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liver Flashcards

1
Q

what are the symptoms of primary biliary cholangitis

A

fatigue
itch without rash
xanthelasma

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2
Q

what is the treatment for PBC

A

urseodeoxycyclic acid

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3
Q

how is PBC diagnosed

A

need 2 of 3
positive AMA
cholestatic LFTs
liver biopsy

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4
Q

what happens to patients with PBC

A

most will not develop symptoms

many developing liver failure will be unfit for transplant

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5
Q

blood flows into the liver via what

A

liver has dual blood supply

blood flows in from the portal vein and hepatic artery

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6
Q

what is classed as portal hypertension

A

pressure above the normal range 5-8mmHg

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7
Q

what are the causes of hypertension in the liver

A

prehepatic-blockage of the portal vein before the liver due to portal vein thrombosis or occlusion secondary to congenital portal venous abnormalities
intrahepatic-due to distortion of the liver architecture
presinusoidal eg, schistomiasis of non-cirrhotic portal hypertension
post sinusoidal eg.cirrhosis causes include cirrhosis, alcoholic hepatitis and congenital hepatic fibrosis

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8
Q

what signs would you see in compensated cirrhosis

A 
spider naevi
palmar erythema 
gynaecomastia 
clubbing 
maybe hepatomegaly 
splenomegaly
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9
Q

what signs would you see in decompensated cirrhosis

A

jaundice
ascites
encephalopathy
bruising

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10
Q

how would you treat cirrhosis

A

remove or treat the underlying cause

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11
Q

what are the complications of cirrhosis

A

variceal bleeding
jaundice
ascites
liver failure

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12
Q

what is the first line drug in treating ascites

A

spironolactone

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13
Q

where does spironolactone act

A

in the collecting ducts in the kidneys

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14
Q

what is ammonia normally metabolised to and where

A

to urea in the liver

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15
Q

what is hepatic encephalopathy

A

ammonia generated in the intestines form nitrogenous compounds in the diet is taken directly into the systemic circulation rather than being metabolized in the liver

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16
Q

what are oesophageal varices

A

extremely dilated sub-mucosa veins in the lower third of the oesophagus

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17
Q

what are oesophageal varices usually due to

A

portal hypertension, commonly due to cirrhosis

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18
Q

how are oesophageal varices treated prophylactically

A

B blockers non selective eg carvediolol, propanolol

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19
Q

what are the causes of chronic liver disease

A 
alcohol
hep B, hep C
autoimmune hepatitis
primary biliary cholangitis 
haemochromatosis 
NAFLD
primary sclerosing cholangitis 
a 1 anti-trypsin
budd chiari
methotrexate
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20
Q

name 2 diseases that affect the liver chronically but aren’t chronic liver diseases

A

amyloid and rotor syndrome

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21
Q

what is primary sclerosing cholangitis

A

an autoimmune disease of large and medium sized bile ducts

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22
Q

how is primary sclerosing cholangitis diagnosed

A

clinically through cholangitis

diagnosis through imaging of biliary tree

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23
Q

what is haemochromatosis

A

genetic iron overload syndrome

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24
Q

how is haemochromatosis treated

A

venesection-patient gives blood

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25
Q

what is Wilson’s disease

A

lenticulo-hepatic degeneration

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26
Q

how does Wilson’s disease damage the liver

A

deposition of copper in the liver

Wilson’s disease causes fibrosis

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27
Q

what clinical signs can indicate wilsons disease

A

Kaiser Fleisher rings

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28
Q

how is wilsons disease treated

A

copper chelation drugs-pencillamine

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29
Q

what signs can Budd-chiari produce acutely

A

jaundice, tender hepatomegaly

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30
Q

what symptoms can chronic budd-chiari produce

A

ascites

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31
Q

what is methotrexate used to treat

A

rheumatoid arthritis and psoriasis

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32
Q

what does steato mean

A

relating to fatty matter or tissue

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33
Q

what does sclero mean

A

hard/hardening

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34
Q

what is pruritis

A

severe itching of the skin, as a symptom of various ailments

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35
Q

what is anti-microbial antibody used to test for

A

primary biliary cirrhosis

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36
Q

what is anti-nuclear, smooth muscle (actin), liver/kidney microsomal antibody used to test for

