PUD Flashcards
1
Q
What does PUD encompass?
A
Gastric ulcers (GUs) and duodenal ulcers (DUs)
PUD stands for Peptic Ulcer Disease.
2
Q
How are ulcers defined in terms of size and depth?
A
Breaks in the mucosal surface >5 mm in size, with depth to the submucosa
This definition applies to both gastric and duodenal ulcers.
3
Q
What are the most common risk factors for PUD?
A
- H. pylori
- NSAIDs
These factors have estimated odds ratios of 3.7 and 3.3, respectively.
4
Q
What is the odds ratio for chronic obstructive lung disease as a risk factor for PUD?
A
2.34
This indicates a significant association with PUD risk.
5
Q
List additional risk factors for PUD along with their odds ratios.
A
- Chronic renal insufficiency (2.29)
- Current tobacco use (1.99)
- Former tobacco use (1.55)
- Older age (1.67)
- Three or more doctor visits in a year (1.49)
- Coronary heart disease (1.46)
- Former alcohol use (1.29)
- African American race (1.20)
- Obesity (1.18)
- Diabetes (1.13)
These factors contribute to the risk of developing PUD.
6
Q
What medications and procedures are associated with an increased incidence of PUD?
A
- Selective serotonin reuptake inhibitors (SSRIs)
- Gastric bypass surgery
Both have been linked to a higher incidence of peptic ulcers.
7
Q
True or False: DUs and GUs share many common features in terms of pathogenesis, diagnosis, and treatment.
A
True
Despite their differences, GUs and DUs have similar underlying mechanisms.
8
Q
When do gastric ulcers (GUs) typically occur in life?
A
GUs tend to occur later in life, with a peak incidence reported in the sixth decade.
9
Q
What is the gender distribution for gastric ulcers?
A
More than one-half of GUs occur in males.
10
Q
Where do duodenal ulcers (DUs) most often occur?
A
In the first portion of the duodenum (>95%)
DUs are usually located within 3 cm of the pylorus
11
Q
What is the typical diameter of duodenal ulcers?
A
≤1 cm, but can reach 3–6 cm (giant ulcer)
Giant ulcers are a rare occurrence
12
Q
What is the characteristic appearance of duodenal ulcers?
A
Sharply demarcated with depth reaching the muscularis propria
The base often consists of eosinophilic necrosis with surrounding fibrosis
13
Q
What distinguishes gastric ulcers (GUs) from duodenal ulcers?
A
GUs can represent a malignancy and should be biopsied upon discovery
14
Q
Where are benign gastric ulcers most often found?
A
Distal to the junction between the antrum and the acid secretory mucosa
15
Q
What association do benign gastric ulcers have with H. pylori?
A
Associated with antral gastritis
16
Q
What may be observed in NSAID-related gastric ulcers instead of chronic active gastritis?
A
Chemical gastropathy, typified by foveolar hyperplasia, edema of the lamina propria, and epithelial regeneration
17
Q
What are the primary causes of duodenal ulcers (DUs)?
A
H. pylori and NSAID-induced injuries
These account for the majority of DUs.
18
Q
How does gastric acid secretion in DU patients compare to control subjects?
A
Average basal and nocturnal gastric acid secretion appears to be increased
There is substantial overlap between DU patients and control subjects.
19
Q
What is the significance of bicarbonate secretion in DU patients?
A
Bicarbonate secretion is significantly decreased in the duodenal bulb
This is compared to control subjects.
20
Q
What are the main causes of gastric ulcers (GUs)?
A
H. pylori or NSAID-induced mucosal damage
The majority of GUs can be attributed to these factors.
21
Q
What tends to be the gastric acid output in gastric ulcer patients?
A
Normal or decreased
This applies to both basal and stimulated gastric acid output.
22
Q
Where do Type I gastric ulcers occur and what is their association with gastric acid production?
A
In the gastric body; associated with low gastric acid production
They are classified as Type I ulcers.
23
Q
Where do Type II gastric ulcers occur and what is their association with gastric acid production?
A
In the antrum; gastric acid can vary from low to normal
They are classified as Type II ulcers.
24
Q
Where do Type III gastric ulcers occur and what is their gastric acid production status?
A
Within 3 cm of the pylorus; commonly associated with DUs and normal or high gastric acid production
They are classified as Type III ulcers.
25
Where are Type IV gastric ulcers found and what is their association with gastric acid production?
In the cardia; associated with low gastric acid production
## Footnote
They are classified as Type IV ulcers.
26
What dose of aspirin may lead to serious GI ulceration?
75 mg/d
## Footnote
This indicates that even low doses of aspirin can be risky for gastrointestinal health.
27
What infection increases the risk of PUD-associated GI bleeding in chronic users of low-dose aspirin?
H. pylori infection
## Footnote
This infection is a significant risk factor for gastrointestinal complications.
28
List established risk factors for NSAID-induced morbidity.
