GI Flashcards
What are the indications for EGD in a patient with GERD?
“Because of the high sensitivity and specificity of symptoms (>90%), most patients do not need endoscopy or any other diagnostic intervention. Patients with refractory GERD or those with new symptoms over age 45 years (50 by some sources) warrant endoscopy.”
What are the red flag symptoms for GERD?
“Red flag symptoms include dysphagia, weight loss, anemia, aspiration, early satiety or vomiting, and cough”
If a GERD patient has already failed H2-blockers and antacids, what is the next treatment?
“Testing is actually less sensitive than symptoms for GERD with the sensitivity of tests varying between 50% and 70%. Many patients have a false-negative EGD. While H2 blockers should still be first-line treatment in patients with GERD, this patient has already failed cimetidine. Starting a proton pump inhibitor (PPI), like omeprazole, is the next step and is preferred as first-line therapy in patients with severe symptoms”
What is the most common finding on EGD for patients with GERD?
“Most patients with GERD will have negative endoscopic findings (termed nonerosive reflux disease[NERD]—really, we didn’t make this one up). Symptoms do not correlate well with the presence or degree of esophageal inflammation or erosion.”
What is the role of fundoplication in GERD?
“While fundoplication will alleviate symptoms in 80–95% of patients, there is progressive loss of effectiveness over time (only 40% are without medication after 10 years). Adverse effects of surgery include persistent dysphagia (requiring additional interventions in 3–7%), gas, bloating, and inability to belch”
What is Barrett’s esophagus and what are 2 risk factors?
“Barrett esophagus is diagnosed histologically when esophageal mucosal metaplasia has occurred and the usual squamous epithelial cells have changed to columnar epithelium. Risk factors for Barrett include long-standing reflux, male gender (6:1 male:female preponderance), middle age, tobacco use, and white race. Barrett esophagus occurs in 10–15% of patients with erosive esophagitis, and it dramatically increases the risk of esophageal adenocarcinoma (30-fold). However, the absolute risk of adenocarcinoma is still small, about 0.12–2% annually”
What is the CREST syndrome?
“CREST is an acronym for a syndrome that includes Calcinosis cutis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias. Figure 7–1 shows telangiectasias on the palmar digital pad. Up to 60% of patients with CREST have erosive esophagitis. Dysphagia is common and is due to esophageal stricture and/or dysmotility.”
What is the appropriate management for the esophageal dysmotility that is related to the CREST syndrome?
“Severe reflux and dysphagia are hallmarks of CREST syndrome. The esophagus may be amotile with impaired function of the lower esophageal sphincter. The barrier to acid reflux and the motor clearance of refluxing material are affected, requiring chronic and potent acid suppressive medications, such as PPIs” “Steroids could worsen the GI symptoms by irritating the gastric mucosa”
How does eosinophiliac dysphagia present?
“The classic adult patient presents with dysphagia to solids to the extent that it may cause food impaction. Children often present with feeding problems (age 2), recurrent vomiting (age 8), and chronic abdominal pain (age 12) or food impaction (teenage years). Association with childhood asthma is strong and dietary elimination therapy may be helpful in children.”
What is the treatment for eosinophiac dysphagia?
“Treatment in adults (and often children) involves swallowing inhaled corticosteroids (fluticasone), montelukast, and, in severe cases, systemic steroids. Systemic eosinophilia is rare.”
A person develops regurgitation 4 hours after eating. What is the most likely diagnosis?
“Late regurgitation of undigested food is pathognomonic for Zenker diverticulum. A Zenker diverticulum is an outpouching of esophageal mucosa that is acquired and typically becomes symptomatic in middle age or later in life. The diagnosis is confirmed by lateral view of a barium swallow.”
What is nonulcer dyspepsia?
“Nonulcer dyspepsia is an ill-defined condition characterized by the presence of recurring intermittent symptoms of epigastric discomfort and fullness with other associated symptoms in the absence of mucosal lesions or other structural abnormalities of the GI tract. Nonulcer dyspepsia is also known as “functional dyspepsia,” as there are no identifiable structural or anatomic abnormalities of the GI tract. While about 20% of the general population has nonulcer dyspepsia, only about 20% of these seek medical attention”
Name 3 symptoms of nonulcer dyspepsia.
