Pathology of esophageal diseases Flashcards
Non-neoplastic disorders of the esophagus:
Congenital and mechanical disorders:
- Agenesis
- Atresia
- diverticulum: Traction, Pulsion
- Hiatus hernia
Atresia
failure of canalization
Atresia: failure of canalization associated with
tracheo esophageal-fistula
Traction diverticulum:
external forces pulling on the wall
Pulsion diverticulum:
forcible distension
Pulsion diverticulum: e.g?
Zenker diverticulum
Hiatus hernia:
protrusion of upper part of stomach into thorax
via diaphragmatic orifice
Hiatus hernia:cause?
increased intra-abdominal pressure and loss of
diaphragmatic muscular tone with ageing
Hiatus hernia
Predisposing factors:
obesity, lifting heavy loads,
Sequnces of Hiatus hernia:
regurgitation of gastric contents and GERD
Ectopic gastric mucosa most commonly occurs in
upper third of
esophagus
Functional Esophageal obstruction
Abnormal contraction of esophageal muscle
Mechanical Abnormal contraction of esophageal muscle
- webs
- rings/Schatzki ring
Diff btw webs/rings
Webs: thin mucosal membrane that grows across the lumen
Rings or Schatzki ring: a ring of tissue near the end of esophagus
Webs e.g?
Plummer-Vinson syndrome
(Paterson-Brown Kelly syndrome):
Symptoms of
Plummer-Vinson syndrome (Paterson-Brown Kelly syndrome):
Dysphagia, Esophageal webs, Iron deficiency anemia, Angular stomatitis, Atrophic tongue, Brittle nails, Increased incidence of post-cricoid carcinoma
Plummer-Vinson syndrome (Paterson-Brown Kelly syndrome)
Cause?
unclear
Probable mechanisms include iron and nutritional deficiencies,
genetic predisposition, and autoimmunity
Rings or Schatzki ring:
ring of tissue near the end of esophagus
Achalasia (megaesophagus)
LES fails to relax/open → stays contracted → food unable
to pass to stomach → accumulates in lower esophagus → esophagus dilates
(megaesophagus)]
Achalasia (megaesophagus)
Symptoms
triad
1-Incomplete LES relaxation (stays closed),
2-Increased LES tone( contracted),
3-esophageal aperistalsis (no peristalsis)
Primary
Achalasia (megaesophagus)
failure of distal esophageal inhibitory neurons, idiopathic
Secondary
Achalasia (megaesophagus)
Degenerative changes in neural innervation
Secondary
Achalasia (megaesophagus) e.g?
Chagas disease
How Chagas disease can cause achalasia??
Trypanosoma cruzi infection causes destruction of the
myenteric plexus, failure of LES relaxation, and esophageal dilatation
Achalasia-like disease may be caused by:
o diabetic autonomic neuropathy
o infiltrative disorders such as malignancy, amyloidosis, or sarcoidosis
o lesions of dorsal motor nuclei, which may be produced by polio or surgical
ablation
Esophageal varices
localized dilatations of veins
Esophageal varices
Cause
Portal hypertension → results in a porto-systemic shunt → esophageal veins
become congested and dilated →Protrude into esophageal lumen → easily traumatised
by passage of food → acute hemorrhage
Esophageal varices complication
Acute hemorrhage
Esophageal varices
Commonly detected during
Endoscopy
Esophageal lacerations / mucosal injury
Mallory-Weiss tears (most common)
Boerhaave’s syndrome
Mallory-Weiss tears often induced by
severe retching or vomiting or violent coughing
Mallory-Weiss tears
pathophysiology
reflex relaxation of the gastroesophageal musculature
fail during prolonged vomiting, with the result that refluxing
gastric contents cause the esophageal wall to stretch and tear
Mallory-Weiss tears Patients usually present with
hematemesis
Mallory-Weiss tears result in
linear lacerations (superficial and heal quickly without surgical intervention) → longitudinally oriented and usually cross the gastroesophageal junction (lower esophagus)
Boerhaave’s syndrome
Results in
severe transmural esophageal tears (catastrophic and require surgical
intervention)
Boerhaave’s syndrome lead to
Mediastinitis ,
Subcutaneous emphysemia
Boerhaave’s syndrome
Symptoms
Mack let’s triad
- vomiting
- chest pain
- SC emphysemia
Esophagitis
Non-infectious:
▪ Reflux ▪ Barret’s ▪ Eosinophilic ▪ Extremely hot drinks ▪ Chemical (pill, chemotherapy, radiation, acids, alkali, alcohol):
Non-infectious:
▪ Chemical
generally causes
only self-
limited pain, particularly odynophagia (pain with swallowing)
Pill induced esophagitis
Most commonly pills
- doxycycline
- bisphosphates
Esophagitis
Infectious
common in——,
can be primary or———-
immunocompromised
complicate a preexisting ulcer
Infectious esophagitis
Viral?
Fungal?
Others?
