Pancreas Flashcards
What are the 4 parts of the pancreas?
head neck body tail
Major blood supply to pancreas supplied by what vessels?
celiac
SMA
Head and uncinate process of pancreas supplied by what arteries?
pancreaticoduodenal arteries (anterior/posterior)–> come from the GDA –> hepatic artery and SMA inferiorly
Neck, body, and tail of pancreas receive their blood supply from?
splenic artery
Dorsal pancreatic artery arises from?
splenic artery
dorsal pancreatic artery courses posterior to the body
What is the major duct of the pancreas?
duct of Wirsung
What is the accessory duct of the pancreas?
duct of Santorini
When do the ventral/dorsal buds of pancreas fuse?
8 weeks
ventral bud becomes inferior part of head and uncinate process
What’s pancreas divisum?
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
What is annular pancreas?
ventral pancreatic bud migrates and encircles 2nd portion of duodenum
Annular pancreas associated with what abnormalities?
Down’s
cardiac issues
malrotation
intestinal atresia
Sx tx for annular pancreas causing obstruction?
gastric bypass via duodenojejunostomy
Ventral or dorsal pancreatic duct wraps around 2nd portion of duodenum and causes annular pancreas?
ventral
Ectopic pancreas commonly found where?
stomach
duodenum
Meckel’s
What type of cells make up the pancreas?
acinar cells (85%)
islet cells (2%)
Acinar cells of the pancreas secrete what?
inactive zymogens in granules in response to food
What enzyme activates trypsinogen into trypsin?
enterokinase; made in duodenum
This enzyme, made in duodenum, stimulates trypsinogen to active trypsin:
enterokinase
Acinar cells produce two enzymes in active form:
pancreatic lipase
pancreatic amylase
SPINK-1 mutations are assc with development of what?
chronic pancreatitis
What’s the role of HCO3 secreted by pancreas acinar cells in duodenum?
neutralizes acid (HCL) from stomach
pancreatic enzymes are inactivated at low pH
What happens during cephalic phase of eating?
Ach is released
induces acinar cell secretion of enzymes
accnts for 20-25% of daily secretion of pancreatic juice
Phases of eating and pancreatic acid secretions?
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
What cells make CCK?
I cells of duodenum
What’s the main mediator of pancreatic secretions in duodenum?
CCK made by I cells of duodenum
What does secretin do the sphincter of oddi?
relaxes it so pancreatic enzymes can escape
Mortality of acute pancreatitis?
mild is 1%
severe is 10-30%
MCC of death in acute pancreatitis?
multi-organ dysfunction
What are the two top causes of acute pancreatitis?
gallstones
etoh
**accnt for 70-80% of cases
In peds pts, MCC of AP?
abdominal blunt trauma
systemic dx
MC cause of AP in the west?
gallstones (40%)
Two theories causing AP due to gallstones:
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
How does etoh cause AP?
triggers inflammatory cytokines; activates NF-kb pathway which upregulates TNF-a, IL-I, death caspases
What % of pts who have ERCP, develop AP?
5%
**most common complication of ERCP is AP
Metabolic causes of AP?
hyper-TGs; usually > 2000 confirms dx
Clinically hows does AP present?
epigastric, periumbilical pain radiating to the back
constant
Rarely you can see retroperitoneal bleeding assc with severe pancreatitis and they produce these classic ecchymotic patterns;
gray turner sign- flank
cullen sign - peri-umiblical
How do we dx AP?
clinically + elevated pancreatic enzymes (three-fold elevation in amylase/lipase)
Which is more sensitive/specific for AP?
lipase
Best test for pancreatitis evaluation?
CT w/portal venous phase
This predicts severity of AP at presentation and 48 hrs later using 11 parameters:
Ranson’s criteria
severe pancreatitis is established if >3 of the parameters are filled
What are Ranson’s criteria?
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
Disadvantage of Ransons?
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
Aside from Ranson’s score, what other scoring system can we use?
