Gastrointestinal: Pancreas Flashcards

1
Q

How do you know whether the pancreas echogenicity is normal?

A

The pancreas should be hyperechoic relative to the liver

Note: If it is hypoechoic to the liver, consider pancreatitis.

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2
Q

What is the brightest organ on non contrast T1 images?

A

The pancreas

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3
Q

Which portion of the pancreas is retroperitoneal?

A

Head and body (the tail is often intraperitoneal)

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4
Q

What are the major pancreatic changes in cystic fibrosis?

A
  • Fatty replacement (more common, increased T1 signal)
  • Fibrosis (decreased T1 and T2 signal)
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5
Q

Are pancreatic problems more common in pts diagnosed with cystic fibrosis in childhood or adulthood?

A

Adulthood

Note: Cystic fibrosis pts with residual pancreatic exocrine function tend to have bouts of recurrent acute pancreatitis (due to thick secretions). Small pancreatic cysts (1-3 mm) are also common.

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6
Q

What is the most common imaging findings in an adult with cystic fibrosis?

A

Complete fatty replacement of the pancreas

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7
Q

Lipomatous pseudohypertrophy of the pancreas

A

Enlarged pancreas with fatty replacement

Note: This is classically seen in pts with cystic fibrosis, but can also be seen in Shwachman-Diamond syndrome.

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8
Q

Fibrosing colonopathy

A

Wall thinking of the proximal colon as a complication of enzyme replacement therapy in pts with cystic fibrosis

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9
Q

Pediatric pt with persistent diarrhea, short stature, and eczema…

A

Think Shwachman-Diamond syndrome (the second most common cause of pancreatic insufficiency after cystic fibrosis)

Note: Short stature is due to metaphyseal achondroplasia.

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10
Q

Pancreatic lipomatosis

A

The accumulation of fat in the pancreatic parenchyma

Note: This is why the pancreas becomes more fatty as we age.

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11
Q

Differential for pancreatic lipomatosis

A
  • Aging/obesity (most common in adults)
  • Cystic fibrosis (most common in children)
  • Cushing syndrome
  • Chronic steroid use
  • Hyperlipidemia
  • Shwatchman-Diamond syndrome
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12
Q

Dorsal pancreatic agenesis is associated with…

A
  • Diabetes (most beta cells are in the tail)
  • Polysplenia
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13
Q

How can you differentiate severe pancreatic lipomatosis from pancreatic agenesis?

A

In pancreatic agenesis, there will not be a pancreatic duct (but there will be in pancreatic lipomatosis)

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14
Q

Etiology of annular pancreas

A

Embryologic defect (failure of the ventral bud to rotate with the duodenum)

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15
Q

Clinical presentation of annular pancreas

A
  • Duodenal obstruction (pediatric)
  • Pancreatitis (adult)
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16
Q

What determines whether pancreatic trauma is surgical or nonsurgical?

A

The integrity of the pancreatic duct (if the duct is damaged, they need surgery)

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17
Q

Common complications of pancreatic trauma

A
  • Pancreatic duct injury (needs surgery)
  • Pancreatic fistula
  • Abscess formation
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18
Q

MVC

A

Pancreatic laceration

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19
Q

Traumatic pancreatitis in an infant…

A

Suspect non accidental trauma

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20
Q

How can you tell whether peripancreatic fluid is due to pancreatic trauma or aggressive hydration?

A

Look at the liver and IVC (large IVC and periportal edema favor aggressive hydration)

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21
Q

If you suspect a pancreatic duct injury on CT, what’s the next step?

A

MRCP or ERCP

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22
Q

Most common causes of pancreatitis

A
  • Gallstones
  • EtOH
  • Recent ERCP
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23
Q

What medication is classically known to cause pancreatitis?

A

Valproic acid

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24
Q

What is the most common cause of pancreatitis in a child?

A

Trauma

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25
Q

What is the biggest factor in determining prognosis of acute pancreatitis?

A

Degree of pancreatic necrosis

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26
Q

When is the risk for infection greatest during acute pancreatitis?

