pathology REVIEWER digestive system 1

DR. MONTES

QUESTIONS
This refers to the incomplete development of esophagus where a thin
noncanalized cord replaces a segment of esophagus, causing a
mechanical obstruction
Most common site of esophageal atresia
The fistula associated with atresia can cause;
Esophageal atresia is associated with (conditions)
ANSWERS
Esophageal atresia
at or near the tracheal bifurcation and is usually associated with fistula
connecting the upper or lower esophageal pouches to a bronchus or the
trachea
aspiration, suffocation, pneumonia, and severe fluid and electrolyte imbalances
congenital heart defects, genitourinary malformations, and neurologic disease
fistulae

Intestinal atresia though less common than esophageal atresia, is Located in the duodenum and is characterized by a segment of bowel lacking a
commonly located in _____ and characterized by ____ lumen
An incomplete form of atresia in which the lumen is markedly reduced Stenosis
in caliber as a result of fibrous thickening of the wall, resulting in - May involve any part of the GIT but its more common in esophagus
partial or complete obstruction and small intestine
Intestinal atresia

Most common form of congenital intestinal atresia due to failure of the Imperforated anus
cloacal diaphragm to involute
Are saccular or elongated cystic masses that contain redundant Congenital duplication cysts
smooth muscle layers - Maybe present in esophagus, SI and colon
Intestinal duplication
- markedly dilated duplicated segment

This occurs when incomplete formation of the diaphragm allows the Diaphragmatic hernia
abdominal viscera to herniate into the thoracic cavity - when severe can cause pulmonary hypoplasia (incompatible with
life)

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pathology REVIEWER digestive system 1
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Diaphragmatic hernia.
The abdominal contents are in the chest cavity, causing hypoplastic lungs.

This occurs when closure of the abdominal musculature is incomplete Omphalocele

and the abdominal viscera herniate into a ventral membranous sac
Omphalocele

A ventral wall defect similar to omphalocele except that it involves all Gastroschisis
of the layers of the abdominal wall, from the peritoneum to the skin
Developmental rests that common in GIT is termed as ___ Ectopia
The most frequent site of ectopic gastric mucosa is the ___ upper third of the esophagus, where it is referred to as an inlet patch
An ectopia that occurs less frequently and can be found in the Ectopic pancreatic tissue
esophagus or stomach is termed as ____ - nodules are most often asymptomatic but can produce damage and
local inflammation
- if present in the pylorus, inflammation and scarring may lead to
obstruction
- they can mimic invasive cancer
Small patches of ectopic gastric mucosa in the small bowel or colon, Gastric heterotopia
may present with blood loss due to peptic ulceration of adjacent
mucosa
It is a blind outpouching of the alimentary tract that is lined by Diverticulum
mucosa, communicates with the lumen, and includes all 3 layers of the
bowel wall
The most common type of diverticulum is Meckel diverticulum
- located in the ileum
- due to the failed involution of the vitelline duct, which connects the
lumen of the developing gut to the yolk sac
Expound the rule of 2s in meckel diverticulum Occurs in 2% of the population, located approximately 2 feet within the
ileocecal valve, about 2 inches long and twice more common in males
The presence of gastric tissue in meckel diverticulum may result to; peptic ulceration of adjacent small intestinal mucosa and present with occult
bleeding or abdominal pain resembling acute appendicitis or intestinal
obstruction
Meckel diverticulum

Most common site of acquired diverticulae
Congenital hypertrophic stenosis;
This condition generally presents in the 2nd or 3rd week of life as new-
onset regurgitation and persistent, projectile, nonbillous vomiting
In pyloric stenosis, PE reveals;
Curative procedure for pyloric stenosis
Sigmoid colon
More common in males, 1 in every 300- 900 live births, high rate in
monozygotic twins and associated with turner syndrome and trisomy 21
Congenital hypertrophic pyloric stenosis
Hyperperistalsis and firm ovoid abdominal mass (this is due to the hyperplasia
of the pyloric muscularis propria w/c obstructs the gastric outflow.
Surgical splitting of the muscularis (myotomy)

