SAVED
File name .JPG
File alt. text
Image should be px wide x px tall.
Select Image
home - Stomach - Miscellaneous - Gastric Physiology Overview Written by Dr Sebastian Zeki
Nausea and Vomiting:
Understands the pathophysiology of vomiting.
Appreciates the gastrointestinal conditions that cause nausea and
vomiting as well as the range of extra-intestinal causes

Recognises the influence of neurological conditions and metabolic
derangements such as diabetes

Understands the physiology of gastric emptying and how this is
affected by disease, toxins and drugs

Abdominal Pain:
Knows the causes of acute and chronic abdominal pain that arise
from upper gastrointestinal, biliary and pancreatic diseases

Understands the clinical presentations of the various conditions
causing pain and the means by which they can be diagnosed and
treated

Weight Loss:
Knows the significance of weight loss as a consequence of upper
gastrointestinal disease, knows those conditions that present with
loss of weight and how they are managed

Skills
Makes a detailed clinical assessment of patients presenting with
symptoms indicating possible upper gastrointestinal disease,
construct a management plan and be aware of the various avenues
of treatment

Behaviours
Evaluates patients in a structured and timely manner, carries out
appropriate investigations and formulates management plan.

Gastric Physiology Overview

Small Intestine a) Segmentation- Circular muscle contracts with relaxation of muscle either side-Mixes and is propulsiveb) Peristalsis Short burst of longtitudinal contraction which isnt continuous.c) Interdigestive Period: MMC Enteric Reflexes:The enterogastric reflex is activated by intestinal receptors sensitive to hydrogen ion, distension, and osmolarity. This causes a decrease in gastric motility and slows the rate of gastric emptying, protecting the intestine from excessive acidity. The ileocaecal, or ileocolic, reflex is stimulated by distension of the ileum. Increases motility of the ileum and relaxes the ileocaecal sphincter, allowing chyme to pass from the ileum to the caecum. Also, distention of the colon causes the ileocaecal sphincter to contract reflexly, providing protection against reflux of colonic contents. The gastroileal reflex is initiated when the stomach is distended, causing increased ileal motility.The intestino-intestinal inhibitory reflex is caused when a segment of intestine is distended and results in relaxation of the remaining intestine. The colocolic inhibitory reflex is a similar reflex observed in the colon. These are mediated via sympathetic pathways. Defecation is a complex, neurally controlled act that includes voluntary and involuntary elements. Mass movements or coordinated segmental contractions of the colon deliver faecal matter to the rectum. Stretch receptors in the wall of the rectum and anal canal respond and trigger the rectosphincteric reflex. Afferent signals are sent to the cerebral cortex, where the urge to defecate is recognized, to the autonomic ganglia, and to the spinal centers, which provide the efferent innervation of the sphincters. As distension increases, rectal contractions are reflexly induced. When the rectum is distended, the immediate reflex response is relaxation of the internal sphincter and contraction of the external sphincter. If conditions are perceived to be appropriate (ie, socially acceptable) for defaecation, the external sphincter is voluntarily relaxed and defaecation occurs. If conditions are inappropriate, contraction of the external sphincter is voluntarily maintained, the rectal stretch receptors adapt, and the rectum relaxes to accommodate the contained faecal matter. The act of defaecation is facilitated by assuming a squatting or seated position to align and dilate the recto-anal junction and by employing the Valsalva maneuver to increase intra-abdominal pressure 1.5 L per day.High [HCO3-] and low [Cl-]. Secretions come fromGlands of Lieberkuhn: Produce viscous mucus to protect mucosaPaneth Cells: Produce enterokinase to activate pancreatic zymogenGoblet cells: Produce mucus: Lubricates food pH of 8.0 to 8.4 and is secreted at about 60 ml/d. High [K+] and [HCO3-]Low [Na+ and Cl-]. Secretion stimulated by mechanical irritation. Inhibited by sympathetic nerve. ------Gastric accommodation: Mediated by vagus and CCK. Parietal cells G cells Cephalic phase: Vagal stimulation of secretion and motility Gastric phase: Food in the stomach stimulates mechanoreceptors to stimulate G and parietal cells and motility Intestinal Phase: Gastrin secreted if ph <3Gastric secretion and motility (via