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Esophageal Disorders Flashcards

1
Q

What is the function of the esophagus?

A

to transport the bolus from pharynx into the gastric reservoir

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2
Q

Which portion of swallowing is voluntary? involuntary?

A

the inital phase is voluntary but as bolus is pushed backward by the tongue to the hypopharynx the involuntary phase of swallow reflex is triggered

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3
Q

How is the larynx elevated during the initial phase of swallowing?

A

suprathyroid muscles pull thyroid/cricoid up, epiglottis gloses off glottis

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4
Q

What type of muscle is the UES? LES?

A

UES-skeletal

LES-smooth

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5
Q

What is the role of the LES?

A

prevents reflux of acid with it’s tone

reenforced by crural diaphragm

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6
Q

How is the bolus moved from mouth to stomach?

A

ante-grade peristalsis (coordinated and propulsive sequential contraction)
primary peristalsis occurs in concert with appropriately timed relaxation of the sphincters

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7
Q

What is primary peristalsis?

A

triggered by swallow

associated with pharyngeal contraction and UES relaxtion

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8
Q

What is secondary peristalsis?

A

triggered by esophageal peristalsis

contraction start proximal to distention

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9
Q

What are the 2 innervations of the esophagus that generate peristalsis?

A

intrinsic-enteric neural plexus

extrinsic-vagus nerve

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10
Q

What 2 nuclei are involved in neural control of peristalsis?

A

nucleus ambiguous-proximal esoph.

dorsal motor nuclei-distal esoph.

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11
Q

What generates the sequence of peristalsis?

A

central pattern generator of the brainstem

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12
Q

How is peristalsis in smooth muscle regulated physiologically?

A

as a wave of inhibition followed by a wave of excitation

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13
Q

What is the main excitatory neurotransmitter?

A

acetylcholine

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14
Q

What is the main inhibitory neurotransmitter?

A

nitric oxide

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15
Q

What is dysphagia?

A

difficulty to eat (during swallow)
sticks, caught, hung up
NOT like globus sensation (always a lump in the throat)

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16
Q

3 main questions to ask with dysphagia history

A

1: what kind of food
2: intermittent or progressive
3: other symptoms (heart burn, regurg, odynophagia, chest pain)

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17
Q

Main features of esophageal dysphasia

A

sticks/hang ups after swallow
may have chest pain or not
pain can refer to pharynx

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18
Q

Main features of pharyngeal dysphagia

A

difficulty initiating swallow
coughing, choking, nasal regurgitation
canNOT refer to esophagus

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19
Q

3 main mechanical dysphagias

A

peptic stricture
esophageal ring
cancer

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20
Q

3 main neuromuscular dysphagias

A

achalasia
esophageal spasm
dysmotility

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21
Q

What type of dysphagia casues problems with solid food only?

A

mechanical obstruction

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22
Q

What type of dysphagia causes problem with solid or liquid food?

A

neurouscular

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23
Q

3 main features of mechanical obstruction

A 
progressive (age >50 cancer)
chronic heartbutn (peptic stricture)
intermittent (esophageal ring)
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24
Q

2 main features of neuromuscular dysphagia

A

progressive with hearburn/regurg-scleroderma

intermittent and chest pain-spasm

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25
Q

What are the techniques used to diagnose esophageal disorders?

A

upper gi endoscopy
esophageal manometry
radiography/esophagram

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26
Q

What is the Z line?

A

GEJ opening

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27
Q

How does esophageal manometry work?

A

measures esophageal intra-luminal pressures

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28
Q

What are the steps of primary peristalsis in the esophagus?

A

UES relaxes .5s
primary peristaltic wave produces a lumen-occluding contraction with amplitude of 30-150mm HG
Peristlatic duration 3-7s, migrates aborally at a speed of 3-5cm/s
LES relaxes 3-8 s to allow bolus emptying into stomach

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29
Q

What is achalasia?

A

impaired LES relaxation/increased LES tone
loss of peristalsis in the body of the esphagus
due to impared and then loss of inhibitory (NO) activity

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30
Q

Presentation of achalasia?

A

dysphagia ~90%

chest pain, heartburn, regurg, wt loss ~60%

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31
Q

What accomodative behaviors do people with achalasia

A

slow, stereotypical eating movements

avoiding social events with meals

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32
Q

What are the characteristic radiographic findings of achalasia?

A 
bird beak sign
sigmoid shape (end stage)
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33
Q

What else does the differential diagnosis for achalasia contain?

A 
malignancy
other infiltrative disorders
chagas disease
paraneoplastic syndromes
autonomic nerve damage
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34
Q

What are the treatments for achalasia?

