GI Flashcards
0
Q
What are the indications for EGD in a patient with GERD?
A
“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.”
1
Q
What are the red flag symptoms for GERD?
A
“Red flag symptoms include dysphagia, weight loss, anemia, aspiration, early satiety or vomiting, and cough”
2
Q
If a GERD patient has already failed H2-blockers and antacids, what is the next treatment?
A
“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”
3
Q
What is the most common finding on EGD for patients with GERD?
A
“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.”
4
Q
What is the role of fundoplication in GERD?
A
“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”
5
Q
What is Barrett’s esophagus and what are 2 risk factors?
A
“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”
6
Q
What is the CREST syndrome?
A
“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.”
7
Q
What is the appropriate management for the esophageal dysmotility that is related to the CREST syndrome?
A
“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”
8
Q
How does eosinophiliac dysphagia present?
A
“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.”
9
Q
What is the treatment for eosinophiac dysphagia?
A
“Treatment in adults (and often children) involves swallowing inhaled corticosteroids (fluticasone), montelukast, and, in severe cases, systemic steroids. Systemic eosinophilia is rare.”
10
Q
A person develops regurgitation 4 hours after eating. What is the most likely diagnosis?
A
“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.”
11
Q
What is nonulcer dyspepsia?
A
“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”
12
Q
Name 3 symptoms of nonulcer dyspepsia.
A
“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.”
13
Q
What is the preferred test for H. pylori?
A
“13C urea breath test or stool antigen test”
14
Q
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?
A
“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”
15
Q
Which drugs are commonly used to treat nonulcer dyspepsia?
A
“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”
16
Q
In the treatment of nonulcer dyspepsia, are drugs more effective than placebo?
A
“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”
17
Q
What are the lifestyle modifications that may be helpful for nonulcer dyspepsia?
A
“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”
18
Q
What are some of the side effects of PPI’s?
A
“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”
19
Q
A normal hemoglobin excludes the existence of a significant G.I. bleed. True or false?
A
“a normal hemoglobin does not exclude a significant acute bleed, as hemodilution (in the absence of IV fluids) requires several hours”
20
Q
Orthostatic changes are an absolute indication of hypovolemia. True or false?
A
“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”
21
Q
What is the risk of developing a clinically significant G.I. bleed on NSAIDs?
A
“The risk of a clinically significant NSAID-related GI event, including GI bleeding, perforation, or obstruction, is about 1–4% per year.”
22
Q
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?
A
“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”
23
Q
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
A
“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”
24
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”
25
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”
26
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.
27
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.”
28
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%).”
29
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.”
30
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”
31
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”
32
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”
33
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”
34
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”
35
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”
36
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).”
37
What are the current post polypectomy surveillance guidelines?
“1. No polyps or only rectal hyperplastic polyps, repeat in 10 years.
2. 1–2 tubular adenomas less than 1 cm in size with only low-grade dysplasia should have repeat colonoscopy in 5 years.
3. 3–10 tubular adenomas, or villous features or high-grade dysplasia should have surveillance in 3 years.
4. Patients with >10 adenomas should be screened more frequently and familial colon cancer syndromes should be considered.
5. If a sessile polyp is removed in piecemeal fashion, then a repeat exam in 3 months is appropriate to assure complete removal.
6. If prep is not good, repeat colonoscopy at earliest convenience is indicated”
38
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”
39
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.”
40
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”
41
What is the usefulness of serologic testing in the workup of colitis?
Crohn disease is associated with antibodies against saccharomyces (ASCA), while ulcerative colitis (UC) patients are more often positive for ANCA. However, the sensitivity of these tests is only about 60%. Moreover, there is about a 20% overlap (e.g., ANCA positive in Crohn disease), raising further questions about the overall usefulness of these tests. ASCA can also be positive in celiac disease.”
42
How do you address an anal fissure from Crohn's disease?
“Fissures are one of the anal manifestations of Crohn disease and should be approached by treating the underlying disease rather than using surgical techniques, botulinum injection, etc. Botulinum injections, nitroglycerin ointment, and nifedipine have all been used for anal fissures with success, but we need to diagnose this patient and address the underlying disease.”
43
Tell me three facts about Crohn's disease.
