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AP reviewer > GI tract > Flashcards

GI tract Flashcards

1
Q

Gastric ectopia of the esophagus: Histology.

A

Oxyntic mucosa usually.

May undergo intestinal metaplasia.

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2
Q

Sebaceous ectopia in the esophagus: Synonym.

A

Fordyce’s granules.

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3
Q

Pancreatic ectopia in the esophagus: Associations (3).

A

Metaplasia due to reflux.

Trisomy 13 or 18.

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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.

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5
Q

Esophageal atresia: Types.

A

I: No fistula.

II: Proximal fistula only.

III: Distal fistula only.

IV: Proximal and distal fistulae.

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6
Q

Esophageal atresia: Clinical presentation.

A

Choking during feeding; excessive drooling.

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7
Q

Esophageal atresia: Associated syndromes.

A

Down’s syndrome.

VATER syndrome.

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8
Q

Congenital esophageal duplication: Gross pathology.

A

Cyst (most often), diverticulum, or tubule.

May be intramural or extramural.

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9
Q

Congenital esophageal duplication: Histology (2).

A

Lining: Respiratory, gastric, intestinal, or squamous.

Wall: Two layers of muscularis propria.

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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.

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11
Q

Plummer-Vinson syndrome: Other association.

A

Autoimmune diseases.

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12
Q

Esophageal web: Histology.

A

Fibrovascular core without muscle.

Proximal lining: Squamous mucosa.

Distal lining: Squamous or gastric mucosa.

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13
Q

Esophageal ring: Cause.

A

Constriction due, e.g., to reflux or scleroderma.

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14
Q

Esophageal ring: Types.

A

Muscular.

Mucosal.

Schatzki ring: Located at or just above the GE junction.

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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.

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16
Q

Esophageal hernia: Types.

A

Sliding.

Paraesophageal.

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17
Q

Esophageal hernia:

A. Gross pathology.
B. Histology.

A

A. Dilatation, ischemic changes.

B. Chronic inflammation, epithelial regenerative changes, fibromuscular proliferation.

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18
Q

VATER syndrome: Components.

A

Vertebral anomalies.

Anal atresia.

TracheoEsophageal fistula.

Renal defects.

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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.

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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.

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21
Q

Pill esophagitis:

A. Main culprits.
B. Histology.

A

A. Iron, alendronate.

B. Nonspecific ulcer, possibly with prominent endothelial proliferation.

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22
Q

Chemical esophagitis: Locations.

A

Points of compression: Proximal and distal ends, mid-esophagus.

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23
Q

Radiation esophagitis: Gross pathology.

A

Large superficial ulcers.

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24
Q

Radiation esophagitis: Histology.

A

Acanthosis with parakeratosis.

Necrosis.

Atypia of stromal cells: Stellate fibroblasts, plump endothelial cells.

Hyalinized blood vessels.

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25
Q

Esophagitis dissecans superficialis:

A. Endoscopy.
B. Biopsy.

A

A. Whitish strips of peeling mucosa.

B. Intraepithelial splitting with necrotic superficial epithelium, bacterial and fungal colonies.

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26
Q

Esophagitis dissecans superficialis: Causes.

A

Bisphosphonates.

Bullous skin diseases.

Esophageal trauma.

Stricture.

Smoking.

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27
Q

“Black esophagus”.

A

Acute esophageal necrosis: May be associated with severe cardiovascular disease with hemodynamic compromise.

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28
Q

Bullous diseases of the esophagus:

A. Potentially fatal.
B. Rare in this location but more common in the skin.

A

A. Pemphigus vulgaris.

B. Bullous pemphigoid.

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29
Q

Gross pathology of esophageal bullous diseases:

A. Pemphigus vulgaris.
B. Bullous pemphigoid.
C. Lichen planus.

A

A. Bleeding and strictures.

B. Blisters.

C. Papules, plaques, or strictures.

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30
Q

Esophageal erythema multiforme: Gross pathology (2).

A

May resemble peptic or reflux esophagitis.

Pseudomembranes may form.

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31
Q

Esophageal graft-versus-host disease:

A. Typical location.
B. Gross pathology.

A

A. Upper third.

B. Desquamative lesions may cause a web.

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32
Q

Esophageal pemphigus vulgaris:

A. Location of split.
B. Inflammatory cells.

A

A. Suprabasal.

B. Eosinophils.

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33
Q

Esophageal bullous pemphigoid:

A. Location of split.
B. Inflammatory cells.

A

A. Subepithelial.

B. Eosinophils.

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34
Q

Histology of esophageal graft-versus-host disease:

A. Acute.
B. Chronic.

A

A. Karyorrhexis and apoptosis of epithelial cells; variable infiltrate of T cells.

B. Epidermal atrophy; fibrosis of lamina propria.

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35
Q

Immunofluorescence:

A. Pemphigus vulgaris.
B. Bullous pemphigoid.

A

A. Intercellular IgG.

B. IgG or IgA at the basement membrane.

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36
Q

Lymphocytic esophagitis:

A. Definition.
B. Cause.

A

A. At least 30 lymphocytes per hpf.

B. Many, including reflux, candidiasis, achalasia, lichenoid drug eruption.

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37
Q

Eosinophilic esophagitis: Epidemiology (2).

A

More common in males.

Concurrent eosinophilic enteritis is more common in children.

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38
Q

Eosinophilic esophagitis: Endoscopy (4).

A

Webs.

Corrugation.

Ulcers, exudates may be seen.

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39
Q

Eosinophilic esophagitis: Histologic definition.

A

More than 15 eosinophils per hpf.

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40
Q

Eosinophilic esophagitis: Ancillary test.

A

Serum eotaxin-3.

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41
Q

Reflux esophagitis: Endoscopic grading.

A

A through D, with A being the mildest.

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42
Q

Reflux esophagitis: Frequency of endoscopically inapparent cases.

A

30%.

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43
Q

PPI-responsive esophageal eosinophilia.

A

Eosinophilic esophagitis that responds to proton-pump inhibitors.

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44
Q

Barrett’s esophagus: Age groups.

A

Under the age of 15.

Over the age of 40.

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45
Q

Barrett’s esophagus: Special stain.

A

Alcian blue, pH 2.5.

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46
Q

Barrett’s esophagus: Immunohistochemistry.

A

CK7: Superficial and deep staining.

CK20: Bandlike superficial staining.

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47
Q

Intestinal metaplasia of cardia-type mucosa:

A. Distinction from Barrett’s esophagus.
B. Causes.

A

A. Depends on endoscopic impression.

B. Reflux, Helicobacter pylori.

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48
Q

Barrett’s esophagus with low-grade dysplasia: Treatments.

A

Antireflux therapy and close clinical follow-up.

Endoscopic ablation.

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49
Q

Barrett’s esophagus with low-grade dysplasia vs. indefinite for dysplasia: Immunohistochemistry.

A

Low-grade dysplasia may show more staining with p53, racemase, and Ki67.

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50
Q

Barrett’s esophagus with dysplasia vs. regenerative atypia (5).

A

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.

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51
Q

Colchicine and taxane: Histologic effects on the esophagus (4).

A

Increased mitotic figures, including “ring” types.

Apoptosis.

Nuclear stratification.

Loss of nuclear polarity.

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52
Q

Eosinophilic esophagitis: Genetics.

A

Familial cases: Mutation in TSLP (thymic stromal lymphopoietin) on 5q22.

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53
Q

Esophageal adenocarcinoma: Ancillary test.

A

Immunohistochemistry or FISH for HER2 to select patients for trastuzumab therapy.

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54
Q

Esophageal inflammatory fibroid polyp: Histology.

A

Lining: Benign squamous mucosa, possibly ulcerated.

Stroma:
− Variably cellular and variably edematous.
− Eosinophils and plasma cells.
− Prominent vessels with concentric stromal cells.

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55
Q

Esophageal inflammatory fibroid polyp: Mutation.

A

Somatic mutations, similar to those of some GISTs, may occur.

PDGFRα may be mutated.

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56
Q

Granular-cell tumor: Histologic features that suggest malignancy (5).

A

Increased cellularity.

Spindle cells.

Nuclear atypia.

Necrosis.

More than 2 mitotic figures per 10 hpf.

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57
Q

Squamous papilloma of the esophagus: Causes (4).

A

Human papillomavirus.

Reflux esophagitis.

Eosinophilic esophagitis.

Trauma.

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58
Q

Squamous papilloma of the esophagus: Location.

A

Mid or lower esophagus in 95% of cases.

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59
Q

Esophageal squamous dysplasia: Schemes of grading (2).

A

Mild, moderate, severe, or carcinoma in situ.

Low or high.

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60
Q

Esophageal squamous-cell carcinoma: Locations.

A

Mid or lower esophagus in 90% of cases.

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61
Q

Esophageal squamous-cell carcinoma: Tumor configurations.

A

Exophytic: Most common.

Ulcerating.

Purely infiltrating: Least common.

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62
Q

Esophageal squamous-cell carcinoma: Morphology of early lesions (2).

A

May be multifocal.

May be combined with widely scattered variable dysplasia and carcinoma in situ.

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63
Q

Esophageal squamous-cell carcinoma: Effect of irradiation.

A

Calcification keratinizing cells and foreign-body-giant-cell reaction.

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64
Q

Esophageal fibrovascular polyp: Histology.

A

Lining: Benign squamous epithelium.

Core: Collagenous or myxoid; sometimes contains fat.

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65
Q

Esophageal squamous-cell carcinoma: Main determinants of survival (2).

A

Depth of invasion.

Nodal status.

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66
Q

Tylosis:

A. Inheritance.
B. Clinical features (3).

A

A. Autosomal dominant.

B. SCC of the esophagus, hyperkeratosis of palms and soles, oral leukoplakia.

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67
Q

Esophageal squamous-cell carcinoma: Main variants (3).

A

Verrucous.

Sarcomatoid.

Undifferentiated.

