Howden - GERD Flashcards
1
Q
What are most common symptoms of GERD?
A
-
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
2
Q
What do you see here?
A
-
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)
3
Q
What are some more severe symptoms of GERD?
A
- Weight loss
- Dysphagia
- Vomiting
4
Q
What questions might you ask a pt who is not responding well to PPI tx for GERD?
A
- 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?
5
Q
How can pts optimize PPI administration?
A
- 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
6
Q
Which pts with GERD should be referred to a gastroenterologist?
A
- 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)
7
Q
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?
A
- 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
8
Q
What histo changes are associated with reflux?
A
- Eosinophils: can have lymphs and neutros too
- Basal cell hyperplasia due to chronic irritation
- Elongated lamina propria papillae
- Edema/spongiosis
- Subepithelial vascular dilatation
9
Q
What is the difference b/t these 2 images?
A
- 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
10
Q
Can weight loss help relieve GERD symptoms?
A
- 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)
11
Q
When should tx be initiated in pts w/typical GERD symptoms? By whom?
A
- 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
12
Q
What is the role of endoscopy in patients with typical symptoms?
Can medical treatment be safely initiated before (or without) endoscopy?
A
- 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
13
Q
What is the (limited) role of endoscopy in GERD?
A
-
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
14
Q
What is going on here?
A
- 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
15
Q
What is the difference b/t these 2 images? Arrow?
A
- 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
18
Q
What do you see here?
A
- Barrett’s esophagus: typical endoscopic appearance
- Intestinal metaplasia with islands of normal-appearing squamous mucosa
19
Q
What do you see in this esophageal biopsy?
A
- 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
20
Q
Describe the dysplasia in these two esophageal biopsies. How are they different?
A
- 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
21
Q
What do you see in this esophageal biopsy? Arrow?
A
- 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
22
Q
What is going on in this esophageal biopsy?
A
- 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
24
Q
What is a major prognostic indicator for esophageal adenocarcinoma?
A
- 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
25
Q
What is the going on in these two images?
A
- 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
26
Q
What is the difference b/t these two images?
A
- 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)
27
Q
What are the epi and risk factors for SCC of the esophagus?
A
- 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)