“Crohn disease and UC are both relapsing/remitting diseases. Up to 30% of initial exacerbations of Crohn disease will remit without any intervention. While there is a genetic component to inflammatory bowel disease (IBD) (up to a 100-fold increase in risk among first-degree relatives with IBD), no single, autosomal-dominant gene has been identified. half or more of patients with Crohn disease will ultimately require some sort of surgery. Unfortunately, chronic glucocorticoid administration does not lower the rate of relapse. There are many complications of IBD and GI abscesses and fistulae occur with a relatively high frequency (20–40%) in Crohn disease” “Histologically, UC involves only the mucosa and submucosal tissue, while Crohn disease is transmural. All of the other statements are true. UC involves the rectum in 95% of cases and advances proximally.”
44
Name three extra intestinal manifestations of inflammatory bowel disease.
Cholelithiasis. Liver disease. Ankylosing Spondylitis. Arthritis related to IBD (enteropathic arthritis) is fairly common and usually migratory in nature, involving the large joints. Spondyloarthropathy may also be seen. Sclerosing cholangitis and autoimmune hepatitis can occur and may be fatal. Eye disease may include uveitis and episcleritis. Importantly, the main treatment of extraintestinal manifestations is to treat the IBD. IBD spondyloarthropathy and pyoderma gangrenosum are important exceptions, as these do not always improve with treatment of the underlying IBD.”
45
What is toxic megacolon and what symptoms are associated with it?
“Toxic megacolon is a potentially deadly complication of IBD that should be suspected in a patient with IBD who presents with fever, abdominal pain, and shock. Also consider other causes of intestinal obstruction.”
46
What is the emergency management of a patient who has inflammatory bowel disease and presents with fever abdominal pain and bloody diarrhea?
“Thalidomide has been used as chronic therapy for IBD, but it is not indicated in the acute setting. The patient should be stabilized, and this includes IV access and fluid resuscitation. An exacerbation (or relapse) of IBD can be treated with glucocorticoids in the acute setting, and antibiotics are often helpful. It appears that metronidazole has beneficial effects that are not solely due to its antimicrobial properties. In this patient, who may have an abscess or obstruction, further evaluation (e.g., labs and abdominal CT) and surgical consultation are necessary”
47
What is the medical long-term treatment of inflammatory bowel disease?
“Of special note are the 5-ASA drugs (e.g., Pentasa and Asacol). These have fewer side effects than sulfasalazine and are the initial drugs of choice for maintenance, once control of symptoms has been obtained. Systemic steroids (e.g., prednisone) are useful acutely to induce remission but should be tapered and stopped as soon as possible.
Additional drugs for treatment of IBD include cyclosporine, 6-mercaptopurine (6-MP), infliximab, and adalimumab (just say Humira®, it’s much easier), among others. Antidiarrheal drugs such as loperamide are useful to control symptoms. However, be sure to avoid antidiarrheal drugs in patients who may have impending toxic megacolon. Probiotics and lactose avoidance may also be useful (although there is less good evidence for these”
48
Name two contraindications to the use of sulfasalazine.
“Sulfasalazine contains both sulfa and salicylate moieties and thus is contraindicated in patients with sulfa or aspirin allergy.”
49
Name two complications of infliximab use for the treatment of inflammatory bowel disease.
“Anemia will generally improve with the treatment of IBD. Anemia in IBD is often due to a combination of iron deficiency and anemia of chronic disease, but IBD can cause an autoimmune hemolytic anemia as well. All of the rest are common—or particularly severe in the case of sepsis—complications of infliximab. In fact, ongoing infection is an absolute contraindication to the use of infliximab.”
50
Both hypocalcemia and hypothyroidism can cause constipation. True or false?
False. “Secondary causes of constipation, such as hypothyroidism, medication side effects or hypercalcemia, should be ruled out as appropriate. Therefore, a TSH level should be obtained”
51
What are the Rome criteria for irritable bowel syndrome?
“Continuous or recurrent abdominal pain or discomfort, at least 3 days per month in the last 3 months, with symptoms starting at least 6 months prior to diagnosis, and associated with at least 2 of the following:
Relief with defecation
Change in stool frequency
Change in stool form
52
What is the treatment of irritable bowel syndrome?
“Although there is not much evidence for its efficacy, the mainstay of therapy for IBS is fiber. Fiber supplements increase stool volume and frequency and soften stools, thereby alleviating symptoms of constipation. While bowel habits can be successfully changed with bulking agents for constipation or loperamide for diarrhea-predominant IBS, pain is generally not affected by these measures. In fact, increased fiber intake may transiently worsen some symptoms due to fermentation and generation of gas, potentially resulting in flatulence or bloating” 60% of patients will improve with the use of placebos in IBS.
