gastroenterology ob 5

eosinophilic esophagitis

A 51-year-old woman with a history of childhood asthma presented with a sensation of food impaction. Upper gastrointestinal endoscopy revealed classic “feline” esophagus, with mucosal rings (Panel A) and an esophageal stricture near the gastroesophageal junction. Biopsy specimens of the proximal and distal esophagus showed extensive mucosal eosinophilic infiltrates (Panel B, hematoxylin and eosin). The distal esophageal stricture was dilated with the use of a balloon dilator. The patient was treated with a fluticasone inhaler (four 220-μg puffs twice daily), with instructions to swallow and to rinse her mouth. During the next 2 months, her symptoms diminished, and the histologic findings improved. Adult onset of eosinophilic esophagitis is still not recognized by many practitioners. This condition is often confused with gastroesophageal reflux disease and is associated with esophageal strictures. The presence of more than 20 eosinophils per high-power field in an esophageal biopsy specimen is strongly suggestive of this diagnosis. Optimal treatment remains unclear.

The first cases of probable eosinophilic esophagitis were reported in the late 1960s to 1970s. The incidence of eosinophilic esophagitis appears to be increasing. 

• A population-based study evaluated the incidence of eosinophilic esophagitis in Olmsted County Minnesota over thirty years [29]. The incidence increased significantly during the last three of the five-year intervals examined (from 0.35 per 100,000 population between 1991 and 1995 to 9.45 per 100,000 between 2001 and 2005). The prevalence was estimated to be 55 per 100,000 in 2006.

The majority of affected adults have been men in their 20s or 30s, although later presentations have been described.Among children, the disease is also more common in boys (71 percent in the series described above). In another population-based study, children with eosinophilic esophagitis were significantly more likely to be Caucasian (84 percent compared with 73 percent of the surrounding community as a whole). Patients were also more likely to be male (76 versus 48 percent).

PATHOGENESIS —  incompletely understood, Adaptive T-cell immunity driven by type 2 T-helper (Th2) cells, involving interleukin (IL)-13, IL-5, and IL-15 expression appears to play a major role in the pathogenesis of eosinophilic esophagitis.

Genetic factors — A genetic predisposition to eosinophilic esophagitis is supported by evidence of familial clustering. In addition, a possible susceptibility locus has been identified on chromosome 5q22

Eosinophilic esophagitis (EoE) is an allergic disorder characterized by the accumulation of eosinophils in the esophagus. We report association of EoE with variants at chromosome 5q22 encompassing TSLP and WDR36 (rs3806932, combined P = 3.19 x 10(-9)). TSLP is overexpressed in esophageal biopsies from individuals with EoE compared with unaffected individuals, whereas WDR36 expression is unaltered between the two groups. These data implicate the 5q22 locus in the pathogenesis of EoE and identify TSLP as the most likely candidate gene in the region.

Nat Genet. 2010 Apr;42(4):289-91. doi: 10.1038/ng.547. Epub 2010 Mar 7.

Common variants at 5q22 associate with pediatric eosinophilic esophagitis.

CLINICAL MANIFESTATIONS — The clinical manifestations of eosinophilic esophagitis vary with age. Adults and teenagers frequently present with dysphagia and food impactions, whereas in younger children symptoms often include feeding difficulties and abdominal pain.

Clinical manifestations in adults — Common clinical manifestations seen in adults include [5,18,22,29,75-100]:

• Dysphagia
• Food impaction
• Chest pain that is often centrally located and does not respond to antacids
• Gastroesophageal reflux disease-like symptoms/refractory heartburn
• Upper abdominal pain

Clinical manifestations in children — Symptoms in children vary depending in part upon their age [23,105-109]. In one series, the most common presenting symptoms included [23]:

• Feeding dysfunction (median age 2.0 years)
• Vomiting (median age 8.1 years)
• Abdominal pain (median age 12.0 years)
• Dysphagia (median age 13.4 years)
• Food impaction (median age 16.8 years)

