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GI Fellowship > Esophagus > Flashcards

Esophagus Flashcards

1
Q

What are the most common causes of GERD?

A
  1. Weak LES
  2. Increased frequency of transient LES relaxations

Others include: Hiatal hernias, gastric hyperacidity

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2
Q

Which clinical syndrome is associated with oral thrush, dysphagia and odynophagia?

A

candida esophagitis (in HIV)

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3
Q

What clinical syndrome is associated with white mucosal plaques and esophagitis on endoscopy?

A

candida esophagitis (in HIV)

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4
Q

which clinical syndrome associated with histological pattern of elongated pseudohyphae and round forms

A

candida esophagitis (in HIV)

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5
Q

What is the treatment for candida esophagitis (in HIV)?

A

Empiric tx with fluconazole if they have oral thrush and esophageal symptoms. If sys dint get better, do EGD.

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6
Q

Clinical syndrome associated with severe odynophagia and substernal chest pain (not really assoc with dysphagia)

A

CMV esophagitis

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7
Q

clinical syndrome associated with endoscopy showing large and deep esophageal ulcers

A

CMV esophagitis

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8
Q

clinical syndrome associated with histology findings of large cytomegalic cells with granular cytoplasmic inclusions and basophilic intranuclear inclusions surrounded by eosinophilic halos (owls eye appearance). Requires special staining.

A

CMV esophagitis

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9
Q

Tx for CMV esophagitis

A

Ganciclovir, foscarnet

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10
Q

Clinical syndrome associated with dysphagia, odynophagia, and chest pain?

A

HSV esophagitis

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11
Q

Clinical syndrome in which endoscopy shows multiple ulcers less than 2 cm in size, erythema and exudate

A

HSV esophagitis

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12
Q

Why is the biopsy from HSV esophagitis so important?

A

hsv affects epithelial cells at the periphery of the ulcer, the biopsy from the edge of the ulcer will have a higher yield for HSV

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13
Q

wHICH Clinical syndrome is assoc with histologic pattern of multinucleated giant cells, nuclear molding, and margination of the nuclear chromatin?

A

HSV esophagitis

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14
Q

wHICH Clinical syndrome is assoc with histologic pattern of cowdry type a bodies (intranuclear eosinophilic droplet like bodies)?

A

HSV esophagitis

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15
Q

wHICH Clinical syndrome is assoc with histologic pattern of cowdry type b bodies (basophilic intranuclear bodies)

A

HSV esophagitis

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16
Q

What is the treatment for HSV esophagitis?

A

acyclovir, Valacyclovir, famciclovir

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17
Q

Clinical syndrome associated with odynophagia and dysphagia, with endoscopy showing large deep ulcers with no evidence of viral infection on esophageal biopsy and staining.

A

Idiopathic HIV esophageal ulcers

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18
Q

What is the treatment or confirmatory test for idiopathic HIV esophageal ulcers

A

confirm the absence of viral infection, on previous biospies, then repeat EGD to obtain multiple biopsies from the center and edge of the ulcer. Then steroids, thalidomide is effective in healing HIV iodpathic ulcers.

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19
Q

What is the LA classification system used to grade?

A

erosive esophagitis

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20
Q

What is the difference between LA grade and grade B

A

LA grade A is less than 5mm in length, and grade b is more than 5mm length

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21
Q

What is the difference between LA grade C and D

A

C includes more than 1 mucosal fold, but less than 75% of esophageal circumference, while D is greater than 75% circumference.

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22
Q

If the patient has barretts or erosive esophagitis, does they need ph testing

A

No, these findings are diagnostic of GERD

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23
Q

What is the next step in managing patients with severe erosive esophagitis after PPI treatment?

A

Repeat EGD to eval for presence of barretts

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24
Q

What is the purpose of doing a retroflexion during an EGD for patients with esophagitis?

A

To examine the cardia and describe the integrity of the gastroesophageal flap valve and presence of hiatal hernia

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25
Q

what classification system is used to describe the flap valve during an EGD

A

The Hill classification

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26
Q

What test can be used to evaluate for motility disorders?

A

Manometry

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27
Q

What GI testing is required prior to surgical fundoplication>

A

Manometry and Ph monitoring is required prior to fundop to rule out motility disorders.

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28
Q

what is the role of PH monitoring in GERD

A
  1. To document the abnormal esophageal acid exposure in non erosive GERD before fundop surgery,
  2. for people with continue symptoms after reflux surgery
  3. continued sxs despite max PPI dose
  4. for pts with non cardiac chest pain, asthma, or extra-GERD
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29
Q

describe the wireless ph system and function

A

during an egd, a wireless capsule is placed 6cm above GE junction. Pt eats and drinks normally, and ph is recorded. If the pH decreases to less than 4 then thats acid reflux.

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30
Q

What is the difference between the definitions of acid reflux and GERD on ph monitoring?

A

acid reflux is defined as a decrease in pH to <4, while GERD is a total acid exposure time of 6% if the duration of the study.

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31
Q

If a GERD patient is undergoing ph monitoring, how long should the test be if the patient has infrequent symptoms AND NEGATVIE prior studies?

A

prolonged monitoring up to 96 hours is advised if symptoms are infrequent but high clinical suspicion of GERD

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32
Q

Which system is used to correlate the gerd sxs with acid exposure events during ph monitoring?

A

SAP or symptom association index

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33
Q

What SAP or symptom association index SCORE indicates a positve test for reflux

A

SAP > 95%

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34
Q

What are the lifestyle modifications for patients with GERD?

A

Weight loss, stop smoking, elevated HOB, small meals, avoid alcohol and caffeine.

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35
Q

What is treatment for MILD or infrequent GERD?

A

H2 blockers (famotidine-Pepcid), Zantac

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36
Q

What is treatment for Severe GERD?

A

PPI (Omeprazole.
Esomeprazole.
Lansoprazole.
Dexlansoprazole.
Pantoprazole.
Rabeprazole.)

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37
Q

What is the MOA for PPIs?

A

PPIs are prodrugs that are activated by the gastric acid. They covalently bind to and irreversibly inhibit active hydrogen potassium ATPases-

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38
Q

How should PPIs be administered?

