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GIGU2 Exam 2 > Liver, Gallbladder, Pancreas 2 - Dr. Dobson > Flashcards

Liver, Gallbladder, Pancreas 2 - Dr. Dobson Flashcards

1
Q

Choledochal cysts

A

congenital dilation of the common bile duct

before age 10yo, jaundice + biliary colic = recurrent abd pain

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2
Q

Choledochal cysts risk of getting what

A
  1. stones
  2. stenosis + strictures
  3. pancreatits
  4. obstructive biliary complications in liver
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3
Q

Fibropolycystic disease

A

group of lesions causing congenital malformation of the biliary tree

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4
Q

Fibropolycystic disease lesions happen how

A

persistence of fetal periportal ductal plates

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5
Q

Fibropolycystic disease associated with what

A
  1. polycystic renal disease
  2. cholangiocarcinoma
  3. Von Meyenburg complexes (Hamartomas)
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6
Q

Fibropolycystic disease histology

A

Von Meyenburg complexes (Hamartomas)

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7
Q

Caroli disease is what

A

multifocal cystic dilation of large intrahepatic bile ducts

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8
Q

Caroli syndrome is what

A

Caroli disease + congenital hepatic fibrosis

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9
Q

impaired BF to portal vein or extrahepatic veins = inflow (obstruction or thrombosis) SX

A

esophageal varices, splenomegally, GI congestion

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10
Q

Impaired BF in intrahepatic vessels (cirrhosis, sinusoid occlusion) SX

A

Ascities
varices
hepatomegaly
high AST/ ALP

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11
Q

Impaired hepatic vein (outflow) destruction thrombosis = Budd-chiari syndrome, sinusoidal obstructive syndrome SX

A 
Ascities
hepatomegaly
ABD pain
jaundice
high AST /ALP
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12
Q

Hepatic Artery occlusion causes

A

local infarct (pale or hemorhagic)

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13
Q

Hepatic Artery occlusion common causes

A
  • neoplasm
  • polyarteritis nodosa (vasculitis)
  • sepsis
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14
Q

portal vein obstruction causes what

A

well tolerated to catastrophic sx

= ABD pain, portal HTN (varices that can rupture)

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15
Q

extrahepatic portal vein obstruction happens how often and can be caused by what in neonatal

A
  1. 1/3 of cases

2. neonatal umbilical sepsis, umbilical vein catheterization (varices bleeding and ascites years later)

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16
Q

Hepatic Artery occlusion caused by what in adults 6

A
  1. acute diverticulitits ABD infection —-> pyelophlebitis in spleen
  2. hypercoag. state (thrombosis)
  3. trauma
  4. pancreatitis or pancreatic cancer causing splenic vein thrombosis
  5. portal vein invades into it from HCC
  6. cirrhosis
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17
Q

small portal vein obstruction cause

A

schistosomiasis **

prothrombotic state, virus, drugs, chronic biliary obstr., autoimmune

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18
Q

small portal vein obstruction SX

A

upper GI bleed

splenomegaly

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19
Q

most common cause of impaired BF to liver

A

cirrhosis

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20
Q

sinusoidal BF occlusion caused by what 4

A
  1. Sickle cell
  2. DIC
  3. Eclampsia
  4. Diffuse intrasinusoidal tumor
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21
Q

sinusoidal BF occlusion can lead to what

A

massive necrosis, acute liver failure

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22
Q

Peliosis hepatis is what

A
  1. type of sinusoidal dilation, CAUSING —-I EFFLUX of hepatic blood
  2. blood filled cystic spaces in liver
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23
Q

Peliosis hepatis can cause what complication

A

ABD hemorrhage

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24
Q

Hepatic Vein thrombosis is what

A

Budd - Chiari Syndrome

= deadly if not tx

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25
Q

Budd - Chiari Syndrome TRIAD

A
  1. hepatomegaly
  2. ABD pain
  3. ascities
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26
Q

