BMS13 - Gastrointestinal Tract :knife_fork_plate: (Digestion and…
BMS13 - Gastrointestinal Tract :knife_fork_plate:
Liver and Pancreas
The pancreas sits in the fold of the small intestine adjacent to the duodenum which it will discharge it's product into.
The pancreas has two ducts; the
main pancreatic duct
which secretes the
common bile duct
which stems from the
stores and concentrates bile and only releases it when digestive products are about to enter the duodenum.
It concentrates bile using
Na+/K+ ATPase pumps
on the basolateral side, controlling the ions helps
to control water
which affects the concentration of bile.
The Gall bladder is stimulated to release it's contents by the hormone,
by neuroendocrine cells of the stomach. The gall bladder has a simple, columnar epithelium with an irregular brush border.
The pancreas has dual function acting as both an exocrine and endocrine organ.
The exocrine function is formed of secretory acini which are spherical units. These secrete the digestive enzymes e.g. lipases, amylases etc.
The exocrine portion looks like a salivary gland. It produces fifteen enzymes for digestion but in
form and secretes them via merocrine secretion.
The differences between the pancreas and a salivary gland are: centroacinar cells line the centre of the acinus (secrete bicarbonate cells) and the excretory cells are columnar but have no striations.
The endocrine portion is done by the islet of langerhans; to secrete hormones (insulin, glucagon, somatostatin etc.) into the blood and so, they have a profuse blood supply.
Different cells in the islets produce different hormones.
Liver hepatocytes are very complex cells which reflects the functions of liver. These functions include: production of bile (exocrine), detoxification, storage and synthesis whilst in foetuses - it is the site of haematopoiesis.
The liver has three main vessels: the hepatic artery, the hepatic portal vein and the hepatic vein.
The lobes of the liver are arranged in '
'. These lobules are roughly
in shape, with the outer boundary consisting of connective tissue. At the centre of each lobule is a
whilst at each vertices is a
consisting of a branch of the major blood vessels (
hep. artery, hep. portal vein and bile duct
The hepatocytes are arranged in rows with a sinusoid flowing in-between - this is where blood flows toward the central vein. The cells also secrete bile between eachother where it flows to join the bile duct.
These sinusoids are lined with endothelial cells which contain Kupffer cells which are phagocytic in nature so act as part of the immune system.
The space between the endothelial cell and the hepatocyte is called the space of disse. Hepatocytes have microvilli which extend into the space of disse. The microvilli have both absorption (food, drugs etc) and secretive (albumin, fibrinogen etc) roles.
The space of disse may also contain a cell known as a perisinusoidal cell (also known as Hepatic stellate cells or Ito cells). These store Vitamin A in lipid droplets or can transform into myofibroblast in response to stimuli producing large amounts of collagen = cirrhosis.
Hepatocytes are packed full with organelles as they are important in both absorption and secretion of important proteins and factors. The liver does have some ability to regenerate.
Rather than the liver be arranged in lobules, it can be considered '
'. The acinus rather than being a hexagon is two adjacent triangular portions put together.
An example of this is paracetamol poisoning. The toxic by-products get to a high concentration during overdose. These build up around the central vein (zone three) - leading to liver failure.
If the acinus is split into zones, the zone closest to the connective tissue will have the highest oxygen content. The content of oxygen decreases as you move toward the central vein. This is important because in Zone 3 - this is where there will be the largest concentration of liver metabolite (this could be toxic dependent on drugs etc) and in Zone 1 - this is where bacteria and viruses are most likely to attack liver tissue as this is where all the nutrients and oxygen are.
is an important product produced by the liver. Once produced, bile leaves hepatocytes down channels called
which are between the cells.
Bile is a
thick, alkaline fluid
- secreted by the liver to help emulsify fats in the chyme. It flows in the opposite direction to blood.
Bile is synthesised from cholesterol and contains sodium glycocholate, deoxycholate etc. It acts as a detergent; emulsifying fats in the duodenum. As the enzymes that digest food are water-soluble not lipid soluble, emulsifying fats makes these enzymes more efficient,
Bile also has pigments (biliruben and biliverdin) which are breakdown products of haemoglobin.
Mechanisms of GI tract motility and it's control
Gut motility involves a number of inputs to ensure smooth movement of food from when consumed up until the point of defacation.
Muscle in the wall of the tract mainly smooth but can be skeletal, to push food along the tract.
Nervous innervation particularly from the Enteric system and some minor innervation from the ANS.
