GI tract Flashcards
1
Q
Gastric ectopia of the esophagus: Histology.
A
Oxyntic mucosa usually.
May undergo intestinal metaplasia.
2
Q
Sebaceous ectopia in the esophagus: Synonym.
A
Fordyce’s granules.
3
Q
Pancreatic ectopia in the esophagus: Associations (3).
A
Metaplasia due to reflux.
Trisomy 13 or 18.
4
Q
Pancreatic ectopia of the esophagus:
A. Gross pathology.
B. Histology.
A
A. Submucosal mass that may have a central pore.
B. Usually acinar but can contain islet cells also.
5
Q
Esophageal atresia: Types.
A
I: No fistula.
II: Proximal fistula only.
III: Distal fistula only.
IV: Proximal and distal fistulae.
6
Q
Esophageal atresia: Clinical presentation.
A
Choking during feeding; excessive drooling.
7
Q
Esophageal atresia: Associated syndromes.
A
Down’s syndrome.
VATER syndrome.
8
Q
Congenital esophageal duplication: Gross pathology.
A
Cyst (most often), diverticulum, or tubule.
May be intramural or extramural.
9
Q
Congenital esophageal duplication: Histology (2).
A
Lining: Respiratory, gastric, intestinal, or squamous.
Wall: Two layers of muscularis propria.
10
Q
Plummer-Vinson syndrome:
A. Clinical triad.
B. Esophageal lesions.
A
A. Iron-deficiency anemia, cheilitis, glossitis.
B. Proximal webs, predisposition to proximal SCC.
11
Q
Plummer-Vinson syndrome: Other association.
A
Autoimmune diseases.
12
Q
Esophageal web: Histology.
A
Fibrovascular core without muscle.
Proximal lining: Squamous mucosa.
Distal lining: Squamous or gastric mucosa.
13
Q
Esophageal ring: Cause.
A
Constriction due, e.g., to reflux or scleroderma.
14
Q
Esophageal ring: Types.
A
Muscular.
Mucosal.
Schatzki ring: Located at or just above the GE junction.
15
Q
Esophageal ring: Histology.
A
Mucosal: Fibrovascular core with a little muscularis mucosae.
Muscular: More muscle.
Both are lined by squamous mucosa proximally and often by gastric mucosa distally.
16
Q
Esophageal hernia: Types.
A
Sliding.
Paraesophageal.
17
Q
Esophageal hernia:
A. Gross pathology.
B. Histology.
A
A. Dilatation, ischemic changes.
B. Chronic inflammation, epithelial regenerative changes, fibromuscular proliferation.
18
Q
VATER syndrome: Components.
A
Vertebral anomalies.
Anal atresia.
TracheoEsophageal fistula.
Renal defects.
19
Q
Esophageal diverticula: Locations.
A
Above the upper esophageal sphincter (Zenker’s): Most common.
Above the lower esophageal sphincter.
At the midpoint of the esophagus.
20
Q
Best place to look for inclusions of ___ esophagitis.
A. HSV
B. CMV
A
A. At the edge of the ulcer, in squamous cells.
B. At the base of the ulcer, in endothelial cells, fibroblasts, or glandular cells.
21
Q
Pill esophagitis:
A. Main culprits.
B. Histology.
A
A. Iron, alendronate.
B. Nonspecific ulcer, possibly with prominent endothelial proliferation.
22
Q
Chemical esophagitis: Locations.
A
Points of compression: Proximal and distal ends, mid-esophagus.
23
Q
Radiation esophagitis: Gross pathology.
A
Large superficial ulcers.
24
Q
Radiation esophagitis: Histology.
A
Acanthosis with parakeratosis.
Necrosis.
Atypia of stromal cells: Stellate fibroblasts, plump endothelial cells.
Hyalinized blood vessels.
25
Esophagitis dissecans superficialis:
A. Endoscopy.
B. Biopsy.
A. Whitish strips of peeling mucosa.
B. Intraepithelial splitting with necrotic superficial epithelium, bacterial and fungal colonies.
26
Esophagitis dissecans superficialis: Causes.
Bisphosphonates.
Bullous skin diseases.
Esophageal trauma.
Stricture.
Smoking.
27
"Black esophagus".
Acute esophageal necrosis: May be associated with severe cardiovascular disease with hemodynamic compromise.
28
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.
29
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.
30
Esophageal erythema multiforme: Gross pathology (2).
May resemble peptic or reflux esophagitis.
Pseudomembranes may form.
31
Esophageal graft-versus-host disease:
A. Typical location.
B. Gross pathology.
A. Upper third.
B. Desquamative lesions may cause a web.
32
Esophageal pemphigus vulgaris:
A. Location of split.
B. Inflammatory cells.
A. Suprabasal.
B. Eosinophils.
33
Esophageal bullous pemphigoid:
A. Location of split.
B. Inflammatory cells.
A. Subepithelial.
B. Eosinophils.
34
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.
35
Immunofluorescence:
A. Pemphigus vulgaris.
B. Bullous pemphigoid.
A. Intercellular IgG.
B. IgG or IgA at the basement membrane.
36
Lymphocytic esophagitis:
A. Definition.
B. Cause.
A. At least 30 lymphocytes per hpf.
B. Many, including reflux, candidiasis, achalasia, lichenoid drug eruption.
37
Eosinophilic esophagitis: Epidemiology (2).
More common in males.
Concurrent eosinophilic enteritis is more common in children.
38
Eosinophilic esophagitis: Endoscopy (4).
Webs.
Corrugation.
Ulcers, exudates may be seen.
39
Eosinophilic esophagitis: Histologic definition.
More than 15 eosinophils per hpf.
40
Eosinophilic esophagitis: Ancillary test.
Serum eotaxin-3.
41
Reflux esophagitis: Endoscopic grading.
A through D, with A being the mildest.
42
Reflux esophagitis: Frequency of endoscopically inapparent cases.
30%.
43
PPI-responsive esophageal eosinophilia.
Eosinophilic esophagitis that responds to proton-pump inhibitors.
44
Barrett's esophagus: Age groups.
Under the age of 15.
Over the age of 40.
45
Barrett's esophagus: Special stain.
Alcian blue, pH 2.5.
46
Barrett's esophagus: Immunohistochemistry.
CK7: Superficial and deep staining.
CK20: Bandlike superficial staining.
47
Intestinal metaplasia of cardia-type mucosa:
A. Distinction from Barrett's esophagus.
B. Causes.
A. Depends on endoscopic impression.
B. Reflux, Helicobacter pylori.
48
Barrett's esophagus with low-grade dysplasia: Treatments.
Antireflux therapy and close clinical follow-up.
Endoscopic ablation.
49
Barrett's esophagus with low-grade dysplasia vs. indefinite for dysplasia: Immunohistochemistry.
Low-grade dysplasia may show more staining with p53, racemase, and Ki67.
50
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.
51
Colchicine and taxane: Histologic effects on the esophagus (4).
Increased mitotic figures, including "ring" types.
Apoptosis.
Nuclear stratification.
Loss of nuclear polarity.
52
Eosinophilic esophagitis: Genetics.
Familial cases: Mutation in TSLP (thymic stromal lymphopoietin) on 5q22.
53
Esophageal adenocarcinoma: Ancillary test.
Immunohistochemistry or FISH for HER2 to select patients for trastuzumab therapy.
54
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.
55
Esophageal inflammatory fibroid polyp: Mutation.
Somatic mutations, similar to those of some GISTs, may occur.
PDGFRα may be mutated.
56
Granular-cell tumor: Histologic features that suggest malignancy (5).
Increased cellularity.
Spindle cells.
Nuclear atypia.
Necrosis.
More than 2 mitotic figures per 10 hpf.
57
Squamous papilloma of the esophagus: Causes (4).
Human papillomavirus.
Reflux esophagitis.
Eosinophilic esophagitis.
Trauma.
58
Squamous papilloma of the esophagus: Location.
Mid or lower esophagus in 95% of cases.
59
Esophageal squamous dysplasia: Schemes of grading (2).
Mild, moderate, severe, or carcinoma in situ.
Low or high.
60
Esophageal squamous-cell carcinoma: Locations.
Mid or lower esophagus in 90% of cases.
61
Esophageal squamous-cell carcinoma: Tumor configurations.
Exophytic: Most common.
Ulcerating.
Purely infiltrating: Least common.
62
Esophageal squamous-cell carcinoma: Morphology of early lesions (2).
May be multifocal.
May be combined with widely scattered variable dysplasia and carcinoma in situ.
63
Esophageal squamous-cell carcinoma: Effect of irradiation.
Calcification keratinizing cells and foreign-body-giant-cell reaction.
64
Esophageal fibrovascular polyp: Histology.
Lining: Benign squamous epithelium.
Core: Collagenous or myxoid; sometimes contains fat.
65
Esophageal squamous-cell carcinoma: Main determinants of survival (2).
Depth of invasion.
