Esophagus Flashcards

1
Q

Three areas of esophageal narrowing are?

A

cricopharyngeus muscle

aortic notch

GEJ

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2
Q

Why are the three areas of esophageal narrowing important?

A

these are where foreign objects that are swallowed tend to be lodged

swallowed corrosive liquids also tend to cause damage here because of slower passage of material here

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3
Q

Opening of esophagus and ending of pharynx is collared around what muscle?

A

cricopharyngeus mc

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4
Q

Where do the recurrent laryngeal nerves lie in relation to the esophagus?

A

lie in the right and left grooves between trachea and esophagus

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5
Q

Length of esophagus?

A

cervical 5 cm

thoracic is 20 cm

abdominal 2cm

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6
Q

Muscles of the esophagus?

A

outer longitudinal layer

inner circular layer

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7
Q

Muscles of upper esophagus vs lower esophagus?

A

upper 1/3–> striated

lower 2/3—> smooth (most esophageal motility d/o involve the smooth part of esophagus)

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8
Q

Blood supply of esophagus?

A

cervical part—> from inferior thyroid A (from subclavian)

thoracic part—> bronchial arteries (1 right sided bronchial artery and 2 left sided most commonly); also get 2 esophageal branches from aorta

abdominal part–> ascending branch of left gastric A and inferior phrenic a

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9
Q

Right and left recurrent laryngeal nerves turn where?

A

R–> underneath right subclavian A

L–> underneath aortic arch

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10
Q

Venous drainage of esophagus?

A

cervical–> inferior thyroid vein

thoracic–> azygous, hemi-azygous, bronchial veins

abdominal–> coronary veins

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11
Q

PSNS innvervation of the esophagus?

A

vagus n

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12
Q

Swallowing is what type of act?

A

reflexive

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13
Q

What happens when we swallow food?

A

tongue moves bolus in posterior oropharynx

soft palate is elevated

hyoid bone elevated

epiglottis covers larynx

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14
Q

Describe the course of the esophagus?

A

cervical esophagus begins as midline structure; then deviates to the left of trachea as passes thru thoracic inlet

at level of carina it deviates to the right to accomadate aortic arch

then deviates to left as it enters diaphragm at T11

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15
Q

At what level does esophagus enter diaphragm

A

T11

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16
Q

What’s Killian’s triangle?

A

point of weakness in cervical esophagus

transition point between thyropharyngeus and cricopharyngeus muscle

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17
Q

What m. is responsible for generating the high pressure in the UES?

A

circopharyngeus

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18
Q

How do we distinguish esophagus from other alimentary organs?

A

lacks a serosa

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19
Q

What’s a Z line?

A

point where squamous tissue of esophagus transitions to columnar epithelium of stomach

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20
Q

Musculature of the esophagus?

A

has outer longitudinal fibers
has inner circular m fibers

upper 1/3–> striated skeletal muscle
lower 2/3–> smooth muscle fibers

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21
Q

How can we identify the GEJ?

A

squamo-columnar Z line junction helps identify it

transition from smooth esophageal lining to ruggael folds of stomach also helps identify it

the gastro-esophageal fat pad also helps delineate the GEJ

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22
Q

Cervical esophagus supplied by what artery?

A

inferior thyroid artery–> from thyrocervical trunk–> from L/R subclavians

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23
Q

What’s blood supply of circopharyngeus m, which marks the upper portion of the cervical esophagus?

A

superior thyroid artery

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24
Q

Blood supply of thoracic esophagus?

A

4-6 branches directly off the aorta

esophageal branches off of R/L bronchial arteries

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25
Q

Abdominal esophagus receives its blood supply from?

A

left gastric A

paired inferior phrenic arteries

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26
Q

R/L recurrent laryngeal nerves arise from?

A

vagus

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27
Q

R/L recurrent laryngeal nerve loop where?

A

R—> under R-subclavian

L—> under aortic arch

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28
Q

What n innervates the cricopharyngeus m?

A

recurrent laryngeal n

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29
Q

What are the resting pressures of the UES vs the LES?

