2. Melena: dark, tarry stools signify a bleed proximal to the duodenojejunal junction.
B. Pyloric stenosis
1. Congenital pyloric obstruction: occurs in 1:500 live births; more common in boys; multifactorial inheritance 2. Pathogenesis: progressive hypertrophy of the circular
muscles in the pyloric sphincter occurs over the ensuing 2-4 weeks
3. Clinical findings: projectile vomiting of non—bile- stained fluid 2-4 weeks after birth
4. Acquired pyloric obstruction: complication of chronic duodenal ulcer disease
C. Gastritis
1. Acute hemorrhagic (erosive) gastritis
a. Etiology: bleeding results from erosions (breach in the epithelium of the mucosa) and is caused by:
(1) Nonsteroidal anti-inflammatory drugs (NSAIDs)
(2) Smoking tobacco, alcohol, burns, central nervous system injury, uremia, consumption of Anisakis (worm in raw fish)
b. Clinical findings: hematemesis, melena, iron deficiency
2. Chronic atrophic gastritis
a. Type A: involves the body and fundus of the stomach
(1) Most commonly caused by autoimmune destruction of parietal cells (e.g., pernicious anemia)
(2) Complications: achlorhydria with hypergas- trinemia, macrocytic anemia, increased risk of adenocarcinoma
b. Type B: involves the antrum and pylorus of the stomach
(1) Commonly caused by Helicobacter pylori:
produces urease and cytotoxins; colonizes the mucous layer that lines the mucosa
(2) Microscopic findings: chronic inflammatory infiltrate in the lamina propria consisting mainly of lymphocytes with prominent germi- nal follicles; the intestinal metaplasia (goblet cells, Paneth cells) is a precursor of adenocar- cinoma.
(3) Tests used to identify H. pylori: tests that detect urease; serologic tests
Most common cause of gastritis.
NSAIDs
Most common cause of type B chronic atrophic gas- tritis: H. pylori
208 Pathology
TABLE 17-2 Comparison of Gastric Ulcers and Duodenal Ulcers
Feature Gastric Ulcers Duodenal Ulcers
Percent of ulcer cases 25% 75%
Epidemiology Male:female ratio: 1:1; risk Male:female ratio: 2:1; risk increased with blood increased with blood group
group A 0 and MEN I
Smoking does not cause Increased in cirrhosis, COPD, PUD but delays healing renal failure, hyperparathy-
roidism Helicobacter pylori - 80% of cases 90-95% of cases
Pathogenesis Defective mucosal barrier Defective mucosal barrier due due to H. pylori to H. pylori
Mucosal ischemia (reduced Increased acid production PGE), bile reflux, delayed (increased parietal cell mass) gastric emptying
Location Single ulcer on lesser Single ulcer on anterior curvature of antrum; portion of first part of same location for cancer duodenum followed by
single ulcer on posterior portion (danger of perfora- tion into pancreas) Complications Bleeding (most commonly Bleeding (most commonly in
in left gastric artery) gastroduodenal artery) Perforation Perforation (air under
diaphragm, pain radiates to left shoulder)
Gastric outlet obstruction;
pancreatitis
Clinical findings Burning epigastric pain Burning epigastric pain 1-3 soon after eating hours after eating
COPD, chronic obstructive pulmonary disease; MEN, multiple endocrine neoplasia; PGE, prostaglandin E
(4) Complications: cancers associated with H.
pylori (e.g., gastric adenocarcinoma, low-grade B-cell malignant lymphoma)
c. Menetrier's disease: hypertrophic gastropathy (1) Characterized by giant rugal folds caused by
hyperplasia of mucus-secreting cells and hypo- proteinemia
(2) Results in atrophy of parietal cells (achlor- hydria) and risk of adenocarcinoma
D. Peptic ulcer disease (PUD) (Table 17-2)
1. Ulcers are breaches in the mucosa that extend into the submucosa or deeper.
2. Peptic ulcers occur in the stomach or in the first part of the duodenum.
3. All peptic ulcers (gastric or duodenal) are identical in appearance.
a. Gross: clean, sharply demarcated lesions that are slightly elevated at the edges
Most common cause of gastric and duodenal ulcers:
H pylori
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Chapter 17 Gastrointestinal Disorders 209 b. Microscopic: four layers: necrotic debris; inflam-
mation, with neutrophils predominating; granula- tion (repair) tissue; fibrotic tissue
4. Zollinger-Ellison syndrome: malignant islet cell gastrin-secreting tumor
a. Located in pancreatic islet cells; associated with multiple endocrine neoplasia type I (20-30% of cases)
b. Clinical findings: epigastric pain with weight loss, peptic ulceration (single or multiple), diarrhea c. Laboratory findings
(1) Increased basal and maximal output of acid (2) Serum gastrin > 1000 pg/mL
E. Gastric polyps and tumors
1. Gastric polyps: develop in the setting of chronic gastri- tis and achlorhydria
a. Hyperplastic polyps (most common): hamartomas with no malignant potential
b. Adenomatous polyps: neoplastic and usually sessile; potential for malignant transformation if polyps > 2 cm
2. Leiomyoma: stomach is most common gastrointesti- nal (GI) site; may ulcerate or bleed; no malignant potential
3. Gastric adenocarcinoma: intestinal type
a. Epidemiology: decreased incidence in the United States; increased in Japan; occurs most often in men
b. Risk factors: H. pylori, nitrosamines, smoked foods, diet lacking fruits and vegetables (decreased anti- oxidants), type A gastritis, Menetrier's disease, ade- nomatous polyps
c. Precursor lesion: intestinal metaplasia
d. Locations: lesser curvature of pylorus and antrum (50-60% of cases), cardia (25% of cases), body and fundus
e. Gross and microscopic findings: polypoid, ulcer- ated appearance
(1) Early lesions are confined to the mucosa and submucosa.
(2) Advanced lesions extend into the muscle wall.
f. Clinical findings
(1) Weight loss, epigastric pain
(2) Paraneoplastic lesions (acanthosis nigricans, multiple outcroppings of seborrheic keratoses)
g. Common metastatic sites: lymph nodes (especially left supraclavicular node), liver, lungs, ovaries h. Prognosis: overall 5-year survival rate about 20%
4. Gastric adenocarcinoma: diffuse type (less common) a. No association with chronic gastritis or H. pylori b. Characterized by diffuse infiltration of the
stomach wall (linitis plastica) and no peristalsis;
Most common cause of hemateme- sis and melena:
PUD
Most common cause of gastric ade- nocarcinoma:
H. pylori
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210 Pathology
composed of "signet-ring" cells (mucin-filled neo- plastic cells with the nucleus pushed to the
periphery)
c. Hematogenous spread, causing bilateral Kruken- berg tumors in ovaries
5. Primary gastric malignant lymphoma
a. Stomach is the most common site of extranodal malignant lymphomas.
b. Low-grade B-cell lymphoma: MALToma;
H. pylon-related
c. High-grade lymphomas: B- or T-cell lymphomas V. Disorders of the Small and Large Bowels