53
Name three supplements to live show him promise in the treatment of irritable syndrome.
psyllium has an NNT of 11, hyoscyamine has an NNT of 5, and peppermint oil has an NNT of 2.5 (BMJ 2008; 337:a2313). Amazingly, St John wort is actually less effective than placebo! SSRIs and tricyclic antidepressants (TCAs) are also effective.”
54
what is the role of rifaximin, also known as Xifaxam, in the treatment of IBS?
“41% improved on vs. 32% on placebo!). The NNT is 11 (which means 10 patients are paying up to $1200/month for no benefit”
55
What are the symptoms of lactose intolerance?
Lactose intolerant individuals have insufficient levels of lactase, an enzyme that catalyzes the hydrolysis of lactose into glucose and galactose, in their digestive system. In most cases, this causes symptoms which may include abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi (rumbling stomach), or vomiting[1] after consuming significant amounts of lactose.
56
What other diseases should be considered in your differential diagnosis for lactose intolerance?
“bacterial overgrowth syndrome, presents with bloating, diarrhea, dyspepsia, and possible malabsorption and weight loss. It can occur as a result of bowel dysmotility, bowel redundancy or diver-ticula, chronic pancreatitis, etc. gluten-sensitive enteropathy (nontropical or celiac sprue), presents with similar symptoms including malabsorption. Giardia infection, can be chronic and presents with gas, diarrhea, and occasionally constipation. Finally, C. difficile infection (pseudomembranous colitis) can also be chronic in nature with chronic diarrhea and blood loss”
57
What is the diagnostic test for bacterial overgrowth syndrome?
“The d-xylose breath test takes advantage of the fact that the bacteria responsible for bacterial overgrowth syndrome (gram-negative aerobes) catabolize d-xylose. The breath test measures radioactive CO2 that is formed as a result of bacterial breakdown of radioactive d-xylose. The glucose breath test, in which glucose is administered to the patient and breath hydrogen is measured, is also helpful and commonly used. However, it is less sensitive and specific than the d-xylose test and has a 30–40% false-negative rate. Workup of bacterial overgrowth syndrome should also include an upper GI endoscopy and possible small bowel biopsy. GI hypomotility, small bowel dilatation, or small bowel diverticula support the diagnosis of bacterial overgrowth syndrome”
58
What is the most reliable screen for gluten sensitivity and what is the gold standard for diagnosis?
“Tissue transglutaminase antibodies are sensitive and specific for severe gluten-sensitive enteropathy but may be falsely negative in mild-to-moderate cases. Antiendomysial IgA antibodies are also relatively sensitive and very specific for gluten-sensitive enteropathy. Antigliadin antibodies are less sensitive and specific and have fallen out of favor. The definitive test (“gold standard”) is a small bowel biopsy and should be considered if your clinical suspicion is high and the patient has negative antibodies. Patients with positive antibodies should also have and endoscopy; the diagnosis should be confirmed by endoscopy and biopsy before committing the patient to a gluten-free diet for life.”
59
People with a gluten sensitivity can often reintroduce small amounts of gluten into their diet after abstaining without any adverse effects. True or false?
While there is no good data on the benefit of a long-term gluten-free diet in patients who can tolerate small amounts of gluten, several factors argue for continuing a gluten-free diet. The first is that many patients will have subclinical nutrient deficiencies if they reintroduce gluten. For this reason, patients with gluten-sensitive enteropathy should be screened for osteoporosis and take a multivitamin. This is especially true in pediatric patients where deficiencies may lead to stunted growth. The second is that there is some data that patients who reintroduce gluten may have increased mortality from GI lymphoma despite the fact that they are tolerating the gluten well. With a gluten-free diet, antibodies (tissue transglutaminase, antigliadin, antiendomysial) often return to normal levels.”
60
What is the difference in treatment for a patient with bloody diarrhea and fever versus a patient with bloody diarrhea without fever?
“Patients with severe, bloody diarrhea, and fever (T >101 F, >6 stools per day) should be treated with a 3–5-day course of a fluoroquinolone while awaiting stool culture results. Bloody diarrhea in an afebrile patient should suggest Escherichia coli//0157:H7. These patients should not get antibiotics because of an increased risk of hemolytic-uremic syndrome.”