A

30 minutes before meals, and required 3 to 5 days to reach maximal efficacy.

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39
Q

which conditions are PPIs most effective for?

A

erosive esophagitis, heartburn, GERD chets pain,. However they arent very effective for gerd regurgitation.

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40
Q

If patient does not respond to one PPI, what should you do next?

A

Switch to another PPI

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41
Q

what IS THE NAME OF potassium competitive acid blocker that competitively blocks the availability of potassium to engage the hydrogen ATP-ase pump?

A

Vonoprazan (CYP2C19 DEPENDDENT). It is more potent and works faster than PPI, and does not have to be given before meals. Superior to PPI in erosive esophagitis

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42
Q

what is the most common surgical treatent for GERD

A

Laparoscopic fundoplication

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43
Q

which is superior to remission rates for GERD? PPI vs surgery?

A

Same remission rates (ppI have slightly higher remission rates at 5 years). Use surgery if pt does not want to stay on PPI

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44
Q

Besides fundoplication, what other surgical option exists for GERD?

A

Laparoscopic magnetic sphincter augmentation- LINX- small band of magnetic beads that are implanted (lap) around the outside of the LES to augment pressure and keep LES closed.

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45
Q

How is refractory GERD defined?

A

Persistent heartburn ?2 times/week for 3 months despite BID PPI therapy.

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46
Q

what is the goal in patients with refractory GERD?

A

To make an accurate diagnosis, suggest effective therapy, and stop ineffective medications like PPIs

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47
Q

In patients with refractory GERD what another test that can be done as part of the investigation?

A

gastric emptying study

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48
Q

In patients with refractory GERD what another test that can be done besides gastric emptying study as part of the investigation?

A

do an EGD off of the PPI for 2 to 4 weeks to exclude other etiologies and eval for erosive esophagitis or barretts and then do biopsies to rule out EOE

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49
Q

IF A pt has refractory GERD and normal EGD what to do next?

A

do PH testing immediately after EGD.
For those with no proven GERD before do the PH study off PPIs x 7days and for those with a history of proven GERD do the PH and impedance on PPI BID

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50
Q

what is the definition of acid exposure time?

A

The amount of time the ph is below 4

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51
Q

what percentage (MIN %) of acid exposure time is consistent wIth GERD?

A

6%.

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52
Q

If the acid exposure time is less than 4% with positive reflux symptoms what is this called?

A

reflux hypersensitivity

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53
Q

What criteria has to be met to dx a pt with functional heartburn?

A

No priod dx of GERD
NORmal ph study with (-) sxs
normal esophageal manometry

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54
Q

What criteria has to be met to dx a pt with functional heartburn overlapping with GERD?

A

If pt has proven GERD, and the ph study on PPI shows normal acid exposure and (-) sxs, and normal esophageal manometry,

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55
Q

For patients with TRULY refractory GERD and reflux related heartburn, which is the most effective therapy?

A

Nissen Fundop

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56
Q

Should a patient with purely functional heartburn be on PPI/

A

No, stop the PPI

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57
Q

Can a patient with functional heartburn with overlap GERD be on PPI?

A

Yes, you can also consider a trial of TCA or SSRI

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58
Q

FOR FUNCTIONAL HEART BURN WHICH TREATMENTS SHOULD BE AVOIDED?

A

Nissen fundop, endop tx,

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59
Q

Clinical syndrome in which there is reflux episodes on impendance testing and the ph is greater than 4 with GERD sxs?

A

Non-Acid reflux

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60
Q

How is non acid reflux treated?

A

Lifestyle changes, can use baclofen to decrease transient LES relaxations.

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61
Q

what are 4 examples of extra-esophageal reflux?

A

asthma, cough, laryngitis (laryngopharyngeal reflux), dental erosions

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62
Q

What are symptoms of laryngopharyngeal reflux?

A

Hoarseness, throat pain, sensation of lump in throat, phlegm production

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63
Q

What may be seen on endoscopy in pts with laryngopharyngeal reflux?

A

nonspecific signs of edema and erythema of the larynx

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64
Q

How is laryngopharyngeal reflux treated?

A
  1. If GERD sxs, PPI x 3 months
  2. If no GERD sxs, reflux monitiring
  3. Dont do EGD without reflux monitoring to dx GERD
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65
Q

How is barretts esophagus DEFINED?

A

the presence of intestinal metaplasia of >1cm that replaces normal stratified squamous epithelium. This is recognized endoscopically by its salmon colored mucosa

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66
Q

What clinical syndrome associated with histologic findings or intestinal metaplasia and goblet cells?

A

BE

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67
Q

If there is an irregular z line or BE segment that is less than 1 cm how should this be referred to? and is there an increased risk of malignancy?

A

Refer to as specialized intestinal metaplasia of the GEJ, these hasve no increased risk of cancer. dont biopsy

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68
Q

What is the most concerning progression or complication of BARRETTS?

A

ESOPHAGEAL ADENOCARCNOMA. And the risk is higher in those with long segment BE longer than 3 cm

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69
Q

Which barretts patients have the highest risk of esophageal adenocarcionma?

A
  1. Long segment BE
  2. Low grade dysplasia
  3. High grade dysplasia
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70
Q

Which BE patients have the highest risk of progression from low grade dysplasia to high grade or progression to adenocarcinoma?

A
  1. Those with LGD confirmed by a SECOND pathologist have a higher risk than those without the confirmation by a 2nd
  2. MUCH HIGHER in those with persistent LGD on repeat/follow up endoscopy
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71
Q

Which BE patients have the highest risk of progression from to adenocarcinoma? long vs short seg

A

Longer has the highest risk

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72
Q

Screening for BE: Is screening for BE recommended in women? If so, under what circumstances?

A

Not usually recommended in women. but consider If they have chronic reflux and multiple risk factors for BE (age >50, first degree relative with BE or esophageal adenocarcinoma, Caucasian race, obesity, smoking history)

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73
Q

What are the risk factors for Barretts? Which is most important?

