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Gastrointestinal RT > Liver and Biliary Tract Pathology > Flashcards

Liver and Biliary Tract Pathology Flashcards

1
Q

what is cirrhosis of the liver?

A

scarring of the liver after long term damage

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2
Q

what are the 4 main consequences of liver cirrhosis?

A

reduced metabolic capacity
portal hypertension
ascites
shunting of blood by-passing liver

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3
Q

why in liver cirrhosis does ascites occur mainly in the abdomen?

A

because of the low albumin and very higher pressure from portal system
(large hydrostatic pressure of capillaries [Pc], low osmatic drive of capillaries [pieC])

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4
Q

what are the 4 main causes of liver damage?

A

obesity/diabetes
alcohol
viruses
drugs

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5
Q

what happens to the size of the liver in cirrhosis?

A

becomes small shrunken and hard

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6
Q

what is ‘caput medusae’?

A

when the umbilical vein (ligamentum hepes) becomes back in use because of portal hypertension

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7
Q

what is the function of up-regulating of the umbilical vein?

A

to help with the diversion of blood from portal system to systemic system (shunting) in order to combat the high portal pressure

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8
Q

what happens to highly metabolised drugs when there is portal-systemic shunting?

A

increased plasma levels

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9
Q

why is there increased plasma levels of some drugs due to portal-systemic shunting?

A

due to lack of first pass metabolism

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10
Q

what is meant by saturable kinetics of drugs?

A

metabolism increases until a certain point where it then remains at a constant rate- because liver has become saturated

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11
Q

why in liver cirrhosis is the renin-angiotensin-aldosterone system up regulated?

A

because low albumin causes low plasma volume which activates renin production from the kidneys

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12
Q

what can this up-regulation of the RAAS system cause in a patient with a cirrhotic liver?

A 
secondary aldosteronism
(liver is unable to break the aldosterone down anymore)
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13
Q

why do both endothelin and oestrogen concentrations of the plasma increase in patients with cirrhotic livers?

A

because the liver become unable to metabolise endothelin and oestrogen leading to their accumulation

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14
Q

what does the increased oestrogen due to liver cirrhosis cause to males?

A

gynaecomastia

feminisation of men and loss of secondary sexual characteristics

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15
Q

what are the 3 main consequences of cirrhotic liver in respect to the kidneys?

A

water retention
sodium retention
potassium loss

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16
Q

what is produced in response to hormone vasoconstrictors (such as endothelin, aldosterone, angiotensin II) that acts to maintain kidney function?

A

renal vasodilator prostaglandins

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17
Q

why should NSAIDs be avoided if possible in patients in dehydrated states (such as alcoholism/cirrhotic livers)?

A

NSAIDs inhibit vasodilator prostaglandins so will worsen kidney impairment due to vasoconstriction

(due to the high concentration of vasoconstrictors produced because of the dehydration)

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18
Q

if you are prescribing a NSAID for a patient with cirrhotic liver what must be co-prescibred?

A

a proton pump inhibitor

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19
Q

what 2 phases occur in drug metabolism in the liver?

A

phase 1: biotransformation

phase 2: conjugation

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20
Q

what drug metabolism phase is affected early in liver disease and what phase is affected late in liver disease?

A

phase 1 affected early

phase 2 affected late

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21
Q

what is the highly reactive intermediate that knackers your liver and is formed from the metabolism of paracetamol?

A

N-acetyl-p-benzoquinonimine

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22
Q

why are healthy patients unaffected by n-acetyl-p-benzoquinonimine?
(at advised doses of paracetmol)

A

n-acetyl-p-benzoquinonimine is removed quikly with glutathione

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23
Q

what happens if the glutathione runs out and herefore not all the n-acetyl-p-benzoquinomine can be removed?

A

paracetamol overdose

-can lead to fulminant hepatitis

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24
Q

why does being drunk reduce risk of overdosing when taking too many paracetamol tablets?

