ESOPHAGUS and STOMACH

AZESU O. SILVA, MD, DPSP (AP-CP)

Surgical Pathology
ESOPHAGUS
Mouth to stomach- Passage for
food and water
Swallow then coordinated wave of
peristaltic contractions
Motor disorders:
o nutcracker esophagus
Outer longitudinal and inner
circular smooth muscle
lack of coordination
o Diffuse esophageal spasm
wall stress-small
outpouching
(pseudodiverticula = lacks
true muscularis)
NORMAL
hollow muscular highly distensible
tube
epiglottis- (C6), GE junction-(T11 to
T12)
10-11 cm children, 25 cm adult
Endoscopist- esophagus- between
15 and 45 cm from incisor/ GE
junction at 40 cm
points of narrowing:
1. CRICOID CARTILAGE
2. ALONGSIDE AORTIC ARCH
3. PIERCINGDIAPHRAGM
NORMALLY NEGATIVE PRESSURE IN
LUMEN- but with 2 higher pressure
areas, contracted in resting phase:
1. IN PROXIMAL ESOPHAGUS, 3
CM SEGMENTCRICOPHARYNGUS MUSCLE
LEVEL (UES)
2. PROXIMAL TO GE JUNCTION,
2-4 CM SEGMENTDIAPHRAGM LEVEL (LES)

* Physiologic sphincters- no anatomic

landmarks

HISTOLOGY
1. MUCOSA
2. SUBMUCOSA
3. MUSCULARIS PROPRIA
4. ADVENTITIA
MUCOSA
non-keratinizing strat. sq.
epithelium (matured squamous
and basal cells) * specialized cellsmelanocytes, endocrine cells,
dendritic cells, lymphocytes
lamina propria areolar CT, blood
vessels, leukocytes
muscularis mucosa longitudinally
arranged smooth muscle cells
1

SUBMUCOSA

Loose CT, blood vessels,

lymphatics, lymphoid follicles,
nerves (Meissner plexus),
submucosal glands

MUSCULARIS PROPRIA
inner circular and outer
longitudinal muscle layers,
myenteric plexus (Auerbach
plexus)
ADVENTITIA
* No serosa- Intra-abdominal part only *
With fascia- thoracic portion

CONGENITAL ANOMALIES
ECTOPIC TISSUE REST:
1. ECTOPIC GASTRIC MUCOSA
(inlet patch)
MOST COMMON
Located at upper 3rd of
esophagus (proximal
esophagus)
Causes barrett esophagus,
dysphagia and esophagitis
Rarely causes
adenocarcinoma
Also in small bowel and
colon
Presents as occult blood loss
or as peptic ulceration
2. ECTOPIC PANCREATIC TISSUES
(also in stomach, pylorusinflammation, scarring and
obstruction) LESS FREQUENT

IMPAIRED FORMATION OF
DIAPHRAGM
Herniation of abdominal content in
the thorax
Lungs hypoplastic at time of birth
AGENESIS absence of esophagusextremely rare (*Atresia and fistula
formation- more common)
ATRESIA esophagus as thin noncanalized cord with proximal blind pouch
attached to the pharynx and a lower
pouch leading to the stomach. Most
commonly located at or near tracheal
bifurcation. Rarely occurs alone. Usually
associated with fistula.
Assoc. with fistula- connects lower or
upper pouch with bronchus or trachea.
Atresia and fistula, associated
anomalies- congenital heart dse,
neurologic dse, genitourinary dse, GI
malformation
Atresia assoc. with single umbilical
artery
Aspiration and paroxysmal suffocation
from food, hazards. Pneumonia and
severe electrolyte imbalance.
ESOPHAGEAL ATRESIA AND
TRACHEOSEPHAGEAL FISTULA

Type C
most common
Blind upper segment and fistula
between lower segment and
trachea
ESOPHAGEAL MUCOSAL WEBS
ledge like mucosal protrusion,
usually at UE
semicircumferential, eccentric
2