A

risk factors for BE (age >50, first degree relative with BE or esophageal adenocarcinoma, Caucasian race, obesity, smoking history). The most important is first degree relative with BE or esophageal adenocarcinoma.

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74
Q

When should male patients have screening for BE?

A

After 5 years of GERD symptoms and 2 or more risk factors.

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75
Q

What does the Prague classification describe?

A

Barretts esophagus. It reports the length of BE as circumferential extent over maximum extent (C/M).

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76
Q

For nondysplalstic Barretts, how should biopsies be taken?

A

4 quadrant biopsies every 2 cm

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77
Q

For dysplalstic Barretts, how should biopsies be taken? (low grade of high grade)

A

4 quadrant biopsies every every 1 cm

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78
Q

In patients with Barretts esophagus, what is the management for findings of no dysplasia?

A

One EGD with adequate sampling with 4 biopsies every 2 cm. EGD every 3 to 5 years.

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79
Q

In patients with Barretts esophagus, what is the management for findings of indefinite for dysplasia? (mucosal changes that are abnormal but insufficient to call dysplasia)

A

Optimize PPI, repeat EGD in 3 to 6 months

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80
Q

In patients with Barretts esophagus, what is the management for findings of low grade dysplasia?

A
  1. Needs to be confirmed by two pathologists
  2. Confirm with another EGD biopsy in 3 to 6 months
  3. Surveillance EGD yearly until no dysplasia on two exams
    OR
  4. Endoscopic ablation
    OR
  5. EMR if there is nodular dysplasia
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81
Q

In patients with Barretts esophagus, what is the management for findings of high grade dysplasia (confirmed by 2 pathologists)?

A

Confirm with another EGD biopsy in 3 to 6 months with four quadrant, 1cm biopsies

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82
Q

In patients with Barretts esophagus, what is the management for findings of intramucosal esophageal adenocarcinoma (Tumor invades the lamina propria or muscularis mucosa)?

A

EMR and ablation preferred over esophagectomy

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83
Q

In patients with Barretts esophagus, what is the management for findings of submucosal esophageal adenocarcinoma (tumor invades submucosa)?

A

EMR and ablation or esophagectomy (Endoscopic therapy is always the preferred approach)

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84
Q

How often to screen for short segment barrets

A

Q5 years

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85
Q

Clinical situation described by esophageal high grade dysplasia or adenocarcinoma detected prior to the next recommended surveillance EGD in a patient with nondysplastic BE. This may occur due to missed HGD or rapidly progressing adenocarcinoma?

A

Post endoscopy esophageal neoplasia

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86
Q

What is the goal of endoscopic therapy for BE?

A

tO REMOVE ALL NEOPLASOA AND BE Mucosa

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87
Q

How should nodular barretts be treated?

A

Nodular BE should be resected using EMR to get accurate pathology and staging, followed by eradication of flat BE using radiofrequency ablation or cryotherapy

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88
Q

How often does barretts recur after having radiofrequency ablation?

A

20% after 1 year and 33% after 2 years

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89
Q

Following eradication of BE, how often should surveillance EGD should be done for those with either high grade dysplasia or esophageal adenocarcinoma?

A

at 3, 6 and 12 months, then annually

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90
Q

Following eradication of BE, how often should surveillance EGD should be done for those with either low grade dysplasia??

A

At 1 year then 3 years, then q2 years

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91
Q

Does isolated intestinal metaplasia in the cardia require abalation?

A

nO

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92
Q

Cryotherapy can be used to ablate dysplastic (HGD) BE or carcinoma. Wat are side effects of this method?

A

chest pain, dysphagia, mild esophageal strictures

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93
Q

what is the main indication for EMR in barretts?

A

Resection of nodular dysplasia or early esophageal adenocarcinoma extending to the superficial submucosa. It also helps with staging if BE

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94
Q

When is the risk of esophageal strictures following EMR highest?

A

When there is extensive EMR PERFORMED DURING THE SAME SESSION. iF MORE THAN 3CM OF ESOPHAGEAL MUCOSA IS RESECTED, 50% chance of esophageal stricture.

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95
Q

what 2elements increase the risk oF esophageal strictures following EMR?

A

50% risk of strxs if
1. iF MORE THAN 3cm esophageal MUCOSAL length resected
2. If 2/3 of the esophagus circumference is resected
Avoid EMR for large areas of BE AND USE A SUPERFICIAL METHOD

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96
Q

How is eosinophilic esophagitis defined?

A

Chronic inflammatory disorder of the esophagus characterized by dysphagia and food impaction and histologically by an eosinophilic infiltrate in the absence of other causes of esophageal eosinophilia.

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97
Q

What are the 3 main criteria for diagnosis of eosinophilic esophagitis>?

A
  1. Presence of esophageal symptoms
  2. Eosinophilic infiltration limited to the esophagus (>15 eosinophils per HPF) in esophageal biopsies.
  3. Absence of other causes of EOE (like GERD)
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98
Q

What are other causes of having eosinophils in the esophagus?

A

crohns, eosinophilic GI disease, achalasia, graft vs host disease, vasculitis, drug hypersensitivity, esophageal leiomyomatosis, hyper eosinophilic syndrome, parasitic infection, Bullous pemphigoid.

99
Q

what is the first line therapy for PPI?

A

PPI

100
Q

What other conditions are usually associated with EOE?

A

Atopic conditions like food allergy, asthma, allergic rhinitis, atopic dermatitis, allergic conjunctivitis, urticaria, angioedema

101
Q

Which endoscopic findings are suggestive of EOE?

A

Esophageal rings, longitudinal furrows and fragile esophageal mucosa, white patches or specks, esophageal strictures, narrowed esophagus

102
Q

For patients with EOE, what percent will have a normal endoscopy?

A

15%

103
Q

How should biopsies be taken in patients with suspected EOE?

A
  1. Get biopsies in all patients with suspected EOE.
  2. Take 2 to 4 biopsies from the distal and 2 to 4 from the proximal esophagus (place in the same jar).
  3. EOE can be patchy and getting the biopsies from the same level may show different eosinophil counts.
  4. Get biopsies from stomach and duodenum to rule out eosinophilic gastroenteritis. Here separating biopsies into prox and distal can help tell difference between GERD and EOE.
104
Q

How can we differentiate between GERD and EOE on EGD/histology?

