PUD Flashcards
What does PUD encompass?
Gastric ulcers (GUs) and duodenal ulcers (DUs)
PUD stands for Peptic Ulcer Disease.
How are ulcers defined in terms of size and depth?
Breaks in the mucosal surface >5 mm in size, with depth to the submucosa
This definition applies to both gastric and duodenal ulcers.
What are the most common risk factors for PUD?
- H. pylori
- NSAIDs
These factors have estimated odds ratios of 3.7 and 3.3, respectively.
What is the odds ratio for chronic obstructive lung disease as a risk factor for PUD?
2.34
This indicates a significant association with PUD risk.
List additional risk factors for PUD along with their odds ratios.
- 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.
What medications and procedures are associated with an increased incidence of PUD?
- Selective serotonin reuptake inhibitors (SSRIs)
- Gastric bypass surgery
Both have been linked to a higher incidence of peptic ulcers.
True or False: DUs and GUs share many common features in terms of pathogenesis, diagnosis, and treatment.
True
Despite their differences, GUs and DUs have similar underlying mechanisms.
When do gastric ulcers (GUs) typically occur in life?
GUs tend to occur later in life, with a peak incidence reported in the sixth decade.
What is the gender distribution for gastric ulcers?
More than one-half of GUs occur in males.
Where do duodenal ulcers (DUs) most often occur?
In the first portion of the duodenum (>95%)
DUs are usually located within 3 cm of the pylorus
What is the typical diameter of duodenal ulcers?
≤1 cm, but can reach 3–6 cm (giant ulcer)
Giant ulcers are a rare occurrence
What is the characteristic appearance of duodenal ulcers?
Sharply demarcated with depth reaching the muscularis propria
The base often consists of eosinophilic necrosis with surrounding fibrosis
What distinguishes gastric ulcers (GUs) from duodenal ulcers?
GUs can represent a malignancy and should be biopsied upon discovery
Where are benign gastric ulcers most often found?
Distal to the junction between the antrum and the acid secretory mucosa
What association do benign gastric ulcers have with H. pylori?
Associated with antral gastritis
What may be observed in NSAID-related gastric ulcers instead of chronic active gastritis?
Chemical gastropathy, typified by foveolar hyperplasia, edema of the lamina propria, and epithelial regeneration
What are the primary causes of duodenal ulcers (DUs)?
H. pylori and NSAID-induced injuries
These account for the majority of DUs.
How does gastric acid secretion in DU patients compare to control subjects?
Average basal and nocturnal gastric acid secretion appears to be increased
There is substantial overlap between DU patients and control subjects.
What is the significance of bicarbonate secretion in DU patients?
Bicarbonate secretion is significantly decreased in the duodenal bulb
This is compared to control subjects.
What are the main causes of gastric ulcers (GUs)?
H. pylori or NSAID-induced mucosal damage
The majority of GUs can be attributed to these factors.
What tends to be the gastric acid output in gastric ulcer patients?
Normal or decreased
This applies to both basal and stimulated gastric acid output.
Where do Type I gastric ulcers occur and what is their association with gastric acid production?
In the gastric body; associated with low gastric acid production
They are classified as Type I ulcers.
Where do Type II gastric ulcers occur and what is their association with gastric acid production?
In the antrum; gastric acid can vary from low to normal
They are classified as Type II ulcers.
Where do Type III gastric ulcers occur and what is their gastric acid production status?
Within 3 cm of the pylorus; commonly associated with DUs and normal or high gastric acid production
They are classified as Type III ulcers.
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
They are classified as Type IV ulcers.
What dose of aspirin may lead to serious GI ulceration?
75 mg/d
This indicates that even low doses of aspirin can be risky for gastrointestinal health.
What infection increases the risk of PUD-associated GI bleeding in chronic users of low-dose aspirin?
H. pylori infection
This infection is a significant risk factor for gastrointestinal complications.
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
These factors increase the likelihood of serious complications from NSAID use.
List possible risk factors for NSAID-induced morbidity.
- Concomitant infection with H. pylori
- Cigarette smoking
- Alcohol consumption
These factors may contribute to the risk of complications when using NSAIDs.
What effect do SSRIs have on NSAID-induced GI bleeding?
Synergistic effect
SSRIs may increase the risk of GI bleeding due to their impact on platelet aggregation.