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68
Q

Sarcomatoid carcinoma of the esophagus: Epidemiology.

A

Much more common in males than in females.

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69
Q

Sarcomatoid carcinoma of the esophagus: Histology of metastases.

A

May include any or all of the component of the primary tumor.

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70
Q

Esophageal squamous-cell carcinoma: Prognosis (2).

A

Generally poor, but better with polypoid tumors.

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71
Q

Undifferentiated carcinoma of the esophagus:

A. Histology.
B. Immunohistochemistry.

A

A. Undifferentiated cells with vesicular nuclei, prominent nuclei; cytoplasm is often abundant and eosinophilic.

B. Typically cytokeratin positive.

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72
Q

Verrucous carcinoma of the esophagus: Possible associations (2).

A

Achalasia.

Ingestion of acid.

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73
Q

Verrucous carcinoma of the esophagus: Surface.

A

Show parakeratosis and hyperkeratosis.

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74
Q

Verrucous carcinoma of the esophagus vs. benign papillomatous lesions.

A

Benign papillomatous lesions exhibit no pushing pattern of invasion at the deep margin.

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75
Q

High-grade neuroendocrine carcinoma of the esophagus: Histology (3).

A

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.

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76
Q

High-grade neuroendocrine carcinoma of the esophagus vs. metastatic neuroendocrine carcinoma (3).

A

TTF-1 to exclude pulmonary primary.

Clinical history may be required.

Distinction may be clinically irrelevant.

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77
Q

Melanoma of the esophagus: Possible changes in adjacent squamous mucosa (4).

A

Melanosis.

Melanocytosis.

Junctional activity.

Melanoma in situ.

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78
Q

Gastric duplication:

A. Location (2).
B. Gross pathology.

A

A. Usually intramural and on the greater curvature of the stomach.

B. Cystic mass that usually does communicate with the gastric lumen.

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79
Q

Gastric duplication: Lining.

A

More often gastric mucosa but can contain small-intestinal, respiratory, or pancreatic epithelium.

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80
Q

Gastric pyloric stenosis: Epidemiology (2).

A

More common in males and in firstborn children.

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81
Q

Gastric pyloric stenosis: Normal thickness of pyloric sphincter.

A

0.5 cm.

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82
Q

Pancreatic heterotopia in the stomach:

A. Origin.
B. Gross pathology.

A

A. Accessory pancreatic bud.

B. Umbilicated submucosal mass with duct.

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83
Q

Pancreatic heterotopia in the stomach: Histology.

A

Usually contains ducts, acini, and islet cells.

Can under the histologic changes that occur in the pancreas, e.g. inflammation, dysplasia, tumors.

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84
Q

Pancreatic heterotopia in the stomach: Name given to a lesion that consists of ducts only.

A

Adenomyoma.

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85
Q

Pyloric stenosis: Possibly associated mutation.

A

Duplication of 9q.

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86
Q

Sarcomatoid carcinoma of the esophagus: Immunohistochemistry.

A

Cytokeratin is positive in fewer than half of cases.

Vimentin is strong in the stromal component.

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87
Q

Sarcomatoid carcinoma of the esophagus: Histology.

A

Carcinomatous component: Squamous, glandular, or undifferentiated.

Mesenchymal: Spindle cells or with heterologous differentiation.

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88
Q

Gastric xanthelasma: Associations (3).

A

Duodenal reflux, gastritis, previous gastric surgery.

Not associated with hyperlipidemia.

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89
Q

Acute erosive gastritis: Associations (6).

A

NSAIDs.
Chemotherapy.

Alcohol.
Heavy smoking.

Physiologic stress.
Nasogastric intubation.

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90
Q

Mild acute erosive gastritis: Histology.

A

Active gastritis with edema.

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91
Q

Moderate acute erosive gastritis: Histology.

A

Mucosal erosion with fibrinopurulent exudate.

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92
Q

Severe acute erosive gastritis: Histology.

A

Confluent erosions; may resemble ulcer.

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93
Q

Reactive gastropathy: Causes.

A

Ethanol.
NSAIDs.
Steroids and other drugs.

Physiologic stress.

Reflux of duodenal contents.

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94
Q

Reactive gastropathy vs. gastric antral vascular ectasia.

A

Gastric antral vascular ectasia: Fibrin thrombi in the dilated capillaries.

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95
Q

Diffuse antral Helicobacter pylori-associated gastritis:

A. Epidemiology.
B. Location.

A

A. Whites in the United States.

B. Typically antral.

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96
Q

Diffuse antral Helicobacter pylori-associated gastritis: Histology.

A

Active chronic antral gastritis, sometimes with lymphoid aggregates, intestinal metaplasia.

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97
Q

Multifocal antral Helicobacter pylori-associated gastritis:

A. Epidemiology.
B. Location.

A

A. Minorities in the United States; Scandinavians.

B. Antral-body junction.

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98
Q

Diffuse antral Helicobacter pylori-associated gastritis: Histology (3).

A

Minimal chronic inflammation associate with islands of intestinal metaplasia or pyloric pseudometaplasia.

Minimal active inflammation.

Lymphoid follicles with germinal centers may persist.

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99
Q

Types of intestinal metaplasia.

A

Type I: Goblet cells and enterocyte-type absorptive cells.

Type II: Goblet cells and gastric foveolar cells.

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100
Q

Helicobacter heilmannii:

A. Associations (3).
B. Morphology.

A

A. Gastritis, carcinoma, gastric MALT lymphoma.

B. Twice as long (7 μm) as H. pylori; tightly coiled.

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101
Q

Autoimmune gastritis: Location.

A

Body and fundus.

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102
Q

Autoimmune gastritis: Histology.

A

Oxyntic epithelium: Atrophy, pyloric pseudometaplasia, intestinal metaplasia.

Enterochromaffin cells: Hyperplasia, dysplasia, or carcinoid tumors.

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103
Q

Autoimmune gastritis: Laboratory findings (2).

A

Hypergastrinemia.

Autoantibodies to parietal cells or to intrinsic factor.

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104
Q

Atrophic autoimmune pangastritis: Location.

A

Body and antrum.

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105
Q

Atrophic autoimmune pangastritis: Histology.

A

Epithelium: Inflammation (sometimes with. Any lymphocytes), atrophy, apoptosis.

Neuroendocrine cells: Decrease.

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106
Q

Atrophic autoimmune pangastritis: Laboratory findings (2).

A

No hypergastrinemia.

No antibodies to parietal cells or to intrinsic factor.

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107
Q

Lymphocytic gastritis: Associations (3).

A

Helicobacter pylori.

Celiac disease.

Lymphocytic colitis.

Others.

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108
Q

Lymphocytic gastritis: Histology.

A

Surface: More than 25 lymphocytes per 100 gastric foveolar cells.

Background: Chronic gastritis.

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109
Q

Collagenous gastritis: Associations (3).

A

Collagenous colitis.

Celiac disease.

Anemia in some younger patients.

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110
Q

Collagenous gastritis: Histology.

A

Thickened subepithelial collagen plate, sometimes with lymphocytic gastritis.

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111
Q

Eosinophilic gastritis: Epidemiology.

A

Children, adolescents.

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112
Q

Eosinophilic gastritis: Histology.

A

Eosinophils not associated with other inflammatory cells and causing mucosal architectural change or crypt injury.

Eosinophils may infiltrate muscularis mucosae or deeper layers.

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113
Q

Peptic ulcer: Histologic layers.

A

Neutrophils and débris.

Fibrin and necrotic matter.

Active granulation tissue.

Fibrous scar that interrupts the muscularis mucosae.

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114
Q

Hypertrophic gastropathy: Thickness of mucosa.

A

Greater than 1 to 1.5 mm.

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115
Q

Ménétrier’s disease: Symptoms (4).

A

Abdominal pain.

Diarrhea.

Weight loss.

Peripheral edema.

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116
Q

Ménétrier’s disease: Chemical abnormalities (2).

A

Hypoproteinemia.

Hypochlorhydria.

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117
Q

Ménétrier’s disease: Associations (3).

A

Eosinophilia.

Pulmonary infections.

Thrombosis.

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118
Q

Ménétrier’s disease: Possible infectious association.

A

CMV: Children and some cases in the immunosuppressed.

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119
Q

Ménétrier’s disease: Gross pathology (2).

A

Thick gastric wall with cerebriform rugae.

Antral sparing.

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120
Q

Ménétrier’s disease: Histology (4).

A

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.

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121
Q

Zollinger-Ellison syndrome:

A. Cause.
B. Epidemiology.

A

A. Gastrinoma.

B. Can affect anyone but is most common in between ages 20 and 50.

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122
Q

Zollinger-Ellison syndrome: Symptoms.

A

Abdominal pain, diarrhea.

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123
Q

Zollinger-Ellison syndrome: Gross pathology.

A

Thick gastric wall with giant rugae.

Antral sparing.

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124
Q

Zollinger-Ellison syndrome: Histology.

A

Hyperplasia is in the specialized glands.

Thickness ratio of pits to glands exceeds 5 to 1.

The foveolar epithelium is atrophic.

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125
Q

Complications of Zollinger-Ellison syndrome:

A. Histologic.
B. Clinical.

A

A. Hyperplasia of enterochromaffin-like cells, dysplasia of neuroendocrine cells, carcinoid tumors.

B. Peptic ulcers.

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126
Q

Ménétrier’s disease vs. gastric hyperplastic polyp.

A

May depend on clinical history, especially in small biopsies.

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127
Q

Gastritis glandularis et cystica profunda: Synonyms.

A

Diffuse cystic (glandular) malformation.

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128
Q

Gastritis glandularis et cystica profunda: Histology.

A

Mucosal and submucosal cysts lined by mucous cells.

Pyloric or Brunner-type glands.

Fundic-type glands (rare).

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129
Q

Gastritis glandularis et cystica profunda: Significance.

A

May increase risk for gastric carcinoma.

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130
Q

Fundic-gland polyp: Causes (5).

A

Idiopathic (sporadic).

