Tavassoli,Alireza

1. Pancreas Tavassoli,Alireza

2. نام درس :بيمار يهاي پانكراساهداف • 1-بيماري هاي پانكراس رابشناسد • 2-عوامل سبب زاي بيماري هاي پانكراس را بشناسد • 3- راه هاي پيشگيري بيماري هاي پانكراس را بداند. • 4- نحوه مراقبت بيماري هاي پانكراس را فراگيرد. (Surveillance) • 5-عوامل خطرزاي بيماري هايپانكراس را بداند • 6- ويژگي هاي اپيدميولوژيك بيماري هاي پانكراس را بشناسد . • 7-روش هاي تشخیصی بيماري هاي پانكراس رابشناسد. • 8- روش هاي درمان را بداند.

3. neutralize chyme digestive enzymes hormones Normal Anatomy & Physiology

4. Exocrine Function BODY common bile duct TAIL HEAD pancreatic duct ampulla UNCINATE pancreatic enzymes

5. Enzyme Secretion acinus pancreatic duct microscopic view of pancreatic acini duodenum

6. Exocrine Stimulation • The moreproximal the nutrient infusion…the greater the pancreatic stimulation (dog studies) • stomach – maximal stimulation • duodenum – intermediate stimulation • jejunum – minimal / negligible stimulation • Elemental formulas tend to cause less stimulation than standard intact formulas • intact protein > oligopeptides > free amino acids • Intravenous nutrients (even lipids) do not appear to stimulate the pancreas

7. Acute Pancreatitis

8. Clinical Case • A man with acute onset abdominal pain • h/o alcohol intake • Or Gall stone

9. Acute PancreatitisDefinition • Acute inflammatory process involving the pancreas • Usually painful and self-limited • Isolated event or a recurring illness • Pancreatic function and morphology return to normal after (or between) attacks

10. Acute PancreatitisEtiology

11. Cholelithiasis Ethanol abuse Idiopathic Medications Hyperlipidemia ERCP Trauma Pancreas divisum Hereditary Hypercalcemia Viral infections Mumps Coxsackie virus End-stage renal failure Penetrating peptic ulcer Acute PancreatitisAssociated Conditions

12. Acute PancreatitisCausative Drugs • AIDS therapy:pentamidine ,didanosine • Anti-inflammatory:sulindac, salicylates • Antimicrobials:metronidazole, sulfonamides, tetracycline, nitrofurantoin • Diuretics:furosemide, thiazides • IBD:sulfasalazine, mesalamine • Immunosuppressives:azathioprine, 6-mercaptopurine • Neuropsychiatric:valproic acid • Other: calcium, estrogen, tamoxifen,

13. Pancreas divisum

14. Hereditary Pancreatitis • Autosomal dominant with 80% phenotypic penetrance • Recurrent acute pancreatitis, chronic pancreatitis, and 50-fold increased risk of pancreatic cancer

15. PancreatitisBackground • Potentially fatal • Mortality – 10-15% • Necrosis determines the prognosis

16. Background • Mild AP (no necrosis) – 0% • Sterile necrosis – 10% • Infected necrosis – 25% • Overall mortality: 10-15%

17. What do you think? • Amylase or lipase • Ultrasound or CT scan • If yes, When? • ICU or medical ward • Enteral nutrition or TPN • Antibiotics • ERCP • Surgery

18. prematureenzyme activation Acute PancreatitisPathogenesis acinar cell injury failed protectivemechanisms

20. Acute PancreatitisPathogenesis premature enzyme activation autodigestion of pancreatic tissue local vascular insufficiency activation of white blood cells release ofenzymes into the circulation localcomplications distantorgan failure

21. Acute PancreatitisPathogenesis SEVERITY Mild Severe • STAGE 1: Pancreatic Injury • Edema • Inflammation • STAGE 2: Local Effects • Retroperitoneal edema • Ileus • STAGE 3: Systemic Complications • Hypotension/shock • Metabolic disturbances • Sepsis/organ failure

22. Pathophysiology of necrosis infection h/ h/

23. PancreatitisClinical Presentation • Pain:Steady & severe in nature; located in the epigastric or umbilical region; may radiate to the back. Worsened by lying supine; may be lessened by flexed knee, curved-back position. • Vomiting:Varies in severity, but is usually protracted, worsened by ingestion of food or fluid. Does not relieve the pain. Usually accompanied by nausea.