Endocrine influences which link the presence of food to increased motility.
Sphincters allow for a
one way system
for food to travel.
Sphincters not only allow for one-way traffic but also for appropriate delay points.
Upper oesophageal sphincter closes the top of your oesophagus.
Lower oesophageal sphincter closes at the top of the stomach where the oesophagus ends.
This sphincter is formed by the contraction of circular smooth muscle in the wall of the abdominal oesophagus and only relaxes during the swallowing reflex/vomiting.
This sphincter has two special ways of remaining closed to prevent stomach reflux.
The angle at which the oesophagus enters the stomach is rather oblique - this means that pressure within the stomach can keep the sphincter closed by squashing one wall.
As the sphincter lies just beneath the diaphragm - when the diaphragm contracts during inspiration and the high intra-abdominal pressure restricts the opening of the sphincter.
Pyloric sphincter is at the end of the stomach and controls the movement of chyme going from the stomach into the small intestine.
Ileo-caecal sphincter is at the junction between the ileum and the large intestine (colon).
This is made of 'smooth muscle'. It relaxes in response to upstream pressure and constricts in the response to downstream pressure.
Anal sphincters (internal and external) control defecation.
Sphincters are required because of pressure differences. Pressure in the oesophagus is lower than atmospheric pressure and also, a little lower than abdominal pressure. This means food will be forced upwards and downwards at different times - sphincters allow for 'compartmentalisation' so food moves in a single direction.
Swallowing is an important process relying on compartmentalisation for smooth passage of food through the tract - this can be split into three sections:
The first stage is '
'. The tongue helps form a bolus. The bolus goes to the back on mouth, touching the soft palate. This causes a nervous response by the brain stem triggering the swallowing reflex.
The second stage is '
. The upper oesophageal sphincter relaxes whilst the epiglottis closes protecting the trachea to ensure, no food is inhaled to prevent choking.
The third stage is '
'. The bolus moves downwards propelled by gravity and peristalsis.
The oesophagus is split into
striated and smooth
muscle, with a majority being smooth muscle. The striated muscle is supplied by
somatic motor neurons from the brain stem
whilst the smooth muscle is
innervated by the ANS (parasympathetic) via the vagus nerve
. The vagus nerve will then synapse with the enteric nervous system which causes the smooth muscle contraction.
is contraction behind the bolus and relaxation in front of it, this is done as a unidirectional wave pushing the bolus down the oesophagus.
The gastrointestinal tract is lined mostly by the muscularis propria. This consists of a lumen surrounded by mucosa, submucosal plexus, circular muscle, Myenteric plexus and longitudinal muscle.
The submucosal plexus is mostly sensory and deals with responses to local stimuli from the mucosa.
The Myenteric plexus is mainly to do with muscle co-ordination and is influenced by autonomic supply.
Enteric nervous system (ENS)
is a largely independent system. Overall, control is from the ANS with some somatic contribution (upper oesophagus).
The ENS contains motor neurons to smooth muscle, for vasomotion (constriction/dilative), to secretomotion (regulating acid secretion) and to the epithelium particularly enteroendocrine cells which release hormones.
Interneurons for the co-ordination of reflex arcs by connecting layers of the muscularis propria.
The ENS also contains sensory neurons to detect chemical changes e.g. for proton concentration and mechanoreceptors for distension.
When food reaches the stomach it is very squashed and can only hold 50ml, it goes through a number of changes to increase it's storage volume to 1.5 litres.
There is a '
' - this happens due to a reflex arc initiated by the PNS via the brain stem; this reduces pressure and increases volume within the stomach.
in the stomach helps to mix contents to propel it into the pyloric region.
These waves of contraction are controlled by
cells. These waves of contraction get stronger towards to pyloric antrum squirting chyme through the sphincter. As the sphincter is narrow - this causes larger chunks to be regurgitated back into the stomach for more mixing.
Gastric motility is controlled thanks to a number of feedback inputs via the duodenum. If there is an increase in acidity, fats, amino acids and distension - this causes either a neural or hormonal response to reduce gastric emptying.
Controlling gastric emptying
Once, absorption is done - we get a
migrating myoelectic complex
- this triggers peristaltic waves to transport indigestible foodstuffs through the tract into the large intestine and is a cyclic process.
The internal gastric rugae (creases/folds) flatten in order to increase surface area.
Once food reaches the small intestine, the chyme is mixed via
rather than peristalsis. This allows a lateral mixing and leads to a slow transit time to maximise absorption. There is also a small pressure gradient from proximal to distal, helping the movement of chyme in the correct direction.
Chyme moves into the large intestine via the ileo-caecal sphincter. This prevents reflux back into the ileum. Motility is maintained in the colon via:
Haustrations for mixing where circular and longitudinal muscle constrict.
Mass movements for bulk movement due to the contraction of longer segments of circular muscle.
The colon is responsible for water reabsorption and this slowly changes the gut contents to help produce faeces.
Defecation is controlled by the anal sphincters. The internal sphincter is under parasympathetic control (smooth muscle) whilst the external sphincter along with the levator ani are skeletal muscle and are thus under voluntary control.
Gut motility regulated by hormones or neural controls.
Gut motility is sped up by increased parasympathetic firing and slowed by decreased by sympathetic firing.
during the 'inter-digestive period' regulates the background motility in the fast period between meals - controls the migrating myocentric complex.
increases motility during the 'post-meal period' then CCK and GL1-P reduce motility as digestion progresses.
Secretin inhibits gastrin secretion and decreases overall motility.
Gastrointestinal secretions and their control
Water comes from a range of sources in the gastrointestinal tract such as saliva, gastric secretions, diet and intestinal secretions.
A majority of this water is reabsorbed at the level of the small intestine not the colon.
The colon's main function is water reabsorption but only to affect the consistency of stools for defecation.
is a major GI secretion responsible for lubricating food, pH balance, initiating digestion and antimicrobial activity (thanks to lysozymes, igA from plasma cells etc.)
Saliva is produced by salivary glands which contain acinar cells which produce the saliva.
There are three salivary glands which do differ in composition and flow rate. They're are all controlled by the ANS with both sympathetic ( :arrow_up: macromolecular components) and parasympathetic ( :arrow_up: fluid and electrolyte component) increasing saliva production.
The saliva is isotonic with plasma and is dependent on several transporters on the basolateral side of the cell.
Diagram of transporters
Chloride ions build up in the cell and enter the salivary lumen via voltage-gated chloride channels. As they are voltage gated they respond to rises in intracellular calcium for nervous inputs.
As chloride aggregates in the saliva, this attracts cations particularly sodium ions through intercellular junctions. Water will follow sodium - as a result we get a moderately watery, saline saliva.
The salivary secretion is dependent on the
pump. This creates an electrochemical gradient for Na+ so it diffuses into the cell via a co-transporter along with potassium and chloride ions.
Saliva is modified as it passes along ducts before entering the oral cavity.
Some sodium and chloride are reabsorbed whilst potassium and bicarbonate are added. This results in a bicarbonate rich, hypotonic solution.
The exact composition depends on rate of flow through the ducts. If the flow rate is fast/slow, there will be less/more time for reabsorption and secretion altering saliva composition.
Saliva contains many other things such as: other ions, amylase, lysozyme, Immunoglobulin A and mucins (glycoprotein).
Digestion comes in three major phases; cephalic, gastric and intestinal.
The Gastric phase
begins when food reaches the stomach. The stomach secretes acid and pepsinogen in response to food with an increase in gastric motility.
This is under neural, enteric and hormonal control.
Gastric pits in the stomach lining contain parietal cells and chief cells. The chief cells secrete pepsinogen and intrinsic factor (
required for the absorption of Vitamin B-12
) whilst parietal cells secrete HCL. The main enterocytes secrete lipases and water.
works as: the cell can produce carbonic acid using carbonic anhydrase. This means that a proton and bicarbonate form - the proton is pumped into the lumen using ATP whilst bicarbonate is exchanged for chloride ions. Chloride ions then move down their gradient through voltage channels to form HCL in the stomach lumen.
Acid secretion increases upon stimulation thanks to the proton pumps required being stored in
at rest. Once stimulated, these vesicles fuse with the lumenal membrane - increasing the surface area for HCL secretion.
This secretion is regulated by four molecules:
Parietal cell regulation
Acetylcholine on a muscarinic receptor, Histamine on a H2 receptor and Gastrin
are all positive effectors on acid secretion.
is a negative effector, reducing acid secretion.
Acetylcholine is stimulated by the enteric nervous system via the vagus nerve by stomach distension. This acts directly on the parietal cell, on a enterochromaffin cell to secrete histamine which is also a effector or on D cells to secrete the inhibitory somatostatin (negative feedback).
Gastrin is released from g-cells when proteins are sensed in the stomach to increase stomach acid secretion.
