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Chapter 19 Flashcards

1
Q

The exocrine pancreas makes up _% of the organ

A

80-85

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2
Q

What is the exocrine pancreas composed of

A

Acinar cells that secrete enzymes for digestion

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3
Q

In the exocrine pancreas, __ are carried by ducts to duodenum for activation via proteolytic cleavage

A

Pronzymes

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4
Q

What are acinar cellls

A

Pyramid shaped epithelial cells with membrane bound granules rich in proenzymes (zymogens ) like trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase, kallikreinogen, and phospholipase A and B

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5
Q

What is the endocrine pancreas

A

Islet of langerhan

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6
Q

What are inslets of langerhans

A

Cell clusters throughout the gland that secrete insulin, glucagon, and somatostatin

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7
Q

What percentage of the pancreas is endocrine pancreas

A

1-2%

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8
Q

In the embryo, what does the dorsal primordium become

A

Body, tail, and superior/anterior aspect of the head of the pancreas; accessory duct of santorini

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9
Q

In the embryo, what does the ventral primordium become

A

Posterior/inferior part of the head of the pancreas; main pancreatic duct (the duct of wirsung)

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10
Q

What is the most common congenital anomaly of the pancreas

A

Pancreas divisum

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11
Q

Why get pancreas divisum

A

Failure of the ventral and dorsal fetal duct systems to fuse properly

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12
Q

What does the main pancreatic duct of wirsung do

A

Drains only a small portion of the head of the gland through the papilla of vaster

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13
Q

Where do the majority of pancreatic secretions drain

A

Small caliber, minor papilla rather than the papilla of vater

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14
Q

What are people with pancreas divisum predisposed to

A

Chronic pancreatitis

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15
Q

What is an annular pancreas

A

Band like ring of normal pancreatic tissue that encircles the second portion of the duodenum

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16
Q

What can annular pancreas cause

A

Duodenal obstruction

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17
Q

Ectopic pancreas symptoms

A

Usually symptomatic, but at aberrant sites may lead to pain from localized inflammation( or rarely mucosal bleeding)

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18
Q

What are most common sites of ectopic pancreas

A

Stomach, duodenum, jejunum, meckel diverticula, ileum

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19
Q

Genetics of pancreatic agenesis

A

Homozygous mutation of PDX1

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20
Q

What does PDX1 code

A

Gene normally encodes homeobox transcription factor critical for pancreatic development

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21
Q

How does the pancreas protect itself

A

Synthesis of proenzymes packaged in secretory granules-biochemically separate

Duodenal enteropeptidase

Trypsin inhibitors

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22
Q

Duodenal enteropeptidase(enterokinase)

A

In the small bowel activates trypsin which activates other proenzymes-anatomically separate
-intrapancreatic activation of proenzymes is normally minimal

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23
Q

Trypsin inhibitors

A

Secreted by acinar and ductal cells

-serine protease inhibitor Kazan type I (SPINK1) further limits intrapancreatic trypsin activity

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24
Q

Failure of pancreatic protection mechanisms

A

Pancreatitis

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25
Q

Acute pancreatitis

A

Reversible pancreatic parenchymal injury associated with inflammation due to diverse etiologies

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26
Q

80% of acute pancreatitis is caused by what

A

Alcoholism and biliary tract disease

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27
Q

What is th the ratio of male to female with acute pancreatitis caused by alcoholism

A

6:1

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28
Q

What is the ratio of females to males that get acute pancreatitis from biliary disease (cholelithiasis)

A

3:1

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29
Q

Pathogenesis of acute pancreatitis: three initiating events that lead to autodigestions

A

Duct obstruction, primary acinar icell injury, and defective intracellluar transport of proenzymes within acinar cells

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30
Q

Pathogenesis of acute pancreatitis: what causes parenchymal autodigestion

A

Inappropriate release and activation of pancreatic enzymes (trypsinogen)

  • degradation of fat cells (phospholipase), damage to elastic fibers of blood vessels (elastase)
  • pre-kallikrein leads to kallikrein which activated the kinin system and clotting(factor XII) and complements systems
  • produces inflammation and thrombosis which further damage acinar cells and amplify the intrapancreatic activation of digestive enzymes
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31
Q