ASSOCIATIONS WITH OTHER DISORDERS — There is a strong association of eosinophilic esophagitis with allergic conditions such as food allergies, environmental allergies, asthma, and atopic dermatitis. It has been estimated that 28 to 86 percent of adults and 42 to 93 percent of children with eosinophilic esophagitis have another allergic disease 

DIAGNOSIS — The diagnosis of eosinophilic esophagitis should be based upon symptoms, endoscopic appearance, and histological findings. In patients suspected of having eosinophilic esophagitis, the first diagnostic test is typically an upper endoscopy with esophageal biopsies following two months of treatment with a proton pump inhibitor. In addition, other disorders that can cause esophageal eosinophilia, such as gastroesophageal reflux disease (GERD), should be ruled out.

Endoscopy —

• Stacked circular rings (“feline” esophagus) (picture 1): 44 percent
• Strictures (particularly proximal strictures) (picture 2): 21 percent
• Attenuation of the subepithelial vascular pattern: 41 percent
• Linear furrows (picture 3): 48 percent
• Whitish papules (representing eosinophil microabscesses) (picture 1): 27 percent
• Small caliber esophagus: 9 percent

A 14-month-old with failure to thrive and loose stools. Endoscopy demonstrates a thickened furrowed esophagus consistent with eosinophilic esophagitis. These patients commonly have dysphagia with, as well as without, evidence of stricture. Eosinophilic esophagitis is also a common cause of dysphagic in atopic school-aged children. Histology would demonstrate sheets of eosinophils in the lamina propria.

Courtesy of Karen Murray, MD.

Upper endoscopy in a 36-year-old man with dysphagia. Multiple rings are present in the proximal to mid esophagus giving it the appearance of a trachea. Small whitish papules are also visible representing eosinophilic abscesses on histology. The patient's symptoms responded to oral fluticasone.

Courtesy of Eric D Libby, MD.

Nissen fundoplication is a surgical procedure to treat gastroesophageal reflux disease (GERD) and hiatal hernia. In GERD it is usually performed when medical therapy has failed, but with paraesophageal hiatus hernia, it is the first-line procedure. 

Gastroenterology ob 4

EGD
we don't normally do H.Pylori biopsy with endoscopy. For patient has never test for H.Pylori, can use serology test, if patient has complete eradication treatment, use stool antigen test, which has high sensitive, and is cheapest.

Wireless video capsule endoscopy
after take capsule, 2hr clear liquid, 4hr eat light meal.

Indications — The indications for VCE of the small bowel are evolving. The primary indications are for diagnosis of the site of obscure gastrointestinal bleeding in adults (including iron deficiency anemia), suspected Crohn's disease, and small bowel tumors. In addition, VCE is being used to detect small bowel injury associated with the use of nonsteroidal antiinflammatory drugs (NSAIDs), evaluate abdominal pain of unclear etiology, to screen for polyps in patients with familial polyposis syndromes such as Peutz-Jeghers syndrome and familial adenomatous polyposis, and possibly in the assessment of celiac disease. There is also growing experience in children over the age of 10 for the above indications [17] and these indications are now approved for children as young as two years of age. 

preparation--a 12-hour fast without preparation

Both the PillCam SB2 (in SVH) and the EndoCapsule are 11 x 26 mm in size and acquire images from one end of the device at a rate of two frames per second for approximately eight hours.



Capsule ingestion — The video capsule is swallowed with water. Following capsule ingestion, clear liquids may be taken after two hours, and food and medications may be taken after four hours. The sensor arrays are removed after eight hours and the recorded images are downloaded and processed on workstations.No need to collect the capsule.

The overall yield of VCE for obscure gastrointestinal bleeding has been reported to be in the range of 30 to 70 percent.

