Tiemann GERD DSA

Question 1

GERD

Answer 1

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

Question 2

GERDPRESENTATION

Answer 2

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”

Question 3

GERD DIFFERENTIAL DIAGNOSIS

Answer 3

Differential diagnosis:
Gallbladder disease
PUD
Angina
Medications (biphosphonates)
Infections
Radiation

Associated conditions:
Pregnancy
Scleroderma
Prolonged nasogastric intubation
Zollinger-Ellison syndrome

Question 4

GERD DIAGNOSIS

Answer 4

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)

Question 5

EGD AND BARIUM SWALLOW

Answer 5

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

Question 6

INTRAESOPHAGEAL pH MONITORING

Answer 6

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

Question 7

ESOPHAGEAL MANOMETRY

Answer 7

Measures and records amplitude of peristaltic contractions and LES pressures

Useful in diagnosis of dysphagia and motility disorders

Question 8

Non-erosive (typical GERD symptoms, but EGD normal or mild esophagitis)

Answer 8

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

Question 9

Erosive GERD (severe esophagitis or ulceration)

Answer 9

20-30%

High rates of relapse and complications

Question 10

GERD TREATMENT

Answer 10

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

Question 11

GERD MEDICATIONS

Answer 11

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

Question 12

Proton Pump Inhibitors

Answer 12

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

Question 13

Gerd relapse

Answer 13

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

Question 14

Surgery

Answer 14

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

Question 15

GERD COMPLICATIONS: Erosive esophagitis and ulceration

Answer 15

• Perforation very rare

- Overt bleeding rare, but iron-deficiency anemia in 10-20%

Question 16

Gerd complications: Stricture

Answer 16

• 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

Question 17

Gerd complications: Barrett’s esophagus

Answer 17

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

Question 18

GERDEXTRA-ESOPHAGEAL MANIFESTATIONS

Answer 18

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

Question 19

PEPTIC ULCER DISEASE

Answer 19

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

Question 20

PUD clinical presentation

Answer 20

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

Question 21

PUD differential diagnosis

Answer 21

Cholecystitis
Pancreatitis
GERD
Angina
Abdominal angina
IBD
Malignancy

Question 22

PUD diagnostic testing

Answer 22

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

Question 23

H. Pylori

Answer 23

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

Question 24

H. Pylori Diagnosis

Answer 24

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

Question 25

PUD Acid secretory testing

Answer 25

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

Question 26

PUD treatment: Acid neutralization and suppression

Answer 26

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

Question 27

PUD H. Pylori treatment

Answer 27

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

Question 28

NSAID-ASSOCIATED ULCERS

Answer 28

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

Question 29

PUD- post-treatment testing

Answer 29

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

Question 30

PUD COMPLICATIONS

Answer 30

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