61
What is the most common cause of travelers diarrhea?
“Enterotoxigenic E. coli is the most common cause of traveler diarrhea in patients traveling to Mexico. Enterohemorrhagic E. coli is less likely and should be associated with bloody diarrhea. The others are much less likely to be causes of traveler diarrhea.”
62
In a patient with travelers diarrhea and no systemic signs, what is the recommended treatment?
“This patient has non-bloody diarrhea and no systemic signs, so it should be safe to treat him with antidiarrheal agents (e.g., loperamide) and avoid antibiotics. Oral rehydration is the rule unless a patient is too nauseated or has some other reason that he cannot take adequate fluids by mouth. Patients (including children) should eat anything they can tolerate. The concept of “gut rest” is passe and actually leads to increased bowel permeability and more persistent diarrhea. Lactose deserves special mention. The American Academy of Pediatrics has changed their recommendations about lactose in diarrhea. They recommend withholding lactose only in children less than 3 months of age. This seems to be the group in which transient lactase deficiency occurs”
63
What should be considered for patients with antibiotic related diarrhea that tests negative for clostridium antigen?
“Klebsiella oxytoca can produce an antibiotic-related diarrhea that is indistinguishable from C. difficile. In those with a negative stool for Clostridium antigen, consider (1) false-negative test (some of the newer strains of Clostridium are not detected by traditional stool antigen) or (2) K. oxytoca or (3) the C. difficile toxin degenerates rapidly at room temperature (no toxin may be detectable after 2 hours of exposure to room temperatures) or (4) ELISA tests generally only test for Type A antigen. The patient may have an antigen Type B producing strain or there may be a mutation of antigen Type A.”
64
What is the best screening test for hepatitis C?
“The sensitivity and specificity of the present-day HCV antibody test are excellent; thus, this is the best test to perform.”
65
To further assess a patient for cirrhosis who has slightly elevated liver enzymes, fatigue and HCV antibody positive, what test/s are indicated?
Liver biopsy and possibly U/S. Having established that the patient has hepatitis C with elevated liver enzymes, the next step is to determine the severity of his liver disease. Although his liver function tests are reassuring, it does not exclude the possibility of advanced fibrosis or even well-compensated cirrhosis. You would not be incorrect to order ultrasound imaging in addition to the liver biopsy”
66
Hepatitis C virus can be spread through sexual relations. True or false?
“HCV is spread by parenteral contact with infected blood. In contrast to hepatitis B, sexual transmission of HCV is inefficient and appears to be a minor route of spread. Additionally, the efficacy of latex condoms in preventing disease is not known. The NIH and the USPHS do not recommend condom use for patients in a stable, long-term, and monogamous relationship. That said, using condoms will likely reduce an already low risk even further”
67
What are the treatments for hepatitis C virus?
“combination therapy with interferon and ribavirin is the old treatment of HCV. The HCV genotype was a major factor determining the likelihood of achieving sustained virological response (SVR), although not the likelihood of progression to end-stage liver disease. Genotype 1 (including 1a and 1b) is the most difficult to clear, while genotypes 2 and 3 are the most responsive to treatment. Stage of fibrosis is also a factor, with patients with stages 3 and 4 (bridging fibrosis and cirrhosis) being less likely to achieve SVR. Higher baseline viral levels also tend to predict poorer response to treatment. Combination therapy is expensive and is associated with significant toxicities. The major concerns with ribavirin are hemolytic anemia and teratogenicity, while the interferons (standard or the long-acting pegylated forms) have a long list of potential side effects, of which neuropsychiatric problems, such as depression and irritability, are often the most troublesome.
OK now the game changer: Telaprevir and boceprevir are protease inhibitors that have shown benefit in genotype 1 hepatitis C. For now, they are being used in combination with interferon and ribavirin. However, recent studies suggest they may be just as effective without the use of interferon, the side[…]”
68
What is the differential for a patient with a history of fatigue and other symptoms and signs of hepatitis?
“Constitutional symptoms such as fatigue and anorexia can be seen with any form of acute or chronic liver disease; thus, they are not helpful in establishing a differential diagnosis. The first priority is to rule out infectious hepatitis including hepatitis A, B, and acute hepatitis C. Autoimmune hepatitis deserves consideration, particularly in female patients. While HCV infection is a worldwide problem, HBV infection is endemic in Asia and Africa, and the possibility of chronic hepatitis B also warrants special attention in this patient”
69
Which test will be useful in determining if somebody has hepatitis a or B?
