10/8- Pancreatitis Flashcards

1
Q

Familiarize yourself with this picture

A

Vasculature:

  • Splenic a down body/tail of pancreas
  • Hepatic a
  • Portal v
  • Superior/inferior pancreatico-duodenal a
  • Superior mesenteric a/v
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2
Q

What is acute pancreatitis?

  • Mild vs. severe
  • Mortality rates
A

Acute inflammatory process of the pancreas

  • 80% mild, 20% severe

Mortality

  • 25-33% mortality with severe pancreatitis
  • Two peaks of morality:
  • Half within 1-2 wks from multiorgan failure
  • Late peak from infection
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3
Q

What is the pathophysiology of acute pancreatitis?

A
  • Conversion of trypsinogen to trypsin in acinar cells in sufficient quantity
  • Trypsin catalyzes conversion of proenzymes to active enzymes
  • Active enzymes autodigest the pancreas
  • Cycle of releasing more enzymes
  • Microcirculatory injury with resulting edema and ischemia
  • Disruption of pancreatic ducts
  • Cytokine release from PMNs and macrophages
  • Systemic inflammatory response and systemic effects
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4
Q

70% of US cases of acute pancreatitis are related to either _____ or _______

A

70% of US cases of acute pancreatitis are related to either gallstones or chronic alcohol abuse

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5
Q

Gallstones are related to __% of acute pancreatitis cases but only __% of pts with gallstones will get pancreatitis

  • More common with ____
  • Process/pathogenesis
A

Gallstones are related to 40% of acute pancreatitis cases but only 3-7% of pts with gallstones will get pancreatitis

  • More common with stones < 5mm

Process/pathogenesis:

  • Stone obstructs pancreatic duct
  • Stone passage -> edema
  • Reflux of bile
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6
Q

What is seen here?

A

Gallstone throwing shadow

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7
Q

Describe the anatomy of the gallbladder

A
  • Fundus (most distal)
  • Body
  • Hartmann’s pouch (proximal)
  • Neck
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8
Q

Describe the outflow path from the gallbladder

A
  • Cystic duct (with spiral valves), which joins with the common hepatic duct
  • > Bile duct, which combines with the pancreatic duct
  • > Ampulla of Vater

Dumps into duodenum (2nd stage)

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9
Q

Ethanol is related to __% of cases of acute pancreatitis; it affects a ____ (small/large) percentage of alcoholics

  • Often occurs in the setting of _____
  • Possible mechanisms
A

Ethanol is related to 30% of cases of acute pancreatitis; it only affects a small percentage of alcoholics

  • Often occurs in the setting of chronic alcoholic pancreatitis

Possible mechanisms:

  • Relaxatin or spasm of sphincter of Oddi
  • Higher protein concentration in pancreatic juice
  • Direct toxic injury
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10
Q

What are other predisposing factors of acute pancreatitis? (not alcohol or gallstones)

A
  • Hypertriglyceridemia (> 100 mg/dL)
  • Microlithiasis and biliary sludge
  • Drugs:
  • Azathioprine
  • Valproate
  • Tetracycline
  • Furosemide..
  • Hypercalcemia
  • Post-ERCP pancreatitis (5-25% of ERCPs)
  • Trauma (blunt or penetrating)
  • Infections:
  • Mumps
  • CMV
  • VZV
  • Mycoplasma
  • Aspergillus
  • Toxoplasma
  • Hereditary (trypsinogen gene)
  • Autoimmune pancreatitis (IgG4 elevated)
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11
Q

What is necessary to establish acute pancreatitis diagnosis?

A

Combo of at least 2 of the 3:

  • Typical symptoms
  • Elevated amylase/lipase
  • CT findings of pancreatitis
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12
Q

What are typical symptoms of acute pancreatitis?

A

Abdominal pain

  • Steady and moderate to severe
  • Upper abdomen, epigastric

Nausea and vomiting

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13
Q

What are physical exam findings in acute pancreatitis?

A
  • Abdominal tenderness
  • Estravasation fo hemorrhagic exudate (rare)
  • Grey Turner’s sign: ecchymoses in flanks
  • Cullen’s sign: periumbilical ecchymoses
  • Tachycardia, fever
  • Respiratory distress, altered mental status in severe pancreatitis
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14
Q

What is Grey Turner’s sign?

A

Ecchymoses in flanks

  • (rare) finding in acute pancreatitis
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15
Q

What is Cullen’s sign?

A

Periumbilical ecchymosis

  • (rare) finding in acute pancreatitis
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16
Q

What is seen here?

A

Acute pancreatitis: Cullen’s sign?

– periumbilical ecchymosis

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17
Q

What are lab values expected in acute pancreatitis?

A

Amylase

  • 3x serum elevation
  • Rises within 6-12 hrs; half life 10 hrs

Lipase

  • 3x serum elevation
  • Rises within 24 hrs; longer half life
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18
Q

What is the most important imaging technique for diagnosis/complication identification in acute pancreatitis?

