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hepatology Flashcards

1
Q

What are the majority of liver cancers?

A

metastasis

small proportion are hepatocellular carcinomas (HCC)

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2
Q

describe the pathophysiology/aetiology of an hepatocellular carcinoma?

A 
arises as a result of chronic inflammation of the liver (hepatitis and cirrhosis)
hepatitis B and C
chronic alcohol
hereditary haemochromatosis 
primary biliary cirrhosis
aflatoxin 
smoking, FHx, age
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3
Q

what are the symptoms associated with HCC?

A

vague symptoms initially: fatigue, fever, weight loss and lethargy. Rare symptom is a dull ache in RUQ

later symptoms: ascites, signs associated with portal hypertension and jaundice

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4
Q

in terms of time scale how to jaundice compare in HCC and cholangiocarcinoma?

A

jaundice is an early sign in cholangiocarcinoma but a late sign in HCC

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5
Q

what does the liver feel like on examination in someone with HCC?

A

irregular
craggy
tender
enlarged

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6
Q

what does the AST: ALT ratio tell us?

A

if >2 it is likely to be alcoholic liver disease

if around 1 likely to be viral hepatitis

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7
Q

what investigations would you do if you suspect HCC?

A

LFTs, FBC
a-fetoprotein - raised in 70% of cases (can be used to monitor response to treatment
USS - if mass >2 cm and raised AFP then very likely to be cancer
CT and MRI
fine needle aspiration biopsy if still in doubt

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8
Q

why do we try to avoid a biopsy of the liver by fine needle aspiration if we suspect HCC?

A

may help to spread the tumour

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9
Q

what staging systems are used for liver cancer?

A

Barcelona clinic liver cancer staging system (BCLC) - looks at stage, liver function, physical state and cancer related symptoms to guide treatment
Child-Pugh score- predictor of mortality from cirrhosis

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10
Q

what is the surgical management of HCC?

A 
resection 
transplantation if: 
   - one lesion <5cm or 3 lesions <3cm 
   - no extrahepatic manifestations 
   - no vascular infiltration
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11
Q

what is the non-surgical management of HCC?

A

image guided ablation - use USS to guide probe and then use different things to kill tumour e.g. microwave probe or alcohol injections. this induces necrosis of malignant tissue. however only good for small tumours - early stage

transartifical chemoembolization - BCLC stage B tumours - high con chemo drugs injected into the hepatic artery and then embolising agent (Cellulose) is added to induce ischaemia

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12
Q

how can we prevent HCC?

A

Hep B vaccine
education - don’t drink too much alcohol
surveillance of those at risk e.g. hemochromatosis

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13
Q

where are the most common places liver metastasis come from?

A

bowel (via portal circulation), lung, breast, pancreas and stomach

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14
Q

what does raised ALP show?

A

can be raised by liver (biliary obstruction or hepatic metastasis) , bone (pagets, fractures, renal bone disease, osteomalacia) and placental pathologies.

if the raised ALP mirrors raised gGT it is more likely to be hepatic in origin

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15
Q

what does raised gGT show?

A

used to assess if the raised ALP is due to liver or another pathology. associated with cholangiocyte damage and liver disease

more specific to liver damage than ALP

can also be elevated in obesity, hyperlipidaemia, diabetes, congestive cardiac failure, kidney/prostate and pancreas.

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16
Q

if both ALP and aGT are raised what does this suggest?

A

there is damage to the liver - these two are correlated and both linked to liver damage (although each linked to other causes, if they correlate it makes liver damage but more likely)

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17
Q

why do enzyme get raised in liver damage?

A

damage leads to enzymes leaking from liver cells.

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18
Q

when is AST (aspartate aminotransferase ) raised?

A

liver, cardiac, skeletal muscle pathologies

also kidneys and pancreas

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19
Q

when in ALT (alanine aminotransferase) raised?

A

specific to liver pathology. short half life and thus will follow pattern of liver damage and healing quite accurately.

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20
Q

what is meant by a mild, moderate and marked increase in the aminotransferases?

A

mild (<300): cirrhosis, non alcoholic fatty liver, HCC, haemachromatosis/Wilsons

moderate (300-500) chronic/alcohol/autoimmune hepatitis, biliary obstruction

marked (1000s): toxic drug induced (paracetamol), acute viral hepatitis, liver ischaemia

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21
Q

what is gGT more specifically associated with in terms of liver damage?

A

alcohol abuse

enzyme inducing drugs

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22
Q

what are other tests that indicate liver damage?

