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GI Boards November 20th 2024 > GERD > Flashcards

GERD Flashcards

1
Q

The presence of characteristic MUCOSAL INJURY seen at ENDOSCOPY and/or abnormal esophageal ACID exposure demonstrated on a REFLUX MONITORING STUDY is known as?

A

GERD

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2
Q

What are the TWO TYPICAL symptoms of GERD?

A

HEARTBURN and REGURGITATION

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3
Q

What is the actual CAUSITIVE agent of INJURY in REFLUX ESOPHAGITIS?

A

INFLAMMATORY CELLS not the acid itself

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4
Q

Chest pain (ESOPHAGEAL); Globus, Sore throat, Burning tongue, Dental erosions, Sinusitis (oropharynx); Laryngitis, Chronic cough, Asthma (airway) are what type of SYMPTOMS?

A

ATYPICAL GERD symptoms
esophageal vs EXTRAESOPHAGEAL

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5
Q

Erythema and Edema in the POSTERIOR Laryngeal region?

A

Laryngopharyngeal Reflux (LPR)

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6
Q

Can a DIAGNOSIS of LARYNGOESOPAHGEAL REFLUX be made on the basis of laryngoscopy findings alone?

A

NO

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7
Q

When presented with EXTRAESOPHAGEAL symptoms (Globus, Sore throat, Burning tongue, Dental erosions, Sinusitis, Laryngitis, Chronic cough, Asthma what should NOT be the first DIAGNOSIS?

A

GERD (explore non-GERD causes)
UNDERGO REFLUX TESTING BEFORE PPI therapy

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8
Q

In patients who have EXTRAesophageal (atypical) GERD symptoms, what SHOULD be done BEFORE trial of PPI therapy?

A

Explore OTHER CAUSES of manifestations (cough, globus, etc.)

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9
Q

In patients who have MIXED EXTRAesophageal (atypical) GERD symptoms, and TYPICAL symptoms (HEARTBURN, REGURGITATION) what SHOULD be done for therapy?

A

BID PPI for 8-12 weeks

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10
Q

WHEN are ENDOSCOPIC or SURGICAL procedures to FIX REFLUX recommended in a patient with ATYPICAL symptoms of GERD?

A

Only when OBJECTIVE evidence (see mucosal changes on EGD) exists for reflux

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11
Q

How long is a swallow-induced LESrelaxation and can REFLUX occur during these?

A

< 10 seconds
NO! (accompanied by a peristaltic wave)

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12
Q

What is the most COMMON mechanism for PHYSIOLOGIC REFLUX?

A

TLESR (Transient LES Relexation) or the “belch reflex” which occurs during gastric distention to allow trapped air to get our and are >10 seconds long

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13
Q

How can you REDUCE the physiologic TLESR episodes?

A

BACLOFEN (acts on the TLESR inhibitor GABAb receptor)

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14
Q

Do you ROUTINELY TEST for H.pylori in a patient with GERD?

A

NO

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15
Q

If H.pylori is found in a patient, do you treat?

A

ALWAYS

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16
Q

How are H.pylori and GERD, Barrett’s Esophagus and esophageal Adenocarcinoma related?

A

H.pylori is found MUCH LESS in patients with Barret’s or Adenocarcinoma or GERD because it causes GASTRITIS and thus a REDUCTION in REFLUX

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17
Q

What CONDITION is associated with GERD and BARRETT’s ESOPHAGUS?

A

OBESITY

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18
Q

What is done for patients with CLASSIC (typical) GERD symptoms (heartburn, regurgitation) WITHOUT ALARM symptoms (bleeding, weight loss, dysphagia)?

A

8 WEEK trial of PPIs taken ONCE DAILY before meal

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19
Q

WHEN do you do ENDOSCOPY for patient with CLASSIC (typical) GERD symptoms (heartburn, regurgitation) and WITHOUT alarm symptoms (bleeding, weight loss, dysphagia)?

A

AFTER 8 WEEK trial if INADEQUATE to control symptoms OR if symptoms return 2-4 weeks after PPI is STOPPED

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20
Q

Can GERD or EoE be DIAGNOSED on EGD if PPIs have NOT been stopped?

A

NO!!

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21
Q

Troublesome REFLUX-RELATED symptoms in the ABSENCE of endoscopically visible MUCOSAL BREAKS?

