Dr Ghassan Ali AlKizwini Consultant GIT Surgeon Stomach amp Duodenum LEARNING OBJECTIVES the student should be able to Describe gross and microscopic anatomy and pathophysiology ID: 916733
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Stomach & Duodenum
Assistant Professor Dr. Ghassan Ali Al-KizwiniConsultant GIT Surgeon
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LEARNING OBJECTIVES: the student should be able to• Describe gross and microscopic anatomy
and pathophysiology of the stomach in relation to disease.• Decide on the most appropriate investigation
of patients with
complaints relating to the stomach and duodenum.
• Recognize the critical importance of
gastritis
and
Helicobacter pylori
in upper gastrointestinal disease.
• Investigate and treat
peptic ulcer
disease and its complications.
• Recognize the presentation of
gastric cancer
and understand the principles involved in its treatment.
• Know causes of
duodenal obstruction
and the presentation of
duodenal tumours
.
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Functions of the stomach: Act as reservoir for the ingested food.Breaks down foodstuffs mechanically and starts the process of digestion, before passing it to the duodenum
Anatomy of the stomach & duodenum: Blood supply: Arteries:
Rt. gastric artery
Lt. gastric artery
Gastroduodenal artery
Rt. gastroepiploic artery
Lt gastroepiploic artery
Vasa
brevia
(short gastric arteries)
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Anatomy of the stomach & duodenum: Blood supply: Veins:Equivalent to the arteries.
Those on the lesser curve mainly drain into the portal vein.Those on the greater curve mainly drain into the splenic vein
Lymphatics:
Are important in surgery of gastric cancer to assess tumour spread.
Nerve supply:
Intrinsic nerves
: Myenteric plexus of Auerbach
Submucosal plexus of Meissner
Extrinsic nerve supply:
Parasympathetic: Vagus nerve (CN X)
Sympathetic: derived from the coeliac ganglia
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Micro-anatomy of the stomach & duodenum:Epithelial mucus secreting cells
Specialized cells Parietal cells Chief cells
Endocrine cells
G-cells
Enterochromaffin-like (ECL) cells
D-cells
(Somatostatin)
Duodenal endocrine cells
The neurons
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Gastric acid secretion Hydrogen ions are produced by the parietal cell by the proton pump (Hydrogen-Potassium ATPase
).The role of Histamine, Vagus Nerve & Gastrin
H
2
-receptor antagonists
Proton Pump Inhibitors (PPI
s
)
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Summary-The anatomy and physiology of the stomach● The stomach acts as a reservoir
for food and commences the process of digestion● Gastric acid
is produced by a
proton pump
in the
parietal cells
, which in turn are controlled by
histamine
acting on the H2-receptors
● The histamine is produced by the endocrine gastric
ECL cells
in response to a number of factors, particularly
gastrin
and the
vagus
●
Proton pump
inhibitors
abolish gastric acid production, whereas
H2-receptor antagonists
only markedly reduce it
● The gastric
mucous layer
is essential to the integrity of the gastric mucosa
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INVESTIGATION OF THE STOMACH AND DUODENUMFlexible endoscopyContrast radiologyUltrasonography
CT scanning and Magnetic Resonance ImagingCT/ Positron emission tomographyLaparoscopyGastric emptying studies
Angiography
Tests for Helicobacter pylori
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Helicobacter pylori This organism has proved to be of major importance in the aetiology of a number of common gastroduodenal diseases such as chronic gastritis,
peptic ulceration and gastric cancer.
In
1980
Warren
and
Marshall
ingested the organism to confirm that it is the cause of gastritis that they succeed in causing in themselves. (received Nobel prize 2005)
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Helicobacter pylori/ characteristics & pathological effects Has the ability to
hydrolyse urea, within the gastric mucosa resulting in the production of
ammonia
, a strong alkali. This will stimulate antral G cells to release of
Gastrin
via a negative-feedback loop.
Infection with H. pylori leads to the
disruption of the gastric mucous barrier by the enzymes produced by the organism
.
Some strains of H. pylori produce
cytotoxins
, notably the
Cag A
and
Vac A
products.
H. pylori is now classed by the
WHO
as a
class 1 carcinogen.
It is
difficult to explain
how the organism is involved in
duodenal ulceration
, since the normal duodenum is
not colonized
, but the increased Gastrin level 2ndary to increased production of Ammonia, and the modestly increased gastric acid secretion supports the responsibility for ulcer formation.
