Ch 19 Flashcards
what is a annular pancreas
congenital anomaly
abnormal rotation of the pancreas
The central pancreas may have two lobes that migrate in the opposite direction to fuse w/ the dorsal portion
can lead to duodenal obstruction
what is a pancreas divisum
MC congenital anomaly due to the failure of ventral and dorsal bud fusion after rotation
The ventral/dorsal pancreas do not join/fuse w/ the ductal system, –> not a shared ductal system w/ the pancreas and CBD
associated w chronic pancreatitis
what are the pathogenesis pathways for acute pancreatitis
- toxic release of enzymes, cytokines and other mediators into the circulation–> cause SIR - increase WBC, DIC, edema, and ARDS. Shock may occur bc the SIR syndrome and acute renal tubular necrosis
- Once tissue damage begins, trypsin can directly/indirectly active factors in the blood (coagulation, complement, kallikrein and fibrinolytic pathways) –> inflam and small-vessel thrombosis –> further damage to acinar cells and amplify intrapancreatic enzyme activation
what do acute and chronic pancreatitis have in common
due to injury due to autodigestion by its own enzymes when protective mechanisms are disrupted/overloaded
what is the etiology and prognosis of acute pancreatitis
western countries
w/ alcoholism - > men
w/ biliary tract dz- > women
The systemic organ failure and pancreatic necrosis are prognostic indicators
what is the presentation of acute pancreatitis
Abd pain is the cardinal manifestation
= constant, intense, and may refer to the upper or mid back and occasionally to the L shoulder
The pt may also present w/ cullen’s sign (through round L) and grey turner’s sign (subQ tissue)
what are cullen and grey turner signs
how do they occur
what info do they provide
cullen’s sign (through round L) periumbilical ecchymosis
grey turner’s sign (subQ tissue) flank ecchymosis
increased pancreatic enzymes –> diffuse necrosis and inflam w/ retroperitoneal and intraabd bleeding.
The cullens and grey turner signs are not specific, however they are associated w/ severe acute pancreatitis and high mortality
what is relationship of gallstones and acute pancreatitis
Gallstones are present in 35-60% acute pancreatitis cases and can cause gallstone pancreatitis in about 5% of pts
what labs/imaging studies are used to assess acute pancreatitis
elevated lipase (most specific and sensitive marker) and also elevated amylase (which has a short t1/2 so may return to normal before lipase doesn).
10% of cases have glycosuria, decreased Ca2+ due to saponification of necrotic fat
CT scan for direct visualization of the enlarged/inflamed pancreas (at levels L1-L4)
what will be seen on imaging for severe acute cases of pancreatitis
what is the outome
CT will present w/ necrotizing pancreatitis w/ several acute peripancreatic fluid collections AND gallstones in GB w/ NO choledocholithasis
- multiple organ system failure and the pt may pass from complications of pancreatitis even w/ supportive care
what is the morphology of acute pancreatitis
ranges from limited inflam/edema to extensive necrosis and hemorrhage
the extent of injury is based on the duration/severity of the dz
The basic changes in morphology include: microvascular leak/edema, fat necrosis, acute inflam, damage/ autodigestion of pancreatic parenchyma and BV destruction w/ intestinal hemorrhage
where does fat necrosis occur in acute pancreatitis
in the omentum and mesentery of the bowel next to the pancreas and beyond the abd cavity (subQ fat) bc of systemic lipase release
The peritoneal cavity contains serous, slightly turbid, brown-tinged fluid w/ fat globules that reflect digestion of adipose tissue
what is the Tx for acute pancreatitis
put the pancreas to “rest.”
NPO, supportive IV fluids and analgesia
Most pt recover however 5% w/ severe cases die w/i the first week of illness.
what are complications of continued damage in acute pancreatitis
sterile pancreatic abscesses and pancreatic pseudocysts
In 40-60% pt w/ acute necrotizing pancreatitis, the acellular debris can become infected by gram (-) organism
ARDS and acute renal failure
.
what is the cause of chronic pancreatitis
prolonged inflam of the pancreas associated w/ irreversible destruction of the exocrine parenchyma, fibrosis and in late stages loss of endocrine parenchyma
The MCC is long term EtOH use
TGF-B is produced by activated macrophages
what is the fxn of TGF-B in chronic pancreatitis
scar formation and fibrosis of the lung, liver and kidneys
also = anti-inflam cytokine so it limits and stops the inflam response by inhibiting lymphocyte prolif and the activity of other leukocytes
what increases suspicion of chronic pancreatitis?
