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43 Cards in this Set

  • Front
  • Back
What are the 2 areas at high pressure during rest?
upper ES - at cricopharyngeus
lower ES - 2-4 cm
What are the layers of the normal esosphagus
mucosal epithelium (SS)
lamina propria
muscularis mucosa
muscularis propria
What is the Z line?
irregular serrated junction between the SS and columnar epithelium

proximmal to the gastroesophageal by 2-3 cm
Esophageal Atresia
esophagus is thin, non-canalized
T-E fistula
associated with congenital heart disease

multiple forms - most common is upper eso ending in pouch with lower eso attached to trachea
- These kids regurgitate alot - predisposition to pneumonia

treat with surgery - with late complications of GERD and esophagitis
Ectopic Gastric Tissue
orange-red spots, post cricoid
remebles gastric mucosa with glands and a sharp border with surrounding SS epithelium

can ulcerate and become inflammed
Ectopic Pancreatic Tissue
aka pancreatic heteropia

located at GE junction in 15% of people

congenital and independent of Barrett's eso

not significant unless becomes neoplastic
Esophageal Webs
protrusions of mucosa into the lumen
usually in upper esophagus

SS epithelium with fibrous core
women over 40
causing episodic dysphagia
idiopathic or occuring after radiotherapy

Schatzki ring - in lover esophagus
Esophageal Stenosis
fibrous thickening of the esophageal wall, mainly the submucosa - atrophy of the muscularis. Epithelium may be ulcerated

caused by severe injury/inflammation with scaring, or GERD, scleroderma, or radiation

rarely caused by esophageal webs

progressive dysphagia - progressing to total obstruction
failure for LES to relax
lack of progressive peristalsis
increased LES resting tone

due to T cell mediated destriction of mysenteric ganglion cells

idiopathic or due to Chagas disease (trypanosoma cruzi) or Polio, diabetes, amyloidosis, sarcoidosis, surgery
Symptoms of Achalasia
progressive dilation of esophagus above LES
slightly increased risk for esophageal SCC
increased risk for Candida, diverticula, aspiration, GERD, peptic ulceration

Tx with esophagomyotomy
Pathogenesis of Achalasia
myenteric lymphocytic inflamation
marked depletion of ganglion cells in Auerbach plexux, replacement of nerves by fibrous tissue and muscle

squamous mucosa is hyperplastic with papillomatosis and basal cell hyperplasia (similar to GERD)
CD3 T cell present

DDx: visceral neuropathies, normal aging, psuedoachalasia
achalasia like syndrome
associated with neoplasms (adenocarcinoma)

also caused by scleroderma and amyloidosis
Hiatal Hernia
characterized by seperation of diaphragmatic crura and widening of th space between the muscular crura and the esophageal wall

sliding type is more common than the nonaxial type

increasing incidence with age
-heartburn or regurgitation made worse by bending forward, laying on back, and obesity

can ulcerate, bleeding, perforation, and strangulation of hernias
Lacerations (Mallory Weiss tear)
longitudinal tears at GE junction and in proximal gastric mucosa

due to severe retching associated with alcoholsm

can be mucosal or full thickness

support vasocontrictors, transfusions and balloon tamponade

Boerhaave syndrome - esophageal rupture - lethal
Esophageal Diverticula
- immediately above the LES
due to lack of coordination in peristalsis and LES relaxation
- causes regurgitation of massive amounts of fluid at night/aspiration

- near mid esophagus
-previously thought to be due to TB, mediastinal lymphadenitis and scarring
- due to motor dysfunction or congenital

Zenker's diverticulum
- above esophageal sphincter in posterior wall
- due to cricopharyngeal motor dysfunction or weakness
- food accumulates or is regurgitated and aspirated
- seen in the elderly
Esophageal Varices
dilated tortuous vessels develop from portal hypertension
collaterals in lower esophagus take blood diverted from portal vein through the coronary veins of the stomach into azygous veins into vena cava

hepatic schistosomiasis

can cause massive hemorrhage - 40% die on first episode of bleeding, 40% die on second bleed

Tx. with sclerotherapy/ballon tamponade

DDx: gastritis esophageal laceration, peptic ulcer
defined as epithelial damage and inflammation

Most common cause is GERD
-many causes for GERD, like CNS depressants, hypothyroidism, pregnancy, alcohol, tobacco, NG intubation, sliding hiatal hernia, delayed gastic emptying
pain may be mistaken for MI

long term consequences include minor bleeding, stricture, Barrett's esophagus, Barrett's ulcer.

due to chronic exposure to gastic juices impairs repair
bile reflux may be a factor

