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Peptic Ulcer Disease- MWEBAZA VICTOR pdf
1. M W E B A Z A
VICTOR
MBchB
Ugandan
Peptic ulcer disease
Surgical department
KIU/WC- MUBENDE R.RHosp site
October/2021.
2. Anatomy of the stomach®
The stomach, is an intraperitoneal digestive organ located
between the oesophagus and the duodenum.
It has a ‘J’ shape, and features a lesser and greater
curvature. The anterior and posterior surfaces are smoothly
rounded with a peritoneal covering.
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3. Anatomical Position
The stomach lies within the superior aspect of the
abdomen. It primarily lies in the epigastric and umbilical
regions, however, the exact size, shape and position of the
stomach can vary from person to person and with position
and respiration.
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4. The stomach has four main anatomical divisions; the
cardia, fundus, body and pylorus:
Cardia – surrounds the superior opening of the stomach at
the T11 level.
Fundus – the rounded, often gas filled portion superior to
and left of the cardia.
Body – the large central portion inferior to the fundus.
Pylorus – This area connects the stomach to the
duodenum. It is divided into the pyloric antrum, pyloric
canal and pyloric sphincter. The pyloric sphincter
demarcates the transpyloric plane at the level of L1.
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8. 1.
2.
Sphincters of the Stomach
There are two sphincters of the stomach, located at each
orifice. They control the passage of material entering and
exiting the stomach.
Inferior Oesophageal Sphincter. at the T11 level which
marks the transition point between the oesophagus and
stomach
Pyloric Sphincter. The pyloric sphincter lies between the
pylorus and the first part of the duodenum. It controls of
the exit of chyme (food and gastric acid mixture) from
the stomach.
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9. 1.
2.
Greater and Lesser Omenta
Greater omentum – hangs down from the greater
curvature of the stomach and folds back upon itself
where it attaches to the transverse colon It contains
many lymph nodes and may adhere to inflamed areas ,
therefore playing a key role in gastrointestinal immunity
and minimising the spread of intraperitoneal infections.
Lesser omentum– continuous with peritoneal layers of
the stomach and duodenum, this smaller peritoneal fold
arises at the lesser curvature and ascend to attach to the
liver. The main function of the lesser omentum is to
attach the stomach and duodenum to the liver.
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11. 1.
2.
3.
4.
Neurovascular Supply
The arterial supply to the stomach comes from the celiac
trunk and its branches. Anastomoses form along the lesser
curvature by the right and left gastric arteries and along the
greater curvature by the right and left gastro-omental arteries:
Right gastric – branch of the common hepatic artery,
which arises from the coeliac trunk.
Left gastric – arises directly from the coeliac trunk.
Right gastro-omental – terminal branch of the
gastroduodenal artery, which arises from the common
hepatic artery.
Left gastro-omental – branch of the splenic artery, which
arises from the coeliac trunk.
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12. 1.
2.
The veins of the stomach run parallel to the arteries. The right
and left gastric veins drain into the hepatic portal vein. The
short gastric vein, left and right gastro-omental veins ultimately
drain into the superior mesenteric vein.
Innervation
The stomach receives innervation from the autonomic nervous
system:
Parasympathetic nerve supply arises from the anterior and
posterior vagal trunks, derived from the vagus nerve.
Sympathetic nerve supply arises from the T6-T9 spinal cord
segments and passes to the coeliac plexus via the greater
splanchnic nerve. It also carries some pain transmitting
fibres.
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13. Lymphatics
The gastric lymphatic vessels travel with the arteries along
the greater and lesser curvatures of the stomach. Lymph
fluid drains into the gastric and gastro-omental lymph
nodes found at the curvatures.
Efferent lymphatic vessels from these nodes connect to the
coeliac lymph nodes, located on the posterior abdominal
wall.
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15. Definition
Peptic ulcer disease (PUD) refers to a
destruction of mucosal defect in the portions
of the gastrointestinal tract (gastric or
duodenal) exposed to gastric acid secretion.
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16. 1.
2.
3.
4.
5.
Common sites for peptic ulcers:
The first part of the duodenum.
The lesser curve of the stomach.
In the stoma following gastric surgery.
The oesophagus.
Even in a Meckel’s diverticulum, which contains ectopic gastric
epithelium.
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17. 1.
2.
3.
In general, the ulcer occurs at a junction between different types of
epithelium, the ulcer occurring in the epithelium least resistant to acid
damage.
These can be:
Acute or chronic.
Superficial or deep (sometimes penetrating ulcers).
Acute stress ulcer.