Acute pancreatitis : duct obstruction

A
  • raises intrapancreatic ductal pressure and leads to accumulation of enzymes rich fluid in the intertitium
  • lipase (secreted in an active form) has potential for local fat necrosis
  • death of pancreatic tide releases “danger signals’ locally that stimulate parenchymal release of proinflammatory cytokines
  • interstitial edema through a leaky microvascularization
  • inflammation and interstitial edema compromise vascular flow, increased ischemia to the ongoing parenchyma injury
  • due to gallstones, periampullarry neoplasms, choledochoceles (congenital cystic dilation of the common bile duct), parasites (espicially ascaris lumbricoides and clonorchis sinesis) and possible pancreatic divisum
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32
Q

Acute pancreatitis: primary acinar cell injury

A

Leads to release of digestive enzymes->inflammation and autodigestion

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33
Q

What causes primary acinar cell injury

A
  • oxidative stress: free radicals-> membrane lipid oxidation-?AP1 and NFKB==pro-inflammatory
  • Low ca: trypsin cleaves and inactivated itself
  • high Ca autoinhibition is abrogated and activation of trypsinogen by trypsin is favored
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34
Q

Acute pancreatitis: defective proenzyme transport

A

Exocrine enzymes are misdirected to lysosomes rather than to secretion

Lysosomal hydrolysis of the proenzyme leads to activation and release

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35
Q

What is the most likely etiology of acute pancreatitis

A

Alcohol consumption

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36
Q

How does alcohol cause acute pancreatitis

A
  • direct toxic effect on acinar cells

- alcohol induced oxidative stress->free radicals->lipid peroxidation->free radicals->AP1 and NFKB==pro-inflammatory

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37
Q

Alcohol consumption and acute pancreatic causes transiently increased contraction of what

A

Sphincter of oddi (muscle at papilla of vater)

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38
Q

Acute pancreatitis: chronic alcohol consumption causes secretion of what

A

Protein rich pancreatic fluid causing inspissated protein plugs that block small ducts

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39
Q

Does chronic alcohol consumption commonly cause acute pancreatitis

A

Most do not, those who do, do after many years of abuse

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40
Q

What are some other triggers of acute pancreatitis

A

Metabolic disorders:hyperTG, hyperCa, hyperPTH

Genetic lesions:40% increased risk f prostate cancer

Medications:furosemide, azathioprine, estrogens

Trauma or ischemia to acinar cells

Infection:mumps

Hereditary pancreatitis: characterized by recurrent attacks of severe acute pancreatitis and ultimately leading to chronic pancreatitis

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41
Q

Hereditary pancreatitis

A

Recurrent attacks of severe acute pancreatitis and ultimately leading to chronic pancreatitis

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42
Q

Shared feature of hereditary pancreatitis

A

Shared feature of most forms is a defect that increases or sustains the activity to trypsin

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43
Q

Genetic mutations of hereditary pancreatitis

A

PRSS1

PSINK1

CFTR

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44
Q

PRSS! Hereditary pancreatitis

A

Gain fo function mutation of trypsinogen making trypsin resistant to self inactivation or prone to activation

Most common

AD

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45
Q

SPINK1 hereditary pancreatitis

A

Loss of function preventing inhibition of trypsin

AR

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46
Q

CFTR hereditary pancreatitis

A

Decreased bicarbonate secretion leads to protein plugins, duct obstruction, and pancreatitis

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47
Q

Patients with hereditary pancreatisi have a 40% chance of developing __ __

A

Pancreatic cancer

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48
Q

Morphology acute pancreatitis

A

Microvascular leakage leads to edema

Fat necrosis by lipolysis enzymes, released fatty acids combine with Ca that give a granular blue look to fat cells (saponofication)

Proteolytic destruction of the pancreatic parenchyma

Vascular injury with subsequent interstitial hemorrhage that appears red black with foci of yellow white chalky fat necrosis

Peritoneal cavity: serous, slightly turbid, brown fluid with fat globules

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49
Q

Acute pancreatitis presentation

A

Constant abdominal pain, may refer to upper back or L shoulder

Anorexia, nausea, vomiting

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50
Q

Labs acute pancreatitis

A

Increased plasma levels of amylase (24 hours), lipase (72096 hours)

