Therapy

1. Peptic Ulcer Disease
Chalelgn K.

2. Overview
• Peptic ulcer disease (PUD) refers to ulceration of the
mucosa anywhere in the GI tract exposed to acid and
pepsin.
• They can range in size from a few millimeters to a few
centimeters
• The 2 most common forms/locations of PUD are
– Duodenal ulcer
– Gastric ulcer

3. Overview

4. Anatomical View of Duodenal and Gastric
Ulcers
.

5. Etiology and Pathophysiology

6. Etiology and Pathophysiology
• Hydrochloric acid and pepsin are the primary substances that
cause gastric mucosal damage in PUD.
• Three different stimuli (eg, histamine, acetylcholine, and gastrin)
cause acid secretion through interactions with the histaminic,
cholinergic, and gastrin receptors on the surface of parietal cells.
• Gastric acid output occurs in two stages:
– (a) basal acid output during fasting, and
– (b) maximal acid output in response to meals.

7. Etiology and Pathophysiology
• After stimulation by histamine, acetylcholine, and gastrin, acid is secreted by
the H+-K+-ATPase+ (proton) pump, located on the luminal side of parietal
cells.
• Pepsinogen released from chief cells in the body of the stomach is converted
to pepsin in an acidic environment.
• pepsin initiates protein digestion and collagen proteolysis and serves as a
signal for the release of other digestive enzymes such as gastrin and
cholecystokinin.
• The proteolytic activity of pepsin appears to influence ulcer formation.

8. Etiology and Pathophysiology
• Common causes of PUD
– Helicobacter pylori (H.pylori) infection
– Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
– Critical illness (stress-related mucosal damage)
• Uncommon causes of PUD
– Idiopathic (non-H.pylori, non- NSAID)
– Hypersecretion of gastric acid (e.g. Zollinger Ellison syndrome)
– Viral infections
– Radiation therapy
– Chemotherapy

9. Helicobacter Pylori (HP)-Associated
• Helicobacter pylori (HP) is a spiral shaped, gram negative,
flagellated bacteria first associated with PUD in the early 1980’s
• Found in most people with duodenal and gastric ulcers
– About 95% of those with duodenal ulcers
– About 80% of those with gastric ulcers
• HP is primarily spread through the fecal to oral route
• People are most often infected during childhood

10. Helicobacter Pylori (HP)-Associated
• Mechanisms by which HP causes mucosal injury are not entirely clear
• However, occurs through a combination of the following
mechanisms:
– HP catalyzes urea  ammonia is produced  ammonia erodes the
mucous barrier and causes epithelial damage
– HP produces cytotoxins as well
– HP produces mucolytic enzymes

11. NSAID-Induced
• In long-term NSAID users, there is:
– a 10% - 20% prevalence of gastric ulcers and
– a 2% - 5% prevalence of duodenal ulcers
• Mechanisms for NSAID-induced ulceration
– NSAIDs are weak acids and are non-ionized at gastric pH
• Diffuse freely across the mucous barrier into gastric epithelial cells  H+
ions are liberated and cause cellular damage

12. NSAID-Induced…..continued
– NSAIDs inhibit cyclooxygenase activity and therefore decrease
prostaglandin production which results in a:
• Reduction in gastric and mucosal blood flow
• Decrease in mucous and bicarbonate secretion
• Decrease in cellular repair and replication
– These mechanisms cause mucosal injury and decrease
mucosal defense mechanisms

13. NSAID-Induced….continued
• 1% - 2% of NSAID users will develop an ulcer or ulcer complications with 1 year
• Aspirin is the most ulcernogenic of all NSAIDs.
– Even with low dose aspirin (81-162mg/day), ulcers occur in 0.6% - 1.2% of
patients per year.
• The risk of developing an NSAID-related complication is greater in patients:
– Greater than 60 years old
– With a prior history of PUD
– Taking high dose NSAIDs or multiple NSAIDs, including low dose aspirin
– Who are concurrently taking
• Corticosteroids
• Anticoagulants
• Oral bisphosphonates
• Anti-platelet agents
• SSRIs (Selective Serotonin Reuptake Inhibitors)