Composed of squamous mucosa

and vascular submucosa
Congenital, or in long standing
reflux esophagitis, chronic GVHD
and blistering skin disease
If accompanied by: iron def
anemia, glossitis, cheilosis =
PATERSON-BROWN-KELLY OR
PLUMMER-VINSON SYNDROME with
risk of postcricoid esophageal
carcinoma
Main symptom- dysphagia with
incompletely chewed food

NORMAL

fibrous thickening, submucosa,

with atrophy of muscularis propria,
thin ulcerated lining epithelium
Occasionally congenital
most common cause severe injury
with inflammatory scarring (chronic
GE reflux, irradiation, caustic
injury)
Develops slowly in adulthood
progressive dysphagia (solid then
fluid)

NORMAL

STENOSIS

WEB

ESOPHAGEAL RING or Schatzki ring

concentric and thicker plates,
distal esophagus
A ring- above the GE junction
B ring - at the squamocolumnar
junction (with Gastric type mucosa)
Mucosa, submucosa and
hypetrtophied muscularis propria,
Gastric type mucosa (B ring)
NORMAL

ESOPHAGEAL RING

WEBS AND RINGS

common in female, 40 yo,
uncertain etiology
Main symptom- episodic dysphagia
Pain is infrequent
ESOPHAGEAL STENOSIS

LESIONS ASSOCIATED WITH MOTOR

DYSFUNCTION
ACHALASIA
HIATAL HERNIA
DIVERTICULUM
MALLORY-WEISS TEAR
ACHALASIA
failure to relax
Major abnormalities: aperistalsis,
partial or complete relaxation of
LES with swallowing, increased
resting tone of LES
PRIMARY: UNCERTAIN ETIOLOGY
MOSTLY
Dysfunction of inhibitory neurons
containing NO2 and vasoactive
intestinal peptide (VIP), neural
innervation degenerative changes
(vagus nerve)
SECONDARY: Chagas disease (T
cruzi) myenteric plexus
destruction, failure of peristalsis
and esophageal dilatation
ACAHALASIA LIKE DISEASE
o diabetic autonomic
3

neuropathy
Disorders of dorsal motor
nuclei- polio, surgical
ablation (amputation,
excision)
Infiltrative disordermalignancy, amyloidosis,
sarcoidosis

Treatment
Myotomy, pneumatic balloon
dilatation
Botulinum toxin (botox)- inhibits
LES cholinergic neurons

crura and widening of the space

between the muscular crura and
esophageal wall causing protrusion
of upper portion of stomach into
the thoracic cavity
PREDISPOSING FACTORS:
Muscle weakening and loss of
elasticity with age
Pregnancy
Obesity
Abdominal ascites
Diaphragmatic hernias may be congenital
or acquired.
1. Acquired hiatal hernias
- non-traumatic (more common)
(1) sliding hiatal hernia(2)
paraesophageal hiatal hernia
*(a mixed variety is also possible). traumatic hernia
1. AXIAL OR SLIDING HIATAL HERNIA(95%) protrusion of stomach, bell shaped
dilatation bounded below by
diaphragmatic narrowing
2. NON-AXIAL PARAESOPHAGEAL HIATAL
HERNIA (ROLLING)- separate portion of
stomach along greater curvature enters
thorax through widened foramen
SLIDING HERNIA, 9% suffer from heart
burn, attributed to incompetence of LES,
positions favoring reflux (bending
forward, supine) and obesity
- Reflux esophagitis is frequent.
ROLLING HERNIA, strangulation and
obstruction
BOTH- ULCER, BLEEDING, PERFORATION

MORPHOLOGY
Progressive dilatation above LES,
wall with normal thickness
Absent myenteric ganglia, but may
or may not be reduced at LES area
Ulcer, inflammation or fibrotic
thickening above the LES
Development of SQUAMOUS CELL
CARCINOMA (5% OF CASES)
HIATAL HERNIA
separation of the diaphragmatic
4

