Diseases of the Esophagus Flashcards
1
Q
Acts as a conduit for the transport of food
A
Esophagus
2
Q
How long is the esophagus in cm?
A
18-26 cm long hollow muscular tube
3
Q
In order for the esophagus to accommodate food it distends by how much?
A
To accommodate food:
o lumen distends up to 2 cm AP and 3 cm laterally
4
Q
What are the four layers of the esophagus?
A
esophageal wall: 4 layers
o innermost mucosa
o submucosa
o muscularis propria
o outermost adventitia
o NO SEROSA
5
Q
Where does the esphagus begins?
A
Origin: neck at the level of the cricoid cartilage
6
Q
Where does the esophagus ends?
A
Ends after passage through the hiatus in the right crus of the diaphragm by joining the stomach below
7
Q
Esophageal diseases can be manifested
by i________________.
A
mpaired function or pain
8
Q
What are the key functional impairments of the esophagus?
A
Key functional impairments are
swallowing disorders and excessive gastroesophageal reflux.
9
Q
The remains central to the evaluation of esophageal
symptoms.
A
clinical history
A thoughtfully obtained history will often expedite management.
Important details include
- weight gain or loss,
- gastrointestinalbleeding,
- dietary habits including the timing of meals,
- smoking,
- and alcohol consumption.
10
Q
The major esophageal symptoms are
A
- heartburn
- regurgitation,
- chest pain
- dysphagia,
- odynophagia, and
- globus sensation.
11
Q
__________
o Most common symptom
o Discomfort or burning sensation behind the sternum
o intermittent symptom most commonly experienced after eating, during exercise, and while lying recumbent
o relieved with drinking water or antacid
o but can occur frequently
A
HEARTBURN
12
Q
_____________
o Effortless return of food or fluid into the pharynx without nausea and retching
o Patients report a sour or burning fluid in the throat or mouth that may also contain undigested food particles.
o Bending, belching, or maneuvers that increase intraabdominal pressure can provoke regurgitation
A
REGURGITATION
13
Q
________
Preceded by nausea and retching
A
VOMITING
14
Q
___________
Is a behavior in which recently swallowed food is regurgitated and then swallowed repetitively for up to 1 hour
A
RUMINATION
15
Q
_______
o Pressure type sensation in the mid chest radiating to the mid back, arms and jaw (Esophageal Pain)
o common esophageal symptom with characteristics similar to cardiac pain, sometimes making this distinction difficult.
A
CHEST PAIN
16
Q
What is the most common cause of chest pain in esophageal dse?
A
Gastroesophageal reflux is the most common cause of esophageal chest pain
17
Q
**The similarity to cardiac pain in chest pain brought about by esophageal symptoms is likely because_______________________
A
the two organs share amnerve plexus and the nerve endings in the esophageal wall have poor discriminative ability among stimuli
18
Q
_________
o Food sticking or lodging in the chest
o Solid and liquid food VS solid food only
A
DYSPHAGIA
19
Q
How to distinguised dysphagia?
A
o Important distinctions are between uniquely solid food dysphagia as opposed to liquid and solid, episodic versus constant dysphagia, and progressive versus static dysphagia.
20
Q
If the dysphagia is for liquids as well as solid food, it suggests a__________________.
**
A
motility disorder such as achalasia
21
Q
Conversely, uniquely solid food dysphagia is suggestive ________________
A
of a stricture,
ring, or tumor
22
Q
___________________
o Pain by swallowing (pill)
o pain either caused by or exacerbated by swallowing.
o more common with pill or infectious esophagitis than with reflux esophagitis
A
ODYNOPHAGIA
23
Q
o When odynophagia does occur in GERD
it is likely related to an ___________________
A
esophageal ulcer or deep erosion.
24
Q
______________
o Perception of lump or fullness in the throat irrespective of swallowing (anxiety)
o often relieved by the act of swallowing
o As implied by its alternative name (globus hystericus), globus sensation often occurs in the setting of anxiety or obsessive-compulsive disorders
A
GLOBUS SENSATION / GLOBUS HYSTERICUS
25
\_\_\_\_\_\_\_\_\_\_\_\_
o **Excessive salivation** from **vagal reflex triggered by acid in the stomach**
**o not a common symptom**
o Afflicted individuals will **describe the unpleasant sensation of the mouth rapidly filling with salty thin fluid,** often in the **setting of concomitant heartburn.**
WATER BRASH
26
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_, also known as \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_) is
the best test for the evaluation of the proximal gastrointestinal tract.
Modern instruments produce high-quality color images of the esophageal,
gastric, and duodenal lumen..
Endoscopy esophagogastroduodenoscopy (EGD
endoscopes also have an instrumentation
c**hannel through which biopsy forceps, sclerotherapy**
**catheters, balloon dilators, or cautery devices can be utilized.** The key
advantages of endoscopy over barium radiography are: (1) increased
sensitivity for the detection of mucosal lesions, (2) vastly increased
sensitivity for the detection of abnormalities mainly identifiable by
an abnormal color such as Barrett’s metaplasia, (3) the ability to
obtain biopsy specimens for histologic examination of suspected
abnormalities, and (4) the ability to dilate strictures during the
examination. The main disadvantage of endoscopy is that it usually
necessitates the use of conscious sedation with medicines such as
midazolam (Versed), meperidine (Demerol), or fentanyl.
27
The key
advantages of endoscopy over barium radiography are:
(1) increased sensitivity for the detection of mucosal lesions,
(2) vastly increased sensitivity for the detection of abnormalities mainly identifiable by
an abnormal color such as Barrett’s metaplasia,
(3) the ability to
**obtain biopsy** specimens for histologic examination of suspected
abnormalities, and
(4) the ability to **dilate strictures during the**
* *examination.** l.
