11-20 DSA Peptic Ulcer Disease & GERD (Tieman) Flashcards
What are some epidemiological characteristics of GERD?
Most common and costly GI disease (10 billion dollars/year in 2000)
Impairs quality of life similar to arthritis, CHF, HTN and MI
Occurs across all age groups and both sexes, although complications increase with age and male sex
What is the pathophysiology of GERD?
Failure of the body’s normal protective mechanisms to prevent reflux of gastric contents into the esophagus with resultant damage to the esophagus
What are the clinical SXs of GERD?
Symptoms:
- asymptomatic sometimes
- heartburn
- effortless regurgitation of gastric conetnts
- sleep disturbances due to coughing or heartburn
- water brash - sudden salivation
- dysphagia (alarm sx)
- odynophagia (alarm sx)
What are the extra-esophageal manifestations of GERD?
Asthma
Laryngitis, laryngeal ulcer
chronic cough
recurrent pneumonitis
non-cardiac chest pain (mimics angina)
Why is asthma considered an extra-esophageal manifestation of GERD?
◦Reflux often silent and asymptomatic
◦Significant co-existence between GERD and asthma in adults
◦Any adult with new-onset asthma, without allergic component, and with poor response to bronchodilators or steroids should be investigated for GERD
In addition to asthma, what are some other conditions that are associated with causing GERD?
◦Pregnancy
◦Scleroderma
◦Prolonged nasogastric intubation
◦Zollinger-Ellison syndrome
How is GERD usually dx’ed?
PE is usually non-specific, labs aren’t helpful
Diagnostic testing:
- trial of PPIs
EGD
Ba esophogram/swallow (for alarm Sx)
esophageal pH monitoring
Sx recording
Esophageal motility studies - if dx is in doubt
How effective is a PPI trial in dx of GERD?
◦Trial of PPI’s
80% sensitivity and specificity for GERD if response in 2 weeks or less
What sorts of information is provided by a Ba swallow test? What kinds of conditions is it helpful for diagnosis?
Anatomic information, eg. Diverticulae, stricture, hiatal hernia, webs, Schatzki’s ring,
Physiologic information, eg. Esophageal motility, reflux
How is an EGD useful for GERD? When is it indicated?
EGD, abbr for Esophagogastroduodenoscopy
Visualizes mucosa and allows biopsy
High specificity for esophagitis, Barrett’s esophagus, cancer
Indicated in “alarm symptoms” of odynophagia, dysphagia, bleeding, weight loss, abnormal barium swallow, or long-standing symptoms
What is this?
EGD Esophagitis
How is intraesophageal pH monitoring done?
Probe secured 5 cm above LES
Records time and pH
Pt goes about ADL and marks episodes of symptoms
}8-24 hours
When is an intraesophageal pH monitoring test considered abnormal?
}if pH<4 more than 5% of time
When is intraesophageal pH monitoring useful in establishing a Dx of GERD?
◦Symptoms resistant to medical therapy
◦Extra-esophageal manifestations with asymptomatic GERD
◦Before surgery in questionable cases
◦After surgery if symptoms persist or recur
Describe the 3 intraesophageal test results shown below:
- physiologic - WNL
- upright reflux pattern
- Combined reflux pattern
What does esophageal manometry test? What is it useful in Dx of?
Measures and records amplitude of peristaltic contractions and LES pressures
}
Useful in diagnosis of dysphagia and motility disorders
Below is an image of a normal esophageal manometry. Describe how it would be different for achalasia.
What are the 2 basic subsets of GERD?
Non-erosive
Erosive
What is the prevalence and and typical symptoms of non-erosive GERD?
}Non-erosive (typical GERD symptoms, but EGD normal or mild esophagitis)
◦70-80%
What are the 3 subsets of non-erosive GERD?
Abnormal pH monitoring—respond to PPI’s
Normal reflux pattern on pH monitoring, but symptoms correlate with reflux (increased sensitivity)
Normal reflux pattern with poor symptom correlation - need to look for another cause for symptoms
What is the prevalence and typical presentation of erosive GERD?
Erosive (severe esophagitis or ulceration)
◦20-30%
◦High rates of relapse and complications
What is the goal of GERD treatment?
◦Relieve symptoms and prevent esophagitis and complications in a cost-effective manner
What are the lifestyle modifications that are helpful in controlling GERD?
Elevate head of bed
Avoid alcohol, large meals late at night, spices, chocolate
Weight loss
Avoid tight-fitting clothes
Stop smoking
Avoid esophagitic drugs
What classes of medications are helpful in controlling GERD?
antacids
prokinetics
H2RA
PPI
What is the most effective antacid for GERD?
Require frequent doses, Gaviscon most effective
What are some prokinetic meds that are helpful in controlling GERD? Are they frequently used?
Bethanacol, metaclopramide
Not used frequently because of side effects
What is the timeframe for the effectiveness of H2RAs? Does increased dosage increase their effectiveness?
