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Esophageal and Motility Disorders Flashcards

1
Q

What are the pathological findings of adenocarcinomas of the esophagus?

A

gross: flat patches to nodular masses, adjacent to Barrett’s mucosa
microscopically: moderate or well differentiated, usually mucin producing (intestinal type mucosa) with foci of squamous or endocrine differentiation
* can rarely have signet-ring cells, papillary structures, paneth cells, endocrine cells*

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2
Q

What are the microscopic findings of esophageal squamous cell carcinoma?

A

moderate to well differentiated

keratinization of tumor cells

angiolymphatic invasion

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3
Q

What is a hiatus hernia?

A

a protrusion of the stomach through the diaphragmatic hiatus into the chest

predisposes to GERD

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4
Q

What is the epidemiology of Barrett’s esophagus?

A

present in up to 10% of GERD patients

more common in men and non-Black patients

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5
Q

Which colonic reflex can be induced by cholera toxin?

A

giant peristaltic contraction

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6
Q

What is ogilvie’s syndrome?

A

also called acute colonic pseudo-obstruction

characterized by the presence of marked colonic dilation in the absence of mechanical bowel obstruction that occurs frequently in post-operative setting

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7
Q

What is the most common GI manifestation of scleroderma?

A

esophageal dysmotility

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8
Q

What is the pathophysiology of Hirschsprung’s disease?

A

normally, neural crest cells migrate to digestive tract to form enteric nervous system

Hirschsprung’s disease = cells fail to populate the distal digestive tract –> no NO containing neurons (thus sphincter cannot relax)

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9
Q

Complications of gastroesophageal reflux disease include the following:

a) exposure to refluxate can lead to mucosal inflammation and injury (esophagitis)
b) esophageal stricture formation
c) epithelial metaplasia (Barrett’s esophagus)
d) all of the above

A

d) all of the above

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10
Q

What is adenocarcinoma of esophagus?

A

malignant epithelial tumor with glandular differentiation

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11
Q

What are the symptoms of diabetic gastroparesis?

A

post-prandial regurgitation, nausea, vomiting, abdominal pain, early satiety

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12
Q

What does this histology show?

A

basal cell hyperplasia, vascular extension upwards

suggestive of reflux esophagitis

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13
Q

What condition is associated with adenocarcinoma of esophagus?

A

Barrett’s esophagus

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14
Q

An esophageal biopsy has columnar epithelium interspersed with distended, barrel-shaped cells with mucin filled cytoplasm. What is the most likely diagnosis?

A

Barrett’s esophagus

the mucin-filled cells are goblet cells

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15
Q

Which of the following medications is not associated with pill esophagitis?

a) Cimetidine
b) Clindamycin
c) Potassium
d) Iron

A

a) Cimetidine

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16
Q

What is the venous drainage of different parts of the esophagus?

A

inferior thyroid vein (upper 1/3)

azygous vein (middle 1/3) –> empties to superior vena cava

gastric vein (lower 1/3) –> empties to portal system

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17
Q

What do these endoscopic findings suggest?

A

eosinophilic esophagitis

left is esophageal rings, right is esophageal furrows

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18
Q

What is the contractile activity of the gastric fundus?

A

tonic (sustained) and phasic (short duration) contractions that transfer ingested food to the antrum and increase intragastric pressures

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19
Q

What does this esophageal biopsy suggest?

A

Barrett’s esophagus

  • columnar/mucinous metaplasia*
  • goblet cells*
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20
Q

What is esophageal stricture?

A

narrowing of the esophagus that may impair swallowing

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21
Q

What are the commoncauses of infectious esophagitis? How can they be differentiated?

A

candida –> white plaques or exudates

herpes simplex virus –> shallow punched out ulcers

cytomegalovirus –> deeper serpiginous ulcers

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22
Q

What are the three major mechanisms of reflux?

A

1) transient lower esophageal sphincter relaxations
2) abdominal strain (associated with weakened sphincter)
3) free reflux across an atonic LES

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23
Q

How should Barrett’s esophagus be monitored?