* Advanced age
* History of ulcer
* Concomitant use of glucocorticoids
* High-dose NSAIDs
* Multiple NSAIDs
* Concomitant use of anticoagulants or clopidogrel
* Serious or multisystem disease
## Footnote
These factors increase the likelihood of serious complications from NSAID use.
29
List possible risk factors for NSAID-induced morbidity.
* Concomitant infection with H. pylori
* Cigarette smoking
* Alcohol consumption
## Footnote
These factors may contribute to the risk of complications when using NSAIDs.
30
What effect do SSRIs have on NSAID-induced GI bleeding?
Synergistic effect
## Footnote
SSRIs may increase the risk of GI bleeding due to their impact on platelet aggregation.
31
What is the role of prostaglandins in the gastroduodenal mucosa?
Maintaining mucosal integrity and repair
## Footnote
Prostaglandins are essential for protecting the gastric mucosa from injury.
32
What role do neutrophils play in NSAID-induced mucosal injury?
Initiation of mucosal injury via adherence to gastric microcirculation
## Footnote
Neutrophil adherence is crucial in the early stages of injury.
33
What are single nucleotide polymorphisms (SNPs) associated with in NSAID-induced mucosal injury?
Genes including cytochrome P450 subtypes, IL-1β, angiotensinogen, and SLCO1B1
## Footnote
These SNPs need confirmation in larger studies.
34
How does topical use of NSAIDs affect the mucosa?
Increases epithelial surface permeability
## Footnote
This can lead to mucosal injury through various mechanisms.
35
Why do aspirin and many NSAIDs cause cell injury in the stomach?
They remain in a nonionized lipophilic form in the acidic environment
## Footnote
This allows NSAIDs to cross lipid membranes and become trapped intracellularly.
36
What is one consequence of NSAIDs altering the surface mucous layer?
Permitting back diffusion of H + and pepsin
## Footnote
This leads to further epithelial cell damage.
37
What is a risk associated with enteric-coated or buffered NSAID preparations?
Risk of peptic ulceration
## Footnote
These preparations can still contribute to mucosal injury.
38
How do NSAIDs produce additional proinflammatory mediators?
Through activation of the lipoxygenase pathway
## Footnote
This results in increased levels of TNF and leukotrienes.
39
What is the relationship between H. pylori and NSAIDs in the pathogenesis of PUD?
Complex interplay as independent and synergistic risk factors
## Footnote
Both factors can increase the risk of PUD and complications.
40
What effect does the eradication of H. pylori have on NSAID-induced complications?
Reduces likelihood of GI complications in high-risk individuals
## Footnote
This brings their risk levels closer to those of average-risk individuals.
41
What role does cigarette smoking play in the pathogenesis of PUD?
Cigarette smoking is implicated in increased frequency of ulcers, decreased healing rates, impaired response to therapy, and increased ulcer-related complications
## Footnote
The exact mechanism is unknown, but theories include altered gastric emptying and increased risk for H. pylori infection.
42
What is the genetic predisposition related to peptic ulcer disease (PUD)?
First-degree relatives of DU patients are three times as likely to develop an ulcer
## Footnote
Increased frequencies of blood group O and nonsecretor status are also implicated.
43
Which blood group is preferentially bound by H. pylori?
Blood group O
## Footnote
This binding may be a factor in ulcer development among those with this blood type.
44
What are potential susceptibility genes for NSAID-induced PUD?
Genes encoding cytochrome P450 2C9 and 2C8 (CYP2C9 and CYP2C8)
## Footnote
Studies have not consistently demonstrated this association.
45
How does psychological stress relate to PUD?
Psychological stress has been thought to contribute to PUD, but studies have shown conflicting results
## Footnote
Certain personality traits like neuroticism are associated with PUD and nonulcer dyspepsia.
46
What dietary factors are associated with peptic diseases?
No convincing studies indicate a specific diet associated with ulcer formation
## Footnote
Certain foods and beverages may cause dyspepsia.
47
List chronic disorders strongly associated with PUD.
* Advanced age
* Chronic pulmonary disease
* Chronic renal failure
* Cirrhosis
* Nephrolithiasis
* α1-antitrypsin deficiency
* Systemic mastocytosis
## Footnote
These conditions have a strong correlation with PUD.
48
What disorders have a possible association with PUD?
* Hyperparathyroidism
* Coronary artery disease
* Polycythemia vera
* Chronic pancreatitis
* Former alcohol use
* Obesity
* African-American race
* Three or more doctor visits in a year
## Footnote
These associations are less definitive than those of strong association.
49
What are the two predominant causes of PUD?
* H. pylori infection
* NSAID ingestion
## Footnote
PUD not related to these causes is on the rise.
50
What is the common symptom in many GI disorders, including DU and GU?
Abdominal pain
## Footnote
Abdominal pain has a poor predictive value for the presence of either DU or GU.
51
What percentage of patients with PUD do not have abdominal pain?
