oesophagus and stomach phil thirkell + asfand baig
TRANSCRIPT
Oesophagus and StomachPHIL THIRKELL + ASFAND BAIG
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
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
Smooth MuscleNarrow, rod shaped cellsNo striationsOne nucleus per cell
Striated MuscleTubular cellsStriationsMultiple nuclei
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)
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
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
Stomach Anatomy
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
Parietal Cell
Stimulation of Acid Secretion
Stimulates acid secretion Inhibits acid secretion
Histamine Somatostatin
Gastrin Prostaglandins
Acetylcholine Enteric hormones - VIP
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
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
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
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
Stomach Pharmacology
Antacids
Alginates
Bismuth chelates
Prostaglandin analogues
H2 antagonist
Proton pump inhibitors
H. pylori eradication therapy
Antacids React chemically to neutralise stomach acid (acid + base salt + water + carbon dioxide)
Magnesium hydroxide
Calcium Carbonate
e.g. Rennie
S/E - gas
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
Bismuth Chelates
Binds pepsin to prevent acid secretion
Coats the mucosa
Increases prostaglandin production
S/E – can cause black tongue and black faeces
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
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)
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
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