Esophageal and Gastric Pathology Flashcards
What kind of cells line the esophagus?
non keratinized stratified squamous epithelium
What are the bridges one sees on microscopy of the esophagus?
tight junctions between esophageal epithelium
What kind of cell lines the fetal esophagus?
respiratory type ciliated columnar epithelium –> common embryologic derivation of the trachea and esophagus
Is the GEJ an anatomical or functional sphincter?
functional –> no clear muscle group but still functions as a sphincter
Where are minor salivary glands located?
in the pharynx, esophagus and no where distally
What is the function of minor salivary glands?
lubrication and enzymes like amylase
Is the LES an anatomical or functional sphincter?
functional –> no clear muscle group but still functions as a sphincter due to controlled contraction of smooth muscle via neural input
What is an esophageal duplication cysts?
a congenital abnormality involving a “branched” esophagus that has all layers (can be squamous or respiratory type cells as it has to do with embryologic divergence of the two structures)
Where are inlet patches found?
cervical esophagus –> multiple glandular types of mucosa
What is the significance of inlet patches?
none –> just a developmental abnormality
What is esophagitis?
injury to the mucosal lining of the esophagus
Do all people have chest/mid epigastric pain with esophagitis?
no
How do we detect esophagitis?
endoscopy and biopsy –> may appear reddish when mild to ulcerated when severe
What kinds of cells are involved in esophagitis?
neutrophils and eosinophils // lymphocytes are normal b/c of MALT (but can be an inflammatory mediator too)
What is the endoscopic finding in reflux esophagitis?
linear erythema with variable linear ulcers w/neutrophils and reactive epithelium
Dysphagia
difficulty on swallowing
What are the endoscopic/histologic findings of Herpes esophagitis?
ulcers “punched out”, multinucleated squamous cells, intranuclear inclusions
What are the endoscopic/histologic findings of CMV esophagitis?
ulcers, intranuclear AND intracytoplasmic inclusions (vs herpes which only has intranuclear)
What are the endoscopic/histologic findings of candida esophagitis?
white “cheesy” plaques, keratin debris, admixed yeast and psuedohyphae
What are the endoscopic/histologic findings of eosinophilic esophagitis?
white papules of intraepithelial eosinophils (12-15/hpf), ring esophagus/felinization/trachealization, stricture
T/F the incidence of eosinophilic esophagitis is falling in children and adults.
F –> rising
Pathogenesis of eosinophilic esophagitis
atopic allergic response to antigen in food or air
Tx of eosinophilic esophagitis
oral swish and low dose steroids
Dyspepsia
pain in the upper abdomen associated with feeding
Name 3 skin disorders that can present as esophagitis.
pemphigus, pemphigoid, lichenoid reactions
Schatzki Ring
muscular ring covered by squamous epithelium that can cause dysphagia –> 10% of people
Odynophagia
pain on swallowing
Pathogenesis Achalasia
LES has high tone impeding progress of bolus into stomach and dilates over time due to increased pressure and food –> food stasis with enzymes can increase risk of carcinoma/dysplasia progression
Pathogenesis Scleroderma/Crest
selective ATROPHY (not fibrosis) of inner circular muscle layer –> lower esophagus only
Pathogenesis Mallory Weiss Tear
with repeated wrenching vomiting, a rip may occur in distal esophagus causing massive bleeding
Where are most common cancers of GI tract?
colorectal
4 categories of benign esophageal tumors
papilloma, granular cell, mixed, leiomyoma
4 categories of malignant esophageal tumors
squamous and adenocarcinoma, malignant nerve sheath, adenoid cystic, leiomyosarcoma
Worldwide, what is the most common esophageal tumor?
squamous cell carcinoma
In the occident, what is the most common esophageal tumor?
adenocarcinoma
Risk factors for adenocarcinoma
reflux, diet, obesity, male, microbiome
“DORMM”
Are the esophagus and stomach sterile?
the esophagus isn’t, the stomach is
T/F >50% of those with Barrett’s have no symptoms
T
T/F >99% of BE develops before initial endoscopy
T (BE = barrett’s)
Pathogenesis of Barrett’s risk factors
obesity promotes GERD mechanically and by secreting inflammatory factors, high fat diet has delayed gastric emptying + MHC variants + long segment BE
T/F screening for BE based on reflux symptoms is effective
F –> will miss >50% w/only reflux screening
How do we identify BE histologically?
goblet cells/intestinal metaplasia
When is the length of intestinal metaplasia in BE established?
at the initiation of the injury
Do short segments convert to long segments in BE?
NO
Which has a higher risk of cancer in BE? long/short segment
long segment
When may surgical resection become necessary w/regards to esophagus dysplasia/cancer?
once invasion has developed
Staging of esophageal adenocarcinoma?
TNM
What term is used for peri-esophageal fat?
adventitia
Does the esophagus have a serosal surface?
no –> adventitia
What are the endoscopic findings of esophageal BE/dysplasia/cancer?
salmon colored tongue of glandular mucosa
What some etiologic factors in squamous cell carcinoma of the esophagus?
ETOH, smoking, moldy foods, achalasia, lye, diverticulum
Is HPV a prominent etiologic factor in squamous cell carcinoma of the esophagus?
No
How common is squamous cell carcinoma of the esophagus in the US?
quite rare actually
What set of genes increases risk of squamous cell carcinoma of the esophagus?
alcohol dehydrogenases
What would a geographic high risk area for squamous cell carcinoma of the esophagus look like?
low altitude, drought, low vegetable intake
What is the staging system used in squamous cell carcinoma of the esophagus?