The Intestinal phase
is where a majority of digestion and absorption takes place. Once food enters the small intestine, it secretes hormones which inhibit motility and gastric secretion but stimulate pancreatic and biliary secretions into the duodenum.
This is under enteric and hormonal control
The Cephalic stage
occurs before food has reached the stomach. It can be considered a feed-forward reflex. The smell, presence or taste of food increases the production and secretion of saliva and gastric secretions.
This is under neural control.
Other endocrine factors affecting gastric secretion:
is secreted by the duodenum in response to fats (causes bile release) and it decreases gastric secretion and motility. This is also the main satiety factor.
Regulates pancreatic exocrine secretions from acinar cells. The pancreas and the gall bladder have a common bile duct which leads to the duodenum controlled by the sphincter of oddi. The pancreas produces an
to neutralize stomach acid and
many digestive enzymes
(stored inactive in zymogen granules so they don't digest the pancreas) - these are released by exocytosis.
The alkaline secretion is controlled by a number of transporters. Energy is received via the Na+/K+ ATP pump, this creates an electrochemical gradient for sodium so it enters the cell via a bicarbonate-dependent co-transporter. Bicarbonate can then enter the lumen thanks to an anion exchanger. The main source of bicarbonate is from the breakdown of carbonic acid. Defect in the chloride channel (CTFR) leads to cystic fibrosis.
Pancreatic duct cell
Cholecytokinin controls this by stimulating the release of enzymes when fats are sensed in the stomach. Secretin controls the release of the alkaline fluid in response to low pH due to high acid secretion.
is secreted by the duodenum in response to stomach acid. This inhibits gastric secretions.
is secreted from the pyloric antrum and its release is stimulated by protein, coffee and alcohol whilst it is inhibited by low gastric pH. It induces gastric secretions and increase motility.
Gastric-inhibitory polypeptide (GIP) and Glucagon-like peptide 1 (GLP-1)
are incretins (Gut hormones). Stimulated by the present of fat and chyme in the small intestine after eating. Incretins potentiate glucose-induced insulin release after meals which inhibits gastric secretion/motility. These also promote satiety.
The small intestine also secretes mucus (goblet cells),
(crypt cells use the Na+/K+ ATP pumps),
is also known as the hunger hormone. When the stomach is empty, ghrelin is secreted - this increase stomach acid secretion and motility; promoting appetite.
secretes bicarbonate and some potassium thanks to the negative potential differential set up in the lumen by sodium and chloride ions. More sodium tends to be absorbed in to the cell from the lumen thanks to a Na+ channel compared to Chloride ions, this gives the lumen a negative potential compared to the cell. Therefore K+ ions diffuse down their gradient into the lumen via intercellular junctions.
If GI secretions did not work properly, there could be a range of health consequences:
Digestion and Absorption in the GI
Digestion is segmented into different regions of the tract due to the need for various enzymes and their activity. The aim of digestion is to break down macromolecules into monomers/dimers for absorption.
Absorption occurs mainly at the level of the small intestine by the use of various transporters some requiring energy (ATP) if done against a concentration gradient.
The enterocytes of the small intestine are specialised for the absorptive process. The cells have tight junctions between each other and have microvilli to maximise surface area.
There are an array of transporters (many sodium dependent) in order to drive the absorption of vital solutes (e.g. Glucose). There are also many enzymes on the surface for the breakdown of macromolecules.
There are many Na+/K+ ATP pumps to maintain a low intracellular sodium. This helps to create electrochemical gradient from outside the cell to the inside to assist with the sodium dependent transporters. This also drives water absorption into the intracellular space.
Stomach chyme which enters the duodenum has low pH and contains solubilised proteins and carbohydrates. Further secretions are required for more digestion.
Digestion and absorption of
Enterokinase is secreted by the duodenal enterocytes activates pancreatic trypsinogen into trypsin. Trypsin activates the
of the pancreas.
Trypsin and Chymotrypsin (endopeptidases) cleave peptide bonds producing short peptides. Carboxypeptidases (exopeptidases) cleave amino acids from the carboxyl ends whilst aminopeptidases cleave residues on the amino-end of peptides.
relies on pepsinogen (the precursor of pepsin) secreted by the chief cells in the stomach. Pepsinogen is activated via HCL (parietal cell) into pepsin which breaks down protein into peptides.
Protein is then absorbed via amino acids using a Na+ dependent transporter and then diffuse through the cytoplasm into a capillary. If protein is still in a small peptide form - these are absorbed using a proton dependent transporter and then hydrolysed into amino acids via cytoplasmic enzymes.
