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EXOCRINE PANCREAS PANCREATITIS

EXOCRINE PANCREAS PANCREATITIS. INFLAMMATION OF THE PANCREAS 1.ACUTE PANCREATITIS 2.CHRONIC PANCREATITIS. ACUTE PANCREATITIS. ETIPATHOGENESIS ETIOLOGICAL FACTORS A. METABOLIC ALCOHOL HYPERLIPOPROTEINEMIA. ACUTE PANCREATITIS. HYPERCALCEMIA DRUGS- THIAZIDE

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EXOCRINE PANCREAS PANCREATITIS

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  1. EXOCRINE PANCREASPANCREATITIS INFLAMMATION OF THE PANCREAS 1.ACUTE PANCREATITIS 2.CHRONIC PANCREATITIS

  2. ACUTE PANCREATITIS ETIPATHOGENESIS ETIOLOGICAL FACTORS A. METABOLIC ALCOHOL HYPERLIPOPROTEINEMIA

  3. ACUTE PANCREATITIS HYPERCALCEMIA DRUGS- THIAZIDE DIURETICS GENETICS

  4. ETIOLOGY B.MECHANICAL GALL STONES TRAUMATIC INJURY PEROPERATIVE INJURY

  5. ETIOLOGY C.VASCULAR SHOCK ATHEROEMBOLISM POLYARTERITIS NODOSA

  6. ETIOLOGY D.INFECTIOUS MUMPS COXACKIE VIRUS MYCOPLASMA PNEUMONIAE 80% OF CASES ALCOHOLISM AND GALL STONES 20% CASES NO APPARENT CAUSES

  7. PATHOGENESIS AUTODIGESTION OF PANCREATIC SUBSTANCE BY INAPPROPRIATE ACTIVATION OF PANCREATIC ENZYMES & CELLULAR INJURY RESPONSE MEDIATED BY PROINFLAMMATORY CYTOKINES.

  8. PATHOGENESIS OF ACUTE PANCREATITIS

  9. NORMAL ENZYME RELEASE PROENZYME FROM ZYMOGEN GRANULES - INTO PANCREATIC DUCTS INTO DUODENUM .TRYPSIN ACTIVATE THEM INTO ENZYMES

  10. NORMAL ENZYME RELEASE IN ACUTE PANCREATITIS – PROENZYMES ARE ACTIVATED &RELEASED FROM ZYMOGEN GRANULES INTO ACINAR CELLS

  11. NORMAL ENZYME RELEASE AUTOACTIVATION OF TRYPSINOGENINZYMOGEN GRANULES, ACTIVATION BY CATHEPSIN B IN LYSOSOMES WITHIN THE ACINAR CELLS.

  12. PATHOGENESIS ENZYMES- DISINTEGRATE ACINAR CELLS & FAT TISSUE IN & AROUND PANCREAS DAMAGE ELASTIC FIBERS OF BLOOD VESSELS -?

  13. PATHOGENESIS ACTIVATED TRYPSIN ALSO ACTIVATE PRECALLIKREIN TO KALLIKREIN-ACTIVATION OF HAGEMAN FACTOR- THROMBOSIS OF SMALL BLOOD VESSELS

  14. PATHOGENESIS DAMAGED ACINAR CELLS RELEASEPOTENT CYTOKINES – ATTRACT NEUTROPHILS & MACROPHAGES MORE CYTOKINES ESPECIALLY TUMOUR NECROSIS FACTOR

  15. PATHOGENESIS INTERLEUKIN 1 NITRIC OXIDEPLATELET ACTIVATING FACTOR INTO PANCREATIC TISSUE & CIRCULATION – LOCAL & SYSTEMIC INFLAMMATORY RESPONSE.

  16. PATHOGENESIS HEREDITORY PANCREATITIS-MUTATION IN TRYPSINOGEN GENE(AUTOSOMAL DOMINANT DISORDER) –

  17. PATHOGENESIS INACTIVATION OF TRYPSIN DOES NOT OCCUR – CASCADE OF AUTODIGESTION OF PANCREAS OCCUR.

  18. PANCREATIC DUCT OBSTRUCTION GALL STONES – FOUND IN 70 – 80 % CASES, OR INTRAPANCREATIC STONES ( IN ALCOHOLISM). OBSRUCTION - INTERSTITIAL OEDEMA- IMPAIRED BLOOD FLOW- ISCHEMIC DAMAGE TO ACINAR CELLS

  19. PANCREATIC DUCT OBSTRUCTION ALCOHOL- INCREASE PROTEIN RICH PANCREATIC EXOCRINE SECRETION-INSPISSATED PROTEIN PLUGS-OBSTRUCTION, CONTRACTION OF SPHINCTER OF ODDI, DIRECT TOXIC EFFECTS ON ACINAR CELLS.