What is the role of prostaglandins in the gastroduodenal mucosa?
Maintaining mucosal integrity and repair
Prostaglandins are essential for protecting the gastric mucosa from injury.
What role do neutrophils play in NSAID-induced mucosal injury?
Initiation of mucosal injury via adherence to gastric microcirculation
Neutrophil adherence is crucial in the early stages of injury.
What are single nucleotide polymorphisms (SNPs) associated with in NSAID-induced mucosal injury?
Genes including cytochrome P450 subtypes, IL-1β, angiotensinogen, and SLCO1B1
These SNPs need confirmation in larger studies.
How does topical use of NSAIDs affect the mucosa?
Increases epithelial surface permeability
This can lead to mucosal injury through various mechanisms.
Why do aspirin and many NSAIDs cause cell injury in the stomach?
They remain in a nonionized lipophilic form in the acidic environment
This allows NSAIDs to cross lipid membranes and become trapped intracellularly.
What is one consequence of NSAIDs altering the surface mucous layer?
Permitting back diffusion of H + and pepsin
This leads to further epithelial cell damage.
What is a risk associated with enteric-coated or buffered NSAID preparations?
Risk of peptic ulceration
These preparations can still contribute to mucosal injury.
How do NSAIDs produce additional proinflammatory mediators?
Through activation of the lipoxygenase pathway
This results in increased levels of TNF and leukotrienes.
What is the relationship between H. pylori and NSAIDs in the pathogenesis of PUD?
Complex interplay as independent and synergistic risk factors
Both factors can increase the risk of PUD and complications.
What effect does the eradication of H. pylori have on NSAID-induced complications?
Reduces likelihood of GI complications in high-risk individuals
This brings their risk levels closer to those of average-risk individuals.
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
The exact mechanism is unknown, but theories include altered gastric emptying and increased risk for H. pylori infection.
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
Increased frequencies of blood group O and nonsecretor status are also implicated.
Which blood group is preferentially bound by H. pylori?
Blood group O
This binding may be a factor in ulcer development among those with this blood type.
What are potential susceptibility genes for NSAID-induced PUD?
Genes encoding cytochrome P450 2C9 and 2C8 (CYP2C9 and CYP2C8)
Studies have not consistently demonstrated this association.
How does psychological stress relate to PUD?
Psychological stress has been thought to contribute to PUD, but studies have shown conflicting results
Certain personality traits like neuroticism are associated with PUD and nonulcer dyspepsia.
What dietary factors are associated with peptic diseases?
No convincing studies indicate a specific diet associated with ulcer formation
Certain foods and beverages may cause dyspepsia.
List chronic disorders strongly associated with PUD.
- Advanced age
- Chronic pulmonary disease
- Chronic renal failure
- Cirrhosis
- Nephrolithiasis
- α1-antitrypsin deficiency
- Systemic mastocytosis
These conditions have a strong correlation with PUD.
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
These associations are less definitive than those of strong association.
What are the two predominant causes of PUD?
- H. pylori infection
- NSAID ingestion
PUD not related to these causes is on the rise.
What is the common symptom in many GI disorders, including DU and GU?
Abdominal pain
Abdominal pain has a poor predictive value for the presence of either DU or GU.
What percentage of patients with PUD do not have abdominal pain?
Approximately two-thirds
Up to 87% of patients with NSAID-induced mucosal disease can present with complications without antecedent symptoms.
How is epigastric pain in DU and GU typically described?
Burning or gnawing discomfort
It can also be described as an ill-defined, aching sensation or as hunger pain.
When does typical pain in DU occur after a meal?
90 minutes to 3 hours
This pain is frequently relieved by antacids or food.
What symptom is most discriminating for DU patients?
Pain that awakes the patient from sleep (between midnight and 3 a.m.)
Two-thirds of DU patients describe this complaint.
How do elderly patients typically present with PUD?
They are less likely to have abdominal pain and may present with a complication
Complications include ulcer bleeding or perforation.
How may the pain pattern in GU patients differ from DU patients?
Discomfort may be precipitated by food
Nausea and weight loss occur more commonly in GU patients.
What does constant dyspepsia that is no longer relieved by food or antacids suggest?
A penetrating ulcer
This may involve the pancreas.
What does sudden onset of severe, generalized abdominal pain indicate?
Perforation
This is a critical symptom that requires immediate attention.
