Pathology Ch. 19: The Pancreas

Front 1

Most common congenital anomaly of the pancreas

Back 1

Pancreas Divisum

Front 2

Anomaly caused by a failure of the fetal duct systems of the ventral and dorsal pancreatic primordia to fuse? Where does the bulk of the pancreas drain

Back 2

Pancreas Divisum:
It drains through a dorsal duct and the small calliber papilla

Front 3

In pancreas divisum, what happens to the main pancreatic duct

Back 3

It becomes short and drains only a small portion of the pancreas

Front 4

Most common location of ectopic pancreas

Back 4

Submucosa of the stomach and duodenum

Front 5

Band-like ring ring of normal pancreatic tissue that completely encircles what portion of the duodenum? What may this cause?

Back 5

Annular pancreas:
Around the 2nd part of the duodenum
Duodenal obstruction

Front 6

Trypsin inhibitors are what type of protease inhibitors

Back 6

serine

Front 7

Several mechanisms of protection against self-digestion in the pancreas

Back 7

Synthesized as Inactive proenzymes
Enzymes are within membrane bound zymogen-granules within the acinar cells.
Proenzymes must be activated by trypsin
Trypsin inhibitors are present within acinar and ductal secretions
Acinar cells are resistant to enzyme action

Front 8

Activates trypsinogen into trypsin

Back 8

Duodenal enteropeptidase(enterokinase)

Front 9

The pancreas arises from the fusion of dorsal and ventral outpouchings of? The majority of the pancreas is derived from?

Back 9

the foregut
the dorsal primordium of the foregut

Front 10

Gives rise to the posterior/inferior part of the head of the pancreas

Back 10

Ventral primordium of the foregut

Front 11

Type of exocrine cell of the pancreas

Back 11

Acinar

Front 12

Account for approximately 80% of cases in acute pancreatitis

Back 12

Alcohol and biliary disease

Front 13

Reversible pancreatic parenchymal injury associated with inflammation

Back 13

Acute pancreatitis

Front 14

Most cases of idiopathic pancreatitis are caused by germline mutations of

Back 14

Cationic trypsinogen gene:
This mutation abrogates a critical fail-safe mechanism by altering a site on the cationic trypsinogen molecule that is essential for the cleavage of trypsin by trypsin itself. When this site is mutated, trypsin becomes resistant to cleavage by another trypsin molecule.

Front 15

Viral infection that may cause acute pancreatitis? Parasite?

Back 15

mumps
Ascaris lumbricoides

Front 16

The serine protease inhibitor Kasal type 1 gene encodes for?

Back 16

A trypsin inhibitor

Front 17

Fat necrosis in pancreatitis is due to What appearance do the released fatty acids give on microscopic examination

Back 17

activation of lipase
They combine with Ca2+ to form insoluble salts that impart a blue appearance

Front 18

Pancreatitis with mild inflammation, interstitial edema, and focal areas of fat necrosis

Back 18

Acute interstitial pancreatitis

Front 19

In acute necrotizing pancreatitis, where may foci of fat be found

Back 19

within the pancreas, but also on the omentum and mesentery of bowel, and even outside the abd cavity, such as in subcutaneous fat

Front 20

Extensive parenchymal necrosis with dramatic hemorrhage within the gland

Back 20

Hemorrhagic pancreatitis

Front 21

Pancreatitis with microvascular edema, interstitial inflammation, necrosis of fat, proteolytic destruction of pancreatic parenchyma, and destruction of blood vessels w/ hemorrhage

Back 21

Acute necrotizing pancreatitis

Front 22

What pancreatic cells are destroyed in acute necrotizing pancreatitis

Back 22

acinar, ductal, and islets of Langerhans

Front 23

the inappropriate activation of what, is an important triggering event in acute pancreatitis

Back 23

trypsinogen

Front 24

Besides the digestive enzymes, what else does trypsin activate?

Back 24

Converts prekalikrein to kalikrein, thus activating kinin: inflammation and vasodilation/increased vascular permeability
Activates Hageman factor (XII):
Clotting factor

Front 25

Mechanism of injury in acute pancreatitis caused by certain viruses, drugs, trauma, or ischemia.

Back 25

Primary acinar cell injury.

Front 26

Initiates local inflammation and promotes the development of interstitial edema via leaky microvasculature

Back 26

Injured tissues periacinar fibroblasts, and leukocytes release proinflammatory factors such as IL-1, IL-6, TNF, PAF, and substance P.

Front 27

At what time is pancreatic amylase elevated during pancreatitis? Lipase?

Back 27

24 hrs
72-96 hrs

Front 28

How does hypocalcemia occur in pancreatitis?

Back 28

Due to the amount of fatty acids of necrotic fat cells combining with Ca2+ to form insoluble salts.
This is a poor prognostic sign

Front 29

In half of pts with acute necrotizing pancreatitis, the necrotic debris become infected with?

Back 29

gram- organisms

Front 30

How defective transport of digestive enzymes lead to acute pancreatitis?

Back 30

Pancreatic proenzymes are delivered to the intracellular compartmentcontaing lysosomal hydrolases, which activate the proenzymes, leading to injury.

Front 31

What primarily causes activated enzymes?

Back 31

acinar cell injury from:
Duct obstruction
Primary injury (virus, drugs,trauma)
Defective intracellular transport

Front 32

How does duct obstruction lead to acute pancreatitis?

Back 32

Cholelithiasis causes ampulla obstruction which increases intrapancreatic ductal pressure and lead to accumulation of enzyme rich fluid which cannot be entirely inactivated by anti-trypsin. This leads to injury, edema, impaired blood flow, and ischemia, which cause acinar injury, and activate enzymes.

