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GI-II, Exam 1 > 11-20 DSA Peptic Ulcer Disease & GERD (Tieman) > Flashcards

11-20 DSA Peptic Ulcer Disease & GERD (Tieman) Flashcards

1
Q

What are some epidemiological characteristics of GERD?

A

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

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2
Q

What is the pathophysiology of GERD?

A

Failure of the body’s normal protective mechanisms to prevent reflux of gastric contents into the esophagus with resultant damage to the esophagus

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3
Q

What are the clinical SXs of GERD?

A

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)
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4
Q

What are the extra-esophageal manifestations of GERD?

A

Asthma

Laryngitis, laryngeal ulcer

chronic cough

recurrent pneumonitis

non-cardiac chest pain (mimics angina)

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5
Q

Why is asthma considered an extra-esophageal manifestation of GERD?

A

◦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

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6
Q

In addition to asthma, what are some other conditions that are associated with causing GERD?

A

◦Pregnancy

◦Scleroderma

◦Prolonged nasogastric intubation

◦Zollinger-Ellison syndrome

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7
Q

How is GERD usually dx’ed?

A

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

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8
Q

How effective is a PPI trial in dx of GERD?

A

◦Trial of PPI’s

–80% sensitivity and specificity for GERD if response in 2 weeks or less

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9
Q

What sorts of information is provided by a Ba swallow test? What kinds of conditions is it helpful for diagnosis?

A

–Anatomic information, eg. Diverticulae, stricture, hiatal hernia, webs, Schatzki’s ring,

–Physiologic information, eg. Esophageal motility, reflux

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10
Q

How is an EGD useful for GERD? When is it indicated?

A

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

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11
Q

What is this?

A

EGD Esophagitis

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12
Q

How is intraesophageal pH monitoring done?

A

Probe secured 5 cm above LES

Records time and pH

Pt goes about ADL and marks episodes of symptoms

}8-24 hours

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13
Q

When is an intraesophageal pH monitoring test considered abnormal?

A

}if pH<4 more than 5% of time

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14
Q

When is intraesophageal pH monitoring useful in establishing a Dx of GERD?

A

◦Symptoms resistant to medical therapy

◦Extra-esophageal manifestations with asymptomatic GERD

◦Before surgery in questionable cases

◦After surgery if symptoms persist or recur

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15
Q

Describe the 3 intraesophageal test results shown below:

A
  1. physiologic - WNL
  2. upright reflux pattern
  3. Combined reflux pattern
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16
Q

What does esophageal manometry test? What is it useful in Dx of?

A

Measures and records amplitude of peristaltic contractions and LES pressures

}

Useful in diagnosis of dysphagia and motility disorders

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17
Q

Below is an image of a normal esophageal manometry. Describe how it would be different for achalasia.

A
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18
Q

What are the 2 basic subsets of GERD?

A

Non-erosive

Erosive

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19
Q

What is the prevalence and and typical symptoms of non-erosive GERD?

A

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

◦70-80%

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20
Q

What are the 3 subsets of non-erosive GERD?

A

–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

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21
Q

What is the prevalence and typical presentation of erosive GERD?

A

Erosive (severe esophagitis or ulceration)

◦20-30%

◦High rates of relapse and complications

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22
Q

What is the goal of GERD treatment?

A

◦Relieve symptoms and prevent esophagitis and complications in a cost-effective manner

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23
Q

What are the lifestyle modifications that are helpful in controlling GERD?

A

–Elevate head of bed

–Avoid alcohol, large meals late at night, spices, chocolate

–Weight loss

–Avoid tight-fitting clothes

–Stop smoking

–Avoid esophagitic drugs

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24
Q

What classes of medications are helpful in controlling GERD?

A

antacids

prokinetics

H2RA

PPI

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25
Q

What is the most effective antacid for GERD?

A

–Require frequent doses, Gaviscon most effective

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26
Q

What are some prokinetic meds that are helpful in controlling GERD? Are they frequently used?