14. Stress-Related Mucosal Damage SRMD
• Stress-Related Mucosal Damage SRMD occurs most frequently in
critically ill patients due to mucosal defects caused by gastric
mucosal ischemia and intraluminal acid.
• The ulcers are usually superficial, but SRMD may also penetrate
into the submucosa and cause significant GI bleeding.
• Physiologically stressful situations that lead to SRMD include:
– sepsis, organ failure, prolonged mechanical ventilation, thermal injury, and
surgery.

16. Zollinger-Ellison Syndrome (ZES)
• ZES is characterized by gastric acid hypersecretion and recurrent
peptic ulcers that result from a gastrin-producing tumor
– More than 50% of gastrinomas are malignant
• ZES is suspected for patients with multiple ulcers and recurrent or
refractory PUD often accompanied by esophagitis or ulcer
complications
• Only accounts for 0.1% to 1% of those with duodenal ulcer

17. Other Potential Factors in the Development of PUD
• Cigarette smoking
– Increases the risk of developing PUD and its complications
– Impairs ulcer healing and increases the risk of recurrence
– Ulcer risk is proportional to the number of cigarettes smoked per day
• Psychological stress
– People who develop PUD tend to be more adversely affected by stress
– However, controlled trials are conflicting and have failed to document a
direct cause-effect relationship
– Stress may induce behavioral risks such as smoking and the use of
NSAIDs or may alter the inflammatory response or resistance to HP
infection
• Dietary factors
– Certain foods (e.g. coffee, tea, carbonated beverages, beer, milk, spices)
may cause dyspepsia but do not increase the risk of developing PUD

18. Clinical Presentations
Signs and Symptoms
•Symptoms depend on ulcer location, ulcer etiology, and patient age
•Many patients, particularly the elderly, have few or even no symptoms
•NSAID-induced ulcers are often silent
– Complications such as bleeding and perforation are often the initial
presentation

19. Clinical Presentations
• Pain localized to the epigastrium is the most common
symptom
• The pain is described as burning, distressing, cramping, or hunger
• A typical nocturnal pain that wakes the patient from sleep
(especially between 12 and 3am)
• The severity of ulcer pain varies from patient to patient.

20. Clinical Presentations
• Episodes of pain usually occur in clusters, lasting up to
a few weeks followed by a pain-free period or
remission lasting weeks to years
• Changes in the character of pain may suggest the
presence of complications
• Pyrosis (heartburn), belching, and bloating may
accompany the pain

21. Clinical Presentations
Gastric Ulcer
•Pain often does not follow a consistent pattern; not
predictable
•Food will sometimes cause pain
•Nausea, vomiting, anorexia, and weight loss are more common
with gastric ulcer than duodenal ulcer

22. Clinical Presentations
Duodenal Ulcer
•Pain more likely follows a consistent pattern compared to gastric
ulcer Epigastric pain occurs in 60% - 90% of patients with duodenal ulcers
•Food often relieves pain but the pain usually returns 1-3 hrs after
eating
•Nocturnal epigastric pain often occurs
•40% - 70% have additional non-specific dyspeptic complaints
(belching, bloating, abdominal distension, food intolerance)

23. Complications
• Major complications of PUD include:
– Bleeding
• Occurs in about 15% of patients with active PUD
– Perforation
• Occurs in about 7% of patients with active PUD
– Mortality
• Mortality from acute bleeding is about 6% - 10%

24. Diagnosis
• The diagnosis of PUD depends on visualizing the ulcer crater
by either upper GI radiography or upper endoscopy
– Upper GI radiography with barium was the initial diagnostic
procedure but has been replaced with upper endoscopy
• There are multiple laboratory tests that can be performed to
diagnosis an H.pylori infection