A

alcohol has used up all the enzyme paracetamol needs for metabolism, so paracetamol isn’t metabolised as quickly and acetyl-p-benzoquinomine is formed at a much slower rate

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25
Q

why does being a long term alcoholic increase risk of overdosing when taking too many paracetamol tablets?
(if not currently drunk)

A

as a long term alcoholic your body has more receptors and so the paracetamol will be metabolised much quicker and acetyl-p-benzoquinomine is formed at a much faster rate

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26
Q

why does liver failure increase risk of overdosing when taking normal doses of paracetamol?

A

liver failure reduces glutathione stores, so even though paracetamol is being metabolised at a normal rate, there isn’t enough glutathione to remove the acetyl-p-benzoquinomine

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27
Q

what is Hy’s Rule?

A

if ALT/AST > 5x Upper Limit Normal
and
Bilirubin > 3mg/dl
the drug is causing liver disease

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28
Q

which diuretic is best for people with liver cirrhosis to remove excess fluid?

A

spironolactone

due to potassium-sparing effects

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29
Q

what type of excretion route do you want the drugs you are prescribing to a patient with liver cirrhosis to have?

A

renal excretion

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30
Q

what is acute liver disease?

A

rapid development of hepatic dysfunction without prior liver disease
(less than 6 months duration of symptoms)

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31
Q

in acute liver disease how do you get the liver to recover without scarring or ongoing damage?

A

remove stimulus

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32
Q

what do liver function tests measure?

A

ALT
AST
Alk Phos
GGT

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33
Q

what do true liver function tests measure?

A

bilirubin
albumin
prothrombin time

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34
Q

what happens to prothrombin time if there is liver disease?

A

increases

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35
Q

what does acute liver failure do on top of acute liver disease?

A

causes encephalopathy and prolonged coagulation

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36
Q

what must be abnormal for acute liver disease?

A

LFTs

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37
Q

where is pain most likely to be felt in acute liver disease?

A

right upper quadrant

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38
Q

what are the 8 clinical features you might expect with acute liver disease?

A 
none
jaundice
lethargy
nausea
anorexia
pain
itch
arthralgia (although usually more chronic)
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39
Q

what are the 7 main causes of acute liver disease?

A 
viral
drugs
shock liver
cholangitis
alcohol
malignancy
chronic liver disease
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40
Q

what are the most common viral causes of hepatitis?

A 
hep A
hep B
hep C
hep D
hep E
cytomegalovirus
epstein-barr virus
toxoplasmosis
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41
Q

what drug is an important cause of acute liver disease?

A

paracetamol

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42
Q

how are hep B and C passed?

A

blood and some body fluids

-mainly sex and passed through needles

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43
Q

how are hep A and E passed?

A

faecal-oral route

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44
Q

when can hep D cause infection?

A

only hepatitis B is also present

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45
Q

what is shock liver caused by?

A

sudden hypoperfusion leading to massive hepatocyte necrosis

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46
Q

what is Budd Chairi?

A

a rare cause of acute liver disease caused by obstruction of hepatic veins

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47
Q

who does Budd Chairi typically present in?

A

young women starting oral contraceptives

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48
Q

what are 2 rare causes of acute liver disease that are disease of pregnancy?

A

acute fatty liver of pregnancy

cholestatsis of pregnancy

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49
Q

what are the 4 main factors for liver disease?

A

direct toxicity
nutrition
immunological
genetic predisposition

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50
Q

what is haemochromatosis?

A

a genetic condition where iron levels accumulate in the body

patient absorbs more iron from their food than they should

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51
Q

what is non-alcoholic steatoic hepatitis caused by?

A

usually due to unhealthy lifestyle (high in fats) causing ongoing inflammation in the liver

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52
Q

what is the treatment of acute liver disease?

A
  • rest (usually up to 3 months, may be 6)
  • fluids
  • no alcohol
  • increase calories (but high fat food poorly tolerated)
  • sodium bicarbonate bath, cholestryamine or uresodeoxycholic acid- for itch
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53
Q

why is hyoglycaemia a very serious clinical sign of acute liver disease?

A

because the liver usually makes glucose until the very end

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54
Q

what is fulminant hepatic failure?