• Small bowel angiectasia – 22 percent
• Small bowel ulcerations – 10 percent
• Small bowel tumors – 7 percent
• Small bowel varices – 3 percent
• Blood in the small bowel with no lesion identified – 8 percent
• Esophagogastric lesions (eg, esophagitis, gastritis) – 11 percent
• Colonic angiectasia – 2 percent

VCE should not be used in patients with known or suspected strictures, Capsule retention has been described in up to 5 percent of patients who underwent a capsule study for Crohn's disease, even after performing an initial small bowel study.

Magnetic resonance imaging — Patients should not undergo magnetic resonance imaging (MRI) until passage of the capsule has been confirmed due to concern that it could result in damage to the gastrointestinal tract. Perforation!!!!

Contraindications — The procedure may be contraindicated in patients with the following conditions, albeit these contraindications may not be absolute:

• Dementia (in patients who cannot cooperate with swallowing of the capsule or who may inadvertently damage the equipment)
• Gastroparesis (the capsule can be placed in the duodenum by endoscopy to avoid this problem)
• An esophageal stricture, swallowing disorders that could prevent passage of the capsule (eg, Zenker's diverticulum) (the capsule can be placed in the duodenum by endoscopy to avoid this problem)
• Partial or intermittent small bowel obstruction (unless a surgeon is involved, the patient understands the risks, and the patient has been cleared for surgery)
• Those who are inoperable or refuse surgery
• Patients who have defibrillators or pacemakers (this is a recommendation in the package insert, but does not appear to be a significant clinical problem)
• Women who are pregnant

diabetes patient preparation for colonoscopy
if patient is taking insulin, stop short act insulin in the morning and only take half dose long act insulin the night before.
actually prefer higher glucose than low glucose.

EGD
snakeskin pattern in gastric mucosa indicate mild portal hypertension
http://www.gastrointestinalatlas.com/English/Stomach/Portal_Hypertensive_Gastropath/portal_hypertensive_gastropath.html

Endoscopic appearance of portal hypertensive gastropathy
 in a 65-year-old man with cirrhosis. Note the characteristic
 snakeskin appearance of the gastric mucosa.

Management of anticoagulants in patients undergoing endoscopic procedures

Low-risk procedures, high or low-risk conditions — No change in anticoagulation is recommended for low-risk procedures, though we suggest that elective procedures be delayed in patients taking vitamin K antagonists (eg, warfarin) if the INR or prothrombin time is in the supratherapeutic range.

High-risk procedures, low-risk conditions — In patients at low risk for thromboembolism undergoing high-risk endoscopic procedures, vitamin K antagonists (eg, warfarin) should be discontinued five days before the procedure. The INR should be confirmed to be below 1.4 before the procedure. The vitamin K antagonist can usually be reinstituted on the night of the procedure.

Patients taking an oral direct thrombin or factor Xa inhibitor (dabigatran, rivaroxaban, or apixaban) with normal renal function typically discontinue the drug one to two days prior to the procedure. These drugs have rapid onsets of action (hours) and short half-lives (9 to 17 hours) [5]. These drugs can usually be reinstituted following the procedure. (See "Management of anticoagulation before and after elective surgery", section on 'Dabigatran' and "Management of anticoagulation before and after elective surgery", section on 'Rivaroxaban and apixaban'.)

In patients in whom a sphincterotomy has been performed, the risk of bleeding persists for three to five days, and when sessile polyps are resected, the risk of bleeding may persist for more than two weeks. It is reasonable to delay attaining therapeutic levels of anticoagulation in these situations until five days or two weeks postprocedure, respectively.

High-risk procedures, high-risk conditions — For patients at high risk for thromboembolism undergoing high-risk procedures, vitamin K antagonists (eg, warfarin) should be discontinued five days before the procedure, and bridge therapy should be considered. Similarly, patients taking dabigatran should have the drug stopped one to two days prior to the procedure, assuming normal renal function. We suggest consulting the clinician prescribing the anticoagulant to discuss the options for bridge therapy. (See "Management of anticoagulation before and after elective surgery", section on 'Dabigatran'.)

