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Robbins Pathology GI (Chptr 16,17,18,19) > Chapter 19- Pancreas > Flashcards

Chapter 19- Pancreas Flashcards

1
Q

Which cells in the pancreas are responsible for the majority of secreted enzymes and what is the that percentage

A

Acinar cells account for 80-85% of exocrine (digestion) enzymes

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2
Q

How does the embryological origin of the pancreas lead to congenital abnormalities

A
  • Ventral outpouch gives rise to posterior head/main pancreatic duct
  • Dorsal outpouch gives rise to body, tail, superior head/accessory duct
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3
Q

What is the most common congenital abnormality of the pancreas

A

Pancreas divisium

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4
Q

What is occurring during the process of pancreas divisium formation

A

Failure of the fetal systems of the ventral and dorsal out-pouches do not fuse

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5
Q

What is the structural abnormality and result of pancreas divisium

A

Because the ducts do not form, the majority of the pancreatic secretions drains in the duodenum drains through the minor papilla and not through the duct of Wirsung like normal

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6
Q

What is the clinical consequences as a result of pancreas divisum

A

Increased susceptibility to acute pancreatitis and subsequent chronic pancreatitis

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7
Q

What is annular pancreas

A

Band like ring of normal pancreatic tissue that completely surrounds the second part of the duodenum

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8
Q

What is the clinical consequence of annular pancreas

A

Produces duodenal obstruction

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9
Q

What is the gene commonly seen when there is pancreatic agenesis

A

PDX1

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10
Q

What is the state of reversibility of acute pancreatitis

A

Reversible

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11
Q

What are the two major pathways of acute pancreatitis and what percentage of cases seen do they make up

A

80% of cases are:

  • Biliary tract disease
  • Alcoholism
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12
Q

What is the gender ratio of biliary tract disease causing acute pancreatitis

A

3:1 females

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13
Q

What is the gender ration of alcoholism causing acute pancreatitis

A

6:1 male

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14
Q

What is the pathogenesis that is causing acute pancreatitis

A

Inappropriate release and activation of pancreatic enzymes which causes an inflammatory reaction

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15
Q

What is the process/enzymes present during acute pancreatitis that are released prematurely

A

-Activation of trypsin causes the activation of phospholipases and proelastases, which damage the fat and vessel of the pancreas

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16
Q

How does acute pancreatitis lead to clotting and complement system involvement

A

Trypsin activates prelalikrein, which activates:

  • Coagulation factor 7
  • Complement fixation
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17
Q

What are the three main mechanisms involved during acute pancreatitis

A

1-Pancreatic duct obstruction
2-Primary acinar cell injury
3-Defective intracellular transport of proenzymes within acinar cells

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18
Q

What are pancreatic duct obstructions during acute pancreatitis commonly caused by

A

Gallstones and biliary sludge

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19
Q

Which two organisms can readily cause pancreatic duct obstruction

A
  • Ascaris lumbricoides

- Clonorchis sinensis

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20
Q

Which enzyme is released in the activated form from the pancreas and what is the result

A

Lipase is secreted in the activated form, so has the potential to cause local fat necrosis

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21
Q

What is the result of primary acinar cell injury during acute pancreatitis

A

Release of digestive enzymes, oinflammation and autodigestion of pancreatic tissue

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22
Q

What is the trigger that is linked to the inappropriate activation of enzymes during acute pancreatitis

A

Calcium influx, which is the regulator of trypsin activation

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23
Q

How can damage of acinar cells with regards to intracellular transporting cause damage in acute pancreatitis

A

Proenzymes are delivered to the lysosomes, where they are activated by the hydrolases and released

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24
Q

What is the effect of alcohol on the pancreas

A
  • Contraction of the sphincter of Oddi
  • deposition of protein plugs
  • Toxic to acinar cells
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25
Q

