Chapter 17: GIT-Esophagitis

Question 1

What is *Mallory-
Weiss tears*

Answer 1

Longitudinal tears in the esophagus near the gastroesophageal junction are termed *Mallory-
Weiss tears*, and aremost often associated with severe retching or vomiting secondary to acute
alcohol intoxication

Question 2

Mallory-
Weiss tears, and are most often associated with what?

Answer 2

severe retching or vomiting secondary to acute
alcohol intoxication

Question 3

What is the pathogenesis of Mallory-Weiss tears?

Answer 3

Normally, a reflex relaxation of the gastroesophageal musculature precedes the antiperistaltic contractile wave associated with vomiting.

It is speculated that this relaxation
fails during prolonged vomiting,with the result thatrefluxing gastric contents overwhelm the
gastric inlet and cause the esophageal wall to stretch and tear.

Question 4

What is the morphology of Mallory-Weiss tears?

Answer 4

The roughly linear lacerations
of Mallory-Weiss syndrome are longitudinally oriented and range in length from millimeters to
several centimeters.

These tears usually cross the gastroesophageal junction but may also be
located in the proximal gastric mucosa.

Question 5

Up to 10% of upper GI bleeding, which often presents
as hematemesis ( Table 17-1 ), is due to what?

Answer 5

• *superficial esophageal laceration**s such as those
• *associated with Mallory-Weiss syndrome**.

Question 6

What is the treatment of Mallory Weiss tears?

Answer 6

These do not generally require surgical intervention,
and healing tends to be rapid and complete.

In contrast, Boerhaave syndrome, characterized by
distal esophageal rupture and mediastinitis, occurs rarely and is a catastrophic event.

Question 7

What is Boerhaave syndrome?

Answer 7

characterized by
distal esophageal rupture and mediastinitis, occurs rarely and is a catastrophic event.

Question 8

TABLE 17-1 – Esophageal Causes of Hematemesis

Answer 8

• Lacerations (Mallory-Weiss syndrome)
• Esophageal perforation (cancer or Boerhaave syndrome)
• Varices (cirrhosis)
• Esophageal-aortic fistula (usually with cancer)
• Chemical and pill esophagitis
• Infectious esophagitis (Candida, Herpes)
• Benign strictures
• Vasculitis (autoimmune, cytomegalovirus)
• Reflux esophagitis (erosive)
• Eosinophilic esophagitis
• Esophageal ulcers (many etiologies)
• Barrett esophagus
• Adenocarcinoma
• Squamous cell carcinoma
• Hiatal hernia

Question 9

The stratified squamous mucosa of the esophagus may be damaged by a variety of irritants
including what?

Answer 9

• alcohol,
• corrosive acids or alkalis,
• excessively hot fluids, and
• heavy smoking.
• The esophageal mucosa may also be injured when medicinal pills lodge and dissolve in the esophagus rather than passing into the stomach intact, a condition termed pill-induced esophagitis.

Question 10

What is pill-induced​ esophagitis.

Answer 10

The esophageal mucosa may also be injured when medicinal pills lodge and dissolve in the esophagus rather than passing into the stomach intact, a condition termed pill-induced​ esophagitis.

Question 11

What is the outcome when esophagitis is due to chemical injury?

Answer 11

generally only causes self-limited pain, particularly dysphagia (pain with swallowing).

Hemorrhage, stricture, or perforation may occur in
severe cases.

Question 12

Iatrogenic esophageal injury may be caused by what?

Answer 12

• cytotoxic chemotherapy,
• radiation therapy, or
• graft-versus-host disease.

Question 13

Infections may occur in otherwise healthy individuals but are most frequent in those who are debilitated or immunosuppressed as a result of disease or therapy.

In these patients, what esophageal infection is common?

Answer 13

• Herpes simplex viruses,
• cytomegalovirus (CMV), or
• fungal organisms

The esophagus may also be involved by the desquamative skin diseases bullous

pemphigoid and epidermolysis bullosa and, rarely, Crohn disease

Question 14

Among fungi, what is the most common infection most frequent in those who are debilitated or immunosuppressed as a result of disease or therapy causing esophagitis?

Answer 14

• candidiasis is most common,
• although mucormycosis and
• aspergillosis may occur.

Question 15

What is the morphology of chemical and infectious esophagitis?

Answer 15

varies with etiology.

Question 16

What is mostly present in the morphology of esophagitis?

Answer 16

Dense infiltrates of neutrophils are present in most cases but may be absent following injury induced by chemicals (lye, acids, or detergent), which may result in outright necrosis of the esophageal wall.

