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