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GI > 16. Pancreas: Acute, Chronic, and AI Pancreatitis > Flashcards

16. Pancreas: Acute, Chronic, and AI Pancreatitis Flashcards

1
Q

What is the annual incidence for acute pancreatitis?

Overall mortality

A

4.9 to 35 per 100,000

5%

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2
Q

What are the main causes of mortality from AP in the first two weeks?

A

SIRS: systemic inflammatory response syndrome

Organ failure

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3
Q

What is the definition of SIRS?

A

Two or more abnormalities in the temperature, HR, respiration, or WBC count NOT related to infection

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4
Q

What is the main cause of mortality from AP after the first two weeks?

A

Sepsis and its complications

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5
Q

What are the main causes of AP?

A 
Gallstones ***
Smoking
Alcohol
Hypertriglyceridemia
Pancreas divisum
Autoimmune pancreatitis 
Hypercalcemia
Post-ERCP
Genetic
Intraductal papillary nucinous neoplasm and pancreatic cancer
Drugs
Trauma
Ischemia
Pregnancy
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6
Q

What is the most common cause of AP in the world? (25-40% of all cases)

A

Gall stones

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7
Q

What % of people with gallstones develop pancreatitis?

A

3-7%

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8
Q

What % of alcoholics develop pancreatitis? What % of cases in the US?

A

10%
30%
**usually after MANY years of alcohol abuse

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9
Q

What level of TGs is a RF for AP? What % of AP cases?

A

> 1000 mg/dl

1-4% of AP cases

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10
Q

What is pancreas divisum?

A

Congenital condition where the dorsal and ventral drainage is separate and the major drainage is through the minor papilla

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11
Q

What % of people with pancreas divisum develop pancreatitis?

A

Less than 5% (not a major risk factor)

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12
Q

Why is risk for pancreatitis increased post-ERCP (Endoscopic retrograde cholangiopancreatography)

A

Pancreatic duct can be disrupted due to proximity to the bile duct
**pancreatitis in 3-5% of ERCPs w/o manometry

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13
Q

What are four mutations that can increase the risk for pancreatitis?

A
  1. PRSS1 (Serine protease 1)
  2. CFTR (cytic fibrosis transmembrane conductance regulator)
  3. SPINK1 (serine protease inhibitor Kazal type 1)
  4. CTRC (Chymotrypsin C)
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14
Q

How does alcohol act as an inciting event for AP?

A
  1. Increased effect of CCK on activating TFs, NF-kB, and protein-1
  2. Acetaldehyde and ox stress activate pancreatic stellate cells
  3. Generation of acetalehyde and and fatty acid ethyl esters
  4. Sensitization of acinar cells to premature activation of zymogens by CCK
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15
Q

How do gallstones act as an inciting event for AP

A
  1. Reflux of bile into the pancreatic duct

2. Ampullary obstruction from stones or edema

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16
Q

How does hypertriglyceridemia act as an inciting event for AP?

A

Free fatty acid release by pancreatic lipase

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17
Q

How do genetics act as inciting events for AP?

A

Premature activation of pancreatic zymogens
- CTFR gene mutations, more concentrated and acidic pancreatic juice production -> ductal obstruction or altered acinar cell function

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18
Q

What are the main early acute changes in AP that all inciting events lead to?

A
  1. Intraacinar activation of proteolytic enzymes
  2. Microcirculatory injury
  3. Leukocyte chemoattraction
  4. Release of cytokines and oxidative stress
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19
Q

What does intraacinar activation of proteolytic enzymes involve?

A
  1. Generation of large amounts of active trypsin within the pancreas
  2. Vacuoles containing active trypsin rupture
  3. Overwhelming of natural defense mechanisms
  4. Pancreatic autodigestion from intrapancreatic release of active enzymes
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20
Q

What are the normal defense mechanisms that are overwhelmed in the setting of intraacinar activation of proteolytic enzymes?

