Gi Liver Path Louisville 2011

Front 1

What is normally first result of noxious factor acting on hepatocyte

Back 1

decrease in atp and hydropic degeneration

Front 2

What causes zone 1 necrosis

Back 2

Phosphorous

Front 3

What causes zone 2 necrosis

Back 3

yellow fever

Front 4

What causes zone 3 necrosis

Back 4

CCL4, ischemia

Front 5

what are 4 kinds of cirrhosis

Back 5

biliary, cardiac, alcoholic, postnecrotic

Front 6

What are 3 causes of microvesicular fatty degeneration: is this type acute or chronic?

Back 6

reye's (children treated with aspirin after flu like illness), tetracycline, pregnancy:
acute

Front 7

What are 3 causes of macrovesicular fatty degen?
Acute or chronic?

Back 7

alcohol, obesity, diabetes
Chronic

Front 8

What is councilman body?

Back 8

Single cell hepatocyte necrosis

Front 9

What are zones of lobule with respect to central vein

Back 9

z3, z2, z1

Front 10

Which cells are the main players in cirrhosis?

Back 10

the Normally quiescent stellate cells

Front 11

Where do stellate cells live?

Back 11

In the space of disse

Front 12

Where is the space of disse?

Back 12

Between the endothelial layer and the hepatocyte layer

Front 13

List the steps in cirrhosis: starting with hepatocyte apoptosis or necrosis

Back 13

First: apop/nec
2) mac enters area and produces pdgf, tnf alpha for proliferation of stellate cells; tgfB for fibrinogenesis; Et-1 for contraction
3) in repsonse, stellate cells begin to act like myofibroblast

Front 14

To have true cirrhosis, you need two histological findings: what are they?

Back 14

regenerative Nodules and bridging septa (fibrosis)

Front 15

What stain highlights collagen

Back 15

Trichrome

Front 16

micronodular cirrhosis would be what?

Back 16

alcoholic

Front 17

macronodular

Back 17

necrotic (massive hepatitis)

Front 18

What is an example of only fibrosis (without the nodule)

Back 18

congenital hepatic fibrosis (organization is still there)

Front 19

What is an example of only nodules

Back 19

(partial nodular transformation): after slight ischemia

Front 20

Again, 4 types of cirrhosis

Back 20

biliary, cardiac, alcoholic, postnecrotic

Front 21

Biliary:

Back 21

begins around central vein (can recognize but fibrosis around it

Front 22

cardiac cirrhosis pattern

Back 22

The portal triad is in the middle of the nodule

Front 23

alcoholic

Back 23

most damage takes place around sinusoids (there is nothing in the middle)

Front 24

postnecrotic

Back 24

this is haphazard fibrosis

Front 25

Nutmeg liver seen in what?

Back 25

cardiac cirrhosis

Front 26

Post necrotic cirrhosis causes
3 types?
members of types?

Back 26

cryptogenic, post hepatitic (viral or toxic, metabolic (A1 antitrypsin def, Fe build up, Cu deposits in Wilson's disease-this has parkinson type symptoms)

Front 27

4 places where blood will back up due to portal hypertension (and what names used to describe them)? Mnemonic for 3 not including the organ?

Back 27

umbililical veins (periumbilical caput madusa),internal hemeorrhoids, Esophageal varices, splenomegaly (GUT, BUTT, CAPUT)

Front 28

LECTURE 2

Back 28

Bilirubin

Front 29

What are steps in hemoglobin breakdown?

Back 29

hemoglobin taken up by retic endo system; heme group separated and turned into biliverdin, then biliverdiin becomes bilirubin

Front 30

what enzyme works on biliverdin?

Back 30

biliverdin reductase

Front 31

What does biliverdin reductase make?

Back 31

unconjugated bilirubin

Front 32

what does this attach to?

Back 32

albumin

Front 33

What molecule is added to bilirub in liver

Back 33

glucuronate

Front 34

What gives yellow color to stool and pee?

Back 34

urobilinogen which is produced when bacteria change conjugated bilirubin in gut into urobilinogen.

Front 35

What happens to conj bilirub in gut

Back 35

bacteria remove glucuronate from bilirubin

Front 36

what are normal levels of total bilirubin, direct, indirect

Back 36

total: 0.1-1.3, Dir less than 0.3, indirect 0.1-1.0

Front 37

What is kernaicterus

Back 37

brain deposition of bilirubin

Front 38

What are 4 congenital hyperbilirubinemias? Are they life threatening?

