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DMH Part 1 > Disorders of the Esophagus and Stomach > Flashcards

Disorders of the Esophagus and Stomach Flashcards

1
Q

Esophagitis

A

Injury of the esophageal mucosa with subsequent inflammation.

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2
Q

Esophageal Disorders

A
  • Reflux Esophagitis
  • Eosinophilic Esophagitis
  • Infection
  • HSV
  • CMV
  • Candida
  • Mallory Weiss Tear
  • Esophageal SCC
  • Esophageal Adenocarcinoma
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3
Q

Reflux Esophagitis

A

Chronic regurgitation of gastric contents into the esophagus producing various degrees of tissue damage. The acid-peptic action of gastric juices is critical to the development of injury to the esophageal mucosa.

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4
Q

Reflux Esophagitis - Pathogenesis

A
  • Decreased efficacy of esophageal antireflux mechanisms.
  • Inadequate / slowed esophageal clearance of refluxed material.
  • Presence of a sliding hiatal hernia.
  • Delayed gastric emptying and increased gastric volume.
  • Reduced reparative capacity of esophageal mucosa by protracted exposure to acid
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5
Q

Reflux Esophagitis - Clinical Features

A
  • Commoner in adults >40 years of age.
  • Also occurs in infants and children.
  • Cardinal features: Dysphagia, Heart burn, Regurgitation of sour “brash”
  • Hematemesis and melena
  • Chest pain (it may be severe enough to mimic a myocardial infarct)
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6
Q

Reflux Esophagitis - Gross Findings

A

•vary according to the degree of severity from mild edema and hyperemia to erosions and ulcers.

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7
Q

Reflux Esophagitis - Microscopic Findings

A
  • Uncomplicated: Epithelial basal zone hyperplasia, exceeding 20% of the epithelial thickness; eosinophils, lymphocytes with or without neutrophils within the epithelium; congestion and elongation of lamina propria papillae, extending into the top third of the epithelium.
  • Severe cases: Erosions and ulcers covered by fibrinopurulent debris.
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8
Q

Reflux Esophagitis - Complications

A

•Bleeding, stricture formation and Barrett’s esophagus.

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9
Q

Barrett’s Esophagus

A

•Condition in which the distal squamous esophageal mucosa is replaced by columnartype epithelium (glandular mucosa) as a complication of prolonged reflux esophagitis.

  • 10% of symptomatic GERD patients will develop BE
  • Portends increased risk of esophageal adenocarcinoma.
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10
Q

Barrett’s Esophagus - Pathogenesis

A

The proposed theory is that long standing gastroesophageal reflux leads to inflammation and ulceration with healing by reepithelialization and ingrowth of immature pluripotent stem cells. These stem cells, in a low pH environment, differentiate into a gastric or intestinal type of epithelium that is more acid resistant.

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11
Q

Barrett’s Espohagus - Gross Findings

A

Tongues of red velvety glandular mucosa contrasting with the pale pink squamous mucosa within esophagus. Length 3cm: Long segment BE.

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12
Q

Barrett’s Espohagus - Microscopic Findings

A
  • The hallmark of diagnosis is intestinal metaplasia of esophagus characterized by goblet cells (Intracytoplasmic pale blue mucin vacuole with remaining cytoplasm assuming the shape of a wine goblet).
  • Dysplasia is recognized by the presence of cytological and architectural abnormalities (enlarged, crowded and stratified hyperchromatic nuclei, glandular proliferation and crowding with loss of intervening stroma).
  • Precursor of adenocarcinoma.
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13
Q

Barrett’s Espohagus - Diagnostic Criteria

A
  • Endoscopic identification of tongues of salmon-colored glandular mucosa projecting into pearly white squamous lined esophagus >/= 1cm in length
  • AND • Histologic documentation of intestinal metaplasia, characterized by goblet cells within this salmon-colored patch
  • Presently, intestinal metaplasia (goblet cells) is required for the diagnosis of Barrett’ s esophagus because intestinal metaplasia is the only type of esophageal columnar epithelium that clearly predisposes to malignancy
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14
Q

Barrett’s Espohagus - Risk Factors

A

• Well established risk factors for BE:

– Age >50

– White Male

– Chronic GERD with frequent symptoms

– Current or past history of smoking

– Central obesity

– First degree relative with BE and/or EAC

• Patients with multiple risk factors undergo screening for BE.

