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Gastrointestinal Tract

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Parietal cells found in fundus and body. Secrete HCl & intrinsic factor ... normal fundus. antrum ( pylorus) emptying. into the 1ST of duodenum. Stomach ... – PowerPoint PPT presentation

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Title: Gastrointestinal Tract


1
Gastrointestinal Tract
2
Gastrointestinal Tract
3
  • Stomach
  • Glands
  • Parietal cells found in fundus and body
  • Secrete HCl intrinsic factor
  • Chief cells are more at fundus and body
  • Secrete pepsinogen I II
  • Congenital Anomalies
  • 1. Diaphragmatic Hernia
  • A defect in the diaphragm ? away from the hiatal
    orifice (not hiatal hernia)
  • Portions of stomach small intestine herniates
  • Results in respiratory impairment pulmonary
    hypoplasia

4
Stomach - Normal
IF
5
Stomach - Normal
6
  • Stomach
  • . 2. Congenital Hypertrophic Pyloric Stenosis
  • Hypertrophy of the circular muscle of the pylorus
  • Results in Regurgitation vomiting in the
    neonatal period
  • VGP-visible Gastric peristalsis palpable mass
    in the epigastrium
  • males, multifactorial inheritance.
  • Rx A full thickness muscle splitting incision
    (pyloro-myotomy) is curative (Hellers operation)

7
Stomach - Normal
normal fundus
esophagus
antrum ( pylorus) emptying into the 1ST of
duodenum
8
  • Stomach
  • Acute Gastritis inflammation of gastric mucosa
  • acute presence of neutrophils
  • Chronic lymphocytes and plasma cells
  • Caused by ingestion of strong acids or alkalies,
    NSAIDs, cancer chemotherapy, irradiation,
    alcohol, uremia, severe stress shock states
  • Proposed mechanisms ? acid production with ?
    surface bicarbonate buffer
  • Morphology Mucosal edema, hyperemia, PML
    infiltration, erosions (not deeper than
    muscularis mucosa) hemorrhages

9
Acute Gastritis
  • Gastric mucosa demonstrates infiltration by
    Neutrophils

10
Acute Gastritis
  • diffusely hyperemic gastric mucosa
  • causes for acute gastritis
  • alcoholism
  • drugs
  • infections, etc.

11
  • Stomach
  • Chronic Gastritis Chronic mucosal inflammation
  • Leading to mucosal atrophy, intestinal metaplasia
    dysplasia.
  • Pathogenesis
  • Chronic infection by Helicobacter pylori (90)
    MCC of chronic gastritis, Elaboration of urease ?
    produces ammonia that buffers gastric acid,
    protecting organism from acid
  • Other diseases associated with H. pylori
    Infection
  • Peptic ulcer disease
  • Gastric carcinoma
  • Gastric lymphoma
  • Autoimmunity (gt10) Antibodies to parietal cells
    cause parietal cell destruction (HCl intrinsic
    factor)

12
  • Stomach
  • Chronic Gastritis
  • Morphology
  • Autoimmune ? diffuse mucosal damage of the
    body-fundic mucosa
  • H. pylori ?affect antral mucosa
  • Histology Lymphocytic plasma cell infiltrate
    of the lamina propria
  • atrophy, regeneration, metaplasia (to intestinal
    type mucosa) dysplasia.
  • H. pylori detected on the mucosal surface
  • Clinically
  • Mild abdominal discomfort, nausea, vomiting
    hypochlorhydria, hypergastrinemia rarely
  • Overt pernicious anemia (in autoimmune)
    gastritis).
  • Long-term risk of cancer is 2-4

13
H. pylori
  • small curved to spiral rod-shaped bacterium is
    found in the surface epithelial mucus of most
    patients with active gastritis
  • The rods are seen here with a methylene blue
    stain.

14
Autoimmune gastritis
  • Autoimmune gastritis - pernicious anemia
  • Chronic atrophic gastritis is associated with
    Abs
  • - intrinsic factor
  • - patietal cell
  • bright green IF- in the parietal cells of the
    gastric mucosa.