Approximately two-thirds
## Footnote
Up to 87% of patients with NSAID-induced mucosal disease can present with complications without antecedent symptoms.
52
How is epigastric pain in DU and GU typically described?
Burning or gnawing discomfort
## Footnote
It can also be described as an ill-defined, aching sensation or as hunger pain.
53
When does typical pain in DU occur after a meal?
90 minutes to 3 hours
## Footnote
This pain is frequently relieved by antacids or food.
54
What symptom is most discriminating for DU patients?
Pain that awakes the patient from sleep (between midnight and 3 a.m.)
## Footnote
Two-thirds of DU patients describe this complaint.
55
How do elderly patients typically present with PUD?
They are less likely to have abdominal pain and may present with a complication
## Footnote
Complications include ulcer bleeding or perforation.
56
How may the pain pattern in GU patients differ from DU patients?
Discomfort may be precipitated by food
## Footnote
Nausea and weight loss occur more commonly in GU patients.
57
What does constant dyspepsia that is no longer relieved by food or antacids suggest?
A penetrating ulcer
## Footnote
This may involve the pancreas.
58
What does sudden onset of severe, generalized abdominal pain indicate?
Perforation
## Footnote
This is a critical symptom that requires immediate attention.
59
What symptoms suggest gastric outlet obstruction?
Pain worsening with meals, nausea, and vomiting of undigested food
## Footnote
These symptoms can indicate a blockage in the stomach.
60
What do tarry stools or coffee-ground emesis indicate?
Bleeding
## Footnote
These symptoms are associated with gastrointestinal bleeding.
61
What is the most frequent finding in patients with GU or DU?
Epigastric tenderness
## Footnote
GU refers to gastric ulcer, and DU refers to duodenal ulcer.
62
What signs suggest dehydration secondary to vomiting or active GI blood loss?
Tachycardia and orthostasis
## Footnote
These vital sign changes are critical indicators of fluid loss.
63
What does a severely tender, board-like abdomen suggest?
Perforation
## Footnote
This finding is a serious complication that requires immediate medical attention.
64
What does the presence of a succussion splash indicate?
Retained fluid in the stomach
## Footnote
This suggests a potential gastric outlet obstruction.
65
What is the most common complication observed in PUD?
GI bleeding
## Footnote
PUD stands for peptic ulcer disease.
66
In which age group does bleeding and complications of ulcer disease occur more often?
>60 years of age
67
What is a likely reason for the higher incidence of GI bleeding in the elderly?
Increased use of NSAIDs
68
What percentage of mortality in PUD-related bleeding is due to nonbleeding causes?
Up to 80%
69
List three nonbleeding causes of mortality in PUD-related bleeding.
* Multiorgan failure (24%)
* Pulmonary complications (24%)
* Malignancy (34%)
70
What percentage of patients with ulcer-related hemorrhage bleed without any preceding warning signs or symptoms?
>50%
71
What is the second most common ulcer-related complication?
Perforation
## Footnote
Reported in 6–7% of PUD patients with an estimated 30-day mortality of >20%
72
What are the classic symptoms associated with perforation?
Acute abdominal pain, tachycardia, abdominal rigidity
## Footnote
This classic triad may not be present in elderly or immunosuppressed patients
73
Which organ do DUs typically penetrate into?
Pancreas
## Footnote
This can lead to pancreatitis
74
Which organ do GUs typically penetrate into?
Left hepatic lobe
## Footnote
Gastrocolic fistulas associated with GUs have also been described
75
The least common ulcer-related complication, occurring in 1–2% of patients.
Gastric outlet obstruction
76
What can cause relative obstruction in gastric outlet obstruction?
Ulcer-related inflammation and edema in the peripyloric and duodenal region.
77
What is a fixed, mechanical obstruction in gastric outlet obstruction caused by?
Scar formation in the peripyloric areas.
78
What interventions may be required for fixed mechanical obstruction?
Endoscopic (balloon dilation with or without placement of a biodegradable stent) or surgical intervention (stricturoplasty or gastrojejunostomy).
79
What are some signs and symptoms of gastric outlet obstruction?
* New onset of early satiety
* Nausea
* Vomiting
* Increase of postprandial abdominal pain
* Weight loss
80
The most commonly encountered diagnosis among patients seen for upper abdominal discomfort
functional dyspepsia (FD) or essential dyspepsia
81
What is often required to document the presence of a gastroduodenal ulcer?
A radiographic study or an endoscopic procedure
## Footnote
Radiographic studies include barium studies, which are rarely done today.
82
What is the sensitivity of older single-contrast barium meals for detecting a duodenal ulcer?
Up to 80%
## Footnote
A double-contrast study provides detection rates as high as 90%.
83
What factors decrease the sensitivity for detection of duodenal ulcers?
Small ulcers (<0.5 cm), presence of previous scarring, postoperative patients
## Footnote
These factors affect the ability to accurately detect ulcers.
84
How does a duodenal ulcer typically appear in radiographic studies?