what is the prognosis
are repeated occurrences of abd pain, persistent back pain, calcifications, pseudocyst, pancreatic exocrine insuf and DM
poor long-term outcome, with 50% mortality rate 20-25 yrs later
The significant morbidity/mortality can be due to the pancreatic exocrine insuf, chronic malabs and DM
what is AI pancreatitis
Type 1 =IgG4 which secrete plasma cells in the pancreas and is one of the manifestations of IgG related dz
Type 2 is restricted to the pancreas, except in a few forms of UC
Both types may mimic pancreatic carcinoma and present as a mass lesion in the pancreatic head on imaging
how does inheritance come into play for pancreatitis
what genes may be involed and what are their fxns
hereditary factor = defect that causes increase/sustains the activity of trypsin
present w/ recurrent attacks of severe acute pancreatitis beginning in childhood
Pt w/ PRSS1 mutations have a 40% increased risk for developing pancreatic CA.
what are congenital cyst
thin-walled cysts that result from anomalous pancreatic duct development
A thining fibrous capsule filled w/ clear serous fluid
may be sporadic/inherited conditions, such as AD polycystic kidney dz and von hippel-lindau dz
what are pseudocysts
= most of the pancreatic cysts
The lack an epithelial lining and form after multiples recurrences of acute pancreatitis, esp when superimposed on chronic alc pancreatitis
can also be due to trauma
resolve spontaneously, become infected or compress/perforate neighboring structures
what are the neoplasms of the pancreas that appear cystic
serous cystic neoplasm
mucinous cystic neoplasm
solid-pseudopapillary neoplasm
intraductal papillary mucinous neoplasms
what are characteristics of Serous cystic neoplasms
benign, F, 60-70s, pancreatic tail
what are characteristics of Mucinous cystic neoplasms:
benign, borderline or carcinoma, 95% F, pancreatic tail
what are characteristics of Solid-pseudopapillary neoplasm:
young F, pancreatic tail, locally aggressive
what are characterisitics of Intraductal papillary mucinous neoplasms: (IPMNs):
connected to duct system, MALE, pancreatic HEAD and progress to CA
explain the progression of PanIN to invasive carcinoma
(Invasive CA arise form noninvasive precursor lesions (pancreatic intraepithelial neoplasia -PanIN))
what is the etiology of pancreatic carcinoma
> 60 yo,
african american, japanese american, native american, hawaiian and ashkenazi jew
what is the prognosis of pancreatic carcinoma
Survival after dx of advanced pancreatic CA is short
> 80% cases are unresectable by the time of dx bc of the invasion of vessels and other structures/distant metastasis
However pt who have a tumor that can be successfully resected can survive a longer period
what is the use of CA 19-9 and carcinoembryonic antigen
the longer survival w/ resection of the tumor shows the importance of early detection
However there is no marker for pancreatic CA for detection
CA 19-9 and carcinoembryonic antigen: lacks specificity and sensitivity- It is seen to be elevated in pt w/ pancreatic CA and is useful in monitoring response to tx.
what are the RF for pancreatic carcinoma
cigarette smoke (doubles risk of pancreatic CA)
chronic pancreatitis (association of chronic inflam, tissue repair and neoplasia)
visceral obesity and high body mass index
DM (modest RF)
how do pancreatic carcinomas present
silent until invasion to neighboring structures
Pain is usually the first sign but by the time the pain appears the CA is far beyond curabl
wt loss, anorexia and generalized malaise and weakness tends to be a sign for advanced dz.
migratory thrombophlebitis (trousseau sign)
Tumor associated inflam and coagulation factors from tumor cells cause increased risk of thromboembolism and disseminated CA
what is the morphology of pancreatic carcinoma
adenocarcinoma and a dense desmoplastic reaction
where do the most of the tumors occur on the pancreas
how does this affect presentation
60% of cancers present in the head of the gland, which are associated w/ obstructive jaundice
These obstruct the distal CBD –> distention of the biliary tree = Courvoisier sign- palpable GB w/ mild painless jaundice
besides the head of the pancreas, where can tumors occur on the pancreas
15% present in the body and 5% in the tail. 20% may involve the whole gland.
what are common sites of invasion for pancreatic carcinoma
tends to grow along Ns and invade BVs and retroperitoneum
The perineural, lymphatic and large vessel invasion is common
direct invasion- spleen, adrenals, transverse colon and stomach
peripancreatic, gastric, mesenteric, omental and portohepatic LNs are commonly involved as well
Distant metastasis = liver and lungs
