This document presents in a very organized and easily accessible way all the informations about diseases and pathology of the gastrointestinal tract. It contains images that facilitate learning. Is has all the informations presented in Robbins and Cortan Pathologic Basis of Diseases.
The liver, the gallbladder, the pancreas, the gastrointestinal tract
4 de abril de 2022
31
2021/2022
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Temas
disease
medicine
pathology
gastrointestinal
esophagus
stomach
illness
histology
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The Gastrointestinal Tract
[Congenital Abnormalities]
ESOPHAGUS
ESOPHAGEAL OBSTRUCTION
Structural (mechanical) obstruction or functional obstruction (caused by disruption of peristaltic
contractions)
Nutcracker esophagus: loss of coordination of inner circular layer and outer longitudinal layer
smooth muscle high-amplitude contraction of the distal esophagus
Diffuse esophageal spasm: repetitive and simultaneous contractions of distal esophagus
Hypertensive lower esophageal sphincter: lower sphincter dysfunction (high resting pressure of
incomplete relaxation), WITHOUT altered patterns of contraction
Esophageal dysmotility epiphrenic diverticulum (above the lower sphincter)
Impaired relaxation or spasm of the cricopharyngeal muscle Zenker (or pharyngoesophageal)
diverticulum (above the upper sphincter)
o In ages >50 yo
o Can accumulate food mass production regurgitation and halitosis
Mechanical obstruction causes: progressive dysphagia ( starts with inability to swallow solids)
Esophageal stenosis (lumen narrowing): benign
o Caused by chronic gastroesophageal reflux or irradiation inflammation and scarring
fibrous thickening of the submucosa atrophy of the muscularis propria and
secondary epithelial damage
Esophageal mucosal webs
o Idiopathic ledge-like protrusions of the mucosa, composed of fibromuscular connective
tissue and overlying epithelium, semi-circumferential lesions
o In women >40 yo
o Associated with gastroesophageal reflux, chronic graft-versus-host disease or blistering
skin disease
o In the upper esophagus: mucosal webs + iron deficiency anemia + glossitis + cheilosis
Paterson-Brown-Kelly or Plummer-Vinson syndrome
o Symptoms: nonprogressive dysphagia associated with incompletely chewed food
Schatzki (or esophageal) rings:
o Circumferential lesions
o Include the mucosa, submucosa , and hypertrophic muscularis propria
o A rings: covered by squamous mucosa, located above the gastroesophageal junction
o B rings: contain gastric cardia-type mucosa, located at the squamocolumnar junction
ACHALASIA
Triad: incomplete LES relaxation + increased LES tone + esophagus aperistalsis
Normal relaxation of lower esophageal sphincter (LES) caused by: release of NO and vasoactive
intestinal polypeptides from inhibitory neurons, and interruption of normal cholinergic signaling
Primary achalasia: distal esophageal inhibitory neuronal ganglion degeneration
o Increased tone and inability to relax the LES
o Degeneration of the extraesophageal vagus nerve
, Secondary achalasia
o In Chagas disease, caused by Trypanosoma cruzi infection destruction of myenteric
plexus, peristalsis failure, and esophageal dilation
o Associated immune-mediated destruction of inhibitory esophageal neurons: with HSV1
infection or Sjögren syndrome
Treatment: laparoscopic myotomy, pneumatic balloon dilation, botulinum neurotoxin (Botox,
inhibit LES cholinergic neurons)
ESOPHAGITIS
LACERATIONS
Mallory-Weiss tears:
o Longitudinal mucosal tears ranging from mm too cm, near the gastroesophageal
junction (Can also be located in proximal gastric mucosa
o Caused by retching and vomiting secondary to acute alcohol intoxication
o Causes upper GI bleeding (hematemesis)
Boerhaave syndrome
o Less common, more serious
o Transmural tearing and rupture of distal esophagus
o Causes severe mediastinitis and severe chest pain (mistaken for MI)
o Requires surgery
CHEMICAL AND INFECTIOUS
Damage of the mucosa caused by: alcohol, acids or alkalis (secondary to accidental ingestion of
household cleaning products by children), hot fluids, smoking
Pill-induced esophagitis: mucosal injury caused by dissolved medication in the esophagus rather
than in the stomach, located at site of strictures
Iatrogenic esophagitis: caused by chemotherapy, radiation therapy, graft-versus-host disease
Symptoms: odynophagia (pain on swallowing), hemorrhage, stricture, perforation
Infections mainly caused by HSV (in healthy individuals), also by CMV and fungi (in
immunocompromised)
Histology
o Dense neutrophils infiltrates (but NOT in chemicals-induced injury)
o With irradiation: intimal proliferation and luminal narrowing of submucosal and mural
blood vessels (radiation-induced vascular damage)
o Infections: pathogenic organisms invade the lamina propria cause ulcers (containing
nonpathogenic oral bacteria) and necrosis of overlying mucosa
o Candida: gray-white pseudomembrane (fungal hyphae and inflammatory cells covering
