Introduction to hepatology Flashcards
Why might a patient have acute abnormal liver tests?
What does acute mean?
<6 weeks
Causes
- Drugs
- VIral Hepatitis (A,B,C,E)
- Autoimmune hepatitis
- Wilsons disease
Why might a patient have subacute abnormal liver tests?
What does acute mean?
6-26 weeks (6 months)
Causes
- Drugs
- VIral Hepatitis (A,B,C)
- Autoimmune hepatitis
- Wilsons disease
Why might a patient have chronic abnormal liver tests?
What does acute mean?
> 6 months
Causes
- Viral hepatitis (B,C)
- Alcohol
- NAFLD
- Autoimmune hepatitis
- Wilsons disease
- Haemochromatosis
- A1 antitrypsin deficiency
What does a liver panel investigate?
Bilirubin- which has prognostic value
Liver enzymes- ALT, AST, ALP, GGT
Albumin
PT and INR- which have prognostic value
What does the PT measure?
The extrinsic coagulation pathway
- factor II, V, VII, and fibrinogen
How do we screen for viral hepatitis?
Hep A- Hep A IgM
Hep B- Hep B surface antigen
Hep C- Hep C antibody
Hep E- Hep E IgG and IgM
How do we screen for autoimmune hepaititis and primary biliary cholangitis ?
Autonimmune Hep- ANA, SMA, LKM
Primary biliary cholangitis- AMA
How do we screen for the following disorders?
- Alpha-1-antitrypsin deficiency
- Wilsons disease
- Genetic haemochromatosis
- Alpha 1 antitrypsin
- Copper and caeruloplasmin
- Ferritin
You review a patients liver panel and notice that the ALT and AST are significantly raised compared to the bilirubin and ALP.
What kind of picture is this?
What may be the cause?
Hepatitic picture
- Drugs
- Viral hepatitis: A,B,C,E
- Autoimmune hepatitis
You review a patients liver panel and notice that the Bilirubin and ALP are significantly raised compared to the AST and ALT
What kind of picture is this?
What may be the cause?
Cholestatic picture
Biliary obstruction Viral Hep A, B, E Drug-induced liver injury (DILI) Primary biliary cholangitis Primary sclerosing cholangitis
(remember things that cause hepatitis can cause cholestatic dysfunction)
Outline the routes of transmission of Hep A, B, C, E
Hep A and E
- orofaecal matter (in the developing world)
Hep B and C
- bodily fluids so high-risk sex, IV drug use, recipients of blood products before screening
Hep E
- in the UK it is mainly a zoonotic disease acquired through eating uncooked pork or shellfish
What is cirrhosis?
Generally irreversible scarring of the liver causing chronic liver disease
The main feature is damage to the portal vein (which is formed by the superior mesenteric and splenic vein) causing increased pressure in portal circulation (portal hypertension)
What are the features of decompensated cirrhosis?
- Variceal bleeding
- Ascites
- Hepatic encephalopathy
What are the signs of chronic liver disease you would look for on examination?
Hands
- Liver flap, palmar erythema, dupuytrens contracture
Jaundice
Spider naevi, caput medusae
Splenomegaly
How does the survival of those compensated and decompensated cirrhosis differ?
Compensated
- have a median survival of 9 years
Decompensated
- median survival of 1.5 years
- development of complications: ascites, variceal bleeding, hepatic encephalopathy, jaundice
How do you manage ascites in cirrhosis?
- Salt restiriction
- Fluid restriction if low Na
- Diuretics (spironolactone and furosemide)
- Large volume paracentesis (LVP) with albumin cover
If refractory
- recurrent LVP
- TIPS procedure
- Liver transplant
- Long term drains (in palliative care)
In the haemodynamically stable patient how do you manage variceal bleeding in the acute scenario?
- Correct coagulopathy (INR)
- Correct thrombocytopenia
- IV Terlipressin (a vasopressin analogue which will reduce portal HTN and bleeding)
- IV antibiotics (GI bleed increases risk of SBP due to increased bacteria translocation)
- If you suspect variceal bleeding endoscope in theatre with patient intubated and anaesthetist present (even if out of hours)
On endoscopy, a patient has stigmata of variceal bleeding
How can you manage this to stop the bleeding?