A

Weeks 3-4 (anti-inflammatory period), due to translocation of intestinal flora

Note: Infection rarely occurs during the first 2 weeks (pro-inflammatory period).

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27
Q

What is the most important finding:

A. Pancreatic hemorrhage
B. Pancreatic necrosis
C. Pancreatic fluid collection
D. Infected pancreatic necrosis

A

D. Infected pancreatic necrosis

Note: Once a necrotic pancreas becomes infected, mortality is very high (50-70%).

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28
Q

Fluid collection around the pancreas 2 weeks after acute pancreatitis…

A

Acute peripancreatic fluid collection

Note: At 4 weeks, this starts being called a pseudocyst.

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29
Q

Fluid collection around the pancreas 5 weeks after acute pancreatitis…

A

Pseudocyst

Note: Prior to 4 weeks, this is called an acute peripancreatic fluid collection.

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30
Q

Fluid around the pancreas 3 weeks after acute necrotizing pancreatitis…

A

Acute necrotic collection

Note: After 4 weeks, this starts being called walled-off necrosis.

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31
Q

Fluid around the pancreas 6 weeks after acute necrotizing pancreatitis…

A

Walled-off necrosis

Note: Prior to 4 weeks, this is called an acute necrotic collection.

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32
Q

What are common vascular complications of acute pancreatitis?

A
  • Splenic vein/portal vein thromboses
  • Gastroduodenal artery/splenic artery pseudoaneurysms
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33
Q

What are common nonvascular complications of acute pancreatitis?

A

Abscess/infection

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34
Q

Pancreatic fluid collection containing gas with history of recent acute pancreatitis…

A

Concerning for infection (high mortality)

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35
Q

Where does the pancreatic duct enter the duodenum?

A
  • The major pancreatic duct (Wirsung) drains to the inferior duodenal papilla
  • The minor pancreatic duct (Santorini) drains to the superior duodenal papilla

Note: Santorini is Smaller and drains Superiorly.

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36
Q

What anatomic variant is this?

A

Pancreatic divisum (the most common anatomic variant of the pancreas)

Note: The main pancreatic duct now drains to the minor (superior) papilla. These pts are at increased risk for pancreatitis.

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37
Q

Pts with pancreatic divisum are at increased risk for…

A

Pancreatitis

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38
Q

What is the most common cause of chronic pancreatitis?

A

EtOH (followed by gallstones)

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39
Q

Early imaging signs of chronic pancreatitis

A
  • Loss of T1 signal (normally the pancreas is the T2 brightest organ in the body)
  • Delayed enhancement
  • Dilated side branches
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40
Q

Late imaging findings of chronic pancreatitis

A
  • Dilatation and beading of the pancreatic duct with calcifications (most characteristic)
  • Uniform atrophy (but can have focal enlargement)
  • Pseudocyst formation (30%)
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41
Q
A

Chronic pancreatitis

42
Q

How can you differentiate pancreatic ductal dilatation in chronic pancreatitis from that in pancreatic cancer?

A

Irregular duct dilatation where the duct is less than 50% of the AP gland diameter favors chronic pancreatitis

Uniform duct dilatation where the duct is greater than 50% of the AP gland diameter favors pancreatic cancer (due to obstructive atrophy)

43
Q

Complications of chronic pancreatitis

A

Pancreatic cancer (20 years of chronic pancreatitis = 6% risk of pancreatic cancer)

44
Q

Most common cystic lesion in the pancreas

A

Psudocyst

45
Q

Are simple pancreatic cysts common?

A

No, true epithelial lined pancreatic cysts are rare and tend to occur with syndromes

46
Q

Simple pancreatic cysts are associated with…

A
  • Von Hippel Lindau
  • Polycystic kidney disease
  • Cystic fibrosis
47
Q

What are the main categories of cystic pancreatic neoplasms that do not communicate with the pancreatic duct and their typical age groups?

A
  • Solid pseudopapillary epithelial neoplasm (daughter lesion, female in 30s)
  • Mucinous cystic neoplasm (mother lesion, female in 50s)
  • Serous cystic neoplasm (grandmother lesion, female in 70s)
48
Q

75 y/o female

A

Serous cystadenoma (microcystic grandmother lesion)

49
Q

What is the most common location for a pancreatic serous cystadenoma?