25. Testing for H. pylori
• There are multiple tests that can be performed to test for
the presence of H. pylori
• Invasive testing (Requires endoscopy with biopsy)
– Histology
– Culture
– Rapid urease testing
• Noninvasive testing
– Serological test
– Urea breath test
– Fecal antigen test

26. Testing for H. pylori
Invasive Testing
•All of these tests require biopsy to be acquired via endoscopy
•Histology
– Microbiologic examination using various stains
– Excellent sensitivity and specificity but it is invasive, expensive and
requires trained personnel
•Culture
– Culture of biopsy
– Costly, time consuming, and technically difficult

27. Testing for H. pylori
Invasive Testing-Rapid Urease Testing
– Rapid urease tests detect the presence of ammonia in the
biopsy sample
– The ammonia is generated by H.pylori urease activity
– Test of choice at endoscopy
– Greater than 90% sensitive and specific
– Easily performed with rapid results
– Tests for active HP infection

28. Testing for H. pylori
Noninvasive Tests -Antibody Detection/Serological Test
•A simple blood test
– Laboratory-based (more accurate than office-based tests)
– Office-based
•Detects IgG antibodies to H. pylori in the serum
•Quick, noninvasive, inexpensive
•Can’t be used to distinguish between an active infection or past
exposure because antibodies persist for long periods of time
– Most patients remain seropositive for 6 months to 1 year after HP
eradication
•Can’t be used to determine if eradication is successful

29. Testing for H. pylori
Noninvasive Tests-Urea Breath Test
Detects the exhalation of radioactive CO2 following
ingestion of 13
C or 14
C radiolabeled urea
•H. pylori hydrolysis of the radiolabeled urea results in
radiolabeled CO2 production
•97% sensitivity and 95% specificity

30. Testing for H. pylori
Noninvasive Tests -Fecal Antigen Test
•Polyclonal antibody test that detects the presence of H.pylori
antigen in the stool
•Sensitivity and specificity similar to urea breath test
•The urea breath and fecal antigen tests may be falsely negative in
patients who have recently taken
– Antibiotics (up to 4 weeks)
– Bismuth compounds (up to 4 weeks)
– Antisecretory agents (up to 2 weeks)
•The urea breath and fecal antigen tests can be used as an initial
screen to determine if a patient is infected

31. Testing for H. pylori
Tests for Confirming Eradication
•The urea breath (preferred) and fecal antigen tests can be used to
confirm eradiation of H.pylori in a patient who has been treated
•The serological test can not be used to determine eradication because
antibodies last for an extended period after the infection has been
cleared
•However, confirming eradication is not practical or cost effective
•Indications for confirming eradication include:
– Continued dyspeptic symptoms
– H. pylori-associated MALT (mucosal associated lymphoid tissue)
lymphoma
– Resection for gastric cancer

32. Treatment
Goals of Therapy
•Choice of treatment depends on etiology (e.g. HP or
NSAIDs) and whether treatment is for initial management
or prevention of recurrence
•Overall goals
– Relief of pain
– Healing of ulcer
– Prevention of recurrence
– Prevent or reduce complications

33. Pharmacologic Therapy
Goals for an active HP positive ulcer
• To eradicate the HP
• To heal the ulcer
• To ultimately cure the disease
– Use multi-drug regimens containing antibiotics and anti-secretory agents (usually
proton pump inhibitors (PPIs)) and sometimes bismuth preparations
Goals for an NSAID-induced peptic ulcer or Non HP peptic Ulcer
• To heal the ulcer as quickly as possible
– Can use PPIs, H2-receptor antagonists, or sucralfate
– Antacids are not used as monotherapy to heal peptic ulcers
– Misoprostol can be used to reduce the risk of NSAID-induced PUD

34. Non-pharmacologic Therapy
• Eliminate or reduce psychological stress
• Smoking cessation
• Eliminate or reduce NSAID use
• Avoid foods that cause dyspepsia
• Avoid foods and beverages that cause dyspepsia or exacerbate
ulcer symptoms (eg, spicy foods, caffeine, and alcohol).
• Emergency surgery may be required for: Bleeding, Perforation or
obstruction.

