ACUTE
PANCREATITIS
DR ARPITA SINGH
INTRODUCTION
ETIOLOGY
PATHOGENESIS
DEFINITION & SPECTRUM
 Inflammatory disease of the pancreas
associated with little or no fibrosis
 Mild self limiting inflammation to critical
disease
 SIRS
 MODS
INCIDENCE :
WORLD SCENARIO
 49.3 PER 100000
POPULATION PER
YEAR IN USA
INDIAN SCENARIO
 50 PER 100000
POPULATION PER
YEAR
CLASSIFICATION
 MILD
 MODERATE
 SEVERE
 CRITICAL
ETIOLOGY I
METABOLIC
 ALCOHOL
 Hyperlipoproteinaemia
 Hypercalcaemia
 Drugs
 Genetics
 Scorpion venom
ETIOLOGY II
MECHANICAL
 CHOLELITHIASIS
 ERCP
 Post operative
 Pancreatic divisum
 Pancreatic duct obstruction
 Pancreatic ductal bleeding
 Post traumatic
 Duodenal obstruction
ETIOLOGY III
VASCULAR
 Post operative in
cardiopulmonary
bypass
 PAN
 Atheroembolism
INFECTIONS
 Mumps
 Coxsackie B
 CMV
 Cryptococcus
EVENTS IN
AP:
 ACINAR CELL
EVENTS
 CYTOKINE
ACTIVATION
ALCOHOLIC PANCREATITIS
 MOST COMMON cause
 AMOUNT & PATTERN is more important
BILIARY TRACT DISEASE
 HYPOTHESIS, not yet THEORY
1. OPIE’S COMMON CHANNEL
hypothesis
2. TRANSIENT incompetence of the
sphincter due to stone lodgement
3. DUCTAL HYPERTENSION
DRUG INDUCED PANCREATITIS
 AZATHIOPRINE
 SULPHONAMIDES
 Na VALPROATE
 FUROSEMIDE
 6 MERCAPTO PURINE
 TETRACYCLINE
 STATINS
 DIGOXIN
METABOLIC FACTORS
 HYPERTRIGLYCERIDAEMIA
 HYPERCALCAEMIA
 SCORPION VENOM
MISCELLANEOUS
 PANCREATIC TUMOUR
 IDIOPATHIC
PATHOPHYSIOLOGY WILL DETERMINE THE
COURSE OF CLINICAL FEATURES
ACUTE PANCREATITIS ,INTRODUCTION, AETIOPATHOLOGY

ACUTE PANCREATITIS ,INTRODUCTION, AETIOPATHOLOGY