Lecture 79 - Path of Esophageal Disease Flashcards
Normal Histology of the esophagus:
what type of epithelium is the mucosa?
whats missing form the adventia? why is this important?
Mucosa — non keratinized stratified squamous epithelium
Adventitia: Lack's Serosa Therefore easier for cancers to spread once there
Normal Anatomy/Function
– what are three areas of anatomical narrowing in the esophagus?
Three Anatomical Narrowings: Cricoid Carilage, Aortic Arch/Bronchial bifurcation, Diaphragm
Achalasia:
pathophysiology?
what is seen on histo?
what infection may be seoncdary cause of achalasia
Failure of relaxation of the LES due to loss of myenteric (auerbach) plexus
Secondary achalasia – may arise from T. Cruzi (chagas) or malignancy
Histological findings of GERD?
what else might be on the ddx?
DDx:
Eosinophilic Esophagitis – (EoE)
Chemical Injury, Infectious esophagitis, GERD with Barrett’s Esophagus
Mucosal injury and repair; inflammation (typically eosinophilic)
Decreased thickness of surface over papillae
Prominent basal layer (stem cells)
what % of GERD patients get barrett’s esophagus?
what is barrett’s esophagus?
10% of patients with GERD
Over time: metaplasia to an epithelium more like the intestine which is better equipped to handle acid
Metaplasia: Stratified squamous epithelium —> non ciliated columnar epithelium with goblet cells
May progress to dysplasia and adenocarcinoma
what are the required findings to make a diagnosis of Barrett’s Esophagus?
Dx Requirements:
1) endoscopy appearance of pink/salmon columnar mucosa in tubular esophagus, (but just bc it is columnar doesn’t mean its intenstinal (could be gastric))
2) Histological findings of intestinal metaplasia — Glandular epithelium with Goblet Cells
what is common mutation in dysplasia in the progression of BE to carcinoma?
what is this progrsesion
P53 mutation – common and early event
BE Metaplasia—> Low grade dysplasia –> high grade dysplasia –> Adenocarcinoma
features of low grade dysplasia ?
eatures which indicated Increased replication at the expense of function:
Increased cell turn over – dark nuclei – “picket fence”
Mucin depletion
Mitoses moving up the gland
Intestinal metaplasia with pale goblets cells
Features of high grade dysplasia:
High Grade Dysplasia \
Architectureal distortion -- cribiforming "swiss-cheese" look (cribriform = pierced with small holes) Severe cytological and nuclear abnormalities --- loss of polarity; high variability
lots of mitosis
Adenocarcinoma of the Esophagus
- associatd with what precursor?
- histology?
- what third of the esophagus does it commonly occur?
Risk factors: Reflux and barrett’s esophagus (95% of cases)
Derives from glandular mucosa --> glandular dysplasia --> Cancer Invasion of atypical glands into underlying tissues Distal third of esophagus
Squamous Cell Carcinoma –
risk factors?
Histology?
Risk factors: Smoking, drinking, acid ingestion, and caustic burns, exposure increases (such as in achalasia)
Dysplasia: Squamous cells with impaired maturation with atypia
Carcinoma: cells break out of normal distribution, invade underlying tissues
Staging of Esophgeal cancers:
where are the first mets?
- Depth of invasion – (for GI tract cancers in general)
Risk of mets increase with increased depth of invasion === confers to prognosis
– if it invades to surrounding structurs — unresectable
First mets are usually to LNs
three most common agents of infectious esophagitis?
Candida – most commony
HSV – 2nd
CMV
Gross and Histological findings of candiasis of infectious esophagitis?
what specific stain can be used?
Gross: White plaques – disruption and falling off the sqmamous
Micro – squamous debris, active esophagitis (PMNs),
GMS Stain -- fungal forms are black
HSV infectious esophagitis –
Gross:
where should the bx be taken from?
Indicative histological finding?
what specific stain can be used?
ulcers and erosion
virus will be at the interface of the ulcer and squamous epithelium
Micro: Multinucleated cells at the interface
Immuno stain for herpes virus:
