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Appendix > Pancreas > Flashcards

Pancreas Flashcards

1
Q

What are the 4 parts of the pancreas?

A

head neck body tail

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2
Q

Major blood supply to pancreas supplied by what vessels?

A

celiac

SMA

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3
Q

Head and uncinate process of pancreas supplied by what arteries?

A

pancreaticoduodenal arteries (anterior/posterior)–> come from the GDA –> hepatic artery and SMA inferiorly

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4
Q

Neck, body, and tail of pancreas receive their blood supply from?

A

splenic artery

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5
Q

Dorsal pancreatic artery arises from?

A

splenic artery

dorsal pancreatic artery courses posterior to the body

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6
Q

What is the major duct of the pancreas?

A

duct of Wirsung

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7
Q

What is the accessory duct of the pancreas?

A

duct of Santorini

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8
Q

When do the ventral/dorsal buds of pancreas fuse?

A

8 weeks

ventral bud becomes inferior part of head and uncinate process

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9
Q

What’s pancreas divisum?

A

failure of organogenesis in pancreas development
(normally dorsal and ventral buds fuse and form a common duct with enters duodenum with CBD)

failure of dorsal and ventral buds to fuse–> divisum

ventral pancreatic duct and CBD drain via major papilla
dorsal pancreatic duct drains via minor papilla

(most pancreas secretions exit via dorsal duct, but small caliber of minor papilla causes partial obstruction)

buildup of back pressure causes relapsing acute or chronic pancreatitis

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10
Q

What is annular pancreas?

A

ventral pancreatic bud migrates and encircles 2nd portion of duodenum

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11
Q

Annular pancreas associated with what abnormalities?

A

Down’s

cardiac issues

malrotation

intestinal atresia

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12
Q

Sx tx for annular pancreas causing obstruction?

A

gastric bypass via duodenojejunostomy

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13
Q

Ventral or dorsal pancreatic duct wraps around 2nd portion of duodenum and causes annular pancreas?

A

ventral

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14
Q

Ectopic pancreas commonly found where?

A

stomach

duodenum

Meckel’s

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15
Q

What type of cells make up the pancreas?

A

acinar cells (85%)

islet cells (2%)

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16
Q

Acinar cells of the pancreas secrete what?

A

inactive zymogens in granules in response to food

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17
Q

What enzyme activates trypsinogen into trypsin?

A

enterokinase; made in duodenum

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18
Q

This enzyme, made in duodenum, stimulates trypsinogen to active trypsin:

A

enterokinase

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19
Q

Acinar cells produce two enzymes in active form:

A

pancreatic lipase

pancreatic amylase

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20
Q

SPINK-1 mutations are assc with development of what?

A

chronic pancreatitis

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21
Q

What’s the role of HCO3 secreted by pancreas acinar cells in duodenum?

A

neutralizes acid (HCL) from stomach

pancreatic enzymes are inactivated at low pH

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22
Q

What happens during cephalic phase of eating?

A

Ach is released

induces acinar cell secretion of enzymes

accnts for 20-25% of daily secretion of pancreatic juice

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23
Q

Phases of eating and pancreatic acid secretions?

A

cephalic phase–> 25%, mediated by ACh release of enzymes

gastric phase–> vasovagal reflexes due to gastric distention cause release of enzymes (10%)

intestinal phase–> 70% of pancreatic juice released during this phase, mediated by CCK release

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24
Q

What cells make CCK?

A

I cells of duodenum

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25
Q

What’s the main mediator of pancreatic secretions in duodenum?

A

CCK made by I cells of duodenum

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26
Q

What does secretin do the sphincter of oddi?

A

relaxes it so pancreatic enzymes can escape

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27
Q

Mortality of acute pancreatitis?

A

mild is 1%

severe is 10-30%

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28
Q

MCC of death in acute pancreatitis?

A

multi-organ dysfunction

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29
Q

What are the two top causes of acute pancreatitis?

A

gallstones
etoh

**accnt for 70-80% of cases

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30
Q

In peds pts, MCC of AP?

A

abdominal blunt trauma

systemic dx

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31
Q

MC cause of AP in the west?