A

autoimmune hepatitis

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37
Q

what is raised serum IgG a sign of

A

primary biliary cirrhosis

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38
Q

what is raised serum IgM a sign of

A

autoimmune hepatitis

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39
Q

what are increased viral markers a test of

A

Hepatitis A,B,C,D,E

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40
Q

what does a-fetoprotein test for

A

hepatocellular carcinoma

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41
Q

what does serum iron, transferrin saturation, serum ferritin test for

A

hereditary haemochromatosis

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42
Q

what does serum and urinary copper, serum caeruloplasmin test for

A

Wilson’s disease

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43
Q

how would you test for cirrhosis

A

a1-antitrypsin

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44
Q

what would a1-antitrypsin test for

A

cirrhosis and emphysema

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45
Q

how would you test for primary sclerosing cholangitis

A

anti-nuclear cytoplasmic antibodies

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46
Q

what would anti-nuclear cytoplasmic bodies test for

A

primary sclerosing cholangitis

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47
Q

what would markers of liver fibrosis indicate

A

non-alcoholic fatty liver disease

hepatitis C

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48
Q

what would genetic analyses test for

A

HFE gene in hereditary haemochromatosis

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49
Q

what are the true liver function tests

A

bilirubin
albumin
prothrombin time

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50
Q

what are measured in LFTs

A

ALT/AST
alkaline phosphatase (ALP)
GGT
Bilirubin

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51
Q

what is acute liver disease

A

any insult to the liver causing damage
in previously normal liver
acute liver failure defined as causing encephalopathy and prolonged coagulation

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52
Q

how are hep B and C transmitted

A

blood

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53
Q

what are the causes of acute liver disease

A 
viral A,B,C,D,E, CMV, EBV and toxoplasmosis 
drugs
shock liver
cholangitis 
alcohol 
malignancy 
chronic liver disease 
PARACETAMOL
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54
Q

good questions for probing more into an alcohol history

A

ask when they last had a drink
what did you drink
what strength

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55
Q

acute liver investigations

A

LFTS (inc albumin and bilirubin)

prothrombin time

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56
Q

treatment of liver disease

A

rest, up to 3 months for recovery may be up tp 6
fluids, no alcohol
increase calories, high fat foods poorly tolerated
for itch-sodium bicarbonate bath, cholestryamine or uresodeoxycholic acid

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57
Q

what metabolic considerations are needed for acute liver disease

A

monitor and supplement K, PO4 and Mg, hypoglycaemia is a very serious clinical sign

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58
Q

why is paracetamol toxic in high quantities

A

when paracetamol is metabolised a toxin called NAPQI is made, this can be mopped up by glutathione but at high overdoses the glutathione can be all used up

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59
Q

what is the name of the dangerous toxin made by the metabolism of paracetamol

A

NAPQI

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60
Q

what drugs can cause liver disease

A

co-amoxiclav
flucloxacillin
NSAID

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61
Q

fulminant hepatic failure has what symptoms

A

jaundice and encephalopathy in a patient with a previously normal liver

62
Q

what are the common causes of fulminant hepatic failure

A 
paracetamol 
fulminant viral 
drugs 
HBV
Non A-E
rare but Wilsons, Budd Chiari, malignancy
63
Q

fulminant hepatic failure treatment

A

supportive
inotropes and fluids
renal replacement
transplantation

64
Q

categories for super-urgent transplantation for acute liver failure due to paracetamol

A

ph 100 (inr 6.5) + creatinine 300 or anuria + grade 3 or 4 encephalopathy
lactate >3.5 )3.0 after resus >24 hr after ingestion
any 2 of 3 from category 2 plus life-threatening deterioration without sepsis

65
Q

how is hep A transmitted

A

faecal oral-route

66
Q

can you get acute or chronic Hep A

A

just acute hepatitis A, no chronic infection

67
Q

what is hep A associated with

A

poor hygiene/overcrowding

some cases in gay men and injecting drug users

68
Q

how is Hep E transmitted

A

faecal oral route

69
Q

which is more common in Uk Hep A or E

A

Hep E

70
Q

which Hep is there no available vaccination

A

hep E

71
Q

does hep E produce acute or chronic hepatitis

A

acute but can be chronic in immunocompromised patients

72
Q

how is hep E spread in the UK

A

zoonose from pigs, rabbit or deer

73
Q

how do you get Hep D

A

only get Hep D after getting hep B

74
Q

what is co-infection of Hep D

A

co-infection where you get hep B and D at the same time

75
Q

what is it called when you get hep D after getting hep B

A

superinfection

76
Q

what is superinfection (in relation to hep)