Budd - Chiari Syndrome associated conditions : 5

A
  1. myeloproliferative neoplasms
  2. inherited hypercoag.
  3. anti-phospholipid AB syndrome
  4. PNH (proxysmal nocturnal hemoglobinuria)
  5. HCC
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27
Q

Sinusoidal obstruction syndrome is what

A

pyrrolizidine alkaloid in bush tea from Jamaica = veno-occlusive disease*

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28
Q

Sinusoidal obstruction syndrome caused by what + mortality rate

A
  1. post hematopoietic stem cell transplant*
  2. chemo
    = 80% mortality
    = jamaican tea
    = vano-occlusive disease
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29
Q

Sinusoidal obstruction syndrome DX

A
  1. biposy gold standard only risky
  2. hepatomegaly, jaundice, ascitis, WG,
  3. attenuated hepatic venous flow (Doppler US)**
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30
Q

which organ is effected most after an organ transplant

A

liver

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31
Q

jaundice in preg caused by

A

Viral hep (20% fatal if HEV)

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32
Q

acute liver failure in preg also caused by

A

HSV

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33
Q

liver abscesses in preg caused by

A

Listeria

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34
Q

3 serious liver complications in preg.

A
  1. eclampsia / preeclampsia
  2. acute fatty liver
  3. intrahepatic cholestasis
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35
Q

4 sx of eclampsia / preeclampsia that happen

A
  1. maternal HTN
  2. proteinuria
  3. peripheral edema
  4. coagulation abnormal
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36
Q

eclampsia / preeclampsia what you see in pt with this (acronym)

A

HELLP

  1. Hemolysis
  2. Elevated Liver enzymes (AST /ALP)
  3. Low Plts
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37
Q

preeclampsia becomes eclampsia when

A

when hyperreflexia and convulsions happen

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38
Q

eclampsia / preeclampsia most dangerous in who

A

women with acute fatty liver of preg

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39
Q

acute fatty liver of preg sx and tx and complications

A
  1. bleeding, N/V, jaundice, coma
  2. termination of preg
  3. hepatic failure and death
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40
Q

intrahepatic cholestasis of preg sx

A

pruritus in 2nd or 3rd trimester, darkening urine, light color stools

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41
Q

intrahepatic cholestasis of preg labs, histology

A
  1. low bilirubin,

2. canicular cholestasis

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42
Q

intrahepatic cholestasis of preg tx and associated with what risk

A
  1. resolved 2-3 weeks after delivery

2. fetal loss, and recur in future preg

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43
Q

liver infarction risk

A

RARE (dual BS, 1/3 hepatic A, 2/3 portal vein)

= bile ducts can die if hepatic A obstructed since they get O2 from artery only)

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44
Q

most common cause of varices

A

portal vein occlusion

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45
Q

obliterative portal venopathy caused by

A

HIV

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46
Q

sinusoidal dilations caused by

A

peliosis hepatis

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47
Q

passive liver congestion caused by

A

right heart failure

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48
Q

chronic vs acute transplant rejection

A

acute : cellular

chronic : vascular

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49
Q

nutmug liver formed from

A

hypoperfusion, retrograde congestion

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50
Q

Focal Nodular Hepatis (FNH) : what and looks like

A

altered BF causing hyperplastic changes, and a mass development in liver
= single well marked lesion, central scar with no capsule (less then 5cm)

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51
Q

Focal Nodular Hepatis (FNH) : histology

A

“map like pattern”

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52
Q

Cavernous hemangioma of liver : prevalence and location and risk

A
  1. most common benign liver neoplasm, F
  2. subcapsular location
  3. hemorrhage
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53
Q

Hepatocellular adenoma is what , who, from what (Strong link or association)

A

benign neoplsm ,
young women,
oral contraceptives + anabolic steroids, obesity

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54
Q

Hepatocellular adenoma risk

A

rupture hemorrhage

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55
Q

Hepatocellular adenoma 3 subtypes

A
  1. HNF1-a adenoma: F, HCC can happen , fatty looking
  2. Inflammatory adenoma: F, obesity, malignant risk if from B-catenin, amyloid
  3. B-Catenin Adenoma : malignant risk to HCC, oral contraceptives, anabolic steroids
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56
Q

