Diseases of the pancreas csbrp
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Diseases of the pancreas csbrp
- 2. Pancreas - Normal anatomy Transversely oriented Retroperitoneal Extends from the duodenum to the splenic hilum 20 cm in length and weighs ~90 gm Separated into four parts: (Based on adjacent vasculature) Head Neck Body & Tail
- 3. Pancreas - Normal anatomy The pancreatic duct system: highly variable Main pancreatic duct - Wirsung Accessory pancreatic duct - Santorini Ampulla of Vater - common channel for biliary and pancreatic drainage - The main pancreatic duct joins the common bile duct proximal to the papilla of Vater
- 5. Greek word pankreas = “all flesh” Lobulated organ Two components: Exocrine & Endocrine Exocrine portion – 80% to 85% Endocrine portion – 1% Pancreas - Normal anatomy
- 6. Exocrine portion: Secretes inactive proenzymes Trypsinogen Chymotrypsinogen Procarboxypeptidase Proelastase Kallikreinogen & Prophospholipase A and B Pancreas - Normal physiology
- 7. Endocrine portion: 1 million, islets of Langerhan Secrete: Insulin Glucagon & Somatostatin Pancreas - Normal physiology
- 8. Self-digestion of pancreatic tissue is prevented by several mechanisms: Enzymes occur as inactive proenzymes The enzymes are membrane-bound Enterokinase is required for activation Trypsin cleaves proenzymes Trypsin inhibitors in acinar and ductal secretions Acinar cells are resistant to many enzymes Pancreas - Normal physiology
- 9. AGENESIS: PDX1 mutations on chromosome 13q PANCREAS DIVISUM: Most common, 3% to 10%, chronic pancreatitis ANNULAR PANCREAS: 2nd portion of the duodenum, duodenal obstruction ECTOPIC PANCREAS: 2% of PMs, stomach and duodenum, jejunum, Meckel diverticula, and ileum Pancreas - Congenital Anomalies
- 11. Annular pancreas
- 12. Pancreatitis Inflammation of the pancreas Injury to exocrine pancreas Severity may range form mild self limiting illness to life threatening acute inflammatory process
- 13. Pancreatitis Acute pancreatitis: Reversible Gland returns to normal if underlying pathology is removed Chronic pancreatitis: Irreversible By definition it’s irreversible loss of exocrine parenchyma
- 14. Acute Pancretitis Reversible pancreatic parenchymal injury associated with inflammation M:F = 1:3 (with biliary tract disease 6:1) Biliary tract disease & gall stones account for 80% of cases Alcohol binge as precipitant – vary 60% in some places to 5% in other areas
- 15. Etiologic Factors in Acute Pancreatitis Metabolic alcoholism hyperlipoproteinemias hypercalcemia Drugs (azathioprine) Genetic Mutations in cationic tryprinogen and trypsinogen inhibitor gene Mechanical Gall stones Trauma Operative procedures Vascular shock Atheroembolism vasculitis Infections mumps
- 16. Etiologic Factors in Acute Pancreatitis – less common causes Ampullary carcinomas Ascaris lumbricoides Clonarchis sinensis Hereditory pancreatitis
- 17. Hereditary Pancreatitis Recurrent attacks of severe pancreatitis Begins in childhood Most of them are due to genetic mutations Trypsinogen gets activated with in the pancreas
- 18. Acute pancreatitis - Morphology The basic alterations are: Microvascular leakage causing edema Necrosis of fat by lipolytic enzymes Acute inflammation Proteolytic destruction of pancreatic parenchyma and Destruction of blood vessels and subsequent interstitial hemorrhage
- 20. Fat necrosis Foci of fat necrosis may also be found in extra-pancreatic collections of fat Omentum Mesentery of the bowel Subcutaneous fat
- 21. Chicken soup exudate In the majority of cases the peritoneal cavity contains a serous, slightly turbid, brown-tinged fluid in which globules of fat can be identified In its most severe form, hemorrhagic pancreatitis, extensive parenchymal necrosis is accompanied by dramatic hemorrhage within the substance of the gland
- 22. Red-black hemorrhage interspersed with foci of yellow-white, chalky fat necrosis
- 24. Pathogenesis Autodigestion of the pancreatic substance by inappropriately activated pancreatic enzymes
- 25. Pathogenesis Inappropriate activation of trypsinogen is an important triggering event in acute pancreatitis
- 26. Pathogenesis Inappropriate activation of Trypsin With resultant activation of other proenzymes Prekallikrein (kinin system) Hageman factor (Clotting, compliment sys)
- 27. Pathogenesis - Alcoholism Alcohol consumption may cause pancreatitis by several mechanisms: 1 - Secretion of protein-rich pancreatic fluid 2 - Increases pancreatic exocrine secretion 3 - Contraction of the sphincter of Oddi and 4 - Direct toxic effects on acinar cells
- 28. Clinical features: 1 Pain abdomen 2 Anorexia, nausea, and vomiting 3 leukocytosis, hemolysis, disseminated intravascular coagulation, 4 Fluid sequestration 5 ARDS 6 diffuse fat necrosis. 7 Peripheral vascular collapse and shock 8 acute renal tubular necrosis
