Stomach Anatomy and Pathology

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Stomach Anatomy and Pathology

• Week 4- Feeling Tired
• Skye Poulton

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• The stomach is Intraperitoneal
• Lesser omentum has superior attachment to liver
  by lesser curvature
• Greater omentum suspended from greater curvature
  of stomach and loops back up to attach to
  transverse colon

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• Body Types effects shape and position of stomach

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• Has four regions
• Cardia
• Fundus
• Body
• Pyloric

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Blood Supply

• The rich arterial supply of the stomach arises
  from the celiac trunk and its branches
• Most blood is supplied by anastomoses formed
  along the lesser curvature by the right and left
  gastric arteries, and along the greater curvature
  by the right and left gastro-omental
  (gastroepiploic) arteries.
• The fundus and upper body receive blood from the
  short and posterior gastric arteries.
• The veins of the stomach parallel the arteries in
  position and course

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• Gastric Innervation
• Receives Parasympathetic innervations from
  medulla via vagus nerves
• Receives Sympathetic innervations from celiac
  ganglia arising from T5 T9
• Lymphatic Drainage
• mainly to the gastric lymph nodes,
  pancreaticosplenic lymph nodes, pyloric lymph
  nodes and pancreatic-oduodenal lymph nodes
• then drainage accompany the large arteries to the
  celiac lymph nodes

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Histology

• Glandular Epithelium
• Gastric Pits and Glands
• Extra layer in muscularis Propria- Inner Oblique
  Layer

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Structure of Glands

• Surface/Neck mucous cells-  secrete protective
  bicarbonate ions
• Parietal Cells- most numerous in the isthmus of
  the glands, secrete gastric acid (HCL) as well
  as intrinsic factor.
• Chief, peptic or zymogenic cells- located towards
  the bases of the gastric glands. Secrete gastric
  lipase and pepsinogen.
• Neuroendocrine cells- part of the diffuse
  neuroendocrine system, secrete serotonin and
  other hormones
• Stem cells- divide continuously to replace all
  other types of cell in the glands. Not easily but
  become very prominent with plentiful mitotic
  figures after damage to the mucosa has occurred,
  e.g. after an episode of gastritis.
• ie. important histopathology feature

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Stomach- Pathologies

• Acute Gastritis - a transient mucosal
  inflammatory process that may be asymptomatic or
  cause variable degrees of epigastric pain,
  nausea, and vomiting. In more severe cases there
  may be mucosal erosion, ulceration, hemorrhage,
  hematemesis, melena, or, rarely, massive blood
  loss.
• Pathophysiology The gastric lumen is strongly
  acidic with pH close to 1. This harsh
  environment contributes to digestion but also has
  the potential to damage the gastric mucosa, if
  any of the protective mechanisms that have
  evolved are disrupted.

• Reduced mucin synthesis in the elderly
• NSAIDs prevents synthesis of prostaglandins,
  which enhance bicarbonate secretion, inhibit acid
  secretion, promote mucin synthesis, and increase
  vascular perfusion
• urease-secreting H. pylori inhibitions gastric
  bicarbonate transporters by ammonium ions.
• Direct cellular injury due to excessive alcohol
  consumption, NSAIDs, radiation therapy, and
  chemotherapy.

This diagram illustrates the progression from
more mild forms of injury to ulceration that may
occur with acute or chronic gastritis
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Chronic Gastritis

• In contrast to acute gastritis, the symptoms are
  typically less severe but more persistent.
• The most common cause of chronic gastritis is
  infection with H. Pylori. Although the mechanism
  is incompletely defined, it is clear that
  infection results in increased acid production
  and disruption of normal gastric and duodenal
  protective mechanisms.
• Four features are linked to H. pylori virulence
• Flagella, which allow the bacteria to be motile
  in viscous mucus
• Urease, which generates ammonia from endogenous
  urea and thereby elevates local gastric pH
• Adhesins that enhance their bacterial adherence
  to surface foveolar cells
• Toxins, such as cytotoxin-associated gene A
  (CagA), that may be involved in ulcer or cancer
  development by poorly defined mechanisms
• Other chronic irritants, including psychologic
  stress, caffeine, alcohol, and tobacco
• Peptic Ulcer Diseases- chronic reoccurring
  lesions
• complication of chronic Gastritis the imbalances
  of mucosal defenses and damaging forces