A

jaundice and encephalopathy in a patient with previous normal liver

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55
Q

out of the hepatitis viruses which is the most likely to cause fulminant hepatic failure?

A

hepatitis B

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56
Q

what is the treatment of fulminant hepatic failure?

A 
supportive
inotropes and fluids
renal replacement
management of raised ICP
possible transplantation
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57
Q

what is the main clinical manifestation of hepatitis viruses?

A

liver disease

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58
Q

how long does it take for patients with hep A to recover and rid their body of the virus?

A

usually within 3 months

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59
Q

how can all viral hepatitis infection be confirmed?

A

blood serology

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60
Q

which hepatitis’ have a vaccine?

A

hep A

hep B

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61
Q

when is chronic infection of hep B most likely to result?

A

if first exposure is in childhood

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62
Q

what 4 groups of people have a higher than average risk of hep B in the UK?

A
  1. people born in areas of intermediate/high prevalence
  2. people with multiple sexual partners
  3. people who inject drugs
  4. children of infected mothers
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63
Q

what antigen is present in the blood of all individuals infected with Hep B?

A

HBsAg

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64
Q

if HBsAg is in the blood of an individual for over 6 months what does this mean?

A

chronic Hep B infection

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65
Q

what 2 makers indicate an individual with hep B is highly infectious?

A

HBeAg (usually)

high titre of HBV DNA

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66
Q

when does a patient have anti-HBs?

A

if a patient is immune to hep B- natural infection or vaccination

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67
Q

what marker does a patient who gained immunity through natural infection to hep B have that a patient who gained immunity through vaccination doesnt?

A

anti-HBc

as well as the anti-HBs that vaccination also gives

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68
Q

what marker of Hep B is best at giving an indicator of prognosis?

A

HBV DNA

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69
Q

why do individuals with hep B need to be monitored regularly even if at first their viral load is very low?

A

relationship with infection is dynamic and so later on in disease progression they might have a very high HBV DNA load

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70
Q

what can be given a post-exposure prophylaxis for an individual who has come into contact with another individual with Hep B?

A

vaccine + HBIG

HBIG = hyperimmune Hep B immunoglobulin

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71
Q

which is more easily transmitted by sex- hep B or C?

A

hep B

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72
Q

if patient has antibody to hep C virus what does this mean?

A

past or active infection

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73
Q

if a patient has hep C RNA what does this mean?

A

active infection

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74
Q

compare the nucleic acid present in hep B compared to hep C?

A

hep B= DNA

hep C= RNA

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75
Q

once a patient with hep B has chronic infection can they have a spontaneous cure?

A

yes

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76
Q

once a patient with hep C has chronic infection can they have a spontaneous cure?

A

no

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77
Q

what is the progression of disease from chronic hepatitis?

A

chronic hepatitis
cirrhosis
hepatocellular carcinoma or chrnoic liver failure
death

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78
Q

compare the chances of hep B and hep C becoming a chronic infection?

A

hep C is more likely to become chronic than resolve

hep B is more likely to resolve than become chronic (unless child is infected at birth)

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79
Q

if child is infected at birth with hep B what is the likely progression?

A

likely to become chronic rather than resolve

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80
Q

what is the management of acute viral hepatitis?

A
  • supportive
  • no antivirals given
  • monitor for encephalopathy
  • monitor for resolution
  • notify public health
  • immunisation of contacts
  • test for other infections if at risk
  • vaccinate against other infections if at risk
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81
Q

what is the management of chronic viral hepatitis?

A
  • antivirals
  • vaccination of other infections
  • infection control
  • reduced alcohol intake
  • hepatocellular carcinoma awareness/screening
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82
Q

compare the number of antivirals on the market for hep C compared to hep B?

A

hep B= 6 antivirals

hep C= 8 antivirals

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83
Q

what is a complete contraindication to the treatment of chronic hepatitis with antivirals?

A

hepatocellularcarcinoma

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84
Q

as HBV DNA load at initial infection increases what happens to the risk of hepatocellular carcinoma if infection becomes chronic?

