What are most common symptoms of GERD?
- Heartburn: burning, retrosternal discomfort (experienced in the chest, NOT the abdomen)
1. Can be, and usually is, chronic
- Regurgitation: effortless movement of fluid up into the chest, and even into the back of the throat
What do you see here?
- Erosive esophagitis: pretty much makes the dx of GERD, but most pts will have a normal-appearing esophagus
1. 90-95% specific to GERD: clinical standard for excluding other causes
2. Only 20-60% of pts w/acid esophageal reflux via pH testing are found to have endoscopic findings consistent with esophagitis
- Compare to normal (attached here): white, grey
- NOTE: there is an LA grading system for severity (from A being least severe to D, or most severe)
What are some more severe symptoms of GERD?
- Weight loss
What questions might you ask a pt who is not responding well to PPI tx for GERD?
- What symptom(s) does he have?
- Was the diagnosis of GERD correctly established before PPI treatment was begun?
- Was there an initial response to the PPI?
How can pts optimize PPI administration?
- Generally, best taken BEFORE FOOD
- Should be taken on a regular, ONCE DAILY basis
- Although many pts are on twice-daily PPI therapy for GERD, this is often unnecessary
Which pts with GERD should be referred to a gastroenterologist?
- Pts with atypical symptoms
- Pts with unresponsive symptoms (to PPI)
- Pts w/alarm features: need to take adequate history
1. Change in the nature of chronic symptoms
2. Dysphagia, vomiting, unexplained weight loss, family hx of cancer, concerns about cancer, anemia
- Pts with typical chronic GERD symptoms, but no prior endoscopy (maybe – if it has been years)
65-yo man with 10-yr hx of chronic GERD. Smoker. Takes PPI. Endoscopy 10 years ago w/grade B esophagitis. What should you do?
- Advise to take PPI each morning before eating
- Advise to stop smoking (not really evidence that stopping smoking does anything, but still advise pts to do so)
- See gastroenterologist -> repeat upper endoscopy to evaluate erosive esophagitis, verify no Barrett’s or cancer
What histo changes are associated with reflux?
- Eosinophils: can have lymphs and neutros too
- Basal cell hyperplasia due to chronic irritation
- Elongated lamina propria papillae
- Subepithelial vascular dilatation
What is the difference b/t these 2 images?
- LEFT: normal
- RIGHT: gastroesophageal reflux
1. Sm # of intraepithelial eosinophils
2. Basal cell thickening due to chronic irritation (INC production)
3. Lengthening of stromal papillae
Can weight loss help relieve GERD symptoms?
- Dietary modification doesn’t contribute a great deal in GERD, unless the patient is overweight or obese (or if pt notes a distinct trigger to their symptoms, e.g., pts with EoE)
When should tx be initiated in pts w/typical GERD symptoms? By whom?
- In pts with typical symptoms and no alarm features, treatment can and should be initiated in the primary care setting
- Primary care physicians are very comfortable doing this
What is the role of endoscopy in patients with typical symptoms?
Can medical treatment be safely initiated before (or without) endoscopy?
- No urgent need for endoscopy in pts with typical symptoms -> medical tx can be safely initiated w/o endoscopy
- Reserve specialist referral (endoscopy) for pts with:
1. Atypical/unusual symptoms
2. Poorly responsive symptoms
3. Alarm features: dysphagia, unexpected weight loss, family history of cancer, etc.
4. Requirement for Barrett’s screening: reflux symptoms for >5 yrs. w/o endoscopy should probably have one
What is the (limited) role of endoscopy in GERD?
- Might confirm diagnosis of GERD
1. Good specificity: erosive esophagitis (90-95%)
2. Poor sensitivity (most pts will not have erosions)
- Can evaluate some other symptoms, e.g. dysphagia
- Can help to rule out other conditions
1. Ex: eosinophilic esophagitis (which can only be diagnosed by endoscopy and biopsy)
- Screening for Barrett’s esophagus
What is going on here?
- Eosinophilic esophagitis (EoE): predominantly in young male patients
- Hx of atypical heartburn, intermittent dysphagia, and recurrent food impaction
- Ringed appearance to esophagus (trachealization)
- Linear furrows and narrow caliber lumen
- Eosinophilic infiltrate on biopsy; white spots are micro-abscesses filled w/eosinophils
- May respond to PPI's (first-line) or may need topical steroids (if don't respond to PPI's)
- NOTE: this is a spectrum of disease -> overlap b/t EoE and GERD
What is the difference b/t these 2 images? Arrow?