- 29. Lab findings: 1 Elevated Serum amylase (with in 24hrs) 2 Lipase (72hrs) 3 Glycosuria 4 Hypocalcemia (poor prognosis)
- 30. Macroamylasemia Normal persons with high serum amylase Because of large size they can not be excreted in urine May be mistaken for acute pancreatitis
- 32. Recurrent bouts of inflammation leads to loss of pancreatic parenchyma and replacement by fibrosis Primary causes: Alcohol abuse Hypercalcemia / hyperlipoproteinemia Pancreas divisum Hereditary pancreatitis Chronic Pancreatitis
- 33. Chronic Pancreatitis - Pathology Loss of lobular appearance of pancreas Loss of exocrine tissue (typically not islets) Irregularly distributed fibrosis Reduced size of pancreas Inflammation Destruction of ducts – ductal dilatation Pseudocysts (25% of cases)
- 34. Chronic Pancreatitis - Gross Normal White areas of fibrosis
- 37. Sequelae - Acute Pancreatitis Systemic complications Shock Organ failure DIC Pancreatic abscesses Pseudocysts Duodenal obstruction
- 38. Sequelae - Chronic Pancreatitis Duct obstruction Pseudocysts Malabsorption (Steatorrhea, Vit deficiency) Secondary diabetes
- 39. Pancreatic Pseudocysts Localized collections of pancreatic secretions (within or adjacent to pancreas) Virtually all arise after a bout of acute or chronic pancreatitis Lack a true epithelial lining Lined by macrophages, fibrosis Different from sterile pancreatic abscesses Collections of neutrophils following liquefactive necrosis of pancreatic parenchyma
- 40. Pancreatic Pseudocyst - Gross
- 41. Pancreatic Pseudocyst - Micro
- 43. Cullen’s sign
- 47. E N D
Editor's Notes
- The adult pancreas is a transversely oriented retroperitoneal organ extending from the “C” loop of the duodenum to the hilum of the spleen ( Fig. 19-1 ). On average, the pancreas measures 20 cm in length and weighs 90 gm in men and 85 gm in women.[1] The vasculature adjacent to the pancreas can be used to separate the pancreas into four parts: the head, neck, body, and tail.
- The pancreatic duct system is highly variable. The main pancreatic duct, also known as the duct of Wirsung, most commonly drains into the duodenum at the papilla of Vater, whereas the accessory pancreatic duct, also known as the duct of Santorini, most often drains into the duodenum through a separate minor papilla approximately 2 cm cephalad (proximal) to the major papilla of Vater ( Fig. 19-1A ). In most adults the main pancreatic duct joins the common bile duct proximal to the papilla of Vater, thus creating the ampulla of Vater, a common channel for biliary and pancreatic drainage. This ductal architecture can differ significantly from person to person.
- FIGURE 19-1 Pancreatic ductal anatomy. A, The normal ductal anatomy. B, The ductal anatomy in pancreatic divisum. (Adapted from Gregg JA et al.: Pancreas divisum: results of surgical intervention. Am J Surg 145:488–492, 1983.)
- Although the organ gets its name from the Greek pankreas, meaning “all flesh,” the pancreas is, in fact, a complex lobulated organ with distinct exocrine and endocrine components. The exocrine portion, which produces digestive enzymes, constitutes 80% to 85% of the pancreas. The endocrine portion is composed of about 1 million clusters of cells, the islets of Langerhans. The islet cells secrete insulin, glucagon, and somatostatin and constitute only 1% to 2% of the organ. Diseases of the endocrine pancreas are described in detail in Chapter 24 .
- The pancreas secretes its exocrine products as enzymatically inert proenzymes. They include trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase, kallikreinogen, and prophospholipase A and B.[1] Self-digestion of pancreatic tissue is prevented by several mechanisms:
- Endocrine portion – 1% 1 million, islets of Langerhans Secrete insulin, glucagon & somatostatin
- Self-digestion of pancreatic tissue is prevented by several mechanisms: • The majority of the enzymes are synthesized as inactive proenzymes (with the exception of amylase and lipase). • The enzymes are sequestered in membrane-bound zymogen granules in the acinar cells. • Activation of proenzymes requires conversion of inactive trypsinogen to active trypsin by duodenal enteropeptidase (enterokinase). Trypsin cleaves proenzymes to yield products such as chymotrypsin, elastases, and phospholipases. • Trypsin inhibitors including serine protease inhibitor Kazal type l (SPINK1, also known as pancreatic secretory trypsin inhibitor, PSTI) are present within acinar and ductal secretions. • Acinar cells are remarkably resistant to the action of trypsin, chymotrypsin, and phospholipase A2.
