Transcript THE GASTROINTESTINAL TRACT (GIT)

GASTROINTESTINAL
PATHOLOGY
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ESOPHAGUS
• Location: posterior mediastinum
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• Distensible muscular tube
• 23-25 cm in length
• Upper esophageal sphincter & lower
esophageal sphincter
• Mucosa, submucosa, muscularis propria
• Transports food & liquids from pharynx to
stomach
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ESOPHAGUS: CONGENITAL ANOMALIES &
CONSTRICTIONS
• Atresia =
noncanalized
segment of
esophagus
• Fistula = connection
between esophagus
& trachea
•Hazards:
aspiration, pneumonia & suffocation
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ESOPHAGUS: CONGENITAL ANOMALIES &
CONSTRICTIONS
•Webs & Rings: Main Sx: dysphagia
•Uncommon, mid age women of unknown etiology
•Ledge- like mucosal protrusions
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• Webs:
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• Upper esophageal
mucosal narrowings
• Plummer-Vinson/
Paterson- Brown-Kelly
synd Perimenopausal
female + anemia +
glossitis  risk
esophageal ca
Schatzki’s rings:
Lower gastroesophageal
junction
narrowings
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MC acquired (MCC: GE reflux, chemical injury,
scleroderma, & radiation injury)
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ACHALASIA
• Aperistalsis, failure of relaxation of LES &
inc resting tone of LES  dysphagia,
regurgitation, & esophageal dilatation
• Predisposes to:
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Aspiration pneumonia
Candida esophagitis
Diverticula
Ca (~ 5%)
• MC is primary (neuronal degeneration): in
young adults, remains for life
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ACHALASIA
• 2o achalasia:
– Chagas’ dse (T. cruzi)
– Lesions of vagal motor nuclei
– Diabetic autonomic neuropathy
– Infiltrative disorders
• Morphology: progressive esophageal
dilatation above LES, & diminished
myenteric ganglia
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HIATAL HERNIA
• Upward protrusion of
part of stomach
through diaphragmatic
(esophageal) hiatus
• Clinically:
• Affects up to 20% of
adults
• <10% symptomatic
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Complications:
Reflux esophagitis
Ulceration
Bleeding
Perforation
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HIATAL HERNIA patterns:
• Sliding hiatal
(>90%) px
stomach slides
through a widened
hiatus
• Rolling/
paraesophageal
(<10%) part of
stomach (fundus)
herniates alongside
esophagus into
thorax, vulnerable
to strangulation,
may be caused by
previous sx
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MALLORY-WEISS
SYNDROME
• Lacerations at GE junction
• 2o episode of excessive vomiting + spasm
of LES
• MC in alcoholics
• Clinical: 5-10% of UGI bleeding
– Mallory-Weiss tears hematemesis
• Morphology: irregular longitudinal tear in
EG junction. May involve only mucosa, or
may rarely penetrate wall
– Tear penetrates all layers (Boerhaave’s synd)
mediastinitis or peritonitis
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ESOPHAGEAL VARICES
• Collateral bypass channels in lower
part of esophagus between branches
of left gastric vein & azygos veins
• Seen in long-standing portal HPN
(alcoholic cirrhosis- 90%)
• Morphology: Tortuous, dilated veins
w/in submucosa of lower esophagus,
raising the mucosa & tend to rupture
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ESOPHAGEAL VARICES
• Clinically:
• Asymptomatic until rupture 
catastrophic bleeding (hematemesis
& melena)
• Rarely subsides spontaneously
• 40-50% fatality rate for each episode
of bleeding
• 90% chance of recurrence in
survivors
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ESOPHAGITIS
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Incidence: 5% adults (US), 80% (Iran)
Predisposing Factors:
Reflux of gastric contents (reflux esophagitis)
Infections (immunosuppressed patients)
Ingestion of irritants: alcohol, hot tea, smoking
Uremia
Ca chemotx, Radiotx
Prolonged gastric intubation
Systemic desquamative disorders: pemphigoid
GVH dse
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REFLUX ESOPHAGITIS
• Clinical Features
• 24 hr pH studies:
– pH <4 > 4.5% of the
time
• Predisposing factors:
– LES tone, hiatal hernia
– Heartburn &
regurgitation
– Hematemesis or melena
– Strictures  dysphagia
– Barrett’s esophagus
• Morphology:
• Hyperplasia
• Elongation of
papillae
• Intraepithelial eos
• Ulceration & hge in
severe cases
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BARRETT’S ESOPHAGUS
• Squamous ep replaced by columnar ep w/
intestinal metaplasia (goblet cells)
• Long- segment Barrett’s esophagus =
>2cm segment 30- 40 fold inc risk of
adenoca
• Short- segment Barrett’s esophagus =
<2cm segment  some inc risk of
adenoca
• Columnar ep w/o goblet cells =
“columnar lined esophagus w/o intestinal
metaplasia”  significance ?
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BARRETT’S ESOPHAGUS
• Pathogenesis:
• Long-standing GERD  damage to
the squamous ep  repair 
proliferation of pleuripotent basal
cells  differentiate into gastric type
ep (mucus-secreting cells) 
mutations  intestinal metaplasia
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ESOPHAGEAL
ADENOCARCINOMA
• ~50% of esophageal Ca (USA)
• Clinically:
– arise in Barrett’s patients w/ long standing GE
reflux dse (GERD)
– dysphagia, wt loss, bleeding
– overall 5-year survival is 15%
• Mostly in distal 1/3 of esophagus
• Gross: polypoid, ulcerative or infiltrative
• Histologic types: tubular (intestinal),
signet ring cell
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SQUAMOUS CELL
CARCINOMA
• M>F, >50 y/o, highest
incidence in Asia, 90%
of esoph Ca worlwide
• Related to:
• Upper 1/3- 20%
• Middle 1/3- 50%
• Lower 1/3- 30%
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cigarette smoking
Alcohol
Nitrosamines
fungus contaminated
foods
– nutritional deficiencies
– HPV
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SQUAMOUS CELL
CARCINOMA
• Mode of Spread:
– Local- into mediastinal structures
– Submucosal lymphatics to nearby LN
• Insidious onset:
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Dysphagia
weight loss
Hemorrhage
TE fistula
• Overall 5-yr survival: 5%
• Pathologic staging - best indicator of
prognosis for esophageal ca
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