GI tract Flashcards
Gastric ectopia of the esophagus: Histology.
Oxyntic mucosa usually.
May undergo intestinal metaplasia.
Gastric ectopia in the esophagus:
A. Synonym.
B. Location.
C. Clinical features.
A. Inlet pouch.
B. Cervical esophagus.
C. Older patients may have peptic symptoms.
Sebaceous ectopia in the esophagus: Synonym.
Fordyce’s granules.
Pancreatic ectopia in the esophagus: Associations (3).
Metaplasia due to reflux.
Trisomy 13 or 18.
Pancreatic ectopia of the esophagus:
A. Gross pathology.
B. Histology.
A. Submucosal mass that may have a central pore.
B. Usually acinar but can contain islet cells also.
Esophageal atresia: Types.
I: No fistula.
II: Proximal fistula only.
III: Distal fistula only.
IV: Proximal and distal fistulae.
Esophageal atresia: Clinical presentation.
Choking during feeding; excessive drooling.
Esophageal atresia: Associated syndromes.
Down’s syndrome.
VATER syndrome.
Congenital esophageal duplication: Gross pathology.
Cyst (most often), diverticulum, or tubule.
May be intramural or extramural.
Congenital esophageal duplication: Histology (2).
Lining: Respiratory, gastric, intestinal, or squamous.
Wall: Two layers of muscularis propria.
Plummer-Vinson syndrome:
A. Clinical triad.
B. Esophageal lesions.
A. Iron-deficiency anemia, cheilitis, glossitis.
B. Proximal webs, predisposition to proximal SCC.
Plummer-Vinson syndrome: Other association.
Autoimmune diseases.
Esophageal web: Histology.
Fibrovascular core without muscle.
Proximal lining: Squamous mucosa.
Distal lining: Squamous or gastric mucosa.
Esophageal ring: Cause.
Constriction due, e.g., to reflux or scleroderma.
Esophageal ring: Types.
Muscular.
Mucosal.
Schatzki ring: Located at or just above the GE junction.
Esophageal ring: Histology.
Mucosal: Fibrovascular core with a little muscularis mucosae.
Muscular: More muscle.
Both are lined by squamous mucosa proximally and often by gastric mucosa distally.
Esophageal hernia: Types.
Sliding.
Paraesophageal.
Esophageal hernia:
A. Gross pathology.
B. Histology.
A. Dilatation, ischemic changes.
B. Chronic inflammation, epithelial regenerative changes, fibromuscular proliferation.
VATER syndrome: Components.
Vertebral anomalies.
Anal atresia.
TracheoEsophageal fistula.
Renal defects.
Esophageal diverticula: Locations.
Above the upper esophageal sphincter (Zenker’s): Most common.
Above the lower esophageal sphincter.
At the midpoint of the esophagus.
Best place to look for inclusions of ___ esophagitis.
A. HSV
B. CMV
A. At the edge of the ulcer, in squamous cells.
B. At the base of the ulcer, in endothelial cells, fibroblasts, or glandular cells.
Pill esophagitis:
A. Main culprits.
B. Histology.
A. Iron, alendronate.
B. Nonspecific ulcer, possibly with prominent endothelial proliferation.
Chemical esophagitis: Locations.
Points of compression: Proximal and distal ends, mid-esophagus.
Radiation esophagitis: Gross pathology.
Large superficial ulcers.
Radiation esophagitis: Histology.
Acanthosis with parakeratosis.
Necrosis.
Atypia of stromal cells: Stellate fibroblasts, plump endothelial cells.
Hyalinized blood vessels.
Esophagitis dissecans superficialis:
A. Endoscopy.
B. Biopsy.
A. Whitish strips of peeling mucosa.
B. Intraepithelial splitting with necrotic superficial epithelium, bacterial and fungal colonies.
Esophagitis dissecans superficialis: Causes.
Bisphosphonates.
Bullous skin diseases.
Esophageal trauma.
Stricture.
Smoking.
“Black esophagus”.
Acute esophageal necrosis: May be associated with severe cardiovascular disease with hemodynamic compromise.
Bullous diseases of the esophagus:
A. Potentially fatal.
B. Rare in this location but more common in the skin.
A. Pemphigus vulgaris.
B. Bullous pemphigoid.
Gross pathology of esophageal bullous diseases:
A. Pemphigus vulgaris.
B. Bullous pemphigoid.
C. Lichen planus.
A. Bleeding and strictures.
B. Blisters.
C. Papules, plaques, or strictures.
Esophageal erythema multiforme: Gross pathology (2).
