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GASTROENTEROLOGY > PANCREATITIS 1.2 > Flashcards

PANCREATITIS 1.2 Flashcards

1
Q

What is the management for hypertriglyceridemia in acute pancreatitis?

A

IV Insulin, control of diabetes, lipid-lowering agents (statins, fenofibrates), weight loss, and avoidance of lipid-raising drugs.

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2
Q

What nutritional therapy is recommended for acute pancreatitis?

A

Low-fat solid diet and early enteral nutrition (within 24 hours if symptoms improve).

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3
Q

What is the purpose of enteral nutrition in acute pancreatitis?

A

Maintains gut barrier integrity, limits bacterial translocation, is less expensive, and has fewer complications.

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4
Q

When should imaging be considered for local complications in acute pancreatitis?

A

If the patient shows clinical deterioration despite standard therapy.

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5
Q

What are the local complications of acute pancreatitis?

A

Necrosis, pseudocyst, pancreatic duct disruption, perivascular complications, and extrapancreatic infections.

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6
Q

What are the systemic complications of acute pancreatitis?

A

Pulmonary (e.g., ARDS), cardiovascular (e.g., hypotension), renal (e.g., acute tubular necrosis), metabolic (e.g., hyperglycemia), and CNS (e.g., psychosis).

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7
Q

What are the types of pancreatic fluid collections?

A

Acute necrotic collection, walled-off necrosis, and pancreatic pseudocyst.

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8
Q

What is the management for infected necrosis in acute pancreatitis?

A

Antibiotics with or without pancreatic drainage and/or necrosectomy.

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9
Q

What is the diagnostic method for pancreatic duct disruption?

A

MRCP or ERCP.

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10
Q

What is the treatment for pancreatic duct disruption?

A

Placement of a bridging pancreatic stent for at least 6 weeks.

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11
Q

What are the key perivascular complications in acute pancreatitis?

A

Splenic vein thrombosis with gastric varices, pseudoaneurysms, and portal or superior mesenteric vein thrombosis.

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12
Q

What is the imaging modality for perivascular complications?

A

Mesenteric angiography.

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13
Q

What percentage of hospital-acquired infections occur in acute pancreatitis?

A

0.2

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14
Q

What are the most common causes of recurrent acute pancreatitis?

A

Alcohol and cholelithiasis.

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15
Q

What are the infectious causes of pancreatitis in AIDS?

A

CMV, Cryptosporidium, and Mycobacterium avium complex.

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16
Q

What are the drug-related causes of pancreatitis in AIDS?

A

Pentamidine, TMP-SMX, and protease inhibitors.

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17
Q

What is the most effective treatment for pancreatic duct leaks?

A

Bridging pancreatic stents with or without parenteral nutrition and octreotide.

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18
Q

When is conservative management indicated for sterile necrosis?

A

When there is no clinical deterioration or signs of infection.

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19
Q

What are the follow-up care considerations for acute pancreatitis?

A

Management of diabetes, exocrine pancreatic insufficiency, and prevention of recurrent cholangitis.

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20
Q

What defines a pancreatic pseudocyst?

A

Persistent fluid collections after 4 weeks, with less than 10% requiring intervention.

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21
Q

What is the role of prophylactic antibiotics in necrotizing pancreatitis?

A

No role; empiric antibiotics are considered only for decompensated patients.

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22
Q

What are the metabolic complications of acute pancreatitis?

A

Hyperglycemia, hypertriglyceridemia, hypocalcemia, and encephalopathy.

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23
Q

What is Purtscher’s retinopathy in the context of acute pancreatitis?

A

Sudden blindness caused by microvascular occlusion.

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24
Q

What cardiovascular complications can mimic myocardial infarction in acute pancreatitis?

A

Nonspecific ST-T changes on ECG.

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25
Q

What is the management for splenic vein thrombosis in acute pancreatitis?

A

Embolization.

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26
Q

When should repeat imaging be performed in necrotizing pancreatitis?

A

To monitor for complications like thrombosis, hemorrhage, or abdominal compartment syndrome.

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27
Q

What is the primary treatment goal for recurrent acute pancreatitis?

A

Identifying and addressing the underlying cause, such as alcohol use or biliary tract disease.

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28
Q

What is the timeline for persistent fluid collections to be considered pseudocysts?

A

After 4 weeks of persistent fluid collections.

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29
Q

What are the clinical signs of pancreatic ascites?

A

Elevated amylase and lipase in ascitic fluid.

30
Q

What systemic marker indicates early feeding can begin in acute pancreatitis?

A

Improvement in abdominal pain, absence of nausea, and vomiting.

31
Q

How can hypertriglyceridemia trigger acute pancreatitis?

A

By causing excessive free fatty acid release, leading to pancreatic injury.

32
Q

What imaging finding differentiates walled-off necrosis from acute necrotic collections?

A

Walled-off necrosis develops a defined capsule over time, usually after 4 weeks.

33
Q

What drugs are used to manage metabolic complications like hyperglycemia in acute pancreatitis?

A

Insulin and, if needed, oral hypoglycemic agents.

34
Q

What is the mechanism of heparin in managing hypertriglyceridemia-induced pancreatitis?

A

Heparin releases lipoprotein lipase, which helps lower triglyceride levels.

35
Q

When is plasmapheresis used in hypertriglyceridemia-induced pancreatitis?

A

In severe cases unresponsive to conventional therapies.

36
Q

What is the pathophysiology of chronic pancreatitis?

A

Stellate cell activation leads to cytokine expression, extracellular matrix protein production, chronic inflammation, fibrosis, and destruction of exocrine and endocrine tissue.

37
Q

What are the cardinal manifestations of chronic pancreatitis?