10% glycosuria

Hypocalcemia due to deposition of Ca soap formation in necrotic fat (saponification)

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51
Q

Full blown acute pancreatitis

A

Acute abdomen (intense pain)

Peripheral vascular collapse

Shock due to activation of systemic inflammatory response syndrome (SRS)

  • leukocytosis, disseminated intravascular coagulation, edema, ARDS (shock and acute renal tubular necrosis may occur)
  • LIFE THREATENING EMERGENCY
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52
Q

Treatment acute pancreatitis

A

Total restriction of oral intake to rest the pancreas

IV fluids and pain meds

Nutrition+volume support

Function returns to normal if resolved

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53
Q

Complications acute pancreatitis

A

5% will die int he first week of severe acute pancreatitis

ARDS and acute renal failure

Sterile pancreatic abscess

Pancreatic pseudocyst

Infection of necrotic debris by gram -ve pathogens from alimentary tract

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54
Q

Chronic pancreatitis

A

Prolonged inflammation of the pancreas due to irreversible destruction of exocrine parenchyma, fibrous and eventually, the endocrine parenchyma

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55
Q

Who gets chronic pancreatitis

A

Middle age males

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56
Q

Causes of chronic pancreatitis

A

Long term alcohol use

Longstanding obstruction by calculi or neoplasm

Autoimmune injury

25% of chronic pancreatitis has a genetic component

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57
Q

Chronic pancreatitis often follows repeated bouts of __ ___

A

Acute pancreatitis

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58
Q

Chronic pancreatitis leads to perilobular fibrosis, duct distortion and altered secretions that can lead to what

A

Loss of parenchyma

Fibrosis

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59
Q

In chronic pancreatitis there is production of fibrogenic inflammatory mediators TGFB and PDGF

A

Induces activation and proliferation of periacinar myofibroblasts (pancreatis stellate cells)->deposition of collagen and fibrosis

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60
Q

Morphology chronic pancreatitis

A

Fibrosis, atrophy and dropout of acini

Variable dilation of pancreatic ducts

Pancreas is hard with focal calcification

Relative sparing of islet of langerhans

Chronic pancreatitis caused by alcohol abuse is characterized by ductal dilation, intraluminal protein plugs and calcification

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61
Q

Symptoms chronic pancreatitis

A

Usually silent, but there may be recurrent attacks of pain and/or jaundice

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62
Q

What triggers chronic pancreatitis

A

ETOH, overeating (increased demand) or opiates that increase tone of sphincter of oddi

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63
Q

With chronic pancreatitis, ____ __ and ___ eventually develop due to destruction of exocrine and endocrine organ

A

Pancreatic insufficiency

DM

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64
Q

Prognosis chronic pancreatitis

A

Not usually life threatening

20-25 year=50% mortality

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65
Q

How diagnose chronic pancreatitis

A

Clinical suspicion

Amylase levels are not always elevated and fever not always present due to acinar cells

Visualization of calcification in the pancreas via CT or ultrasonography

Weight loss and edema due to hypoalbuminemia from malabsorption

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66
Q

Complications chronic pancreatitis

A

Malabsorption, DM, pseudocysts (10%)

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67
Q

Autoimmune pancreatitis

A

Pathogenically distinct form of chronic pancreatitis that is associated with the presence of IgG4 secreting plasma cells int he pancreas

IgG

68
Q

Characterization autoimmune pancreatitis

A

Duct-centric mixed inflammatory cell infiltrate, venulitis, and increased numbers of IgG4 secreting plasma cells

