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liver Flashcards

0
Q

portal triad and waht contaisn it

A

hepatic artery
portal vein
duct

hepatoduodenal ligaent

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1
Q

cells of liver

A

hepatocytes
cholangiocytes:intercellualr channels–>bile canaliculi
nonparenchy
–kupffer (macrophages)
–sinusoidal endothelial cells- no RBC; leaky barrier
–pit cells
–hepatic stellate cells -collagen synth

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2
Q

splenic vein branches

A

short gastric
pancreatic
L gastroepiploic
IMV

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3
Q

SMV

A

inferior pancreatoduodenal

R gastroepiploic

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4
Q

portal vein

A

superior pancreatic duo

L gastric

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5
Q

biliary system

A

canals of hering–>bile ductules–>terminal ducts–>segmental bile ducts–>R and L lobal ducts–>common hepatic ducts + cystic duct–>common bile duct–>sphincter of oddi

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6
Q

acinus

A

blood supply of a small portion of parenchyma that drains a particular bile duct

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7
Q

lobule

A

blood supply by several separated portal vein branches, each of which also supplies adjacent lobules

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8
Q

bile compromises

A

conjugated bilirubin
cholesterol, phospholipids
bile salts
water, electrolytes

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9
Q

what converts 1% conj bilirubin to urobilinogen

A

intestinal bacteria

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10
Q

places glucose 6 p can go

A

synthesis of glycogen
anaerobic glyclysis
pentose-phosphate shunt

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11
Q

what proteins are not made by liver

A

Igs

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12
Q

what else makes alk P

A

bone

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13
Q

gGT

A

biliary epithelium

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14
Q

liver disease changes bioavailablity of circulating vasoactive substances and endothelial dysfunction

A

eNOS increase in splanchnic and decrease in liver AND increase production of VC–>splanchnic dilation and liver resistance

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15
Q

PHTN syndrome

A

central VS of cns and kidney–>brain dysfunction and hepatorenal syndrome

vasodilation of splanchnic–>arterial hypotension–>decrease in PVR, hypervolemia–> well perfused skin, low BP

vasodilation of intrapulm circ–>dec O2–>hepatopulm

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16
Q

hyperdynamic circulation means that

A

system very suceptible to very minor changes
septicemia–>endotoxin medicated vasoC
Nsaids–>block kidney fx
diurectics–>increase VS

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17
Q

these drugs may improve cirrhosis

A

bblockers to decrease shear stress on hepatic/splanic vessels–>decrease endothelial damage–>decrease enos

a agonist–>VD

anti inflam agents

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18
Q

child pugh predicts

A 
outcome of tx, variceal hemorrhage etc
scored for freq of abnoramilties
A: 5-6
B: 7-9
C: 10-15--decompensated cirrhosis
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19
Q

TIPS not recommendedchilds

A

grade b-c

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20
Q

ALT>AST

A

hepatitis

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21
Q

AST>ALT

A

alcohol or cirrhosis

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22
Q

dx test for ascites

A

SAAG
culture
cytology
CBC and HGB

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23
Q

SAAG >1.1

A

almost alaways decompensated cirrhosis

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24
Q

tx ascites

A

tx underlying liver dz
consider transplant if prognosis is poor
decrease dietary Na intake, fluid restriction, and diuretics

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25
Q

in diuretic ressistance patients

A

paracentesis
shunts:TIPS
extracorporeal ultrafilitartin of ascitic fluid
liver transplant

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26
Q

sequela of ascites

A

hepatic hydrothorax- fluid enters chest via diaphragmatic defects
umbilicl, inguinal hernias
spontaenous bacterial peritonitis: translocation of bacteria from mesenteric LN–>bacteremia–>bacterascites
hepatorenal fx (poor px)