DIVERTICULA
OUTCPOUCHING of alimentary tract
that contains all visceral layers
False diverticulum- mucosa and
submucosa Only
3 regions:
o 1. ZENKERDIVERTICULUMabove the UES
o 2. TRACTION DIVERTICULUMmidpoint
o 3. EPIPHRENIC
DIVERTICULUM- above the
LES
ZENKER DIVERTICULUM- disordered
cricopharyngeal motor dysfunction w/ or
w/o GERD and diminished luminal size of
UES.
TRACTION DIVERTICULUM- Scarring sec to
lymphadenitis (TB), causes traction to
esophagus.
EPIPHRENIC DIVERTICULUMDiscoordinated peristalsis and LES
relaxation.

ZENKERS DIVERTICULUM

ESOPHAGITIS
LACERATIONS (MALLORY WEISS
SYNDROME)
- longitudinal tears in the
esophagus at the esophago-gastric
junction or gastric cardia, severe retching
or vomiting, in alcoholics
- relaxation fails to occur during
prolonged vomiting
- Underlying hiatal hernia is a
predisposing factor
- Infection may lead to
inflammatory ulcer or to mediastinitis
5

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- Distal esophageal rupture,

BOERHAAVE SYNDROME
MALLORY-WEISS TEAR

ESOPHAGEAL VARICES
prolonged or severe portal hypertension
due to formation of collateral bypass
channels wherever portal and caval
system communicate
Develops in 90% of cirrhotic patients
- Alcoholic cirrhosis
- Hepatic schistosomiasis
Dilated veins- in submucosa of distal
esophagus and proximal stomach
Also dilated venous channels beneath the
esophageal epithelium
ESPHAGEAL VARICES

Clinically- no symptoms until they

rupture
half of cirrhotic patients die from
rupture of varices.
ESOPHAGITIS
Normally submucosal glands- bicarbonate
and mucin- mucosal protection
inflammation of esophageal mucosa
physical chemical and biological agents
REFLUX ESOPHAGITIS associated with the
clinical condition-GERD- - decreased
efficiency of esophageal anti-reflux
mechanisms, LES tone- CNC depressant,
pregnancy
- In Sliding hiatal hernia
- Inadequate slowed esophageal
clearance or refluxed material
- Delayed gastric emptying and
increased gastric volume
- Reduction of reparative capacity
by protracted exposure to gastric acid. Gastric juice and bile (severe cases) from
duodenum
Morphology
Hyperemia- inflamm cells (N,E,L) in
squamous epithelial layer
6

 Basal zone hyperplasia >20 % of wall

thickness
elongation or lamina propria papillae
with capillary congestion

REFLUX ESOPHAGITIS-GERD

REFLUX ESOPHAGITIS-GERD

hematamesis, melena, stricture, barrett

esophagus
BARRETT ESOPHAGUS
Complication of long standing GERD
In 10% of symptomatic GERD patients
Simple most important risk factor for
ESOPHAGEAL ADENOCARCINOMA.
Distal squamous mucosa is replaced by
metaplastic columnar epithelium as
response to injury.
Criteria:1. Endoscopic evidence of
columnar epithelial lining above the GE
junction 2. Histologic evidence of
intestinal metaplasia of columnar
epithelium
Classification:
1. 2.