28
The main disadvantage of endoscopy is that it usually
necessitates the use of conscious sedation with medicines such as
midazolam (Versed), meperidine (Demerol), or fentany
29
\_\_\_\_\_\_\_\_\_\_
o combine an endoscope with an ultrasound transducer to **create a transmural image** of the tissue surrounding the endoscope tip
o The key advantage of EUS over alternative radiologic imaging techniques
much greate resolution attributable to the proximity of the ultrasound transducer to the area being examined.
o Available devices can provide either radial imaging (360-degree, cross-sectional) or a curved linear image
can guide fine-needle aspiration of imaged structures such as lymph nodes or tumors
o Major esophageal applications of EUS:
1. To stage esophageal cancer, to evaluate dysplasia in Barrett’s esophagus
2. To assess submucosal tumors
EUS (ENDOSCOPIC ULTRASOUND)
30
What is the key advantage of EUS over alternative radiologic imaging techniques ?
much greate resolution attributable to the proximity of the ultrasound transducer to the area being examined.
Available devices can provide either radial imaging (360-degree, cross-sectional) or a curved linear image
**can guide fine-needle aspiration of imaged structures such as lymph nodes or tumors**
31
What are the major esophageal applications of EUS:
1. To stage esophageal cancer, to evaluate dysplasia in Barrett’s esophagus
2. To assess submucosal tumors
32
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_, entails **positioning a
pressure sensing catheter** within the esophagus and then observing
the **contractility following test swallows**.
Esophageal manometry, or motility testing
33
How does the the upper and lower
esophageal sphincters appear in esophageal manometry?
as zones of high pressure that relax on
swallowing
34
How does the the intersphincteric esophagus appear in esophageal manometry?
they exhibits peristaltic
contractions.
35
\_\_\_\_\_\_ is used to diagnose motility disorders
(**achalasia, diffuse esophageal spasm) and to assess peristaltic **integrity prior to the surgery for reflux disease.
This can also
be combined with **intraluminal impedance** monitoring. Impedance recordings utilize a catheter with a series of paired electrodes.
Esophageal luminal contents in contact with the electrodes decrease
(liquid) or increase (air) the impedance signal allowing detection of anterograde or retrograde transit of esophageal bolus transit.
Manometry
Technological
advances have rebranded esophageal manometry as **high-resolution ****esophageal pressure topography **
36
\_\_\_\_\_\_\_\_\_\_\_\_\_\_ of the esophagus, stomach, and duodenum
**can demonstrate:**
**1.barium reflux**
**2. hiatal hernia**
* *3. mucosal granularity
4. erosions**
**5. ulcerations**
**6.strictures.**
The sensitivity of this
compared with **endoscopy** for detecting esophagitis reportedly ranges from **22–95%**, with higher grades of esophagitis (i.e., ulceration or stricture) exhibiting greater detection rates.
Conversely, 8 PART 14 Disorders of the Gastrointestinal System
the sensitivity for detecting esophageal strictures
**is greater than that of endoscopy**, especially when the study is
done in conjunction with barium-soaked bread or a 13-mm barium
tablet.
These studies also provide an **assessment of esophageal
function and morphology**that**may be undetected on endoscopy.**
**Hypopharyngeal pathology** and disorders of the **cricopharyngeal
muscle**are better appreciated in here, particularly
with **videofluoroscopic recording.**
Contrast radiography
NOTE: adiography is that it rarely obviates the need for
endoscopy. Either a positive or a negative study is usually followed
by an endoscopic evaluation either to clarify findings in the case of
a positive examination or to add a level of certainty in the case of a
negative one.
37
**GERD** is often diagnosed in the **absence of endoscopic esophagitis,**
which would otherwise define the disease.
This occurs in the settings
of partially treated disease, an abnormally sensitive esophageal
mucosa, or without obvious explanation.
In such instances, this can d**emonstrate excessive esophageal exposure to refluxed
gastric juice, the physiologic abnormality of GERD**. This can be
done by ambulatory **24- to 48-hour esophageal pH** recording using
either a wireless pH-sensitive transmitter that is anchored to the
esophageal mucosa or with a transnasally positioned wire electrode
with the tip stationed in the distal esophagus. Either way, the outcome
is **expressed as the percentage of the day that the pH was less
than 4**(***indicative of recent acid reflux***), with values**exceeding 5%
indicative of GERD.**
It is useful with **atypical symptoms
or an inexplicably poor response to therapy.**
REFLUX TESTING
38
What can be added to pH monitoring to detect reflux
events irrespective of whether or not they are acidic, potentially
increasing the sensitivity of the study?
Intraluminal impedance
monitoring
39
\_\_\_\_\_\_\_\_ is a herniation of viscera, most commonly **the stomach**,
into the mediastinum through the esophageal hiatus of the
diaphragm.
Hiatus hernia
40
One of the four types of hiatus hernia comprising at least 95% of the overall total.
sliding hiatal hernia
41
A\_\_\_\_\_\_\_\_\_ is one in which the gastroesophageal junction
and gastric cardia slide upward as a result of **weakening of the
phrenoesophageal ligament** attaching the gastroesophageal junction
to the diaphragm at the hiatus. True to its name, this
**enlarge with increased intraabdominal pressure, swallowing, and
respiration.**
The incidence of this **increases with age** and
conceptually, **results from wear and tear:** **increased intraabdominal**
**pressure** from abdominal obesity, pregnancy, etc., and hereditary
factors predisposing to the condition.
The main significance of this is the propensity of affected individuals to have GERD.
sliding hiatal hernia
42
Types II, III, and IV hiatal hernias are all subtypes of paraesophageal
hernia in which the herniation into the mediastinum includes a
**visceral structure** other than the gastric cardia.
With type II and III
paraesophageal hernias, the\_\_\_\_\_\_\_ with the
distinction being that in type II, the \_\_\_\_\_\_\_\_\_\_
while type III is a\_\_\_\_\_\_\_\_\_\_\_\_
. With type IV hiatal hernias, \_\_\_\_\_\_\_\_\_\_\_herniate into the mediastinum, **most commonly the colon**.
gastric fundus also herniates
gastroesophageal junction remains fixed at the hiatus,
mixed sliding/paraesophageal hernia.
viscera other than the stomach
43
With
\_\_\_\_\_\_\_\_\_\_\_\_paraesophageal hernias, the **stomach inverts as it
herniates**and large paraesophageal hernias**can lead to an upside
down stomach, gastric volvulus, and even strangulation of the
stomach.** Because of this risk, surgical repair is often advocated for
large paraesophageal hernias.
type II and III
44
A lower esophageal mucosal ring, also called a _____ , is a thin
membranous narrowing at the **squamocolumnar mucosal junction**
( Fig. 292-2 ). Its **origin is unknown** but these are demonstrable
in about **15% of people** and are usually **asymptomatic.**
B ring
45
When the
lumen diameter is **less than 13 mm**, distal rings are usually associated
with **episodic solid food dysphagia** and are called \_\_\_\_\_\_\_\_. Patients typically present **older than 40 years**, consistent with
an **acquired rather than congenital origin**. This is one of the
**most common causes of intermittent food impaction**, also known as
**“steakhouse syndrome**” as **meat is a typical instigator.**
Symptomatic
rings are easily treated by dilatation.