A

–Bethanacol, metaclopramide

–Not used frequently because of side effects

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27
Q

What is the timeframe for the effectiveness of H2RAs? Does increased dosage increase their effectiveness?

A

–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

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28
Q

When used in combination with PPIs, what are H2RA really useful for?

A

–suppress nocturnal acid reflux

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29
Q

What are some important DDIs to keep in mind with H2RAs?

A

–Cimetidine and ranitidine raise levels of theophylline, phenytoin, lidocaine, quinidine and warfarin (Cytochrome P-450 system)

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30
Q

When should PPIs be taken?

A

◦Require active proton pump, therefore given before meals

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31
Q

How long are PPIs active for? What increases their effectiveness?

A

◦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

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32
Q

What are the possible ROA for PPIs?

A

PO and IV

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33
Q

What is the most effective PPI?

A

esomeprazole

34
Q

What are some DDIs to keep in mind with PPIs?

A

◦Omeprazole interferes with metabolism of diazapam and warfarin

35
Q

What are the influences for a relapse of GERD? What do these patients need?

A

◦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

36
Q

What is the surgery for GERD?

A

◦Laparoscopic Nissen Fundoplication

37
Q

Who is laparoscopic nissen fundoplication indicated for?

A

–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)

38
Q

What is the success rate of the laparoscopic Nissen fundoplication surgery?

A

–90-95% successful, but up to 60% return to taking some meds within 10-15 years

39
Q

What are the complications for the Nissen fundoplication surgery?

A

–gas bloat, dysphagia, recurrent GERD symptoms

40
Q

What are some complications associated with GERD?

A

Erosive esophagitis and ulceration

Stricture

Barrett’s Esophagus

41
Q

What are the major results of erosive esophagitis and ulceration?

A

◦Perforation very rare

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

42
Q

How common is stricture due to GERD?

A

◦Develop in 10-20% of patients with esophagitis

43
Q

What are the major SXs of stricture due to GERD?

A

◦Progressive dysphagia with good appetite and little or no weight loss (vs. esophageal CA)

44
Q

What is the morphology of strictures related to GERD?

A

◦Smooth, tapered, circumferential in distal esophagus

◦Short (Schatzki’s ring) to long (5-6 cm)

45
Q

How are strictures treated?

A

dilatation

46
Q

How prevalent is Barrett’s esophagus? What is it associated with?

A

◦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)

47
Q

How is Barrett’s esophagus treated? Why does it need consistent f/u?

A

◦Rarely regresses with medical or surgical therapy

◦Requires periodic surveillance and biopsies

◦Predisposes the patient to adenocarcinoma of esophagus (vs. squamous cell CA)

48
Q

What is peptic ulcer disease?

A

Peptic=pepsin + acid cause caustic damage to epithelium of stomach and/or duodenum

49
Q

How prevalent is peptic ulcer disease/PUD?

A

10% of population will develop PUD

500,000 new cases and 4 million recurrences/yr.

50
Q

What are some interesting but probably low yield tid-bits about the history of PUD?

A

◦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

51
Q

What is the clinical presentation of PUD?

A

◦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

52
Q

What are the 2 different etiologies behind the epigastric/ upper abdominal pain symptoms of PUD? What are the triggers and symptoms for each?

A

–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

53
Q

What are some differential Dx’s to consider with PUD?

A

◦Cholecystitis

◦Pancreatitis

◦GERD

◦Angina

◦Abdominal angina

◦IBD

◦Malignancy

54
Q

What are the 2 areas of Dx testing for PUD?

A

Anatomic - Ba swallow/UGI series, EGD

Etiologic - H. pylori, acid secretory testing, NSAID

55
Q

For anatomic Dx testing of PUD, which test is preferred?

A

–Barium swallow/UGI Series

–EGD (preferred)

–Higher sensitivity and specificity and allows biopsy for H. Pylori or gastric ulcer

56
Q

What’s this?

