Escolar Documentos
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Cultura Documentos
the Stomach
Aiman Zaher, MD
Objectives
At the end of this segment, when given a
clinical presentation, gross specimen and/or
photomicrograph, students will be able to:
Compare and contrast the clinical presentations,
etiologies, pathogenesis, gross and microscopic
changes found in developmental, inflammatory,
circulatory, mechanical, and neoplastic disorders
of the stomach.
Objectives
At the end of this segment, when given a
clinical presentation, gross specimen and/or
photomicrograph, students will be able to:
Predict the clinical complications associated with
diseases of the stomach.
Define the words in the glossary.
Glossary
Peptic ulcers
Phytobezoars
Pyloric stenosis
Rugae
Trichobezoars
Ulcers in cancer
Normal Anatomy
Robbins
7th Edition,
Fig. 17-12a
Rugae = longitudinal
infoldings of both mucosa
and submucosa on the
inner surface of the
stomach
Gastric wall comprised of a
mucosa, submucosa,
muscularis propria, and
serosa
Congenital
Anomalies
Congenital Anomalies
Heterotopic rests
Pancreatic rests located in the pylorus become
inflamed leading to obstruction
Gastric rests in duodenum or more distal sites
undergo peptic ulceration, leading to bleeding
Gastric rests in upper esophagus lead to
inflammation and discomfort
Diaphragmatic hernia
Results from defective closure of the diaphragm,
usually on the left
May be asymptomatic or cause respiratory
problems for newborns
Congenital Anomalies
Pyloric Stenosis (Congenital Hypertrophic Pyloric Stenosis)
Incidence 1/300-900 live births
M:F = 3-4:1
May be associated with Turner Syndrome, Trisomy 18
and esophageal atresia
Presents as regurgitation and persistent projectile
vomiting at 2-3 weeks of age
Results from hypertrophy and possibly hyperplasia of
muscularis propria of pylorus
(Pyloric stenosis can also be acquired in adults as a
complication of antral gastritis, peptic ulcer, carcinoma,
or prolonged pyloric spasm.)
Pyloric Stenosis
-Morphology
PJ Goldblatt, MD
Hypertrophy of
Muscularis Propria
Inflammatory
Diseases
Gastritis
Definition
Inflammation of the gastric mucosa
Histologic diagnosis!
Acute Gastritis
Definition
An acute mucosal inflammatory process, with
neutrophilic infiltrate, that is usually transient.
There may be hemorrhage into the mucosa or
sloughing of the mucosa.
Severe erosive form is an important cause of
severe GI bleeding
Acute Gastritis
Etiology
Frequently associated with, among others:
Often, idiopathic
Acid secretion +
+ back diffusion
Bicarbonate
buffer
+
Direct
Mucosal
Injury
Disruption
of
Mucus layer
Acute Gastritis
Blood flow
PJ Goldblatt, MD
PJ Goldblatt, MD
PJ Goldblatt,
MD
Acute Gastritis
Clinical Features
broad range of signs and symptoms that depend on the
severity of the the condition
Asymptomatic
Epigastric pain, nausea & vomiting
Hemorrhage, massive hematemesis, melena, or fatal blood loss
Chronic Gastritis
Definition
Chronic mucosal inflammatory changes leading to
atrophy and metaplasia (usually without erosions)
Chronic Gastritis
Etiology
Many causes but two important types:
90% of patients with antral chronic gastritis:
Helicobacter pylori infected
Motile, gram negative curvilinear rods that elaborate
urease (buffers gastric acid) & toxins and have adhesins
to bind to the epithelium
Colonization rate increases with age: 50% of adults over
50 in the US
Chronic Gastritis
Pathogenesis
H. pylori (urease NH4+ + toxins) + Host (acid + peptic
enzymes) Chronic Inflammation
Antibodies Gland destruction + Mucosal atrophy
acid intrinsic factor (which can lead to pernicious
anemia)
Chronic Gastritis
Morphology
PJ Goldblatt, MD
Chronic Gastritis
Clinical Features
Usually only a few symptoms: nausea, vomiting,
upper abdominal discomfort
H. pylori
Most infected person have gastritis, but are
asymptomatic
Hypochlorhydria, but NOT achlorhydria and pernicious
anemia (parietal cells never completely destroyed)
Gastrin normal to slightly elevated
Antibiotics are treatment of choice
Autoimmune Form
Hypo to achlorhydria (severe loss of parietal glands)
Hypergastrinemia
10% have pernicious anemia
Chronic Gastritis
Clinical Complications
H. pylori
H. pylori predisposes to peptic ulcers in duodenum and
stomachMost patients with a peptic ulcer are infected.
Risk of gastric carcinoma and lymphoma
Autoimmune Form
Often seen in association with other autoimmune
disorders (Hashimoto thyroiditis, Addison disease, and
type I diabetes)
Significant risk for the development of gastric
carcinoma (2-4%) and endocrine tumors (carcinoid
tumor)
Peptic Ulcers
Definition
A breach in the mucosa that extends into the
submucosa or deeper.
Chronic relapsing and solitary lesions, <4 cm
diameter (except in Zollinger-Ellison Syndrome)
Location
Can occur anywhere in the GI tract where there is
exposure to acid/peptic juices, but most common
in the duodenum and stomach
Peptic Ulcers
About 10% of American men and 4%
American women will develop them.