“Nonulcer dyspepsia is characterized by all the other symptoms and also includes such symptoms as abdominal distention, borborygmi (i.e., grandpa’s tummy gurgling heard across the room at Thanksgiving), epigastric or substernal pain, anorexia, nausea, vomiting, and abdominal tenderness.”
What is the preferred test for H. pylori?
“13C urea breath test or stool antigen test”
A patient begins to have diarrhea shortly after beginning a regimen involving a PPI and an H2 blocker to treat nonulcer dyspepsia. Which of the two drugs is most likely the culprit and why?
“Diarrhea is a common adverse effect of PPIs that occurs in at least 5–7% of patients. Discontinuation leads to a rapid resolution in the majority of cases. While reduced stomach acidity from PPIs or H2 blockers may result in bacterial colonization of the proximal GI tract, the early onset and severity of symptoms described argue against bacterial overgrowth as the etiology of this patient’s symptoms. While PPIs can elevate gastrin levels, the hypergastrinemia seen is not comparable to levels seen in Zollinger-Ellison syndrome, which can also cause diarrhea. Stool studies and empiric therapy with antidiarrheals may be considered if discontinuing the PPI does not improve symptoms”
Which drugs are commonly used to treat nonulcer dyspepsia?
“There are no drugs that have great evidence to support their use in nonulcer dyspepsia. PPIs and H2 blockers are often used. Prokinetic agents may be helpful, and in the United States this means metoclopramide or erythromycin. Cisapride has been removed from the market secondary to cardiac arrhythmias (QT prolongation with torsades de pointes). Metoclopramide, of course, is associated with tardive dyskinesia and extrapyramidal reactions. Erythromycin causes GI side effects and prolonged QT”
In the treatment of nonulcer dyspepsia, are drugs more effective than placebo?
“Up to 60% of patients in placebo-controlled trials respond to placebo, making it difficult to prove efficacy of medications. As the above number suggests, spontaneous resolution of symptoms is common, while many patients will have a chronic, intermittent course characterized by symptom-free periods. Most patients will not develop serious pathology”
What are the lifestyle modifications that may be helpful for nonulcer dyspepsia?
“avoid tobacco, caffeine products, and alcohol) and limit or avoid aggravating medications (NSAIDs). Patients should chew their foods slowly and eat more frequent, small meals. Finally, if there is underlying psychiatric morbidity, relaxation training or treatment of specific diseases can be helpful”
What are some of the side effects of PPI’s?
“PPIs are not benign drugs and have been associated with (1) increased risk of hip fracture in the elderly, (2) increased risk of pneumonia, (3) increased risk of Clostridium difficile colitis, and (4) diarrhea as noted above. Stop them as soon as possible”
A normal hemoglobin excludes the existence of a significant G.I. bleed. True or false?
“a normal hemoglobin does not exclude a significant acute bleed, as hemodilution (in the absence of IV fluids) requires several hours”
Orthostatic changes are an absolute indication of hypovolemia. True or false?
“Orthostatic vital signs are not that useful in determining a patient’s volume status. Many hypovolemic patients are not orthostatic and many patients who are euvolemic have orthostatic changes (e.g., patients on antihypertensives and the elderly). So, use orthostatic vital signs to confirm your clinical suspicion, but do not use them as an absolute guide to the patient’s volume status (JAMA 1999;281:1022–1029”
What is the risk of developing a clinically significant G.I. bleed on NSAIDs?
“The risk of a clinically significant NSAID-related GI event, including GI bleeding, perforation, or obstruction, is about 1–4% per year.”
Patients who have suffered a G.I. bleed from an ulcer due to an and said she’d be continued and aunt acids in definitely. True or false?
“Patients with uncomplicated and small (<1 cm) duodenal or gastric ulcers who have received adequate treatment of H. pylori or NSAID-induced ulcer do not need long-term therapy directed at ulcer healing as long as they are asymptomatic following therapy. Antisecretory drugs can be discontinued after 4–6 weeks in these patients”
After in endoscopic examination identifies an ulcer, it is necessary to do a follow-up endoscopic evaluation to confirm it’s healing. True or false
“While nonhealing ulcers may be due to a neoplasm, the vast majority of duodenal ulcers are benign. Therefore, neither endoscopic nor radiologic documentation of healing is necessary”
Name three risk factors for cancer in patients with gastric ulcers.