Schatzki rings
46
\_\_\_\_\_\_\_\_\_\_\_\_ higher in the esophagus can be of congenital
or inflammatory origin. Asymptomatic cervical esophageal webs
are demonstrated in about 10% of people and typically **originate
along the anterior aspect of the esophagus**. When circumferential,
they **can cause intermittent dysphagia to solids similar to Schatzki**
rings and are **similarly treated with dilatation**.
Web-like constrictions
47
The combination of
**symptomatic proximal esophageal web**s and **iron-deficiency anemia**
in **middle-aged women** constitutes \_\_\_\_\_\_\_\_\_\_\_\_\_\_
Plummer-Vinson syndrome.
48
49
\_\_\_\_\_\_\_\_\_\_\_\_ are categorized by location with the most
common being **epiphrenic, hypopharyngeal (Zenker’s), and mid
esophageal.**
Esophageal diverticula
50
\_\_\_\_\_\_\_ are false diverticula
involving **herniation of the mucosa and submucosa through the
muscular layer of the esophagus.**These lesions result from**increased
intraluminal pressure associated with distal obstruction.**
Epiphrenic and Zenker’s diverticula
51
In the case
of \_\_\_\_\_\_\_, the obstruction is a **stenotic cricopharyngeus muscle
(upper esophageal sphincter)**and the**hypopharyngeal herniation**
most commonly occurs in an area of **natural weakness known as
Killian’s triangle**
Zenker’s
52
\_\_\_\_\_\_\_\_\_\_ are usually
**asymptomatic** but when they enlarge sufficiently to retain food and
saliva they can be associated with d**ysphagia, halitosis, and aspiration.**
Treatment is by surgical diverticulectomy and cricopharyngeal
myotomy or a marsupialization procedure in which an endoscopic
stapling device is used to divide the cricopharyngeus.
Small Zenker’s diverticula
53
\_\_\_\_\_\_\_\_ are usually associated with **achalasia or
a distal esophageal stricture**.
Epiphrenic diverticula
54
\_\_\_\_\_\_\_\_\_\_\_\_may be
caused by **traction from adjacent inflammation (classically tuberculosis)**
in which case they are **true diverticula** **involving all layers
of the esophageal wall,** or by pulsion associated with esophageal
motor disorders.
Mid-esophageal diverticula
Mid-esophageal and epiphrenic diverticula are
usually **asymptomatic** until they enlarge sufficiently to retain food and cause dysphagia and regurgitation.
Symptoms attributable to the diverticula tend to correlate more with the underlying esophageal
disorder than the size of the diverticula. Large diverticula can
be removed surgically, usually in conjunction with a **myotomy**
if the underlying cause is achalasia.
55
\_\_\_\_\_\_\_\_\_ has poor survival because of the **abundant esophageal lymphatics**
leading to **regional lymph node metastases**.
Diffuse intramural esophageal
56
\_\_\_\_\_\_\_ diverticulosis is a rare entity that results from dilatation of the
excretory ducts of submucosal esophageal glands ( Fig. 292-4 ).
Esophageal candidiasis and proximal esophageal strictures are commonly
found in association with this disorder.
Diffuse intramural
57
Examples of small (left ) and large (middle, right **) Zenker’s diverticulum** arising from **Killian’s triangle** in the distal hypopharynx.
**Smaller diverticul**a are evident only during the **swallow, whereas larger ones retain food and fluid.**
58
Intramural esophageal pseudodiverticulosis associated
with chronic obstruction. Invaginations of contrast into the esophageal wall
outline deep esophageal glands.
59
It is about 10 times less common than colorectal
cancer but **kills about one-quarter as many patients**. These statistics
emphasize both the **rarity and lethality** of this.
Esophageal ca
60
One
notable trend is the shift of dominant esophageal cancer type from
**squamous cell to adenocarcinoma**, strongly linked to\_\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_\_\_
reflux disease
and Barrett’s metaplasia.
Note: Other distinctions between cell types are
the predilection for **adenocarcinoma to affect white males in the
distal esophagus**and**squamous cell to affect black males in the
more proximal esophagus**with the added risk factors of**smoking,**
**alcohol consumption, caustic injury, and human papilloma virus
infection** (Chap. 91).
61
The typical presentation of esophageal cancer is of \_\_\_\_\_\_\_\_. Associated symptoms may
include **odynophagia, iron deficiency, and, with mid-esophageal
tumors, hoarseness**from**left recurrent laryngeal nerve injury.**
Generally, these are indications of locally invasive or even metastatic
disease manifest by tracheoesophageal fistulas, and vocal cord
paralysis. Even when detected as a small lesion, esophageal cancer has poor survival **because of the abundant esophageal lymphatics
leading to regional lymph node metastases.**
progressive
solid food dysphagia and weight loss
62
\_\_\_\_\_\_\_\_\_\_\_\_ are uncommon and usually discovered
incidentally. In decreasing frequency of occurrence, cell types
include leiomyomas, fibrovascular polyps, squamous papillomas,
granular cell, lipomas, neurofibromas, and inflammatory fibroid
polyps. These generally **become symptomatic only when they are
associated with dysphagia**and merit removal only under the same
circumstances.
