Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

GI2 E1 > pancreas > Flashcards

pancreas Flashcards

robbins (73 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

composition of the endocrine pancreas

A

contain islets of langehans,

secrete insulin, glucagon, and somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

most common congenital anomaly of the pancreas

A

pancreas divisum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where is ectopic pancreatic tissue most commonly found

A

most to least =

stomach+duodenum
jejunum
meckel diverticula
ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

prognosis of having an ectopic pancreas

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what germline mutation is associated with pancreatic agenesis

A

PDX1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

intrapancreatic trypsin activation of prophospholipase causes what

A

degrade fat cells of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

intrapancreatic trypsin activation proelastase causes what

A

damage elastic fibers of BVs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

causes of pancreatic obstruction

A 
cholelithiasis
ampullary obstruction
chronic alc
ductal concretions
parasites- Ascaris lumbricoides, Clonorchis sinensis
pancreas divisum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what vascular etiologies can cause acute pancreatitis

A

shock, atheroembolism, vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what infections can cause acute pancreatitis

A

mumps

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how can primary acinar cell injury lead to acute pancreatitis
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,
26
how can defective intracellular transport of proenzymes within the acinar cells lead to acute pancreatitis
(caused by alc or obstruction) panreatic proenzymes are incorrectly sent to the intracellular compartment containing lysosomal hydrolases leading to intracellular activation--> acinar cell injury
27
etiology of EtOH toxicity pancreatitis
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
28
acinar cell injury --> activated enzymes --> _____ (4) ---> acute pancreatitis
1. interstitial inflammation and edema 2. proteolysis 3. fat necrosis 4. damage to vessel walls, hemorrhage
29
what genetic mutations are associated with predisposition to pancreatitis
``` CFTR= cystic fibrosis PRSS1= serine protease 1 SPINK1= serine peptidase inhibitor, CASR= Ca-sensing receptor CTRC= chymotrypsin C CPA1= carboxypeptidase A1 ```
30
what metabolic disorders predisopose one to developing acute pancreatitis
hypertriglyceridemia hypercalcemia hyperparathyroid
31
what meds predispose one to developing acute pancreatitis
``` furosemide azathioprine 2-3-dideoxyinosine estrogens etc. ```
32
hereditary pancreatitis is associated with ____ attacks of ____ often beginning _____ and ultimately leading to _____
reccurent severe acute pancreatitis in childhood chronic pancreatitis
33
what three genes are associated with hereditary pancreatitis and what do they have in common
PRSS1 (AD) *most* SPINK1 (AR) CFTR = all increase or sustain the activity of trypsin
34
patient with hereditary pancreatitis have a 40% lifetime risk of developing ___
pancreatic CA
35
characteristic morphology of acute pancreatitis
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
clinical presentation of acute pancreatitis
constant and intense abd pain referred to the upper back and occasionally the left shoulder anorexia, N/V, elevated amylase and lipase
37
prognosis of acute pancreatitis
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
lab findings associated with acute pancreatitis
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
define chronic pancreatitis
prolonged pancreatic inflammation with irreversible destruction of the exocrine parenchyma, fibrosis, and destruction of endocrine parenchyma in the late stages
40
population associated with chronic pancreatitis
middle aged males
41
most common cause of chronic pancreatitis and other causes
alcohol abuse -long standing obstruction, autoimmune, hereditary
42
etiology of chronic pancreatitis
repeated episodes of acute pancreatitis will initiate a sequence of perilobular fibrosis, duct distortion and altered pancreatic secretions
43
chronic pancreatic injury leads to local production of ______ that activate ___ (aka ___) to promote ___ and ____
inflammatory mediators (TGF-B, PDGF) periacinar myofibroblasts/pancreatic stellate cells fibrosis and acinar cell loss
44
etiology of autoimmune pancreatitis
IgG4 secreting plasma cells in the pancreas can mimic signs of pancreatic carcinoma
45
characteristic morphology of chronic pancreatitis
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
clinical features of chronic pancreatitis
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
diagnostic tools for chronic pancreatitis
visualize calcification by CT or US
48
prognosis of acute pancreatitis
poor morbidity with insufficiency, chronic malabsorption, and DM if survive, severe chronic pain is a problem can develop pancreatic pseudocysts or CA
49
trx for IgG4 autoimmune ds
glucocorticoids (immune suppressant)
50
necrotic and hemorrhagic material that are rick in pancreatic enzymes and lack an epithelial lining
pseudocyst
51
75% of cysts in the pancreas are
pseudocysts
52
when do pseudocysts usually arise
usually following a bout of acute pancreatitis, particularly one superimposed on chronic alcoholic pancreatitis post trauma to the pancreas
53
where do pseudocysts usually occur
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
prognosis of pseudocyst
many spontaneously resolve | many become secondarily infected, larger ones may compress or even perforate into adjacent structures
55
prognosis of cystic neoplasms
range from harmless benign to precursors that become lethal CA
56
serous cystic neoplasms ``` where histology genetic mutation population prognosis trx ```
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
mucinous cystic neoplasms ``` where histology genetic mutation population prognosis trx ```
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
intraductal papillary mucinous neoplasms (IPMNs) ``` where histology genetic mutation population prognosis trx ```
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
solid-pseudopapillary neoplasm ``` where histology genetic mutation population prognosis trx ```
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
pancreatic CA is synonymous with
infiltrating ductal adenocarcinoma of the pancreas
61
prognosis of pancreatic CA
one of the highest mortality rates of any CA 5 year survival less than 5%
62
invasive pancreatic CA is though to arise from well-defined noninvasive precursor lesions in ____, called ______
small ducts | pancreatic intraepithelial neoplasia
63
compare the three stages of progression in invasive carcinoma in the colon and the pancreas
COLON nonneoplastic epithelium --> ademona -->invasive carcinoma PANCREAS nonneoplastic epithelium--> PanIN --> invasive carcinoma
64
sequence of genetic mutations that leads to pancreatic carcinoma
KRAS mutations CDKN2A TP53, SMAD4, BRCA2
65
sx of pancreatic CA
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
genetic mutations seen in pancreatic CA
KRAS = x MAPK CDKN2A= most frequently inactivated tumor suppressor gene SMAD4= x TGF-B TP53
67
population associated with pancreatic CA
older adults, mostly 60s-80s blacks and Ashkenazi Jews
68
strongest environmental influence lead others
cigarette smoke doubles the risk fatty diets
69
___ and ___ are associated with pancreatic CA, either caused by it or cause it
chronic pancreatitis | DM
70
genetic mutations associated with pancreatic CA
BRCA2 | CDKN2A
71
(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,
head common body and tail
72
pancreatic CA can lead to ______, also known as ______, due to elaboration of platelet-activating factors and procoagulants from the carcinoma or necrotic products
migratory thrombophlebitis Trousseau sign
73
dx and trx for pancreatic CA
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions