PANCE Blueprint GI and Nutrition (9%)

Peptic ulcer disease

Gastric ulcer: Patient will present with → abdominal discomfort that is worse with meals and gets better an hour or so later after eating.

Duodenal ulcer: Patient will present with → abdominal discomfort that improves with meals and gets worse an hour or so later after eating.

What is a risk factor for an increased incidence of duodenal and gastric ulcers, as well as a decrease in rate of healing?
Cigarette smoking

A peptic ulcer is an erosion in a segment of the GI mucosa (versus gastritis which is inflammation), typically in the stomach (gastric ulcer) or the first few centimeters of the duodenum (duodenal ulcer), that penetrates through the muscularis mucosae

Nearly all ulcers are caused by Helicobacter pylori infection or NSAID use. Symptoms typically include burning epigastric pain that is often relieved by food

  • Zollinger-Ellison syndrome (gastrinoma) is the result of an unregulated release of gastrin resulting in gastric acid hypersecretion. Up to 50% of patients complain of diarrhea along with peptic ulcer disease. diagnosed with serum gastrin levels (> 150 pg/mL is suggestive - > 200 pg/mL is diagnostic)
  • Cigarette smoking is a risk factor for the development of ulcers and their complications. Also, smoking impairs ulcer healing and increases the incidence of recurrence

Pain with food = gastric ulcer

Pain after food = duodenal ulcer

Persistent or ↑ symptoms after PPI = Look for H.Pylori

  • A biopsy is the gold standard for diagnosis of H.Pylori – serology is not reliable
  • The second most reliable is urea breath test and fecal antigen testing

Treatment for H.Pylori:  PPI + Amoxicillin 1g PO BID + Metronidazole or Clarithromycin 500 mg PO BID

  • Think baseball "CAP" = Clarithromycin + Amoxicillin + PPI
  • Patients with NSAID-associated ulcers should be treated with a PPI for a minimum of eight weeks
  • PPI therapy for four to eight weeks in patients with H. pylori-negative ulcers that are not associated with NSAID use
  • Zollinger-Ellison syndrome: PPI and resect the tumor
CAP = Clarithromycin + Amoxicillin + PPI

CAP = Clarithromycin + Amoxicillin + PPI

IM_NUR_Peptic_ucler_assessment_V1.3_ Peptic ulcers are caused by an erosion of the mucosal wall of the gastrointestinal tract. These ulcers develop when excess hydrochloric acid and digestive enzymes (pepsin) disrupt the gastric mucosal barrier, causing breakdown. A bacteria called Helicobacter pylori (H. pylori) may also contribute to peptic ulcer formation; however, not everyone who is infected with this bacteria will develop an ulcer. Patients with this condition may present with abdominal pain, heartburn, GI distress, black, tarry stools, and weight loss.

zollinger-ellison-syndrome-mechanisms-and-symptoms_5965_1490642054 Zollinger-Ellison syndrome (ZES) is caused by gastrin-secreting tumors, known as gastrinomas. The sequelae of this disease are the result of excess gastric acid production, which leads to abdominal pain, heartburn, diarrhea and ulcers in patients. These ulcers present most commonly in the proximal duodenum, and less commonly in the distal duodenum and jejunum. Furthermore, these are usually solitary ulcers. Patients may present with gastrointestinal bleeding as well. Abdominal pain and heartburn occur secondary to gastroesophageal reflux disease (GERD), which develops in roughly 50% of patients with Zollinger-Ellison syndrome. The gastrinomas of this disease can be sporadic and can occur without any other disease present. However, an important correlation of this disease is that 25% of cases are associated with multiple endocrine neoplasia type 1 (MEN 1).

IM_MED_HelicobacterPylori_V1.2_ASSETS Helicobacter pylori is a gram-negative bacillus with multiple flagella that causes gastritis and peptic ulcer disease (PUD). H. pylori are the most common cause of gastric and duodenal ulcers. It survives in the stomach's acidic environment by producing urease, which converts urea to ammonia and makes the stomach more alkaline. It disrupts the stomach's mucous layer which leaves the underlying tissue susceptible to damage and also elicits an inflammatory reaction resulting in chronic gastritis. As a result, long term complications include gastric adenocarcinoma and MALT lymphoma. Detection of H. pylori infection is made by IgG serology, stool antigen assay, urease positive breath test or an endoscopic biopsy. Treatment is a combination of two antibiotics, typically clarithromycin and either amoxicillin or metronidazole, as well as a proton-pump inhibitor (PPI).

Helicobacter pylori Picmonic

IM_PHM_PPI_v1.5_ Proton pump inhibitors are a class of drugs that act directly on the H+/K+/ATPase pump to prevent the secretion of acid. They are indicated for GERD, peptic ulcer disease, treatment of gastritis and for gastrinomas, such as Zollinger-Ellison syndrome. These drugs are easy to remember, as they share a common suffix, "prazole," exemplified by the medication omeprazole.

Common side effects of these medications include hip fracture, as this drug class decreases calcium absorption, as well as pneumonia, due to bacterial overgrowth in a less acidic environment.

Proton Pump Inhibitors (PPIs)

IM_NUR_Sucralfate_V1.2_ Sucralfate (Carafate) is an antiulcer agent used in patients with duodenal ulcers. This medication works by creating a barrier that protects existing ulcers from stomach acid and pepsin, allowing the ulcer(s) to heal. Patients should be instructed to take sucralfate on an empty stomach and at least two hours before or after a meal. An oral suspension may be recommended for patients with difficulty swallowing large pills.