A

GERD can cause mild eosinophilia in the distal esophagus (less than 15 per HPF), while EOE causes SIGNIFICANT eosinophilia (grater than 15 HPF) in the distal and proximal esophagus.

105
Q

which clinical syndrome is associated with histologic findings of eosinophilic infiltration >15 per HPF, eosinophilic micro abscesses or superficial crusts, basal cell hyperplasia, subepithelial fibrosis?

A

EOE

106
Q

What is the treatment goal for EOE (Histology/Endo)?

A
  1. To achieve symptom resolution
  2. Histologic remission (less than 15 eosinophils per HPF
  3. Improve endoscopic appearance (lumen diameter > 15mm
107
Q

which EOE meds are FDA approved?

A

None

108
Q

what are the benefits and efficacy of PPIs in EOE?

A
  1. PPIs have anti-inflammatory and anti-secretory effects
  2. Can induce histologic remission in 50% of patients
  3. BID dosing is better than daily
109
Q

How long should PPI be continued in patients with EOE?

A

After a 6 to8 week trial of PPI, if the patient is responding then tx should continue longterm to maintain remission

110
Q

In patients with EOE who do no respond to PPIs, what other treatment options should we consider next?

A

Topical steroids
1. Swallowed fluticasone
2. Swallowed budesonide
(Oral viscous budesonide, Budesonide orodispersible tablets)

111
Q

What is a well known side of effect of use of PO topical steroids in patients with EOE?

A

20% can get esophageal candidiasis

112
Q

In treating EOE patients with steroids, what treatment consideration should be made for patients with severe EOE (strictures, food impaction or releapse)

A

Continue topical steroids for maintenance therapy

113
Q

In treating EOE patients with steroids, if topical steroids are not effective, what should be considered next?

A
  1. PO steroids Prednisone
  2. Can also consider Dupilumab (Dupixent)
114
Q

what non pharmacological therapy can be used in EOE pts?

A
  1. Food elimination (6 food)- getting rid of the foods that commonly cause allergy (milk, wheat, soy, eggs, nuts, seafood, sesame).
115
Q

what nonpharm treatment option is available for EOE strictures? is it effective?

A

Endoscopic dilation is effective in 90% of EOE stricture for sxs. It doesnt change the # of eosinophils but its effective for sxs. Use balloon dilators.

116
Q

what are common complications of dilating eoe stricutres?

A

chest pain (2%, esophageal tears and perforations (0.3%)

117
Q

Which clinical syndrome is described as a radiologic abnormality, that appears as a posterior indentation at the level of the cricoid cartilage on barium swallow?

A

Cricopharyngeal bar

118
Q

What causes a cricopharyngeal bar?

A

Increased upper esophageal sphincter pressure and decreased compliance (likely 2/2 sphincter fibrosis)

119
Q

What symptoms are associated with the cricopharyngeal bar?

A

orppharyngeal dysphagia to solids and or liquids, cough , choking, throat pain with swallowing.

120
Q

What manometry findings are seen in patients with cricopharyngeal bar?

A

Increased intrapharyngeal bolus pressure, and failure of the upper esophageal sphincter to relax normally.

121
Q

In a patient with dysphagia and a negative work up, what is the significance of finding a cricopharyngeal bar?

A

It is significant, and the patient should be considered for endoscopic dilation. Response to dilation is immediate.

122
Q

How is a zenkers diverticulum treated?

A

by surgical or endoscopic cricopharyngeal myotomy

123
Q

which is the most common type of esophageal cancer in the US?

A

Esophageal adenocarcinoma, more common in white men

124
Q

What are the 4 main risk factors for patients with esophageal adenocarcinoma?

A

GERD, Barretts, smoking, obesity

125
Q

which type of esophageal cancer is more common in blacks? Whites?

A

SCC for blacks, adeno for whites

126
Q

What are the main risk factors for patients with esophageal SCC?

A

caustic injury, smoking, alcohol, achalasia (chronic stasis), radiation, vit c deficiency, plummer Vinson syndrome, HPV

127
Q

What RARE causes of Esophageal SCC is associated with AD disease, with hyperkeratosis of the palms and feet?

A

Tylosis

128
Q

How is esophageal cancer diagnosed?

A

Endoscopy and biopsy, then staging with PET/CT, EUS +/- FNA

129
Q

What is the treatment for esophageal cancer for small and early tumors (T1a or T1b)?

A

EMR if there are no region lymph nodes or mets. EMR with ablation is preferred over esophagectomy in t1 tumors due to lower adverse events.

130
Q

which features suggest low risk of advanced esophageal tumor?

A
  1. less than 500 um invasion of the submucosa for adenocarcinoma
  2. good to moderate differentiation
  3. absence of lymphatic invasion
131
Q

Under what circumstance is esophagectomy indicated over EMR+ ablation?

A

In esophageal cancer pts with T2, T3 cancers without LN involvement.

132
Q

Under what circumstance is chemoradiotherapy indicated over esophagectomy ?

A

chemorads therapy is indicated in pts with locally advanced or metastatic cancers.

133
Q

Under what 2 circumstances do we recommend screening for esophageal cancer?

A
  1. In patients with Tylosis starting at age 30, and every 1 to 3 years
  2. In patients with a caustic esophageal injury 15 to 20 years after ingestion, repeat q1 to 3 years
134
Q

is screening for esophageal cancer in pts with achalasia recommended?

A

nO

135
Q

Which type of caustic ingestion is associated with liquefactive necrosis as a mechanism of tissue injury?

A

Alkaline ingestion

136
Q

Which type of caustic ingestion is associated with coagulative necrosis as a mechanism of tissue injury?

A

Acidic ingestion

137
Q

Which type of caustic ingestion (alkaline or acidic) is usually more severe?

A

Alkaline (also more common in western countries)

138
Q

What are the most concerning signs for patients with a caustic ingestion?