A
  1. Pancreatic secretory trypsin inhibitor
  2. Autolysis of prematurely activated trypsin
  3. Mesotrypsin and enzyme Y lysis of trypsin
  4. Nonspecific antiproteases (A1AT, alpha2 macroglobulin)
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21
Q

What is involved in the microcirculatory injury seen in early acute changes in AP

A
  1. Damage of vascular endothelium and pancreatic interstitium
  2. Vasoconstriction, capillary stasis, ischemia, and decreased oxygen saturaiton
  3. Increased vascular permeability and pancreatic gland swelling
  4. Possible role of ischemia-reperfusion injury
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22
Q

What is involved in leukocyte chemoattraction seen as an early acute change in AP?

A

Complement activation and C5a release

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23
Q

What is involved in release of cytokines and oxidative stress as early acute changes in AP?

A 
TNF
IL-1, 6, 8
Prostaglandins, PAF, leukotrienes 
Proteolytic and lipolytic enzymes 
Reactive oxygen metabolites
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24
Q

What are the components of the systemic response in AP?

A
  1. SIRS
  2. Renal failure
  3. Myocardial depression
  4. Bacterial translocation from the gut
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25
Q

What are the clinical manifestations of AP?

A 
Acute onset of persistent, severe epigastric abdominal pain
Pain radiating to back in 50% of cases
Nausea and vomiting in 90% of cases 
No pain in 5-10% of cases 
Ileus can be present (gut hypomotility)
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26
Q

What are the laboratory findings in AP?

A
  1. Amylase elevated in 6-12 hours

2. Lipase elevated in 4-8 hours, peaks at 24

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27
Q

When does lipase return to normal after AP?

A

8-14 days

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28
Q

What are two inflammatory markers that will rise along with amylase and lipase in AP?

A

CRP

Leukocytosis

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29
Q

What is the best way to look for the MCC of AP?

A

Abdominal ultrasound: evaluate for gallstones in the gallbladder (cholelithiasis) and bile duct (choledocholithiasis)
**visualization can be obscured by bowel gas

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30
Q

What modality is good for detecting necrosis related to AP but NOT gallstones?

A

CT

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31
Q

What has a higher sensitivity to early AP than CT, with a better visualization of the bile duct and pancreatic duct?

A

MRI

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32
Q

Diagnosis of AP required at least 2 of the following:

A
  1. Constant epigastric or LUQ pain with radiation to the back or flanks
  2. Serum amylase and/or lipase > 3 x the upper range of normal
  3. Characteristic abdominal imaging findings
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33
Q

What % of people with AP have local or systemic complications?

A

20%

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34
Q

What are the two main local complications or AP?

A

Acute peripancreatic fluid collection ( pseudocysts (>4wk)

Acute necrotic collection ( walled off necrosis (>4wk)

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35
Q

What are the main systemic complications of AP?

A

SIRS

Organ failure–acute respiratory failure, shock, renal failure

36
Q

What is the classification of AP?

A

Mild: absence of organ failure and local/systemic complications
Moderate: transient organ failure resolving in 48 hr and/or local or systemic complications w.o organ failure over 48 hr
Severe: Failure of one or more organs over 48 hr

37
Q

What are the components of AP treatment?

A
  1. Pain control
  2. IV fluids
  3. Nutrition
  4. ECRP
  5. Cholecystectomy for gallstone AP
  6. Endoscopic necrosectomy or surgery
  7. Rectal indomethacin to prevent post-ERCP pancreatitis
  8. Pancreatic stint
38
Q

What is an acute peripancreatic fluid collection after 4 weeks?

A

Pseudocysts

39
Q

What is aggressive IV hydration most beneficial in AP?

A

Early hydration in the first 12-24 hours

40
Q

What is an acute necrotic collection called after 4 weeks?

What is preferred to normal saline for AP?

A

Walled off necrosis

Lactated Ringer’s solution–less SIRS due to less bicarb

41
Q

What type of nutrition is preferred in AP?