What symptoms suggest gastric outlet obstruction?
Pain worsening with meals, nausea, and vomiting of undigested food
These symptoms can indicate a blockage in the stomach.
What do tarry stools or coffee-ground emesis indicate?
Bleeding
These symptoms are associated with gastrointestinal bleeding.
What is the most frequent finding in patients with GU or DU?
Epigastric tenderness
GU refers to gastric ulcer, and DU refers to duodenal ulcer.
What signs suggest dehydration secondary to vomiting or active GI blood loss?
Tachycardia and orthostasis
These vital sign changes are critical indicators of fluid loss.
What does a severely tender, board-like abdomen suggest?
Perforation
This finding is a serious complication that requires immediate medical attention.
What does the presence of a succussion splash indicate?
Retained fluid in the stomach
This suggests a potential gastric outlet obstruction.
What is the most common complication observed in PUD?
GI bleeding
PUD stands for peptic ulcer disease.
In which age group does bleeding and complications of ulcer disease occur more often?
> 60 years of age
What is a likely reason for the higher incidence of GI bleeding in the elderly?
Increased use of NSAIDs
What percentage of mortality in PUD-related bleeding is due to nonbleeding causes?
Up to 80%
List three nonbleeding causes of mortality in PUD-related bleeding.
- Multiorgan failure (24%)
- Pulmonary complications (24%)
- Malignancy (34%)
What percentage of patients with ulcer-related hemorrhage bleed without any preceding warning signs or symptoms?
> 50%
What is the second most common ulcer-related complication?
Perforation
Reported in 6–7% of PUD patients with an estimated 30-day mortality of >20%
What are the classic symptoms associated with perforation?
Acute abdominal pain, tachycardia, abdominal rigidity
This classic triad may not be present in elderly or immunosuppressed patients
Which organ do DUs typically penetrate into?
Pancreas
This can lead to pancreatitis
Which organ do GUs typically penetrate into?
Left hepatic lobe
Gastrocolic fistulas associated with GUs have also been described
The least common ulcer-related complication, occurring in 1–2% of patients.
Gastric outlet obstruction
What can cause relative obstruction in gastric outlet obstruction?
Ulcer-related inflammation and edema in the peripyloric and duodenal region.
What is a fixed, mechanical obstruction in gastric outlet obstruction caused by?
Scar formation in the peripyloric areas.
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).
What are some signs and symptoms of gastric outlet obstruction?
- New onset of early satiety
- Nausea
- Vomiting
- Increase of postprandial abdominal pain
- Weight loss
The most commonly encountered diagnosis among patients seen for upper abdominal discomfort
functional dyspepsia (FD) or essential dyspepsia
What is often required to document the presence of a gastroduodenal ulcer?
A radiographic study or an endoscopic procedure
Radiographic studies include barium studies, which are rarely done today.
What is the sensitivity of older single-contrast barium meals for detecting a duodenal ulcer?
Up to 80%
A double-contrast study provides detection rates as high as 90%.
What factors decrease the sensitivity for detection of duodenal ulcers?
Small ulcers (<0.5 cm), presence of previous scarring, postoperative patients
These factors affect the ability to accurately detect ulcers.
How does a duodenal ulcer typically appear in radiographic studies?
As a well-demarcated crater, most often seen in the bulb
This characteristic appearance aids in diagnosis.
What does a benign gastric ulcer typically appear as?
A discrete crater with radiating mucosal folds originating from the ulcer margin
This appearance helps differentiate it from malignant ulcers.
What size gastric ulcers are more often malignant?
Ulcers >3 cm in size or those associated with a mass
Size and association with a mass are key indicators of malignancy.
What is the appropriate initial testing for individuals <45 years of age with ulcer symptoms?
Testing for H. pylori and antibiotic therapy
This approach is recommended before embarking on a diagnostic evaluation.
True or False: Barium studies are commonly used as a first test for documenting an ulcer.
False
Barium studies are rarely used as a first test in today’s environment.
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.
Endoscopy allows for direct visualization of the mucosa.
What additional procedures can endoscopy facilitate?
Photographic documentation of a mucosal defect and tissue biopsy.
Biopsies are used to rule out malignancy or H. pylori.
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.
What is the sensitivity and specificity of several biopsy urease tests for H. pylori?
> 90–95%.