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15
Q

Barrett’s Esophagus - Clinical Manifestations

A

*same as reflux esophagitis

  • Commoner in adults >40 years of age.
  • Also occurs in infants and children.
  • Cardinal features: Dysphagia, Heart burn, Regurgitation of sour “brash”
  • Hematemesis and melena
  • Chest pain (it may be severe enough to mimic a myocardial infarct)
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16
Q

Barrett’s Esophagus - Complications

A

Include ulceration, bleeding, development of strictures and a 30-40 fold risk for the development of carcinoma.

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17
Q

Eosinophilic Esophagitis

A

Characterized by infiltration of esophageal mucosa by a large number of eosinophils, particularly superficially.

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18
Q

Eosinophilic Esophagitis - Pathogenesis

A

Majority of individuals are atopic with other allergic conditions such as asthma and moderate peripheral eosinophilia. Etiology is believed to be allergy to food.

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19
Q

Eosinophilic Esophagitis - Clinical Features

A

Typical history of dysphagia and food impaction. Adults and children.

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20
Q

Eosinophilic Esophagitis - Complications

A

Stricture formation, esophageal dysmotility

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21
Q

Endoscopic Features of EoE

A
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22
Q

Microscopic Features of EoE

A
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23
Q

Eosinophilic Esophagitis - Management

A
  • Identification of allergens and dietary restriction
  • Proton pump inhibitors: Mechanism of action is by blocking recruitment of eosinophils and release of eotaxin
  • Topical steroids
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24
Q

Chemical Induced Eosinophilic Esophagitis

A

Ingestion of mucosal irritants (ETOH, corrosive acids or alkalis) excessively hot fluid and heavy smoking; induced injury ranges from mild erythema and edema to severe necrosis and inflammation. Localized esophageal erosions may result from pharmaceutical tablets or capsules “sticking” to the mucosa (Pill-induced esophagitis).

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25
Q

Infection

A
  • In debilitated and immunocompromised patients: -HSV and CMV are the most common viral etiologies. Both produce punch out ulcers. Nuclear inclusions of HSV are found in the remaining epithelium at the edge of the ulcer. Nuclear and cytoplasmic inclusions of CMV are found in endothelial and stromal cells at the base of the ulcer.
  • Candida is the most common fungus infecting the esophagus. Grossly it forms a gray-white pseudomembrane, which under the microscope has inflammatory debris, neutrophils and yeasts with pseudohyphi.
  • Others: Uremia, radiation, GVHD and desquamative dermatologic conditions of pemphigoid and epidermolysis bullosa.
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26
Q
A
  • HSV
  • margination of chromatin, ring around pink center
  • giant cells with multiple nuclei
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27
Q
A
  • CMV
  • individual cells are enlarged
  • intranuclear inclusion
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28
Q

HSV vs. CMV

A
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29
Q
A

•Candida Esophagitis

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30
Q

Mallory-Weiss Tear

A
  • Longitudinal mucosal tear near gastroesophageal junction (GEJ)
  • Associated with severe retching or vomiting secondary to acute alcohol intoxication; due to failure of GEJ musculature to relax before anti-peristaltic wave of vomiting.
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31
Q

Esophageal Neoplasms

A
  • Benign: Rare and most are of mesenchymal origin.
  • Malignant: Squamous cell carcinoma and Adenocarcinoma
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32
Q

Esophageal Squamous Cell Carcinoma - Epidemiology

A

•Geographic variability: High incidence in Northern Iran, North China, Puerto Rico, South Africa and Eastern Europe and relatively uncommon in the USA

  • Male to female ratio of 4:1.

Age of disease is generally older than 50.

African Americans are affected more than are Caucasians

  • The incidence in the USA is rapidly declining
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33
Q

Dietary Factors Associated with Esophageal Squamous Cell Carcinoma

A
  • Vitamins deficiency (A, C, riboflavin, thiamine, pyridoxine)
  • Deficiency of trace metals (zinc, molybdenum)
  • Fungal contamination of foodstuffs
  • High content of nitrites/nitrosamines
  • Betel chewing
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34
Q

Lifestyle Factors Associated with Esophageal Squamous Cell Carcinoma

A

•Alcohol, tobacco and urban environment: Majority of cases in USA and Europe are linked to alcohol and tobacco use, which act synergistically.

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35
Q

Esophageal Disorders Associated with Esophageal Squamous Cell Carcinoma

A

•Long-standing esophagitis, achalasia and Plummer-Vinson syndrome (esophageal webs, iron deficiency anemia and glossitis)

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36
Q

Genetic Predisposition Associated with Esophageal Squamous Cell Carcinoma

A
  • Long-standing celiac disease
  • Ectodermal dysplasia, epidermolysis bullosa
  • Tylosis palmaris at plantaris
  • Racial predisposition
  • HPV-DNA is frequently found in esophageal squamous cell carcinoma from high incidence regions: its presence in similar cancers in North America is infrequent.
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37
Q

Esophageal Squamous Cell Carcinoma - Gross Findings

A

Three growth patterns:

a) fungating,
b) flat, diffusely infiltrating and
c) excavating ulcer.

•Half are located in the middle third with the others about evenly split in the upper and lower thirds of the esophagus.

38
Q

Esophageal Squamous Cell Carcinoma - Microscopic Findings

A

•Malignant squamous cells with cytoplasmic keratinization, keratin pearl formation, nuclear pleomorphism and mitoses.

39
Q

Esophageal Squamous Cell Carcinoma - Clinical Features

A
  • Symptoms vary from none in early stages to dysphagia, obstruction, invasion into adjacent organs in late stages.
  • Prognosis is stage-dependent at the time of diagnosis.
  • Rich lymphatic network of esophagus promotes circumferential and longitudinal dissemination of tumor cells such that tumor nodules can be found far away from the main tumor mass.
  • Metastasis occur via lymphatics with those in the upper third going to cervical lymph nodes; those in the middle third to mediastinal, tracheobronchial lymph nodes and those in the lower third spreading to celiac and gastric lymph nodes.
40
Q

Esophageal Adenocarcinoma - Epidemiology

A

•Male to female ratio is 7:1.

  • The age at which it occurs is generally over 40.
  • Caucasians are affected more than are African-Americans.

•The tumor rises from dysplasia in the setting of Barrett’s esophagus.

41
Q

Esophageal Adenocarcinoma - Etiology and Pathogenesis

A
  • Clonal progression of dysplastic cells in BE to overt carcinoma occurs with accumulation of further chromosomal abnormalities.
  • Environmental factors (primarily GERD) is the major cause.
42
Q

Esophageal Adenocarcinoma - Gross Findings

A

•Early lesions are composed of flat or raised patches of intact mucosa; nodular or mass lesions that may ulcerate and infiltrate are seen in advanced cancers.

43
Q

Esophageal Adenocarcinoma - Microscopic Findings

A

•Malignant glands with intracytoplasmic mucin and varying degrees of differentiation.

44
Q

Esophageal Adenocarcinoma - Clinical Features

A
  • Symptoms of dysphagia, odynophagia, progressive weight loss, vomiting and bleeding often occur in advanced disease.
  • Less than half the patients give a history of symptoms of reflux disease.
  • Diagnosis is made by endoscopic biopsy and imaging techniques. It invades adjacent structures and metastases are via lymphatics.
  • Prognosis is stage-dependent at the time of diagnosis.
45
Q

Gastritis

A

Inflammation of the gastric mucosa

46
Q

Gastric Disorders

A
  • Acute Gastritis
  • Chronic Gastritis
  • H.pylori
  • autoimmune
  • Peptic Ulcer Disease
  • Hypertrophic Gastropathy
  • Benign Tumors
  • polyps
  • inflammatory/hyperplastic
  • adenoma
  • mesenchymal - GIST

•Malignant Tumors

  • adenocarcinomas
  • lymphoreticular malignancies
  • carcinoid tumors
  • mesenchymal
47
Q

Acute Gastritis

A

Acute mucosal inflammatory process usually of a transient nature.