A

get hep D after getting hep B

77
Q

who is at higher risk of hep B

A

people born in areas of intermediate/high prevalence
multiple sex partners
inject drug users
children to infected mothers

78
Q

what is HBsAg

A

hep B surface antigen

79
Q

when is HBsAg present

A

in the blood of all infectious individuals

80
Q

what is also USUALLY present in highly infectious individuals with hep B

A

HBeAg

81
Q

what is ALWAYS present in high titre in highly infectious individuals with hep B

A

Hep B virus DNA

82
Q

what are present in immunity with Hep b

A

anti-HBs

83
Q

what is likely to be present in recently infected cases

A

Hep B igM

84
Q

how is Hep B prevented/controlled

A 
safe blood transfusions
safe sex
needle exchange 
prevention of needle stick injuries 
screening of pregnant women
85
Q

if you have been exposed to Hep B what do you do for post-exposure prophylaxis

A 
can give vaccine 
plus HBIG (hyperimmune HepB immunoglobulin)
86
Q

is there a vaccine available for hep C

A

no

87
Q

if patient at risk of hep C or with signs of chronic liver disease

A

test for antibody to Hep C virus

88
Q

if test for antibody to hep C virus and positive what does this indicate

A

past or active infection

89
Q

how would you differentiate between past or active infection in hep C

A

test for Hep C virus RNA by PCR

90
Q

what does a test for Hep C virus RNA by PCR negative indicate

A

past infection

91
Q

which two tests would have to be positive to indicate a active infection of hep C

A

positive antibody to Hep C virus and positive test for hep C virus RNA by PCR

92
Q

can you get acute or chronic hepatitis with hep B and C

A

both

93
Q

how long is infection of hepatitis before it is chronic

A

6 months or less=acute more than that =chronic

94
Q

does chronic hep C usually resolve

A

no once chronic infection is established, spontaneous cure IS NOT seen

95
Q

pattern of infected children at birth in hep B is similar to what

A

hep C in that high levels of chronic infection is seen

96
Q

how is acute viral hepatitis treated

A 
symptomatic treatment 
no antivirals given 
monitor for encephalopathy 
monitor for resolution-hep B, C or Hep E
notify public health 
vaccinate against other infections if at risk
97
Q

how is the drug used to treat HCV chosen

A

depending on genotype of HCV

98
Q

what are some of the side effects to inferon alpha

A

flu like symptoms
autoimmune disease eg SLE
psychosis

99
Q

what can ribavirin cause

A

anaemia (made worse by telaprevir and boceprevir)

100
Q

what can telepravir and boceprevir

A

rash which can be very severe

anaemia

101
Q

what are the options for treatment of chronic hep B

A

1-peginterferon alone

2-suppressive antiviral drug eg.entecavir, tenofovir

102
Q

what is the advantage of suppressive antivirals such as entecavir and tenofovir

A

they are safer less side effects than peginterferon

103
Q

what is the disadvantage to suppressive antiviral drugs like entecavir, tenofavir

A

they are suppression not cure and resistance can develop

104
Q

what are the aims/benefits of hep B therapy

A

reduction in HBV DNA (suppression)
loss of HBeAg
loss of HBsAg (cure)

105
Q

what new therapies are being used in hepatitis C

A

new antivirals simeprevir, ledipasvir, daclatasvir

move is towards all oral, interferon free courses of a few moths with high SVRs (sustained virological response)

106
Q

what plasma proteins does the liver produce

A

all main plasma proteins except gamma (y) globulins

107
Q

what does albumin transport

A

fatty acids, bilirubin and drugs

108
Q

what do alpha globulins transport

A

lipoproteins, lipids, hormones and bilirubin

109
Q

what does retinol binding protein transport

A

transports vitamin A

110
Q

give two examples of b globulins

A

transferrin and fibrinogen

111
Q

what does LDL transport

A

cholesterol transport to peripheral tissues

112
Q

what do chylomicrons transport

A

transport of exogenous fat to liver

113
Q

how does HDL reverse cholesterol transport

A

cholesterol is esterified with fatty acids and transported back to liver where it is excreted as bile salts via biliary system or faeces

114
Q

where can cholesterol be metabolised and excreted

A

ONLY THE LIVER

115
Q

what vitamins does the liver store

A

vitamin A, D, B12 and iron

116
Q

where is cholesterol located in a lipoprotein

A

in the core

117
Q

what causes prehepatic jaundice

A

excess production of bilirubin after haemolysis

118
Q

what causes post hepatic jaundice

A

from a blocked bile duct (gallstone)
increased conjugated bilirubin in plasma
pale coloured stools due to reduction of faecal bile pigments
dark urine due to excretion of water soluble bilirubin conjugates