May resemble peptic or reflux esophagitis.
Pseudomembranes may form.
Esophageal graft-versus-host disease:
A. Typical location.
B. Gross pathology.
A. Upper third.
B. Desquamative lesions may cause a web.
Esophageal pemphigus vulgaris:
A. Location of split.
B. Inflammatory cells.
A. Suprabasal.
B. Eosinophils.
Esophageal bullous pemphigoid:
A. Location of split.
B. Inflammatory cells.
A. Subepithelial.
B. Eosinophils.
Histology of esophageal graft-versus-host disease:
A. Acute.
B. Chronic.
A. Karyorrhexis and apoptosis of epithelial cells; variable infiltrate of T cells.
B. Epidermal atrophy; fibrosis of lamina propria.
Immunofluorescence:
A. Pemphigus vulgaris.
B. Bullous pemphigoid.
A. Intercellular IgG.
B. IgG or IgA at the basement membrane.
Lymphocytic esophagitis:
A. Definition.
B. Cause.
A. At least 30 lymphocytes per hpf.
B. Many, including reflux, candidiasis, achalasia, lichenoid drug eruption.
Eosinophilic esophagitis: Epidemiology (2).
More common in males.
Concurrent eosinophilic enteritis is more common in children.
Eosinophilic esophagitis: Endoscopy (4).
Webs.
Corrugation.
Ulcers, exudates may be seen.
Eosinophilic esophagitis: Histologic definition.
More than 15 eosinophils per hpf.
Eosinophilic esophagitis: Ancillary test.
Serum eotaxin-3.
Reflux esophagitis: Endoscopic grading.
A through D, with A being the mildest.
Reflux esophagitis: Frequency of endoscopically inapparent cases.
30%.
PPI-responsive esophageal eosinophilia.
Eosinophilic esophagitis that responds to proton-pump inhibitors.
Barrett’s esophagus: Age groups.
Under the age of 15.
Over the age of 40.
Barrett’s esophagus: Special stain.
Alcian blue, pH 2.5.
Barrett’s esophagus: Immunohistochemistry.
CK7: Superficial and deep staining.
CK20: Bandlike superficial staining.
Intestinal metaplasia of cardia-type mucosa:
A. Distinction from Barrett’s esophagus.
B. Causes.
A. Depends on endoscopic impression.
B. Reflux, Helicobacter pylori.
Barrett’s esophagus with low-grade dysplasia: Treatments.
Antireflux therapy and close clinical follow-up.
Endoscopic ablation.
Barrett’s esophagus with low-grade dysplasia vs. indefinite for dysplasia: Immunohistochemistry.
Low-grade dysplasia may show more staining with p53, racemase, and Ki67.
Barrett’s esophagus with dysplasia vs. regenerative atypia (5).
Regenerative atypia:
− Background of active inflammation.
− Maturation at the surface.
− Greater uniformity of atypical cells.
− Nuclei and cytoplasm are equally enlarged.
− Cytoplasm tends to be eosinophilic rather than basophilic.
Colchicine and taxane: Histologic effects on the esophagus (4).
Increased mitotic figures, including “ring” types.
Apoptosis.
Nuclear stratification.
Loss of nuclear polarity.
Eosinophilic esophagitis: Genetics.
Familial cases: Mutation in TSLP (thymic stromal lymphopoietin) on 5q22.
Esophageal adenocarcinoma: Ancillary test.
Immunohistochemistry or FISH for HER2 to select patients for trastuzumab therapy.
Esophageal inflammatory fibroid polyp: Histology.
Lining: Benign squamous mucosa, possibly ulcerated.
Stroma:
− Variably cellular and variably edematous.
− Eosinophils and plasma cells.
− Prominent vessels with concentric stromal cells.
Esophageal inflammatory fibroid polyp: Mutation.
Somatic mutations, similar to those of some GISTs, may occur.
PDGFRα may be mutated.
Granular-cell tumor: Histologic features that suggest malignancy (5).
Increased cellularity.
Spindle cells.
Nuclear atypia.
Necrosis.
More than 2 mitotic figures per 10 hpf.
Squamous papilloma of the esophagus: Causes (4).