A
  • subcutaneous emphysema (means esophageal perforation)
  • rebound abdominal tenderness and guarding (gastric perforation)
139
Q

How should patients with caustic ingestions be managed?

A

NPO, supportive care
- DONT give emetics and dont do gastric lavage
- If signs of perforation, CXR and chest CT
- If hoarseness, stridor, consider ET intubation

140
Q

In a patient who is asymptomatic with history of ingesting a small amount or a weak caustic substance, is EGD required?

A

EGD can be deferred and pt discharged within 6 to 12 hours. Otherwise should be done within 24 to 48 hours of ingestions.

141
Q

What are the main contraindications to EGD in patients with caustic ingestion?

A

respiratory distress, severe chest pain, suspicion or confirmation of esophageal perforation

142
Q

which type of ingestion should we avoid an EGD? why? and during what time frame

A

Avoid EGD within 5 to 15 days of corrosive ingestion due to tissue softening and increased risk of perforation.

143
Q

what other treatment options are available for patients with caustic ingestion?

A

Sucralfate, PPI

144
Q

WHAT ARE THE LATE COMPLICATIONS OF CAUSTIC ingestion?

A

Strictures (so do a barium swallow prior to endoscopy). You can use wire guided balloon dilation for these bad strictures.

145
Q

How often should a patient with history of caustic injury be screened for SCC?

A

15 to 20 years after exposure, then every 1 to 3 years

146
Q

Pertaining to high resolution manometry, which value measures LES pressure by evaluating a continuous or interrupted 4-second relaxation in a 10 second window and then measuring the median value.

A

Integrated Relaxation Pressure

147
Q

Pertaining to high resolution manometry, which value measures the vigor (power) of the distal esophageal contraction (normal range 450 to 8000).

A

Distal contractile integral (DCI)

148
Q

Which Distal contractile integral (DCI) values indicate failed peristalsis?

A

DCI values below 100

149
Q

Which Distal contractile integral (DCI) values indicate weak peristalsis?

A

DCI values between 100-450 (ineffective swallows)

150
Q

Which Distal contractile integral (DCI) values indicate hypercontractile pattern peristalsis?

A

DCI >8000

151
Q

WHICH value measures the contiguity of peristalsis using 20mmHg isobaric contour ?

A

Contractive wave integrity

152
Q

after what length of time is a peristalsis break (discontinuity of peristalsis) considered a large break and is deemed ineffective swallows?

A

Greater than 5 seconds

153
Q

WHICH value measures from the onset of swallow to the contractile deceleration point?

A

Distal latency

154
Q

A distal latency less than what amount indicates premature/spastic contraction?

A

Less than 4.5 seconds

155
Q

which clinical syndrome is associated with the esophageal content is trapped between two simultaneous contracting esophageal segments, seen as a vertical isobaric pressure band at IC >30mmhg?

A

Pan esophageal Pressurization

156
Q

How is penesophageal pressurization different from intrabolus pressurizaiton?

A

Intrabolus pressurization is seen as compartmentalization of intrabolus pressure at an IC ?20MMHG that precede the esophageal contraction above the Esophagogastric junction

157
Q

How is the median (IRP) Integrated Relaxation Pressure DIFFERENT in disorders of the EGJ outflow (achalasia) and disorders of peristalsis (spasms, hypercontractile, etc)?

A

Disorders of the EGJ have elevated MEDIAN IRP, while disorders of peristalsis have normal MEDIAN IRP.

158
Q

Which type of achalasia is associated with 100% failed peristalsis and no pan esophageal pressurization?

A

Type 1 achalasia (classic)

159
Q

Which type of achalasia is associated with 100% failed peristalsis and greater than 20% pan esophageal pressurization?

A

Type 2 achalasia

160
Q

Which type of achalasia is associated with no evidence of peristalsis and greater than 20% swallows with premature/spastic contractions?

A

Type 3 achalasia (spastic achalasia)

161
Q

Which type of achalasia is associated with greater than 20% swallows with increased intrabolus pressure in supine position?

A

EGJ outflow obstruction

162
Q

which peristalsis disorder is associated with 100% failed peristalsis (DCI<100)?

A

Absent contractility

163
Q

which peristalsis disorder is associated with >20% swallows with premature/spastic contractions?

A

distal esophageal spasms

164
Q

which peristalsis disorder is associated with >20% swallows with hypercontractile pattern (DCI >8000)?

A

Hypercontractile esophagus

165
Q

which peristalsis disorder is associated with >70% ineffective swallows (DCI<100) or weak DCI (100-450), OR break >5 sec or more tan 50% failed peristalsis

A

In effective esophageal motility

166
Q

What is the pathophysiology of achalasia ?

A

achalsia results from the selective loss of post ganglionic inhibitory neurons containing nitric oxide and substance P., leads to continuous cholinergic stimulation and high LES pressure

167
Q

Which clinical syndrome shows histology with inflammatory infiltrate around the ganglion cells in the myenteric plexus of the LES?

A

Achalasia

168
Q

Normally the esophagus contracts and relaxes in a series. In achalasia, there is loss of relaxation, and then abnormal contraction. The resulting dysmotility of the esophagus is confined to what two areas? why?

A

It is confined to the mid and distal esophagus where smooth muscle forms the muscular layer of the esophagus

169
Q

which infection can cause achalasia?

A

Chagas disease (Trypanosoma cruzi)

170
Q

What things can cause a pseudoachalasia?

A
  1. Tumor at GE junction or cardia, invading the myenteric plexus of the LES
  2. Paraneoplastic achalasia afrom extraintestinal malignancy (lung cancer. Patient will have POSITIVE ANTINEURONAL ANTIBODIES
171
Q

When should pseudo achalasia be suspected over just regular achalasia?

A

Older patient, with QUICK AND SHORT duration of symptoms, less than 6 months AND rapid weight loss. In this group, perform cross sectional imaging of the chest and abdomen +/- EUS of the distal esophagus and gastric cardia

172
Q

if you suspect a tumor causing psueodoachalasia, what should be done in terms of workup?

