Pancreatitis Flashcards
Epidemiology
Annual incidence of 4.9 to 35/100,000
Overall mortality of 5%
What is the complication time frame of acute pancreatitis?
First two weeks: Systemic Inflammatory Response Syndrome (SIRS), organ failure
After two weeks: Sepsis and its complications
What is SIRS?
2 or more abnormalities: temperature, HR, respiration, WBC count in the absence of infection
What are the various etiologies of acute pancreatitis?
Mechanical: Gallstones, Sludge
Toxic: Ethanol, scorpion venom
Metabolic: Hyperlipidemia (hypertriglyceremia), hypercalcemia
Drugs: Many but azathioprine most common
Infection: Mumps
Trauma: Blunt or penetrating injury
Congenital: Pancreas divisum (failure of duct fusal)
Genetic: CFTR or others
What percent of patients with gallstones develop AP?
What percent of AP cases due to gallstones?
How do gallstones result in AP?
3-7% of patients with gallstones develop acute pancreatitis (AP)
Responsible of 35-40% cases
Reflux of bile into the pancreatic duct due to the obstruction of the ampulla
Edema resulting from passage of a stone
What percent of alcoholics develop AP?
What percetn of AP is due to alcohol?
How does alcohol result in AP?
10% of alcoholics develop AP
30% of cases of AP in the US
Usually after many years of alcohol abuse
Increased effect of CCK on transcription factors
Premature activation of zymogens
Generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters
How high does hypertriglyceremia have to be to result in AP?
What percent of AP cases?
>1000
1-4% of AP cases
What is wrong in an annular pancreas?
What does it result in?
What is wrong in a pancreas divisum?
What does it result in?
Ring around the duodenum
Duodenal obstruction
Dorsal duct empties into minor papilla
Ventral duct empties in major papilla
Risk factor for recurrent AP can lead to CP
What causes chemical injury to acinar cells?
What causes infectious injury to acinar cells?
What causes mechanical injury of acinar cells?
Triglycerides: FFA damages acinar cells
Medications
CMV, Mumps
Seat belt trauma, posterior penetration of duodenal ulcer
What are the genetic causes of AP?
How does each cause AP?
Serine protease 1 (80% of hereditary pancreatitis unrelated to CF)
Recurrent acute to chronic
Trypsin activation within the pancreas
CFTR – Cystic Fibrosis
Concentrated secretion
Leads to ductal obstruction or altered acinar cell function
Serine protease inhibitor Kazal type 1 (SPINK1)
Mutation results in a pancreatic secretory inhibitor
Binds and inhibits 20% of trypsin activity
What are the early acute changes of AP?
Intraacinar activation of proteolytic enzymes
Generation of large amounts of active trypsin within pancreas
Vacuoles containing active trypsin rupture
Pancreatic autodigestion
What are the local changes involved in AP?
Microcirculatory injury: Damage to endothelium; Vasoconstriction, ischemia, hypoxia
Inflammatory cytokines produced
Leukocyte chemoattraction
Increased vascular permeability and injury: Induce thrombosis and hemorrhage, leading to necrosis
Overwhelms normal protective mechanisms
What are systemic changes involved in AP?
SIRS
ARDS: Phospholipase A digest lecithin (major surfactant component)
Myocardial depression due to vasoactive peptides
Renal failure due to hypovolemia and hypotension
Bacterial translocation from gut due to compromised gut barrier
Majority do not have systemic complications
What are the clinical manifestations for AP?
Acute onset of persistent, severe epigastric abdominal pain
Pain radiates to back in approximately 50% of cases (retroperitoneal)
Nausea and vomiting: 90% of patients
No pain in 5-10%
Ileus can be present
Intraabdominal hemorrhaging with ecchymosis
What are Cullen’s sign and Grey-Turner’s sign?
What do they increase the risk of?
Intrabdominal hemorrhaging with ecchymosis
Cullen’s Sign: Periumblical
Grey-Turner’s Sign: Flanks
Increased risk for systemic symptoms