“HBsAg is helpful to assess for HBV infection (acute and chronic) and anti-HAV antibodies will rule out acute hepatitis A infection. A positive total anti-HAV (positive IgG) with a negative IgM would indicate past infection, while a positive IgM would suggest acute HAV infection. Interpreting the HBV antigens (Ag) and antibodies (Ab) can be confusing, and Table 7–5 may help”
70
How do you do long-term monitoring of somebody with hepatitis B virus?
“The HBe antigen reflects viral replication. Loss of HBeAg indicates decreased viral replication and less of a risk of progression to cirrhosis. Loss of HBeAg may occur spontaneously; it is also the therapeutic endpoint of antiviral treatments of HBV infection (interferon, lamivudine, adefovir). If she is negative for HBeAg and is anti-HBe antibody positive (anti-HBe +) or has low or undetectable levels of HBV DNA, she has a low level of viral replication and will not benefit further from anti-retro viral treatment.
71
What is the risk of hepatocellular carcinoma in a patient with hepatitis B virus and what is the monitoring of such patients?
“Even asymptomatic HBV carriers with minimal liver disease are at risk for hepatocellular carcinoma, and screening is recommended in chronic HBV carriers (men >40 years old, women >50 years old, in those with family a history of HCC, in cirrhotic patients and in those of African ancestry >20 years of age).”
72
What are the side effects of interferon therapy for hepatitis B?
“Depression, Aggression and homicidal behavior, Myalgias, Leukopenia...Flu-like symptoms of myalgias, malaise, fever, chills, headache, and weight loss are particularly common”
73
What is the most likely diagnosis for a patient who presents with edema, ascites and spider angiomas on his abdomen?
“This patient likely has portal hypertension given his ascites and stigmata of liver disease (spider angiomata/telangiectasias). Blood is shifted toward the spleen because of the increased portal pressure (the blood, like the rest of us, likes the path of least resistance). Shunting of blood through the spleen results in thrombocytopenia through increased platelet destruction. “A” is wrong since liver patients often have anemia. “C” is incorrect because liver patients frequently have a low albumin.”
74
In performing the diagnostic paracentesis for a patient with ascites what marker is important to determine it's cause?
“The ascitic fluid albumin is needed to calculate the serum-ascites albumin gradient (SAAG), which is helpful to distinguish between ascites resulting from portal hypertension from ascites due to other causes. Lactate and pH have been proposed as markers for spontaneous bacterial peritonitis (SBP) but have proven to be unreliable. Measurement of triglycerides is useful to confirm chylous ascites; however, in the absence of grossly milky-appearing fluid, there is no need to perform this test”
“In addition to albumin, all ascitic fluid should be sent for cell count and cultures. A cell count showing >250 polymorphonuclear leukocytes/mm3 is presumptive evidence of SBP. Gram stain is nearly useless since bacterial counts are low enough that bacteria are rarely seen on Gram stain”
75
What is a SAAG and what does it mean?
“The SAAG can tell us whether the fluid is a transudate or exudate. The SAAG is simply the difference between the serum albumin and the ascitic fluid albumin, or 3.3–1.9 = 1.4, in this case. A SAAG of > 1.1 indicates portal hypertension with 97% accuracy. Remember this by remembering that a high SAAG means high pressure in the portal system.
Ascites from any cause of portal hypertension will have a high SAAG. Aside from cirrhosis, portal hypertension also may result from schistosomiasis, sarcoidosis, portal vein thrombosis (Budd-Chiari syndrome), congenital hepatic fibrosis, CHF, myxedema, etc. Causes of a low SAAG include serositis from connective tissue disorders, nephrotic syndrome, pancreatic-related ascites, and peritoneal carcinomatosis among others”
76
What is in the initial approach to management of ascites due to portal hypertension?