Delayed onset (6-10 hours) but may be effective, especially if used for longer period (12 weeks)
6-8 hours of effectiveness, may require re-dosing
Increased dosage does not increase effectiveness
When used in combination with PPIs, what are H2RA really useful for?
suppress nocturnal acid reflux
What are some important DDIs to keep in mind with H2RAs?
Cimetidine and ranitidine raise levels of theophylline, phenytoin, lidocaine, quinidine and warfarin (Cytochrome P-450 system)
When should PPIs be taken?
◦Require active proton pump, therefore given before meals
How long are PPIs active for? What increases their effectiveness?
◦10-14 hours of action, may require second dose
◦Prolonged therapy and/or increased dosage increase effectiveness, as well as adding nighttime dose of H2RA
Almost 100% healing
What are the possible ROA for PPIs?
PO and IV
What is the most effective PPI?
esomeprazole
What are some DDIs to keep in mind with PPIs?
◦Omeprazole interferes with metabolism of diazapam and warfarin
What are the influences for a relapse of GERD? What do these patients need?
◦80% with severe esophagitis relapse, especially younger patients
◦Lesser relapse rates with milder disease
◦Require maintainence therapy
50-60% can be maintained on H2RA therapy
PPI’s generally more effective
Start at 50% of treatment dose, but may need to go up
What is the surgery for GERD?
◦Laparoscopic Nissen Fundoplication
Who is laparoscopic nissen fundoplication indicated for?
Indicated in good-risk patients who respond well to medical therapy, but need long-term maintainence
Also indicated in patients with extra-esophageal GERD manifestations not responsive to medical therapy and patients with complications of GERD (eg. stricture, Barrett’s)
What is the success rate of the laparoscopic Nissen fundoplication surgery?
90-95% successful, but up to 60% return to taking some meds within 10-15 years
What are the complications for the Nissen fundoplication surgery?
gas bloat, dysphagia, recurrent GERD symptoms
What are some complications associated with GERD?
Erosive esophagitis and ulceration
Stricture
Barrett’s Esophagus
What are the major results of erosive esophagitis and ulceration?
◦Perforation very rare
◦Overt bleeding rare, but iron-deficiency anemia in 10-20%
How common is stricture due to GERD?
◦Develop in 10-20% of patients with esophagitis
What are the major SXs of stricture due to GERD?
◦Progressive dysphagia with good appetite and little or no weight loss (vs. esophageal CA)
What is the morphology of strictures related to GERD?
◦Smooth, tapered, circumferential in distal esophagus
◦Short (Schatzki’s ring) to long (5-6 cm)
How are strictures treated?
dilatation
How prevalent is Barrett’s esophagus? What is it associated with?
◦Occurs in 5-10% of symptomatic GERD patients
Higher frequency in middle-aged, white men
3:1 men:women
◦May be asymptomatic, but usually associated with severe long-standing esophagitis (>10 years)
How is Barrett’s esophagus treated? Why does it need consistent f/u?
◦Rarely regresses with medical or surgical therapy
◦Requires periodic surveillance and biopsies
◦Predisposes the patient to adenocarcinoma of esophagus (vs. squamous cell CA)
What is peptic ulcer disease?
Peptic=pepsin + acid cause caustic damage to epithelium of stomach and/or duodenum
How prevalent is peptic ulcer disease/PUD?
10% of population will develop PUD
500,000 new cases and 4 million recurrences/yr.
What are some interesting but probably low yield tid-bits about the history of PUD?
◦Increasing incidence through 19th and early 20th centuries in the US, but decreasing since mid-1900’s
◦Treated with rest and diet through early 1900’s
◦1950-1980’s treated with antacids or acid suppression
High recurrence rate
◦1984-present, role of H. Pylori and NSAID’s appreciated
What is the clinical presentation of PUD?
◦Can be asymptomatic until complication occurs
◦Epigastric/upper abdominal pain
◦Significant overlap in symptoms of duodenal and gastric ulcers
◦PE and labs usually not helpful unless chronic low-grade bleeding causes iron-deficiency anemia
What are the 2 different etiologies behind the epigastric/ upper abdominal pain symptoms of PUD? What are the triggers and symptoms for each?
Duodenal
2-3 hours after eating, relieved by food or antacid, often at night and in clusters, appetite and weight preserved
Gastric
Immediately after eating, not relieved with food or antacid, often with anorexia and wt. loss, not at night
What are some differential Dx’s to consider with PUD?
◦Cholecystitis
◦Pancreatitis
◦GERD
◦Angina
◦Abdominal angina
◦IBD
◦Malignancy
What are the 2 areas of Dx testing for PUD?
Anatomic - Ba swallow/UGI series, EGD
Etiologic - H. pylori, acid secretory testing, NSAID
For anatomic Dx testing of PUD, which test is preferred?
Barium swallow/UGI Series
EGD (preferred)
Higher sensitivity and specificity and allows biopsy for H. Pylori or gastric ulcer
What’s this?
UGI - gastric ulcer
What’s this?