Familial adenomatous polyposis.

Attenuated familial adenomatous polyposis.

MUTYH-associated polyposis syndrome.

Proton-pump inhibitors.

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131
Q

Fundic-gland polyps: Mutations (2).

A

APC.

β-Catenin.

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132
Q

Fundic-gland polyposis associated with FAP syndrome:

A. Number of polyps.
B. Location.

A

A. Hundreds.

B. Mostly on the greater curvature, with antral sparing.

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133
Q

Gastric adenocarcinoma with chief-cell differentiation: Histology.

A

Anastomosing cords of oxyntic epithelial cells that infiltrate generally only the mucosa.

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134
Q

Gastric adenocarcinoma with chief-cell differentiation: Prognosis.

A

May persist or recur if incompletely excised.

No reports of metastasis; may be benign.

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135
Q

Gastric carcinoma: Main types (2).

A

Intestinal: Exophytic; resembles colonic carcinoma.

Diffuse: Infiltrative.

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136
Q

Gastric dysplasia: Main types (2).

A

Flat.

Adenomatous.

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137
Q

Gastric adenomas: Types (5).

A

Common: Tubular, tubulovillous, villous.

Rare: Antral-foveolar type, pyloric-type.

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138
Q

Intestinal type of gastric adenocarcinoma:

A. Epidemiology (2).
B. Associations (2).

A

A. Found more often in elderly men and in countries with high incidence of gastric cancer.

B. Dietary practices; H. pylori.

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139
Q

Intestinal type of gastric adenocarcinoma: Histologic origin.

A

Intestinal metaplasia; dysplastic precursor.

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140
Q

Diffuse type of gastric adenocarcinoma:

A. Epidemiology.
B. Associations (2).

A

A. More common in younger patients and in women.

B. H. pylori (possibly); germline mutations of CDH1 (E-cadherin).

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141
Q

Diffuse type of gastric adenocarcinoma:

A. Histologic origin.
B. Prognosis.

A

A. May arise from undifferentiated cells in the neck of the gastric gland.

B. Worse than that of the intestinal type.

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142
Q

Early gastric carcinoma:

A. Definition.
B. Survival.

A

A. Invasion of submucosa but not of muscularis propria.

B. 95%.

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143
Q

Gastric carcinoma: Molecular testing.

A

Testing for HER2 for selection of patients for trastuzumab therapy.

Also relevant to adenocarcinomas of the gastric cardia, gastroesophageal junction, and the lower esophagus.

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144
Q

Gastric carcinoma: Best predictor of survival.

A

Depth of invasion.

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145
Q

Gastric carcinoma: Survival for tumors that involve the subserosa.

A

50%.

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146
Q

Gastric neuroendocrine tumors: Types.

A

1: Associated with atrophic gastritis.
2: Associated with Zollinger-Ellison syndrome.
3: Sporadic.
4: High-grade neuroendocrine carcinoma.

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147
Q

Gastric neuroendocrine tumors: Categories.

A

Sporadic tumors.

Tumors arising in a background of hypergastrinemia.

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148
Q

Sporadic gastric neuroendocrine tumors:

A. Number.
B. Behavior.

A

A. Usually solitary.

B. Can invade or metastasize.

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149
Q

Hypergastrinemia-related gastric neuroendocrine tumors:

A. Relative frequency.
B. Number.
C. Behavior.

A

A. More common than sporadic tumors.

B. Multiple.

C. Indolent.

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150
Q

Hypergastrinemia-related gastric neuroendocrine tumors:

A. Cause.
B. Histologic origin.

A

A. Achlorhydria.

B. Enterochromaffin-like cells: Progression from hyperplasia to nodular hyperplasia to dysplasia to neoplasia.

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151
Q

Gastric neuroendocrine tumors:

A. Which ones respond to antral resection?
B. Which ones tend to be larger?

A

A. Hypergastrinemia-related tumors.

B. Sporadic tumors.

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152
Q

Gastric neuroendocrine tumors: Grading scheme of the WHO.

A

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.

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153
Q

Gastric neuroendocrine tumors: Classification of smaller Grade 1 tumors.

A

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.

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154
Q

Diagnostic criteria of well-differentiated (gastric) neuroendocrine carcinoma.

A

A grade 1 tumor that is larger than 2 cm

  • or -

That invades the muscularis propria or beyond

  • or -

That has metastasized.

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155
Q

Diagnostic criteria of high-grade (gastric) neuroendocrine carcinoma.

A

Any tumor of grade 2 or grade 3.

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156
Q

Gastric neuroendocrine tumors: Histologic distinction between sporadic and hypergastrinemia-related.

A

Hypergastrinemia-related tumors: Immunohistochemistry shows endocrine-cell hyperplasia in the adjacent mucosa.

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157
Q

Classification of gastric neuroendocrine proliferations by size.

A

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.

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158
Q

Classification of gastric neuroendocrine proliferations: When applicable (2).

A

When analyzing the mucosa adjacent to a gastric neuroendocrine tumor.

Not to be performed on antral mucosa.

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159
Q

Gastric lymphoma:

A. Most common type.
B. Most common location.

A

A. Diffuse large B-cell lymphoma.

B. Antrum.

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160
Q

Gastric marginal-zone lymphoma: Possible cell types (6).

A

Small lymphocytes with round nuclei.

Centrocyte-like cells.

Monocytoid B cells.

Plasma cells.

Centroblasts, immunoblasts.

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161
Q

Gastric marginal-zone lymphoma: Definition of lymphoepithelial lesion.

A

At least three B lymphocytes within the epithelium of the gastric glands.

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162
Q

Gastric marginal-zone lymphoma vs. lymphocytic gastritis (2).

A

Lymphocytic gastritis:
− Usually no lymphoepithelial lesions.
− Intraepithelial lymphocytes are T cells, not B cells.

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163
Q

Normal rotation of bowel during development.

A

Counterclockwise around the superior mesenteric artery.

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164
Q

Intestinal malrotation: Gross pathology (2).

A

Small intestine may be pushed to one side of abdomen.

Cecum may be on left side.

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165
Q

Intestinal malfixation: Gross pathology.

A

Fixation band may cause intestinal torsion and infarction.

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166
Q

Omphalocele: Causes (2).

A

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.

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167
Q

Omphalocele: Associations.

A

Other malformations of the gastrointestinal tract.

Cardiovascular defects.

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168
Q

Omphalocele: Gross pathology (3).

A

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.

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169
Q

Gastroschisis: Possible cause.

A

Vascular accident before 12 weeks of development.

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170
Q

Gastroschisis: Gross pathology.

A

Extra-abdominal viscera are not covered.

Umbilical cord is not affected.

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171
Q

Intestinal atresia:

A. Most common location.
B. Least common location.

A

A. Duodenum.

B. Colon.

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172
Q

Intestinal atresia: Risk factors (2).

A

Twin gestation.

Maternal use of cocaine.

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173
Q

Intestinal atresia: Presentation.

A

Bilious vomiting in soon after birth.

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174
Q

Intestinal atresia: Variations in gross pathology (3).

A

Imperforate septum occlude lumen.

Absence of lumen: Fibrotic cord.

Absence of bowel segment and its mesentery.

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175
Q

Intestinal stenosis: Variations in gross pathology (2).

A

Perforate septum.

Narrow lumen.

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176
Q

Intestinal atresia and stenosis: Histology (2).

A

Proximal to the defect: Ischemia, necrosis, granulation tissue, submucosal fibrosis, hypertrophy of lamina propria (all due to dilatation).

Blind segment: Meconium, lanugo, mucin.

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177
Q

Meckel’s diverticulum:

A. Cause.
B. Prevalence.

A

A. Failure of involution of the vitelline duct.

B. 1% to 4%.

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178
Q

Meckel’s diverticulum: Prevalence (3).

A

On the antimesenteric surface of the small bowel.

Infants: Within 30 cm of the ileocecal valve.

Adults: Within 100 cm of the ileocecal valve.

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179
Q

Meckel’s diverticulum:

A. Length.
B. Histology.

A

A. 2-15 cm.

B. Usually normal small-bowel mucosa; 80% contain ectopic pancreatic or gastric tissue.

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180
Q

Volvulus:

A. Definition.
B. Most common location.

A

A. Twisting of a segment of bowel around its mesentery.

B. Sigmoid colon.

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181
Q

Volvulus: Predisposing factors (3).

A

Congenitally long mesentery.

Meckel’s diverticulum.

Congenital band.

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182
Q

Volvulus: Gross pathology and histology.

A

Variable ischemia; possible necrosis.

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183
Q

Intussusception:

A. Epidemiology.
B. Predisposing factors (2).

A

A. Twice as common in males.

B. None in children; intraluminal mass in adults.

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184
Q

Intussusception: Histology (2).

A

Ischemia.

Recurrent cases: Intramural vascular proliferation can mimic vascular tumor.

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185
Q

Gastric marginal-zone lymphoma: Translocation.

A

t(11;18).

API2−MALT1.

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186
Q

Enterohemorrhagic Escherichia coli: Seasonal distribution of infections.

A

Most common in the summer.

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187
Q

Enterohemorrhagic E. coli: Effect of toxin.

A

Inhibits protein synthesis, thereby damaging epithelial and endothelial cells.

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188
Q

Salmonella spp.: Location of replication.

A

Within intracellular vacuoles of enterocytes and macrophages.

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189
Q

Typhoid fever:

A. Complications (3).
B. Mortality in the untreated.

A

A. Massive hemorrhage, perforation, peritonitis.

B. About 15%.

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190
Q

Salmonella spp.: Incubation period for gastroenteritis.

A

A few hours.

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191
Q

Salmonella spp.: Gross pathology of gastrointestinal infections.

A

Longitudinal oval ulcers with elevated edges, located over Peyer’s patches.

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192
Q

Campylobacter spp.: Frequent association.

A

Drinking untreated mountain water.

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193
Q

Campylobacter spp.: Incubation period for diarrhea.

