Pancreatitis Flashcards
During the first two weeks of pantreatitis, what issues do we see?
What about after two weeks?
First two weeks: (SIRS), organ failure
–>SIRS: two or more abnormalities in the temperature, heart rate, respiration, or white bloodcell count not related to infection
After two weeks: sepsis and its complications
Causes of ACUTE panreatitis
Gall stones, alcohol, scorpion venom, Hyperlipidemia, cholesterol, viruses, trauma, pancres divisum, CFTR, or other genetics
ACUTE PANCREATITIS:
GALLSTONES
3-7% of patients with gallstones develop acute pancreatitis (AP), responsible for _____ of cases of acute pancreatitis
35-40%
Alcohol use and Acute pancreatits
• Alcohol
10% of alcoholics develop AP
30% of cases of AP in the United States
Usually after many years of alcohol abuse
TG and acute pancreatitis
Hypertriglyceridemia
> 1000 mg/dL
1-4% of AP cases
What is pancreas divisum?
Embryologic defect, pancrease forms ring aound the small intestine and blocks passage of food
The main and small duct dont fuse together
Genetic cause of Acute Pancreatitis
Serine protease 1 (PRSS1)
• Hereditary pancreatitis, recurrent AP in childhood/early adolescence
• Present in up to 80 % of with hereditary pancreatitisunrelated to CF
• Primary defense against pancreatitis is to control trypsin
activity, either by prevention of premature activation of
trypsinogen to trypsin, or by the destruction, inhibition,
or elimination of trypsin from the pancreas
Mutation impairs above step
Serine protease 1 (PRSS1)
• Cystic fibrosis transmembrane conductance regulator (CFTR) defect can lead to Acute Pancreatits
Mutation may result in production of :
Leads to ductal obstruction or _______ function
more concentrated or acidic pancreatic juice
altered acinar cell
Genetic cause of acute pancreatitis
Encodes a pancreatic secretory trypsin inhibitor
Binds and inhibits about 20 % of trypsin activity
Serine protease inhibitor Kazal type 1 (SPINK1)
• Inflammation of the pancreas; different etiologies but all same after?
after inciting event or pancreatitis begins
• Inciting event (varies) => early acute changes (similar) => systemic response
(similar)
Early acute changes in acute pancreatitis:
•______ activation of proteolytic enzymes
Intraacinar
IN acute pancreatitis:
We get Intraacinar activation of proteolytic enzymes: this leads to
• Generation of large amounts of active______ within pancreas
trypsin
What causes pancreatic autodigestion
• Vacuoles containing active trypsin rupture
Leads to activation of further trypsin, chymotrypsin, elastase
• Pancreatic autodigestion from intrapancreatic release of active enzymes
Key pathogeneis is acute pancreatitis
MIcrocirculatory injury
Inflammatory cytokines produced
Leukocyte chemoattraction (PMN)
increased vascular permeability and injury (leads to hemorrhage and necrosis)
–> overwhelms normal protective mechanisms
What happens from the systemic response in acute pahtogenesis?
- (SIRS)
- ARDS: phospholipase A digests lecithin, a major component of surfactant
- Myocardial depression due to vasoactive peptides
- Renal failure due to hypovolemia and hypotension
- Bacterial translocation from gut due to compromised gut barrier
How do gallstones cause acute pancreatitis?
reflux of bile to pancreatic duct d/t ampulla obstruction (stones)
edema occurs from passage of stone
How does alcohol cause acute pancreatits?
Increases effect of CCK on transcripton factors and induce premature activation of zymogens
generate more toxic metabolites
What ways can acinar cells be damaged and lead to acute pancreatitis?
Chemical injury: TGs release FFA that damage acinar cells and parncreatic capillary endothelium
INfectious injury to acinar cells: CMV or mumps
Mechanical injury to acinar cells: seat belt trauma or posterior penetration of duodenal ulcer
Pt comes in with perisitant, severe EPIgastric pain radiating to the back
She has been nauseous and vomitting. What could be the issue?
Acute Pancreatitis: pain radiates to back 50% of tim and 90% pt feel nauseus and vomit
Cullens sign and Grey-Turner sign are both severe echymossis can be caused by:
acute pancreatitis
What lab findings are there in acute pancreatitis?
Amylase: elevated w/in 6-12 hrs with short 1/2 life
LIpse: elevated 4-8 hours and pesaks at 24 and back to normal 8-14 days
What must be present to diagnose acute pancreatitis?
Presence of at least two of the following:
• Constant epigastric or right upper quadrant
abdominal pain with radiation to the back, chest, or flanks
• Serum amylase and/or lipase > 3 times the upper range of normal
• Characteristic abdominal imaging findings
What complications can we have with acute pancreatisis
w/in first 4 weeks
over 4 weeks
Acute peripancreatic fluid collection (< 4weeks)
pseudocysts (> 4 weeks)
Acute necrotic collection; Infection
Pancreatic pseudocyst present after 4 weeks and what is concerning about this complication of acute pancreatitis?
potential space for bacterial to grow and we can’t access this space with antibiotics
What do we do for treatement of Acute Pancreatitis
• Pain control
• Aggressive intravenous fluids; pt losing lots of fluids
• Antibiotics if evidence of infection
• Nutrition* helps a ton
• Address underlying cause
If stone: endoscopic removal or surgery
Causes of chornic pancreatitis
• Alcohol abuse
• Cigarette smoking
• Ductal obstruction
Pancreas divisum
• Ampullary obstruction
• Autoimmune pancreatitis
• Genetic pancreatitis
Pathogenesis of chronic pancreatitis
Progressive fibro-inflammatory process
resulting in permanent structural damage
What are three differences between Acute and Chronic Pancreatitis?
AP is usually painful, CP can be asymptomatic in 20-45%
Serum amylase and lipase may be normal or only mildly elevated in CP
CP is patchy, AP is more diffuse
How can chornic pancreatits result in duct scarring and obstruction?
Proteinaceous ductal plugs:
• Increased pancreatic protein secretion =>
plugs within ducts => nidus for calcification =>
stones within the ducts => duct scarring and obstruction
How do you diagnose chronic pancreatitis
imaging; pancreatic calcification, ductal dilation, enlargement of pancreas, fluid collection
How does chornic pancreatic insufficiency present?
• Pancreatic insufficiency
Fat malabsorption: > 90% of pancreatic function lost
Diabetes mellitus: late in the disease
• Pain from pseudocysts (ductal disruption)
What are long term complications of chronic pancretitis
Bile duct/duodenal compression or infections from pseudocyst
• Increased risk of pancreatic adenocarcinoma
Treatement for Chronic pancreatits
- Alcohol and smoking abstinence
- Analgesics
- Diabetes treatment
- Pancreatic enzyme supplementation
- May decrease pain
- Addresses steatorrhea
- Decompression of dilated pancreatic duct
What do we look for if we suspect autoimmune pancreatits?
• One form of IgG4-related disease
IgG4-positive plasma cells in tissue
Elevated serum IgG4 levels in some patients
Can affect multiple organs
What do you treat autoimmune pancreatitis with?
Treat with corticosteroids
- Pancreatic mass that can mimic cancer
- Mild abdominal pain +/- attacks of AP and CP
- Pancreatic duct strictures
AUTOIMMUNE PANCREATITIS