How can chronic alcoholism cause damage to the pancreas

A

-Deposition of protein plugs that result in obstruction of the pancreatic ducts

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26
Q

What is the mechanism that alcohol can cause direct toxicity to the pancreas

A

Damages the acinar cells, which causes inflammation,

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27
Q

Which metabolic conditions are known to cause acute pancreatitis

A
  • Hypertriglycerides
  • Hypercalcemic
  • HyperPTH
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28
Q

Which drugs are known to cause acute pancreatitis

A
  • Furosemide
  • azathioprine
  • 2,3-dideoxyinosine
  • Estrogens
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29
Q

Which infections are known to cause acute pancreatis

A

Mumps (damages acinar cells)

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30
Q

What is the main underlying factor that is seen in Hereditary forms of acute pancreatitis

A

-Defect that causes the increased activation or sustained activity of trypsin

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31
Q

Most hereditary cases of acute pancreatitis are caused by what kind of mutations and in which gene

A

Gain of function in the trypsinogen gene (aka PRSS1)

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32
Q

What is the lifelong risk percent of hereditary pancreatitis

A

40%

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33
Q

What are iatrogenic injuries that can cause acute pancreatitis

A
  • Operative injury

- Endoscopic procedure with dye injection

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34
Q

What are the vascular events that can cause acute pancreatitis

A
  • Shock
  • Atheroembolism
  • Vasculitis
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35
Q

What is the most common cause of hereditary cases and what is the pattern of inheritance

A
  • Gain of function mutation in PRSS1 (aka trypsin)

- Autosomal dominant

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36
Q

What are the histological morphologies seen in acute interstitial pancreatitis, and what is the cause

A

-Fat necrosis (lipase caused), which combine with calcium to form granular blue fat cells

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37
Q

What are the histological morphologies seen in acute necrotizing pancreatitis, and what is the cause

A

Substance is red-black from the hemorrhage, with white chalky fat necrosis scattered within

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38
Q

During acute necrotizing pancreatitis, what is a seconadary area commonly affected and morphologically what is seen there

A

-Peritoneal cavity contains serous, turbid, brown tinges fluid containing fat globules

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39
Q

What is the cardinal manifestation of acute pancreatitis

A

-abdominal pain

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40
Q

How is the pain during acute pancreatitis characterized

A

-constant but intense pain in the upper back, sometimes including the left shoulder

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41
Q

What are the diagnostic features seen for acute pancreatitis

A

Elevated lipase (72 to 96 hours) and amylase (first 24 hours) in the plasma

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42
Q

What are the systemic consequences that are possible due to acute pancreatitis

A
  • DIC
  • Acute respiratory distress
  • acute renal tubular necrosis
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43
Q

What is the management plan taken with acute pancreatitis

A

Resting the pancreas but restriction of oral intake, IV fluids, and analgesia

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44
Q

What is a major complication secondary to acute pancreatitis and what is the percentage

A

40-60% develop gram negative infection of the necrotic debris

45
Q

What is the state of reversibility in chronic pancreatitis

A

Irreversible

46
Q

What is the most common cause of chronic pancreatitis

A

Alcohol abuse

47
Q

What are the very general features seen in chronic pancreatitis

A

Irreversible damages of the exocrine parenchyma and fibrosis. The endocrine may be involved in late stages

48
Q

Which immunological cytokines are predominately involved in chronic pancreatitis

A

TGF-beta

Platelet-derived growth factor

49
Q

What is the immunological effect seen in chronic pancreatitis

A

-TGF beta and PDGF causes proliferation of pariacinar myofibroblasts that result in fibrosis and collagen Deposition

50
Q

During autoimmune pancreatitis, what is commonly associated

A

IgG4 secreting plasma cells in the pancreas

51
Q

What condition may be mimicked by autoimmune pancreatitis, and what is the way to determine

A

Autoimmune pancreatitis mimics pancreatic carcinoma, but will actually respond to steroid therapy

52
Q

Morphologically, how is chronic pancreatitis characterized

A
  • ductal dilation and intraluminal protein plugs and calcification
  • Dilated ducts
  • Acinar loss
53
Q