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27
Q

main cause of jaundice

A

viral hepatitis

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28
Q

hep A

A

+ stranded RNA picornavirus w/o envelope

feval oral

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29
Q

dx hep a

A

HAV IgM

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30
Q

HBV

A

small DNA virus of hepadnavirus
–partially dsDNA + viral envelope + core, DNA polymerase and x particle

sexual transfer
mom–>child

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31
Q

clinical presentation of hepB

A

acute infection
CLD
extrahep-rash, gnitis, arthritis, vasculitis, angioneurogenic edema

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32
Q

testing hbv

A

+HbsAg= acute infection if anti-HBc (IgM is )+
+HBsAg w/ sx and - Igm- early acute
+HBsAg w/o sx- mild CLD
+anti-HVs(afe)–recovery/immunity
+HV DNA- best indicator for active viral replicatin

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33
Q

tx HBV

A

entecavir, tenofovir

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34
Q

HDV

A

defective RNa virus–requires HBV first

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35
Q

HEV

A

single stranded + RNA hepevirus

pigs are reservoir

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36
Q

HEV transmission

A

fecal oral

rare instates, but leading cause of jaundice in endemic areas–usually affects both sexes

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37
Q

clinical presenation of HEV

A

incubation 2-9 weeks
may cause acute liver failure
chronic form possible

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38
Q

mortality in HEV

A

increase sa ton in pregnancy esp third trimester

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39
Q

testing HEV

A

RNA for active rep + IGM= acute, +IGG= past hep

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40
Q

hep v

A

single + sRNa virus, eveloped, flavivirus

1-6 types

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41
Q

how do HCV invaide

A

interact with surface proteins hepatocyte
enter cell by endocytosis
uncoat in the low endosomal ph
viral envelope fuses with endosome mebrane releasing RNa into cyto
rna interacts with ribo
single polyprotein produced
cleaved by proteases to mature viral protein
replicate
assembly
budding

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42
Q

risk of HCV

A

40-80%

higher than HBV

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43
Q

HCV can prodyuce

A

cryoglobinemia–accum of Igg related products in dependent ares- becoem insoluble in cold temp

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44
Q

screening tests

A

ELISA + RNA detection

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45
Q

anti HCV + HCV RNA +

A

active infection

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46
Q

anti HCV + , HCV RNA=

A

past infection

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47
Q

ANTI HCV -, HCV RNA+

A

acute HCV immunp sup

false positive RNA

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48
Q

HHC affects many organs

A 
pituitary
thyroid
parathyroid
heart
liver
panc
gonads
joints
blood skin
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49
Q

pathiphys A1AT def

A

lung: A1AT blocks lung elastase in alveoli
- -if they lack this–>lung disease and COPD

liver: cuumulation of wrongly folded A1AT in cell ER–>cell damage–>apoptosis–>fibrosis and cirrhosis

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50
Q

what type of disease is A1AT

A

AR with codomiannt expression
M, S, and Z alleles on SERPINA1 gene on Ch16 (or >100 identified alleles)

most normal MM, Z abnormal

51
Q

screening for A1At

A

recommended in patients with asthma and COPD

52
Q

adults vs children presentaing

A

adults: lung > liver
kids: neonatal jaundice, hepatomegaly, failure to thrive, or acute LF

53
Q

dx A1AT def

A

decrease serum A1AT (but can increase with iflam because it is an APP)
protein phenotyping
liver bx (nor req)
PAS + diastase resistant gloubles

54
Q

most Fe in body found within

A

hemoglobin

55
Q

most storage of Fe

A

macrophages and hepatocytes- small amounts in myoglbin

56
Q

hepcidin

A

hormone produced in liver–>responds to Fe levels in blood

stimulates Fe transport into cells (macrophages, enterocytes, hepatocytes)

57
Q

ferroportin

A

main Fe export protein on enterocytes, Mo, and hepatocytes

58
Q

HFE protein

A

found on hepatocytes; sensory for circulating Fe

59
Q

decrease in hepcidin

A

increase in circulating Fe

60
Q

increase in hepicdin

A

increase in Fe transport into cells but decrease in export out because destruction of ferroportin

