Pathology - Pancreas and Gallbladder Flashcards

1
Q

-Major metabolic cause of acute pancreatitis?-Other causes?

A

-ALCOHOL-hyperliporproteinemia-hypercalcemia-drugs (thiazides)-genetic

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2
Q

-Major mechanical cause of acute pancreatitis?-Other causes?

A

-GALLSTONES-trauma-latrogenic injury (perioperative injury ; endoscopic procedures with dye injection)

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3
Q

Vascular causes of acute pancreatitis?

A

-shock-atheroembolism-vasculitis (polyarteritis nodosa, SLE, Henoch-Schonlein purpura)

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4
Q

Infectious causes of acute pancreatitis?

A

-mumps-coxsackievirus-mycoplasma pneumonia

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5
Q

which enzyme is usually primary issue with acute pancreatitis?Why?

A

-trypsin-this enzyme activates all the other pancreactic enzymes

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6
Q

Classic acute pancreatitis presentation?

A

epigastric pain with radiation to the back

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7
Q

Acute pancreatitis - LABS

A

-first 24 hrs increase serum amylase (but NOT specific to pancreas)-72-96 hours inc serum lipase (more specific)-hypocalcemia - bc the enzymes digest fat = ppt of calcium soaps (poor prognosis)

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8
Q

Does serum amylase or lipase stay elevated for long in acute pancreatitis?

A

lipase

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9
Q

If serum amylase is elevated for longer than 2-4 days (normal) then what does that suggest?

A

pancreatic pseudocyst (amylase rich fluid collecting around pancreas)

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10
Q

Primary concern with acute pancreatitis? WHY?

A

SHOCK - develop respiratory issues (ARDS) –> high mortality

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11
Q

Mildest form of acute pancreatitis?

A

acute INTERSTITIAL pancreatitis = trivial inflammation and edema (organ can return to normal fucntion if treated)

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12
Q

Serious forms of acute pancreatitis?

A

-acute NECROTIZING pancreatitis-acute HEMORRHAGIC pancreatitis(medical emergency –> SHOCK … and all that. - may still restore function but probs not- FYI chronic pancreattiis = irreversible damage)

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13
Q

What is the pain like in acute necrotizing or hemorrhagic pancreatitis?Progression?

A

-constant pain radiating to UPPER back-Shock & acute tubular necrosis –> loss of blood volume and vasodilation (vasoactivators-inc effect of blood volume loss) –> DIC, ARDS…. all that stuff

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14
Q

What are potential outcomes (sequelae) of acute pancreatitis?

A

-multiple acute bouts = chronic pancreatitis-sterile pancreatic abscess -*PSEUDOCYST - collection of blood, debris, tissue, fluid tht forms 1-4 weeks after onset (not true cyst bc no epithelial lining)-infected pancreatitic necrosis

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15
Q

Defining feature of chronic pancreatits?

A

-fibrosis = irreversible loss of or damage to tissue

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16
Q

Major cause of chronic pancreatitis?

A

ALCOHOL again

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17
Q

Less common causes of chronic pancreattis?

A

-long-standing obstruction of pancreatic duct (pseudocysts, stones…)-Familial hereditary pancreatitis: mutations in PRSS1 or SPINK1 (associated with both acute and chronic)-Cystic fibrosis - mutation in CFTR gene = thick secretions

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18
Q

90-95% of chronic pancreatitis are due to?Other 5% cause?

A

alcoholidiopathicgall stones

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19
Q

Acute pancreatitis pathogenesis initiation?Over time pathogenesis?

A

-sequence of fibrosis around pancreatic lobules, duct distortion, and altered pancreatic secretions-with multiple episodes = loss of pancreatic parenchyma and fibrosis

20
Q

Pathogenic events?

A

-ductal obstruction by concretions (ductal plugs –> calcification, alcohol=more protein in secretions)-toxic metabolites - especially alcohol= lipids accumulate in cells–> death and fibrosis

21
Q

How does alcohol predispose patient to pancreatitis?

A

-decreased bicarbonate secretion-inc protein secretion===>favors formation of inspissated ductal secretions that, in turn, leads to ductal obstruction with inflammation, fibrosis, and atrophy

22
Q

What happens to acinar cells in chronic pancreatitis?