A

Abdominal pain, steatorrhea, weight loss, diabetes mellitus, and pancreatic cancer.

38
Q

What is the most feared complication of chronic pancreatitis?

A

Pancreatic cancer.

39
Q

What is the TIGAR-O classification of chronic pancreatitis?

A

Toxic-metabolic, Idiopathic, Genetic, Autoimmune, Recurrent acute pancreatitis, Obstructive.

40
Q

What are toxic-metabolic causes of chronic pancreatitis?

A

Alcohol use, tobacco smoking, hypercalcemia, hyperlipidemia, and chronic renal failure.

41
Q

What are genetic causes of chronic pancreatitis?

A

Mutations in PRSS1, CFTR, CASR, CTRC, and SPINK1 genes.

42
Q

What are the two types of autoimmune pancreatitis?

A

Type 1 autoimmune pancreatitis (IgG4-related disease) and Type 2 autoimmune pancreatitis (idiopathic duct-centric chronic pancreatitis).

43
Q

What is the histological hallmark of Type 1 autoimmune pancreatitis?

A

Lymphoplasmacytic infiltrate, storiform fibrosis, and abundant IgG4-positive cells.

44
Q

What is the histological hallmark of Type 2 autoimmune pancreatitis?

A

Granulocytic epithelial lesions (GEL) without IgG4-positive cells.

45
Q

What are common imaging findings in Type 1 autoimmune pancreatitis?

A

Diffuse pancreatic enlargement, hypoechoic rim (capsule sign), and bile duct strictures.

46
Q

What are the Mayo Clinic HISORt criteria for diagnosing autoimmune pancreatitis?

A

Histology, Imaging, Serology (elevated IgG4), Other organ involvement, and Response to glucocorticoid therapy.

47
Q

What is the initial glucocorticoid therapy for autoimmune pancreatitis?

A

Prednisone 40 mg/day for 4 weeks, tapered by 5 mg per week.

48
Q

What are the key clinical features of chronic pancreatitis?

A

Abdominal pain, maldigestion symptoms (steatorrhea), fat-soluble vitamin deficiencies, metabolic bone disease, and diabetes mellitus.

49
Q

What is the best initial imaging modality for chronic pancreatitis?

A

Abdominal CT scan.

50
Q

What are typical findings on CT in chronic pancreatitis?

A

Pancreatic calcifications, dilated ducts, and an atrophic pancreas.

51
Q

What is the most sensitive functional test for chronic pancreatitis?

A

Secretin stimulation test.

52
Q

When does the secretin stimulation test become abnormal?

A

When ≥60% of pancreatic exocrine function is lost.

53
Q

What are complications of chronic pancreatitis?

A

Chronic pain, exocrine insufficiency, diabetes, splanchnic thrombosis, osteoporosis, biliary strictures, pseudocyst, and pancreatic cancer.

54
Q

What are causes of GI bleeding in chronic pancreatitis?

A

Peptic ulceration, gastritis, pseudocyst erosion, hemosuccus pancreaticus, and variceal bleeding.

55
Q

What are the treatment options for steatorrhea in chronic pancreatitis?

A

Pancreatic enzyme replacement (25,000-50,000 units of lipase per meal) and proton pump inhibitors for better absorption.

56
Q

What are the treatment options for abdominal pain in chronic pancreatitis?

A

Pregabalin, endoscopic therapy, celiac plexus block, and surgery for ductal decompression.

57
Q

What is the role of pancreatic enzyme therapy in abdominal pain?

A

It has no consistent benefit for pain relief.

58
Q

What endoscopic treatments are available for chronic pancreatitis?

A

Sphincterotomy, pancreatic duct stenting, stone extraction, and pseudocyst drainage.

59
Q

What is the role of smoking in chronic pancreatitis?

A

Smoking is an independent, dose-dependent risk factor that increases susceptibility to pancreatic autodigestion and fibrosis.

60
Q

What are the manifestations of exocrine pancreatic insufficiency in chronic pancreatitis?

A

Steatorrhea, malabsorption, and fat-soluble vitamin deficiencies (A, D, E, K).

61
Q

What genetic mutation carries the highest risk for chronic pancreatitis?

A

SPINK1 mutation increases risk 20-fold.

62
Q

What complications of chronic pancreatitis are associated with splanchnic thrombosis?

A

Variceal bleeding and pseudocyst formation.

63
Q

What metabolic bone diseases are associated with chronic pancreatitis?

A

Osteopenia and osteoporosis.

64
Q

What is the hallmark imaging feature of a pseudocyst?

A

A well-defined, fluid-filled sac in or around the pancreas.

65
Q

What is hemosuccus pancreaticus?

A

Arterial bleeding into the pancreatic duct, causing GI bleeding.

66
Q

What is the cornerstone of management for chronic pancreatitis?

A

Screening for and managing complications, as no therapies can reverse or delay disease progression.

67
Q

What imaging findings suggest pancreatic cancer in a patient with chronic pancreatitis?

A

Pancreatic mass, ductal obstruction, or atrophic pancreas on CT or MRI.

68
Q

What are clinical signs that should prompt suspicion of pancreatic cancer in chronic pancreatitis?

A

Abdominal pain, weight loss, high HbA1c, and new-onset diabetes.

69
Q

What is the most common cause of chronic pancreatitis in adults?

A

Alcohol use.

70
Q

What is the most common cause of chronic pancreatitis in children?

A

Cystic fibrosis.

71
Q

What are common symptoms of maldigestion in chronic pancreatitis?

A

Steatorrhea and weight loss.

72
Q

What cytokines are involved in pancreatic stellate cell activation?

A

TNF-alpha, IL-1, IL-6, and TGF-beta.

GASTROENTEROLOGY (5 decks)

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