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
Give (3) key differences between chronic and acute pancreatitis
- AP is painful, CP often asymptomatic
- Serum amylase and lipase may be normal or only mildly elevated in CP
- CP is patchy, whereas AP is more diffuse
What is the role of increased pancreatic protein secretion in chronic pancreatitis
- increased protein secretion creates ductal plugs in the pancreas
- the plugs serve as a nidus for calcification
- this creates stones in the ducts, leading to duct scarring and obstruction
Describe the clinical manifestations of chronic pancreatitis
- Pancreatic insufficiency (not seen in acute pancreatitis)
- fat malabsorption when 90% of pancreatic function is lost
- diabetes mellitus late in the disease (due to loss of islet cells)
- Pain from pseudocysts (ductal disruption)
Give two key complications of chronic pancreatitis
- compression or infection from pseudocysts
- increased risk of pancreatic adenocarcinoma
Describe the treatment strategy for chronic pancreatitis
- Analgesics for pain control
- Encourage alcohol and smoking abstinence
- Supplement pancreatic enzymes to address steatorrhea -> this may also reduce pain by decreasing demand on the pancreas itself
- Surgical decompression of dilated pancreatic duct
What is the treatment approach for autoimmune pancreatitis
give corticosteroids!
(but this is risky with concurrent infection)
Describe the clinical presentaiton of autoimmune pancreatitis
Pancreatic mass (mimics cancer)
mild abdominal pain with possible attacks of AP or CP
Pancreatic duct strictures
What is the most common cause of AP in the US?
Gallstones
Immunologically, what is observed in autoimmune pancreatitis?
IgG4+ plasma cells in the tissue
Elevated serum IgG4 is sometimes seen
May present in multiple organs (not just the pancreas)