LONG SEGMENT extending cephalad

more than 3 cm from the manometric GE
junction
SHORT SEGMENT- extending less than
3cm cephalad.
Pathogenesis is unclear but it appears to
be as a result of alteration in the
differentiation of the stem cells of the
esophageal mucosa.
Esophageal squamous epithelium is
replaced by metaplastic epitheliumGoblet cells and intestinal columnar cells.
Important is to search also for dysplasia,
low grade or high grade.
50% of patient with High grade dysplasia
may already have adenocarcinoma
Clinical- 40-60 yo, white males, local
ulceration, bleeding, stricture
Long segment- 30-40 fold inc risk for
Adenocarcinoma
Short segment- unknown risk
BARRETT ESOPHAGUS

EOSINOPHILSEARLYHISTOLOGICABNORMALITY
NEUTROPHILSMORESEVEREINJURY,INULCER
Most common in adults 40 yo
Infant and children also
Dysphagia, heart burn, regurgitation of
sour tasting gastric content (less
frequently)
Complications: ulceration,
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BARRETT ESOPHAGUS

margins of ulcer
CMV-linearulcerationofmucosa
- intranuclear and cytoplasmic inclusion,
capillary endothelium and stromal cells,
base of ulcer
Pathogenic bacteria- 10-15 % of
infectious esophagitis
- Invasion of lamina propria and
necrosis of squamous epithelium
- Polymicrobial, oral flora
MORPHOLOGY
Chemicals- MILD ERYTHEMA, EDEMA,
SLOUGHING OF THE MUCOSA, NECROSIS
- Medication sticking in esophagus
Irradiation-submucosal and mural blood
vessel with marked intimal proliferation
and luminal narrowing, fibrotic
submucosa, mucosal atrophy, flattening
of papillae, thinning of epithelium
GVHD- apoptosis of basal cells,
separation of epithelium and lamina
propria, atrophy, and fibrosis of lamina
propria with minimal inflammation
CANDIDIASIS

INFECTIOUS AND CHEMICAL ESOPHAGITIS

ORIGINS:
Mucosalirritantsalcohol,corrosivealkaliand acid and heavy
smoking
Cytotoxic anticancer therapy
Infection followed by bacteremia or
Viremia: HSV, CMV (common offenders in
immunocompromised patients)
Fungal infection candidiasis,
mucormycosis, aspergillosis
Uremia in setting of renal failure
following irradiation, systemic GVHD,
autoimmune dse, desquamative
dermatologic conditions, Chron disease
Morphology
Final common pathway is severe acute
inflammation, superficial necrosis and
ulceration with granulation tissue
formation and eventual fibrosis
Candidiasis- fungus and grey white
pseudomembrane, entire esophagus
Herpesvirus-punchedoutulcer
- Nuclear inclusion in degenerating
epithelial cells,
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Candidiasis
Herpes virus

CMV

TUMORS
ADENOCARCINOMA (western) AND
SQUAMOUS CELL CARCINOMA
(worldwide)
ADENOCARCINOMA
arises in the background of BARRET
ESOPHAGUS and long standing GERD
Increased risk: Documented dysplasia,
tobacco use, obesity, prior radiation
therapy
Decreased risk: fruit and vegetable diet
Distal third, and may invade distal gastric
cardia
Mucin production, gland formation
(intestinal type), signet ring cells (gastric
cancer like), small poorly differentiated
cells (like small cell CA in lung)
Pain, difficulty in swallowing,
progressive weight loss, hematamesis,
chest pain, vomiting (already with
submucosal lymphatic invasion)
5 year survival:
- Mucosa and submucosa- 80 %
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P
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- Deeper or advanced- <25 %

SQUAMOUS CELL CARCINOMA
RISK FACTORS:
- Plummer-Vinson syndrome,
alcohol, tobacco use, previous radiation
exposure (10 years)
- HPV infection (in high risk)
In middle third of esophagus usually
In situ- then Polypoid exophytic, diffuse or
ulcerative
Lymph node metastasis:
- Upper third- cervical
- Middlethird-mediastinal,paratracheal,
tracheobronchial
- Lower third- gastric and celiac
Dysphagia, odynophagia, obstruction
Weight loss, hemorrhage, sepsis

STOMACH
AZEUS O. SILVA, MD, DPSP (AP-CP)
CASE #1 CLINICAL HISTORY:
- MALE, 50 Y.O.- Massive hematamesis,
epigastric pain, nausea - Alcohol intake,
previous- Heavy smoker- Aspirin for
Rheumatoid Arthritis
Endoscopy: hyperemic with focal
hemorrhage, inflammation with
superficial sloughing of gastric mucosa