Dx with symptoms, pH monitoring, histology examination
Reflux Esophagitis
inflammatory cells in epithelial layer
basal cell hyperplasia
extension of the lamina propria
ballooned squamous cells
vascular dilation
intraepithelial eosinophils
What is the biopsy criteria for GERD?
increased thickness of the basal layer, increased height of the papillae, and inflammation with intraepithelial eosinophils
biopsies distal to the Z line in patients with GERD shows carditis

caused by H pylori gastritis and GERD

increases incidence of gastric cardia cancer
dysplasia rarely diagnosed
Barrett's esophagus
squamous epitlelium is replaced with columnar epithelium (and goblet cells) - more resistant to acid, pepsin and bile

major risk factor for adenocarcinoma
more common in med, CF patients, and after chemo

has a red velvety appearance
Dx by endoscopy and biopsy
Tx with antacid therapy and frequent endoschopy
Pathogenesis of Barrett's Esophagus
squamous epithelium is replaced by columnar cells and goblet cells

-goblet cells are definitive ID for Barretts Eso

lamina propria is fibrotic and it has mild chronic inflamation
muscularis mucosa is thickened
erosions/ulceration may mimic carcinoma
Barrett's related dysplasia
Barrett's is a precursor to esophageal adenocarcinoma
NOT linked to SCC

step-wise process of dysplasia
usually patchy and irregular, thickend, velvety mucosa
Barrett's low grade dysplasia
anti-reflux therapy and intensive surveilance
the bigger it is the higher chance of transforming to adenocarcinoma
Barrett's High Grade dysplasia
50% risk for invasive adenocarcinoma
on diagnosis rebiopsy to exclude missed carcinoma - consider esophagectomy

biopsy should be reviewed by a second experienced consultant
DDx of Esophageal Dysplasia
intramucosal adenocarcinoma

reactive inflammation (PMN's)
Eosinophilic Esophagitis
disease of childhood mostly
young caucasian males

increased frequency of diagnosis
Allergic Esophagitis in Children
resembles RE but pH tests show no acid in esophagus

does not respond to antacids

associated with dysphagia, failure to thrive, peripheral eosinophilia
High numbers of eosinophils in esophagus
-DDx - rule out relfux disease
Chemical Esophagitis
caused by ingestion of strong alkalis, acids, detergents, or chemotherapy

can turn into Barrett's esophagus - rarely SCC

mucosal or transmural injury with hemorrhage, necrosis, possible bacteral infectio
restricted to immunocompromised patients, diabetics, HIV, chemo, or transplant recipients

Mostly Candada, HSV, or CMV
Acute Esophagitis
manifested by increased neutrophils in the submucosa as well as in the squamous mucosa
most common cause of infectious esophagitis
immunocomprimised, and associated with antibiotic therapy

grey-white pseudomembrane or plaques in mid esophagus
mucosa is red and swollen, may be ulcerated
-- Thrush" --

densely atte pseudohyphae and budding spores, exudate, necrosis

positive for PAS and GMS
numerous inclusions atypical in HIv patients

look like unched out mucosal ulcers (similar to HSV)
virus present in endothelium and enlarged cells at ulcer base

Intranuclear inclusions surrounded by clear halo
macrophage aggregations

inclusions are NOT seen in SCC
opportunistic infection in IC patients

usually also have secondary bacterial and fungal infections

shallow vesicles and ulcers coalsce into extensive areas of erosion
ulcers have necrotic debris and exudates with neutrophils
inclusions IN multinucleates squamous cells at margins (different than CMV)
inclusions usually Cowdry type A, and ground glass inclusions
Esophageal Carcinoma
low incidence by numbers are increaseing
shifting from SCC to AC (equal occurrance)
usually presents as advanced/metastatic disease
Eitiology/Epidemiology of Squamous cell carcinoma
most common - adults over 50, and men
geographically high in Iran and Asia, south Africa, Eastern europe, and Puerto Rico

caused by Vit. A, C, thiamine, B6, riboflavin, zinc, molybdenum, nitrates, Betel nuts, tobacco

associated with achalasia, other SCC;s, chronic esophagitis, Plummer-Vinson syndrome, celiac disease, epidermolysis bullosa, radiation, HPV

begins in dysplasia
Symptpms/appearance of SCC
dysphagia, anorexia, weight loss

invasion of muscularis propria, adjacent structures, lymph node metastasis

protruded (usually), can also be flat or excavated

moderately to well differentiated
tumor clusters surround a main mass
focal glandular or small cell differentiation
progression from Barrett's esophagus
increasing in incidence
more common in men and whites
-- common in people with hiatal hernia, smokers, and alcohol users --
Symptoms/Appearance of Adenocarcinoma
invasion through wall often with lymph node involvement

distal esophagus with invasion of cardia
flat patches or nodular masses

moderate to well differentiated
next to Barretts with high grade dysplasia
Granular Cell Tumor
solitary in lower esophagus

treat with excision

look like sheets of uniform cells and abundant eosinophillic cytoplasm
most common benign tumor
small tumors near gastroesophageal junction

circumsised solitary mass
bulges into lumen, grey-white, and whorled
rarel ulcerated