Acute pancreatitis  intro
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  • Due to the retroperitoneal and deep location, pain arising from pancreas is often characterized as penetrating through to the back.The neck divides the pancreas into approximately two equal halves.
  • Pancreatic peudocyst commonly develop in the lesser sac The posterior aspect of the stomach usually forms the anterior wall of the pseudocyst and the base of transverse colon forms the inferior wall of pseudocyst. Hence these regions can be used to drain the pseudocyst.
  • Common Hepatic arterygastroduodenal artery  superior pancreaticoduodenal artery anterior and posterior branches Superior Mesenteric artery inferior pancreaticoduodenal arteries anterior and posterior branchesThe superior and inferior pancreaticoduodenal arteries by its branches supply the head of pancreas and the medial aspect of the C- loop of duodenum, hence it is not possible to resect the head of pancreas without resecting duodenum.Splenic artery runs along the posterior superior border of body and tail of pancreas, while the superior mesenteric artery give rise to inferior pancreatic artery which runs along the inferior border of pancreas.The splenic and inferior pancreatic arteries are joined by three branches, which run perpendicularly through the parenchyma of the body and tail of pancreas
  • The superior aspect of head is drained directly in to the portal vein.The posterior-inferior aspect is drained into inferior mesenteric vein.The anterior-inferior aspect is drained into right gastroepiploic vein and middle colic vein  superior mesenteric vein.
  • Variations in portal venous anatomy. The superior mesenteric vein joins the splenic vein and then continues toward the portahepatis as the portal vein. The inferior mesenteric vein often joins the splenic vein near its junction with the portal vein, but sometimes joins the superior mesenteric vein; or the three veins merge as a trifurcation to form the portal vein.
  • Lymphatic drainage from pancreas is diffuse and widespread. This provides egress to tumor cells arising from the pancreas. This diffuse lymphatic drainage contributes to the fact that pancreatic cancer often presents with positive lymph nodes and a high incidence of local recurrence.
  • Pancreas is supplied by sympathetic and parasympathetic nervous system.Parasympathetic nervous system stimulates endocrine and exocrine secretion while sympathetic system inhibits the secretion.Somatic innervation is by celiac ganglia.
  • In 1/3rd of individuals the pancreatic duct and bile duct remain distinct to the end of the papilla, in another 1/3rd the two ducts fuse at the papilla and in the remaining 1/3rd a true common channel is present for a distance of several millimeters.
  • because alcohol causes spasm of sphincter of Oddi.Initial effect of alcohol is increase in secretion and later inhibition. This leads elevation of pancreatic enzymes that can precipitate in the ducts, leading to pressure build up. lead to pancreatic ischemic injury
  • It is associated post op with billroth II gastrectomy and jejunostomy as it cause increased intraduodenal pressure, which can lead to blackflow of activated enzymes in to pancreas.
  • Mumps, coxsackievirus, and m.pneumocniae are believed to be capable of inducing pancreatitis by infecting acinar cells. But they haven’t been isolated from diseased pancreas. Though in 30% of cases there is increase in the antibody titers of mumps and coxsackievirus. This could be a non specific reaction to pancreatitis.

Acute pancreatitis  intro Acute pancreatitis intro Presentation Transcript

  • Acute Pancreatitis
  • Anatomy • The pancreas is a retroperitoneal organ that lies in an oblique position, sloping upward from the C-loop of the duodenum to the splenic hilum. • Weighs about 75 to 100gm • Length is about 15 to 20cm • It can be divided into Head, Uncinate process, neck, body and tail. • Neck lies over L1 and L2 vertebrae
  • Anatomical Relations • The neck of the pancreas lies directly over the portal vein. • At the inferior border of the neck, the superior mesenteric vein joins the splenic vein and then continues as the portal vein. • The common bile duct runs in a deep groove on the posterior aspect of the head. • The body and tail lie just anterior to the splenic artery and vein. • The body overlies the aorta at the origin of the superior mesenteric artery.
  • Arterial Supply
  • Venous Drainage
  • Variations of Portal Vein
  • Lymphatic Drainage
  • Nervous Supply
  • Pancreatic Duct • Embryologically pancreas develops from a ventral bud and a dorsal bud. • The duct of ventral bud is called as duct of Wirsung, which is joined by common bile duct. • The duct of dorsal bud is called as duct of Santorini and it drains directly into the duodenum. • With the gut rotation, the two buds and their respective ducts fuse. The ventral bud becomes the inferior portion of head and uncinate process while the dorsal bud becomes the body and tail of pancreas.
  • • Most of the pancreas drains through the duct of Wirsung, the main pancreatic duct, and drains into duodenum through ampulla of Vater/ major papilla. • In 60% of the people the duct of Santorini persists as the lesser pancreatic duct and drains into duodenum through lesser papilla. • The lesser papilla is usually about 2 cms proximal to ampulla of Vater. • In 30% the duct of Santorini ends as blind accessory duct and does not empty into duodenum.