Back 38

Gilbert, crigler-najjar, dubin-johnson, rotor;
Gilbert, dubin-johnson, rotor's: NO
Crigler najjar type 1: deadly by 2 or 3
Type II is less severe

Front 39

What is Gilbert

Back 39

Defect in transport of bilirubin from blood into hepatocyte

Front 40

Crigier Najjar Syndrome?

Back 40

Defect in glucuronyl transferase (so can't conjugate bilirubin)

Front 41

Dubin-Johnson/Rotor

Back 41

Can't transport conj bilirubin from hepatocyte into biliary tree.

Front 42

What are two categories of hyperbilirubinemia? How else can you designate?

Back 42

conj and unconj; pre hep,hep, post hep

Front 43

If I said unconjugated, hepatic

Back 43

gilbert, crigier najjar

Front 44

unconj, prehep

Back 44

hemolytic

Front 45

conj hepatic

Back 45

dubin johson

Front 46

Is bile excretion by hepatocytes active or passive

Back 46

active

Front 47

1st phase of excretion

Back 47

bile salt active excretion

Front 48

2)

Back 48

atp Na/K and diffusion driven entrance of water and elecrolytes

Front 49

Phase 3

Back 49

secretin interacts to determine how much water is secreted and ductules and how much electrolytes are reabsorbed in ductules

Front 50

Where does secretin act?

Back 50

ductules

Front 51

bile acid deficiency poop issues

Back 51

steatorrhea,

Front 52

cholestasis is what?

Back 52

decrease in canalicular bile flow

Front 53

Can have two types. What are they?

Back 53

intra and extra hepatic

Front 54

intrahepatic would show what?

Back 54

bile granules in hepatocytes; could also see bile plug in ductules

Front 55

extrahepatic would show what?

Back 55

biliary cirrhosis (central vein in center---kills near the portal triad)

Front 56

INtracellular cholestasis caused by

Back 56

1) postnecrotic cirrhosis
2) dubin johnson
Pregancy (prob at canaliculi
chlorpromazine; benign recurrent jaundice both work at cnaliculi

primary biliary cirrhosis: bile ductules

Primary sclerosing cholangitis or cholangiocarcinoma blocks ductules/ducts

Front 57

primary biliary cirrhosis
pathogenesis?
special lab result?
color of poop?

Back 57

chronic, non suppurative, destructive cholangitis

path: autoimmune
speical lab: anti mitochondrial antibody including IgM
color: whitish
labs: inc alk phosph, inc cholest, inc direct bili

Front 58

Secondary biliary cirrhosis
large duct or small duct?
labs same or different than primary?
special histology?

Back 58

Large duct
same
distended bile ducts

Front 59

Gallstones
real name?
types

Back 59

Cholelithiasis
cholesterol, calcium bilirubinate, calcium carbonate

Front 60

ways gall stones can have problems with cholesterol

Back 60

cholesterolosis

Front 61

Chronic cholecystitis can have a special histological sign....what is it?

Back 61

rokitansky sinus (a mucosal herniation)

Front 62

Lecture 3 Hepatitis

Back 62

Correct

Front 63

In liver how long is still considered acute?

Back 63

6months

Front 64

Viruses: 2 types wrt liver

Back 64

1) hepatropic: replicate mainly in liver
2) Nonhepatotropic: rep outside liver

Front 65

Hepatropic viruses
what are most important

Back 65

A,B,C

Front 66

nonhepatotropic viruses

Back 66

EBV, CMV, Adenovirus, YF

Front 67

HAV

Back 67

Fecal oral transmission, inc period 15-40 days

Front 68

HBV

Back 68

parenteral, or sexual
50-80 inc period
acute hepttis, can lead to hepatocellular carcinoma

Front 69

HCV

Back 69

parenteral, transfusion
inc prd 18-90 days

Front 70

HDV

Back 70

Requires hep b for replication

Front 71

HAV
RNA or DNA?

Back 71

RNA
IgG ab protective

Front 72

HBV
makeup?
best way to diagnose acute
last to rise?
Which is protective?

Back 72

contains a core with DNA polymerase, DNA, and core antigen, e antigen
Then outside is a surface ag coat

IgM anticore
Igg antiS
Igg antiS

Front 73

What can you expect to see in a carrier?

Back 73

more surface ag, some DNA and antigen e

Front 74

hepd

Back 74

needs hepb surface ag to replicate

Front 75

IgG tells you what?
What doesn't it tell you?