A

annual endoscopic examination with multiple biopsies

evaluate biopsies for dysplastic changes

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24
Q

What are the three subtypes of achalasia?

A

1) absent esophageal body contractility
2) panesophageal pressurization
3) spastic esophageal body contractions

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25
Q

A patient presents with odynophagia (painful swallowing). On exam, you note white plaques in the esophagus. What is the most likely diagnosis?

A

candida infection of the esophagus

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26
Q

What are the symptoms of eosinophilic esophagitis/esophageal eosinophilia?

A

food impaction and dysphagia (adults), feeding intolerance or GERD-like symptoms in children

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27
Q

What non-pharmalogical modifications can help with GERD?

A

postural maneuvers (upright after meals and during sleep)

chewing gum or oral lozenges to increase saliva

dietary changes

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28
Q

What is the gross appearance of Barrett’s esophagus?

A

red velvety GI type mucosa between pale squamous mucosa of lower esophagus and lush pink gastric mucosa

may have “tongues” extending up from GE junction or broad band displacing the GE junction

may have preserved squamous “islands”

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29
Q

After eating and digesting, how are remaining food contents ejected from the stomach?

A

migrating motor complexes that cycle every 90 minutes

high amplitude cotnractile waves that propel residual gastric contents

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30
Q

What is the pathogenesis of reflux esophagitis?

A

normally: lower esophageal sphincter provides barrier to prevent reflux of gastric contents to esophagus

in RE: acid, pepsin, bile, and alkaline duodenal contents are refluxed into the esophagus due to decreased in sphincter tone (in 50% of cases) or other factors (increased gastric emptying time, antral gastritis, abnormal antral mobility)

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31
Q

What are the radiographic findings of the GI effects of scleroderma?

A

diffuse small bowel dilatation and wide mouthed intestinal diverticulae

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32
Q

How does the external anal sphincter contribute to fecal continence?

A

through phasic contractions (especially during increases in intraabdominal pressure)

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33
Q

What are the complications of Ogilvie’s syndrome?

A

colonic ischemia, perforation

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34
Q

What are giant peristaltic contractions?

A

heightened peristaltic reflexes in the colon with high amplitudes and long durations

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35
Q

What is the difference between erosion and ulceration?

A

ulceration = loss of superficial epithelium down to muscularis mucosa

erosion = loss of superficial epithelium above muscularis mucosa

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36
Q

What are risk factors for developing adenocarcinoma of esophagus?

A

Barrett’s esophagus

reflux esophagitis

tobacco exposure and obesity

genetic mutations (in p53, bet-catenin, and ERB-B2)

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37
Q

What are the clinical manifestations of scleroderma-associated intestinal dysmotility?

A

diarrhea, abdominal pain, maldigestion, small bowel bacterial overgrowth

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38
Q

What is the contractile activity of the antrum?

A

generates high amplitude, phasic contractions that forcefully proopel ingested contents against a closed pylorus

leads to grinding of materials to particle size

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39
Q

What is the difference in control between the proximal colon and the anorectum?

A

proximal colon motility is involuntary

anorectal activity is voluntary

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40
Q

What is the gastrocolic reflex?

A

a motility pattern in the colon in the fed state

increase in colonic motility within 30 minutes of a meal

stimulated by presence of food in the duodenum, related to cholecystokinin release

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41
Q

What is dysphagia?

A

difficulty swallowing

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42
Q

What action defines esophageal body motility?

A

the presence of peristalsis

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43
Q

What are the long-term sequellae of Barrett’s esophagus?

A

15% become adenocarcinoma of esophagus

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44
Q

What is the small bowel motility pattern of scleroderma?

A

markedly diminished or absent contractile activity

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45
Q

What are predisposing causes of reflux esophagitis?

A

hiatus hernia, pyloric stenosis, increased intrabdominal pressure (ex. obesity, pregnancy)

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46
Q

What is the pathogenesis of Barrett’s esophagus?

A

gastroesophageal reflux leads to ulceration of squamous mucosa

ulcer is re-epithelialized by stem cells that differentiate into gastric or intestinal type epithelium

47
Q

What is an example of a malignant mesenchymal tumor?