35. Treatment of H. pylori-Positive Ulcers
• Multi-drug regimens that include antimicrobials and anti-secretory agents
are used to eradicate H. pylori infection
• H. pylori has been developing resistance to some antibiotics, particularly
clarithromycin
– First-line therapies should have an eradication rate of greater than 80%
– Regional bacterial resistance patterns need to be taken into account when
recommending therapy
– If a second course of H. pylori eradication therapy is needed, the second regimen
should contain different antibiotics
• H.pylori eradication regimens
– Triple Therapy
– Bismuth-based Quadruple Therapy
– Non-Bismuth Quadruple “Concomitant” Therapy
– Sequential Therapy
– Hybrid Therapy
– Salvage Therapy

36. Triple Therapy
• Standard triple therapy regimen contains
– Amoxicillin 1000mg twice a day PLUS Clarithromycin 500mg
twice a day PLUS a PPI dosed once to twice a day
– Given for 10 to 14 days
• 14 day regimens are generally preferred as 14 day regimens
significantly increases the eradication rate
• If the patient is allergic to penicillin, then
metronidazole 500mg twice a day can be substituted
for the amoxicillin

37. Triple Therapy
• Standard triple therapy is considered first-line in areas
where the clarithromycin resistance rate of H. pylori is less
than 15% and no prior macrolide exposure is documented.
• Adding probiotics (specifically Saccharomyces boulardii and
Lactobacillus) to triple therapy has been shown to increase
eradication rates and decrease adverse effects of
treatment, particularly diarrhea

38. Bismuth-based Quadruple Therapy
• Bismuth-based quadruple-therapy contains
– Tetracycline 500mg 4 times a day PLUS Metronidazole 250-500mg 4
times a day PLUS Bismuth subsalicylate 525mg 4 times a day PLUS
a PPI once or twice a day OR H2-receptor antagonist twice a day
– PPIs generally produce higher H. pylori eradication rates and are
preferred over H2RA
– All medications except the PPI should be taken with meals (PPIs 30
minutes before meal)
– Bismuth-based quadruple regimens are given for 10 to 14 days

39. Bismuth-based Quadruple Therapy
• May be used as first-line therapy in areas where the
clarithromycin resistance rate is 15%
≥
• May also be considered for first-line therapy in those with
penicillin allergy or in those who have been previously
treated with a macrolide antibiotic
• May also be used if first-line standard triple therapy fails
(e.g. as second-line therapy or salvage therapy)

40. Non-bismuth quadruple (or “concomitant”)
• Non-bismuth quadruple (or “concomitant”)
therapy (PPI, clarithromycin, amoxicillin, metronidazole) for
10–14 days is another recommended first-line therapy.
• “Concomitant” therapy means that all four drugs are given at
the same time twice daily for the entire duration of therapy.
There is lack of evidence in North America for this regimen.

41. Sequential Therapy
• Newer HP eradication therapy where the antibiotics are administered in
a sequence rather than at the same time
• Sequential therapy contains:
– A PPI twice a day for 10 days AND
– Amoxicillin 1000mg twice day days 1 – 5, followed by Clarithromycin 500mg twice
day PLUS Tinidazole 500mg OR Metronidazole 500mg twice a day days 6 – 10.
– Given for 10 days total (5 days for each antibiotic regimen)
• Adherence and tolerance rates of sequential therapy are similar to triple
therapy but the cost is lower

42. Hybrid therapy
• Hybrid therapy combines the strategies of concomitant
and sequential therapy.
• It involves 7 days of dual therapy (PPI and amoxicillin)
followed by 7 days of quadruple therapy
(PPI, amoxicillin, clarithromycin, metronidazole).
• There is lack of evidence in North America with this
regimen.