A

low albumin
high INR
total protein (albumin and globulins) can be raised in active hepatitis and in chronic inflammation

low albumin + high protein = myeloma
low albumin + normal protein = infection
low both = advanced cirrhosis , malnutrition

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23
Q

what are the normal liver functions?

A

nutrition - glycogen store, gluconeogenesis, glucogenolysis and makes cholesterol
Absorption of fats and fat soluble vitamins (bile)
Makes clotting factors
immune function - kupfer cells, acute phase response
detoxification - CYP450 enzymes
makes albumin and binding proteins

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24
Q

what is fulminant hepatic failure?

A

clinical syndrome resulting from massive necrosis of liver cells leading to impairment of liver function

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25
Q

what is hyperacute liver failure?

A

very rapid onset - encephalopathy within 7 days of jaundice onset

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26
Q

what are the causes of acute liver failure?

A

infection: viral (Hep A, B,C, CMV), yellow fever, malaria
drugs: isoniazid, paracetamol, ethanol, mushroom toxins
vascular: DIC, veno-occlusion
genetic: autoimmune hepatitis, haemachromatosis, primary biliary cirrhosis, wilsons (however mainly chronic), alpha1 antitrypsin deficiency
malignancy
pre-eclampsia

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27
Q

what are the signs of acute liver failure?

A

jaundice
fetor hepaticus (breath that smells like pear drops)
flapping tremor
constructional apraxia (cant copy 5 point object)
hepatic encephalopathy
oedema/ascites

may have signs of chronic - suggesting acute on chronic

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28
Q

how do we classify acute liver failure?

A

type 1: rapidly progressive deterioration (survival 2 weeks)

type 2: steady deterioration (survival 6 months)

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29
Q

what is pathogenesis of hepatic encephalopathy?

A

nitrogenous waste builds up (liver function impaired so urea cycle is not working properly)
astrocytes aim to remove nitrogenous waste by converting glutamate to glutamine
glutamine effects osmotic pressure -cerebral oedema results

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30
Q

what are the different grades of hepatic encephalopathy?

A

grade 1: altered mood/behaviour, dyspraxia, sleep disturbance, no flap

grade 2: increased drowsiness, confusion and slurred speech, liver flap

grade 3: flap, restless, almost unconscious (stupor)

grade 4: coma

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31
Q

what investigations would you do to find the cause of acute liver failure?

A

LFTs - look at ratio of AST:ALT, gGT, bilirubin etc
glucose and paracetamol levels
virology screen - Ab for Hep B/C/CMV /EBV
a1 antitrypsin deficiency screen
screen for autoAb
ferritin levels - haemochromatosis
serum copper and caeruloplasmin and 24 hour urinary copper - wilsons.

USS, CXR, dopler of portal vein

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32
Q

list some hepatotoxic drugs

A

paracetamol, methotrexate, isoniazid, azathioprine, oestrogen, salicyclates, tetracycline

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33
Q

what drugs should be avoided in acute liver failure?

A

drugs that constipate (opiates, diuretics - risk of encephalopathy)
hepatotoxic drugs
oral hypoglycaemics
warfarins effects will be enhanced

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34
Q

how is acute liver failure managed?

A

manage in ITU
correct underlying cause

- monitor temperature, resp rate, pulse , BP, pupils, urine output, FBC, U&amp;Es and LFTs daily 
- monitor glucose 1-4 hourly

glucose given IV to avoid hypoglycaemia
give thiamine and folate supplements
treat any seizures with lorazepam

treat complications

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35
Q

what is given for paracetamol overdose?

A

N-acetyl cysteine

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36
Q

why may PPIs be given in acute liver failure?

A

reduce risk of stress ulceration

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37
Q

how are the complications of acute liver failure managed?

A

cerebral oedema: mannitol
ascites: fluid restriction, low salt, diuretic
bleeding: vit K, FFP, blood or platelets
encephalopathy: lactulose to clear gut bacteria so there are fewer nitrogen forming gut bacteria
IV albumin
splanchnic vasoconstrictors
sepsis - Tazocin - avoid gentamicin (renal failure)

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38
Q

what is cirrhosis?

A

a condition where the liver has become progressively replaced by scar tissue due to chronic inflammation. the damage is irreversible. there is loss of hepatic architecture with fibrosis and nodular regeneration

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39
Q

what are the causes of chronic liver failure/cirrhosis?

