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Block 10 Week 4 > Usera: Exocrine Pancreas > Flashcards

Usera: Exocrine Pancreas Flashcards

1
Q

The major pancreatic duct (which joins the common bile duct & empties into the small intestine)

A

Duct of Wirsung

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2
Q

Accessory pancreatic duct emptying into the duodenum

A

Duct of Santorini

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3
Q

Congenital absence of the pancreas may be due to defects in this gene

A

PDX1 - transcription factor necessary for pancreatic development

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4
Q

What is a consequence of pancreatic agenesis?

A

DM

malabsorption

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5
Q

Most common congenital anomaly of the pancreas
A congenital anomaly in the anatomy of the ducts of the pancreas in which a single pancreatic duct is not formed, but rather remains as two distinct dorsal and ventral ducts

A

pancreas divisum

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6
Q

Rare, congenital anomaly that may not become apparent until adult life
Developmental malformation in which the pancreas forms a ring around the duodenum, leading to a risk of duodenal obstruction

A

annular pancreas

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7
Q

Pancreatic tissue in location other than the pancreas
Present in approximately 2% of autopsies
Stomach, duodenum, jejunum, Meckel diverticulum, ileum
Located within the submucosa
Consists of acini and occasionally islet cells
Pathogenesis is unknown

A

Ectopic pancreas

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8
Q

What is pancreatitis? What are the two general categories?

A

inflammation of the pancreas with injury of the exocrine pancreatic tissue; can be acute, in which the exocrine tissue can return to normal function is the pancreatitis is removed, or chronic if there is irreversible injury with loss of pancreatic exocrine tissue

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9
Q

Reversible pancreatic parenchymal injury associated with inflammation

A

Acute pancreatitis

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10
Q

What are the two most common causes of acute pancreatitis?

A

biliary tract disease (gallstones)
alcohol

  • *biliary tract disease a more common cause in women, alcohol more likely in men
  • *other causes include trauma, hypercalcemia, hyperlipidemia, drugs, mumps, etc
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11
Q

(blank) are present in 35-60% of cases of acute pancreatitis

A

gallstones

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12
Q

What types of things can cause an obstruction of the pancreatic ductal system leading to acute pancreatitis?

A

Periampullary neoplasm (cancer of the pancreatic head)
Pancreatic divisum
Choledochocele (congenital cystic dilatation of the CBD)
Biliary sludge
Parasites (Ascaris, Clonorchis)

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13
Q

Infection with this virus can cause acute pancreatitis

A

mumps virus

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14
Q

3 metabolic disorders that can lead to acute pancreatitis

A

alcohol
hyperlipoproteinemia (hyper TAGs)
hypercalcemia

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15
Q

3 forms of ischemic injury that can lead to acute pancreatitis

A

shock
vasculitis
atheroembolism

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16
Q

What types of trauma can cause acute pancreatitis?

A 
gallstones
iatrogenic injury (during operation)
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17
Q

What gene is associated with acute pancreatitis?

A

PRSS1 & SPINK1

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18
Q

So, list three major causes of acute pancreatitis?

A

duct obstruction
acinar cell injury (alcohol, drugs, trauma, ischemia, viruses)
defective intracellular transport (alcohol, metabolic injury, duct obstruction)

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19
Q

As a consequence of acinar cell injury, enzymes are released from damaged acinar cells. What are the long term effects of these activated enzymes?

A

interstitial inflammation & edema
proteolysis
fat necrosis
hemorrhage

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20
Q

What are some histological findings in acute pancreatitis?

A

necrosis of the pancreatic parenchyma
fat necrosis
areas of hemorrhage

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21
Q

How do people with acute pancreatitis present clinically?

A

abdominal pain AND back pain
epigastric tenderness
nausea & vomiting
low-grade fever

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22
Q

What are the most valuable lab findings for acute pancreatitis?