A

leiomyosarcoma

48
Q

What are the pathological criteria for diagnosis of eosinophilic esophagitis?

A

prominent intraepithelial eosinophils (15+ in 2 or more high power fields)

microabscesses

large clusters near surface

49
Q

Which of the following are true of eosinophilic esophagitis?

a) it is a female predominant disease
b) atopic conditions are not usually associated with eosinophilic esophagitis
c) this is a self limited disease which usually resolves after a few months
d) pathophysiology involves exposure to food allergens

A

d) pathophysiology involves exposure to food allergens

50
Q

What are esophageal defensive mechanisms against GERD?

A

1) competent gastroesophageal junction
2) effective esophageal emptying of refluxed materials from the esophagus
3) neutralization of refluxed acid by salivary bicarbonate
4) an intact mucosa

51
Q

What are the two types of Barrett’s esophagus?

A

long-segment: metaplastic changes involving more than 3 cm in length of esophagus

short-segment: metaplastic changes involving less than 3 cm of esophagus

52
Q

What are the characteristic features of high grade dysplasia?

A

severe atypia, architectural complexity

villiform configuration of mucosal surface

nuclear pleomorphism and hyperchromatism

nuclear stratification to crypt luminal surface

53
Q

What are examples of precursor lesions?

A

squamous dysplasia, Barrett’s related dysplasia

54
Q

What part of the esophagus may be affected by portal vein hypertension?

A

the lower 1/3

this region drains into the gastric vein, which feeds the portal system

55
Q

What are the risk factors for pill esophagitis?

A

position of patient, size of medication, amount of fluid ingested with medication, increased age, abnormal esophageal anatomy

56
Q

What conditions are associated with development of eosinophilic esophagitis/esophageal eosinophilia?

A

atopic dermatitis, allergic rhinitis, asthma, modest peripheral eosinophilia

57
Q

What is the clinical presentation of achalasia?

A

progressive dysphagia (liquids and solids), regurgitation, chest pain, supine aspiration, weight loss

58
Q

What is the neurogenic control of the lower esophageal sphincter?

A

controlled by the myenteric plexus

excitatory neurons produce acetylcholine for resting tone

inhibitory neurons produce nitric oxide and vasoactive intestinal polypeptide (VIP) for LES relaxation

59
Q

IAre mass movements regulated by slow wave activity?

A

no - possibly under ANS control

60
Q

What factors/conditions are associated with Barrett’s esophagus?

A

GERD, sliding hiatal hernia, esophageal stricture, lye ingestion, chemotherapy, bile/pancreatic juice reflux, peptic ulceration, decreased resting pressure of lower esophageal sphincter

61
Q

What is the definition of Barrett’s esophagus?

A

a condition where distal squamous mucosa is replaced by metaplastic specialized (intestinalized columnar) epithelium as a response to longstanding chronic injury/esophagitis

irreversible, acquired metaplastic condition

62
Q

How is lower esophageal sphincter resting pressure maintained?

A

myogenic resting tone

neurogenic factors (myenteric plexus)

63
Q

What are the threatments for achalasia?

A

botulinum toxin injection, dilation of the LES, surgical myotomy/per oral myotomy

64
Q

What is the motor activity of the transverse and descending colon?

A

mass movements caudally

mass movement = lumen obliterating, intermittent contractions of the colonic circular muscle layer that propels fecal matter short distances along the colon

65
Q

On histology, an esophageal biopsy is found to have neutrophils in the epithelial layer, basal cells that make up 30% of epithelial thickness, and ballooned squamous cells. What is the most likely pathogenesis?

A

reflux esophagitis

66
Q

When medications induce esophageal injury, where along the esophagus is the injury most likely to occur?

A

at the level of the aortic arch

due to mild extrinsic compression

67
Q

Which colonic reflex is activity by food in the duodenum?

A

gastrocolic reflex

68
Q

How is esophageal motor function evaluated clinically?