Question 17

Dense infiltrates of neutrophils are present in most cases but may be absent following injury induced by chemicals (lye, acids, or detergent), why?

Answer 17

which may result in outright necrosis of the esophageal wall.

Question 18

Pill-induced esophagitis frequently occurs where?

Answer 18

at the site of strictures that impede passage of luminal contents.

When present, ulceration is accompanied
by superficial necrosiswith granulation tissueandeventual fibrosis.

Question 19

What are the morphological changes seen inEsophageal irradiation ?

Answer 19

causes damage similar to that seen in other tissues and includes:

• intimal proliferation and
• luminal narrowing of submucosal and
• mural blood vessels.
  
  • The mucosal damage is, in part, often secondary to radiation-induced vascular injury as discussed

in Chapter 9 .

Question 20

Infection by fungi or bacteria can either result to what?

Answer 20

cause damage or complicate a preexisting ulcer.

Question 21

Nonpathogenic oral bacteria are frequently found where?

Answer 21

in ulcer beds

Question 22

while pathogenic organisms,
which account for about 10% of infectious esophagitis, may invade up to where?

Answer 22

may invade the lamina propria and
cause necrosis of overlying mucosa.

Question 23

What is the characteristic of Candidiasis, in its most advanced form?

Answer 23

adherent, gray-white pseudomembranes composed of densely matted fungal hyphae
and inflammatory cells covering the esophageal mucosa.

Question 24

Wh atoften provides a clue as to the infectious agent in viral esophagitis.

Answer 24

endoscopic appearance

Question 25

Herpesviruses typically cause what?

Answer 25

punched-out ulcers ( Fig. 17-4A ).

Question 26

What is being demonstrated in Biopsy
specimens of esophagitis caused by Herpesvirus?

Answer 26

nuclear viral inclusions within a rim of degenerating epithelial cells at the margin of the ulcer ( Fig. 17-4B ).

Question 27

What is the appearance of CMV in esophagitis?

Answer 27

In contrast, CMV causes shallower ulcerations and
characteristic nuclear and cytoplasmic inclusions within capillary endothelium and stromal cells ( Fig. 17-4C ).

Question 28

Although the histologic appearance is characteristic,what is sensitive and specific ancillary diagnostic tools?

Answer 28

immunohistochemical stains for virus-specific antigens are a sensitive and specific ancillary
diagnostic tool

Answer 29

Histologic features of esophageal graft-versus-host disease are similar to those in the skin
and include basal epithelial cell apoptosis, mucosal atrophy, and submucosal fibrosis without
significant acute inflammatory infiltrates. The microscopic appearances of esophageal
involvement in bullous pemphigoid, epidermolysis bullosa, and Crohn disease are also similar
to those in the skin ( Chapter 25 ).

Question 30

What are the microscopic appearances of esophageal
involvement in bullous pemphigoid, epidermolysis bullosa, and Crohn disease?

Answer 30

are also similar
to those in the skin ( Chapter 25 ).

Question 31

Answer 31

FIGURE 17-4 Viral esophagitis.

• A, Postmortem specimen with multiple herpetic ulcers in the distal esophagus.
• B, Multinucleate squamous cells containing Herpesvirus nuclear inclusions.
• C, Cytomegalovirus-infected endothelial cells with nuclear and cytoplasmic nclusions.

Question 32

The stratified squamous epithelium of the esophagus is resistant to abrasion from foods but is
sensitive to what?

Answer 32

acid.

Submucosal glands, which are most abundant in the proximal and distal esophagus, contribute to mucosal protection by secreting mucin and bicarbonate.

More importantly, constant lower esophageal sphincter tone prevents reflux of acidic gastric contents, which are under positive pressure and would otherwise enter the esophagus.

Question 33

Where is the Submucosal glands most abundant in the esophagus?

Answer 33

proximal and distal esophagus

contribute to mucosal protection by secreting mucin and bicarbonate.

Question 34

What is the most frequent cause of esophagitis and the most common outpatient GI diagnosis in the United States. [6]

Answer 34

Reflux of gastric

contents into the lower esophagus

Note: The associated clinical condition is
termed gastroesophageal reflux disease (GERD) .

Question 35

What is the pathogenesis of GERD?

Answer 35

• Reflux of gastric juices is central to the development of mucosal injury in GERD.
• In severe cases, reflux of bile from the duodenum may exacerbate the damage
• . Conditions that decrease lower esophageal sphincter tone or increase abdominal pressure contribute to GERD

Question 36

What are the Conditions that decrease lower esophageal sphincter tone or increase abdominal pressure contribute to GERD ?

