Pancreatitis

Question 1

What is seen in the first 2 weeks of pancreatitis?

Answer 1

SIRS (systemic inflammatory response syndrome) = two or more abnormalities in the temperature, heart rate, respiration or WBC count NOT related to infection
Organ failure

Question 2

What is seen after 2 weeks in pancreatitis?

Answer 2

Sepsis and its complications

Question 3

What are some common causes of acute pancreatitis?

Answer 3

Gallstones (most common cause in US) 
Ethanol
Scorpion venom
Hyperlipidemia (triglycerides > 1000mg/dL) 
Azathioprine 
Viruses-mumps
Blunt or penetrating trauma
Pancreas Divisor 
CRTR and other genetic mutations

Question 4

What is one common genetic cause of acute pancreatitis?

Answer 4

Serine protease 1 (PRSS1) - recurrent AP in childhood/early adolescence
Mutation impairs the ability to control trypsin activity by allowing premature activation or inhibiting the destruction or elimination

Question 5

What are two other genetic causes of acute pancreatitis?

Answer 5

CFTR mutation –> production of more concentrated or acidic pancreatic juice –> ductal obstruction or altered acinar cell function

Serine protease inhibitor Kazal type 1 (SPINK1) –> encodes pancreatic secretory trypsin inhibitor –> binds and inhibits about 20% of trypsin activity

Question 6

What are some early acute changes common to acute pancreatitis?

Answer 6

Intraacinar activation of proteolytic enzymes 
Microcirculatory injury 
Inflammatory cytokines produced
Leukocyte chemoattraction
Increased vascular permeability 
Overwhelms normal protective mechanisms

Question 7

What is the common systemic response of acute pancreatitis?

Answer 7

SIRS
ARDS - phospholipase A digests lecithin 
Myocardial depression 
Renal failure - hypovolemia, hypotension
Bacterial translocation from gut d/t compromised gut barrier

Question 8

Explain how acute pancreatitis can lead to gallstones.

Answer 8

Ampulla obstruction due to stones –> reflux of bile into the pancreatic duct

Question 9

How does alcohol cause AP?

Answer 9

Increased effect of CCK on transcription factors
CCK also induces premature activation of zymogens
Generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters

Question 10

What are some things that may cause chemical injury to acinar cells leading to AP?

Answer 10

Triglycerides – release of free fatty acids damages acinar cells and pancreatic capillary endothelium
Medications – thiazides, sulfa drugs, azathioprine, valproic acid

Question 11

What are some common clinical manifestations of AP?

Answer 11

Acute onset, persistent, severe epigastric abdominal pain
Pain radiates to the back (50%)
Nausea and vomiting (90%)
No pain (5-10%)
Ileum can be present (decreased bowel sounds)

Question 12

What is Cullen’s Sign? Grey-Turner’s Sign?

Answer 12

Cullen’s Sign = Central intra-abdominal hemorrhaging

Grey-Turner’s Sign = Flanks, more severe, may have ARDS, renal failure

Question 13

What are some lab finding that help diagnose AP?

Answer 13

Amylase: elevated w/i 6-12 hours, short half life
Lipase: elevated w/i 4-8 hours, peaks at 24 hours, normal in 8-14 days

Question 14

What is needed to make a diagnosis of AP?

Answer 14

At least 2 of the following:

1. Constant epigastric or RUQ abdominal pain with radiation to the back, chest or flanks
2. Serum amylase and/or lipase > 3 times the upper range of normal
3. Characteristic abdominal imaging findings

Question 15

What is the best diagnostic tool for the pancreas?

Answer 15

Cat scan

Question 16

What are some possible complications of AP?

Answer 16

20% have local or systemic complications
Local complications = acute peripancreatic fluid collection ( psueudocysts (>4 week)
Acute necrotic collect – infection

Question 17

What is the treatment for AP?

Answer 17

Pain control 
Agressive IV fluids
Antibiotics if evidence of infection
Nutrition improves recovery 
Address underlying cause (i.e. if stone, removal)

Question 18

What are some causes of chronic pancreatitis?

Answer 18

Alcohol abuse
Cigarette smoking
Ductal obstruction (pancreas divisum)
Ampullarf obstruction
Autoimmune pancreatitis
Genetic pancreatitis

Question 19

What are some differences between AP and CP?

Answer 19

AP is usually painful, CP can be asymptomatic (20-45%)
Serum amylase and lipase may be normal or mildly elevated in CP
CP is patchy, AP is more diffuse

Question 20

How do proteinaceous ductal plugs lead to CP?

Answer 20

Increase pancreatic protein secretion –> plugs within ducts –> nidus for calcification –> stones within the ducts –> duct scarring and obstruction

Question 21

What are some clinical manifestations of CP?

Answer 21

Pancreatic insufficiency –> fat malabsorption, DM
Pain from pseudocysts (ductal disruption)
Bile duct/duodenal compression or infections from pseudocyst
Increased risk of pancreatic adenocarcinoma

Question 22

What is the treatment for CP?

Answer 22

Alcohol and smoking abstinence
Analgesics
Diabetes treatment
Pancreatic enzyme supplementation (may decrease pain and address steatorrhea) 
Decompressing of dilated pancreatic duct

Question 23

What is found in autoimmune pancreatitis?

Answer 23

IgG4 positive plasma cells in tissue
Elevated serum IgG4 levels in some patients
Can effect multiple organs

Question 24

How does a patient with autoimmune pancreatitis present?

Answer 24

Pancreatic mass that can mimic cancer
Mild abdominal pain +/- attacks of AP and CP
Pancreatic duct strictures