“Occurrence in ethnic groups raised in endemic areas (Asians, Latinos, etc.)
Helicobacter pylori infection
Absence of recent NSAID use
Absence of concomitant duodenal ulcer or a prior history of duodenal ulcer (duodenal ulcers require higher acid secretion, which is incompatible with the pangastritis typical of most gastric cancers)
Giant ulcers (>2–3 cm)
Absence of a protracted ulcer history—in general, the longer the ulcer history, the lower the risk that a gastric ulcer is cancer. Gastric ulcers require acid and gastric cancer usually develops in the setting of atrophic pangastritis”
How effective are the agents used to identify h. Pylori infection?
“Sensitivity of serologic testing for H. pylori is 90–100%. But this does not indicate current infection and may reflect prior infection. Breath testing is 88–95% sensitive with most false negatives the result of the use of antibiotics and antacids, including H2 blockers and PPIs. Thus, make sure that the patient has been off antibiotics for at least a month prior to testing and has not taken acid suppressors for 2 weeks prior to testing. This also holds true for CLO testing. Stool antigen testing (94% sensitive, 92% specific) is also available to help with the noninvasive documentation of H. pylori infection or eradication”
What is the role of metronidazole in the treatment of H pylori?
“There is resistance to metronidazole, so it should only be used when the patient is penicillin allergic OR taking quadruple therapy.
Why does a serum IgG antibody test not helpful for testing ERADICATION of H pylori infection after treatment?
“Only 57% of patients are antibody negative to H. pylori a year after successful treatment. Thus, antibody titers cannot document eradication. All of the other tests mentioned are functional tests for the presence of H. pylori. The CLO test is done on biopsy specimens and documents the presence of urea splitting. The same is true for the breath urea test and the radioactive CO2 blood test. In both of these tests, urea is ingested. If H. pylori is present, radioactive CO2 is generated that can be measured in the blood or breath.”
Are NSAIDs more common to cause gastric or duodenal ulcers?
“NSAIDs are more frequently found to be the cause of gastric ulcers (up to 30%) compared to duodenal ulcers (up to 20%).”
Name two medications that was stuck in the esophagus and can cause esophagitis.
“Many medications can cause “pill esophagitis,” including potassium chloride, ferrous sulfate, alendronate, tetracycline antibiotics, and ascorbic acid. Aspirin and other NSAIDs can also cause esophagitis. Smaller pills are less likely to cause problems. In addition to not being irritating, loratadine is tiny.”
In a patient with recurrent ulcers that seem be refractory to therapy, what should this raise your index of suspicion for?
“Some sort of screening test for gastrinoma is warranted in a patient who has recurrent or refractory ulcers. Zollinger-Ellison syndrome is the name given to the state in which there is acid hypersecretion secondary to increased gastrin production, usually from a gastrin-producing tumor (gastrinoma). Up to 1% of patients with PUD have a gastrinoma. Serum gastrin levels should be obtained with the patient fasting and off PPIs, as PPIs will increase gastrin levels. If the serum gastrin is elevated, further investigations will need to be performed. Other reasons to consider obtaining a serum gastrin level include ulcers in unusual locations, family history of ulcers, and ulcers associated with reflux esophagitis”
What’s the difference between a Boerhaave’s tear and a Mallory-Weiss tear?
“A Mallory-Weiss tear occurs after repeated trauma to the lower esophageal and gastric mucosa from forceful retching. This can be differentiated from a Boerhaave tear by the (generally) self-limited nature of the bleeding and the absence of other symptoms. A Boerhaave tear is of a similar etiology but occurs higher in the esophagus and is associated with mediastinitis, fever, shock, and death if intervention is not forthcoming”
What is superior mesenteric artery syndrome?
“SMA syndrome is more likely to occur in a patient who has lost significant weight, resulting in thinning of the mesenteric fat pad. The patient has a bruit in the abdomen on PE. Here’s the pathophysiology: the SMA runs above the duodenum and becomes stretched and partially occluded in response to meals (as the stomach and duodenum expand), leading to mesenteric ischemia and food aversion. SMA syndrome can be diagnosed using Doppler ultrasound to demonstrate increased velocity of blood in the SMA”
What’s the next step in a patient over 50 who is asymptomatic, yet positive for fecal occult blood?