Human papillomavirus.
Reflux esophagitis.
Eosinophilic esophagitis.
Trauma.
Squamous papilloma of the esophagus: Location.
Mid or lower esophagus in 95% of cases.
Esophageal squamous dysplasia: Schemes of grading (2).
Mild, moderate, severe, or carcinoma in situ.
Low or high.
Esophageal squamous-cell carcinoma: Locations.
Mid or lower esophagus in 90% of cases.
Esophageal squamous-cell carcinoma: Tumor configurations.
Exophytic: Most common.
Ulcerating.
Purely infiltrating: Least common.
Esophageal squamous-cell carcinoma: Morphology of early lesions (2).
May be multifocal.
May be combined with widely scattered variable dysplasia and carcinoma in situ.
Esophageal squamous-cell carcinoma: Effect of irradiation.
Calcification keratinizing cells and foreign-body-giant-cell reaction.
Esophageal fibrovascular polyp: Histology.
Lining: Benign squamous epithelium.
Core: Collagenous or myxoid; sometimes contains fat.
Esophageal squamous-cell carcinoma: Main determinants of survival (2).
Depth of invasion.
Nodal status.
Tylosis:
A. Inheritance.
B. Clinical features (3).
A. Autosomal dominant.
B. SCC of the esophagus, hyperkeratosis of palms and soles, oral leukoplakia.
Esophageal squamous-cell carcinoma: Main variants (3).
Verrucous.
Sarcomatoid.
Undifferentiated.
Sarcomatoid carcinoma of the esophagus: Epidemiology.
Much more common in males than in females.
Sarcomatoid carcinoma of the esophagus: Histology of metastases.
May include any or all of the component of the primary tumor.
Esophageal squamous-cell carcinoma: Prognosis (2).
Generally poor, but better with polypoid tumors.
Undifferentiated carcinoma of the esophagus:
A. Histology.
B. Immunohistochemistry.
A. Undifferentiated cells with vesicular nuclei, prominent nuclei; cytoplasm is often abundant and eosinophilic.
B. Typically cytokeratin positive.
Verrucous carcinoma of the esophagus: Possible associations (2).
Achalasia.
Ingestion of acid.
Verrucous carcinoma of the esophagus: Surface.
Show parakeratosis and hyperkeratosis.
Verrucous carcinoma of the esophagus vs. benign papillomatous lesions.
Benign papillomatous lesions exhibit no pushing pattern of invasion at the deep margin.
High-grade neuroendocrine carcinoma of the esophagus: Histology (3).
Small-cell subtype: Similar to other small-cell neuroendocrine carcinomas.
Large-cell subtypes also exist.
Neuroendocrine carcinoma may coexist with more common types, e.g. SCC.
High-grade neuroendocrine carcinoma of the esophagus vs. metastatic neuroendocrine carcinoma (3).
TTF-1 to exclude pulmonary primary.
Clinical history may be required.
Distinction may be clinically irrelevant.
Melanoma of the esophagus: Possible changes in adjacent squamous mucosa (4).
Melanosis.
Melanocytosis.
Junctional activity.
Melanoma in situ.
Gastric duplication:
A. Location (2).
B. Gross pathology.
A. Usually intramural and on the greater curvature of the stomach.
B. Cystic mass that usually does communicate with the gastric lumen.
Gastric duplication: Lining.
More often gastric mucosa but can contain small-intestinal, respiratory, or pancreatic epithelium.
Gastric pyloric stenosis: Epidemiology (2).
More common in males and in firstborn children.
Gastric pyloric stenosis: Normal thickness of pyloric sphincter.
0.5 cm.
Pancreatic heterotopia in the stomach:
A. Origin.
B. Gross pathology.
A. Accessory pancreatic bud.
B. Umbilicated submucosal mass with duct.
Pancreatic heterotopia in the stomach: Histology.
Usually contains ducts, acini, and islet cells.
Can under the histologic changes that occur in the pancreas, e.g. inflammation, dysplasia, tumors.
Pancreatic heterotopia in the stomach: Name given to a lesion that consists of ducts only.
Adenomyoma.
Pyloric stenosis: Possibly associated mutation.
Duplication of 9q.
Sarcomatoid carcinoma of the esophagus: Immunohistochemistry.
Cytokeratin is positive in fewer than half of cases.