The small intestinal wall is permeable to peptides in infants to allow for easy absorption of antibodies and growth factors from colostrum.
Digestion and absorption of
Complex carbohydrates must be cleaved into simple sugars in order to be absorbed. However, some polysaccharides such as cellulose and inulin cannot be directly digested.
Carbohydrate digestion begins in the mouth using salivary amylase. Pancreatic amylase is released into the duodenum and further cleaves carbohydrates into simpler sugars. The small intestine has small membrane bound disaccharides which also help in the breaking down of complex sugars. These work best at neutral pH so the role of bile in neutralising stomach acid is vital.
Pancreatic amylase can only cleave straight and not branched glycosidic bonds producing oligosaccharides, maltose and maltriose.
The di/tri-saccharides are then broken down my brush-border enzymes into monosaccharides.
Absorption of these monomers are dependent on transporters found in the membrane of enterocytes. For glucose and galactose, there is a Na+ dependent cotransporter (dependent on Na+/K+ pump to create a Na+ gradient) whilst fructose uses GLUT5 transporters and moves via facilitated diffusion. Once in the cell, the monomers are absorbed into the blood using GLUT2 transporters.
Digestion and absorption of
Fat digestion requires pancreatic lipase, colipase, bile salts and the correct pH. Bile salts help to increase the surface area of lipids by emulsification because fats are not water soluble.
Bile salts are reabsorbed in the terminal ileum (95%) via the portal vein and re-extracted by hepatocytes in the liver and returned to the gall bladder. A small amount of bile is lost the faeces but new bile production accommodates for the small loss.
The emulsification in conjunction with pancreatic lipase helps to form micelles. Micelles are monoglycerides and fatty acid droplets which can then be absorbed by the enterocytes.
Absorption of fatty acids and monoglycerides into the enterocytes occurs by diffusion. The smooth endoplasmic reticulum resynthesises triglyceride and uses it to form chylomicrons. The packaging of chylomicrons are dependent on beta-lipoprotein; they are then released and taken up by lacteals (lymph).
Microbiota in the colon can produce vitamin K and folic acid which are absorbed here also. Many vitamins (A, D, E etc) are fat soluble so will also be absorbed in the small intestine along with lipid.
Things can go wrong in digestion and absorption which could lead to some illnesses:
Malabsorption could occurs as result of a person's inability to cleave macromolecules due to lack of pancreatic enzyme deliver, lack of bile salts or poor co-ordination of the tract with motility and secretion delivery.
This could lead to no absorption of lactose (lack of lactase leading to alactasaemia), incomplete lipid digestion and absorption (lack of bile to form micelles, no beta-lipoprotein to form chylomicrons etc.), lack of water absorption (due to high solute load in the lumen) and a lack of minerals and vitamins (could lead to aneamia).
Anaemia can be caused by a lack of iron or vitamin B-12
. pH in the stomach helps to stabilise the ferrous ion and without it; could lead to a
lack of haemoglobin leading to microcytic RBCs
. Vitamin B-12 relies on intrinsic factor from the parietal cells of the stomach for transport - insufficient factor can cause an immune response in which the body attacks the parietal cells producing less factor.
This disturbs erythropoiesis, giving us fewer but macrocytic RBCs
This can lead to
of two forms: osmotic and secretory.
Osmotic diarrhoea is caused by malabsorption: undigested fats have a laxative effect but also a solute imbalance causing more water to remain in the lumen.
Secretory diarrhoea is a result of bacterial infections e.g. cholera which increases the activity of secretory crypt cells in the intestine.
Diarrhoea can also be caused by mucosal damage e.g. Coeliac's disease causes the hypersensitivity of crypts due to gluten allergy.
Pharmacology of gastric acid control
Gastric acid can lead to damage of the stomach and duodenal walls leading to peptic ulcers. Ulcers are single lesions in areas of the tract which have been over-exposed to peptic juices.
Ulcers give a burning sensation often at night which goes away after a meal but then returns later. They can lead to a number of complications such as penetration and exposure of the liver/pancreas, perforation of the peritoneal cavity or heavy bleeding of the GI tract.
The Oxyntic gland in the gastric pits is responsible for the gastric secretions (pepsin and HCL) which can potential cause an ulcer.
A number of factors could influence ulcer formation:
Acid hypersecretion causing an ulcer is rare unless in the case of zollinger-ellison syndrome (a gastrin-secreting tumour leading to hypersecretion) which is a rare disease.