Answer 36

• alcohol and
• tobacco use,
• obesity,
• central nervous system depressants,
• pregnancy,
• hiatal hernia (discussed below)
• delayed gastric emptying, and increased gastric volume.

In many cases, no definitive cause is identified

Question 37

What is the morphology of GERD?

Answer 37

• hyperemia
  
  • ​may be the only alteration
• eosinophils
  
  • ​significant disease
• Basal zone hyperplasia
  
  • ​may also be present

Question 38

What is the mucosal histology in mild GERD?

Answer 38

.

In mild GERD the mucosal histology is often unremarkable.

Question 39

What is the mucosal histology in severe GERD?

Answer 39

With more significant
disease, eosinophils are recruited into the squamous mucosa followed by neutrophils, which
are usually associated with more severe injury ( Fig. 17-5A ).

Basal zone hyperplasia
exceeding 20% of the total epithelial thicknessandelongation of lamina propria papillae, such
that they extend into the upper third of the epithelium, may also be present.

Question 40

Answer 40

FIGURE 17-5 Esophagitis.

• A, Reflux esophagitis with scattered intraepithelial eosinophils. Although mild basal zone expansion can be appreciated, squamous cell maturation is relatively normal.
• B, Eosinophilic esophagitis is characterized by numerous intraepithelial eosinophils. Abnormal squamous maturation is also apparent.

Question 41

GERD is most common in what age?

Answer 41

adults over age 40 but also occurs in infants and children.

Question 42

What is the mostcommon clinical symptoms of GERD?

Answer 42

• dysphagia,
• heartburn,
• and, less frequently, noticeable regurgitation of sour-tasting gastric contents.
• Rarely, chronic GERD is punctuated by attacks of severe chest pain that may be mistaken for heart disease.

Question 43

What is the treatment for GERD?

Answer 43

Treatment with proton pump inhibitors or H2 histamine receptor antagonists, which reduce gastric acidity, typically provides symptomatic relief.

Question 44

The severity of symptoms in GERD is not closely related to the degree of histologic damage, the latter tends to increase with disease duration.

T or F

Answer 44

TRUE

Question 45

Complications of reflux
esophagitis include what?

Answer 45

• esophageal ulceration,
• hematemesis,
• melena,
• stricture development, and
• Barrett esophagus.

Question 46

What is Hiatal hernia?

Answer 46

is characterized by separation of the diaphragmatic crura and protrusion of the
stomach into the thorax through the resulting gap.

Congenital hiatal hernias are recognized in
infants and children, but many are acquired in later life.

Hiatal hernia is symptomatic in fewer
than 10% of adults, and these cases are generally associated with other causes of LES
incompetence.

Symptoms, including heartburn and regurgitation of gastric juices, are similar to
GERD.

Question 47

What are the symptoms of eosinophilic esophagitis?

Answer 47

The incidence of eosinophilic esophagitis is increasing markedly. [7]

Symptoms include:

• food impaction and
• dysphagia in adults and
• feeding intolerance or GERD-like symptoms in children.

Question 48

What is the cardinal histologic feature of EOSINOPHILIC ESOPHAGITIS?

Answer 48

is large numbers of intraepithelial eosinophils, particularly superficially ( Fig. 17-5B ).

Question 49

What can help differentiate eosinophilic esophagitis
from GERD, Crohn disease, and other causes of esophagitis?

Answer 49

is large numbers of intraepithelial eosinophils, particularly superficially ( Fig. 17-5B ).

Question 50

What are the Clinical characteristics of EOSINOPHILIC ESOPHAGITIS?

Answer 50

• particularly failure of high-dose proton pump inhibitor treatment and
• the absence of acid reflux, are also necessary for diagnosis.

Question 51

The majority of individuals with eosinophilic esophagitis are what?

Answer 51

• atopic and
• many have
  
  • atopic dermatitis,
  • allergic rhinitis,
  • asthma, or
  • modest peripheral eosinophilia.

Question 52

What are the treatments for EOSINOPHILIC ESOPHAGITIS?

Answer 52

Treatments include dietary restrictions to prevent exposure to food allergens, such

as cow’s milk and soy products, and topical or systemic corticosteroids.

Question 53

What is Barrett esophagus?

Answer 53

is a complication of chronic GERD that is characterized by intestinal metaplasia within the esophageal squamous mucosa.

The incidence of Barrett esophagus is
rising, and it is estimated to occur in as many as 10% of individuals with symptomatic GERD.

Question 54

Barrett esophagus is most common in what race, age and sex?

Answer 54

white males and it typically presents between 40 and 60 years of age.

Question 55

What is the greatest concern in Barrett esophagus?

Answer 55

confers an increased risk of
esophageal adenocarcinoma.