10

 ACUTE EROSIVE HEMORRHAGIC

GASTRITIS
PATHOGENESIS
Considerations: inc acid secretion, dec
bicarbonate buffer production, reduced
blood flow, disruption of adherent mucus
layer, direct damage to the epithelium
Mucosal insults: bile acid and lecithin
regurgitation from proximal duodenum,
inadequate synthesis of prostaglandin
Biopsy: neutrophilic infiltrates within
epithelium, (+) superficial mucosal
erosion (without crossing of the
muscularis mucosa), fibrinous exudate in
glandular lumen, H. pylori (-), atrophy (-),
Intestinal metaplasia (-)

DIAGNOSIS:
ACUTE GASTRITIS

ACUTE GASTRIC ULCERATION

focal, acutely developing gastric
mucosal defect- NSAID TX COMPLICATION
(cyclooxygenase inhibition)
TYPES
Stress ulcers- shock, sepsis and severe
trauma Curling ulcers- severe burns and
trauma
- proximal duodenum* Splanchnic
vasoconstriction inc Hcl
11

 Cushing ulcer- intracranial disease

(stimulation of vagal nuclei, inc acid
secretion)
- gastric, duodenal, esophageal - high
incidence of perforation

the lumen of the stomach.

Endoscopy: antral-body-fundic mucosa
(Pangastritis), reddened, coarse

Prostaglandin
IMPORTANCE: Favors production of
mucus and bicarbonate Inhibits acid
secretion by parietal cells Vasodilatory
action, PGE and I improves mucosal blood
flow

Gross

Shallow erosion superficial to deep Less

than 1 cm in diameter (acute) Ulcer
base- brown to black
- extravasated blood (acid digestion) transmural infiltration- local serositis
Can be found anywhere in stomach
Rugal folds- normal Non-indurated base
and margins Single or Multiple mostly
Sharply demarcated- normal adjacent
mucosa

1.

2.

Microscopy
NECROTIC AREA INFLAMMATORY
CELLS GRANULATION TISSUE
FIBROSIS
* Heals with complete re-epithelialization
CASE #2 CLINICAL HISTORY:
- FEMALE, 40 Y.O.
- NAUSEA, VOMITTING, UPPER
ABDOMINAL DISCOMFORT
- Normal to inc serum Gastrin level
GASTRIN
is a peptide hormone that stimulates
secretion of gastric acid (HCl) by the
parietal cells ofthe stomach
aids in gastric motility
released by G cells in the antrum of the
stomach, duodenum, and the pancreas.
Gastrin binds to cholecystokinin B
receptors to stimulate the release of
histamines in enterochromaffin-like cells,
and it induces the insertion of
+ +
K /H ATPase pumps into the apical
membrane of parietal cells (which in turn
+
increases H release into the stomach
cavity).
Its release is stimulated by peptides in

PANGASTRITIS

Biopsy: lymphocytes and plasma cells in

lamina propria, thin and flattened , Noninvasive H. pylori (+), atrophy (+),
Intestinal metaplasia (+), lymphoid
aggregates with germinal centers within
mucosa, intraepithelial neutrophils and
pit abscess, subepithelialplasma cells
Regenerative changes- mitotic figures in
gland neck, EC enlargement,
hyperchromatic nuclei, high N:C ratio,
mucus depletion
Parietal cells are prominent but
decreased in number
G cell hyperplasia
P

12

DIAGNOSIS:
- CHRONIC GASTRITIS WITH
HELICOBACTER PYLORI INFECTION
- CHRONIC ATROPHIC GASTRITIS WITH
INTESTINAL METAPLASIA HELICOBACTER
PYLORI, PRESENT