A

gallstones (40%)

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32
Q

Two theories causing AP due to gallstones:

A

a—-> pancreatic duct obstruction due to GS, back up of pancreatic juices, duct dilatation

b—> bile salt reflux into pancreas from common channel with CBD: bile salts cause necrosis of acinar cells

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33
Q

How does etoh cause AP?

A

triggers inflammatory cytokines; activates NF-kb pathway which upregulates TNF-a, IL-I, death caspases

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34
Q

What % of pts who have ERCP, develop AP?

A

5%

**most common complication of ERCP is AP

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35
Q

Metabolic causes of AP?

A

hyper-TGs; usually > 2000 confirms dx

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36
Q

Clinically hows does AP present?

A

epigastric, periumbilical pain radiating to the back

constant

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37
Q

Rarely you can see retroperitoneal bleeding assc with severe pancreatitis and they produce these classic ecchymotic patterns;

A

gray turner sign- flank

cullen sign - peri-umiblical

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38
Q

How do we dx AP?

A

clinically + elevated pancreatic enzymes (three-fold elevation in amylase/lipase)

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39
Q

Which is more sensitive/specific for AP?

A

lipase

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40
Q

Best test for pancreatitis evaluation?

A

CT w/portal venous phase

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41
Q

This predicts severity of AP at presentation and 48 hrs later using 11 parameters:

A

Ranson’s criteria

severe pancreatitis is established if >3 of the parameters are filled

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42
Q

What are Ranson’s criteria?

A

can have one with gallstone related dx and one w/out

age >55
glucose >200
WBC >16
LDH >350
AST >250
after 48 hrs;
hct drop >10 %
Ca <8
Base deficit >4
BUN increase >5
Fluid requirement >6 L
Pao2 <60
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43
Q

Disadvantage of Ransons?

A

doesn’t predict severity of disease at time of presentation, need the 48 hrs parameters

**used to rule out AP, has a high negative predictive value

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44
Q

Aside from Ranson’s score, what other scoring system can we use?

A

APACHE II score

> 8 acute pancreatitis

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45
Q

What defines severe pancreatitis?

A

presence of local pancreatic complications like;

necrosis, pseudocyst, abscess or any evidence of organ failure

CRP>150 also assc with severe pancreatitis

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46
Q

Main cornerstone of tx for AP?

A

aggressive IVF w/crystalloids

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47
Q

How does AP effect the lungs?

A

most common systemic complication of AP is hypoxemia cause by acute lung injury

48
Q

When do we use ERCP for AP?

A

when you suspect AP due to biliary obstruction

49
Q

What % of pts with acute biliary pancreatitis will have recurrence?

A

30%

50
Q

Sterile vs infected peripancreatic fluid collections in AP:

A

acute abdominal fluid in a pt with AP is common

usually fluid collection is sterile

if fever, WBC develop, has become infected –> aspiration needed to confirm

if infection present, drain fluid and start ABX

51
Q

What’s pancreatic necrosis in AP?

A

nonviable pancreatic parenchyma or fat

can be focal or diffuse

CT best to dx it; see low attenuation of HU

52
Q

What % of pts with AP develop pancreatic necrosis?

A

20%

53
Q

Whats the problem of pancreatic necrosis in pts with AP?

A

risk of infection

usually due to bacterial translocation from enteric bacteria E.coli, klebsiella, enteroccocus

54
Q

What do you do if you suspect an infected pancreatic necrosis in someone with AP?

A

FNA

gram stain/culture will confirm the dx

then start abx once dx confirmed

55
Q

In pts with confirmed pancreatic necrosis that have AP, what abx have shown good penetrance into pancreatic tissue?

A

carbapenems

56
Q

Abx of choice of infected pancreatic necrosis in pts with AP?

A

carbapenems

57
Q

Definitive tx for infected pancreatic necrosis?

A

necrosectomy

**mortality after open necrosectomy is 25-30%

pts who have necrosectomy within first 14 days have mortality of 70%

pts who have necrosectomy between 14-29 days have 45% mortality

> 30 days, 8% mortality

58
Q

What’s a pancreatic pseudocyst?

