Gastrointestinal system Flashcards
What does the nervous system in the GI tract consist of?
Intrinsic (enteric) system
Extrinsic system: sympathetic, parasympathetic
Where is the intrinsic nervous system of the GI tract found?
In the wall of the GI tract
2 plexuses of GIT intrinsic nervous system
Myenteric (Auerbach’s) plexus = between circular and longitudinal muscle layers, mainly motor
Submucosal (Meissner’s) plexus = within submucosa, mainly sensory
What does the enteric nervous system respond to?
Responsible for majority of gut SECRETION and MOTILITY
Respond to gut transmitters: Cholecystokinin Substance P Vasoactive intestinal peptide (VIP) Somatostatin
Input of enteric nervous system apart from gut transmitters
From autonomic (extrinsic) nervous system
Sympathetic: fibres terminate in the submucosal and myenteric plexuses
What does stimulation of the GIT SYMPATHETIC nervous system lead to?
Vasoconstriction
Inhibit secretion of glandular tissue
Contraction of sphincters
Inhibit circular muscle of bowel, hence DECREASING MOTILITY
What does stimulation of the GIT PARASYMPATHETIC nervous system lead to?
Parasympathetic: fibres terminate in MYENTERIC plexus ONLY
Increase secretion of glandular tissue
Relaxation of sphincters
Stimulate circular muscle of bowel, hence INCREASING motility
Hormones and neurotransmitters regulating GI motility and secretion
Gastrin Secretin Cholecystokinin (CCK) Pancreatic polypeptide Gastric inhibitory polypeptide (GIP) Motilin Enteroglucagons Neurotensin
Which glands secrete saliva?
PAROTID (25%) = watery lacking mucus, Na and Cl- lower than plasma, K+ and bicarb levels higher, high enzyme conc (salivary amylase and IgA), affected by aldosterone
SUBMANDIBULAR (70%) = more viscous (mixed serous and mucosal)
SUBLINGUAL (5%) = contain mucoproteins
(numerous saliva glands present over tongue and palate)
Functions of saliva
Lubrication (mucus) to help with swallowing Speech Taste Antibacterial: lysozyme, IgA Starch digestion: amylase
2-stage process of saliva formation within salivary glands
1) ISOTONIC fluid of similar composition to ECF secreted by ACINAR component of salivary gland
2) Isotonic fluid is modified as it moves along the duct. Na and Cl- removed, K+ and HCO3- added by ATP transport proteins
Why is saliva DILUTE during LOW rates of secretion?
Plenty of time for ductal modification
Why is saliva more CONCENTRATED during HIGH rates of secretion?
Na, Cl- and HCO3- content increases
What is saliva secretion controlled by?
Autonomic nervous system
Reflex stimulated by salivary nuclei in MEDULLA
What is saliva secretion STIMULATED by?
Stimulation of mechanoreceptors and chemoreceptors in mouth
Higher centres in CNS i.e. smelling/thinking about food
Parasympathetic impulses stimulate saliva secretion through which cranial nerves?
Facial and glossopharyngeal nerves
3 phases of swallowing
ORAL = voluntary
PHARYNGEAL = involuntary, superior constrictor raises soft palate (preventing food from entering nasopharynx), initiates peristalsis pushing food through upper oesophageal sphincter (respiration inhibited to prevent food entering resp system)
OESOPHAGEAL = peristalsis continues
Pressure of oesophegeal sphincter
15-25mmHg (high) in region 2cm above and 2cm below diaphragm
Note: it’s a physiological sphincter, not anatomical
Factors preventing reflux from stomach into oesophageus
Physiological oesophageal SPHINCTER
RIGHT CRUS of diaphragm compresses oesophagus as it passes through oesophageal hiatus
ACUTE ANGLE at which oesophagus enters the stomach acts as a VALVE
Closure of sphincter is under VAGAL control, but hormone GASTRIN causes sphincter to CONTRACT
Which hormones cause the oesophageal sphincter to RELAX?
Secretin
CCK
Glucagon
What is the gastric mucosa divided into?