A

chronic alcohol abuse
chronic hep B/C ingection
haemachromatosis, a1-antitrypsin deficiency, wilsons
non-alcoholic fatty liver disease
autoimmune: primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis
drugs: amiodarone, methotrexate, methyl dopa

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40
Q

what are the signs of chronic liver failure?

A

high oestrogen: gynecomastia, spider naevi , palmar erythema

hypoalbumin: leukonychia, ascites

terrys nails: distal 1/3 of nail reddened by telangiectasia

clubbing , dupuytrons contractures

hepatomegaly or small liver

low clotting: straie

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41
Q

what are the complications of hepatic failure?

A 
hypoglycaemia 
coagulopathy - increased INR
encephalopathy - liver flap
hypoalbumin - oedema , can lead to renal failure
low immune factors - sepsis /infection
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42
Q

what are the complications of cirrhosis?

A

hepatic failure
portal hypertension
HCC risk

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43
Q

how would you investigate the cause and complications of cirrhosis?

A

LFTs
albumin + INR levels
WCC and platelets - if low suggest hyposplenism
USS and duplex - fatty liver, hepatic vein thrombosis

causes:

  • iron and ferritin levels - haemachromatosis
  • caeruloplasmin - wilsons
  • A fetoprotein
  • A1 antitrypsin deficiency
  • serology for virus
  • autoAb

biopsy for definite diagnosis

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44
Q

how can we manage chronic liver failure?

A

general : improve nutrition, stop alcohol, avoid NSAIDs, sedative and opiates.

colestyramine helps pruritis

treat specific causes or complications

USS and alpha fetoprotein every 3-6 months to screen for HCC

liver transplant - definite cure

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45
Q

why is peritonitis a complication of cirrhosis? how can we treat bacterial peritonitis ?

A

ascites develops due to low albumin and portal hypertension
fluid stasis favours bacterial growth
can confirm diagnosis by ascetic tap - fluid sent to MC&S

treat with cefotaxime/tazocin and metronidazole

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46
Q

how does the child-pugh grade work?

A

points are given for level of bilirubin, albumin, prothrombin time, ascites and encephalopathy. the higher the points the higher the grade. if score is >8 the risk of variceal bleeding is much higher

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47
Q

what is hereditary haemochromatosis?

A

autosomal recessive disease
abnormal iron metabolism - increased iron absorption from the gut and then deposition of iron in joints, liver, heart, pancreas, pituitary , adrenals and skin

caused by HFE gene

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48
Q

how does hemochromatosis present?

A

early: lethargy, MCP joint arthralgia, erectile dysfunction
later: grey pigmented skin , signs of chronic liver disease, dilated cardiomyopathy, signs of bronze diabetes, signs of pituitary dysfunction

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49
Q

how can secondary hemochromatosis occur?

A

if transfusions are given e.g. in thalassemia

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50
Q

what investigations would you do for haemochromatosis?

A

raised LFTs, raised serum ferritin, HFE genotype
Xray of hands - chondrocalcinosis of MCPJ
Liver MRI - Fe overload
liver biopsy - confirms perl’s stain
ECHO/ECG - cardiomyopathy

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51
Q

what are the irreversible complications of haemachromatosis?

A

cirrhosis, diabetes, hypogonadotrophic hypogonadism, arthropathy

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52
Q

what are the reversible complications of haemachromatosis?

A

cardiomyopathy

skin pigmentation

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53
Q

how do we manage haemochromatosis?

A

Venesect: reduces ferritin levels - returns life expentancy to normal but any cirrhosis that has already occurred is irreversible

monitor LFTs, glucose , screen for HCC

advice a low iron diet

screen first degree relatives

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54
Q

what is the pathogenesis behind a1 antitrypsin deficiency?

A

autosomal recessive
a1antitrypsin is a glycoprotein of the family of serine protease inhibitors that is usually made in the liver
normally functions in controlling inflammatory cascades.

therefore deficiency leads to uncontrolled inflammatory cascades
e.g. normally protects lungs against elastase made my neutrophils therefore excess elastase results in emphysema

in the liver there is a build up of abnormal protein resulting in cirrhosis and HCC

can also cause pancreatitis, gall stones and is associated with Wegners

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55
Q

what are the symptoms of a1 antitrypsin deficiency ?

A

dyspnoea - due to emphysema

jaundice - due to cirrhosis and cholestasis

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56
Q

how would you test for a1 antitrypsin deficiency?

A

serum a1 antitrypsin levels - usually low
liver biopsy - will show diastase resistant globules
genetic testing
phenotyping - look at protiens by isoelectric focussing
CT of lung

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57
Q

why does smoking worsen a1 antitrypsin deficiency?