What are some triggers of attacks for chronic pancreatitis

A
  • Alcohol ingestion
  • overeating
  • Opiates/drugs (increased tone of sphincter of Oddi)
54
Q

What is the long term prognosis for patients with chronic pancreatitis

A

Poor

55
Q

What are the clinical features of chronic pancreatitis that normally lead to morbidity and mortality

A
  • Exocrine insufficiency
  • Chronic malabsorption
  • diabetes mellitus
56
Q

What are the general characteristics of congenital cysts

A

Unilocular, thin-walled cysts that develop from the anomalous development of the pancreatic ducts

57
Q

Congenital cysts usually contain which kind of fluid

A

Clear, serous fluid

58
Q

Which two conditions are commonly associated with the formation of congenital cysts

A
  • Von Hippel-Lindau

- Polycystic kidney disease

59
Q

Congenital cysts located in the kidney, liver and pancreas are commonly associated with which condition

A

-Autosomal dominant polycystic kidney disease

60
Q

Congenital cysts located in the pancreas, liver, and pancreas, along with neoplasms in the retina, cerebellum/Brian stem are commonly associated with which condition

A

Von-Hippel Lindau

61
Q

What are the general characteristics of pseudocysts

A

-Collections of necrotic and hemorrhagic material with pancreatic enzymes and lacking epithelial lining

62
Q

What is the common form of cysts seen in the pancreas

A

Pseudocysts (75%)

63
Q

When do pseduocysts commonly occur

A

Following bouts of acute pancreatitis

64
Q

What is the complications that arise form pseudocysts

A

-Spontaneously resolve, but can become infected or impinge on other structures

65
Q

Which percentages of pancreatic cysts are neoplastic

A

5-15%, most are pseudocysts

66
Q

What is the common location fo serous cystic neoplasms

A

Tail of the pancreas

67
Q

What are the serous cystic neoplasms containing

A

-Glycogen rich cuboidal cells, containing clear, thin, straw colored fluid

68
Q

Which population is most commonly seen to contain serous cystic neoplasms

A

-Females between 60 and 70

69
Q

What is the prognosis of patients with serous cystic neoplasms

A

-Almost always benign and resection is curative

70
Q

Which gene is commonly seen in serous cystic neoplasm

A

Inactivation of VHL

71
Q

What is the patient population see to contain mutinous cystic neoplasm

A

95% female

72
Q

What is the location that contains mutinous cystic neoplasms

A

Tail of the pancreas

73
Q

What are the physical characteristics of the mucinous cystic neoplasm

A

Large cystic cavities containing mucin and lined with columnar mucin producing epithelium with a thick “ovarian” stroma

74
Q

What percentage of mucinous cystic neoplasm contain invasive adenocarcinoma

A

1/3

75
Q

What is the prognosis in those patients with mucinous cystic neoplasms

A

Not good, as half of the 1/3 of patients with invasive adenocarcinoma from their mucinous cystic neoplasm will die

76
Q

Which genes are commonly mutated in mucinous cystic neoplasm

A

KRAS and TP53

77
Q

What is the location that intraductal papillary mucinous neoplasms (IPMNs) are commonly found

A

Larger ducts of the head of pancreas

78
Q

Which patient population is affected by intraductal papillary mucinous neoplasms (IPMNs)

A

Male

79
Q

What are the distinguishing features of IPMNs that allow it to be differentiated from other mucinous cysts

A
  • Absence of “ovarian stroma”

- Involvement of the pancreatic duct

80
Q

What is the prognosis of intraductal papillary mucinous neoplasms (IPMNs)

A

Can developing into invading adenocarcinoma

81
Q

What are the genes commonly associated with IPMNs

A

GNAS, KRAS, TP53, SMAD4, RNF43

82
Q

Which patient population is commonly infected with solid-pseudopapillary neoplasms