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pathology REVIEWER
Acquired stenosis in adult can occur as a consequence of;
This dse condition results when the normal migration of neural crest
cells from cecum to rectum is arrested prematurely or when the
ganglion cells undergo premature death
This mutation accounts for the majority of familial cases and
approximately 15% of sporadic cases
Morphology of Hirschsprung dse
This technique is commonly used to confirm the presence of ganglion
cells at the anastomotic region
Clinical features of Hirschsprung dse
Identified as the major threats to life involved in Hirschsprung dse
In Hirschsprung dse, the primary mode of tx is
In contrast to congenital megacolon, this may occur at any age as a
result of Chagas disease, obstruction by a neoplasm or inflammatory
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DR. MONTES
Antral gastritis or PUD close to pylorus
Pyloric stenosis
Markedly thickened muscle at pyloric channel
Hirschsprung dse
- Aka congenital aganglionic megacolon
- This produces a distal intestinal segment that lacks both the
Meissner submucosal and the Auerbach myenteric plexus
(aganglionosis)
- Absent coordinated peristaltic contractions and (+) fxnal
obstruction dilatation of the proximal colon of the affected
segment
- males are affected preferentially while disease tends to be more
extensive in females
Heterozygous loss-of-function mutations in the receptor tyrosine kinase RET
rectum is always affected and sigmoid as well (length varies)
aganglionic region grossly normal or contracted appearance
innervated proximal colon may undergo progressive dilation
may reach diameters as much as 20 cm.
Dilation may stretch and thin the colonic wall to the point of rupture
Mucosal inflammation or shallow ulcers may also be present
intraoperative frozen-section analysis of transmural sections
Hirschsprungs Disease
Hirschsprungs disease. Note absence of ganglion cells in myenteric plexus.
neonatally, often with a failure to pass meconium in the immediate
postnatal period
Obstructive constipation follows
enterocolitis, fluid and electrolyte disturbances
surgical resection of the aganglionic segment and anastomosis of the normal
colon to the rectum
- take years for patients to attain normal bowel function and
continence
Acquired megacolon
- of these, only Chagas dse is associated with loss of ganglia
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pathology REVIEWER digestive system 1
DR. MONTES
stricture, toxic megacolon complicating ulcerative colitis, visceral
myopathy, or in association with functional psychosomatic disorders
Normal esophagus
Squamous esophagus

Glandular stomach

Normal esophageal squamous mucosa

Normal GE junction; squamous mucosa on the right, and gastric cardiac

glandular mucosa on the left

Describe the normal esophagus Hollow, highly distensible muscular tube that extends from the pharynx to the
gastro-esophageal (GE) junction at the level of the T11 or T12 vertebra
- Newborn: 10 to 11 cm. ; Adults: 23 to 25cm
Physiologic narrowing in esophagus 1. Proximally at the cricoid cartilage
2. Midway- alongside the aortic arch & at the anterior, crossing the left main
bronchus
3. Distally where it pierces the diaphragm
The 2 higher pressure areas in the esophagus are; 1. Upper esophageal sphincter (UES)
- 3-cm segment in the proximal esophagus at the level of the
cricopharyngeal muscle
2. lower esophageal sphincter (LES)
- 2- to 4-cm segment just proximal to the anatomic esophago-gastric
junction, at the level of the diaphragm
4 layers of the wall of the esophagus 1. mucosa- Non-keratinizing stratified squamous epithelia and lamina
propria
2. sub- mucosa- Loose connective tissue containing blood vessels,
lymphatics, leukocytes with occasional lymphoid follicles, nerve fibers
3. muscularis propria- Proximal 6 to 8 cm contains striated muscle fibers
from the cricopharyngeus
4. adventitia devoid of serosal coat
Functions of esophagus 1. Conducts food and fluids from the pharynx to the stomach
2. Prevents reflux of gastric contents into the esophagus

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pathology REVIEWER digestive system 1
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Refers to the difficulty in swallowing seen in deranged esophageal Dysphagia
motor function and with diseases that narrow or obstruct the lumen
Pain in swallowing Odynophagia
A retrosternal burning pain resulting from reflex regurgitation of Heartburn
gastric content in the lower esophagus
What is hematemesis Vomiting of blood
Black stool (upper GI tract in origin) Melena
Lack of coordination between the longitudinal layer and circular layer Nutcracker esophagus cause periodic short-lived esophageal obstruction
contraction results to
Types of diverticula in esophagus that causes obstruction a. Zenkers diverticulum- located just above the UES
b. Traction divertivulum- located at the midpoint area
c. Epiphrenic diverticulum- located just above the LES
3 types of esophageal diverticula

Another cause of esophageal obstruction that is generally caused by Stenosis

fibrous thickening of the submucosa and is associated with atrophy of - Most commonly caused by inflammation and scarring by chronic
the muscularis propria as well as secondary epithelial damage GERD
Esophageal Stenosis