A

Up to 1 week.

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194
Q

Frequent location of colitis due to ___.

A. Enterohemorrhagic E. coli.
B. Campylobacter spp.

A

A. Right colon.

B. Ileocecal valve.

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195
Q

Campylobacter spp.: Cause of severe systemic illness.

A

Campylobacter fetus.

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196
Q

Bacteria that cause focal active colitis (3).

A

Shigella spp.

Campylobacter spp.

Salmonella spp. (sometimes).

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197
Q

Bacteria that cause hyperplasia of lymphoid follicles.

A

Salmonella spp.

Yersinia enterocolitica.

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198
Q

Bacterial enterocolitis vs. idiopathic inflammatory bowel disease (5).

A 
Idiopathic inflammatory bowel disease:
− More diffuse active inflammation.
− Less hemorrhage.
− Basal plasmacytosis.
− More crypt-architectural distortion.
− Fewer suppurative granulomas (than seen in yersiniosis).
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199
Q

Causes of diarrhea in AIDS patients.

A

Infections.

AIDS enteropathy.

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200
Q

AIDS-related enteropathy: Definition (4).

A

Chronic diarrhea.

Malnutrition.

Wasting.

No evidence of gastrointestinal infection.

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201
Q

AIDS-related enteropathy: Complications (2).

A

Malabsorption due to loss of microvilli.

Death due to large ulcers proceeding from erosions.

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202
Q

Giardiasis: Associated inherited immunodeficiencies (2).

A

Common variable immunodeficiency.

Selective IgA immunodeficiency.

203
Q

Sites of gastrointestinal infection by ___.

A. CMV.
B. HSV.

A

A. Esophagus, stomach, intestines.

B. Esophagus, low rectum, anus, perianal skin.

204
Q

Cholera: Incubation period.

A

A few hours to 2 days.

205
Q

Coccidiosis: Organisms (3).

A

Cyclospora cayetanensis.

Cystoisospora belli.

Cryptosporidium spp.

206
Q

Cyclospora infection: Associations.

A

Travelers’ diarrhea.

Ingested of contaminated fresh fruit.

207
Q

Region of the gastrointestinal tract most frequently affected by ___.

A. Mycobacterium tuberculosis.
B. Mycobacterium avium complex.

A

A. Ileocecal region.

B. Anywhere.

208
Q

Histology of mycobacterial gastroenteritis:

A. Mycobacterium tuberculosis.
B. Mycobacterium avium complex.

A

A. Necrotizing granulomas, Langhans’ giant cells.

B. Foamy macrophages stuffed with bacteria fill the lamina propria.

209
Q

Yersinia enterocolitica: Risk factors for fatal infection.

A

Immunosuppression.

Iron overload.

210
Q

Adenovirus: Histology of colitis.

A

Dystrophic goblet cells with amorphous nuclei that rarely contain diagnostic (smudgy) inclusion bodies.

211
Q

Candida spp.: Definition of blastoconidium.

A

A budding yeast form, 3-5 μm.

212
Q

Gastrointestinal histoplasmosis: Types of inflammation (2).

A

Granulomatous.

Histiocytic.

213
Q

Gastrointestinal syphilis:

A. Site.
B. Histology.

A

A. Rectum or anus.

B. Dense mononuclear infiltrate that includes many plasma cells; lymphoid aggregates; no crypt-architectural distortion or marked acute inflammation.

214
Q

Use of ___ stain to detect intestinal protozoa.

A. Giemsa (3)
B. trichrome

A

A. Cryptosporidium, Cystoisospora, microsporidia.

B. Giardia (distinction from mucus).

215
Q

Mycobacterium-avium-complex enteritis vs. Whipple’s disease.

A

Whipple’s disease:
− “Fat vacuoles”.
− Positive for PAS-D, not for AFB.

216
Q

Intestinal spirochetosis: Stains.

A

Silver stain.

Immunohistochemical stain for Treponema spp.

217
Q

Candida spp.: True hypha vs. pseudohypha.

A

True hypha: No indentation at true septa.

Pseudohypha (elongated blastoconidium): Indentation at false septa.

218
Q

Whipple’s disease: Main sites (3).

A

Gastrointestinal system.

Joints.

Central nervous system.

219
Q

Whipple’s disease: Prognosis.

A

Often fatal without antibiotics.

220
Q

Whipple’s disease: Gross pathology of the bowel (3).

A

Mucosa: Yellow plaques, shallow ulcers.

Wall: Thickening.

221
Q

Whipple’s disease: Gross pathology outside the bowel (3).

A

Lymphadenopathy.

Hepatosplenomegaly.

Plaques in mesenteric fat and peritoneum.

222
Q

Whipple’s disease: Histology (3).

A

Foamy macrophages filled with bacilli.

“Fat vacuoles”, some of which are dilated lymphatic vessels.

Foreign-body granulomas or lipogranulomas.

223
Q

Whipple’s disease: Inflammatory infiltrate.

A

Little or none.

224
Q

Waldenström’s macroglobulinemia in the bowel: Histology.

A

Foamy macrophages.

Dilated lymphatics filled with eosinophilic matter.

225
Q

Gliadin-containing cereal grains.

A

Wheat, rye, barley.

226
Q

Celiac disease can cause deficiency of which nutrients (3)?

A

Iron.

Folate.

Calcium.

227
Q

Celiac disease: Preferred tests.

A

Antibodies to tissue transglutaminase.

In those who lack the above: Antibodies to deaminated gliadin peptides.

228
Q

Celiac disease: HLA types.

A

DQ2: 98%.

DQ8: 2%.

229
Q

Celiac disease: Typical number of intraepithelial lymphocytes.

A

More than 40 per 100 enterocytes.

230
Q

Celiac disease: Histology of crypts (3).

A

Elongation and hyperplasia.

Increased mitotic activity.

231
Q

Celiac disease: When to consider workup for clonality.

A

When there are ulcers in the small intestine.

In cases of refractory sprue.

232
Q

Normal length ratio of villi to crypts.

A

3:1 to 5:1.

233
Q

Celiac disease: Endoscopic finding.

A

Scalloping of the valvulae conniventes.

234
Q

Lymphocytic enterocolitis.

A

Concurrent lymphocytic colitis.

Celiac-disease-like changes in the proximal small intestine.

No response to gluten-free diet.

235
Q

Refractory sprue: Definition and cause.

A

No response to gluten-free diet for 12 months.

Allergic reaction to protein other than gluten.

236
Q

Types of refractory sprue: Intraepithelial lymphocytes.

A

Type II:
− Some may appear atypical.
− Loss of CD8 and CD5.
− Monoclonality of T-cell receptors.

237
Q

Types of refractory sprue: Treatment.

A

Type I: Azathioprine, prednisone, budesonide, or mesalamine.

Type II: May respond to cladribine, anti-CD52, or chemotherapy and stem-cell transplantation.

238
Q

Types of refractory sprue: Prognosis.

A

Type II: 50% mortality rate; most cases progress to enteropathy-associated T-cell lymphoma.

239
Q

Tropical sprue: Treatment.

A

Broad-spectrum antibiotics and vitamins.

240
Q

Autoimmune enteritis:

A. Gene and chromosome.
B. Associations (2).

A

A. FOXP3 on the X chromosome.

B. X-linked type: Immune dysregulation, polyendocrinopathy.

241
Q

Autoimmune enteritis: Targets of autoantibodies (4).

A

Enterocytes.

Goblet cells.

Parietal cells.

Smooth-muscle cells.

242
Q

Autoimmune enteritis: Clue to diagnosis (3).

A

No goblet cells.

No increase in intraepithelial lymphocytes.

No response to gluten-free diet.

243
Q

Abetalipoproteinemia:

A. Histology.
B. Peripheral blood.

A

A. Enterocytes with intracytoplasmic vacuoles.

B. Acanthocytes.

244
Q

Celiac disease: Progression of recovery.

A

From distal to proximal, with the duodenum recovering last.

245
Q

Primary adenocarcinoma of the small intestine: Risk factors (6).

A

Familial adenomatous polyposis.
Attenuated FAP.
MUTYH-associated polyposis syndrome.

Lynch’s syndrome.
Peutz-Jeghers syndrome.

Crohn’s disease.

246
Q

Primary adenocarcinoma of the small intestine: Locations.

A

Most: Near major duodenal papilla.

Associated with Crohn’s disease: Ileum.

247
Q

Gastrointestinal carcinoid tumors: Sites (5).

A

Appendix (#1).

Ileum.

Rectum.

Stomach.

Colon.

248
Q

Carcinoid tumors of the bowel: Presentations (4).

A

Incidental.

Weight loss.

Obstruction.

Carcinoid syndrome.

249
Q

Carcinoid syndrome associated with carcinoid tumors of the bowel:

A. Prevalence.
B. Most common site of carcinoid tumor.

A

A. 10%.

B. Ileum.

250
Q

Carcinoid syndrome:

A. Hormonal mediators.
B. Associated lesion.

A

A. 5-HT, 5-HIAA.

B. Lesion of right heart in 50% of cases.

251
Q

Significance ___ in carcinoid tumors of the bowel:

A. cytologic features
B. vascular invasion
C. perineural invasion

A

None of these factors predict behavior of the tumor.

252
Q

Atypical carcinoid: Synonyms (2).

A

Grade 2 neuroendocrine tumor.

Intermediate-grade neuroendocrine tumor.

253
Q

Grade 2 neuroendocrine tumor: Criteria (2).

A

2-20 mitotic figures per 10 hpf.

More than 2% to 20% of nuclei positive for Ki-67.

254
Q

Carcinoid tumors of the bowel: Relevance of immunohistochemistry to site.

A

Hindgut tumors are often negative for chromogranin.

255
Q

Gangliocytic paraganglioma: Cellular components (3).

A

Neuroendocrine cells.

Spindle cells with Schawann-cell differentiation.

Ganglion cells.