A

smoking increases elastase production by neutrophils

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58
Q

what management is required for a1 antitrypsin?

A 
stop smoking 
can give IV a1 AT
supportive treatment of liver and lungs 
may need lung/liver transplant 
regular screens for HCC
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59
Q

what the pathophysiology of primary biliary cirrhosis?

A

an autoimmune disease leading to damage of interlobular bile ducts by granulomatous inflammation.

leads to cholestasis, fibrosis and cirrhosis and portal hypertension

caused by unknown environmental triggers and genetic predisposion

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60
Q

which auto Ab are present in primary biliary cirrhosis?

A

anti mitochondrial

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61
Q

what age does primary biliary cirrhosis mainly present?

A

50 years

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62
Q

what symptoms are associated with primary biliary cirrhosis?

A 
often asymptomatic (ALP raised on routine test)
lethargy and sleepiness
jaundice and pruritus 
skin pigmentation and xanthomas 
hepatosplenomegaly
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63
Q

what are the complications associated with primary biliary cirrhosis?

A

cirrhosis of liver and HCC
osteoporosis
malabsorption of fat - steatorrhoea
osteomalacia (less vit D due to fat absorption)
coagulopathy (less vit K due to low fat absorp)

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64
Q

what is found on investigating primary biliary cirrhosis?

A

LFTS: ALP and gGT raised, slightly raised AST and ALT
in late disease: raised bilirubin, low albumin, increased prothrombin time (INR)

USS can rule out extra-hepatic cholestasis
USS can also show liver to be normal, fatty or cirrhosis

fibroscan - degree of cirrhosis

biopsy - not usually needed but can show granulomatous inflammation around bile ducts

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65
Q

how do we treat primary biliary cirrhosis?

A

specific:
Ursodeoxycholic acid - high dose - emulsifies bile to prevent it blocking up ducts
liver transplant for end stage

Supportive:
Colestyramine for pruritus 
codeine for diarrhoea 
osteoporosis prevention 
Fat soluble vitamin prophylaxis - ADEK

monitor regularly LFTs and ultrasound

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66
Q

what is primary sclerosing cholangitis?

A

A disease of bile ducts that causes progressive cholestasis, inflammation and strictures/fibrosis

67
Q

what is the cause of primary sclerosing cholangitis?

A

primary cause is unknown but thought to have an autoimmune element involved
associated with UC

68
Q

what are the symptoms of primary sclerosing cholangitis?

A

pruritis and fatigue

later symptoms associated with ascending cholangitis, cirrhosis and hepatic failure

69
Q

what cancers is an individual with primary sclerosing cholangitis at an increased risk of?

A

bile duct
gall bladder
liver
colon

70
Q

what markers are raised in primary sclerosing cholangitis?

A

bilirubin

ALP

71
Q

how do we manage primary sclerosing cholangitis?

A 
Colestyramine for pruritus 
Ursodeoxycholic acid can protect against colon cancers and improve LFTs
Abx for any ascending cholangitis 
cholecystectomy for gall bladder polyps
liver transplant at end stage disease

yearly colonoscopy to check for cancer
yearly ultrasound to check gall bladder and liver cancers.

72
Q

what group of people does autoimmune hepatitis most commonly affect?

A

young and middle aged women

73
Q

what is the antigen in autoimmune hepatitis?

what auto-ab is it associated with?

A

hepatocyte surface antigen

anti-smooth muscle Ab

74
Q

what is the presentation of someone with autoimmune hepatitis?

A

acute hepatitis: mild jaundice
signs of autoimmunity: malaise, fever, rash, polyarthritis, pleurisy, glomerulonephritis

complications of cirrhosis
complications of immunosuppressive drug therapy

75
Q

what do we find on investigations of someone with autoimmune hepatits?

A

bilirubin, AST, ALT and ALP all raised
hypergammaglobulinaemia (anti smooth muscle Ab)
anaemia
reduced WCC and platelets - indicated hypersplenism

liver biopsy will confirm diagnosis

76
Q

how do we treat autoimmune hepatitis?

A

prednisolone, azathioprine

liver transplant - for decompensated cirrhosis or failure to respond to medical therapy

77
Q

what conditions are associated with autoimmune hepatitis?

A 
pernicious anaemia 
autoimmune haemolysis 
primary sclerosisng cholangitis
UC
glomerulonephritis 
diabetes mellitus
78
Q

what is wilsons disease?

