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These are a drug class, containing alkaline chemicals, such as aluminium hydroxide and magnesium carbonate, used to aid in neutralising the excess acidic contents of the stomach. Common brands include Gaviscon and Milk of Magnesia.
Retrosternal pain or precordial pain is simply 'pain behind the sternum', i.e. in the epigastric region.
This is the radiating, burning pain caused by the reflux of gastric acid into the oesophagus via the lower oesophageal sphincter (from now on referred to as the LOS). Its occurrence is more likely after a large meal or drinking session, where the stomach contents can be found closer to the LOS. The pain of severe heartburn can often be mistaken for a heart attack. 
Ranitidine, known commercially as Zantac; and its sister drug cimetidine, are histamine H2-receptor antagonists, otherwise known as antihistamines, and are most commonly used orally.  It prevents the binding of histamine (which is released from mast cells and is the most effective stimulant of parietal cells) that would otherwise incur the release of H+ into the gastric lumen.
A patient swallows a solution of barium sulphate, a contrast medium. Highly insoluble barium sulphate particles are mixed with pectin - a larger molecule to improve motility. It also helps to bind the solution to the mucosa in the GI tract.  This is then visible (opaquely) on X-Ray. Multiple images are captured every second to analyse peristalsis and the passage of the medium. Conditions that can be highlighted via this technique include hiatus hernias (often a cause of GORD), 'Swan neck oesophagus' and various tumours and ulcers.
H.Pylori & Peptic Ulcers
Helicobacter Pylori is a gram negative bacterium listed as the cause of peptic ulcers. It colonises the antrum of the stomach, using its flagellum for motility and to bury down into the gastric mucosa. Approximately Â¾ of the third world's population are "infected" with H.Pylori while only around one in five people infected in 1st world countries. Symptoms however, will only be present in 20 percent of these cases.
It is shielded from the natural gastric acid secretions by the juxtamucosal layer. This layer contains alkaline bicarbonate secretions from antral cells. H.Pylori produces urease, which breaks down urea to carbon dioxide and ammonia. The ammonia increases the surrounding pH essential for the bacterium's survival and is also toxic to gastric epithelial cells, causing degradation of this layer. 
Ammonia is converted to the ammonium ion using H+ from water. The remaining OH- ion combines with carbon dioxide to form bicarbonate, also serving to increase alkalinity around the bacterium.
The urease producing ability of H Pylori is useful in its detection. A patient will swallow a solution of urea, containing an isotope of carbon, either 13C or 14C. The bacterium's urease will break this down and one of the waste products will be carbon dioxide, containing one of said isotopes, that is detectable in the breath approximately 30 minutes later. Thus its presence is indicative of H Pylori colonisation. 
H.Pylori, like the presence of other bacteria, induces an inflammatory response. This manifests itself in stimulating the G-cells in the stomach to produce gastrin. This will increase HCl production. The numbers of parietal cells will increase to cope with this additional demand, further increasing the acidity of the stomach's contents. H.Pylori infection will therefore potentially result in antral gastritis and peptic ulcers. 
Drugs such as aspirin and other NSAIDS (Non-steroidal anti inflammatory drugs) are not recommended for those with heartburn /ulcer like symptoms. They inhibit prostaglandin production which would normally protect the mucosal lining, by stimulating the production of bicarbonate and mucous, as well as increasing blood flow. Thus inhibition increases the risk of peptic ulcers and microbleeds. 
Peptic ulcers can be divided into five different types, depending on their location. They can either be acute or chronic. The main symptom is pain, yet some bleeding can occur, either noticed in expulsion by mouth (haematemesis) or blackened in the stool.
Upper GI tract / Foregut
The foregut is the section of the digestive system whose oxygenated blood is supplied by the branches of the celiac trunk. It runs from the distal third of the oesophagus to the ampulla of Vater in the duodenum. The upper GI tract is a more colloquial term used to describe the oesophagus and stomach.
Image of part of the foregut. 
Other structures of the foregut (not pictured) include: liver, gall bladder, trachea, distal 1/3 of the oesophagus. Note that only the superior region of the pancreas is supplied by the celiac trunk and is therefore included in the foregut.
Anatomy & Microanatomy of the Upper GI tract
The upper GI tract is composed of four different layers: Mucosa, submucosa, muscularis propria and tunica adventitia.
Microanatomy of the GI tract 
The mucosa is mainly lined with stratified squamous epithelium (non-keratinised) in the oesophagus and simple columnar in the stomach - relative to their function. The mucosa is comprised of the muscularis mucosa, lamina propria and the epithelium.
The circular and longitudinal muscles work in tandem to move/squeeze food down the oesophagus (peristalsis). The muscle in the distal 1/3 is smooth muscle under involuntary control, as opposed to the proximal 1/3 which is skeletal muscle, to aid in voluntary swallowing. The pressure the food exerts on the oesophagus stimulates the production of mucous from glands in the submucosa, which is made up of areolar connective tissue.
This submucosal secretion is regulated by the enteric nervous system in the submucosal plexus. The contractions (and thus motility) are regulated in the myenteric plexus.
The adventitia is made up of fibrous connective tissue.