15
  • Stomach
  • Peptic Ulcer Disease
  • Ulcer - a breach in mucosa extends thru
    muscularis mucosae into submucosa or deeper
  • 1) Acute Gastric Ulcers
  • acute erosive gastritis erosions ABOVE the
    muscularis mucosa
  • Caused by Severe stress ( Stress Ulcers)
  • Shock, extensive burns (Curlings ulcers)
  • Severe head injuries (Cushings ulcers)
  • patients in Intensive Care Units, use of NSAIDs.
  • Morphology Multiple, small (lt1 cm) ulcers,
    normal adjacent mucosa
  • Clinically Upper GIT hemorrhage.
  • Treatment treat underlying cause

16
Stress ulcers
  • small, shallow gastric ulcerations known as
    "stress ulcers"
  • patients with a variety of stressful conditions,
    including trauma, burns, sepsis, and shock.
  • Anti-inflammatory drugs such as aspirin and
    NSAIDs may play a role in their appearance.

17
  • 2) Peptic ulcers - chronic
  • Characterized by Solitary, chronic ulcers,
  • Ratio of duodenal gastric 4 1 (Duodenal
    ulcer is more common)
  • Morphology Sharply punched out mucosal defect
    With sharp borders clean ulcer base.
  • Surrounding mucosa shows chronic gastritis
    radial convergence of rugal folds towards the
    ulcer niche (unlike malignant ulcer)
  • Clinically Epigastric pain 1-3 hours after meals
    worse at night nausea vomiting belching
    occult blood in the stools.
  • Complications
  • Perforation - accounts for 2/3rds of ulcer
    deaths
  • Hemorrhage - accounts for 25 of ulcer deaths
  • Obstruction - causes severe crampy abdominal pain
  • Malignant transformation is extremely rare

18
Peptic Ulcerpathogenesis
19
Gastric ulcer
  • larger 3 x 4 cm gastric ulcer
  • This ulcer is much deeper with more irregular
    margins
  • Complications of gastric ulcers (either benign or
    malignant) include
  • pain
  • Bleeding (MC)
  • Perforation (most dangerous)
  • obstruction.

20
Gastric ulcer
  • Microscopically
  • the ulcer here is sharply demarcated, with normal
    gastric mucosa on the left falling away into a
    deep ulcer whose base contains inflamed, necrotic
    debris
  • Arterial branch at the ulcer base is eroded and
    bleeding.

21
  • 3). Hypertrophic Gastropathy
  • Characterized by Giant enlargement of the gastric
    rugal folds
  • Caused by hyperplasia of epithelial cells ( not
    due to inflammation )
  • ?risk of cancer
  • Includes 3 variants
  • A) Menetriers disease
  • Hyperplasia of surface mucous cells
  • glandular atrophy
  • excessive loss of proteins in gastric secretion
    (protein-losing Gastropathy)
  • B) Hypersecretory Gastropathy
  • Hyperplasia of parietal and chief cells
  • Secondary to excessive gastrin stimulation.
  • C) Zollinger - Ellison Syndrome
  • Caused by Gastrinoma of Pancreas secreting
    gastrin ? elevated serum gastrin levels
  • multiple peptic ulcerations in stomach, duodenum,
    jejunum
  • Hypertrophic rugal folds Parietal cell
    hyperplasia ? excess gastric acid production

22
  • Benign Tumors of the stomach
  • 1) Gastric polyps
  • Most of the polyps ( 90) are non-neoplastic
    polyps
  • (hyperplastic /or inflammatory)
  • no malignant potential.
  • Gastric polyps must be biopsied
  • 2) Adenomatous Polyps
  • true neoplasms with proliferative dysplastic
    epithelium
  • Have malignant potential, common in old age
  • MC associated with chronic gastritis or familial
    polyposis syndromes