Benign esophageal tumors
63
The most common congenital esophageal anomaly is \_\_\_\_\_\_\_\_\_\_\_\_, occurring in about 1 in 5,000 live births. This can occur
in several permutations, the common denominator being **developmental
failure of fusion**between the**proximal and distal esophagus**
associated with a **tracheoesophageal fistula**, most commonly with
the distal segment excluded. Alternatively, there can be an **H-type
configuration**in which esophageal fusion has occurred, but with a
tracheoesophageal fistula. This is usually recognized
and corrected surgically within the first few days of life. Later life
complications include **dysphagia from anastomotic strictures or
absent peristalsis and reflux**, which can be severe.
esophageal
atresia
Note: Less common
developmental anomalies include congenital esophageal stenosis, webs, and duplications.
64
\_\_\_\_\_\_\_ can also result from congenital abnormalities that cause
**extrinsic compression of the esophagus**.
Dysphagia
65
In\_\_\_\_\_\_\_\_the esophagus
is compressed by an **aberrant right subclavian arter**y arising from
the descending aorta and passing behind the esophagus. Alternatively
vascular rings may surround and constrict the esophagus.
Heterotopic gastric mucosa, also known as an esophageal inlet
patch, is a focus of gastric type epithelium in the proximal cervical
esophagus; the estimated prevalence is 4.5%. The inlet patch
is thought to result from incomplete replacement of embryonic
columnar epithelium with squamous epithelium. The majority of
patches are asymptomatic, but acid production can occur as most
contain fundic type gastric epithelium with parietal cells.
dysphagia lusoria,
66
Esophageal motility disorders are diseases attributable to \_\_\_\_\_\_\_\_\_\_\_\_\_\_ commonly associated with **dysphagia,
chest pain, or heartburn**. The major entities are achalasia,
diffuse esophageal spasm (DES), and GERD.
Motility disorders can
also be secondary to broader disease processes as is the case with
pseudoachalasia, Chagas’ disease, and scleroderma.
esophageal
neuromuscular dysfunction
67
\_\_\_\_\_\_\_\_\_\_\_\_ is a rare disease caused by **loss of ganglion cells within the
esophageal myenteric plexus** with a population incidence of about
**1:100,000** and usually presenting between age **25 and 60.** With longstanding
disease, **virtual aganglionosi**s is noted. Excitatory (cholinergic)
ganglionic neurons are variably affected and inhibitory (nitric
oxide) ganglionic neurons are necessarily involved. Functionally,
i**nhibitory neurons mediate deglutitive lower esophageal sphincter**
(LES) **relaxatio**n and the sequential propagation of peristalsis. Their
absence **leads to impaired deglutitive LES relaxation and absent
peristalsis.**
Achalasia
68
Increasing evidence suggests that the ultimate cause of
ganglion cell degeneration in achalasia is an \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
autoimmune process
attributable to a latent infection with human herpes simplex virus 1
combined with genetic susceptibility.
69
\_\_\_\_\_\_\_\_\_\_\_\_ is characterized by progressive dilatation
and **sigmoid deformit**y of the **esophagus with hypertrophy of the LES.**
Clinical manifestations may include **dysphagia, regurgitation,
chest pain, and weight loss.**
**Most patients report solid and liquid
food dysphagia**. Regurgitation occurs when food, fluid, and secretions
are **retained in the dilated esophagus**.
Long-standing achalasia
Note: Patients with advanced
achalasia are at **risk for bronchitis, pneumonia, or lung abscess
from chronic regurgitation and aspiration.**
70
\_\_\_\_\_\_\_\_\_\_\_ is frequent
early in the course of achalasia, thought to r**esult from esophageal
spasm.**
Patients describe a squeezing, pressure-like retrosternal pain,
sometimes radiating to the neck, arms, jaw, and back. Paradoxically,
some patients complain of **heartburn that may be a chest pain
equivalent.**
Chest pain
Note:Treatment of achalasia is less effective in relieving chest
pain than it is in relieving dysphagia or regurgitation.
71
The differential diagnosis of achalasia includes\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
DES, Chagas’
disease, and pseudoachalasia.
72
\_\_\_\_\_\_\_\_\_\_\_\_\_\_is endemic in areas
of central Brazil, Venezuela, and northern Argentina, spread by
the bite of the **reduvid (kissing) bug** that transmits the protozoan,
**Trypanosoma cruzi.**
The chronic phase of the disease develops years
after infection and **results from destruction of autonomic ganglion**
cells throughout the body, including the **heart, gut, urinary tract,**
**and respiratory tract.**
Chagas’ disease
73
Tumor infiltration, most commonly seen
with **\_\_\_\_\_\_\_\_\_\_\_\_\_** can **mimic
idiopathic achalasia**. The resultant**“pseudoachalasia”** accounts for
up to **5% of suspected cases** and is more likely with **advanced age,**
**abrupt onset of symptoms (\<1 year), and weight loss**. Hence, endoscopy
should be part of the evaluation of achalasia. When the clinical
suspicion for **pseudoachalasia** is **high and endoscopy nondiagnostic,**
**CT scanning or endoscopic ultrasonography may be of value.**
Rarely, pseudoachalasia can result from a paraneoplastic syndrome
with circulating antineuronal antibodies.
**carcinoma in the gastric fundus or distal esophagus**
74
Achalasia is diagnosed by\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_; The barium swallow x-ray appearance
is of a dilated esophagus with poor emptying, an air-fluid
level, and tapering at the LES giving it a **beak-like appearance**
( Fig. 292-5 ).
barium swallow x-ray and/or esophageal
manometry
75
What is the role of endoscopy in diagnosing achalasia ?
has a relatively minor role other than
to **exclude pseudoachalasia. **
76
Occasionally, an\_\_\_\_\_\_\_\_\_\_\_\_\_\_ is observed.
In long-standing achalasia, the esophagus may assume a **sigmoid
configuration.**
epiphrenic diverticulum
77
The diagnostic criteria for achalasia with esophageal
manometry are \_\_\_\_\_\_\_\_\_\_\_\_\_\_
High-resolution manometry has somewhat advanced this diagnosis;
three subtypes of achalasia are differentiated based on the pattern of
pressurization in the nonperistaltic esophagus ( Fig. 292-6 ).
impaired LES relaxation and absent peristalsis.
78
Because
\_\_\_\_\_\_\_\_\_\_identifies early disease before esophageal dilatation and
food retention, it is the **most sensitive diagnostic test.**
There is **no known way of preventing or reversing achalasi**a.