EGD - gastric ulcer
What are the salient microbiological details about H. pylori? (Gram, shape, biochem)
◦Gm -, flagellated, spiral bacterium
◦Produces urease which splits urea into CO2 and ammonia
What is the prevalence of H. pylori infections?
◦Endemic in lower socioeconomic groups and developing countries
◦In US, 20% of population <age>age 60 infected</age>
◦20% of infected individuals develop ulcers
80% of duodenal ulcers associated with H. Pylori
60% of gastric ulcers associated with H. Pylori
◦Successful eradication of H. Pylori reduces ulcer recurrences from routine to <10%/year
How is a H. pylori infection dx’ed?
Biopsy
Serology for IgG Ab
Urea breath test
Stool antigen
How is a biopsy done for a H. pylori infection?
Requires EGD–invasive
Special stains for histological diagnosis
Agar gel slide test for urease
Both highly sensitive unless pt. recently treated with PPI’s
Is serology useful to test for H. pylori infection after AB therapy has been completed?
◦Serology tests IgG antibodies to H. Pylori
Shows whether H. Pylori has been present, but not useful to show eradication, as antibodies drop slowly
What are some drawbacks associated with using urea breath testing or stool antigen testing for H. pylori infections?
Other than asking your patient to poop in a bag?
Both breath test and stool antigen have high false – if done within 7-14 days of PPI therapy
How does the C13 urea breath test work?
When is acid secretory testing useful in dx’ing PUD?
◦Not used often
Useful when looking for hypersecretory states or achlorhydria
- Refractory ulcers after successful eradication of H. Pylori
- Elevated gastrin levels
- Unusual location or number of ulcers
- Rugal fold hypertrophy on EGD
Basal rate and stimulated rate included
What are some hypersecretory conditions that can cause PUD-like symptoms?
- Zollinger-Ellison Syndrome (Gastrinoma)
- Antral G-cell Hyperplasia
- Systemic mastocytosis
- Myeloproliferative disorders
- Idiopathic
What is the main treatment goal for PUD?
acid neutralization and suppression
How is acid neutralization and suppression achieved with PUD?
Use of antacids, H2RA, and PPIs
How are antacids helpful for PUD? What are some common ADRs and ADIs?
◦Antacids
May be useful for symptom control
Mg=diarrhea, Ca and Al=constipation
Shouldn’t be used with NSAID’s, increased complications
What are some important DDIs associated with H2RAs?
Cimetidine and ranitidine raise levels of theophylline, phenytoin, lidocaine, quinidine and warfarin
What are some important DDIs assocaited with PPIs?
Inhibits absorption of ketaconazole, increase absorption of digoxin
Omeprazole may raise levels of drugs metabolized by cytochrome p-450 system
What are the 2 treatment therapies for H. pylori infections?
◦Triple therapy (antisecretory + 2 antibiotics)
- or -
◦Quadruple therapy (high-dose therapy for HP resistant to clarithromycin)
What is in triple therapy for H. pylori infections?
◦Triple therapy (antisecretory + 2 antibiotics)
PPI bid
Metronidazole 500 mg. bid
Amoxacillin 1000 mg bid
Or
Clarithromycin 500 mg bid
What is in quadruple therapy for H. pylori infections?
◦Quadruple therapy (high-dose therapy for HP resistant to clarithromycin)
PPI bid
Bismuth 2 tablets qid
Tetracycline 500 mg qid
Metronidazole 500 mg tid
Continue PPI for another 4-6 weeks, especially if symptomatic
How effective is triple or quadruple therapy in treating H. pylori infections?
◦> 80% successful in eradicating H. Pylori and healing ulcer
What is the treatment for NSAID-associated ulcers?
Stop NSAID, if possible
- consider prophylactic therapy in high risk pts if they need to be started on NSAID
PPI, or PPI maintenance therapy if NSAID can’t be d/c’ed
Check for H. pylori infection and treat
Is switching to a COX-2 inhibitor in an NSAID-associated ulcer an effective way to get ulcers to heal?
no data suggests this
What will happen to most NSAID-associated ulcers?
◦Most will heal if NSAID discontinued
◦50-60% heal, even if NSAID continued, especially if ulcer duodenal
Who are the high-risk patients for NSAID-associated ulcers? What should they be treated with?
◦High-risk=Prior ulcers, smoking, cirrhosis, chronic illnesses, elderly
◦PPI or misoprostol for these patients
After treatment for PUD wraps up, what should you do?
}Post-treatment testing
◦Repeat EGD for gastric ulcers to assess complete healing and/or re-biopsy to r/o malignancy
◦H. Pylori testing for persistent symptoms
How is post-Tx testing for H. pylori done?
4 weeks after last PPI treatment
Biopsy +/- agar gel test, if EGD indicated
C13 urea breath test or stool antigen, if EGD not necessary
Antibody test not useful because of slow decrease in antibody level over time
What are the complications of PUD?
Refractory ulcers - may require surgery
Bleeding - 80% stop, 20% require endoscopic or surgical intervention
Perforation - most require surgical intervention
Obstruction - initially treat with intense medical therapy; surgery if not resolved medically
