Tiemann GERD DSA Flashcards
GERD
Failure of the body’s normal protective mechanisms to prevent reflux of gastric contents into the esophagus with resultant damage to the esophagus
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
GERDPRESENTATION
May be asymptomatic
Heartburn
- Epigastric/lower chest with radiation to neck, throat or back
- 2 days/week or more
- Post-prandial, especially after large meals, alcohol, rich or spicy foods, citrus, chocolate
Effortless regurgitation of gastric contents
- Increases with supine position, bending over, full stomach
Sleep disturbances—may wake up coughing or with heartburn
Water brash (sudden onset of salivary secretions in mouth)
Dysphagia (difficulty swallowing)
Odynophagia (pain on swallowing)
- Dysphagia and Odynophagia are called “alarm symptoms”
GERD DIFFERENTIAL DIAGNOSIS
Differential diagnosis: Gallbladder disease PUD Angina Medications (biphosphonates) Infections Radiation
Associated conditions: Pregnancy Scleroderma Prolonged nasogastric intubation Zollinger-Ellison syndrome
GERD DIAGNOSIS
PE usually non-specific
Lab usually not helpful
Diagnostic testing:
- Trial of PPI’s (80% sensitivity and specificity for GERD if response in 2 weeks or less)
- EGD
- Barium esophogram (EGD and Ba Swallow should be done initially if “alarm symptoms” present)
- Esophageal pH monitoring and symptom recording
- Esophageal motility studies (pH and motility studies usually reserved for more complicated cases, where diagnosis is in doubt)
EGD AND BARIUM SWALLOW
Usually used together, provide different information
Barium swallow:
- Anatomic information, eg. Diverticulae, stricture, hiatal hernia, webs, Schatzki’s ring,
- Physiologic information, eg. Esophageal motility, reflux
EGD:
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
INTRAESOPHAGEAL pH MONITORING
Probe secured 5 cm above LES
Records time and pH
Pt goes about ADL and marks episodes of symptoms
18-24 hours
Abnormal if pH under 4 more than 5% of time
Useful in establishing GERD when:
Symptoms resistant to medical therapy
Extra-esophageal manifestations with asymptomatic GERD
Before surgery in questionable cases
After surgery if symptoms persist or recur
ESOPHAGEAL MANOMETRY
Measures and records amplitude of peristaltic contractions and LES pressures
Useful in diagnosis of dysphagia and motility disorders
Non-erosive (typical GERD symptoms, but EGD normal or mild esophagitis)
70-80%
3 subsets
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
Erosive GERD (severe esophagitis or ulceration)
20-30%
High rates of relapse and complications
GERD TREATMENT
GOAL
Relieve symptoms and prevent esophagitis and complications in a cost-effective manner
MEDICAL Lifestyle modifications Elevate head of bed Avoid alcohol, large meals late at night, spices, chocolate Weight loss Avoid tight-fitting clothes Stop smoking Avoid esophagitic drugs
GERD MEDICATIONS
Antacids
Require frequent doses, Gaviscon most effective
Prokinetics
- Bethanacol, metaclopramide
- Not used frequently because of side effects
H2RA
- 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
- May be used with PPI’s to suppress nocturnal acid reflux
- Cimetidine and ranitidine raise levels of theophylline, phenytoin, lidocaine, quinidine and warfarin (Cytochrome P-450 system)
PPIs
Proton Pump Inhibitors
Require active proton pump, therefore given before meals
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
IV forms available
Esomeprazole most effective (slight margin)
Omeprazole interferes with metabolism of diazapam and warfarin
Gerd relapse
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
Surgery
Laparoscopic Nissen Fundoplication
- 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)
- 90-95% successful, but up to 60% return to taking some meds within 10-15 years
- Complications = gas bloat, dysphagia, recurrent GERD symptoms
Endoscopic plication techniques presently being evaluated
GERD COMPLICATIONS: Erosive esophagitis and ulceration
- Perforation very rare
- Overt bleeding rare, but iron-deficiency anemia in 10-20%
Gerd complications: Stricture
- Develop in 10-20% of patients with esophagitis
- Progressive dysphagia with good appetite and little or no weight loss (vs. esophageal CA)
- Smooth, tapered, circumferential in distal esophagus
- Short (Schatzki’s ring) to long (5-6 cm)
- Treated with dilatation
Gerd complications: Barrett’s esophagus
May be asymptomatic, but usually associated with severe long-standing esophagitis (>10 years)
Occurs in 5-10% of symptomatic GERD patients
Higher frequency in middle-aged, white men
3:1 men:women
Squamous esophageal mucosa replaced by columnar epithelium with intestinal metaplasia
Rarely regresses with medical or surgical therapy
Predisposes the patient to adenocarcinoma of esophagus (vs. squamous cell CA)
Requires periodic surveillance and biopsies
GERDEXTRA-ESOPHAGEAL MANIFESTATIONS
Asthma
- 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
Laryngitis, laryngeal ulcer
Chronic cough
Recurrent pneumonitis
Non-cardiac chest pain mimics angina
PEPTIC ULCER DISEASE
Peptic=pepsin + acid cause caustic damage to epithelium of stomach and/or duodenum
10% of population will develop PUD
500,000 new cases and 4 million recurrences/yr.