A

greater risk of cancer

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85
Q

for chronic hepatitis, how is alpha interferon administered?

A

peginterferon injections

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86
Q

what are the common side effects of peginterferon?

A

flu-like symptoms

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87
Q

what are the less common, but more severe side effects of peginterferon?

A

thyroid disease
autoimmunde disease
psychiatric disease

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88
Q

what are the side effects of older HCV antivirals such as ribavirin, telaprevir and boceprevir?

A

anaemia

telaprevir and boceprevircan also cause a sever rash

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89
Q

what are the 2 options for chronic hep B therapy?

A
  1. peginterferon alone

2. suppressive antiviral drugs

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90
Q

what are the advantages of peginterferon treatment of chronic hep B?

A

sustained cure possible from a few months of therapy

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91
Q

what are the disadvantages of peginterferon treatment of chronic hep B?

A

only minority gain benefit
side effects
injections

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92
Q

what are the advantages of suppressive antiviral drug therapy for chronic hep B?

A

safer than peginterferone therapy

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93
Q

what are the diseadvantages of suppressive antiviral drug therapy for chronic hep B?

A

suppression not cure

resistance can develop

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94
Q

what are the 3 virological aims in terms of chronic hep B therapy?

A
  1. reduction in HBV DNA (suppression)
  2. loss of HBeAg (further suppression)
  3. loss of HBsAg (cure)
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95
Q

what are the 6 main aims of chronic hep B therapy?

A
  1. virological aims
  2. improved liver biochem
  3. improved histopathology
  4. reduced infectivity
  5. reduced progression to cirrhosis and primary hepatocellular carcinoma
  6. reduced mortality
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96
Q

what is a hepatitic C therapy response defined as?

A

SVR: sustained virological response (cure as relapse is rare)

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97
Q

what defines sustained virological response?

A

loss of HCV RNA in blood sustained to 6 months after end of therapy

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98
Q

even if patients have sustained virological response what must be continued if the patient already has cirrhosis?

A

6 monthly ultrasound screening for hepatocellular carcinoma

even though risk has been reduced, because the liver is cirrhotic patient still has significant risk

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99
Q

what ribs protect the liver?

A

7-11

100
Q

what ligament on the anterior surface of the liver separates the right and left lobe?

A

falciform ligament

101
Q

in the acinar concept of the liver, what zone is closest to the central vein? what zone is furthest from the central vein?

A

zone 3 = closest to central vein

zone 1 = furthest from central vein

102
Q

what are the 3 main consequences of acute liver failure?

A

complete recovery
chronic liver disease
death from liver failure

103
Q

what is the phrase that means jaundice within the sclera of the eyes?

A

icterus

104
Q

what are the 3 classes of jaundice?

A

pre-hepatic
hepatic
post-hepatic

105
Q

what type of bilirubin is excess in the blood in pre-hepatic jaundice?

A

unconjugated bilirubin

106
Q

what type of bilirubin is excess in the blood in hepatic jaundice?

A

both unconjugated and conjugated bilirubin

107
Q

what type of bilirubin is excess in the blood in post-hepatic jaundice?

A

conjugated bilirubin

108
Q

what can cause pre-hepatic jaundice?

A

haemolysis of all causes

109
Q

what can cause post-hepatic jaundice?

A

all obstructions of the biliary tree

eg gallstones, strictures, tumours

110
Q

what is cirrhosis of the liver defined by?

A

bands of fibrosis separating regenerative nodules of hepatocytes
-prevent regeneration

111
Q

what are the 2 subgroups of cirrhosis?

A

macronodular or micronodular

112
Q

which sub group of cirrhosis is caused by alcohol abuse?

A

micronodular

113
Q

what are the differences between rectal varices and haemorrhoids?

A

anorectal varices= dilation of portal-systemic anastomosis due to portal hypertension
haemorrhoids = prolapse of rectal venous plexus (not due to portal hypertension)

114
Q

what are the 3 main complications of cirrhosis?

