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Pancreas 1 Presentation Transcript

  • 1. Title: Pancreas.Objectives: to1. Describe shortly the anatomy , histology, andembryology of pancreas.2. Explain congenital anomalies of pancreas.3. Study both acute and chronic pancreatitis.
  • 2. Anatomy: From Greek word (pankreas) , meaning "all flesh“. Retroperitoneal organ extending from "C" loop ofduodenum to hilum of spleen . Divided into three parts: head, body, and tail. Main pancreatic duct (duct of Wirsung) drainsinto duodenum at major papilla of Vater.
  • 3.  Accessory pancreatic duct (duct of Santorini)drains into duodenum through a separate minor papilla. In many adults, main pancreatic duct merges withcommon bile duct thus creating ampulla of Vater.
  • 4. Histology: Complex lobulated organ with distinct exocrineand endocrine components. The exocrine portion: composed of acini(produce enzymes needed for digestion), ductulesand ducts. it constitutes 80% to 85% of pancreas. The endocrine portion: composed of about 1 millionclusters of cells( islets of Langerhans); secrete insulin,glucagon, and somatostatin. it constitute 1% to 2%of pancreas.
  • 5. PANCREAS Stained with H&E : 1 – acinus 2 - islet of Langerhans3 - interlobular connective tissue septa 4 - blood vessels
  • 6. Embryology: pancreas arises from fusion of dorsaland ventral outpouchings of foregut.o The majority of gland ( body, tail, superior/anterioraspect of head, and accessory duct of Santorini )is derived from dorsal primordium .o Ventral primordium gives rise to posterior/inferiorpart of head and duct of Wirsung .
  • 7. Congenital Anomalies:1. AGENESIS : Very rare, pancreas is totally absent (agenesis),incompatible with life. The transcription factor IPF1 (PDX1) is criticalfor development of pancreas. Germ line homozygous mutation in IPF1 gene onchromosome 13 reported in these patient.
  • 8. 2. PANCREAS DIVISUM: Clinically significant. Caused by failure of duct systems of dorsal andventral primordia to fuse. So bulk of pancreas (formed by dorsal primordium)drains through duct of Santorini. Duct of Wirsung is very short and drains only smallportion of head of pancreas.
  • 9.  Accumulated pancreatic secretionspredispose patients to chronic pancreatitis.
  • 10. 3. ANNULAR PANCREAS: develops when one portion of ventral pancreaticprimordium becomes fixed, while other portionis drawn around duodenum. When this portion fuses with head of pancreas,it forms bandlike ring that completely encirclessecond portion of duodenum . present with signs and symptoms of duodenal obstructionsuch as gastric distention and vomiting.
  • 11. 4. ECTOPIC PANCREAS : Found in 2% of routine postmortem examination. Favored sites are stomach and duodenum,followed by jejunum, and ileum. Usually located in submucosa. Histologically: pancreatic acini , occasionally with isletsof Langerhans. May be visualized as a sessile mass. May cause pain from localized inflammation, or rarelymay cause mucosal bleeding. 2% of islet cell tumors arise in ectopic pancreatic tissue.
  • 12. Pancreatitis:Acute pancreatitis: Reversible lesion. Ranging in severity from edema and fat necrosis ; toparenchymal necrosis with severe hemorrhage.Etiologic Factors :Metabolic: Alcoholism, Hyperlipoproteinemia , andHypercalcemia.Drugs: thiazide diuretics.Genetic : mutation in genes encoding pancreatic enzymesand their inhibitors [ trypsinogen (PRSS1) andtrypsin inhibitor (SPINK1) genes ].
  • 13. Mechanical : Trauma , Gallstones , andIatrogenic injury (perioperative,and endoscopic procedures )Vascular:ShockAtheroembolismPolyarteritis nodosaInfectious:MumpsCoxsackie virusMycoplasma pneumoniaeIdiopathic : 10% to 20% of cases.
  • 14. Morphology:Gross: areas of red-black hemorrhage, withfoci of yellow-white chalky fat necrosis .Microscope:(1) microvascular leakage causing edema.(2) fat necrosis by lipolytic enzymes.(3) acute inflammatory reaction.(4) proteolytic destruction of pancreatic parenchyma.(5) destruction of blood vessels with subsequentinterstitial hemorrhage.
  • 15. Acute pancreatitis: low power shows : hemorrhage, paranchymalnecrosis, fat necrosis , and acute inflammatory cells .
  • 16. Pathogenesis: pancreatic enzymes present in acinar cellsin proenzyme form and have to be activated. Lysosomal hydrolases permitting proenzyme activation,and local release of activated enzymes. Mechanisms of activation:1. pancreatic duct obstruction.2. primary acinar cell injury.3. defective intracellular transport of proenzymeswithin acinar cells.