2 most common primary epithelial tumors of liver

A
  1. HCC

2. cholangiocarcinoma

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57
Q

pediatric liver tumor most common

A

hepatoblastoma

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58
Q

nonepithelial tumor of liver

A

angiosarcoma

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59
Q

rare primary hepatic lymphoma

A

Diffuse Large B-cell lymphoma (DLBCL)

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60
Q

hepatoblastoma associated with 2 diseases

A
  1. Familial Adenomatous polyposis

2. Beckwith-Wiedemann syndrome

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61
Q

hepatoblastoma SX

A

abnormal ABD swelling (can see jaundice and pruritus)

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62
Q

hepatoblastoma complication

A

20% of times tumor has gone to lungs by the time of DX

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63
Q

Hepatocellular Carcinoma (HCC)
prevalence
what has made this increase in rate in western countries

A
  1. most common primary malignancy to hepatocytes (esp. chronic liver disease with cirrhosis)
  2. HCV and Metabolic syndrome + alcolol**
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64
Q

Aflatoxin is what and from what

A

fungi toxin in crops = aspergillus flavus and aspergillus parasiticus

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65
Q

noncirrhotic livers that can cause HCC

A

aflatoxin, adenomas

66
Q

fibrolamellar carcinoma is what and histology

A

type of HCC (more survivor rate)

cirrhosis tumor with fibrous band (large polygonal cells + granular cytoplasm, dense collagen bundles

67
Q

unresectable tumors tx

A

image guided tumor ablation with alcohol or radiofequency waves

68
Q

intrahepatic cholangiocarcinoma is what

A

adenocarcinoma

69
Q

extrahepatic cholangiocarcinoma

A

biliary adenocarcinoma

70
Q

intrahepatic cholangiocarcinoma most common locations and reason

A

= SE asia (thiland, Laos, Camboidia)

= liver fluke infection high

71
Q

intrahepatic cholangiocarcinoma sx and spreads

A

spreads to perineural and LN

none usually accidental, or cholastasis, feel liver mass

72
Q

extrahepatic cholangiocarcinoma sx

A

biliary tree obstruction sx

73
Q

angiosarcoma hepatic, associated with what

A

vinyl chloride, arsenic, thorotrast exposure

74
Q

Lymphoma in liver usually associated with

A

DLBCL mostly and then

MALToma

75
Q

Metastatic liver associated with

A

primary hepatic neoplasia (however if from some other place mostly from colon, breast, lung, pancreas)

76
Q

liver secretes how much bile per day and GB can store how much

A

1L per day

and 50mL storage in GB

77
Q

GB formed from what embryonically

A

superior bud of the hepatic diverticulum

78
Q

CCK function and secreted by

A
  1. SM in GB to contract and release bile, relax muscular sphincter of Oddi
  2. from duodenal cells
79
Q

most common anomaly in gallbladder congenital defect

A

fundus folding = phrygian cap

80
Q

most common disease causing biliary tract disease

A

Cholelithiasis

81
Q

2 types of gallstones

A
  1. cholesterol stones (developed countries, high in native Americans)
  2. pigment stones (developing countries, bacterial infection, parasitic infection, chronic red cell hemolysis)
82
Q

cholesterol gallstones contain what and from where

A

from gallbladder, 100% to 50% cholesterol + calcium carbonate, phosphates, bilirubin

83
Q

cholesterol gallstones with a lot of cholesterol look like :

cholesterol gallstones with a lot of calcium carbonate look like :

A
  1. radiolucent

2. radiopaque

84
Q

black stones have what + from where + look like

A 
= oxidized calcium salts (unconjugated bilirubin )
= ca carbonate
= ca phosphate
cholesterol a little 
FROM : sterile GB bile
LOOK : radiopaque
85
Q

brown stones have what and from where + look like

A

= same as black + more cholesterol + calcium salts
FROM : infected large bile ducts
LOOK : radiolucent