Nodal status.
66
Tylosis:
A. Inheritance.
B. Clinical features (3).
A. Autosomal dominant.
B. SCC of the esophagus, hyperkeratosis of palms and soles, oral leukoplakia.
67
Esophageal squamous-cell carcinoma: Main variants (3).
Verrucous.
Sarcomatoid.
Undifferentiated.
68
Sarcomatoid carcinoma of the esophagus: Epidemiology.
Much more common in males than in females.
69
Sarcomatoid carcinoma of the esophagus: Histology of metastases.
May include any or all of the component of the primary tumor.
70
Esophageal squamous-cell carcinoma: Prognosis (2).
Generally poor, but better with polypoid tumors.
71
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.
72
Verrucous carcinoma of the esophagus: Possible associations (2).
Achalasia.
Ingestion of acid.
73
Verrucous carcinoma of the esophagus: Surface.
Show parakeratosis and hyperkeratosis.
74
Verrucous carcinoma of the esophagus vs. benign papillomatous lesions.
Benign papillomatous lesions exhibit no pushing pattern of invasion at the deep margin.
75
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.
76
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.
77
Melanoma of the esophagus: Possible changes in adjacent squamous mucosa (4).
Melanosis.
Melanocytosis.
Junctional activity.
Melanoma in situ.
78
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.
79
Gastric duplication: Lining.
More often gastric mucosa but can contain small-intestinal, respiratory, or pancreatic epithelium.
80
Gastric pyloric stenosis: Epidemiology (2).
More common in males and in firstborn children.
81
Gastric pyloric stenosis: Normal thickness of pyloric sphincter.
0.5 cm.
82
Pancreatic heterotopia in the stomach:
A. Origin.
B. Gross pathology.
A. Accessory pancreatic bud.
B. Umbilicated submucosal mass with duct.
83
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.
84
Pancreatic heterotopia in the stomach: Name given to a lesion that consists of ducts only.
Adenomyoma.
85
Pyloric stenosis: Possibly associated mutation.
Duplication of 9q.
86
Sarcomatoid carcinoma of the esophagus: Immunohistochemistry.
Cytokeratin is positive in fewer than half of cases.
Vimentin is strong in the stromal component.
87
Sarcomatoid carcinoma of the esophagus: Histology.
Carcinomatous component: Squamous, glandular, or undifferentiated.
Mesenchymal: Spindle cells or with heterologous differentiation.
88
Gastric xanthelasma: Associations (3).
Duodenal reflux, gastritis, previous gastric surgery.
Not associated with hyperlipidemia.
89
Acute erosive gastritis: Associations (6).
NSAIDs.
Chemotherapy.
Alcohol.
Heavy smoking.
Physiologic stress.
Nasogastric intubation.
90
Mild acute erosive gastritis: Histology.
Active gastritis with edema.
91
Moderate acute erosive gastritis: Histology.
Mucosal erosion with fibrinopurulent exudate.
92
Severe acute erosive gastritis: Histology.
Confluent erosions; may resemble ulcer.
93
Reactive gastropathy: Causes.
Ethanol.
NSAIDs.
Steroids and other drugs.
Physiologic stress.
Reflux of duodenal contents.
94
Reactive gastropathy vs. gastric antral vascular ectasia.
Gastric antral vascular ectasia: Fibrin thrombi in the dilated capillaries.
95
Diffuse antral Helicobacter pylori-associated gastritis:
A. Epidemiology.
B. Location.
A. Whites in the United States.
B. Typically antral.
96
Diffuse antral Helicobacter pylori-associated gastritis: Histology.
Active chronic antral gastritis, sometimes with lymphoid aggregates, intestinal metaplasia.
97
Multifocal antral Helicobacter pylori-associated gastritis:
A. Epidemiology.
B. Location.
A. Minorities in the United States; Scandinavians.
B. Antral-body junction.
98
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.
99
Types of intestinal metaplasia.
Type I: Goblet cells and enterocyte-type absorptive cells.
Type II: Goblet cells and gastric foveolar cells.
100
Helicobacter heilmannii:
A. Associations (3).
B. Morphology.
A. Gastritis, carcinoma, gastric MALT lymphoma.
B. Twice as long (7 μm) as H. pylori; tightly coiled.
101
Autoimmune gastritis: Location.
Body and fundus.
102
Autoimmune gastritis: Histology.
Oxyntic epithelium: Atrophy, pyloric pseudometaplasia, intestinal metaplasia.
Enterochromaffin cells: Hyperplasia, dysplasia, or carcinoid tumors.
103
Autoimmune gastritis: Laboratory findings (2).
Hypergastrinemia.
Autoantibodies to parietal cells or to intrinsic factor.
104
Atrophic autoimmune pangastritis: Location.
Body and antrum.
105
Atrophic autoimmune pangastritis: Histology.
Epithelium: Inflammation (sometimes with. Any lymphocytes), atrophy, apoptosis.
Neuroendocrine cells: Decrease.
106
Atrophic autoimmune pangastritis: Laboratory findings (2).
No hypergastrinemia.
No antibodies to parietal cells or to intrinsic factor.
107
Lymphocytic gastritis: Associations (3).
Helicobacter pylori.
Celiac disease.
Lymphocytic colitis.
Others.
108
Lymphocytic gastritis: Histology.
Surface: More than 25 lymphocytes per 100 gastric foveolar cells.
Background: Chronic gastritis.
109
Collagenous gastritis: Associations (3).
Collagenous colitis.
Celiac disease.
Anemia in some younger patients.
110
Collagenous gastritis: Histology.
Thickened subepithelial collagen plate, sometimes with lymphocytic gastritis.
111
Eosinophilic gastritis: Epidemiology.
Children, adolescents.
112
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.
113
Peptic ulcer: Histologic layers.
Neutrophils and débris.
Fibrin and necrotic matter.
Active granulation tissue.
Fibrous scar that interrupts the muscularis mucosae.
114
Hypertrophic gastropathy: Thickness of mucosa.
Greater than 1 to 1.5 mm.
115
Ménétrier's disease: Symptoms (4).
Abdominal pain.
Diarrhea.
Weight loss.
Peripheral edema.
116
Ménétrier's disease: Chemical abnormalities (2).
Hypoproteinemia.
Hypochlorhydria.
117
Ménétrier's disease: Associations (3).
Eosinophilia.
Pulmonary infections.
Thrombosis.
118
Ménétrier's disease: Possible infectious association.
CMV: Children and some cases in the immunosuppressed.
119
Ménétrier's disease: Gross pathology (2).
Thick gastric wall with cerebriform rugae.
Antral sparing.
120
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.
121
Zollinger-Ellison syndrome:
A. Cause.
B. Epidemiology.
A. Gastrinoma.
B. Can affect anyone but is most common in between ages 20 and 50.
122
Zollinger-Ellison syndrome: Symptoms.
Abdominal pain, diarrhea.
123
Zollinger-Ellison syndrome: Gross pathology.
Thick gastric wall with giant rugae.
Antral sparing.
124
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.
125
Complications of Zollinger-Ellison syndrome:
A. Histologic.
B. Clinical.
A. Hyperplasia of enterochromaffin-like cells, dysplasia of neuroendocrine cells, carcinoid tumors.
B. Peptic ulcers.
126
Ménétrier's disease vs. gastric hyperplastic polyp.
May depend on clinical history, especially in small biopsies.
127
Gastritis glandularis et cystica profunda: Synonyms.
Diffuse cystic (glandular) malformation.
128
Gastritis glandularis et cystica profunda: Histology.
Mucosal and submucosal cysts lined by mucous cells.
Pyloric or Brunner-type glands.
Fundic-type glands (rare).
129
Gastritis glandularis et cystica profunda: Significance.
May increase risk for gastric carcinoma.
130
Fundic-gland polyp: Causes (5).
Idiopathic (sporadic).
Familial adenomatous polyposis.
Attenuated familial adenomatous polyposis.
MUTYH-associated polyposis syndrome.
Proton-pump inhibitors.
131
Fundic-gland polyps: Mutations (2).
APC.
β-Catenin.
132
Fundic-gland polyposis associated with FAP syndrome:
A. Number of polyps.
B. Location.
A. Hundreds.
B. Mostly on the greater curvature, with antral sparing.
133
Gastric adenocarcinoma with chief-cell differentiation: Histology.
Anastomosing cords of oxyntic epithelial cells that infiltrate generally only the mucosa.
134
Gastric adenocarcinoma with chief-cell differentiation: Prognosis.
May persist or recur if incompletely excised.
No reports of metastasis; may be benign.
135
Gastric carcinoma: Main types (2).
Intestinal: Exophytic; resembles colonic carcinoma.
Diffuse: Infiltrative.
136
Gastric dysplasia: Main types (2).
Flat.
Adenomatous.
137
Gastric adenomas: Types (5).
Common: Tubular, tubulovillous, villous.
Rare: Antral-foveolar type, pyloric-type.