- Congenital Anomalies: The complex process by which the dorsal and ventral pancreatic primordia fuse during pancreatic development frequently gives rise to congenital variations in pancreatic anatomy.[3] Most of these do not directly cause disease; however, such variations, especially in ductal anatomy, may present particular problems to endoscopists and surgeons. For example, failure to recognize aberrant ductal anatomy may lead to the inadvertent ligation of a pancreatic duct during surgery, causing serious sequelae such as pancreatitis. AGENESIS Very rarely the pancreas may be totally absent (agenesis), a condition associated with other severe malformations that are usually incompatible with life. PDX1 (pancreatic and duodenal homeobox-1 gene) encodes a transcription factor critical for the development of the pancreas.[3] Homozygous PDX1 mutations on chromosome 13q12.1 have been reported in a person with pancreatic agenesis.[3,][4] PANCREAS DIVISUM Pancreas divisum is the most common congenital anomaly of the pancreas, with an incidence of 3% to 10%.[4] This anomaly is caused by a failure of fusion of the fetal duct systems of the dorsal and ventral pancreatic primordia.[4] As a result, the bulk of the pancreas (formed by the dorsal pancreatic primordium) drains through the dorsal pancreatic duct and the small-caliber minor papilla (see Fig. 19-1B ).[4] The duct of Wirsung in persons with divisum, normally the main pancreatic duct, is very short (1 to 2 cm) and drains only a small portion of the head of the gland through the larger caliber major papilla of Vater. Although controversy exists about the clinical significance of pancreatic divisum, it has been suggested that the relative stenosis caused by the bulk of the pancreatic secretions passing through the minor papilla predisposes individuals to the development of chronic pancreatitis.[4,][5] ANNULAR PANCREAS Annular pancreas is a band-like ring of normal pancreatic tissue that completely encircles the second portion of the duodenum. Annular pancreas is often associated with other congenital anomalies and may present early in life or in adults with signs and symptoms of duodenal obstruction such as gastric distention and vomiting.[4,][6] ECTOPIC PANCREAS Aberrantly situated, or ectopic, pancreatic tissue is found in about 2% of careful routine postmortem examinations. The favored sites for ectopia are the stomach and duodenum, followed by the jejunum, Meckel diverticula, and ileum.[4] These embryologic rests are a few millimeters to centimeters in size and are located in the submucosa. Histologic examination reveals that they are composed of normal-appearing pancreatic acini, glands, and sometimes islets of Langerhans. Though usually incidental, ectopic pancreas may cause pain from localized inflammation, or, rarely, may incite mucosal bleeding. Approximately 2% of islet cell neoplasms ( Chapter 24 ) arise in ectopic pancreatic tissue. The pathogenesis of ectopic pancreas has not been established.
- FIGURE 19-1 Pancreatic ductal anatomy. A, The normal ductal anatomy. B, The ductal anatomy in pancreatic divisum. (Adapted from Gregg JA et al.: Pancreas divisum: results of surgical intervention. Am J Surg 145:488–492, 1983.)
- In acute pancreatitis the gland can return to normal if the underlying cause of the pancreatitis is removed.[9,][10] By contrast, chronic pancreatitis is defined by the irreversible loss of exocrine pancreatic parenchyma.[7,][11]
- Biliary tract disease and alcoholism account for approximately 80% of cases in Western countries ( Table 19-1 ). [8] [9] [10][12] Gallstones are present in 35% to 60% of cases of acute pancreatitis, and about 5% of patients with gallstones develop pancreatitis. The proportion of cases of acute pancreatitis caused by excessive alcohol intake varies from 65% in the United States to 20% in Sweden to 5% or less in southern France and the United Kingdom.[13] The male-to-female ratio is 1 : 3 in the group with biliary tract disease and 6 : 1 in those with alcoholism.
- The morphology of acute pancreatitis ranges from trivial inflammation and edema to severe extensive necrosis and hemorrhage. The basic alterations are (1) microvascular leakage causing edema, (2) necrosis of fat by lipolytic enzymes, (3) acute inflammation, (4) proteolytic destruction of pancreatic parenchyma, and (5) destruction of blood vessels and subsequent interstitial hemorrhage. The extent of each of these alterations depends on the duration and severity of the process.
- Alcohol consumption may cause pancreatitis by several mechanisms: 1 - Secretion of protein-rich pancreatic fluid, which leads to the deposition of inspissated protein plugs and obstruction of small pancreatic ducts. 2 - Alcohol also transiently increases pancreatic exocrine secretion and 3 - Contraction of the sphincter of Oddi (the muscle at the ampulla of Vater), and 4 - It has direct toxic effects on acinar cells
- Grey-Turner’s sign