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GI > Esophageal and Gastric Pathology > Flashcards

Esophageal and Gastric Pathology Flashcards

1
Q

Describe the developmental process of the esophagus

A

Starts out as a single tube with trachea. Then laryngotracheal diverticulum forms…becomes epithelial ridges and eventually forms full trachea

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2
Q

How does epithelium change over course of fetal development?

A

From psedustratified columnar to columnar epithelium with mutinous secretion to non-keratinizing stratified squamous epithelium

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3
Q

Describe the embyronic development process of the stomach

A

Fusiform dilitation of the foregut and rotation

There is no epithelial changes

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4
Q

What is esophageal atresia?

A

Esophagus “not perforated”– basically the tube forms a dead end

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5
Q

Which is the most common developmental anomaly?

A

Esophageal atresia where esophagus not continuous and part that should be connected is continuous with stomach

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6
Q

What is a tracheoesophageal fistula?

A

Narrowing of tube with connection between esophagus and trachea

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7
Q

Esophogeal duplication: How does it present?

How is it treated?

A

It’s discovered after birth due to regurgitation during feeds. It requires prompt surgical repair because it is incompatible with life

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8
Q

Gastric Ectopia (inlet patch)

A

Presence of ectopic gastric mucosa in upper 1/3 of esophagus

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9
Q

Intantile hypertrophic pyloric stenosis: Epidemiology and presentation

A

More common in white males

Presents between 3rd/6th week of life with regurgitation, projectile vomiting

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10
Q

What are the types of obstruction? How do they present?

A

Webs– eccentric thin membranes often in proximal region
Ring: Diaphragm of tissue located in distal esophagus
Schatzki ring: both mucosa/submucosa
Often are asymptomatic

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11
Q

What is a pulsion diverticula?

A

Diverticulum due to increased intraluminal pressure. Located in proximal/distal esophagus
Secondary to motility disturbances such as achalasia

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12
Q

Describe a traction diverticula

A

Extrinsic inflammation retracts/pulls bowel outwards
Located in mid esophagus
Less common

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13
Q

Name some of the etiologies of esophagitis

A

Mechanical (achalasia), reflux, corrosive injuryies, pills/drugs, infections, allergies, radiation, GVHD, systemic disorders

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14
Q

What is mechanism of injury in achalasia?

A

Injury to myenteric plexus from toxins, trauma, viruses, bacteria, autoimmune

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15
Q

How does achalasia appear on barium swallow?

A

“Bird’s beak”– dilatation of esophagus with acute tapering at LES and narrowing of GEJ

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16
Q

What is boerhaave syndrome?

A

Rupture of the esophagus post vomiting due to sudden increase in intraluminal esophageal pressure

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17
Q

What are Mallory-Weirs tears?

A

Mucosal lacerations in distal esophagus and proximal stomach due to retching, vomiting, straining, coughing (often after heavy alc use)

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18
Q

How does viral esophagitis appear grossly?

On high magnification?

A

Gross: Shallow punched out ulcers
Histo: Herpes=Multinucleated squamous epithelial cells with intranuclear inclusions. CMV=big cells with nuclear/cytoplasmic inclusions

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19
Q

How does candida esophagitis appear? Both gross and high power.

A

Gross: Lots of white patches
Histology: pseudo hyphae and budding yeast

20
Q

How does eosinophilic esophagitis appear on endoscopy?

A

“Trachealization”– ringed appearance with linear furrows

21
Q

How does eosinophilic esophagitis present? Eli and symptoms

A

Epi: Children or adults, males, concurrent with other allergic conditions
Px: feeding difficulty, nausea, vomiting, dysphagia as a result of fibrosis of submucosa

22
Q

How does scleroderma-caused esophageal sclerosis appear on high power?

A

Inner circular layer of smooth muscle is not well observed due to deposition of collagenous material– atrophy/fibrosis leads to LES defect, GERD, pulmonary infections

23
Q

Which esophageal cancer is most common in the Western hemisphere? World wide?

A

Western hemisphere: adenocarcinoma

Worldwide: Squamous cell carcinoma

24
Q

Esophageal carcinoma: Epidemiology

A

Associated with Barrett’s esophagus

RFs: males, age, longstanding reflux, obesity

25
Q

How is Barrett’s esophagus diagnosed?