A

portal hypertension (hepatic)
ascites
liver failure

115
Q

what type of cause of portal hypertension is a portal vein thrombosis?

A

pre-hepatic portal hypertension

116
Q

what type of cause of portal hypertension is hepatomegaly?

A

pre-hepatic portal hypertension

117
Q

what type of cause of portal hypertension is right sided heart failure?

A

post-hepatic portal hypertension

118
Q

what type of cause of portal hypertension is budd chairi (hepatic vein outflow obstruction)?

A

post-hepatic portal hypertension

119
Q

why can chronic liver disease cause oedema?

A

reduced albumin synthesis resulting in hypoalbuminaemia

120
Q

why can chronic liver disease causes ascites?

A

hypoalbinaemia
secondary hyperaldosteronism
portal hypertension

121
Q

why can chronic liver disease cause haematemesis?

A

ruptured oeophageal varices due to portal hypertension

122
Q

why can chronic liver disease cause spider naevi?

A

impaired ability to metabolise oestrogen causing hyperoestrogenism

123
Q

why can chronic liver disease cause gynaecomastia?

A

impaired ability to metabolise oestrogen causing hyperoestrogenism

124
Q

why can chronic liver failure cause purpura and bleeding?

A

reduced clotting factor synthesis

125
Q

what is purpura?

A

bleeding of small blood vessels that cause purple spots on the skin

126
Q

why can chronic liver failure cause a coma?

A

failure to eliminate toxic gut bacterial metbaolites

127
Q

why can chronic live failure cause increased infection?

A

reduced kupffer cell number and function

128
Q

what is the pathogenesis of alcoholic liver disease?

A
  1. increased peripheral release of fatty acids and increased synthesis of fatty acids and triglyceride within hepatocytes
  2. acetaldehyde (a product of alcohol metabolism) is responsible for liver cell injury
  3. increased collagen synthesis by fibroblasts and stellate (ito) cells
129
Q

when is alcoholic liver disease reversible?

A

fatty liver stage (2-3 days of drinking)
hepatitis stage (4-6 weeks of drinking)
ONLY IF CESSATION OF ALCOHOL

130
Q

when is alcoholic liver disease irreversible?

A 
fibrosis stage (months- years of drinking)
cirrhosis stage (years of drinking
131
Q

why is liver disease irreversible after fibrosis stage?

A

because of collagen deposition around hepatocytes

132
Q

what is NASH? (non-alcoholic steatoheaptitis)

A

pathologically identical to alcoholic liver disease but occurs in patient with diabetes, obesity or hyperlipidaemia insteaf of drinkers

133
Q

why does hepatitis B cause liver damage?

A

due to antiviral host immune response

134
Q

if you have HBsAg in your blood but are asymptomatic what are you known as?

A

a carrier

135
Q

which is more likely to progress to hepatocelular carcinoma if it becomes chronic- hep B or hep C?

A

hep B

136
Q

what autoantibodies is primary biliary cirrhosis associated with?

A

anti- mitochondria antibodies

AMA

137
Q

why do you use a biopsy within primary biliary cirrhosis?

A

to stage disease

138
Q

what autoantibodies is autoimmune heaptitis associated with?

A

type 1: anti-nuclear antibodies (ANA)
anti-smooth-muscle antibodies (ASMA)
type 2: anti-liver-kidney-microsomal antibodies (anti-LKM-1)
anti-liver-cytosolic antibodies (anti-LC-1)

139
Q

what is primary sclerosing cholangitis?

A

a chronic inflammatory process affecting intra and extra hepatic bile ducts which leads to periductal fibrosis, duct destruction and fibrosis

140
Q

what is primary haemochromatosis?

A

an autosomal recessive condition which causes excess iron within the liver due increased absorption of iron from food

141
Q

what is secondary haemochromatosis?

A

excess iron within the liver caused by iron overload from diet, transfusions or iron therapy

142
Q

how is haemochromatosis treated?

A

venesection

143
Q

what can haemochromatosis cause within the liver?