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Autoimmune gastritis

• the most common cause of atrophic gastritis, and
  the most common form of chronic gastritis in
  patients without H. pylori infection.
• Autoimmune gastritis is characterized by
• Antibodies to parietal cells and intrinsic factor
  that can be detected in serum and gastric
  secretions
• Reduced serum pepsinogen I concentration
• Antral endocrine cell hyperplasia
• Vitamin B12 deficiency
• Defective gastric acid secretion
• Pathogenesis believed that CD4 T cells directed
  against parietal cell components, including the
  H,K-ATPase, are the principal agents of injury.
  This is supported by the observation that
  transfer of H,K-ATPase-reactive CD4 T cells
  into mice results in gastritis and production of
  autoantibodies.
• Loss of parietal cells ? absence of acid
  production ? gastrin release ? hypergastrinemia
  and hyperplasia of antral gastrin-producing G
  cells.
• Loss of parietal cells ? lack of intrinsic factor
  ? B12 deficiency and a slow-onset megaloblastic
  anaemia (pernicious anaemia).
• Gastric Gland destruction ? consequential chief
  cell destruction ? reduced serum pepsinogen
  concentration

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Atrophy, Metaplasia and Dysplasia

• Long-standing chronic gastritis that involves the
  body and fundus may ultimately lead to
  significant loss of parietal cell mass. This
  atrophy may be associated with intestinal
  metaplasia, recognized by the presence of goblet
  cells, and is strongly associated with increased
  risk of gastric adenocarcinoma.
• Chronic gastritis exposes the epithelium to
  inflammation-related free radical damage and
  proliferative stimuli. Over time this can lead to
  the accumulation of genetic alterations that
  result in carcinoma. Pre-invasive in situ lesions
  can be recognized histologically as dysplasia.
• Dysplasia- in the form of Polyps, and adenomas
  almost always occur on a background of chronic
  gastritis with atrophy and intestinal metaplasia.
  

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Adenocarcinoma

• Adenocarcinoma is the most common malignancy of
  the stomach, comprising over 90 of all gastric
  cancers.
• Unfortunately early symptoms resemble those of
  chronic gastritis.
• Although specific sequences of events have not
  been defined, it is clear that chronic
  inflammation promotes neoplastic progression.
• While the majority of gastric cancers are not
  hereditary, many genetic mutations have been
  identified

• mutations in CDH1, and the subsequent loss of
  E-cadherin function, a protein that contributes
  to epithelial intercellular adhesion, is a key
  step in the development of diffuse gastric
  cancer.
• BRCA2 mutations are at increased risk of
  developing diffuse gastric cancer.
• several genes including TGFßRII, BAX, IGFRII, and
  p16/INK4a have also been described in sporadic
  intestinal-type gastric cancer.
• Genetic variants of pro-inflammatory and immune
  response genes, including those that encode
  IL-1ß, TNF, IL-10, IL-8, and Toll-like receptor 4
  (TLR4), are associated with elevated risk of
  gastric cancer when accompanied by H. pylori
  infection
• p53 mutations are present in the majority of
  sporadic gastric cancers of both histologic
  types.

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Hypertrophic Gastropathies

• Hypertrophic gastropathies are uncommon diseases
  characterized by giant cerebriform enlargement of
  the rugal folds due to epithelial hyperplasia
  without inflammation.
• As might be expected, the hypertrophic
  gastropathies are linked to excessive growth
  factor release. The two most well-understood
  examples
• Zollinger-Ellison syndrome is caused by
  gastrin-secreting tumors, gastrinomas, that are
  most commonly found in the small intestine or
  pancreas.
• Ménétrier disease is a rare disorder caused by
  excessive secretion of transforming growth factor
  a (TGF-a)

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• Vitamin B12 has no appreciable toxicity level.
  So no risk to her health of continuing B12
  injections.

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References

• Kumar. V., et L. (2010). Robbins and Cotran
  pathologic basis of disease, 8th Edn.
  Philadelphia Saunders/Elsevier.
• Moore, K.L.  Agur, A.M.R. (2007). Essential
  clinical anatomy. 3rd edn. Baltimore Lippincott
  Williams Wilkins.
• Young, B. et al. (2006). Wheater's functional
  histology  A text and colour atlas. 5th edn. New
  York Churchill Livingstone.