An uncommon condition described as ledge-like protrusions of the Webs

mucosa that may cause obstruction most frequently in women above - semicircumferential, eccentric lesions that protrude less than 5 m
40 yrs old
Upper esophageal webs accompanied by iron-deficiency anemia, Paterson-Brown-Kelly or Plummer-Vinson syndrome
glossitis, and cheilosis are part of the
Most common location of webs Upper esophagus
Microscopically, webs are composed of fibrovascular connective tissue and overlying epithelium
The most common sx of web is Dysphagia
This is similar to webs, but are circumferential and thicker Schatzki rings
o A ring located above the GE junction and covered by squamous
mucosa
o B ring located at the squamocolumnar junction and may have
gastric cardia-type mucosa
This is characterized by the Increased tone of the LES, as a result of achalasia
impaired smooth muscle relaxation, is an important cause of
esophageal obstruction
The triad of ruling out achalasia is consists of 1. Incomplete relaxation of the LES
2. Increased LES tone
3. Aperitalsis of the esophagus
Primary achalasia is caused by; by failure of distal esophageal inhibitory neurons, and is, by definition,
idiopathic
Secondary achalasia may arise in what condition? Chagas disease, in which Trypanosoma cruzi infection causes destruction of
the myenteric plexus, failure of peristalsis, and esophageal dilatation

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pathology REVIEWER digestive system 1
DR. MONTES
Other causes of achalasia Diabetic autonomic neuropathy
Infiltrative disorders malignancy, amyloidosis, sarcoidosis
Lesions of dorsal motor nuclei, particularly polio or surgical ablation
Treatment options for primary and secondary achalasia include; laparoscopic myotomy and pneumatic balloon dilatation and Botulinum
neurotoxin (Botox) injection, to inhibit LES cholinergic neurons, can also be
effective
achalasia

Longitudinal tears near the G-E junction that are most often Mallory-Weiss tears,
associated with severe retching or vomiting secondary to acute
alcohol intoxication are termed as ______
Morphology
- Linear lacerations longitudinally oriented and range in length from
millimeters to several centimeters
- Usually cross the GE junction but may also be located in the
proximal gastric mucosa
- May involve only the mucosa or penetrate the entire wall

This type of laceration characterized by distal esophageal rupture and Boerhaave syndrome
mediastinitis that occurs rarely and is a catastrophic event
This occurs when the esophageal mucosa may be injured when Pill- induced esophagitis
medicinal pills lodge and dissolve in the esophagus rather than
passing into the stomach intact
Esophagitis caused by infectious agent may be brought by; Herpes simplex viruses, cytomegalovirus, or fungal organisms
- Most common fungal agent is candida
Fungal infection characterized by adherent gray-white Candidiasis
pseudomembranes composed of densely matted fungal hyphae and
inflammatory cells covering the esophageal mucosa
This virus typically cause punched-out ulcers Herpes viruses
Candida Esophagitis

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pathology REVIEWER
This virus causes shallower ulcerations and characteristic nuclear and
cytoplasmic inclusions within capillary endothelium and stromal cells
What contribute to mucosal protection by secreting mucin and
bicarbonate?
The most frequent cause of esophagitis and the most common
outpatient GI diagnosis in the US
Conditions that contribute to GERD include;
In reflex esophagitis, this is the only alteration, evident to the
endoscopist as redness (grossly)
Microscopic morphology in a more significant dse
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DR. MONTES
Herpetic Esophagitis
note marked ulceration and hemorrhage
Herpes, from the points of view of the endoscopist and the pathologist. Might
these large nucleolated cells be exfoliated as Tzanck cells?
Herpetic
Inclusions
CMV
Submucosal glands which are most abundant in the proximal and distal
esophagus
Reflux of gastric contents into the lower esophagus clinically known as GERD
Alcohol and tobacco use, obesity, CNS depressants, pregnancy, hiatal hernia,
delayed gastric emptying, and increased gastric volume
hyperemia
eosinophils are seen in the squamous mucosa followed by neutrophils,
which are usually associated with more severe injury
Basal zone hyperplasia exceeding 20% of the total epithelial thickness
and elongation of lamina propria papillae
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pathology REVIEWER digestive system 1
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Linear erosions
Typical of reflux
esophagitis

Reflux esophagitis.
Note rete peg elongation and basal layer hyperplasia.

