gastric motility and secretions Flashcards
To understand the three basic mechanical movements of the stomach and how each of these three movements are regulated.
storing: increase in volume without rise in pressure. (1) receptive relaxation (prior to reception of food) and (2) gastric accomodation (stomach fills/distension without increase in pressure). NO and vagus important in both. loss of vagal input = impaired ability of stomach volume to increase without an increase in pressure.
churning: breaking down (2mm) to increase SA for digestion.
emptying: rate depends on what you ate!
HCl in duodenum - secretin - impaired gastric emptying. (stops too much acid going to the duodenum)
Fat in duodenum- CCK - impaired gastric emptying
Prtn in stomach- gastrin - impaired gastric emptying
Duodenal distension - ENS - impaired gastric emptying
Vagal- Ach, opioid, 5-HT impair gastric emptying. NO, VIP promote gastric emptying.
To understand how vomiting is coordinated and stimulated. (emesis)
Centrally controlled at the medulla in the emetic center.
Also at the chemoreceptor trigger zone which will feed the emetic center info.
Important: 5HT, Dopa, Ach.
Gut: 5HT specifically.
Motion sickness** histamine and Ach.
Know the following pathophysiological conditions and how the physiology of the stomach is altered during these conditions: gastroesophageal reflux disease (GERD) and pyloric stenosis.
you know GERD.
Pyloric stenosis: narrowing of pyloric sphincter caused by thickending of pyloric muscle due to poorly controlled DM or congenital conditions. Leads to impaired motility of stomach (gastroparesis)
List the cellular make-up and the secretions of the mucosal surface of the stomach: parietal, chief, neck, enterochromaffin-like (ECL), G, D, and superficial epithelial cells.
parietal: HCL for prtn digestion, sterillization, and nutrient absorption. IF for vitamin B12 absorption.
chief: pepsinogen for prtn digestion.
neck: mucus and bicarb for protection.
ECL enterochromaffin-like cells: promote HCL secretion.
G cells: gastrin to promote HCL secretion.
D cells: somatostatin to suppress HCL secretion.
Nerve cells: Ach to promote mucus secretion, promote bicarb secretion, promote Hcl secretion.
Describe how neuronal, paracrine, and endocrine pathways regulate acid secretion in the stomach
Endocrine regulation —> gastrin
Gastrin increase acid secretion directly by acting on parietal cells to increase activity of H/K/ATPase. Indirectly- acts on ECL cells to release histamine to act on parietal cells to increase activity of H/K/ATPase.
Neurocrine regulation —> Ach
Ach increase acid secretion directly by releasing from neurons and acting on parietal cells to increase activity of H/K/ATPase. Indirectly Ach acts on ECL cells to release histamine to act on parietal cells to increase activity of H/K/ATPase.
Paracrine regulation —> histamine is main. Also PGE2 and Somatostatin.
Histamine from ECL cells acts on parietal cells to increase activity of H/K/ATPase.
PGE2: decrease acid secretion by decreasing activity of H/K/ATPase.
Somatostatin: released by D cells to inhibit the release of gastrin by G cells —> less histamine released from ECL cell and less activity of H/K/ATPase.
List the functions of gastric acid.
- Protein digestion (conversion of pepsinogen to pepsin)
- Provide sterile environment.
- Prevent bacterial and fungal growth.
- Facilitate absorption.
- Promote bile and pancreatic enzyme flow.
Identify positive and negative regulators of gastric acid secretions, the cells which release these regulators, and the target of the secreted regulators.
promote: histamine, gastrin, acetylcholine
from ECL, G cell and nerve cells
*suppress is somatostatin from D cell
Characterize the differences in the four phases of gastric acid secretion and how they are regulated.
4 phases: interdigestive phase, cephalic phase, gastric phase, intestinal phase
Interdigestive phase: lowest in the early morning and rises throughout day. pH 3-6. Depends on number of parietal cells, body weight or presence of food in stomach.
Cephalic phase: 30% of acid secretion. Activated by sight or smell of food triggering a vagal response resulting in acid secretion.
Gastric phase: 50 – 60% of gastric secretion occurs during this phase. Distension in the stomach stimulates vagal n leading to acid secretion. Negative feedback if pH below 1 via gastric D cells.
Intestinal phase: 10% of gastric secretion occurs during this phase. Mediated by presence of peptides in duodenum –> release gastrin to increase activity of parietal cell.
Describe the steps of how pepsinogen is converted in lumen of the stomach to the active protease pepsin.
- Pepsinogen secreted by chief cells acid hydrolysis (via gastric acid) pepsin.
- Regulator: acetylcholine (main), also: gastrin, histamine, CCK, secretin, VIP, NE, and PGE2. Regulation is similar to that of gastric acid secretion.
- Extra: pepsin is irreversibly inhibited when pH gets too high (too basic).
Identify the site of intrinsic factor secretion and its physiological role.
- Site of secretion: parietal cells of stomach.
- Physiological role: important for vitamin B12 absorption.
o Complexes with vitamin B12 in duodenum complex interacts with receptor on surface epithelial cells of ileum absorbed via endocytosis.
List the two key stimuli for mucus secretion by epithelial and neck cells of the stomach, the physiological role of mucus in the stomach, and the components of mucus.
- Stimuli: acetylcholine, prostaglandins.
- Physiological role:
o Protection at surface of epithelium (maintains surface at relatively normal pH so that pepsinogen is not activated until it reaches deeper into the lumen).
o Buffering capacity. - Components:
o Mucus (mucin, phospholipids, electrolytes, and water)
o Bicarbonate.
Describe the role of secretin in the stomach and its target cells.
secretin –> impaired gastric emptying when HCl is in the duodenum
inhibit the parietal cells –> dont want acid in the duodenum
Know the following pathophysiological conditions and how the physiology of the stomach is altered during these conditions: gastroesophageal reflux disease (GERD), pyloric stenosis, pyloric obstruction, gastritis, H. pylori infection, peptic ulcers, and Zollinger-Ellison syndrome
- Pyloric obstruction: results in activation of emetic response.
- Gastritis:
o What it is: infiltration of inflammatory cells without break in mucosal barrier damage of mucosal barrier.
o Causes: nonsteroidal antiinflammatory drug use (ex: aspirin), infectious agents (ex: H. pylori), increased # of parietal cells, high serum gastrin levels (Zollinger-Ellison syndrome), loss of acid-mediated negative feedback on gastrin secretion, rapid gastric emptying, cigarette smoking, alcohol use, decreased mucosal bicarbonate secretion, GERD.
o Disease process: can lead to ulceration.
H. pylori infection:
o What it is: bacterial that colonize luminal surface of gastric epithelium inflammation and ulceration.
o Disease process: fecal-oral transmission, mechanism of inflammation is unknown. Note: organism itself doesn’t invade epithelial tissue to cause damage; the inflammatory response to organism causes damage to surrounding tissue.
o Note: H. pylori produce urease, which allows for production of bicarb and ammonia to set-up a buffering environment around organisms to protect from gastric acid.
Peptic ulcers:
o What it is: inflammation that breaks through mucosal lining.
o What causes it: similar causes as gastritis (ulcers are the next severe form of gastritis).
o Disease process: can lead to perforation of GI tissue, hemorrhage, cancer, etc.
Zollinger-Ellison syndrome gastrin producing tumor
o What it is: high serum gastrin levels.
o Causes: tumors in duodenum/pancreas (gastrinomas).
o Disease process: too much gastrin too much gastric acid production peptic ulcers.
