PANCREATITIS 1.2 Flashcards
What is the management for hypertriglyceridemia in acute pancreatitis?
IV Insulin, control of diabetes, lipid-lowering agents (statins, fenofibrates), weight loss, and avoidance of lipid-raising drugs.
What nutritional therapy is recommended for acute pancreatitis?
Low-fat solid diet and early enteral nutrition (within 24 hours if symptoms improve).
What is the purpose of enteral nutrition in acute pancreatitis?
Maintains gut barrier integrity, limits bacterial translocation, is less expensive, and has fewer complications.
When should imaging be considered for local complications in acute pancreatitis?
If the patient shows clinical deterioration despite standard therapy.
What are the local complications of acute pancreatitis?
Necrosis, pseudocyst, pancreatic duct disruption, perivascular complications, and extrapancreatic infections.
What are the systemic complications of acute pancreatitis?
Pulmonary (e.g., ARDS), cardiovascular (e.g., hypotension), renal (e.g., acute tubular necrosis), metabolic (e.g., hyperglycemia), and CNS (e.g., psychosis).
What are the types of pancreatic fluid collections?
Acute necrotic collection, walled-off necrosis, and pancreatic pseudocyst.
What is the management for infected necrosis in acute pancreatitis?
Antibiotics with or without pancreatic drainage and/or necrosectomy.
What is the diagnostic method for pancreatic duct disruption?
MRCP or ERCP.
What is the treatment for pancreatic duct disruption?
Placement of a bridging pancreatic stent for at least 6 weeks.
What are the key perivascular complications in acute pancreatitis?
Splenic vein thrombosis with gastric varices, pseudoaneurysms, and portal or superior mesenteric vein thrombosis.
What is the imaging modality for perivascular complications?
Mesenteric angiography.
What percentage of hospital-acquired infections occur in acute pancreatitis?
0.2
What are the most common causes of recurrent acute pancreatitis?
Alcohol and cholelithiasis.
What are the infectious causes of pancreatitis in AIDS?
CMV, Cryptosporidium, and Mycobacterium avium complex.
What are the drug-related causes of pancreatitis in AIDS?
Pentamidine, TMP-SMX, and protease inhibitors.
What is the most effective treatment for pancreatic duct leaks?
Bridging pancreatic stents with or without parenteral nutrition and octreotide.
When is conservative management indicated for sterile necrosis?
When there is no clinical deterioration or signs of infection.
What are the follow-up care considerations for acute pancreatitis?
Management of diabetes, exocrine pancreatic insufficiency, and prevention of recurrent cholangitis.
What defines a pancreatic pseudocyst?
Persistent fluid collections after 4 weeks, with less than 10% requiring intervention.
What is the role of prophylactic antibiotics in necrotizing pancreatitis?
No role; empiric antibiotics are considered only for decompensated patients.
What are the metabolic complications of acute pancreatitis?
Hyperglycemia, hypertriglyceridemia, hypocalcemia, and encephalopathy.
What is Purtscher’s retinopathy in the context of acute pancreatitis?
Sudden blindness caused by microvascular occlusion.
What cardiovascular complications can mimic myocardial infarction in acute pancreatitis?
Nonspecific ST-T changes on ECG.
What is the management for splenic vein thrombosis in acute pancreatitis?
Embolization.
When should repeat imaging be performed in necrotizing pancreatitis?
To monitor for complications like thrombosis, hemorrhage, or abdominal compartment syndrome.
What is the primary treatment goal for recurrent acute pancreatitis?
Identifying and addressing the underlying cause, such as alcohol use or biliary tract disease.
What is the timeline for persistent fluid collections to be considered pseudocysts?
After 4 weeks of persistent fluid collections.
What are the clinical signs of pancreatic ascites?
Elevated amylase and lipase in ascitic fluid.
What systemic marker indicates early feeding can begin in acute pancreatitis?
Improvement in abdominal pain, absence of nausea, and vomiting.
How can hypertriglyceridemia trigger acute pancreatitis?
By causing excessive free fatty acid release, leading to pancreatic injury.
What imaging finding differentiates walled-off necrosis from acute necrotic collections?
Walled-off necrosis develops a defined capsule over time, usually after 4 weeks.
What drugs are used to manage metabolic complications like hyperglycemia in acute pancreatitis?
Insulin and, if needed, oral hypoglycemic agents.
What is the mechanism of heparin in managing hypertriglyceridemia-induced pancreatitis?
Heparin releases lipoprotein lipase, which helps lower triglyceride levels.
When is plasmapheresis used in hypertriglyceridemia-induced pancreatitis?
In severe cases unresponsive to conventional therapies.
What is the pathophysiology of chronic pancreatitis?
Stellate cell activation leads to cytokine expression, extracellular matrix protein production, chronic inflammation, fibrosis, and destruction of exocrine and endocrine tissue.
What are the cardinal manifestations of chronic pancreatitis?
Abdominal pain, steatorrhea, weight loss, diabetes mellitus, and pancreatic cancer.