TNM
Another name for an isolated patch of glycogenated squamous mucosa in the esophagus.
glycogenic acanthosis –>benign
What part of the stomach mucosa makes acid and pepsinogen?
oxyntic –> basically fundus and body and cardia
What part of the stomach mucosa makes gastrin?
antrum
Does the antrum have rugae?
no –> smooth
Does the antrum have MALT?
no
Pathogenesis of acute gastritis
epithelial injury resulting in breakdown of mucosal barrier allowing gastric luminal contents to back diffusely into the lamina causing ulcerations and bleeding
Etiologic factors in acute gastritis
alcohol, severe stress (“cushing type” ulcers in burn patients and head trauma patients), shock, radiation, caustic agents, NSAIDs
Histologic features of acute gastritis
fibrin, erosion, ulcer beds, no chronic inflammation, may have neutrophils, blood
What distinguishes an erosion from an ulcer?
ulcer goes all the way through mucosa vs. erosion is just surface epithelium
What is implied if there are lymphocytes in the gastric lamina propria?
chronic gastritis
What is chronic gastritis without activity vs with activity?
without = lymphocytes with = lymphocytes + neutrophils
4 tests for H.pylori
biospy with thiazine stain, CLOtest (pH/urease), blood test for Ab, breath test
How do we get duodenal ulcers with H.pylori?
antral H.pylori can kill off D cells reducing inhibition of acid production
What is atrophic chronic gastritis?
loss of parietal and chief cells –> autoimmune or migration of antral H.pylori – // can increase risk of carcinoma and lymphoma
Autoimmune gastritis pathogenesis
auto antibodies against H+ pump –> antibody and cell mediated killing follows
What is another word for gastric atrophy?
antralization
What are the negative effects of autoimmune gastritis?
- rise in gastric pH due to loss of inhibition of G cells –> proliferation of ECL cells –> carcinoid tumors
- reduced B12 absorption b/c no intrinsic factor production –> pernicious anemia
- long term low acid production
Histologic features of ECL clusters
round nuclei, chromogranin
–> microscopic ball = microcarcinoid
endoscopic mass = macrocarcinoid
H.pylori or autoimmune gastritis? begins in antrum
H.pylori
H.pylori or autoimmune gastritis? involves body and fundus
autoimmune –> antrum NOT effected
H.pylori or autoimmune gastritis? acute and chronic
both
H.pylori or autoimmune gastritis? + CLO
H.pylori
H.pylori or autoimmune gastritis? -CLO
autoimmune
H.pylori or autoimmune gastritis? antiparietal antibodies
usually autoimmune (rarely H.pylori)
H.pylori or autoimmune gastritis? microcarcinoid
autoimmune
2 categories of malignancies in stomach
lymphoma and carcinoma
2 categories of benign growths of stomach
polyps, enlarged folds
What is the most common stomach malignancy?
carcinoma
T/F gastric cancer prevalence is increasing in the USA
F –> unlike esophagus, on the decline
Fundic gland polyps
usually incidental, most common polyp, single/multiple, benign, always in those with FAP gene (familial adenomatous polyposis), sporadic ones occur via beta catenin mutations
What mutation can lead to sporadic fundic gland polyps?
beta catenin mutation
Histologic features of fundic gland polyps
oxyntic mucosa, dilation of glands, no proliferation
Hyperplastic gastric polyp
usually antral, single/multiple, usually arise on underlying gastritis, low risk of neoplastic transformation, inflamed and proliferating mucosa
Etiologies of enlarged gastric folds
lymphoma, gastric cancer, metastatic breast lobular cancer, diffuse gastritis, benign increase called hypertrophic gastropathy
What is the normal ratio of parietal/chief cells to surface foveolar cell compartment?
3:1
What cell layer is expanded in hypertrophic gastropathies?
epithelium
In what condition is parietal cell compartment expanded?
ZES/MEN
*probably not testable b/c only in notes: pathogenesis of Metrier’s disease
foveolar/epithelial expansion in stomach leads to lots of mucin production –> abnormal protein signaling –> loss of protein –> secretion of serum albumin –> loss of pressure, body edema
Most common primary lymphoma in stomach
extra nodal marginal zone b cell lymphoma
Pathogenesis of extra nodal marginal zone b cell lymphoma
H.pylori –> stomach MALT –> proliferation and mutations –> indolent or large cell lymphoma
Can we treat extra nodal marginal zone b cell lymphoma with antibiotics?
yes, if it is indolent/small then it will respond to antibiotics
2 types of gastric cancer
intestinal type, signet ring type
What are the features of intestinal type gastric cancer
repeated injury/chronic gastritis –> metaplasia/dysplasia –> glands
Does signet ring type gastric cancer undergo dysplasia/metaplasia sequence?
NO, no injury or gastritis so no metaplasia/dysplasia –> instead, 2 e cadherin mutations
M:F Intestinal gastric cancer
M>F
M:F Signet Ring gastric cancer
M = F
Avg Age: Intestinal gastric cancer
58
Avg Age: Signet Ring gastric cancer
48
Diet and geographic effects: Intestinal gastric cancer
both have an association
Diet and geographic effects: Signet Ring gastric cancer
no association
Does ETOH increase risk of intestinal gastric cancer?
No
Does Vitamin C increase risk of intestinal gastric cancer?
No –> protective
Does processed meat increase risk of intestinal gastric cancer?
yes –> 50g/day = 2.5x increase
Do vegetables increase risk of intestinal gastric cancer?
No –> 100g/day = 1/3 risk
Presentation of gastric cancers
enlarged folds, ulcers, glands
Presentation of pure genetic signet ring gastric cancer
leather bottle stomach/linitus plastica