48
Q

Acute Gastritis - Pathogenesis

A
  • It has been associated with heavy use of NSAIDs particularly aspirin: ETOH consumption, heavy smoking, chemotherapy, uremia, severe stress, systemic infection, shock, ingestion of acids or alkalis, trauma and after distal gastrectomy with reflux of bilious material.
  • Ultimate damage is thought to result from the following mechanisms:
  • Disruption of the adherent mucous layer
  • Stimulation of acid secretion with hydrogen ion back diffusion
  • Decreased production of bicarbonate
  • Reduced mucosal blood flow – hypoxic injury
  • Direct damage to the epithelium
49
Q

Acute Gastritis - Gross Findings

A

•wide morphologic spectrum varying from localized to diffuse mucosal edema and erythema to frank erosion with hemorrhage

50
Q

Acute Gastritis - Microscopic Findings

A

•vary from mild mucosa congestion, edema and acute inflammation to erosions to frank ulcerations. The presence of concurrent erosions and hemorrhage is termed acute erosive hemorrhagic gastritis.

51
Q

Acute Gastritis - Clinical Course

A

•varies depending on the severity of the anatomic changes from asymptomatic to mild epigastric pain, nausea, vomiting to severe hematemesis with potentially fatal blood loss.

52
Q

Chronic Gastritis

A

•It is defined as chronic mucosal inflammatory changes leading eventually to mucosal atrophy and intestinal metaplasia, usually in the absence of erosions. Chronic gastritis is notable for distinct causal subgroups and for patterns of histological alterations that vary in different parts of the world.

53
Q

Chronic Gastritis Etiology and Epidemiology

A
  • Infectious: Helicobacter pylori (most important etiologic association)
  • Immunologic: Autoimmune gastritis
  • Toxic: Alcohol and cigarette
  • Chemical: Reflux of bilious duodenal secretions after antrectomy and gastroenterostomy
  • Motor and mechanical: Obstruction, bezoars and gastric atony
  • Other: Radiation, granulomatous conditions, amyloidosis, GVHD
54
Q

Chronic Gastritis - H. pylori

A
  • Worldwide distribution, more prevalent in underdeveloped countries.
  • Colonization rates increase with age.
  • Motile, curved, non-spore forming gram negative rod
  • Colonizes the surface of gastric-type epithelium, only. Non-invasive infection

– Antrum and cardia

– May become pangastritis

– Bacillus transmitted by fecal-oral route

55
Q

Chronic Gastritis - H. pylori Pathogenic Factors

A
  • Produces urease, which hydrolyses urea to ammonia and bicarbonate, thus producing an alkaline microenvironment in the acid stomach
  • Binds to gastric epithelial cells via a bacterial adhesin
  • Strains that co-express the cag A gene are strongly associated with duodenal ulcer; such gene encodes for an 87-kD vacuolating cytotoxin.
  • This along with bacterial lipopolysaccharide (endotoxin) and other protein products, appear to act as proinflammatory substances.
  • Elicits a local and systemic immune response
56
Q

Chronic Gastritis - H. pylori Complications

A
  1. Peptic ulcer disease
  2. Gastric adenocarcinoma, intestinal type
  3. Mucosa associated lymphoid tissue lymphoma (MALToma)
57
Q

Chronic Gastritis - Autoimmune

A
  • CD4+ T cell mediated immune response against parietal cells. Development of autoantibodies to parietal cells, intrinsic factor and acid producing enzyme H+ ,K+ -ATPase
  • Loss of parietal cells leads to achlorhydria causing G cell hyperplasia and secondary hypergastrinemia that leads to Enterochromaffin-like (ECL) cell hyperplasia (in gastric body and fundus) and carcinoid tumors
  • Loss of intrinsic factor leads to vitamin B12 deficiency causing pernicious anemia and subacute combined degeneration of spinal cord. Achlorhydria leads to iron deficiency anemia
  • It is seen in association with other autoimmune diseases such as Hashimoto’s thyroiditis and Addison’s disease
58
Q

Chronic Gastritis Gross Findings (regardless of etiology)

A

•The mucosa varies from normal to slight erythema and boggy appearance. With H. pylori gastritis, these findings occur in any area of the stomach in a patchy manner; with autoimmune gastritis, they are confined to the body and fundus in a diffuse and confluent manner.