Examples include PyloriTek, CLOtest, Hpfast, and Pronto Dry.
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.
What was the main form of therapy for peptic ulcers before the role of histamine was understood?
Neutralization of secreted acid with antacids
What are antacids primarily used for now?
Symptomatic relief of dyspepsia
What are the most commonly used agents in antacids?
Mixtures of aluminum hydroxide and magnesium hydroxide
What side effect can aluminum hydroxide produce?
Constipation and phosphate depletion
What side effect can magnesium hydroxide cause?
Loose stools
What combination do many commonly used antacids (e.g., Maalox, Mylanta) contain?
Both aluminum hydroxide and magnesium hydroxide
Why should magnesium-containing antacids be avoided in chronic renal failure patients?
Possible hypermagnesemia
What potential risk does aluminum have in chronic renal failure patients?
Chronic neurotoxicity
What are two potent antacids mentioned in the text?
Calcium carbonate and sodium bicarbonate
What syndrome can long-term use of calcium carbonate lead to?
Milk-alkali syndrome
What are the effects of milk-alkali syndrome?
Hypercalcemia and hyperphosphatemia with possible renal calcinosis and progression to renal insufficiency
What potential issue may sodium bicarbonate induce?
Systemic alkalosis
What are the four H 2 receptor antagonists currently available?
Cimetidine, ranitidine, famotidine, nizatidine
What do all H 2 receptor antagonists significantly inhibit?
Basal and stimulated acid secretion
What is the common therapeutic use of H 2 receptor antagonists?
Treatment of active ulcers in combination with antibiotics
Which H 2 receptor antagonist was the first to be used for acid peptic disorders?
Cimetidine
What are some weak antiandrogenic side effects of cimetidine?
Reversible gynecomastia and impotence
What monitoring is indicated with long-term use of cimetidine?
Monitoring of drugs such as warfarin, phenytoin, and theophylline
What are some rare reversible adverse effects of cimetidine?
Confusion, elevated serum aminotransferases, creatinine, and serum prolactin
How do the potencies of ranitidine, famotidine, and nizatidine compare to cimetidine?
They are more potent H 2 receptor antagonists than cimetidine
What is a common dosing regimen for ulcer prevention with H 2 receptor antagonists?
Once a day at bedtime
What are the comparable nighttime dosing regimens for H 2 receptor antagonists?
- Cimetidine 800 mg
- Ranitidine 300 mg
- Famotidine 40 mg
- Nizatidine 300 mg
What rare systemic toxicities can occur with H 2 receptor antagonists?
Pancytopenia, neutropenia, anemia, thrombocytopenia
Which H 2 receptor antagonists can bind to hepatic cytochrome P450?
Cimetidine and ranitidine
True or False: Patients may develop tolerance to H 2 blockers.
True
Fill in the blank: H 2 receptor antagonists are often used for the treatment of _______ in combination with antibiotics.
[active ulcers]
How are omeprazole and lansoprazole administered?
As enteric-coated granules in a sustained-release capsule that dissolves at pH of 6.
What is a unique formulation of lansoprazole?
Orally disintegrating tablet that can be taken with or without water.
What is the purpose of sodium bicarbonate in omeprazole formulations?
To protect omeprazole from acid degradation and promote rapid gastric alkalinization.
What types of formulations are available for pantoprazole and rabeprazole?
Enteric-coated tablets
Pantoprazole is also available as a parenteral formulation for intravenous use.
What is the time frame for the maximum acid inhibitory effect after administration of PPIs?
Between 2 and 6 hours after administration.
How long can the duration of inhibition last after taking PPIs?
72–96 hours.
What percentage of acid production is inhibited after one week of daily PPI therapy?
> 95%.
What is the half-life of PPIs?
~18 hours.
What can happen after discontinuation of PPIs in H pylori negative individuals?
Rebound gastric acid hypersecretion may occur.
What is the mechanism behind rebound gastric acid hypersecretion?
Gastrin-induced hyperplasia and hypertrophy of histamine-secreting ECL cells.
How can rebound hypersecretion be prevented?
Gradual tapering of the PPI and switching to an H2 receptor antagonist.
What impact do PPIs have on vitamin B12 absorption?
IF production is inhibited, but vitamin B12 deficiency anemia is uncommon.
Which drugs may be interfered with by PPIs due to significant hypochlorhydria?
