Oesophagus and Stomach PHIL THIRKELL + ASFAND BAIG.
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Transcript of Oesophagus and Stomach PHIL THIRKELL + ASFAND BAIG.
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Oesophagus and StomachPHIL THIRKELL + ASFAND BAIG
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Anatomy Blood supply to the oesophagus and stomach?
◦ Coeliac artery – a branch off the abdominal aorta
Which embryonic structure does the oesophagus derive from?◦ Foregut◦ Endoderm
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Histology
Upper 1/3 oesophagus•Striated muscle
Middle 1/3 oesophagus•Striated muscle and Smooth muscle
Lower 1/3 oesophagus•Smooth muscle
Cell Type•Non- Keratinised Stratified Squamous Epithelium
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Smooth MuscleNarrow, rod shaped cellsNo striationsOne nucleus per cell
Striated MuscleTubular cellsStriationsMultiple nuclei
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Gastro-oesophageal Junction How can you tell where the junction is?
◦ Change from non-keratinised stratified squamous to simple columnar
What forms the lower oesophageal sphincter?◦ Compression from the diaphragm (right crus)◦ Angle of entry into the stomach◦ Intra-abdominal pressure◦ Mucosal folds (but I don’t know how these help form the junction)
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Pathology Gastro-Oesophageal Reflux Disease
◦ Failure of lower sphincter causes reflux of acid◦ Oedema/white cell infiltration◦ Increases risk of cancer
Barrett’s Oesophagus◦ Metaplasia from stratified squamous to simple columnar◦ Goblet cells
◦ Produce mucus to protect against acid environment
◦ Considered a pre-malignant condition◦ Association with adenocarcinoma
Oesophageal Cancer◦ Late presentation◦ Can cause obstruction◦ Poor prognosis◦ Risk Factors:
◦ Age, male, FH, smoking, alcohol, reflux, Barrett’s, hot drinks
Oesophageal Varices◦ Dilated veins of portal system◦ Form due to portal hypertension◦ Risk of bleeding◦ Difficult to treat
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Stomach Functions of the stomach?
◦ Storing food◦ Killing bacteria◦ Regulate food entry into duodenum◦ Dissolve and partially digest macromolecules into food◦ To secrete intrinsic factor
◦ the only indispensable role of the stomach
What are the folds in the stomach?◦ Rugae – same name for the folds in the bladder, which do the same – allow increase in size without
increasing the pressure within
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Stomach Anatomy
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Stomach Secretions Contents of stomach secretions?
◦ Hydrochloric acid◦ Enzymes – pepsinogen, gastric lipase◦ Mucus◦ Bicarbonate◦ Water◦ Intrinsic Factor
Chief cell◦ Pepsinogen
Parietal cell◦ HCl
G-cell◦ Gastrin
Mucus cell◦ Mucus
D-cell◦ Somatostatin
ECL-cell◦ Histamine
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Parietal Cell
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Stimulation of Acid Secretion
Stimulates acid secretion Inhibits acid secretion
Histamine Somatostatin
Gastrin Prostaglandins
Acetylcholine Enteric hormones - VIP
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Dysphagia difficulty swallowing
Disease of mouth/tonsils
Inflammation or cancer
Stricture
Pharyngeal pouch
Hiatus hernia
Achalasia – problem with peristalsis co-ordination. (sorry to those I told wrong, I was getting confused with oesophageal atresia)
Goitre
Infections (oesophagitis)
Aortic aneurysm
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Peptic Ulcer Causes:
◦ Helicobacter pylori◦ NSAIDs◦ Crohn’s disease◦ Cancer◦ Zollinger-Ellison syndrome
◦ A non-beta islet cell, gastrin-producing tumour of the pancreas. Loads of gastrin causes huge acid secretion all the time, making patients really prone to ulcers
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Peptic Ulcer Epigastric pain – what happens on eating?
◦ A gastric ulcer gets worse on eating. Food enters stomach, acid is released and it comes into contact with the ulcer, aggravating it and causing pain.
◦ A duodenal ulcer is made better on eating as the pyloric sphincter closes and bicarbonate is released from the pancreas. The pain then starts again after 2-3 hours when the contents of the stomach is released and the acid comes into contact with the ulcer.
Nausea
Bloating/flatulence
Epigastric tenderness
Anaemia – chronic bleeding from the ulcer
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Why do NSAIDs cause ulcers?
Normally, prostaglandins are released when gastric mucosa is damaged, causing increased production of mucus and bicarbonate.
Cyclo-oxygenase enzyme 1 (COX-1) creates prostaglandins.
NSAIDs inhibit COX-1, reducing prostaglandin production. This decreases the mucus and bicarbonate secretion
This increases the damage by acid on gastric mucosa ulcers
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Stomach Pharmacology
Antacids
Alginates
Bismuth chelates
Prostaglandin analogues
H2 antagonist
Proton pump inhibitors
H. pylori eradication therapy
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Antacids React chemically to neutralise stomach acid (acid + base salt + water + carbon dioxide)
Magnesium hydroxide
Calcium Carbonate
e.g. Rennie
S/E - gas
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Alginates Polysaccharide which reacts with stomach contents to make a raft which floats on the surface to prevent reflux and protects mucosa
E.g. Sodium alginate
Gaviscon is combined antacid and alginate
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Bismuth Chelates
Binds pepsin to prevent acid secretion
Coats the mucosa
Increases prostaglandin production
S/E – can cause black tongue and black faeces
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Prostaglandin Analogues Misoprostol
Inhibits acid secretion
Increases mucosal blood flow to generate HCO3
S/E: diarrhoea and stomach cramps
Can’t be used in pregnancy – causes uterine contractions and can cause a termination◦ women of child-bearing age should be using contraceptives if prescribed misoprostol as gastric acid
treatment
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H2-receptor antagonists (anti-histamines)
Blocks the histamine receptor on the parietal cell to reduce acid secretion
e.g. Cimetidine, ranitidine, nizatidine
(not loratidine – only blocks H1, so used in allergies)
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Proton Pump Inhibitors◦ e.g. omeprazole, lansoprazole, pantoprazole
Block the H+/K+-ATPase pump of the gastric parietal cell
Used in patients with reflux, GORD, NSAID ulcers and as 2° prevention in pts who’ve had ulcers
Used to control Zollinger-Ellison until something else can be done about it
Acts systemically, in that it is absorbed into the blood stream, circulates and then acts on the parietal cells – instead of just acting directly on them in the stomach lumen
In acidic conditions the drug can bind to the ATPase, but in neutral conditions it cant.
S/E - ↑risk of infection due to ↓ acid secretion to kill bacteria, decreased vitamin B12 absorption due to less acid, decreased calcium absorption.
Nausea + vomiting
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H. Pylori eradication 1 week of:
◦ 1 proton pump inhibitor – omeprazole, lansoprazole
◦ 2 antibiotics – amoxicillin and either: clarithromycin or metronidazole
Can’t use serology to check if the eradication therapy has worked because the antibodies will still be there even if all the bacteria are now dead