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Pathology of Peptic Ulcer

Normal
Stomach
Esophagus & Stomach Normal
Benign tumors
usually small, polypoid and
asymptomatic, but may be confused
with malignancies
Most common- leiomyomas – GIST
Smooth muscle tumors
Leiomyoma
Most common benign tumor of
esophagus
Minute tumors 1-2 mm are often near
the gastroesophageal junction and are
asymptomatic
Median age 35 years,
2/3 men
Gross
Circumscribed, mural, solitary mass,
2-5 cm, bulges into lumen,
may be polypoid;
gray-white and whorled cut surface;
Micro
similar to classic leiomyomas;
circumscribed lesion
composed of intersecting fascicles of
bland spindle cells with variable fibrosis
Other benign tumors
Fibromas
Lipomas
Hemangiomas
Neurofibromas
Lymphangiomas
Fibrovascular polyps
Squamous papillomas
Inflammatory polyps
Esophageal Carcinoma
shift from squamous cell carcinoma
arising in upper/middle third of
esophagus to adenocarcinomas arising
in distal esophagus
Since most patients are asymptomatic
during early stages, they often present
with advanced or metastastic disease
Metastases usually to liver, lungs,
pleura
Squamous cell carcinoma

Most common type of esophageal


cancer
Highest incidence in northern Iran,
northern China (? due to polycyclic
aromatic hydrocarbons,
Causes
deficiency of
vitamins A, C, thiamine, B6, riboflavin
zinc, molybdenum;
fungal contamination,
nitrates / nitrosamines,
Betel nuts,
alcohol, tobacco, urban environment
Other causes

achalasia,
corrosive strictures,
long standing esophagitis,
Plummer-Vinson syndrome,
HPV in high risk regions
Symptoms
Usually men age 50+ in low risk areas;
more common in blacks (4:1) in US
dysphagia, anorexia, weight loss (due
to advanced stage at presentation)
90% in mid/lower esophagus
Often multifocal
Most present with invasion into
muscularis propria
Gross
(a) deep irregular ulcers with nodular
margins that may perforate and enter
trachea, aorta or mediastinum;
(b) gray-white plaque-like thickenings
of mucosa that cause thick, rigid
esophageal wall and luminal narrowing
or
(c) polypoid exophytic lesion
Esophageal Carcinoma
Micro
most are moderate to well
differentiated;
tumor clusters may exist several cm
from main mass due to lymphatic
spread through submucosa ;
may have focal glandular or small cell
differentiation or lymphoid stroma
Superficial squamous cell
carcinoma
Tumor confined to mucosa and submucosa (T1)
regardless of lymph node status
Intramucosal tumors have no lymph node
involvement vs. 30% of submucosal tumors
Account for 20% of resections in US/Western
Europe
Patients may also have bronchial or
oropharyngolaryngeal carcinoma
5 year survival is 85% without vs. 40% with
nodal involvement
Gross:
polypoid masses,
thin plaques or
eroded mucosal depressions
Micro:
invasive nests with irregular borders
Staging (clinical and
pathologic)
Primary tumor (T)
TX: primary tumor cannot be assessed
T0: no evidence of primary tumor
Tis: carcinoma in situ
T1: tumor invades lamina propria or
submucosa
T2: tumor invades muscularis propria
T3: tumor invades adventitia
T4: tumor invades adjacent structure
Regional lymph nodes (N)
 
NX: regional lymph nodes cannot be assessed
N0: no regional lymph node metastases
N1: regional lymph node metastases
Distant Metastasis (M)
 
MX: distant metastasis cannot be assessed
M0: no distant metastasis
M1: distant metastasis 
 
Stage grouping and 5 year
survival
Stage 1 : T1 N0 M0, 80-90%
Stage 2A: T2 or T3, N0 M0, 40-50%
Stage 2B: T1 or T2, N1 M0, 25-40%
Stage 3 : T3 N1 M0 or T4 any N M0,
15-25%
Stage 4 : Any T, any N, M1, < 5%
Stage 4a: Any T, any N, M1a
Stage 4b: Any T, any N, M1b
Features to report