Vimentin is strong in the stromal component.
Sarcomatoid carcinoma of the esophagus: Histology.
Carcinomatous component: Squamous, glandular, or undifferentiated.
Mesenchymal: Spindle cells or with heterologous differentiation.
Gastric xanthelasma: Associations (3).
Duodenal reflux, gastritis, previous gastric surgery.
Not associated with hyperlipidemia.
Acute erosive gastritis: Associations (6).
NSAIDs.
Chemotherapy.
Alcohol.
Heavy smoking.
Physiologic stress.
Nasogastric intubation.
Mild acute erosive gastritis: Histology.
Active gastritis with edema.
Moderate acute erosive gastritis: Histology.
Mucosal erosion with fibrinopurulent exudate.
Severe acute erosive gastritis: Histology.
Confluent erosions; may resemble ulcer.
Reactive gastropathy: Causes.
Ethanol.
NSAIDs.
Steroids and other drugs.
Physiologic stress.
Reflux of duodenal contents.
Reactive gastropathy vs. gastric antral vascular ectasia.
Gastric antral vascular ectasia: Fibrin thrombi in the dilated capillaries.
Diffuse antral Helicobacter pylori-associated gastritis:
A. Epidemiology.
B. Location.
A. Whites in the United States.
B. Typically antral.
Diffuse antral Helicobacter pylori-associated gastritis: Histology.
Active chronic antral gastritis, sometimes with lymphoid aggregates, intestinal metaplasia.
Multifocal antral Helicobacter pylori-associated gastritis:
A. Epidemiology.
B. Location.
A. Minorities in the United States; Scandinavians.
B. Antral-body junction.
Diffuse antral Helicobacter pylori-associated gastritis: Histology (3).
Minimal chronic inflammation associate with islands of intestinal metaplasia or pyloric pseudometaplasia.
Minimal active inflammation.
Lymphoid follicles with germinal centers may persist.
Types of intestinal metaplasia.
Type I: Goblet cells and enterocyte-type absorptive cells.
Type II: Goblet cells and gastric foveolar cells.
Helicobacter heilmannii:
A. Associations (3).
B. Morphology.
A. Gastritis, carcinoma, gastric MALT lymphoma.
B. Twice as long (7 μm) as H. pylori; tightly coiled.
Autoimmune gastritis: Location.
Body and fundus.
Autoimmune gastritis: Histology.
Oxyntic epithelium: Atrophy, pyloric pseudometaplasia, intestinal metaplasia.
Enterochromaffin cells: Hyperplasia, dysplasia, or carcinoid tumors.
Autoimmune gastritis: Laboratory findings (2).
Hypergastrinemia.
Autoantibodies to parietal cells or to intrinsic factor.
Atrophic autoimmune pangastritis: Location.
Body and antrum.
Atrophic autoimmune pangastritis: Histology.
Epithelium: Inflammation (sometimes with. Any lymphocytes), atrophy, apoptosis.
Neuroendocrine cells: Decrease.
Atrophic autoimmune pangastritis: Laboratory findings (2).
No hypergastrinemia.
No antibodies to parietal cells or to intrinsic factor.
Lymphocytic gastritis: Associations (3).
Helicobacter pylori.
Celiac disease.
Lymphocytic colitis.
Others.
Lymphocytic gastritis: Histology.
Surface: More than 25 lymphocytes per 100 gastric foveolar cells.
Background: Chronic gastritis.
Collagenous gastritis: Associations (3).
Collagenous colitis.
Celiac disease.
Anemia in some younger patients.
Collagenous gastritis: Histology.
Thickened subepithelial collagen plate, sometimes with lymphocytic gastritis.
Eosinophilic gastritis: Epidemiology.
Children, adolescents.
Eosinophilic gastritis: Histology.
Eosinophils not associated with other inflammatory cells and causing mucosal architectural change or crypt injury.
Eosinophils may infiltrate muscularis mucosae or deeper layers.
Peptic ulcer: Histologic layers.
Neutrophils and débris.
Fibrin and necrotic matter.
Active granulation tissue.
Fibrous scar that interrupts the muscularis mucosae.
Hypertrophic gastropathy: Thickness of mucosa.
Greater than 1 to 1.5 mm.
Ménétrier’s disease: Symptoms (4).
Abdominal pain.
Diarrhea.
Weight loss.
Peripheral edema.
