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GI > Liver Pathology and Hepatitis > Flashcards

Liver Pathology and Hepatitis Flashcards

1
Q

What are the major areas of the liver (4)

A

right lobe
left lobe
caudate lobe
quadrate lobe

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2
Q

What is the vascular entry into the liver

A

enters through the parenchyma via branches of the hepatic portal vein and hepatic artery

it will empty into the hepatic sinusoid

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3
Q

What is the vascular mode of exit from the liver

A

drainage of the sinusoid through the central vein

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4
Q

How is the liver divided based on the oxygen supply

A

it is divided into 3 parts

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5
Q

zone 1 of liver oxygen supply

A

encircles the portal tracts where the oxygenated blood from the hepatic artery enters. closer to the portal triad

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6
Q

zone 2 of liver oxygen supply

A

located in between the central vein and portal triad

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7
Q

zone 3 of liver oxygen supply

A

located around the central veins where oxygenation is poor

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8
Q

How can you classify diseases of the liver

A

acute
chronic
focal
diffused
mild
severe
reversible
irreversible

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9
Q

Most cases of acute liver disease is caused by what

A

viral hepatitis

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10
Q

Y/N: Do mild cases of liver disease need medical attention

A

no

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11
Q

what is hepatitis

A

hepatitis is an inflammatory process causing liver death by necrosis or by triggering apoptosis

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12
Q

What causes hepatitis

A

infection with one or several types of the virus
exposure to drugs or alcohol

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13
Q

What drugs may cause hepatitis

A

isoniazid
acetaminophen

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14
Q

what are the different types of hepatitis

A

HAV
HBV
HCV
HDV
HEV

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15
Q

how long is acute hepatitis

A

< 6 months

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16
Q

how long is chronic hepatitis

A

> 6 months

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17
Q

HAV characteristics

A

Acute
No lipid bi-layer
mode of transmission = fecal-oral route
ssRNA

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18
Q

HBV characteristics

A

Can be acute or chronic
has a lipid bi-layer
mode of transmission = sex, blood, perinatal tube
dsDNA

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19
Q

HCV characteristics

A

Can be acute or chronic
has a lipid bi-layer
mode of transmission = blood transfusion
ssRNA

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20
Q

HDV characteristics

A

Mainly chronic
mode of transmission = sex blood, perinatal
need co or super infection
ssRNA
(HBV is a precursor)

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21
Q

HEV

A

Mainly acute but can progress to chronic
no lipid bilayer
mode of transmission = fecal-oral route
no envelope, ssRNA
(similar to A but no vaccine for it specifically)

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22
Q

What is the role of perforins in the pathogenesis of hepatitis

A

forms pores on hepatocytes

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23
Q

What is the role of granzymes in the pathogenesis of hepatitis

A

induce apoptosis

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24
Q

how do granzymes induce apoptosis

A

cytotoxic t-cells activate:
caspases
mitochondrial pathway

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25
Q

What activates cytotoxic T-cells

A

MHC-1

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26
Q

cytotoxic t-cells induce damage via 2 ways

A
  1. preforin & granzyme
  2. increased accumulation of viral proteins
    (RNA/DNA polymerase, antigen, capsia)
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27
Q

What is the mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA)

A

(7)
1. Attachment
2. Entry
3. Uncoating
4. Translation
5. Replication
6. Maturation and assembly
7. Release

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28
Q

What is the mechanism of replication for HBV (dsDNA)

A

(9)
1. Attachment
2. Entry
3. Uncoating
4. NUCLEAR IMPORT
5. TRANSCRIPTION
6. Translation
7. REVERSE TRANSCRIPTION
8. Maturation and assembly
9. Release

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29
Q

What is the ATTACHMENT mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA)

A

it binds to the receptor on the suface

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30
Q

What is the ENTRY mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA)

A

by endocytosis

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31
Q

Where is the UNCOATING mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA) taking place

A

in the ribosome and removes the capsid and lipid bilayer

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32
Q

What is the TRANSLATION mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA)

A

of viral protein to RNA/DNA

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33
Q

What is the REPLICATION mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA)

A

it is highly dependent on RNA polymerase to increase ssRNA

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34
Q

Where is the MATURATION AND ASSEMBLY mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA) happening

A

in the endoplasmic reticulum

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35
Q

What is the RELEASE mechanism of replication for HAV, HEV, HCV, and HDV (ssRNA)