59
Q

Chronic Gastritis Microscopic Findings (regardless of etiology)

A
  • The lamina propria has a lympho-plasmacytic inflammatory infiltrate with neutrophils (activity) within the glandular and surface epithelium.
  • There are regenerative epithelial changes, variable gland loss and ultimate mucosal atrophy.
  • Intestinal metaplasia of either small or large bowel type, with a risk for development of dysplasia and adenocarcinoma

*With H. pylori: the bacterium is found in mucous layer overlying the gastric epithelium (including ectopic gastric mucosa) and does not invade the tissue

*With autoimmune gastritis: loss of parietal cells, G-cell and mucin secreting cell hyperplasia, carcinoid

60
Q

Chronic Gastritis Clinical Features (regardless of etiology)

A
  • Usually asymptomatic, but upper abdominal discomfort, nausea, and vomiting can occur.
  • Patients with environmental causes (H. pylori) often develop hypochlorhydria but not achlorhydria; gastrin levels are usually normal or modestly elevated.
  • Patients with longstanding autoimmune gastritis, characteristically develop hypochlorhydria or achlorhydria and hypergastrinemia as well as autoantibodies to parietal cells and intrinsic factor.
61
Q

Peptic Ulcer Disease

A

An ulcer is a disruption of the surface mucosa extending beyond the muscularis mucosae. They are chronic, most often solitary lesions that occur at any level of the GI tract, exposed to the aggressive action of acid-peptic juices.

62
Q

Peptic Ulcer Disease - Epidemiology

A
  • The lifetime likelihood of developing a peptic ulcer is ~10% for American men and ~4% for American women
  • Genetic influences play little or no role.
  • Top most etiologic association for gastric and duodenal ulcers: H. pylori, NSAIDs, cigarette smoking.
63
Q

Peptic Ulcer Disease - Pathogenesis

A
  • Appear to be produced by an imbalance between the gastroduodenal mucosal defense mechanisms and the damaging forces.
  • Mucosal exposure to gastric acid and pepsin is essential for the development of peptic ulcers.
64
Q

Peptic Ulcer Disease - Etiology

A
  • H. pylori: Plays an important role in the pathogenesis of PUD: its products directly damage mucosal epithelial cells. The products of the inflammatory cells it attracts also destroy epithelial cells and produce capillary thrombosis. The chronically inflamed mucosa is more susceptible to acid injury. Despite this, only about 10-20% of infected people develop PUD. Antibiotic therapy promotes healing of ulcers and prevents recurrence. In patients with duodenal ulcers, H. pylori is limited to the stomach; it is believed that the ammonia H. pylori produces stimulates gastrin release, thereby paradoxically increasing acid production.
  • NSAID’s: they suppress mucosal prostaglandin synthesis; aspirin is also a direct irritant.
  • Cigarette smoking: impairs mucosal blood flow and healing.

Corticosteroids, in high dose and with repeated use promote ulcer formation. Alcoholic cirrhosis, COPD, CRF and hyperparathyroidism are associated with a higher incidence of duodenal ulcer. Hypercalcemia (present in the latter two conditions) is believed to be ulcerogenic.

65
Q

Peptic Ulcer Disease - Gross Findings

A

•Anatomical location with decreasing frequency:

  • Duodenum, first portion, anterior and posterior wall -Stomach, lesser curvature and antrum-pyloric region -Within Barrett’s mucosa
  • At gastroenterostomy margin (stomal ulcer)
  • In duodenum, stomach or jejunum (Zollinger-Ellison syndrome)
  • Within or adjacent to Meckel’s diverticulum that contains gastric mucosa
  • Usually single, however 10-20% of gastric ulcer patients have a concomitant duodenal ulcer.
  • The majority are small (<2cm), round to oval in shape (size alone does not differentiate between a peptic ulcer from an ulcerated gastric cancer.
  • Edge of ulcer is at mucosal level or slightly elevated with mucosal folds radiating from the ulcer edge.
  • Ulcer base is smooth and “clean” because peptic secretions digest any exudate.
  • In contrast, malignant ulcer has heaped up edges without radiating mucosal folds. The base of malignant ulcer contains necrotic debris. Penetrates muscularis mucosae into muscularis propria and may perforate gastric wall to the extent that the ulcer bed may be formed by adherent pancreas, fat or liver
66
Q

Gross features of benign versus malignant ulcer

A
67
Q

Peptic Ulcer Disease - Microscopic Findings

A

•Most active peptic ulcers display the following zones:

  • Ulcer base has amorphous, fibrinoid eosinophilic debris.
  • Inflammatory infiltrate with neutrophils.
  • Granulation tissue with mixed inflammation Fibrous / collagenous scar.

*Note: chronic gastritis is almost always coexistent.