43. Levofloxacin-Based Triple Therapy
• Levofloxacin-based Triple Therapy contains:
– Amoxicillin 1000mg twice a day PLUS Levofloxacin 500mg
once a day PLUS a PPI twice a day
– Given for 10 days
• This regimen is an option for salvage therapy in
patients who have persistent H. pylori infection
– This therapy regimen needs validation in North America

44. Salvage Therapy
• If initial treatment fails to eradicate H. pylori, second-line (salvage)
treatment should:
– (1) use antibiotics that were not included in the initial regimen,
– (2) be guided by region-specific or individual antibiotic resistance testing,
and
– (3) use an extended treatment duration of 10–14 days.
• Patients failing clarithromycin triple therapy can be treated with either
bismuth quadruple therapy or the levofloxacin triple regimen for 14
days.
• Other salvage regimens may also be successful.
• Penicillin allergy testing is recommended for patients who report
penicillin allergy because many patients are not truly allergic.

45. Drug Regimens Used to Eradicate Helicobacter pylori
Regimen Duration Drug #1 Drug #2 Drug #3 Drug #4
Proton pump
inhibitor–based triple
therapy
14 days PPI once or twice
daily
Clarithromycin 500
mg twice daily
Amoxicillin 1 g twice
daily or metronidazole
500 mg twice daily
Bismuth quadruple
therapy
10 14 days
− PPI or H2RA once or
twice daily
Bismuth
subsalicylate 525 mg
four times daily
Metronidazole
250 500 mg four
−
times daily
Tetracycline 500
mg four times daily
Non-bismuth
quadruple or
“concomitant”
therapy
10 14 days
− PPI once or twice
daily on days 1 10
−
Clarithromycin 250–
500 mg twice daily
on days 1 10
−
Amoxicillin 1 g twice
daily on days 1 10
−
Metronidazole
250 500 mg twice
−
daily on days 1 10
−
Sequential therapy 10 days PPI once or twice
daily on days 1 10
−
Amoxicillin 1 g twice
daily on days 1 5
−
Metronidazole 250–500
mg twice daily on days
6 10
−
Clarithromycin
250 500 mg twice
−
daily on days 6 10
−
Hybrid therapy 14 days PPI once or twice
daily on days 1 14
−
Amoxicillin 1 g twice
daily on days 1 14
−
Metronidazole 250–500
mg twice daily on days
7 14
−
Clarithromycin
250 500 mg twice
−
daily on days 7 14
−
Levofloxacin triple 10 14 days
− PPI twice daily Levofloxacin 500 mg
daily
Amoxacillin 1 g twice
daily
Levofloxacin
sequential
10 days PPI twice daily on
days 1 10
−
Amoxicillin 1 g twice
daily on days 1 10
−
Levofloxacin 500 mg
once daily on days
6 10
−
Metronidazole 500
mg twice daily on
days 6 10
−
LOAD 7 10 days
− Levofloxacin 250 mg
once daily
Omeprazole (or other
PPI) at high dose
once daily
Nitazoxanide (Alinia)
500 mg twice daily
Doxycycline 100
mg once daily

46. Treatment of NSAID-Induced Ulcers
• Ideally, discontinue the NSAID and treat with standard healing
regimens of a PPI, H2-receptor antagonist, or sucralfate
– PPIs are usually preferred because they provide the fastest symptom relief
and ulcer healing
• If the NSAID needs to be continued:
– Consider: Reducing the dose of the NSAID OR Change NSAID to one of the
following
• Acetaminophen, A nonacetylated salicylate (salsalate, trisalicylate)
• A partially selective COX-2 inhibitor (etodalac, nabumetone, meloxicam, diclofenac,
celecoxib)
– Use a PPI to treat the ulcer
• When an NSAID needs to be continued, PPIs are the drugs of choice to treat and heal
the ulcer

47. Reducing the Risk of NSAID-Induced Ulcer & GI
Complications
• Strategies to reduce the risk of NSAID-induced ulcers
– In GI toxicity high risk patients, use either a PPI or misoprostol as co-
therapy along with the NSAID
– Use a selective COX-2 inhibitor instead of a nonselective NSAID
• When selecting a strategy, cardiovascular risk of the patient
must also be considered

