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GI > Pathology- Liver > Flashcards

Pathology- Liver Flashcards

1
Q

where is the liver

A

in the upper right hypochondrian

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2
Q

what is the periportal zone

A

area nearest blood supply- receives most oxygenated blood

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3
Q

what is the mid acinar zone

A

zone between periportal and pericentral

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4
Q

whyacinar zone furthest from blood supply most at risk to injury

A

as is cut off from the blood supply

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5
Q

what happens when the liver is acutely injured

A

liver is very resistant- Some liver insults can produce severe parenchymal necrosis but heal entirely by restitution

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6
Q

when does liver injury leave permanent damage

A

when injury chronic

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7
Q

what is the pathogenesis of liver disease

A

insult- inflammation- fibrosis- cirrhosis

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8
Q

what can cause insult to hepatocytes

A

viral, drug, toxin, antibody

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9
Q

what is acute liver failure

A

acute onset of jaundice (raised bilirubin)

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10
Q

what can cause acute liver failure

A

viruses, alcohol, drugs, bile duct obstruction

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11
Q

what is acetoaminophen toxitiy

A

poisoning of the liver, seen in suicides- confluent necrosis produces massive acute necrosis and liver failure

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12
Q

what are the possible outcomes of acute liver failure

A

complete recovery, chronic liver disease, death from liver failure

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13
Q

how is jaundice classified

A

site; pre, hepatic and post hepatic

type: conjugated, unconjugated

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14
Q

what is pre-hepatic jaundice

A

when there is too much haemolysis resulting in too much bilirubin being delivered to the liver

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15
Q

what can cause pre hepatic jaundice

A

haemolysis of all causes, haemolytic anaemias, unconjugated bilirubin, sickle cell disease

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16
Q

what is unconjugated bilirubin

A

not water soluble as not bound to other substances

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17
Q

what is hepatic jaundice

A

when the liver cells are injured or dead

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18
Q

what causes hepatic jaundice

A

acute liver failure, alcoholic hepatitis, cirrhosis (decompensated), bile duct loss, pregnancy

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19
Q

what is post hepatic jaundice

A

when the bile cannot escape into the bowl

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20
Q

what can cause post hepatic jaundice

A

congenital biliary atresia, gall stones blocking the common bile duct, strictures of the common bile duct, tumours at head of pancreas

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21
Q

is cirrhosis reversible

A

no

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22
Q

what are the characteristic features of cirrhosis

A

bands of fibrosis seperating regenerative nodules of hepatocytes, alteration of microvasculature, loss of hepatic function

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23
Q

what are the causes of cirrhosis

A

alcohol, hep b and c, iron overload, gallstones, cirrhosis, autoimmune liver disease

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24
Q

why is liver function impaired in cirrhosis

A

as healthy areas cut off from circulation and cannot receive or transmit substances in blood

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25
Q

what are the complications of cirrhosis

A

portal hypertension,
ascites,
liver failure

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26
Q

how can portal hypertension present

A

oesophageal varices, caput medusa, haemorrhoids

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27
Q

what makes up the portal vein

A

superior mesenteric and splenic vein

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28
Q

what are the other clinical features of chronic liver disease and cirrhosis

A

oedema (reduced albumin)
ascites (reduced albumin and increased aldosterone and portal hypertension)
haematemesis (ruptured varices)
spider naevi and gynaecomastia
coma (toxins still in blood)
purpura and bleeding (reduced clotting factor synthesis
infection (reduced kupffer cells)

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29
Q

what does alcohol cause in the liver

A

fatty liver- releases fatty acids and triglycerides

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30
Q

what injurs hepatocytes in alcoholic liver disease

A

acetaldehyde- metabolite of ethanol

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31
Q

what causes the laying down of collagen in alcoholic liver disease

A

fibroblasts

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32
Q

when does alcohol injury become irreversible

A

after months-years

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33
Q

what is steatosis

A

fatty liver

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34
Q

is a fatty liver reversible

A

yes

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35
Q

what else can cause a fatty liver

A 
NASH
Pregnancy
Drugs
Nutritional
Diabetes (type 2)
HepCV (type 3)
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36
Q

what are the features of alcoholic hepatitis

A

Hepatocyte necrosis
Neutrophils
Mallory Bodies
Pericellular fibrosis

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37
Q

what is massons trichrome

A

in alcoholic cirrhosis when defined bands of cirrhosis separates regenerative nodules

