The document discusses acute and chronic pancreatitis, including causes such as alcohol abuse, gallstones, and trauma. It describes clinical features such as severe epigastric pain and elevated serum amylase and lipase levels. Diagnostic tests include blood tests, imaging like CT scans and MRCP, and endoscopic ultrasound. Treatment depends on the severity and includes IV fluids, analgesics, antibiotics, and surgery for complications like pseudocysts or obstruction.

2. Alcohol abuse Biliary tract diseases Drugs Trauma Viral infections Metabolic disorders Connective tissue diseases

3. Idiopathic in 30% of acute pancreatitis 25 – 40% of chronic pancreatitis

4. Severe constant epigastric pain  back Elevated serum Amylase, Lipase levels Ascites, pleural effusion Hypercalcemia, hypocalcemia Hypertriglyceridemia (Serum amylase maybe normal) Chronic pancreatitis: Normal enzyme levels

5. Serum Amylase: rises within 24 hrs; remains elevated 1-3 days; 3x ULN; 85% of patients will have elevated amylase levels Amylase also found in salivary glands, liver, small intestines, kidneys and fallopian tubes Amylase elevated in CA of lungs, esophagus, breast, and ovary Lipase: single best enzyme

7. Plain radiography: 1. sentinel loop (localized ileus of jejunum) 2. air fluid levels 3. colon cut off sign (distension of transverse colon) 4. duodenal distension 5. mass (pseudocyst)

8. UGIS: widened C loop Ultrasonography: edema, inflammation, calcifications, cysts, mass lesions CT Scan EUS (Endoscopic Ultrasound) MRCP ERCP

9. Interstitial: mild and self-limiting Necrotizing: degree of necrosis correlates with the severity of clinical manifestations

10. Gallstones: 30-60% Alcohol: 15-30% Others

13. Initial Phase: Intrapancreatic digestive enzyme activation andacina cell injury Second phase: activation, chemoattraction, sequestration of neutrophils  intrapancreatic inflammation Third phase: due to the effects on the distant organs of activated proteolytic enzymes and cytokines  proteolysis, edema, insterstitial hemorrhage, vasgular damage, coag necrosis

14. Cellular necrosis  liberation of bradykinin, histamine and vasoactive substances  vasodilation, increased vascular permeability and edema  lungs (ARDS , SIRS), multiorgan failure

15. Pain: constant, severe, boring; epigastrium  back, chest, flanks: supine and relieved by trunk flexing and knees drawn up. Nausea, vomiting, abdominal distention Fever, tachycardia, hypotension Hypovolemia; shock Cullen’s sign Turner’s sign

16. Amylase: 3x ULN; return to N in 72 hrs; higher in gall stones Lipase: elevated for 7-14 days; higher in alcohol-related Leukocytosis Hyperglycemia Hypocalcemia Hyperbilirubinemia

17. Hypertriglyceridemia LDH, AST Alkaline phosphatase Hypoxemia

21. Self-limited in 85-90% Conventional measures: IV fluids, analgesics, colloids, no oral alimentation Role of antibiotics – controversial Somatostatin, H2 blockers, glucagon, steroids Resumption of feeding: decrease/resolution of pain, resolution of organ dysfunction, patient feels hungry

22. Chronic inflammation, fibrosis, progressive destruction of exocrine, and later endocrine function Complications: chronic pain, steatorrhea, DM

23. Alcohol: as little as <50g/d prolonged consumption Idiopathic: 15% genetic defects Clinical Features: 1. pain – related to food intake 2. maldigestion – diarrhea, steatorrhea, weight loss

25. Amylase and Lipase not usually elevated Secretin test: best sensitivity/specificity; abN when 60% of exocrine function is lost Radiography: calcifications Ultrasonography CT scans MRCP ERCP

27. Enzyme therapy to control diarrhea Octreotide – somatostatin analogue that inhibits pancreatic secretion; decrease pain in large-duct disease Endoscopic treatment: sphincterotomy, stenting, stone extraction, drainage of pseudocyst