Pathophysiology of Gallstone Formation and Pancreatitis Robert F. Schwabe olumbia.edu S.N.S
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1 Pathophysiology of Gallstone Formation and Pancreatitis Robert F. Schwabe olumbia.edu
2 - Gallbladder/Bile and Pancreas both are essential for digestion of food -A large percentage of the population have gallstones (up to 30% of people >50y) and about surgeries and $6 billion cost/year in the US - Gallbladder and Pancreas physiology are linked as gallstones cause a large percentage of acute pancreatitis cases
3 Pancreatic secretions and bile are required for digestion Bile: Emulsifica ation of fat Pancreatic secretions: -Digestion of proteins, carbohydrates and fat -Neutraliz zation of the acidic chyme
4 Bile - Secreted by hepatocytes - Transported through the biliary system - Stored and concentrated in the gallbladder - Released into duodenum after ingestion of food (mediated by CCK)
5 Bile composition Cholesterol Phospholipids Bile Salts (Lecithin) Miscellaneous (Pigment, Protein) 0.7% 4% H 2 0 1% 12% 84.3%
6 Bile salts are conjugated with glycine or taurine to increase their solubility at lower ph Primary bile salts Dehydroxylation Secondary bile salts Dehydroxylation
7 Important functions of bile 1. Emulsification of fats in the intestine 2. Cholesterol excretion a. Bile salts are generated from cholesterol l and their synthesis thus decreasess the cholesterol pool bchl b. Cholesterol lis excreted tdinto bile
8 Formation and secretion of bile acids 1. Synthesis ( g) Cholesterol Cyp7a 2. Enterohepatic ti circulation (5-10x daily) AB BC transporters ABCG11 ABCG11 Various proteins located at the bas solateral membrane that mediate transport of bile acids, cholesterol and pho ospholipids p into bile Pool =2-3g Bile acids ABCG11 Fecal loss g (equals hepatic synthesis) S.N.S
9 Why do we have a mechanismm for enterohepatic circulation of bile acids? Reabsorption and redelivery of bile acids allows to very quickly replenish the pool of bile acids in the liver/gallbladder llbl The digestive tract is prepared for the next meal within a relatively l short time.
10 FXR Bile The Nuclear salts is a sensor are receptors hepatoxic of bile FX ac cids XR at plays high and prevents an concentrations important bile acid role in bile salt toxicity metabolism Cholesterol Bile acids Cyp7a FXR Synthetic FXR Agonists (Moschetta et al, Nat Med 2004) ABCG11 Hepatocyte FXR stimulation: 1. Decreased bile salt synthesis 2. Increased bile salt secretion Lowers intracellular bile acid pool increasing bile acid secretion into bile may prevent gallstone formation
11 Secretion of cholesterol HDL SR-BI Synthesis LDL LDL-R Cholesterol l Export into Periphery (VLDL) Bi le ABCG5/8 acids
12 The nuclear receptor LXR is a cholesterol sensor and lowers intracellular cholesterol levels Cholesterol Cholesterol Bile acids Cyp7a ABCG5/8 LXR Bile acids LXR stimulation: 1. Increased bile salt synthesis decreases cholesterol 2. Increased cholesterol secretion ABCG5/8
13 Cholesterol requires bile salts for solubilization S.N.S
14 Excess cholesterol precipitates to form cholesterol crystals and stones
15 Composition of Gallbladder bile Composition of Gallbladder Bile Healthy controls Patients with Gallstones
16 Where do gallstone develop? Very large stones Unlikely Bile to ducts: pass into the duct but more likely to cause local problems -Constant tflow -Bile is not concentrated Smaller stones Can pass into the duct and cause biliary colic/cholestasis/ pancreatitis ludge Gallbladder: (viscous aggregate of -Stasis of bile -Bile is concentratedce rystals and mucus) an pass into the duct but is much ess likely to cause problems as it an easier pass the papilla S.N.S
17 Factors influencing the prevalence of gallstones Age under 30y 1-6% 50-60y 9-30% Female gender/ sex hormones Men under % Women under % Men 50-60y 9-22% Women 50-60y 16-30% Environmental and genetic factors Female Pima Indians >25y 73% Low prevalence in Asia and Africa Obesity Non-obese women 10% PREGNANCY 2. Trim 3. Trim 4-6w pp 5.1% 7.9% 10.2% Obese women 30% S.N.S
18 Cholesterol stones: - Great majority of all stones in the US (>80%) - either pure cholesterol stones or mixed stones (more th han 50% cholesterol content) 1 cm Mi Main contributing tibti factors: -Decreased bile acids Super -Increased biliary cholesterol -Gallbladder factors allowing for stasis/ nucleation rsaturation