A

Enteral over parenteral

**avoid probiotics

42
Q

What should be preformed within 24 hr of admission for AP and acute cholangitis?

A

ERCP

*not needed in most patients with gallstone pancreatitis with no evidence of ongoing biliary obstruction

43
Q

What should be given after ERCP to prevent pancrreatitis?

A

Rectal indomethacin

44
Q

What is the role of a pancreatic stint post-ERCP?

A

Allows the pancreas to drain and prevents inflammation from blocking the drainage

45
Q

What are the etiologies for CP?

A
  1. Constant alcohol abuse
  2. Cigarette smoking
  3. Ductal obstruction
  4. Ampullary obstruction
  5. AIP
  6. Idiopathic
  7. Genetic
  8. Tropical
  9. Congenital
46
Q

What gene mutation causes hereditary acute pancreatitis, or recurrent AP in early childhood?

A

PRSS1 (serine protease 1)

47
Q

What are the three gene variants assocaited with CP?

A

SPINK1
CFTR
PRSS1

48
Q

What gene variant is associated with hereditary chronic pancreatitis, with an autosomal dominant pattern of inheritance?

A

PRSS1

49
Q

Hereditary pancreatitis from PRSS1 mutation causing CP has an increased risk for:

A

pancreatic cancer, beginning in the 50s

50
Q

Where is tropical pancreatitis found? Who is affected?

A

South india
Children affected
**Cassava fruit implicated

51
Q

What are two congenital causes of CP?

A

Pancreas divisum

Biliary cysts

52
Q

What is the pathogenesis of CP?

A
  1. Progressive fibroinflammatory process resulting in permenant structural damage
  2. Proteinaceous ductal plugs
  3. ischemia
  4. Autoimmune
  5. Decreased antioxidants
53
Q

What are the main differences between AP and CP?

A

AP painful, CP can be asymptomatic
Serum amylase and lipase tend to be normal in CP
CP is patchy, AP is more diffuse

54
Q

What causes the proteinaceous ductal plugs that can cause CP? Result?

A 
Increased pancreatic protein secretion
Plugs in ducts
Nidus for calcification 
Stones in ducts 
Duct scarring and obstruction
55
Q

What is likely to perpetuate rater than initiate CP?

A

Ischemia

56
Q

What are the main clinical manifestations of CP?

A
  • Abdominal pain after eating, most continous later in course (no pain in 20-45% of patients)
  • Pancreatic insufficiency
57
Q

What are the two main components of pancreatic insufficiency seen with CP, starting with the one seen first?

A
  1. Fat malabsorption: seen when over 90% of the pancreatic function is lost
  2. Diabetes mellitus: late in disease
58
Q

What is the presentation of fat malabsorption?

A

Steatorrhea: greasy, foul smelling stools

59
Q

When is it more common to get diabetes mellitus as a consequence of CP?

A

Chronic, calcifying disease

Family hx of diabetes

60
Q

What imaging modalities are used for CP?

A

Abdominal plain films–see pancreatic calcifications

Abdominal ultrasound, CT, MRI: calcifications, ductal dilation, enlargement of the pancreas, fluid collections

61
Q

What imaging finding is pathopneumonic for CP?

A

Calcifications in the pancreas

62
Q

What is DIRECT pancreatic function testing?

A

Stimulation of the pancreas with a meal (Lundh test) or horomones (secretin or CCK)
Duodenal fluid collected to quanitfy pancreatic secretory content (enzymes, bicarb)
**DONE RARELY

63
Q

What do indirect pancreatic function testing generally measure?

A

Consequences of pancreatic insufficiency

64
Q

What is measured as INDIRECT pancreatic function tests?

A
  1. Fecal elastase and chymotrypsin (both remain stabile in transit, but elastase more so) **
  2. Serum trypsinogen: less sensitive and specific without ADVANCED exocrine insufficiency
  3. Fecal fat
  4. Secretin MRI
  5. Pancreolauryl test
  6. 13C breath test
65
Q

How does the pancreolauryl test work (indirect pancreatic function test)?

