Download chronic peptic ulcer pm 1946-00248

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Although noted, it is important to stress that this ulcer was an extremely large one;
now one would rarely encounter an ulcer bigger than approx. 2cm in diameter. Many
of the macroscopic features are in fact complications that arose from the ulceration.
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Often what a chronic ulcer situation becomes is a race between the supply of blood
for sufficient healing of the eroded tissue versus the erosion of the tissue and the
blood vessels themselves. What ends up happening is that the end arteries become
inflamed and close off, cutting off the blood supply to the ulcerated area, inhibiting
healing and allowing deeper and deeper erosion of the tissue; or as in this case, the
blood vessels become eroded and can no longer control the amount of blood
entering the bowel, causing haemorrhage and anaemia in the case of our patient.
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The microscopy for this case was unfortunately unavailable but some images were
obtained from a similar case for a general indication: slightly inflamed foveolar cells,
colonization of H. pylori bacteria, and areas of necrosis and granulation tissue at the
edge of the ulceration (the tissue about to be digested and the tissue trying to
undergo repair) and haemorrhage.
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The most common cause of chronic gastric ulcers is a Helicobacter pylori infection
(responsible for up to 80%). Its pathogenesis is well-summarized into 3 phases in the slide but
can be elaborated on.
Phase 1 : Active Phase
One of the main and most important characteristics of Helicobacter pylori is that it’s
urease positive. It is in this way that the motile bacteria – protected in the mucus
lining of the stomach – increase the gastric pH by producing ammonia via urease
action, increasing the wear on the stomach wall.
Phase 2: Stationary Phase
The bacteria attach themselves to fructose-containing receptors on mucous surface
cells of pyloric region of the stomach. This provides them with stability within the
mucus layer during peristaltic and churning motions of the stomach.
The attachment of the bacteria results in production of cytotoxic proteases via
neutrophil polymorph reactions incurring further break down of the protein in the
stomach wall.
Phase 3: Colonization Phase
Involves bacterial detachment from receptors, increase in number by replication
within the protective mucosal blanket and remain in the stomach via attachment to
glycoproteins on the surface epithelium, production of urease and consequent
burying into protective mucus barrier and high motility (flagella allow for easier,
more efficient burrowing).
The histologically significant signs of this particular aetiology can be found throughout the
entire stomach but to a varying degree – the area with the highest level of involvement being
the antrum of the stomach. Gradual glandular atrophy, replacement of the epithelium and
wall with fibrosis and intestinal metaplasia (i.e. transformation of stomach epithelium to
something resembling intestinal epithelium) are some features that can be expected in areas
of involvement.
A complication of gastric ulcers by any aetiology is gastric cancer, though ulceration as a
result of a cancer is the more likely pathogenesis.
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Chemical injury was thought to be the only aetiology for many years before the
discovery of helicobacter (its first culture experiments in 1982). Fairly simple
pathogenesis: direct damage to the mucosal lining of the stomach via the increased
level of HCl, disruption of the protective mucus layers (breakdown making the
stomach unable to protect itself from secreted HCl) and the degranulation of mast
cells in an immune response mechanism, the release of their contents often causing
as much damage as the initial stimulus.
Upon histological investigation, one would find increase amounts of foveolar (surface
epithelial) cells, vasodilation as a result of the mast cells and other stimuli, oedema as
a result of vasodilation, scanty accumulation of inflammatory cells.
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There are quite a number of ways to diagnose a ulceration or H. pylori infection.
Blood test
This sample of venous blood would be tested for the presence of H. pylori
antibodies created by the immune system in an effort to fight the bacteria
(although this response is noted, it does little for the containment of the
infection but does help with opsonisation).
Urea Breath Test
This involves the swallowing of a capsule or liquid containing urea “labeled”
with a modified carbon atom. After a few minutes, patient breathes into a
container. If H. pylori present, the carbon atom will be found in the breath as
the urease produced by the H. pylori breaks down urea into CO2 and NH3
during its metabolic processes.
Endoscopy
Endoscope (a tube fitted with a camera) is passed through the mouth to the
stomach and duodenum. Inspection of the lining of the upper GIT can occur as
well as the sampling of tiny sections of tissue as in biopsies (useful in gastric
ulcers to check for malignancy).
Barium Contrast X-ray
This happens when a contrast or dye is swallowed preceding the x-ray
imaging. This is done to help determine the severity and size of an ulcer which
is not always very clear with an endoscopy because it is either too far down in
the duodenum or hidden by a fold.
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This is a strategic arrangement of the possible complications to gastric ulcers – they
are arranged in order of most frequent to least frequent; their heights, however, do
not correspond to a specific number or exact proportional difference.
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The nature of H. pylori as an infectious organism is covered in this slide: its
characteristics and their importance; relating structure to function.
It is a gram negative bacteria, spiral Rod-shaped with unipolar multiple flagella. Its
flagella give it motility and allow it to provide protection for itself in viscous mucus
lining of the stomach. It swims to an area within the layer that has an almost neutral
pH and in this way increases its chances of survival and colonization. H. pylori is
urease positive which means that the bacteria have the ability to synthesize urea into
CO2 and NH3 thereby elevating gastric pH. The bacteria are microaerophilic which
means they require oxygen to survive. They have adhesins that enhance the ability of
the bacteria to adhere to foveolar cells.
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