A

Cross sectional imaging of the chest and abdomen +/- EUS of the distal esophagus and gastric cardia

173
Q

What work up is needed for achalasia?

A
  1. EGD to rule out mechanical obstruction and GEJ tumor
  2. Barium swallow (dilated esophagus and tight LES bird beaks appearance)
  3. Esopahgeal manometry
174
Q

Wat are the two key features of manometry that suggest achalasia?

A
  1. Absent esophageal peristalsis (all swallows either fail or are premature)
  2. EGJ outflow abnormality: absent or incomplete LES relaxation with elevated IRP
175
Q

in what situations can you get false negative manometry for achalasia?

A

When using conventional manometry with out the use of pressure topography. This is due to significant esophageal shortening during swallowing resulting in distal sensor recording the low pressure in the gastric cardia instead of the LES (Misinterpreted as LES relaxation).

176
Q

Using conventional manometry with out the use of pressure topography can lead to false negative manometry for achalasia. How can this be avoided?

A

Use high resolution manometry with pressure topography corrects for esophageal shortening and gives accurate measurements of LES relaxation

177
Q

which type of achalasia has a better response to treatment compared to the others?

A

Type 2, responds better to treatment with pneumatic dilation compared to lasproscopic myotomy.

178
Q

For which type of achalasia is POEM (per oral endoscopic myotomy) more effective ?

A

In type 3 achalasia due to the ability to perform an extended myotomy that treats the entire contracted segment of the LES in the distal esophagus.

179
Q

which score system is used to assess symptoms for patients with achalasia?

A

Eckardt

180
Q

When to use medical over surgical management of pts with achalasia? Which medical management options are used for patients with achalasia?

A
  1. Provides temp relief but use in those who cant tolerate surgery ir endotherapy
  2. Nifedipine, isosorbide nitrates sildenafil
181
Q

describe the process of pneumatic dilation for Achalsasia

A

Baloon dilator is used to break the muscular fibers of the LES, pass it over the GEJ and then inflate for 30 to 60 seconds. start at 30 fo rmost pts

182
Q

what percentage of pts have an immediate response rate to pneumatic dilation?

A

70% to 90%

183
Q

which predictors are associated with poor response to pneumatic dilation?

A
  1. Less than 40 y/o
  2. Male
  3. Pre-dilation LES pressure >20mmHG
  4. Type 3 achalasia
184
Q

How is botox used to treat achalasia? How effective is it?

A

Botox inhibits the excitatory acetylcholine releasing neurons that leads to decreased LES pressure. Its injected into 4 quadrants of the esophagus at the level of the LES 1cm above normal z line. 70to 90% have an initial response rate

185
Q

If the Heller myotomy is used to treat achalasia, how effective is this for an immediate response? and what should be done after the myotomy?

A

Myotomy is more than 85% effective
Have to do partial fundoplication post myotomy to decrease risk of GERD

186
Q

WHAT are contraindications to POEM (per oral endoscopic myotomy)?

A
  1. History of esophageal or mediastinal radiotherapy
  2. Coagulopathy
  3. Low platelets
  4. Severe pulmonary disease
  5. Prior esophageal mucosal ablative therapies
  6. Cirrhosis with portal hypertension
187
Q

which achalasia patients should be initially considered for botox vs dilation or myotomy?

A

If they are high surgery risk do botox

188
Q

Which clinical syndrome is associated with a normal IRP, and manometry shows >20% swallows with premature contractions?

A

Distal esophageal spasm (cork screw esophagus)

189
Q

Which clinical syndrome is associated with a DCI of ?8000 in at leat 2 swallows and a normal LES and IRP??

A

Hypercontractile esophagus (Jackhammer, Nutcracker)

190
Q

How are both Hypercontractile esophagus (Jackhammer, Nutcracker) and Distal esophageal spasm (cork screw esophagus) treated?

A
  1. Control GERD with PPI
  2. Trial of TCA, CCB, Nitrates, sildenafil, Botox
191
Q

which clinical syndrome is associated with esophageal symptoms but has normal appearing esophagus and LES on EGD, but has elevated IRP in both the supine and upright positions, and increased intrabolus pressure in >20% of swallows with normal peristalsis?

A

Functional Esophagogastric Junction Outflow Obstruction (EGJOO)

192
Q

In patients with scleroderma, esophageal symptoms develops in 50%6 of pts. Pts can present with severe GERD and dysphagia. What is seen on manometry?

A

Weak or absent esophageal contractions in the distal 2/3 of the esophagus, and low LES pressure.

193
Q

what are the main causes of Functional Esophagogastric Junction Outflow Obstruction (EGJOO)?

A
  1. Fundoplication (tight rap)
  2. paraoesophageal HERNIA
  3. Eosinophilic esophagitis
  4. infiltrative esophageal process
  5. chronic opiate use
  6. early achalasia
194
Q

what options for investigation should be sought in patients with manometry findings of Functional Esophagogastric Junction Outflow Obstruction (EGJOO)?

A
  1. Times barium swallow
  2. EndoFLIP
195
Q

For patients with Barrett’s esophagus who have a raised lesions , whats the treatment recommendation?

A

Current Barrett’s esophagus guidelines recom-
mend resection of any raised lesions in the setting of Barrett’s esophagus. Radiofrequency
ablation should be performed after resection of
raised lesions or in the setting of flat Barrett’s
esophagus (ie, no raised lesions) with dysplasia.
Typically, after the raised lesion is resected, endoscopic eradication therapy with ablation
would be performed.

196
Q

In the setting of Barretts esophagus, esophagitis and chronic inflammation, if
indefinite dysplasia is found on biopsies, what is the best way to manage this?

A

In the setting of esophagitis and chronic inflammation, the diagnosis of dysplasia can be difficult to ascertain, often leading to a pathology read
showing indefinite dysplasia. For someone who is not on a proton pump inhibitor, the next best
step would be to start a proton pump inhibitor and repeat the upper gastrointestinal endoscopy with biopsy in 8 to 12 weeks to confirm dysplasia versus inflammation artifact.

197
Q

In the setting of nondysplastic Barrett’s esophagus, what is the he current recommendation is to perform surveillance endoscopy?