NOTE Check for dysplasia or neoplasia,

WHY? LONG STANDING CHRONIC
GASTRITIS
Metaplasia Dysplasia In-situ Carcinoma
GASTRIC CANCER - associated with
autoimmune gastritis and H. pylori assoc.
Chronic gastritis

CHRONIC GASTRITIS
less severe but more persistent
Nausea and upper abdominal discomfort
vomiting (sometimes), hematamesis
(uncommon)
Most common cause of CG is infection
(H. pylori)
Most common cause of CG without H.
pylori infection- autoimmune gastritismost common cause of ATROPHIC
GASTRITIS
CHRONIC GASTRITIS
Other causes: 1. RADIATION
13

P
P
P

P
P
P

CHRONIC BILE REFLUX

MECHANICAL INJURY
SYSTEMIC DISEASES- CHRON DISEASE,
AMYLOIDOSIS, GVHD
Helicobacter pylori
Non-spore forming curvilinear gram neg
rod, 3.5 x 0.5 um
Does not invade mucosa, intense inflamm
reaction and immune response. Inc
production of proinflamm cytokines (IL-1,
TNF -from epith cells, PMN recruitment)
Produces bacterial products that cause
epithelial injury and induces inflammation
(urease, phospholipase)
Enhances gastric acid secretion
Some of its protein are immunogenic (T
and B cells) - causes T cell-driven
activation of B-cells- GASTRIC LYMPHOMA
HUMANS ARETHEONLYKNOWNHOST
ORAL-ORAL, FECAL-ORAL,
ENVIRONMENTAL SPREAD
H. PYLORI
VIRULENCE:
- FLAGELLA- motility in mucus
- UREASE- generates ammonia
from endogenous urea, elevates local
gastric pH
- ADHESINS- adherence to foveolar
cells
- TOXINS- cytotoxin-associated
gene A (CagA) maybe associated with
ulcer and cancer development by poorly
defined mechanism.
predominantly antral gastritis with high
acid production, despite hypogastrinemia
increased risk of duodenal cancer
IMBALANCE IN GASTRODUODENAL
MUCOSAL DEFENSE AND DAMAGING
FORCES THAT OVERCOME THOSE
DEFENSES
CASE #3 CLINICAL HISTORY:
- FEMALE, 45 Y.O.
- NAUSEA, VOMITTING, UPPER
ABDOMINAL DISCOMFORT
- CBC-dec HGB, dec HCT, dec RBC
- PBS- macrocytic anemia with
hypersegmented polymorphonuclear cells

Diffuse mucosal damage, body and

fundus Thin and rugal fold almost lost
Incomplete mucosal atrophy Multiple
small polyps and nodules

Microscopy
- Parietal and chief cells, severe loss or
absent- G cell hyperplasiaEnterochromaffin like cell hyperplasia PERSISTING GLANDS, CYSTIC DILATATION

Diagnosis:
CHRONIC GASTRITIS

- inc Gastrin level

- Hyperchlorhydria or achlorhydria
or hypergastrinemia
Gross
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 AUTOIMMUNE TYPE OF CHRONIC

GASTRITIS
ASSOCIATIONS
ACID PRODUCTION
Epithelial cells damage
OTHER LESION
MUCOSAL DAMAGE
PEPTIC ULCER
GASTRIC LYMPHOMA
CARCINOID TUMOR (ECL hyperplasia)
ASSOCIATIONS

P
P
P
P
P

layers of stomach, middle aged women

REACTIVE GASTROPATHY- edema,
glandular hyperplasia, regenerative
changes,
- NSAID, bile reflux
GVHD- lamina propria lymphocytes,
bone marrow transpalntation
REACTIVE GASTROPATHY-mucosal
histologic changes (foveolar hyperplasia,
loss of mucin, glandular regenerative
changes etc) without neutrophils
PEPTIC ULCER DISEASE
A BREACH IN THE MUCOSA OF THE
ALIMENTARY TRACT THAT EXTEND
THROUGH THE MUSCULARIS MUCOSA
INTO THE SUBMUCOSA OR DEEPER.
*Erosion- (-) muscularis mucosa breach
Commonly involves duodenum and
stomach Acute and chronic ulcers