A

A rare autosomal recessive disorder characterised by excess copper deposition in tissues. there is increased copper absorption from the small intestine and decreased hepatic copper excretion

79
Q

when does someone with wilsons disease present? and how does presentation differ depending on age at which they first present?

A

onset of symptoms usually between 10-25 years
children usually present with liver disease first whereas if the disease presents in young adults first then the signs are often neurological

80
Q

discuss the features of wilsons (include liver, neurological, renal, haematology, dermatology and eyes)

A

liver: hepatitis and cirrhosis
neurological: basal ganglia degeneration - speech and behaviour problems at first, asterixis (flap), chorea, dementia and parkinsonism

renal tubular acidosis
haemolysis

blue nails

kayser Fleischer rings - dark rings with circle iris - in eyes

81
Q

describe the pathogenesis behind wilsons disease

A

There is an impairment of the packaging of copper into caeruloplasmin in the liver. this is required for the excretion of copper into bile. Therefore copper is absorbed by the intestine and transported to the liver but cannot be excreted so copper accumulates in the liver.

82
Q

what is found on investigations in Wilsons disease?

A

increased 24 hour urinary copper excretion
reduced serum caeruloplasmin
molecular genetic testing confirms disease

83
Q

how is wilsons managed?

A

penicillamine (chelates copper)
avoid eating food high in copper - liver, nuts, mushrooms
screen siblings
liver transplant

84
Q

what is alcoholic liver disease?

A

A term used to describe the array of changes that occur to the liver due to alcohol over consumption

85
Q

what are the risk factors associated with developing alcoholic liver disease?

A 
women are 2x more likely
amount consumed
pattern of drinking 
hep C infection
malnourishment
genetic predisposition
86
Q

describe the pathogenesis behind alcoholic liver disease.

A

alcohol –> acetylaldehyde –> acetate
(each stage NAD to NADH)

the excess NADH stimulates fatty acid synthesis - promotes fatty liver
the acetylaldehyde is toxic to the liver - hepatitis
this results in inflammation and reduced liver functions - less apoprotein to export fat (fatty liver), less clotting factors, less acute phase proteins, less albumin, less urea cycle (encephalopathy) , less conjugation of bilirubin (jaundice)

excessive hepatitis - results in necrosis and scarring of liver - eventually leads to cirrhosis - portal hypertension and increased risk of HCC

87
Q

what are the signs associated with alcoholic liver disease?

A

low albumin: ascites/oedema, leukonychia

portal hypertension: ascites, splenomegaly, hepatomegaly, bleeding varices, caput medusa

excess oestrogen (less breakdown): palmer erythema, gynaecomastia, spider Neiva, testicular atrophy

high ammonia - liver flap, neglects (weight loss, appearance), altered mood/sleep

coagulopathy: purpura (small red non-blanching spots - small bleeds/bruises), striae

dupuytrens contractures
gastritis / peptic ulcers
signs of anaemia

from history: hides the fact they drink, lost interest in other activities, complains of loss of appetite and sleepiness , cant handle normal routine

88
Q

What is CAGE?

A 
C= cut down - have you ever felt the need to cut down?
A = annoyed - have you ever been annoyed by people criticising you for drinking
G = guild - have you ever felt guilty about drinking
E = Eyeopener - ever needed a drink to steady nerves in a morning

these are a set of questions to ask that would indicate alcoholic

89
Q

what is the difference between hepatic encephalopathy and wernickes korsakoff?

A

hepatic encephalopathy - excess ammonia due to liver dysfunction and impaired urea cycle

wernickes korsakoff - B12 deficiency due to gut damage and poor diet

90
Q

how would you manage someone with alcoholic liver disease?

A
  • stop drinking alcohol - may need to be weened off due to withdrawal symptoms
  • refer to dietician - avoid salts (reduce oedema), healthy diet, vitamin supplements (B12, folate and thiamine)
  • Disulfiram - treat chronic alcohol dependence by making drinking unpleasant
  • corticosteroids for inflammation
    colchicine - to reduce fibrosis
  • diazepam to reduce withdrawal symptoms e.g. seizures
  • furosemide may help with oedema
  • counselling / support groups

liver transplant

91
Q

what are the signs of alcohol withdrawal?

A 
increased HR, tremor, confusion, seizures, hallucinations
nausea and vomiting
sweating 
agitation/anxiety 
headache
92
Q

how does disulfiram work?

A

inhibits acetaldehyde dehydrogenase (converts acetaldehyde to acetate)

acetylaldehyde gives people the feeling of a hangover
this will build up and make drinking unpleasant

93
Q

what is the TWEAK screening questions?