A

Young women

83
Q

What are the physical characteristics of solid-pseudopapillary neoplasms

A

Large, well circumcribed malignant cyst with hemorrhagic contents
-Grow in solid sheets but are poorly cohesive

84
Q

What are the clinal signs of a solid-pseudopapillary neoplasm

A

-Abdominal discomfort due to their large size

85
Q

Which gene is almost always associated with the solid-pseudopapillary neoplasm

A

Hyper-activation of WNT signaling due to CTNNB1 (Beta-catenin)

86
Q

What is the prognosis of solid pseudopapillary neoplasms

A

Good, as they are only locally invasive, most are cured by surgical resection

87
Q

What is the prognosis in patients with infiltrating ductal adenocarcinoma

A

Aka pancreatic cancer

-Highest mortality of any cancer

88
Q

What are invasive pancreatic cancers believed to arise from

A

Well defined pancreatic intraepithelial neoplasms (aka PanIN)

89
Q

What is the relation of telomere length in PanIN

A

Dramatic shortening of the telomere length

90
Q

What is the order genetic abnormalities that allow the change from PanIN to invasive carcinoma

A

1-Telomere shortening, KRAS activation
2-Inactivation of CDKNA2
3-Inactivation of TP53, SMAD4, BRCA2

91
Q

What is the most commonly mutated oncogene in pancreatic cancer and what percent

A

KRAS in 90-95%

92
Q

Which pathway is activated through mutations in KRAS

A

MAPK and PI3K/AKT

-aka growth factor pathway and tyrosine kinase

93
Q

What is the most commonly inactivated tumor suppressor gene in pancreatic carcinomas and which percentage

A

CDKNA2/p16 in 95%

94
Q

What is the result of a loss of function in p16/CDKN2A

A

Loss of the cell cycle regulator

95
Q

What are the three tumor suppressor genes that are commonly associated with transition from PanIN to carcinoma

A
  • CDKN2A (95%)
  • SMAD4 (55%)
  • TP53 (75%)
96
Q

What role does SMAD4 mutation have in the transition from PanIN to carcinoma in the pancreas

A

TGFBeta pathway is activated

97
Q

Which carcinoma is most likely if diagnosis markers comes back with mutations in SMAD4

A

Pancreatic carcinoma (rarely seen out of this cancer)

98
Q

Activation of which genetic signaling pathway is activated in pancreatic carcinoma

A

Hedgehog signaling pathway

99
Q

Which patient population is commonly affected by pancreatic carcinoma

A

60-80 year old, black or ashkenazi jew

100
Q

What is the strongest environmental influence on pancreatic cancer and what is the increased risk

A

Smoking, and doubles the risk

101
Q

What are the preexisting conditions that are risk factors for pancreatic cancer

A
  • DM

- Acute pancreatitis

102
Q

What is a first sign that may arise in a patient with pancreatic carcinoma

A

Diabetes mellitus in older patients

103
Q

Which genetic factor seems to be involved in the development of pancreatic carcinomas, especially in Ashkenazi Jews

A

BRCA2

104
Q

Families with increase in which cancer is commonly developing pancreatic carcinomas, and what is the reasoning

A

Melanomas due to CDKN2A loss of function mutations

105
Q

What portion of the pancreas is the common location for the formation of cancers

A

Head of the pancreas

106
Q

What are the two morphological distinguishing features of pancreatic adenocarcinoma

A
  • Highly invasive

- intense host reaction with dense fibrosis (aka desmoplastic response)

107
Q

What are the common morphologies seen in ductal adenocarcinomas in the head of the pancreas

A

-Obstruction of the biliary tree, leading to distention and development of jaundice

108
Q

What is the prognosis and time of discovery of pancreatic adenocarcinomas in the tail of the pancreas

A

Very bad and late because there is no obstruction of the biliary tree

109
Q

What are the common sites of metabolism for ductal adenocarcinomas

A

Liver, lungs, nerves, and blood vessels

Robbins Pathology GI (Chptr 16,17,18,19) (32 decks)

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