All these ulcers can perforate and bleed.
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18.
Aetiology and predisposing factors
Gastric acid levels are higher in patients having duodenal ulcer.
Patients with gastric ulceration have relatively normal levels of gastric acid
secretion.
Gastrinoma (Zollinger–Ellison syndrome).
All ulcers can be healed in the absence of acid (it is clear that acid is
important).
Genetic factors may be involved.
Social stress has also been implicated.
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19.
It is now widely accepted that infection withH. pylori is the most important
factor in the development of peptic ulceration.
The other factor of major importance at present is ingestion of NSAIDs.
Cigarette smoking predisposes to peptic ulceration and increases the
relapse rate after treatment with gastric antisecretory agents.
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20. Duodenal ulceration
Incidence
There have been marked changes in the last two decades in the incidence of
duodenal ulceration.
First, even before the introduction of H2-receptor antagonists, the incidence
of duodenal ulceration and the frequency of elective surgery for the condition
were falling.
Now patients presenting with a duodenal ulcer at gastroscopy are less
common.
In part, this may relate to the widespread use of gastric antisecretory agents
and eradication therapy for patients with dyspepsia.
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21. Second, the peak incidence is now in a much older age group than
previously and, although it is still more common in men, the difference is
less marked.
It is now observed more frequently in some developing nations.
The relationship withH. pylori appears convincing.
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22. Pathology
Most duodenal ulcers occur in the first part of the duodenum.
A chronic ulcer penetrates the mucosa and into the muscle coat, leading to
fibrosis.
The fibrosis causes deformities such as pyloric stenosis.
Sometimes there may be more than one duodenal ulcer.
The situation in which there is both a posterior and an anterior duodenal
ulcer is referred to as ‘kissing ulcers’.
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23. Anteriorly placed ulcers tend to perforate, posterior duodenal ulcers tend to
bleed (by eroding a large vessel such as the gastroduodenal artery).
Occasionally, the ulceration may be so extensive that the entire duodenal cap
is ulcerated and devoid of mucosa.
Malignancy in this region is uncommon .
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24. Gastric ulceration
Incidence
H. pylori and NSAIDs are the most important aetiological factors.
It is also associated with smoking.
It is less common than duodenal ulceration.
The incidence is equal between both sexes.
The population with gastric ulcers tends to be older.
They are more prevalent in low socioeconomic groups and considerably
more common in the developing world than in the west.
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25. Pathology
Gastric ulcers tend to be larger than duodenal ones.
Fibrosis, when it occurs, may result in hourglass contraction of the stomach.
Large chronic ulcers may erode posteriorly into the pancreas and, on other occasions,
into major vessels such as the splenic artery.
Less commonly, they may erode into other organs such as the transverse colon.
Chronic gastric ulcers are much more common on the lesser curve (especially at the
incisura angularis).
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26. Hour glass contracture: It occurs exclusively in
women,
is due to cicatricial contracture of lesser curve ulcer.
Here stomach is divided into two compartments.
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27.
Malignancy in gastric ulcers
Chronic duodenal ulcers are not associated with malignancy but, in contrast,
gastric ulcers are.
Two clinical extremes must be distinguished.
First, a benign chronic gastric ulcer undergoes malignant transformation.
Second, biopsies reveal malignancy since the beginning.
It is fundamental that any gastric ulcer should be regarded as being
malignant, no matter how classically it resembles a benign gastric ulcer.
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28. Multiple biopsies should always be taken, perhaps as many as 10 well-
targeted biopsies, before an ulcer can be tentatively accepted as being
benign.
Even then it is important that further biopsies are taken while the ulcer is
healing and when healed.
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29.
Other peptic ulcers
Pre-pyloric gastric ulcer.
Pyloric channel ulcers are similar to duodenal ulcers.
Both pre-pyloric and pyloric ulcers may be malignant, and biopsy is essential.
Stomal ulcers occur after a gastroenterostomy or a gastrectomy of the
Billroth II type.
The ulcer is usually found on the jejunal side of the stoma.
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30. Clinical features of peptic ulcers
Pain
Described as gnawing or burning, and may radiate to the back. Eating may sometimes
relieve the discomfort. The pain is normally intermittent rather than intractable.
Periodicity
Symptoms may disappear for weeks or months to return again.
Vomiting
It is not a notable feature unless stenosis has occurred.
Alteration in weight
Weight loss.
Bleeding
All peptic ulcers may bleed. The bleeding may be acute or chronic.