  • • In 10% the duct of Wirsung and Santorini fail to fuse, this results in majority of pancreas draining through the duct of Santorini and lesser papilla. This is know as pancreas divisum • In minority of patients with pancreas divisum the lesser papilla can be inadequate to handle the flow of pancreatic juice resulting in outflow obstruction leading to pancreatitis.
  • Ampulla Of Vater
  • Sphincter Of Oddi
  • Histology • Pancreas secretes approximately 500ml to 800ml of pancreatic juice per day. • Exocrine pancreas accounts for 85% • Endocrine pancreas accounts only for 2% • only approximately 20% of the normal pancreas is required to prevent insufficiency. • The acinar cells secrete amylase, proteases, and lipases enzymes • The centroacinar and intercalated duct cells secrete the water and electrolytes
  • Endocrine Function Hormones Islet Cell Functions Insulin Beta Cell Decreased gluconeogenesis, glycogenolysis, fatty acid breakdown, and ketogenesis Increased glycogenesis, protein synthesis Glucagon Alpha Cell Opposite effects of insulin; increased hepatic glycogenolysis and gluconeogenesis Somatostatin Delta Cell Inhibits GI secretion Inhibits secretion and action of all GI endocrine peptides Inhibits cell growth Pancreatic polypeptide PP Cell Inhibits pancreatic exocrine secretion and secretion of insulin Facilitates hepatic effect of insulin
  • Hormones Islet Cell Functions Amylin Beta Cell Counterregulates insulin secretion and function Pancreastatin Beta Cell Decreases insulin and somatostatin release Increases glucagon release Decreases pancreatic exocrine secretion Ghrelin Epsilon Cell Decreases insulin release and insulin action
  • Pancreatitis Acute Pancreatitis Acute Relapsing Pancreatitis Chronic Pancreatitis
  • Acute Pancreatitis • Inflammatory disease of pancreas that is associated with little or no fibrosis of the gland. OR • An acute condition presenting with abdominal pain and is usually associated with raised pancreatic enzymes levels in the blood or urine as a result of pancreatic inflammation.
  • Acute v/s Chronic • Acute pancreatitis is reversible pancreatic parenchymal injury associated with inflammation. • Chronic pancreatitis is defined as inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis, and, in the late stages, the destruction of endocrine parenchyma.
  • Clinical Classification Acute Pancreatitis Mild Severe
  • • Mild acute pancreatitis: Interstitial oedema of the gland and minimal organ dysfunction. • 80% of case fall under Mild category, which has about 1% mortality. • Severe acute pancreatitis: pancreatic necrosis, severe systemic inflammatory response and often multi-organ failure. • Mortality rate is as high as 20 to 50%
  • Aetiology • • • • • • Alcohol Biliary tract disease Hyperlipidemia Hereditary Hypercalcemia Trauma o External o Surgical o ERCP • Ischemia o Hypoperfusion o Atheroembolic o Vasculitis • Pancreatic duct obstruction o Neoplasms o Pancreas divisum o Ampullary and duodenal lesions • • • • Infections Venom Drugs Idiopathic
  • Aetiology Others 5% Incidence Alcohol 25% Biliary Tract Diseases 70%
  • Biliary Tract disease • Choledocholithiasis is the most common form of associated biliary abnormality • Various Theories: o o o o Common channel hypothesis Sphincter Incompetence Ductal Pressure Colocalization theory
  • Alcohol • Pancreatitis can result with single or little alcohol intake. • Usually > 2 years of intake, and often history of > 10 years. • In individuals taking 100 to 150gm/day of alcohol, 10 to 15% can develop pancreatitis. • It can become recurrent with continued alcohol intake. • Theories: secretion with blockage mechanism • It is a metabolic toxin to pancreatic acinar cells. • Alcohol also transiently decreases blood flow to pancreas
  • Tumors • Should be considered in a non alcoholic patient with no demonstrable biliary tract disease. • 1 to 2% of patients with acute pancreatitis have pancreatic carcinoma • It could be the first clinical manifestation of periampullary tumor.
  • Iatrogenic • Pancreatic biopsy, biliary duct exploration, distal gastrectomy and splenectomy are associated with acute pancreatitis. • It is associated post op with billroth II gastrectomy and jejunostomy. • ERCP results in pancreatitis in 2 to 10% of cases.
  • Drug Induced • • • • • • • • • • Thiazides furosemide estrogens azathioprines l-asparaginase 6-marcaptopurine methyldopa sulfonamides tetracyclines pentamide • • • • • procainamide nitrofurantoin dideoxyinosine valproic acid acetylcholinesterase inhibitors
  • Infections • Mumps, coxsackievirus, and m.pneumoniae are believed to be capable of inducing pancreatitis by infecting acinar cells. • Infection by ascaris lumbricoides, and clonorchis sinensis are also implicated.
  • Hereditary • Cationic trypsinogen/PRSS1: It is a missense mutation, which results in premature, intrapancreatic activation of trypsinogen. • It accounts for about two-thirds of cases of hereditary pancreatitis • A failure to express a normal trypsinogen inhibitor, pancreatic secretory trypsin inhibitor (PSTI) or SPINK1, is a cause of familial pancreatitis.