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Flashcards in Peptic Ulcers Deck (17):

What is a peptic ulcer?

A chronic, solitary lesion/sores in an area of GI tract exposed to acid/peptic juices.


Symptoms of a peptic ulcer?

Epigastirc burning sensation (relieved by eating is deudenal), heart burn and bloating.


Name 3 complications of peptic ulcers.

Penetration - ulcer burrows into pancreas or liver.
Perforation - ulcer opens into peritoneal cavity.
Upper GI bleeding - ulcer erodes into an artery.


Explain, with regards to secreted substances of the stomach, what happens to encourage peptic ulcers to form.

Mucous cells release mucous and bicarbonate.
Parietal cells produce HCl which converts pepsinogen to pepsin/

When the balance between acid/pepsin and mucosal defence is disturbed - ulcers may form.


Name 6 risk factors for peptic ulcers.

1) Helicobater pylori
3) Zollinger-Ellison syndrome
4) Smoking
5) Stress
6) Acid hypersecretion - NO, except in Zollinger-Ellison Syndrome.


Explain the causes of GASTRIC ulcers.

Normal to low levels of gastric acid.
Defect in gastric mucosal resistance.
75% infected with H pylori - through the entire gastric epithelium = epithelium damage.


Explain the causes of DEUODENAL ulcers.

Hight secretion of acid/pepsin (due to infection in gastric atrium) which causes gastric METAPLASIA in deuodenum which can be infected by H pylori (95%).


Describe Helicobacter pylori.

Spiral shaped bactrium that causes gastritis.
Grows on surface of epithelial cells - under mucosal layer to protect from pH of stomach.
Causes increased secretion of gastrin and pepsin.
Increased incidence with age.
Genetic susceptibility.
Certain strains are especially pathogenice (cag pathogenicity island)
H pylori secretes urease which converts endogenous urea to HCO3 and CO2...protect itself from gastric acid.
Test - drink radioactive labelled urea - and measure labelled CO2 in breath.


Explain Koch's posturate.

How to determine if H pylori is the main cause.

Must be present in all animals suffering but not in healthy ones.
If injected into healthy ones then it would cause them to become unhealthy.


Expain the regulation of acid secretion.

Nerves secrete ACh act on mast cells and M receptors. Gastrin from blood vessels acts on mast cells and G receptors. mast cells release histamine...H2 receptor...HCl secretion, (PGE2 = negative action).
HCL secreted from H+/K+ ATPase pump into the gastric lumen.


Explain proton pump inhibitors.

Omeprazole. Prudrug that inhibits parietal cell H+/K+ATPase pump irreversibly.

At pH7 = inactive.
At Causes a 90% inhibition of acid secretion.

Use if NSAID or Z-E syndrome associated ulcers.


Explain H2 receptor blockers.

Selectively blocks H2 receptors on parietal cells.
Decrease acid secretion by 90%
Good for heart burn.
BUT cimetidine can inhibit cyt p450 - retard metabolism of other drugs.


Explain how sucralfate works.

It enhances mucosal protection.
Binds to negative sulphonated sucrose to Hcl which forms a viscous adhesive which binds to positive groups in ulcer crater.
Buffers acid and stimulates secretion of mucus, pGs and HCO3-.
Decrease number and adherance of pylori.
BUT constipation, and decreased absorption of some drugs.

Good for deuodenal ulcers or stress induced.


Explain how Bismuth Chelate works.

Enhances mucosal protection.
Coats ulcer, absorbs pepsin and stimulates mucus, HCO3- and PG secretion.
Used in combination with other antibacterials.
SE: blackens mouth, vomiting.


Explain how antacids work.

Neutralise gastric acid by inhibiting pepsin.
Symptomatic relief and some healing.

Sodium bicarbonate (can lead to systemic alkalosis).
Magnesium carbonate - diarrhoea.
Aluminium hydroxide - constipation.


Explain how misoprotil works.

Stable PGE1 analogue - good if NSAID induced.
SE: diarrhoea, abdominal cramps.
Avoid in pregancy - can cause uterine contractions.


Explain antimicrobial therapy.

Use to eradicate H. plyori and prevent ulcer relapse.
Combine with an H2 blocker (cimetidine) or with omeprazole - which increases gastric pH, stabalises antibiotic and decreases resistance.