Therapy is directed at **reducing LES pressure so that gravity** and **esophageal pressurization promote esophageal emptying**. Peristalsis
rarely, if ever, returns. LES pressure can be reduced by pharmacologicals
therapy, forceful dilatation, or surgical myotomy. No large,
controlled trials of the therapeutic alternatives exist and the optimal
approach is debated. **Pharmacologicals therapies are relatively
ineffective but are often used as temporizing therapies.**Nitrates or
calcium channel blockers are administered before eating, advising
caution because of their **effects on blood pressure**.
**Botulinum
toxin**, injected into the LES under endoscopic guidance,**inhibits
acetylcholine release from nerve endings and improves dysphagia**
in about 66% of cases for at least 6 months. Sildenafil, or alternative
phosphodiesterase inhibitors, effectively decrease LES pressure, but
practicalities limit their clinical use in achalasia.
manometry
79
The only durable therapies for achalasia
are\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_\_\_\_\_\_
pneumatic dilatation and Heller
myotomy.
80
\_\_\_\_\_\_\_\_\_\_\_\_, with a
reported efficacy ranging from 32–98%,
is an **endoscopic technique using a noncompliant,
cylindrical balloon dilator**
positioned across the LES and inflated
to a diameter of 3–4 cm.
The major
complication is perforation with a
reported incidence of 1–5%.
Pneumatic dilatation
81
The most
common surgical procedure for achalasia
is \_\_\_\_\_\_\_\_\_\_\_\_\_\_ usually
performed in conjunction with an antireflux
procedure (partial fundoplication);
good to excellent results are reported in
62–100% of cases.
laparoscopic Heller myotomy,
Note :Occasionally, patients
with advanced disease fail to respond
to pneumatic dilatation or Heller myotomy.
In such refractory cases, esophageal
resection with gastric pull-up or
interposition of a segment of transverse
colon may be the only option other than
gastrostomy feeding.
In untreated or inadequately treated achalasia, esophageal dilatation
predisposes to stasis esophagitis. Prolonged stasis esophagitis is
the likely explanation for the association between achalasia and esophageal
squamous cell cancer. Tumors develop after years of achalasia,
usually in the setting of a greatly dilated esophagus with the overall
squamous cell cancer risk increased 17-fold compared to controls.
82
The barium swallow x-ray appearance
is of a dilated esophagus with poor emptying, an air-fluid
level, and tapering at the LES giving it a beak-like appearance
( Fig. 292-5 )
Achalasia with esophageal dilatation, tapering at the
gastroesophageal junction and an air-fluid level within the esophagus.
The example on the left shows sigmoid deformity with very advanced disease
83
\_\_\_\_\_\_\_\_ is manifested by episodes of dysphagia and chest pain
attributable to **abnormal esophageal contractions with normal
deglutitive LES relaxation**. Beyond that, there is little consensus.
The pathophysiology and natural history of thisare ill defined.
DES
84
Radiographically,\_\_\_\_\_\_\_\_\_\_\_\_\_ has been characterized by tertiary contractions
or a **“corkscrew esophagus**” ( Fig. 292-7 ), but in many
instances these abnormalities are actually **indicative of achalasia.**
Manometrically, a variety of defining features have been proposed
including **uncoordinated (“spastic”) activity in the distal esophagus,**
**spontaneous and repetitive contractions, or high amplitude and
prolonged contractions.**
DES
Diffuse esophageal spasm. The characteristic “corkscrew”
esophagus results from spastic contraction of the circular muscle in the
esophageal wall; more precisely, this is actually a helical array of muscle.
These findings are also seen with spastic achalasia.
Note: Greatest consensus exists with the concept
that **simultaneous contractions define DES.**
All of these definitions
lead to patients with a variety of disorders being diagnosed as
DES. In fact, high-resolution manometry suggests that DES, when
defined in a restrictive fashion ( Fig. 292-8 ), is actually much less
common than achalasia and suspected cases are often incorrectly
categorized achalasia.
85
Radiographically, a **“corkscrew esophagus,**” “**rosary bead esophagus,”**
**pseudodiverticula, or curling** can be indicative of _______ but
these **are also found with spastic achalasia**. Given these vagaries of
defining this, and the resultant heterogeneity of patients identified
for inclusion in therapeutic trials, it is not surprising that trial
results have been disappointing. Only small, uncontrolled trials
exist, reporting response to nitrates, calcium channel blockers,
hydralazine, botulinum toxin, and anxiolytics. The only controlled
trial showing efficacy was with an anxiolytic. Surgical therapy (long
myotomy or even esophagectomy) should be considered only
with severe weight loss or unbearable pain. These indications are
extremely rare.
DES,
86
Manometric studies done to evaluate chest pain and/or dysphagia
often report minor abnormalities (hypertensive or hypotensive
peristalsis, hypertensive LES, etc.) that are insufficient to diagnose
either achalasia or DES. These findings are of unclear significance.
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
are common among such individuals. A lower visceral pain threshold and symptoms of irritable bowel syndrome are noted in
more than half of such patients. Consequently, therapy for these
individuals should either target the most common esophageal
disorder, GERD, or more global conditions such as depression or
somatization neurosis that are found to be coexistent.
NONSPECIFIC MANOMETRIC FINDINGS
Reflux and psychiatric diagnoses, particularly anxiety and depression,
87
The current conception of\_\_\_\_\_\_\_\_\_\_\_ is to encompass a family of conditions
with the commonality that they are caused by the **gastroesophageal
reflux**resulting in**either troublesome symptom**s or an
**array of potential esophageal and extraesophageal manifestations.**
With respect to the esophagus, the spectrum of
injury includes **esophagitis, stricture, Barrett’s esophagus, and adenocarcinoma**
GERD
88
. Of particular concern is the rising incidence
of \_\_\_\_\_\_\_\_\_\_\_-, an epidemiologic trend that
parallels the increasing incidence of GERD.
esophageal adenocarcinoma
89
The best defined subset of GERD patients, albeit a minority overall,
have\_\_\_\_\_\_\_\_-
This occurs when refluxed gastric acid and
pepsin cause necrosis of the esophageal mucosa causing erosions
and ulcers. Note that some degree of gastroesophageal reflux is
normal, physiologically intertwined with the mechanism of belching
**(transient LES relaxation**), but this results from **excessive
reflux, often accompanied by impaired clearance of the refluxed**
**gastric juice.** Restricting reflux to that which is physiologically
intended depends on the anatomic and physiologic integrity of the
esophagogastric junction, a complex sphincter comprised of both
the LES and the surrounding crural diaphragm.
esophagitis.