86
Q

risk factors of cholesterol cholelithiasis

A
  • F
  • Fertile
  • Fat
  • Forty
  • Fair skinned
  • FH
87
Q

risk factors of pigment cholelithiasis

A
  • clinorchia sinensis
  • Ascaris Lumbricoides
  • E. Coli
88
Q

types of stones that are more dangerous

A

smaller ones, they can travel and obstruct `

89
Q

consequences of cholelithiasis

A
  • cholecystitis
  • cholangitis
  • cholestasis
  • pancreatits
  • GB carcinoma
90
Q

Gallstone ileus other name and what

A

Bouvert syndrome = large stone eroding into SI causing obstruction

91
Q

cholecystitis is what

A

inflammation of the gallbaldder

92
Q

acute cholecystitis : what + SX

A

obstruction in neck of GB or cystic duct by stone
= RUQ/ epi pain, fever, tachy, N/V,
= no jaundice, can have elevated alk phosphatase

93
Q

acute calculous cholecystitis : what is it and tx

A

FROM GALLSTONES

resolve on its own or emergency surgery

94
Q

acute acalculous cholecystitis : dx and sx

A

NOT FROM GALLSTONES
hard to dx since pt have sx not referrable to GB, failure to recognize early can lead to death = gangrene and perforation can happen

95
Q

acute acalculous cholecystitis : how pt can get this

A

= rare : S. Typhi and staph,
= severe atherosclerotic ischemic disease
= ascending biliary tree infection

96
Q

chronic cholecystitis happens usually from

A

no other previous cholecystitis usually, however can be from repeated mild to severe acute cholecystitis

97
Q

carcinoma of GB prevalence and risks

A

= most common extrahepatic biliary tract malignancy , Female
= gallstones (95% of cases), chronic bacterial or parasitic infections have been risks in Asia

98
Q

most carcinomas in GB are located where and what type and common sites of spread

A
  1. fundus
  2. adenocarcinomas
  3. lungs, liver, cystic duct, bile ducts, GI, peritoneum, porta-hepatic LNs
99
Q

sterile perintonitis

A

leakage of bile or pancreatic enzymes into peritoneum

100
Q

bacteria superinfection to the peritoneum happens when

A

perforation or rupture of biliary tree system

101
Q

granulomatous reaction to the peritoneum happens how

A

ruptured dermoid cysts releasing keratins

102
Q

spontaneous bacterial peritonitis happens how

A

from ascites and cirrhosis

103
Q

Idiopathic Retroperitoneal Fibrosis is what and happens how + SX

A

= fibroinflammatory process surrounding the abd aorta and ureters, higher in M
= IgG4 related disease
= back + ABD pain

104
Q

Idiopathic Retroperitoneal Fibrosis DX and labs

A

= radiologic imaging, bilateral impingement on ureters, hydronephrosis
= soft tissue in retroperitoneum,
= ureter obstruction —-> acute renal failure \
= high C-reactive P, HIGH erythrocyte sedimentation rates

105
Q

Idiopathic Retroperitoneal Fibrosis can happen from what

A

= IgG4 related disease

= radiation therapy from tumors or lymphoma

106
Q

Idiopathic Retroperitoneal Fibrosis histology

A

= dense fibrosis and chronic inflammation (small lymphocytes)
= high IgG4/IgG plasma cell ratio

107
Q

primary tumor of the Peritoneum

A

Mesotheliomas : desmoplastic small round cell tumor localized at some place= can metastasize into peritoneal carcinomatosis

108
Q

location of the pancreas

A

from C-loop of duodenum to the hilum of the spleen

109
Q

2 ducts from pancreas emptying into the duodenum

A
  1. pancreatic duct —-> Major duodenal papilla (sphincter of oddi, connection to the bile duct)
  2. accessory pancreatic duct —–> minor duodenal papilla
110
Q

uncinate process

A

ventral pancreas that rotates during development with bile duct attached to it
= fuses with the dorsal pancreas (tail and body)