Bridge therapy — Bridge therapy may be indicated in the periendoscopic period in patients on anticoagulants who are at high risk for thromboembolic complications. The American Heart Association and the American College of Cardiology recommend the following [1]:

• Atrial fibrillation – Bridge therapy is not required for a patient with isolated atrial fibrillation, but is recommended for a patient with atrial fibrillation and a mechanical valve, a history of a cerebrovascular accident or transient ischemic attack, or a history of systemic embolism.
  
  Patients with atrial fibrillation and a bileaflet aortic valve do not require bridge therapy, but should have their anticoagulant restarted within 24 hours.
• Valvular heart disease – Bridge therapy is recommended for patients with a mechanical mitral valve or a mechanical aortic valve with any of the following: atrial fibrillation, previous thromboembolic event, left ventricular dysfunction, hypercoagulable condition, mechanical tricuspid valve, or more than one mechanical valve.

SUMMARY AND RECOMMENDATIONS

• The risk of bleeding from endoscopic procedures can be classified as high or low. In general, diagnostic procedures are low-risk, whereas therapeutic procedures are high-risk (table 1). 
• The probability of a thromboembolic complication following reversal or discontinuation of anticoagulation or antiplatelet agents depends upon the preexisting condition for which the medication was prescribed (table 2). 
• For low-risk procedures, the American Society of Gastrointestinal Endoscopy (ASGE) guidelines suggest making no changes in anticoagulation (Grade 2C). We suggest that elective procedures be delayed if the INR or prothrombin time is in the supratherapeutic range (Grade 2C). (See 'Low-risk procedures, high or low-risk conditions' above.)
• In patients undergoing high-risk endoscopic procedures, we suggest discontinuing vitamin K antagonists (eg, warfarin) five days before the procedure and dabigatran, rivaroxaban, or apixaban one to two days before the procedure in patients with normal renal function (Grade 2C). (See 'High-risk procedures, low-risk conditions' above.)

• Bridge therapy is not required for patients at low-risk for thromboembolism. (See 'High-risk procedures, low-risk conditions' above.)
• For patients at high-risk for thromboembolism, we suggest bridge therapy (Grade 2C). (See 'High-risk procedures, high-risk conditions' above and 'Bridge therapy' above.)

• The management of patients taking antiplatelet agents is discussed in detail elsewhere. (See "Management of antiplatelet agents in patients undergoing endoscopic procedures".)
• Other disorders of hemostasis that may require treatment prior to gastrointestinal procedures, including von Willebrand's disease, hemophilia A and B, renal failure, liver failure, and thrombocytopenia, are discussed in detail elsewhere. (See "Endoscopic procedures in patients with disorders of hemostasis".)

gastroenterology ob 3

ERCP

• risk of pancreatitis 10-20%, after procedure, normally stay overnight to observe 
• tiny stone < 6mm can probably pass on it own. 
•  gallbladder pain attack often related to eating fatty food. 

crohn's disease
1st line treatment, mesalamine(Asacol)
2nd line or flare up, predinisone
before treat with 6-mp(mercaptopurine) or azathioprine (AZA), all patient need to check TPMT test to avoid possible bone marrow toxicity and liver toxicity.

6-TG and 6-MMP are toxic metabolites, 6-TG level between 230-400 may correlate to response and remission of IBD, but >400 will correlate with bone marrow suppression, 6-mmp greater than 5700, will correlate with liver toxicity.
89% of population has wild type TPMT, while 11% are heterozygous and has low TPMT enzyme activity, and only 27% of mutant TPMT associated with enzyme deficiency. so, even TPMT testing is performed, CBC and liver function must still be obtained.

recommendation: 

• all patient undergo baseline TPMT genotype testing, especially african american since they have lower WBC count. 
• homozygous mutant TPMT should avoid use heterozygous should start with low dose 
• normal genotype may use more aggressive dose by beginning with the target weight based dose. 
• all patients should have a CBC and liver chemistries at least every other week for 6-8 wks after beginning, and at least once every 3 months thereafter.  