A

tells you the likelihood someone has a drinking problem

1) increased tolerance ? 2 points
2) worry about your drinking ? 2 points
3) have you ever seen alcohol as an EYE opener in morning ? 1 point
4) do you get Amnesia after drinking ? 1 point
5) have you felt the need to cut (KUT) down? 1 point

score of 2 or more suggests alcohol problem

more sensitive questionnaire than CAGE sometimes

94
Q

what is non-alcoholic fatty liver disease? (what does it include and what causes it)

A

most commonest type of liver disease in developed world. Largely caused by obesity and describes a range of diseases including steatosis (fat in liver), steatohepaitis (fat with inflammation) and fibrosis and liver cirrhosis
i.e. this disease describes the hepatic manifestations of metabolic syndrome and hence insulin resistance is thought to be key in the pathogenesis

95
Q

what are the factors associated with non-alcoholic fatty liver disease?

A 
obesity 
hyperlipidaemia 
type 2 diabetes
jejunoileal bypass 
sudden weight loss/starvation
96
Q

what symptoms/signs are associated with non-alcoholic fatty liver disease?

A

usually asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity (appears whiter) on USS

97
Q

how do we manage non-alcoholic fatty liver disease?

A

weight loss
monitoring
research into gastric banding or insulin sensitising drugs (metformin)

98
Q

Is hep A self limiting or chronic?

A

usually a benign self limiting disease

serious outcome is very rate

99
Q

what type of virus is hepatitis A?

A

RNA picornavirus

100
Q

what is the incubation period for hepatitis A?

A

2-4 weeks

101
Q

how is hepatitis A transmitted?

A

faecal oral

often in institutions

102
Q

what symptoms does someone with hep A experience?

A

acute onset jaundice, hepatosplenomegaly

flu like symptoms

103
Q

is there a vaccine for hepatitis A?

A

yes - initial dose and then booster dose 6 - 12 months later

104
Q

who should be vaccinated against Hepatitis A?

A

people with chronic liver disease
people with haemophilia
people with HIV

travelling to areas of high prevalence
men who have sex with men
injecting drug users
occupational risk: sewage workers,

105
Q

what type of virus is hepatitis B?

A

double stranded DNA hepadnavirus

106
Q

how is hep B transmitted?

A

body fluids
blood
verticle transmission from mum

107
Q

what is the incubation period of hep B?

A

6 to 20 weeks

108
Q

what are the symptoms of Hep B?

A

fever, malaise, jaundice

109
Q

what are the complications of hepatitis B?

A 
chronic hepatitis (5-10%)
fulminant liver failure (1%) 
HCC
glomerulonephritis
polyarteritis nodosa
cryoglobulinaemia
110
Q

is there a vaccine for hepatitis B?

A

yes - contains HBsAg (surface antigen)

111
Q

how is the vaccine for hepatitis B given?

A

3 doses of the vaccine

booster dose after 5 years

112
Q

who should be vaccinated against hepatitis B?

A

at risk groups: health care workers, IV drug users, sex workers, individuals receiving blood transfusions regularly
chronic liver disease
chronic kidney disease - in case dialysis is needed

113
Q

does everyone respond well to the hepatitis B vaccine?

A

No some people fail to respond

risk factors include age, over 40, obesity, smoking, alcohol, immunosuppression

114
Q

why do we check anti-HBs levels?

A

check patients for immunisation
only do this for high risk groups e.g. health care workers and chronic kidney disease
check 1-4 months after immunisation

115
Q

what is the treatment of hepatitis B?

A

pegylated interferon alpha - reduces viral replication in up to 30% of carriers. - first line

however other antivirals are available - tenofovir, entecavir

116
Q

what blood tests will confirm hepatitis B infection?

A

raised aminotransferases in hepatitis B infection
HBsAg (surface antigen) - first marker to appear - implies acute disease
if this marker is still present after 6 months it indicates chronic disease.
anti- HBs indicates immunity (this will be negative in chronic disease)

117
Q

what does the anti HBc indicate?

A

antibodies against Hep B core antigen
igM anti HBc goes away after 6 months
IgG anti HBc persists

HbeAg results from the breakdown of core antigen from infected liver - therefore a marker of infectivity

118
Q

what does antiHBs positive and all other markers negative indicate for Hep B infection?

A

previous immunisation

119
Q

what does anti HBc positive and HBsAg negative suggest for hep B infection?

A

previous Hep B infection

now cleared

120
Q

what does anti HBc and HBsAg positive suggest?