REFLUX/GERD

Eosinophils in
reflux
esophagitis

Most common clinical sxs of GERD dysphagia, heartburn, and less frequently, regurgitation of sour-tasting gastric
contents

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pathology REVIEWER
Tx for GERD includes
This condition is characterized by separation of the diaphragmatic
crura and protrusion of the stomach into the thorax through the
resulting gap
Sxs of hiatal hernia include;
The cardinal histologic feature of hiatal hernia that that differentiate it
from GERD, Crohn disease, and other causes of gastritis)
Clinical characteristic important in the dx of hiatal hernia from GERD
Majority of individuals with hiatal hernia have conditions like;
Treatment for hiatal hernia includes
A complication of chronic GERD that is characterized by intestinal
metaplasia within the esophageal squamous mucosa
A pre-invasive lesion detected in 0.2 to 2% of persons with Barrett
esophagus
Morphology of barrett esophagus
2 Classifications of barrett esophagus based on endoscopic findings
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DR. MONTES
proton pump inhibitors or H2 histamine receptor antagonists, which reduce
gastric acidity, typically provides symptomatic relief
Hiatal hernia
Hiatal hernia
food impaction and dysphagia in adults and feeding intolerance or GERD-like
symptoms in children
large numbers of intraepithelial eosinophils, particularly superficially
failure of high-dose proton pump inhibitor treatment and the absence of acid
reflux
atopic dermatitis, allergic rhinitis, asthma, or modest peripheral eosinophilia
dietary restrictions to prevent exposure to food allergen and topical or
systemic corticosteroids
Barrett esophagus
- It confers an increased risk of esophageal adenocarcinoma
- It suggests that barrett epith is more similar to adenoca than to a
normal esoph, thus considered pre- malignant condition
Epithelial dysplasia
- most individuals with Barrett esophagus do not develop esophageal
tumors
one or several tongues or patches of red, velvety mucosa extending
upward from the GE junction
metaplastic mucosa alternates with residual smooth, pale squamous
(esophageal) mucosa and interferes with light-brown columnar (gastric)
mucosa distally
Diagnosis requires both endoscopic and histological evidences
Goblet cells, define intestinal metaplasia and are necessary for diagnosis
of Barrett esophagus
Increased epithelial proliferation, often with atypical mitoses, nuclear
hyperchromasia and stratification, irregularly clumped chromatin,
increased nucleo-cytoplasmic ratio, and a failure of epithelial cells to
mature as they migrate to the esophageal surface are present in both
grades of dysplasia
Gland architecture is frequently abnormal and is characterized by
budding, irregular shapes, and cellular crowding
1. long segment 3 cm or more of the esophagus is involved
2. short segment less than 3 cm is involved
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pathology REVIEWER digestive system 1
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Normal white Squamous mucosa

Pink abnormal Glandular mucosa

Barrett Esophagus

Barrett Esophagus
Note goblet cell metaplasia

Squamous mucosa

Carcinoma arising in Barretts

esophagus

Barretts esophagus

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pathology REVIEWER digestive system 1
DR. MONTES
Barretts esophagus with dysplasia. Note lack of mucin, nuclear
hyperchromasia,, and variation in size and shape.

Sequence: barrett dysplasia carcinoma

High power
view of dysplasia in Barretts esophagus.
Note nuclear variation, prominent nucleoli, and increased mitoses.

Technique recommended for detection of dysplasia in barrett Periodic endoscopy with biopsy
esophagus v Treatment options include surgical resection, or esophagectomy
An important cause of bleeding from diseases that impede the flow of Esophageal Varices
venous blood from the GIT to the liver via the portal vein cause portal - develop in 90% of cirrhotic patients, most commonly in association
hypertension with alcoholic liver disease
- hepatic schistosomiasis is the second most common cause of
varices
Esophageal varices in venogram appear; tortuous dilated veins within the submucosa of the distal esophagus and
proximal stomach
1.