angiodysplasia

eosinophilic esophagitis
http://www.medscape.org/viewarticle/560078

hepatic encephalopathy
MELD score(billirubin, creatinine, INR) patient MELD score 34, 3 month mortality >70%, transfer for liver transplantation, need 6 month sober.
Model for End-stage Liver Disease (MELD)

standard drink
12oz beer=5oz wine=1.5oz spirits=14 grams of alcohol
significant alcohol consumption >210 grams/wk in men and >140 gram/wk in women that equal 15 drinks/wk in men or 12 drinks/wk in women

multiple stomach polyps

ERCP
1,cholangiocarcinoma patient present w/ jaundice, previous history of gall bladder stone, ct 9 month ago show stones, but ct scan from this admission show long stricture in common bile duct, highly suspect soft tissue mass, possible cholangiocarcinoma, ercp went through this obstruction hardly, and did cytobrush, leave a 7cm 7fr stent for palliative purpose.
2,bile leak (another interesting story)

gastroenterology observership 2

40 year old female has hepA infection, jaundice at young age, no family history of liver disease, she had her liver enzyme up and down since 10 years ago, recently high alt ast, high cholesterol, TG, her weight is stable, recently ultrasound show mild fatty liver
NASH? LIVER BIOPSY?

NASH nonalcoholic steatohepatitis (NASH)
Patients with nonalcoholic fatty liver disease (NAFLD) have hepatic steatosis, with or without inflammation and fibrosis. In addition, no secondary causes of hepatic steatosis are present.
NAFLD is subdivided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). In NAFL, hepatic steatosis is present without evidence of significant inflammation, whereas in NASH, hepatic steatosis is associated with hepatic inflammation that may be histologically indistinguishable from alcoholic steatohepatitis.

Prevalence — Nonalcoholic fatty liver disease (NAFLD) is seen worldwide and is the most common liver disorder in Western industrialized countries, where the major risk factors for NAFLD, central obesity, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome are common.
In the United States, studies report a prevalence of NAFLD of 10 to 46 percent, with most biopsy-based studies reporting a prevalence of NASH of 3 to 5 percent.
Worldwide, NAFLD has a reported prevalence of 6 to 35 percent (median 20 percent).

Patients with NAFLD (particularly those with NASH) often have one or more components of the metabolic syndrome.
■Obesity
■Systemic hypertension
■Dyslipidemia
■Insulin resistance or overt diabetes

Laboratory findings — Patients with NAFLD may have mild or moderate elevations in the aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Patients with NAFLD may have an elevated serum ferritin concentration or transferrin saturation . There is evidence that a serum ferritin greater than 1.5 times the upper limit of normal in patients with NAFLD is associated with a higher nonalcoholic fatty liver disease activity score (and thus, NASH) and with advanced hepatic fibrosis.

Rule out other disorders — Differentiating NAFLD from the other items in the differential diagnosis begins with a thorough history to identify potential causes such as significant alcohol use, starvation, medication use, and pregnancy-related hepatic steatosis.

We test all patients with hepatic steatosis for hepatitis C virus infection. We also test for hepatitis A and B. We do this to both to rule out these infections in patients with elevated aminotransferases and to determine immunity to guide future immunizations.
We also rule out other chronic liver diseases such as autoimmune hepatitis and hemochromatosis.
We obtain the following tests in all patients:
■Anti-hepatitis C virus antibody
■Hepatitis A IgG
■Hepatitis B surface antigen, surface antibody, and core antibody
■Plasma iron, ferritin, and total iron binding capacity
■Serum gammaglobulin level, antinuclear antibody, antismooth muscle antibody, and anti-liver/kidney microsomal antibody-1

Radiographic examinations:obtain an ultrasound

Role of liver biopsy: While liver biopsy is the gold standard for diagnosing NAFLD, in many cases a presumptive diagnosis can be made based upon the patient's history, laboratory tests, and imaging findings, provided other disorders have been excluded. However, some patients will continue to have an unclear diagnosis following a noninvasive evaluation. In such cases, a liver biopsy is indicated.