24. Pancreatitiscon’t…… • Fever: Rarely exceeds 39 C. • Abdominal Finding:Rigidity, tenderness, guarding, distended Abd, decreased or absent peristalsis and paralytic ileus.Fatty stools-(steatorrhea) • Laboratory Finding:Elevation of WBC count- 20-50,000. lipase and amylase(5 to 40 times); elevated(glucose, bilirubin, alkaline phosphatase.,Urine amylase).Abnormal low serum CA, Na & Mg.-due to dehydration. Binding of Ca in areas of fat necrosis.

25. Acute Pancreatitis

26. Acute Pancreatitis

27. Acute Pancreatitis

28. Acute Pancreatitis

34. Acute PancreatitisDifferential Diagnosis • Choledocholithiasis • Perforated ulcer • Mesenteric ischemia • Intestinal obstruction • Ectopic pregnancy

35. Acute PancreatitisDiagnosis • Symptoms & Signs • Abdominal pain • Laboratory • Elevated amylase or lipase • > 3x upper limits of normal • Imaging • Abnormal sonogram or CT

36. Acute PancreatitisDiagnosis • EtOH: history • Gallstones: abnormal LFTs & sonographY • Hyperlipidemia: lipemic serum, Tri>1,000 • Hypercalcemia: elevated Ca • Trauma: history • Medications: history

37. Abdominal Exam • Abdominal tenderness and rigidity • Bowel sounds decreased • Palpable upper abdominal mass Acute fluid collections and pseudocysts • Skin Exam • Erythematous skin Nodule (Subcutaneous Fat Necrosis) • Cullen's Sign (periumbilical discoloration) • Turner's Sign (flank discoloration) * due to exudation of blood-stained fluid into the subcutaneous tissue, usually 72 h into the illness.

39. Acute PancreatitisClinical Manifestations PANCREATIC PERIPANCREATIC Adjacent viscera: SYSTEMIC Mild: edema, inflammation, fat necrosis Severe:phlegmon, necrosis, hemorrhage, infection, abscess, fluid collections Retroperitoneum, perirenal spaces, mesocolon, omentum, and mediastinum ileus, obstruction, perforation Cardiovascular: hypotension Pulmonary: pleural effusions, ARDS Renal: acute tubular necrosis Hematologic: disseminated intravascular coag. Metabolic:hypocalcemia, hyperglycemia

40. Serum Amylase elevated Nonspecific Returns to normal in 48-72 hours Normal amylase does not exclude pancreatitis Level of elevation does not predict disease severity Serum Lipase elevated Specific for pancreatic disease Returns to normal in 7-14 days Diagnosis: Biochemical

41. White Blood Cells increased to 15k-20k Hypertriglyceridemia (15%) liver Function Tests (ALP) (AST) ,elevated (LDH) elevated (Poor prognosis) Hyperglycemia Albumine (Poor prognosis) Serum Electrolytes Hypocalcemia (25%) Diagnosis: Biochemical

42. Another criteria often used to assess the severity of pancreatitis is the (APACHE-II) . Acute Physiology And Chronic Health Evaluation age and vital signs Specific laboratory parameters, Chronic health status The main advantage is the immediate assessment of the severity of pancreatitis. A score of eight or more at admission is usually considered indicative of severe disease

44. Predictors of Severity • Why are they needed? • Appropriate triage & therapy • compare results of studies of the impact of therapy • When are they needed? • optimally, within the first 24 hours • Which is the best?

45. AT ADMISSION Age > 55 years WBC > 16,000 Glucose > 200 AST > 250 IU/L LDH > 350 IU/L WITHIN 48 HOURS HCT drop > 10% BUN > 5 Arterial PO2 < 60 mm Hg Base deficit > 4 mEq/L Serum Ca < 8 Fluid sequestration > 6L Ranson CriteriaAlcoholic Pancreatitis Number <2 1% 3-4 16% 5-6 40% 7-8 100% Mortality

46. Glasgow CriteriaNon-alcoholic Pancreatitis • WBC > 15,000 • Glucose > 180 • BUN > 16 • Arterial PO2 < 60 mm Hg • Ca < 8 • Albumin < 3.2 • LDH > 600 U/L • AST or ALT > 200 U/L

47. CT Severity Index Balthazar et al. Radiology 1990.

48. Useful markers of severe disease. • Pleural effusion • BMI (High body mass index) • Necrosison contrast-enhanced CT-SCAN • CRPlevel greater than 150 mg/L at 48 h • Infection of the necrotic tissue after the first week of illness is the major determinant of later outcome.

49. Pancreatic necrosis

50. CT-guided percutaneous fine-needle aspiration of the pancreatic tail