History:
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
PUD clinical presentation
Can be asymptomatic until complication occurs
Epigastric/upper abdominal pain
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
Significant overlap in symptoms of duodenal and gastric ulcers
PE and labs usually not helpful unless chronic low-grade bleeding causes iron-deficiency anemia
PUD differential diagnosis
Cholecystitis Pancreatitis GERD Angina Abdominal angina IBD Malignancy
PUD diagnostic testing
Anatomic:
Barium swallow/UGI Series
EGD
Higher sensitivity and specificity and allows biopsy for H. Pylori or gastric ulcer
Unlike in GERD, these tests are not usually used together, and EGD is preferred for the reasons stated.
Etiologic:
H. Pylori
Acid secretory testing—basal and stimulated
NSAID
H. Pylori
Gm -, flagellated, spiral bacterium
Produces urease which splits urea into CO2 and ammonia
Endemic in lower socioeconomic groups and developing countries
In US, 20% of population under age 40 and 50% >age 60 infected
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 under 10%/year
H. Pylori Diagnosis
Biopsy
- Requires EGD–invasive
- Special stains for histological diagnosis
- Agar gel slide test for urease (Both highly sensitive unless pt. recently treated with PPI’s)
Serology tests IgG antibodies to H. Pylori (Shows whether H. Pylori has been present, but not useful to show eradication, as antibodies drop slowly)
Urea breath test (C13 or C14)
Stool antigen
- Both breath test and stool antigen have high false – if done within 7-14 days of PPI therapy
PUD Acid secretory testing
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
Hypersecretory conditions: Zollinger-Ellison Syndrome (Gastrinoma) Antral G-cell Hyperplasia Systemic mastocytosis Myeloproliferative disorders Idiopathic
PUD treatment: Acid neutralization and suppression
Antacids
- May be useful for symptom control
- Mg=diarrhea, Ca and Al=constipation
- Shouldn’t be used with NSAID’s, increased complications
H2RA
- Cimetidine and ranitidine raise levels of theophylline, phenytoin, lidocaine, quinidine and warfarin
PPI
- Inhibits absorption of ketaconazole, increase absorption of digoxin
- Omeprazole may raise levels of drugs metabolized by cytochrome p-450 system
PUD H. Pylori treatment
Triple therapy (antisecretory + 2 antibiotics): PPI bid Metronidazole 500 mg. bid Amoxacillin 1000 mg bid Or Clarithromycin 500 mg bid
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
> 80% successful in eradicating H. Pylori and healing ulcer
NSAID-ASSOCIATED ULCERS
Stop NSAID, if possible
- No data suggesting switching to Cox-2 inhibitor is effective in getting ulcer to heal
PPI
- Most will heal if NSAID discontinued
- 50-60% heal, even if NSAID continued, especially if ulcer duodenal
Check for H. Pylori and treat, if HP present
May require PPI maintainence therapy if NSAID needs to be continued
Consider prophylactic therapy in high-risk pt. needs to be started on NSAID
- High-risk=Prior ulcers, smoking, cirrhosis, chronic illnesses, elderly
- PPI or misoprostol for these patients
PUD- 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
- 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
PUD COMPLICATIONS
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