138
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.
139
Intestinal type of gastric adenocarcinoma: Histologic origin.
Intestinal metaplasia; dysplastic precursor.
140
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).
141
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.
142
Early gastric carcinoma:
A. Definition.
B. Survival.
A. Invasion of submucosa but not of muscularis propria.
B. 95%.
143
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.
144
Gastric carcinoma: Best predictor of survival.
Depth of invasion.
145
Gastric carcinoma: Survival for tumors that involve the subserosa.
50%.
146
Gastric neuroendocrine tumors: Types.
1: Associated with atrophic gastritis.
2: Associated with Zollinger-Ellison syndrome.
3: Sporadic.
4: High-grade neuroendocrine carcinoma.
147
Gastric neuroendocrine tumors: Categories.
Sporadic tumors.
Tumors arising in a background of hypergastrinemia.
148
Sporadic gastric neuroendocrine tumors:
A. Number.
B. Behavior.
A. Usually solitary.
B. Can invade or metastasize.
149
Hypergastrinemia-related gastric neuroendocrine tumors:
A. Relative frequency.
B. Number.
C. Behavior.
A. More common than sporadic tumors.
B. Multiple.
C. Indolent.
150
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.
151
Gastric neuroendocrine tumors:
A. Which ones respond to antral resection?
B. Which ones tend to be larger?
A. Hypergastrinemia-related tumors.
B. Sporadic tumors.
152
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.
153
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.
154
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.
155
Diagnostic criteria of high-grade (gastric) neuroendocrine carcinoma.
Any tumor of grade 2 or grade 3.
156
Gastric neuroendocrine tumors: Histologic distinction between sporadic and hypergastrinemia-related.
Hypergastrinemia-related tumors: Immunohistochemistry shows endocrine-cell hyperplasia in the adjacent mucosa.
157
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.
158
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.
159
Gastric lymphoma:
A. Most common type.
B. Most common location.
A. Diffuse large B-cell lymphoma.
B. Antrum.
160
Gastric marginal-zone lymphoma: Possible cell types (6).
Small lymphocytes with round nuclei.
Centrocyte-like cells.
Monocytoid B cells.
Plasma cells.
Centroblasts, immunoblasts.
161
Gastric marginal-zone lymphoma: Definition of lymphoepithelial lesion.
At least three B lymphocytes within the epithelium of the gastric glands.
162
Gastric marginal-zone lymphoma vs. lymphocytic gastritis (2).
Lymphocytic gastritis:
− Usually no lymphoepithelial lesions.
− Intraepithelial lymphocytes are T cells, not B cells.
163
Normal rotation of bowel during development.
Counterclockwise around the superior mesenteric artery.
164
Intestinal malrotation: Gross pathology (2).
Small intestine may be pushed to one side of abdomen.
Cecum may be on left side.
165
Intestinal malfixation: Gross pathology.
Fixation band may cause intestinal torsion and infarction.
166
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.
167
Omphalocele: Associations.
Other malformations of the gastrointestinal tract.
Cardiovascular defects.
168
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.
169
Gastroschisis: Possible cause.
Vascular accident before 12 weeks of development.
170
Gastroschisis: Gross pathology.
Extra-abdominal viscera are not covered.
Umbilical cord is not affected.
171
Intestinal atresia:
A. Most common location.
B. Least common location.
A. Duodenum.
B. Colon.
172
Intestinal atresia: Risk factors (2).
Twin gestation.
Maternal use of cocaine.
173
Intestinal atresia: Presentation.
Bilious vomiting in soon after birth.
174
Intestinal atresia: Variations in gross pathology (3).
Imperforate septum occlude lumen.
Absence of lumen: Fibrotic cord.
Absence of bowel segment and its mesentery.
175
Intestinal stenosis: Variations in gross pathology (2).
Perforate septum.
Narrow lumen.
176
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.
177
Meckel's diverticulum:
A. Cause.
B. Prevalence.
A. Failure of involution of the vitelline duct.
B. 1% to 4%.
178
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.
179
Meckel's diverticulum:
A. Length.
B. Histology.
A. 2-15 cm.
B. Usually normal small-bowel mucosa; 80% contain ectopic pancreatic or gastric tissue.
180
Volvulus:
A. Definition.
B. Most common location.
A. Twisting of a segment of bowel around its mesentery.
B. Sigmoid colon.
181
Volvulus: Predisposing factors (3).
Congenitally long mesentery.
Meckel's diverticulum.
Congenital band.
182
Volvulus: Gross pathology and histology.
Variable ischemia; possible necrosis.
183
Intussusception:
A. Epidemiology.
B. Predisposing factors (2).
A. Twice as common in males.
B. None in children; intraluminal mass in adults.
184
Intussusception: Histology (2).
Ischemia.
Recurrent cases: Intramural vascular proliferation can mimic vascular tumor.
185
Gastric marginal-zone lymphoma: Translocation.
t(11;18).
API2−MALT1.
186
Enterohemorrhagic Escherichia coli: Seasonal distribution of infections.
Most common in the summer.
187
Enterohemorrhagic E. coli: Effect of toxin.
Inhibits protein synthesis, thereby damaging epithelial and endothelial cells.
188
Salmonella spp.: Location of replication.
Within intracellular vacuoles of enterocytes and macrophages.
189
Typhoid fever:
A. Complications (3).
B. Mortality in the untreated.
A. Massive hemorrhage, perforation, peritonitis.
B. About 15%.
190
Salmonella spp.: Incubation period for gastroenteritis.
A few hours.
191
Salmonella spp.: Gross pathology of gastrointestinal infections.
Longitudinal oval ulcers with elevated edges, located over Peyer's patches.
192
Campylobacter spp.: Frequent association.
Drinking untreated mountain water.
193
Campylobacter spp.: Incubation period for diarrhea.
Up to 1 week.
194
Frequent location of colitis due to ___.
A. Enterohemorrhagic E. coli.
B. Campylobacter spp.
A. Right colon.
B. Ileocecal valve.
195
Campylobacter spp.: Cause of severe systemic illness.
Campylobacter fetus.
196
Bacteria that cause focal active colitis (3).
Shigella spp.
Campylobacter spp.
Salmonella spp. (sometimes).
197
Bacteria that cause hyperplasia of lymphoid follicles.
Salmonella spp.
Yersinia enterocolitica.
198
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).
```
199
Causes of diarrhea in AIDS patients.
Infections.
AIDS enteropathy.
200
AIDS-related enteropathy: Definition (4).
Chronic diarrhea.
Malnutrition.
Wasting.
No evidence of gastrointestinal infection.
201
AIDS-related enteropathy: Complications (2).
Malabsorption due to loss of microvilli.
Death due to large ulcers proceeding from erosions.
202
Giardiasis: Associated inherited immunodeficiencies (2).
Common variable immunodeficiency.
Selective IgA immunodeficiency.
203
Sites of gastrointestinal infection by ___.
A. CMV.
B. HSV.
A. Esophagus, stomach, intestines.
B. Esophagus, low rectum, anus, perianal skin.
204
Cholera: Incubation period.
A few hours to 2 days.
205
Coccidiosis: Organisms (3).
Cyclospora cayetanensis.
Cystoisospora belli.
Cryptosporidium spp.
206
Cyclospora infection: Associations.
Travelers' diarrhea.
Ingested of contaminated fresh fruit.
207
Region of the gastrointestinal tract most frequently affected by ___.
A. Mycobacterium tuberculosis.
B. Mycobacterium avium complex.
A. Ileocecal region.
B. Anywhere.
208
Histology of mycobacterial gastroenteritis:
A. Mycobacterium tuberculosis.
B. Mycobacterium avium complex.
A. Necrotizing granulomas, Langhans' giant cells.
B. Foamy macrophages stuffed with bacteria fill the lamina propria.
209
Yersinia enterocolitica: Risk factors for fatal infection.
Immunosuppression.
Iron overload.
210
Adenovirus: Histology of colitis.
Dystrophic goblet cells with amorphous nuclei that rarely contain diagnostic (smudgy) inclusion bodies.
211
Candida spp.: Definition of blastoconidium.
A budding yeast form, 3-5 μm.
212
Gastrointestinal histoplasmosis: Types of inflammation (2).
Granulomatous.
Histiocytic.
213
Gastrointestinal syphilis:
A. Site.
B. Histology.
A. Rectum or anus.
B. Dense mononuclear infiltrate that includes many plasma cells; lymphoid aggregates; no crypt-architectural distortion or marked acute inflammation.
214
Use of ___ stain to detect intestinal protozoa.
A. Giemsa (3)
B. trichrome
A. Cryptosporidium, Cystoisospora, microsporidia.
B. Giardia (distinction from mucus).
215
Mycobacterium-avium-complex enteritis vs. Whipple's disease.
Whipple's disease:
− "Fat vacuoles".
− Positive for PAS-D, not for AFB.