A

UES–> has a steady state of tone at 60 mmHg, prevents steady air flow into esophagus

LES–> avg is 24 mmHg, remains elevated enough to prevent reflux of stomach content

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30
Q

What are the three types of esophageal peristalsis?

A

primary–> progressive, generate pressures of 40-80 mmHg, generated by voluntary swallowing

secondary–> progressive, but are generated from distention or irritation of esophagus (clears esophagus from material that was left behind after primary peristalsis)

tertiary–> non-progressive, non-peristaltic, cause esophageal spasms b/c they represent uncoordinated esophageal contraction

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31
Q

Intrinsic innervation of esophagus provided by ?

A

Auerbach’s plexus–> between muscle layers

Meissner’s plexus–> submucosal layer

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32
Q

What causes esophageal diverticula to form?

A

due to primary motor disturbances of the UES and LES

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33
Q

Where do we commonly see esophageal diverticula form?

A

pharyngoesophageal (Zenker’s)

mid-esophageal (parabronchial)

epiphrenic (sub-diaphragmatic)

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34
Q

What is the difference between a true and false diverticulum?

A

true divertic—> involves all layers of esophagus

false divertic—> only mucosa and submucosa only

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35
Q

What are pulsion vs traction diverticulum?

A

pulsion—> false diverticula (caused by increased intraluminal pressures )

traction—> true (due to external inflammatory mediastinal lymph nodes adhered to esophagus, and as they heal they contract and pull the esophagus in the process)

***Zenker’s and epiphrenic diverticula are pulsion diverticula

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36
Q

What is a pharyngo-esophageal diverticulum?

A

Zenker’s

false diverticula;pulsion; due to elevated intra-luminal pressures

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37
Q

What is the most common esophageal divertic?

A

Zenker’s

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38
Q

Who gets Zenker’s and where do they get it?

A

men in 70s

get it at Killian’s triangle; junction between thyropharyngeus and cricopharyngeus

**MC location is left-posterior

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39
Q

What’s cricopharyngeal achalasia?

A

Zenkers’s

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40
Q

Most serious complication from a Zenker’s?

A

aspiration pneumonia

lung abscess

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41
Q

Why do we need lateral views to visualize a Zenker’s?

A

usually protrudes posteriorly, in pre-tracheal space

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42
Q

Tx for Zenker;s?

A

surgical vs endoscopy is gold standard–> can do diverticulectomy vs diverticulopexy–>done via incision on left neck

in all cases a myotomy is performed on thyropharyngeus and cricopharyngeus

(open left cervical incision was done in the past)

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43
Q

When do you perform a diverticulectomy vs diverticulopexy for Zenker’s?

A

old frail pts, who won’t heal well–> diverticulopexy via left cervical incision

in most pts with good tissue, healthy, and >5 cm—> diverticulectomy done

***monitor for 2-3 days, NPO

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44
Q

What’s the Dohlman procedure?

A

endoscopic approach to repair of Zenker’s

done in pts with diverticula between 2-5 cm

doesn’t remove the pouch
wides opening of pouch and divides the cricopharyngeus

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45
Q

What kind of diverticula are epiphrenic diverticula?

A

false, pulsion

usually found in distal esophagus

**more common right side and have a wide opening

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46
Q

What are some causes of achalasia?

A

idiopathic
infectious/neurogenic
(stress, trauma, weight reduction, Chagas dx)

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47
Q

Pathophysiology of achalasia?

A

failure of LES to relax on pharyngeal swallowing

increased esophageal pressure

esophageal dilatation

loss of progressive peristalsis

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48
Q

What is the risk of Ca with achalasia?

A

over a 20 year period, a pt will have 8% chance of developing ca

squamous cell ca most common (air-fluid levels in esophagus causes mucosal irritation and induce metaplasia)

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49
Q

Sxs of achalasia?

A

dysphagia–> begins with liquids, progresses to solids
regurgitation
weight loss

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50
Q

Esophagram shows a dilated esophagus with distal narrowing/tapering referred to as a bird’s beak appearance;

A

achalasia

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51
Q

Gold standard for diagnosing achalasia?

