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Stomach Anatomy and Pathology


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Title: Stomach Anatomy and Pathology

Stomach Anatomy and Pathology
  • Week 4- Feeling Tired
  • Skye Poulton

  • 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

  • Body Types effects shape and position of stomach

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

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

  • 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

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

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

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
  • 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

This diagram illustrates the progression from
more mild forms of injury to ulceration that may
occur with acute or chronic gastritis
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
  • complication of chronic Gastritis the imbalances
    of mucosal defenses and damaging forces

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
  • 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
  • Loss of parietal cells ? absence of acid
    production ? gastrin release ? hypergastrinemia
    and hyperplasia of antral gastrin-producing G
  • 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

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.

  • Adenocarcinoma is the most common malignancy of
    the stomach, comprising over 90 of all gastric
  • 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
  • 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
  • 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
  • p53 mutations are present in the majority of
    sporadic gastric cancers of both histologic

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
  • Zollinger-Ellison syndrome is caused by
    gastrin-secreting tumors, gastrinomas, that are
    most commonly found in the small intestine or
  • Ménétrier disease is a rare disorder caused by
    excessive secretion of transforming growth factor
    a (TGF-a)

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

  • 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.
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