Lectures 1,2: Esophagus Flashcards
Four layers of the esophagus
Mucosa, muscularis mucosae (thin), submucosa, muscularis propria
In which esophageal layer are the salivary glands located?
Muscularis mucosae
Three components of the muscularis propria (progressing downward)
Smooth muscle, myenteric plexus, skeletal muscle
Line between esophagus and stomach
Z line
Stem cells become what kind of cells and then what kind of cells in esophageal renewal?
Stem cells –> basal cells –> mature cells
What can assess by looking at the thickness of the basal cells?
Esophageal surface injury
What is the most dangerous caustic chemical class? What happens upon exposure? Long-term consequences (2)?
Alkalis –> odorless/tasteless and cause rapid injury die to necrosis and saponification –> perforation and death; narrowing and squamous cell carcinoma
Describe pill esophagitis: definition and pathogenesis. What is symptom and the endoscopic finding?
Injury due to prolonged contact of pill to mucosa; esophagus collapses and secretions decrease during sleep; presents with acute chest pain and the finding is “kissing ulcers”
How does a bisphosphonate become corrosive? What kind of medication?
Dissolves in the stomach and refluxes into lower esophagus; bone-building medications
Describe candida esophagitis: how it presents and endoscopic finding
Presents as odynophagia (terrible pain on swallowing) and oral thrush; finding is whitish plaques with normal esophagus inbetween made of desquamated cells and fungi
CMV esophagitis is associated with what state? What does it indicate?
Immunocompromised; viremia
What kinds of cells do CMV infect? What does this cause in the esophagitis?
Mesenchymal cells (NOT squamous cells –> so must biosy BASE of the ulcer); ulcers
T/F: Herpes esophagitis can infect both immunocompetent and immunocompromised hosts
True
Herpes infect what kind of cells? What are three characteristic findings?
Squamous; 1. Cell-cell detachment, 2. Multinucleation; 3. “Ground glass” nuclei
What causes injury in reflux esophagitis?
Gastric acid, pepsin, and duodenal contents (trypsin, bile)
Describe GERD grossly and histologically
Erythematous; congested capillaries (suggest chemical injury)
What are some other manifestations of reflux esophagitis? Take-home point?
Edemic cells (ballooned with large intracellular spaces) and basal cell hyperplasia with eosinophils; VARIABLE reflux histology
Histology of reflux-associated “peptic” ulcer…
PUS = neutrophils, exudate
Three complications of reflux esophagitis
Ulcer –> odynophagia, hematemesis; regeneration –> Barrett esophagus (columnar); stricture –> dysphagia
Describe eosinophilic esophagitis: incidence, presentation, etiology, and treatment
Rising incidence; presents with dysphagia/food impaction; antigen driven (allergic); tx with dietary restriction and PPIs (may be potentiated by acid reflux)
Endoscopic findings of eosinophilic esophagitis (3) and histological findings (2)
Transverse rings; longitudinal furrows, tiny white mucosal plaques; eosinophil aggregates at surface (plaques) and fibrosis
Who usually gets EoE? Who usually gets GERD?
EoE = children and adults; GERD = usually adults
Symptoms of EoE vs GERD
EoE = dysphagia, impaction; GERD = heartburn
Pathogenesis of EoE vs GERD
EoE = IgE and cell mediated injury; GERD = chemical injury
Site of EoE vs GERD
EoE = Pan-esophageal; GERD = distal esophagus
Tx of GERD
Suppression of acid secretion and reflux
Describe Barrett esophagus: definition, what type of “plasia” and symptoms
Columnar-lined esophagus in response to GERD; a form of metaplasia; no symptoms
Barrett esophagus is a risk factor for…
Risk factor for esophageal adenocarcinoma
About what % of chronic GERD patients get Barrett esophagus
10%
What does Barrett esophagus look like grossly and histologically?
Salmon-colored esophagus; stomach-like columnar lining with goblet cells (necessary to be sure it was esophagus)
Barrett esophagus malignant progression. Fast or slow?
Metaplasia –> increasingly dysplastic mucosa (low grade to high grade dysplasia) –> Barrett adenocarcinoma; slow (takes years)
Management of Barrett esophagus (3)
Manage GERD, surveillance, ablation/surgery
Symptoms of Barrett adenocarcinoma and 5-year survival
Symptoms: dysphagia and weight loss; 5-year survival = 15%
Risk factors for squamous cell carcinomas, divided into underdeveloped and industrialized
Developping = dietary deficiencies, aflatoxins, indoor coal burning; Industrialized = alcohol + smoking
Who tends to get squamous cell carcinoma in the US?