216
Intestinal spirochetosis: Stains.
Silver stain.
Immunohistochemical stain for Treponema spp.
217
Candida spp.: True hypha vs. pseudohypha.
True hypha: No indentation at true septa.
Pseudohypha (elongated blastoconidium): Indentation at false septa.
218
Whipple's disease: Main sites (3).
Gastrointestinal system.
Joints.
Central nervous system.
219
Whipple's disease: Prognosis.
Often fatal without antibiotics.
220
Whipple's disease: Gross pathology of the bowel (3).
Mucosa: Yellow plaques, shallow ulcers.
Wall: Thickening.
221
Whipple's disease: Gross pathology outside the bowel (3).
Lymphadenopathy.
Hepatosplenomegaly.
Plaques in mesenteric fat and peritoneum.
222
Whipple's disease: Histology (3).
Foamy macrophages filled with bacilli.
"Fat vacuoles", some of which are dilated lymphatic vessels.
Foreign-body granulomas or lipogranulomas.
223
Whipple's disease: Inflammatory infiltrate.
Little or none.
224
Waldenström's macroglobulinemia in the bowel: Histology.
Foamy macrophages.
Dilated lymphatics filled with eosinophilic matter.
225
Gliadin-containing cereal grains.
Wheat, rye, barley.
226
Celiac disease can cause deficiency of which nutrients (3)?
Iron.
Folate.
Calcium.
227
Celiac disease: Preferred tests.
Antibodies to tissue transglutaminase.
In those who lack the above: Antibodies to deaminated gliadin peptides.
228
Celiac disease: HLA types.
DQ2: 98%.
DQ8: 2%.
229
Celiac disease: Typical number of intraepithelial lymphocytes.
More than 40 per 100 enterocytes.
230
Celiac disease: Histology of crypts (3).
Elongation and hyperplasia.
Increased mitotic activity.
231
Celiac disease: When to consider workup for clonality.
When there are ulcers in the small intestine.
In cases of refractory sprue.
232
Normal length ratio of villi to crypts.
3:1 to 5:1.
233
Celiac disease: Endoscopic finding.
Scalloping of the valvulae conniventes.
234
Lymphocytic enterocolitis.
Concurrent lymphocytic colitis.
Celiac-disease-like changes in the proximal small intestine.
No response to gluten-free diet.
235
Refractory sprue: Definition and cause.
No response to gluten-free diet for 12 months.
Allergic reaction to protein other than gluten.
236
Types of refractory sprue: Intraepithelial lymphocytes.
Type II:
− Some may appear atypical.
− Loss of CD8 and CD5.
− Monoclonality of T-cell receptors.
237
Types of refractory sprue: Treatment.
Type I: Azathioprine, prednisone, budesonide, or mesalamine.
Type II: May respond to cladribine, anti-CD52, or chemotherapy and stem-cell transplantation.
238
Types of refractory sprue: Prognosis.
Type II: 50% mortality rate; most cases progress to enteropathy-associated T-cell lymphoma.
239
Tropical sprue: Treatment.
Broad-spectrum antibiotics and vitamins.
240
Autoimmune enteritis:
A. Gene and chromosome.
B. Associations (2).
A. FOXP3 on the X chromosome.
B. X-linked type: Immune dysregulation, polyendocrinopathy.
241
Autoimmune enteritis: Targets of autoantibodies (4).
Enterocytes.
Goblet cells.
Parietal cells.
Smooth-muscle cells.
242
Autoimmune enteritis: Clue to diagnosis (3).
No goblet cells.
No increase in intraepithelial lymphocytes.
No response to gluten-free diet.
243
Abetalipoproteinemia:
A. Histology.
B. Peripheral blood.
A. Enterocytes with intracytoplasmic vacuoles.
B. Acanthocytes.
244
Celiac disease: Progression of recovery.
From distal to proximal, with the duodenum recovering last.
245
Primary adenocarcinoma of the small intestine: Risk factors (6).
Familial adenomatous polyposis.
Attenuated FAP.
MUTYH-associated polyposis syndrome.
Lynch's syndrome.
Peutz-Jeghers syndrome.
Crohn's disease.
246
Primary adenocarcinoma of the small intestine: Locations.
Most: Near major duodenal papilla.
Associated with Crohn's disease: Ileum.
247
Gastrointestinal carcinoid tumors: Sites (5).
Appendix (#1).
Ileum.
Rectum.
Stomach.
Colon.
248
Carcinoid tumors of the bowel: Presentations (4).
Incidental.
Weight loss.
Obstruction.
Carcinoid syndrome.
249
Carcinoid syndrome associated with carcinoid tumors of the bowel:
A. Prevalence.
B. Most common site of carcinoid tumor.
A. 10%.
B. Ileum.
250
Carcinoid syndrome:
A. Hormonal mediators.
B. Associated lesion.
A. 5-HT, 5-HIAA.
B. Lesion of right heart in 50% of cases.
251
Significance ___ in carcinoid tumors of the bowel:
A. cytologic features
B. vascular invasion
C. perineural invasion
None of these factors predict behavior of the tumor.
252
Atypical carcinoid: Synonyms (2).
Grade 2 neuroendocrine tumor.
Intermediate-grade neuroendocrine tumor.
253
Grade 2 neuroendocrine tumor: Criteria (2).
2-20 mitotic figures per 10 hpf.
More than 2% to 20% of nuclei positive for Ki-67.
254
Carcinoid tumors of the bowel: Relevance of immunohistochemistry to site.
Hindgut tumors are often negative for chromogranin.
255
Gangliocytic paraganglioma: Cellular components (3).
Neuroendocrine cells.
Spindle cells with Schawann-cell differentiation.
Ganglion cells.
256
Gangliocytic paraganglioma:
A. Frequent site.
B. Behavior.
A. Ampullary region.
B. Uncertain malignant potential.
257
Mixed carcinoid-adenocarcinoma:
A. Gross pathology.
B. Portion made up by adenocarcinoma.
A. Often large and infiltrating.
B. Typically more than 50%.
258
Mixed carcinoid-adenocarcinoma:
A. Differential diagnosis.
B. Prognosis.
A. Benign epithelial differentiation within a carcinoid tumor.
B. Acts like adenocarcinoma.
259
Frequent histologic feature of carcinoid tumors of the ___.
A. Small intestine.
B. Rectum.
C. Duodenum.
A. Insular growth.
B. Trabecular growth.
C. Psammoma bodies.
260
Carcinoid tumors of the bowel: Relevance of risk of metastasis to size of tumor.
Less than 1 cm: 2%.
1-2 cm: 50% (ileal), 15% (rectal).
More than 2 cm: 80%.
261
Carcinoid tumors of the bowel: Best indicator of behavior.
Metastasis.
262
Typical behavior of ___.
A. Gastrinoma.
B. Insulinoma.
A. Malignant.
B. Benign.
263
Hirschsprung's disease: Risk factors (2).
Male sex.
Down's syndrome.
264
Hirschsprung's disease: Forms (3).
Short-segment (most common): No more than 3 cm of distal rectum.
Long-segment: Extends beyond sigmoid colon.
Ultra-short: Less than 2 cm; diagnosed by manometry, not by histology.
265
Hirschsprung's disease: Typical histology (3).
No ganglion cells.
Hypertrophic mural nerves (>40 μm).
Thickened muscle layers.
266
Hirschsprung's disease: Special stains (4).
Acetylcholinesterase: Nerve fibers extend into lamina propria.
Calretinin: Absence of staining.
NSE for ganglion cells.
S-100 for Schwann cells.
267
Long-segment Hirschsprung's disease: Histology and special stain.
Mural nerves may not be hypertrophic.
Acetylcholinesterase stain may be falsely negative.
268
Hirschsprung's disease: Mutations.
RET, endothelin receptor B.
269
Hirschsprung's disease vs. hypoganglionosis.
Hypoganglionosis: Some ganglion cells but still too few.
270
Intestinal neuronal dysplasia: Histology.
Hyperplastic plexus.
Giant ganglia containing more than 8 neurons.
271
Eosinophilic gastroenteritis: Definition (3).
Gastrointestinal symptoms.
Eosinophilic infiltration of the gastrointestinal tract.
No known cause such as specific allergy or parasites.
272
Eosinophilic gastroenteritis: Frequent associations (3).
Peripheral eosinophilia.
Elevated serum IL-5.
History of allergies.
273
Eosinophilic gastroenteritis: Types (3).
Mucosal: Diarrhea and malabsorption.
Submucosal: Obstruction.
Mural and serosal: Ascites, eosinophilic peritonitis.
274
Eosinophilic gastroenteritis: Main histologic features (3).
Sheets of eosinophils.
Mucosal changes.
Fibrosis.
275
Allergy to cow's milk: Histology (2).
Villous atrophy.
Neutrophils and eosinophils.