A

via exocytosis and they will effect other hepatocytes

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36
Q

How does the mechanism of replication for HBV (dsDNA) differ from that of HAV, HEV, HCV, and HDV (ssRNA)

A

the inclusion of nuclear import, transcription, and reverse transcription

no replication

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37
Q

What does TRANSCRIPTION do in the mechanism of replication for HBV (dsDNA)

A

makes 2 types of RNA:
viral RNA
pregenomic RNA

VIA RNA POLYMERASE

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38
Q

What does NUCLEAR IMPORT do in the mechanism of replication for HBV (dsDNA)

A

DNA repair enzyme for complete dsDNA

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39
Q

What does REVERSE TRANSCRIPTION do in the mechanism of replication for HBV (dsDNA)

A

RNA to DNA via reverse transcriptase

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40
Q

What are the phases of viral hepatitis

A

(3)
Prodromal
Icteric
Convalescent

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41
Q

what are characteristics of the PRODROMAL phase of viral hepatitis

A

Fever, via:
1. Hepatotoxins and cytokines (IL-1, IL-6, and TNF-alpha) from the liver go into circulation
2. they activate PGE2 and PGF2 in the enteric center of the brain stell

Nausea, and flu-like symptoms via:
leads to retroperistotic action = back flow of food up the esophagus

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42
Q

what are characteristics of the ICTERIC phase of viral hepatitis

A
  1. Icterus in the eyes
  2. yellowish skin discolorations in the palms and soles
  3. dark urine
  4. clay stools
  5. hepatomegaly with pain in the upper right quadrant of the abdomen
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43
Q

what creates the DARK URINE characteristics of the ICTERIC phase of viral hepatitis

A

increased levels of unconjugated bilirubin

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44
Q

what creates the ICTERUS AND YELLOWISH DISCOLORATION characteristics of the ICTERIC phase of viral hepatitis

A
  1. increased bilirubin
  2. increased unconjugated bilirubin
  3. increased bile salts

in circulation make deposits at different areas in the body that build up over time

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45
Q

what creates the CLAY STOOLS characteristics of the ICTERIC phase of viral hepatitis

A
  1. decreased bile =
  2. decreased bilirubin =
  3. decreased urobilinogen =
  4. decreased sterocobilin (what colors stools)
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46
Q

what creates the HEPATOMEGALY characteristics of the ICTERIC phase of viral hepatitis

A
  1. decreased bile production
    due to
  2. decreased bilirubin
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47
Q

what is hepatomegaly

A

enlargement and pain of the liver due to inflammation

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48
Q

what are characteristics of the CONCALESCENT phase of viral hepatitis

A
  1. Body resolving the infection
  2. flu-like symptoms diminish
  3. jaundice, yellow sclera, hepatomegaly, urine, and stool clear up/return to normal
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49
Q

what are extrahepatic manifestations of liver infection

A
  1. arthritis
  2. vasculitis
  3. myocardial and pericarditis
  4. thrombocytopenia
  5. atypical lymphocytes
  6. chronic hepatitis
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50
Q

what is the root cause of extrahepatic manifestations of liver infection

A

Chronic infection of HBV and HCV (HDV because HBV is needed to get to it)

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51
Q

what is the mechanism of extrahepatic manifestations of liver infection

A

antibodies make deposits of immune complex into different tissues around the body causing inflammation in those areas

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52
Q

what are the pathways to get CHRONIC HEPATITIS as an extrahepatic manifestations of liver infection from HBV HCV or HDV?

A
  1. fibrosis leads to the risk of cirrhosis
  2. regeneration of cells by mitosis = lots of replication = hepatocellular carcinoma
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53
Q

What are the characteristics of acute hepatitis?

A
  1. minimal portal tract inflammation
  2. lobular hepatitis or apoptosis
  3. mononuclear cell infiltrate
  4. confluent necrosis around central vein progressing to central-portal necrosis
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54
Q

What are the characteristics of chronic hepatitis?