A

NERD (Non-Erosive Reflux Disease)

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22
Q

What medication CLASS can RAPIDLY provide relief for heartburn BUT cannot be used to HEAL REFLUX ESOPHAGITIS?

A

H2 Blockers (cimetidine, famotidine, nizatidine) - develop tolerance with REGULAR use

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22
Q

How LONG MUST you STOP PPIs for before performing an EGD to be able to DIAGNOSE GED/NERD/EoE?

A

2-4 WEEKS

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23
Q

First-Line therapy for LA Grade C & D Esophagitis?

A

PPIs (metabolized by CYP2C19)

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24
Q

Which of the PPIs is the MOST POTENT?

A

RABEPRAZOLE (followed by ESOMEPRAZOLE)

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25
Q

Which of the PPIs is the WEAKEST?

A

PANTOPRAZOLE

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26
Q

What is the FIRST STEP in management of REFRACTORY GERD?

A

Optimization of PPI therapy

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27
Q

WHEN are PPIs MOST EFFECTIVE?

A

When taken 30-60 minutes BEFORE MEALS
(because they’ll be in the blood stream just as the PARIETAL cells start secreting acid which is what PPIs need to work)

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28
Q

Is the use of PPIs associated with ANY adeverse events (cardiovascular, cancer, renal, anticoagulation interference, etc.?)

A

NO!! (only mild entericinfections)

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29
Q

Patients with OBJECTIVE evidence of SEVERE reflux esophagitis, LARGE hiatal hernias, or PERSISTENT GERD symptoms would benefit from this?

A

FUNDOPLICATION (surgery)

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30
Q

What is the GERD recurrence rate after SURGERY (fundoplication) that requires return to PPI therapy?

A

10-30% in 5 years

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31
Q

In patients with REGURGITATION GERD symptoms who FAIL PPI therapy and who want an ALTERNATIVE to fundoplication, what do you recommend?

A

MAGNETIC Sphincter Augmentation (MSA)

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32
Q

In patients who have TROUBLESOME HEARTBURN or REGURGITATION GERD symptoms, who do NOT have SEVERE reflux esophagitis (LA Grades C&D), HIATAL HERNIAS < 2 cm and who want an ALTERNATIVE to surgery, what do you recommend?

A

TIF

33
Q

What is the SURGICAL procedure of CHOICE for GERD in OBESE patients?

A

Roux-en-Y gastric bypass

34
Q

How does SLEEVE GASTRECTOMY affect GERD?

A

Can CAUSE it or WORSEN GERD

35
Q

What is meant by a STEP-UP approach for treating GERD in the 65% of women who have this during PREGNANCY?

A

LIFE STYLE modifications –> SUCRALFATE –> H2 (famotidine) –> PPIs (EXCEPT omeprazole)

36
Q

Is there a BENEFIT of treating GERD with SUCRALFATE outside of PREGNANCY?

A

NO

37
Q

Which TWO PPIs should be AVOIDED when during PREGNANCY?

A

OMEPRAZOLE and ESOMEPRAZOLE (during breastfeeding)

38
Q

What is REFLUX HYPERSENSITIVITY?

A

PERSISTENT REFLUX events that evoke symptoms of HEARTBURN when there is no longer ACID refluxing - esophageal REFUX monitoring

39
Q

When a patient has persistent GERD-SYMPTOMS and extraesophageal causes (cardiac, biliary), non-reflux disorders (achalasia, EoE), reflux hypersensitivity and ACID has been neutralized by PPIs, what is the condition called?

A

FUNCTIONAL heartburn

40
Q

What is C4M6 Barrett’s Esophagus?

A

LONG-SEGMENT Barrett’s Esophagus (C=circumferential extent and M=extent in cm)

41
Q

In a patient in whom GERD is SUSPECTED but NO OBJECTIVE evidence on EGD, whats the NEXT diagnostic step?

A

pH MONITORING OFF PPIs to be able to establish the diagnosis of GERD

42
Q

On pH MONITORING, what constitutes PATHOLOGIC REFLUX?

A

ACID EXPOSURE >6% of the time (< 4% is NORMAL)

43
Q

In a patient with an ESTABLISHED diagnosis of GERD whose symptoms have NOT ADEQUATELY responded to BID PPI therapy, what is the DIAGNOSTIC recommendation?

A

ph IMPEDANCE (catheter only) study ON PPI therapy - to detect ACIDIC and NON-ACIDIC reflux episodes (bile, etc.)