48. GI and Cardiovascular Safety Issues with NSAIDs
• There is no difference in cardiovascular risk between the
selective COX-2 inhibitors, the partially selective NSAIDs, and the
non-selective NSAIDs with the exception of naproxen
– When compared with all the other NSAIDs, naproxen has the best
cardiovascular safety profile

49. GI and Cardiovascular Safety Issues with
NSAIDs
• Guidelines take both CV risk and GI toxicity risk into account
when recommending a strategy to reduce the risk of developing
a peptic ulcer in those who need chronic NSAID therapy

50. Treatment of Non-H. pylori, Non-NSAID
Ulcers
• Very few patients have non-H. pylori, non-NSAID
(idiopathic) peptic ulcers
• If an idiopathic peptic ulcer is confirmed, treatment
with standard ulcer healing therapy should be
initiated
– Standard H2-receptor antagonist or sucralfate dosage
regimens heal the majority of gastric and duodenal ulcers in
6 to 8 weeks
– Standard PPI dosage regimens heal the majority of gastric
and duodenal ulcers in 4 weeks

51. Maintenance Therapy with Anti-Secretory Agents
• Maintenance therapy (to maintain ulcer healing,
prevent recurrence and complications) with anti-
secretory agents like PPIs is only indicated in the
following groups of high risk patients:
– Those who have failed H. pylori eradication
– Those who have a history of ulcer related complications
– Those who have frequent recurrences of H. pylori-negative
ulcers
– Those who are heavy smokers
– Those who NSAID users

52. Stress Related Mucosal Damage (SRMD)
• Two independent risk factors for SRMD include:
– patients with respiratory failure (mechanical ventilation for >48
hours) or
– coagulopathy defined as
• a platelet count <50,000 cells/ mm3
• an international normalized ratio of more than 1.5, or
• a partial thromboplastin time of more than two times normal.
• Patients with these risk factors should receive stress induced
Ulcers prophylaxis.

53. Stress Related Mucosal Damage (SRMD)
• Other risk factors include:
– severe burns (>35% of body surface area)
– multiple trauma
– surgery, or organ failure
– History of GI ulceration or bleeding within 1 year of admission,
– Two of the following risk factors:
• sepsis, ICU stay for more than 1 week, occult bleeding lasting 6 or more days
• use of high dose corticosteroids (> 250 mg/day of hydrocortisone or equivalent
• It is not cost effective to use prophylaxis for all patients;
– reserved for those patients at high risk of SRMD.

54. Stress Induced Ulcers Prophylaxis
• Adverse effects, drug interactions, and frequent dosing make antacids and
sucralfate less favorable compared to H2-receptor antagonists (H2RAs) and
PPIs for the prevention of SRMB.
• Clinical trials demonstrate that H2RAs significantly reduce the risk of GI
bleeding in critically ill patients.
– However, tolerance can develop within 42 hours with the use of H2RAs.
• PPIs provide more consistent acid suppression and unlike H2RAs tolerance does
not develop.
• Both H2RAs and PPIs may be given by mouth, nasogastric tube, or
intravenously

55. Treatment of Gastric Acid Hypersecretion from
Zollinger-Ellison Syndrome (ZES)
• PPIs are the oral drugs of choice for managing gastric acid
hypersecretion from ZES
• Treatment should be started with omeprazole 60mg per day or an
equivalent dose of another PPI
– This PPI daily dose should be divided and the PPI given every 8 to 12
hours

56. Treatment of Refractory Ulcers
• Ulcers are considered refractory to therapy when symptoms, ulcers,
or both persist beyond 8 to 12 weeks despite conventional
treatment as previously described or when several courses of H.
pylori eradication therapy fail
• Patient should undergo an upper endoscopy to assess the situation
• Treatment depends on cause and may include additional H. pylori
eradication attempts, higher PPI dosages, or surgery

57. Pharmacologic Agents
• Proton Pump Inhibitors
• H2-Receptor blockers
• Anti-acids
Read about from previous slides (GERD
pharmacotherapy)