Ménétrier’s disease: Chemical abnormalities (2).
Hypoproteinemia.
Hypochlorhydria.
Ménétrier’s disease: Associations (3).
Eosinophilia.
Pulmonary infections.
Thrombosis.
Ménétrier’s disease: Possible infectious association.
CMV: Children and some cases in the immunosuppressed.
Ménétrier’s disease: Gross pathology (2).
Thick gastric wall with cerebriform rugae.
Antral sparing.
Ménétrier’s disease: Histology (4).
Hyperplasia is in the superficial mucosa:
− Hyperplastic foveolar cells secrete much mucus.
− Expansion of pits produces cysts.
− Hyperplastic muscularis mucosae.
The fundic glands are atrophic.
Mixed inflammation.
Zollinger-Ellison syndrome:
A. Cause.
B. Epidemiology.
A. Gastrinoma.
B. Can affect anyone but is most common in between ages 20 and 50.
Zollinger-Ellison syndrome: Symptoms.
Abdominal pain, diarrhea.
Zollinger-Ellison syndrome: Gross pathology.
Thick gastric wall with giant rugae.
Antral sparing.
Zollinger-Ellison syndrome: Histology.
Hyperplasia is in the specialized glands.
Thickness ratio of pits to glands exceeds 5 to 1.
The foveolar epithelium is atrophic.
Complications of Zollinger-Ellison syndrome:
A. Histologic.
B. Clinical.
A. Hyperplasia of enterochromaffin-like cells, dysplasia of neuroendocrine cells, carcinoid tumors.
B. Peptic ulcers.
Ménétrier’s disease vs. gastric hyperplastic polyp.
May depend on clinical history, especially in small biopsies.
Gastritis glandularis et cystica profunda: Synonyms.
Diffuse cystic (glandular) malformation.
Gastritis glandularis et cystica profunda: Histology.
Mucosal and submucosal cysts lined by mucous cells.
Pyloric or Brunner-type glands.
Fundic-type glands (rare).
Gastritis glandularis et cystica profunda: Significance.
May increase risk for gastric carcinoma.
Fundic-gland polyp: Causes (5).
Idiopathic (sporadic).
Familial adenomatous polyposis.
Attenuated familial adenomatous polyposis.
MUTYH-associated polyposis syndrome.
Proton-pump inhibitors.
Fundic-gland polyps: Mutations (2).
APC.
β-Catenin.
Fundic-gland polyposis associated with FAP syndrome:
A. Number of polyps.
B. Location.
A. Hundreds.
B. Mostly on the greater curvature, with antral sparing.
Gastric adenocarcinoma with chief-cell differentiation: Histology.
Anastomosing cords of oxyntic epithelial cells that infiltrate generally only the mucosa.
Gastric adenocarcinoma with chief-cell differentiation: Prognosis.
May persist or recur if incompletely excised.
No reports of metastasis; may be benign.
Gastric carcinoma: Main types (2).
Intestinal: Exophytic; resembles colonic carcinoma.
Diffuse: Infiltrative.
Gastric dysplasia: Main types (2).
Flat.
Adenomatous.
Gastric adenomas: Types (5).
Common: Tubular, tubulovillous, villous.
Rare: Antral-foveolar type, pyloric-type.
Intestinal type of gastric adenocarcinoma:
A. Epidemiology (2).
B. Associations (2).
A. Found more often in elderly men and in countries with high incidence of gastric cancer.
B. Dietary practices; H. pylori.
Intestinal type of gastric adenocarcinoma: Histologic origin.
Intestinal metaplasia; dysplastic precursor.
Diffuse type of gastric adenocarcinoma:
A. Epidemiology.
B. Associations (2).
A. More common in younger patients and in women.
B. H. pylori (possibly); germline mutations of CDH1 (E-cadherin).
Diffuse type of gastric adenocarcinoma:
A. Histologic origin.
B. Prognosis.
A. May arise from undifferentiated cells in the neck of the gastric gland.
B. Worse than that of the intestinal type.
Early gastric carcinoma:
A. Definition.
B. Survival.
A. Invasion of submucosa but not of muscularis propria.
B. 95%.
Gastric carcinoma: Molecular testing.
Testing for HER2 for selection of patients for trastuzumab therapy.
Also relevant to adenocarcinomas of the gastric cardia, gastroesophageal junction, and the lower esophagus.
Gastric carcinoma: Best predictor of survival.
Depth of invasion.
Gastric carcinoma: Survival for tumors that involve the subserosa.
50%.
Gastric neuroendocrine tumors: Types.
1: Associated with atrophic gastritis.
2: Associated with Zollinger-Ellison syndrome.
3: Sporadic.
4: High-grade neuroendocrine carcinoma.
Gastric neuroendocrine tumors: Categories.
Sporadic tumors.
Tumors arising in a background of hypergastrinemia.
Sporadic gastric neuroendocrine tumors:
A. Number.
B. Behavior.
A. Usually solitary.
B. Can invade or metastasize.
Hypergastrinemia-related gastric neuroendocrine tumors:
A. Relative frequency.
B. Number.
C. Behavior.
A. More common than sporadic tumors.
B. Multiple.
C. Indolent.
Hypergastrinemia-related gastric neuroendocrine tumors:
A. Cause.
B. Histologic origin.
A. Achlorhydria.
B. Enterochromaffin-like cells: Progression from hyperplasia to nodular hyperplasia to dysplasia to neoplasia.
Gastric neuroendocrine tumors:
A. Which ones respond to antral resection?
B. Which ones tend to be larger?
A. Hypergastrinemia-related tumors.
B. Sporadic tumors.
Gastric neuroendocrine tumors: Grading scheme of the WHO.
Grade 2: 2-20 mitotic figures per hpf, and >2-20% of nuclei are positive for Ki-67.
Grade 1: Fewer of both.
Grade 3: More of both.
Gastric neuroendocrine tumors: Classification of smaller Grade 1 tumors.
Smaller than 1 cm and confined to mucosa and submucosa: Benign well-differentiated NET.
1-2 cm and confined to mucosa and submucosa: Well-differentiated NET of uncertain malignant potential.
Diagnostic criteria of well-differentiated (gastric) neuroendocrine carcinoma.
A grade 1 tumor that is larger than 2 cm
- or -
That invades the muscularis propria or beyond
- or -
That has metastasized.
Diagnostic criteria of high-grade (gastric) neuroendocrine carcinoma.
Any tumor of grade 2 or grade 3.
Gastric neuroendocrine tumors: Histologic distinction between sporadic and hypergastrinemia-related.
Hypergastrinemia-related tumors: Immunohistochemistry shows endocrine-cell hyperplasia in the adjacent mucosa.
Classification of gastric neuroendocrine proliferations by size.
Linear hyperplasia: A line of at least 5 endocrine cells.
Nodular hyperplasia: At least 5 endocrine cells form a cluster smaller than 150 μm.
Endocrine-cell dysplasia: 150 μm-0.5 mm.
Neuroendocrine tumor: Larger than 0.5 mm.
Classification of gastric neuroendocrine proliferations: When applicable (2).
When analyzing the mucosa adjacent to a gastric neuroendocrine tumor.
Not to be performed on antral mucosa.
Gastric lymphoma:
A. Most common type.
B. Most common location.
A. Diffuse large B-cell lymphoma.
B. Antrum.
Gastric marginal-zone lymphoma: Possible cell types (6).
Small lymphocytes with round nuclei.
Centrocyte-like cells.
Monocytoid B cells.
Plasma cells.
Centroblasts, immunoblasts.
Gastric marginal-zone lymphoma: Definition of lymphoepithelial lesion.
At least three B lymphocytes within the epithelium of the gastric glands.
Gastric marginal-zone lymphoma vs. lymphocytic gastritis (2).
Lymphocytic gastritis:
− Usually no lymphoepithelial lesions.
− Intraepithelial lymphocytes are T cells, not B cells.
Normal rotation of bowel during development.
Counterclockwise around the superior mesenteric artery.
Intestinal malrotation: Gross pathology (2).
Small intestine may be pushed to one side of abdomen.
Cecum may be on left side.
Intestinal malfixation: Gross pathology.
Fixation band may cause intestinal torsion and infarction.
Omphalocele: Causes (2).
Failure of the intestines to return to the abdominal cavity during the 10th week of development.
Incomplete closure of the abdominal wall during the 4th week of development.
Omphalocele: Associations.
Other malformations of the gastrointestinal tract.
Cardiovascular defects.
Omphalocele: Gross pathology (3).