APACHE II score
> 8 acute pancreatitis
What defines severe pancreatitis?
presence of local pancreatic complications like;
necrosis, pseudocyst, abscess or any evidence of organ failure
CRP>150 also assc with severe pancreatitis
Main cornerstone of tx for AP?
aggressive IVF w/crystalloids
How does AP effect the lungs?
most common systemic complication of AP is hypoxemia cause by acute lung injury
When do we use ERCP for AP?
when you suspect AP due to biliary obstruction
What % of pts with acute biliary pancreatitis will have recurrence?
30%
Sterile vs infected peripancreatic fluid collections in AP:
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
What’s pancreatic necrosis in AP?
nonviable pancreatic parenchyma or fat
can be focal or diffuse
CT best to dx it; see low attenuation of HU
What % of pts with AP develop pancreatic necrosis?
20%
Whats the problem of pancreatic necrosis in pts with AP?
risk of infection
usually due to bacterial translocation from enteric bacteria E.coli, klebsiella, enteroccocus
What do you do if you suspect an infected pancreatic necrosis in someone with AP?
FNA
gram stain/culture will confirm the dx
then start abx once dx confirmed
In pts with confirmed pancreatic necrosis that have AP, what abx have shown good penetrance into pancreatic tissue?
carbapenems
Abx of choice of infected pancreatic necrosis in pts with AP?
carbapenems
Definitive tx for infected pancreatic necrosis?
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
What’s a pancreatic pseudocyst?
has no epithelium
contains granulation tissue and collagen
(*** develop in 5-15% of pts that develop peri-pancreatic fluid collections after AP)
How long after AP episode do pancreatic pseudocysts tend to form?
4-8 weeks
Fluid cytology that suggests a pancreatic pseudocyt is?
high amylase
low CEA
absent mucin
In majority of pancreatic pseudocysts what do we do?
we do nothing
70% regress spontaneously
Tx for symptomatic pancreatic pseudocysts?
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
What is a cyst gastrostomy?
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
How do we treat pancreatic pseudocysts close to pancreatic head and duodenum?
cysto-duodenostomy
***for some cysts not in tact with stomach or duodenum, a Roux-en-y cysto-jejunostomy is performed
What’s a pancreaticopleural fistula?
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
Describe chronic pancreatitis?
persistent inflammation
irrerversible fibrosis
atrophy of pancreatic parenchyma
What’s the most common cause of chronic pancreatitis?
alcohol consumptions (70-80%)
Mutations in what gene have been shown to cause hereditary chronic pancreatitis?
PRSS1 on chromosome 7
mutations of this gene lead to intra-acinar trypsinogen activation
SPINK1 mutations also implicated in hereditary chronic pancreatitis
CFTR is a gene that regulates what?
HCO3 and Cl secretions in respiratory and pancreatic secretions
- *homozygous CFTR mutations cause CF
- **heterozygous CFTR mutations predispose to chronic pancreatitis
What do we see on Ct findings of chronic pancreatitis?
dilated pancreatic duct
calcifications
atrophy of parenchyma
When we see pancreatic duct dilatation in chronic pancreatitis, how is it described?
chain of lakes
Pancreatic duct dilatation in chronic pancreatitis, is often described as a chain of lakes pattern due to multiple strictures, how do we treat?
modified Puestow procedure
side to side pancreaticojejunostomy
What is a modified puestow procedure?
side to side pancreatico-jejunostomy
What is the benefit of a modified Puestow procedure for duct dilatation in chronic pancreatitis?
allows for parenchymal preservation
preserved endocrine/exocrine function of pancreas
Describe the Frey procedure?
local resection of the pancreatic head with longitudinal pancreatico-jejunostomy
When is a Frey procedure performed?
pts w/dilated pancreatic ducts secondary to benign stricture in the head of pancreas
What are the most common cystic neoplasms of the pancreas?
