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acute pancreatitis is the sudden inflammationand hemorrhaging of the pancreas due to destruction by its own digestive enzymes—a process fittinglycalled autodigestion. most of the time the disease is actually relativelymild, but it can easily become severe, so it's critical to diagnose and treat it quickly. the pancreas is a long, skinny gland the lengthof a dollar bill and is located in the upper

crash diet gallstones, abdomen, or the epigastric region, behindthe stomach. it plays endocrine roles—for example, alphaand beta cells make hormones like insulin and glucagon that are secreted into the bloodstream,but it also plays exocrine roles— for example, acinar cells make digestive enzymes that aresecreted into the duodenum to help digest

food. these pancreatic digestive enzymes break downmacromolecules like carbohydrates, lipids and proteins found in food, but these macromoleculesare also found in the cells of the pancreas. to protect the pancreas, the acinar cellsmanufacture inactive forms of the enzymes called proenzymes, or zymogens. these zymogens are normally activated by proteaseswhich cleave off a polypeptide chain, which is kind of like pulling the pin on a grenade. for additional security, the zymogens arekept away from sensitive tissues in storage vesicles called zymogen granules, and arepackaged with protease inhibitors that prevent

enzymes from doing damage if they become prematurelyactive. to digest a meal, these zymogens are releasedinto the pancreatic duct, and delivered to the small intestine where they are activatedby the protease trypsin. trypsin is a pancreatic digestive enzyme thatis produced as the zymogen trypsinogen. normally, trypsinogen isn’t activated untilit is cleaved by protease enteropeptidase which is found in the duodenum. but if trypsinogen and these zymogens becomeactivated too early, then it can cause acute pancreatitis, and this might happen as a resultof any injury to the acinar cells, or anything that prevents the normal secretion of theproenzymes into the duodenum.

the two leading causes of acute pancreatitisare alcohol abuse and gallstones. with alcohol abuse it goes like this: alcoholincreases zymogen secretion from acinar cells while decreasing fluid and bicarbonate productionfrom the ductal epithelial cells. as a result, the pancreatic juices becomereally thick and viscous, potentially forming a plug that can block the duct. a blocked duct is bad news because pancreaticjuices start backing up, increasing the pressure, and leading to distention of the duct itself. at the cellular level, one consequence ofthis is that membrane trafficking becomes chaotic.

zymogen granules might fuse with lysosomesbringing trypsinogen into contact with lysosomal digestive enzymes. trypsinogen might then be turned into activatedtrypsin which begins the cascade of digestive enzyme activation and autodigestion of thepancreas—which is acute pancreatitis. alcohol also contributes to pancreatitis inother ways, though, for example, stimulating acinar cells to release inflammatory cytokineswhich attracts a strong immune reaction. neutrophils arrive quickly at the scene, andoften release superoxide and their own proteases, which contribute to the problem. finally, it’s thought that high consumptionand subsequent oxidative metabolism of alcohol

may produce enough reactive oxygen speciesto overwhelm cellular defenses and damage the cells. with gallstones what happens is that theysometimes get lodged at the sphincter of oddi which blocks the release of pancreatic juices,which is pretty similar to the alcohol-induced protein plug. but the causes of acute pancreatitis are variedand most of the important ones can remembered with the mnemonic “i get smashed”: where‘i’ refers to unknown, or idiopathic, causes; ‘g’ is obstruction by gallstones,‘e’ is ethanol abuse; ‘t’ is a pancreatic trauma, which is more likely if the traumais the result of a puncture injury (like a

knife wound not a punch); ‘s’ is the useof steroids; ‘m’ is an infection of the mumps virus, ‘a’ is the result of autoimmunediseases; the second ‘s’ is the result of scorpion sting—which is probably themost exciting item on this list and one of the more rare causes; ‘h’ is a cheat andstands for both hypertriglyceridemia and for hypercalcemia; ‘e’ is trauma from a procedurecalled an endoscopic retrograde cholangiopancreatography or ercp which is a technique used to diagnoseand treat various biliary and pancreatic diseases; and finally ‘d’ stands for drugs, likesulfa drugs, reverse-transcriptase inhibitors, and protease inhibitors. so in acute pancreatitis, there is pancreatictissue destruction that results from the proteases