69
Q

Treatment autoimmune pancreatitis

70
Q

Congenital cysts cause

A

Due to anomalous development of the pancreatic ducts

71
Q

Congenital cysts are unilocular and thin walled with _ _ lining

A

Cuboidal epithelial

72
Q

Congenital cysts have a thin fibrous capsule with __ __ _

A

Clear serous fluid

73
Q

Genetics congenital cysts

A

AD polycystic kidney disease

74
Q

What is ongeital cysts

A

Cyst in liver, kidney, and pancreatic cysts

75
Q

Congenital cysts VHL

A

Tumors in retina, cerebellum/brain stem+pancrea, liver, kidney

76
Q

What are the most common pancreatic cysts

A

Pseudocysts

77
Q

Pseudocysts can occur __ the pancreas

A

Outside

Also inside

78
Q

Describe pseudocysts

A

Localized collections of necrotic and hemorrhagic material rich in pancreatic enzymes

79
Q

Why are pseudocysts called pseudo

A

Lack an epithelial lining

80
Q

Why get pseudocysts

A

When areas of intrapancreatic or peripancreatic hemorrhagic fat necrosis are walled off by fibrousand granulation tissue

81
Q

Treat pseudocysts

A

Spontaneously resolve

82
Q

Prognosis pseudocysts

A

Spontaneously resolve, can become infected or compress or penetrate adjacent structures

83
Q

Morphology pseudocysts

A

Walled off areas of fat necrosis

Encircled by fibrosed granulation tissue

Occur after acute pancreatitis or trauma

84
Q

Serous cystic neoplasms

A

Entirely benign and multicystic

85
Q

Where are serous cystic neoplasms usually

A

Int he tail of the pancreas

86
Q

Morphology serous cystic neoplasm

A

Small, lined by glycogen rich cuboidal cells, and contain clear, thin straw colored fluid

87
Q

Serous cystic neoplasms account for _% of all cystic neoplasms of the pancreas

88
Q

Serous cystic neoplasms male or female

89
Q

Age serous cystic neoplasm

90
Q

Presentation serous cystic neoplasms

A

Presents with nonspecific abdominal pain, often an incidental finding on imaging

91
Q

Treat serous cystic neoplasm

A

Surgery is curative

92
Q

Genetic serous cystic neoplasm

A

VHL inactivation (a tumor suppressor)

93
Q

Mutinous cystic neoplasms

A

Precancerous

94
Q

Mutinous cystic neoplasm men or women

95
Q

Where are mutinous cystic neoplasms

A

Tail of pancreas

96
Q

Pain and growth with mucinous cystic neoplasm

A

Painless, slow growing

97
Q

Morphology mucinous cystic neoplasm

A

Filled with thick, tenacious mucin and lined by a columnar mucin-producing epithelium associated with a dense stroma similar to ovarian stroma

98
Q

Treat mucinous cystic neoplasm non invasive

A

Surgical resection is curative bc non invasive

99
Q

There is 50% mortality associated with __ __ arising in a mucinous cystic neoplasm

A

Invasive carcinoma

EARLY DETECTION CRITICAL

100
Q

Genetics mucinous cystic neoplasm

A

KRAS oncogene

TP53 and RNF43 tumor supressor genes

101
Q

Intraductal papillary mucinous neoplasm

A

Precancerous mucin producing neoplasm involving the larger ducts of the pancreas

102
Q

Male or female intraductal papillary mucinous neoplasms

103
Q

Where are intraductal papillary mucinous neoplasms

A

Head»tail

104
Q

What percentage of intraductal papillary mucinous neoplasms are multifocal

105
Q

Morphological differences with mucinous cystic neoplasm

A

No dense ovarian stroma

Involvement of a pancreatic duct

106
Q

Genes intraductal papillary mucinous neoplasms

A

GNAS and KRAS oncogenes

TP53, SMAD4, RNF43 tumor suppressor genes

107
Q

Treatment intraductal papillary mucinous neoplasm

A

Surgerical resection curative

108
Q

Intraductal papillary mucinous neoplasm can progress to

A

Invasive cancer with a higher mortality rate

-early detection and treatment is critical

109
Q

Solid pseudopapillary neoplasm

A

Precancerous

Large, well-circumscribed malignant neoplasms with solid and cystic components filled with hemmorhagiv debris