19 Pigment stones: - much less common in US than Cholesterol stones - contain pigment = bilirubin 1 cm usually due to increased hemolyis -or due to decreased bilirubin conjugation Main causes S.N.S Chronic Hemolysis Decreased bilirubin conjugation (cirrhosis, bacterial infections) excess bilirubin decreased bilirubin solubility
20 x-ray Appearance of Gallstones Radio-opaque Radioluscent 27% = Cholesterol Stones 73% = Pigment Stones 83% = Cholesterol Stones 17% = Pigment Stones
21 Factors Favoring Cholesterol Gallstones SUPERSATURATION STASIS NUCLEATION Hepatic Production of Lith hogenic Bile A. Excess cholesterol secretion 1. Obesity 2. Estrogens 3. Crash diet 4. Genetic factors/ethnicity (Pimas) - Point Mutation in ABCA8 accounts probably for 10% of gallstones (Nat. Genetics 2007) S.N.S
22 Factors Favoring Cholesterol Gallstones Hepatic Production of Lithogenic Bile BD B. Decreased dsecretion of fbile Aid Acids 1. Decreased bile salt synthesis despite diminished pool, e.g. Cyp7a mutations (rare) 2. Decreased bile acid return to liver (ileal resection) Gallbladder Factors 1. Stasis (TPN, fasting, progestins) 2. Nucleation (increased mucopr roteins)
23 Natural History 80% of all gallbladder stones will never cause symptoms of Gallstones Ultrasound 1-4% of gallbladder stones/year cause symptoms (e.g. colic, pancreatitis, cholecystitis) Ultrasound Dilated Duct Int traductal stone (not always visible) ERCP
24 Schematic diagram for the management of gallstone disease Gallstones Asymptomatic Endoscopic retrograde cholangio- pancreatography p y( (ERCP) Follow-up Complicated Symptomatic Uncomplicated Laparosco opic Cholecyste ectomy +/-ERCP Ursodiol Good success -Visualize with biliary small Ch tree olesterol and stones Very high pancreatic recurrence ducts rate -Extract stones Only if contraindications for surgery: Observation Ursodiol Possibly emergency surgery S.N.S
25 SUMMARY GALLSTONES. Over 80% of gallstones are CHOLESTEROL stones caused by a ysbalance between cholesterol and bile acids in bile. FASTING (Gallbladder stasis), OBESITY (increased cholesterol ecretion) and ESTROGEN (increas sed cholesterol secretion) promote allstone formation. SMALLER GALLSTONE pass easier into the duct and are more ikely to cause symptoms (colic, pancreatitis, cholecystitis). 80% of gallstones remain unsymptomatic. Therapy of choice hi for symtopatic gallstone disease is laparoscopic holecystectomy S.N.S
26 PANCREAS PHYSIOLOGY
27 Pancreas macro- and microanatomy S.N.S
28 Major functional units ACINUS Digestive enzyme secretion (Trypsin, Elastase, Amylase, Lipase ) DUCTULE Water, bicarbonate secretion
29 HC0 3 concentration and ph increase with increased pancreatic secretion The increase in HC0 3 serves to buffer the acidic ph of food after it passes into the duodenum. Ion (me Eq/L) Meal-stimulated secretion 8.0 ph Secretory rate (ml/min) S.N.S
30 Bicarbonate secretion is regulated through hormonal and neural mechanisms Cephalic phase Food cues Dorsal Vagal Complex Gastric phase Distention ntestinal phase Vagal Afferents Vagal Efferents Ach Secretin duodenal ph<4.5 ph sensitive Secretin-releasing factor Secretin S-cells H 2 0, NaHC0 3 CFTR S.N.S
31 Regulation of Enzyme Secretion is mediated by Neural Mechanisms Cephalic phase Food cues Gastric phase Distention CCK-sensing Vagal Afferents Dorsal Vagal Complex Vagal Efferents Ach, VIP, GRP Intestinal phase CCK -RF Proteins, AA, FA CCK (I-cells) Digestive Enzymes S.N.S
32 Activation of pancreatic enzymes in the intestine SPIN Ent NK terokinase Trypsinogen Trypsinogen Trypsin Trypsin Trypsinogen Trypsin Chymotrypsinogen Chymotrypsin Proelastase 2 Mechanisms to prevent Procarboxyp autod peptidase digestion: -Trypsinogen activation Prophosp occurs pholipase outside of the pancreas -Pancreatic inhibitor prevents trypsinogen activation Procolipase Elastase Carboxypeptidase Phospholipase Colipase S.N.S
33 PATHOGENESIS OF PANCREATITIS Activation of pancreatic c enzymes within the pancreas and the resulting autodigestion is the most important mechanism that triggers pancreatitis
34 Classification of pancreatitis Functional and morphologic changes CHRONIC EtOH Outcome: Pain Endocrine insufficiency Exocrine insufficiency Time ACUTE RECURRENT e.g. sludge, SOD Outcome: Recovery or death ACUTE e.g. stone, EtOH Outcome: Recovery or death S.N.S
35 Acute Pancreatitis - Clinically severe - Typically starts with moderate to severe abdominal pain -Complications such as pancreatic necrosis, infection, shock and multi-organ failure develop in some patients