90
Three dominant
mechanisms of esophagogastric junction incompetence are recognized:
(1) transient LES relaxations (a vagovagal reflex in which LES
relaxation is elicited by gastric distention),
(2) LES hypotension, or
(3) anatomic distortion of the esophagogastric junction inclusive
of hiatus hernia.
Of note, the third factor, esophagogastric junction
anatomic disruption, is both significant unto itself and also because
it i**nteracts with the first two mechanisms.**
91
\_\_\_\_\_\_\_\_\_\_\_\_\_-
account for at least 90% of reflux in normal subjects or GERD
patients without hiatus hernia, but patients with hiatus hernia
have a more heterogeneous mechanistic profile.
Transient LES relaxations
92
Factors tending to
exacerbate reflux regardless of mechanism are:
abdominal obesity,
pregnancy, gastric hypersecretory states, delayed gastric emptying,
disruption of esophageal peristalsis, and gluttony.
93
Consequently,
two causes of prolonged acid clearance are \_\_\_\_\_\_\_\_\_\_\_\_\_.
impaired peristalsis and
reduced salivation
94
Impaired peristaltic emptying can be attributable
to \_\_\_\_\_\_\_\_\_\_\_\_\_.
disrupted peristalsis or superimposed reflux associated with
a hiatal hernia
Note: With superimposed reflux, fluid retained within
a sliding hiatal hernia refluxes back into the esophagus during
swallow-related LES relaxation, a phenomenon that does not normally
occur.
95
\_\_\_\_\_\_\_\_\_\_\_\_\_ are the typical
symptoms of GERD.
Somewhat less common
are **dysphagia and chest pain**. In each case, multiple
potential mechanisms for symptom genesis
operate that extend beyond the basic concepts
of mucosal erosion and activation of afferent
sensory nerves. Specifically, hypersensitivity
and functional pain are increasingly recognized
as confounding factors. Nonetheless the dominant
clinical strategy is of empirical treatment
with acid inhibitors, reserving further evaluation
for those who fail to respond. Important
exceptions to this are patients with chest pain
Heartburn and regurgitation
96
Extraesophageal syndromes with an established
association to GERD include \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
A multitude of other conditions including pharyngitis,
chronic bronchitis, pulmonary fibrosis,
chronic sinusitis, cardiac arrhythmias, sleep
apnea, and recurrent aspiration pneumonia have
proposed associations with GERD. However,
in both cases it is important to emphasize
the word association as opposed to causation.
In many instances the disorders likely coexist because of **shared
pathogenetic mechanisms rather than strict causality.**
chronic
cough, laryngitis, asthma, and dental erosions.
97
Potential
mechanisms for extraesophageal GERD manifestations are of either
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
regurgitation with direct contact between the refluxate and supraesophageal
structures or via a vagovagal reflex wherein reflux activation
of esophageal afferent nerves triggers efferent vagal reflexes
such as bronchospasm, cough, or arrhythmias.
98
What are the differential diagnoses for GERD?
Infectious esophagitis
Pill esophagitis
Eosinophilic esophagitis
Peptic ulcer disease- 10% with abdominal pain
Non-ulcer dyspepsia
Biliary tract disease
Coronary artery disease
Esophageal motor disease
99
the most severe histologic consequence
of GERD is \_\_\_\_\_\_\_\_\_\_\_\_\_\_with the associated risk
of **esophageal adenocarcinoma**, and the incidence of these lesions
has increased, not decreased in the era of potent acid suppression.
Barrett’s metaplasia
100
Barrett’s metaplasia, endoscopically recognized by tongues of
reddish mucosa extending proximally from the gastroesophageal
junction
101
adenocarcinoma developing within an area of Barrett’s
esophagus.
102
Histopathology of Barrett’s metaplasia and Barrett’s with high-grade
dysplasia. H&E, hematoxylin and eosin.
103
\_\_\_\_\_\_\_\_\_\_\_\_\_ are routinely advocated as GERD
therapy.
Lifestyle modifications
Broadly speaking, these fall into three categories:
(1) avoidance of foods that reduce lower esophageal sphincter
pressure, making them “refluxogenic” (these commonly include
**fatty foods, alcohol, spearmint, peppermint, tomato-based**
**foods, possibly coffee and tea)**; (2) avoidance of acidic foods
that are inherently irritating; and (3) adoption of behaviors to
minimize reflux and/or heartburn.
104
\_\_\_\_\_\_\_\_\_\_\_\_\_ is increasingly recognized in adults
and children around the world. Population-based studies suggest
the **prevalence to be in excess of 1:1000** with a predilection for white
males. The increasing prevalence of tihis s attributable to a **combination
of an increasing incidence and a growing awareness of the
condition.**There is also an incompletely understood, but important,
overlap betweent this and GERD that delays or confuses diagnosis
of the disease in many cases.
This is diagnosed based on the combination of **typical esophageal
symptoms and esophageal mucosal biopsies**demonstrating esophageal
**squamous epithelial infiltration with eosinophils.**
Eosinophilic esophagitis (EoE)
105
Current evidence indicates that ________ is an allergic
disorder induced by **antigen sensitization in susceptible individuals.**
Studies have demonstrated an important role for **dietary allergens in
both the pathogenesis and treatment** of this. Aeroallergens may also
contribute but there is much less evidence in this regard. The natural
history of the disorder is uncertain as are the consequences of not
treating asymptomatic or minimally symptomatic patients.
EoE
106
\_\_\_\_\_\_\_\_\_\_\_ should be strongly considered in children and adults with
dysphagia and food impactions, **regardless of the presence or
absence of heartburn**. Other symptoms may include atypical chest
pain and heartburn, particularly heartburn that is refractory to esophagal mucosa (generally ≥ 15 eosinophils per high-power
field) ( Fig. 292-12 ). Fibrosis, narrow caliber esophagus, and stricture
can occur with EoE, but the predictive variables for these are
not known. Complications of disease include food impaction and
esophageal perforation.