256
Q

Gangliocytic paraganglioma:

A. Frequent site.
B. Behavior.

A

A. Ampullary region.

B. Uncertain malignant potential.

257
Q

Mixed carcinoid-adenocarcinoma:

A. Gross pathology.
B. Portion made up by adenocarcinoma.

A

A. Often large and infiltrating.

B. Typically more than 50%.

258
Q

Mixed carcinoid-adenocarcinoma:

A. Differential diagnosis.
B. Prognosis.

A

A. Benign epithelial differentiation within a carcinoid tumor.

B. Acts like adenocarcinoma.

259
Q

Frequent histologic feature of carcinoid tumors of the ___.

A. Small intestine.
B. Rectum.
C. Duodenum.

A

A. Insular growth.

B. Trabecular growth.

C. Psammoma bodies.

260
Q

Carcinoid tumors of the bowel: Relevance of risk of metastasis to size of tumor.

A

Less than 1 cm: 2%.

1-2 cm: 50% (ileal), 15% (rectal).

More than 2 cm: 80%.

261
Q

Carcinoid tumors of the bowel: Best indicator of behavior.

A

Metastasis.

262
Q

Typical behavior of ___.

A. Gastrinoma.
B. Insulinoma.

A

A. Malignant.

B. Benign.

263
Q

Hirschsprung’s disease: Risk factors (2).

A

Male sex.

Down’s syndrome.

264
Q

Hirschsprung’s disease: Forms (3).

A

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
Q

Hirschsprung’s disease: Typical histology (3).

A

No ganglion cells.

Hypertrophic mural nerves (>40 μm).

Thickened muscle layers.

266
Q

Hirschsprung’s disease: Special stains (4).

A

Acetylcholinesterase: Nerve fibers extend into lamina propria.

Calretinin: Absence of staining.

NSE for ganglion cells.

S-100 for Schwann cells.

267
Q

Long-segment Hirschsprung’s disease: Histology and special stain.

A

Mural nerves may not be hypertrophic.

Acetylcholinesterase stain may be falsely negative.

268
Q

Hirschsprung’s disease: Mutations.

A

RET, endothelin receptor B.

269
Q

Hirschsprung’s disease vs. hypoganglionosis.

A

Hypoganglionosis: Some ganglion cells but still too few.

270
Q

Intestinal neuronal dysplasia: Histology.

A

Hyperplastic plexus.

Giant ganglia containing more than 8 neurons.

271
Q

Eosinophilic gastroenteritis: Definition (3).

A

Gastrointestinal symptoms.

Eosinophilic infiltration of the gastrointestinal tract.

No known cause such as specific allergy or parasites.

272
Q

Eosinophilic gastroenteritis: Frequent associations (3).

A

Peripheral eosinophilia.

Elevated serum IL-5.

History of allergies.

273
Q

Eosinophilic gastroenteritis: Types (3).

A

Mucosal: Diarrhea and malabsorption.

Submucosal: Obstruction.

Mural and serosal: Ascites, eosinophilic peritonitis.

274
Q

Eosinophilic gastroenteritis: Main histologic features (3).

A

Sheets of eosinophils.

Mucosal changes.

Fibrosis.

275
Q

Allergy to cow’s milk: Histology (2).

A

Villous atrophy.

Neutrophils and eosinophils.

276
Q

Systemic mastocytosis of the gastrointestinal tract:

A. Associated mutation.
B. Definition of mast-cell aggregate.

A

A. D816V in KIT.

B. More than 15 mast cells.

277
Q

Systemic mastocytosis of the gastrointestinal tract: Histological confounder.

A

Obscuring eosinophils (80% of cases).

278
Q

Idiopathic constipation: Histology (3).

A

Ganglion cells are present.

Argyrophilic neurons may be lost.

Interstitial cells of Cajal may be decreased.

279
Q

Acute graft-versus-host disease:

A. Timing.
B. Initial site of involvement.

A

A. Usually occurs within 100 days after transplantation.

B. Skin.

280
Q

Gastrointestinal graft-versus-host disease: Initial histology.

A

Necrosis of single cells in the bases of crypts gives rise to lacunae that contain apoptotic débris.

281
Q

Gastrointestinal graft-versus-host disease: Intermediate histology.

A

Apoptosis in many crypts; crypt abscesses; ulcers with secondary fungal infection.

282
Q

Gastrointestinal graft-versus-host disease: Late histology.

A

Mucosal atrophy, fibrosis, or regeneration.

283
Q

Gastrointestinal graft-versus-host disease vs. effect of mycophenolate mofetil.

A

Mycophenolate mofetil:
− More likely to have eosinophils.
− Less likely to have apoptotic débris within lacunae.

284
Q

Graft-versus-host disease: Mediating cell.

A

The cytotoxic T cell.

285
Q

Crohn’s disease of the small bowel: Gene.

A

IBD-1, a.k.a. NOD2/CARD15.

286
Q

Ulcerative colitis: Feared acute complications (2).

A

Toxic megacolon.

Perforation.

287
Q

Crohn’s disease: Gross pathology (3).

A

Fat-wrapping.

“Stovepipe” bowel.

“Cobblestoning” of mucosa.

288
Q

Crohn’s disease: Radiography.

A

“String sign” due to luminal stenosis.

289
Q

Crohn’s disease: Histology of inflammation (4).

A

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
Q

Crohn’s disease: Histology of stromal changes (3).

A

Hypertrophy of muscularis mucosae.

Submucosal neuronal hyperplasia.

Mural fibrosis.

291
Q

Crohn’s disease: Serologic test.

A

Antibodies to Saccharomyces cerevisiae are found in about half of patients.

292
Q

Ulcerative colitis: Site.

A

Always involves the rectum.

Does not have to involve the whole colon; “backwash” ileitis is not a required finding.

293
Q

Ulcerative colitis: Histology of inflammation (2).

A

Dense lymphoplasmacytic and neutrophilic infiltrate that usually goes no deeper than the submucosa.

Cryptitis, crypt abscesses, crypt regeneration, and crypt-architectural distortion.

294
Q

Ulcerative colitis: Features that may make it “primary inflammatory bowel disease of an indeterminate type” (2).

A

Pancolitis with involvement of the terminal ileum.

Ulcers that extend into the muscularis propria.

295
Q

Ulcerative colitis: Antibody.

A

pANCA.

296
Q

Lymphocytic colitis: Number of lymphocytes.

A

More than 15 per 100 superficial epithelial cells.

297
Q

Diversion colitis: Leading cause.

A

Hartmann pouch constructed during a proximal partial colectomy.

298
Q

Diversion colitis: Histology (4).

A

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
Q

Diversion colitis: Treatment (3).

A

Restoration of fecal stream.

Enemas of short-chain fatty acids.

Surgical excision in refractory cases.

300
Q

Causes of active ileitis (4).

A

Minimal and focal:
− Bowel preparation.
− Trauma and prolapse.

Significant:
− Crohn’s disease.
− NSAIDs.

301
Q

Ileal pouch:

A. Purpose.
B. Clinical indications.

A

A. To restore continence after colectomy.

B. Ulcerative colitis, FAP.

302
Q

Ileal pouchitis: Clinical features.

A

Bloody and foul-smelling effluent.

Fever and malaise.

303
Q

Ileal pouchitis: Histologic features (4).

A

Granulation tissue.

Architectural change.

Ulcers.

Loss of normal lymphoid follicles.

304
Q

Ileal pouch: Histologic features that suggest Crohn’s disease (3).

A

Ulcers and non-necrotizing granulomas in the afferent limb.

Pyloric-gland metaplasia.

305
Q

Risk for colon cancer in ___.

A. Ulcerative colitis.
B. Crohn’s disease.

A

A. 20% in 30 years.

B. 3% in 20 years.

306
Q

Dysplasia in inflammatory bowel disease: Gross pathologic types (2).

A

Flat dysplasia.

Dysplasia-associated lesion or mass: Polyp or plaque.

307
Q

Dysplasia in inflammatory bowel disease: Grading.

A

Negative for dysplasia.

Indefinite for dysplasia.

Low-grade dysplasia.

High-grade dysplasia.

308
Q

Dystrophic goblet cell.

A

One in which the mucin vacuole does not communicate with the lumen.

309
Q

Dysplasia-associated lesion or mass vs. sporadic adenoma: Histology.

A

Not possible to make the distinction.

310
Q

Clinical features favoring dysplasia-associated lesion or mass over sporadic adenoma (2).

A

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
Q

Ancillary studies favoring dysplasia-associated lesion or mass over sporadic adenoma (3).

A

IHC: Positive for p53, negative for bcl-2.

Molecular: Loss of heterozygosity in chromosome 3p.

312
Q

Radiation colitis:

A. Dose of radiation.
B. Other risk factors (3).

A

A. Usually more than 450 Gy.

B. Diabetes, cardiovascular disease, chemotherapy.

313
Q

Radiation colitis: Symptoms (3).

A

Diarrhea.

Abdominal pain.

Bowel obstruction in chronic radiation colitis.

314
Q

Acute radiation colitis: Histology (5).

A

Edema.

Vascular ectasia.

Acute cryptitis.

Superficial ulcers.

Epithelial cytomegaly and atypia.

315
Q

Chronic radiation colitis: Histology (5).

A

Stromal fibrosis with atypical fibroblasts.

Thickened subepithelial collagen.

Glandular atrophy and distortion.

Vascular changes.

Increased plasma cells in the lamina propria.

316
Q

Ischemic colitis: Clinical features.

A

Usually acute onset.

Abdominal pain, nausea, vomiting, diarrhea, or lower-gastrointestinal bleeding.

317
Q

Ischemic colitis: Pharmacological causes (2).

A

NSAIDs.

Oral contraceptives.

318
Q

Ischemic colitis: Infectious mimics.

A

Enterohemorrhagic E. coli.

Clostridium difficile.

319
Q

Mild ischemic colitis: Histology (4).

A

Superficial hemorrhage.

Patchy mucosal necrosis.

