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BSMS302 > 1. Intro to Hepatology and LFTs > Flashcards

1. Intro to Hepatology and LFTs Flashcards

1
Q

Acute causes of abnormal liver tests

A 
(6 weeks or less)
drugs
viral hepatitis (A,B,C,E)
Autoimmune hepatitis
Wilsons disease
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2
Q

Subacute causes of abnormal liver tests

A 
(6-26 weeks)
drugs
viral hepatitis (A,B,C)
Autoimmune hepatitis
Wilson's disease
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3
Q

Chronic causes of abnormal liver tests

A 
(>26 weeks)
Viral hepatitis (B, C)
Alcohol
NAFLD (non-alcoholic fatty liver disease)
haemochromatosis
A1 antitrypsin deficiency
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4
Q

Wilson’s disease

A

Wilson’s disease is a autosomal recessive disease in which copper builds up in the body.

Symptoms are typically related to the brain and liver.Liver-related symptoms include vomiting, weakness, fluid build up in the abdomen, swelling of the legs, yellowish skin, and itchiness. Brain-related symptoms include tremors, muscle stiffness, trouble speaking, personality changes, anxiety, and hallucinations.
Treated by low copper diet and chelating agent e.g. zinc

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5
Q

Liver tests

A

Wilson’s disease is a autosomal recessive disease in which copper builds up in the body.

Symptoms are typically related to the brain and liver.Liver-related symptoms include vomiting, weakness, fluid build up in the abdomen, swelling of the legs, yellowish skin, and itchiness. Brain-related symptoms include tremors, muscle stiffness, trouble speaking, personality changes, anxiety, and hallucinations.
Treated by low copper diet and chelating agent e.g. zinc

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6
Q

Liver tests -proteins

A

bilirubin 17micromol/l

liver enzymes:
Aspartate aminotransferase (AST) 40iu/l
alanine aminotransferase (ALT) 40iu/l
Alkaline phosphatase (ALP) 200iu.l
Gamma GT 50 iu/l

Albumin 40gm/l

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7
Q

Effects of certain diseases on LFTS

A

transaminases increase if hepatitis

ALP and GGT go up if cholestitis

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8
Q

Liver tests - clotting

A

Prothrombin time
INR (measurement of ratio of measured PT to normal)

Measures extrinsic coagulation pathway - II, V, VII, X and fibrinogen

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9
Q

What to do if LFTs are abnormal?

A

Do a liver screen
Hepatitis serology - Hepatitis A IgM, hepatitis B surface antigen, hep C antibody, Hep E IgG and IgM

ANA, SMA, LKM for autoimmune hepatitis
AMA for primary biliary cholangitis

Alpha 1 antitrypsin (in case of deficiency)

Copper, caeruloplasmin for Wilson’s disease

Ferritin (genetic haemachromatosis)
Ultrasound

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10
Q

What tests are included in hepatitis serology?

A

Hepatitis A IgM, hepatitis B surface antigen, hepatitis C antibody, Hepatitis E IgG and IgM

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11
Q

What to do to look for autoimmune hepatitis?

A

Screen for ANA (antinuclear antibodies), SMA(smooth muscle antibodies) LKM (liver kidney microsome antibodies)

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12
Q

What does AMA screen look for?

A

Antimitochondrial antibodies, like in primary biliary cholangitis

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13
Q

hepatitic disease elevated bloods

A

AST and ALT massively increased but bilirubin normal

Things that start as hepatitic can become cholestatic

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14
Q

Cholestatic elevated bloods

A

bilirubin and ALP raised but AST and ALT normal

e.g. biliary obstruction

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15
Q

Hepatitic causes of abnormal liver tests

A

Viral hepatitis A,B,C,E
Drug induced liver injury (DILI)
Autoimmune hepatitis

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16
Q

Cholestatic causes of abnormal liver tests

A 
Biliary obstruction
Viral hepatits A,B,E
DILI
Autoimmune hepatitis
Primary biliary cirrhosis cholangitis
Primary sclerosing cholangitis
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17
Q

Is cirrhosis reversible?

A

Cirrhosis is generally irreversible
Feature of chronic liver disease
The main feature of cirrhosis is increased pressure in the portal circulation, also known as portal hypertension

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18
Q

Liver failure - what can develop?