A

UGI - gastric ulcer

57
Q

What’s this?

A

EGD - gastric ulcer

58
Q

What are the salient microbiological details about H. pylori? (Gram, shape, biochem)

A

◦Gm -, flagellated, spiral bacterium

◦Produces urease which splits urea into CO2 and ammonia

59
Q

What is the prevalence of H. pylori infections?

A

◦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

60
Q

How is a H. pylori infection dx’ed?

A

Biopsy

Serology for IgG Ab

Urea breath test

Stool antigen

61
Q

How is a biopsy done for a H. pylori infection?

A

–Requires EGD–invasive

–Special stains for histological diagnosis

–Agar gel slide test for urease

–Both highly sensitive unless pt. recently treated with PPI’s

62
Q

Is serology useful to test for H. pylori infection after AB therapy has been completed?

A

◦Serology tests IgG antibodies to H. Pylori

–Shows whether H. Pylori has been present, but not useful to show eradication, as antibodies drop slowly

63
Q

What are some drawbacks associated with using urea breath testing or stool antigen testing for H. pylori infections?

A

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

64
Q

How does the C13 urea breath test work?

A
65
Q

When is acid secretory testing useful in dx’ing PUD?

A

◦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

66
Q

What are some hypersecretory conditions that can cause PUD-like symptoms?

A
  • Zollinger-Ellison Syndrome (Gastrinoma)
  • Antral G-cell Hyperplasia
  • Systemic mastocytosis
  • Myeloproliferative disorders
  • Idiopathic
67
Q

What is the main treatment goal for PUD?

A

acid neutralization and suppression

68
Q

How is acid neutralization and suppression achieved with PUD?

A

Use of antacids, H2RA, and PPIs

69
Q

How are antacids helpful for PUD? What are some common ADRs and ADIs?

A

◦Antacids

–May be useful for symptom control

–Mg=diarrhea, Ca and Al=constipation

–Shouldn’t be used with NSAID’s, increased complications

70
Q

What are some important DDIs associated with H2RAs?

A

Cimetidine and ranitidine raise levels of theophylline, phenytoin, lidocaine, quinidine and warfarin

71
Q

What are some important DDIs assocaited with PPIs?

A

–Inhibits absorption of ketaconazole, increase absorption of digoxin

–Omeprazole may raise levels of drugs metabolized by cytochrome p-450 system

72
Q

What are the 2 treatment therapies for H. pylori infections?

A

◦Triple therapy (antisecretory + 2 antibiotics)

  • or -

◦Quadruple therapy (high-dose therapy for HP resistant to clarithromycin)

73
Q

What is in triple therapy for H. pylori infections?

A

◦Triple therapy (antisecretory + 2 antibiotics)

–PPI bid

–Metronidazole 500 mg. bid

–Amoxacillin 1000 mg bid

–Or

–Clarithromycin 500 mg bid

74
Q

What is in quadruple therapy for H. pylori infections?

A

◦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

75
Q

How effective is triple or quadruple therapy in treating H. pylori infections?

A

–◦> 80% successful in eradicating H. Pylori and healing ulcer

76
Q

What is the treatment for NSAID-associated ulcers?

A

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

77
Q

Is switching to a COX-2 inhibitor in an NSAID-associated ulcer an effective way to get ulcers to heal?

A

no data suggests this

78
Q

What will happen to most NSAID-associated ulcers?

A

◦Most will heal if NSAID discontinued

◦50-60% heal, even if NSAID continued, especially if ulcer duodenal

79
Q

Who are the high-risk patients for NSAID-associated ulcers? What should they be treated with?

A

◦High-risk=Prior ulcers, smoking, cirrhosis, chronic illnesses, elderly

◦PPI or misoprostol for these patients

80
Q

After treatment for PUD wraps up, what should you do?

A

}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

81
Q

How is post-Tx testing for H. pylori done?

A

–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

82
Q

What are the complications of PUD?

A

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

GI-II, Exam 1 (8 decks)

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