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Acute pancreatitis is classified as mild, moderately severe, or severe. Mild acute pancreatitis does not involve organ failure or local or systemic complications, usually resolves within 1 week, and has a low mortality rate. Twenty percent of patients with acute pancreatitis develop moderately severe or severe disease.

Moderately severe acute pancreatitis involves local or systemic complications such as necrosis or transient organ failure for less than 48 hours.

Clinical Presentation and Diagnosis The diagnosis of acute pancreatitis requires two of the following three criteria: 1 acute-onset abdominal pain characteristic of pancreatitis severe, persistent for hours to days, and epigastric in location, often radiating to the back ; 2 serum lipase or amylase levels elevated to three to five times the upper limit of normal; and 3 characteristic radiographic findings on contrast-enhanced CT Figure 9 , MRI, or transabdominal ultrasonography.

The presence of high fever and leukocytosis is part of the cytokine cascade and does not necessarily indicate infection. Because acute pancreatitis is most commonly caused by biliary disorders, patients with acute pancreatitis should undergo transabdominal ultrasonography. Transabdominal ultrasonography is preferred over CT because it has a higher sensitivity for detection of gallstones, avoids the risks associated with intravenous contrast, and is more cost effective.

However, abdominal air can limit the visualization of the pancreas in patients with acute pancreatitis. Magnetic resonance cholangiopancreatography MRCP may be considered in patients who do not have abnormal findings on ultrasonography. CT may be indicated if the diagnosis is in question or if clinical symptoms are not alleviated within the first 48 hours. Acute liver-enzyme elevation at presentation suggests biliary obstruction. Serum amylase and lipase levels may be elevated in conditions other than acute pancreatitis, such as kidney disease, acute appendicitis, cholecystitis, intestinal obstruction or ischemia, peptic ulcer, or gynecologic disorders.

Enzyme levels may be falsely low or normal in patients with hypertriglyceride-induced pancreatitis because of lipemicserum interference with laboratory assays. A systematic review of 18 multiple-factor scoring systems, including the Ranson criteria and the Acute Physiologic Assessment and Chronic Health Evaluation APACHE II score, for predicting outcome in acute pancreatitis found these systems to have limited clinical value and accuracy.

Scoring systems only identify severe disease as it develops, without enough lead time for intervention, and they are too cumbersome for routine use. Data suggest serum hematocrit, elevated blood urea nitrogen levels, and the presence of SIRS to be as accurate as complex scoring systems in predicting outcome, and they are easier to use. CT scan showing acute pancreatitis with peripancreatic fat stranding and inflammation.

The hazy appearance of the mesenteric fat surrounding the pancreas in this image is called fat stranding, and the blurring of the margins of the pancreas is consistent with peripancreatic edema, features seen with inflammatory changes of acute pancreatitis. Mainstays of management include fluid resuscitation, pain management, and antinausea medication.

More rapid fluid resuscitation boluses may be needed in patients with severe volume depletion. Routine use of antibiotics is not warranted in acute pancreatitis, unless there is evidence of extrapancreatic infection, such as ascending cholangitis, bacteremia, urinary tract infection, or pneumonia.

Use of prophylactic antibiotics in patients with sterile pancreatic necrosis to prevent infected necrosis is not recommended. In mild acute pancreatitis, oral feedings can be started as soon as nausea and vomiting are controlled and clinical symptoms begin to subside.

Enteral feeding should begin within 72 hours if oral feeding is not tolerated; it is usually required in patients with moderately severe or severe acute pancreatitis. Feeding with a nasojejunal tube has traditionally been preferred, but data suggest that nasogastric feedings are likely equally effective and easier to administer.

Enteral feeding promotes a healthy gut-mucosal barrier to prevent translocation of bacteria into inflamed tissues. If a biliary cause of acute pancreatitis is suspected, serial liver chemistry tests and clinical symptoms can show whether the biliary obstruction is ongoing or resolving. Endoscopic retrograde cholangiopancreatography ERCP is not indicated in patients with gallstone pancreatitis unless there is persistent elevation of liver chemistries or if choledocholithiasis is seen on imaging studies.

Patients with cholangitis should undergo ERCP within 24 hours of admission. Patients with uncomplicated gallstone pancreatitis should be considered for cholecystectomy before discharge. There is no value in rechecking serum amylase and lipase levels after the diagnosis is established.

Complications There are two overlapping phases of acute pancreatitis with two peaks in mortality. The early phase is the first week of the disease, when the body is responding to local pancreatic injury and the cytokine cascade, and SIRS and organ failure are possible.

The late phase occurs after the first week and may persist for weeks to months in patients with moderately severe or severe acute pancreatitis. Significant risk for infection in peripancreatic fluid collections and necrosis occurs in the late phase.

Proper classification of fluid collections in acute pancreatitis is important to guide management. An international consensus group updated the Atlanta classification and definitions of acute pancreatitis and its complications in to try to promote consistency in diagnosis and management.

Four types of fluid collections were defined: 1. Acute peripancreatic fluid collections are collections that occur in edematous interstitial pancreatitis no necrosis within the first 4 weeks, are thought to occur because of rupture of main or side branch ducts as a result of inflammation, are sterile, and usually resolve spontaneously. Pancreatic pseudocysts are acute peripancreatic fluid collections that have persisted for longer than 4 weeks,.

Walled-off necrosis Figure 11 occurs after 4 weeks, when the body liquifies the necrosis and contains it within a well-defined wall. Contrast-enhanced CT may not be able to distinguish solid from liquid content in fluid collections; therefore, necrotic collections are frequently misdiagnosed as pancreatic pseudocysts. Pancreatic pseudocysts do not require drainage. CT scan showing acute pancreatitis with hypoperfusion of the body of the pancreas as indicated by lack of enhancement following intravenous contrast infusion necrosis and normal perfusion of the pancreatic tail.

CT scan showing maturation and liquefaction of pancreas necrosis of nearly the entire pancreas over 4 weeks in duration with a well-defined rim or wall arrows , known as walled-off necrosis.

Phases of chronic hepatitis B infection. It is assumed that patients progress through the phases in sequence, although not all patients develop HBeAgnegative chronic hepatitis B, and only patients with vertical transmission of hepatitis B have a clinically recognized immune-tolerant phase.

Risk factors for the development of cirrhosis and hepatocellular carcinoma in patients with chronic HBV infection are listed in Table Treatment is advised for patients with acute liver failure, infection in the immune-active phase or reactivation phase, and cirrhosis, and in immunosuppressed patients.

Treatment thresholds in chronic immune-active or reactivation HBV. Firstline treatment is entecavir or tenofovir. Lamivudine, adefovir, and telbivudine are less commonly used due to resistance. Pegylated interferon can be used for 48 weeks in patients with. This self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefully before answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choice questions.

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