffin Like (ECL) Cells?
Neuroendocrine cells utilized at the CCK-B receptors (Gastrin) and M3 receptors (acetylcholine).
-Release histamine
-Found in close proximity to parietal cells
What is the Enterochromaffin Cell Different Subtype?
Found in the gut.
-Release serotonin
-Believed to be responsible for peristalsis.
-Can cause and be stimulated by gastric distention and cause N&V, and abdominal pain.
-Being studied for association with IBS and other GI disorders (chronic constipation)
What do Chief Cells secrete?
-Inactive Pepsinogen.
-Lipase
Located in deep mucosal layer of stomach.
When Pepsinogen reacts with ____from Parietal Cells, it becomes activated to ____ to break down proteins.
When Pepsinogen reacts with HCL from parietal cells, it becomes activated to pepsin to break down proteins.
What do D Cells secrete?
Somatostatin.
-Somatostatin will bind to G-Cells and inhibit further Gastrin Release.
What stimulates D Cells?
Stimulated by increase intraluminal H+ concentration
-Increased Fats/Proteins in Duodenum
What are the 3 Phases of Digestion?
1) Cephalic
2) Gastric
3) Intestinal
Describe the Cephalic Phase of Digestion.
-1/3rd of stomach acid (no food present)
-Sight of food (occipital), thought of food (pre-frontal), smell and taste of food (olfactory)
-Messages to hypothalmus-medulla-dorsal nuclei of Vagus nerve to parietal cells of stomach.
Describe the Gastric Phase of Digestion.
-Accounts for remaining 2/3rds of acid
-Distention of stomach affects stretch receptors stimulate response from Vagus Nerve to the CNS and down again
via the long reflex arc, or short reflex arc via submucosal and mesenteric plexus
*HCL acid release is stimulated my multiple paths
Describe the Intestinal Phase of Digestion.
Stimulated by the presence of chyme.
Parietal cells are stimulated to secrete acid (H+) by _______ (acting on gastrin/CCK-B receptor), ________ (M3 receptor), and _______ (H2 receptor).
Parietal cells are stimulated to secrete acid (H+) by gastrin (acting on gastrin/CCK-B receptor), acetylcholine (M3 receptor), and histamine (H2 receptor).
Acid is secreted across the parietal cell canalicular membrane by the ______ proton pump into the gastric lumen.
Acid is secreted across the parietal cell canalicular membrane by the H+/K+-ATPase proton pump into the gastric lumen.
Gastrin is secreted by _______ cells into blood vessels in response to ____________.
Gastrin is secreted by antral G cells into blood vessels in response to intraluminal dietary peptides.
Within the gastric body, gastrin passes from the blood vessels into the ___________ of the fundic glands, where it binds to __________ receptors on parietal cells and enterochromaffin-like (ECL) cells.
Within the gastric body, gastrin passes from the blood vessels into the submucosal tissue of the fundic glands, where it binds to gastrin-CCK-B receptors on parietal cells and enterochromaffin-like (ECL) cells.
The vagus nerve stimulates _______neurons of the enteric nervous system to release ______, which binds to _________ receptors on parietal cells and ECL cells.
The vagus nerve stimulates postganglionic neurons of the enteric nervous system to release acetylcholine (ACh), which binds to M3 receptors on parietal cells and ECL cells.
Stimulation of ECL cells by ______ (CCK-B receptor) or ________(M3 receptor) stimulates release of ____________.
Stimulation of ECL cells by gastrin (CCK-B receptor) or acetylcholine (M3 receptor) stimulates release of histamine.
Within the gastric antrum, vagal stimulation of postganglionic enteric neurons enhances gastrin release ______ or ________.
Directly or Indirectly
How does vagal stimulation directly enhance gastrin release?
Directly by stimulation of antral G cells (through gastrin-releasing peptide, GRP)
How does vagal stimulation indirectly enhance gastrin release?
Indirectly by inhibition of somatostatin secretion from antral D cells.
Antral D cells are stimulated to release _____ by the rise in intraluminal H+ concentration and by CCK that is released into the bloodstream by duodenal I cells in response to ___________ and ____.
Antral D cells are stimulated to release somatostatin by the rise in intraluminal H+ concentration and by CCK that is released into the bloodstream by duodenal I cells in response to proteins and fats.
Binding of ______________ to receptors on adjacent antral G cells inhibits further ________ release.
Binding of somatostatin to receptors on adjacent antral G cells inhibits further gastrin release.
