Gastric ulcers are also called peptic (pepsin) ulcers.
Prostaglandins are important for mucus production in the stomach. The mucus protects gastric cells from gastric juices. Non-steroidal (and steroidal) agents prevent prostaglandin production and subsequently prevent mucus production. The cells exposed to the gastric juices can be damaged => gastric ulceration. Neoplasia, chronic inflammation and chronic hyperacidity (gastrinoma, mastocytosis, head trauma) can also cause ulcers. Both young and old animals are at greater risk.
For how prostaglandins affect the mucous layer more directly, check this video at the 5 minute mark.
The esophagus and nonglandular portion of the stomach (camelids, horses) can also be damaged by stomach acids with vomiting and perhaps with certain forms of exercise (equine).
Deep ulcers can perforate, leading to peritonitis.
The gastric lining can repair itself, so not all damage leads to ulcers or problems.
One of the earliest signs of gastric ulceration is low serum protein. Abdominal pain and anorexia are often associated. Animals are often lethargic (low energy) and have vomiting and/or diarrhea.
Later signs include weight loss and anemia.
In non-ruminants, ulcers can be visualized endoscopically.
Fecal occult blood tests can be useful in herbivores; carnivores and omnivores eat too much meat for the test to be useful.
Ulcers are treated by:
(1) stopping NSAID use
(2) protecting the ulcers with sucralfate – this drug creates a sticky gel when exposed to acidic environments; quick relief that lasts about 6 hours
(3) neutralizing acid by binding HCl with antacids – quick relief but may cause rebound effects
(4) blocking HCl production
(a) antihistamines – block the histamine receptor that signals HCl production. Ex – famotidine; takes 1-2 days to work in humans; these are weaker than the proton pump inhibitors as the other mediators can still stimulate some pump function
(b) proton pump inhibitors – directly blocks the HCl pump. Ex- omeprazole; takes 2-3 days to work in humans
(4) misoprostol is a synthetic prostaglandin used to prevent or repair damage
In a recent study, misoprostol was more effective than omeprazole in treating equine glandular ulcers. These seem to be different then the more common squamous ulcers that do respond well to omeprazole. As the glandular stomach should have less acid exposure, other mechanisms may be more in play than damage due to acid. Glandular ulcers may be increasing in prevalence.
Drug treatment is harder in ruminants as many drugs do not make it through the rumen or are too expensive for cattle.
- The gastric mucus layer can be thinned by NSAIDs, leading to gastric ulcers.
- Gastric ulcers can be treated by antacids (bind acid), sucralfate (coat the ulcer), antihistamines (decrease pump stimulation) or proton pump inhibitors (block acid production).
How nsaids create ulcers – simple but useful depiction; same as above
Understanding gastric acid production– very useful; includes therapy
Ulcers pathophysiology and treatment – set to classical music
Horse stomach acid – nice short overview (different gastric structure than dogs)
Gastric cells and secretions – shorter but scientific version
Alpha -1 proteinase inhibitor– explanation of this test
Gastric acid physiology– more anatomy, physio with neurotransmitters, hormones and feedback loops
Aspirin and prostaglandins – more about how the drugs work
Abomasal ulcers in cattle– DVM 360, 2008
Abomasal ulcers in calves – Dairyherd, 2018
Gastrointestinal protectants in dogs and cats – ACVIM white paper (consensus statement), JVIM, 2018
Consensus statement on Equine gastric ulcer syndrome – European discussion, JVIM, 2015
New thoughts on gastric ulcers in horses – KER, 2016
Sucralfate actions- more than I ever knew
Drugs for peptic ulcers– slideshow about humans; includes drug side effects and drugs we don’t currently use
Helicobacter and SA gastric ulcers, JVIM, 2000