23
  • Malignant - Tumors
  • 1. Gastric Carcinoma
  • Incidence 4-fold decline in incidence over the
    last 70 years (for unknown reasons).
  • Risk Factors
  • Diet Nitrites (from food preservatives), smoked
    and salted foods, deficiency of fresh fruits and
    vegetables.
  • Host Factors Chronic gastritis (autoimmune H.
    pylori), Adenomatous polyps, partial gastrectomy
    pts.
  • Genetic Factors blood group A, close relatives
    of stomach cancer patients, certain racial groups
    (Japanese)
  • Classification
  • A) Early Gastric Carcinoma Confined to the
    mucosa submucosa, despite lymph node spread
  • Associated with very good prognosis (gt90 5-year
    survival)

24
  • B) Advanced Gastric Carcinoma Has extended
    beyond the submucosa Spread is by local
    invasion, lymphatics, blood (to liver lungs)
  • Krukenberg tumor bilateral ovarian metastases
    (stomach, breast, pancreas, and even gallbladder
    )
  • Virchow node left supraclavicular node with
    mets.
  • Sister Mary Joseph nodule metastasize to the
    periumbilical region (subcutaneous malignant
    nodule)
  • Histologic types
  • Intestinal type, glandular, expansile growth
    pattern
  • Gastric type, diffuse signet ring infiltrating
    pattern
  • Pathologic stage is the most important prognostic
    indicator
  • 2) Gastrointestinal Stromal Tumor (GISTs)
  • Arise from Interstitial cells of Cajal
  • c-KIT (CD117) CD34- positive

25
  • 3. Carcinoid (neuroendocrine) tumors
  • made of Enterochromaffin-like (ECL) cell tumors
  • Associated with multiple endocrine neoplasia type
    1 (MEN1) Zollinger-Ellison syndromes
  • 4) Gastric Lymphoma
  • MC site for extranodal lymphoma
  • majority (gt80) are associated with H. pylori
    chronic gastritis

26
Stomach gastric carcinoma
  • Gastric adenocarcinoma in the U.S., most gastric
    cancers are discovered at a late stage when the
    neoplasm has invaded and/or metastasized.
  • All gastric ulcers and All gastric masses must
    be biopsied,
  • In contrast, virtually all duodenal peptic ulcers
    are benign.

27
Stomach gastric carcinoma
  • Malignant gastric ulcer
  • This ulcer on biopsy proved to be malignant, so
    the stomach was resected

28
  • Linitis plastica
  • a diffuse infiltrative gastric adenocarcinoma
  • stomach looks like a shrunken "leather bottle"
    appearance
  • markedly thickened gastric wall
  • very poor prognosis.

29
Case - 1
  • A 48-year-old man has had vague abdominal
    discomfort for a number of years. There is no
    history of hematemesis, but he has occasional
    nausea and vomiting. An upper GI endoscopy is
    performed. There is no evidence for ulceration or
    a mass lesion, and gastric biopsies are taken.
    Images 8.1 and 8.2 demonstrate the gastric mucosa
    at low and high magnification. The surface of the
    gastric mucosa at high magnification is seen in
    images 8.3 and 8.4.

30
1.1
31
1.2
32
1.3
33
1.4
34
Case - 2
  • A 55-year-old woman, with a history of epigastric
    pain relieved by food, complained of episodes of
    hematemesis that have occurred in the past week.
    Upper GI endoscopy with biopsies was performed
    (image 3.1). The specimen shown here is from the
    subsequent partial gastrectomy (image 3.2). The
    lesion appears as a cup-shaped ulcer filled with
    blood clot. The ulcer, which was found to extend
    almost through the gastric wall, is lined by
    necrotic debris and acute inflammatory cells
    overlying a base of granulation tissue and
    fibrosis (images 3.3 and 3.4) with a large vessel
    at the base (image 3.5).

35
2.1
36
3.2
37
3.3
38
Case -3
  • A 60-year-old man complained of anorexia,
    vomiting, and vague abdominal pain accompanied by
    weight loss of 15 kg over the past two months.
    Physical examination revealed supraclavicular
    lymphadenopathy. An abdominal CT scan revealed
    that the stomach wall was thickened . He became
    progressively cachectic and died. At autopsy, the
    stomach was diffusely thickened and leather-like
    . Microscopic sections of the gastric wall are
    shown .

39
3.1
40
3.2
41
3.3
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