  • 17. Clinical Features and Diagnosis : Pain is constant and intense , often radiated to upper back. Systemic features due to release of toxic enzymes andcytokines into circulation resulting in : leukocytosis,hemolysis, DIC , ARDS, and diffuse fat necrosis. Peripheral vascular collapse and shock withacute renal tubular necrosis due to profound fluid loss.
  • 18. Lab. findings: Marked elevation of serum amylase levels duringfirst 24 hours, followed within 72 to 96 hours byrising serum lipase level. Glycosuria: in 10% of cases. Hypocalcemia: result from precipitation of calcium soapsin fat necrosis, if persistent it is poor prognostic sign. Direct visualization of enlarged inflamed pancreasby radiographic means.
  • 19. Treatment: Resting the pancreas by total restriction oforal food and fluids intake. Supportive therapy.Prognosis: Most patients recover fully. 5% die from shock during first week of illness. ARDS and ARF are ominous complications. In surviving patients sequel include: sterile pancreaticabscess and pancreatic pseudo cyst .
  • 20. CHRONIC PANCREATITIS: Inflammation of pancreas with destruction ofexocrine parenchyma, and fibrosis. In late stages: destruction of endocrine parenchyma. Irreversible impairment in pancreatic function.Etiology:1. Most common cause is Long-term alcohol abuse.
  • 21. 2. Less common causes include:o Long-standing obstruction of pancreatic duct by:calculi, trauma, neoplasms, or pancreas divisum.o Tropical pancreatitis: in Africa and Asia, attributedto malnutrition.o Hereditary pancreatitis: germ line mutations in PRSS1 orSPINK1 genes.o Idiopathic: as in cystic fibrosis.
  • 22. Pathogenesis: Four hypotheses:1. Ductal obstruction by concretions:accumulation of pancreatic enzymes.2. Toxic-metabolic:toxins including alcohol and its metabolites,can exert direct toxic effect on acinar cells.3. Oxidative stress:Alcohol-induced oxidative stress may generatefree radicals in acinar cells.4. Necrosis-fibrosis:in hereditary pancreatitis autolysis-resistant trypsinmolecule causes acute pancreatitis, repeated episodesof acute pancreatitis almost later develop chronicpancreatitis.
  • 23. Morphology:Gross: pancreas is hard, sometimes with extremelydilated ducts and visible calcified concretions.Microscope: Parenchymal fibrosis. Reduced number and size of acini with sparing ofislets of Langerhans. Dilation of pancreatic ducts. Chronic inflammatory infiltrate around lobules and ducts. Ductal epithelium may be atrophied or hyperplasticor may show squamous metaplasia. Islets of Langerhans become embedded insclerotic tissue, eventually they may too disappear.
  • 24. Chronic pancreatitis : Markedly-diminished pancreatic parenchyma with relativelyincrease in fattty tissue. The interstitimum: increases in fibrous component alongwith chronic inflammatory cells.
  • 25. Clinical Features and Diagnosis : Repeated attacks of mild or moderate abdominal pain,or persistent abdominal and back pain. The disease may be entirely silent until pancreaticinsufficiency and diabetes mellitus develop. In others, recurrent attacks of jaundice or indigestion. Attacks may be precipitated by alcohol abuse, orover eating .
  • 26. Lab. Findings: Mild-to-moderate elevations of serum amylase. Elevation in serum levels of alkaline phosphatase. Visualization of calcifications within pancreas byCT scan and US. Hypoalbuminemia and hypoalbuminemic edema frommalabsorption caused by pancreatic exocrine insufficiency .
  • 27. Prognosis: Long -term outlook is poor, with mortality rateover 20 to 25 years is 50%. Severe pancreatic exocrine insufficiency and chronicmalabsorption may develop, as can diabetes mellitus. Pancreatic pseudocysts develop in 10% of patients. Hereditary pancreatitis have 40% risk of developingpancreatic cancer ; other forms predisposition is unclear.
  • 28. Summary :1. Pancreas is retroperitoneal organ dividedinto three parts: head, body, and tail.2. It has distinct exocrine and endocrine components.3. Congenital anomalies include : Agenesis , divisum ,annular , and ectopic pancreas.4. Pancreatitis can be acute reversible, or chronicirreversible lesion.
  • 29. Questions:1. Enumerate congenital anomalies of pancreas, andwrite short notes on one of them?2. Write short assay on pathogenesis of chronicpancreatitis?THANK YOU