68
Q

Peptic Ulcer Disease - Clinical Course

A
  • Chronic, recurrent epigastric pain, worst at night and usually 1-3 hrs after a meal, typically relieved by alkalis or food;
  • uncommonly there is nausea, vomiting, belching and significant weight loss.
  • With penetrating ulcers, the pain may be referred to the back, to the left upper quadrant or to the chest, mimicking an MI.
  • Complications include bleeding, perforation, gastric outlet obstruction and intractable pain.
69
Q

Peptic Ulcer Disease - Diagnosis

A

•Clinical history, imaging techniques, endoscopy In older patients with suspected gastric ulcer, endoscopic biopsy or brushes are performed to rule out malignancy

70
Q

Hypertrophic Gastropathy

A

•Giant cerebriform enlargement of rugal folds, secondary to hyperplasia of epithelial cells without significant inflammation. It’s very rare. The recognized 2 variants are as follows:

  • Menetrier’s Disease
  • Zollinger- Ellison Disease
  • hypertrophic hypersecretory gastropathy
71
Q

Menetrier’s Disease

A
  • Diffuse hyperplasia of surface mucous/foveolar cells of body and fundus with accompanying glandular (parietal and chief cell) atrophy.
  • Spares antrum.
  • Associated with increased secretion of transforming growth factor α.
  • Most common in Adults in 4-6th decade, but may happen in children
  • Presents with protein losing enteropathy.
  • Diarrhea, weight loss and peripheral edema may be present.
  • Gastric secretions contain excessive mucous and little or no acid There often is hypoalbuminemia and peripheral edema Metaplasia may develop and with it the risk for malignancy
72
Q

Zollinger-Ellison Syndrome

A
  • Gastric gland (mucus and parietal cell) hyperplasia secondary to excessive gastrin secretion, in the setting of a gastrinoma (Zollinger-Ellison syndrome) .
  • The hyperacidity predisposes patients to extensive peptic ulceration (especially duodenal), chronic diarrhea and carcinoid tumors in stomach.
  • Associated with MEN I in 25% of patients.

These conditions are of clinical importance because:

a) they may mimic an infiltrating carcinoma or lymphoma on radiographic and endoscopic examination and
b) the risk of peptic ulcer in the latter condition.

73
Q

Gastric Tumors - Polyps

A

•any nodule or mass arising from the mucosa, that protrudes above its level. They may be pedunculated (attached to the stomach by a thin stalk) or sessile (flat).

74
Q

Gastric Tumors - Inflammatory/Hyperplastic

A
  • benign
  • >90%
  • usually small, may be single or multiple, occur in a background of chronic gastritis and have NO malignant potential
75
Q

Gastric Tumors - Adenoma

A
  • benign
  • 10%
  • Vary in size, usually single, most are located in the antrum, risk of MALIGNANT change increases with polyp size, occur in a background of chronic gastritis and intestinal metaplasia. May be sessile or pedunculated. Microscopically they are composed of dysplastic epithelium similar to colon polyps. Increased incidence in FAP
  • NOTE: Because gastric polyps cannot be reliably classified grossly, biopsy for histological examination is mandatory.
76
Q

Gastric Tumors - Mesenchymal

A
  • benign
  • 2%
  • leiomyomas, leiomyoblastomas, lipomas and stromal tumors.
  • They may protrude into the mucosa as a polypoid mass.
77
Q

Gastric Tumors - Adenocarcinoma Epidemiology and Classification

A
  • malignant
  • 90-95%
  • Incidence varies with geographic location (Japan, Eastern Europe > US and Canada)
  • Steady decline in incidence and mortality worldwide.
  • H. pylori infection mucosal atrophy, intestinal metaplasia and dysplasia are recognized precursor lesions.
  • PUD does not increase risk of gastric carcinoma.
  • Carcinoma of gastric cardia (close to GEJ) is similar to esophageal adenocarcinoma with GERD, BE and dysplasia as the precursor lesions. Rising in incidence.