A

barium esophagram and esophageal manometry

69
Q

What are the three phases of the migrating motor complexes in the small intestine?

A

phase I: motor inactivity

phase II: intermittent phasic, non-propagating contractions

phase III: burst of phasic contractions of maximum frequency and amplitude that propagates in a caudal direction

70
Q

What is the function of the internal anal sphincter?

A

it maintains resting tone, primary deterrent for involuntary egress of stool

remains tonically contracted when there is no neural inhibition

71
Q

What nerves innervate the external anal sphincter?

A

pudendal nerves from S2-S4

72
Q

What is odynophagia?

A

pain upon swallowing

73
Q

What are the main functions of the esophagus?

A

propel food from pharynx to stomach (via peristalsis)

secrete mucin for lubrication (via mucinous lined submucosal glands)

74
Q

What are the symptoms of squamous cell carcinoma of esophagus?

A

vague symptoms at first

later stages: progressive dysphagia, anorexia and weight loss

75
Q

What is dyspepsia?

A

indigestion/bad digestion

76
Q

What is the effect of a vagotomy on gastric motor function?

A

loss of acommodation reflex –> accelerated liquid emptying

interrupts antral contractile activity –> delayed mechanical digestion and emptying of solids

77
Q

How does the content of a meal alter the rate of gastric emptying?

A

liquids empty fastest, solids take longer due to mechanical digestion

fat, glucose, and hypertonic fluids empty slower

78
Q

What is another term for benign epithelial tumor?

A

squamous papilloma

79
Q

What size particles can pass through the pylorus?

A

1-2 mm

80
Q

What is the effect of nitric oxide inhibition on lower esophageal sphincter function?

A

it prevents relaxation induced by swallowing

  • mimics achalasia*
  • nitric oxide normally causes relaxation of the LES*
81
Q

What are the excitatory neurons of peristalsis? Inhibitory?

A

excitatory: cholinergicenteric neurons
inhibitory: nitric oxide generating neurons

82
Q

A patient presents with odynophagia (painful swallowing). On exam, you note shallow punched out ulcers in the esophagus. What is the most likely diagnosis?

A

herpes simplex virus infection of the esophagus

83
Q

What are the triggers of lower esophageal sphincter opening?

A

swallowing (primary peristalsis), esophageal distension (secondary peristalsis), or gastric distension (transient lower esophageal relaxation)

84
Q

What are the pathological findings of reflex esophagitis?

A

1) acute inflammatory cells in epithelial layer (eosinophils, neutrophils, excess T cells)
2) basal cell hyperplasia (>15% of epithelial thickness, elongated lamina propria)
3) ballooned squamous cells, vascular dilation, or multinucleated squamous epithelial giant cells

85
Q

What is metaplasia?

A

conversion of one differentiated epithelium into another differentiated type of epithelium

86
Q

What is a latency gradient of the esophagus?

A

the process of an inhibitory phase lengthening caudally down the esophagus

prevents all parts of the esophagus from contracting simulaneously, allows for coordinated movement

87
Q

What are the microscopic findings associated with Barrett’s esophagus?

A

esophageal squamous epithelium is replaced by columnar epithelium of gastrointestinal type (stomach, small bowel, colon) with goblet cells (mucin-filled cytoplasm)

may be villiform or contain paneth cells or pancreatic acini

definitive diagnosis = columnar mucosa with intestinal goblet cells

88
Q

How does esophageal cancer spread?

A

to adjacent tissue

metastatically (common) –> paraesophageal, paratracheal, parabronchial, mediastinal/deep cervical lymph nodes, liver, lungs, adrenals most common sites

89
Q

If an annual exam for Barrett’s esophagus finds low grade dysplasia, what should the next step be?

A

3-month course of intensive acid suppression treatment

if it persists after that, antireflex surgery or ablation therapy is performed

90
Q

What is the motor activity of the ascending colon?

A

ring contractions that migrate towards the head (opposite direction of normal intestinal transit) –> allows for retention/storage of fecal material

91
Q

What is the definition of reflux esophagitis?