- HSV ,CMV
- candida, mucormycosis, aspergillosis
- Tuberculosis, Crohn’s disease
Candidiasis
adherent, gray-white pseudo membranes composed of densely matted
fungal hyphae and inflammatory cells covering the mucosa
Reflux esophagitis aka
gastroesophageal reflux disease (GERD) → (reflux of gastric juices)
gastroesophageal reflux disease (GERD)
Causes
Decreased LES tone, increased abdominal pressure, Delayed gastric emptying and increased gastric volume , Alcohol and tobacco use, Chocolate / fatty foods, Obesity, CNS depressants, Pregnancy, Hiatal hernia,
GERD Pathogenesis:
gastric acid + pepsin+ refluxed bile
GERD
Morphology (histo):
hyperaemia,
linear streaks (erosions, ulcers),
hyperplasia of epithelium and thickened basal layer,
elongated sub-epithelial papillae,
mixed inflammatory cells with scattered eosinophils (few)
GERD common at — yrs
40
GERD symptoms
Heartburn, dysphagia, sour-tasting gastric contents
Rarely: attacks of severe chest pain (may be mistaken by heart disease)
GERD treatment
proton pump inhibitors (reduces gastric acidity for symptomatic relief)
GERD complications
esophageal ulceration, hematemesis, melena (bloody/black stool), stricture development, Barrett esophagus
Barret esophagus (complication of chronic GERD) Characterized by
1-Intestinal metaplasia : change of normal esophageal epithelium [strat squamous] to intestinal [simple
columnar w/ goblet cells]
2-epithelial dysplasia
change of normal esophageal epithelium [strat squamous] to intestinal [simple
columnar w/ goblet cells] especially in
distal esophagus
Barret esophagus affect
White males; 40 and 60 years
Barret esophagus increases risk of
esophageal adenocarcinoma
Barret esophagus
Gross:
Tongues or patches of red,
velvety mucosa extending upward from the
gastroesophageal junction (indicates change to intestinal epithelium)
Barret esophagus
histology:
presence of goblet cells in esophageal mucosa
Goblet stain
Alcian blue stain shows the
blue- staining intestinal goblet cells) → DIAGNOSTIC
Barret esophagus
diagnosis:
- abnormal mucosa above the GE junction (endoscopy) and
- histologically documented gastric or intestinal metaplasia (biopsy) needed for diagnosis
- symptoms of GERD
epithelial dysplasia
preinvasive lesion that develops in 0.2% to 1% of individuals with Barrett esophagus
➢ low grade or high grade or Intramucosal carcinoma
What is recommended to do with patients w/ barret esophagus
screening for dysplasia
high-grade dysplasia and intramucosal carcinoma, always require therapeutic
intervention
Eosinophilic esophagitis
➢ Chronic immunologically mediated disorder
Eosinophilic esophagitis
Symptoms
Food impaction, dysphagia, feeding intolerance
➢ Patients also have atopy, atopic dermatitis, allergic rhinitis, asthma, peripheral
eosinophilia
Eosinophilic esophagitis
Gross: Endoscopy reveals
circumferential rings
Eosinophilic esophagitis
Histology:
Infiltration by numerous eosinophils in proximal esophagus (much more
than GERD)
Eosinophilic esophagitis
Treatment
Poor response to proton pump inhibitors (treated w/ dietary restrictions)
Most common Benign esophageal tumors:
Leiomyomas (smooth muscle)
Rarer Benign esophageal tumors:
lipomas, hemangiomas, fibromas
Benign esophageal tumors:
Squamous papilloma: linked to
human papilloma virus (HPV)
Malignant esophageal tumors (cancers)
- Esophageal squamous cell carcinoma (SCC) (most common)
- Esophageal adenocarcinoma (AC)
- Keratosis palmoplantaris (tylosis) / esophageal cancer syndrome
- Metastatic neoplasms to esophagus
Esophageal squamous cell carcinoma (SCC)
More common in:
Affects:
Asia and Africa
adults older than 45 years, M:F=4:1, six times more in African Americans than whites
Esophageal squamous cell carcinoma (SCC)
risk factors:
alcohol, tobacco,
poverty,
caustic esophageal injury,
achalasia,
Plummer-Vinson syndrome,
frequent consumption of very hot beverages,
radiation therapy, Vitamin and mineral deficiencies, Lye strictures, Viruses (HPV 16, 18),
Genetic factors (Palmoplantar keratoderma /Tylosis)
Esophageal squamous cell carcinoma (SCC) mostly occurs in
middle third of esophagus
Esophageal squamous cell carcinoma (SCC)
gross
❖ Early lesions
: small, gray-white plaque like thickenings (superficial)
Esophageal squamous cell carcinoma (SCC)
gross
❖ Later:
polypoid,
ulcerated or diffusely infiltrative lesions that
spread within esophageal wall, where they can cause thickening, rigidity, and
luminal narrowing
Esophageal squamous cell carcinoma (SCC)
histology
normal squamous epithelium and mild, moderate, or severe esophageal
squamous dysplasia
Esophageal squamous cell carcinoma (SCC)
symptoms
dysphagia to solids [80%], odynophagia (pain on swallowing), obstruction,
extreme weight loss (as consequences of both impaired nutrition and tumor-associated
cachexia), hemorrhage and sepsis (due to tumor ulceration)
Esophageal adenocarcinoma (AC) Seen in
In the western world (USA, UK, Canada, Australia), incidence of SCC has reduced and AC
is higher
- Esophageal adenocarcinoma (AC)
Arises in a background of
Barrett esophagus and long-standing GERD
Esophageal adenocarcinoma (AC)
➢ risk factors:
Affect?
documented dysplasia, tobacco, obese, radiation therapy
➢ whites; M:F = 7:1
Esophageal adenocarcinoma (AC)
➢ pathogenesis
Barret esophagus progresses to AC
through the stepwise acquisition of genetic and
epigenetic changes (chromosomal abnormalities and
TP53 mutation are often present in early stages)