A

CT

  • Not always necessary (mild cases)
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19
Q

What is expected in CT of acute pancreatitis?

A
  • Peri-pancreatic inflammatory changes
  • Peri-pancreatic fluid collections
  • Pancreatic necrosis
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20
Q

What is the benefit of using abdominal x-ray for suspected acute pancreatitis?

A
  • Evaluate for other causes of abdominal pain
  • Sentinel loop: localized ileus of a segment of small intestine
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21
Q

What are the benefits/uses of abdominal ultrasound in the evaluation of acute pancreatitis?

A

Visualize:

  • Gallstones
  • Dilated bile duct (choledocholithiasis)
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22
Q

What is choledocholithiasis?

A

Dilated bile duct

23
Q

What will be helpful in determining the cause of acute pancreatitis?

A

History:

  • Alcohol
  • Medications

Labs:

  • Liver tests
  • Calcium
  • TG
  • IgG4

Ultrasound:

  • Gallstones
  • Dilated bile duct

CT

  • Pancreatic mass of cyst
24
Q

What are predictors/methodsof assessing severity in cases of acute pancreatitis?

A

Severe Acute Pancreatitis:

SIRS: 2+ of the following:

  • P > 90, R > 20, or PaCO2 < 32
  • T < 36 or T > 38
  • WBC < 4,000 or WBC > 12,000

Organ failure (pulmonary, renal, cardiovascular)

Pancreatic necrosis

Scoring systems

25
Q

What is Ranson’s Criteria?

  • At admission
  • During initial 48 hrs
A

At admission:

  • Age > 55 yo
  • WBC > 16,000/mm3
  • Blood glucose > 200 mg/dL
  • Serum LDH > 350 IU/L
  • Serum AST > 250 IU/L

Initial 48 hrs:

  • Hematocrit decrease > 10%
  • BUN increase > 5 mg/dL
  • Serum Ca < 8 mg/dL
  • Arterial pO2 < 60 mmHg
  • Serum base deficit (24 - HCO3) > 4 mEq/L
  • Fluid sequestration > 6 L
26
Q

How is Ranson’s criteria scored?

  • Mortality
  • Shortcomings
A

Scoring:

  • 1 pt for each positive
  • Severe pancreatitis is 3+ points
  • Mortality:
  • 0-2: 2%
  • 3-4: 15%
  • 5-6: 40%
  • 7-8: 100%
  • Cumbersome and requires 48 hrs to calculate…
27
Q

What is the CT scoring index for acute pancreatitis?

A

Balthazar grades (A-E) associated with certain CT findings:

Grade A: Normal pancreas

Grade B:

  • Enlargement of pancreas
  • Irregular contour
  • Inhomogenous attenuation

Grade C: peripancreatic inflammation + B

Grade D: associated single fluid collection + C

Grade E: 2+ peripancreatic fluid collections or gas in pancrease + C

28
Q

What is seen here?

A

Grade A (normal pancreas)

29
Q

What is seen here?

A

CT of acute pancreatitis: Grade B

  • Enlargement of pancreas
  • Irregular contour
  • Inhomogeneous attenuation
30
Q

What is seen here?

A

CT of acute pancreatitis: grade C

  • Peripancreatic inflammation in addition to Grade B:
  • Enlargement of pancreas
  • Irregular contour
  • Inhomogenous attenuation
31
Q

What is seen here?

A

CT of acute pancreatitis: Grade D

  • Associated single fluid collection in addition to Grade C criteria:
  • Peripancreatic inflammation
  • Enlargement of pancreas
  • Irregular contour
  • Inhomogenous attenuation
32
Q

What is seen here?

A

CT of acute pancreatitis: Grade E

  • 2+ peripancreatic fluid collections or gas in pancreas in addition to Grade C:
  • Peripancreatic inflammation
  • Enlargement of pancreas
  • Irregular contour
  • Inhomogenous attenuation
33
Q

What is the BISAP score?

A

1 point for each:

  • BUN > 25 mg/dL
  • Impaired mental status
  • SIRS
  • Age > 60 yo
  • Pleural effusion
34
Q
A
35
Q

What are the two main scoring systems in predicting SAP (Severe Acute Pancreatitis)?

A
  1. Ranson’s
  2. BISAP
36
Q

How do you manage acute pancreatitis?

A
  • Aggressive IVF resuscitation (first 24 hours most important)
  • Pain control with opiates
  • Close monitoring
  • Prophylactic antibiotics not typically indicated (controversial topic with necrotizing pancreatitis)
  • “Pancreatic rest”
  • Historical management strategy that patients with pancreatitis should be kept NPO with slow advancement of diet after improvement in pain
  • No longer considered standard of care
  • Nutritional support
  • Increased metabolism and protein catabolism with severe acute pancreatitis
  • Enteral nutrition better than parenteral nutrition (TPN) – reduced infections & mortality
  • No TPN!!!
  • Early initiation of enteral feeding
  • Nasogastric feeding may be ~ to nasojejunal feeding
  • If gallstone cause, treat it (later slide)
37
Q

How do you manage acute pancreatitis associated with gallstones?