A

carrier for hep B

121
Q

who are at risk of hepatitis C?

A

IV drug users

those who received blood transfusions prior to 1991

122
Q

what type of virus is hepatitis C?

A

RNA flavivirus

123
Q

what is the incubation period for hep C?

A

6-9 weeks

124
Q

how is hepatitis C transmitted?

A

blood - needle stick
verticle
sexual intercourse

125
Q

what percentage of people with Hep C infection develop acute hepatitis?

A

less than 20%

126
Q

what are the complications of hepatitis C infection?

A

chronic infection - in 80% (only 15-20% clear the virus)
cirrhosis
HCC
cryoglobulinaemia
porphyria cutanea tarda (PCT) - type of porphyria

127
Q

how is hepatitis C treated?

A

curable
pegylated interferon alpha and ribavirin are used
- 12 week treatment course
- blood tests throughout to check patient compliance and check for side effects.

need to take IFN and ribavirin once a week. take paracetamol with IFN to keep fever down.

128
Q

what are the side effects of ribavirin (hep C treatment)?

A

haemolytic anaemia, cough, insomnia, low Hb

women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic

129
Q

what are the side effects of interferon alpha (hep C treatment)?

A 
flu like symptoms
depression 
fatigue
leukopenia
thrombocytopenia
130
Q

how is portal hypertension defined?

A

> 20mmHg in portal system

131
Q

what are the causes of portal hypertension?

A

pre hepatic: portal vein thrombosis (e.g. pancreatitis)
hepatic: cirrhosis, schistosomiasis, sarcoidosis
post hepatic: right heart failure, constrictive pericarditis

132
Q

where are the 3 places where the portal system and venous system anastomose?

A

oesophagus - left and short gastric veins (portal) with inferior oesophageal veins (azygous vein, systemic)

caput medusa - periumbilical veins (portal) and superficial abdo wall veins (systemic)

rectal - superior rectal veins (portal) with inferior and middle rectal veins (systemic)

133
Q

what are the consequences of portal hypertension?

A

SAVE:

  • splenomegaly
  • ascites
  • varices
  • encephalopathy
134
Q

how does hepatic encephalopathy occur?

A

reduced hepatic function means that there is an increase in nitrogenous waste circulating. these are shunted to the systemic system.
astrocytes convert glutamate to glutamine –> cerebral oedema

135
Q

what are the features of hepatic encephalopathy?

A 
asterixis, ataxis 
confusion 
dysarthria 
constructional apraxia 
seizures
136
Q

what are the precipitants of hepatic encephalopathy?

A

HEPATICS:

  • haemorrhage e.g. varices
  • electrolytes (reduced K, Na) - (give K sparring diuretics in liver failure)
  • poisons: diuretics, sedatives
  • Alcohol
  • tumour: HCC
  • infection: pneumonia, UTI
  • constipation - build up of bacteria which produce nitrogen
  • sugar low
137
Q

how do we manage hepatic encephalopathy?

A

nurse at 20 degrees head up
correct any precipitants
avoid sedatives
lactulose + PO4 enemas to reduce nitrogen forming bowel bacteria - 2 to 4 soft stools per day
consider rifaximin orally to kill microflora in gut

138
Q

what is the pathogenesis behind ascites?

A

low oncotic pressure from loss of albumin + back pressure to portal hypertension
reduced circulating volume and so RAS activation and more fluid retention

139
Q

what are the causes of ascites? divide these into serum ascites albumin gradient of >1.1g/dL and <1.1g/dL

A

> 1.1g/dL - pre hepatice, hepatic and post hepatic e.g. cirrhosis. other causes of hypoalbumin e.g. kwashiorkor

<1.1g/dL - neoplasia (peritoneal or visceral), inflammation (pancreatitis), nephrotic syndrome , infection (TB peritonitis) (diabetic nephropathy too)

140
Q

what investigations would you want to do for someone with ascites?

A

FBC, U&Es, LFTs, INR, chronic hepatitis screen

USS - confirm ascites, liver, portal vein duplex

Ascitic tap - MSC and acid fast bacilli test, cytology (cancer), biochem (albumin, LDH, glucose, protein) , SAAG (serum albumin - ascites albumin)

liver biopsy

141
Q

how would you treat ascites?

A

daily weights - aim for <0.5kg/day reduction
fluid restriction (<1.5L/day) and Na restriction
spironolactone and furosemide (if poor response)

consider albumin infusion

transjugular intrahepatic portosystemic shunt (TIPSS)

142
Q

what is transjugular intrahepatic portosystemic shunt (TIPSS) ?

