Pathology of Exocrine Pancreas -Lyons

what part of the pancreas is NOT retroperitoneal

tail

pancreas extends from where to where

C loop of duodenum → hilum of spleen

normal pancreas

what comprises 80% of pancreas

acini → produce bicarb (ductal cells) and digestive enzymes, proenzymes that need alkaline pH

digests starch into maltose (disaccharide)

amylase

digests triglycerides into monoglycerides and free FA

target for orlistat

lipase

most cases of acute pancreatitis can be traced to

biliary tract disease (gallstones) or alcoholism

reversible lesions, inflammation of pancreas

35-60% of cases also have gallstones

range from edema and fat necrosis to parenchymal necrosis with severe hemorrhage

• oft autodigestion

• trypsin → activates others

acute pancraetitis

what activates trypsinogen into trypsin

enterokinase in small intestine epithelial cell

head of pancreas in relation to duodenum

posterior

scorpion stings

can cause acute pancreatitis

clinical presentation of acute panc

epigastric abdominal pain, rad to back

partly relieved by sitting up and leaning forward

Cullen sign, Grey-Turner sign

N/V

Labs for acute panc

elevated serum and urine amylase

elevated serum lipase (more spec)

may see hypocalcemia

• fat necrosis, saponification

leads to contraction of sphincter of oddi and obstruction of panc drainage

alcoholism

criteria for dx of panc

>= 2/3

ab pain consistent with the disease

serum lipase/amylase >3x ULN

characteristic imaging findings

cullen and greyturner sign

imaging for acute pancreatitis

US

CT if unclear

MRI

patients with acue panc and concurrent acute cholangitis should

undergo ERCP within 24h admission

if no cholangitis/jaundice, ___________ rather than ERCP should screen for choledocholiathiasis

MRCP or EUS

edematous pancreas bc acute pancreatitis

edematous panc with pseudocyst in tail of panc

normal panc with distinct borders

proposed mechanism: panc duct obstruction

blocks up → interstitial edema → impaired blood flow and ischemia → acinar cell injury

proposed mechanism: acinar cell injury

alcohol/drugs/trauma/ischemia/virus/hypercalcemia → releases intracellular proenzymes and lysosomal hydrolases → activation of enzymes → further acinar cell injury

proposed mechanism: defective intracellular transport of proenzymes in acinar cells

→ delivery of proenzymes to portion of cell containing lysosomal hydrolases → intracellular activation of enzymes → acinar cell injury

gross findings in acute pancreatitis

mild: swollen/edematous

severe: autodigestion → hemorrhagic (very vascular), liquefactive necrosis, fat necrosis (yellow nodules)

microscopic acute pancreatitis

diffuse interstilial edema bc microvascular leakage

interstitial hemorrhage from blood vessel destruction

liquefactive necrosis of pancreatic parenchyma

gat necrosis of pancreatic and peripancreatic fat

dystrophic calcification, early and extensively

immune respons to acute pancreatitis

initially neutrophils

→ macrophages

→ lymphocytes

acute pancreatitis

normal left, necrotic on right. red tinge in middle is hemorrhage

acute pancreatitis

complications of acute panc

shock

infection/abscess

pseudocyst

calcifications

ARDS

DIC

subcutaneous fat necrosis/pancreatic panniculitis

localized area of necroti and hemorrhagic tissue with enzymes surrounded by fibrous and granulation tissue that develop, try to wall off

NO epithelial lining

high amylase within cysts but normal to mild elevated in serum

pseudocysts

C * HOBBS

Calcium <8

HCT >10%

Oxygen <60

BUN >5

Base deficit >4

Sequestration of fluid >6L

24 mmol/L - serum bicarb

base deficit

fluid input - fluid output

fluid sequestration

how he would ask a ranson criteria q

1

predisposing factors for chronic pancreatitis

alcohol, cystic fibrosis/genetics (kids), idiopathic

chronic panc:

repeated/persistent acute panc with irreversible destruction of pancreatic parenchyma and replacement of parenchyma with ________

fibrosis,

dystrophic calcification

why would someone with chronic panc have decreased duodenal pH

decreased bicarb secretion from the damage

chronic panc have inc risk of

panc adenocarcinoma

imaging on chronic pancreatitis

“chain of lakes” due to alternatin stenosis and dilated from fibrosis and calcifications

micro of chronic panc

fibrosis, inflammation, protein plugs in ducts

gross chronic panc

hard firm white pancreas

pink fibrosis, remnants of islets

chronic panc

irreg dilated ducts and side branches

chronic panc

pancreatic adenocarcinom arises from

pancreatic ducts, precursor dysplasia (PanIN pancreatic intraepithelial neoplasia)

doubles the risk of pancreatic adenocarcinoma

smoking

most pancreatic adenocarcinoma arises in

head of pancreas

progression to cancer

tumor in body or tail of pancreas may present as

diabetes

tumor in head of pancreas may present as Courvoisier sign:

obstructive jaundice

pale stools

distended and nontender palpable gallbladder

Trousseau syndrome/sign of malignancy

migratory thrombophlebitis with swelling and tenderness of extremities due to platelet aggregating factors and procoagulants from tumor or its necrotic products

tumor marker for pancreatic cancer

CA 19-9 (may be in others), not for screen but response to tx

gross panc adenocarcinoma

poor delineated, gray white hard mass

local infiltrate

micro panc adenocarcinoma

individual tubular glands surrounded by stroma

atypia and desmoplasia

mucin production is specific for what in panc adenocarcinom

ductal origin

pancreatic adenocarcinoma. SMV abutted but not encased

pancreatic adenocarcinoma

normal on left

small irregular glands

panc adenocarcinoma.

poorly differentiated glands and extensive desmoplasia (collagenous stroma)

pancreatic adenocarcinoma

tx pancreatic adenocarcinoma

surgery, whipple

chemo

radiation

bad prognosis

whipple procedure