A

drop out - dec numbers and sizeACINAR LOSS IS A CONSTANT FEATURE

23
Q

progressive inflammatory disease of pancreatitis is characterized by what clinical triad?

A

diabetessteatorrheacalcifications (radiology)

24
Q

non neoplastic cysts:

A

-congenital-pseudocyst

25
Q

neoplastic cysts:

A

-microcystic serous cystadenomas (older women-benign)-mucinous cystic neoplasms (younger women-malignant potential)-solid pseudopapillary tumor-rare adolescent girls and young women)**-intraductal papillary mucinous cystic neoplasms (IPMNS) - more men and in head of pancreas

26
Q

congenital cyst-type?-what about it?

A

-non-neoplastic-has cuboidal epithelium-component of von Hippel-Lindau disease = cysts in pancreas, liver and kidney; angiomas in retina and cerebellum or brain stem-BASICALLY they have a greater risk of having more cysts or cancers in many places

27
Q

Most common non-neoplastic cyst?

A

pseudocyst

28
Q

Pseudocysts-type?-how to get?-features/what abou ti?

A

-non-neoplastic-unilocular cyst = lacks true epithelial lining but is fluid filled (collection of pancreatic secretions-develop after acute or chronic pancreatitis-hemorrhage and infection complications

29
Q

Where do neoplastic cystic pancreatic tumors arise from?

A

pancreatic duct tissue

30
Q

What does a pancreatic serous cystadenoma look like grossly?

A

honey comb like

31
Q

Intraductal papillary mucinous neoplasms–dangerousness?-men or woemn?-where in pancreas?-what happens to epithelium?

A

-super bad - benign, malignant or boderline malignant-MEN>women-head of pancreas > tailchanges:1) cuboid to columnar2) papillary infoldings3) papillary epithelium with architectural and cytologic changes4) significant atypia and budding off of clusters of cells

32
Q

pancreatic cancer - prognosis?

A

-poor prognosis - most dead within first year

33
Q

pancreatic cancer - who gets most often, comobidiites? race?

A

-elderly-men-African americans-diabetics

34
Q

major risk factor for pancreatic cancer?other factors?

A

-SMOKING**-hereditary pancreatitis-high fat diet-chronic pancreatitis-diabetes

35
Q

90% of pancreatic cancers have what gene mutiation?

A

K-Ras (usually due to smoking)

36
Q

Most common location for pancreatic cancer?

A

head

37
Q

risk factors for gallbaldder stones:

A

-diet (cholesterol stones common)-pregnancy-oral contraceptives

38
Q

3 types of gallstones:

A

1) cholesterol stones (biliary hypersecretion of cholesterol/supersaturation of bile with cholesterol)2) pigmented stones (mostly bilirubin calcium salts)3) mixed

39
Q

4 processes that cause (cholesterol) stones:

A

-supersaturation (lots of cholesterol or bile)-gallbladder hypomotility (slow flow of bile)-crystal nucleating -accretion within the gallbladder mucous layer

40
Q

Pigmented gallstones- risk factors:

A

-chronic hemolytic syndromes-biliary tract infection (bacterial or parasitic)-ileal disease (resection or bypass)-CALCIUM PRECIPITATION OF BILIRUBIN

41
Q

gross appearance term for high levels of cholesterol in the gallbladder?-what is going on?

A

-strawberry gallbladder (cholesterolosis)-cholesterol laden macrophages build up under epithelium = bumpy white/yellow

42
Q

common acute types of cholecystitis:

A

1) Acute calculous cholecystitis2) acuet acalculous cholecystits-postop-sever burn or trauma-mutli organ failure-sepsis-prolonged hyperalimentation-postpartum

43
Q

stones in the gallbladder most likely?

A

CHRONIC cholecystits

44
Q

special types of chronic cholcestitis:

A

-porcelain gallblader - stiff wall with dystrophic calicification-hydrops of the gallbladder-stone blocks and GB enlarges and atrophic - filled wtih clear fluid

45
Q

main concern with acute and chronic cholecystitis?

A

Gb perforation or rupturesuperinfection or peritonitislocal abscess formation

46
Q

Most common cancer type of the gallbladder?

A

adenocarcinoma