111
Q

exocrine vs endocrine pancreas

A
  1. exocrine : 80%, zymogens

2. islets of Langerhans cells clusters, secreting insulin and glucagon

112
Q

congenital anomalie of pancreas most common

A
  1. Pancreas divisum : ventral and dorsal bud dont fuse, so the majority of tail and body of pancreas only drain from the minor papilla
    = can cause chronic pancreatitis
113
Q

annular pancreas

A

= many also have pancreas divisum
= bilobed ventral lobe each going around the foregut endoderm in opposite directions to the dorsal lobe —–> duodenal obstruction can happen

114
Q

ectopic pancreas

A

area not supposed to be in, stomach, duodenum,
= can cause pain if local inflammation
= rare to cause mucosal bleeding

115
Q

most enzymes are packed how in the pancreas

A

into secretory granules as inactive proenzymes = zymogens

116
Q

proenzymes are activated how and by what

A
  1. enteropeptidase (enterokinase) = activates Trypsin in the DUODENUM
  2. Trypsin activates proenzymes
117
Q

acinar and ductal cells of the pancreas secrete what

A

trypsin inhibitors like SPINK1 (Serine proteas inhibitor Kazal type 1

118
Q

severe acute pancreatitis causes what SX and things to happen

A
  1. enzymes and cytokines released into circulation
    = systemic inflammation, leukocytosis, DIC, edema, acute respiratory distress
    = acute renal necrosis
119
Q

severe acute pancreatitis can present how and tx

A
  1. severe sudden epigastric pain, high serum lipase

2. fluid hyrdation, pain meds, bowel rest, emergency surgery

120
Q

PE sx on severe acute pancreatitis

A
  1. Cullens sign : periumbilical ecchymosis
  2. Grey Turners sign : flank ecchymosis
  3. jaundice, abd distension
121
Q

ecchymosis from pancreatitis happen how

A

from free pancreatic enzymes causing diffusion of fat necrosis and retroperitoneal / intraabdominal bleeding

122
Q

diffusion of fat necrosis and inflammation in Cullens sign happens how

A

from retroperitoneum to umbilicus (Through the round ligament)

123
Q

diffusion of fat necrosis and inflammation in Grey Turners sign happens how

A

from retroperitoneum to the subQ tissues of flanks

124
Q

sx of high mortality in sever acute pancreatitis

A

eccymosis signs

125
Q

radiation of pain in acute pancreatitis + 2 other labs that are elevated besides lipase * and amylase (10 % of pts and if fat necrosis)

A
  1. upper / mid back + left shoulder
  2. Glycosuria (10% of pts)
    Hypocalcemia (if saponification of necrotic fat)
126
Q

trypsin activated in the pancreas can do what

A
  1. activate proenzymes = autodigestion
  2. blood components : coag, complement, fibrinolytic pathways = inflammation + small vessels thrombosis , causing more duct cell destruction and trypsin activation
127
Q

CFTR and acute pancreatitis

A

X bicarbonate secretion + obstruct ducts with mucus = duct destruction and trypsin activation

128
Q

PRSS1 and acute pancreatitis

A

cationic trypsin (mutated serine protease 1), = X self inactivation of trypsin

129
Q

SPINK1 and acute pancreatitis

A

serine peptidase inhibitor kazal type 1 : INHIBITS trypsin activation (mutated)

130
Q

CASR and acute pancreatitis

A

ca- sensing R in ECF : X not working so alters Ca concentrations in ducts + trypsin gets activated

131
Q

CTRC and acute pancreatitis

A

Chymotrypsin C (caldecrin) : degrades trypsin , protects pancreas from destruction from trypsin (mutated)

132
Q

CPA1 and acute pancreatitis

A

Carboxypeptidase A1 : exopeptidase regulates zymogen activation by trypsin (mutated)

133
Q

stages of acute pancreatitis in sx

A
  1. microvascular leak and edema
  2. fat necrosis
  3. acute inflammation
  4. damage + autodigestion (pancreatic parenchyma)
  5. BV destruction + interstitial hemorrhage
134
Q

brown fluid in peritoneum

A

fat cells digested from lipase

135
Q

acute pancreatitis tx

A

bowel rest : NPO (IV fluids, analgesia)

most recover

136
Q

40% to 60% acute necrotizing pancreatitis pts get what

A

acellular debri gets infected (gram- from gI) = further complicating disease

137
Q

lungs and acute pancreatitis

A

ARDS

138
Q

most common cause of chronic pancreatitis and what is it

A
  1. long term alcohol use

2. irreversible destruction of exocrine parenchyma, fibrosis + later loss of endocrine parenchyma