STAGES OF FIBROSIS — Noninvasive tests of hepatic fibrosis attempt to predict the stage of hepatic fibrosis that would be seen histologically. There are several histologic scoring systems for chronic liver disease. Many use five-point scales, such at the Metavir score (see "Histologic scoring systems for chronic liver disease", section on 'Metavir score'):
■F0: No fibrosis
■F1: Portal fibrosis without septa
■F2: Few septa
■F3: Numerous septa without cirrhosis
■F4: Cirrhosis 
Patients are typically considered to have significant fibrosis if their fibrosis score is ≥F2.

SEROLOGIC TESTS for fibrosis— A variety of serologic markers have been evaluated to predict the degree of fibrosis in the liver, and panels have been developed that combine assays of multiple markers to improve predictive ability.

The most studied panels are the aspartate aminotransferase (AST) to platelet ratio (APRI), FibroTest/FibroSure, Hepascore, and FibroSpect.

Panels of indirect markers of fibrosis: AST to platelet ratio index — The APRI is based on the AST level and platelet count and is easy to calculate. The APRI is calculated using the AST elevation (which is the AST level divided by the upper limit of normal [ULN] for the lab) and the platelet count per mm3 divided by 1000.
APRI = (AST elevation/platelet count) x 100
As an example, a patient with an AST level of 90 int. unit/L in a lab with an ULN = 45 int. unit/L and a platelet count of 120,000/mm3 would have an APRI of: (2/120) x 100 = 1.67

FibroTest, FibroSure, and ActiTest:FibroTest involves assessment of alpha-2-macroglobulin, alpha-2-globulin (haptoglobin), gammaglobulin, apolipoprotein A1, GGT, and total bilirubin Hepascore — Hepascore involves a combination of bilirubin, GGT, hyaluronic acid, alpha-2-macroglobulin, age, and sex. 

AST/ALT ratio — The AST/ALT ratio is approximately 0.8 in normal subjects. Some studies have suggested that a ratio >1 suggests the presence of cirrhosis.

RADIOLOGIC TESTS: Ultrasound-based transient elastography Magnetic resonance elastography (MRE) Acoustic radiation forse impulse (ARFI) imaging

COMBINING TESTS — Using multiple serologic panels or combining serologic panels with radiographic imaging may improve the ability to correctly assess the degree of a patient's fibrosis [14,166,167]. In addition, it may be possible to improve the diagnostic performance of these panels if they are used in stepwise combination. We typically use a combination serologic testing and tissue elastography. The specific tests chosen will depend on local availability. (See 'Choice of test' above.) The aspartate aminotransferase (AST) to platelet ratio (APRI) has been combined with FibroTest/FibroSure, a strategy referred to as "SAFE" biopsy (sequential algorithm for fibrosis evaluation). In one study, the combination had good overall accuracy for significant fibrosis and reduced the need for liver biopsy in patients with chronic hepatitis C virus (HCV). (See 'FibroTest, FibroSure, and ActiTest' above.) FibroTest has also been evaluated in combination with ultrasound-based transient elastography. In a study of 183 patients with chronic HCV, the combination of these tests demonstrated an area under the ROC curve of 0.88 for F ≥2, 0.95 for F ≥3, and 0.95 for F = 4. When the elastography and FibroTest results agreed, liver biopsy examination confirmed the stage of fibrosis in 84 percent of cases for F ≥2 fibrosis, in 95 percent for F ≥3 fibrosis, and in 94 percent for F = 4 fibrosis. Thus, it is likely that a combination of serum biomarkers and elastography will improve the accuracy of fibrosis detection.