276
Systemic mastocytosis of the gastrointestinal tract:
A. Associated mutation.
B. Definition of mast-cell aggregate.
A. D816V in KIT.
B. More than 15 mast cells.
277
Systemic mastocytosis of the gastrointestinal tract: Histological confounder.
Obscuring eosinophils (80% of cases).
278
Idiopathic constipation: Histology (3).
Ganglion cells are present.
Argyrophilic neurons may be lost.
Interstitial cells of Cajal may be decreased.
279
Acute graft-versus-host disease:
A. Timing.
B. Initial site of involvement.
A. Usually occurs within 100 days after transplantation.
B. Skin.
280
Gastrointestinal graft-versus-host disease: Initial histology.
Necrosis of single cells in the bases of crypts gives rise to lacunae that contain apoptotic débris.
281
Gastrointestinal graft-versus-host disease: Intermediate histology.
Apoptosis in many crypts; crypt abscesses; ulcers with secondary fungal infection.
282
Gastrointestinal graft-versus-host disease: Late histology.
Mucosal atrophy, fibrosis, or regeneration.
283
Gastrointestinal graft-versus-host disease vs. effect of mycophenolate mofetil.
Mycophenolate mofetil:
− More likely to have eosinophils.
− Less likely to have apoptotic débris within lacunae.
284
Graft-versus-host disease: Mediating cell.
The cytotoxic T cell.
285
Crohn's disease of the small bowel: Gene.
IBD-1, a.k.a. NOD2/CARD15.
286
Ulcerative colitis: Feared acute complications (2).
Toxic megacolon.
Perforation.
287
Crohn's disease: Gross pathology (3).
Fat-wrapping.
"Stovepipe" bowel.
"Cobblestoning" of mucosa.
288
Crohn's disease: Radiography.
"String sign" due to luminal stenosis.
289
Crohn's disease: Histology of inflammation (4).
Required for diagnosis:
− Non-necrotizing granulomas and/or
− Transmural lymphoid aggregates away from a deep ulcer.
Other features:
− Neutrophilic infiltrates and crypt abscesses.
− "Rosary bead" of lymphoid aggregates along the serosa.
290
Crohn's disease: Histology of stromal changes (3).
Hypertrophy of muscularis mucosae.
Submucosal neuronal hyperplasia.
Mural fibrosis.
291
Crohn's disease: Serologic test.
Antibodies to Saccharomyces cerevisiae are found in about half of patients.
292
Ulcerative colitis: Site.
Always involves the rectum.
Does not have to involve the whole colon; "backwash" ileitis is not a required finding.
293
Ulcerative colitis: Histology of inflammation (2).
Dense lymphoplasmacytic and neutrophilic infiltrate that usually goes no deeper than the submucosa.
Cryptitis, crypt abscesses, crypt regeneration, and crypt-architectural distortion.
294
Ulcerative colitis: Features that may make it "primary inflammatory bowel disease of an indeterminate type" (2).
Pancolitis with involvement of the terminal ileum.
Ulcers that extend into the muscularis propria.
295
Ulcerative colitis: Antibody.
pANCA.
296
Lymphocytic colitis: Number of lymphocytes.
More than 15 per 100 superficial epithelial cells.
297
Diversion colitis: Leading cause.
Hartmann pouch constructed during a proximal partial colectomy.
298
Diversion colitis: Histology (4).
Large lymphoid aggregates and follicles.
Dense lymphoid infiltrate in the lamina propria.
Mild active inflammation may be seen.
Normal crypt architectural except in longstanding cases.
299
Diversion colitis: Treatment (3).
Restoration of fecal stream.
Enemas of short-chain fatty acids.
Surgical excision in refractory cases.
300
Causes of active ileitis (4).
Minimal and focal:
− Bowel preparation.
− Trauma and prolapse.
Significant:
− Crohn's disease.
− NSAIDs.
301
Ileal pouch:
A. Purpose.
B. Clinical indications.
A. To restore continence after colectomy.
B. Ulcerative colitis, FAP.
302
Ileal pouchitis: Clinical features.
Bloody and foul-smelling effluent.
Fever and malaise.
303
Ileal pouchitis: Histologic features (4).
Granulation tissue.
Architectural change.
Ulcers.
Loss of normal lymphoid follicles.
304
Ileal pouch: Histologic features that suggest Crohn's disease (3).
Ulcers and non-necrotizing granulomas in the afferent limb.
Pyloric-gland metaplasia.
305
Risk for colon cancer in ___.
A. Ulcerative colitis.
B. Crohn's disease.
A. 20% in 30 years.
B. 3% in 20 years.
306
Dysplasia in inflammatory bowel disease: Gross pathologic types (2).
Flat dysplasia.
Dysplasia-associated lesion or mass: Polyp or plaque.
307
Dysplasia in inflammatory bowel disease: Grading.
Negative for dysplasia.
Indefinite for dysplasia.
Low-grade dysplasia.
High-grade dysplasia.
308
Dystrophic goblet cell.
One in which the mucin vacuole does not communicate with the lumen.
309
Dysplasia-associated lesion or mass vs. sporadic adenoma: Histology.
Not possible to make the distinction.
310
Clinical features favoring dysplasia-associated lesion or mass over sporadic adenoma (2).
Patient under 40 with UC for more than 10 years.
Lesion larger than 1 cm in area of colitis with dysplasia in the adjacent flat mucosa.
311
Ancillary studies favoring dysplasia-associated lesion or mass over sporadic adenoma (3).
IHC: Positive for p53, negative for bcl-2.
Molecular: Loss of heterozygosity in chromosome 3p.
312
Radiation colitis:
A. Dose of radiation.
B. Other risk factors (3).
A. Usually more than 450 Gy.
B. Diabetes, cardiovascular disease, chemotherapy.
313
Radiation colitis: Symptoms (3).
Diarrhea.
Abdominal pain.
Bowel obstruction in chronic radiation colitis.
314
Acute radiation colitis: Histology (5).
Edema.
Vascular ectasia.
Acute cryptitis.
Superficial ulcers.
Epithelial cytomegaly and atypia.
315
Chronic radiation colitis: Histology (5).
Stromal fibrosis with atypical fibroblasts.
Thickened subepithelial collagen.
Glandular atrophy and distortion.
Vascular changes.
Increased plasma cells in the lamina propria.
316
Ischemic colitis: Clinical features.
Usually acute onset.
Abdominal pain, nausea, vomiting, diarrhea, or lower-gastrointestinal bleeding.
317
Ischemic colitis: Pharmacological causes (2).
NSAIDs.
Oral contraceptives.
318
Ischemic colitis: Infectious mimics.
Enterohemorrhagic E. coli.
Clostridium difficile.
319
Mild ischemic colitis: Histology (4).
Superficial hemorrhage.
Patchy mucosal necrosis.
Dilated vessels
"Decapitated" glands.
320
Severe ischemic colitis: Histology (3).
Crypt dropout.
Acute inflammation, including cryptitis.
Coagulative necrosis.
321
Late lesions of ischemic colitis: Histology.
Replacement of mucosa by granulation tissue and fibrosis.
322
Microscopic colitis: Causes (3).
Idiopathic.
Drugs, e.g. ticlopidine.
Infection, e.g. Brainerd diarrhea.
323
Microscopic colitis: Epidemiology.
Collagenous colitis is more common in women.
324
Collagenous colitis: Histology (3).
Thickened subepithelial collagen.
Increased intraepithelial lymphocytes.
Increased plasma cells in the superficial lamina propria.
325
Microscopic colitis: Possible aberrant histologic findings (6).
```
Subepithelial giant cells.
Cryptitis.
Ulcers.
Paneth-cell metaplasia.
Pseudomembranes.
Architectural change.
```
326
Collagenous colitis: Possible complication.
"Fracture" of colon during endoscopic insufflation, leading to pneumatosis coli.
327
Cord colitis syndrome: Association.
Cord-blood stem-cell transplantation.
328
Cord colitis syndrome: Histology.
Granulomatous inflammation and changes similar to those of idiopathic inflammatory bowel disease.
Affects upper and lower gastrointestinal tract.
329
Cord colitis syndrome:
A. Treatment.
B. Possible cause.
A. Usually responds to antibiotics.
B. Bradyrhizobium enterica.
330
Syndromes of mucosal prolapse: Endoscopy.
Mucosal erythema, ulcer, or polypoid lesion.
331
Syndromes of mucosal prolapse: Histology (4).
Fibromuscular obliteration of the lamina propria.
Mucosal architectural change and misplacement.
Mucosal capillary ectasia.
Sometimes: Erosion with inflammatory pseudomembrane.
332
Collagenous colitis: Significance of metaplasia.
Paneth-cell metaplasia:
− Seen in collagenous colitis with more severe diarrhea.
− May cause confusion with idiopathic inflammatory bowel disease.
333
Entamoeba histolytica: Chemical resistance.
Resists gastric acid and chlorination.
334
Entamoeba histolytica: Complications of infection in the colon (3).