A

acute and chronic inflammatory process due to reflux of gastric or duodenal contents into lower esophagus (w/o vomiting or belching) secondary to failure of anti-reflux mechanisms

may be erosive or non-erosive

92
Q

How is small bowel dysmotility treated?

A

dietary modification, nutritional support, intermittent antibiotics for secondary bacterial overgrowth

93
Q

What are the complications of reflux esophagitis?

A

erosion and ulceration, strictures, Barrett’s esophagus

94
Q

What are predisposing factors for squamous cell carcinoma of the esophagus?

A

tobacco, alcohol, ingestion of corrosives, anatomical abnormalities (hiatal hernia, diverticula), leukoplakia and Plummer-Vinson syndrome

95
Q

What endoscopy findings are associated with reflux esophagitis?

A

hyperemia, patches (like leukoplakia), erythema, edema, linear ulcers at distal esophagus

over half of patients appear normal on endoscopy

96
Q

What are examples of benign mesenchymal tumors?

A

leiomyoma, neurofibroma, lipoma, granular cell tumor

97
Q

If an annual exam for Barrett’s esophagus finds high grade dysplasia, what should the next step be?

A

esophagectomy

98
Q

What is the local peristaltic reflex of the small intestine?

A

bolus in GI lumen stimulates mucosal afferents

motor neurons with excitatory transmitters (acetylcholine and substance P) are activated above the bolus

motor neurons with inhibitory transmitters (NO, VIP) are activated below the bolus

net result = contraction above and relaxation below bolus, aboral propagation

99
Q

What are the symptoms of reflex esophagitis?

A

heartburn, dysphagia, sensation of acid in the mouth, retrosternal pain

100
Q

What is the most common cause of esophagitis?

A

reflux esophagitis

101
Q

What are the characteristic features of low grade dysplasia?

A

preservation of crypt architecture with minimal distortion

atypical nuclei in only basal half of crypts

variable hyperchromasia

overlapping cell borders, nuclear crowding, irregular nuclear contours

maturation towards lumen

102
Q

What are the treatments for eosinophilic esophagitis?

A

dietary restrictions to prevent exposure to common food allergens

topical or systemic corticosteroids

103
Q

What is the gross pathology of esophageal squamous cell carcinoma?

A

fungating/exophytic/polypoid lesions

ulcerative lesions

infiltrative lesions (thickens esophageal wall)

104
Q

What is the primary treatment for gastroparesis?

A

dietary modification with frequent, smaller meals with low fat and fiber content

105
Q

What is the difference in endoscopy findings between adults and children with eosinophilic esophagitis?

A

adults: fibrostenotic features (concentric rings, distinct strictures, narrow esophagus)
children: inflammatory features (edema, white exudates, furrowing)

106
Q

What is Hirschsprung’s disease?

A

a congenital disorder where the internal anal sphincter fails to relax, which produces a functional obstruction of the anorectum leading to proximal colonic dilation (“megacolon”)

107
Q

A patient presents with odynophagia (painful swallowing). On exam, you note deep serpiginous ulcers in the esophagus. What is the most likely diagnosis?

A

cytomegalovirus infectionof the esophagus

108
Q

What are the histological findings of the GI tract in scleroderma?

A

atrophy of the muscularis propria

109
Q

What are the two main motility patterns of the small intestine?

A

fed pattern: segmentation (non-propagated focal contractions at multiple levels)

fasting pattern: migrating motor complex

110
Q

What are the treatments for Ogilvie’s syndrome?

A

supportive care

IV neostigmine, ACE-Inhibitor

decompressionif severe

111
Q

What is another term for malignant epithelial tumor?

A

carcinoma (including adenocarcinoma and squamous cell carcinoma)

112
Q

What is the accomodation reflex of the stomach? How is it mediated?

A

active relaxation of the gastric body and fundus during a meal

mediated by the vagus nerve

113
Q

What are key non-pathology based factors that differentiate eosinophilic esophagitis from GERD, Chron’s disease, or other causes of esophagitis?

A

failure of high-dose PPI treatment

absence of acid reflux

GI (10 decks)

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