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GI2 E1 > pancreas > Flashcards

pancreas Flashcards

robbins

1
Q

composition of the exocrine pancreas

A

= >80% of the pancreas

composed of acinar cells that secrete enzymes for digestion, i.e. trypsinogen, chymotrypsinogen, procarcboxypeptidase, proelastase, kallikreinogen, prophospholipase A+B

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2
Q

composition of the endocrine pancreas

A

contain islets of langehans,

secrete insulin, glucagon, and somatostatin

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3
Q

why are congenital anomalies so common in the pancreas

A

the dorsal and ventral foregut outpouchings have a very complex way that they fuse

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4
Q

dorsal pancreatic primordium gives rise to

A

body
tail
superior/anterior part of the head of the pancreas

drains though accessory duct of the santorini

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5
Q

ventral pancreatic primordium gives rise to

A

poster/inferior part of the head of the pancreas

drains through main pancreatic duct to papilla of vater

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6
Q

most common congenital anomaly of the pancreas

A

pancreas divisum

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7
Q

normal pancreatic drainage

A

where the main pancreatic duct (of Wirsung) joins the common bile duct just proximal to the papilla of vater, and the accessory pancreatic duct (of Santorini) drains into the duodenum through a separate minor papilla

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8
Q

what is pancreatic divisum

A

failure of fetal duct systems–> the bulk of the pancreas drains into the duodenum through the small caliber minor papilla

which means it backs up bc the sphincter is so small

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9
Q

individuals with pancreatic divisum are predisposed to _____ because of the inadequate drainage of the pancreatic secretions through the minor papilla

A

chronic pancreatitis

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10
Q

what is annular pancreas

A

a band like ring of normal pancreatic tissue that completely encircles the second portion of the duodenum

can lead to duodenal obstrunction

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11
Q

where is ectopic pancreatic tissue most commonly found

A

most to least =

stomach+duodenum
jejunum
meckel diverticula
ileum

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12
Q

prognosis of having an ectopic pancreas

A

usually an incidental finding, but also can cause localized into or incite mucosal bleeding

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13
Q

what germline mutation is associated with pancreatic agenesis

A

PDX1

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14
Q

what is the role of trypsin in the protection of the pancreas from self-digestion

A

most proenzymes are activated by trypsin,

trypsin is activated by duodenal enteropeptidase within the small bowel

acinar and ductal cells secrete trypsin inhibitors, including SPINK1, which further limits intrapancreatic trypsin activity

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15
Q

acute pancreatitis = ____ pancreatic perenchymal injury, due to EtOH toxicity, obstruction, vascular injury, mutations, or infection

A

reversible

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16
Q

___ and ____ account for ~ 80% of acute pancreatitis in the west

A

alcoholism (mostly male) and biliary tract ds (mostly female)

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17
Q

etiology of acute pancreatitis

A

inappropriate release and activation of pancreatic enzymes, which destroy pancreatic tissue and elicit an inflammatory response

intrapancreatic trypsin activation

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18
Q

intrapancreatic trypsin activation of prophospholipase causes what

A

degrade fat cells of the pancreas

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19
Q

intrapancreatic trypsin activation proelastase causes what

A

damage elastic fibers of BVs

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20
Q

intrapancreatic trypsin activation prekalikrein causes what

A

activates the kinin system–> activated clotting and complement systems –> inflammation and small essel thromboses–> damage to acinar cells,

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21
Q

how can pancreatic duct obstruction lead to acute pancreatitis

A

pancreatic duct obstruction –> accumulation of fluid in the interstitium that has proenzymes and active lipase –> fat necrosis –> edema –> impaired bloow flow –> ischemia

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22
Q

causes of pancreatic obstruction

A 
cholelithiasis
ampullary obstruction
chronic alc
ductal concretions
parasites- Ascaris lumbricoides, Clonorchis sinensis
pancreas divisum
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23
Q

what vascular etiologies can cause acute pancreatitis

A

shock, atheroembolism, vasculitis

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24
Q

what infections can cause acute pancreatitis

A

mumps

A. lumbricoides and C. sinensis parastial infections can lead to pancreatic obstruction –> acute pancreatitis

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25
Q

how can primary acinar cell injury lead to acute pancreatitis

A

release of digestive enzymes, inflammation, and autodigestion of pancreatic tissues

caused by ischmiea–> oxidative free radicals –> activate AP1 and NF-KB
increased Ca influx–> triggers inappropriate activation of enzymes
alc, drugs, trauma,

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26
Q

how can defective intracellular transport of proenzymes within the acinar cells lead to acute pancreatitis

A

(caused by alc or obstruction)

panreatic proenzymes are incorrectly sent to the intracellular compartment containing lysosomal hydrolases
leading to intracellular activation–> acinar cell injury

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27
Q

etiology of EtOH toxicity pancreatitis

A

alc consumption increases contraction of the sphincter of Oddi and chronic alc ingestion leads to deposition of thick protein plugs and obstruction of small pancreatic ducts

also direct toxicity to acinar cells

cause oxidative stress–> alter intracellular Ca levels–> promote intracinar trypsin activation

