acute pancreatitis

Inflammation of the pancreas of abrupt onset, often accompanied by gallstones and alcohol ingestion.

Epidemiology
15-fold increase from 1960s to present, possibly due to widened diagnostic criteria, with 40 admissions/105/year.

Aetiology
See table.
Clinical findings
Abdominal pain, nausea, vomiting, hypotension.
Diagnosis
Contrast-enhanced CT (method of choice), ultrasonography.
Lab
Increased amylase, increased lipase.
Management
Supportive bowel rest with parenteral nutrition.

Prognotic instruments
Ranson’s criteria, modified Glasgow criteria, APACHE II.

Prognosis
25% have complications; 9% die of pancreatitis, sepsis, pulmonary failure, etc.
Acute pancreatitis aetiology
• Acute ischaemia—thrombosis, embolism, vasculitis, shock.
• Alcohol.
• Drugs—thiazide diuretics, azathioprine, oestrogens, sulfonamides, furosemide, methyldopa, pentamidine, procainamide.
• Gallstones—biliary tract disease.
• Genetic—defective genes encoding critical enzymes or proteins.
• Infection—mumps, coxsackieviruses, Mycoplasma pneumoniae.
• Metabolic defects—hypertriglyceridemia, hyperparathyroidism, hypercalcaemia.
• Obstruction—ampullary tumours, congenital defects of pancreas or biliary tree, parasites.
• Toxins—scorpion bites.
• Trauma—blunt, iatrogenic injury during heart surgery or ERCP.
• Vascular defects.
• Idiopathic.
Pathogenesis
Autodigestion of pancreas by inappropriately activated pancreatic enzymes—e.g., trypsin from trypsinogen—which activates other proenzymes. Possible pathways of enzyme activation:
(1) Pancreatic duct obstruction
Increased intrapancreatic ductal pressure results in accumulation of enzyme-rich interstitial fluid; lipase (one of the few enzymes secreted in activated form) results in fat necrosis, while injured tissues release cytokines, leading to local inflammation, oedema.
(2) Primary acinar cell injury—e.g., mumps, other viral infections, drugs, trauma, ischaemia, shock.
(3) Defective intracellular transport of proenzymes—aberrant cell packaging of enzymes has been shown to occur in alcohol and duct obstruction.

acute pancreatitis

Inflammation of the pancreas of abrupt onset, often with gallstones and alcohol ingestion Epidemiology 109,000 hospitalizations, 2251 deaths–US; 10-fold ↑ from 1960s to 1980s–reason unclear;
? alcohol abuse; ? widened diagnostic criteria; ± 250 admissions/10⁶ population/yr, higher in certain populations–eg, 4-22% in AIDS Pts Etiology Obstruction, toxins or drugs, trauma, metabolic defects, infection, vascular defects, idiopathic Diagnosis Abdominal pain, ↑ amylase, ↑ lipase, ultrasonography, contrast-enhanced CT Management Supportive, bowel rest with parenteral nutrition Prognosis Ranson's criteria, modified Glasgow criteria, APACHE II Prognosis 25% have complications, 9% die of pancreatitis, sepsis, pulmonary failure, etc. See Chronic pancreatitis.

a·cute pan·cre·a·ti·tis

(ă-kyūt' pan'krē-ă-tī'tis) Inflammation of the pancreas, frequently involving destruction of tissue by pancreatic enzymes. When severe, may lead to local necrosis, hemorrhage, and shock.

Fitz,

Reginald Heber, U.S. physician, 1843-1913. Fitz syndrome - Synonym(s): acute pancreatitis

单词	acute pancreatitis
释义	DictionarySeepancreatitis acute pancreatitis acute pancreatitis [ə′kyüt ′pan·krē·ə′tīd·əs] (medicine) A disease of unknown etiology that causes sudden liberation of activated pancreatic enzymes that digest the pancreatic parenchyma, leading to dissolution of fat and production of calcium soaps, and rupture of pancreatic vessels with resultant hemorrhage and shock. acute pancreatitis acute pancreatitis Inflammation of the pancreas of abrupt onset, often accompanied by gallstones and alcohol ingestion. Epidemiology 15-fold increase from 1960s to present, possibly due to widened diagnostic criteria, with 40 admissions/105/year. Aetiology See table. Clinical findings Abdominal pain, nausea, vomiting, hypotension. Diagnosis Contrast-enhanced CT (method of choice), ultrasonography. Lab Increased amylase, increased lipase. Management Supportive bowel rest with parenteral nutrition. Prognotic instruments Ranson’s criteria, modified Glasgow criteria, APACHE II. Prognosis 25% have complications; 9% die of pancreatitis, sepsis, pulmonary failure, etc. Acute pancreatitis aetiology • Acute ischaemia—thrombosis, embolism, vasculitis, shock. • Alcohol. • Drugs—thiazide diuretics, azathioprine, oestrogens, sulfonamides, furosemide, methyldopa, pentamidine, procainamide. • Gallstones—biliary tract disease. • Genetic—defective genes encoding critical enzymes or proteins. • Infection—mumps, coxsackieviruses, Mycoplasma pneumoniae. • Metabolic defects—hypertriglyceridemia, hyperparathyroidism, hypercalcaemia. • Obstruction—ampullary tumours, congenital defects of pancreas or biliary tree, parasites. • Toxins—scorpion bites. • Trauma—blunt, iatrogenic injury during heart surgery or ERCP. • Vascular defects. • Idiopathic. Pathogenesis Autodigestion of pancreas by inappropriately activated pancreatic enzymes—e.g., trypsin from trypsinogen—which activates other proenzymes. Possible pathways of enzyme activation: (1) Pancreatic duct obstruction Increased intrapancreatic ductal pressure results in accumulation of enzyme-rich interstitial fluid; lipase (one of the few enzymes secreted in activated form) results in fat necrosis, while injured tissues release cytokines, leading to local inflammation, oedema. (2) Primary acinar cell injury—e.g., mumps, other viral infections, drugs, trauma, ischaemia, shock. (3) Defective intracellular transport of proenzymes—aberrant cell packaging of enzymes has been shown to occur in alcohol and duct obstruction. acute pancreatitis Inflammation of the pancreas of abrupt onset, often with gallstones and alcohol ingestion Epidemiology 109,000 hospitalizations, 2251 deaths–US; 10-fold ↑ from 1960s to 1980s–reason unclear; ? alcohol abuse; ? widened diagnostic criteria; ± 250 admissions/10⁶ population/yr, higher in certain populations–eg, 4-22% in AIDS Pts Etiology Obstruction, toxins or drugs, trauma, metabolic defects, infection, vascular defects, idiopathic Diagnosis Abdominal pain, ↑ amylase, ↑ lipase, ultrasonography, contrast-enhanced CT Management Supportive, bowel rest with parenteral nutrition Prognosis Ranson's criteria, modified Glasgow criteria, APACHE II Prognosis 25% have complications, 9% die of pancreatitis, sepsis, pulmonary failure, etc. See Chronic pancreatitis. a·cute pan·cre·a·ti·tis (ă-kyūt' pan'krē-ă-tī'tis) Inflammation of the pancreas, frequently involving destruction of tissue by pancreatic enzymes. When severe, may lead to local necrosis, hemorrhage, and shock. Fitz, Reginald Heber, U.S. physician, 1843-1913. Fitz syndrome - Synonym(s): acute pancreatitis
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