Pathophysiology of
esophagus
The GIT
 1- esophagus
 2- peritoneal cavity
 3- stomach (1.5l)
 4- gastroesophageal
junction
 5- pylorus
 6- small intestine (4.5 – 6m)
 7- duodenum
 8- jejunum
 9- ileum
 10- ileocoecal valve
 11- large intestine
 ascendent
 transversal
 descendent colon
 rectum + anus
Esophagus - anatomy
 Upper sphincter
(cricopharyngeal
muscle)
 Upper 2/3 – skeletal
muscle, squamous
epithelium
 Lower 1/3 – smooth
muscle
 Lower sphincter
(LES)
 Cylindrical epithelium
in the terminal part
Esophageal diverticula
 true diverticula (traction) –
include muscular layer
 pseudodiverticula – only
mucous layer (e.g. Zenker
diverticulum)
 Combined diverticula
 Localization
 Pharyngoasophageal
 Midthoracic (epibronchial)
 Epiphrenic
true diverticulum pseudodiverticulum
Dysphagia
 Functional
 Inflammation in
gastroesophageal
reflux
 Sclerodermia
 Neuropathy (e.g. in
diabetes)
 Amyotrophic lateral
sclerosis
 Chagas disease
 Achalasia
 Obstructive
 Tumours
 Strictures
 Peptic ulcers
Esophageal achalasia
 The lower sphincter is incapable of relaxation
 This leads into esophageal dilatation and loss of
peristaltic movements
 The primary cause is the disorder of myenteric plexus
(plexus Auerbachi), which produces NO
 Most often, it is caused by autoimune destruction
Chagas disease
 Infection by Trypanozoma cruzi
 About 15 000 000 victims (mostly in latin America)
 Acute stage: local oedema (often paraorbitally)
 Chronic stage: megacolon, megaesophagus, malnutrition, Chagasic
cardiomyopathy, CNS involvment
Hiatal hernias
 sliding
 Lower esophageal sphincter
and upper part of stomach
slides into thoracic cavity
 Low external pressure in the
thoracic cavity leads into the
loss of function of LES and
gastroesophageal reflux
 paraesophageal
 Part of stomach‘s fundus is
squeezed into thoracic cavity
paralelly with esophagus
 This can lead into its
incarceration or strangulation
with necrosis (life-threatening)
 Mostly, it manifests by pain
and vomiting
Hiatal hernias – risk factors
 Wide hiatus
 Obesity
 High intraabdominal pressure
 Gravidity
Gastroesophageal reflux disease
(GERD)
 Retrograde movement of
gastric juice
 Loss of anti-reflux barrier
 LES
 Peristalsis
 Angle between esophagus and
fundus
 Aggressive action of HCl and
proteases (pepsin) cause
damage to the esophagus
 Sometimes, it occurs also in
healthy people
 Frequently accompanies sliding
hiatal hernia
GERD - symptoms
 Heartburn
 Chest pain (meal-related)
 Regurgitation – vomiting
 Dysphagia
GERD - complications
 Reflux esophagitis
 Peptic ulcers in esophagus
 Strictures
 Bleeding
 Barrett‘s esophagus (up to 10%)
 Tumours
Barrett‘s esophagus
 Intestinal metaplasia in chronic GERD
 Change in cellular diferentiation – squamous epithelium -> cylindrical
(columnar)
 Precancerosis (cca 10 times higher relative risk of adenocarcinoma)
 Other risk factors: alcohol intake, high HCl secretion, decrease in motility
Barret‘s esophagus in gastroscopy
Esophageal varices
 During portal hypertension
(caused by e.g. liver cirhosis, liver
tumour, portal thrombosis,
schistosomiasis), blood flows
through anastomoses between
portal and systhemic circulation
instead of through the liver
 That leads into remodelation of
these collaterals and forming of
varices
 They include esophageal varices,
hemorrhoidal varices, swelling of
paraumbilical veins („caput
Medusae“) and collaterals to vena
azygos in the retroperitoneum
Esophageal varices - complications
 Severe bleeding with melena and hematemesis
 Posthemorrhagic anemia
Esophageal varices Bleeding
Esophageal tumours
 Benign
 Leiomyoma
 Hemangioma
 Fibroma
 Malignant
 Adenocarcinoma
 Squamous cell
carcinoma
 Melanoblastoma
T-N-M classification