Sucralfate (Carafate) Picmonic

IM_PHM_H2blockers_v1.8_ H2 blockers are antagonists at the histamine H2 receptor, which are found within the parietal cells of the stomach. These medications can be recalled easily, because of the common suffix found in their drug names, "itidine." These drugs may help to treat GI disorders including indigestion and heartburn (GERD), and promote the healing of ulcers. This drug class exerts its action by blocking histamine H2 receptors in parietal cells of the stomach, leading to reduced acid secretion.

Particular medications within this drug class causing notable side effects are ranitidine and cimetidine, which both cause decreased creatinine clearance via inhibition of tubular secretion. Cimetidine, however, crosses the blood-brain barrier and may lead to headache, dizziness and confusion. Cimetidine is also an anti-androgen, which works as a competitive antagonist at DHT receptors. Furthermore, it is a potent inhibitor of the cytochrome P450 enzyme system, and may decrease the metabolism of other medications.

Question 1
A patient describes abdominal discomfort that improves with meals and gets worse an hour or so later after eating. What do you suspect?
duodenal ulcer
gastric ulcer
Gastric ulcer causes abdominal discomfort that is worse with meals and gets better an hour or so later after eating.
acute cholecystitis
RUQ pain and + Murphy's sign
Question 1 Explanation: 
A duodenal ulcer improves with meals and gets worse an hour or so later after eating.
Question 2
A patient describes abdominal discomfort that is worse with meals and gets better an hour or so later after eating. What do you suspect?
Duodenal ulcer
Gastic Ulcer
Acute pancreatitis
Acute pancreatitis can cause epigastric pain which is usually sudden in onset and gradually intensifies in severity until reaching a constant ache. Patient would usually present at the emergency looking toxic especially when severe.
Question 2 Explanation: 
A gastric ulcer will cause abdominal discomfort that is worse with meals and gets better an hour or so later after eating.
Question 3
Which of the following is not a component of the TRIPLE THERAPY for H. pylori eradication
A proton pump inhibitor
Question 3 Explanation: 
Bismuth is a component of the QUADRUPLE THERAPY for H. pylori eradication. Treatment is composed of Bismuth subsalicylate tetracycline, metronidazole and a PPI. All other options are components of the TRIPLE THERAPY which includes PPI + Clarithromycin + Amoxicillin.
Question 4
A 26-year old lady presents at the outpatient clinic with 11 month history of recurrent epigastric pain which is worse when she’s hungry. It is temporarily relieved by food and antacids. It is also worse at night. It sometimes awakens her. Pain occurs for a few weeks, then goes and occurs again after several weeks. There is history of chronic NSAID ingestion, nausea and anorexia. Which of the following is the most likely diagnosis?
Pain from esophagitis is usually retrosternal. Most patients complain of heartburn due to acid reflux. There is no periodicity and association with food.
Acute pancreatitis
Acute pancreatitis can cause epigastric pain which is usually sudden in onset and gradually intensifies in severity until reaching a constant ache. Patient would usually present at the emergency looking toxic especially when severe. There is no association with chronic NSAID use.
Peptic ulcer disease
Gastroesophageal reflux disease
GERD presents with heartburn which has no periodicity, and regurgitation.
Question 4 Explanation: 
The most common presentation of PUD is that of recurrent epigastric pain which has three notable characteristics: localization to the epigastrium, relationship to food and episodic occurrence (periodicity). Chronic NSAID ingestion can cause PUD.
Question 5
Which of the following is the gold standard for definitive diagnosis of Peptic Ulcer Disease(PUD)
Upper gastrointestinal endoscopy
Double-contrast barium enema
Double-contrast barium enema is not as sensitive as endoscopy for establishing a diagnosis of small ulcers (<0.5cm). It also does not allow for obtaining a biopsy.
Chest radiograph
Chest radiograph may be useful to detect free abdominal air when perforation is suspected. It cannot diagnose PUD.
None of the above
Question 5 Explanation: 
Upper gastrointestinal endoscopy is the gold standard for diagnosing peptic ulcer disease. It allows for visualization of the ulcer and taking a biopsy for histology.
Question 6
Advantages of PPIs over H2 blockers include all of the following except
superior acid suppression
faster healing rates
safe for use in hepatically impaired patients
faster symptom relief
lower and less frequent dosing requirement
Question 6 Explanation: 
Several of the PPIs, namely, lansoprazole and rabeprazole, need to be used with caution in patients with hepatic impairment. PPIs do provide better acid suppression, healing rates, and symptom relief than the H2 blockers. The dose and frequency of dosing are also less for PPIs.
Question 7
Which of the following types of H. pylori testing is not useful to confirm eradication?
stool antigen test
urea breath test
enzyme-linked immunosorbent assay (ELISA) serology
Steiner stain of gastric biopsy specimen
Question 7 Explanation: 
ELISA serology testing, although convenient and commonly used, is not reliable to determine successful eradication of H. pylori. Antibody titers are slow to decline and can therefore lead to many false-positive results even after successful treatment. Serology testing is appropriate for patients never treated for the organism in the past. Steiner stain of gastric biopsy specimen and culture require invasive endoscopy but are sensitive and specific for detection of persistence of H. pylori after treatment. Stool antigen and urea breath tests are also accurate tests to check for persistence of infection. Stool tests are more convenient because they are office based compared with the urea breath test, which requires special equipment not usually available in the office.
There are 7 questions to complete.
Shaded items are complete.

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Gastritis (Prev Lesson)
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