Molecular studies suggest that Barrett epithelium may be more similar to adenocarcinoma than to normal esophageal epithelium, consistent with the view that
Barrett esophagus is a pre-malignant condition.

In keeping with this, epithelial dysplasia,
considered to be a pre-invasive lesion, is detected in0.2% to 2.0% of persons with Barrett
esophagus each year and is associated with prolonged symptoms and increased patient age.

Although the vast majority of esophageal adenocarcinomas are associated with Barrett
esophagus,it is _important to remember that most individuals with Barrett esophagus do not
develop esophageal tumors_

Question 56

What is the morphology of esophagus?

Answer 56

Barrett esophagus can be recognized as one or several tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction.

This metaplastic
mucosa alternates with residual smooth, pale squamous (esophageal) mucosa and interfaces
with light-brown columnar (gastric) mucosa distally ( Fig. 17-6A , B).

Question 57

High-resolution
endoscopes have increased the sensitivity of Barrett esophagus detection.

This has led to
subclassification of Barrett esophagus as what?

Answer 57

1. long segment
2. short segment

Question 58

What is the long segment Barrett esophagus?

Answer 58

long segment, in which 3 cm or more of esophagus

is involved

Question 59

What is short segment of the Barrett esophagus?

Answer 59

or short segment, in which less than 3 cm is involved.

It is not yet clear if the risk
of dysplasia in short segment disease is less than in long segment Barrett esophagus.

Question 60

Diagnosis of Barrett esophagus requires both what?

Answer 60

• endoscopic evidence of abnormal mucosa above the gastroesophageal junction and
• histologically documented intestinal metaplasia.
  
  • Goblet cells, which have distinct mucous vacuoles that stain pale blue by H&E and impart the shape of a wine goblet to the remaining cytoplasm, define intestinal metaplasia and are necessary for diagnosis of Barrett esophagus ( Fig. 17-6C ).

Foveolar mucus
cells, which do not have distinct mucous vacuoles are insufficient for diagnosis.

The requirement for an endoscopic abnormality helps to prevent misdiagnosis if metaplastic goblet
cells within the cardia are included in the biopsy.

Question 61

The requirement for intestinal

metaplasia reflects the fact that this feature correlates with what risk?

Answer 61

neoplastic risk.

Question 62

When dysplasia is present in Barrett esophagus, it is classified as low grade or high grade.

What are present in both grades of dysplasia? (Fig. 17 7A ).

Answer 62

• Increased epithelial proliferation,
• often with atypical mitoses,
• nuclear hyperchromasia and stratification,
• irregularly clumped chromatin,
• increased nuclear-to-cytoplasmic ratio, and a
• failure of epithelial cells to mature as they migrate to the esophageal surface
• Gland architecture is frequently abnormal and is characterized by budding, irregular shapes, and cellular crowding ( Fig. 17-7B ).

Question 63

High-grade dysplasia of the Barrett esophagus exhibits what?

Answer 63

more severe cytologic and architectural changes.

NOTE : Intramucosal carcinoma is characterized by
invasion of neoplastic epithelial cells into the lamina propria

Question 64

Answer 64

FIGURE 17-6 Barrett esophagus.

• A, Normal gastroesophageal junction.
• B, Barrett esophagus. Note the small islands of paler squamous mucosa within the Barrett mucosa.
• C, Histologic appearance of the gastroesophageal junction in Barrett esophagus. Note the transition between esophageal squamous mucosa (left) and Barrett metaplasia, with abundant metaplastic goblet cells (right).

Question 65

Answer 65

FIGURE 17-7 Dysplasia in Barrett esophagus.

• A, Abrupt transition from Barrett metaplasia to low-grade dysplasia. Note the nuclear stratification and hyperchromasia.
• B, Architectural irregularities, including gland-within-gland, or cribriform, profiles in high-grade dysplasia.

Question 66

How can you diagnos Barrett esophagus?

Answer 66

Barrett esophagus can only be identified thorough endoscopy and biopsy, which are usually
prompted by GERD symptoms.

Question 67

Once diagnosed, the best course of management in Barrett esophagus is a matter of debate.

However, most agree that by what management has an important role?

Answer 67

periodic endoscopy with biopsy, for detection of dysplasia, has an important role.

Nevertheless, uncertainties about the potential of
dysplasia to regress, either spontaneously or in response to therapy, complicate clinical
decisions when dysplasia is identified. In contrast, intramucosal carcinoma requires therapeutic
intervention.

Question 68

What are the treatment options for Barrett esophagus?

Answer 68

• surgical resection, or esophagectomy,
• as well as newer modalities such as
  
  • photodynamic therapy,
  • laser ablation, and
  • endoscopic mucosectomy.