A
  • ERCP
  • Urgent: impacted stone; cholangitis, rising/elevated bilirubin
  • Delayed: evidence of choledocholithiais by labs or imaging
  • Cholecystectomy
38
Q

What are localized complications (of acute pancreatitis?)

A

Under 4 wks:

  • Acute fluid collection
  • Acute necrotic collection

Over 4 wks:

  • Pseudocyst
  • Walled-off necrosis
39
Q

What is a pancreatic pseudocyst?

  • Characteristics
  • Timeline
  • Treatment
A

Most commonly encountered chronic complication (of acute pancreatitis?)

  • Develop adjacent to pancreas after 4 weeks
  • Fluid filled
  • Encapsulated wall
  • May require drainage if symptomatic
40
Q

What is the pathophysiology of chronic pancreatitis?

A

- Loss of parenchymal cells (acinar first, then islet), chronic inflammation, fibrosis

- Alcoholic chronic pancreatitis

  • 10% heavy alcohol users (genetic effect)
  • Direct toxic effects of alcohol and metabolites
  • Stimulates stellate cells (fibrosis)
  • Recurrent acute episodes lead to chronic changes
41
Q

What is the etiology of chronic pancreatitis?

A
  • Smoking: chronic pancreatitis and cancer
  • Alcohol: 70%
  • Idiopathic: 10-30%
  • Tropical pancreatitis
  • Genetic (PRSS1, SPINK1, CFTR)
  • Autoimmune pancreatitis
  • Ductal obstruction
42
Q

How does chronic pancreatitis present?

A

- Abdominal pain – most common symptom

  • Exocrine insufficiency
  • Steathorrhea (< 10% pancreas function)
  • Diarrhea and weight loss
  • Endocrine insufficiency
  • Diabetes Mellitus
  • Reduced glucagon – risk of hypoglycemia with insulin treatment
43
Q

How is chronic pancreatitis diagnosed?

A

It’s difficult

  • Tests of pancreatic function
  • Direct: bicarbonate output in duodenum after dose of secretin; not practical
  • Indirect: fecal elastase and fecal fat (72 hr vs. Sudan stain)
  • Tests of pancreatic structure
  • Abdominal x-ray: diffuse calcifications
  • CT:
    • Dilated, irregular pancreatic duct
    • Intraductal filling defects
    • Calcifications
    • Irregular contour, heterogeneous parenchyma
  • MRI/MRCP
  • Endoscopic ultrasound (EUS)
  • ERCP
  • Exocrine/endocrine deficiency
  • Abdominal pain alone…

All tests are most useful in advanced chronic pancreatitis

44
Q

What is seen here?

A

Calcification in pancreas on abdominal x-ray

  • Indicative of chronic pancreatitis
45
Q

What is seen here?

A

Calcifications in pancreas??

46
Q

What is the gold standard for diagnosing chronic pancreatitis?

  • What does it show?
A

ERCP

  • Dilated pancreatic duct, filling defects, dilated side branches
  • Invasive
47
Q

What does MRI/MRCP do for the diagnosis of chronic pancreatitis?

A
  • Provides imaging of the pancreatic parenchyma and the pancreatic duct
  • Non-invasive
48
Q

What does endoscopic ultrasound (EUS) do for the diagnosis of chronic pancreatitis?

A
  • Some questions about specificity
  • Completely normal EUS -> chronic pancreatitis unlikely
49
Q

Look at this pic

A
50
Q

Normal?

A

No idea what this is…

51
Q

When can exocrine/endocrine deficiency be used to help diagnose chronic pancreatitis?

A

Advanced disease

  • CT or other tests are likely positive
52
Q

When can abdominal pain alone be used to help diagnose chronic pancreatitis?

A
  • Not advanced disease -> challenging diagnosis
  • Pancreatic protocol CT or MRI/MRCP
  • EUS
53
Q

How should chronic pancreatitis be managed from an abdominal pain standpoint?

What if:

  • ERCP
  • Steatorrhea
  • Diabetes mellitus
A
  • Most common and bothersome symptom
  • Pain medication – risk of addiction
  • Stop ETOH
  • Pancreatic enzymes (non-enteric coated)

Also if:

  • ERCP: pancreatic duct strictures or stones
  • EUS: celiac plexus block (transient, rarely used)
  • Surgery – Puestow, pancreatectomy w/ islet cell transplant
  • Steatorrhea: pancreatic enzyme supplementation
  • Diabetes mellitus: insulin often needed; risk of hypoglycemia
  • Malignancy: pancreatic adenocarcinoma (later cad)
54
Q

What malignancy is associated with chronic pancreatitis?

  • Lifetime risk
  • Increased risk factors
A

Pancreatic adenocarcinoma

  • 4% lifetime risk
  • Smoking increases risk

Difficult to diagnose in setting of chronic pancreatitis

  • Similar symptoms (abdominal pain, weight loss)
  • Clinical suspsicion