A

NO donors/anticholinergic agents
endoscoptic therapy: botulinum toxin injection (inhibits Ach release), pneumatic dilation
operative therapy

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35
Q

Define esophageal spasm

A

dyscoordinated contraction, usually in body, LES usually fine
intermittant, problems with liquids

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36
Q

Describe complete aperistalsis/scleroderma esophagus

A

smooth muscle contraction lost, skeletal muscle still works

also seen w/polio, severe COPD & severe diabetes

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37
Q

What is stratified squamous non-keratinized stratified epithelium resistant to? sensitive to?

A

reistant to: abrasion

Sensitive to: acid

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38
Q

What makes up the pre-epithelial defense?

A

mucus-unstirred water layer-bicarbonate barrier

mucus blocks pepsin but not hydrogen ions

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39
Q

What makes up the epithelial defense?

A

apical cell membrane, intercellular junctional complex

intracellular buffering and H+ extrusion processes

40
Q

What is the pathophysiology of GERD?

A

decreased in normally constant LES tone
reflux of gastric juices leading to mucosal injury
IL-6 production–>more H2O2 in muscle–>increase in PAF and PGE2–>decreased ACh release and LES tone

41
Q

What can lead to an incompetent LES? (3)

A

transient LES strain
strain
hypotonic LES

42
Q

What causes a hiatal hernia?

A

separation of diaphragmatic crura and LES

43
Q

What are the two types of hiatal hernia?

A

sliding/type I-common, asymptomatic usually

paraesophageal/type II

44
Q

What is characteristic histologically of reflux?

A

> 20% of total epithelium basal zone epithelium (normal 10%)

eosinophils are recruited into the squamous mucosa, followed by neutrophils (more severe)

45
Q

What may be seen on endoscopy in a person with GERD?

A

redness, erosions

46
Q

What is the most common cause of esophagitis?

A

reflux of gastricc contents (reflux esophagitis)

47
Q

What are classic symptoms of reflux esophagitis?

A

heartburn
regurgitation
(atypical chest pain, chronic cough, hoarseness also possible)

48
Q

What diagnostic modalities are used for GERD?

A

endoscopy-more specific
ambulatory reflux monitoring-more sensitive
radiography

49
Q

What are the “alarm” symptoms of GERD?

A 
dysphagia
anemia
weight loss
abdominal mass
vomiting
50
Q

How is GERD managed?

A 
lifestyle modifications (wt loss, elevation of bed, avoiding late meals & trigger foods)
pharm (PPIs, anti-secretory drugs)
Operative (fundoplication, substitute devices to enforce LES)
51
Q

What are the major complications of GERD?

A

**Barrett’s esophagus

esophageal ulcer, stricture, bleeding

52
Q

What are the most common causes of esophageal stricture?

A

chronic GERD
radiation
caustic injury
(inflammation and scarring)

53
Q

Features of esophageal stricture

A

difficult eating solids first, then liquids
fibrous thickening of submucosa
atrophy of muscularis propria
secondary epithelial damage

54
Q

What is eosinophilic esophagitis?

A

epithelial infiltration by large numbers of eosinophils, particularly superficially
if far from GEJ can differentiate from GERD

55
Q

Clinical presentation of eosinophilic esophagitis?

A

Adults: dysphagia, most common cause of food impaction, heartburn, nausea
Kids: nausea, burning, food intolerance
failure of acid suppressive treatment & absence of acid reflux

56
Q

What family history information may be pertinent to eosinophilic esophagitis?

A

personal/family history of atopia (atopic dermatitis, rhinitis, asthma)

57
Q

What causes eosinophilic esophagitis?

A

allergic immune reactions to ingested/inhaled allergens that invovles Tcell mediated HSR
eosinophil activation/infiltration
major basic protein, increased IL5 & IL13
tissue remodeling/fibrosis, change in mechanical properties of the esophagus

58
Q

What confirms a diagnosis of eosinophilic esophagitis?

A

> 15 eosinophils/HPF in esophageal mucosa

history of food impaction also extremely important

59
Q

What is the treatment for eosinophilic esophagitis?

A

elimination diet
topical steroids
systemic steroids
endoscopic dilation

60
Q

Features of chemical esophagitis

A

irritants
medicinal pills may lodge and dissolve in esophagus
self-limited pain, odynophagia

61
Q

Who usually gets infectious esophagitis?

A

immunosuppressed/debilitated

overall very rare

62
Q

What are the most common causes of viral esophagitis?

A

HSV

CMV

63
Q

Key features of HSV esophagitis?

