Chapter 1
Gastrointestinal disorders

1. A. Peptic ulcer disease
2. B. Gastroesophageal reflux disease
3. C. Irritable bowel syndrome
4. D. Inflammatory bowel disease (CD and UC)
   1. a. Crohn's disease
   2. b. Ulcerative colitis
5. E. Diverticular disease
6. F. Acute pancreatitis
7. G. Celiac sprue
8. H. Pseudomembranous colitis
9. References

A. Peptic ulcer disease

Clinical synopsis

Peptic ulcer disease (PUD) is a general term describing a group of acid-peptic disorders of the upper gastrointestinal (GI) tract including the esophagus, stomach, and duodenum. A peptic ulcer is defined as a circumscribed loss of tissue or break that occurs in the GI mucosa extending through the GI tract smooth muscle. There is an imbalance between gastric acid and pepsin and mucosal defense factors, including prostaglandins, which protect the stomach by increasing the production of gastric mucus and reducing the production of gastric acid.

There are three types of peptic ulcers: gastric ulcer, which occurs in the stomach; duodenal ulcer, which occurs in the duodenum; and esophageal ulcer, which occurs in the esophagus. Most peptic ulcers are asymptomatic; however, the more commonly seen symptoms in symptomatic ulcers are midepigastric pain, dyspepsia (indigestion), nausea, fullness, nocturnal pain, anorexia, and weight loss. One of the distinguishing features of gastric ulcer is the presence of stomach pain after eating. When pain occurs hours after eating or on an empty stomach accompanied with pain at night, it is duodenal ulcer (Peters et al. 2010). The classical epigastric pain in a duodenal ulcer occurs when acid is produced and secreted in the absence of food in the stomach.

The two most common causes of PUD are chronic nonsteroidal anti-inflammatory drugs (NSAIDs) use and Helicobacter pylori (H. pylori), a Gram-negative bacterium, which resides in the GI mucosal lining and in certain individuals can erode the mucosa resulting in ulceration. Even though the majority of duodenal ulcers are caused by H. pylori, only 5-10% will develop ulcers (Malfertheiner et al. 2009; Peters et al. 2010). The definitive diagnosis of PUD is generally made by an upper GI endoscopy (Peters et al. 2010).

Diagnostics/lab values

If it is certain that the ulcer is not caused by chronic NSAID use, a blood test to detect the presence of H. pylori antibodies is a noninvasive test. Although the test has high sensitivity and specificity when lab serology is used, it cannot discriminate if it is a current infection or previous exposure. Additionally, IgG testing may be positive for many years after treatment and eradication of the bacteria. Saliva can also be used but there is low sensitivity and specificity (Meurer and Bower 2002). Urea breath test (UBT) and fecal antigen test are the other preferred methods for diagnosing the presence of H. pylori before administration of antibiotic and antisecretory drugs (Peters et al. 2010). The UBT is utilized to confirm the eradication of H. pylori. Recurrence of H. pylori infection usually is defined by a positive result on urea breath or stool antigen testing six or more months after documented successful eradication therapy (Ables et al. 2007).

Medications

Management of PUD can differ depending upon whether the etiology is NSAID use or H. pylori infection. Antibiotics are used to eradicate H. pylori infection. Proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) provide quick pain relief and accelerated healing of the ulcer (Table 1.1). H2 receptor blockers reduce histamine-stimulated gastric acid secretion by competitively inhibiting H2 receptors on the parietal cells in the stomach. These agents have a limited effect on gastric acid secretion after food ingestion and are effective in healing ulcers in 6-12 weeks. Antacids are used for the treatment of dyspepsia. PPIs provide rapid symptomatic relief with accelerated healing of duodenal ulcers, thus providing the most rapid symptom relief and highest percentage of esophageal healing of all agents used in gastroesophageal reflux disease (GERD) management. They are the drug of choice for patients with frequent daily symptoms, patients with moderate to severe GERD symptoms, patients not responding to H2RAs, and patients with complicated disease, including Barrett's esophagus and esophagitis.

Table 1.1 Medications for peptic ulcer disease and gastroesophageal reflux disease.

For NSAID-induced peptic ulcer, an H2 antagonist or PPI is prescribed. Antacids are recommended for the epigastric pain. Antibiotics are not prescribed.

Management of non-NSAID-induced peptic ulcer that is positive to H. pylori includes systemic antibiotics and H2 antagonists or PPIs. Over the years, resistance to antibiotics is emerging. The goal of treating ulcers is the elimination of H. pylori, which will increase healing of the ulcer, improve symptoms, and reduce recurrence. Although the management of H. pylori is being continuously investigated, currently, the accepted protocol for H. pylori eradication (Box 1.1) is quadruple or triple therapy; usually, it is triple therapy. The drawback of therapy is low adherence because of the vast number of medications that have to be taken for 14 days; H. pylori cannot be eradicated with just one antibiotic or medication.

Box 1.1 Therapy for H. pylori Management (http://www.fpnotebook.com/GI/ID/HlcbctrPylr.htm; Ables et al. 2007; Chey and Wong, 2007; Peters et al. 2010).

Quadruple Therapy

• Metronidazole (Flagyl) 250 mg four times a day +
• Tetracycline 500 mg four times a day +
• Bismuth subcitrate (Pepto-Bismol) 525 mg four times a day +
• Antisecretory drug (up to 6 weeks): omeprazole (Prilosec) 20 mg twice a day OR esomeprazole 20-40 mg daily OR lansoprazole (Prevacid) 20 mg twice a day OR pantoprazole (Protonix) 40 mg twice a day OR rabeprazole (Aciphex) 20 mg twice a day

Triple Therapy

• Amoxicillin 500 mg twice a day
• Clarithromycin (Biaxin) 1000 mg twice a day
• Metronidazole (Flagyl) 500 mg twice a day (only use if allergic to penicillin)
• Prevpac is a combination product containing pantoprazole, clarithromycin, and amoxicillin.

Helicobacter pylori has been found in dental biofilms, and its appearance varies from one site to another in the oral cavity (Kilmartin 2002). Individuals with gastric H. pylori were positive for oral H. pylori also (Anand et al. 2006). Other studies have found that patients with the presence of H. pylori in dental plaque had a greater prevalence of gastric infection (Lui et al. 2009). It has been theorized that antibiotics used to eliminate gastric H. pylori do not eliminate H. pylori in dental plaque and can be a source of future reinfection (Anand et al. 2006).

Dental drug-drug interactions/adverse reactions

Common dental drug-peptic ulcer disease drug interactions are listed in Table 1.2.

Table 1.2 Dental drug-drug interactions (www.rxlist.com; Peters et al. 2010).