Vol. 60, 1909 - University of North Carolina at Chapel Hill

The chief causative factors of gastric
ulcer, so far as our present knowledge, are
localized loss of nutrition, mechanical irritation
and chemical destruction.
Pathology.—The macroscopic appearance
of the serous membrane or external surface
of a non-perforating ulcer is that of a lump
or nodule in the wall of the stomach, usually,
almost invariably, in the course of a
bloodvessel. From the interior, it presents
a funnel shape, "the edges clean cut, the
base smooth, or it may show little islands
sometimes covered with coagulated blood,
or tough, dark mucus." The size of the
ulcer varies from that of a pea to several
centimeters. The most usual seat is at or
near the pylorus, though it may be in any
part of the stomach wall.
The microscopic appearance of a fresh
ulcer: "The glandular tubules present a
trough shape as if cut off. In old ulcers a
reactive inflammation sets in at the periphery
and leads to the formation of a calloused
margin;" the fibrous framework is
thickened, the glandular epithelium has
undergone a change, and the lab cells have
been replaced by cubical or cylindrical
cells. Their nuclei are not recognizable by
ordinary staining; their protoplasm has
undergone a hyaline degeneration, "the
sub-mucous is permeated by a profuse,
small-cell infiltration and a strong, vascular
network." "The layers of the muscularis
are separated l)y fibrillary, intermedi-
ate tissue. '
"
The entire process is surround-
ed by a zone of irritation. There is always
a tendency for the floor of the ulcer to adhere
to the tissue Iieneath it. Cicatrization
begins and the fibrous network is soon covered
by the mucous membrane, though it
may continue to contact beneath the membrane,
thus causing a constant source of
irritation and distorted shape to the walls
of the stomach, especially when adhesions
to neighboring viscera have taken place.
Necrosis continuesuntil cicatriza tion takes
place and so long as peptic gastric juice
comes in contact wilh the ulcer. There is
a tendency to thrombosis caused by the
corrosive effect of the gastric juice, but this
thrombus is destroyed as soon as sufficient
juice comes in contact with it, thus producing
hemorrhage. If the necrosis extends
to the serosa, an adhesion to neighboring
organs is formed witli peri-gastritis: or if in
the dependent part of the stomach, perforation
into the cavity occurs and is followed
by general j)eritonitis, frecjuently by death.
Sometimes there is perforation which is
stopped by adhesions to the omentum, and
sometimes a circumscribed abscess forms.
Symptoms.—The symptoms of a tyjiical
gastric ulcer are pain, tenderness, vomiting,
ORIGINAL COMMUNICATIONS. 15
hemorrhage, constipation and increased
hydrochloric acid. As the development of
the ulcer is gradual, so will the symptoms
be insidious. In most, if not all cases of
peptic ulcer, we have a well developed pain
or great discomfort after eating. The time
of the appearance of the pain depends upon
the seat of the ulcer, and the severity depends
very largely upon the quantity and
the quality of the food. The pain is due
to mechanical, chemical and thermic irritation.
Coarse foods and foods not well masticated
produce more pain than liquids.
The food causes a secretion of hydrochloric
acid, and larger particles take up less acid
than finely divided particles: hence, we
have more pain from this source. The ulcer
produces more or less irritation to the ner\-es
of the stomach which causes an increased
amount of acid to be secreted. The excess
of hydrochloric acid and the irritation of the
ulcer causes a firm contraction of the pylorus
and prolonged retention of food;
hence, fermentation of starches and fats
which distends the walls of the stomach,
thus increasing the tension of the ulcer,
with exaggerated pain, often reversed peris-
talsis and vomiting. The pain is also increased
by swallowing food that is very hot
or very cold. I'sually, the pain ceases as
soon as the stomach is empty either from
vomiting or food passing into the intestines.
If the ulcer is in the fundus of the stomach,
the pain will come on immediately
after eating; if near the pylorus, a little
later; if in the duodenum, still later. Vomiting
seldom occurs when the stomach is
empty, generally after meals—and is usually
caused by a spasm of the pylorus and
reversed peristalsis. The siiasm is produced
by the irritating effect of the hydrochloric
acid add the food particles coming in contact
with the raw surface of the ulcer. The
vomited material consists of undigested
liarticlesof food (usually starches and fats,
as the proteids have been digested by the
abundant gastric juice), mucus and, sometimes,
streaks of blood, occult blood and
free hydrochloric acid. There is more or
less tenderness in the epigastric region.
Hoaz lavs considerable stress uii the pressure
points in the median line half way between
the umbilicus and the ensiform cartilage
and the dorsal points over the 10th and
12th dorsal vertebrae. There is an excess
of hydrochloric acid in most cases of ulcer,
esi>ecially if there is much irritation caused
by the nicer. This is a nervous or irritation
hyperchlorhydria. Constipation usually accompanies
excessive hydrochloric acid.
Many cases of ulcer run their course without
distinct hemorrhage. It is said that
hemorrhage occurs in from about .% to 40
per cent. Hemorrhage may be independent