Gastric ulcers also develop when protective forces break down. Alterations in mucosal blood flow are a common risk factor
for the development of gastric ulcers, and can result from many different processes. Administration of non-steroidal anti-inflammatory
drugs (NSAIDs) and glucocorticoids decrease local prostaglandin production thereby reducing mucosal blood flow, limiting the
epithelium's capacity to protect itself from the injurious effects of acid. Recent investigations in other species on the
effects of NSAIDs have suggested that this class of drugs can also impair ulcer healing through inhibition of angiogenesis
(necessary for granulation tissue formation in the ulcer bed) and epithelial proliferation. Hypovolemia, shock, vascular thrombosis,
or other processes that interrupt gastric blood flow (e.g. gastric dilatation/volvulus) also can cause mucosal ulceration.
Other diseases associated with ulcers can disrupt normal mucosal architecture, and likely also alter blood flow; examples
include gastric neoplasms and inflammatory stomach diseases. For some of the diseases that are associated with ulcers, for
example liver disease and hypoadrenocorticism in dogs, the mechanisms contributing to ulcer formation are not well-characterized,
but are still likely to involve aberrations in mucosal protective functions.
Clinical signs and physical examination
The most common clinical sign of gastric ulcers in dogs and cats is vomiting, which may or may not have blood in it. Blood
in the vomitus can appear fresh, or digested to create the classic "coffee grounds" appearance. It must be pointed out that
the appearance of fresh or digested blood in vomitus does not definitively indicate that an ulcer is the source of blood as
blood emanating from the nasopharynx or esophagus could be swallowed and vomited. Clients may report seeing melena if there
has been large-scale bleeding, but not seeing melena doesn't exclude the possibility of gastrointestinal bleeding. Other clinical
signs associated with gastric ulcers include anorexia, weight loss, increased salivation, and abdominal pain. Abdominal pain
in some animals could be a reflection of peritonitis from a perforation, or near perforation. Clinical signs attributed to
underlying disease (e.g. polyuria/polydipsia with renal failure or hepatic disease) may be present in addition to those that
are more directly referable to the presence of the ulcer. It is also important to understand that there may be no overt clinical
signs directly suggestive of gastric ulcers, likely making the incidence of gastric ulceration in dogs and cats underestimated.
Mucous membrane pallor may be seen if bleeding is severe, and the presence of masses in animals with other features suggestive
of ulcers should prompt at least needle cytology to exclude a mast cell tumor as the primary cause of an ulcer.
There are no pathognomonic clinical pathology abnormalities seen in patients with gastric ulcers, but several that can be
highly suggestive in a patient with other supportive historical and physical examination findings. Anemia, which can be regenerative
or non-regenerative, will be seen in some animals. Some patients may have microcytosis and hypochromasia (neither evident
without indices or examination of a blood smear), with or without anemia, suggestive of iron deficiency if there has been
chronic gastric bleeding. Inflammatory leukograms are possible reflecting the inflammation that often accompanies ulcers.
Platelet numbers are usually normal, but can vary depending on the underlying cause of ulcers; chronic ulcers may be associated
Serum biochemistry abnormalities will be variable and sometimes reflect the underlying cause and severity of the gastric ulcer.
Increases in liver enzyme activity and abnormalities in the indirect indicators of hepatic function (decreases in one or more
of albumin, cholesterol, BUN and glucose) may be seen in patients with ulcers attributed to liver disease; cholestatic liver
diseases may be accompanied by hypercholesterolemia. Albumin and globulin concentrations may be decreased as a consequence
of intraluminal bleeding, and in some patients, an increase in BUN without an increase in creatinine may be seen with large-scale
gastric hemorrhage. Results of a urinalysis don't overtly suggest the presence of an ulcer, but could be important to rule
out urinary tract causes of, or contributions to, anemia or hypoalbuminemia; results of a urinalysis could also suggest the
presence of liver disease (e.g. low urine specific gravity and biurate crystals). Patients with suspected, or confirmed,
gastric ulcers without any other identified risk factor may be candidates for measurement of fasting serum gastrin concentrations
to rule out gastrinomas.
Patients with gastric ulcers can have chronic, low-grade blood loss that is not overtly apparent. For patients that do not
have overt signs of gastrointestinal bleeding, but for which bleeding is suspected as a cause of anemia or microcytosis, a
fecal occult blood test can help confirm the intestinal tract as a site of blood loss. Substantial amounts of blood in the
proximal intestinal tract are needed to produce melena, so normal stools do not at all exclude gastrointestinal hemorrhage
in the suspect patient as noted previously above.
The initial suspicion of gastric ulcers is usually aroused by the presence of compatible clinical signs and laboratory abnormalities,
particularly in a patient that has an identifiable risk factor in the history (e.g. NSAID or glucocorticoid administration)
or laboratory data base (liver disease or renal failure). However, few patients actually have a definitive diagnosis established,
but are instead empirically treated.