“The initial approach to the management of ascites due to portal hypertension is sodium restriction and diuretics. The goal is a 2-g sodium diet (which is impossible to follow). The majority of patients will not have an adequate response to sodium restriction alone, so it is reasonable to begin diuretics at the outset. Spironolactone, which is an aldosterone antagonist, is useful because portal hypertension is a state of hyperaldosteronism. Spironolactone tends to cause hyperkalemia, an effect that can be mitigated by the coadministration of furosemide. Once-daily doses are appropriate for initial therapy; adjustments are made based on the patient’s electrolytes, renal function, and response to treatment. NSAIDs should be avoided, due to sodium retention and GI bleeding”
77
How does one diagnosed spontaneous bacterial. Peritonitis?
“>250 polymorphonuclear leukocytes/mm3 in the ascites fluid) and has clinical findings to suggest infection. This patient could become unstable quickly, so discharge from the emergency department is not recommended. Increasing doses of diuretics and/or large-volume paracentesis may be required, but these interventions should only be considered in the setting of hospital admission. Broad-spectrum antibiotics are the standard of care for SBP, and IV third-generation cephalosporins (ceftriaxone, cefotaxime) are typically the first-line agents in hospitalized patients” “In addition, albumin in the dose of 1.5 g/kg on day 1 followed by 1 g/kg on day 3 reduces the chance of renal failure and death and therefore should be given to all patients with SBP”
78
The patient with known hepatitis who develops neurologic changes consistent with hepatic encephalopathy, what causes should be investigated?
“High-protein diets are associated with hepatic encephalopathy as is up regulation of GABA receptors in the CNS. Similarly, a GI bleed delivers a large protein load to the GI tract. Thus, any patient with hepatic encephalopathy should be evaluated for a GI bleed. Other causes of acute hepatic encephalopathy include constipation, sedative use (e.g., benzodiazepines), and hypokalemic metabolic alkalosis. An elevated ammonia level is associated with hepatic encephalopathy, although there is not a direct linear correlation between serum ammonia level and mental status”
79
What is the treatment of hepatic encephalopathy in the hospital?
“The mechanism of action of lactulose is dependent on bacterial metabolism of lactulose into lactic and acetic acids. This reduces the pH of the colon leading to precipitation of nonabsorbable ammonia in the colon, which reduces serum ammonia levels. Enemas (soap suds, etc.), on the other hand, may help acutely by removing colonic contents. Oral antibiotics (neomycin, metronidazole and others) should be reserved for patients who do not respond to lactulose. Their efficacy is more limited”
80
What problems do you need to worry about in a patient with end-stage liver disease?
“Patients with end-stage liver disease tend to have a lack of vitamin K-dependent clotting factors (and thus elevated PT/INR) and have thrombocytopenia due to shunting of blood from the liver to the splanchnic bed because of elevated portal pressures. However, 50,000 platelets are generally considered adequate. Additionally, it is likely that there is platelet dysfunction in cirrhosis, although the clinical significance is not clear”
81
What can be used in management of a patient with continued alcohol abuse and end-stage liver disease?
Nadolol and isosorbide dinitrate “will reduce portal pressures and reduce the risk of variceal bleeding. pentoxifylline, has anti-TNF activity and reduces mortality when used acutely (at least in the first 4 weeks after an event of alcoholic hepatitis). vitamin K, is indicated because of liver failure-induced coagulopathy.” “Prednisolone (40 mg/day) and tapered over 2–4 weeks may have some benefit in severe alcoholic hepatitis. The evidence is contradictory”
82
At which point should albumin be replaced when doing a paracentesis on a patient with significant ascites?
“It is still unclear who needs albumin replacement. There is clearly no need for albumin in patients who have less than 5 L of fluid removed. However, for patients who have more than 5 L of fluid removed, the standard of care is replacement with albumin although the data are limited”
83
Name a marker for biliary cirrhosis.
“AMA (antimitochondrial antibodies are found in primary biliary cirrhosis (95% sensitive and 98% specific). antismooth muscle antibodies, are found in autoimmune hepatitis. reduced levels of alpha1-antitrypsin, are found in hepatitis from alpha1-antitrypsin deficiency (surprise!). polyclonal antibodies, are found in autoimmune hepatitis”
84
What is Gilbert syndrome?
“Gilbert syndrome is the most common inherited disorder of bilirubin metabolism, affecting up to 5% of Caucasians. It is characterized by isolated mild unconjugated hyperbilirubinemia, with serum bilirubin levels usually less than 3 mg/dL. However, bilirubin levels in patients affected with Gilbert syndrome can increase with fasting or during febrile illnesses, though rarely exceeding 6mg/dL.
85
Tell me about nonalcoholic fatty liver disease.