119
Q

what are the three types of benign liver masses

A

Haemangioma
Focal Nodular hyperplasia
Adenoma
also liver cysts

120
Q

what are the types of malignant tumours in the liver

A

primary liver cancers-hepatocellular carcinoma
cholangiocarcinoma
or metastases

121
Q

which is the commonest benign liver tumour

A

haemangioma

122
Q

what are the clinical features of a haemangioma

A 
commonest liver tumour 
hypervascualr tumour 
usually single small 
wel demarcated capsule
asymptomatic
123
Q

do you need to biopsy a haemangioma

A

no diagnosis is made based on imaging-ultrasound and CT

124
Q

what is focal nodular hyperplasia

A

benign nodule formation of normal liver disease

125
Q

what is focal nodular hyperplasia associated with

A

congenital vascular anomaly associated with osler weber rendu and liver haemangioma
classically-central scar containing a large artery, radiating branches to the periphery (hub and spoke)

126
Q

what cells are present on histology of focal nodular hyperplasia

A

sinusoids, bile ductules and kupffer cells

127
Q

is focal nodular hyperplasia symptomatic

A

no

128
Q

when is focal nodular hyperplasia more common

A

in young and middle aged women

129
Q

what does a focal nodular hyperplasia look like on imaging

A

us-nodule with varying echogenicity

ct-hypervascular mass with a central scar

130
Q

how is focal nodular hyperplasia treated

A

no treatment necessary

131
Q

what are the features of a hepatic adenoma

A

benign neoplasm composed of normal hepatocytes no portal tract, central veins or bile ducts

132
Q

what are hepatic adenomas associated with

A

contraceptive hormones

133
Q

what are the symptoms or hepatic adenoma

A

usually asymptomatic but may have RUQ pain

134
Q

how can hepatic adenomas change over time

A

may present with rupture, haemorrhage or malignant transformation(v rare)

135
Q

what is contained in hepatic adenoma

A

most are solitary fat containing lesions

136
Q

which lobe are hepatic adenomas usually present in

A

the right lobe

137
Q

what are the symptoms of hepatic adenoma

A

symptoms (pain bleeding) are size related

138
Q

what are multiple adenomas associated with

A

glycogen storage diseases

139
Q

what does hepatic adenoma look like on imaging

A

us-filing defect
ct-diffuse arterial enhancement
MRI-hypo or hyper intesnse lesion

140
Q

how do you treat adenomas

A

stop hormones if that is what is causing them
observe
if no regression then surgical excision

141
Q

what are the differences in adenoma and focal nodular hyperplasia

A

adenoma-purely a hepatocyte tumour but FNH-contains all the liver ultrastructure including RES and bile ductules
malignant degeneration in adenoma but no malignant risk in FNH
adenoma may cause pain and bleed
FNH-ay cause pain but minima bleeding risk

142
Q

what are the 5 types of cystic lesions

A

simple, hydatid, atypical, polycystic lesion, pyogenic or amoebic abscess

143
Q

simple cyst appears how

A

liquid collection lined by an epithelium

no biliary tree communication

144
Q

how do simple cysts present

A

generally no symptoms but symptoms can be related to intracystic haemorrhage, infection, rupture, compression

145
Q

is a simple cyst connected to biliary tree

A

no biiary tree communication, liquid collection of pus lined by an epithelium, solitary and unilocualted

146
Q

how are simple cysts managed

A

no follow up necessary-if symptomatic or uncertain diagnosis then consider surgery

147
Q

what is a hydatid cyst

A

echinoccocus granulosus

148
Q

how can a hydatid cyst present

A

patients may present with disseminated disease or erosion of cysts into adjacent structure and vessels

149
Q

how is a diagnosis of a hydatid cyst made

A

clinical diagnosis based on history appearance and serologic testing detection of anti-echinococcus antibodies

150
Q

what is the most common form of treatment for a hydatid cyst

A

surgery or with albendazole or percutaneous drainage-PAIR but surgery is the most common

151
Q

what is polycystic liver disease

A

numerous cysts throughout liver parenchyma due to embryonic ductal plate malformation of the intrahepatic biliary tree

152
Q

what are the tHree types of PLD

A

von meyenburg complexes (VMC)
polycystic liver disease
autosomal dominant PLD

GI (13 decks)

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