EoE
107
Histopathology of eosinophilic esophagitis (EoE)
showing **dense infiltration of the esophageal squamous epithelium**
**with eosinophils**.
108
Eosinophilic inflammation can also be seen with gastroesophageal
reflux disease (GERD); the optimal discriminatory threshold for
EoE is\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
greater than 15 eosinophils per high-power field.
109
INFECTIOUS ESOPHAGITIS
With the increased use of immunosuppression for organ transplantation
as well as chronic inflammatory diseases and chemotherapy
along with the AIDS epidemic, infections with Candida species,
Herpesvirus, and cytomegalovirus (CMV) have become relatively
common.
INFECTIOUS ESOPHAGITIS
110
Although rare, infectious esophagitis also occurs among
the nonimmunocompromised, with \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. Among AIDS patients,
infectious esophagitis becomes more common as the CD4 count
declines; cases are rare with the **CD4 count \>200 and common when
\<100.** HIV itself may also be associated with a self-limited syndrome
of acute esophageal ulceration with oral ulcers and a maculopapular
skin rash at the time of seroconversion. Additionally, some patients
with advanced disease have deep, persistent esophageal ulcers
treated with oral glucocorticoids or thalidomide. However, with
the widespread use of protease inhibitors, a reduction in these HIV
complications has been noted.
herpes simplex and Candida
albicans being the most common pathogens
111
Regardless of the infectious agent, __________ is a characteristic
symptom of infectious esophagitis; dysphagia, chest pain, and
hemorrhage are also common.
odynophagia
Note: Odynophagia is uncommon with
reflux esophagitis, so its presence should always raise suspicion of
an alternative etiology
112
\_\_\_\_\_\_\_\_\_\_- is normally found in the throat, but can become pathogenic
and produce esophagitis in a compromised host;
This also occurs with esophageal stasis
secondary to esophageal motor disorders and diverticula. Patients
complain of **odynophagia and dysphagia**. If **oral thrush is present,**
**empirical therapy is appropriate**, but coinfection is common,
and persistent symptoms should lead to prompt endoscopy with
biopsy, which is the most useful diagnostic evaluation. This has a characteristic appearance of **white plaques with
friability.** Rarely,this is complicated by bleeding,
perforation, stricture, or systemic invasion.
CANDIDA ESOPHAGITIS
Candida C. albicans is most
common.
Note: TX
Oral fluconazole
(200 mg on the first day, followed by 100 mg daily) for 7–14 days
is the preferred treatment. Patients refractory to fluconazole may
respond to itraconazole. Alternatively, poorly responsive patients
or those who cannot swallow medications can be treated with an
intravenous echinocandin (caspofungin 50 mg daily for 7–21 days).
Amphotericin B (10–15 mg IV infusion for 6 h daily to a total dose
of 300–500 mg) is used in severe cases.
113
\_\_\_\_\_\_\_\_\_\_\_\_ may cause esophagitis. Vesicles
on the **nose and lips** may coexist and are suggestive of this
etiology.
Herpes simplex virus type 1 or 2
Note: Varicella-zoster virus can also cause esophagitis in children with chickenpox or adults with zoster.
Culture or polymerase chain reaction
(PCR) assays are helpful to identify acyclovir-resistant strains.
The infection is often self-limited after a 1–2 week period. Acyclovir
(400 mg orally 5 times a day for 14–21 days) or valacyclovir (1 g
orally tid for 7 days) reduces this morbidity. In patients with severe
odynophagia, intravenous acyclovir, 5 mg/kg every 8 h for 7–14 days,
foscarnet (90 mg/kg intravenously bid for 2–4 weeks) or oral famciclovir
are used.
114
The characteristic
endoscopic findings are vesicles and **small, punched-out ulcerations.**
Because these infections are limited to **squamous
epithelium,** biopsies from the ulcer margins are most likely to reveal
the **characteristic ground glass nuclei, eosinophilic Cowdry’s type A**
**inclusion bodies, and giant cells.**
HERPETIC ESOPHAGITIS
115
\_\_\_\_\_\_\_\_\_\_\_ occurs **only in immunocompromised** patients,
particularly **transplant recipients**.
This is usually activated from a
latent stage or may be acquired from transfusions. Endoscopically,
this lesions appear as **serpiginous ulcers** in an otherwise normal
mucosa, particularly in the **distal esophagus**. Biopsies of the ulcer
bases have the highest diagnostic yield for finding the **pathognomonic
large nuclear or cytoplasmic inclusion bodies.**Immunohistology
with monoclonal antibodies to CMV and in situ hybridization tests
are useful for early diagnosis.
CMV esophagitis
NOTE : Ganciclovir, 5 mg/kg every 12 h intravenously,
is the treatment of choice. Valganciclovir (900 mg bid), an
oral formulation of ganciclovir, or foscarnet (90 mg/kg every 12 h
intravenously) can also be used. Therapy is continued until healing,
which may take 3–6 weeks.
116
Most cases of _______________ are from **instrumentation of
the esophagus or trauma**.
Alternatively, forceful vomiting or retching
can lead to **spontaneous rupture at the gastroesophageal junction**
**(Boerhaave’s syndrome**).
More rarely, corrosive esophagitis
or neoplasms lead to perforation. Instrumental perforation from
endoscopy or nasogastric tube placement typically occurs in the
**hypopharynx or at the gastroesophageal junction.** Perforation may
also result at the **site of stricture in the setting of endoscopic food
disimpaction or esophageal dilation**.
This causes
pleuritic retrosternal pain that can be associated with pneumomediastinum
and subcutaneous emphysema.
ESOPHAGEAL PERFORATION
Note: CT of the chest is most sensitive in
detecting mediastinal air. Esophageal perforation is confirmed by
a contrast swallow; usually Gastrografin followed by thin barium.
