GI- Clinical - GERD Flashcards
What are the 4 main contents of gastric reflux?
Gastric acid (HCl)
Pepsin (ogen)
Gastric Lipase
Gastrin
Pepsin(ogen) is the primary enzyme secreted by the stomach-with its primary purpose: degradation (in presence of acid)
protein
HCl
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
Physiologic reflux
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
GERD
The majority of patients with GERD do/do not seek medical attention?
What % of Americans have GERD?
do not
20%
GERD is a viscious promoting disease?
self
What role does gastrin play as concerning the closing pressure of the LES?
decreases LES closing pressure
What are the 3 main contributors of GERD and what is the most common?
- Flow into stomach impaired (esophageal motility disorder, web/ring)
- Flow out of the stomach (sticture, liver/gallbladder/pancreatic mass blocking)
- backflow of stomach contents (most common)
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
Esophageal web
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
Esophageal “Schatzki” rings
What can cause impeded flow out of the stomach:
stricture
liver/gallbladder/pancreatic mass
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…)
is not
incompetent
What 3 issues can contribute to incompetent gastro-esophageal junction?
LES dysfunction
hiatal hernia
increase intra-abdominal pressure (obesity, pregnancy)
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
LES
peppermint
tone
What pregnancy hormones can relax the LES and what else does pregnancy do to increase risk of GERD?
relaxin, progesterone
+ ↑intraabdom. pressure from fetus
Hiatal hernia=diaphragmatic hernia (not uncommon over yrs; occasionally due to injury/excessive ; less commonly-congenital) also increases risk of GERD
50
lifting
What are some medications that can increase the risk of GERD?
progesterone
antihistamines
anticholinergics
calcium channel blockers
tricyclic antidepressants
nitrates
Which hiatal hernia is more at risk for cutting off blood supply and leading to necrosis- more urgent?
paraesophageal hiatus hernia
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?
hiatal hernia
- LES pressure is often low
- Gastric pouch- intra-thoracic reservoir
- Diaphragm- no esophageal pinch
Besides causing heartburn/reflux symptoms, what else might a patient with a large hiatal hernia complain of:
mid chest discomfort around the nipple line
wheezing, coughing, SOB
What innervation of the esophagus and stomach maintains normal LES pressures & peristaltic movement through the GI tract?
vagus
What are all of these examples of:
BARIUM SWALLOW + GERD
What are the 3 most common symptoms of GERD?
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)
What are the 5 Atypical symptoms of GERD?
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)
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?
Empiric treatment (lifestyle, +/- PPI’s* once/ day or H2 blockers*) for 6-8 weeks and then as needed
What if the initial treatment does not work ?
increase PPI to 2X a day and referr to GI for EGD
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)?
labs (H.pylori, CBC, CMP…), CXR, empiric treatment with lifestyle and PPI’s and refer to GI, ENT if DX unclear or no response
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) ?
Endoscopy (EGD) to r/o strictures, erosive esophagitis, Barrett’s esophagus, malignancy
What are 3 evaluations methods for GERD?
EGD
Nasopharyngoscopy (view of normal and LPR voice box)
24 hr probe
The majority/minority of patients with symptoms of GERD who undergo EGD will show abnormalities, such as Erosive Esophagitis (only seen in 30%)?
minority
note: erosive esophagitis
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
majority
Which population of GERD patients commonly have a poor response to PPIs?
Non-Erosive Reflux Disease=NERD
Describe the progressive process of GERD?
erosive esophagitis can next lead to:
peptic strictures ulcers
Barret’s esophagus can lead to :
adenocarcinoma
What is the first non-surgical treatment and prevention of GERD?
lifestyle changes
↓fatty foods, eat smaller meals, no food within 2-3 hrs of lying supine
After lifestyle change, what other non-surgical treatments are recommended?
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
What does Gaviscom do to treat acid reflux?
creates a cap over the gastric contents
What are the 4 integrative supplements that Dr. Bennett mentioned she uses to treat GERD?
marshmallow, slippery elm, licorice (if no HTN), aloe vera
IF YOU BLOCK ACID, DO YOU STOP REFLUX?
IF YOU DON’T STOP REFLUX, WHAT OTHER SUBSTANCE(S) IS/ARE STILL REFLUXED?
Gastrin and Pepsin
What are the long-term risks for using PPIs involving the kidneys?
↑Chronic Kidney Disease (28x increased risk!!!) & Acute Interstitial Nephritis
Review the other complications of taking PPIs long term?
↑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?
What happens after somone uses H2 blockers for 4 to 6 weeks or more?
tachyphylaxis = decreasing efficacy, tolerance
What are the 4 surgical options for GERD?
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
Which surgical option is the gold standard and has two forms?
Open/laparoscopic Nissen fundoplication (partial-toupet, full)-gold standard
Which surgical method is more effective for morbidly obese with GERD?
Bariatric Surgery
What is pictured?
Esphageal webs and rings
What is pictured?
Barrett’s esophagus
(intestinal metaplasia)
What is pictured?
esophageal scarring
What is pictured?
What is pre-cancerous, dysplastic changes in esophageal epithelium 2nd to chronic acid exposure?
Barrett’s esophagus
What is silent reflux?
VI. LARYNGOPHARYNGEAL REFLUX (LPR)
What is a key symptom of LPR (LARYNGOPHARYNGEAL REFLUX)?
71% Chronic hoarseness
What are some other symptoms of LPR?
58% Wheezing, asthma, SOB
51% Chronic, non-productive cough
47% Globus sensation
42% Chronic throat clearing (esp after eating)
35% Dysphagia
How is LPR different from GERD?
GASEOUS/VAPORIZED REFLUXATE OF ACID, PEPSIN AND BILE SALTS
Esophagus can handle reflux episodes/day without tissue damage
Larynx and oropharynx develop damage after only episodes/day
50
3
How do GERD and LPR symptoms differ as concerning:
heartburn
body position
which sphincter is affected
throat related symptoms?
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
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
are not
Pepsin
acidic
Asthma
What is the main driver for LPR?
Pepsin
ENT often diagnoses pt.→because of upper airway symptoms, cough,
Higher rates of laryngeal and laryngeal cancer
hoarseness
polyps
What is the first non-invasive test for LPR and what does it detect?
Peptest
detects high pepsin levels in oropharynx
What are the diagnostic criteria for REFLUX SYMPTOM INDEX (RSI) TO SCREEN FOR LPR?
0-5: Normal
>13: Likely LPR
What are the 4 treatment options for LPR?
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)
