Lectures

Acute Pancreatitis

by Carlo Raj, MD
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    Acute pancreatitis, by definition, everything in your pancreas is going absolutely crazy. In your head, you should be thinking about the pancreas and divide it into two physiologic organs. And by that, I mean you divide it into exocrine pancreas and you divide it into endocrine pancreas. Initially, when there's damage that has taken place to the pancreas, all these enzymes that are being released and, in your head, you should also be thinking about, "Whoa, those enzymes from the pancreas that are responsible for protein digestion include trypsin, carboxypeptidase, endopeptidase and so forth, trypsin being the most potent. If you're dealing with the enzymatic or exocrine pancreas and you wish to metabolize your lipid and then that discussion takes you to lipase. In any case, that's a lot of enzymes within the pancreas, is it not? And all these enzymes are being released locally, you might have utmost enzymatic destruction resulting in a term called autodigestion. Important etiologies that we'll take a look at: alcohol being quite common. This pain that the patient's feeling is not only epigastric, but then also radiating to the back. When the time is right, I will then then give you a list of differentials quickly to have you differentiate between different types of epigastric pain. Gallstones could also be a possible cause of pancreatitis and we'll talk about that in greater detail and it's a nice little story. In other words, you had a gallstone that was in my gallbladder, ended up in my biliary tree and eventually makes its way to the the second part of the duodenum in which it may then cause what's known as compression atrophy. Other causes also, hypercalcemia, may cause damage to the pancreas. And, for example, if you have a patient that has a type 4...

    About the Lecture

    The lecture Acute Pancreatitis by Carlo Raj, MD is from the course Pancreatic and Biliary Tract Diseases.


    Included Quiz Questions

    1. Cystic fibrosis
    2. Hemochromatosis
    3. Wilson disease
    4. Phenylketonuria
    5. IgA deficiency syndrome
    1. Hypertriglyceridemia
    2. Alcohol
    3. Drugs
    4. Hereditary pancreatitis
    5. Gall stones
    1. Hydrochlorothiazide
    2. Spironolactone
    3. Digoxin
    4. Propranolol
    5. Furosemide
    1. Acute pancreatitis
    2. Acute cholecystitis
    3. Acute hepatitis
    4. Acute appendicitis
    5. Acute peptic ulcer disease
    1. ERCP
    2. MRCP
    3. Upper GI endoscopy
    4. USG guided FNAC
    5. X-ray abdomen
    1. Cullen's sign
    2. Cushing's sign
    3. Caput medusa
    4. Kosher's sign
    5. Sitkovsky's sign
    1. Chronic pancreatitis
    2. Acute pancreatitis
    3. Blunt trauma to abdomen
    4. Retroperitoneal hemorrhage
    5. Ruptured ectopic pregnancy
    1. Foramen of Winslow
    2. Right hepatic duct
    3. Left hepatic duct
    4. Cystic duct
    5. Neck of the gall bladder
    1. Pancreatic Amylase
    2. Salivary amylase
    3. Pepsin
    4. Gamma glutamyl transferase
    5. AST

    Author of lecture Acute Pancreatitis

     Carlo Raj, MD

    Carlo Raj, MD


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