Treatment includes nasogastric suction and parenteral broadspectrum
antibiotics with prompt surgical drainage and repair in
noncontained leaks. Conservative therapy with NPO status and
antibiotics without surgery may be appropriate in cases of minor
instrumental perforation that are detected early. Endoscopic clipping
or stent placement may be indicated in nonoperable cases such as
perforated tumors.
117
spontaneous rupture at the gastroesophageal junction
Boerhaave’s syndrome
118
\_\_\_\_\_\_\_\_\_\_ is a major
complication of esophageal perforation, and prompt recognition
is key to optimizing outcome.
Mediastinitis
119
Vomiting, retching, or vigorous coughing can cause a nontransmural
tear at the gastroesophageal junction that is a common cause of
upper gastrointestinal bleeding.
Most patients present with hematemesis.
Antecedent vomiting is anticipated but not always evident.
Bleeding usually abates spontaneously, but protracted bleeding may respond to local epinephrine or cauterization therapy, endoscopic
clipping, or angiographic embolization. Surgery is rarely needed.
MALLORY-WEISS TEAR
120
\_\_\_\_\_\_\_\_\_can complicate treatment for thoracic cancers,
especially **breast and lung**, with the risk proportional to radiation
dosage. Radiosensitizing drugs such as doxorubicin, bleomycin,
cyclophosphamide, and cisplatin also increase the risk. **Dysphagia
and odynophagia may last weeks****to months** after therapy.
The
esophageal mucosa becomes erythematous, edematous, and friable.
Submucosal fibrosis and degenerative tissue changes and stricturing
may occur years after the radiation exposure.
Radiation esophagitis
Radiation exposure
in excess of 5000 cGY has been associated with increased risk of
esophageal stricture. Treatment for acute radiation esophagitis is
supportive. Chronic strictures are managed with esophageal dilation.
121
\_\_\_\_\_\_\_\_\_\_
Caustic esophageal injury from ingestion of alkali or, less commonly,
acid can be accidental or from attempted suicide. Absence
of oral injury does not exclude possible esophageal involvement.
Thus, early endoscopic evaluation is recommended to assess and
grade the injury to the esophageal mucosa. Severe corrosive injury
may lead to esophageal perforation, bleeding, stricture, and death.
Glucocorticoids have not been shown to improve the clinical outcome
of acute corrosive esophagitis and are not recommended.
Healing of more severe grades of caustic injury is commonly associated
with severe stricture formation and often requires repeated
dilatation.
CORROSIVE ESOPHAGITIS
122
\_\_\_\_\_\_\_\_\_occurs when a swallowed pill fails to traverses
the entire esophagus and **lodges within the lumen**. Generally,
this is attributed to poor **“pill taking habits”**: **inadequate liquid with
the pill,**or**lying down immediately after taking a pil**l.
Pill-induced esophagitis
123
The most
common location for the pill to lodge is in the\_\_\_\_\_\_\_\_\_\_\_\_\_ Extrinsic compression from these
structures halts the movement of the pill or capsule. Since initially
reported in 1970, more than 1000 cases of pill esophagitis have been
reported, suggesting that this is not an unusual occurrence.
mid-esophagus near
the crossing of the aorta or carina.
124
A wide
variety of medications are implicated with the most common being \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
However, virtually any pill can result in pill
esophagitis if taken carelessly.
doxycycline, tetracycline, quinidine, phenytoin, potassium chloride,
ferrous sulfate, nonsteroidal anti-inflammatory drugs (NSAIDs),
and bisphosphonates.
125
Typical symptoms of pill esophagitis are the **\_\_\_\_\_\_\_\_** Characteristically, the pain will
develop over a period of hours or will awaken the individual from
sleep. A classic history in the setting of ingestion of recognized pill
offenders obviates the **need for diagnostic testing in most patients.**
When endoscopy is performed, l**ocalized ulceration or inflammation
is evident.** Histologically, acute inflammation is typical. Chest
**CT imaging will sometimes reveal esophageal thickening consistent
with transmural inflammation.** Although the condition usually
resolves within days to weeks, **symptoms may persist for months**
and **stricture can develop in severe cases**. No specific therapy is
known to hasten the healing process, but antisecretory medications
are frequently prescribed to remove concomitant reflux as
an aggravating factor. When healing results in stricture formation,
dilatation is indicated.
**sudden onset
of chest pain and odynophagia.**
126
\_\_\_\_\_\_ may lodge in the esophagus causing complete
obstruction, causing an i**nability to handle secretions (foaming
at the mouth) and severe chest pain**.
Food or foreign bodies
127
Food impaction may occur due to \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ If it does not spontaneously resolve,
impacted food is dislodged endoscopically. Use of meat tenderizer
enzymes to facilitate passage of a meat bolus is discouraged because
of potential esophageal injury. Glucagon (1 mg IV) is sometimes
tried before endoscopic dislodgement. After emergent treatment
patients should be evaluated for potential causes of the impaction
with treatment rendered as indicated.
stricture, carcinoma, Schatzki ring, eosinophilic esophagitis,
or simply inattentive eating.
128
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ was initially described as a manifestation of **scleroderma
or other collagen vascular diseases** and thought to be specific for
these disorders. However, this nomenclature subsequently proved
unfortunate and has been discarded because an estimated half of
qualifying patients **do not have an identifiable systemic disease,**
and **reflux disease is often the only identifiable association**. When
scleroderma esophagus occurs as a manifestation of a collagen
vascular disease, the histopathologic findings are of infiltration
and destruction of the esophageal muscularis propria with collagen
deposition and fibrosis.
SCLERODERMA AND COLLAGEN VASCULAR DISEASES
Scleroderma esophagus (hypotensive LES and absent esophageal
peristalsis)
129
\_\_\_\_\_\_\_\_\_
A host of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ can affect the oropharynx and esophagus, particularly
the proximal esophagus with blisters, bullae, webs, and strictures.
Glucocorticoid treatment is usually effective. Erosive lichen planus,
Stevens-Johnson syndrome, and graft-versus-host disease can also
involve the esophagus. Esophageal dilatation may be necessary to
treat strictures.
DERMATOLOGIC DISEASES
dermatologic disorders (pemphigus vulgaris, bullous
pemphigoid, cicatricial pemphigoid, Behçet’s syndrome, epidermolysis
bullosa)
130