110
Q

Solid pseudopapillary neoplasms men or women, age

A

Young women

111
Q

Presentation solid pseudopapillary neoplasm

A

Abdominal discomfort owing to their large size

112
Q

Morphology solid pseudopapillary neoplasm

A

Grow in sold sheets or pseudopapillary projections, poorly cohesive

113
Q

Genetics solid pseudopapillary neoplasm

A

CTNNB1 (B catenin) oncogene mutation leads to hyperactivation of WNT signaling

114
Q

Treatment solid pseudopapillary neoplasm

A

Surgical resection usually curative, though some may be locally aggressive

115
Q

Pancreatic intraepithelial neoplasia

A

Well defined non invasive precursor lesions in small ducts that may give rise to invasive pancreatic cancers

No neoplastic epithelium->pancreatic intraepithelial neoplasia->invasive carcinoma

116
Q

Epithelial cells in pancreatic intraepithelial neoplasia show dramatic __ ___

A

Telomere shortening

117
Q

Infiltrating ductal adenocarcinoma

A

Pancreatic carcinoma

118
Q

Infiltrating ductal adenocarcinoma is the _th leading cause of cancer death in the USA

119
Q

What are the top causes of cancer death in USA

A

Lung, colon, breast, pancreatic

120
Q

Pancreatic cancer is one of the most aggressive of the ___ __

A

Solid malignancies

121
Q

Prognosis infiltrating ductal adenocarcinoma

A

5 year survival <5% (usually caught in advanced stage)

122
Q

Ribs factors for infiltrating ductal adenocarcinoma

A

Cirgarette smoke 2x risk-leading preventable cause

High fat diet, chronic pancreatitis family history, diabetes mellitus

Chronic pancreatitis and diabetes mellitus are both risk factors and complications

Ashkenazi jews (BRCA2) and african Americans>caucasiona

123
Q

Location infiltrating ductal adenocarcinoma

A

60% head of pancreas

15% body pancreas

5% tail

20% diffuse involvement

124
Q

Head of pancreas infiltrating ductal adenocarcinoma

A

Obstruct distsal common bile duct leading to jaundice
(Extrahepatic biliary obstruction and an elevation in direct bilirubin and alkaline phosphatase and no inflammation)
PAINLESS JAUNDICE

125
Q

Body pancreas infiltrating ductal adenocarcinoma

A

Body and tail do not impinge on structures and remain clinically silent
May be large and widely disseminated at discovery

126
Q

Morphology infiltrating ductal adenocarcinoma

A

Hard, stellate, gray white, poorly defined masses

127
Q

Morphology infiltrating ductal adenocarcinoma

A

Poorly differentiated
Glands lined with pleomorphic cuboidal columnar epithelium
Forms abortive tubular structures or cell clusters

128
Q

Aggressive infiltrating ductal adenocarcinoma

A

Aggressive, deeply infiltrating growth pattern, elicits an intense desmoplastic response with dense stromal fibrosis

129
Q

Infiltrating ductal adenocarcinoma often grow along __ or invade __ _ and the __

A

Nerves

Blood vessels

Retroperitoneum

130
Q

Who gets pancreatic cancer infiltrating ductal adenocarcinoma

A

Older adults 80% 60-80

131
Q

Presentation pancreatic carcinoma

A

Clinically silent until they invade into adjacent structures

-most present with pain and advanced disease-palliative disease

132
Q

With pancreatic carcinoma there is migratory thrombophlebitis (__ sign) in 10% due to elaboration of platelet activating factors and procoagulants from carcinoma or it necrotic products

133
Q

Pancreatic carcinoma after diagnosis is

A

Buried and progressive

134
Q

What percent of pancreatic carcinomas are respectable

135
Q

Screening tests for pancreatic carcinoma

A

No reliable
-serum levels of several antigens (CA19-9 antigen) are often elevated in them
Not specific or sensitive

136
Q

What can we use CA19 antigen and carcinoembryonic antigen for if not screening for pancreatic carcinoma

A

Follow individuals patients response to treatment

137
Q

How confirm pancreatic carcinoma diagnosis

A

Imaging (endoscopic ultrasonography andcomputed tomography) but not for screening

138
Q

Genetics pancreatic carcinoma

A

KRAS oncogene

CDKN2A tumor suppressor

SMAD4 tumor suppressor

TP53 tumor suppressor

DNA methylation abnormalities

Germline BRCA2 mutation

139
Q

Pancreatic cancer KRAS oncogene mutation

A

Chromosome 12p

Point mutations constitutively activate this GTP-binding protein which normally interacts with tyrosine kinase to augment cell growth and survival via MAPK and PI3K/AKT