Which patients to biopsy — Specifically, we obtain a biopsy if the patient:
■Has peripheral stigmata of chronic liver disease (suggestive of cirrhosis)
■Has splenomegaly (suggestive of cirrhosis)
■Has cytopenias (suggestive of cirrhosis)
■Has a serum ferritin >1.5 times the upper limit of normal (suggestive of NASH and advanced fibrosis)
■Is >45 years of age with associated obesity or diabetes (increased risk of advanced fibrosis)

NAFLD activity score — The NAFLD activity score (NAS) is a validated score that is used to grade disease activity in patients with NAFLD. The NAS is the sum of the biopsy's individual scores for steatosis (0 to 3), lobular inflammation (0 to 2), hepatocellular ballooning (0 to 2), and fibrosis (0 to 4). An NAS of 1 or 2 corresponds to NAFL, 3 to 4 corresponds to borderline NASH, and a score ≥5 corresponds to NASH.

DIFFERENTIAL DIAGNOSIS Alternative causes of hepatic steatosis — There are multiple causes of hepatic steatosis that should be considered in a patient with suspected nonalcoholic fatty liver disease (NAFLD).
Causes of hepatic steatosis in addition to NAFLD include:
■Alcoholic liver disease
■Hepatitis C (particularly genotype 3)
■Wilson disease
■Lipodystrophy
■Starvation
■Parenteral nutrition
■Abetalipoproteinemia
■Medications (amiodarone, methotrexate, tamoxifen, glucocorticoids, valproate, anti-retroviral agents for HIV)
■Reye syndrome
■Acute fatty liver of pregnancy
■HELLP (hemolytic anemia, elevated liver enzymes, low platelet count) syndrome
■Inborn errors of metabolism (LCAT deficiency, cholesterol ester storage disease, Wolman disease) A standard drink in the United States (12 oz [360 mL] of beer, 5 oz [150 mL] of wine, 1.5 oz [45 mL] of 80-proof spirits) contains approximately 14 grams of alcohol (figure 1), so the limits above roughly translate to >15 drinks per week for men and >10 drinks per week for women.

SUMMARY AND RECOMMENDATIONS
■Nonalcoholic fatty liver disease (NAFLD) refers to the presence of hepatic steatosis when no other causes for secondary hepatic fat accumulation (eg, heavy alcohol consumption) are present. NAFLD may progress to cirrhosis and is likely an important cause of cryptogenic cirrhosis. (See 'Definitions' above.) NAFLD is subdivided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). In NAFL, hepatic steatosis is present without evidence of significant inflammation, whereas in NASH, hepatic steatosis is associated with hepatic inflammation that may be histologically indistinguishable from alcoholic steatohepatitis.
■Most patients with NAFLD are asymptomatic, although some patients with NASH may complain of fatigue, malaise, and vague right upper abdominal discomfort. Patients are more likely to come to attention because laboratory testing revealed elevated liver aminotransferases or hepatic steatosis was detected incidentally on abdominal imaging.
■Patients with NAFLD may have mild or moderate elevations in the aspartate aminotransferase and alanine aminotransferase, although normal aminotransferase levels do not exclude NAFLD.
■Radiographic findings in patients with NAFLD include increased echogenicity on ultrasound, decreased hepatic attenuation on computed tomography, or an increased fat signal on magnetic resonance imaging.
■A definitive diagnosis of NAFLD requires all of the following: •Demonstration of hepatic steatosis by imaging or biopsy •Exclusion of significant alcohol consumption •Exclusion of other causes of hepatic steatosis
■Other causes of hepatic steatosis include (see 'Differential diagnosis' above): •Significant alcohol use •Hepatitis C (particularly genotype 3) •Wilson disease •Lipodystrophy •Starvation •Parenteral nutrition •Abetalipoproteinemia •Medications •Reye syndrome •Acute fatty liver of pregnancy •HELLP (hemolytic anemia, elevated liver enzymes, low platelet count) syndrome •Inborn errors of metabolism
■Radiologic findings are often sufficient to make a diagnosis of NAFLD, provided other causes of hepatic steatosis have been excluded. However, liver biopsy may be indicated if the diagnosis is not clear or to assess the degree of hepatic injury.

gastroenterology observership 1

colonoscopy 
medicine: midazolam+fentanyl (most common)
patient with a lot of pain medication, use propofol for deeper sedation

Barrette esophagus:

 A, Lower esophageal sphincter and squamocolumnar junction; B, endoscopic view.