A

asymptomatic for years

then stimulates fibrosis and cirrhosis if not treated

144
Q

what does haemochromatosis predispose to?

A

hepatocellular carcinoma, diabetes, cardiac failure, impotence

145
Q

what are the 2 major results of alpha-1-antitrypsin deficiency?

A

emphysema

cirrhosis

146
Q

what type of inheritance is alpha-1-antitrypsin deficiency?

A

autosomal recessive

147
Q

what are the 2 types of primary cancers within the liver?

A 
hepatocellular adenoma- benign
hepatocellular carcinoma (hepatoma)- malignant
148
Q

who is more likely to get primary biliary cirrhosis- M or F?

A

females

149
Q

who is more likely to get autoimmune hepatitis- M or F

A

females

150
Q

who is more likely to get primary sclerosing cholangitis- M or F?

A

males

151
Q

who is more likely to have haemochromatosis- M or F?

A

males

152
Q

who is mre likely to get hepatocellular adenoma- M or F?

A

females

153
Q

how long does liver disease has to be ongoing to be classed as chronic?

A

6 months

154
Q

why do stellate cells start to produce collagen?

A

in response to cytokines produced from kupffer cells during times of inflammation

155
Q

how do you diagose simple steatosis?

A

ultrasound

156
Q

what is the treatment for simple steatosis?

A

weight loss and exercise

157
Q

how do you diagnose NASH?

A

liver biopsy

158
Q

what are the increased risks due to simple steatosis of the liver?

A

increased cardiovascular risks not liver risks

159
Q

what are the main symptoms of PBC?

A

fatigue
itch without rash
xanthelasma

160
Q

what is the treatment for PBC?

A

ureseodeoxycholic acid

161
Q

what is the biomodal age distribution of type 1 autoimmune hepatitis?

A

10-20

45-70

162
Q

compare the LFTs of AIH and PBC?

A

PBC- cholestatic picture

AIH- hepatic picture

163
Q

how do you confirm autoimmune hepatitis?

A 
liver biopsy
(autoimmune antibodies don't confirm)
164
Q

what is the treatment of AIH?

A

corticosteroids eg prednisolone

azathioprine

165
Q

for children with autoimmune hepatitis what treatment should you try first and why?

A

azathioprine monotherapy to try reduce effects of steroids (eg reduced bone growth)

166
Q

what is the main feature of a patient with primary sclerosing cholangitis?

A

recurrent cholangitis

167
Q

how do you diagnose primary scelrosing cholangitis?

A

imaging of the biliary tree

168
Q

what is the treatment of alpha 1 anti-trypsin deficiency?

A

supportive

169
Q

what is a serious adverse effect of methotrexate?

A

progressive fibrosis of liver and lungs

170
Q

what is cardiac cirrhosis?

A

cirrhosis of the liver secondary to high right heart pressures

171
Q

what are the 4 groups of collateral pathways from the portal system to systemic system?

A

esophageal plexus
umbilical vein
retroperitoneal collateral vessels
rectal venous plexus

172
Q

what are the signs of decompensated liver failure?

A 
all the signs of compensated liver failure plus:
jaundie
ascites
encephatlopathy
easy bruising
(ie problems with function)
173
Q

when you press spider naevi how should the vessels refill?

A

from the middle to the edges

174
Q

what is the treatment for ascited?

A 
improve underlying liver disease
reduce salt intake, maintain nutrition
diuretics (spironolactone first)
paracentesis
TIPSS
transplantation
175
Q

what is trans-jugular porto-systemic shunt?

A

a minimally invasive procedure which results in equalising pressures in portal and systemic systems

176
Q

how does spontaneous bacterial peritonitis occur?

A

translocated bacterial infection caused by ascites

177
Q

what is the treatment of spontaneous bacterial peritonitis?

A

antibiotics
terlipressin
maintain renal perfusion

178
Q

in encephalopthy what should you use to clear gut?

A

lactulose

179
Q

why should you use lactulose in encephalopathy?