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28
Q

acinar cell injury –> activated enzymes –> _____ (4) —> acute pancreatitis

A
  1. interstitial inflammation and edema
  2. proteolysis
  3. fat necrosis
  4. damage to vessel walls, hemorrhage
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29
Q

what genetic mutations are associated with predisposition to pancreatitis

A 
CFTR= cystic fibrosis
PRSS1= serine protease 1
SPINK1= serine peptidase inhibitor, 
CASR= Ca-sensing receptor
CTRC= chymotrypsin C
CPA1= carboxypeptidase A1
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30
Q

what metabolic disorders predisopose one to developing acute pancreatitis

A

hypertriglyceridemia
hypercalcemia
hyperparathyroid

31
Q

what meds predispose one to developing acute pancreatitis

A 
furosemide
azathioprine
2-3-dideoxyinosine
estrogens
etc.
32
Q

hereditary pancreatitis is associated with ____ attacks of ____ often beginning _____ and ultimately leading to _____

A

reccurent
severe acute pancreatitis
in childhood
chronic pancreatitis

33
Q

what three genes are associated with hereditary pancreatitis and what do they have in common

A

PRSS1 (AD) most
SPINK1 (AR)
CFTR

= all increase or sustain the activity of trypsin

34
Q

patient with hereditary pancreatitis have a 40% lifetime risk of developing ___

A

pancreatic CA

35
Q

characteristic morphology of acute pancreatitis

A

microvascular leak and edema

fat necrosis (of pancreas, omentum, or mesentery)

acute inflammation

destruction of pancreatic parenchyma, acinar and duct cells, and islets of langerhan (more severe forms)

destruction of BVs and interstitial hemorrhage (more severe forms)

pancreas is red-black from hemorrhage with foci of yellow-white fat necrosis

most severe form=hemorrhagic pancreatitis

36
Q

clinical presentation of acute pancreatitis

A

constant and intense abd pain referred to the upper back and occasionally the left shoulder

anorexia, N/V,
elevated amylase and lipase

37
Q

prognosis of acute pancreatitis

A

full blown acute pancreatitis is a medical emergency

–> explosive release of toxins into the systemic circulation–> leukocytosis, DIC, edema, and acute respiratory distress –> shock and acute renal tubular necrosis
can lead to systemic organ failure

5% die within the first week
40-60% with necrotic pancreatitis will get a G+ infection

38
Q

lab findings associated with acute pancreatitis

A

marked elevation of serum amylase in the first 24 hours
rising serum lipase between 72-96 hours

glycosuria in 10% of cases
hypocalcemia from precipitation of calcium soaps in necrotic fat

39
Q

define chronic pancreatitis

A

prolonged pancreatic inflammation with irreversible destruction of the exocrine parenchyma, fibrosis, and destruction of endocrine parenchyma in the late stages

40
Q

population associated with chronic pancreatitis

A

middle aged males

41
Q

most common cause of chronic pancreatitis

and other causes

A

alcohol abuse

-long standing obstruction, autoimmune, hereditary

42
Q

etiology of chronic pancreatitis

A

repeated episodes of acute pancreatitis will initiate a sequence of perilobular fibrosis, duct distortion and altered pancreatic secretions

43
Q

chronic pancreatic injury leads to local production of ______ that activate ___ (aka ___) to promote ___ and ____

A

inflammatory mediators (TGF-B, PDGF)

periacinar myofibroblasts/pancreatic stellate cells

fibrosis and acinar cell loss

44
Q

etiology of autoimmune pancreatitis

A

IgG4 secreting plasma cells in the pancreas

can mimic signs of pancreatic carcinoma

45
Q

characteristic morphology of chronic pancreatitis

A

fibrosis, atrophy and dropout of acini, and variable dilation of pancreatic ducts

acinar loss is a constant feature while loss of islets of langerhan is more variable

caused by alc abuse: characterized by ductal dilation and intraluminal protein plugs and calcification

46
Q

clinical features of chronic pancreatitis

A

follows repeated bouts of acute pancreatitis

repeated attacks of abd pain or persistant abd/back pain

pain precipitated by alc abuse, overeating, or use of opiates and other drugs that increase sphincter of oddi tone

can also be silent until insufficiency or DM develop

can have mild fever, elevations of serum amylase, weight loss, edema due to low albumin

gallstone obstruction–> jaundice or elevations in serum alkaline phosphatase

47
Q

diagnostic tools for chronic pancreatitis

A

visualize calcification by CT or US

48
Q

prognosis of acute pancreatitis

A

poor

morbidity with insufficiency, chronic malabsorption, and DM

if survive, severe chronic pain is a problem

can develop pancreatic pseudocysts or CA

49
Q

trx for IgG4 autoimmune ds

A

glucocorticoids (immune suppressant)