Granulomatous masses that can mimic carcinoma.
Perforation.
Fistulae.
335
Entamoeba histolytica: Most frequent sites of ulcers in the large intestine.
Cecum.
Appendix.
Rectosigmoid.
336
Entamoeba histolytica: Typical orientation of colonic ulcers.
Perpendicular to the long axis of the colon.
337
Entamoeba histolytica vs. histiocytes.
Histocytes:
− Smaller.
− Larger, more irregular nucleus.
− Less intense staining with PAS.
338
Aoncotheca philippinensis:
A. Synonym.
B. Geography.
A. Capillaria philippinensis.
B. Asia, Middle East, Africa.
339
Aoncotheca philippinensis:
A. Disease.
B. Diagnosis.
A. Protein-losing enteropathy.
B. Identification of eggs, larvae, or worms in stool.
340
Aoncotheca philippinensis: Sites of infection (2).
Jejunum, upper ileum.
341
Strongyloides stercoralis: Histology of autoinfection.
Filiform larvae in the bowel wall.
342
Diphyllobothrium latum: Residence.
Small intestine.
343
Trichuris trichiura:
A. Residence.
B. Morphology of adult.
A. Cecum, ascending colon.
B. Whiplike, 4 cm.
344
Lymphangiectasia: Forms.
Primary: Congenital obstruction.
Secondary: Inflammation, malignancy.
345
Lymphangiectasia: Manifestations (2).
Protein-losing enteropathy.
Lymphatic obstruction.
346
Pneumatosis intestinalis: Forms.
Acute: Gas-forming intestinal organisms.
Chronic: Pulmonary disease.
347
Pneumatosis intestinalis: Causative bacteria (3).
Clostridium perfringens.
Enterobacter aerogenes.
Escherichia coli.
348
Pneumatosis intestinalis: Association in infants.
Necrotizing enterocolitis.
349
Pneumatosis intestinalis: Manifestations in adults (3).
Diarrhea.
Flatulence.
Increased mucus in the stool.
350
Pneumatosis intestinalis: Radiography.
Ring of gas in the wall of the bowel.
351
Pneumatosis intestinalis: Typical location of gas-filled cysts.
Near the mesenteric border.
352
Pneumatosis intestinalis: Histology.
Gas-filled cysts that usually have no endothelial lining.
Variable inflammatory response.
Overlying mucosa may show ischemic changes.
353
Melanosis coli: Pigment and its location.
Lipofuscin in histiocytes of the lamina propria.
354
Melanosis coli: Special stains (3).
Positive: PAS, AFB, Fontana-Masson.
Negative: Iron stains.
355
Brown-bowel syndrome:
A. Pigment and its location.
B. Typical association.
C. Symptoms.
A. Lipofuscin in smooth-muscle cells.
B. Deficiency of vitamin E.
C. Abdominal pain, diarrhea.
356
Pseudomelanosis duodeni: Pigment and its location.
Iron in the tips of duodenal villi.
357
Pseudomelanosis duodeni: Associations (4).
Iron-containing compounds.
Hypertension.
Diabetes mellitus.
End-stage renal disease.
358
Inflammatory polyp of the colon: Histology (4).
Variable mixture of inflamed stromal tissue and hyperplastic epithelium.
Fibromuscular hyperplasia.
Thick-walled or ectatic blood vessels.
Sometimes: Bizarre stromal cells.
359
Serrated adenoma:
A. Typical location.
B. Distinguishing histology (2).
A. Left colon.
B. Eosinophilic cytoplasm, gastric foveolar metaplasia.
360
Sessile serrated polyp: Histologic features (10).
Basal dilatation of crypts.
Branching of crypts.
Horizontal orientation of crypts.
Prominent serration.
Misplacement of glands.
Epithelial-to-stromal ratio exceeding 50%.
No thickening of basement membrane at surface.
Persistent atypia in the upper third of the crypt.
Mitotic figures in the upper third of the crypt.
Dystrophic goblet cells.
361
Sessile serrated polyp: Number of histologic features needed for diagnosis.
4.
362
Sessile serrated polyp: Significance (2).
May progress to colon cancers with microsatellite instability.
Multiple in the serrated polyposis syndrome.
363
Sessile serrated polyp: Surveillance interval (3).
Less than 10 mm: 5 years.
At least 10 mm: 3 years.
With cytologic dysplasia: 3 years.
364
Serrated adenoma: Surveillance interval.
3 years.
365
Colon cancer: Major molecular pathways (2).
Chromosomal instability: 85%.
Mutator phenotype (microsatellite instability): 15%.
366
Colon cancer of the chromosomal-instability pathway:
A. Typical ploidy.
B. Affected chromosomes (3).
C. Associated syndrome.
A. Aneuploid.
B. 5, 17, 18.
C. Familial adenomatous polyposis.
367
Colon cancer of the mutator-phenotype pathway:
A. Typical gross pathology (2).
B. Typical ploidy.
C. Associated syndrome.
A. Large, right-sided.
B. Diploid.
C. Lynch's syndrome.
368
Lynch's syndrome: Sites of non-colonic carcinomas (6).
Central nervous system.
Urinary tract.
Biliary tract.
Ovary.
Stomach, small intestine.
Endometrium.
369
Lynch's syndrome: Amsterdam II criteria.
At least 3 relatives with LS-related tumors.
Colo-rectal carcinoma in 2 generations.
LS-related tumor occurring in patient under 50.
370
Familial colorectal cancer syndrome, type X:
A. Definition.
B. Mutant protein.
A. Applied to one who fulfills the Amsterdam II criteria but has no mutated mismatch-repair gene.
B. Some: Epithelial-cell adhesion molecule (EPCAM).
371
Colonic adenocarcinoma: Grading.
I: Well-formed glands in a desmoplastic stroma.
II: Less well-formed glands; focal cribriform pattern.
III: No glands; solid sheets.
372
Mucinous adenocarcinoma of the colon: Prognosis.
Worse, but only if at least 75-80% of the tumor has extracellular mucus.
373
Colorectal cancer of Lynch's syndrome: Histology.
Many lymphocytes around and within the tumor.
Poorly differentiated: Undifferentiated or medullary.
Many tumors are of the mucinous or signet-ring type.
374
Bethesda criteria for colorectal carcinoma: Purpose.
To determine which tumors should be tested for MSI-H.
375
Bethesda criteria for colorectal carcinoma: The criteria (5).
Patient under 50.
LS-related tumor at any time, any age.
MSI-H histology in a patient under 60.
Colorectal carcinoma in a first-degree relative.
Patient with at least 2 relatives with an LS-related tumor at any age.
376
Effect of MSI-H histology on ___.
A. Prognosis.
B. Treatment.
C. Surveillance.
A. Better prognosis.
B. Irinotecan is used rather than 5-FU.
C. Surveillance for other LS-related tumors.
377
Another reason why testing for MSI-H should be done.
To catch those who have MSI-H but do not meet the Amsterdam II criteria.
378
Tests for MSI-H (3).
PCR for microsatellite stability.
IHC for enzymes of mismatch repair.
Sequencing of genes of mismatch repair.
379
Colorectal carcinoma: Relevance of site of tumor to prognosis.
Worse if left-sided.
380
Causes of loss of MSH6 by immunohistochemistry (3).
Germline mutation of MSH2/MSH6.
Deficiency of MLH1/PMS2 + somatic mutation of MSH6.
Previous chemotherapy.
381
Familial adenomatous polyposis:
A. Inheritance.
B. Onset of polyps.
C. Natural course.
A. Autosomal dominant.
B. Usually around puberty.
C. Death from colorectal carcinoma.
382
Familial adenomatous polyposis:
A. Gene and its location.
B. Mutations associated with attenuated FAP.
A. APC on 5q21.
B. Mutations near the 3' end, near the 5' end, or in exon 9.
383
Familial adenomatous polyposis: Ocular abnormality.
Congenital hypertrophy of the retinal pigmented epithelium.
384
Familial adenomatous polyposis: Leading cause of death after colectomy.
Periampullary carcinoma.
385
Gardner's syndrome:
A. Benign tumors (3).
B. Extra-colonic sites of malignant tumors (2).
A. Osteomas, epidermal cysts, fibromatosis.
B. Duodenum, thyroid.
386
Turcot's syndrome vs. pseudo-Turcot's syndrome.
Turcot's: Familial adenomatous polyposis with medulloblastoma.
Pseudo-Turcot's: Lynch's syndrome with glioblastoma.
387
Muir-Torre syndrome:
A. Defective protein.
B. Location of colonic adenomas.
A. Mismatch-repair enzymes.
B. Proximal colon.
388
Muir-Torre syndrome: Skin tumors.
Sebaceous neoplasms.
BCC.
SCC.
389
MUTYH-associated polyposis syndrome:
A. Inheritance.
B. Gene and its function.
A. Autosomal recessive.
B. MYH encodes an enzyme of excision repair.
390
MUTYH-associated polyposis syndrome: Relation to familial adenomatous polyposis (2).
