Acute Pancreatitis :- Causes, Pathogenesis, Morphology, Signs & Symptoms, Diagnosis & Management

pancreatitis is divided into two forms acute pancreatitis and chronic pancreatitis both of these forms are initiated by injuries that lead to auto digestion of the pancreatic tissue by its own enzymes under normal circumstances pancreas has several mechanisms that protect it from self-digestion including the following most digestive enzymes are synthesized as inactive pro enzymes also known as zymogens which are packaged within secretory granules zymogen granules have an acidic ph and a low calcium level which prevent premature activation of zymogens most pro enzymes are activated by trypsin which itself is activated by duodenal enterokinas in the small intestine thus intrapancreatic activation of proenzymes is normally minimal moreover a signer and pancreatic ductal cells secrete trypsin inhibitors which further limits intrapancreatic trypsin activity so pancreatitis occurs when these protective mechanisms are deranged or overwhelmed acute pancreatitis is characterized by reversible pancreatic parenchymal injury associated with inflammation it can return back to normal after resolution of the episode acute pancreatitis is a relatively common condition the annual incidence in western countries is about 10 to 20 cases per 100 000 people gallstones and alcohol account for the vast majority of cases in western countries acute pancreatitis ranges from mild and self-limiting to extremely severe disease in severe disease there is extensive pancreatic and pure pancreatic necrosis along with hemorrhage which carries a high mortality rate now let's discuss about the etiology of acute pancreatitis most common causes of acute pancreatitis include the following gallstones alcohol following endoscopic retrograde calangio pancreatography which is a technique used to diagnose and treat conditions involving the liver gallbladder biliary system and the pancreas about 10 percent of pancreatitis cases are a diapathic meaning that they do not have a clear ideology less common causes of acute pancreatitis include the following trauma infections with certain viruses including mumps hiv adenovirus and coxac eb virus pancreatic tumors congenital pancreatic abnormalities such as pancreas division a condition that leads to formation of two main pancreatic ducts metabolic abnormalities like hypercalcemia and hypertriglyceridemia certain types of venom like scorpion sting and spider venom and certain drugs including the following azathioprine and mercaptopurine didnocene estrogens antibiotics like tetracycline valproic acid furosemide sulfonamides amino salicylates corticosteroids metronidazole and ace inhibitors in addition to these factors hereditary factors also play a role in acute pancreatitis in certain individuals now let's discuss about the pathogenesis of acute pancreatitis acute pancreatitis results from inappropriate activation and release of pancreatic enzymes that destroy the pancreatic tissue and elicit an acute inflammatory response but how this inappropriate activation of pancreatic enzymes occurs in acute pancreatitis is not completely understood however there is evidence that at least three major initiating events pancreatic duct obstruction primary assigner cell injury and defective intracellular transport of pro enzymes within a siner cells pancreatic duct obstruction is most commonly caused by gallstones and biliary sludge other causes of pancreatic duct obstruction include pancreatic cancer colidocacyl or congenital cystic dilation of the common bile duct parasites such as ascorous lumbricoids and pancreas division whatever the cause obstruction leads to accumulation of enzyme-rich fluid in the pancreatic interstitial tissue which raises intrapancreatic ductal pressure unlike other enzymes lipus is produced in its active form therefore accumulation of lypis leads to local fat necrosis and adipocyte death this will stimulate myofibroblasts and leukocytes to secrete pro-inflammatory cytokines which will result in inflammation and edema which compromise the local blood flow leading to vascular insufficiency and ischemic injury to assiner cells causing release and activation of pancreatic enzymes primary assigner cell injury can be caused by many factors including oxidative stress and increased calcium flux which causes activation of zymogens whatever the cause primary assigner cell injury leads to release and activation of zymogens causing inflammation and auto digestion of the pancreatic tissue defective intracellular transport of pro-enzymes within a cynor cells is seen in animal models with acute pancreatitis in normal assigner cells digestive enzymes and lysosomal hydrolases are transported in separate pathways however in pancreatitis some hydrolases and digestive enzymes are transported together leading to activation of those enzymes alcohol consumption may cause acute pancreatitis through all of these mechanisms alcohol transiently increases the contraction of sphincter of body leading to transient obstruction and chronic alcohol ingestion results in the secretion of protein-rich pancreatic fluid that leads to deposition of protein plugs and obstruction of small pancreatic ducts in addition alcohol has a direct toxic effect on assigner cells alcohol-induced oxidative stress may generate free radicals within a cynor cells leading to membrane lipid oxidation oxidative stress