A

to reduce time bacteria have to produce ammonia ie reduce transit time

180
Q

what is the last resort for oesophageal varice bleeding? (ie if nothing else works)

A

balloon tamponade

181
Q

why do cholesterol gallstones form?

A

imbalance between the ratio of cholesterol to bile salts

182
Q

what are the 4 predisposing factors to cholesterol gallsontes?

A

female
obesity
diabetes
genetic

183
Q

why do pigment gallstones form?

A

excess bilirubin present within stone due to exces haemolysis

184
Q

what is cholecystitis?

A

inflammation of the gallbladder

185
Q

what is cholecystitis usually associated with?

A

gallstones

186
Q

why is the usual pathogenesis of acute cholecystitis?

A

gallstones obstructing outflow of bile
this becomes infected and may cause empyeme rupture and peritonitis
intense adhesions are formed

187
Q

what is the wall of the gallbladder like in chronic cholecystitis?

A

thickened

but not distended

188
Q

what is the most common carcinoma of the gallbladder?

A

adenocarcinoma

-still rare

189
Q

what are carcinomas of the gallbladder generally associated with?

A

gallstones

190
Q

what is the most common carcinoma of the bile ducts?

A

adenocarcinoma (cholangiocarcinoma)

-still rare

191
Q

what are carcinomas of the bile ducts (cholangiocarcinomas) generally associated with?

A

ulcerative cholitis and primary sclerosing cholangitis

192
Q

in non-cirrhotic patients what is the most common solid liver tumour?

A

hemangioma (benign)

193
Q

what are the 4 main benign focal nodules?

A

hemangioma
focal nodular hyperplasia
adenoma
liver cysts

194
Q

what are the 6 primary liver cancer?

A 
hepatocellular carcinoma
cholangiocarcinoma
fibrolamellar carcinoma
hepatoblastoma
angiosarcoma
haemangioendothelioma
195
Q

what is the treamtent for a hemangioma?

A

none

196
Q

what is a hemangioma?

A

a benign vascular tumour within a well demarcated capsule

197
Q

what is a focal nodular hyperplasia?

A

a benign nodule formation of normal liver tissue

198
Q

what do focal nodular hyperplasia lesions classically have in the centre?

A

a central scar containing an unusually large artery with radiating branches to the perphery

199
Q

why do focal nodular hyperplasia lesions form?

A

as a response to a vascular abnormality

200
Q

who are focal nodula hyperplasia lesions most common in?

A

young and middle aged women

201
Q

what does hyperintense mean on MRI?

A

brighter than surrounding tissue

202
Q

what does hypointense mean on MRI?

A

darker than surrounding tissue

203
Q

what does isointense mean on MRI?

A

same colour as surrounding tissue

204
Q

what is the treatment for focal nodular hyperplasia?

A

none

205
Q

what is a hepatic adenoma?

A

a benign neoplasm composed of normal hepatocytes but with no portal tract, central ceins or bile ducts

206
Q

who is hepatic adenomas more common in-M or F?

A

females

207
Q

what are hepatic adenomas associated with?

A

contraceptive hormones especially high oestrogen pills

208
Q

sometime hepatic adenomas can by symptomatic, what can they present as?

A

RUQ pain

209
Q

what can be the complications of a hepatic adenoma?

A

rupture
haemorrhage
malignant transformation

210
Q

what is adenomatosis?

A

a rare conditions with multiple adenomas

211
Q

if a a hepatic adenoma is contraceptive pill driven what wilhappen if the pill is discontinued?

A

regression

212
Q

what is the treatment of hepatic adenoma?

A

stop hormones

observe every 6 months for 2 years and if no regression then surgical excision

213
Q

what are the main differences between adenomas and focal nodular hyperplasia?

A

adenoma is purely a hepatocyte tumour which FNH contains all liver ultrastructure

adenomas can bleed and become malignant while FNH can’t do either

214
Q

which is a simple liver cyst?

A

liquid collection lined by an epithelium

215
Q

what is a hydatid cyst?

A

a multilobular cyst

ie contains many irregular cavities

216
Q

what parasite can cause hydatid cysts in the liver?