Ketoconazole, ampicillin, iron, digoxin.
Which PPIs inhibit hepatic cytochrome P450?
Omeprazole, lansoprazole.
What caution should be taken when using PPIs with other medications?
Caution with theophylline, warfarin, diazepam, atazanavir, phenytoin.
What is the association between long-term PPI use and community-acquired pneumonia?
Higher incidence.
What is the increased risk percentage of C. difficile infection associated with PPI use according to a meta-analysis?
74% increased risk.
What is postulated to play a role in the increased risk of infection with PPI use?
PPI-induced changes in the host microbiome.
What condition is associated with PPI use and specifically with lansoprazole?
Collagenous colitis.
What is the association found in a population-based study regarding long-term use of PPIs?
Development of hip fractures in older women
The absolute risk of fracture remained low and may be zero despite the observed increase associated with the dose and duration of acid suppression.
What deficiencies have been implicated with long-term use of PPIs?
Iron, vitamin B12, and magnesium deficiency
A meta-analysis found a 40% increase in hypomagnesemia in PPI users compared to nonusers.
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
These recommendations are not evidence-based or recommended by expert opinion.
What negative effect might PPIs have on clopidogrel?
Inhibition of the antiplatelet effect
Evidence is mixed regarding this interaction, with earlier studies showing a small increase in mortality and readmission rates for coronary events.
What is the mechanism of interaction between PPIs and clopidogrel?
Competition for the same cytochrome P450 (CYP2C19)
The influence of this drug interaction on mortality is not clearly established.
What is a recommended separation time for administering PPIs and clopidogrel?
12 hours
Some have suggested giving the PPI 30 minutes before breakfast and clopidogrel at bedtime.
What additional side effects have been associated with long-term PPI use?
Increased cardiac risks, dementia, acute and chronic kidney injury
Data are often retrospective and confounding variables were not consistently eliminated.
What is particularly important regarding the use of PPIs in patients aged ≥65 years?
Higher risk for long-term side effects
This is partly due to the higher prevalence of concomitant chronic diseases in this age group.
What should be done when discontinuing a PPI in long-term users?
Taper gradually over 1-2 weeks
Abrupt withdrawal may result in rebound hyperacidity, and a transition to an H2 blocker may be considered.
True or False: High-dose H2 blockers are as effective as PPIs for GI protective therapy.
False
High-dose H2 blockers do not appear to be as effective as PPIs.
What is sucralfate?
A complex sucrose salt substituted by aluminum hydroxide and sulfate
Sucralfate is insoluble in water and forms a viscous paste in the stomach and duodenum.
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
EGF stands for Epidermal Growth Factor.
What is the most common toxicity associated with sucralfate?
Constipation (2–3% incidence)
Other rare toxicities include hypophosphatemia and gastric bezoar formation.
In which patients should sucralfate be avoided?
Patients with chronic renal insufficiency
This is to prevent aluminum-induced neurotoxicity.
What is the standard dosing of sucralfate?
1 g qid
‘qid’ stands for ‘four times a day’.
What are common adverse effects of bismuth-containing preparations?
Black stools, constipation, and darkening of the tongue
Long-term high doses may lead to neurotoxicity.
What is the role of stable prostaglandin analogues in treating PUD?
They enhance mucosal defense and repair
They were developed due to their central role in maintaining mucosal integrity.
What is the most common toxicity noted with prostaglandin analogues?
Diarrhea (10–30% incidence)
Other major toxicities include uterine bleeding and contractions.
What is the standard therapeutic dose of misoprostol?
200 μg qid
Misoprostol is contraindicated in women who may be pregnant.
What types of drugs were historically used for treating acid peptic disorders but are rarely used today?
Anticholinergic agents and tricyclic antidepressants
Their use declined due to toxicity and the development of potent antisecretory agents.
Who should be treated for H. pylori infection according to consensus conferences?
Patients with documented PUD
Should patients with a history of documented PUD and positive H. pylori tests be treated?
Yes, they should be treated
What percentage of patients with gastric MALT lymphoma experience complete remission after H. pylori eradication?
Between 60 and 90%
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%
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
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
What does the ACG recommend for patients who have undergone resection of early gastric cancer?
Eradication of H. pylori
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
What conditions do the ACG clinical guidelines recommend testing for H. pylori eradication?