A

surveillance endoscopy within 3 to 5 years.

198
Q

In the setting of HIGH GRADE DYSPLASIA in BARRETTS, which will provide the most accurate evidence of depth of tissue invasion?

A

In the setting of nodular Barrett’s esophagus, the lesion is most likely high-grade dysplasia or early-stage esophageal adenocarcinoma. Endoscopic
mucosal resection of the nodule will provide the most accurate evidence of tissue invasion as the pathologic assessment can evaluate the mucosa
and submucosal layers. Endoscopic ultrasound can assess tissue invasion depth, but
accuracy in dysplasia or early-stage esophageal adenocarcinoma (T1) is limited.

199
Q

Which 6 food groups are associated with eosinophilic
esophagitis ?

A

The 6 food groups associated with eosinophilic
esophagitis are dairy, eggs, fish/shellfish, nuts, soy,
and wheat.

200
Q

In young patients with a history of asthma, eczema, and allergies, dysphagia is most
often caused by what?

A

eosinophilic esophagitis.

201
Q

What is the most likely adverse outcome related
to An esophageal dilation??

A

Postprocedural pain

202
Q

in pts taking swallowed topical steroids for EOE, whats the most common side effects of using this med?

A

Candida esophagitis occurs in approximately 5% to 15% of individuals on swallowed topical steroids.

203
Q

for pts with EoE and
heartburn symptoms (or esophageal changes distally), what is the best iniital tx?.

A

PPIs are often the first choice in
treatment of EoE, especially in individuals with
heartburn symptoms.

204
Q

Coughing while eating likely indicates what type of-
dysphagia?

A

Coughing while eating likely indicates oropharyngeal dysphagia.

205
Q

whats the best test to evaluate oropharyngeal dysphagia?

A

The
best test to evaluate oropharyngeal dysphagia

is a modified barium swallow.

206
Q

which condition is associated with a pt presenting with dysphagia, skin rash and proximal muscle weakness, elevated creatine kinase level and positive ANA
and anti-SAE antibody?

A

In cases of dermatomyositis, the most likely reason for trouble swallowing is oropha-
ryngeal dysphagia.

207
Q

In this young patient without history of gastrointestinal
reflux disease, heartburn, or regurgitation, but has mid-esophageal ulceration, what the dx and cause?

A

In this patient without history of gastrointestinal
reflux disease, heartburn, or regurgitation, the
most likely etiology of mid-esophageal ulceration
in pill-induced esophagitis. A young person with acne may be prescribed an antibiotic (doxycy-
cline), which makes this the most likely etiology. The most likely etiologies of pill-induced esophagitis include antibiotics, nonsteroidal anti-inflammatory drugs, and bisphosphonates. The other medications are not known to cause esophagitis.

208
Q

What is the most likely etiology of mid-esophageal ulceration without evidence of distal esophagitis?

A

The most likely etiology of mid-esophageal ulceration without evidence of distal esophagitis is pill-induced esophagitis. The most likely etiologies of pill-induced esophagitis include antibiotics, nonsteroidal anti-inflammatory drugs, and bisphosphonates.

209
Q

which clinical syndrome with dysphagia patients in their seventh or eighth decade of life
and presents with regurgitation, halitosis, and dysphagia?

A

Zenker’s diverticulum. This is typically seen in patients in their seventh or eighth decade of life and presents with regurgitation, halitosis, and dysphagia.

210
Q

whats the age group Associated with pts with zenkers diverticulum?

A

70s and 80s year ols

211
Q

which esophageal layers does zenkers go through?

A

A Zenker’s diverticulum is a sac-like out-pouching of the mucosa and submucosa through
Killian’s triangle, an area of muscular weakness between the transverse fibers of the cricopharyngeus muscle and the oblique fibers of the lower inferior constrictor muscle.

212
Q

Esophageal dysmotility typical-
ly causes issues with dysphagie to what things?

A

solids and liquids

213
Q

best management of a Schatzki’s ring?

A

The most important management is to disrupt the ring of tissue, which can be done via balloon dilation. dilation. Other possible methods of disruption of the ring include
tissue biopsy and cautery using a needle knife; however, the majority of Schatzki rings respond adequately to balloon dilation.

214
Q

which clinical finding is associated with heterotopic gastric mucosa of the upper
esophagus, found incidentally and do not cause symptoms?

A

An inlet patch, otherwise
known as heterotopic gastric mucosa of the upper
esophagus. Inlet patches range in size from 2 mm
to 4.5 cm and can be solitary or multiple. Most
inlet patches are found incidentally and do not cause symptoms. Because most are asymptomatic, further therapy is not necessary. Argon

215
Q

which clinical syndrome is seen when esophageal ulcerations are noted in the presence of multinucleated giant cells?

A

Viral esophagitis (herpes esophagitis)

216
Q

Which conditions is assoc with the presence of persistent, dysphagia and nonpainful sensation in the throat without structural lesions, occurrence of symptoms between meals, absence of dysphagia or odynophagia, and absence of a gastric inlet patch?

A

This presentation demonstrates a typical case oglobus sensation that meets the criteria including
presence of persistent, nonpainful sensation in
the throat without structural lesions, occurrence of symptoms between meals, absence of dysphagia or odynophagia, and absence of a gastric inlet patch. The mainstay of treatment for globus sensation remains explanation and reassurance.

217
Q

for a patient with typical GERD symptoms, whats the tx?

A

This presentation represents typical symptoms of GERD without warning signs or symptoms, for which an 8-week
trial of single-dose proton pump inhibitor (PPI) therapy is recommended.

218
Q

for pts with suspected GERD who did not respond with PPI therapy, after they have an EGD to rule out erosive reflux
disease, what should be next?

A

manometry

219
Q

When is Evaluation with upper GI endoscopy would recommended in GERD?

A

Evaluation with upper GI endoscopy would be recommended if warning signs or symptoms (dysphagia, weight loss, anemia, signs of upper
GI bleeding) were present and/or if the patient
did not derive symptom response with PPI
therapy.

220
Q

at what point should Antireflux surgery such as Nissen fundoplication be considered in patients with established objective GERD?

