GI- Clinical - GERD Flashcards

1
Q

What are the 4 main contents of gastric reflux?

A

Gastric acid (HCl)

Pepsin (ogen)

Gastric Lipase

Gastrin

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2
Q

Pepsin(ogen) is the primary enzyme secreted by the stomach-with its primary purpose: degradation (in presence of acid)

A

protein

HCl

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3
Q

What is being described, physiologic reflux or GERD?

Some degree of GER/LES relaxation is adaptive ie to allow humans to release air swallowed & gas, <50 events/24hr

Minimally symptomatic LES relaxations are very brief

Rarely occurs at night

Does not lead to tissue damage

A

Physiologic reflux

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4
Q

What is being described, physiologic reflux or GERD?

LES relaxations are frequent (>50/24hr) and occur > 2x/wk Symptomatic

Prolonged: commonly> 1- 2 hrs

Often associated with risk factors/ other medical conditions

Often occurs at night/while sleeping If prolonged→tissue damage

A

GERD

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5
Q

The majority of patients with GERD do/do not seek medical attention?

What % of Americans have GERD?

A

do not

20%

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6
Q

GERD is a viscious promoting disease?

A

self

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7
Q

What role does gastrin play as concerning the closing pressure of the LES?

A

decreases LES closing pressure

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8
Q

What are the 3 main contributors of GERD and what is the most common?

A
  1. Flow into stomach impaired (esophageal motility disorder, web/ring)
  2. Flow out of the stomach (sticture, liver/gallbladder/pancreatic mass blocking)
  3. backflow of stomach contents (most common)
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9
Q

What is being described as concerning impaired flow into the stomach?

  • spiderweb shaped
  • semi-circumferential lesion
  • older women
  • fibrovascular connective tissue and epithelium
  • associated with Paterson-Brown-Kelly/ Plummer-Vinson Syndrome
A

Esophageal web

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10
Q

What is being described as concerning impaired flow into the stomach?

  • Circumferential folds
  • thicker, includes mucosa and submucosa
  • Type A Usually above GE junction
  • type B at squamocolumnar junction
A

Esophageal “Schatzki” rings

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11
Q

What can cause impeded flow out of the stomach:

A

stricture

liver/gallbladder/pancreatic mass

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12
Q

Primary etiology for GERD=IS/ IS NOT due to excessive acid production

Usually 2nd to gastro-esophageal junction (due to: LES dysfunction, hiatal hernia, incr. intra-abd pressure…)

A

is not

incompetent

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13
Q

What 3 issues can contribute to incompetent gastro-esophageal junction?

A

LES dysfunction

hiatal hernia

increase intra-abdominal pressure (obesity, pregnancy)

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14
Q

Review risk factors for GERD:

Obesity/wt gain=↑intraabdominal pressure on the

Foods =caffeine, ETOH, tobacco, , chocolate, meds* → ↓LES

Eating habits:

= Eating large meals ➙ distended stomach overwhelms LES closing pressure Fatty meals (stay in stomach longer and incr risk of reflux) & spicy or acidic foods (direct irritant to esophagus and likely relax LES too)

Eating within 2-3 hrs of bedtime→gravity aids reflux

A

LES

peppermint

tone

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15
Q

What pregnancy hormones can relax the LES and what else does pregnancy do to increase risk of GERD?

A

relaxin, progesterone

+ ↑intraabdom. pressure from fetus

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16
Q

Hiatal hernia=diaphragmatic hernia (not uncommon over yrs; occasionally due to injury/excessive ; less commonly-congenital) also increases risk of GERD

A

50

lifting

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17
Q

What are some medications that can increase the risk of GERD?

A

progesterone

antihistamines

anticholinergics

calcium channel blockers

tricyclic antidepressants

nitrates

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18
Q

Which hiatal hernia is more at risk for cutting off blood supply and leading to necrosis- more urgent?

A

paraesophageal hiatus hernia

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19
Q

Which hernia is more common and can have symptoms of GERD?

And what 3 physiologic changes can occur that result in this type of hernia?

A

hiatal hernia

  1. LES pressure is often low
  2. Gastric pouch- intra-thoracic reservoir
  3. Diaphragm- no esophageal pinch
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20
Q

Besides causing heartburn/reflux symptoms, what else might a patient with a large hiatal hernia complain of:

A

mid chest discomfort around the nipple line

wheezing, coughing, SOB

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21
Q

What innervation of the esophagus and stomach maintains normal LES pressures & peristaltic movement through the GI tract?