- BAND LIGATION
- if a complete blood bath, balloon tamponade will decompress varices and gives time to stabilise patient
- TIPS (also decompresses pressure)
What drug is used as secondary prophylaxis of variceal bleeding?
- Non-selective B blocker e.g. propanolol, carvedilol
What is hepatorenal syndrome?
What are the signs?
A type of renal fialure seen in patients with severe liver disease, caused by cirrhosis. Rapid renal impairment caused by reduced renal perfusion
Type 1 and 2
Increase in serum creatinine by 50% from baseline within 3 months
(remember that the primary problem here is with the liver, if the kidneys were removed and given to a patient with functioning liver they would work just fine)
How do you manage hepatorenal syndrome?
Treat underlying cause
Terlipressin
Liver transplant
What is liver failure?
Hepatic encephalopathy (confusion, reduced GCS)
Coagulopathy (iNR>1.5)
Jaundice
It is life threatening
Describe heaptic encephalopathy
- Why does it happen?
- How is it diagnosed?
- How is it treated?
Liver cannot adequately remove toxins from the blood so there is build up of ammonia (this is produced by gut bacteria, protein degradation)
It is a diagnosis of exclusion
Treat underlying cause: constipation, diuretics, infection, sedative, GI bleed
Lactulose (removes ammonia)
Non-absorbable antibiotics (Rifaximin- eliminates gut bacteria)
How do we classify the development of liver failure?
By time
Acute development of coagulopathy encephalopathy <4 weeks
Subacute 4-12 weeks
Acute on chronic
- acute liver failure in a patient with underlying chronic liver disease (e.g. alcohol)
Describe acute liver failure
- context
- pathognomonic features
- presentation
- prognosis
- causes
- No preexisting liver disease
- coagulopathy, encephalopathy
- jaundice, abnormal LFTs, cerebral edema, increased risk of infections, hepatorenal syndrome, intracranial hypertension
- good survival without liver transplant (50-60)
- PARACETAMOL DRUGS (50%), non-paracetamol drugs (15%), Hep A, Hep B
Describe subacute liver failure
- prognosis
- causes
- Poor spontaneous survival (10-15%)
- Caused by non paracetamol drug induced liver innjur
What is the toxic dose of paracetamol?
Recommended dose is 4g/day
Toxic >15g
In pre-existing liver disease the toxic dose is lower
Outline the pathogenesis of paracetamol toxicity
Glucuronidation and sulphation pathways are rapidly saturated which leads to increased metabolism to NAPQI
usually glutathione breaks down this toxic metabolite but in overdose glutathione stores are depleted so toxic metabolite build up
How would a patient with paracetamol overdose present?
- nausea
- vomiting
- RUQ pain
- confusion
- Jaundice and liver failure develop 3-4 days later
Highly raised liver enzymes
Raised PT
How can you prevent acute liver failure in paracetamol overdose?
Administer NAC (N-acetyl cysteine) which replenishes glutathione - glutathione is required to inactivate NAPQI and when levels depleted -> hepatocellular death takes place
Important to give within 16 hours
Dont withhold to confirm diagnosis
What is severe alcoholic hepatitis?
- most serious form of alcohol related injury
- characterised by jaundice and coagulopathy
- 40% mortality if left untreated
Discrimant function score used to determine prognosis - Treat steroids (+ pentoxifylline)
Describe non-alcoholic fatty liver disease
- pathology
- risk factors
- A spectrum of disorders that resembles alcoholic liver disease but occur in the absence of alcohol abuse. The underying mechanism if insulin resistance
- fatty liver –> non-alcohol steatohepatitis (NASH) –> cirrhosis
- obesity, T2DM, HTN, hyperlipidaemia (elevated TG)
How could you identify paracetamol induced acute liver failure on blood gas/boods?
Acidotic
- pH<7.3 after resuscitation
- arterial lactate >3.5 (after 4 hours); >3 (after 12 hours)
Coagulopathic
- INR>6.5
- PT> 100seconds
Serum creatinine >300mmol/L
Encephalopathic (Grade 3/4)
How might a non-paracetamol induced acute liver failure appear?
Age
- <11yo; >40yo
Jaundice
- longer than 7 days before onset of confusion
PT >50s (INR>3.5)
Serum bilirubin >300
Aetiology: Non-Hep A/Hep B; halothane hepatitis; idiosyncratic drug reactions