also promotes the fusion of zymogen granules with lysosomes and mitochondrial damage which increases intracellular calcium levels leading to inappropriate activation of zymogens however it is important to note that most drinkers never develop pancreatitis during their lifetime thus key aspects of the pathophysiology of alcohol-induced pancreatitis remain unexplained this image is from the robin's textbook of pathology it is a summary of what we have discussed in the pathogenesis part you can pause the video and go through it before we proceed into the next section now let's see what are the morphologic features in acute pancreatitis the morphology of acute pancreatitis ranges from mild inflammation and edema to extensive necrosis and hemorrhage basic alterations are microvascular leak and edema fat necrosis acute inflammation destruction of pancreatic perinchema and destruction of blood vessels and interstitial hemorrhage in the milder form acute interstitial pancreatitis histologic alterations are limited to mild inflammation and interstitial edema and focal areas of fat necrosis in the pancreas and pure pancreatic fat released fatty acids may combine with calcium to form insoluble salts in the more severe form acute necrotizing pancreatitis there is necrosis of the siner and ductal tissues as well as the eyelets of langerhans vascular injury can lead to hemorrhage macroscopically the pancreatic substance is red black and contains interspersed fossee of chalky fat necrosis in the most severe form acute hemorrhagic pancreatitis there is extensive parenchymal necrosis accompanied by hemorrhage within the substance of the gland now let's discuss about the clinical features of acute pancreatitis upper abdominal pain is the cardinal feature in acute pancreatitis the pain usually begins in the epigastric region acute pancreatitis is a differential diagnosis in any patient with upper abdominal pain abdominal pain is often accompanied by nausea and vomiting as inflammation spreads throughout the peritoneal cavity the pain becomes more intense involvement of the retroperitoneum may lead to back pain and patient may give a history of previous similar episodes physical examination may reveal upper abdominal tenderness in severe disease patient will have tachycardia and hypotension along with oliguria widespread tenderness and guarding and reduced or absent bowel sounds specific clinical signs that support a diagnosis of severe necrotizing pancreatitis include periumbilical bruising or cullen's sign and flank bruising or gray turner's sign now let's discuss about the diagnosis of acute pancreatitis blood tests and imaging tests are the mainstay of diagnosis sarah mammalis is an extremely sensitive test if it is three times more the normal limit however other conditions that increase sarah mammalis should be excluded these include upper gastrointestinal perforation biliary peritonitis and intestinal infarction in addition to sarah mammalis urinary amylose is also elevated in acute pancreatitis serum lypus is also raised in acute pancreatitis and remains elevated for a longer period of time than amylose however the accuracy of serum lipus is not significantly greater than amylose crp level is important in assessing the disease severity and prognosis other baseline investigations include a full blood count serum creatinine and electrolytes blood glucose arterial blood gas analysis and liver biochemistry imaging tests include an erect chest x-ray to exclude gastro-duodenal perforation a supine x-ray may reveal gallstones and pancreatic calcification abdominal ultrasound scan is important to identify possible biliary causes for pancreatitis such as gallstones it also detects pancreatic swelling and necrosis in severe pancreatitis the pancreas made difficult to be identified due to the gas-filled bowel loops mri is useful in assessing the degree of pancreatic damage it also identifies gallstones within the biliary tree and helps differentiate between solid and liquid inflammatory masses endoscopic retrograde colangio pancreatography is used as a treatment measure to remove bile duct stones in selected cases of gallstone-related pancreatitis finally let's come to the treatment of acute pancreatitis early fluid losses in acute pancreatitis may be large and require intravenous fluid administration urinary catheterization is essential to monitor the circulatory volume and to assess the renal function arterial and central venous catheterization may be necessary to facilitate close monitoring of hemodynamic status and to permit repeated sampling of arterial blood gases nasogastric suction is essential to prevent abdominal distension and vomitus in order to prevent aspiration pneumonia in addition prophylactic antibiotics and analgesics such as tramadol are also given low molecular weight heparin should be given for prophylaxis of deep vein thrombosis feeding of a patient with acute pancreatitis is usually by nasal gastric administration of food however some people may not tolerate naso gastric feeding for these patients postpolaric feeding is indicated total parenteral nutrition is not indicated for the patients with acute pancreatitis due to the high risk of infection okay that is all i wish to discuss in this video hope it made sense if you have any question or doubt regarding this topic feel free to post them in the comment section thanks for watching see you soon in the next video