A

vagus

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22
Q

What are all of these examples of:

A

BARIUM SWALLOW + GERD

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23
Q

What are the 3 most common symptoms of GERD?

A

Heartburn(pyrosis) (burning sensation retrosternally, usually postprandial)-common symptom

Food or acidic reflux into back of throat or mouth-common symptom

Dysphagia (=difficulty swallowing➙common with long standing GERD)

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24
Q

What are the 5 Atypical symptoms of GERD?

A

Chest pain (can mimic angina)

Water brash (hypersalivation sensed by pt needing to swallow excessive saliva)

Globus sensation (constant perception of lump in throat)

Odynophagia (pain with swallowing➙uncommon with GERD)

Extraesophageal=LPR(recurring cough, wheezing, asthma, shortness of breath, throat clearing and postnasal drip sensation, choking episodes esp supine, laryngitis, dental erosions)

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25
Q

If one has typical GERD symptoms of heartburn/regurg and no red flags (unexplained wt loss, anorexia, persistent vomiting, dysphagia, odynophagia, noncardiac chest pain, iron def. anemia, GI bleed, onset age >50)

what is the treatment recommendation?

A

Empiric treatment (lifestyle, +/- PPI’s* once/ day or H2 blockers*) for 6-8 weeks and then as needed

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26
Q

What if the initial treatment does not work ?

A

increase PPI to 2X a day and referr to GI for EGD

27
Q

What if a patient has atypical symptoms (cough, hoarseness, wheeze, dyspepsia, persistent nausea or bloating, epigastric pain) and no red flags

(unexplained wt loss, anorexia, persistent vomiting, dysphagia, odynophagia, noncardiac chest pain, iron def. anemia, GI bleed, onset age >50)?

A

labs (H.pylori, CBC, CMP…), CXR, empiric treatment with lifestyle and PPI’s and refer to GI, ENT if DX unclear or no response

28
Q

What if there are red flags (unexplained wt loss, anorexia, persistent vomiting, dysphagia, odynophagia, noncardiac chest pain, iron def. anemia, GI bleed, onset age >50) ?

A

Endoscopy (EGD) to r/o strictures, erosive esophagitis, Barrett’s esophagus, malignancy

29
Q

What are 3 evaluations methods for GERD?

A

EGD

Nasopharyngoscopy (view of normal and LPR voice box)

24 hr probe

30
Q

The majority/minority of patients with symptoms of GERD who undergo EGD will show abnormalities, such as Erosive Esophagitis (only seen in 30%)?

A

minority

note: erosive esophagitis

31
Q

The minority/majority of patients with GERD symptoms who undergo EGD, will have Non-Erosive Reflux Disease=NERD (70%)

Poor response to PPI’s is common

High % of ‘treatment-resistant’ GERD 17%-24% of NERD pt’s develop erosive esophagitis over time

A

majority

32
Q

Which population of GERD patients commonly have a poor response to PPIs?

A

Non-Erosive Reflux Disease=NERD

33
Q

Describe the progressive process of GERD?

A
34
Q

erosive esophagitis can next lead to:

A

peptic strictures ulcers

35
Q

Barret’s esophagus can lead to :

A

adenocarcinoma

36
Q

What is the first non-surgical treatment and prevention of GERD?

A

lifestyle changes

↓fatty foods, eat smaller meals, no food within 2-3 hrs of lying supine

37
Q

After lifestyle change, what other non-surgical treatments are recommended?

A

Diet: limit caffeine/acidic foods/alcohol/ tobacco/chocolate/high fat/peppermint

Drugs: acid neutralizers (ie Tums), PPI’s (ex. omeprazole/lansoprazole/esomeprazole/ pantoprazole) QD or BID for 6-8 weeks; pro-kinetic agents (ex. domperidone, metoclopramide), H2 blockers (ex. ranitidine), sodium alginate “raft” (Gaviscon Advanced)

Weight loss if overweight or obese

Limit heavy exertion within 2-3 hrs of eating and

avoid tight-fitting clothes

Bed wedge/elevate head bed 6 inches & sleep on L side

38
Q

What does Gaviscom do to treat acid reflux?

A

creates a cap over the gastric contents

39
Q

What are the 4 integrative supplements that Dr. Bennett mentioned she uses to treat GERD?

A

marshmallow, slippery elm, licorice (if no HTN), aloe vera

40
Q

IF YOU BLOCK ACID, DO YOU STOP REFLUX?

IF YOU DON’T STOP REFLUX, WHAT OTHER SUBSTANCE(S) IS/ARE STILL REFLUXED?

A

Gastrin and Pepsin

41
Q

What are the long-term risks for using PPIs involving the kidneys?