Dilated vessels

“Decapitated” glands.

320
Q

Severe ischemic colitis: Histology (3).

A

Crypt dropout.

Acute inflammation, including cryptitis.

Coagulative necrosis.

321
Q

Late lesions of ischemic colitis: Histology.

A

Replacement of mucosa by granulation tissue and fibrosis.

322
Q

Microscopic colitis: Causes (3).

A

Idiopathic.

Drugs, e.g. ticlopidine.

Infection, e.g. Brainerd diarrhea.

323
Q

Microscopic colitis: Epidemiology.

A

Collagenous colitis is more common in women.

324
Q

Collagenous colitis: Histology (3).

A

Thickened subepithelial collagen.

Increased intraepithelial lymphocytes.

Increased plasma cells in the superficial lamina propria.

325
Q

Microscopic colitis: Possible aberrant histologic findings (6).

A 
Subepithelial giant cells.
Cryptitis.
Ulcers.
Paneth-cell metaplasia.
Pseudomembranes.
Architectural change.
326
Q

Collagenous colitis: Possible complication.

A

“Fracture” of colon during endoscopic insufflation, leading to pneumatosis coli.

327
Q

Cord colitis syndrome: Association.

A

Cord-blood stem-cell transplantation.

328
Q

Cord colitis syndrome: Histology.

A

Granulomatous inflammation and changes similar to those of idiopathic inflammatory bowel disease.

Affects upper and lower gastrointestinal tract.

329
Q

Cord colitis syndrome:

A. Treatment.
B. Possible cause.

A

A. Usually responds to antibiotics.

B. Bradyrhizobium enterica.

330
Q

Syndromes of mucosal prolapse: Endoscopy.

A

Mucosal erythema, ulcer, or polypoid lesion.

331
Q

Syndromes of mucosal prolapse: Histology (4).

A

Fibromuscular obliteration of the lamina propria.

Mucosal architectural change and misplacement.

Mucosal capillary ectasia.

Sometimes: Erosion with inflammatory pseudomembrane.

332
Q

Collagenous colitis: Significance of metaplasia.

A

Paneth-cell metaplasia:
− Seen in collagenous colitis with more severe diarrhea.
− May cause confusion with idiopathic inflammatory bowel disease.

333
Q

Entamoeba histolytica: Chemical resistance.

A

Resists gastric acid and chlorination.

334
Q

Entamoeba histolytica: Complications of infection in the colon (3).

A

Granulomatous masses that can mimic carcinoma.

Perforation.

Fistulae.

335
Q

Entamoeba histolytica: Most frequent sites of ulcers in the large intestine.

A

Cecum.

Appendix.

Rectosigmoid.

336
Q

Entamoeba histolytica: Typical orientation of colonic ulcers.

A

Perpendicular to the long axis of the colon.

337
Q

Entamoeba histolytica vs. histiocytes.

A

Histocytes:
− Smaller.
− Larger, more irregular nucleus.
− Less intense staining with PAS.

338
Q

Aoncotheca philippinensis:

A. Synonym.
B. Geography.

A

A. Capillaria philippinensis.

B. Asia, Middle East, Africa.

339
Q

Aoncotheca philippinensis:

A. Disease.
B. Diagnosis.

A

A. Protein-losing enteropathy.

B. Identification of eggs, larvae, or worms in stool.

340
Q

Aoncotheca philippinensis: Sites of infection (2).

A

Jejunum, upper ileum.

341
Q

Strongyloides stercoralis: Histology of autoinfection.

A

Filiform larvae in the bowel wall.

342
Q

Diphyllobothrium latum: Residence.

A

Small intestine.

343
Q

Trichuris trichiura:

A. Residence.
B. Morphology of adult.

A

A. Cecum, ascending colon.

B. Whiplike, 4 cm.

344
Q

Lymphangiectasia: Forms.

A

Primary: Congenital obstruction.

Secondary: Inflammation, malignancy.

345
Q

Lymphangiectasia: Manifestations (2).

A

Protein-losing enteropathy.

Lymphatic obstruction.

346
Q

Pneumatosis intestinalis: Forms.

A

Acute: Gas-forming intestinal organisms.

Chronic: Pulmonary disease.

347
Q

Pneumatosis intestinalis: Causative bacteria (3).

A

Clostridium perfringens.

Enterobacter aerogenes.

Escherichia coli.

348
Q

Pneumatosis intestinalis: Association in infants.

A

Necrotizing enterocolitis.

349
Q

Pneumatosis intestinalis: Manifestations in adults (3).

A

Diarrhea.

Flatulence.

Increased mucus in the stool.

350
Q

Pneumatosis intestinalis: Radiography.

A

Ring of gas in the wall of the bowel.

351
Q

Pneumatosis intestinalis: Typical location of gas-filled cysts.

A

Near the mesenteric border.

352
Q

Pneumatosis intestinalis: Histology.

A

Gas-filled cysts that usually have no endothelial lining.

Variable inflammatory response.

Overlying mucosa may show ischemic changes.

353
Q

Melanosis coli: Pigment and its location.

A

Lipofuscin in histiocytes of the lamina propria.

354
Q

Melanosis coli: Special stains (3).

A

Positive: PAS, AFB, Fontana-Masson.

Negative: Iron stains.

355
Q

Brown-bowel syndrome:

A. Pigment and its location.
B. Typical association.
C. Symptoms.

A

A. Lipofuscin in smooth-muscle cells.

B. Deficiency of vitamin E.

C. Abdominal pain, diarrhea.

356
Q

Pseudomelanosis duodeni: Pigment and its location.

A

Iron in the tips of duodenal villi.

357
Q

Pseudomelanosis duodeni: Associations (4).

A

Iron-containing compounds.

Hypertension.

Diabetes mellitus.

End-stage renal disease.

358
Q

Inflammatory polyp of the colon: Histology (4).

A

Variable mixture of inflamed stromal tissue and hyperplastic epithelium.

Fibromuscular hyperplasia.

Thick-walled or ectatic blood vessels.

Sometimes: Bizarre stromal cells.

359
Q

Serrated adenoma:

A. Typical location.
B. Distinguishing histology (2).

A

A. Left colon.

B. Eosinophilic cytoplasm, gastric foveolar metaplasia.

360
Q

Sessile serrated polyp: Histologic features (10).

A

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
Q

Sessile serrated polyp: Number of histologic features needed for diagnosis.

A

4.

362
Q

Sessile serrated polyp: Significance (2).

A

May progress to colon cancers with microsatellite instability.

Multiple in the serrated polyposis syndrome.

363
Q

Sessile serrated polyp: Surveillance interval (3).

A

Less than 10 mm: 5 years.

At least 10 mm: 3 years.

With cytologic dysplasia: 3 years.

364
Q

Serrated adenoma: Surveillance interval.

A

3 years.

365
Q

Colon cancer: Major molecular pathways (2).

A

Chromosomal instability: 85%.

Mutator phenotype (microsatellite instability): 15%.

366
Q

Colon cancer of the chromosomal-instability pathway:

A. Typical ploidy.
B. Affected chromosomes (3).
C. Associated syndrome.

A

A. Aneuploid.

B. 5, 17, 18.

C. Familial adenomatous polyposis.

367
Q

Colon cancer of the mutator-phenotype pathway:

A. Typical gross pathology (2).
B. Typical ploidy.
C. Associated syndrome.

A

A. Large, right-sided.

B. Diploid.

C. Lynch’s syndrome.

368
Q

Lynch’s syndrome: Sites of non-colonic carcinomas (6).

A

Central nervous system.
Urinary tract.
Biliary tract.

Ovary.
Stomach, small intestine.
Endometrium.

369
Q

Lynch’s syndrome: Amsterdam II criteria.

A

At least 3 relatives with LS-related tumors.

Colo-rectal carcinoma in 2 generations.

LS-related tumor occurring in patient under 50.

370
Q

Familial colorectal cancer syndrome, type X:

A. Definition.
B. Mutant protein.

A

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
Q

Colonic adenocarcinoma: Grading.

A

I: Well-formed glands in a desmoplastic stroma.

II: Less well-formed glands; focal cribriform pattern.

III: No glands; solid sheets.

372
Q

Mucinous adenocarcinoma of the colon: Prognosis.

A

Worse, but only if at least 75-80% of the tumor has extracellular mucus.

373
Q

Colorectal cancer of Lynch’s syndrome: Histology.

A

Many lymphocytes around and within the tumor.

Poorly differentiated: Undifferentiated or medullary.

Many tumors are of the mucinous or signet-ring type.

374
Q

Bethesda criteria for colorectal carcinoma: Purpose.

A

To determine which tumors should be tested for MSI-H.

375
Q

Bethesda criteria for colorectal carcinoma: The criteria (5).

A

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
Q

Effect of MSI-H histology on ___.

A. Prognosis.
B. Treatment.
C. Surveillance.

A

A. Better prognosis.

B. Irinotecan is used rather than 5-FU.

C. Surveillance for other LS-related tumors.

377
Q

Another reason why testing for MSI-H should be done.

A

To catch those who have MSI-H but do not meet the Amsterdam II criteria.

378
Q

Tests for MSI-H (3).

A

PCR for microsatellite stability.

IHC for enzymes of mismatch repair.

Sequencing of genes of mismatch repair.

379
Q

Colorectal carcinoma: Relevance of site of tumor to prognosis.

A

Worse if left-sided.

380
Q

Causes of loss of MSH6 by immunohistochemistry (3).

A

Germline mutation of MSH2/MSH6.

Deficiency of MLH1/PMS2 + somatic mutation of MSH6.

Previous chemotherapy.

381
Q

Familial adenomatous polyposis:

A. Inheritance.
B. Onset of polyps.
C. Natural course.

A

A. Autosomal dominant.

B. Usually around puberty.

C. Death from colorectal carcinoma.

382
Q

Familial adenomatous polyposis:

A. Gene and its location.
B. Mutations associated with attenuated FAP.

A

A. APC on 5q21.

B. Mutations near the 3’ end, near the 5’ end, or in exon 9.

383
Q

Familial adenomatous polyposis: Ocular abnormality.