A
  1. mononuclear portal tract infiltration
  2. interface hepatitis spills out into other hepatocytes
  3. fibrosis bridge fibrosis and cirrhosis
  4. bile duct proliferation
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55
Q

What are the histological characteristics of chronic hepatitis? (HBV)

A

Ground glass
ER swollen by HBsAg (a viral protein that fills up the hepatocyte)

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56
Q

What are the histological characteristics of chronic hepatitis? (HCV)

A
  1. lymphoid aggregates or fully formed follicles in the portal tract
  2. fatty changes of scattered hepatocytes
  3. ballooned or swollen/rounded hepatocytes
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57
Q

How do you test for HAV

A

Anti-HAV IgM test
Anti-HAV IgG test

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58
Q

What markers to focus on with HAV testing

A

IgG
IgM

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59
Q

In HAV testing, IgM indicates what?

A

Active infection

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60
Q

In HAV testing, IgG indicates what?

A

recovery or vaccination

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61
Q

How do you test for HBV

A

3 antigens:
AHBsAg
HBeAg
HBcAg

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62
Q

what does AHBsAg detect

A

surface antigen

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63
Q

what does HBeAg detect

A

e antigen

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64
Q

what does HBcAg detect

A

core antigen

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65
Q

what is the treatment for HAV

A

supportive care
rehydration
rest

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66
Q

what is the treatment for HBV

A

vaccine with HBsAg to stimulate antibodies
HBsAb for prevention (serum immunoglobins)

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67
Q

what are the tests for HCV?

A

ELISA
HCV RNA with PCR

68
Q

what is the gold standard test for HCV ?

A

RNA test with PCR

69
Q

what is the test for HDV

A

anti-HDV IgM or IgG for active infection
vaccine for HBV

70
Q

T/F: IgG is a protective antibody for HDV

A

FALSE

71
Q

what is the test for HEV

A

Anti HEV IgM for active infection
Anti HEV IgG for recovery or vaccination

72
Q

what is the treatment for HEV

A

supportive care
rehydration
rest
no vaccine

73
Q

(alcoholic liver disease) Toxin-induced liver disease

A

liver injury caused by excess amount of alcohol

74
Q

Toxin-induced liver disease often has a comorbidity of what forms of hepatitis?

A

HCV
HBV

75
Q

How many grams of alcohol consumption is recommended

A

14g

76
Q

what is the normal metabolic pathway of alcohol metabolism

A

ethanol > acetaladehyde > AcytlCoA > water + CO2

77
Q

where is the normal metabolic pathway of alcohol metabolism

A

hepatocyte

78
Q

acetaladehyde converts to AcetylCoA where

A

Mitochondria

79
Q

what 2 substrates are involved in normal alcohol metabolism

A

ADH
ALDH

80
Q

what is the metabolic pathway of alcohol metabolism when binge drinking

A

the addition of CYP450 to CYP2E1
H2O2 Catalase

81
Q

WHERE is the metabolic pathway of alcohol metabolism when binge drinking with CYP450

A

Hepatocyte + ER

82
Q

What is a byproduct of CYP450 and CYP2E1

A

ROS

83
Q

WHERE is the metabolic pathway of alcohol metabolism when binge drinking with C2O2 Catalase

A

peroxisome

84
Q

what is the route of alcohol metabolism

A

stomach > small intestine > liver > hepatocyte

85
Q

How does the route of alcohol metabolism lead to the liver

A

portal vein

86
Q

What percentage of alcohol is absorbed in the liver

A

80%

87
Q

the synthesis of alcohol decreases what

A

NAD. It is needed to transform ActylCoA to ATP
without it goes through FA synthesis and stored in the body as triglycerides

88
Q

what effect does liver injury have on the colon decrease gut bacteria

A

damages good bacteria

89
Q

filtration of toxins in the liver occurs how

A

by kupffer cells in the sinusoid

90
Q

ROS, fat storage, and LPS may lead to what

A

liver cirrhosis

91
Q

LPS

A

gram negative bacteria from kupffer cells in the liver

92
Q

ethanol can cause what to the mitochondria and cell membrane

A

damage and dysfunction

93
Q

alcohol stimulated sinusodial endothelial cells to release endothelin. in return this does what?