*Incidence:

  • Intestinal type: ~55 years of age; male to female ratio: 2:1
  • Diffuse type: ~48 years of age; with equal male to female ratio
78
Q

Gastric Tumors - Adenocarcinoma - Pathogenesis Environmental

A

•Diet, low socio-economic status, cigarette smoking Host Factors: H. pylori infection leading to chronic gastritis and intestinal metaplasia which may become dysplastic; autoimmune gastritis, partial gastrectomy and gastric adenomas

79
Q

Gastric Tumors - Adenocarcinoma - Pathogenesis Genetic

A
  • Diffuse gastric cancer: Loss of function mutation in tumor suppressor gene CDH1, with loss of E-cadherin expression.
  • Familial or sporadic.
  • Intestinal type: Wnt-β-catenin signaling pathway mutations. Increased incidence in FAP.
80
Q

Gastric Tumors - Adenocarcinoma Classification

A
  • Intestinal type: arise from dysplastic intestinal metaplastic mucosa; incidence in the USA is diminishing
  • Diffuse type: arises de novo from native mucous cells; incidence remains steady
81
Q

Gastric Tumors - Adenocarcinoma Pathologic Features

A
  • Intestinal type: the majority grow as an exophitic, flat or excavated lesion, on the lesser curvature of the antro-pyloric region less often in the cardia and body and fundus. Microscopically, there is gland formation resembling adenocarcinomas from the colon.
  • Diffuse type: they diffusely infiltrate the stomach wall, giving it a “leather bottle” shape and consistency, also known as linitis plastica. Microscopically they are poorly differentiated; they infiltrate in small cell clusters and a single cell pattern where the nucleus is pushed peripherally by a mucin vacuole (so called “signet ring” cell)
82
Q

Gastric Tumors - Adenocarcinoma Clinical Features

A
  • In the early stages it is asymptomatic.
  • Weight loss, abdominal pain, anorexia and chronic blood loss may occur late in the disease. Depending on location, they may produce gastric outlet obstruction. It invades the stomach wall and metastasize to regional lymph nodes, liver and distant sites.
83
Q

Gastric Tumors - Adenocarcinoma Unusual Presentations

A
  • In females, as metastases to the ovaries (known as Krukenberg tumor)
  • Metastasis to the supraclavicular sentinel node (Virchow node)
  • Prognosis: depends on the depth of invasion and extent of metastases:
  • Early type: invades mucosa and submucosa with or without regional lymph node involvement and has a 90-95% 5-year survival
  • Late type: invades beyond the submucosa and has < 15% 5-year survival.
84
Q

Gastric Lymphoma

A
  • Most are non-Hodgkin’s type
  • The GI is the most common site of extranodal lymphomas
  • Most are of the mucosa-associated lymphoid tissue (MALTomas) and related to chronic H. pylori infection
  • Most are of B-cell type, either low grade or high grade
  • Extranodal marginal zone B-cell lymphoma, aka MALToma
  • Epstein Barr virus related B-cell lymphomas in immunosuppressed patients
  • Diffuse large B-cell lymphoma
85
Q

Carcinoid Tumors

A
  • Stomach carcinoids arise from epithelial neuroendocrine cells and are rare
  • They are usually small and discovered as an incidental lesion.
  • Associated with endocrine cell hyperplasia, autoimmune chronic atrophic gastritis, MEN-1, ZE syndrome.
  • Better prognosis.
86
Q

MALToma

A

• Lymphoma of Mucosa associated lymphoid tissue: Low grade lymphoma of mature B cells

– Secondary to chronic inflammation due to long term H. pylori infection

– 75-80% lymphomas regress with H.pylori eradication treatment

• Failure of H.pylori eradication to induce remission is associated with progression of disease

87
Q

Neuroendocrine Tumor (Carcinoid) Gastrin vs. Nongastrin

A
88
Q

Gastrointestinal Tumor (GIST)

A
  • Most common mesenchymal tumor of stomach and abdomen - can be maignant or benign
  • Located in muscularis propria
  • Arise from interstitial cells of Cajal (pacemaker cells)
  • May be sporadic, familial or syndromic (Carney triad, Carney-Stratakis syndrome)
  • May be incidental or present with mass effects, if big
89
Q

Gastrointestinal Tumor (GIST) - Pathogenesis

A
  • >80% have oncogenic gain of function mutation of receptor tyrosine kinase KIT
  • Next most common mutation: receptor tyrosine kinase PDGFRA (platelet derived growth factor alpha) – Constitutive activation of tyrosine kinase receptors with increased proliferation and survival of cells –> tumor
90
Q

GIST

A
  • surface untouched, mucosa intact
  • invasion of muscularis propria
  • spindle cells
91
Q

Adenocarcinoma Intestinal vs. Diffuse

A

DMH Part 1 (35 decks)

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