A

Pancreatic head (70%)

Note: Mucinous cystic neoplasm almost always occurs in the body/tail.

50
Q

What is the most common location for a pancreatic mucinous cystic neoplasm?

A

Pancreatic body and tail (almost always)

Note: Serous cystadenoma usually occurs in the pancreatic head (70%).

51
Q

Which pancreatic tumor communicated with the pancreatic duct?

A

Intraductal papillary mucinous neoplasms (both side branch and main branch types)

52
Q

Which pancreatic neoplasm often has a central scar and/or central calcifications?

A

Serous cystadenoma (20%)

Note: Mucinous cystic neoplasm calcifications are usually peripheral.

53
Q

Unilocular cyst with a lobulated contour in the pancreatic head…

A

Think serous cystadenoma

Note: These are more often multiloculated/microcystic, but can be unilocular and are more common in the pancreatic head.

54
Q

Serous cystadenoma is associated with…

A

Von Hippel Lindau

55
Q

Treatment for mucinous cystic neoplasm of the pancreas

A

Surgical excision (this is a premalignant lesion)

56
Q

Which pancreatic neoplasm tends to be unilocular with peripheral calcifications?

A

Mucinous cystic neoplasm (macrocystic mother lesion)

Note: Calcifications in 20% of cases.

57
Q

Is pancreatic serous cystadenoma benign or malignant?

A

Benign

58
Q

Is mucinous cystic neoplasm of the pancreas benign or malignant?

A

Benign, but premalignant

59
Q

Is solid pseudopapillary epithelial neoplasm of the pancreas benign or malignant?

A

Malignant, low grade

60
Q
A

Mucinous cystic neoplasm (macrwocystic mother lesion)

61
Q

Young female

A

Solid pseudopapillary epithelial neoplasm (daughter lesion)

62
Q

Autoimmune pancreatitis is associated with…

A

IgG4 disease

63
Q

Treatment for autoimmune pancreatitis

A

Steroids

64
Q
A

Think autoimmune pancreatitis

Note: “Sausage shaped” with peripheral capsule-like delayed enhancement.

65
Q
A

Groove pancreatitis (paraduodenal pancreatitis)

Note: Soft tissue in the pancreaticoduodenal groove.

66
Q

Young male with history of malnutrition

A

Tropic pancreatitis (increased risk of adenocarcinoma)

Note: Calculi in dilated pancreatic ducts in a young pt with history of malnutrition.

67
Q

18 y/o without history of malnutrition

A

Think hereditary pancreatitis (SPINK-1 gene mutation)

Note: These pts have an increased risk of adenocarcinoma.

68
Q

What is the most common parasitic cause of pancreatitis?

A

Ascaris infection

69
Q

Common manifestations of IgG4 disease

A
  • Autoimmune pancreatitis
  • Retroperitoneal fibrosis
  • Sclerosing cholangitis
  • Inflammatory pseudotumor
  • Riedel’s thyroiditis
70
Q

How can you differentiate autoimmune pancreatitis from chronic pancreatitis?

A

Autoimmune pancreatitis has no ductal dilatation and no calcifications

71
Q

Which type of intraductal papillary mucinous neoplasm has the highest rate of malignancy

A

Main duct IPMN

Note: Side branch IPMNs are common and rarely malignant.

72
Q

What features of an intraductal papillary mucinous neoplasm are concerning for malignancy?

A
  • Main duct dilatation > 1 cm
  • Diffuse or multifocal involvement
  • Enhancing nodules
  • Solid hypovascular mass
73
Q

Which pancreatic tumor often has early, hemangioma-like peripheral enhancement?

A

Solid psudopapillary epithelial neoplasm

74
Q
A

Main duct IPMN

75
Q

Red arrow

A

Side branch IPMN

Note: There is also a main-duct IPMN here.

76
Q

What are the two major types of solid pancreatic cancer?