Diagnosed middle-aged to older adults.
M:F; gastric 1.5-2:1; Duodenal 3:1; women
after menopause.
Recently, decreased incidence of duodenal
ulcers for unknown reasons, but not gastric
ulcers
Peptic Ulcers
Etiology and Pathogenesis
Appear to be produced by imbalances between
the gastroduodenal mucosal defense mechanisms
and the damaging forces of gastric acid and
pepsin.
Hyperacidity is not a pre-requisite since only a
minority have it with duodenal ulcers, and even
fewer with gastric ulcers
Ulceration occurs when
mucosal blood flow decreased
gastric emptying is delayed
epithelial restitution is impaired
Robbins
7th Edition,
Fig 17-7
GRIPE
GRIPE
GRIPE
Peptic Ulcers
Clinical Features
Zollinger-Ellison Syndrome
Multiple peptic ulcerations in the stomach,
duodenum, and jejunum
Due to excess gastrin secretion by a tumor
(gastrinoma), leading to excess gastric acid
production
Mechanical
Gastric Dilation
Etiology and Pathogenesis
Outlet obstruction
pyloric stenosis
paralytic ileus
intralumenal concretions e.g. bezoars
Trichobezoar
Other bezoars
PJ Goldblatt, MD
Hypertrophic Gastropathy
Definition
Characterized by cerebriform enlargement of the
gastric rugal folds
Caused by mucosal epithelial hyperplasia, without
inflammation
Hypertrophic Gastropathy
Types
Mntriers disease:
occurs in males in the 4th-6th decades
hyperplasia of mucous cells, with atrophy of glands
gastric secretions contain excessive mucus and little acid
protein loss hypoproteinemia (protein-losing
gastropathy)
Hypertrophic-hypersecretory gastropathy:
hyperplasia of parietal and chief cells in gastric glands
Morphology
PJ Goldblatt, MD
Neoplasms
Benign Processes
Hyperplasic Polyps
Mucosal masses that project above the level of
the surrounding mucosa, single or multiple
Majority in patients with achlorhydria, atrophic
gastritis and pernicious anemia
Most often seen with chronic gastritis
No malignant potential
Benign Processes
Adenomas
True neoplasms with proliferative dysplastic
epithelium
Have malignant potential
Usually single and in the antrum
Sessile or pedunculated
Incidence goes up with age, especially the 70s
M:F 2:1
40% have malignant foci when removed and risk of
malignancy in adjacent mucosa as high as 30%
Associated with chronic gastritis with intestinal
metaplasia and autoimmune gastritis
Gastric Carcinoma
Epidemiology
90-95% of malignant tumors of the stomach are
carcinoma
Second most common tumor in the world
Incidence particularly high in Japan, parts of South
America, China, Portugal, Russia, and Bulgaria; but 4-6X
less common in the US, UK, Canada, Australia
Gastric Carcinoma
Risk Factors
Environmental: Nitrites (from food preservatives),
smoked and salted foods, pickled vegetables,
deficiency of fresh fruits and vegetables, cigarette
smoking
Host Factors: chronic atrophic gastritis,
adenomatous polyps, partial gastrectomy and H.
pylori infection (risk increased 5-6X)
Genetic Factors: more common in persons with
blood group A, family history of gastric cancer
Gastric Carcinoma
Classification
Depth of Invasion
Greatest impact on clinical outcome
Early form confined to mucosa and submucosa. Good
prognosis (90-95% 5-year survival rate with surgical
treatment)
Advanced form has extended into muscular wall.
Spread is by local invasion, lymphatics, blood (to liver
and lungs) and trans-celomic. Bad Prognosis (<15% 5year survival)
Gastric Carcinoma
Classification
According to Macroscopic Growth Pattern:
Present in both early and advanced forms
Gastric Carcinoma
Location
Curvatures
40% - Lesser Curvature
12% - Greater Curvature
Other
50-60% - Pylorus and Antrum
25% - Cardia
Remander Body and Fundus
th
Edition
GRIPE
GRIPE
Web Path
Web Path
Web Path
Web Path
Web Path
Gastric Carcinoma
Clinical Features
Insidious disease
Asymptomatic until late in the course
Weight loss, abdominal pain, anorexia, vomiting, altered
bowel habits
Sometimes dysphagia, anemia, and hemorrhage
Early detection important
Japan uses endoscopic screening programs, resulting in 35% of
newly diagnosed gastric carcinoma being found in an early stage
US & Europe only catch 10-15% in the early stage
Gastric Carcinoma
Clinical Complications
Local invasion of pancreas, duodenum, and
retroperitoneum
At death, peritoneum seeded and mets to liver and lungs
common.
Metastasis to regional and distant nodes
Frequently mets to Virchows node (supraclavicular node) as
the first clinical manifestation
Prognosis
Determined by depth of penetration and extent of nodal
involvement, not histology
Surgical resection w/ or w/out adjuvant chemotherapy
and radiation
References
Kumar, Abbas, & Fausto: ROBBINS & COTRAN
PATHOLOGIC BASIS OF DISEASE, 7th Edition,
pp. 810-827.