As a well-demarcated crater, most often seen in the bulb
## Footnote
This characteristic appearance aids in diagnosis.
85
What does a benign gastric ulcer typically appear as?
A discrete crater with radiating mucosal folds originating from the ulcer margin
## Footnote
This appearance helps differentiate it from malignant ulcers.
86
What size gastric ulcers are more often malignant?
Ulcers >3 cm in size or those associated with a mass
## Footnote
Size and association with a mass are key indicators of malignancy.
87
What is the appropriate initial testing for individuals <45 years of age with ulcer symptoms?
Testing for H. pylori and antibiotic therapy
## Footnote
This approach is recommended before embarking on a diagnostic evaluation.
88
True or False: Barium studies are commonly used as a first test for documenting an ulcer.
False
## Footnote
Barium studies are rarely used as a first test in today's environment.
89
What is the primary purpose of endoscopy in examining the upper GI tract?
To provide the most sensitive and specific approach for examining the upper GI tract.
## Footnote
Endoscopy allows for direct visualization of the mucosa.
90
What additional procedures can endoscopy facilitate?
Photographic documentation of a mucosal defect and tissue biopsy.
## Footnote
Biopsies are used to rule out malignancy or H. pylori.
91
Why is endoscopic examination particularly useful?
To identify lesions too small to detect by radiographic examination, evaluate atypical radiographic abnormalities, or determine if an ulcer is a source of blood loss.
92
What is the sensitivity and specificity of several biopsy urease tests for H. pylori?
>90–95%.
## Footnote
Examples include PyloriTek, CLOtest, Hpfast, and Pronto Dry.
93
List three types of studies routinely used to detect H. pylori.
* Serologic testing
* 13 C- or 14 C-urea breath test
* Fecal H. pylori antigen test.
94
What was the main form of therapy for peptic ulcers before the role of histamine was understood?
Neutralization of secreted acid with antacids
95
What are antacids primarily used for now?
Symptomatic relief of dyspepsia
96
What are the most commonly used agents in antacids?
Mixtures of aluminum hydroxide and magnesium hydroxide
97
What side effect can aluminum hydroxide produce?
Constipation and phosphate depletion
98
What side effect can magnesium hydroxide cause?
Loose stools
99
What combination do many commonly used antacids (e.g., Maalox, Mylanta) contain?
Both aluminum hydroxide and magnesium hydroxide
100
Why should magnesium-containing antacids be avoided in chronic renal failure patients?
Possible hypermagnesemia
101
What potential risk does aluminum have in chronic renal failure patients?
Chronic neurotoxicity
102
What are two potent antacids mentioned in the text?
Calcium carbonate and sodium bicarbonate
103
What syndrome can long-term use of calcium carbonate lead to?
Milk-alkali syndrome
104
What are the effects of milk-alkali syndrome?
Hypercalcemia and hyperphosphatemia with possible renal calcinosis and progression to renal insufficiency
105
What potential issue may sodium bicarbonate induce?
Systemic alkalosis
106
What are the four H 2 receptor antagonists currently available?
Cimetidine, ranitidine, famotidine, nizatidine
107
What do all H 2 receptor antagonists significantly inhibit?
Basal and stimulated acid secretion
108
What is the common therapeutic use of H 2 receptor antagonists?
Treatment of active ulcers in combination with antibiotics
109
Which H 2 receptor antagonist was the first to be used for acid peptic disorders?
Cimetidine
110
What are some weak antiandrogenic side effects of cimetidine?
Reversible gynecomastia and impotence
111
What monitoring is indicated with long-term use of cimetidine?
Monitoring of drugs such as warfarin, phenytoin, and theophylline
112
What are some rare reversible adverse effects of cimetidine?
Confusion, elevated serum aminotransferases, creatinine, and serum prolactin
113
How do the potencies of ranitidine, famotidine, and nizatidine compare to cimetidine?
They are more potent H 2 receptor antagonists than cimetidine
114
What is a common dosing regimen for ulcer prevention with H 2 receptor antagonists?
Once a day at bedtime
115
What are the comparable nighttime dosing regimens for H 2 receptor antagonists?
* Cimetidine 800 mg
* Ranitidine 300 mg
* Famotidine 40 mg
* Nizatidine 300 mg
116
What rare systemic toxicities can occur with H 2 receptor antagonists?
Pancytopenia, neutropenia, anemia, thrombocytopenia
117
Which H 2 receptor antagonists can bind to hepatic cytochrome P450?
Cimetidine and ranitidine
118
True or False: Patients may develop tolerance to H 2 blockers.
True
119
Fill in the blank: H 2 receptor antagonists are often used for the treatment of _______ in combination with antibiotics.
[active ulcers]
120
How are omeprazole and lansoprazole administered?
As enteric-coated granules in a sustained-release capsule that dissolves at pH of 6.
121
What is a unique formulation of lansoprazole?