Pro-inflammatory cytokine production

Epithelial cells damage
Inflam cells
SEROLOGY
Characteristics:
Reduced pepsinogen I concn.
Antral endocrine cell hyperplasia
Vit B 12 def
Defective gastric acid secretion
(achlorhydria)
Autoantibodies- against COMPONENTS
OF GASTRIC GLAND PARIETAL CELLS,
ACID PRODUCING ENZYME (H-K-ATPase),
GASTRIN RECEPTORS, INTRINSIC FACTOR
Pernicious anemia + autoimmune
gastritis- Assoc with hashimoto
thyroiditid, Type I DM etc.
UNCOMMON FORMS OF GASTRITIS
ALLERGIC GASTROENTEROPATHYantral, mucosa only, children
LYMPHOCYTIC GASTRITIS- body, Immune
mediated, CD8 cells, mucosa and lamina
propria
GRANULOMATOUS GASTRITIS- antral,
intramucosal, CHRON disease,
Sarcoidosis, TB, Histoplasmosis,
Anisakiasis, foreign body reaction,
systemic vasculitis
UNCOMMON FORMS OF GASTRITIS
EOSINOPHILIC- antral and pyloric, all

CHRONIC
PEPTIC ULCER- solitary, any portion
exposed to acid/peptic juice
Locations:
Duodenum, first portion
Stomach, usually antrum
GE junction in GE reflux or Barrett disease
Margins of gastrojejunostomy
15

P
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P
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P
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P
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Duodenum, stomach and/or jejunumZOLLINGER- ELLISON syndrome

Within or adjacent to an ileal Meckel
diverticulum that contain ectopic gastric
mucosa
They often appear without any
precipitating factor becomes active
heals spontaneously
Imbalance bet gastroduodenal defense
and damaging forces (gastrin and pepsin)
Hyperacidity is not a prerequisite
Ulceration occurs: mucosal defense
fails ( dec mucosal blood flow, delayed
gastric emptying, impaired epithelial
restitution
Tendency to recur due to infection with H.
pylori
Thrombotic occlusion- bacterial platelet
activating factor Damage of cellsleakage of nutrient- sustained bacillus

Morphology
98 % of peptic ulcer are located In the
st
1 portion of the duodenum Wall
penetration, adheres to pancreas,
omental fat or liver ACTIVE ULCERBase and margins, Necrotic fibrinoid
necrosis
Non-specific inflammatory infiltrates,
neutrophil predominance
Active granulation tissue formation
Fibrous scar

Chronic gastritis is universal among

patients with PUD Always positive for H.
pylori Gastritis remains after ulcer has
healed Recurrence of the ulcer not
related to gastritis
*in acute erosive gastritis or stress ulceradjacent mucosa is generally normal
ACUTE GASTRIC ULCERATION
NSAID medication, stress ulcer
Located mainly in stomach and
occasionally in the duodenum
Ranges from erosion to ulceration
Commonly encountered in shock,
extensive burns, sepsis or severe trauma;
in intracranial injury raising intracranial
16

pressure; following intracranial surgery

Curling ulcer- Proximal duodenum
associated with severe burns trauma
Cushing ulcer- gastric, esophageal and
duodenal arising in patient with
intracranial injury, operation or tumor
Factors are shared with acute
gastritis- impaired oxygenation, NSAID
medication, decreased prostaglandin
Intracranial injury- direct stimulation of
vagal nerve- inc acid STRESSsplanchnic vasoconstriction(Splanchnic
vessels are blood vessels supplying and
draining viscera.
MORPHOLOGY
Stress ulcers- LESS THAN 1 CM USUALLY
Circular, brown base (extruded acid
digested blood) Margin and base are not
indurated Gastric rugal mucosa is
essentially normal Suffusion of blood
and inflammatory reaction maybe noted
No scarring and no thickened blood
vessels healing