the mucosa)
o Herpes viruses punched-out ulcers, nuclear viral inclusions with degenerating
epithelial cells at the margin of the ulcer
o CMV shallow ulcerations, inclusions within the capillary endothelium and stroma cells
o G-V-H disease: basal epithelial cell apoptosis, mucosal atrophy, submucosal fibrosis, NO
inflammatory infiltrates
REFLUX ESOPHAGITIS
Submucosal glands secrete mucin and bicarbonate protect mucosa from acidity
LES tone prevents reflux of acidic gastric content
Gastroesophageal reflux disease (GERF): most frequent cause of esophagitis
o Caused by decrease LES tone or increased intraabdominal pressure (coughing, bending,
straining)
, o Associated with alcohol, tobacco, obesity, CNS depressants, pregnancy, hiatal hernia
Histology:
o Sometimes only hyperemia (redness)
o Eosinophils followed by neutrophils infiltration in the mucosa
o Basal zone hyperplasia (>20 % of epithelial thickness), elongation of lamina propria
papillae (extend into upper thirds of the epithelium)
Clinical features
o Most common in individuals >40 yo
o Heartburn, dysphagia, and regurgitation of sour-tasting gastric content
o Chronic GERD: severe chest pain (mistaken for MI)
Complications: ulceration, hematemesis, melena, stricture, Barrett esophagus
Hiatal hernia:
o Symptoms similar to GERD: heart-burn, regurgitation of gastric juices
o Separation of diaphragmatic crura and protrusion of stomach into the thorax through
the resulting gap
EOSINOPHILIC ESOPHAGITIS
Abundant intraepithelial eosinophils, mainly superficially
Unlike GERD
o NO prominent acid reflux
o NO relief with high doses of proton pump inhibitors
Atopic symptoms: atopic dermatitis, allergic rhinitis, asthma
ESOHAGEAL VARICES
Portal hypertension collateral channels (varices) development where portal and caval
systems communicate submucosal (and subepithelial) congested venous plexus
Caused by
o Cirrhosis associated with alcoholic liver disease
o Hepatic schistosomiasis
Varices: dilated veins within the submucosa of the distal esophagus and proximal stomach
o Collapse in the absence of blood (not visible postmortem)
Variceal rupture hemorrhage into the esophageal wall ulcerated and necrotic mucosa
o Lead to death most of the times
Prophylaxis with beta-blockers reduce portal blood flow reduce risk of hemorrhage
BARRETT ESOPHAGUS
Is a complication of GERD
Intestinal metaplasia within the esophageal stratified squamous mucosa, with goblet cells
Precursor lesion to cancer increases the risk of developing esophageal adenocarcinoma
o But most individuals DO NOT develop esophageal tumors
Histology
o Several patches of red/velvet mucosa extending upward from the gastroesophageal
junction
o Mucosa: alternation between pale squamous (esophageal) and brown columnar (gastric)
o Goblet cells: mucous vacuoles, pale blue on H&E stain
When dysplasia is present
o Atypical mitoses, nuclear hyperchromasia, irregular clumped chromatin, increased
nuclear-to-cytoplasm ratio, no epithelial cells maturation
o High-grade: more severe cytologic changes, abnormal glands (irregular shapes, budding,
glands-within-glands or cribriform shapes)
, Progress epithelial cells invade the lamina propria --> intramucosal (invasive)
carcinoma
Arrow: transition from Barrett metaplasia to low-grade dysplasia (nuclear stratification and
hyperchromasia)
Gland-within-gland in high-grade dysplasia
ESOPHAGEAL TUMORS
Adenocarcinoma or squamous cell carcinoma (more common)
Leiomyoma: mesenchymal tumor, most common benign tumor of the esophagus
Diagnosis usually takes place after lymphatic infiltration (late stage)
ADENOCARCINOMA
Mainly arise from Barrett esophagus
Most common in men
Risk factors
o Obesity-related GERD Barrett esophagus
o Tobacco use, radiations
Reduced risk with:
o Diet rich in fresh fruits and vegetables
o H. pylori infection (cause gastric atrophy reduced acid secretion and reflux reduce
incidence of Barrett esophagus)
Barrett esophagus dysplasia invasive carcinoma + genetic and epigenetic mutations (in
early stages: TP53 mutation, and CDKN2A or p16/INK4a downregulation by hypermethylation)
adenocarcinoma
Histology
o In the distal third of the esophagus, and may involve the gastric cardia
o Flat or raised patches of around 5 cm in intact mucosa
o Barrett esophagus adjacent to the tumor
o Tumors produce mucin and form glands
o Infiltration of signet-ring cells (similar to diffuse gastric cancers)
SQUAMOUS CELL CARCINOMA
Most common in men, >45 yo
Risk factors:
o Alcohol, tobacco, consumption of hot beverages, Plummer-Vinson syndrome,
mediastinal radiations, diets poor in fruits or vegetables, consumption of fermented
milk (fungus-contaminated food)
o HPV infection
Amplification of transcription factor gene SOX2, overexpression of cyclin D1, loss of function of
tumor suppressors (TP53, E-cadherin, NOTCH1)
Histology
o In the middle third of the esophagus
o Well differentiated
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