A

Endoscopy: columnar type mucosa on endoscopy
Biopsy: shows intestinal metaplasia (i.e goblet cells)
NEED BOTH

26
Q

What is the difference between short segment and long segment Barrett’s esophagus? What’s the clinical significance

A

Short is less than 3cm. Long is greater than 3cm

Long segment BE carries much higher risk of developing adenocarcinoma

27
Q

Describe the epidemiology of esophageal squamous cell carcinoma

A

Most common worldwide; males more commonly affected
RFs: tobacco, alcohol, vitamin dificiency, food/water rich in nitrates
HPV IS NOT A RF

28
Q

Which part of esophagus is most commonly affected?

A

Middle third

29
Q

What are the different types of squamous cell carcinoma on histology?

A

Keratinizing (appear pinker)– they are more differentiated

Non-keratinizing– poorly differentiated

30
Q

What is chyme? How is it formed?

A

Rhythmic contractions of gastric musculature breaks down ingested food particles and mixes it with gastric fluid. The result is called chyme

31
Q

What are the three phases of gastric acid secretion?

A

Cephalic phase: thought of food leads to stimulation of vagus nerve causing parietal cells to secrete acid
Intestinal phase: As food bolus enters stomach, gastric dilitation occurs that causes gastrin/histamine release by endocrine cells
Intestinal phase: Once food exits stomach, negative regulation by intestinal hormones prevents further acid secretion

32
Q

Compare/contrast acute vs. chronic gastritis

A

Acute: Mucosal barrier breakdown, may see neutrophils. Causes: stresses (cushings, curling, toxic, circulatory)
Chronic: Observe inflammatory cells. Causes: H Pylori, autoimmune

33
Q

How does acute gastritis appear histologically?

A

Observe surface erosion/fibrin

Lack of chronic inflammatory cells

34
Q

How does a chronic H Pylori gastritis appear histologically?

A

Can do special stain to detect– CLOtest detects ureas.

Otherwise, observe superficial inflammation (lymphocytes/plasma cells)

35
Q

What is atrophic gastritis? What are etiologies?

A

Loss of parietal/chief cells of gastric glands that can progress to lymphoma/carcinoma
Etiology: Autoimmune or H pylori

36
Q

How does autoimmune atrophic gastritis appear histologically?

A

Antralized gastric glands– destruction of parietal cells and intestinal metaplasia of surface epithelium

37
Q

How does autoimmune gastritis lead to carcinogenesis?

A

Loss of parietal cells but gastrin signaling still intact: get ECL hyperplasia

Intestinal metaplasia from autoimmune destruction leads to dysplasia and eventually adenocarcinoma

38
Q

How does autoimmune gastritis appear grossly?

A

Loss of rugal folds, mucosal atrophy

39
Q

What is the difference between funds glandular polyp and hyper plastic polyp?

A

Site of enlargement: glands vs. epithelium

40
Q

What is cause of hypertrophic gastropathy? How does it appear grossly and microscopically?

A

ZE Syndrome:
Observe diffuse hypertrophy of rugal folds
On high power, see hyperplasia of parietal cells . Epithelial compartment is not expanded

41
Q

Marginal Zone B Cell Lymphoma (MALT)

A

asd;fljk

42
Q

What are the two types of gastric adenocarcinomas?

A

Intestinal type: Gland forming

Signet ring type: single cells

43
Q

What is the difference in progression between intestinal type and Signet ring type adenocarcinomas?

A

Intestinal: Chronic gastritis–>Metaplasia–>dysplasia–>adenocarcinoma

Signet ring: no chronic gastritis, instead mutation involving E-cadherin

44
Q

Diffuse type gastric carcinoma: How does it appear grossly and histologically?

A

Gross: leather bottle stomach (linnets plastica)
HIsto: Signet ring cells

45
Q

GI Stromal Tumors: Where do most arise? How do most arise? (cell or origin, mutation)

A

70% arise in stomach

Arise from ICC cells; defined by reactivity to c-KIT (a tyrosine kinase)

46
Q

How are GI Stromal tumors treated?

A

Imatinib/gleevec, which targets tyrosine kinase receptor

47
Q

How do GI Stromal tumors appear grossly? Histologically?

A

Gross: submucosal with areas of hemorrhage and necrosis
Histo: Subepithelial, spindle cells

GI (41 decks)

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