Anatomy of the Stomach 
H.Pylori colonises the pyloric antrum of the stomach, hence its name.
The stomach can be found in three of the abdominal regions: the epigastric, umbilical and the left hypochondrium. The LOS can be found approximately level with spinous level T10, the pyloric sphincter around L1.
From Acid Secretion, Dr David Burleigh 
Parietal cells secrete HCl to acidify the contents of the stomach to between pH 1.5 and 3.5. This is done via an H+/K+ ATPase pump. The activity of this pump is increased by the action of Acetylcholine, gastrin and histamine; and inhibited by prostaglandins. (See diagram below)  Parietal cells also secrete intrinsic factor which is essential for B12 absorption.
Chief cells secrete pepsinogen, the precursor to pepsin. The conversion is made feasible within the low pH of the stomach acid.
G cells are innervated by the vagus nerve and secrete gastrin, a hormone that stimulates the production of HCl by parietal cells.
It is thought that pleuripotent stem cells are present at the bottom of these gastric glands to regenerate the epithelium at the end of their lifespan. (So far this is only proven in mice) see 
The combined effect of peristalsis and gastric juices is to convert food boluses to chyme.
Pathophysiology of GORD & Barrett's Oesophagus
GORD is mainly caused by the failure of the body's own natural anti-reflux mechanisms. The most important is the LOS, a sphincter that opens to allow food to pass from into the stomach, a process otherwise known as 'transient lower oesophageal sphincter relaxation'. The weaker this sphincter, the more relaxed it becomes, and so the more likely stomach contents can enter the oesophagus. 
When the LOS (and sometimes part of the stomach) rises above the diaphragm as in a hiatus hernia, it is no longer assisted by the diaphragm, thus increasing the level of gastric reflux into the oesophagus. There are two types of hiatus hernia, rolling (20%) and sliding (80%). The latter being where the gastro-oesophageal junction ascends superiorly above the diaphragm into the thorax. In a rolling hiatus hernia, the gastro-oesophageal junction stays in the abdomen, but part of the stomach rises to become level with the oesophagus. 
In Barrett's oesophagus, the presence of acid in the oesophagus causes the epithelia to change from stratified squamous to simple columnar (metaplasia). The diagnosis is made by endoscopy and a biopsy. It can be treated using a 'HALO360' ablation technique, whereby the columnar layer of Barrett's epithelium is stripped away, thus reducing the long term risk of cancer. 
Appearance of Barrett's 
What are the signs and symptoms of GORD and how is it diagnosed?
The major symptom is heartburn, especially at night or lying down where reflux is aided by gravity. This can lead to a "bad taste in the mouth" due to the acid reaching the mouth. Consistent reflux may result in oesophagitis and in rare cases progress to cancer. A hiatus hernia will also predispose someone to reflux. Other symptoms include painful swallowing (odynophasia), excessive saliva production and excessive burping.
Treatment often occurs without diagnosis. However, endoscopy can be used to confirm oesophagitis, hiatus hernias and Barrett's oesophagus (a complication of GORD). Barium swallows are also used, as discussed.
The intensity of reflux (as well as diagnosing GORD if endoscopy is normal) can be documented by intraluminal pH monitoring over a 24 hour period. A reflux episode, where symptoms may be experienced, is defined as the pH dropping below 4 with a frequency greater than 4%. 
Treatment & Management of GORD & Drug Mechanisms
The "triple therapy" includes 2 antibiotics to relieve the H.Pylori infection. Usually amoxicillin and clarithromycin are used, yet metronidazole can be used in case of a penicillin allergy). The third drug is a proton pump inhibitor such as omeprazole. If this fails, quadruple therapy can be used; this adds a bismuth salt to the drug inventory.
However around 70% of H.Pylori cases show some antibiotic resistance, so ampicillin-sulbactam is used in the presence of amoxicillin-resistant strains of H.Pylori in quadruple therapy. 
Omeprazole works by inhibiting the H+/K+ ATPase proton pump, thus preventing release of H+ into the stomach by up to 90%. Therefore it is cited as the most effective drug for treating peptic ulcers, as it inhibits acid release regardless of ACh, histamine or gastrin stimulation.
Patients are given antacids and the triple therapy as previously described. Sometimes they take drugs that increase the rate of gastric emptying, known as prokinetics, such as domperidome and metoclopramide, to decrease the risk of reflux.
Smoking is not recommended as it slows down the rate of which the affected mucosa can regenerate.
Weight loss will decrease the effects of heartburn, as central obesity forces the stomach contents superiorly towards the oesophagus.
Not sleeping lying down will reduce the effect of reflux due to gravity, and eating smaller meals will decrease the time taken for gastric emptying.
Avoiding calcium channel blockers is recommended as they have the effect of relaxing the LOS.
Surgery is a last resort, only feasible when the patient does not improve with therapy, is in extreme pain and intraluminal pH monitoring proves high levels of reflux. 
The main procedure is a 'Nissen fundoplication', whereby the fundus of the stomach is wrapped around the gastro-oesophageal junction, reinforcing the action of the LOS and keeping it below the diaphragm. 88% of patients remain symptom free after 10 years, yet the most common complication is a recurrent hiatus hernia.