A

serum lipase is specific for pancreatitis - the rise parallels the increase in amylase, but remains elevated for 14 days while serum amylase rises w/i 2-24 hrs and then returns to normal w/i 2-3 days
**lipase is more useful here, bc amylase is secreted by other organs too

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23
Q

Why is full-blown acute pancreatitis a medical emergency?

A

leukocytosis, hemolysis, DIC
acute respiratory distress syndrome
diffuse fat necrosis
may have peripheral vascular collapse or shock with ATN

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24
Q

How to treat acute pancreatitis?

A

rest –> total restriction of oral intake (nothing by mouth)
IV fluids
analgesics

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25
Q

What are the sequelae or complications of acute pancreatitis?

A

5% die
pancreatic abscess
pancreatic pseudocyst

26
Q

Inflammation of the pancreas with IRREVERSIBLE destruction of the exocrine pancreatic parenchyma, fibrosis and, in later stages, destruction of endocrine pancreatic parenchyma

A

chronic pancreatitis

27
Q

What is the most common cause of chronic pancreatitis?

A

chronic alcohol abuse (in adults)

CF (in children)

28
Q

Who gets chronic pancreatitis?

A

middle aged males

29
Q

What are some other causes of chronic pancreatitis?

A

long-standing obstruction
hereditary pancreatitis - PRSS1 or SPINK1 mutations
CFTR gene mutations (very common in CF)

30
Q

How do CFTR mutations cause chronic pancreatitis?

A

they decrease bicarbonate secretion by pancreatic ductal cells & promote plugging of the ducts/ductules

31
Q

How can alcohol cause chronic pancreatitis?

A

alcohol increases the protein in ductal juice, which may calcify, leading to increased viscosity & ductal obstruction

32
Q

What will the pancreas look like grossly with chronic pancreatitis?

A

fibrosis & calcification

33
Q

What are some of the histological findings of chronic pancreatitis?

A

preservation of lobules & acini, surrounding parenchymal fibrosis
reduced number & size of acini with relative sparing of islets
variable dilation of the pancreatic ducts
chronic inflammation

34
Q

What is the “hot” lab test that is currently done to look for AUTOIMMUNE pancreatitis?

A

ordering an IgG4 after a duct-centric biopsy

35
Q

How does chronic pancreatitis present clinically?

A

repeated attacks of mild to severe abdominal pain
persistent abdominal & back pain
jaundice
silent w development of diabetes or pancreatic insufficiency

36
Q

Patients with chronic pancreatitis may precipitate their attacks by doing these things…

A

alcohol use
overeating
use of drugs that increase the tone of the sphincter of Oddi

37
Q

What are the long-term consequences/complications of chronic pancreatitis?

A 
usu not immediately life-threatening
pancreatic exocrine insufficiency w/ malabsorption
diabetes
chronic pain
10% may have pancreatic pseudocysts
38
Q

Result from anomalous development of the pancreatic ducts
Unilocular, thin-walled, up to 5 cm in diameter
Lined by uniform cuboidal epithelium
Enclosed by a thin fibrous capsule
Filled with clear serous fluid

A

congenital cysts

39
Q

What types of syndromes are associated with congenital cysts of the pancreas?

A

ADPKD

von Hippel-Lindau disease

40
Q

Fluid collection (filled with proteins, etc) and lined by granulation tissue, with NO epithelial lining
Necrotic-hemorrhagic material rich in pancreatic enzymes
Single or multiple, Small or large
Most communicate with the pancreatic ductal system
Approximately 75% of pancreatic cysts
Can be caused by acute pancreatitis, chronic pancreatitis, & related to trauma

A

pancreatic pseudocyst

**granulation tissue very specific for pancreatic pseudocyst

41
Q

What are some complications of pancreatic pseudocysts?