Orally disintegrating tablet that can be taken with or without water.
122
What is the purpose of sodium bicarbonate in omeprazole formulations?
To protect omeprazole from acid degradation and promote rapid gastric alkalinization.
123
What types of formulations are available for pantoprazole and rabeprazole?
Enteric-coated tablets
## Footnote
Pantoprazole is also available as a parenteral formulation for intravenous use.
124
What is the time frame for the maximum acid inhibitory effect after administration of PPIs?
Between 2 and 6 hours after administration.
125
How long can the duration of inhibition last after taking PPIs?
72–96 hours.
126
What percentage of acid production is inhibited after one week of daily PPI therapy?
>95%.
127
What is the half-life of PPIs?
~18 hours.
128
What can happen after discontinuation of PPIs in H pylori negative individuals?
Rebound gastric acid hypersecretion may occur.
129
What is the mechanism behind rebound gastric acid hypersecretion?
Gastrin-induced hyperplasia and hypertrophy of histamine-secreting ECL cells.
130
How can rebound hypersecretion be prevented?
Gradual tapering of the PPI and switching to an H2 receptor antagonist.
131
What impact do PPIs have on vitamin B12 absorption?
IF production is inhibited, but vitamin B12 deficiency anemia is uncommon.
132
Which drugs may be interfered with by PPIs due to significant hypochlorhydria?
Ketoconazole, ampicillin, iron, digoxin.
133
Which PPIs inhibit hepatic cytochrome P450?
Omeprazole, lansoprazole.
134
What caution should be taken when using PPIs with other medications?
Caution with theophylline, warfarin, diazepam, atazanavir, phenytoin.
135
What is the association between long-term PPI use and community-acquired pneumonia?
Higher incidence.
136
What is the increased risk percentage of C. difficile infection associated with PPI use according to a meta-analysis?
74% increased risk.
137
What is postulated to play a role in the increased risk of infection with PPI use?
PPI-induced changes in the host microbiome.
138
What condition is associated with PPI use and specifically with lansoprazole?
Collagenous colitis.
139
What is the association found in a population-based study regarding long-term use of PPIs?
Development of hip fractures in older women
## Footnote
The absolute risk of fracture remained low and may be zero despite the observed increase associated with the dose and duration of acid suppression.
140
What deficiencies have been implicated with long-term use of PPIs?
Iron, vitamin B12, and magnesium deficiency
## Footnote
A meta-analysis found a 40% increase in hypomagnesemia in PPI users compared to nonusers.
141
What should be checked in patients needing long-term PPIs after 1-2 years of use?
Complete blood count, vitamin B12 level, and magnesium level
## Footnote
These recommendations are not evidence-based or recommended by expert opinion.
142
What negative effect might PPIs have on clopidogrel?
Inhibition of the antiplatelet effect
## Footnote
Evidence is mixed regarding this interaction, with earlier studies showing a small increase in mortality and readmission rates for coronary events.
143
What is the mechanism of interaction between PPIs and clopidogrel?
Competition for the same cytochrome P450 (CYP2C19)
## Footnote
The influence of this drug interaction on mortality is not clearly established.
144
What is a recommended separation time for administering PPIs and clopidogrel?
12 hours
## Footnote
Some have suggested giving the PPI 30 minutes before breakfast and clopidogrel at bedtime.
145
What additional side effects have been associated with long-term PPI use?
Increased cardiac risks, dementia, acute and chronic kidney injury
## Footnote
Data are often retrospective and confounding variables were not consistently eliminated.
146
What is particularly important regarding the use of PPIs in patients aged ≥65 years?
Higher risk for long-term side effects
## Footnote
This is partly due to the higher prevalence of concomitant chronic diseases in this age group.
147
What should be done when discontinuing a PPI in long-term users?
Taper gradually over 1-2 weeks
## Footnote
Abrupt withdrawal may result in rebound hyperacidity, and a transition to an H2 blocker may be considered.
148
True or False: High-dose H2 blockers are as effective as PPIs for GI protective therapy.
False
## Footnote
High-dose H2 blockers do not appear to be as effective as PPIs.
149
What is sucralfate?
A complex sucrose salt substituted by aluminum hydroxide and sulfate
## Footnote
Sucralfate is insoluble in water and forms a viscous paste in the stomach and duodenum.
150
What are the mechanisms of action of sucralfate?
It acts by several mechanisms:
* Serving as a physicochemical barrier
* Promoting trophic action by binding growth factors
* Enhancing prostaglandin synthesis
* Stimulating mucus and bicarbonate secretion
* Enhancing mucosal defense and repair
## Footnote
EGF stands for Epidermal Growth Factor.
151
What is the most common toxicity associated with sucralfate?
Constipation (2–3% incidence)
## Footnote
Other rare toxicities include hypophosphatemia and gastric bezoar formation.
152
In which patients should sucralfate be avoided?
Patients with chronic renal insufficiency
## Footnote
This is to prevent aluminum-induced neurotoxicity.
