GI: Stomach and Duodenum Flashcards

1
Q

How is a peptic ulcer diagnosed?

A

Peptic ulcers are diagnosed not by symptoms but instead by the presence of a mucosal break 5 mm or larger in the stomach or duodenum.

Upper endoscopy is the gold standard for diagnosis of peptic ulcer disease.

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2
Q

What type of peptic ulcers DO NOT require endoscopic follow-up?

A

Duodenal ulcers and low-risk gastric ulcers (for example, a young patient on NSAIDs) do not typically require endoscopic follow-up.

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3
Q

How do you manage dyspepsia for people UNDER the age of 50-55 and with NO RED FLAG SYMPTOMS?

A

For patients younger than age 50 to 55 years who present with dyspepsia without alarm features, testing and treating for Helicobacter pylori infection or a trial of proton pump inhibitor therapy should be pursued before any further testing is done.

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4
Q

How do you manage dyspepsia in someone older than 50-55 and/or with red flag symptoms and/or persistent symptoms despite eradication of H. pylori?

A

Further structural testing should be performed in patients older than 50 to 55 years, those with alarm features at any age, or those with persistent dyspeptic symptoms despite eradication of H. pylori and/or a trial of PPI therapy. Upper endoscopy is considered the gold standard for the exclusion of upper gastrointestinal structural causes of dyspepsia.

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5
Q

What are the indications for H. pylori testing?

A

Clearly established indications for Helicobacter pylori testing are:

  • active peptic ulcer disease (gastric and/or duodenal ulcer)
  • confirmed history of peptic ulcer disease
  • gastric mucosa–associated lymphoid tissue lymphoma
  • uninvestigated dyspepsia in patients younger than age 60 years without alarm symptoms
  • following endoscopic resection of early gastric cancer.
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6
Q

Is GERD in itself an indication for H. pylori testing?

A

Gastroesophageal reflux disease is not a clinical indication for Helicobacter pylori testing.

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7
Q

How do you test and treat for H. pylori? What medications should be avoided when testing?

A

**Noninvasive tests that identify ACTIVE infection include the urea breath test and fecal antigen test.

  • To improve the diagnostic accuracy of the urea breath test and fecal antigen test, antimicrobial agents and bismuth should be avoided for 28 days prior to testing. PPIs should be avoided for 7 to 14 days prior to testing, and H2 blockers should be avoided for 1 to 2 days prior to testing.
  • Serum testing for IgG antibodies to H. pylori does not identify active infection in populations with low prevalence of disease; however, it remains popular given its ease of administration, rapidity of results, and low cost. Given its marginal sensitivity (85%) and specificity (79%), antibody testing should not be used when there is a low background prevalence of H. pylori (prevalence <20%).
  • Invasive (endoscopic) tests for H. pylori include the rapid urease test, histology, and culture; all invasive testing modalities identify active infection.

**Owing to the increased risk of false-negative endoscopic and fecal antigen test results in patients with bleeding PUD, serologic antibody testing should also be performed as a second test in this clinical setting, and treatment should be pursued if either test modality is positive.

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8
Q

Treatment of H. pylori

A

Patients should be asked about previous treatment with a macrolide antibiotic. Use of a clarithromycin-containing regimen as first-line therapy should be limited to patients with no prior macrolide exposure who do not reside in areas with high clarithromycin resistance. In these situations, bismuth quadruple therapy should be considered for first-line therapy.

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9
Q

How do you confirm eradication of H. pylori?

A

Noninvasive testing to confirm eradication of Helicobacter pylori (with the urea breath test or fecal antigen test) should be performed given the high rate of treatment failure (roughly 25% in the United States); antibody testing is not appropriate for confirming eradication because antibodies can remain in the serum long after H. pylori has been eradicated.

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10
Q

What are the two causes of atrophic gastritis?

A

The two forms of atrophic gastritis are H. pylori–associated and autoimmune.

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11
Q

How is atrophic gastritis treated?

A

H. pylori–associated atrophic gastritis typically resolves with H. pylori eradication. Autoimmune atrophic gastritis, however, has no cure.

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12
Q

What are the clinical manifestations of atrophic gastritis?

A

Important clinical manifestations include pernicious anemia, iron deficiency anemia, and hypergastrinemia, which result from the long-term effects of the associated parietal cell loss and subsequent development of achlorhydria.

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13
Q

What is lymphocytic gastritis? How is it treated?

A

Lymphocytic gastritis is a rare, benign chronic inflammatory condition of the gastric mucosa. Clinical manifestations may include dyspepsia, iron deficiency anemia, and diarrhea.