A

Antireflux surgery such as Nissen fundoplication should only be considered in patients with established objective GERD.

221
Q

in a pt with extraesophageal symptoms in the absence of typical reflux symptoms and absence of warning signs or symptoms, what is the pretest probability of laryngopharyngeal
reflux? and what is the next best step in evaluation for gastroesophageal reflux?

A

in the absence of typical reflux symptoms and absence of warning signs or symptoms.

The pretest probability of laryngopharyngeal
reflux is low in this patient, and the next best step
is objective evaluation for gastroesophageal reflux
disease with ambulatory reflux monitoring before a trial of proton pump inhibitor therapy.

222
Q

For patients with EGD showing LA Grade D severe erosive reflux disease should you do PPI or 4 quad biopsies?

A

severe erosive reflux
disease for which double-dose proton pump inhibitor therapy for 8 weeks is recommended
followed by an upper endoscopy to evaluate for healing of the esophagitis and surveillance for potential underlying Barrett’s esophagus. In the set-
ting of esophagitis, 4-quadrant biopsies are not indicated and can yield a false-positive diagnosis of intestinal metaplasia (Barrett’s esophagus).

223
Q

If the EGD shows erosive esophagitis, is ambulatory reflux monitoring necessary?

A

Cases that demonstrate erosive esophagitis are indicative of gastroesophageal reflux disease; thus, ambulatory reflux monitoring is unnecessary.

224
Q

Are H2 receptor antagonists effective at healing erosive esophagitis ?

A

H2 receptor antagonists are not very effective at healing erosive esophagitis but may be used for mild symptoms of gastroesophageal reflux disease in the absence of esophagitis.

225
Q

how is functional heart
burn defined in the Rome IV criteria?

A

typical heartburn symptoms in the presence of normal upper endoscopy findings, normal ambulatory reflux testing, and negative association between symptoms and reflux events.

226
Q

What clinical condition is defined by elevated
acid exposure on ambulatory reflux monitoring in
the presence of normal upper endoscopy findings.?

A

Nonerosive reflux disease

227
Q

Which condition associated wit this pic?

A

lichen planus

228
Q

what is the main difference between Functional heartburn
and Nonerosive reflux disease?

A

Functional heartburn is everything normal on investigation (normal upper endoscopy findings, normal ambulatory reflux testing) AND has negative association between symptoms and reflux events, WHEREAS nonerosive reflux disease, has elevated acid exposure on ambulatory reflux monitoring in the presence of normal upper endoscopy findings..

229
Q

What is The recommended management of functional
heartburn?

A

The recommended management of functional heartburn is neuromodulation in the form of a low-dose antidepressant and/or behavioral therapy. In addition, PPI therapy should be tapered
off as tolerated. Antireflux surgery such as Nissenfundoplication is not indicated for functional heart-
burn.

230
Q

prior to antireflux surgery, what studies should be done and why?

A

its important to exclude a major esophageal motor disorder, such as achalasia, on high-resolution esophageal manometry before proceeding with antireflux surgery, as achalasia is a contraindication to antireflux surgery.

231
Q

clinical syndrome assoc with presence of persistent, nonpainful sensation in
the throat without structural lesions, occurrence of symptoms between meals, absence of dysphagia or odynophagia, and absence of a gastric inlet
patch.

A

globus sensation

232
Q

what is the potential cause of GERD in patients with hiatal hernia?

A

a disrupted antireflux barrier in the setting of a large hiatal hernia. Intraabdominal strain and retained bolus in the hiatal hernia are the primary drivers of gastroesophageal reflux disease (GERD) in this setting and cannot be reversed with PPI
therapy.

233
Q

which type of of achalasia is characterized by
inadequate lower esophageal sphincter relaxation
(elevated median IRP), 100% failed peristalsis
with panesophageal pressurization in 20% or
more of swallows?

A

achalasia type 2, which is characterized by
inadequate lower esophageal sphincter relaxation
(elevated median IRP), 100% failed peristalsis
with panesophageal pressurization in 20% or
more of swallows.

234
Q

how do you differentiate type 1 achalasia from type 2?

A

Both have median IRP elevated with 100% failed peristalsis but type 1 is without panesophageal pressurization and type 2 is with panesophageal pressurization in 20% or more of swallows.

235
Q

what is The recommended first-line treatment for type 3 achalasia?

A

The recommended first-line treatment for type 3 achalasia is a myotomy across the lower esophageal sphincter with proximal extension along the spastic segment in the esophagus. This is generally achieved via peroral endoscopic myotomy. Endoscopic botulinum toxin injection can be trialed for patients who are not candidates for myotomy.

236
Q

which clinical syndrome is characterized by intact lower esophageal sphincter relaxation (normal median IRP) with more than 70% of swallows ineffective or at least 50% swallows failed.?

A

ineffective esophageal motility, is intact lower esophageal sphincter relaxation (normal median IRP) with more than 70%
of swallows ineffective or at least 50% swallows failed. An ineffective swallow is defined as havin a distal contractile integral less than 450 mmHg-s-
cm or a fragmented swallow with a peristaltic break

greater than 5 cm.

237
Q

Which entity is associated with at least 20% of esophageal contractions having a DCI of over 8000?

A

Hypertensive peristalsis or jackhammer esophagus

238
Q

which clinical entity is associated with all swallows with DCI <100?

A

absent peristalsis (Failed contractions)

239
Q

Which clinical syndrome shows at least 50% of esophageal peristalsis are weak or failed?

A

Ineffective esophageal motility

240
Q

Which clinical syndrome shows at least 50% of esophageal peristalsis with normal DCI, have a peristaltic break (time/space between the UES and LES), more than 5cm (fragmented)?

A

fragmented peristalsis

241
Q

An esophageal distal latency of less than how many seconds is considered to be premature contractions?

A

Less than 4.5 seconds is premature (spasm)

242
Q

clinical syndrome in which a pt with distal latency <4.5 sec for at least 20% or 2 swallows?

A

distal esophageal spasm

243
Q
A

GI Fellowship (11 decks)

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