Mutation of MYH predisposes to acquired mutation of APC.
Can mimic FAP or attenuated FAP clinically.
391
Familial adenomatous polyposis:
A. Earliest lesion in the colon.
B. Gastric polyps.
A. The one-gland adenoma.
B. Fundic-gland polyps, adenomas.
392
Familial adenomatous polyposis: When workup should occur in patient with no known risk factors or family history.
When a patient has had a cumulative total of 10 of more adenomas.
393
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.
394
Familial adenomatous polyposis: Molecular test.
Gene sequencing to determine exact location of mutation of APC gene.
396
Peutz-Jeghers syndrome:
A. Inheritance.
B. Onset of polyps.
A. Autosomal dominant.
| B. During infancy.
397
Peutz-Jeghers syndrome: Gene and its location.
STK-11 on 19q13.3.
399
Peutz-Jeghers syndrome: Characteristic gonadal tumors (2).
Ovarian sex-cord tumor with annular tubules.
Testicular Sertoli-cell tumors.
400
Peutz-Jeghers syndrome: Other sites of malignancy (2).
Pancreas, breast.
401
Peutz-Jeghers syndrome: Benign finding.
Hyperpigmentation of skin and mucous membranes.
402
Isolated juvenile polyps:
A. Maximum.
B. Frequent fate of polyps.
A. Up to 5 juvenile polyps in the colon and rectum.
B. Auto-amputation.
403
Juvenile polyposis syndrome: Criteria (3).
Any of the following:
At least 6 juvenile polyps.
Presence of juvenile polyps throughout the GI tract.
Any juvenile polyp in one with a family history of juvenile polyposis syndrome.
404
Juvenile polyposis syndrome: Forms.
Nonfamilial: May be associated with other congenital anomalies.
Familial: Many varieties, mostly autosomal dominant.
405
Juvenile polyposis syndrome:
A. Onset.
B. Presentations (3).
A. Childhood.
B. Rectal bleeding, bowel obstruction, prolapse of polyp into anal canal.
406
Juvenile polyposis syndrome:
A. Number of polyps.
B. Sites of polyps.
A. Between 6 and several hundred.
B. Distal colon and rectum (90%), stomach.
407
Juvenile polyp: Gross pathology.
Globose or mushroom-shaped and often ulcerated.
408
Juvenile polyp: Histology (4).
Hamartomatous overgrowth of lamina propria.
Dilated glands may form cysts.
Inflamed stroma and (often) surface.
Sometimes: Increased ganglion cells and hypertrophic nerves.
409
Juvenile polyp: Incidence of dysplasia.
Up to 20%.
410
Juvenile polyposis syndrome: Genes and their locations (2).
SMAD4 (MADH4) on 18q21.1.
BMPR1A on 10q23.3 (if concurrent hereditary hemorrhagic telangiectasia).
411
PTEN hamartoma-tumor syndromes (2).
Cowden's syndrome.
Ruvalcaba-Myhre-Smith syndrome.
412
Cowden's syndrome:
A. Inheritance.
B. Sites of tumors (4).
A. Autosomal dominant.
B. Gastrointestinal tract, thyroid, breast, skin of face.
413
Cowden's syndrome: Facial anomalies (3).
Arched palate.
Beaked nose.
Retinal gliomas.
414
Peutz-Jeghers syndrome: Sites of gastrointestinal polyps.
Mostly in the small intestine but also in the colon.
415
Cowden's syndrome: Onset of tumors.
Between ages 20 and 40.
416
PTEN hamartoma-tumor syndromes: Histology of polyps (4).
May resemble juvenile polyps.
May resemble rectal mucosal prolapse.
Ganglioneuromas and lipomas may occur.
417
PTEN: Location of gene.
10q23.
418
Cronkhite-Canada syndrome:
A. Inheritance.
B. Onset.
A. Not inherited.
B. Late adulthood.
419
Cronkhite-Canada syndrome: Findings outside the gastrointestinal tract (3).
Alopecia.
Hyperpigmentation.
Nail dystrophy.
420
Cronkhite-Canada syndrome: Mortality and typical cause of death.
60%; cachexia.
421
Cronkhite-Canada syndrome:
A. Sites of polyps.
B. Gross pathology.
A. Anywhere in the GI tract, but esp. in stomach and colon.
B. May mimic primary IBD; cut surface is often gelatinous.
422
Cronkhite-Canada syndrome:
A. Histology of polyps.
B. Histology of adjacent mucosa.
A. Similar to that of juvenile polyps.
B. Edematous and may be rich in eosinophils.
423
Intestinal ganglioneuromatosis: Causes (5).
Juvenile polyposis syndrome.
PTEN hamartoma-tumor syndromes.
Tuberous sclerosis.
Neurofibromatosis.
MEN IIB.
424
Serrated polyposis syndrome: Possible genetic abnormalities (2).
Defect in hypermethylation of DNA.
Mutation in MYH.
425
Benign fibroblastic polyp of the colon: Synonym.
Colorectal perineurioma.
426
Benign fibroblastic polyp of the colon: Histology (2).
Small, tightly packed spindle cells in the lamina propria.
Spindle cells are often oriented parallel to the muscularis mucosae.
Mucosa may resemble hyperplastic polyp or SSP.
427
Benign fibroblastic polyp of the colon: Immunohistochemistry.
Negative: Neural markers, including S100.
428
Elastosis and elastofibromatous change of the colon: Histology.
Increased elastin fibers and fibrous tissue, often centered on a blood vessel.
Can cause a polypoid mass.
429
Mucosal neuroma:
A. Distinction from ganglioneuroma.
B. Immunohistochemistry.
A. A ganglioneuroma contains ganglion cells as well as spindle cells.
B. Positive for S100.
430
Mucosal neuroma: Associations.
Most cases: None (sporadic).
Neurofibromatosis.
431
Ruvalcaba-Myhre-Smith syndrome: Findings outside the gastrointestinal tract (4).
Macrocephaly.
Mental deficiency.
Characteristic facies.
Penile macules.
432
Peutz-Jeghers syndrome: Histology of colonic polyps.
Hamartomatous overgrowth of muscularis mucosae.
Arborizing architecture.
Dysplasia is rare.
433
Gastrointestinal stromal tumor:
A. Most common sites.
B. Presentation.
A. Stomach, small intestine.
B. Ulceration and bleeding in about half of cases.
434
Gastrointestinal stromal tumor: Carney's triad.
Epithelioid GIST.
Pulmonary chondroma.
Extraadrenal paraganglioma.
435
Gastrointestinal stromal tumor: Criteria for very low risk (2).
Smaller than 2 cm.
Fewer than 5 mitotic figures per 50 hpf.
436
Gastrointestinal stromal tumor: Criteria for low risk (2).
2-5 cm.
Fewer than 5 mitotic figures per 50 hpf.
437
Gastrointestinal stromal tumor: Criteria for intermediate risk (2,2).
Smaller than 5 cm, 6-10 mitotic figures per 50 hpf.
5-10 cm, fewer than 5 mitotic figures per hpf.
438
Gastrointestinal stromal tumor: Criteria for high risk (2,1,1).
Larger than 5 cm, more than 5 mitotic figures per 50 hpf.
Any tumor larger than 10 cm.
Any tumor with more than 10 mitotic figures per hpf.
439
Risk of adverse outcome of high-risk gastrointestinal tumor in the ___.
A. Stomach.
B. Small intestine.
A. 46%.
B. 77%.
440
Colorectal gastrointestinal stromal tumors.
Rare but tend to show high-risk histology.
441
Gastrointestinal stromal tumor: Recommended immunohistochemical panel.
CD117.
CD34.
Desmin, actin.
S-100.
442
Gastrointestinal stromal tumor: Useful newer stain.
DOG-1 is both sensitive and specific for GIST.
443
Gastrointestinal stromal tumor: Most frequently mutated genes (2).
KIT.
PDGFRA.
444
Gastrointestinal stromal tumor: Locations of mutations in KIT.
Exons 9, 11, 13, 17.
445
Gastrointestinal stromal tumor: Relevance to location of mutation in KIT to treatment.
Exon 11: Usually responsive to imatinib.
Exon 9: Only half of patients respond; a higher do may be needed.
Exons 13 and 17: Usually no response.
446
Gastrointestinal stromal tumor: Locations of mutations in PDGRA.
Exons 12, 14, 18.
447
Gastrointestinal stromal tumor: Most common mutation in PDGFRA and relevance to treatment.
D842V in exon 18 is highly resistant to imatinib and sunitinib.
448
CD117-negative gastrointestinal stromal tumor:
A. Incidence.
B. Immunohistochemistry (1,3).
A. 4% of GISTs.
B. Positive for DOG-1; negative for CD117, c-Kit, and CD34.
449
CD117-negative gastrointestinal stromal tumor:
A. Frequent chromosomal abnormality.
B. Frequent histology.
C. Frequent sites (2).
A. Loss of 14 or of 14q.
B. Epithelial.
C. Omentum, peritoneum.
450
CD117-negative gastrointestinal stromal tumor: Treatment.