A

has no epithelium

contains granulation tissue and collagen

(*** develop in 5-15% of pts that develop peri-pancreatic fluid collections after AP)

59
Q

How long after AP episode do pancreatic pseudocysts tend to form?

A

4-8 weeks

60
Q

Fluid cytology that suggests a pancreatic pseudocyt is?

A

high amylase

low CEA

absent mucin

61
Q

In majority of pancreatic pseudocysts what do we do?

A

we do nothing

70% regress spontaneously

62
Q

Tx for symptomatic pancreatic pseudocysts?

A

transgastric or transduodenal endoscopic drainage supported for pts with cyts in close proximity to stomach and duodenum (<1 cm)

surgical drainage then done for pts who have failed endoscopic techniques

63
Q

What is a cyst gastrostomy?

A

in pts with pancreatic pseudocysts, closely attached to stomach, a cyst gastrostomy is performed

anterior gastrostomy made, cyst is then located, and it is drained via stomach posterior wall using a stapler, anterior gastrostomy repaired in two layers

64
Q

How do we treat pancreatic pseudocysts close to pancreatic head and duodenum?

A

cysto-duodenostomy

***for some cysts not in tact with stomach or duodenum, a Roux-en-y cysto-jejunostomy is performed

65
Q

What’s a pancreaticopleural fistula?

A

posterior pancreatic duct disruption into the pleural space

accumulate fluid in thorax

see elevated lipase/amylase in thorax

Tx–> drain the chest, ocreotide, IV nutrition

66
Q

Describe chronic pancreatitis?

A

persistent inflammation

irrerversible fibrosis

atrophy of pancreatic parenchyma

67
Q

What’s the most common cause of chronic pancreatitis?

A

alcohol consumptions (70-80%)

68
Q

Mutations in what gene have been shown to cause hereditary chronic pancreatitis?

A

PRSS1 on chromosome 7

mutations of this gene lead to intra-acinar trypsinogen activation

SPINK1 mutations also implicated in hereditary chronic pancreatitis

69
Q

CFTR is a gene that regulates what?

A

HCO3 and Cl secretions in respiratory and pancreatic secretions

  • *homozygous CFTR mutations cause CF
  • **heterozygous CFTR mutations predispose to chronic pancreatitis
70
Q

What do we see on Ct findings of chronic pancreatitis?

A

dilated pancreatic duct

calcifications

atrophy of parenchyma

71
Q

When we see pancreatic duct dilatation in chronic pancreatitis, how is it described?

A

chain of lakes

72
Q

Pancreatic duct dilatation in chronic pancreatitis, is often described as a chain of lakes pattern due to multiple strictures, how do we treat?

A

modified Puestow procedure

side to side pancreaticojejunostomy

73
Q

What is a modified puestow procedure?

A

side to side pancreatico-jejunostomy

74
Q

What is the benefit of a modified Puestow procedure for duct dilatation in chronic pancreatitis?

A

allows for parenchymal preservation

preserved endocrine/exocrine function of pancreas

75
Q

Describe the Frey procedure?

A

local resection of the pancreatic head with longitudinal pancreatico-jejunostomy

76
Q

When is a Frey procedure performed?

A

pts w/dilated pancreatic ducts secondary to benign stricture in the head of pancreas

77
Q

What are the most common cystic neoplasms of the pancreas?

A

MCNs

78
Q

MCNs contain mucin producing epithelial and how are they described histologically?

A

contain mucin-rich cells

contain ovarian-like stroma (Estronge and progesterone staining are positive in most cases)

79
Q

Where do we find most MCNs?

A

body and tail

80
Q

What are some characteristics on CT imaging of MCNs that might qualify them as malignant?

A

eggshell calcifications

large tumor

81
Q

Cytology of MCNs shows what?

A

rich in mucin

high CEA

low amylase

82
Q

Do MCNs have malignant potential?

A

yes

surgery is standard of care

83
Q

How do we treat MCNs?

A

surgery

84
Q

How do invasive MCNs compare to ductal adenocarcinomas of pancreas?

A

slower growing

less nodal involvement

less aggressive

85
Q

Compared to MCNs, serous cystic neoplasms of the pancreas tend to be located where?