A

punched out ulcers

nuclear inclusions, multinucleate cells

64
Q

Key features of CMV esophagitis?

A

shallow ulcerations

cytoplasmic and nuclear inclusions

65
Q

Most common cause of fungal esophagitis?

A

candida (mucormycosis & aspergillosis also possible)

gray/white pseudomembranes

66
Q

How common is bacterial esophagitis?

A

10% infectious esophagitis

67
Q

What are the main causes of Iastrogenic esophagitis?

A

chemo
GVHD (very rare)
radiation-due to blood vessel thickening/ischemic injury

68
Q

What skin disorders are commonly associated with esophagitis?

A

bullous pemphigoid & epidermolysis bullosa (desquamative skin disease)
lichen planus
crohn’s disease

69
Q

What is Barrett’s esophagus?

A

squamous epithelium replaced by metaplastic columnar mucosa w/goblet cells (intestinal)
incidence increasing

70
Q

What can cause barrett’s esophagus?

A

chronic GERD (10% of GERD pts have)

71
Q

How often does epithelial dysplasia develop from BE?

A

.2-1% pts w/BE/yr

72
Q

Is barrett’s esophagus symptomatic?

A

NO

73
Q

What genes likely play a role in BE?

A

Cdx-expressed in 100% of BE

p53, Cyclin D1 later carcinogenesis

74
Q

What defines adenocarcinoma?

A

intramucosal carcinoma is characterized by invasion of neoplastic epithelial cells into the lamina propria

75
Q

What is the morphology of BE?

A

tongues/patches of red velvety mucosa extending upward from the GEJ, alternates with normal esophageal mucosa

76
Q

How does BE present?

A

endoscopic & histologic evidence of metaplasia
white adult male bwn 40-60 w/long term reflux sx
asymptomatic most often

77
Q

What do you do about BE?

A

periodic endoscopy with biopsy

78
Q

What are the risk factors of esophageal adenocarcinoma?

A 
western countries
dysplasia in BE
tobacco
obesity
radiation therapy
79
Q

Who usually gets esophageal adenocarcinoma?

A

white middle aged men

80
Q

How does adenocarcinoma present?

A 
dysphagia
odynophagia
progressive wt loss
vomiting
found during BE surviellance
81
Q

What is the survival rate for adenocarcinoma?

A

5yr sruvival 80% if only superficial

<25% 5yr survival overall due to advanced age at time of dx

82
Q

What genes are associated with adenocarcinoma?

A 
chromosomal abnormalities
p53
cyclin D1, cyclin E
c-ERB-B2
increased expression of TNF and NFKB (suggests chronic inflammation contributes)
83
Q

What is the morphology of adenocarcinoma?

A

flat or raised patches in otherwise intact mucosa
usually DISTAL 1/3, may invade gastric cardia
tumors typically produce mucin and form dense glands

84
Q

What is the common presentation of squamous cell carcinoma of the esophagus?

A

african american male adults older than 45 yo

85
Q

What are risk factors for SCC?

A 
alcohol
tobacco
poverty
caustic injury
achalasia/plumer-vinson syndrome
frequent consumption of hot beverages
radiation therapy
86
Q

What coutnries have the highest incidence of SCC?

A

iran, turkmenistan, china, hong kong, argentina, brazil, south africa

87
Q

What SCC risk factors are found in endemic regions?

A 
nutritional deficiencies
mutagenic compounds (in fungus contaminated food)
HPV infection
88
Q

What is the morphology of SCC of hte esophagus?

A

MIDDLE 1/3 of esophagus
small, grey plaque like thickenings
lead to tumor masses that protrude into and obstruct the lumen
may invade respiratory tree or aorta
usually moderately to well differentiated

89
Q

What are the main symptoms of SCC?

A 
usually large at time of DX 
dysphagia
odynophagia
obstruction
first sx may be caused by aspiration of food through a TE fistula
90
Q

What does detection of esophageal tumors occur so late?

A

patients may adjust by altering their diet from solid to liquid foods

91
Q

Why does extreme wt loss and debilitation occur during SCC?

A

impaired nutrition and effects of tumor itself

92
Q

What is the survival rate for SCC?

A

75% 5yr survival if superficial
overall 5yr survival <9% due to late detection
lymph node involvement-poorer prognosis

93
Q

Which lymph nodes are associated with the upper 1/3 of the esophagus?

A

cervical

94
Q

Which lymph nodes are associated with the middle 1/3 of the esophagus?

A

mediastinal, paratracheal, tracheobronchial

95
Q

Which lymph nodes are assoicated with the lower 1/3 of the esophagus?

A

gastric and celiac nodes

GI (20 decks)

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