- Unexplained iron deficiency anemia
- Idiopathic thrombocytopenic purpura
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
What is the most effective duration for combination therapy in eradicating H. pylori?
14 days
Combination therapy for 14 days provides the greatest efficacy.
Name five agents frequently used in the treatment of H. pylori.
- Amoxicillin
- Metronidazole
- Tetracycline
- Clarithromycin
- Bismuth compounds
These agents are commonly used to treat H. pylori infections.
True or False: Dual therapy is recommended for H. pylori treatment.
False
Dual therapy is not recommended due to eradication rates of <80–85%.
What was the first effective triple regimen against H. pylori?
Bismuth, metronidazole, and tetracycline
This combination was the first triple regimen found effective against H. pylori.
What are the potential drawbacks of triple therapy for H. pylori?
- Poor patient compliance
- Drug-induced side effects
These drawbacks can affect the effectiveness of the treatment.
What is the name of the prepackaged formulation containing lansoprazole, clarithromycin, and amoxicillin?
Prevpac
Prevpac is taken twice per day for 14 days.
What are the instructions for taking Helidac?
Four times per day with an antisecretory agent for at least 14 days
Helidac contains BSS, tetracycline, and metronidazole.
True or False: Clarithromycin-based triple therapy should be used in settings with high H. pylori resistance.
False
Clarithromycin-based triple therapy should be avoided where H. pylori resistance exceeds 15%.
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
These factors are crucial in selecting an appropriate treatment regimen.
What is a common issue with shorter regimens (7–10 days) for H. pylori treatment?
Less effective than 14-day regimens
Shorter administration courses have not proved as successful as the 14-day regimens.
What is the benefit of adding acid suppression in H. pylori treatment?
Provides early symptom relief and enhances bacterial eradication
Acid suppression aids in the success of H. pylori treatment.
What side effects can bismuth cause?
Black stools, constipation, darkening of the tongue
Bismuth is a component of some triple therapy regimens.
What is the most feared complication associated with amoxicillin?
Pseudomembranous colitis
This complication occurs in <1–2% of patients.
What other side effects can amoxicillin lead to?
Antibiotic-associated diarrhea, nausea, vomiting, skin rash, allergic reaction
These are common adverse effects of amoxicillin.
What effect do probiotics have when used with antibiotics?
May ameliorate some of the antibiotic side effects
Probiotics can help manage gastrointestinal side effects.
What rare side effects are reported with tetracycline?
Rashes, hepatotoxicity, anaphylaxis
These side effects are very rare.
What is a significant concern when treating patients who may not need therapy?
Potential for development of antibiotic-resistant strains
This is a critical consideration in antibiotic prescribing.
What is the most common cause of treatment failure in compliant patients?
Antibiotic-resistant strains
This highlights the importance of antibiotic resistance in treatment outcomes.
What should be included in the decision-making for H. pylori treatment?
Asking the patient about prior antibiotic exposure
This helps assess potential antibiotic resistance.
What is a common reason for the failure of H. pylori eradication with triple therapy in compliant patients?
Infection with a resistant organism
Resistance to treatment can complicate eradication efforts.
What should be the next step if triple therapy fails for H. pylori?
Quadruple therapy, substituting clarithromycin for metronidazole or vice versa
Quadruple therapy is often recommended as a salvage option.
What is the cure rate of the combination of PPI, amoxicillin, and rifabutin for resistant H. pylori strains?
86% cure rate
This regimen is considered effective against resistant strains.
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
These regimens are alternatives when initial treatments fail.
True or False: There is a universally accepted treatment regimen for patients in whom two courses of antibiotics have failed.
False
There is no consensus on treatment after multiple failures.
What should be considered if eradication of H. pylori is still not achieved in a compliant patient?
Culture and sensitivity of the organism
This approach helps tailor further treatment based on resistance patterns.
What factors may lower H. pylori eradication rates?
- Patient’s country of origin
- Cigarette smoking
Eradication rates can vary significantly based on these factors.
What is a promising new approach to H. pylori treatment that has been explored?
Sequential therapy
This involves alternating medications over a set duration.
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
This regimen is shorter and easier to take.
What innovative approach has been explored to improve eradication rates of H. pylori?
Pretreatment with N-acetylcysteine
This aims to disrupt H. pylori biofilm and reduce antibiotic resistance.
What effect did certain probiotics have on antibiotic-associated side effects?