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38
Q

what are the possible outcomes of alcoholic liver disease

A 
cirrhosis 
portal hypertension- varices and ascites 
malnutrition 
hepatocellular carcinoma
social disintegration
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39
Q

what is NASH

A

non alcoholic steatohepatitis

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40
Q

what are the features of NASH and what causes it

A

pathologically identical to alcoholic liver disease

diabetes, obesity, hyperlipidaemia

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41
Q

what is now the commonest cause of liver cancer

A

NASH because of obesity

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42
Q

what viruses other than hep can cause viral heptatitis

A

ebstein barr,
yellow fever,
herpes simplex,
cytomegalovirus

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43
Q

what is delta agent

A

hepatitis D

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44
Q

how is Hep a spread

A

faecal oral

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45
Q

what is the incubation period of hep a

A

2-6 weeks

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46
Q

what does it mean the hep a is directly cytopathic

A

infection causes structural changes in a host cell

47
Q

is there a carrier state in hep B

A

No- recovery or death (death v rare)

48
Q

what is the usual outcome for hep a infection

A

mild illness followed by full recovery

49
Q

what type of degeneration is seen in the liver during hep a

A

ballooning degeneration- sign of hepatocyte injury

50
Q

how is hep B spread

A

blood, blood products, sexually, vertically (utero)

51
Q

what damages the liver in Hep b

A

the antiviral immune response

52
Q

is there a carrier state in hep b

A

yes

53
Q

what are the outcomes of hep b infections

A

acute hepatitis followed by resolution

acute hep with liver failure, death

chronic inflammation either:

  • non progressive
  • progressive, cirrhosis, liver failure

hepatocellular carcinoma

54
Q

is there a vaccine for hep b

A

ye

55
Q

how is hep c spread

A

blood, blood products, possibly sexually

56
Q

does hep c have a long/ short incubation period

A

short

57
Q

why is there not a vaccine for hep c

A

as lots of virus subgroups, need a good antigen to develop vaccine

58
Q

what is the usually course of hep c

A

usually assymptomatic, tends to become chronic

59
Q

what does hep c increase your risk of

A

heptocelullar carcinoma

60
Q

what does chronic viral hepatitis look like on microscopy

A

dense portal chronic inflammation - portal triad surrounded by inflammatory cells: mainly lymphocytes

61
Q

what are inflammatory cells in acute inflammation

A

neutrophils

62
Q

what is piecemeal necrosis and what causes it

A

interface hepatitis- when inflammatory cells infiltrate into the liver and obscure the border of the portal area

seen in chronic viral hepatitis

63
Q

what is a councilman body

A

a dead hepatocyte

64
Q

what is bridging fibrosis

A

when fibrosis caused by chronic viral hepatitis bridges between two portal areas

65
Q

what does bridging fibrosis do to the liver

A

causes it to shrink- scar tissue is hard and contracts

66
Q

what are the micro and macro nodules found in cirrhosis

A

macrondule> 3mm in diameter

micronodule <3mm in diameter

67
Q

what are the outcomes of hep B

A

fulminant (severe or sudden onset) acute infection -> death

chronic hepatitis

cirrhosis-> from progressive to chronic

hepatocellular carcinoma increased risk

asymptomatic (carrier)

68
Q

what is the outcome of hep c

A

chronic hepatitis

death

69
Q

what autoimmune diseases can cause chronic hepatitis

A

primary biliary cirrhosis

autoimmune hepatitis

primary sclerosing cholangitis

70
Q

who is more likely to get primary biliary cirrhosis

A

females 90%

71
Q

what might be seen on biopsy of primary biliary cirrhosis

A

granulomas and bile duct loss

72
Q

how is PBC staged

A

biopsy

73
Q

what does primary biliary cirrhosis involve pathologically

A

chronic portal inflammation causes destruction of the bile duct- bile ducts inflamed, granulomas around ducts