Some tumors respond to imatinib.
451
Fibromatosis: Immunohistochemistry.
Depending on staining technique, may show false positivity for CD117.
452
Gastrointestinal leiomyosarcoma: Most frequent sites (3).
Stomach, small intestine, colon.
453
Gastrointestinal schwannoma: Frequent histologic feature.
Cuff of lymphocytes.
454
Malignant neuroectodermal tumor:
A. Synonym.
B. Mutations.
A. Osteoclast-rich tumor resembling clear-cell sarcoma.
B. EWSR-CREB1 or EWSR-ATF1.
455
Malignant neuroectodermal tumor: Immunohistochemistry (1,1,1).
Positive: S-100.
Variable: Melanoma markers.
Negative: CD117.
456
Familial gastrointestinal stromal tumor:
A. Inheritance.
B. Genetic basis.
A. Autosomal dominant.
B. Germline mutation in KIT and PDGFRA.
457
Familial gastrointestinal stromal tumor: Possible associations (4).
Nevi.
Perineal hyperpigmentation.
Urticaria pigmentosa.
Systemic mast-cell disease.
458
Familial gastrointestinal stromal tumor: Course.
Indolent.
459
Carney-Stratakis syndrome: Tumors (3).
Multiple epithelioid GISTs in the stomach.
Paragangliomas.
Pheochromocytomas.
460
Carney-Stratakis syndrome:
A. Gene.
B. Treatment.
A. Succinate dehydrogenase.
B. Relatively resistant to imatinib.
461
Gastrointestinal stromal tumors associated with neurofibromatosis, type I:
A. Site.
B. Histology (2).
C. Behavior.
A. Small intestine.
B. Spindle-cell type; "skeinoid" fibers.
C. Usually benign.
462
Gastrointestinal stromal tumors in children:
A. Gender preference.
B. Site and histology.
C. Behavior.
A. More frequent in females.
B. Gastric; epithelioid.
C. Indolent.
463
Mantle-cell lymphoma of the gastrointestinal tract: Incidence (2).
Involvement of gastrointestinal tract occurs in 10-20% of patients with mantle-cell lymphoma.
Involvement of gastrointestinal tract is clinically occult in up to 80% of cases.
464
Intestinal lymphomas that can present as lymphomatous polyposis (3).
Mantle-cell lymphoma.
Marginal-zone lymphoma.
Follicular lymphoma.
465
Enteropathy-associated T-cell lymphoma: Typical gross pathology.
Ulcers and strictures in the jejunum.
466
Enteropathy-associated T-cell lymphoma: Histologic types (2).
Pleomorphic.
Monomorphic.
467
Pleomorphic enteropathy-associated T-cell lymphoma: Immunohistochemistry.
Positive: CD3.
Negative: CD4, CD5, CD56.
CD8 is negative in 20% of cases.
468
Monomorphic enteropathy-associated T-cell lymphoma: Immunohistochemistry.
Positive: CD3, CD56, CD8.
469
Enteropathy-associated T-cell lymphoma: Association with celiac disease.
Much stronger with the pleomorphic type.
470
Intestinal reactive lymphoid hyperplasia: Most frequent sites (3).
Terminal ileum.
Duodenum.
Rectum.
471
Terminology of anal squamous intraepithelial lesions.
Anal canal: LGAIN, HGAIN.
Perianal skin: LSIL, HSIL.
472
Anal carcinoma: Location.
Above the dentate line.
473
Anal carcinoma: Typical histology (2).
SCC or some variant thereof (95%).
Half of the SCCs are nonkeratinizing.
474
Anal carcinoma: Basaloid squamous-cell carcinoma.
Consists of tumor islands with peripheral palisading, but not to the degree of BCC.
475
Anal carcinoma: Uncommon histology (3).
Colorectal-type carcinoma.
Salivary-type carcinomas.
Undifferentiated neuroendocrine-type carcinomas.
476
Paget's disease of anal mucosa: Stains (4).
PAS.
Mucicarmine.
Alcian blue.
Often: CEA.
477
Paget's disease of anal mucosa: Origins (3).
Apocrine cells.
Adenocarcinoma of the rectosigmoid.
Adenocarcinoma of the anal canal.
478
Adenocarcinoma involving the anal canal: Origins (5).
Rectum.
Anal canal.
Perianal duct or glands.
Paget's disease.
Chronic perianal fistula.
479
Adenocarcinoma arising in a perianal fistula: Type.
Usually mucinous adenocarcinoma.
480
Anal melanoma may mimic ___ clinically.
a hemorrhoid
481
How many appendices resected for appendicitis turn out to be normal?
About 15%.
482
Mucocele of the appendix.
Gross term only.
Most cases are due to mucinous cystadenoma or cystadenocarcinoma.
483
Non-neoplastic cause of appendiceal mucocele:
A. Name.
B. Size.
C. Typical cause.
A. Retention cyst.
B. Less than 1 cm (anything larger is a neoplasm until proved otherwise).
C. Sterile obstruction of the appendiceal lumen.
484
Mucinous cystadenoma of the appendix: Association.
About 20-25% are associated with a separate primary colonic adenocarcinoma.
485
Mucinous cystadenoma of the appendix: Gross pathology.
Appendix often resembles a sausage.
Expansion of mucin may produce diverticula.
486
Mucinous cystadenoma of the appendix: Histology.
Lining: Columnar cells showing dysplasia, usually low-grade.
Contents: Mucin.
487
Adenocarcinoma of the appendix: Gross pathology.
Forms a mass that may be confined to the base of the appendix or that may expand so as to obliterate the appendix.
488
Adenocarcinoma of the appendix: Histology.
Mucinous cystadenocarcinoma: Mucinous cystadenoma with invasion.
Nonmucinous adenocarcinoma: Identical to that of colonic adenocarcinoma.
489
Pseudomyxoma peritonei:
A. Causes.
B. Composition.
A. Benign or malignant neoplasms of the appendix.
B. May contain almost no cells.
490
Pseudomyxoma peritonei: Predictors of worse prognosis (4).
Diffuse distribution.
Malignant primary tumor.
Cellular mucus.
High-grade dysplasia or malignancy.
491
Pseudomyxoma peritonei: Typical causes of death (2).
Sepsis.
Bowel obstruction.
Not cancer.
492
Pseudomyxoma peritonei: Relevance to ovarian mucinous tumors (2).
Ovarian mucinous tumors can accompany pseudomyxoma peritonei.
The appendix is still the usual the source of pseudomyxoma peritonei.
493
Myxoglobulosis:
A. Significance.
B. Histology (2).
A. May be found in appendiceal mucoceles, including mucinous neoplasms.
B. Lamellated and often calcified; appendiceal lining may show pseudosynovial metaplasia.
494
Carcinoid tumors of the appendix: Variants.
Insular.
Tubular.
Goblet-cell.
495
Goblet-cell carcinoid: Synonyms.
Crypt-cell carcinoma.
Goblet-cell adenocarcinoma.
496
Goblet-cell carcinoid: Histology.
Cells that resemble mature goblet cells form discrete clusters, strands, and microglands.
497
Goblet-cell carcinoid: Immunohistochemistry.
Positive: Pancytokeratin.
Negative or focal: Neuroendocrine markers.
498
Goblet-cell carcinoid: Signs of differentiation into a carcinoma of higher grade (4).
Solid growth.
Complex infiltrative pattern.
Nuclear atypia with increased mitotic activity.
Dissecting mucus.
499
Tubular carcinoid: Immunohistochemistry.
Positive for neuroendocrine markers.
Often positive for glucagon.
500
Carcinoid tumor of the appendix vs. fibrous obliteration.
Fibrous obliteration: Neuroendocrine cells are few and scattered.
501
Tubular carcinoid vs. signet-ring carcinoma.
Signet-ring carcinoma:
− More infiltrative.
− More pleomorphism.
− More mitotic activity.
502
Carcinoid tumors of the appendix: Indications for right hemicolectomy (5).
Size greater than 2 cm.
Invasion beyond muscularis propria.
Vascular invasion.
Incomplete excision.
Coexisting adenocarcinoma.
503
Cancers that metastasize to the stomach:
A. Most common origins (3).
B. Endoscopy.
A. Melanoma, lung, breast.
B. Target-shaped lesion.
504
Pancreaticobiliary carcinoma vs. primary ampullary carcinoma (2).
Primary ampullary carcinoma:
− Usually arises in an adenoma.
− Better prognosis.
505
Cancers that metastasize to the small intestine:
A. Most common origin.
B. Endoscopy.
C. Another frequent metastasis.
A. Melanoma.
B. Obstructive mass.
C. Bronchogenic SCC to the proximal jejunum.
