Transcript Slide 1

STOMACH Cell types:
Mucosal surface & foveolae:
Surface foveolar cells - secrete mucous
Mucous neck cells - progenitor cells
Glands:
Mucous cells - secrete mucous & pepsinogen II
Parietal cells - secrete HCl & IF
Chief cells - secrete pepsinogen I & II
Endocrine cells - secrete peptide & amine
hormones
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Congenital Anomalies
CONGENITAL ANOMALIES
Diaphragmatic Hernia:
Defect in diaphragm, away from
esophageal hiatus
Portions of stomach & SI herniate 
pulmonary hypoplasia & respiratory
impairment
CONGENITAL ANOMALIES
Heterotopic rests:
Location: Anywhere in the GIT
MC: Pancreatic & gastric
S/S: Usually asymptomatic but may cause
ulceration
CONGENITAL ANOMALIES
 Congenital Hypertrophic Pyloric Stenosis:CHiPs
 M > F (3:1), 1 in 200 infant males, multifactorial
inheritance
 Cause:
Hypertrophy & hyperplasia of circular muscle of pylorus
 regurgitation, projectile non- bilious vomiting
commences at 2 - 6 wks of age
May be due to defective autonomic regulation
 Dx: Visible peristalsis & palpable mass in RUQ
 Tx: Pyloromyotomy is curative
ACUTE GASTRITIS
Other Causes:
Ingestion of strong acids or alkali
Ca chemotx
Radiation
Ischemia & shock
NGTs
- Reduced mucosal blood flow
- Direct damage to mucosal epithelium
ACUTE GASTRITIS
Clinically:
Asymptomatic to epigastric pain of varying
severity, up to acute abdomen w/
hematemesis & shock
major cause of massive hematemesis
(esp. alcoholics)
Common in those who take daily aspirin
for RA
ACUTE GASTRITIS
Morphology:
Mucosal edema & congestion, PMN
infiltration (milder cases)
Erosions (not deeper than muscularis
mucosa) & hges (acute erosive gastritis)
/ dysplasia
CHRONIC GASTRITIS
Pathogenesis:
Autoimmune: Abs to parietal cells
parietal cell destruction ( HCl & IF)
Environmental:
Chronic infection by H. pylori
Alcohol, tobacco, radiation, bile reflux, Crohn’s
disease, uremia, gastric atony
CHRONIC GASTRITIS
Gross:
Red mucosa (thickened or flattened)
Autoimmune  fundus & body
H pylori  antrum & body
Bile reflux  antrum
CHRONIC GASTRITIS
 Histology:
 Others:
 Lympho & plasma cell
infiltrates in LP
(superficial or
involving entire
mucosal thickness)
 Regenerative atypia
 Intestinal metaplasia
 Atrophy
 Dysplasia
CHRONIC GASTRITIS
Clinical:
Mild abdominal discomfort, nausea,
vomiting, hypochlorhydria
Autoimmune gastritis:
Hypo- / a- chlorhydria, hypergastrinemia, ~
10%  overt PA, long-term risk of Ca is 24%
Helicobacter pylori
 ~ 50% of
asymptomatic
American adults > 50
yrs are infected
 Dx: CLO test
 Diseases Association:
 Chronic gastritis
 PUD
 Gastric ca/ lymphoma
PEPTIC ULCERS
Usually solitary ~ 0.6 - 4 cm
MC: duodenum & antrum
Ratio of duodenal: gastric PU is ~ 4 : 1
~ 4 M Americans have PU
Life-time incidence in USA is 10% for men
& 4% for women
PEPTIC ULCERS
 Clinical:
 Complications:
 Epigastric pain 1-3 hrs
PC & worse at night;
nausea; vomiting;
belching, weight loss
 Hemorrhage - 25% of
ulcer deaths
 Perforation - ~ 2/3 of
ulcer deaths
 Obstruction - causes
severe crampy abdominal
pain
 Malignant transformation
extremely rare
HYPERTROPHIC GASTROPATHTY
 Zollinger-Ellison Syndrome:
 Hypertrophic rugal folds
 Parietal cell hyperplasia
 Peptic ulcers
 Markedly elevated serum gastrin levels
 Caused by a gastrin secreting tumor
(gastrinoma)
 Pancreas is the usual primary site
HYPERTROPHIC GASTROPATHY
 Menetrier’s disease:
 Affects men in 4th to 6th decades
 Epigastric pain, anorexia, vomitting, wt. loss &
peripheral edema
 Diffuse rugal hypertrophy
 Marked foveolar hyperplasia, smooth muscle
proliferation in LP, glandular atrophy
 Hypochlorhydria
 Protein-losing enteropathy
GASTRIC POLYPS
 Mucosal masses projecting above level of
surrounding mucosa
 > 90% non-neoplastic polyps - no malignant
potential
 Hyperplastic polyps:
 MC type of gastric polyp
 Small sessile polyps
 May be multiple
 No dysplasia  no malignant potential
GASTRIC POLYPS (CONT.)
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 Adenomatous polyps (Adenomas):
May be sessile or pedunculated
Usually solitary
May reach 3-4 cm in dia
Contain proliferating dysplastic epithelium
Are true neoplasms
Up to 40% contain a focus of ca at time of biopsy
Patients with autoimmune gastritis or colonic polyposis
Syndromes have an increased incidence
Gastric polyps need to be biopsied
GASTRIC CARCINOMA
Worldwide distribution variable
US 2.5% of all Ca deaths
5-6 fold decline in incidence over last 70
yrs (for unknown reasons)
GASTRIC CARCINOMA
Classification:
 According to Depth of invasion:
 Early Gastric Ca:
 Confined to mucosa & submucosa
 Very good prognosis - ~ 90% 5-year survival, even
w/ limited LN spread
 Advanced Gastric Ca:
 Extended beyond submucosa
 Spread by local invasion, lymphatics, blood (to liver,
lungs & bone)
 Virchow node
 Bilateral ovarian metastases - Krukenberg
 Poor prognosis (<15% 5-year survival)
GASTRIC CARCINOMA
Classification:
According to Gross Pattern:
Exophytic
Flat/depressed
Excavated (ulcerative)
According to Histologic Pattern:
Intestinal type, glandular, expansile
Diffuse type, “signet ring cell”, infiltrating
(linitis plastica)
GASTRIC CARCINOMA
Classification:
Pathologic stage is the most important
prognostic indicator
Less Common Gastric Tumors:
Lymphomas (~ 5%)
Stromal tumors (~ 2%)
Carcinoid tumors (rare)
GASTRIC CARCINOMA
 Risk Factors:
 Diet: Nitrites (food preservatives), smoked &
salted foods, deficiency of fresh fruits &
vegetables
 Host Factors: chronic gastritis (autoimmune & H.
pylori), adenomatous polyps, partial
gastrectomy
 Genetic Factors: only ~ 4% of patient’s w/ gastric
CA have a family Hx