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pathology REVIEWER
Clinical features of esophageal varices
Methods of treatment for esophageal varices
Death may result in esophageal varies as a consequence of;
This tumor typically arises in a background of Barrett esophagus and
long-standing GERD
These organisms are associated with a decreased risk of
adenocarcinoma, perhaps by causing gastric atrophy and reducing
acid reflux
Genetic mutation related to adenocarcinoma in the early stages
Most adenocarcinoma in esophagus arise in the;
Morphology of adenoca.
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DR. MONTES
Produce no symptoms until they rupture, then massive hematemesis
occur
Factors that trigger rupture: inflammatory erosion of the overlying thinned
out mucosa, increased tension in progressively dilated veins, vomiting
with increased vascular hydrostatic pressure
sclerotherapy by endoscopic injection of thrombotic agents; endoscopic
balloon tamponade; or endoscopic rubber band ligation
hemorrhage or following hepatic coma triggered by hypovolemic shock
Adenocarcinoma
H. pylori
Mutation or overexpression of p53 gene
- Additional genetic changes include:
o Amplification of c-ERB-B2, cyclin D1, and cyclin E genes;
mutation of the retinoblastoma tumor suppressor gene;
and allelic loss of the CDK inhibitor p16/INK4a
distal 3rd of the esophagus and may invade the adjacent gastric cardia
appears as flat or raised patches in otherwise intact mucosa, large
masses up to 5 cm or more may develop
tumors may infiltrate diffusely or ulcerate and invade deeply
Microscopically, Barrett esophagus is frequently present adjacent to the
tumor
Most are mucin-producing glandular tumors exhibiting intestinal-type
features
ADENOCARCINOMA
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pathology REVIEWER
Clinical features of adenoca
Squamous cell carcinoma
Common site of SCC in the esophagus
Morphology of SCC
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DR. MONTES
commonly present with pain or difficulty in swallowing, progressive weight
loss, hematemesis, chest pain, or vomiting
the tumor has usually spread to submucosal lymphatic vessels when the
sxs appear
advanced stage at diagnosis, overall 5- year survival is <25%
occurs in adults over age 45 and affects males 4 times more frequently
than females
Risk factors include: alcohol and tobacco use, poverty, caustic
esophageal injury, achalasia, tylosis, Plummer-Vinson syndrome, and
frequent consumption of very hot beverages
Predisposition: Previous radiation therapy to the mediastinum,
Nutritional deficiencies, as well as polycyclic hydrocarbons, nitrosamines,
and other mutagenic compounds, such as those found in fungus-
contaminated foods, HPV infection in high risk areas, loss of several
tumor suppressor genes, including p53 and p16/INK4a is involved
occur in the middle 3rd of the esophagus
Begins as carcinoma in- situ termed as squamous dysplasia
Early lesions appear as small , gray-white plaque-like thickenings
Over months to years they grow into tumor masses that may be polypoid
or exophytic and protrude into and obstruct the lumen
tumors are either ulcerated or diffusely infiltrative lesions that spread
within the esophageal wall and cause thickening, rigidity and luminal
narrowing
Most are moderately to well differentiated
Less common histologic variants include verrucous SCCA, spindle cell
carcinoma, and basaloid SCCA
Tumors located in the upper 3rd also metastasize to the cervical LNs;
those in the middle mediastinal, paratracheal and tracheobronchial
LNs; lower 3rd gastric and celiac group of LNs
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pathology REVIEWER digestive system 1
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DYSPLASIA IN-SITU INFILTRATION

Infiltrating nests of keratinizing esophageal squamous cell carcinoma

SCCA- Clinical features Insidious onset and ultimately produces dysphagia, odynophagia, and
obstruction
Extreme weight loss and debilitation result from both impaired nutrition
and effects of the tumor itself
Hemorrhage and sepsis may accompany tumor ulceration
Lymph node metastases which are common are associated with poor
prognosis
overall 5-year survival remains a dismal 9%
The first sxs encountered by pxs with SCCA are caused by aspiration of food via a tracheo-esophageal fistula
Benign tumors in esophagus are generally _________ in origin and mesenchymal in origin and arise within the esophageal wall
arise in _____
Benign tumors take the form of polyps usually composed of fibrous fibrovascular polyps or pedunculated lipomas, respectively
and vascular tissue are called ______ and _____ respectively
These are sessile lesions with a central core of connective tissue and Squamous papillomas
a hyperplastic papilliform squamous mucosa
Uncommonly, papillomas are associated with HPV infection Condyloma
Mass of inflamed granulation tissue, growing either as an inflammatory inflammatory pseudotumors
polyp or an infiltrative mass in the wall of the esophagus may
resemble a malignant lesion
BENIGN TUMORS of the esopgaus LEIOMYOMAS
FIBROVASCULAR POLYPS
CONDYLOMAS (HPV)
LIPOMAS
GRANULATION TISSUE (PSEUDOTUMOR)
v The very BEST way to classify ALL tumors of a major organ is to
remember its basic HISTOLOGY
The author of this document wishes you a successful examination. Dont forget to check your notes and books if anything seems confusing. This is
not intended to replace your review materials, instead this is primarily designed to assist you in your study regimen.

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