“NAFLD is more common in women and is among the most common causes of elevated liver enzymes. NAFLD refers to a spectrum of histologic findings that range from simple steatosis to an aggressive injury pattern. NAFLD often occurs in association with obesity, dyslipidemia, and/or glucose intolerance, hypothyroidism, and occurs more commonly in women than men. While most patients with NAFLD will not develop progressive liver disease, a minority are at risk to develop cirrhosis. Female gender and the presence of diabetes increase the risk of progression to cirrhosis”
86
Give the ALT in alcoholic liver disease, what can you predict about the AST?
“In alcohol-related liver disease, the AST is generally 2x the ALT.”
87
What are some characteristics of mesenteric thrombosis and bowel ischemia?
“Patients with small bowel ischemia from either embolism or mesenteric thrombosis will generally present with severe abdominal pain and an exam that is unremarkable. Late in the course there will be guarding, rebound, and other peritoneal signs as the bowel perforates. However, early in the course of the illness, severe pain with a relatively benign exam is consistent with the presentation of bowel ischemia. However, abdominal pain plus lactic acidosis should raise the suspicion that there may be bowel ischemia”
88
What is the antibiotic treatment of choice for acute cholecystitis?
“The most appropriate antibiotic choice available for this patient is ampicillin/sulbactam (Unasyn). The main organisms that need to be covered are gram-negative organisms and anaerobes (E. coli, Enterococcus, Klebsiella, and Enterobacter). Ampicillin/sulbactam will cover all of these organisms. “A” is incorrect because clindamycin, while it covers gram positives and anaerobes, does not cover most gram-negative organisms. Additionally, many enterococci are resistant. “B” is incorrect because vancomycin only covers gram-positive organisms. “C” is incorrect because gentamicin does not cover anaerobic organisms. Other antibiotic options for treating this patient include cefotetan and cefoxitin, among others”
89
What is the treatment of choice for cholecystitis?
“Studies have shown improved outcome in patients with severe gallstone pancreatitis and/or cholangitis that receive early (within 72 hours after admission) ERCP with biliary sphincterotomy.”
90
What is the most common adverse events from an ERCP?
“pancreatitis is the most common, with an incidence of about 5% of patients after ERCP. In fact, elevations in pancreatic enzymes (mostly not significant) occur in up to 75% of patients post-ERCP. The others are less common and in order of descending incidence are bleeding, perforation, sepsis, and contrast allergy (rare).”
91
What are some common causes of pancreatitis?
“The most common causes of acute pancreatitis are ethanol ingestion, biliary tract disease, and endoscopic procedures with biliary tract disease being the most common cause in the United States. Common viruses that can cause pancreatitis include HIV, hepatitis viruses, EBV, and Coxsackieviruses. Many other drugs can also cause pancreatitis: of note are didanosine (DDI), some diuretics, some NSAIDs, some antibiotics, etc.
92
Meperidine is superior to morphine in the treatment of biliary tract diseases. True or false?
“There is no evidence that meperidine is superior to morphine even in gallbladder and pancreatic disease. Meperidine is more likely than morphine to cause seizures in this patient. Meperidine is more likely than morphine to cause confusion and agitation in elderly patients” “Meperidine (and tramadol) may cause a serotonin syndrome when combined with an SSRI. This is not a problem with morphine. The rest are all true. There is no evidence to support the tradition that meperidine is superior to morphine in biliary or pancreatic disease. Meperidine is metabolized into normeperidine that can cause agitation and seizures”
93
What is the routine treatment of pancreatitis?
“The routine treatment of pancreatitis includes avoiding oral intake (NPO status), administering IV fluids, and providing pain management”
94
What are the Ranson criteria?
This can be remembered by the mnemonic "WALLS FOr CHUB" (think of the ice cream brand and the stereotypical patient).
```
At admission:
W = WBC
A = Age
L = LDH
L = Liver enzyme (AST)
S = Sugar
After 48hrs:
F = Fluid requirement
O = PaO2
C = Calcium
H = Haematocrit
U = Urea
B = Base deficit
Interpretation: If the score ≥ 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely.
Or
Score 0 to 2 : 2% mortality
Score 3 to 4 : 15% mortality
Score 5 to 6 : 40% mortality
Score 7 to 8 : 100% mortality..