Tumor type
Histologic grade
Depth of invasion
Tumor size
Anatomic site
Angiolymphatic
invasion
Contd…

Perineural invasion
Margin involvement (proximal, distal, radial)
Lymph node involvement (total involved,
total examined)
Other features (esophagitis, Barrett’s
esophagus, dysplasia, specific types of
infection)
Adenocarcinoma
30-40% of primary esophageal cancers;
increasing incidence over past 20 years for
unknown reasons
Previously confused with gastric carcinomas,
particularly in lower 1/3 of esophagus
Age 40+, median 50’s, usually white men
In Barrett’s esophagus patients, 73% had
hiatal hernia, 63% were smokers, 45%
alcohol users
Tend to invade via submucosal
lymphatics, emphasizing importance of
margin evaluation
Similar prognosis as squamous cell
carcinoma when grouped by stage
Gross
usually distal esophagus with invasion
of gastric cardia;
appear as flat patches to nodular
masses
Deep ulcerative lesions
Micro
Mucin producing glandular tumors
Intestinal type features
Signet ring cells – gastric types – less
common
Clinical features
Over 40 yrs
More common in men
More in whites
Dysphagia
Progressive weight loss
Bleeding
Chest pain
vomiting
Prognostic factors
depth of invasion,
lymph node metastases,
status of resection margins
Mucosal protection
(a) mucus secretion: mucus is relatively
impermeable to H+;
also fluid with acid or pepsin exits
gastric glands as “jets” and penetrates
surface mucus layer without contacting
surface epithelial cells
(b) bicarbonate secretion creates pH
neutral microenvironment adjacent to
cell surface
(c) intercellular tight junctions prevent back-
diffusion of H+; disruptions are quickly
repaired
(d) rich blood flow supplies bicarbonate and
nutrients and removes acid
(e) muscularis mucosa limits injury; if intact,
repair occurs in hours/days vs. weeks if not
intact
Acute gastritis
Acute mucosal inflammatory process,
usually transient
May be accompanied by local
hemorrhage or mucosal sloughing
Severe erosive disease may cause
acute GI bleeds
Associated with heavy use of NSAIDs
(non-steroidal anti-inflammatory drugs,
including aspirin),
excessive alcohol use,
heavy smoking,
cancer chemotherapy,
bile reflux,
uremia,
systemic infections (Salmonella),
severe stress (trauma, burns, surgery),
ischemia and shock,
acid/alkali ingestion as part of suicide attempts,
gastric irradiation
mechanical trauma (nasogastric tube), distal
gastrectomy
Major cause of massive hematemesis in
alcoholics
Occurs in 25% of those who take daily aspirin for
rheumatoid arthritis
Acute Gastritis
Acute Esophagitis & Gastritis
Micro:
mild:
modest edema of lamina propria,
slight vascular congestion, intact
epithelium,
scattered neutrophils;
severe:
erosion and hemorrhage in mucosa
Symptoms:
none, or
Pain in epigastrium
nausea and vomiting
Hemorrhage & massive hemetemesis
melena
Chronic gastritis
Chronic mucosal inflammatory changes
leading to mucosal atrophy and epithelial
metaplasia, usually without erosions
Most cases are type B or non-autoimmune
gastritis

Increases with age; in Europe/Japan, affects


50% at age 60+
Histology does not correlate well with
symptoms
Associations
Chronic Helicobacter pylori infection,
toxins (alcohol, tobacco),
reflux of bilious duodenal secretions
(post-antrectomy or other),
obstruction (bezoars, atony),
radiation
Helicobacter pylori gastritis
Present in 90% with chronic gastritis
affecting the antrum
non-spore forming, curvilinear gram
negative rod, 3.5 x 0.5 microns
Colonizes 50% of asymptomatic
American adults by age 50; 80% of
Puerto Rican adults
Most people with H. pylori infection in
North America have gastritis but no
symptoms
Has adapted to niche provided by
gastric mucus by
motility (flagella) to swim through
viscous mucous,
urease to buffer gastric acid,
adhesin to bind to gastric epithelial
cells (better binding with cells that
express type O antigen)
H. pylori sits on surface or in lumen,
needs acid to survive, otherwise urease
causes pH to be too high
Biopsy - Toludine blue stain, silver stain
Urease test, Breath test.
Helecobacter pylori
Micro