61
Q

HFE-HC type 1

A

hereditary impairment of synthesis of fx of hepcidin
AR mutation on chr 6
1:7 hetero for C282Y and 1:3 hetero for H63D

62
Q

what happens in HFEHC

A

impaired hepcidin synthesis–>increase circulating Ge–>incrase transferrin sat–>progressive Fe deposition in parencyma of liver, etc

63
Q

tx HFE HC

A

phelbotomy

64
Q

NonHFE HC

A

not assocaited with hepcidin function
transferrin saturdation is slightly increased or low
iron accumulates in RES and othe rcells
not responsive to phebotomy

65
Q

dx hemochrom

A

increase LFT, inc ferritin, dec transferring, but inc trans sat (>45), decrease TIBC

66
Q

wilson’s disease

A

AR disease involving accumulation of Cu in body secondary to defective secretion by a mutated Cu transporting Ptype ATPase on golgi in hepato

67
Q

job of defective Cup transporting p typeprotein

A

chaperon Cu into bile by binding apoceruloplasmin to form ceruloplasmin which transports cu

68
Q

wilsons dz presentation

A 
liver 
portal htn
nonhemolytic anemia**
cns: mental dysability
renal dysfx
cardiac
bone 
heme
69
Q

kayser fleischer ring

A

cu depposit in descement membrane of cornea–>sunflower cataract seen in 95% of patients with neuropsych sx
usually normal vision

70
Q

labs wilson

A

decrease in ceruoplasmin
decrease total Cu (because mostly bound to ceruplasmin)
but increase free total Cu fraction

71
Q

tx willsons

A

d-pencillamine and trientine (chelators), zinc-absorption of excess Cu in the body, liver transplant

72
Q

criggler najjer syndrome

A

ar disorder with decrease to absent UGT (more severe filbert)–type 1 incompatible with life, type 2 less severe

UCBemia in children

73
Q

dubin johnson

A

D
ar disorder of apical canalicular membrane proteins resp for excretion of bili into intrahepatic ducts
obstructive with increase CB
black liver

74
Q

rotor

A

similar to dubin with no black liver

75
Q

oxidative metabolism alch

A

acetate is end product–>uses up O2 and NADH and produces centrilovular hypoxia in a region already low in O2

76
Q

microsomal oxidation

A

not used much in normals but more in alcoholics, which is bad because acetyladehyde makes percentral zone produce collagen and also is the pathway used to oxidate tyelnol

77
Q

alcohol increases

A

pmn infiltration

78
Q

cytokines in alcohol

A

tnf and il6

79
Q

HCT

A

may be only abnormal liver test

80
Q

two measures of how bad alcholic liver disease is

A

MDF (pt and bili) >32 predicts 30 mortiality

MELD, >18 predicts 30 day mortality and >5 can get transplant

81
Q

tx alch hepato

A

supprotive
prenisolone for severe or hepatic enceph
tnf inhibitor that decreses risk of renal disease
abstinance is key1

82
Q

NAFL

A

steatosis

benign, reversible

83
Q

NASH

A

fatty liver _ hepatocyte death

84
Q

cirrhosis

A

regenerative nodules + fibrosis

85
Q

abnormal production of hormones produced by fat

A

decreased adiponectin–>block FA uptake–>increase FA oxidation and lipid export–>increase insulinsensitivty

increase TNFa–>proapoptotic, recruits wbc, increase insulin R

86
Q

liver function tests

A

AST, ALT ALT can suggest statosis

negative tsts other dz

87
Q

gold standard of estimating severity

A

bx

88
Q

tx NASH

A 
weight loss
increase insulin sens with metformin or proglitazone
vitamin E/proglitazone
change diet
coffee
89
Q