```
95
What is the preferred method of drainage for a pancreatic pseudocyst
“The formation of a fistula with the stomach using an endoscope is actually the preferred method of drainage. The one major contraindication to endoscopic treatment is a pseudoaneurysm. Injury to an artery can cause significant bleeding that is difficult to control.”
96
Gallstones identified on incidental examination should indicate the need for cholecystectomy. True or false?
“Asymptomatic gallstones do not need special attention since 70–80% remain asymptomatic. Only 2–3% of patients will present with acute cholecystitis or other complications and therefore prophylactic cholecystectomy is not indicated. American Indian populations have high risk of stone associated gallbladder cancer and are an exception to this rule. Diabetics or sickle cell disease patients have higher risk of complications from gallstones but still should not have their gallbladder removed if asymptomatic. Family history of complication from gallstones is not an indication for prophylactic cholecystectomy”
97
What is the best test to assess gastric emptying?
“The most widely used test for diagnosing gastroparesis is radionucleotide scan. The patient is given standardized meal containing 99m technetium sulfur colloid in low-fat eggs, and nuclear activity is measured at 2 and 4 hours, respectively. If radioactivity in the stomach is >50% at 2 hours or >10% at 4 hours, the patient is considered to have delayed gastric emptying. You can do a liquid phase gastric emptying study if you suspect dumping syndrome, but it is not necessary to evaluate for gastroparesis. radiolabeled CO2 breath test, correlates well with nuclear scintigraphy and is easier to perform in the community setting. However, a radiolabeled CO2 breath test requires normal small bowel, pancreas, liver, and lung function”
98
What is the best treatment for a patient with a diagnosis of diabetic gastroparesis?
“The treatment of diabetic gastroparesis is often difficult and frustrating for patients and clinicians. Although not proven in prospective trials, most experts believe improved glucose control with dietary and lifestyle modification is the key to long-term success in diabetic gastroparesis. Cisapride was removed from the market because of prolongation of the QT interval”
99
A high-fiber diet is a staple of the treatment for diabetic gastroparesis. True or false?
False. “Fiber and raw vegetables can form gastric bezoars (phytobezoar) in gastroparesis and this is commonly seen on endoscopy. Bezoars cause early satiety and bloating and add to the symptom burden of gastroparesis. If a bezoar is found, it can be dissolved using cellulase (Kanalase®) or N-acetylcysteine orally”
100
What is the last resort treatment for diabetic gastroparesis?
“The last resort in severe, unremitting gastroparesis with weight loss and brittle diabetic control can be to place percutaneous endoscopic jejunostomy. The patient is then placed on jejunal feedings temporarily while diabetic control and nutritional balance are regained (if possible).”
101
what diagnostic test is central to evaluating diverticulitis?
“CT scan is very sensitive and specific for diverticulitis and can simultaneously evaluate for other causes of abdominal pain. In general, CT scan is indicated if the patient has peritoneal signs or mass suggesting diverticular abscess formation. In a patient who has had previously documented attacks and who has none of the above symptoms, empiric treatment is appropriate. Surgical and/or GI consults may be indicated but are premature at this point”
102
What is the management of mild diverticular attack?
“Mild attacks of diverticulitis can be managed on an outpatient basis. Our patient has small abscess that requires inpatient therapy. In addition, he is immunosuppressed by his diabetes, and all immunosuppressed patients with diverticulitis should be admitted for IV antibiotics since they are more likely to develop complications and need surgery” “Antibiotic regimens for diverticulitis must include both gram-negative and anaerobic coverage. Some common regimens include ciprofloxacin + metronidazole, ampicillin/sulbactam, amoxicillin/clavulanate, ampicillin + gentamicin + clindamycin, and ceftriaxone + metronidazole.”
103
How often will a patient have a second attack of diverticulitis after the first one within five years?
“Antibiotic regimens for diverticulitis must include both gram-negative and anaerobic coverage. Some common regimens include ciprofloxacin + metronidazole, ampicillin/sulbactam, amoxicillin/clavulanate, ampicillin + gentamicin + clindamycin, and ceftriaxone + metronidazole.” “Perforation of diverticulitis is rare and occurs in only 5–10% of patients within 2 years of the initial event. Diverticular bleeding happens in 3–5% of patients with diverticulosis and the risk is not increased with diverticulitis; if GI bleeding occurs during an episode of presumed diverticulitis, other diagnoses should be strongly considered”