A

Coagulopathy and encephalopathy

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19
Q

Onset of liver failure and development of coagulopathy/encephalopathy

A

Acute within 4 weeks
Subacute between 4-12 weeks
Acute on chronic in setting of underlying chronic liver disease

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20
Q

Hyperacute liver failure

A

1 week from jaundice to encephalopathy, ,lowe severity of jaundice, very severe coagulopathy, high intercranial hypertension, good survival rate without emergency liver transplantation

usually caused by paracetamol, hep A and E

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21
Q

Acute liver failure

A

1-4 weeks from jaundice to encephalopathy, moderate jaundice, moderate coagulopathy, high intercranial hypertension, moderate survival rate without emergency liver transplantation

usually caused by hep B

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22
Q

Subacute liver failure

A

4-12 weeks from jaundice to encephalopathy, highly severe jaundice, low coagulopathy, with or without intercranial hypertension, poor survival rate without emergency liver transplantation

non-paracetamol drug-induced liver injury

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23
Q

In acute liver failure…

A

no pre-existing liver disease, coagulopathy, confusion (hepatic encephalopathy)

jaundice
abnormal LFTs
cerebral oedema
increased risk of infections
renal failure (hepatorenal syndrome)
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24
Q

hepatorenal syndrome triad

A

altered liver function, abnormalities in circulation, and kidney failure.

25
Q

How does liver failure affect encephalopathy?

A

the more acute the liver failure the more swollen the brain

26
Q

Paracetamol overdose

A

most common cause of acute liver failure - 70,000 cases and 130 deaths a year in UK

Intentional overdose

recommended dose 4g/day, toxic dose>15g
lower toxic dose if pre-existing liver disease, alcohol excess

27
Q

paracetamol metabolism

A

Usually sulfated or glucuronidate to make safe metabolites
but some undergoes CYP-mediated N-hydroxylation and rearrangment to become NAPQI which undergoes toxic reactions with proteins and nucleic acids

In overdose, metabolism is shunted to NAPQI

28
Q

How can paracetamol overdose be treated?

A

with N-acetyl cysteine (NAC) which replenishes glutathione and allows more of the glucuronidation

Start NAC immediately if paracetamol OD is suspected, even if don’t have paracetamol levels

If receive N-acetyl cysteine within 16 hours, then liver failure rarely develops. Some benefit even up to 36 hours

In severe cases liver transplant only option

29
Q

How does paracetamol overdose present?

A

Nausea, vomiting, RUQ pain, confusion

Jaundice and liver failure after 3-4 days

Very high liver enzymes and prothrombin time

If receive N-acetyl cysteine within 16 hours, then liver failure rarely develops. Some benefit even up to 36 hours

In severe cases liver transplant only option

30
Q

In cirrhosis…

A 
Portal hypertension - varices, ascites, hepatic encephalopathy 
Jaundice
Spiders
Enlarged spleen/pancytopenia
Renal failure (HRS)
Hepatocellular cancer
31
Q

What is liver cirrhosis?

A

Irreversible scarring of the liver

32
Q

What are compensated cirrhosis and decompensated cirrhosis?

A

Compensated cirrhosis is cirrhosis developed from chronic liver disease in which there are no complications and has a median survival rate of 9 years, whereas decompensated cirrhosis has complications and a medial survival of 1.6 years

33
Q

What complications develop in decompensated cirrhosis?

A

Variceal haemorrhage, ascites, encephalopathy, jaundice

34
Q

How can decompensated cirrhosis be treated

A

Orthotopic liver transplant (OLT) otherwise median survival is around 1.6 years before death

35
Q

Stages of cirrhosis

A

1 - compensated without varices, median survival >12 years, and 1 year mortality

2- compensated with varices - 3% 1 year mortality

3- decompensated with ascites without variceal haemorrhage - 20% 1 year mortality, and around 2 year median survival

4- decompensated with/out ascites with variceal haemorrhage - 57% 1 year mortality

36
Q

What characteristics of cirrhosis increase 1 year mortality and decrease survival rate?

A

Whether varices are present +
Whether it is decompensated ++
Whether there is variceal haemorrhage +++

37
Q

Managing ascites in cirrhosis

A

Restrict salt
Restrict fluid if sodium is low
Diuretics - furosemide and spironolactone
Large volume paracentesis (LVP) with albumin cover

38
Q

How to treat refractory ascites

A 
Recurrent LVP (large volume paracentesis)
transjugular intrahepatic portosystemic shunt
consider liver transplant
long-term drains (if palliative) still undergoing research
39
Q

Treating variceal bleed

A

make them haemodynamically stable, correct coagulopathy and thrombocytopenia

IV terlipressin (vasopressin analogue) and IV antibiotics

Endoscopy in theatre with anaesthetist present - variceal banding

If blood bath - balloon tamponade

Non-selective Beta blockers for secondary prophylaxis (propanolol and carvedilol)

40
Q

Hepatorenal syndrome

A

A type of AKI

Functional and fairly rapid renal impairment due to reduced renal perfusion - nothing wrong with the kidney itself

Increase in serum creatinine by 50% from baseline within 3 months

Type 1 and 2

Terlipressin to treat underlying cause

Liver transplant

41
Q

What is terlipressin used to treat?