Back 75

was infected
doesn't tell you if infection is current

Front 76

IgM anti HAV?
Igg anti HAV

Back 76

Acute hep
immune to hep A

Front 77

Hb surbace ag?

Back 77

Acute or chronic hep B

Front 78

IgM anti hbc

Back 78

Acute hep B

Front 79

IgG anti Hbc

Back 79

past exposure to Hep B (if hbsag is neg)
Chronic hep B (if hbsag is pos)

Front 80

Anti hbs

Back 80

immune to hep B

Front 81

hbe ag

Back 81

acute hep B, infectious

Front 82

anti hbe

Back 82

convalescence or continued infectious

Front 83

hbv dna

Back 83

continued infectious state

Front 84

IgM anti HCV

Back 84

acute hep c infection

Front 85

igg anti hcv

Back 85

past exposure or carrier state

Front 86

hcv rna

Back 86

continued infectious state

Front 87

IgM anti delta

Back 87

acute delta infection (high titre with pos hbsag)

Front 88

Igg anti delta

Back 88

past delta infection (low titre with neg IgM anti d)

Front 89

Where will viral hepatitis cause damage, initially

Back 89

periportal area

Front 90

where else could happen?
name 4 others?

Back 90

hydropic degeneration
fatty change (especially with hep c)
cholestasis
apoptosis(councilman)

Front 91

How much is difference in chronic hep?

Back 91

only the fibrosis (bridging necrosis)

Front 92

Chronic hepatitis definition?

Back 92

Necroinflammatory disease of the liver continuing for more than six months (evidence is high alt plus other enzymes)

Front 93

Lecture 4
chemical hepatitis

Back 93

Correct

Front 94

If the xenobiotic is toxic what are phase 1 rxns

Back 94

hydrolysis, reduction, oxidation

Front 95

phase 2 rxns?

Back 95

glucuronidation
sulfation
methylation
conjugation

Front 96

direct injury?
ex?

Back 96

directly acting and causing problem.
Carbon tetrachloride
Chlorpromazine (metabolized to form free radicals)

Front 97

Indirect?

Back 97

Autoimmune, Hypersensitivity

Front 98

Cholestasis

Back 98

Steroid hormones
chlorpromazine

Front 99

submassive necrosis

Back 99

halothane,
hepatitis b,
high dose of tylenol
(many things cause this, have to use history)

Front 100

peliosis

Back 100

enlarged blood vessels in liver

Front 101

alcohol hepatitis

Back 101

more often have neutrophils and mallory bodies.
mallory body: intracellular inclusion bodies of cytokeratin filaments

Front 102

Lecture 5 Liver neoplasia

Back 102

yes

Front 103

Which is linked with oral contraceptives?
Is this link with progestogen compounds?
What does the histology look like?

Back 103

Liver cell adenoma
NO
Hepatocytes without normal architecture

Front 104

How does HBV cause carcinoma

Back 104

integration into DNA

Front 105

paraneoplastic syndromes of HCC

Back 105

insulin like substance
erythropoeitin like sub
parathyroid like sub

Front 106

oncocytoid (fibrolamellar) HCC
Is this more aggressive or less aggressive?
Seen in younger or older patients?

Back 106

Means there are layers of fibrin and hepatocytes
less aggressive
younger patients than usual hcc

Front 107

what is the embryonal liver neoplams?
Can the tumors be mixed or is it always the same tissue? why?

Back 107

Hepatoblastoma
different, because embryonic tissue

Front 108

what is marker for liver metastasis?

Back 108

alpha feto protein

Front 109

What is second most common type of hepatic neoplasm?

Back 109

biliary tract carcinoma

Front 110

Biliary tract carcinoma
name components you can find in BTC?

Back 110

mucin, CEA, NO bile

Front 111

what are components of HCC?

Back 111

NO mucin, a feto prot, Bile

Front 112

What is a klatskin tumor
does this cause gallbladder extension? why

Back 112

hilar adenocarcinoma
NO, because it occurs proximal to where the cystic duct joins the common duct

Front 113

courvoisier's tumor?
What sign will there be?

Back 113

carcinoma of ex hepatic bile duct distal to gallbladder.
gallbladder enlargement which is courvoisier sign.

Front 114

CD31 stains for what?
what others could you use?

Back 114

Angiosarcoma (the endothelial cells are malignant)
Factor 8, cd 56