Columnar epithelium = secrete protective mucus layer
Gastric glands = intersperse mucosa, contain secretory cells
Types of secretory cells in gastric mucosa
MUCUS cells = secret mucus, located at OPENING of gastric glands
PEPTIC (chief) cells = at BASE of gastric glands, secrete PEPSINOGEN
PARIETAL (oxyntic) cells = secrete HCl and INTRINSIC FACTOR
NEUROENDOCRINE cells = secrete peptides regulating GI motility and secretion i.e. GASTRIN
Predominant cell types in various regions of stomach
FUNDUS and BODY = PEPTIC and PARIETAL cells
ANTRUM and pylorus = MUCUS and NEUROendocrine
CARDIA = gastric glands composed almost completely of MUCUS cells
How much secretion does the stomach produce per day?
~2-3L per day
What does gastric secretion contain?
HCl Pepsinogen Mucus Intrinsic factor Salt, water
pH of stomach acid
pH 1-3
Roles of stomach acid
Tissue breakdown
Convert pepsinogen to active pepsin
Form soluble salts with Ca and iron (to aid their absorption)
Immune defence mechanism by killing microorganisms
What is gastric acid secreted by?
Parietal cells
What happens when parietal cells are activated?
Deep clefts form in the apical membrane
These canaliculi allow acid to be secreted into stomach
How are the H+ and Cl- ions pumped from the parietal cell?
H+ ions pumped by H+/K+ ATPase (K+ going into cell)
Cl- ions pumped by 2 routes:
1) Chloride channel
2) Cl-/K+ co-transport system (K+ going out of cell)
How are H+ ions produced in the stomach?
By oxidative processes
This also produces a OH- ion
What happens to the hydroxyl ion produced by parietal cells?
It results in the formation of HCO3- in a reaction catalysed by carbonic anhydrase
It is then exchanged for Cl- on basolateral surface of the cell
What can the production of HCO3- by parietal cells be influenced by?
Prostaglandins
How is acidity of gastric acid maintained?
By H+/K+ ATPase pump on parietal cells
as part of the process, bicarb ions will be secreted into surrounding vessels
What happens to the Na and Cl- ions in parietal cells?
Na+ and Cl- ions are ACTIVELY SECRETED from parietal cells into the canaliculus
This sets up a NEGATIVE POTENTIAL across the membrane
Hence, Na+ and K+ ions diffuse across into the canaliculus
What happens to the bicarbonate ions secreted by parietal cell into surrounding vessels?
Carbonic acid is formed
This dissociates into H+ ions, which leave the cell via the H+/K+ antiporter pump
Na+ ions are actively absorbed at the same time
This leaves H+ and Cl- ions in the canaliculus. These mix and are secreted into the lumen of the oxyntic gland
Factors protecting stomach from digestion
ALKALINE MUCUS secreted from cells at neck of gastric glands form a layer (mucosal barrier) over gastric epithelium
Tight epithelial junctions prevent acid from reaching deeper tissues
Prostaglandin E secretion increases thickness of mucus layer, stimulating HCO3- production and increasing blood flow in mucosa (bringing nutrients to any damaged areas)
3 phases of gastric acid secretion
CEPHALIC (smell/taste of food) = 30% of acid produced, VAGAL cholinergic stimulation causing HCl secretion and GASTRIN release from G cells
GASTRIC (stomach distension) = 60% of acid produced, stomach distension/low H+/peptides causes GASTRIN release
INTESTINAL (food in duodenum) = 10% of acid, high acidity/distension/hypertonic solutions in duodenum INHIBITS gastric acid secretion via enterogastrones (CCK, secretin) and neural reflexes
Factors increasing gastric acid production
VAGAL NERVE stimulation
GASTRIN release
HISTAMINE release (indirectly following gastrin release) from enterochromaffin-like cells
How does vagal activity stimulate gastric secretion?