“Current recommendations suggest screening for colorectal cancer in all patients over the age of 50 years. Testing for fecal occult blood is one of the accepted methods. However, it should only be performed as screening test in asymptomatic individuals. Moreover, the use of aspirin and/or NSAIDs and foods such as undercooked meat may increase the number of false-positive tests and should thus be avoided. However, once you have a guaiac-positive stool, you must proceed to colonoscopy in a patient over age 50. A CBC is also important to determine if the patient is anemic. Since the patient currently has no symptoms referable to upper GI pathology, evaluation of the upper GI tract should only be considered if the colonoscopy is negative”
Does iron cause a false positive Guaiac test?
“Iron causes stool to darken. No. Guaiac tests rely on the presence of hemoglobin in the stool, not iron. Don’t blame a positive guaiac on an iron supplement”
A patient had a negative colonoscopy three years ago but was found to have adenomatous polyp’s on the exam. If fecal occult blood testing was positive in a screening exam, what should the course of action be?
“Adenomatous polyps, such as this patient had, are considered precancerous. Recommended follow-up of an adenomatous polyp is by colonoscopy every 3–5 years. So, he did not truly have a “negative” colonoscopy 3 years ago. Plus, we are not doing the colonoscopy in this case for screening; it is diagnostic. We may find another source of his bleeding. If his previous colonoscopy were completely normal (no adenomatous polyps), you could argue for stopping the aspirin and NSAIDs and following up with serial fecal occult blood tests. In this alternative scenario, persistently positive guaiac tests would lead to colonoscopy as well”
What does the US preventive services task force recommend regarding screening for colon cancer?
“US Preventive Services Task Force recommends routine screening for colorectal cancer, starting at age 50 years for average-risk patients (this does NOT apply to high-risk patients—positive family history, known adenomatous polyps, etc.). Any of the following modalities is acceptable: annual fecal occult blood testing (FOBT) alone, annual FOBT with sigmoidoscopy every 5 years +/—dual contrast barium enema every 5 years, and colonoscopy every 10 years (without annual FOBT).”
What are the current post polypectomy surveillance guidelines?
“1. No polyps or only rectal hyperplastic polyps, repeat in 10 years.
- 1–2 tubular adenomas less than 1 cm in size with only low-grade dysplasia should have repeat colonoscopy in 5 years.
- 3–10 tubular adenomas, or villous features or high-grade dysplasia should have surveillance in 3 years.
- Patients with >10 adenomas should be screened more frequently and familial colon cancer syndromes should be considered.
- If a sessile polyp is removed in piecemeal fashion, then a repeat exam in 3 months is appropriate to assure complete removal.
- If prep is not good, repeat colonoscopy at earliest convenience is indicated”
What I need to know about hereditary non-polyposis colon cancer?
“Patients with HNPCC (Lynch syndrome) are at increased risk of developing colon cancer. About 2–3% of colon cancers occur in patients with Lynch syndrome. Transformation from an adenoma to cancer is faster in patients with Lynch syndrome. In addition, many of the neoplasms are located in the right colon. Compared to sporadic colon cancer patients, those with Lynch syndrome are younger at the time of diagnosis, more frequently present with multiple colon tumors, and are more likely to have extracolonic tumors—especially endometrial cancer. This is a genetic disorder, and the occurrence of colorectal and/or endometrial cancer in three relatives before the age of 50 should suggest HNPCC. The current recommendation is to perform surveillance colonoscopies at least every 3 years in these patients”
What are the recommendations by the ACS regarding screening for colon cancer in somebody with a first degree relative with colon cancer?
“the American Cancer Society (ACS) recommends screening colonoscopy at age 40 or 10 years before the age of diagnosis for any patients with a first-degree relative with colon cancer diagnosed under age 60 (e.g., if mom had colon cancer at 48, start your screening at 38). The ACS recommends screening colonoscopy at age 40 for patients with a first-degree relative with colon cancer over the age of 60.”
A patient presents with chronic abdominal pain and a painless anal fissure. What’s your working Dx and your next step?
“The patient’s history and physical findings with a painless, anteriorly located anal fissure and diarrhea are consistent with Crohn disease. The best next step in her evaluation is colonoscopy with inspection of the terminal ileum. You may want to do some stool testing before colonoscopy; and testing for Giardia, C. difficile toxin, and other pathogens would be reasonable”