139
Q

chronic pancreatitis cytokine involved in fibrosis

A

TGF-B causing fibrosis after injury from inflammation, activated by M,

140
Q

autoimmune pancreatitis type 1 and type 2

A

TYPE 1 : IgG4 plasma cells in pancreas (IgG related disese)

TYPE 2: mass in head on imaging = looks like carcinoma (pts with UC)

141
Q

risks of chronic pancreatitis

A
  1. repeated acute pancreatitis with persistent back / abd pain
  2. calcifications
  3. exocrine insufficiency
  4. DM
142
Q

hereditary pancreatitis with high risk of becoming cancer

A

PRSS-1 mutation (40% chance)

143
Q

most common cysts on pancreas

A

nonneoplastic pseudocysts

144
Q

Congenital cysts in pancreas

A

rare, thin walled cyst from anomaly in pancreatic duct development
= serous fluid filled fibrous capsule

145
Q

congenital cycts can be associated with what 2 conditions

A
  1. Polycystic Kidney Disease

2. von Hippel -Lindau disease

146
Q

nonneoplastic pseudocysts lining and from what and tx

A

no epithelial lining
from acute pancreatitis, esp from chronic alcoholic pancreatitis, trauma
= spontaneously resolve (can compress adjacent structures, or get infected)

147
Q

serous cystic neoplasm what, prevalence, location

A

benign, Female, 6th-7th decade, pancreas tail

148
Q

Mucinous cystic neoplasms what, prevalence, location

A

carcinomas, 95% Female, tail

149
Q

Solid-pseudopapillary neoplasms what, prevalence, location

A

young women, tail, some can be locally aggressive

150
Q

Intraductal papillary mucinous neoplasms (IPMNs) what, prevalence, location

A

connected to duct system in pancreas,
Men
Head of pancreas
can become cancer

151
Q

pancreatic cancer 5yr survival rate

A

10%

152
Q

pancreatic cancer high risk groups

A

AA, Japanese, Native Americans, Hawaiians, Jews

153
Q

strongest risk of pancreatic cancer + other risks

A

smoking *

  • chronic pancreatitis
  • visceral obesity, high BMI
  • DM
154
Q

invasice pancreatic cancers come from what

A

noninvasive precursor lesions (Pancreatic intraepithelial neoplasms (PanIN)

155
Q

PanIN stages

A
  1. telomere shortening, KRAS activated
  2. CDKN2A inactivated
  3. TP53, SMAD4, BRCA2 inactivated
  4. invasive carcinoma
156
Q

Pancreatic ductal adenocarcinomas 4 genes involved

A

KRAS, TP53, CDKN2A, SMAD4 (C/G to T/A or CpG>TpG mutations) = from methylation

157
Q

Pancreas cancers 1st sx and when and most common location

A

pain, when it has invaded into adjacent structures, so beyond cure at that point, head

158
Q

head pancreatic cancer sx and what you see in imaging

A

distal common bile duct obstruction, = obstructive jaundice, Courvoiser sign* = palpable mass felt above GB nontender

159
Q

pancreatic cancer speads most common to

A

lung and liver

grow along nerves and invade into BVs + retroperitoneum

160
Q

pancreatic cancer type

A

adenocarcinoma with dense desmoplastic reaction

161
Q

Migratory thrombophlebitis

A

Trousseau sign** = 10% pts with pancreatic cancer , tumor associated inflammation and coag factors = high risk of thromboembolism in BVs

162
Q

some serum markers for pancreatic cancer

A

CA19-9 Ag + Carcinoembryonic Ag not specific enough, Early detection is key for survival and tx with resection

GIGU2 Exam 2 (4 decks)

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