Front 33

How does chronic alcohol ingestion cause pancreatitis?

Back 33

1. secretion of protein-rich fluid that obstructs small pancreatic ducts.
2. Transiently increases pancreatic exocrine secretion and contraction of the sphincter of oddi
3. Direct toxic affect on acinar cells.

Front 34

many of the systemic features of severe acute pancreatitis can be attributed to?

Back 34

Release of toxic enzymes, cytokines, and other mediators that activate systemic inflammatory response, resulting in leukocytosis, hemolysis, DIC, acute respiratory sydrome, and shock.

Front 35

Inflammation of the pancreas with irreversible destruction of the exocrine parenchyma, fibrosis, and in late stages, the endocrine parenchyma

Back 35

chronic pancreatitis

Front 36

Most common cause of chronic pancreatitis

Back 36

alcohol

Front 37

Mutations in the CFTR gene often lead to?

Back 37

Chronic pancreatitis:
Due to decreased bicarb secretion, which promotes protein plugging.

Front 38

Events that cause the development of chronic pancreatitis

Back 38

1. Ductal obstruction by concretions:
Increase in protein concentrations of the pancreatic juice. Prominent in chronic alcoholics.
2. Toxic effects on acinar cells
3. Oxidative stress

Front 39

Promote the activation of periacinar myofibroblasts, resulting in deposition of collagen and fibrosis

Back 39

TGF-B and PDGF:

This predominates in chronic pancreatitis

Front 40

Characterized by parenchymal fibrosis, reduced size and number of acinar cells, variable dilation of the pancreatic ducts, and relative sparing of the islets of langerhans

Back 40

chronic pancreatitis

Front 41

Loss of what cells is a constant feature of chronic pancreatitis

Back 41

acinar cells

Front 42

Presentation of ductal epithelium in chronic pancreatitis

Back 42

may be hyperplastic, atrophied, or may show squamous metaplasia

Front 43

Chronic pancreatitis characterized by a duct-centric mixed inflammatory cell infiltrate, venulitis, and increased numbers of IgG4-producing plasma cells. Txmt?

Back 43

Lymphoplasmocytic sclerosing pancreatitis
AutoImmune
Steroids

Front 44

In chronic pancreatitis, development of what disease may be associated with destruction of the islets of langerhans

Back 44

diabetes

Front 45

Syndrome of vascular neoplasms are found in the retina and cerebellum or brain stem in association with congenital cysts in the pancreas, liver, and kidneys

Back 45

von Hippel-Lindau disease

Front 46

Believed to result from anamolous development of the pancreatic ducts

Back 46

Congenital cysts

Front 47

Congenital cysts are usually lined by?

Back 47

uniform cuboidal epithelium

Front 48

Localized collections of necrotic-hemorrhagic material rich in pancreatic enzymes. When do they usually occur?

Back 48

Psuedocyts, because they have no epithelial lining
Occur during an episode of acute pancreatitis in the setting of chronic pancreatitis.

Front 49

Most common type of cyst in the pancreas

Back 49

pseudocysts

Front 50

Pseudocysts are formed by the walling off of?

Back 50

areas of peripancreatic hemorrhagic fat necrosis with fibrous tissue

Front 51

Manysurgically resected mucinous cystic neoplasms harbor an associated ?

Back 51

invasive adenocarcinoma

Front 52

Benign cystic neoplasms composed of glycogen rich cuboidal cells surrounding small cysts containing clear, thin, fluid

Back 52

serous cystadenomas

Front 53

Mucinous cystic neoplasms usually arise in what area of the pancreas? Lined by what type of epithelium?

Back 53

Body or tail
Columnar mucin producing epi with associated dense stroma similar to ovarian stroma.

Front 54

Mucin producing intraductal neoplasms? How do they differ from mucinous cystic neoplasms?

Back 54

Intraductal papillary mucinous neoplasms (IPMNs):
Occur in the head of the pancreas, rather than the body or tail.
Lack the dense "ovarian" stroma

Front 55

Individuals present with metastatic fat necrosis caused by release of lipase into the systemic circulation.

Back 55

Acinar cell carcinomas:
Prominent acinar cell differentiation, formation of zymogen granules, and production of exocrine enzymes.

Front 56

Precursor lesions to pancreatic carcinoma. Show dramatic shortening of?

Back 56

PanIn:
pancreatic intraepithelial neoplasias
Telomeres

Front 57

Most frequently altered oncogene in pancreatic CA

Back 57

KRAS:
Impair GTP activity of the K-ras protein, causing it to be constitutively active.

Front 58

Most frequently inactivated tumor suppressor gene in pancreatic CA

Back 58

p16/CDKN2A

Front 59

Strongest environmental influence in pancreatic cancer

Back 59

cigarette smoking

Front 60

Most pancreatic CA arise in what part of the pancreas? What may this cause?

Back 60

Head:
Causes obstruction of the common bile duct leading to marked dilation of the biliary tree and jaundice.

Front 61

Ampulla of vater

Back 61

Joining of the common bile duct and pancreatic duct just prior to emptying in the papilla of vater

Front 62

Carcinomas in this part of the pancreas are often silent and therefore very disseminated by the time they are discovered

Back 62

Body and tail

Front 63

Two features characteristic of pancreatic ca

Back 63

highly invasive
elicits an intense non-neiplastic host rxn composed of fibroblasts, lymphocytes, and extracellular matrix (desmplastic response).

Front 64

The vast majority of pancreatic carcinomas are?

Back 64

ductal adenocarcinomas that form ductal glands and secrete mucin