Decreased side effects including nausea, dysgeusia, diarrhea, and abdominal discomfort/pain
This enhances the tolerability of H. pylori therapies.
What is the most likely explanation for recurrent infection within the first 6 months after therapy?
Recrudescence instead of reinfection
This indicates that the original infection may not have been fully cleared.
What is the first step in the therapy of an active NSAID-induced ulcer?
Stopping the injurious agent
Ideally, the injurious agent should be stopped as the first step in the therapy of an active NSAID-induced ulcer.
Which agents are indicated for the treatment of NSAID-induced ulcers?
Acid inhibitory agents (H2 blockers, PPIs)
Treatment with one of the acid inhibitory agents is indicated if stopping NSAIDs is not possible.
Which medication is the only one that can heal gastric ulcers (GUs) or duodenal ulcers (DUs) independent of NSAID cessation?
PPIs
Only PPIs can heal GUs or DUs, regardless of whether NSAIDs are discontinued.
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
These strategies aim to prevent NSAID-induced injury.
Name two nonselective NSAIDs associated with a lower likelihood of GI and CV toxicity.
- Naproxen
- Ibuprofen
These nonselective NSAIDs are associated with lower GI and CV toxicity, although higher dosages may negate this benefit.
What is the recommended dosage of misoprostol for primary prevention of NSAID-induced ulceration?
200 μg qid
Misoprostol can be used for primary prevention if PPIs are not tolerated.
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
High-dose H2 blockers (e.g., famotidine 40 mg bid) have shown promise in prevention, but PPIs are superior.
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
COX-2 inhibitors like celecoxib and rofecoxib have increased CV events and were withdrawn from the market.
True or False: The CLASS study showed that celecoxib’s advantage in preventing GI complications remains unaffected by low-dose aspirin use.
False
The advantage of celecoxib was offset when low-dose aspirin was used simultaneously.
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
This approach is recommended for moderate GI risk patients without cardiac risk factors.
What should be considered for any patient on long-term traditional NSAID therapy?
H. pylori testing and treatment if positive
This is important regardless of risk status.
Name two combination pills that include NSAID gastroprotective agents.
- Double-dose famotidine with ibuprofen
- Diclofenac with misoprostol
- Naproxen with esomeprazole
These combination pills are designed to improve compliance, though their clinical benefit over separate pills is not established.
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
Efforts continue toward developing safer NSAIDs to reduce GI complications.
What is the initial recommended approach for a patient under 50 years with dyspepsia without alarming signs?
An empirical therapeutic trial with acid suppression
This approach has been common practice, but is evolving with new recommendations.
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
This includes either H2 receptor antagonists or PPIs.
How should H. pylori eradication be documented?
Using a validated monoclonal stool antigen test or a urea breath test (UBT)
The test must be conducted at least 7 days after stopping antisecretory agents.
H pylori eradication should be documented 4 weeks after completing antibiotics
Why is serologic testing not useful for documenting H. pylori eradication?
Antibody titers fall slowly and often do not become undetectable
This makes serologic testing unreliable for this purpose.
What considerations should be made for patients with complicated ulcer disease?
Long-term acid suppression may be necessary
This may make documentation of H. pylori eradication less critical.
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
Even if initial biopsies are negative, follow-up is essential.
What percentage of gastric ulcers eventually found to be malignant undergo significant (usually incomplete) healing?
About 70%
This highlights the importance of monitoring GUs closely.
What is the healing rate for gastric ulcers (GUs) and duodenal ulcers (DUs) with conventional therapy?
More than 90%
This indicates the effectiveness of standard treatment protocols.
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
Other factors like compliance and persistent H. pylori must be excluded first.
What factors should be excluded in refractory ulcers?
NSAID use, cigarette smoking, and malignancy
These factors can significantly impact ulcer healing.
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
Gastric acid analysis can help rule these out.
What is the effective higher dose of PPI for refractory ulcers?
Omeprazole 40 mg/d or lansoprazole 30–60 mg/d
This dosage is effective for healing and maintaining remission.
What rare etiologies of refractory ulcers might be diagnosed by biopsies?
Ischemia, Crohn’s disease, amyloidosis, sarcoidosis, lymphoma, eosinophilic gastroenteritis, and infections
Infections can include cytomegalovirus (CMV), tuberculosis, or syphilis.