44
Q

Should you perform REFLUX MONITORING OFF PPIs solely as a DIAGNOSTIC test for GERD if there is OBJECTIVE (EGD) evidence of LA Grade C or D esophagitis or presence of LONG-SEGMENT BARRETT’s Esophagus?

A

NO!! (because severe esopahgitis an long-segment Barrett’s ARE considered OBJECTIVE EVIDENCE of GERD)

45
Q

What test allows you to make DIAGNOSIS of REFLUX HYPERSENSITIVTY?

A

COMBINED ph-IMPEDANCE study (pH montoring ONLY measures when reflux pH is < 4 whereas impedence monitoring identifies ALL reflux)

46
Q

In a REFLUX monitoring test, a SYMPTOM INDEX (SI) >50% or Symptom Association Probability (SAP) >95% indicate what?

A

SIGNIFICANT ASSOCIATION between RFLUX episodes and SYMPTOMS

47
Q

The condition in which there is NORMAL esophageal acid exposure but POSITIVE Symptom Index (SI >50%) or Symptom Association Probability (SAP >95%) for heartburn and reflux episodes is called?

A

REFLUX HYPERSINSITIVITY

48
Q

Biopsies of the EGJ show Specialized Intestinal Metaplasia?

A

Barrett’s Esophagus

49
Q

High-Grade Dysplasia in Barrett’s Esophagus increases the risk of ADENOCARCINOMA by what percentage per year?

A

5-8% per YEAR

50
Q

Whenever DYSPLASIA of ANY GRADE is detected on Barrett’s biopsies, what MUST BE DONE NEXT?

A

CONFIRMED by a SECOND PATHOLOGIST with EXPERTICE in GI PATHOLOGY

51
Q

What QUALIFIES as SCREENING EGD for Barrett’s Esophagus?

A

CHRONIC GERD symptoms AND ≥3 RISK FACTORS (age >50, Obese, Smoker, Family History, White, Male)

52
Q

Once BARRETT’s is DIAGNOSED, what is RECOMMENDED for SURVEILLACE EGD for DYSPLASIA?

A

BOTH WHITE LIGHT and CHROMO endoscopy AND a STRUCTURED BIOPSY protocol

53
Q

What QUALIFIES as a STRUCTURED BIOPSY PROTOCOL surveillance for a patient with BARRETT’s esophagus (Seattle Protocol)?

A

4 QUADRANT biopsies every 2 cm for NO DYSPLASIA
4 QUADRANT biopsies every 1 cm for POSITIVE DYSPLASIA

54
Q

In NON-DYSPLASTIC Barrett’s Esophagus, what is the SURVEILLANCE interval for SHORT-SEGMENT (< 3 cm) vs LONG-SEGMENT (≥3 cm) Barrett’s Esophagus?

A

SHORT-SEGMENT: every 3 YEARS
LONG-SEGMENT: every 5 YEARS

55
Q

Medication-wise, what should a Barrett’s patient be on?

A

ONCE-A-DAY PPI

56
Q

Should anti-reflux SURGERY be performed for cancer PREVENTION in a patient with Barrett’s?

A

NO!!

57
Q

What is RECOMMENDED for a patient with confirmed Barrett’s esophagus with HIGH-GRADE dysplasia?

A

ERADICATION THERAPY

58
Q

What are the THREE grades of T1a lesions that can ALL be removed endoscopically and are limited to the MUCOSA?

A

m1, m2(< 2% LN mets), m3 (4-7% LN mets)

59
Q

What are the THREE grades of T1b lesions that CANNOT be removed endoscopically (except sm1) and are limited to the SUBMUCOSA?

A

sm1(13% LN mets), sm2(26% LN mets), sm3 (67% LN mets)

60
Q

What is the ONLY EXCEPTION where a T1b lesion CAN be resected endoscopically?

A

As an ALTERNATIVE to ESOPHAGECTOMY T1b sm1 (good-moderate differentiation), NO lymphovascular invasion (no poorly differentiated tumors)

61
Q

What is the BEST METHOD for T-STAGING a tumor in the GIT?

A

EMR or ESD (staging & therapeutic), NOT EUS

62
Q

Preferred TREATMENT of Barrett’s Esophagus with DYSPLASIA?