A
  • Ductal adenocarcinoma (hypovascualr)
  • Islet cell/neuroendocrine (hypervascular)
77
Q

Jaundice and migratory thrombophlebitis in an elderly pt with an enlarged gallbladder…

A

Think pancreatic ductal adenocarcinoma

Note: This is Trousseau syndrome (migratory thrombophlebitis in the setting of malignancy).

78
Q

When does peak pancreatic parenchymal enhancement occur?

A

40 seconds

Note: The peak liver enhancement occurs later at 60 seconds (portal venous phase) due to dependence on portal blood flow.

79
Q

What is the most common location for pancreatic ductal adenocarcinoma?

A

Pancreatic head (67%)

80
Q

MRI appearance of pancreatic ductal adenocarcinoma

A

T1 hypointense mass relative to the intensely T1 bright pancreatic parenchyma

81
Q

What contrast phase will a pancreatic neoplasm be most visible?

A

Pancreatic parenchymal phase at 40 seconds

Note: This is before the portal veinous phase (at 60 seconds) when pancreatic cancers may be isodense to background parenchyma.

82
Q

Is pancreatic adenocarcinoma involving the gastroduodenal artery resectable?

A

Yes, the GDA comes out in a Whipple anyway

83
Q

What is the most important part of staging pancreatic cancer?

A

Is the SMA or celiac axis involved?

Note: If these are involved, the cancer is not resectable.

84
Q

What tumor marker is elevated in pancreatic cancer?

A

CA 19-9

85
Q

What are the classic imaging findings of pancreatic cancer that may be seen on an upper GI series?

A

Mass effect on the duodenum:

  • Inverted 3 sign (narrowing of the 2nd part of the duodenum to look like a backwards “3”)
  • Wide duodenal sweep
86
Q

Which hereditary syndromes are associated with pancreatic cancer?

A
  • HNPCC
  • BRCA mutation
  • Ataxia-telangiectasia
  • Peutz-Jeghers
87
Q

When is a pancreatic adenocarcinoma considered a periampullary tumor?

A

If it originates within 2 cm of the major duodenal papilla

Note: Any tumor (pancreas, bile duct, duodenum) that meets this criteria is considered a periampullary tumor.

88
Q

Best test to evaluate a periampullary tumor

A

MRI/MRCP

89
Q

There is an increased risk of periampullary carcinomas in ______

A

Gardner’s syndrome

90
Q

Islet cell neuroendocrine tumors are associated with…

A
  • MEN 1
  • Von Hippel Lindau
91
Q

What is the most common type of islet cell neuroendocrine tumor?

A

Isulinoma (75%)

Note: These are almost always benign (90%). Gastrinoma is the second most common (30-60% of these are malignant).

92
Q

Small pancreatic head mass in a pt with recently diagnosed jejunal ulcer…

A

Think gastrinoma (pancreatic islet cell neuroendocrine tumor secreting gastrin)

93
Q

What is the most common pancreatic islet cell neuroendocrine tumor associated with MEN 1?

A

Gastrinoma

94
Q

Zollinger-Ellison syndrome

A

Severe peptic ulcer disease secondary to a gastrinoma (gastrin secreting pancreatic neuroendocrine tumor)

95
Q

Are nonfunctional pancreatic neuroendocrine tumors usually benign or malignant?

A

Malignant (80%)

96
Q

Classic imaging appearance of a nonfunctional pancreatic neuroendocrine islet cell tumor

A

Large pancreatic mass with calcifications

97
Q

Where are gastrinomas most likely to occur?

A

Near the duodenal papilla in the gastrinoma triangle

98
Q

History of remote trauma

A

Think intrahepatic accessory spleen

Note: It should follow spleen on all MRI sequences (including restricting diffusion like normal spleen).

99
Q

What nuclear imaging studies can be used to diagnose an intrahepatic accessory spleen?

A
  • Heat treated RBCs
  • Sulfur colloid
100
Q

Pancreatic mass with tiger-stripe appearance on arterial phase imaging…

A

Think intrapancreatic accessory spleen

Note: The spleen demonstrates tiger striping on arterial phases.