NAFL to cirrhosis

A

> 10 years, 3%

90
Q

NASH + fibrosis to cirrhosis

A

5,10 years, 30%

91
Q

autoimmune HLADR3

A

fibrosis and cirrhosis

92
Q

antibodies for AIH

A

ana often + but nto specific

usually either SMA or microsaomal but not both

93
Q

polyclonal gammopathy

A

IgG>IgM>IGa

94
Q

liver bz shows

A

plasma cells

95
Q

LFT >1000

A

viral hep
AiH
shock liver
acute drug or toxin liver injury

96
Q

LFT >10000

A

acetaminophen tox/shock liver

97
Q

other autoimmune dz

A

primary biliary cirrhosis
franulomatous destruction of interlobular bile ducts–>progressive ductopenia–>progressive cholestasis–>cirrhosis and liver failure

98
Q

PE of PBC

A 
hyperpih
excoriations from prutitis
jaundice
xanthomas
hepatosplen
99
Q

labs PBL

A

lFTs cholestatic (ALP/GCT»>AST/ALT)
AMA*****antimitochondrial antibody
ANA+

100
Q

tx of PBC

A

ursodeoxycholic acid works–improves LFTs and survive

101
Q

PSC vs PBC

A

PSC0 macroscopic bile duct abnoramlity

PBC- microscopic

102
Q

major comp of PSC

A

cholangiocarcoma (mc!)

103
Q

ABCDE chronic hep

A 
AiD
B virus
Cvirus
Drug induced
Etoh
104
Q

portal triad and central vein collagen types

A

I, III

105
Q

percellular reticulin in lobules collagen types

A

IV

106
Q

causes of hepatic injury

A

toxin accum
inflam
ischemia

107
Q

injury leads to

A

activiaton of hepatic stell cells–>proliferate, multiply, interact with kuppfer cells–>hepatocyte apoptosis & pro fibrosis (TGF B), loss of fenestrating–>cirrhosis

108
Q

pathway of fibrosis

A

portal fibrosis–>periportal fibrosis–>inflammation that allows fibrosis to swpill over–>bridign fibrosis–>cirrhosis

109
Q

main benign liver tumor

A

hemangioma

110
Q

hepatocyte beign vs malignant

A

benign-hepatic adenoma, focal nodular hyperplasia

malignant- hepatocellular carcinoma, hepatoblastoma

111
Q

biliary epithelium benign and malignant

A

benign- bile duct adenoma, biliary hamartoma

malignant- choiangiocarcoma

112
Q

mesenchymal benign vs malignant

A

benign-hemangioma, angiomylipoma

malignant- angiosarcoma

113
Q

biliary hamartoma is

A

normal tissue an abnormal location

114
Q

hepatocellular adenoma

A

MC primary malignant
HNF1a –associated with MODY3
associated with oral contraceptive, steroids, or pregnancy

RUQ mass, pain, hemorrhage

115
Q

focular nodualr hyperplasia

A

multiple fibrus septae with central scar

116
Q

hepatoblastoma- least common malignant

A

kids; moms notice diapers arent fitting
produces hcg so virilization and precocious puberty
surgery and chemo

117
Q

hepatocellular carcinoma

A 
90% malig cancer
80% with HBV or HCV (90% in west)
travecular and acinar
bile in neoplastic cells
compesnated -->decompensated wth rising afetoprotein level
118
Q

what doesnt work with HCC

A

chemo and radioRx–need liver transplant

119
Q

special subset HCC

A

fibrolammelar hepato–age 20-40, no association with CLD or cirrhosis

120
Q

cholangiocarcinoma

A

adenocarcinoma arising from intra and extra hepatic bile duct epithelium
main site ampulla; no relation to cirrhosis
a/w pSC, choledocal cysts, liver flukes, etc

121
Q

CEA

A

increased in bile duct carcinoma

122
Q

mucin production

A

in bile duct carcinoma

none in HCC

123
Q

bile duct carcinoma vs hepatocellualr carcinoma spreads through

A

HCC-veins

BD-lymphatics

124
Q

gross appearance HCC vs BD

A

HCC-soft and hem

BD-hard whitish

GI (12 decks)

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