  20. PATHOLOGY 4 BASIC ALTERATIONS 1. PROTEOLYTIC DESTRUCTION OF PANCREATIC SUBSTANCE 2.NECROSIS OF BLOOD VESSELS- HAEMORRHAGE

  21. PATHOLOGY 3.NECROSIS OF FAT BY LIPOLYTIC ENZYMES THROUGHOUT ABDOMINAL CAVITY 4. ACUTE INFLAMMATORY REACTION

  22. GROSS BLUE BLACK HAEMORRHAGE INTERSPERSED WITH GREY WHITENECROTIC SOFTENING, SPRINKELED WITH YELLOW WHITE CHALKY FAT NECROSIS

  23. GROSS FAT NECROSIS IS ALSO SEEN IN OTHER INTRAABDOMINAL FAT DEPOTS, OUTSIDE ABDOMINAL CAVITY

  24. GROSS PERITONEAL CAVITY CONTAINS SEROUS SLIGHTLY TURBID BROWN TINGED FLUID WITH GLOBULES OF FAT – MAY BECOME SUPPURATIVE

  25. ACUTE PANCREATITIS

  26. ACUTE NECROTISING PANCREATITIS

  27. ACUTE NECROTISING PANCREATITIS

  28. ACUTE PANCREATITIS- FAT NECROSIS

  29. SEQUELA OF ACUTE PANCREATITIS & CLINICAL FEATURES PANCREATIC PSEUDOCYST-MASSIVE ENLARGEMENT MAY OCCUR OVER MONTHS TO YEARS. CLINICAL FEATURES-ACUTE ABDOMEN- PAIN LOCALIZED IN THE EPIGASTRIUM WITH RADIATION TO THE BACK

  30. SYSTEMIC COMPLICATIONS • include ards, multiple organ dysfunction syndrome, dic, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage)

  31. LOCOREGIONAL COMPLICATIONS • INCLUDE PANCREATIC PSEUDOCYST AND PHLEGMON / ABSCESS FORMATION, SPLENIC ARTERY PSEUDOANEURYSMS, HEMORRHAGE FROM EROSIONS INTO SPLENIC ARTERY AND VEIN, THROMBOSIS OF THE SPLENIC VEIN, SUPERIOR MESENTERIC VEIN AND PORTAL VEINS (IN DESCENDING ORDER OF FREQUENCY), DUODENAL OBSTRUCTION, COMMON BILE DUCT OBSTRUCTION, PROGRESSION TO CHRONIC PANCREATITIS

  32. SEQUELA OF ACUTE PANCREATITIS & CLINICAL FEATURES MEDICAL EMERGENCY TO BE DIFFERENCIATED FROM OTHER CAUSES OF ACUTE ABDOMEN.

  33. SEQUELA OF ACUTE PANCREATITIS & CLINICAL FEATURES SHOCK IS THE COMMON FEATURE HAEMORRHAGE,RELEASE OF VASODILATORY AGENTS LIKE BRADYKININ & PROSTAGLANDINS

  34. LABORATORY FINDINGS 1. SERUM AMYLASE- RAISES WITHIN 12 HOURS FALL TO NORMAL WITHIN 48 – 72 HOURS 2. SERUM LIPASE –INCREASED

  35. LABORATORY FINDINGS BOTH FINDINGS ARE HIGHLY SENSITIVE & SPECIFIC FOR ACUTE PANCREATITIS. HYPOCALCEMIA, JAUNDICE HYPERGLYCEMIA & GLYCOSURIA IN FEW CASES

  36. PROGNOSIS MORTALITY RATE- 20 – 40 % CAUSES OF DEATH- ?

  37. CHRONIC PANCREATITIS REPEATED BOUTS OF MILD TO MODERATE PANCREATICINFLAMMATION WITH CONTINUED LOSS OF PANCREATIC PARENCHYMA & REPLACEMENT BY FIBROUS TISSUE.

  38. CT SCAN ENLARGED INFLAMMED PANCREAS PANCREATIC PSEUDOCYST

  39. ETIOPATHOGENESIS NOT KNOWN

  40. ETIOPATHOGENESIS HYPERSECRETION OF PROTEIN FROM ACINAR CELLS IN THE ABSENCE OF INCREASED FLUID SECRETION PRECIPITATION OF PROTEINS ADMIXED WITH CELLULAR DEBRIS- FORM DUCTAL PLUGS.

  41. ETIOPATHOGENESIS IN ALCOHOLICS THESE PLUGS ENLARGE TO FORM LEMINAR AGGREGATES CONTAINING CALCIUM CARBONATE(STONES)

  42. ETIOPATHOGENESIS IN ALCOHOLIC PERSON DECREASE SECRETION OF PROTEIN LITHOSTATIN-CALCIFICATION IS FAVOURED –SMALL DUCT OBSTRUCTION- CHRONIC NECROSIS - FIBROSIS

  43. TROPICAL PANCREATITIS IN SOUTHEAST ASIA, PARTS OF AFRICA CAUSE IS PROTEIN CALORIE MALNUTRITION

  44. ONE THIRD PATIENTS WITH IDIOPATHIC CHRONIC PANCREATITIS HAVEMUTATION IN CYSTIC FIBROSIS TRANSEMEMBRANE CONDUCTANSE REGULATORY GENE

  45. TROPICAL PANCREATITIS IN SOUTHEAST ASIA, PARTS OF AFRICA CFTR GENE MEDIATES SECRETION OF BICARBONATE RICH ALKALINE PANCREATIC JUICE -NORMAL

  46. CFTR GENE MUTATION CAUSES :REDUCED INTRALUMINAL FLUID, LOWER THAN NORMAL pH- REDUCES THE SOLUBILITY OF SECRETED PROTEINS- THICKENED VISCOUS SECRETION – OBSTRUCT DUCTS.

  47. PATHOLOGY OF CHRONIC PANCREATITIS GROSS- DENSELY FIBROTIC ORGAN WITH EXTENSIVE ATROPHY OF THE EXOCRINE PANCREATIC TISSUE .

  48. PATHOLOGY OF CHRONIC PANCREATITIS THE GLAND BECOMES HARD WITH EXTREMELY DILATED DUCTS- VISIBLE WITH CALCIFIED CONCRETIONS

  49. CHRONIC PANCREATITIS

  50. CHRONIC PANCREATITIS

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