Treatment is directed at the underlying condition, which in most cases is celiac disease or H. pylori infection.Endoscopic surveillance is not required; however, small-bowel and colon biopsies should be obtained to determine the extent of the inflammation and to identify underlying conditions.

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14
Q

Do the following conditions require endoscopic surveillance?

  • Lymphocytic gastritis
  • Atrophic gastritis
  • intestinal metaplasia
  • Atrophic gastritis
A
  • Lymphocytic gastritis: No
  • Atrophic gastritis: No
  • intestinal metaplasia:Not unless they have a family history of gastric cancer or are from an area with high gastric cancer
  • Atrophic gastritis: No
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15
Q

What is the preferred agent for treatment and prophylaxis of NSAID and aspirin related GI injury?

A

PPIs are the preferred agent for treatment and prophylaxis of NSAID- and aspirin-related gastrointestinal injury.

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16
Q

What is gastroparesis and what are the symptoms of it?

A

Gastroparesis is a heterogeneous clinical syndrome that is diagnosed based on the presence of specific symptoms and objective documentation of delayed delivery of the stomach contents into the proximal small bowel in the absence of a mechanical obstruction. Commonly reported symptoms include early satiety, postprandial fullness, nausea, vomiting, upper abdominal pain, bloating, and weight loss.

17
Q

How do you assess for gastroparesis?

A

**Upper EGD: structural assessment of the upper gastrointestinal tract

**The standard test for assessment of gastric emptying is the scintigraphic gastric emptying of solids. A 4-hour emptying study is more accurate than a 2-hour study.

**A wireless motility capsule is also available to assess gastric emptying and offers the advantage of also providing small-bowel and colon transit information.

18
Q

Top three drugs impacting gastric emptying

A
  • Opioid analgesics
  • Anticholinergic agents
  • Tricyclic antidepressants
19
Q

What are some other medical causes that cause. gastroparesis?

A

Patients diagnosed with gastroparesis should be assessed for diabetes, thyroid dysfunction, neurologic disease, previous gastric or bariatric surgery, and autoimmune disorders. Patients should be asked about viral illness prior to symptom onset to identify a postviral gastroparesis.

20
Q

How is gastroparesis treated?

A
  • On demand anti-emetics
  • Diet
  • Treating diseases that cause it
  • Other:
  • prompt identification and treatment of dehydration, electrolyte disturbances, and micronutrient deficiencies
  • Dietary modification and optimization of glycemic control in patients with diabetes should be the first treatment intervention.
  • Specific diet recommendations include small, low-fat meals consumed four to five times per day. Insoluble fiber (found in fresh fruits, fresh vegetables, and bran) should be avoided. High-calorie liquids can be used to increase the liquid nutrient component of meals. Carbonated beverages, alcohol, and tobacco smoking should be minimized or ideally avoided.
21
Q

Talk about the 3 kinds of polyps, when do you need to worry?

A

There are: 1) Fundic gastric polyps and 2) those associated with familial adenomatous polyposis or MYH associated polyposis

  • FGP: usually caused by PPIs, benign and do not require surveillance. Usually 1-5mm in size and <10 in number.
  • FAP/MYH: usually >30, have dysplasia, and should be removed if >10mm in size, followed by a colonoscopy to find polyps there
  • Adenomatous/Hyperplastic; associated with intestinal metaplasia, h. pylori, resect if >5mm
22
Q

What is the imaging modality of choice for gastric sub epithelial tumors?

A

Endoscopic ultrasound is the imaging modality of choice for evaluation of gastric subepithelial lesions.

23
Q

What is the most common type of gastric cancer?

A

Gastric adenocarcinoma accounts for more than 90% of gastric cancers and is subdivided into intestinal and diffuse histology. Intestinal type predominates and is often related to environmental factors. Diffuse gastric cancer is more often seen in women and young patients.

24
Q

Is gastric cancer screening recommended? If so, in whom?

A

Gastric cancer screening for average-risk patients is not recommended in the United States. Patients with a genetic gastric cancer predisposition should undergo syndrome-specific surveillance.

25
Q

What is the screening/surveillance after adenomatous polyp removal?

A

Surveillance upper endoscopy is recommended 1 year after adenomatous gastric polyp removal and, if negative, every 3 to 5 years.

26
Q

Screening/surveillance for intestinal metaplasia?

A

There is insufficient evidence to support surveillance for individuals with gastric intestinal metaplasia; however, surveillance can be considered in patients who have intestinal metaplasia as well as an increased risk owing to ethnicity or family history. Surveillance in intestinal metaplasia should incorporate a biopsy protocol that maps the entire stomach.