- LEFT: reflux
- RIGHT: EoE -> can be up to 70 eosinophils per high-power field (HPF; cut-off 20)
1. Can get micro-abscesses of eos (arrow)
2. Overlap w/reflux (edema, basal hyperplasia), but usually >20 eos per HPF, and usually affects the entire esophagus
What is the role of diet in EoE?
- Some people treat this with elimination diets
- 6 most common foodstuffs that cause this: milk, soy, wheat, egg, peanut, and seafood
What is Barrett's esophagus? Epi? Dx?
- Intestinal metaplasia of distal esophagus that predisposes pt to esophageal adenocarcinoma
1. 1 case in 300 pt-years in pts who do not have dysplasia -> most Barrett’s pts will never devo this cancer
- Male + white + obesity (poster = 65-yo, white, male w/20-yr hx of heartburn)
1. Rare in women: esophageal adenocarcinoma also rare in F (about same risk as man getting breast cancer)
- DX: endoscopy + biopsies
What do you see here?
- Barrett's esophagus: typical endoscopic appearance
- Intestinal metaplasia with islands of normal-appearing squamous mucosa
What do you see in this esophageal biopsy?
- Barrett's esophagus: metaplastic columnar mucosa above gastroesophageal junction
- Goblet cells are diagnostic in US, but diagnosis varies from country-to-country
- Need to ensure biopsy is all from esophagus, and NOT from stomach
Describe the dysplasia in these two esophageal biopsies. How are they different?
- LEFT: low-grade dysplasia (goblet cells)
1. Hyperchromasia, INC N:C ratio (arrow) + start to lose polarity (nuclei no longer at basal side of epithelium)
2. Normal glandular epi on right (arrowhead)
- RIGHT: high-grade dysplasia (abnormal gland architecture; almost a carcinoma in situ)
1. Failure of epi cells to mature as they migrate to the esophageal surface
2. Abnormal architecture: glands start to blend together
3. Nuclear hyperchromasia
4. INC nuclear to chromatin ratio
5. Abnormal mitoses
- NOTE: p53 a major player in progression
What do you see in this esophageal biopsy? Arrow?
- Abrupt transition from Barrett metaplasia (left) to low-grade dysplasia (arrow)
- Note the nuclear stratification and hyperchromasia
- Looks almost like a tubular adenoma of the colon
What is going on in this esophageal biopsy?
- High-grade dysplasia: architectural irregularities, including gland-within-gland, or cribriform, profiles
- Cribriform: anatomical structure pierced by numerous small holes, in particular the plate of the ethmoid bone through which the olfactory nerves pass
What are the risk factors for esophageal adenocarcinoma? Protective factors?
- RISK FACTORS: most cases arise from Barrett's esophagus
- PROTECTIVE: fresh fruits and veggies
1. Some H. pylori infections assoc w/DEC risk (if they affect gastric corpus and cause atrophy and reduced acid secretion) -> DEC reflux
What is a major prognostic indicator for esophageal adenocarcinoma?
- Penetration into the submucosal lymphatic vessels
1. By the time symptoms appear, usually already happened (even though this can take awhile) -> overall 5-yr survival at advanced stage <25%
- In contrast, 5-year survival approximates 80% in the few patients with adenocarcinoma limited to the mucosa or submucosa
What is the going on in these two images?
- LEFT: adenocarcinoma -> usually distal and, as in this case, involves the gastric cardia
- RIGHT: squamous cell carcinoma -> most frequently found in mid-esophagus, where it commonly causes strictures
What is the difference b/t these two images?
- LEFT: adenocarcinoma -> invasive here, with glands all the way down to the muscle
- RIGHT: squamous cell carcinoma -> keratinizing cells (pearls), intercellular bridges (another image attached here)
What are the epi and risk factors for SCC of the esophagus?
- EPI: adults >age 45
1. M 4x more frequently than F
2. 8x more in AA
- RISK FACTORS: alcohol and tobacco use, poverty, caustic esophageal injury, achalasia
1. Previous radiation to mediastinum: 5-10 or more years after exposure
2. Pocket of extremely high esophageal SCC incidence in W Kenya linked to traditional fermented milk (mursik), which contains the carcinogen acetaldehyde (young men)