Stress and smoking could potentially be factors but are relatively minor causes.
Prolonged use of non-steroidal anti-inflammatory drugs (NSAIDS) e.g. ibuprofen and aspirin are said to increase ulcer incidence. This is because they reduce the amount of prostaglandins which are important in mucosal defence against bacteria such as Helicobacter Pylori.
Helicobacter Pylori is the most common cause of ulcer. The bacterium causes gastritis which weakens mucosal defence.
Ulcers are usually a result of an imbalance between acid/pepsin secretion and mucosal defence. Gastric ulcers and duodenal ulcers are developed in different ways but both by H. Pylori.
Gastric ulcers are due to H. Pylori infection in the main body of the stomach called the corpus. Usually the level of gastric acid is normal but there is some sort of defect in the mucosa. This causes a multifocal gastritis in which, glandular cells in the stomach are replaced by fibrous tissue.
Duodenal ulcers are due to H. Pylori infection in the pyloric antrum - there is usually increased secretion of gastric acid and this will get into the duodenum along with the bacteria leading to a metaplasia of the mucosa.
Helicobacter Pylori is a spiral shaped bacterium which causes gastritis. It grows beneath the mucus layer causing the increased release of gastrin/pepsin. Some strains are pathogenic due to the
type four insertion of CagA protein
The bacterium secretes urease which converts urea into bicarbonate and carbon dioxide. It surrounds itself in a 'bubble' of bicarbonate to protect itself from the acidic secretion.
The bacterium was proven to be the cause of ulcers using
. This is the process in proving that a bacterium/virus causes a particular form of disease.
The main mediators controlling gastric acid secretion are histamine, acetylcholine and gastrin via the enterochromaffin-like cells affecting parietal cell behaviour. Prostaglandins inhibit acid secretion of the parietal cells and also cause bicarbonate and mucus release in the lumen (both by binding to the EP3 receptor).
Acidic secretion is controlled by a proton pump (H+/K+ ATPase Pump) which pumps acid into the lumen.
The drugs used to reduce this are called
. This drug irreversibly blocks the H+/K+ pump by binding to sulphydryl groups and is inactive at neutral pH and is activated at a pH less than three. The drug is then metabolised into it's active form - sulphenamide.
In order to prevent ulcers, you can either reduce acid secretion or improve mucosal defences:
As histamine is a major propagator of acidic secretions, we can also use
H2 receptor blockers
H2 receptor blockers selectively block H2 receptors on parietal cells examples are:
cimetidine, ranitidine and famotidine
. These drugs inhibit cytochrome P450 which retards certain drug metabolisms (warfarin etc.)
There are drugs which improve mucosal defence e.g.
sucralate and bismuth chelate
by coating the ulcer and protecting it from gastric acid.
They do this by stimulating secretion of mucus, prostaglandins and bicarbonate. Bismuth chelate also has a chemotherapeutic effect against H. Pylori so that is an added advantage.
Antacids neutralise gastric acid by inhibiting pepsin action. Long term use may cause systemic alkalosis. Examples are:
Sodium bicarbonate, Magnesium carbonate and Aluminium hydroxide
Prostaglandins (PGE2 & PGI2) help to maintain the mucosal integrity. NSAIDs inhibit prostaglandin synthesis so affect mucosal defence.
is a PGE1 analogue taken with NSAIDs to prevent damage and promote healing of the mucosa.
are used to remove H. Pylori from the stomach to prevent ulcer relapse.
Antibiotics (amoxicillin, clarithromycin, metranidazole) are used in conjunction with omeprazole and bismuth chelate. H. Pylori often has a strong resistance to these antibiotics so bismuth chelate is added to further protect the mucosa.
Gastro-oesophageal reflux disease (GORD) is caused by acidic reflux from the stomach in the base of oesophagus.
The main risk of GORD is towards the lower oesophageal sphincter - causes the loss of muscular tone (atonic) or transient relaxations of the sphincter. May also increase intra-abdominal pressure.
Can also lead to tooth erosion - if acid is able to reach the oral cavity. Acid removes pellicle protection and is able to displace saliva (has a lower surface tension) causing excessive demineralisation.
Usually treated using
proton pump inhibitors
antacids plus alginate
(alginate forms a foam layer on top of the chyme preventing reflux),
(5-HT4 agonist) increase muscular tone of the sphincter and stimulate gastric motility.