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Helicobacter pylori/ DetectionTests using the organism’s obligate urease activity include:
the 13C and 14C breath tests
the CLO test (Campylobacter Like Organism test) performed on gastric biopsies.
The organism can also be detected histologically using the Giemsa or the Warthin–Starry stains, and cultured using appropriate media.
Serological tests to detect previous or current
infection
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Helicobacter pylori/ EradicationHypochlorhydria produced by proton pump inhibitors
combined with antibiotics is effective in eradicating the organism. Commonly used eradication regimes include a
proton pump inhibitor
and two antibiotics, such as
metronidazole
and
amoxycillin
.
High eradication rates (of
90%
) can be achieved with combinations that include the antibiotic
clarithromycin
, although future resistance will become a problem.
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GastritisDescribes any histologically confirmed inflammation of the gastric mucosa.According to the underlying aetiology, gastritis is classified into:
Autoimmune gastritis
H. pylori gastritis
Reflux gastritis
Erosive gastritis
Stress gastritis
Ménétrier’s disease
Lymphocytic gastritis
Eosinophilic gastritis
Granulomatous gastritis
Acquired immunodeficiency syndrome (AIDS) gastritis
Phlegmonous gastritis
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Peptic UlcerWhat is an “Ulcer”? ..&..Is it really “
Peptic ” ?!!!Site: common sites include the
first part of the duodenum
and the
lesser curve of the stomach
.
Acute and Chronic peptic ulcer
: it is really a spectrum of disease from the superficial gastric and duodenal ulceration, frequently seen at endoscopy, to deep chronic penetrating ulcers.
The cause
: high gastric acid output…!!!, genetic factor…., social stress…,
H. pylori
,
NSAIDs
, cigarette smoking.
Does
duodenal
differs from
gastric ulcer
regarding incidence, pathology, clinical presentation, the risk of malignancy, diagnosis or treatment?
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Other sites for peptic ulcersPre-pyloric gastric ulcer
Pyloric channel ulcers Both carry the risk of malignancy and biopsy is essential.
Stomal ulcers
occur after a gastroenterostomy
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Clinical features of peptic ulcersGastric and duodenal ulceration cannot be really differentiated depending on symptoms or clinical features.
Pain: epigastric, often gnawing قضم, حفر, نخر and may radiate to the back. Periodicity
: Symptoms may disappear for weeks
Vomiting
Alteration in weight
Bleeding
: all peptic ulcers may bleed. Chronic bleeding presents with microcytic anemia
Clinical examination
: is either –ve or may reveal epigastric tenderness, unless complications develops like gastric outlet obstruction or perforation.
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Investigation of the patient with suspected peptic ulcer G
astroduodenoscopy: (certain technical details; like taking biopsies, CLO test, J maneuver, ..etc.)Treatment of peptic ulceration/ Principles
The
majority
of uncomplicated peptic ulcers are treated
medically
.
Surgical
treatment of
uncomplicated
peptic ulceration is now seldom performed.
Surgical treatment
is now mainly used for complications.
H. pylori e
radication therapy
.
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Medical TreatmentModifications to the patient’s lifestyle.
Drugs: A. Antisecretory drugs
H
2
-receptor antagonists
Proton Pump Inhibitors
(PPIs)
Both drug categories don’t cause serious side-effects.
Relapse is common after stopping them.
Drugs: B. Eradication therapy
:
If a patient has a peptic ulcer and
H. pylori is the principal etiological factor
(essentially the patient not taking NSAIDs)
It is more economical than prolonged courses of
antisecretory
drugs and definitely safer than surgery.
A
PPI + 2 antibiotics
for 10-14 days followed by 4 weeks course of PPI alone will achieve this target.
A patient on
NSAIDs
,
should
not
be prescribed an eradication therapy
Zollinger–Ellison syndrome
should be treated with proton pump inhibitors unless the tumour can be managed by surgery.
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Surgical treatment of uncomplicated peptic ulcerationDuodenal Ulcer Surgeries/ types
1. Vagotomies:Truncal Vagotomy & Drainage procedure*Selective Vagotomy & Drainage procedure*
* (Pyloroplasty or Gastro- Jejunostomy)
Highly Selective Vagotomy
2. Gastrectomies:
Distal Gastrectomy & Gastro- duodenostomy (Billroth 1 operation)
Distal Gastrectomy & Gastro- jejunostomy (Billroth 11 or Polya operation)
3. Mixed:
Vagotomy & Antrectomy
4. Drainage only
Gastro- jejunostomy alone
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