and inflammatory response of the body, andthis can cause tiny blood vessels to become leaky and sometimes rupture. ultimately, all of the extra fluid or edemacauses the capsule of the pancreas to swell, and unfortunately there can be some activationof lipases which go on to destroy the fat around the pancreas, or peripancreatic fat. all of the digestion and bleeding can actuallyliquify the pancreatic tissue, a process called liquefactive hemorrhagic necrosis. in addition to destroying the pancreas, pancreatitiscan cause serious complications, like the formation of a pancreatic pseudocyst.

a pancreatic pseudocyst forms when fibroustissue surrounds liquefactive necrotic tissue of the pancreas, and this fibrous tissue developsa cavity that fills up with pancreatic juice. abdominal pain, loss of appetite and a palpable,tender mass which follows a bout of acute pancreatitis are suggestive of a pancreaticpseudocyst. in addition serum amylase, lipase and bilirubinmight sometimes be elevated. an abdominal ct scan is the best way to imagea pancreatic pseudocyst. since they swell in size pancreatic pseudocystshave the potential to rupture causing hemorrhage and a release of pancreatic enzymes into theabdominal cavity which would lead to a massive inflammatory reaction.

that pseudocyst can also get infected, oftenby e. coli, and turn into a very dangerous pancreatic abscess. this presents similarly to a pseudocyst, butwith the hallmarks of an infection including a high fever and high white blood cell count. other complications of acute pancreatitisinclude serious internal bleeding or hemorrhage from a damaged blood vessel which can quicklydevelop into hypovolemic shock. another troubling complication is systemicactivation of blood coagulation factors or disseminated intravascular coagulation (ordic) where tiny blood clots begin to develop throughout the body, using up all of the clottingfactors, which paradoxically make it easier

to bleed as well—basically upsetting thebalance of clotting homeostasis and potentially damaging various vital organs. finally, acute pancreatitis can lead to acuterespiratory distress syndrome, or ards, which is where massive pancreatic inflammation leadsto leaky blood vessels throughout the body, which makes it hard to breath. ards is the leading cause of death among individualswith acute pancreatitis. in addition to general symptoms like nauseaand vomiting, another distinctive sign of acute pancreatitis is hypocalcemia, particularlywhen there is a lot of fat necrosis because that process tends to consume calcium.

there might also be bruising around the bellybutton, or the periumbilical region, called cullen’s sign, and along the flank of thebody which is between the hip bone and the ribs, called grey turner’s sign. these happen as necrosis induced hemorrhagingspreads to the soft tissues of those body areas. diagnosis of acute pancreatitis can be madebased on clinical findings, lab data, and imaging. the first clinical clue is intense pain inthe epigastric region, which can radiate to the back.

lab data would show an increase in serum digestiveenzymes including amylase and lipase, of which lipase is more specific to pancreatitis. finally, an imaging study like a ct scan mightshow evidence of pancreatitis such inflammation, necrosis, and the formation of pseudocysts. and while it is not directly diagnostic youcan also use ultrasound to look for offending gallstones if they are suspected. treatment of acute pancreatitis is focusedon pain control and making sure that the person’s getting adequate fluids and electrolytes. generally speaking, one treatment goal isto rest the bowels, so therefore many individuals

are therefore told to avoid food, and getnourished through iv fluids instead. finally, it’s very important to treat thecomplications by offering things like oxygen therapy and antibiotics as needed. alright, as a quick recap, your pancreas producesboth hormones for the endocrine system and digestive enzymes for the exocrine system. when the pancreatic acinar cells are damagedor the the pancreatic ducts are blocked, often because of alcohol abuse or gallstones, theinactive zymogens that the pancreas produces can be prematurely converted to active digestiveenzymes. acute pancreatitis happens when these enzymesdigest the pancreas.