A

FIRST: EMR/ESD of ANY VISIBLE abnormality.
SECOND: RFA (prevents progression to neoplasia and cancer)

63
Q

What is meant by ENDOSCOPIC ERADICATION THERAPY of BARRETT’s ESOPHAGUS with DYSPLASIA (regardless of what grade)?

A

EMR/ESD + RFA

64
Q

AFTER endoscopic ERADICATION therapy for Barrett’s Esophagus and COMPLETE elimination of intestinal metaplasia, how long do you perform SURVEILLANCE on these patients?

A

LIFE-LONG (due to frequent RECURRENCE)

65
Q

After COMPLETE ELIMINATION of Barrett’s (intestinal metaplasia) for patients with HIGH-GRADE dysplasia or INTRAMUCOSAL CARCINOMA prior to having the complete ablation done, is HOW FREQUENT do you perform SURVEILLANCE EGD?
What if the just had LOW-GRADE dysplasia prior to eradiction?

A

3 months; 6 months; 12 months; ANNUALLY
For low-grade dysplasia eradication: 1 year; 3 years; every 2 YEARS thereafter

66
Q

When Barrett’s Esophagus RECURS after complete eradication, WHERE does the recurrence occur?

A

AT the EGJ or 1 cm ABOVE

67
Q

When performing SURVEILLANCE EGD after complete Barrett’s eradication, where and how do you biopsy?

A

4 QUARDRANT biopsies AT the EGJ (squamocolumnar area) and 2-3 cm of PROXIMAL NEO-SQUAMOUS epithelium

68
Q

What are the EREFS (Endoscopic Reference Scores) for EoE?

A

Exudsates
Rings
Edema
Furrows
Strictures

69
Q

Histology findigs of ≥15 Eosinophills per HPF, Eosinophil Microabscesses, Basal Zone Hyperplasia, Dilated Intracellular spaces, Subepithelial Fibrosis, MAST cells?

A

EoE (not specific, can see in GERD too)

70
Q

What component of EoE causes PERSISTENT symptoms?

A

MAST cells

71
Q

ALLERGIC conditions such as ATOPIC dermatitis, ASTHMA and RHINITIS are all associated with this GI disorder?

A

EoE

72
Q

The CHANGE of what, impacts symptoms of EoE the most?

A

DIET (elemental diet shown to improve symptoms the most, hence allergens in food) - IL-4 Th2 cytokyne stimulates esophageal Eotaxin-3

73
Q

What immune component attracts EOSINOPHILS to the ESOPHAGUS?

A

EOTAXIN-3 (released by IL-4)
IL-5 makes eosiniphills and IL-13, IL-4 makes EOTAXIN-3 that attracts the eosinophils to the esophagus

74
Q

30%-50% of patients with EoE respond to what TREATMENT?

A

PPIs (because EOTAXIN-3 can be blocked by PPIs)
Topical STEROIDS 6-8 weeks (budesonide, fluticasone) work but EoE RECURS

75
Q

Which DIET treats 91% of EoE patients?
Which DIET treats 72% of EoE patients?

A

91%: ELEMENTAL (super expensive)
72%: ELIMINATION (foods: MILK, GRAINS, Eggs, Soy, Nuts, Seafood)

76
Q

Besides treating patients with PPIs for EoE (blocks EOTAXIN-3) what else is available which DIRECTLY blocks IL-4 & IL-13 PRODUCTION of EOTAXIN-3?

A

DUPILUMAB

77
Q

If DYSPHAGIA persists in EoE patients after treatment, what else can be done?

A

Esophageal DILATION

78
Q

Middle-Aged WHITE woman with ESOPHAGEAL and BUCCAL whitish PLAQUES with STRICTURES that are not resolved by PPIs or DILATION and on biopsy you see SUBEPITHELIAL LYMPHOCYTIC INFILTRATES and CIVATTE BODIES?

A

LICHEN PLANUS

79
Q

BELOW what diameter do most people experience DYSPHAGIA and therefore EGD DILATION should be aimed for what DIAMETER?

A

Below < 13 mm = dysphagia
Dilate 15-18 mm 45-54 F

80
Q

What is the DIFFERENCE in DILATION method between an esophageal STRICTURE and a SCHATZKI ring?

A

STRICTURE is dilated GRADUALLY no more than 3 mm/session, repeat in 1-4 weeks.
SCHATZKI ring is dilated ABRUPTLY to tear it in one session

GI Boards November 20th 2024 (11 decks)

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