A

causes vasoconstriction and contraction of stellate cells

94
Q

vasoconstriction and contraction of stellate cells do what

A

increase the pressure of the portal and central vein causing hypertension

95
Q

what are key histological findings of hepatic steatosis

A

micro-vesicular nodules that become macro vesicuilar globules

96
Q

alcoholic hepatitis causes what

A

hepatocyte ballooning and necrosis

97
Q

Mallory-Denk bodies are clumps of

A

keratin and proteins

98
Q

what is steatofibrosis

A

scarring from fat storage caused by alcohol

99
Q

alcohol steatofibrosis begins with

A

central vein sclerosis and spreads outward

100
Q

in alcohol steatofibrosis clusters of hepatocytes resemble

A

chicken wire fence

101
Q

What is the most important way to diagnose alcohol steatofibrosis

A

liver biopsy
But
blood test, liver function test, and ultrasound/CT is an option

102
Q

what are the most common causes of chronic liver disease

A

steatosis
steatohepatitis
fibrosis
cirrhosis

103
Q

What causes non-alcoholic liver disease

A

fat deposition in the liver
it is not related to alcohol or a viral cause

104
Q

what systemic diseases can cause non-alcoholic liver disease

A

obesity
hypertension
diabetes
hypertyriglyceridemia
hyperlipidemia

105
Q

what is the pathogenesis of non-alcoholic liver disease

A

strong association with insulin resistence
Unsaturated FA are vulnerable to ROS which increases free radicals

106
Q

what is the end result of non-alcoholic liver disease

A

steatohepatitis

107
Q

steatohepatitis is called what without alcohol

A

NASH

108
Q

what is the difference between NASH and alcoholic hepatitis

A

alocholic:
less steatosis
more balloon hepatocytes
neutrophil infiltration
obliteration of the central veins
can progress to cirrhosis
more AST

NASH:
more ALT

109
Q

what is liver cirrhosis

A

Inflammation and damage of the liver caused by the development of fibrotic and scar tissue

110
Q

what are the risk factors of liver cirrhosis

A

excessive alcohol consumption
prolonged attack of HBV, HCV, HCD
medications
drugs
fatty liver

111
Q

What are common histological notes of liver cirrhosis

A

regenerative nodules
fibrotic tissue and collagen

112
Q

what cells mediate fibrosis

A

hepatic stellate cells (HSC)

113
Q

where are HSCs located

A

between the sinusoid and hepatocyte (perisinusoidal space)

114
Q

what do healthy HSCs do

A

Store vitamin A
Quiescent or dormant mode
Natural wound healing

115
Q

What do injured HSCs do

A

lose vitamin A
secrete TGF-beta1 (produces collagen)
increases the build-up of fibrotic tissue
EFFECTS LEAD TO FIBROSIS

116
Q

What are the complications of liver cirrhosis

A

Portal hypertension
Esophageal varices
Portosystemic Shunt
Hepatorenal failure
Hepatic encephalopathy
Asterixis
Decreased estrogen metabolism
Jaundice
Bleeding
Increased Liver enzymes
Hypoalbuminemia
(12)

117
Q

What happens in portal hypertension

A

sinusoidal and portal veins become compressed
increase in pressure

118
Q

What happens in ascites

A

high portal hypertension pushes fluid from the the blood into peritoneal spaces (large cavities) and its excess of fluid is what causes it

119
Q

what happens in in esophageal varices

A

collateral vessels are formed as an alternative circulation pathway to bypass the obstructed flow within the liver

120
Q

what happens in portosystemic shunt

A

blood to the liver is diverted because of high pressure and shunts away to a point of low resistance back toward the heart.

121
Q

what happens in hepatorenal failure

A

a change in portal flow trigger renal vasoconstriction
lowers kidney blood flow
reduces filtration
leads to kidney failure
followed by liver failure

122
Q

what happens with hepatic encephalopathy

A

loss/reduced kidney function
less detoxification
toxins accumulate and enter the brain
mental deficit

123
Q

what happens in asterixis

A

ammonia produced din the GI gets into circulation
reaches the brain
get a tremor/jerky reaction when hands are extended
increased build up = coma

124
Q

what happens in decreased estrogen metabolism

A

increase in blood due to damage = gynecomastia
spider angiomata and palmar erythema

125
Q

what happens in jaundice

A

increased conjugated and unconjugated bilirubin

126
Q

what are the factors of liver cirrhosis

A

(2)
compensated
decommpensated

127
Q

what is compensated liver cirrhosis

A

liver can still function
asymptomatic with weight loss, weakness or fatigue

128
Q

what is decompensated liver cirrhosis

A

extensive fibrosis
liver cant function

129
Q

how do you diagnosis liver cirrhosis

A

the gold standard is to do a liver biopsy

130
Q

what are common lab findings of liver cirrhosis

A

elevated serum bilirubin
elevated liver enzymes (AST, ALP, GGT)
thrombocytopenia

131
Q

what are treatment options for liver cirrhosis

A

prevent further damage by not drinking alcohol and to get an antiviral treatment of HBV, HDV, and HCV

liver transplant

132
Q

What is jaundice

A

a yellow discoloration of due to bilirubin in the skin, mucus membrane, and the eyes

