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Medicine > acute and chronic pancereatitis (pathology) > Flashcards

acute and chronic pancereatitis (pathology) Flashcards

1
Q

pancreas parenchima

A

80% exocrine

1-2% langrhans islands, endcrine

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2
Q

exocrine cells

A

acinic cells
proenzymes: trypsinogen + chymotrypsinogen
active enzemys: amylase+ lipase

ductular (small ducts) cells: bicarbonate 2-7mm

ductal (large ducts) cells: mucin

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3
Q

exocrine self digestion defense mechanism

A

proenzymes
zymogenic granular secrition
entrokinase dependant activation

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4
Q

chymotryapsinogen activator?

A

tyrapsin

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5
Q

trypsinogen activator?

A

entrokinase in brush border

trypsin (high ca+2)

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6
Q

trypsin inhibition?

A

acinar and ductal secretions: serine protease inhibitor kazal type 1 (SPINK1)

auto self inhibition of trypsin (low ca+2)

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7
Q

acute pancreatitis etiology

A

metabolic: alchohol, drugs, hyperlipoproteinemia

mechanical:
obstructions- gallstones,tumors
injuries- endoscopic

vascular- shock, emboli

infections- mumps, m.pneumoniae

idiopathic

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8
Q

genetic etiology of acute pancreatitis

A

cationic trypsinogen (serine protease 1 PRSS1, 7q35)
GOF- self inactivation cleavage site germline mutation
AD 0.8 penetrance

CFTR (7q31)
LOF
duct obstruction

SPINK1
GOF
AR

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9
Q

etiology of acute pancreatitis

A

30-60% due to gall stones

alcholism

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10
Q

acute pancreatitis - duct obstruction pathopysiology

A 
obstruction
interstitial edema
impaired blood flow 
ischemia
acinar cell injury
activation of enzymes
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11
Q

acute pancreatitis -defective intracellular transport pathopisiology (not prooven yet)

A

transport of pancreatic proenzymes to lysosome

activation of enzymes

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12
Q

alchol (usually chronic) induced acute pancreatitis pathopysiology

A

contraction of spinchter of oddi-obstruction

higher exocrine viscosity- obstruction

free radicals -> ca+2 is up -> self activation of trypsin

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13
Q

acute pancreatitis morphology

A

microvascular leakage -edema

necrosis of fat (lypase and amylase endocrinic dissemination) ->
saponification- ca+2 + phospholipds addhition

destruction of BV- hemmorage

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14
Q

chronic pancreatitis 2 types

A

calcific / obstructive

autoimmune

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15
Q

calcific / obstructive chronic pancreatitis definition

A

chronic inflammation with irreversible changes in structure which lead to 100% loss of exocrine activity

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16
Q

calcific / obstructive chronic pancreatitis etiology

A

long standing obstruction
chronic alchoholism 10-20
smoking (strongest advansor of acute to chronic pancreatitis)

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17
Q

calcific / obstructive chronic pancreatitis chimokins

A

IL 8
TGFb
PDGF
all proliferate myofibroblasts -> collagen deposition and fibrosis

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18
Q

calcific / obstructive chronic pancreatitis morphology

A

fibrosis and chronic inflammation infiltrations
acini atrophy
relative sparing of endocrin pancease
dialition of ducts

19
Q

PRSS1 heredetary pancreatitis morphology

A

lipomatous atrophy

20
Q

autoimmune chronic pancreatitis types

A

type 1-
elevated IGg4
infiltration by IGg4 plasma cells (peri-ductal!)
obliterative phlebitis- narrowing venuls due to inflammation and fibrosis
no calcification in ducts

type 2-
neutrophilic epithelial infiltration (granulocytic epithelial lessions)

both exocrine and endocrine disfunction

21
Q

autoimmune chronic pancreatitis treatment

A

prominant recover after oral steroids

22
Q

pancreatic pseudocyst

A

necrotic hemorrhagic material rich in p.enzymes
solitary
no epithel - “pseudo”

23
Q

pancreatic pseudocyst locations

A

in pancease

peripancreatic tissue
lesser omental sac
retroperitoneal

24
Q

pancreatic neoplasms

A

endocrine

exocrine
solid
cyctic

25
Q

pancreatic cyctic neoplasms

A

solid pseudopapillary tumor
serous cyst neoplasm
mucinous cytic neoplasms
intraductal papillary mucinuos neoplasms (IPMN)

26
Q

solid pseudopapillary tumor epidimeology

A

young females

childhood

27
Q

solid pseudopapillary tumor morpholgy

A

large (abdominal discomffort)
resective
mostly bening

28
Q

solid pseudopapillary tumor etiology

A

CTNNB1

29
Q

serous cyst neoplasm epidemiology

A

M:F 2:1

60’s

30
Q

serous cyst neoplasm favored lacation

A

2/3 in body tail region

31
Q

serous cyst neoplasm morphology

A 
many
tightly packed
small
thin walled
cyts (da!) 
honecomb appearance
32
Q

serous cyst neoplasm etiology

A

von hipple-lindau gene mutes 40% of cases

33
Q

IPMN epidemiology

A

M3:F2

60’s

34
Q

IPMN morphology

A

main pancreatic duct of branches , mostly in head
dialition of ducts (grossl visible)
papillary intraductal mucin producing epithelial tumors (adenoma to cacinoma insitu)

35
Q

IPMN etiology

A

Petz-heghers
familial adenomatous polyposis syndromes
1/3 with history of malignancy (aspecialy gastric or colonic)

GNAS, 80%, 20q13, alfa stimulatory G protein subunit GOF
KRAS @ RNF43
TP53 @ SMAD4 when invasive

36
Q

mucinous cytic neoplasms epidemiology

A

females

perimenopausal

37
Q

mucinous cytic neoplasms favord location

A

tail

body

38
Q

mucinous cytic neoplasms etiology

A

RNF43
KRAS
TP53

39
Q

pancreatic ductal carcinoma epidemiology

A 
mostly elderly (60's >80%)
5yr survival <5%
familial clusters (10% of cases)
40
Q

pancreatic ductal carcinoma causes (risks)

A

smoking
chronic pancreatitis
heredetary pancreatitis (40% life time risk)
obesity and diabetes

41
Q

pancreatic ductal carcinoma familial clusters etiology

A 
HNPCC (lynch syndrome)
BRCA2, PALB2 (breast and ovary cancer)
Peutz-jegher
li fraumeni (p53)
CDKN2A
42
Q

pancreatic ductal carcinogenesis precursor lessions

A

IPMN
Mucinous cystic neoplasms
pancreatic intraepithelial neoplasias (PanIN)-90%!

43
Q

pancreatic ductal carcinoma mulecular alternations

A

kras 90% oncogene
cdkn2a 30%
smad4 55% supressor
p53 60% supressor

Medicine (17 decks)

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