Esophageal Epithelium Changes and GERD progression Flashcards
To understand and memorize the structural and functional changes in esophageal epithelium related to GERD, including specialized intestinal metaplasia and Barrett’s esophagus. These flashcards aim to reinforce knowledge on cellular adaptations, molecular defenses, and the progression from acid reflux to potential malignancy.
Think of genes adapting for survival in acidic conditions.
What gene expression changes occur in Barrett’s esophagu to support acid defense?
Barrett’s esophagus overexpresses genes involved in mucosal defense and repair and Barrett’s cells maintain physiological intracellular pH even after prolonged reflux exposure.
Gene overexpression helps maintain cell health despite acid exposure.
Why would tighter junctions help in an acidic environment?
How do claudin 18 tight junctions in Barett’s esophagus contribute to acid protection?
Claudin 18 tight junctions in Barrett’s esophagus provide greater protection against acid permeation compared to claudin 18-deficient tight junctions in esophageal squamous epithelium.
Stronger tight junctions limit acid infiltration between cells.
Think of mucus as a protective coating.
What type of mucus is produced in specialized intestinal metaplasia, and why is it significant?
Specialized intestinal metaplasia produces thick adherent mucus, which is not present in normal squamous esophageal cells, providing extra protection against acid.
Thicker mucus prevents acid from reaching epithelial cells.
Consider the role of bicarbonate in acid buffering.
What is unique about the anion secretion in intestinal metaplasia?
Intestinal metaplasia secretes anions, including bicarbonate, at levels more than fivefold higher than in esophageal squamous epithelium. This helps neutralize acid.
High bicarbonate secretion protects against acid damage.
Think about tiny pockets where new cells are made.
What are the key cellular features of specialized intestinal metaplasia?
Specialized intestinal metaplasia is a well-organized tissue layer with small pockets called crypts. Stem cells at the bottom of these crypts create new cells that multiply and replace older cells, which eventually shed into the inner space of the esophagus.
Crypts help maintain a steady supply of new cells to replace old ones.
Consider the metaplasia that happens due to smoking.
Give an example of metaplasia in other parts of the body related to chronic irritation.
An example of metaplasia is the squamous metaplasia in the trachea or bronchi, often seen in chronic smokers as an adaptation to irritation.
Chronic irritation in smokers’ airways can lead to squamous metaplasia in the bronchi.
Survival rates decline from localized to metastatic stages.
Provide the 5-year survival rates based on the stage of esophageal adenocarcinoma.
Localized (mucosa/submucosa): ~80% survival;
Regional lymph nodes: ~50% survival; Distant metastases: ~25% survival.
Explain the importance of early detection in esophageal adenocarcinoma prognosis.
Early detection improves survival rates significantly. Superficial, non-invasive lesions have around 80% 5-year survival compared to 25% for advanced cases.
5-year survival drops sharply once cancer spreads beyond the esophagus.
Which lymph nodes are typically checked for spread in esophageal adenocarcinoma?
In esophageal adenocarcinoma, lymph node spread often involves the gastric and celiac lymph nodes for cancers in the lower esophagus. For cancers higher up, doctors may check paratracheal, cervical, and supraclavicular lymph nodes.
Different lymph nodes are assessed depending on the tumor’s location along the esophagus.
What factors are associated with poor prognosis in esophageal adenocarcinoma?
Poor prognosis is linked to lymph node metastasis, invasion beyond the submucosa, and advanced cancer stage at diagnosis.
Advanced cancer stage, lymph node spread, and tissue invasion worsen prognosis.
Hint: It’s like a shield with multiple layers.
What’s the superhero layer in your esophagus that protects against food friction?
Stratified squamous epithelium. Multiple layers, with a tough, keratinized surface, providing a barrier against mechanical and chemical irritation.
Stratified squamous epithelium. Multiple layers, with a tough, keratinized surface, providing a barrier against mechanical and chemical irritation.
The gastro-what?
What is the primary factor causing acid reflux? What’s the ‘gate’ that slips up?
Decreased gastroesophageal sphincter tone lets stomach acid sneak up into the esophagus.
The lower sphincter controls acid backflow; when weak, reflux occurs.
The sphincter is like a bouncer that doesn’t keep acid out when it’s too relaxed.
What’s the ‘extreme makeover’ the esophagus pulls to survive acid?
With chronic acid exposure, the esophageal lining changes from squamous to glandular cells, forming Barrett’s esophagus.
Barrett’s esophagus is like the esophagus putting on an ‘acid-proof’ suit.
It’s like a ‘danger zone’ for cells.
Why is ‘dysplasia’ a big red flag in GERD?
Dysplasia signals abnormal cell growth and higher cancer risk, marked by rapid division, enlarged nuclei, and failure to mature properly.
Dysplasia is considered pre-neoplastic and needs monitoring.
Think glandular growth gone bad.
What cancer can develop from GERD if metaplasia and dysplasia go unchecked?
Adenocarcinoma. Chronic acid exposure leads to changes that, over time, may progress into invasive glandular cancer.
From acid to adenocarcinoma—it’s the ultimate ‘bad transformation.’
