Acute liver failure Flashcards

1
Q

What is acute liver failure?

A

Rapid onset of liver dysfunction without prior disease. Generally lasting less than 6 months.

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2
Q

What are the main functions of the liver?

A
Protein metabolism, Lipid metabolism
Carbohydrate metabolism
Imunological defence
Bilirubin metabolism
Hormone and drug metabolism
Bile acid secretion
Storage
Protein synthesis
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3
Q

What are the true liver function tests?

A

Bilirubin, albumin and prothrombin. MOST important as they are prognostic markers

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4
Q

What are the liver ‘damage’ liver function tests?

A

GGT, AKP, ALT/AST and bilirubin

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5
Q

What percentage of patients with cirrhosis have normal LFTs?

A

17%

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6
Q

What are the features of acute liver failure?

A

1) Encephalopathy,
2) Coagulopathy (prolonged prothrmbin time)
3) Jaundice

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7
Q

What are the common symptoms of acute liver failure?

A
None!
Jaundice
Lethargy
nausea
Itchy
Pain (capsule stretching)
Abnormal LFTs
Anorexia
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8
Q

What are the causes of acute liver failure?

A

1) Viral (Hep A-E, CMV, EBV and toxoplasmins)
2) Drugs (many)
3) Shock liver
4) Cholangitis
5) Alcohol
6) Malignancy
7) Chronic liver disease
8) Paracetamol
RARE: Budd Chiarri, AFLP, Cholestasis of pregnancy

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9
Q

What is Shock liver?

A

Inadequate perfusion of the liver. (Hypotention- check the vascular patency of the hepatic artery)

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10
Q

What is Budd Chiarri?

A

Occlusion of hepatic veins which drain the liver.

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11
Q

What is AFLP?

A

Acute fatty liver disease of pregnancy

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12
Q

When you ask a patient about paracetamol what else should you ask?

A

Preparations
OTC drugs which contain paracetamol.
Even 4g/day for 2 weeks can change liver function.

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13
Q

What are the directly toxic causes of liver failure?

A

Drugs, alcohol, virus and hypoperfusion (shock liver)

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14
Q

What are the immunologic causes of liver failure?

A

Primary Billary Cirrhosis

Autoimmune hepatitis

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15
Q

What are the nutritional causes of liver failure?

A

NASH, Malnutrition, refeeding syndrome.

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16
Q

What are the genetic causes of liver failure?

A

Wilsons disease and haemachromatosis (insidious onset and can present with HHC)

17
Q

What are the investigations to consider in acute liver failure?

A
Bilirubin, Prothrombin, Albumin.
LFTs
Ultrasound including vascular
Virology
Immunological serology
Rarely a liver biopsy.
18
Q

When is a liver biopsy indicated?

A

Struggling to get a clear diagnosis or looking at the patients prognosis

19
Q

Acute liver failure history?

A

Duration
Drugs (OTC, illicit, herbal and food supplements)
Alcohol, unusual hobbies, travel, sexual history.

20
Q

What is the treatment for acute liver failure?

A

Supportive. Rest 3-6 months.
Fluids and NO alcohol.
Increase calories (high protein, low fat)
Observe for FHF

21
Q

What is puritus and what is the cause?

A

Severe itching of the skin caused by increase in bilirubin- often post hepatic picture.

22
Q

What is the treatment for puritus?

A

Sodium bicarbonate bath
Cholestyramine (prevents bile salt reabsorption)
Uresodeoxycholic acid (reduces cholesterol absorption)

23
Q

What are the metabolic considerations in acute liver failure? WHat should people be eating?

A

Patients are in a hypermetabolic state and require increased nutritional requirements but are often not hungry.
35-40 calories/Kg/day
1.2-1.5g protein/kg/day.
Monitor K, PO4 and Mg for signs of refeeding syndrome.
Monitor blood glucose for hyper/hypoglycemia
Consider NG feeding in some patients

24
Q

What are the features of a hepatic drug reaction?

A

Occurs about 6 weeks post exposure- the first effect may not have been noticed.
Often the liver is predisposed. Eg NASH.
Caused by any drug, many mechanisms and variation in LFT abnormalities.
Effects CP450 => free radiacl production and lipid peroxidation.

25
How does paracetamol toxicity come about?
Paracetamol is metabolised to NAPQI (toxic) as it comsumes most of the GLUTATHIONE. Glutathione is usually recycled in the liver but when bound to NAPQI it is not.
26
How is Paracetamol toxicity treated?
NAC is given which is the precursor to glutathione. You need to give it faster then it is being used.
27
What are the common drugs which cause liver reactions?
Co-amoxiclav, Flucloxacillin, NSAIDs Fat burners/protein powders Paracetamol containing drugs (statins can change LFts but don't normally cause liver damage.)
28
What is Fulminant Hepatic failure?
Rapid development of encephalopathy in a previously normal liver
29
What are the causes of FHF?
Paracetamol Viral Drugs RARE: AFLP, mushrooms, malignancy, Wilsons disease, Budd Chiari
30
What are the clinical features of fulminant hepatic failure?
``` Encephalopathy => cerebral oedema (may require decompression) Spontaneous hypoglycemia Coagulopathy Circulatory failure Renal failure => dialysis Infection ```
31
What is the treatment for fulminant hepatic failure?
Supportive: Fluids and Ionotropes to increase BP. Renal replacement, Manage raised Intra cranial pressure Transplant
32
What are the survival outcomes of fulminant hepatic failure?
75%, 65% if require transplant.
33
What should you do if you suspect fulminant hepatic failure?
Refer quickly to a 24 hour transplant centre (Edinburgh) Monitor closely (bloods every 6 hours) If they need transplant get it within 24 hours (Die within 48-72 hours) Consider intubating to reduce cerebral oedema and effects
34
What are the guidelines for transplant called?
Kings Collage Criteria for Acetaminophen (paracetamol toxicity) There are also guidelines for non paracetamol fulminant liver failure