Diseases of the pancreas csbrp
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Transcript of Diseases of the pancreas csbrp
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Diseases of the Pancreas
Dr.CSBR.Prasad, M.D.
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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
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Pancreas - Normal anatomyThe 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
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Greek word pankreas = “all flesh” Lobulated organ Two components: Exocrine & Endocrine
Exocrine portion – 80% to 85% Endocrine portion – 1%
Pancreas - Normal anatomy
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Exocrine portion: Secretes inactive proenzymes
Trypsinogen Chymotrypsinogen Procarboxypeptidase Proelastase Kallikreinogen & Prophospholipase A and B
Pancreas - Normal physiology
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Endocrine portion: 1 million, islets of Langerhan Secrete:
Insulin Glucagon & Somatostatin
Pancreas - Normal physiology
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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
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AGENESIS: PDX1 mutations on chromosome 13qPANCREAS 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
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Annular pancreas
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Pancreatitis Inflammation of the pancreas Injury to exocrine pancreas Severity may range form mild self limiting
illness to life threatening acute inflammatory process
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Pancreatitis Acute pancreatitis: Reversible
Gland returns to normal if underlying pathology is removed
Chronic pancreatitis: IrreversibleBy definition it’s irreversible loss of
exocrine parenchyma
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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
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Etiologic Factors in Acute PancreatitisMetabolic 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
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Etiologic Factors in Acute Pancreatitis – less common causes
Ampullary carcinomasAscaris lumbricoidesClonarchis sinensisHereditory pancreatitis
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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
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Acute pancreatitis - MorphologyThe 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
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Fat necrosis Foci of fat necrosis may also be found in
extra-pancreatic collections of fat Omentum Mesentery of the bowel Subcutaneous fat
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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
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Red-black hemorrhage interspersed with foci of yellow-white, chalky fat necrosis
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PathogenesisAutodigestion of the pancreatic substance by
inappropriately activated pancreatic enzymes
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PathogenesisInappropriate activation of trypsinogen is an
important triggering event in acute pancreatitis
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Pathogenesis Inappropriate activation of Trypsin With resultant activation of other
proenzymes Prekallikrein (kinin system) Hageman factor (Clotting, compliment sys)
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Pathogenesis - AlcoholismAlcohol consumption may cause pancreatitis
by several mechanisms:1 - Secretion of protein-rich pancreatic fluid2 - Increases pancreatic exocrine secretion3 - Contraction of the sphincter of Oddi and 4 - Direct toxic effects on acinar cells
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Clinical features:1 Pain abdomen2 Anorexia, nausea, and vomiting 3 leukocytosis, hemolysis, disseminated
intravascular coagulation, 4 Fluid sequestration5 ARDS6 diffuse fat necrosis. 7 Peripheral vascular collapse and shock8 acute renal tubular necrosis
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Lab findings:1 Elevated Serum amylase (with in 24hrs) 2 Lipase (72hrs)3 Glycosuria4 Hypocalcemia (poor prognosis)
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Macroamylasemia Normal persons with high serum amylase Because of large size they can not be
excreted in urine May be mistaken for acute pancreatitis
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Chronic Pancreatitis
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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
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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)
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Chronic Pancreatitis - Gross
NormalWhite areas of fibrosis
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Chronic Pancreatitis- Micro
Normal
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Sequelae - Acute Pancreatitis Systemic complications
Shock Organ failure
DIC Pancreatic abscesses Pseudocysts Duodenal obstruction
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Sequelae - Chronic Pancreatitis Duct obstruction Pseudocysts Malabsorption (Steatorrhea, Vit deficiency) Secondary diabetes
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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
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Pancreatic Pseudocyst - Gross
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Pancreatic Pseudocyst - Micro
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Pancreatic Pseudocyst
vs. congenitalcyst
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Cullen’s sign
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Grey-Turner’s sign
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