MCNs
MCNs contain mucin producing epithelial and how are they described histologically?
contain mucin-rich cells
contain ovarian-like stroma (Estronge and progesterone staining are positive in most cases)
Where do we find most MCNs?
body and tail
What are some characteristics on CT imaging of MCNs that might qualify them as malignant?
eggshell calcifications
large tumor
Cytology of MCNs shows what?
rich in mucin
high CEA
low amylase
Do MCNs have malignant potential?
yes
surgery is standard of care
How do we treat MCNs?
surgery
How do invasive MCNs compare to ductal adenocarcinomas of pancreas?
slower growing
less nodal involvement
less aggressive
Compared to MCNs, serous cystic neoplasms of the pancreas tend to be located where?
HEAD
What do we see on CT scan with serous cystic neoplasms of pancreas?
central calcifications w/sunburst appearance
Tx for serous cystic neoplasms of pancreas?
generally considered benign
resected when >4 cm, pt is symptomatic, rapidly growing lesions, Ca can’t be excluded
Whats the cytology fluid analysis of serous cystic neoplasms of pancreas?
low amylase
low CEA
negative mucin
What are the three types of IPMNs (intraductal papillary mucinous neoplasms)?
side branch IPMN
main duct IPMN
mixed type IPMN
What’s a side branch IPMN?
dilation of a side branch of the main pancreatic duct that communicate with the main duct but do not involve the main duct
What do you do for side branch IPMN?
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
What is the risk of invasive malignancy with side branch IPMN?
10-15 %
What is the treatment for main duct IPMNs?
surgical resection
there is a 30-50% risk of harboring cancer
Cancer risk for main duct IPMNs vs side branch IPMNs?
side branch–> 10-15 % ( >3 cm we resect, otherwise we surveillance)
main branch–> 30-50%, surgery is mandated
Fluid analysis of IPMNs shows what?
high CEA
high amylase
high mucin
What is a mixed-type IPMN?
side branch IPMN which extends to involve the main pancreatic duct to a varying degree
What do we do with mixed-type IPMNs?
treat them like main branch IPMN
harbor 30-50% chance of malignancy
surgery needed
What’s the treatment for mixed-type IPMNs?
surgery (they harbor 30-50% of malignancy, same as main duct IPMNs)
What is the surgical tx for main duct IPMNs?
partial pancreatectomy
What determines survival for IPMNs?
degree of invasiveness
Avg age of pancreatic ca diagnosis?
72
males slightly more affected
Most notable risk factor for developing pancreatic adenocarcinoma is?
smoking
smokers have a 1-3 fold increase risk for developing Ca compared to non-smokers
What are some genetic mutations associated with developing pancreatic cancer?
PRSS1 gene mutation Peutz-Jegers syndrome (STKK1) CF (CFTR) BRC2 Lynch Syndrome FAP
Courvoisier sign ?
painless jaundice
suspect pancreatic Ca
Virchow’s node?
left supra-clavicular node in pancreatic ca
Sister Mary Joseph nodule?
peri-umbilical node in pancreatic Ca
Blumer’s shelf?
peri-rectal pancreatic tumor involvement on DRE
What tumor marker is most sensitive for pancreatic Ca?
Ca- 19-9
Imaging test of choice to evaluate for pancreatic Ca?
multimodal CT
How do we get biopsies for suspected pancreatic ca?
EUS-FNA
Which pancreatic ca stages are treated with surgery?
Stage 1A to 2B
tumors confined to pancreas or peripancreatic tissue without evidence of celiac or SMA involvement, and no evidence of mets
Which pts with pancreatic ca (in terms of staging) do we not operate on?
pts with stage 3 (T4 disease)–> involving celiac/SMA
pts with stage 4–> mets
Whats the role of laparoscopy in pancreatic ca staging?
in pts that appear resectable on imaging, 30% are deemed non-resectable after staging laparoscopy
For tumors involving the head of the pancreas, surgical treatment is what?
pancreaticoduodenemectomy WHIPPLE
MOst common complication following pancreaticoduodenectomy is?
delayed gastric emptying