Present in superficial mucus layer and


along microvilli of epithelial cells;
are NOT invasive;
are usually not seen in areas of
intestinal metaplasia;
associated with chronic inflammatory
infiltrate with germinal centers (follicular
gastritis) and plasma cells in lamina
propria;
Peptic ulcer disease
Ulcers: breach in mucosa of GI tract
Extends from muscularis mucosae into
submucosa or deeper
Peptic ulcer: chronic, usually solitary,
due to acid-peptic juices
Remitting relapsing lesions
Middle aged to older adults
M : F – 3 : 1 for duodenal ulcers
2 : 1 for gastric ulcers
Sites:
Duodenum – 1st part
antrum,
GE junction,
margins of gastrojejunostomy,
adjacent to Meckel diverticulum
containing ectopic gastric mucosa,
lower esophagus
Causes:
Imbalance b/w mucosal defense mech &
damaging forces
mucosal injury due to
Helicobacter pylori infection – all duodenal
ulcers & 2/3 rd gastric ulcers
NSAID use,
alcohol, bile/pancreatic juice reflux
smoking, corticosteroids use,
Zollinger-Ellison syndrome (multiple peptic
ulcerations in stomach, duodenum and
jejunum due to excess gastrin secretion by
a tumor),
Impaired defenses –
ischemia,shock Hyperacidity present in
a minority of duodenal ulcers and only
rarely in gastric ulcers
Gross
usually < 4 cm,
Round to oval, punched out defect
clean base (due to peptic enzymes),
surrounded by erythematous mucosa
Presence of thrombosed artery or blood
vessel at base
Scarring – puckering of surrounding mucosa
Micro
gastritis; H. pylori;
Ulcer may be transmural or limited to
mucosa and submucosa
4 zones in active ulceration-
1) thin layer of necrotic debris
2) nonspecific acute inflammation
3) granulation tissue
4) fibrosis
Clinical features
Epigastric pain – burning or aching
worse at night
Usually 1 to 3 hrs after meals
Relieved by alkalis or food
Referred pain- back or lt upper quadrant
Anemia
Frank hemorrhage
Perforation
Nausea, vomiting, belching, wt. loss
Gastric Ulcer
Peptic ulcer - Endoscopy
Duodenal Peptic Ulcer
Gastric Ulcer
Gastric Ulcer
Gastric Ulcer
Benign Vs Malignant ulcer
Young adults Older age
Duration – wks or years Wks or months
Normal or hyperacidity
Locatn- lesser curvature -
Normal or hypoacidity
pre or pyloric
Size < 4 cm Greater curvature pre or
pyloric region
Punched out edges
Usually >4 cm
Positive response to
antacids
Rolled out edges
No response to antacids
Complications

Bleeding- frequent & life threatening


Perforation
Obstruction from - Edema or scarring
Pain – excessive
Perforation:
Acute gastric ulcer
Causes:
NSAIDs, steroid use,
severe physiologic stress (shock,
extensive burns, sepsis, severe trauma,
increased intracranial pressure, post-
intracranial surgery, intensive care unit),
post-chemotherapy,
post-radiation therapy
Stress ulcers
Cushing ulcers:
ulcers in esophagus to duodenum
associated with intracranial injury or
surgery;
have high incidence of perforation
Curling ulcer: stress ulcer in proximal
duodenum associated with severe
burns or trauma
Stress ulcers heal in days-weeks
Morphologic types of
Carcinoma Stomach
Fungating

Ulcerating

Diffuse
Fungating Carconoma Stomach
Gastric Adenocarcinoma
Linitis Plastica – Schirrhous
Carcinoma diffuse.
Spread of Gastric Ca
“You get ulcer, not from what you eat,
but from what’s eating you..!”
Toludine Blue stain – H pylori
Urease production test
Hmmmm……… H.pylori

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