153
What is the standard dosing of sucralfate?
1 g qid
## Footnote
'qid' stands for 'four times a day'.
154
What are common adverse effects of bismuth-containing preparations?
Black stools, constipation, and darkening of the tongue
## Footnote
Long-term high doses may lead to neurotoxicity.
155
What is the role of stable prostaglandin analogues in treating PUD?
They enhance mucosal defense and repair
## Footnote
They were developed due to their central role in maintaining mucosal integrity.
156
What is the most common toxicity noted with prostaglandin analogues?
Diarrhea (10–30% incidence)
## Footnote
Other major toxicities include uterine bleeding and contractions.
157
What is the standard therapeutic dose of misoprostol?
200 μg qid
## Footnote
Misoprostol is contraindicated in women who may be pregnant.
158
What types of drugs were historically used for treating acid peptic disorders but are rarely used today?
Anticholinergic agents and tricyclic antidepressants
## Footnote
Their use declined due to toxicity and the development of potent antisecretory agents.
159
Who should be treated for H. pylori infection according to consensus conferences?
Patients with documented PUD
160
Should patients with a history of documented PUD and positive H. pylori tests be treated?
Yes, they should be treated
161
What percentage of patients with gastric MALT lymphoma experience complete remission after H. pylori eradication?
Between 60 and 90%
162
What does the Maastricht IV/Florence Consensus Report recommend for patients with uninvestigated dyspepsia?
A test-and-treat approach if local incidence of H. pylori is >20%
163
Who does the ACG clinical guidelines recommend should be tested and treated for H. pylori?
Individuals aged <60 years with uninvestigated dyspepsia
Patient who will be using NSAID
164
Why do patients on long-term NSAIDs require continued PPI treatment after H. pylori eradication?
Eradication alone does not eliminate the risk of gastroduodenal ulcers
165
What does the ACG recommend for patients who have undergone resection of early gastric cancer?
Eradication of H. pylori
166
In what situations should H. pylori eradication be considered for gastric cancer prevention?
* First-degree relatives of gastric cancer patients
* Previous gastric neoplasm treated by endoscopic or subtotal resection
* Severe pangastritis or body-predominant gastritis
* Gastric acid inhibition for >1 year
* Strong environmental risk factors (heavy smoking, exposure to dust, coal, quartz, cement, or work in quarries)
* H. pylori-positive patients fearing gastric cancer
167
What conditions do the ACG clinical guidelines recommend testing for H. pylori eradication?
* Unexplained iron deficiency anemia
* Idiopathic thrombocytopenic purpura
168
What concerns have been raised regarding the widespread use of antibiotics for H. pylori therapy?
* Increased bacterial resistance rates
* Reported weight gain
* Alteration of the microbiome
169
What is the most effective duration for combination therapy in eradicating H. pylori?
14 days
## Footnote
Combination therapy for 14 days provides the greatest efficacy.
170
Name five agents frequently used in the treatment of H. pylori.
* Amoxicillin
* Metronidazole
* Tetracycline
* Clarithromycin
* Bismuth compounds
## Footnote
These agents are commonly used to treat H. pylori infections.
171
True or False: Dual therapy is recommended for H. pylori treatment.
False
## Footnote
Dual therapy is not recommended due to eradication rates of <80–85%.
172
What was the first effective triple regimen against H. pylori?
Bismuth, metronidazole, and tetracycline
## Footnote
This combination was the first triple regimen found effective against H. pylori.
173
What are the potential drawbacks of triple therapy for H. pylori?
* Poor patient compliance
* Drug-induced side effects
## Footnote
These drawbacks can affect the effectiveness of the treatment.
174
What is the name of the prepackaged formulation containing lansoprazole, clarithromycin, and amoxicillin?
Prevpac
## Footnote
Prevpac is taken twice per day for 14 days.
175
What are the instructions for taking Helidac?
Four times per day with an antisecretory agent for at least 14 days
## Footnote
Helidac contains BSS, tetracycline, and metronidazole.
176
True or False: Clarithromycin-based triple therapy should be used in settings with high H. pylori resistance.
False
## Footnote
Clarithromycin-based triple therapy should be avoided where H. pylori resistance exceeds 15%.
177
What factors influence the choice of a treatment regimen for H. pylori?
* Efficacy
* Patient tolerance
* Existing antibiotic resistance
* Prior antibiotic use
* Cost of the drugs
## Footnote
These factors are crucial in selecting an appropriate treatment regimen.
178
What is a common issue with shorter regimens (7–10 days) for H. pylori treatment?
Less effective than 14-day regimens
## Footnote
Shorter administration courses have not proved as successful as the 14-day regimens.
179
What is the benefit of adding acid suppression in H. pylori treatment?
Provides early symptom relief and enhances bacterial eradication
## Footnote
Acid suppression aids in the success of H. pylori treatment.
180
What side effects can bismuth cause?