50
Q

necrotic and hemorrhagic material that are rick in pancreatic enzymes and lack an epithelial lining

A

pseudocyst

51
Q

75% of cysts in the pancreas are

A

pseudocysts

52
Q

when do pseudocysts usually arise

A

usually following a bout of acute pancreatitis, particularly one superimposed on chronic alcoholic pancreatitis

post trauma to the pancreas

53
Q

where do pseudocysts usually occur

A

most commonly in the lesser omental sac or in the retroperotineum between the stomach an transverse colon or stomach and liver

also in the pancreas, but less commonly

54
Q

prognosis of pseudocyst

A

many spontaneously resolve

many become secondarily infected, larger ones may compress or even perforate into adjacent structures

55
Q

prognosis of cystic neoplasms

A

range from harmless benign to precursors that become lethal CA

56
Q

serous cystic neoplasms

where
histology
genetic mutation
population
prognosis
trx
A

in the tail of the pancreas

small, lined by glycogen rich cuboidal cells and contain thin straw colored film

most common genetic abn = x VHL

women, 60s-70s

mostly benign, including serous cystic neoplasms, including serous cystadenomas

surgery is curative

57
Q

mucinous cystic neoplasms

where
histology
genetic mutation
population
prognosis
trx
A

in tail of pancreas

painless, slow growing LARGE, filled with mucin and lined by columnar mucin-producing epithelium associated with a dense stroma similar to ovarian stroma

most common gene mutation= KRAS , TP53, RNF43

women,

can be precursors to invasive carcinomas, up to a third are associated with invasive adenocarcinoma
half with invasive versions will die

surgery is curative if non-invasive- critical for early dx and trx

58
Q

intraductal papillary mucinous neoplasms (IPMNs)

where
histology
genetic mutation
population
prognosis
trx
A

mucin producing neoplasms that involve the larger ducts of the pancreas, more often in the head

  1. absence of ovarian stroma 2. involvement of the pancreatic duct

genes= GNAS, KRAS, TP53, SMAD4, RNF43

men

can progress to invasive CA-critical for early dx and trx

59
Q

solid-pseudopapillary neoplasm

where
histology
genetic mutation
population
prognosis
trx
A

large, well circumscribed malignant neoplasms, solid and cystic components filled with hemorrhagic debris
grow in pseudopapillary projections

mainly young women, cause abd dicomfort as they grow

always associated w hyper-activation of Wnt s/p CTNNB1 (B catenin) oncogene

trx= surgical resection- most people are cured after

60
Q

pancreatic CA is synonymous with

A

infiltrating ductal adenocarcinoma of the pancreas

61
Q

prognosis of pancreatic CA

A

one of the highest mortality rates of any CA

5 year survival less than 5%

62
Q

invasive pancreatic CA is though to arise from well-defined noninvasive precursor lesions in ____, called ______

A

small ducts

pancreatic intraepithelial neoplasia

63
Q

compare the three stages of progression in invasive carcinoma in the colon and the pancreas

A

COLON

nonneoplastic epithelium –> ademona –>invasive carcinoma

PANCREAS

nonneoplastic epithelium–> PanIN –> invasive carcinoma

64
Q

sequence of genetic mutations that leads to pancreatic carcinoma

A

KRAS mutations
CDKN2A
TP53, SMAD4, BRCA2

65
Q

sx of pancreatic CA

A

silent until the invade into adjacent structures

pain is the sx that brings people in, though by that time it really is too late

jaundice, anorexia, weight loss, malaise
DVT
migratory thrombophlebitis aka Trousseau sign

66
Q

genetic mutations seen in pancreatic CA

A

KRAS = x MAPK
CDKN2A= most frequently inactivated tumor suppressor gene
SMAD4= x TGF-B
TP53

67
Q

population associated with pancreatic CA

A

older adults, mostly 60s-80s

blacks and Ashkenazi Jews

68
Q

strongest environmental influence lead

others

A

cigarette smoke doubles the risk

fatty diets

69
Q

___ and ___ are associated with pancreatic CA, either caused by it or cause it

A

chronic pancreatitis

DM

70
Q

genetic mutations associated with pancreatic CA

A

BRCA2

CDKN2A

71
Q

(pancreas) while most carcinomas of the ____ of the pancreas obstruct the distal __ bile duct, carcinomas of the ___&____ do not impinge on the biliary tract and hence remain ___ for some time,

A

head
common

body and tail

72
Q

pancreatic CA can lead to ______, also known as ______, due to elaboration of platelet-activating factors and procoagulants from the carcinoma or necrotic products

A

migratory thrombophlebitis

Trousseau sign

73
Q

dx and trx for pancreatic CA

A

tests to detect: carinoembryonic Ag and CA19-9 Ag are elevated –> are nonspecific

US and CT are more specific but not useful for screening

fewer than 20% are resectable at the time of diagnosis
most have invaded vessels or metastasized by that point

GI2 E1 (19 decks)

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