enterogastric reflex inhibited if chyme ph<2 On eating:)Peristalsis: Occurs proximal to distal- mixes and grinds the chyme- the pylorus opens as the wave approaches 3)Retropulsion- the wave goes back on itself to continue the mixingIn fasting: Migrating Motor Complex: Antral contraction for 10-20 minutes every 2 hours- the electrical activity starts in the stomach and ends in the ileum- sweeps up debris Gastric motility and secretion Secretin Vagus nerve + Cephalic Phase(sight and smell stimulates vagus nerve) The degree of enzyme secretion in the cephalic phase is about 50% of the maximal response elicited with exogenous CCK and secretin. Vagus nerve modulates secretion by means of cholinergic fibers, which innervate pancreatic acinar cells. The vagus also modulates peptidergic nerve fibers, which innervate duct cells. Gastrin + Evokes a small volume of pancreatic juice containing a high enzyme content. Gastric phase Overlaps the cephalic phase. pH<3 CCK Secretin Phenylalanine and tryptophan and fatty acids of 8 to 10 carbons + Intestinal Phase Secretin potentiates the effect of CCK Phases of Pancreatic Secretion CCK 5 amino acid seqquence at carboxy end that is the same as gastrin Structure Several CCK lengths produced as a result of post translation modification CCK Receptors Types:CCK1 receptors (aka CCK-A) CCK2 receptors (aka CCK-B) identical to the gastrin receptor and is present in the stomach and brain Stimulated by:Ingestion of a meal due to fat and protein; less so with carbs.Controlled by: Negative feedback from pancreatic secretions Increases transient lower oesophageal sphincter relaxations (tLESRs) via the CCK1 receptor 27 amino-acidAmidated at C-terminus Inhibits gastric acid release, gastric motility, and gastrin releaseStimulation of pancreatic fluid and bicarbonate secretion Somatostatin-14 Somatostatin-28 Cyclic peptides G protein-coupled receptor Distributed thourghout entire GI tract and bodyIn GI tract produced by D-cellst1/2 in blood of 3 minutes Stimulated By:Meal ingestion and gastric acid secretion InhibitoryDecreases endocrine and exocrine secretion Decreases blood flowReduces GI motility Resduces gallbladder contractionInhibits secretion of most GI hormones Synthetic peptidesOcreotide (90 min half life)Somatosatin LARLanreotide-PRUses:secretory diarrhoea High output fitula/ stomesGI bleedingDiagnostic imaging of neuuroendocrine tumoursInhibition of tumour growth Somatostatin Pre-pro-gastrin rER Gastrin is synthesized on rER, processed in the Golgi apparatus and packaged in secretory granules, Golgi apparatus Secretory granules G-34 G-17 2 Major gastrin forms Protein, peptides, and amino acids stimulate G-cells G-cells in antrum + H+ - ECL Parietal cell + D-cells Hista-mine Causes of hypergastrinemia Chronic atrophic gastritis PPIZollinger-Ellison syndrome Complications of chronic hypergastrinaemiaGastric carcinoids (occur in gastrinoma (30%) and PA (5%). Doesn’t happen with prolonged PPI useColon and Pancreatic tumours (experimental data)Gastric polypsTrophic effects on the stomach and intestine CCK2 receptor is present on parietal cells and enterochromaffin-like cells (ECL cells) of the stomach.CCK1 receptor is abundant in the pancreas and gallbladder and has a 1000x higher affinity for CCK than for gastrin G-protein linked receptor Gastrin Gallbladder contraction. CCK also relaxes the sphincter of Oddi Limited stimulation of pancreatic secretion directly and indirectly via vagus stimulation. Delays gastric emptying Overall role is to optimise small bowel absorption and giving it time Regulates bowel motility C C K S e c r e t i n g c e l l c o n c Duodenum Ileum + G protein coupled receptors Receptors Secreted by intestine Receptor Location:Duct and acinar cells pancreasBrain cells and vagusSecreted from: small intestine and CNS Overall role:As CCK- Overall role is to optimise small bowel absorption and giving it time Role: Somatostatin 1)Receptive relaxation.Distended oesophagus causes vagally mediated distention of orad stomach. Orad stomach distention only lasts as long as LES relaxation. Hormonal Control Of Gastric Acid Secretion Gastrin Synthesis Cephalic phase Gastric phase Intestinal Phase ColonSegmentation (most common)- haustrations take 30 seconds to peak then relax for 60seconds.Peristalsis also occurs but less commonCan take stool 8-15 hours to reach transverse as above movements are slow.Mass movement- predominant in the transverse to sigmoid colon.- occurs for 15 mins during first hour after eating a meal.Stimualted by gastro and duodenocolic reflexesRectum- segmental and peristaltic contractions Oesophagus