Extra-abdominal viscera are covered by a membranous sac consisting of peritoneum and amnion.
Stomach and liver may accompany intestines.
Umbilical cord arises from the center of the sac.
Gastroschisis: Possible cause.
Vascular accident before 12 weeks of development.
Gastroschisis: Gross pathology.
Extra-abdominal viscera are not covered.
Umbilical cord is not affected.
Intestinal atresia:
A. Most common location.
B. Least common location.
A. Duodenum.
B. Colon.
Intestinal atresia: Risk factors (2).
Twin gestation.
Maternal use of cocaine.
Intestinal atresia: Presentation.
Bilious vomiting in soon after birth.
Intestinal atresia: Variations in gross pathology (3).
Imperforate septum occlude lumen.
Absence of lumen: Fibrotic cord.
Absence of bowel segment and its mesentery.
Intestinal stenosis: Variations in gross pathology (2).
Perforate septum.
Narrow lumen.
Intestinal atresia and stenosis: Histology (2).
Proximal to the defect: Ischemia, necrosis, granulation tissue, submucosal fibrosis, hypertrophy of lamina propria (all due to dilatation).
Blind segment: Meconium, lanugo, mucin.
Meckel’s diverticulum:
A. Cause.
B. Prevalence.
A. Failure of involution of the vitelline duct.
B. 1% to 4%.
Meckel’s diverticulum: Prevalence (3).
On the antimesenteric surface of the small bowel.
Infants: Within 30 cm of the ileocecal valve.
Adults: Within 100 cm of the ileocecal valve.
Meckel’s diverticulum:
A. Length.
B. Histology.
A. 2-15 cm.
B. Usually normal small-bowel mucosa; 80% contain ectopic pancreatic or gastric tissue.
Volvulus:
A. Definition.
B. Most common location.
A. Twisting of a segment of bowel around its mesentery.
B. Sigmoid colon.
Volvulus: Predisposing factors (3).
Congenitally long mesentery.
Meckel’s diverticulum.
Congenital band.
Volvulus: Gross pathology and histology.
Variable ischemia; possible necrosis.
Intussusception:
A. Epidemiology.
B. Predisposing factors (2).
A. Twice as common in males.
B. None in children; intraluminal mass in adults.
Intussusception: Histology (2).
Ischemia.
Recurrent cases: Intramural vascular proliferation can mimic vascular tumor.
Gastric marginal-zone lymphoma: Translocation.
t(11;18).
API2−MALT1.
Enterohemorrhagic Escherichia coli: Seasonal distribution of infections.
Most common in the summer.
Enterohemorrhagic E. coli: Effect of toxin.
Inhibits protein synthesis, thereby damaging epithelial and endothelial cells.
Salmonella spp.: Location of replication.
Within intracellular vacuoles of enterocytes and macrophages.
Typhoid fever:
A. Complications (3).
B. Mortality in the untreated.
A. Massive hemorrhage, perforation, peritonitis.
B. About 15%.
Salmonella spp.: Incubation period for gastroenteritis.
A few hours.
Salmonella spp.: Gross pathology of gastrointestinal infections.
Longitudinal oval ulcers with elevated edges, located over Peyer’s patches.
Campylobacter spp.: Frequent association.
Drinking untreated mountain water.
Campylobacter spp.: Incubation period for diarrhea.
Up to 1 week.
Frequent location of colitis due to ___.
A. Enterohemorrhagic E. coli.
B. Campylobacter spp.
A. Right colon.
B. Ileocecal valve.
Campylobacter spp.: Cause of severe systemic illness.
Campylobacter fetus.
Bacteria that cause focal active colitis (3).
Shigella spp.
Campylobacter spp.
Salmonella spp. (sometimes).
Bacteria that cause hyperplasia of lymphoid follicles.
Salmonella spp.
Yersinia enterocolitica.
Bacterial enterocolitis vs. idiopathic inflammatory bowel disease (5).
Idiopathic inflammatory bowel disease: − More diffuse active inflammation. − Less hemorrhage. − Basal plasmacytosis. − More crypt-architectural distortion. − Fewer suppurative granulomas (than seen in yersiniosis).
Causes of diarrhea in AIDS patients.
Infections.
AIDS enteropathy.
AIDS-related enteropathy: Definition (4).
Chronic diarrhea.
Malnutrition.
Wasting.
No evidence of gastrointestinal infection.