74
Q

what is a granuloma

A

collection of histoctyes

75
Q

what is a histocyte

A

macrophage

76
Q

why does PBC give you a green liver

A

as bile gets trapped in the liver because of the bile duct injury

77
Q

what can untreated PBC lead to

A

cholestasis, liver injury, inflammation, fibrosis, cirrhosis

78
Q

what is cholestasis

A

a reduction or blockage of bile flow

79
Q

who is autoimmune hep more common in

A

females

80
Q

what pathological pattern in seen in autoimmune hep

A

chronic hepatitis pattern- portal inflammation

81
Q

what else in seen histologically in autoimmune hepatitis

A

the presence of numerous plasma cells, antibodies to sooth muscle or LKM, IgG

82
Q

when can LKM be raised

A

in acute of chronic liver fialure

83
Q

what is the process of chronic drug induced hepatitis

A

chronic active process

84
Q

what might drug induced hepatitis trigger

A

autoimmune hepatitis

85
Q

what is primary sclerosing cholangitis

A

chronic inflammatory process affecting intra and extra hepatic bile ducts

86
Q

what does primary sclerosing cholangitis lead to

A

periductal fibrosis, duct destruction, jaundice and fibrosis

87
Q

what is primary sclerosing cholangitis associated with

A

ulcerative collitis

88
Q

who is more likely to get primary scleroing cholangitis

A

males

89
Q

what does primary sclerosing cholangitis increase your risk of

A

malignancy in bile ducts and colon

90
Q

what is seen microscopically of PSC

A

cholangitis= inflammation of the ducts

periductal onion-skinning fibrosis

91
Q

name three liver storage diseases

A

haemochromatosis, wilsons disease, alpha-1-antitrypsin deficiency

92
Q

what is haemochromatosis

A

excess iron in the liver

93
Q

what causes primary haemochromatosis

A

genetic condition, increased absorption of iron

94
Q

what causes secondary haemochromatosis

A

iron overload from diet, transfusions, iron therapy

95
Q

what inheritance pattern does primary haemochromatosis folllow

A

autosomal recessive

96
Q

what processes cause primary haemochomatosis

A

excess absorption of iron from intestine, abnormal iron metabolism

97
Q

in who is primary haemochromatosis worse in- why

A

men as they are homozygotes

98
Q

when and why does primary haemochromatosis produce symptoms

A

iron deposited in liver, asymptomatic for years until deposited in portal connective tissue and stimulated fibrosis

99
Q

what can primary haemochromatosis cause

A

predisposes to carcinoma

causes diabetes, cardiac failure and impotence

100
Q

what is seen on the microscopy of haemochromatosis

A

iron accumulation- brown pigments in the hepatocyte

101
Q

how is iron accumulation in haemochromatosis confirmed via microscopy

A

perls stain- goes blue

102
Q

what happens if haemochromatosis goes left untreated

A

cirrhosis, hepatocelluar carcinoma

103
Q

what is wilson’s disease

A

inherited autosomal recessive disorder of copper metabolism where copper accumulates in the liver and brain

104
Q

what are the clinical signs of wilsons disease

A

kasyer-fleischer rings at corneal limbus, low serum caeruloplasmin

105
Q

what does wilsons disease lead to

A

chronic hepatitis and neurological deterioration

106
Q

what is an alpha-1-antitrypsin deficinecy

A

inherited automsomal recessive disorder of production of an enzyme inhibitor

107
Q

what does an alpha-1-antitrypsin deficiency cause

A

empysema and cirrhosis

108
Q

what is seen microscopically in aplha-1-antitrypsin deficiency

A

cytoplasmic globules of unsecreted globules of protein in liver cells- accumulates in liver and causes hepatocyte damage

109
Q

what are the two main primary tumours of the liver

A

hepatocellular adenoma (benign)

hepatocellular carcinoma (hepatoma)

110
Q

who is more likely to get hepatocellular carcinoma

A

females- associated with oestrogen

111
Q

what is hepatocellular carcinoma associated with

A

HBV, HCV and cirrhosis

112
Q

how does HCC usually present

A

as a mass, pain or obstruction

113
Q

what is the prognosis for HCC

A

usually poor

114
Q

what are the two histopathological types of HCC

A

hepatocytic- looks like hepatocytes

cholangio- looks like bile ducts

GI (64 decks)

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