Healing with complete reepithelialization days to several weeks

Complications of PUD
Bleeding Perforation Obstruction from

edema or scarring
*See table
Tumors
Benign:1. Polyp- nodule or mass
- mucosal polyp- non- neoplastic and
neoplastic
- gastric polyp are uncommon, but found
incidentally in biopsy
Non-neoplastic Polyps
HYPERPLASTIC (90 %) - mixture of
hyperplastic foveolar and cystic,
inflammatory cells glandular epithelium,
seen frequently in chronic gastritis
Adenoma/Adenomatous- proliferative
dysplastic epithelium, malignant potential
- Sessile (without a stalk) or
pedunculated (with stalk) commonly
antral location
Uncommon: fundic gland polyp, Peutzjeghers polyp, juvenile polyp,
hamartomatous polyp, inflammatory
fibroid polyp (eosinophilic granuloma)
Check for carcinoma bec. 40 % of
gastric adenoma contains focus of
carcinoma, specially larger lesions
GASTRIC CARCINOMA
MOST COMMON AND MOST IMPORTANT
MALIGNANT TUMOR OF THE STOMACH
Lauren classification:
Intestinal type- glandular structures
Diffuse type- poorly diff discohesive
malignant cells
FEATURES
Precursor lesion
Morphology
Incidence
Occurrence (*same now)
Pathogenesis
H. pylori infection- initially causes
chronic gastritis followed by atrophy
intestinal metaplasia, dysplasia,
carcinoma
- Increased genomic mutation and DNA
damage HOST (AUTOIMMUNE
GASTRITIS)WHO HISTOLOGIC CLASSIFICATION OF
GASTRIC TUMORS
EPITHELIAL TUMOR- Adenoma,
Adenocarcinoma, Small cell carcinoma
NON-EPITHELIAL- Leiomyoma ,
Schwannoma
17

Intesti

(+)
Glandu
65. y.o.
More co

MALIGNANT LYMPHOMA
Check on tableAlso FACTORS ASSOCIATED WITH
INCREASED INCIDENCE OF GASTRIC
CARCINOMA.
MORPHOLOGY
PYLORUS AND ANTRUM- (50-60%)
Cardia (25 %), body and fundus
(remainder) Lesser curvature
antropyloric region- favored site Greater
curvature- less common- most likely
malignant Early lesion-mucosa and
submucosa Advanced lesion- deeper
(through muscular wall
Exophytic flat or depressed excavated

Exophytic linitis plastica excavated

Intestinal type- neoplastic glands
resemble colonic adenocarcinoma, cells
with apical mucin vacuole and abundant
mucin in gland lumen
Diffuse type- no glands, individual cells
scattered (variant-signet ring) *if signet
ring cells are >50% of the tumor signet
ring cell carcinoma

Most common site for metastasisVirchow (supraclavicular sentinel) nodes

Metastasis to periumbillical areasubcutaneous nodule (SISTER MARY
JOSEPH NODULE)
Metastasis to one or both ovariesKRUKENBERG TUMOR
PROGNOSIS: depends on depth of
invasion extent of nodal and distant
metastasis
Other Tumors
Gastric lymphoma usually B Cell of
MALT, associated with chronic gastritis
and H. pylori
GASTROINTESTINAL STROMAL TUMORmesenchymal
- nerve cells- Schwannoma
- GIST( more common)- from
interstitial cells of Cajal (controls
gastrointestinal peristalsis) - c- KIT and
CD 34
Gastric Neuroendocrine Cell (Carcinoid)
Tumors from Enterochromaffin-like cells
(ECL) in the oxyntic mucosaHYPERGASTRINEMIC STATE
Lipoma- SUBMUCOSA
Metastatic carcinoma- systemic
lymphomas - lung and breast CA
metastasis mimics LINITIS PLASTICA
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