36 Etiology of Acut te Pancreatitis Alcoholic Biliary Idiopathi c Oth her Autoimmune Drug-induced Iatrogenic IBD-related Infectious Inherited Metabolic Neoplastic Structural Toxic Traumatic Vascular
37 Cellular Injury through Activated Enzymes Increased pressure Perturbed environment 1. Blockage of Secretion 2. Activation of Zymogens in Lysosymes (Cathepsin B) Lysosome 3. Organelle Damage and Cell Injury by Activated Enzymes Golgi Complex RER S.N.S
38 Cytokines Play an Important Role in Pancreatic Injury Pancreatic Acinar Cell Systemic complications Insult Cyt tokine prod duction Chemoattraction and activation Inflammation Cel ll Death Neutrophil Macrophage
39 Cytokines Mediate Systemic Complications Liver failure Liver ARDS Lu ungs Shock, Organ failure Microcirculation TNFα IL-1β IL-61 ICA AM-1 IL L-1β T NFα PAF Proinfla ammatory PAF Endothelin INOS ICAM-1
40 Local effects of inflammation and pancreas injury Pancreatic and peripancreatic necrosis Fat necrosis Fluid loss into third space
41 Chronic Pancreatitis - Chronic disease - Pain and malabsorption narethemain symptoms -Weight loss can also be due to food avoidance
42 Etiology of Chro onic Pancreatitis Cystic fibrosis Alcoholic Other Idiopathic Hereditary pancreatitis Hypertriglyceridemia y Autoimmune Fibrocalcific (Tropical)
43 Effects of Chronic Alc cohol on the Pancreas Calcification Fibrosis Decreased blood flow Direct toxic effects Cytotoxic lymphocytes Altered protein synthesis (unfavorable ratio of trypsinogen vs. inhibitors)
44 Hereditary Pancreatitis Spink
45 PANCREATITIS CLINICAL CONSIDERATONS
46 Laboratory parameters are crucial to establish the diagnosis of acute pancreatitis Amylase Lipase is and more Lipase specific are than typically Amylase highly and elevated remains in elevated Acute for Pancreatitis a longer perio od Other causes of hyperamylasemia and hyperlipasemia: Parotitis
47 MAGING DIAGNOSIS is important to judge severity and clinical course of pancreatitis Interstitial pancreatitis Necrotizing pancreatitis Higher rate of complications (bacterial infection, organ failure) and mortality If CT is performed within 24h of first symptoms, necrosis may not yet be present
48 PROGNOSIS OF ACUTE PANCREATITIS Admission Ranson s s severity scor re & mortality Age > 55 years WBC > 16,000 mm 3 Glucose > 200 mg/dl LDH > 350 IU/L AST > 120 IU/L Systemic disease During first 48h Hct decrease >10% BUN increase > 5 mg/dl Ca 2+ < 8 mg/dl PaO 2 < 60 mm Hg Base deficit > 4 meq/l Negative fluid balance > 6L Causative 100 Treatment: - Stone extraction in severe Most biliary patients pancreat with - (Cessation 80 of Alcohol intake) severe pancreatitis titis % 60 Supportive Treatment: Mortality - Enteral feeding 40 (nasogastric tube) - Intravenous 20hydration - Pain medication - Intubation 0in case 0 of to respiratory 2 3 to problems 5 6 to 8 9 to 11 Fat necrosis Score S.N.S
49 Acute Pancreatitis Complications Grey-Turner sign Pancreatic Ascites: No epithelial lining Amylase ARDS Obstructing Pseudocyst S.N.S
50 Acute Pancreatitis Complications Infected Necrosis Tr reatment + Anti biotic
51 Chronic Pancreatitis: Diagnostic relies on imaging gand functional tests x-ray and fecal fat have a low sensitivity to detect CP! (EUS) Amylase and Lipase are often within the normal range!! S.N.S
52 Chronic Pancreatitis: Diagnostic tests Imaging ERCP/EUS Most sensi itive Functional Secretin test CT Ultrasonogram Less sensitive Fecal chymotrypsin Serum trypsinogen Abdominal x-ray Least Fecal fat Blood glucose
53 Imaging of Chronic Pancreatitis Abdominal X-ray Abdominal Ultrasound CT scan ERCP S.N.S
54 Chronic Pain and Malabsorption/Malnutrition are the most common Symptoms of Chronic Pancreatitis
55 Exogenous proteases may not only improve maldigestion but also CCK release and pain in chronic pancreatitis Exogenous Protease Food Lesss pain Exogenous Proteases degrading g CCK-RF CCK CCK-RF cell
56 SUMMARY PANCREATITIS 1. ACUTE PANCREATITIS is a clinically severe disease mostly caused by EtOH and GALLSTONES 2. CHRONIC PANCREATITIS causes pain and malabsorption and ist most commonly caused by E toh 3. The diagnosis of ACUTE PANCREATITIS (but not CHRONIC Pancreatitis) is best made by det tection of elevated AMYLASE and LIPASE 4. Imaging (e.g. CT) can reveal severity of acute pancreatitis (interstitial vs. necrotic) 5. CHRONIC PANCREATITIS is diagnosed by imaging (x-ray, Ultrasound, CT, ERCP) or functional tests (secretin, fecal fat) S.N.S
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