Older males who smoke and drink and live in urban environments, higher in African Americans
Symptoms of squamous cell metaplasia (4)
Progressive dysphagia, weight loss, hemoptysis, hoarseness
Most people who die of squamous cell carcinoma die of what kind of complication? 5-year survival?
Local; 5-year survival 5-10%
Muscles of upper esophageal sphincter
Cricopharyngeus and lower fibers of inferior pharyngeal constrictor
Two phases of swallowing (describe)
Oral (voluntary): bolus propelled backward by tongue; Pharyngeal phase: soft palate elevates to close off nasopharynx and larynx moves antero-superiorly to bring larynx away from bolus, then larynx closes and UES relaxes
Describe pressure wave of lower esophageal sphincter
Starts at a resting pressure (closed), then relaxes (receptive relaxation), and finally contracts before returning to rest
How long does it take food to get down the esophagus
6-7 seconds
What is a test to examine esophageal pathology?
Esophageal manometry
How does progesterone affect the LESp?
Lowers the LESp
Symptoms of esophageal disorder
Dysphagia, heartburn, odynophagia, chest pain, regurgitation, ‘atypical’ symptoms (hoarseness, cough, wheeze)
Esophageal disorders tests (5)
Barium esophagram (structural lesion), endoscopy with biopsy (visualize esophageal mucosa), endoscopic ultrasound (imaging lesions), esophageal monometry (pressures/contraction), acid reflux (pH) studies (measures pH for 24 hours)
Can barium swallow ever demonstrate GE reflux?
Yes, if they reflux at that moment
Can esophageal manometry demonstrate GE reflux?
Can demonstrate tendency for GE reflux
What is the best test for reflux?
Acid reflux/pH studies
Esophageal diseases (2 classes, 3 subtypes for 1 class)
Gastroesophageal reflux disease (GERD) and motor disorders (achalasia, scleroderma, esophageal spasm)
GERD: define and symptoms. Is all reflux a disease?
Reflux of gastric contents into the esphagus; heartburn (worse with food, lying down), chest pain, etc; not a disease unless there is dammage
Do you always see GERD macroscopically?
2/3 of the time, no (but may be apparent histologically)
Pathogenesis of GERD is a balance between aggressive (acid) and defensive factors. What are the defensive factors?
- Anti-reflux barrier = most important and includes LES and crural diaphragm; 2. Esophageal acid clearance which includes saliva, peristalsis, gastric emptying, intact esophageal mucosa, lack of hiatal hernia
Define hiatal hernia. Treatment?
Acid pocket within proximal stomach and loss of crural pinch; associated with increased transient LES relaxations; tx = surgical
Two types of hiatal hernia
Sliding and para-esophageal (not associate with heartburn, but more pain/dysphagia)
Consequences of GERD (4)
Mucosal injury, stricture, Barrett’s metaplasia, esophageal adenocarcinoma
Structural problems are associated with…what’s on the diff dx?
Solid foods; progressive: carcinoma (rapid), peptic stricture (gradual w/ GERD hx), intermittent: web/ring
Motility disorders are associated with…what’s on the diff dx?
Solids and liquids; progressive: achalasia (tonically shut LES, no heartburn), scleroderma (heartburn hx where SM is replaced by fibrous tissue), intermittent: spasm (with chest pain)
Achalasia: pathogenesis, manometric findings, sx
Loss of inhibitory ganglion cells within myenteric plexus, LES remains tonically contracted; hypertensive LES w/ impaired relaxation and aperistaltic esophagus; sx = dysphagia, regurgitation, weight loss, chest pain
Achalasia: barium swallow finding
Bird-beak w/ aperistaltic body
Achalasia: tx
Botox toxin, pneumatic (balloon) dilation, most effective = heller myotomy (cut SM of esophagus to relax LES)
Pseudo-achalasia (2 causes)
Chagas’ disease due to T. cruzii infection and cancer of GE junction
Scleroderma: define and manometry findings
CT disorder because SM replaced by fibrotic tissue; tonically open with poor peristalsis
Diffuse esophageal spasm: sx, X-ray finding, manometry, tx
Sx: chest pain, odynophagia; X-ray: corkscrew esophagus; manometry: simultaneous, repetitive contractions w/ normal LES; tx: muscle relaxants, Ca2+ channel blockers, nitrates
Nutcracker esophagus: define and sx
Very high amplitude contractions (>180 mmHg) but normal peristalsis; sx = pain