A

manometry

52
Q

Surgical tx for achalasia?

A

modified laparoscopic heller myotomy

53
Q

Barium esophagram showing a corck-screw esophagus indicates what?

A

Diffuse esophageal spasm

54
Q

Surgical tx for DES?

A

long myotomy, extending proximally and down to LES

Dor fundoplication done to prevent healing of myotomy and prevent reflux

55
Q

This hypermotility disorder is associated with the most pain, results in high amp contractions;

A

nutcracker esophagus

56
Q

In this esophageal hypermotility d/o, pressures as high as 400 mgHg of pressure can be seen;

A

nutcracker esophagus

57
Q

Tx for nutcracker esophagus?

A

medical (CCBs, nitrates, anti-spasmodics)

avoidance of coffee, cold and hot foods

58
Q

Barrett’s esophagus?

A

normal stratified squamous epithelium of distal esophagus turns into gastric columnar epithelium in response to acid reflux

59
Q

What factor responsible for Barrett’s?

A

chronic GERD

60
Q

What is the risk of developing esophageal ca in Barrett’s?

A

40-fold increase in developing esophageal Ca

61
Q

For all pt’s with barret’s esophagus, what is recommended annually?

A

endoscopy

**for pts with low grade dysplasia–> endoscopy Q 6 months

62
Q

What do we do for people with high grade dysplasia Barrett/s?

A

resection

63
Q

What congenital anatomic vascular variant can cause compression of esophagus and cause a so -called vascular ring?

A

when right subclavian artery comes off of the descending aorta and travels behind the esophagus

64
Q

What’s a pulmonary artery sling?

A

L-pulm artery comes off of the right pulm artery and causes anterior compression of esophagus

65
Q

Whats dysphagia lusoria?

A

aberrant right subclavian artery thats comes off of descending aorta and can cause posterior compress of esophagus

66
Q

What is a Schatzkis ring?

A

seen in the GEJ junction

concentric narrowing, makes lower esophagus less distensible

67
Q

How do we diagnose Schaztkis rings?

A

barium esophagram

pt is prone, turned slightly to right

68
Q

Tx for Schatizkis ring?

A

oral papain or meperidine used to dissolve lodged pieces of food

oral dilation then performed

69
Q

How do we distinguish esophageal webs from a Shatzkis ring?

A

webs–> involve mucosa and submucosa, and have squamous type epithelium below and above the web

shtazki ring–> makde of epithelium, and have esophageal mucosa above and gastric mucosa below web

70
Q

Esophageal webs assc with what syndrome?

A

plummer vinson syndrome

edentulous, malnourished, middle aged women, glossitis, spoon shaped fingernails, Fe-deficiency anemia

71
Q

What caustic substance is ingested more commonly acidic or alkali liquids?

A

alkali –>more damaging

72
Q

What parts of esophagus are prone to injury more commonly after caustic substance ingestion?

A

UES
mid-esophagus by aorta
LES

correlate to anatomic narrowings

73
Q

How do alkaline substance dissolve esophageal tissue?

A

liquefactive necrosis

***acid ingestions cause coagulative necrosis

74
Q

Esophageal perforation is a surgical emergency;

A

early detection and repair; within 24 hrs–> 80-90% survival

> 24 hrs; survival decreases to 50%

75
Q

Most esophageal perforations occur from what?

A

EGD

Boarhaves 15%, foreign body ingestion 15%, trauma 10%

76
Q

Mallory Weiss tear?

A

mucosal tear of esophagus after vomitus

77
Q

Boerhavves?

A

esophageal ruptured after emesis

78
Q

For suspected esophageal perforation what contrast do we use to image perforation?

A

BARIUM for thoracic perforations (barium is inert in chest but causes peritonitis in abdomen)

GASTROGRAFFIN for abdominal perforation (can cause life threatening pneumonitis)

79
Q

Most common perforations seen with Booerhaves are seen where?