A, Normal esophageal epithelium; B-D, variants of Barrett’s esophagus.

                                        A, Short-segment and B, long-segment Barrett’s esophagus; A’, B’, endoscopic views.

 Histology of Barrett’s esophagus; A, no dysplasia, B, low-grade dysplasia, and C, high- grade dysplasia.

base on visual change under endoscopy+pathologic diagnosis, if see visual change but pathology not supporting, it is not barrette esophagus.
Barrett's esophagus is the condition in which any extent of metaplastic columnar epithelium that predisposes to cancer development replaces the stratified squamous epithelium that normally lines the distal esophagus.

The condition develops as a consequence of chronic gastroesophageal reflux disease (GERD), and predisposes to the development of adenocarcinoma of the esophagus.

EPIDEMIOLOGY — Barrett's esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years
Barrett's esophagus appears to be uncommon in blacks and Asians.
Obesity is a risk factor for gastroesophageal reflux disease (GERD) and may be a risk factor for Barrett's esophagus
44 percent of patients lacked "troublesome heartburn and/or acid regurgitation during the past three months" suggesting that screening programs based upon reflux symptoms alone may be inadequate to identify patients with Barrett's esophagus.
Familial aggregation of Barrett's esophagus has been described. It is unclear if this is due to common environmental exposures and/or an inherited predisposition. Germline mutations in the MSR1, ASCC1, and CTHRC1 genes have been associated with the presence of Barrett's esophagus and esophageal adenocarcinoma. However, large cohort studies are needed to validate these findings.

CLINICAL FEATURES:  symptoms of associated gastroesophageal reflux disease (GERD), such as heartburn, regurgitation, and dysphagia.

DIAGNOSTIC CRITERIA — Endoscopic examination generally is required to diagnose Barrett's esophagus.
Two criteria must be fulfilled:
■The endoscopist must document that columnar epithelium lines the distal esophagus.
■Histologic examination of biopsy specimens from that columnar epithelium must reveal intestinal metaplasia. Some data suggest that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered "Barrett's esophagus," but most authorities still require the presence of intestinal metaplasia for an unequivocal diagnosis

SUMMARY AND RECOMMENDATIONS
■Barrett's esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years. The specialized intestinal columnar metaplasia typical of Barrett's esophagus causes no symptoms. Most patients are seen initially for symptoms of associated gastroesophageal reflux disease (GERD), such as heartburn, regurgitation, and dysphagia. (See 'Epidemiology' above.)
■Two criteria must be fulfilled to make a diagnosis of Barrett's esophagus: (See 'Diagnostic criteria' above.) •The endoscopist must document that columnar epithelium lines the distal esophagus. •Histologic examination of biopsy specimens from that columnar epithelium must reveal specialized intestinal metaplasia. Some data suggest that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered "Barrett's esophagus," but most authorities still require the presence of specialized intestinal metaplasia for an unequivocal diagnosis.
■It has been proposed that patients with GERD symptoms should be screened endoscopically for Barrett's esophagus. We suggest that patients with multiple risk factors for esophageal adenocarcinoma undergo screening for Barrett's esophagus. However, the evidence supporting this recommendation is weak, and we feel that decisions on when to recommend endoscopic screening should be individualized. Factors known to increase the risk for Barrett's esophagus include white ethnicity, older age, obesity (especially central obesity), and long duration of GERD symptoms.

some info and pics are from
https://gi.jhsps.org/GDL_DiseaseLibrary.aspx?CurrentUDV=31

useful study materials

http://courses.washington.edu/med610/radiology/Luks&TakasugiX-rayTutorial6-8-10.ppt