A

Congenital hypertrophy of the retinal pigmented epithelium.

384
Q

Familial adenomatous polyposis: Leading cause of death after colectomy.

A

Periampullary carcinoma.

385
Q

Gardner’s syndrome:

A. Benign tumors (3).
B. Extra-colonic sites of malignant tumors (2).

A

A. Osteomas, epidermal cysts, fibromatosis.

B. Duodenum, thyroid.

386
Q

Turcot’s syndrome vs. pseudo-Turcot’s syndrome.

A

Turcot’s: Familial adenomatous polyposis with medulloblastoma.

Pseudo-Turcot’s: Lynch’s syndrome with glioblastoma.

387
Q

Muir-Torre syndrome:

A. Defective protein.
B. Location of colonic adenomas.

A

A. Mismatch-repair enzymes.

B. Proximal colon.

388
Q

Muir-Torre syndrome: Skin tumors.

A

Sebaceous neoplasms.

BCC.

SCC.

389
Q

MUTYH-associated polyposis syndrome:

A. Inheritance.
B. Gene and its function.

A

A. Autosomal recessive.

B. MYH encodes an enzyme of excision repair.

390
Q

MUTYH-associated polyposis syndrome: Relation to familial adenomatous polyposis (2).

A

Mutation of MYH predisposes to acquired mutation of APC.

Can mimic FAP or attenuated FAP clinically.

391
Q

Familial adenomatous polyposis:

A. Earliest lesion in the colon.
B. Gastric polyps.

A

A. The one-gland adenoma.

B. Fundic-gland polyps, adenomas.

392
Q

Familial adenomatous polyposis: When workup should occur in patient with no known risk factors or family history.

A

When a patient has had a cumulative total of 10 of more adenomas.

393
Q

Gastric ectopia in the esophagus:

A. Synonym.
B. Location.
C. Clinical features.

A

A. Inlet pouch.

B. Cervical esophagus.

C. Older patients may have peptic symptoms.

394
Q

Familial adenomatous polyposis: Molecular test.

A

Gene sequencing to determine exact location of mutation of APC gene.

396
Q

Peutz-Jeghers syndrome:

A. Inheritance.
B. Onset of polyps.

A

A. Autosomal dominant.

B. During infancy.

397
Q

Peutz-Jeghers syndrome: Gene and its location.

A

STK-11 on 19q13.3.

399
Q

Peutz-Jeghers syndrome: Characteristic gonadal tumors (2).

A

Ovarian sex-cord tumor with annular tubules.

Testicular Sertoli-cell tumors.

400
Q

Peutz-Jeghers syndrome: Other sites of malignancy (2).

A

Pancreas, breast.

401
Q

Peutz-Jeghers syndrome: Benign finding.

A

Hyperpigmentation of skin and mucous membranes.

402
Q

Isolated juvenile polyps:

A. Maximum.
B. Frequent fate of polyps.

A

A. Up to 5 juvenile polyps in the colon and rectum.

B. Auto-amputation.

403
Q

Juvenile polyposis syndrome: Criteria (3).

A

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
Q

Juvenile polyposis syndrome: Forms.

A

Nonfamilial: May be associated with other congenital anomalies.

Familial: Many varieties, mostly autosomal dominant.

405
Q

Juvenile polyposis syndrome:

A. Onset.
B. Presentations (3).

A

A. Childhood.

B. Rectal bleeding, bowel obstruction, prolapse of polyp into anal canal.

406
Q

Juvenile polyposis syndrome:

A. Number of polyps.
B. Sites of polyps.

A

A. Between 6 and several hundred.

B. Distal colon and rectum (90%), stomach.

407
Q

Juvenile polyp: Gross pathology.

A

Globose or mushroom-shaped and often ulcerated.

408
Q

Juvenile polyp: Histology (4).

A

Hamartomatous overgrowth of lamina propria.

Dilated glands may form cysts.

Inflamed stroma and (often) surface.

Sometimes: Increased ganglion cells and hypertrophic nerves.

409
Q

Juvenile polyp: Incidence of dysplasia.

A

Up to 20%.

410
Q

Juvenile polyposis syndrome: Genes and their locations (2).

A

SMAD4 (MADH4) on 18q21.1.

BMPR1A on 10q23.3 (if concurrent hereditary hemorrhagic telangiectasia).

411
Q

PTEN hamartoma-tumor syndromes (2).

A

Cowden’s syndrome.

Ruvalcaba-Myhre-Smith syndrome.

412
Q

Cowden’s syndrome:

A. Inheritance.
B. Sites of tumors (4).

A

A. Autosomal dominant.

B. Gastrointestinal tract, thyroid, breast, skin of face.

413
Q

Cowden’s syndrome: Facial anomalies (3).

A

Arched palate.

Beaked nose.

Retinal gliomas.

414
Q

Peutz-Jeghers syndrome: Sites of gastrointestinal polyps.

A

Mostly in the small intestine but also in the colon.

415
Q

Cowden’s syndrome: Onset of tumors.

A

Between ages 20 and 40.

416
Q

PTEN hamartoma-tumor syndromes: Histology of polyps (4).

A

May resemble juvenile polyps.

May resemble rectal mucosal prolapse.

Ganglioneuromas and lipomas may occur.

417
Q

PTEN: Location of gene.

A

10q23.

418
Q

Cronkhite-Canada syndrome:

A. Inheritance.
B. Onset.

A

A. Not inherited.

B. Late adulthood.

419
Q

Cronkhite-Canada syndrome: Findings outside the gastrointestinal tract (3).

A

Alopecia.

Hyperpigmentation.

Nail dystrophy.

420
Q

Cronkhite-Canada syndrome: Mortality and typical cause of death.

A

60%; cachexia.

421
Q

Cronkhite-Canada syndrome:

A. Sites of polyps.
B. Gross pathology.

A

A. Anywhere in the GI tract, but esp. in stomach and colon.

B. May mimic primary IBD; cut surface is often gelatinous.

422
Q

Cronkhite-Canada syndrome:

A. Histology of polyps.
B. Histology of adjacent mucosa.

A

A. Similar to that of juvenile polyps.

B. Edematous and may be rich in eosinophils.

423
Q

Intestinal ganglioneuromatosis: Causes (5).

A

Juvenile polyposis syndrome.

PTEN hamartoma-tumor syndromes.

Tuberous sclerosis.

Neurofibromatosis.

MEN IIB.

424
Q

Serrated polyposis syndrome: Possible genetic abnormalities (2).

A

Defect in hypermethylation of DNA.

Mutation in MYH.

425
Q

Benign fibroblastic polyp of the colon: Synonym.

A

Colorectal perineurioma.

426
Q

Benign fibroblastic polyp of the colon: Histology (2).

A

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
Q

Benign fibroblastic polyp of the colon: Immunohistochemistry.

A

Negative: Neural markers, including S100.

428
Q

Elastosis and elastofibromatous change of the colon: Histology.

A

Increased elastin fibers and fibrous tissue, often centered on a blood vessel.

Can cause a polypoid mass.

429
Q

Mucosal neuroma:

A. Distinction from ganglioneuroma.
B. Immunohistochemistry.

A

A. A ganglioneuroma contains ganglion cells as well as spindle cells.

B. Positive for S100.

430
Q

Mucosal neuroma: Associations.

A

Most cases: None (sporadic).

Neurofibromatosis.

431
Q

Ruvalcaba-Myhre-Smith syndrome: Findings outside the gastrointestinal tract (4).

A

Macrocephaly.

Mental deficiency.

Characteristic facies.

Penile macules.

432
Q

Peutz-Jeghers syndrome: Histology of colonic polyps.

A

Hamartomatous overgrowth of muscularis mucosae.

Arborizing architecture.

Dysplasia is rare.

433
Q

Gastrointestinal stromal tumor:

A. Most common sites.
B. Presentation.

A

A. Stomach, small intestine.

B. Ulceration and bleeding in about half of cases.

434
Q

Gastrointestinal stromal tumor: Carney’s triad.

A

Epithelioid GIST.

Pulmonary chondroma.

Extraadrenal paraganglioma.

435
Q

Gastrointestinal stromal tumor: Criteria for very low risk (2).

A

Smaller than 2 cm.

Fewer than 5 mitotic figures per 50 hpf.

436
Q

Gastrointestinal stromal tumor: Criteria for low risk (2).

A

2-5 cm.

Fewer than 5 mitotic figures per 50 hpf.

437
Q

Gastrointestinal stromal tumor: Criteria for intermediate risk (2,2).

A

Smaller than 5 cm, 6-10 mitotic figures per 50 hpf.

5-10 cm, fewer than 5 mitotic figures per hpf.

438
Q

Gastrointestinal stromal tumor: Criteria for high risk (2,1,1).

A

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
Q

Risk of adverse outcome of high-risk gastrointestinal tumor in the ___.

A. Stomach.
B. Small intestine.

A

A. 46%.

B. 77%.

440
Q

Colorectal gastrointestinal stromal tumors.

A

Rare but tend to show high-risk histology.

441
Q

Gastrointestinal stromal tumor: Recommended immunohistochemical panel.

A

CD117.

CD34.

Desmin, actin.

S-100.

442
Q

Gastrointestinal stromal tumor: Useful newer stain.

A

DOG-1 is both sensitive and specific for GIST.

443
Q

Gastrointestinal stromal tumor: Most frequently mutated genes (2).

A

KIT.

PDGFRA.

444
Q

Gastrointestinal stromal tumor: Locations of mutations in KIT.

A

Exons 9, 11, 13, 17.

445
Q

Gastrointestinal stromal tumor: Relevance to location of mutation in KIT to treatment.

A

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
Q

Gastrointestinal stromal tumor: Locations of mutations in PDGRA.

A

Exons 12, 14, 18.