27
Q

Screening/surveillance for a GI polyp with low grade dysplasia?

A

Patients with low-grade dysplasia should undergo biopsy every 3 months for the first year, and surveillance should cease when two consecutive endoscopies are negative.

28
Q

Screening/surveillance for high grade dysplasia?

A

The presence of high-grade dysplasia warrants surgical resection. Surveillance after early gastric cancer treatment should be individualized.

29
Q

Diagnostic test of choice for gastric cancer?

A

Upper endoscopy with biopsy is the diagnostic test of choice for gastric cancer.

30
Q

Bariatric surgery complications:

  • What roughly is mortality for all types of bariatric surgery?
  • What factors increase mortality for all bariatric surgeries?
  • What are the major causes of PERIOPERATIVE mortality?
A

In general, mortality rates are low for bariatric surgery and are reported to be 0.3% to 0.4% at 30 days and 0.8% at 2 years. Laparoscopic and restrictive procedures (gastric banding, sleeve gastrectomy) are associated with lower mortality than open and malabsorptive/restrictive procedures (Roux-en-Y gastric bypass, biliopancreatic diversion with duodenal switch). Several clinical factors that increase mortality are a history of deep venous thrombosis or pulmonary embolism, obstructive sleep apnea, impaired functional status, advanced age, and a surgeon and/or hospital with lower volumes of bariatric surgery. The major causes of perioperative mortality are anastomotic leaks, pulmonary embolism, bleeding, and cardiovascular complications.

31
Q

Complications unique to gastric banding?

A

Complications unique to gastric banding include slippage of the gastric band resulting in pouch dilatation, intragastric band erosion with the potential for gastric perforation and/or abscess formation, and esophageal dilatation. Less frequent complications include tube migration, tube disconnection, and port-site infection. Tubing-related small-bowel obstruction is a relatively rare yet serious complication that carries the risk of closed-loop bowel obstruction.

32
Q

Complications unique to sleeve gastrectomy?

A

Complications unique to sleeve gastrectomy include staple-line bleeding, stenosis, and staple-line leakage; leaks are the most concerning complication. Stenosis is typically due to angulation or kinking of the stomach resulting in functional obstruction; it presents as dysphagia to solids and liquids with nausea and vomiting.

33
Q

Complications of vertical banding gastroplasty?

A

The most common complication associated with vertical banding gastroplasty is stenosis at the site of the band placement. Other less common complications include esophagitis, band migration, and staple-line disruption.

34
Q

Complications of Roux-En-Y?

A

Complications following Roux-en-Y gastric bypass include cholelithiasis, nephrolithiasis (due to increased urine oxalate excretion), dumping syndrome, anastomotic stricture, anastomotic ulceration, small-bowel obstruction from internal hernias, and gastrogastric fistula. Although small intestinal bacterial overgrowth can occur following any bariatric procedure, it occurs most often with Roux-en-Y gastric bypass. Similar complications are seen following biliopancreatic diversion with duodenal switch, although most concerning are the nutritional deficiencies.

35
Q

What are the nutrient deficiencies with Roux-en-y or biliopancreatic diversion?

A

Protein-calorie malnutrition can occur 1 to 2 years after malabsorptive procedures (Roux-en-Y gastric bypass or biliopancreatic diversion), typically presenting as rapid weight loss, generalized edema, muscle wasting, and hypoalbuminemia. Micronutrient deficiencies can also develop following bariatric surgery and are more common with malabsorptive procedures (Table 10). Deficiencies may include thiamine (vitamin B1); pyridoxine (vitamin B6); folate; cobalamin (vitamin B12); vitamins C, A, D, E, and K; iron; zinc; selenium; magnesium; and copper. Acceleration in loss of bone mineral density also occurs, primarily with malabsorptive procedures, due to calcium and vitamin D deficiency leading to secondary hyperparathyroidism.

36
Q

What are complications of total and partial gastrectomy as well as Whipple’s procedure?

A

Total and partial gastrectomy for the treatment of PUD, gastric malignancy, and pancreatic tumors can result in a variety of short- and long-term complications. Complications following gastrectomy include intraluminal bleeding, anastomotic leaks, and anastomotic strictures. Delayed gastric emptying, dumping syndrome, and/or fat malabsorption may also develop following partial gastrectomy with or without vagotomy, resulting in symptoms of nausea and vomiting, loss of appetite, bloating and fullness, or early satiety. Pancreaticoduodenectomy (Whipple resection) entails removal of the pancreatic head, duodenum, common bile duct, gallbladder, and distal stomach. Common complications are weight loss, reflux, dumping syndrome, and bacterial overgrowth.