A

echinococcous granulosus

217
Q

what drug is given to patients with hydatid cysts to kill the echinococcus granulosus parasite?

A

albendazole

218
Q

what is the main treatment of hyatid cysts?

A

surgical resection or marsupialization (surgical technique)

219
Q

what are polycystic liver diseases?

A

a range of congenital conditions which results from embryonic ductal plate malformation of the intrahepatic biliary tree
(bile ducts never joined up to the rest of the biliary tree)

220
Q

what are the 3 main types of polycystic liver disease?

A

Von Meyenburg Complexes (VMC
Polycystic Liver disease
Autosomal dominant polycystic kidney disease

221
Q

rarely invasive procedures can be used in patients with PCLD or ADPKD, what are these procedures?

A

defenstration/aspiration

liver transplantation

222
Q

what is the presentation of a liver abscess?

A

high fever
leukocytosis
abdominal pain

223
Q

what history usually proceeds liver abscesses?

A

abdominal or biliary infection

dental procedure

224
Q

what is the management of a liver abscess?

A
  • initial empirical broad spectrum antibiotics
  • aspiration/drainage percutaneously
  • echocardiogram to make sure no infective endocarditis due to bacteraemia
  • operation if no clinical improvement
  • 4 weeks antibiotic therapy with repeat imaging
225
Q

if theres no clinical improvement of a liver abscess what operations can be done?

A

open drainage

resection

226
Q

what is the most important risk factor for hepatocellular carcinoma?

A

cirrhosis

227
Q

what protein is a hepatocellular carcinoma marker?

A

alfa feto protein

228
Q

what treatment can be done for unresectable hepatocelluar carcinomas?

A

radiofrequency ablation
alcohol injection
chemoembolization

229
Q

what is chemoembolization?

A

injecting chemotherapy selectively in hepatic artery and then injecting an embolic agent to block blood supply to tumour

230
Q

what are the 2 main diseases of the biliary tract?

A

cholelithiasis

cholangiocarcinoma

231
Q

what are the 3 possible causes for gallstones?

A

abnormal bile composition (etither excess bilirubin or cholesterol)
bile stasis
infection

232
Q

where do primary bile duct stones develop?

A

in the intrahepatic bile ducts or common bile ducts

233
Q

where do secondary bile duct stones develop?

A

in the gall bladder

much more common

234
Q

what are the 5 risk factors for gall stones?

A 
5 F's
Forty
Female
Fat
Fair (caucasians have a higher incidence)
Fertile (premenopause)
235
Q

what is the main symptoms of bile stones?

A

biliary colic

236
Q

where may the pain of biliary colic present?

A

build up pain in RUQ

radiates to back shoulder

237
Q

what is the pain of biliary colic associated with?

A

indigestion

nausea

238
Q

what are the 5 main reasons for severe acute epigastric pain?

A 
biliary colic
peptic ulcer disease
oesophageal spasm
MI
acute pancreatitis
239
Q

what is acute cholecystitis?

A

inflammation of the gallbladder

240
Q

what is the usual cause of cholecystitis?

A

gall stones causing obstruction of the cystic duct, initially sterile then becomes infected

241
Q

what are the 3 main ways to diagnose gallstones?

A

ultrasound
CT
MRCP/ERCP

242
Q

what is the treatment of acute cholecystitis?

A 
IV antibiotics 
IV fluids
nil by mouth
US to confirm
urgent cholecystectomy
243
Q

if a bile stone migrates into the common bile duct what are the 4 possible consequences?

A

jaundice
cholangitis
acute pancreatitis
gallstone ileus

244
Q

what are the clinical symptoms of a gallstone within the common bile duct?

A

itch
nausea
anorexia

245
Q

what are the clinical signs of af a gallstone within the common bile duct?

A

jaundice, abnormal LFTs

246
Q

what is the only chance of cure of cholangioma?

A

surgical resection

247
Q

what is the first line investigation for cholecystitis/biliary colic?

A

ultrasound

then possible MRCP/ERCP

Gastrointestinal RT (15 decks)

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