A

Ingestion of fluorescein dilaurate with breakfast
Cleaved in proportion to amt of pancreatic cholesterol esterase
Measure the fluorescein excreted in the urin

66
Q

How does the 13C breath test work (indirect pancreatic function test)?

A

Ingested 13C marked substances are hydrolyzed in proportion to the amt of pancreatic lipase-> released as 13CO2 by the lungs

67
Q

Why is CP difficult to diagnose?

A
  1. Laboratory studies and imaging are normal early
  2. Pancreatic calcifications, steatorrhea, and diabetes mellitus are usually seen late in disease
  3. Can be difficult to distinguish from pancreatic cancer
68
Q

What is a ductal disruption that is usually asymptomatic, but can expand and become infected? (seen in 10% of CP patients)

A

Pseudocyst

69
Q

What is the treatment of pseudocytes from CP?

A

Watchful waiting
Endoscopic drainage
Surgical drainage

70
Q

What causes bile duct and/or duodenal obstruction in 5-10% of CP patients

A

Extrinsic comperssion from inflammation and fibrosis in the pancreatic head or pseudocyst

71
Q

What is the treatment for bile duct and/or duodenal obstruction

A

ERCP
Surgery
Surgical or endoscopic psuedocyst drainage

72
Q

How do you treat a pancreatic fistula that may result from CP?

A

Octreotide
ERCP for pancreatic stint placement
Surgery

73
Q

How do you treat splenic vein thrombosis that can result from CP?

A

Splenectomy

74
Q

What is the effect of a pseudoaneurysm (blood leakage from an artery into surrounding tissue) as a complication of CP?

A

Can affect blood vessels near the pancreas (splenic, hepatic, gastroduodenal)

75
Q

What is the treatment for pseudoaneurysm?

A

Angiography with embolization

76
Q

What are the effects of pancreatic enzyme supplimentation in the tx of CP?

A
  1. May decrease pain by decreasing CCK release

2. Address steatorrhea by providing pancreatic lipase

77
Q

What procedures can be done for the tx of CP?

A
  1. Endoscopic or surgical decompression for patients with dilated pancreatic duct
  2. Resection +/- islet cell transplant
  3. Denervation
78
Q

AIP is the etiology of pancreatitis in less than __% of patients

A

5%

79
Q

In AIP, plasma cells are + for __ in tissue and there are elevated serum levels of ___ in some patients

A

IgG4

IgG4

80
Q

What is the clinical presentation of AIP?

A
  1. Pancreatic mass that mimic cancer
  2. Mild abdominal pain +/- attacks of AP and CP
  3. Pancreatic duct strictures (from IgG4 infiltration)
    * *usually presents with a mass and not pain
81
Q

What is the criteria for type 1 AIP?

A 
HISORt criteria
Histology
Imaging
elevated Serologies (IgG4)
Organ involvement 
Response to glucocorticoid Therapy
82
Q

What is characteristic of the histology seen in type I AIP?

A

Lymphoplasmacytic sclerosing pancreatitis
OR
More than 10 IgG4 + cells with at least 2 of:
1. Periductal lymphoplasmacytic infiltrate
2. Obliterative phlebitis
3. Acinar fibrosis

83
Q

What is seen on imaging with Type I AIP?

A

Diffusely enlarged pancreas with featureless borders

Delayed enhancement with or without capsule-like rim

84
Q

What is elevated on serology with Type I AIP?

A

IgG4

85
Q

What is characteristic of Type 2 AIP?

A

Histologically confirmed idiopathic duct centric pancreatitis, often with granulocytic lesions without IgG4 + cells or systemic involvement

  • *unlikely to relapse
  • *likely to be assoicated with IBD
86
Q

What is the treatment for type 2 AIP?

A

Glucocorticoids

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