133
Q

what part of the eyes is bilirubin seen in

A

the conjunctiva over the sclera

134
Q

what happens with the liver is damaged

A

bilirubin metabolism is disrupted
cant release UCB
hepatocytes die
Increased UCB and CB in circulation

135
Q

what are normal levels of total serum bilirubin

A

0.3-1.2mg/dl

136
Q

what level of total serum bilirubin indicates jaundice

A

2-2.5 mg/dl

137
Q

What combination of bilirubin causes jaundice

A

UCB or CB or UCB/CB

138
Q

what disorders cause jaundice

A

extravascular hemolytic anemia
ineffective hematopoiesis

139
Q

what is the normal mechanism for bilirubin metabolism

A

RBCs eaten by macrophages
Heme is broken down (heme + globulin)
heme is broken down (Fe, protoporphyrin, UCB)
Albumin binds to UCB and is taken to the hepatocyte
UGT converts UCB to CB
CB exits with bile
in the duodenum, it is converted to urobilinogen
dark color urine

140
Q

what happens when newborns get jaundice

A

their hepatocytes dont have enough UGT to conjugate enough UCB to keep a normal load

If UBC is too high, Kernicterus causes brain damage or death

141
Q

what is the treatment for jaundice in newborns

A

phototherapy to induce structural changed

142
Q

what is dublin-johnson syndrome

A

an autosomal recessive disorder where there is a low carrier protein and CB builds-up in hepatocytes

143
Q

what carrier protein causes the problem in dublin-johnson syndrome

A

MRP2

144
Q

what carrier protein takes over with a decrease in MRP2

A

MRP3

145
Q

Where does MRP3 direct CB

A

into circulation and not the bile canaliculus

146
Q

What does the CB in dublin-johnson syndrome get excreted as

A

dark urine

147
Q

What does the CB in dublin-johnson syndrome do to the liver

A

makes it dark

148
Q

Jaundice in the form of high CB can be seen as what disorder(s)

A

Dublin-Johnson syndrome
Obsructive Jundice

149
Q

What happens in obstructive jaundice

A

blockage of the bile flow
bile is made up of CB

150
Q

what effect does blockage of the bile flow have in obstructive jaundice

A

gallstones
pancreatic carcinomas
cholangiocarcinomas
parasites

151
Q

what happens when the bile is made up of CB

A

the blockage causes and increase in pressure in the bile ducts

bile leaks through the tight junctions between hepatocytes

bile acids, salts and cholesterols leak into the blood

152
Q

what are the complications of obstructive jaundice

A

pruritus
hypercholesterolemia
xanthomas
dark urine
stratorrhea
fat-soluble vitamin deficiency
(6)

153
Q

What happens with high UCB and CB

A

viral hepaptitis

154
Q

what is viral hepatitis

A

an increase in both UCB and CB in the blood due to hepatocyte infection

155
Q

What is wilson disease

A

an autosomal genetic defect characterized by the accumulation of copper in various tissues due to a lack of the protein carrier ATP7b

156
Q

what tissues can copper accumulate in

A

brain
liver
eyes

157
Q

how much copper does our bodies need per day

A

.75 (the rest is excreted)

158
Q

How is copper excreted

A

90% bile
10% urine

159
Q

what can copper react with in the body and form

A

free radicals
reactive oxygen species

160
Q

what is normal copper metabolism

A

stomach
small intestine
enterocytes
portal vein to the liver

161
Q

what is the special transporter for copper in the liver

A

ATP7b

162
Q

what does wilson disease look like in the liver

A

acute hepatitis to cirrhosis to liver failure

163
Q

what does wilson disease look like in the brain

A

basal gaglia - parkinson’s disease movement
cortex - neuronal death and dementia

164
Q

what does wilson disease look like in the eye

A

cornea - kayser-fleisher ring (green to brown)

165
Q

how do you diagnosis wilson’s disease

A

decreased level of ceruloplasmin in the blood
high level of free copper in the blood and urine

166
Q

what are treatment options for wilson disease

A

penicillamine
zinc and ammonium tetrathiomolybdate
liver transplant

GI (5 decks)

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