Pancreatitis Flashcards

1
Q

During the first two weeks of pantreatitis, what issues do we see?

What about after two weeks?

A

 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

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2
Q

Causes of ACUTE panreatitis

A

Gall stones, alcohol, scorpion venom, Hyperlipidemia, cholesterol, viruses, trauma, pancres divisum, CFTR, or other genetics

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3
Q

ACUTE PANCREATITIS:
GALLSTONES
3-7% of patients with gallstones develop acute pancreatitis (AP), responsible for _____ of cases of acute pancreatitis

A

35-40%

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4
Q

Alcohol use and Acute pancreatits

A

• Alcohol
 10% of alcoholics develop AP
 30% of cases of AP in the United States
 Usually after many years of alcohol abuse

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5
Q

TG and acute pancreatitis

A

Hypertriglyceridemia
 > 1000 mg/dL
 1-4% of AP cases

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6
Q

What is pancreas divisum?

A

Embryologic defect, pancrease forms ring aound the small intestine and blocks passage of food

The main and small duct dont fuse together

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6
Q

Genetic cause of Acute Pancreatitis

A

Serine protease 1 (PRSS1)
• Hereditary pancreatitis, recurrent AP in childhood/early adolescence
• Present in up to 80 % of with hereditary pancreatitisunrelated to CF

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7
Q

• 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

A

Serine protease 1 (PRSS1)

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8
Q

• Cystic fibrosis transmembrane conductance regulator (CFTR) defect can lead to Acute Pancreatits
 Mutation may result in production of :
 Leads to ductal obstruction or _______ function

A

more concentrated or acidic pancreatic juice

altered acinar cell

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9
Q

Genetic cause of acute pancreatitis

 Encodes a pancreatic secretory trypsin inhibitor
 Binds and inhibits about 20 % of trypsin activity

A

Serine protease inhibitor Kazal type 1 (SPINK1)

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10
Q

• Inflammation of the pancreas; different etiologies but all same after?

A

after inciting event or pancreatitis begins
• Inciting event (varies) => early acute changes (similar) => systemic response
(similar)

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11
Q

Early acute changes in acute pancreatitis:
•______ activation of proteolytic enzymes

A

Intraacinar

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12
Q

IN acute pancreatitis:

We get Intraacinar activation of proteolytic enzymes: this leads to
• Generation of large amounts of active______ within pancreas

A

trypsin

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13
Q

What causes pancreatic autodigestion

A

• Vacuoles containing active trypsin rupture
 Leads to activation of further trypsin, chymotrypsin, elastase
• Pancreatic autodigestion from intrapancreatic release of active enzymes

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14
Q

Key pathogeneis is acute pancreatitis

A

MIcrocirculatory injury

Inflammatory cytokines produced

Leukocyte chemoattraction (PMN)

increased vascular permeability and injury (leads to hemorrhage and necrosis)

–> overwhelms normal protective mechanisms

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15
Q

What happens from the systemic response in acute pahtogenesis?

A
  • (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
16
Q

How do gallstones cause acute pancreatitis?

A

reflux of bile to pancreatic duct d/t ampulla obstruction (stones)

edema occurs from passage of stone

17
Q

How does alcohol cause acute pancreatits?

A

Increases effect of CCK on transcripton factors and induce premature activation of zymogens

generate more toxic metabolites

18
Q

What ways can acinar cells be damaged and lead to acute pancreatitis?

A

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

19
Q
A
20
Q

Pt comes in with perisitant, severe EPIgastric pain radiating to the back

She has been nauseous and vomitting. What could be the issue?

A

Acute Pancreatitis: pain radiates to back 50% of tim and 90% pt feel nauseus and vomit

21
Q

Cullens sign and Grey-Turner sign are both severe echymossis can be caused by:

A

acute pancreatitis

22
Q

What lab findings are there in acute pancreatitis?

A

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

23
Q

What must be present to diagnose acute pancreatitis?

A

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

24
Q

What complications can we have with acute pancreatisis

w/in first 4 weeks

over 4 weeks

A

 Acute peripancreatic fluid collection (< 4weeks)

 pseudocysts (> 4 weeks)
 Acute necrotic collection; Infection

25
Q

Pancreatic pseudocyst present after 4 weeks and what is concerning about this complication of acute pancreatitis?

A

potential space for bacterial to grow and we can’t access this space with antibiotics

26
Q

What do we do for treatement of Acute Pancreatitis

A

• 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

27
Q

Causes of chornic pancreatitis

A

• Alcohol abuse
• Cigarette smoking
• Ductal obstruction
 Pancreas divisum
• Ampullary obstruction
• Autoimmune pancreatitis
• Genetic pancreatitis

28
Q

Pathogenesis of chronic pancreatitis

A

Progressive fibro-inflammatory process
resulting in permanent structural damage

29
Q

What are three differences between Acute and Chronic Pancreatitis?

A

 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

30
Q

How can chornic pancreatits result in duct scarring and obstruction?

A

Proteinaceous ductal plugs:
• Increased pancreatic protein secretion =>
plugs within ducts => nidus for calcification =>
stones within the ducts => duct scarring and obstruction

31
Q

How do you diagnose chronic pancreatitis

A

imaging; pancreatic calcification, ductal dilation, enlargement of pancreas, fluid collection

32
Q

How does chornic pancreatic insufficiency present?

A

• Pancreatic insufficiency
 Fat malabsorption: > 90% of pancreatic function lost
 Diabetes mellitus: late in the disease
• Pain from pseudocysts (ductal disruption)

33
Q

What are long term complications of chronic pancretitis

A

Bile duct/duodenal compression or infections from pseudocyst
• Increased risk of pancreatic adenocarcinoma

34
Q

Treatement for Chronic pancreatits

A
  • Alcohol and smoking abstinence
  • Analgesics
  • Diabetes treatment
  • Pancreatic enzyme supplementation
  • May decrease pain
  • Addresses steatorrhea
  • Decompression of dilated pancreatic duct
35
Q

What do we look for if we suspect autoimmune pancreatits?

A

• One form of IgG4-related disease
 IgG4-positive plasma cells in tissue
 Elevated serum IgG4 levels in some patients
 Can affect multiple organs

36
Q

What do you treat autoimmune pancreatitis with?

A

Treat with corticosteroids

37
Q
  • Pancreatic mass that can mimic cancer
  • Mild abdominal pain +/- attacks of AP and CP
  • Pancreatic duct strictures
A

AUTOIMMUNE PANCREATITIS