Direct stimulation of gastric glands via ACh release
Gastrin release from G cells in atrum (stimulate acid and pepsin secretion, and histamine release)
Histamine release from mast cells (stimulates parietal cells via H2 receptors, causing acid production)
Factors decreasing gastric acid production
Somatostatin (inhibit histamine release)
CCK
Secretin
Source, stimulus and action of GASTRIN
Source = G cells in antrum of stomach
Stimulus = stomach distension, extrinsic nerves
(inhibited by low antral pH and somatostatin)
Actions = increase HCl, pepsinogen and IF secretion, increase gastric motility, trophic effect on gastric mucosa
Source, stimulus and action of CCK
Source = I cells in upper small intestine
Stimulus = partially digested proteins and triglycerides (fatty food in duodenum)
Actions = increase secretion of enzyme-rich fluid from pancreas, gallbladder contraction, relaxation of sphincter of Oddi, decrease gastric emptying, trophic effect on pancreatic acinar cells, induce SATIETY
Source, stimulus and action of SECRETIN
Source = S cells in upper small intestine
Stimulus = acidic chyme, fatty acids
Actions = increase secretion of bicarb-rich fluid from pancreas and hepatic duct cells, decrease gastric acid secretino, trophic effect on pancreatic acinar cells
Source, stimulus and action of VIP
Source = Small intestine, pancreas
Stimulus = neural
Actions = stimulate secretion by pancreas and intestines, inhibit acid and pepsinogen secretion
Source, stimulus and action of SOMATOSTATIN
Source = D cells in pancreatic islets and stomach
Stimulus = fat, bile salts, glucose in intestinal lumen
Actions = decrease acid, gastrin and pepsin secretion, decrease pancreatic enzyme secretion, decrease insulin and glucagon secretion, inhibit trophic effects of gastrin, stimulate gastric mucus production, inhibit growth hormone
What type of saliva does parasympathetic stimulation produce?
Water-rich, serous
What type of saliva does sympathetic stimulation produce?
Low volume, enzyme-rich
Where is somatostatin produced?
D cells of pancreatic islets
Enterochromaffin cells of gut
Brain tissue
Note: substances inducing insulin release also induce somatostatin production
Clinical application of somatostatin
Treat pancreatic fistulae (as it reduces pancreatic exocrine secretions)
Clinical manifestations of somatostatinomas
Diabetes mellitus
Gallstones
Steatorrhoea
Resting volume and pressure of stomach
Volume = 50mL
Intragastric pressure = 5-6mmHg
Factors increasing rate of gastric emptying
Increased gastric volume
Gastrin release
Factors decreasing rate of gastric emptying
Hypertonic CHYME
Gastric ACID entering duodenum (vagally-mediated delay in gastric emptying + stimulate bicarb release from pancreas to neutralise acid + secretin release –> inhibit antral contractions + increase contractility of pyloric sphincter)
FATTY food (CCK and GIP released by small intestines –> increase contractility of pyloric sphincter)
PROTEINS (stimulate gastrin release –> increase contractility of pyloric sphincter)
Why do individuals who have undergone truncal vagotomy tend to routinely require either a pyloroplasty or gastro-enterostomy?
Neuronal stimulation of the stomach is mediated via the vagus nerve. The parasympathetic nervous system will tend to favor an increase in gastric motility.
Patients with truncal vagotomy would need pyloroplasty/gastro-enterostomy as they would otherwise have delayed gastric emptying.
Where is the vomiting centre located in the CNS?
Medulla oblongata
Locations of vomiting receptors
Labyrinthine receptors of EAR (motion sickness)
Over-distension receptors of DUODENUM and STOMACH
TRIGGER ZONE of CNS - many drugs (e.g. opiates) act here
Touch receptors in THROAT
Events occurring during vomiting
Respiration inhibited
Larynx closes and soft palate rises
Stomach and pyloric sphincter relax and duodenum contracts, propelling intestinal contents into stomach
Diaphragm and abdominal wall contract –> intragastric pressure increases
Gastro-oesophageal sphincter relaxes and pylorus closes
Stomach contents expelled through the mouth
Stimulation of vomiting centre in medulla leads to motor impulses passing along which cranial nerves?
CN 5, 7, 9, 10
to the intercostals, abdominal muscles and diaphragm
Causes of vomiting
Stimulation of posterior oropharynx
Excessive distension of stomach or duodenum
Stimulation of labyrinth e.g. motion sickness
Severe pain
Raised ICP
Stimulation of chemoreceptor trigger zone by noxious chemicals
Bacterial irritation of upper GI tract
