Etiology of chronic pancreatitis I. ALCOHOL Long-term alcohol abuse: Men 80g, women 40-50g/day for years Fatty food, coffee, smoking, concent

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1 Chronic pancreatitis Definition: Chronic pancreatitis Irreversible destruction of parenchyma Increase of the amount of connective tissue Signs of inflammation Signs of regeneration Decrease of exocrine and endocrine function Forms: 1. Obstructive chronic pancreatitis Diffuse atrophy and fibrosis Removing of obstruction improve the histological picture and function 2. Calcifying pancreatitis metabolic disorder Focal atrophy and fibrosis Segmental dilatation of pancreatic duct Protein plugs and intraductal stones 1

2 Etiology of chronic pancreatitis I. ALCOHOL Long-term alcohol abuse: Men 80g, women 40-50g/day for years Fatty food, coffee, smoking, concentrated form of alcohol- provoke progression Etiology of chronic pancreatitis Effect of alcohol I. Spasm of Sphincter Oddi Ductal destruction: decrease in HCO3 - concentration and volume, increased permeability (Ca duct) Protein plugs, stones irregular inflammation and fibrosis Increase of protein secretion (viscosity ) Defect of biosynthesis of lithostatin (protein matrix of stones) 2

3 Etiology of chronic pancreatitis Effect of alcohol II. Toxic-metabolic hypothesis Fatty degeneration of acinar cells (defect of lipid metabolism intracellular deposits of lipid stimulation of resting fibroblasts) Increased membrane lipid peroxidation acinar cell injury Theory of necrosis fibrosis sequence Interstitial fat necrosis perilobular fibrosis distort of intralobular ducts (stenosis and dilatation) hamper the normal flow protein plugs acinar cell necrosis Etiology of chronic pancreatitis II. Hereditary form Lack of lithostatin (autosomal dominant, incomplete penetration) III. Obstructive chr. Pancreatitis Stenosis of papilla Vateri (tu, scars, pancreas divisum) IV. Autoimmune pancreatitis Ab, Ig, Ly infiltration, association with other autoimmune diseases (Sjögren, PBC, IBD) V. Idiopathic chr. Pancreatitis 15-20% of all cases, genetic abnormality? Slow appearance of exocrine and endocrine dysfunction Pain is not common Atherosclerosis? 3

4 Etiology of chronic pancreatitis VI. Tropical Serin protease inhibitor Kazal type1mutation VII. Drug induced chr. Pancreatitis Phenacetin Antihypertensive drugs Anticonvulsant VIII. Hyperparathyroidism Diagnosis I. CLINICAL MANIFESTATIONS At the beginning the function is maintained and the pain dominates, later the symptoms of exocrine and endocrine insufficiency will become dominant. 4

5 I. PAIN- Dull girdle-likelike Recurring pain Diagnosis II. Consumption of alcohol new foci of necrosis edema increased pancreatic pressure Postprandial stenosis+secretion swelling increased pancreatic pressure Permanent pain Stenosis of duct (stones)- obstruction, swelling, tissue pressure microcirculation Damage of neurilemma of neurons Fibrosis around neurons Diagnosis III. II. MALDIGESTION- insufficiency of exocrine pancreatic function In alcoholics first LIPASE activity Steatorrhoea (fatty stinking stool) Lack of vitamins (soluble in fat) Long chain triglycerides maldigestion III. WEIGHT LOSS Maldigestion Postprandial pain Diabetes mellitus 5

6 Diagnosis IV. Tests of exocrine pancreatic function Direct tests Secretin Lund Indirect tests Diagnosis V. Imaging procedures I. US CT less invasive, less expensive Irregular echo pattern Dilated duct, enlargement, pseudocysta Not sensitive: early stages of chr.pancr. or cc. Sensitivity and specificity: nearly the same Meteorism doesn't disturb Diff. dg: CC - Chr pancr. 6

7 Diagnosis VI. Imaging procedures I. ERCP Most specific and most sensitive (not in early stages) Duct changes, stones, calcification protein plugs Diffdg cc chr. P. MRCP Endoscopic US detection of cc in early stages Complication of chr. pancreatitis Pseudocyst More frequently in alcoholics Spontaneous resolution is rare Main sign: pain Infection is rare Complication: rupture and fistula TH: surgical or endoscopical drainage (cysto-gastrostomy or cysto- duodenostomy) Ascites Leakage from a pseudocyst or disruption Dg elevated amylase and lipase concentration in the ascites fluid TH: Feeding by nasoenteral tube, Somatostatin Pancreatic drainage Resection 7

8 Complication of chr. pancreatitis Fistula Percutan drainage: n the skin: hyperemic opening with erosion, colorless fluid To the pleural space: pleural effusion To the peritoneal space : ascites Splenic vein thrombosis PAIN Conservative treatment Dietary recommendations Treatment Alcohol abstinence Small feeding with the restriction of fat Inhibition of pancreatic secretion Enzyme substitution, H2 rec. bl. Promoting of pancreatic juice excretion Spasmolytics, Nitrats Papillotomy, dilatation of pancreatic duct Treatment of pseudocyst (endoscopic, surgical) Celiac plexus blockade (infiltration with alcohol) Surgical treatment 8

9 Substitution Decrease of HCO - 3 secretion low ph in the duodenum Decreased solubility of bile acids Inactivation of pancreatic enzymes (especially amylase and lipase) TH: H2 receptors blockers, PPI Enterosolvent coating Proteolytic inactivation Chymotrypsin and trypsin inhibitor? Protein rich food Mixing with the food micropellet Trypsin inactivates colipase (connects lipase to micellar bile salts Kiindulás: Pancraes carcinoma 90%-ban a ductalis epithelsejtek (Mucin termelő adenocc 5%.ban acinus sejtek 5%-ban egyéb Localisatio: 1/3-a a fejből 1/3-a testből-farokból Tünetek: Fogyás Hasi fájdalom Icterus-Curvoiser tünet Diabetes mell. 9

10 Pancraes carcinoma Laboratóriumi eltérések: AP, Bi, LDH CA19-9, 9, CEA Diagnosis: Uh: echoszegény CT-dinamikus CT Kezelés Sebészi: palliativ - curativ Endoscopos interventio Chemotherapia: gemcitabine, oxaliplatin, 5 FU Irradiatio: környező szervek sugárérzékenyek Kiegészítő th: táplálás, fájdalomcsillapítás 10