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33. Clinical examination
Examination of the patient may reveal
epigastric tenderness but, except in
extreme cases (for instance gastric
outlet obstruc- tion), there is unlikely to
be much else to find.
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34. 1.
2.
3.
4.
5.
Investigation of the patient with
suspected peptic ulcer
Gastroscopy is done to see the type, location of ulcer,
narrowing if any.
Biopsy also can be taken to look for the presence
of Helicobacter pylori. Usually biopsies are taken from
duodenum, pylorus, antrum, body, fundus.
H. Pylori test
Barium meal X-ray to see niche and notch
US abdomen mainly to rule out other diseases and to
confirm associated diseases.
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35. Barium meal study showing
niche and notch—gastric
ulcer
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44. Complications of Gastric
Ulcer
•
•
•
•
Perforation—most frequent.
Bleeding by erosion into the left gastric and
rarely splenic vessels or to vessels in the wall of
ulcer.
Penetration posteriorly into pancreas, anteriorly
into liver.
Malignant transformation usually into adenocar-
cinoma of stomach (2-5%).
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45. Complications of Duodenal
Ulcer
•
•
•
•
•
Pyloric stenosis: Due to scarring and cicatrisation of
first
part of the duodenum.
Bleeding (10%).
Perforation (5%). Both acute and chronic ulcers can
perforate. Anterior ulcers perforate.
Residual abscess.
Penetration to pancreas.
Note:
• Chronic duodenal ulcer will not turn into malignancy.
• Ulcer which is more than 2 cm is called asgiant
duodenal ulcer.
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46. Treatment of peptic ulceration
The vast majority of uncomplicated peptic ulcers are treated medically.
Surgical treatment of uncomplicated peptic ulceration is now seldom
performed.
Medical treatment aim to reduce gastric acid secretion, using H2-receptor
antagonists or, proton pump inhibitors as well as eradication of H. pylori
infection using antibiotics.
This has now largely given way to eradication therapy.
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47. Medical treatment
Modifications to the patient’s lifestyle.
Eradication therapy
If a patient has a peptic ulcer, H. pylori is the principal
aetiological factor, complete eradication of the organism will cure
the disease and reinfection in adult is uncommon.
Eradication therapy is therefore the mainstay of treatment for
peptic ulceration.
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48. Tripple therapy
-
-Initial treatment typically requires a triple therapy with 2
antibacterial
agents and an acid inhibitor, typically a proton-pump inhibitor (PPI).
-Drug regimens most often include 2 weeks of antibacterial therapy
concomitant with 4 weeks of acid suppression.
-In adults, standard Maastricht triple therapy is a combination of a
PPI,
amoxicillin, and clarithromycin.
In the event eradication fails, a quadruple therapy with PPI,
bismuth,
metronidazole, and tetracycline has been suggested.
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50.
Surgical treatment of peptic ulceration
With the success of medical therapy, surgery has a very limited role in the
management of PUD.
Additional surgical options for refractory or complicated PUD include
vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal
reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly
selective vagotomy.
Currently surgical treatment is reserved only for complications.
Bleeding
Gastric outlet obstruction
Perforation
Malignancy
Intractability
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51. Billroth I gastrectomy. The lower half of the stomach is
removed and the cut stomach anastomosed to the first part
of the duodenum.
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52. Billroth II. Two-thirds of the stomach
removed, the duodenal stump is closed
and the stomach anastomosed to the
jejunum.
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53. Gastroenterostomy. The jejunum is
anastomosed to the posterior, dependent, wall
of the stomach.
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54. Truncal vagotomy. (a) Division of the anterior vagus. (b) Mobilisation of
the oesophagus. (c) Division of the posterior vagus.
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56. Highly selective vagotomy
The anterior and posterior vagus nerves are
preserved but all branches to the fundus
and body of the stomach are divided.
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57. Plain X-ray abdomen in erect position with ground-
glass
appearance and gas under diaphragm—perforation
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59. Duodenal ulcer perforation closed horizontally using
interrupted silk/vicryl sutures with omental patch over it.
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60. Sites of gastric ulcer and duodenal ulcer
bleeding.
Note GU can erode into the left gastric artery.
DU can erode into the gastroduodenal artery.
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64. Truncal vagotomy and gastrojejunostomy. It is
posterior,
vertical, short loop, retrocolic, isoperistaltic GJ of
Mayo.
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65. References
1.
2.
3.
4.
Bailey and Love’s Short Practice of Surgery 26th
Ed
Oxford Textbook of Surgery
SRB’S Manual for surgery, 4th Ed
Teachmeanatomy (TMAnatomy).
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