A

if they expand, they can result in abdominal pain, duodenal or biliary obstruction, vascular occlusion, or fistula formation
can lead to spontaneous infection
pseudoaneurysm
pancreatic ascites & pleural effusion

42
Q

95% in women
Can be associated with invasive carcinoma
Usually arise in the body or tail
Present as painless, slow-growing masses
Cysts are large, filled with thick mucin
Do not connect with pancreatic ductal system
Cysts are lined by columnar mucinous epithelium overlying an ovarian type stroma
Pathologic evaluation for invasive malignancy after complete removal

A

mucinous cystic neoplasm

43
Q

Who gets mucinous cystic neoplasms?

A

women!

44
Q

Do mucinous cystic neoplasms connect with the pancreatic ductal system?

A

no!

45
Q

Mucinous cystic neoplasms of the pancreas are lined by columnar mucinous epithelium overlying a (blank)

A

ovarian type stroma

**thought to come from the same embryologic origin as the ovary

46
Q

Mucin-producing intraductal neoplasm - occurs within the ductal system
Occur more often in MEN
Occur in the pancreatic HEAD
10-20% are multifocal
Involve a larger pancreatic duct
Evaluate for invasive malignancy after surgical resection!!

A

intraductal papillary mucinous neoplasm

47
Q

Who gets intraductal papillary mucinous neoplasms? (IPMN) Where do they occur?

A

men!

in the pancreatic head

48
Q

Benign cystic neoplasm
Glycogen-rich cuboidal cells lining small cysts containing clear (serous) fluid
Represent 25% of all cystic neoplasms of the pancreas
Occur 2X more often in women
7th decade of life
Present as abdominal pain or masses
Surgical resection is curative

A

serous cystadenoma

49
Q

Young women - classic presentation
Head of the pancreas
Large, well-circumscribed with solid and cystic components
Cystic areas filled with hemorrhagic debris
Neoplastic cells in sheets or in papillary projections
Present with abdominal discomfort
Activating mutation of β-catenin

** know this one

A

solid pseudopapillary neoplasm

50
Q

Mutations in this protein lead to solid pseudopapillary neoplasms

A

Beta-catenin

51
Q

Now the 4th leading cause of death in the US

A

pancreatic ductal adenocarcinoma

**high mortality rate w/ a 5 yr survival rate of less then 3-5%

52
Q

Who gets pancreatic cancer? What are the risk factors?

A

people ages 60-80

smoking, diet rich in fats, alcohol, diabetes, & chronic pancreatitis all are risk factors

53
Q

Where does pancreatic cancer occur in the pancreas?

A

most often in the head (60%) 15% in the body

5% in the tail

54
Q

How does pancreatic cancer present grossly?

A

hard, stellate, gray-white, poorly defined masses

55
Q

Most cases of pancreatic carcinoma are highly invasive. Most are (blank) carcinomas. They often grow along & invade (blank), and can invade (blank) and metastasize

A

ductal; nerves; lymphovascular spaces

56
Q

What will you see histologically with pancreatic carcinoma?

A

intense fibroblastic response (desmoplastic response)
Try to look like normal ductal epithelium by forming glands and secreting mucin (poor attempt)
Abortive tubular structures or cell clusters growing in a deeply infiltrative pattern

57
Q

How does pancreatic cancer present clinically?

A 
silent until invasion of other structures, then pain
jaundice if the cancer arises in the head of the pancreas & obstructs the duct
weight loss (very common), fatigue, general malaise, weakness
migratory thrombophlebitis in 10% (Trousseau sign)
58
Q

How do you treat pancreatic cancer?

A

surgical resection!
Whipple procedure

**The most common technique of a pancreaticoduodenectomy consists of the removal of the distal segment of the stomach, the first and second portions of the duodenum, the head of the pancreas, the common bile duct, and the gallbladder, because each of these receive the same blood supply!

59
Q

What will you see endocscopically with IPMN?

A

fishmouth appearance spewing mucin into the ampulla of vader

60
Q

What is the main concern with an IPMN?

A

whether it has progressed to adenocarcinoma

Block 10 Week 4 (8 decks)

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