A

above GEJ on left lateral wall of esophagus

80
Q

Tx of Boorhaves in an unstable pt?

A

debride devitalized tissue

esophageal diversion or resection

creation of an esophagostomy

wide drainage

placing a feeding gastrostomy or feeding jejunostomy

81
Q

Most critical variable that determines surgical management for esophageal perf?

A

degree of inflammation surrounding the perf

less than 24 hrs, tissue is less friable, surgery is recommended

> 24 hrs tissue is more friable

82
Q

Golden timing for repair of esophageal pers?

A

within 24 hrs

83
Q

How do we approach esophageal perforations ?

A

cervical perfs–>approach on same side of perf

thoracic perforations upper 2/3–> right chest incision

thoracic perforations lower 1/3–> left chest incision

abdominal perforations–> approached from abdomen or left chest

84
Q

What is a tracheo-esophageal fistula?

A

it’s an epithelialized tract between trachea and esophagus

85
Q

How do we treat TEF?

A

make pt npo, put in a feeding tube (gastrostomy v jejunostomy)

course of IV abx

2nd stage–> ablate the fistula tract

86
Q

Surgically, how do we remove TEF?

A

expose the fistula tract via thoracic v cervical incision

segmentel tracheal resection, primary repair of esophagus

place muscle flap between trachea/esophagus

87
Q

What’s more common; malignant or benign tumors of the esophagus?

A

malignant tumors more common

***benign tumors make up less than 1 %

88
Q

What are some common benign esophageal tumors?

A

60% are leiomyomas

20% are cysts

5% are polyps

89
Q

Leiomyomas of esophagus?

A

most common benign lesions
more common in men
seen in distal 2/3 of esophagus 80% of time

**classified as GISTs

90
Q

Almost all GIST tumors have a ckit oncogene mutation of?

A

CD117

91
Q

What medication may be of benefit in leiomyomas of esophagus (GISTs)?

A

imatinib

tyrosine kinase inhibitor

92
Q

2nd most common benign lesions of esophagus?

A

esophageal cysts (congenital vs acquire)

93
Q

Most esophageal Ca are what type?

A

squamous cell Ca worldwide

**in US, 70% of diagnosed esophageal ca is adenocarcinoma

94
Q

Who gets esophageal Ca, males or females?

A

squamous cell; male to female 3;1 (mostly AA men)

adenocarcinoma; male to female; 15;1 (mostly white men)

95
Q

Where is squamous cell carcinoma commonly found?

A

upper and mid esophagus 70% of time

96
Q

What causes squamous cell carcinoma (commonly found in upper and mid esophagus)?

A

exposure to envt toxins;

smoking, etoh, nitrosamines, hot liquids, VIt A and zinc deficiencies

caustic ingestion, achalasia, bulimia, plummer vinson, radiation, esophageal diverticula

97
Q

Most esophageal cancers diagnosed in US and western countries is?

A

adenocarcinoma

98
Q

What causes adenocarcinoma?

A

increasing incidence of GERD
Western diet
use of acid suppression meds

99
Q

How does GERD lead to adenocarcinoma?

A

coffee, fats, acidic foods, lead to relaxed LES and increased reflux

to adapt the squamous line distal esophagus transforms to the columnar type tissue of proximal stomach (BARRETTs)

progressive changes from metaplastic barretts to dysplastic changes lead to adenocarcinoma

100
Q

What are some intrinsic esophageal diseases that are considered pre-malignant?

A

Plummer-vinson syndrome; dx of Fe and vitamin deficiency, causes atrophy of esophageal mucosa (assc with increased risk of squamous cell ca)

tylosis–> familial condition, assc with thickening of soles and palms (assc with squamous cell carcinoma)

achalasia–> assc with 16-fold increase in squamous cell ca in late stages of dx

101
Q

What gene mutation assc with increased risk of esophageal ca?

A

P53 mutation

102
Q

Barretts esophagus is assc with 40-fold increase in what esophageal ca?

A

Barretts

103
Q

Why does dysphagia present late in the course of esophageal cancers?

A

b/c the esophagus can distend, 2/3 of the lumen of the esophagus can be obstructed by mass before dysphagia can present

104
Q

Good first test to start with in someone suspect of having esophageal ca and presenting with dysphagia?

A

barium esophagram

can show if lesion is intraluminal or intramural, intrinsic or extrinsic

105
Q

Diagnosis of esophageal Ca is best made by?

A

endoscopic biopsy

106
Q

Most critical study for esophageal ca work up?

A

endoscopic US

107
Q

TNM staging for esophageal cancer:

A

T1–> submucosal
T2–>muscularis propria
T3–>adventitia
T4–>surrounding structures

N0–> no nodes
N1–> any nodes

M0–> no mets
M1a–> regional lymph node mets
M1b–> distant lymph node mets

108
Q

Treatments for squamous cell carcinoma vs adenocarcinoma?

A

SCC–> more common US, more sensitive to chemo-radiotherapy, are mostly treated non surgically

adenocarcinoma–> more common worldwide, need more aggressive surgical approaches

109
Q

After caustic agent ingestion, like lye for example, do we do routine surveillance?

A

15-20 yrs after caustic ingestion

risks of squamous cell carcinoma is 2% after caustic ingestion

110
Q

Best tx option for high grade dysplasia?

A

esophagectomy

111
Q

Why does per-oral endoscopic myotomy have the highest incidence of GERD?

A

it ablates the LES but does not add an anti-reflux component like a Heller

112
Q

What’s a Cameron ulcer?

A

pts with hiatal hernias are prone to developing these due to sliding up GEJ up and down thru the hiatus

113
Q

What is the first surgical step in someone with a perforated esophagus that you are repairing?

A

extend the myotomy

114
Q

Gold standard for diagnosis of achalasia?

A

esophageal manometry

115
Q

In pts who have GERD and wound benefit from a fundoplication procedure, but they also have reduced esophageal motility, wht do you do?

A

can do a partial fundoplication like a Dor, instead of a Nissen

this helps the GERD and doesn’t make the esophageal motility worse

116
Q

Mid-esophageal perforation, how do you approach it?

A

right postero-lateral thoracotomy

117
Q

Perforation of lower third of esophagus, how do you approach?

A

left postero-lateral thoracotomy

118
Q

Surgically how do we remove esophageal leiomyomas?

A

if <5 cm–> endoscopic

if >5 cm–> VATS or laparoscopically

119
Q

Standard for diagnosis esophageal perf?

A

esophagraphy with gastrograffin

120
Q

Traction diverticula are true diverticula and tend to occur where most cmmonly?

A

mid-esophagus

(pulsion diverticula like zenkers and epiphrenic only involve mucosa and submucosa; false; found in cervical and distal esopagus

121
Q

Premature contractions in at least 20% of swallows in setting of normal relaxation of LES:

A

DES

corckscrew appearance on esophagram

tx; initially PPI, CCB initially, botulin injection as second line tx

122
Q

Mgmt of Barrets:

A

BE w/out dysplasia; PPI and surveillance 3-5 yrs

BE w/low grade dysplasia–>endoscopic radiofrequency ablation

BE w/high grade dsyplasia–>endoscopic resection followed by radiofrequency ablation, some cases esophagectomy

123
Q

three types of achalasia based on Chicago classification;

A

type 1; absent peristalsis, LES not relaxed, normal esophageal pressure

type 2; absent peristalsis, LES not relaxed, pan esophageal increase in presure

type 3; absent peristalsis, LES not relaxed, distal esophagus spastic contractions

124
Q

What are the margins of a Heller myotomy performed for achalasia?

A

myotomy 2cm below GE junction

extending 5 cm proximally on esophagus

125
Q

Predominant sx of achalasia?

A

dysphagie to solids and liquids both

126
Q

Tx for Zenkers 2-5 cm?

A

diverticulopexy w/myotomy

diverticulectom w/myotomy

<2 cm–>diverticulopexy alone, or myotomy alone

127
Q

Barretts esophagus will predispose to what type of cancer?

A

adenocarcinoma