A

an artificial channel that is placed between the hepatic portal vein and outflow hepatic vein to reduce build up of pressure and backflow
treats portal hypertension as a result of cirrhosis

143
Q

what are the complications of ascites?

A

dyspnoea - diaphragm cant contract well enough
reduced circulating volume - renal failure
reduced CO because reduced venous return
spontaneous bacterial peritonitis - stasis of fluid in peritoneum allows bacterial growth (Ecoli, strepts, klebsiella)

144
Q

how is spontaneous bacterial peritonitis treated?

A

ascitic tap - MC+S

Tazocin or cefotaxime until sensitivities known

145
Q

what are the complications of splenomegaly?

A

splenic congestion

hypersplenism - leads to low WCC and platelets

146
Q

what are the different types of liver transplant?

A

cadaveric - heart beating or non beating heart

live - right lobe

147
Q

what are the kings college hospital criteria for liver transplantation for paracetamol induced liver failure?

A 
arterial pH <7.3 24 hours after injestion 
OR 
prothrombin time >100s
creatinine >300umol/L
grade 3 or 4 encephalopathy
148
Q

what are the kings college hospital criteria for liver transplantation for non paracetamol liver failure?

A 
Prothrombin time (PT) >100s
OR 3 or 5: 
  1. drug induced
  2. age <10 or >40
  3. 1 week from 1st jaundice to encephalopathy
  4. PT >50s
  5. bilirubin >/=300umol/L
149
Q

how is liver transplantation managed post op?

A

12-24 hours in ITU with enteral feeding starting ASAP and LFTs closely monitored
immunosuppressive -
- ciclosporin and tacrolimus
- and azathioprine/mycophenolate mofetil
- and prednisolone

150
Q

what are the complications of liver transplant?

A

rejection - acute or chronic
sepsis
hepatic artery thrombosis

151
Q

what are the indications for a liver transplant?

A

advanced cirrhosis secondary to :
- alcoholic liver disease, hepatitis (B, C, autoimmune), primary biliary cirrhosis, alpha1 antitrypsin, primary sclerosing cholangitis, HCC

152
Q

what are the contraindications for liver transplant?

A 
extrahepatic malignancy 
multiple tumours
severe cardioresp disease
systemic sepsis
HIV infection 
non-compliance with drug therapy
153
Q

which antibodies are raised in primary biliary cirrhosis ?

A

anti- mitochondrial ab

154
Q

describe the LFTs seen in someone with alcoholic liver disease?

A

AST: ALT >2
MCV raised
AST and ALT both raised but AST more so

155
Q

what are the LFT patterns seen in hepatitis C infection ?

A

raised AST and ALT (but ALT more so

AST:ALT <1

156
Q

what are the LFTs seen in non-alcoholic fatty liver disease?

A

raised AST and ALT but ALT more so.
AST:ALT <1
MCV may be raised or normal

157
Q

describe the link between cirrhosis and renal function?

A
  1. reduced clearance of immune complexes by the liver and so they can become trapped in kidneys - IgA nephropathy and possible glomerulosclerosis
  2. HBV can also cause membranous nephropathy
  3. low albumin –> reduced circulating volume and poor renal perfusion.
  4. splanchnic arterial vasodilation causes a reduction in the circulatory volume
  5. 3 and 4 cause RAS activation - renal arteries are vasoconstricted worsening the problem.
158
Q

what is meant by decompensated cirrhosis?

A

decompensated cirrhosis is when complications such as hepatic encephalopathy, ascites and portal hypertension arise.

159
Q

why may ALT be more than 500?

A

viral infection
ischaemia - e.g due to sepsis and hypotension (ALT will be severely but drop rapidly too)
drugs: paracetamol OD, ecstasy, (never alcohol)
autoimmune

160
Q

what causes cholestasis with non-dilated ducts?

A

cirrhosis

drugs: Abx, NSAIDs, ACEi

161
Q

what advice would you give to alcoholics?

A

warn of effects not only on the liver but on the brain and the heart too.
advice on how to cut down
tell them about different support groups

162
Q

what drugs can cause chronic liver disease?

A

methotrexate, phenytoin, isoniazid

163
Q

what is hepatorenal syndrome?

A

Cirrhosis → splanchnic arterial vasodilatation →
effective circulatory volume → RAS activation → renal
arterial vasoconstriction.
 Persistent underfilling of renal circulation → failure

Surgery sara (10 decks)

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