Black stools, constipation, darkening of the tongue
## Footnote
Bismuth is a component of some triple therapy regimens.
181
What is the most feared complication associated with amoxicillin?
Pseudomembranous colitis
## Footnote
This complication occurs in <1–2% of patients.
182
What other side effects can amoxicillin lead to?
Antibiotic-associated diarrhea, nausea, vomiting, skin rash, allergic reaction
## Footnote
These are common adverse effects of amoxicillin.
183
What effect do probiotics have when used with antibiotics?
May ameliorate some of the antibiotic side effects
## Footnote
Probiotics can help manage gastrointestinal side effects.
184
What rare side effects are reported with tetracycline?
Rashes, hepatotoxicity, anaphylaxis
## Footnote
These side effects are very rare.
185
What is a significant concern when treating patients who may not need therapy?
Potential for development of antibiotic-resistant strains
## Footnote
This is a critical consideration in antibiotic prescribing.
186
What is the most common cause of treatment failure in compliant patients?
Antibiotic-resistant strains
## Footnote
This highlights the importance of antibiotic resistance in treatment outcomes.
187
What should be included in the decision-making for H. pylori treatment?
Asking the patient about prior antibiotic exposure
## Footnote
This helps assess potential antibiotic resistance.
188
What is a common reason for the failure of H. pylori eradication with triple therapy in compliant patients?
Infection with a resistant organism
## Footnote
Resistance to treatment can complicate eradication efforts.
189
What should be the next step if triple therapy fails for H. pylori?
Quadruple therapy, substituting clarithromycin for metronidazole or vice versa
## Footnote
Quadruple therapy is often recommended as a salvage option.
190
What is the cure rate of the combination of PPI, amoxicillin, and rifabutin for resistant H. pylori strains?
86% cure rate
## Footnote
This regimen is considered effective against resistant strains.
191
List two additional regimens considered for second-line therapy for H. pylori.
* Levofloxacin-based triple therapy (levofloxacin, amoxicillin, PPI) for 10 days
* Furazolidone-based triple therapy (furazolidone, amoxicillin, PPI) for 14 days
## Footnote
These regimens are alternatives when initial treatments fail.
192
True or False: There is a universally accepted treatment regimen for patients in whom two courses of antibiotics have failed.
False
## Footnote
There is no consensus on treatment after multiple failures.
193
What should be considered if eradication of H. pylori is still not achieved in a compliant patient?
Culture and sensitivity of the organism
## Footnote
This approach helps tailor further treatment based on resistance patterns.
194
What factors may lower H. pylori eradication rates?
* Patient’s country of origin
* Cigarette smoking
## Footnote
Eradication rates can vary significantly based on these factors.
195
What is a promising new approach to H. pylori treatment that has been explored?
Sequential therapy
## Footnote
This involves alternating medications over a set duration.
196
What does the promising regimen of concomitant therapy consist of?
* PPI twice daily
* Amoxicillin 1 g twice daily
* Levofloxacin 500 mg twice daily
* Tinidazole 500 mg twice daily
## Footnote
This regimen is shorter and easier to take.
197
What innovative approach has been explored to improve eradication rates of H. pylori?
Pretreatment with N-acetylcysteine
## Footnote
This aims to disrupt H. pylori biofilm and reduce antibiotic resistance.
198
What effect did certain probiotics have on antibiotic-associated side effects?
Decreased side effects including nausea, dysgeusia, diarrhea, and abdominal discomfort/pain
## Footnote
This enhances the tolerability of H. pylori therapies.
199
What is the most likely explanation for recurrent infection within the first 6 months after therapy?
Recrudescence instead of reinfection
## Footnote
This indicates that the original infection may not have been fully cleared.
200
What is the first step in the therapy of an active NSAID-induced ulcer?
Stopping the injurious agent
## Footnote
Ideally, the injurious agent should be stopped as the first step in the therapy of an active NSAID-induced ulcer.
201
Which agents are indicated for the treatment of NSAID-induced ulcers?
Acid inhibitory agents (H2 blockers, PPIs)
## Footnote
Treatment with one of the acid inhibitory agents is indicated if stopping NSAIDs is not possible.
202
Which medication is the only one that can heal gastric ulcers (GUs) or duodenal ulcers (DUs) independent of NSAID cessation?
PPIs
## Footnote
Only PPIs can heal GUs or DUs, regardless of whether NSAIDs are discontinued.
203
What are some primary prevention strategies for NSAID-related mucosal injury?
Avoiding the agent, using the lowest dose for the shortest time, using less injurious NSAIDs, using topical NSAIDs, and concomitant medical therapy
## Footnote
These strategies aim to prevent NSAID-induced injury.
204
Name two nonselective NSAIDs associated with a lower likelihood of GI and CV toxicity.
* Naproxen
* Ibuprofen
## Footnote
These nonselective NSAIDs are associated with lower GI and CV toxicity, although higher dosages may negate this benefit.