447
Q

Gastrointestinal stromal tumor: Most common mutation in PDGFRA and relevance to treatment.

A

D842V in exon 18 is highly resistant to imatinib and sunitinib.

448
Q

CD117-negative gastrointestinal stromal tumor:

A. Incidence.
B. Immunohistochemistry (1,3).

A

A. 4% of GISTs.

B. Positive for DOG-1; negative for CD117, c-Kit, and CD34.

449
Q

CD117-negative gastrointestinal stromal tumor:

A. Frequent chromosomal abnormality.
B. Frequent histology.
C. Frequent sites (2).

A

A. Loss of 14 or of 14q.

B. Epithelial.

C. Omentum, peritoneum.

450
Q

CD117-negative gastrointestinal stromal tumor: Treatment.

A

Some tumors respond to imatinib.

451
Q

Fibromatosis: Immunohistochemistry.

A

Depending on staining technique, may show false positivity for CD117.

452
Q

Gastrointestinal leiomyosarcoma: Most frequent sites (3).

A

Stomach, small intestine, colon.

453
Q

Gastrointestinal schwannoma: Frequent histologic feature.

A

Cuff of lymphocytes.

454
Q

Malignant neuroectodermal tumor:

A. Synonym.
B. Mutations.

A

A. Osteoclast-rich tumor resembling clear-cell sarcoma.

B. EWSR-CREB1 or EWSR-ATF1.

455
Q

Malignant neuroectodermal tumor: Immunohistochemistry (1,1,1).

A

Positive: S-100.

Variable: Melanoma markers.

Negative: CD117.

456
Q

Familial gastrointestinal stromal tumor:

A. Inheritance.
B. Genetic basis.

A

A. Autosomal dominant.

B. Germline mutation in KIT and PDGFRA.

457
Q

Familial gastrointestinal stromal tumor: Possible associations (4).

A

Nevi.

Perineal hyperpigmentation.

Urticaria pigmentosa.

Systemic mast-cell disease.

458
Q

Familial gastrointestinal stromal tumor: Course.

A

Indolent.

459
Q

Carney-Stratakis syndrome: Tumors (3).

A

Multiple epithelioid GISTs in the stomach.

Paragangliomas.

Pheochromocytomas.

460
Q

Carney-Stratakis syndrome:

A. Gene.
B. Treatment.

A

A. Succinate dehydrogenase.

B. Relatively resistant to imatinib.

461
Q

Gastrointestinal stromal tumors associated with neurofibromatosis, type I:

A. Site.
B. Histology (2).
C. Behavior.

A

A. Small intestine.

B. Spindle-cell type; “skeinoid” fibers.

C. Usually benign.

462
Q

Gastrointestinal stromal tumors in children:

A. Gender preference.
B. Site and histology.
C. Behavior.

A

A. More frequent in females.

B. Gastric; epithelioid.

C. Indolent.

463
Q

Mantle-cell lymphoma of the gastrointestinal tract: Incidence (2).

A

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
Q

Intestinal lymphomas that can present as lymphomatous polyposis (3).

A

Mantle-cell lymphoma.

Marginal-zone lymphoma.

Follicular lymphoma.

465
Q

Enteropathy-associated T-cell lymphoma: Typical gross pathology.

A

Ulcers and strictures in the jejunum.

466
Q

Enteropathy-associated T-cell lymphoma: Histologic types (2).

A

Pleomorphic.

Monomorphic.

467
Q

Pleomorphic enteropathy-associated T-cell lymphoma: Immunohistochemistry.

A

Positive: CD3.

Negative: CD4, CD5, CD56.

CD8 is negative in 20% of cases.

468
Q

Monomorphic enteropathy-associated T-cell lymphoma: Immunohistochemistry.

A

Positive: CD3, CD56, CD8.

469
Q

Enteropathy-associated T-cell lymphoma: Association with celiac disease.

A

Much stronger with the pleomorphic type.

470
Q

Intestinal reactive lymphoid hyperplasia: Most frequent sites (3).

A

Terminal ileum.

Duodenum.

Rectum.

471
Q

Terminology of anal squamous intraepithelial lesions.

A

Anal canal: LGAIN, HGAIN.

Perianal skin: LSIL, HSIL.

472
Q

Anal carcinoma: Location.

A

Above the dentate line.

473
Q

Anal carcinoma: Typical histology (2).

A

SCC or some variant thereof (95%).

Half of the SCCs are nonkeratinizing.

474
Q

Anal carcinoma: Basaloid squamous-cell carcinoma.

A

Consists of tumor islands with peripheral palisading, but not to the degree of BCC.

475
Q

Anal carcinoma: Uncommon histology (3).

A

Colorectal-type carcinoma.

Salivary-type carcinomas.

Undifferentiated neuroendocrine-type carcinomas.

476
Q

Paget’s disease of anal mucosa: Stains (4).

A

PAS.

Mucicarmine.

Alcian blue.

Often: CEA.

477
Q

Paget’s disease of anal mucosa: Origins (3).

A

Apocrine cells.

Adenocarcinoma of the rectosigmoid.

Adenocarcinoma of the anal canal.

478
Q

Adenocarcinoma involving the anal canal: Origins (5).

A

Rectum.

Anal canal.

Perianal duct or glands.

Paget’s disease.

Chronic perianal fistula.

479
Q

Adenocarcinoma arising in a perianal fistula: Type.

A

Usually mucinous adenocarcinoma.

480
Q

Anal melanoma may mimic ___ clinically.

A

a hemorrhoid

481
Q

How many appendices resected for appendicitis turn out to be normal?

A

About 15%.

482
Q

Mucocele of the appendix.

A

Gross term only.

Most cases are due to mucinous cystadenoma or cystadenocarcinoma.

483
Q

Non-neoplastic cause of appendiceal mucocele:

A. Name.
B. Size.
C. Typical cause.

A

A. Retention cyst.

B. Less than 1 cm (anything larger is a neoplasm until proved otherwise).

C. Sterile obstruction of the appendiceal lumen.

484
Q

Mucinous cystadenoma of the appendix: Association.

A

About 20-25% are associated with a separate primary colonic adenocarcinoma.

485
Q

Mucinous cystadenoma of the appendix: Gross pathology.

A

Appendix often resembles a sausage.

Expansion of mucin may produce diverticula.

486
Q

Mucinous cystadenoma of the appendix: Histology.

A

Lining: Columnar cells showing dysplasia, usually low-grade.

Contents: Mucin.

487
Q

Adenocarcinoma of the appendix: Gross pathology.

A

Forms a mass that may be confined to the base of the appendix or that may expand so as to obliterate the appendix.

488
Q

Adenocarcinoma of the appendix: Histology.

A

Mucinous cystadenocarcinoma: Mucinous cystadenoma with invasion.

Nonmucinous adenocarcinoma: Identical to that of colonic adenocarcinoma.

489
Q

Pseudomyxoma peritonei:

A. Causes.
B. Composition.

A

A. Benign or malignant neoplasms of the appendix.

B. May contain almost no cells.

490
Q

Pseudomyxoma peritonei: Predictors of worse prognosis (4).

A

Diffuse distribution.

Malignant primary tumor.

Cellular mucus.

High-grade dysplasia or malignancy.

491
Q

Pseudomyxoma peritonei: Typical causes of death (2).

A

Sepsis.

Bowel obstruction.

Not cancer.

492
Q

Pseudomyxoma peritonei: Relevance to ovarian mucinous tumors (2).

A

Ovarian mucinous tumors can accompany pseudomyxoma peritonei.

The appendix is still the usual the source of pseudomyxoma peritonei.

493
Q

Myxoglobulosis:

A. Significance.
B. Histology (2).

A

A. May be found in appendiceal mucoceles, including mucinous neoplasms.

B. Lamellated and often calcified; appendiceal lining may show pseudosynovial metaplasia.

494
Q

Carcinoid tumors of the appendix: Variants.

A

Insular.

Tubular.

Goblet-cell.

495
Q

Goblet-cell carcinoid: Synonyms.

A

Crypt-cell carcinoma.

Goblet-cell adenocarcinoma.

496
Q

Goblet-cell carcinoid: Histology.

A

Cells that resemble mature goblet cells form discrete clusters, strands, and microglands.

497
Q

Goblet-cell carcinoid: Immunohistochemistry.

A

Positive: Pancytokeratin.

Negative or focal: Neuroendocrine markers.

498
Q

Goblet-cell carcinoid: Signs of differentiation into a carcinoma of higher grade (4).

A

Solid growth.

Complex infiltrative pattern.

Nuclear atypia with increased mitotic activity.

Dissecting mucus.

499
Q

Tubular carcinoid: Immunohistochemistry.

A

Positive for neuroendocrine markers.

Often positive for glucagon.

500
Q

Carcinoid tumor of the appendix vs. fibrous obliteration.

A

Fibrous obliteration: Neuroendocrine cells are few and scattered.

501
Q

Tubular carcinoid vs. signet-ring carcinoma.

A

Signet-ring carcinoma:
− More infiltrative.
− More pleomorphism.
− More mitotic activity.

502
Q

Carcinoid tumors of the appendix: Indications for right hemicolectomy (5).

A

Size greater than 2 cm.

Invasion beyond muscularis propria.

Vascular invasion.

Incomplete excision.

Coexisting adenocarcinoma.

503
Q

Cancers that metastasize to the stomach:

A. Most common origins (3).
B. Endoscopy.

A

A. Melanoma, lung, breast.

B. Target-shaped lesion.

504
Q

Pancreaticobiliary carcinoma vs. primary ampullary carcinoma (2).

A

Primary ampullary carcinoma:
− Usually arises in an adenoma.
− Better prognosis.

505
Q

Cancers that metastasize to the small intestine:

A. Most common origin.
B. Endoscopy.
C. Another frequent metastasis.

A

A. Melanoma.

B. Obstructive mass.

C. Bronchogenic SCC to the proximal jejunum.

AP reviewer (17 decks)

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