140
Q

What is the most frequently altered oncogene in pancreatic cancer

A

90-95% KRAS

141
Q

CDKN2A tumor suppressor mutation pancreatic cancer

A

Chromosome 9p

Encode p16/INK4a and ARF

142
Q

P16/INK4a

A

Cyclin dependent kinase inhibitor that antagonizes cell cycle progression

143
Q

ARF

A

Protein that augments the function of the p53 tumor suppressor protein

144
Q

CDKN2A may be hypermethylated, implying what

A

Epigenetics

145
Q

What are germline CDKN2A mutations associated with

A

Pancreatic cancer and are almost always observed in individuals from families with an increased incidence of melanoma, which also frequently harbors CDKN2A loss of function mutations

146
Q

Most frequently inactivated tumor suppressor gene in pancreatic cancer

A

95%

CDKN2A

147
Q

SMAD4 tumor suppressor pancreatic cancer

A

Chromosome 18q

Encodes a protein important for TGFB signal transduction

Inactivated in 55% of pancreatic cancers, but rarely mutated in other cancers

148
Q

TP53 tumor suppressor pancreatic cancer

A

Chromosome 17p

FunctionL induce cell cycle arrest in response to DNA damage , inducing apopotosis or cellular senescence

Inactivated in 70-75% of all pancreatic cancer

149
Q

DNA methylation pancreatic carcinoma

A

Hypermethylation of promoter of several tumor suppressor genes (CDKN2A)==transcriptional silencing—>LOF

150
Q

BRCA2 pancreatic cancer

A

1-% of pancreatic cancer in ashkenazi jews

151
Q

Acinar cell carcinoma

A

Acinar cell carcinoma form zymogen granules and produce exocrine enzymes such as trypsin and lipase

152
Q

Acinar cell carcinome: syndrome of metastatic fat necrosis

A

Caused by the release of lipase into the circulation develops in 15% of individuals

153
Q

Pancreatoblastoma

A

Rare neoplasms that occur primarily in children age1-15 years old

154
Q

Morphology pancreatoblastoma

A

Distinct microscopic appearance: squamous islands and mixed with acinar cells

155
Q

Prognosis pancreatoblastoma

A

Malignant, but survival is better than it is for pancreatic ductal adenocarcinomas

156
Q

What is Acute pancreatitis

A

Acute inflammation of the pancreas commonly caused by gallbladder disease or chronic alcohol intake

157
Q

Symptoms of acute pancreatitis

A

Abdominal pain, nausea, vomiting, anorexia, abdominal guarding , rigidity, decreased or absent bowel sounds

158
Q

Risk factor for acute pancreatitis

159
Q

Labs acute pancreatitis

A 
Incred WBC(low grade fever
Jaundice
160
Q

Most likely cause of acute pancreatitis

A

Heavy alcohol and gallstones

161
Q

Skin signs with acute pancreatitis

A

Jaundice, grey turners, Cullen’s sign

162
Q

Which hemodynamics parameters occur as a result of pancreatic hemorrhage associated with acute pancreatitis

A

Hypotension and tachycardia

-could get life threatening shock

163
Q

Complications acute pancreatitis

A 
Infection
Pseudocysts
Hemorrhage
DIC
Hypocalcemia
SIRS
ARDS (acute respiratory discress syndrome)
164
Q

ARDS presentation

A

Widespread systemic inflammation

Dyspnea in patients with acute pancreatitis

165
Q

Pancreatic pseudocyst

A

Circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotizing tissue. It is lined wth granulation tissue
Can extravasation to digest adjoining tissue

166
Q

Hemorrhage acute pancreatitis

A

From acute necrotic destruction parenchyma, fat, o local vessels
Or rupture of pseudocyst

167
Q

Causes of acute pancreatitis GET SMASHED

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hypercalcemia
Hyertg
Ercp
Drugs-valproic acid , asathioprine

Pathology (36 decks)

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