205
What is the recommended dosage of misoprostol for primary prevention of NSAID-induced ulceration?
200 μg qid
## Footnote
Misoprostol can be used for primary prevention if PPIs are not tolerated.
206
What is the efficacy of high-dose H2 blockers in preventing endoscopically documented ulcers compared to PPIs?
High-dose H2 blockers show promise but are inferior to PPIs
## Footnote
High-dose H2 blockers (e.g., famotidine 40 mg bid) have shown promise in prevention, but PPIs are superior.
207
What are COX-2 inhibitors, and how do they compare to standard NSAIDs in terms of selectivity?
Highly selective COX-2 inhibitors are 100 times more selective for COX-2 than standard NSAIDs
## Footnote
COX-2 inhibitors like celecoxib and rofecoxib have increased CV events and were withdrawn from the market.
208
True or False: The CLASS study showed that celecoxib's advantage in preventing GI complications remains unaffected by low-dose aspirin use.
False
## Footnote
The advantage of celecoxib was offset when low-dose aspirin was used simultaneously.
209
For individuals at moderate GI risk without cardiac risk factors, what is the recommended treatment?
COX-2 inhibitor alone or with a nonselective NSAID and PPI or misoprostol
## Footnote
This approach is recommended for moderate GI risk patients without cardiac risk factors.
210
What should be considered for any patient on long-term traditional NSAID therapy?
H. pylori testing and treatment if positive
## Footnote
This is important regardless of risk status.
211
Name two combination pills that include NSAID gastroprotective agents.
* Double-dose famotidine with ibuprofen
* Diclofenac with misoprostol
* Naproxen with esomeprazole
## Footnote
These combination pills are designed to improve compliance, though their clinical benefit over separate pills is not established.
212
What types of safer NSAID formulations are currently being developed?
* Topical NSAIDs
* Rapidly absorbed NSAIDs
* NO-releasing NSAIDs
* Hydrogen sulfide–releasing NSAIDs
* Dual COX/5-LOX inhibitors
* NSAID prodrugs
* Agents sequestering unbound NSAIDs
## Footnote
Efforts continue toward developing safer NSAIDs to reduce GI complications.
213
What is the initial recommended approach for a patient under 50 years with dyspepsia without alarming signs?
An empirical therapeutic trial with acid suppression
## Footnote
This approach has been common practice, but is evolving with new recommendations.
214
What is the recommended therapy for patients with documented H. pylori infection and ulcers?
Triple therapy for 14 days, followed by continued acid-suppressing drugs for total of 4–6 weeks
## Footnote
This includes either H2 receptor antagonists or PPIs.
215
How should H. pylori eradication be documented?
Using a validated monoclonal stool antigen test or a urea breath test (UBT)
## Footnote
The test must be conducted at least 7 days after stopping antisecretory agents.
H pylori eradication should be documented 4 weeks after completing antibiotics
216
Why is serologic testing not useful for documenting H. pylori eradication?
Antibody titers fall slowly and often do not become undetectable
## Footnote
This makes serologic testing unreliable for this purpose.
217
What considerations should be made for patients with complicated ulcer disease?
Long-term acid suppression may be necessary
## Footnote
This may make documentation of H. pylori eradication less critical.
218
What should be done if a gastric ulcer (GU) is suspected to be malignant?
Multiple biopsies should be taken and repeat endoscopy performed at 8–12 weeks
## Footnote
Even if initial biopsies are negative, follow-up is essential.
219
What percentage of gastric ulcers eventually found to be malignant undergo significant (usually incomplete) healing?
About 70%
## Footnote
This highlights the importance of monitoring GUs closely.
220
What is the healing rate for gastric ulcers (GUs) and duodenal ulcers (DUs) with conventional therapy?
More than 90%
## Footnote
This indicates the effectiveness of standard treatment protocols.
221
What constitutes a refractory gastric ulcer?
A GU that fails to heal after 12 weeks or a DU that does not heal after 8 weeks of therapy
## Footnote
Other factors like compliance and persistent H. pylori must be excluded first.
222
What factors should be excluded in refractory ulcers?
NSAID use, cigarette smoking, and malignancy
## Footnote
These factors can significantly impact ulcer healing.
223
What should be considered if refractory ulcers are suspected to be due to a gastric acid hypersecretory state?
Zollinger-Ellison Syndrome (ZES) or idiopathic hypersecretion
## Footnote
Gastric acid analysis can help rule these out.
224
What is the effective higher dose of PPI for refractory ulcers?
Omeprazole 40 mg/d or lansoprazole 30–60 mg/d
## Footnote
This dosage is effective for healing and maintaining remission.
225
What rare etiologies of refractory ulcers might be diagnosed by biopsies?
Ischemia, Crohn’s disease, amyloidosis, sarcoidosis, lymphoma, eosinophilic gastroenteritis, and infections
## Footnote
Infections can include cytomegalovirus (CMV), tuberculosis, or syphilis.