A

HEAD

86
Q

What do we see on CT scan with serous cystic neoplasms of pancreas?

A

central calcifications w/sunburst appearance

87
Q

Tx for serous cystic neoplasms of pancreas?

A

generally considered benign

resected when >4 cm, pt is symptomatic, rapidly growing lesions, Ca can’t be excluded

88
Q

Whats the cytology fluid analysis of serous cystic neoplasms of pancreas?

A

low amylase

low CEA

negative mucin

89
Q

What are the three types of IPMNs (intraductal papillary mucinous neoplasms)?

A

side branch IPMN

main duct IPMN

mixed type IPMN

90
Q

What’s a side branch IPMN?

A

dilation of a side branch of the main pancreatic duct that communicate with the main duct but do not involve the main duct

91
Q

What do you do for side branch IPMN?

A

for asymptomatic small lesions less than 3 cm, observe

lesion <1 cm–> yearly CT/MRI

lesions 1-3 cm–> imaging Q6 months

lesions >3 cm–> surgery due to high risk of malignancy

92
Q

What is the risk of invasive malignancy with side branch IPMN?

A

10-15 %

93
Q

What is the treatment for main duct IPMNs?

A

surgical resection

there is a 30-50% risk of harboring cancer

94
Q

Cancer risk for main duct IPMNs vs side branch IPMNs?

A

side branch–> 10-15 % ( >3 cm we resect, otherwise we surveillance)

main branch–> 30-50%, surgery is mandated

95
Q

Fluid analysis of IPMNs shows what?

A

high CEA
high amylase
high mucin

96
Q

What is a mixed-type IPMN?

A

side branch IPMN which extends to involve the main pancreatic duct to a varying degree

97
Q

What do we do with mixed-type IPMNs?

A

treat them like main branch IPMN

harbor 30-50% chance of malignancy

surgery needed

98
Q

What’s the treatment for mixed-type IPMNs?

A

surgery (they harbor 30-50% of malignancy, same as main duct IPMNs)

99
Q

What is the surgical tx for main duct IPMNs?

A

partial pancreatectomy

100
Q

What determines survival for IPMNs?

A

degree of invasiveness

101
Q

Avg age of pancreatic ca diagnosis?

A

72

males slightly more affected

102
Q

Most notable risk factor for developing pancreatic adenocarcinoma is?

A

smoking

smokers have a 1-3 fold increase risk for developing Ca compared to non-smokers

103
Q

What are some genetic mutations associated with developing pancreatic cancer?

A 
PRSS1 gene mutation
Peutz-Jegers syndrome (STKK1)
CF (CFTR)
BRC2
Lynch Syndrome 
FAP
104
Q

Courvoisier sign ?

A

painless jaundice

suspect pancreatic Ca

105
Q

Virchow’s node?

A

left supra-clavicular node in pancreatic ca

106
Q

Sister Mary Joseph nodule?

A

peri-umbilical node in pancreatic Ca

107
Q

Blumer’s shelf?

A

peri-rectal pancreatic tumor involvement on DRE

108
Q

What tumor marker is most sensitive for pancreatic Ca?

A

Ca- 19-9

109
Q

Imaging test of choice to evaluate for pancreatic Ca?

A

multimodal CT

110
Q

How do we get biopsies for suspected pancreatic ca?

A

EUS-FNA

111
Q

Which pancreatic ca stages are treated with surgery?

A

Stage 1A to 2B

tumors confined to pancreas or peripancreatic tissue without evidence of celiac or SMA involvement, and no evidence of mets

112
Q

Which pts with pancreatic ca (in terms of staging) do we not operate on?

A

pts with stage 3 (T4 disease)–> involving celiac/SMA

pts with stage 4–> mets

113
Q

Whats the role of laparoscopy in pancreatic ca staging?

A

in pts that appear resectable on imaging, 30% are deemed non-resectable after staging laparoscopy

114
Q

For tumors involving the head of the pancreas, surgical treatment is what?

A

pancreaticoduodenemectomy WHIPPLE

115
Q

MOst common complication following pancreaticoduodenectomy is?

A

delayed gastric emptying

Appendix (39 decks)

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