58. Pharmacologic Agents
Misoprostol
• MOA
– A synthetic prostaglandin E1 analog that replaces the protective
prostaglandins that are decreased from prostaglandin inhibiting
therapies such as NSAIDs
• Enhances natural gastromucosal defense mechanisms and healing by
increasing the production of gastric mucous and mucosal secretion of
bicarbonate
• Inhibits basal and nocturnal acid secretion by direct action on the parietal cells
• Agent
– Misoprostol (Cytotec)
• Adverse effects
– Diarrhea, abdominal pain, headache, nausea/vomiting, flatulence,
dysmenorrhea, hypophosphatemia

59. Misoprostol
• Monitoring
– Pregnancy test
– Serum phosphate
• Patient Counseling
– Pregnancy category X
• Is a potential abortifacient

60. Bismuth Preparations
• MOA
– Bismuth exhibits antimicrobial activity against bacterial and
viral gastrointestinal pathogens
• Agents
– Bismuth subsalicylate
– Bismuth subcitrate potassium
• Adverse effects
– Fecal discoloration, tongue discoloration
– Neurotoxicity (rare)

61. Bismuth Preparations
• Monitoring
– No specific monitoring
• Patient counseling
– May cause temporary, harmless darkening of the tongue
and/or stool
– Avoid bismuth subsalicylate if have an aspirin allergy

62. Sucralfate
• MOA
– Thought to form an ulcer-adherent complex at the ulcer site
protecting it from further injury from stomach acid
• Agent
– Sucralfate (Carafate)
• Adverse Effects
– Constipation, bezoar formation, hyperglycemia in diabetes
patients, aluminum toxicity in patients with chronic renal failure
or on dialysis

63. Sucralfate
• Monitoring
– Blood glucose in diabetes patients
– Renal function in elderly patients
• Patient counseling
– Take on an empty stomach
– Do not take antacids 30 minutes before or after taking
sucralfate

64. Drug Dosing
Drug Brand Name Initial Dose Usual Range
Proton pump inhibitors
Omeprazole Prilosec, various 40 mg daily 20–40 mg/day
Omeprazole + sodium
bicarbonate
Zegerid 40 mg daily 20–40 mg/day
Lansoprazole Prevacid, various 30 mg daily 15–30 mg/day
Rabeprazole Aciphex 20 mg daily 20–40 mg/day
Pantoprazole Protonix, various 40 mg daily 40–80 mg/day
Esomeprazole Nexium 40 mg daily 20–40 mg/day
Dexlansoprazole Dexilant 30–60 mg daily 30–60 mg/day
H2-receptor antagonists
Cimetidine Tagamet, various 300 mg four times daily, 400 mg twice
daily, or 800 mg at bedtime
800–1600 mg/day in
divided doses
Famotidine Pepcid, various 20 mg twice daily, or 40 mg at bedtime 20–40 mg/day
Nizatidine Axid, various 150 mg twice daily, or 300 mg at
bedtime
150–300 mg/day
Ranitidine Zantac, various 150 mg twice daily, or 300 mg at
bedtime
150–300 mg/day
Mucosal protectants
Sucralfate Carafate, various 1 g four times daily, or 2 g twice daily 2–4 g/day

65. Evaluation and Management of PUD
Monitor patients for:
Symptomatic relief of ulcer pain.
Potential adverse effects.
Drug interactions.
Symptom persistence or recurrence within 14 days after end of treatment suggests
failure of ulcer healing or HP eradication, or alternative diagnosis such as GERD.
Most patients with uncomplicated HP-positive ulcers do not require confirmation of
ulcer healing or HP eradication.
 Monitor patients taking NSAIDs closely for signs and symptoms of: Bleeding.
Obstruction. Penetration. Perforation.
Follow-up endoscopy justified in patients with: Frequent symptomatic recurrence,
refractory disease, complications, suspected hypersecretory states.

66. Thank You