What is the most feared complication of chronic pancreatitis?
Pancreatic cancer.
What is the TIGAR-O classification of chronic pancreatitis?
Toxic-metabolic, Idiopathic, Genetic, Autoimmune, Recurrent acute pancreatitis, Obstructive.
What are toxic-metabolic causes of chronic pancreatitis?
Alcohol use, tobacco smoking, hypercalcemia, hyperlipidemia, and chronic renal failure.
What are genetic causes of chronic pancreatitis?
Mutations in PRSS1, CFTR, CASR, CTRC, and SPINK1 genes.
What are the two types of autoimmune pancreatitis?
Type 1 autoimmune pancreatitis (IgG4-related disease) and Type 2 autoimmune pancreatitis (idiopathic duct-centric chronic pancreatitis).
What is the histological hallmark of Type 1 autoimmune pancreatitis?
Lymphoplasmacytic infiltrate, storiform fibrosis, and abundant IgG4-positive cells.
What is the histological hallmark of Type 2 autoimmune pancreatitis?
Granulocytic epithelial lesions (GEL) without IgG4-positive cells.
What are common imaging findings in Type 1 autoimmune pancreatitis?
Diffuse pancreatic enlargement, hypoechoic rim (capsule sign), and bile duct strictures.
What are the Mayo Clinic HISORt criteria for diagnosing autoimmune pancreatitis?
Histology, Imaging, Serology (elevated IgG4), Other organ involvement, and Response to glucocorticoid therapy.
What is the initial glucocorticoid therapy for autoimmune pancreatitis?
Prednisone 40 mg/day for 4 weeks, tapered by 5 mg per week.
What are the key clinical features of chronic pancreatitis?
Abdominal pain, maldigestion symptoms (steatorrhea), fat-soluble vitamin deficiencies, metabolic bone disease, and diabetes mellitus.
What is the best initial imaging modality for chronic pancreatitis?
Abdominal CT scan.
What are typical findings on CT in chronic pancreatitis?
Pancreatic calcifications, dilated ducts, and an atrophic pancreas.
What is the most sensitive functional test for chronic pancreatitis?
Secretin stimulation test.
When does the secretin stimulation test become abnormal?
When ≥60% of pancreatic exocrine function is lost.
What are complications of chronic pancreatitis?
Chronic pain, exocrine insufficiency, diabetes, splanchnic thrombosis, osteoporosis, biliary strictures, pseudocyst, and pancreatic cancer.
What are causes of GI bleeding in chronic pancreatitis?
Peptic ulceration, gastritis, pseudocyst erosion, hemosuccus pancreaticus, and variceal bleeding.
What are the treatment options for steatorrhea in chronic pancreatitis?
Pancreatic enzyme replacement (25,000-50,000 units of lipase per meal) and proton pump inhibitors for better absorption.
What are the treatment options for abdominal pain in chronic pancreatitis?
Pregabalin, endoscopic therapy, celiac plexus block, and surgery for ductal decompression.
What is the role of pancreatic enzyme therapy in abdominal pain?
It has no consistent benefit for pain relief.
What endoscopic treatments are available for chronic pancreatitis?
Sphincterotomy, pancreatic duct stenting, stone extraction, and pseudocyst drainage.
What is the role of smoking in chronic pancreatitis?
Smoking is an independent, dose-dependent risk factor that increases susceptibility to pancreatic autodigestion and fibrosis.
What are the manifestations of exocrine pancreatic insufficiency in chronic pancreatitis?
Steatorrhea, malabsorption, and fat-soluble vitamin deficiencies (A, D, E, K).
What genetic mutation carries the highest risk for chronic pancreatitis?
SPINK1 mutation increases risk 20-fold.
What complications of chronic pancreatitis are associated with splanchnic thrombosis?
Variceal bleeding and pseudocyst formation.
What metabolic bone diseases are associated with chronic pancreatitis?
Osteopenia and osteoporosis.
What is the hallmark imaging feature of a pseudocyst?
A well-defined, fluid-filled sac in or around the pancreas.
What is hemosuccus pancreaticus?
Arterial bleeding into the pancreatic duct, causing GI bleeding.
What is the cornerstone of management for chronic pancreatitis?
Screening for and managing complications, as no therapies can reverse or delay disease progression.
What imaging findings suggest pancreatic cancer in a patient with chronic pancreatitis?
Pancreatic mass, ductal obstruction, or atrophic pancreas on CT or MRI.
What are clinical signs that should prompt suspicion of pancreatic cancer in chronic pancreatitis?
Abdominal pain, weight loss, high HbA1c, and new-onset diabetes.
What is the most common cause of chronic pancreatitis in adults?
Alcohol use.
What is the most common cause of chronic pancreatitis in children?
Cystic fibrosis.
What are common symptoms of maldigestion in chronic pancreatitis?
Steatorrhea and weight loss.
What cytokines are involved in pancreatic stellate cell activation?
TNF-alpha, IL-1, IL-6, and TGF-beta.