A

↑Chronic Kidney Disease (28x increased risk!!!) & Acute Interstitial Nephritis

42
Q

Review the other complications of taking PPIs long term?

A

↑C. difficile, Salmonella and Campylobacter enteritis

↑Colonic colonization of multi-drug-resistant bacteria

Community-acquired, pneumonia

↑Microscopic colitis

↑Risk iron/magnesium/calcium/Vit B12 malabsorption and deficiency

↑Hypochlorhydria → ↑osteoclast activity → ↓bone density →↑risk fracture

↑Gastric hyperacidity if stopped abruptly

↓Effectiveness of clopidrogel↑risk of acute MI?

43
Q

What happens after somone uses H2 blockers for 4 to 6 weeks or more?

A

tachyphylaxis = decreasing efficacy, tolerance

44
Q

What are the 4 surgical options for GERD?

A

Open/laparoscopic Nissen fundoplication (partial-toupet, full)-gold standard (90% pt’s satisfied with procedure at 10 years)

LINX © titanium esophageal ring-no long term data beyond 7 yrs

TIF (Transoral Incisionless Fundoplication)-higher risk of recurrence & only 69% satisfaction at 6mo; no long term data >7 yrs

Bariatric surgery (ie gastric bypass) more effective for morbidly obese with GERD

45
Q

Which surgical option is the gold standard and has two forms?

A

Open/laparoscopic Nissen fundoplication (partial-toupet, full)-gold standard

46
Q

Which surgical method is more effective for morbidly obese with GERD?

A

Bariatric Surgery

47
Q

What is pictured?

A

Esphageal webs and rings

48
Q

What is pictured?

A

Barrett’s esophagus

(intestinal metaplasia)

49
Q

What is pictured?

A

esophageal scarring

50
Q

What is pictured?

A
51
Q

What is pre-cancerous, dysplastic changes in esophageal epithelium 2nd to chronic acid exposure?

A

Barrett’s esophagus

52
Q

What is silent reflux?

A

VI. LARYNGOPHARYNGEAL REFLUX (LPR)

53
Q

What is a key symptom of LPR (LARYNGOPHARYNGEAL REFLUX)?

A

71% Chronic hoarseness

54
Q

What are some other symptoms of LPR?

A

58% Wheezing, asthma, SOB

51% Chronic, non-productive cough

47% Globus sensation

42% Chronic throat clearing (esp after eating)

35% Dysphagia

55
Q

How is LPR different from GERD?

A

GASEOUS/VAPORIZED REFLUXATE OF ACID, PEPSIN AND BILE SALTS

56
Q

Esophagus can handle reflux episodes/day without tissue damage

Larynx and oropharynx develop damage after only episodes/day

A

50

3

57
Q

How do GERD and LPR symptoms differ as concerning:

heartburn

body position

which sphincter is affected

throat related symptoms?

A

GERD- esophagitis, heartburn

LPR- esophagitis and heartburn rare

GERD- reflux is nocturnal or supine position

LPR- reflux in daytime or upright

GERD- lower esophageal sphincter

LPR- upper esophageal sphincter

GERD- no throat related

LPR- throat related

58
Q

Most LPR patients are/are NOT obese

Can co-exist with GERD (30%) but often an isolated entity (70%) & only 30-40% respond to PPI’s

likely plays a more important role than HCl acid

Pepsin taken up by oropharyngeal cells and can remain stable for days until reactivated by food/drink to damage tissue proteins

Strong association between LPR and

A

are not

Pepsin

acidic

Asthma

59
Q

What is the main driver for LPR?

A

Pepsin

60
Q

ENT often diagnoses pt.→because of upper airway symptoms, cough,

Higher rates of laryngeal and laryngeal cancer

A

hoarseness

polyps

61
Q

What is the first non-invasive test for LPR and what does it detect?

A

Peptest

detects high pepsin levels in oropharynx

62
Q

What are the diagnostic criteria for REFLUX SYMPTOM INDEX (RSI) TO SCREEN FOR LPR?

A

0-5: Normal

>13: Likely LPR

63
Q

What are the 4 treatment options for LPR?

A

Lifestyle changes (avoiding acidic beverages/foods; limit fatty meals; no strenuous activity/bending over/supine within 2-3 hrs of eating; avoid tight-fitting clothes; quit tob; avoid carbonated beverages; avoid caffeine if possible; limit ETOH)

Elevate trunk/head of bed 6 inches

Consider H2 blockers or PPI’s <8wks

For refractory cases → surgery (Nissen fundoplication)

64
Q
A