Multifocal high-grade dysplasia, which carries a significant risk of progression to intramucosal or
invasive carcinoma, is treated similarly to intramucosal carcinoma.

Many physicians follow lowgrade
dysplasia or a single focus of high-grade dysplasia with endoscopy and biopsy at frequent intervals.

However, management of esophageal dysplasia is evolving, and it is hoped that improved molecular understanding of neoplastic progression may allow development of chemopreventive approaches that reduce incidence of esophageal adenocarcinoma

Question 69

What are esophageal varices?

Answer 69

Instead of returning directly to the heart, venous blood from the GI tract is delivered to the liver via the portal vein before reaching the inferior vena cava.

This circulatory pattern is responsible
for the first-pass effect in which drugs and other materials absorbed in the intestines are
processed by the liver before entering the systemic circulation.

Diseases that impede this flow
cause portal hypertension and can lead to the development of esophageal varices, an
important cause of esophageal bleeding.

Question 70

What is the pathogenesis of ESOPHAGEAL VARICES?

Answer 70

Pathogenesis.

Portal hypertension results in the development of collateral channels at sites where the portal
and caval systems communicate.

Although these collateral veins allow some drainage to occur, they lead to development of a congested subepithelial and submucosal venous plexus within
the distal esophagus.

These vessels, termed varices, develop in 90% of cirrhotic patients, most
commonly in association with alcoholic liver disease. Worldwide, hepatic schistosomiasis is the
second most common cause of varices. A more detailed consideration of portal hypertension is
given in Chapter 18 .

Question 71

Esophageal varices occur 90 % in what condition?

Answer 71

develop in 90% of cirrhotic patients, most commonly in association with alcoholic liver disease.

Question 72

Worldwide, what is the
second most common cause of esophageal varices.

Answer 72

hepatic schistosomiasis

A more detailed consideration of portal hypertension is
given in Chapter 18 .

Question 73

Varices can be detected by what?

Answer 73

venogram ( Fig. 17-8A )

Question 74

In venogram what is the apperance of esophageal varices?

Answer 74

appear as tortuous dilated veins lying primarily within the submucosa of the distal esophagus and proximal
stomach.

Venous channels directly beneath the esophageal epithelium may also become massively dilated.

Question 75

Why are esophageal varices not be grossly obvios in surgical or postmortem specimens?

Answer 75

because they collapse in the absence of blood flow ( Fig. 17-8B ) and, when they are not
ruptured, the overlying mucosa is intact( Fig. 17-8C ).

Question 76

Variceal rupture results in what?

Answer 76

hemorrhage into the lumen or esophageal wall,

in which case the overlying mucosa appears
ulcerated and necrotic.

If rupture has occurred in the past, venous thrombosis, inflammation, and evidence of prior therapy may also be present.

Question 77

Answer 77

FIGURE 17-8 Esophageal varices

• . A, This angiogram shows several tortuous esophageal varices.
• B, Collapsed varices are present in this postmortem specimen corresponding to the angiogram in A. The polypoid areas represent previous sites of variceal hemorrhage that have been ligated with bands.
• C, Dilated varice beneath intact squamous mucosa

Question 78

If rupture of the esophageal varices has occurred in the past, what is present?

Answer 78

venous thrombosis, inflammation,
and evidence of prior therapy may also be present.

Question 79

What are the clinical features of esophageal varices?

Answer 79

While varices are often asymptomatic, they may rupture, causing massive hematemesis.

Question 80

What are the factors that lead to rupture of esophageal varices?

Answer 80

The factors that lead to rupture are not well defined, but

• inflammatory erosion of thinned overlying
• mucosa, increased tension in progressively dilated veins, and
• *increased vascular hydrostatic**
• pressure associated with vomiting are likely to contribute.

Question 81

In any case, hemorrhage due to
variceal rupture is a medical emergency that is treated by any of several methods:

Answer 81

• sclerotherapy by endoscopic injection of thrombotic agents;
• endoscopic balloon tamponade; or
• endoscopic rubber band ligation.

Question 82

Despite the interventions in medical emergency rupture of esophageal varices, as many as half of patients diefrom the first bleeding episode due to what?

Answer 82

either as a direct consequence of hemorrhage or following hepatic coma triggered by hypovolemic shock.

Among those who survive, additional instances
of hemorrhage occur in over 50% within 1 year.

Each episode has a similar rate of mortality.
Thus, over half of deaths among individuals with advanced cirrhosis result from variceal
rupture.

It must be remembered, however, that even when varices are present, they are only
one of several causes of hematemesis.