Pancreatitis - Franco Flashcards
What is the overall mortality rate of acute pancreatitis?
Describe its features during the first two weeks
Describe its features after the first two weeks
5%
<2 weeks: SIRS and organ failure
>2 weeks: sepsis and its complications
List 10 general etiologies of acute pancreatitis
- Mechanical (gallstones, obstruction)
- Toxic (ethanol, scorpion venom)
- Metabolic (hyperlipidemia, hypercalcemia)
- Drugs (azathioprine, estrogen)
- Infection (mumps, hepatitis B, CMV, HIV)
- Trauma (blunt or penetrating abdominal injury)
- Congenital (pancreas divisum)
- Vascular (ischemia, polyarteritis nodosa)
- Miscellaneous (A1AT deficiency, ischemia)
- Genetic (CFTR)
What percentage of patients with gallstones develop acute pancreatitis?
What percentage of patients with pancreas divisum develop acute pancreatitis?
3-7%
<5%
Name and describe (3) genetic causes of acute pancreatitis
Serine protease 1 (PSS1)
- recurrent AP in childhood and early adolescence
- 80% of CF-unrelated hereditary pancreatitis
- PRSS1 is responsible for elimination and inhibition of trypsin in the pancreas
- Mutation impairs PRSS1, leading to AP
Cystic fibrosis (CFTR)
- Mutation results in the producted of concentrated pancreatic juice
- Leads to ductal obstruction or altered acinar cell function
Serine protease inhibitor Kazal type 1 (SPINK1)
- SPINK1 also encodes a pancreatic trypsin inhibitor (approximately 20% of trypsin activity)
Describe the early acute changes of acute pancreatitis
- Intra-acinar activation of proteolytic enzymes
- generation of large amounts of trypsin withink the pancreas
- Formation of vacuoles of active trypsin that eventually rupture, provoking additional activation of zymogens
- Pancreatic autodigestion
Why are diuretics contraindicated in AP?
patients get very volume depleted (hemorrhage, vascular injury, etc)
Give (5) examples of systemic responses to acute pancreatitis
- SIRS
- ARDS: PLA digests lecithin (component of surfactent) -> leads to hypoxia
- Myocardia depression (from vasoactive peptides)
- Renal failure (hypvolemia and hypotension)
- Bacterial translocation (due to compromised gut barrier)
Describe how gallstones might lead to acute pancreatitis
A gallstone may obstruct the ampulla of Vater
Bile refluxes into the pancreatic duct
Explain the role of alcohol in the development of acute pancreatitis
The mechanism is unclear but…
- Increased CCK transcription
- CCK induces premature activation of zymogens
- Alcohol also generates toxic metabolites, such as acetaldehyde and fatty acid ethyl esters
Describe the clinical manifestation of acute pancreatitis
- Acute onset of persistent epigastric pain, radiating to the back (50%)
- Nausea and vomiting
- Ileus (sometimes)
Describe:
Cullen’s Sign
Grey-Turner’s Sign
Both are signs of intra-abdominal hemorrhage
- Cullen’s sign: ecchymoses over the center of the abdomen
- Grey-Turner’s sign: ecchymoses bilaterally over the abdomen
Both are signs of intra-abdominal hemorrhage due to acute pancreatitis
Describe the two key laboratory findings seen in acute pancreatitis
Amylase: elevated within 6-12 hours, 10-hour half life
Lipase: elevated within 4-8 hours, peaks at 24 hours, returns to normal in 8-14 days
What findings are required for diagnosis of acute pancreatitis?
Presence of at least two of the following:
- Constant epigastric or RUQ pain with radiation to the back, chest, or flanks
- Serum amylase and/or lipase 3X upper range of normal
- Characteristic abdominal imaging findings (CT scan or ultrasound)
Describe the treatment approach for acute pancreatitis
- Pain control
- Aggressive IV fluids
- Abx (if evidence of infection)
- Nutrition (improves recovery)
- Address underlying cause (remove stones, if present)
Give several etiologies of chronic pancreatitis
- alcohol abuse
- cigarette smoking
- ductal obstruction (possibly pancreas divisum)
- ampullary obstruction
- autoimmune pancreatitis
- genetic pancreatitis