A

oesophageal varices and hepatorenal syndrome

42
Q

Difference between type 1 and 2 hepatorenal syndrome?

A

Type 1 more acute, type 2 less acute, precipitated by infection sepsis etc

43
Q

Hepatic encephalopathy

A 
Elevated ammonia (which crossess BBB and causes confusion)
diagnosis of exclusion

Treat precipitating cause: constipation, diuretics, infection, sedatives, GI bleed

Lactulose (non-absorbable sugar)
Non-absorbable antibiotics e.g. Rifaximin

44
Q

Acute on chronic liver disease precipitants

A 
Viruses
drugs
alcohol
ischaemia
surgery
sepsis
idiopathies
45
Q

Types of acute on chronic liver failure

A

Type A from chronic liver disease
Type B from compensated cirrhosis
Type C from decompensated cirrhosis (jaundice, ascites, variceal bleeding, hepatic encephalopathy)

46
Q

Result of acute on chronic liver failure

A

hepatic and extrahepatic organ failure

47
Q

Acute on chronic Liver failure causes

A

alcohol
hep C
NAFLD

48
Q

Alcoholic liver disease

A

Normal liver to fatty liver 90-100%
10-35% of fatty liver undergoes alcoholic hepatitis, 40% of which undergoes cirrhosis
8-20% of fatty liver undergoes cirrhosis

49
Q

Severe alcoholic hepatitis

A

most serious form of alcohol related injury

characterised by jaundice and coagulopathy

untreated mortality 40%

Various prognostic scores (discrimant function)

Steroids and pentoxyfilline

50
Q

Risk factors for Hep C virus transmission

A

85% recipients of clotting factors made pre 1987
80% Injection drug use
10-20% long-term haemodialysis
4-6% multiple sex partners
5% recipients of blood transfusion prior to July 1992
4-7% infants born to infected women

51
Q

Factors associated with Hep C disease progression

A

Alochol consumption - 30g/day in men, 20g/day in women (2 drinks a day)

Disease acquisition at >40 years

Male gender

HIV coinfection

Hep B virus coinfection

immunosuppression

52
Q

Hep C natural history

A

female, young age at infection - slow progression, >30 years

Normal liver -> acute infection -> chronic infection in 80% -> chronic hepatitis -> cirrhosis develops in 20% -> risk of carcinoma, 1-4% a year

Fast <20 years with alcohol use or coinfection

53
Q

Types of HCV drugs

A

NS3/4A protease inhibitors (block translation and polyprotein processing)
Grazoprevir, Paritaprevir, Simeprevir, Glecaprevir

NS5A inhibitors - Ledipasvir, Ombitasvir, Daclatasvir, Elbasvir, Velpatasvir, Pibrentasvir

NS5B RNA polymerase inhibitors - Sofosbuvir, Dasabuvir

54
Q

Non-alcoholic fatty liver disease

A

Resembles alcoholic liver disease but occurs in absence of alcohol abuse

Usually associated with metabolic syndrome: type 2 DM, obesity, HTN, and elevated TG

Underlying mechanism is insulin resistance (IR)

55
Q

Spectrum of NAFLD

A

Fatty liver -> nonalcoholic steatohepatitis (NASH) -> cirrhosis

56
Q

Indications for liver transplant in acute liver failure - in context of paracetamol

A

ph<7.3 after fluid resuscitation

Arterial lactate >3.5 mmol at 4 hours or >3.0mmol/l at 12 hours

or
PT >100 seconds (INR>6.5)
serum creatinine >300mmol/l (3.4mg/dl)
Grade 3 or 4 encephalopathy

57
Q

Indications for liver transplant in acute liver failure - no paracetamol

A

PT >100 seconds (INR>6.5) irrespective of grade of encephalopathy or any three of the following:

  1. Age less than 11 or greater than 40
  2. Aetiology of non-A/non-B hepatitse, halothane hepatitis or idiosyncratic drug reactions
  3. Duration of jaundice of more than 7 days before onset of encephalopathy
  4. PT time greater than 50 seconds (INR>3.5)
  5. Serum Bilirubin level greater than 17mg/dL (300micromol/l)
58
Q

Indications for liver transplant in cirrhosis

A

Ascites/SBP (spontaneous bacterial peritonitis)
Variceal bleeding
hepatic encephalopathy
hepatocellular cancer

59
Q

Prognostic scores to prioritise liver transplants in cirrhosis

A

Child Pugh score - encephalopathy, ascites, bilirubin, albumin, PT/INR
MELD and UKELD score: bilirubin, INR, creatinine, Na

BSMS302 (10 decks)

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