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Clinical therapeutics 1 > Liver disease > Flashcards

Liver disease Flashcards

1
Q

Name five of the main functions of the liver

A
  • Metabolism and digestion
  • Immunity
  • Detoxification
  • Storage energy/nutrients
  • Produce proteins
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2
Q

How much of cardiac output does the liver recieve

A

25%

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3
Q

Anatomy of the liver

A
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4
Q

Describe the route of ‘first pass metabolism’

A
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5
Q

Symptoms of liver disease

A
  • Jaundice
  • Ascites
  • Puritis
  • Change in urine colour
  • Blood clotting irregularities
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6
Q

Test for liver disease

A
  • Liver function test LFT
  • Generally blood test
  • For liver enzymes and proteins
  • Then full medical history is assessed
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7
Q

What occurs as a follow up to LFT

A
  • Further investigations e.g. imaging, biopsy, more blood tests
  • Follow progression
  • Monitor response to treatment
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8
Q

Name some standard LFTs

A

ALT alanine transaminase
AST aspartate transaminase
ALP alkaline phosphatase
GGT gamma glutamyltransferase

Bilirubin
Albumin
Prothrombin (clotting)

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9
Q

LFTs enzymes: what are AST and ALT

A
  • Amino transferases: AST (aspartate transaminase) and ALT (alanine transaminase)
  • Inflammation indicators
  • Damaged hepatocytes release both into the blood streatm
  • ALT is more specific to liver
  • AST indicates damage on muscle
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10
Q

What does the AST:ALT ratio tell us

A

> 2 indicates alcoholic liver disease
<1 indicates non-alcoholic liver disease

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11
Q

LFTs enzymes: what is ALP and GGT

A
  • Alkaline phosphates
  • ALP helps diagnose liver and biliary disease, bone disorders
  • GGT gamma glutamyltransferase
  • High levels indicate liver disease/damage to bile ducts
  • GGT level useful for detecting alcohol damage
  • Raised ALP and GGT may indicate block of bile ducts
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12
Q

Raised ALP and GGT may indicate….

A

Raised ALP and GGT may indicate block of bile ducts

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13
Q

LFTs proteins: bilirubin

A
  • Total bilirubin
  • Its a breakdown product of haemoglobin
  • Causes jaundice, levels in blood can predict liver disease
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14
Q

LFTs proteins: albumin

A
  • Its synthesised by the liver and responsible for oncotic pressure in blood and binding of drugs and nutrients
  • Decrease causes fluid retention and indicate liver disease
  • Deficit in albumin can be due to malnutrition
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15
Q

Clotting factors: how do these relate to liver disease and name some

A
  • Prothrombin and prothrombin time
  • Time taken for blood clot following sample
  • Longer PT time indicates reduction in clotting factors produced by the liver
  • Vitamin K deficiency (block of bile extraction)
  • Normally expressed as INR (International Normalised Ratio)
  • Standardised version of PT
  • Target normally 2-3, higher values indicate reduced clotting
  • With high PT/INR score may be repeated following injection of vitamin K
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15
Q
A
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16
Q

Further test for liver disease

A
16
Q

Acute liver disease can lead to what disease

A
  • Acute liver failure ALF
  • ALF is a rare condition where their is rapid deterioration in liver function
16
Q

Difference between acute and chronic liver disease

A
17
Q

Chronic liver disease mostly progresses into..

A
  • Into cirrhosis
  • Where fibrous scars divide liver cells into areas of regenerative tissue called nodules
  • Cirrhosis generally thought to be irreversible although some cases of reversal in Hep B with therapeutic intervention
18
Q

What are the major causes of liver disease

A

Alcohol abuse and chronic viral hepatitis (B and C)

19
Q

Chronic liver disease progression

A
20
Q

Complications associated with severe liver disease

A
  • Symptoms such as fluid retention, ascites, portal hypertension and jaundice often associated with severe liver disease
  • These symptoms may require treatment (not covered)
  • Hepatic encephalopathy
  • Neuropsychological syndrome seen in 70% of patients with cirrhosis
  • End stage liver failure 30% will be severe- coma
  • Characteristic of acute liver failure
21
Q

Stages of alcoholic liver disease

A

Stage 1: Alcoholic fatty liver disease
Normally asymptomatic can occur rapidly
Normally reversible by taking a break from drinking
Stage 2: Alcoholic hepatitis
Mainly due to chronic use over a long period
Progression can be halted by stopping drinking
Stage 3: Cirrhosis
Unlikely to survive (<5 years)unless stop drinking permanently

22
Q

Management of alcoholic liver disease

A
  • Stop drinking alcohol
  • Diazepam - alcohol withdraw symptoms
  • IV thiamine and vitamines
23
Q

Whos at risk of non alcoholic fatty liver disease

A

Diabetes Type II, Obese, Hypertension, Hypercholesterolemia, smokers, over 50

24
Q

Stages of non alcoholic fatty liver disease

A
  • Linked to obesity
  • Stage 1: fatty liver, asymptomatic can be detected by LFTs
  • Stage 2: NASH (non alcoholic steato Hepatitis)
  • Inflammation and pain
  • Stage 3: Fibrosis
  • Stage 4: Cirrhosis
25
Q

Treatment for NAFLD

A
  • No NICE guidelines
  • Improve diet and excercise
  • Avoid reduce alcohol
26
Q

What is viral hepatitis and its types

A
  • Hepatitis is inflammation of the liver
  • Common ones are A B C
  • Rare are D E
  • A and E normally caused by contaminated food/water,
  • B-D generally caused by contact with infected body fluids/blood products
27
Q

Hepatitis A: transmission, symptoms and treatment

A
  • Transmission:
    faecal-oral route;
    Consumption contaminated food (e.g.shellfish)
    Also: sex (esp anal), sharing of needles
  • Symptoms:
    Initial: nausea, vomiting, diarrhoea, malaise, abdominal discomfort, mild fever
    jaundice, liver enlargement, skin rash/itch and pale stools
    acute, self-limiting (3-6 weeks)
  • no treatment required –avoid alcohol while ill
    Vaccination is available
28
Q

Hepatitis B: transmission and symptoms

A
  • Transmission: needles or sex
  • SYM: similar to hepatitis A, take 1-3 months for syms to appear, blood test required for diagnosis
  • Vaccination
29
Q

Hepatitis C: Cause, symptoms, diagnosis, treatment

A
  • Caused by infected blood and blood products mainly drug users
  • Generally asymptomatic or mild until it develops into liver disease or cirhosis
  • Diagnosis via a blood test
  • Treatment: anti viral drugs that inhibit viral replication
30
Q

Max paracetamol dose for an adult

A
  • 4g in 24hrs
  • Overdose and liver damage can occur with as little as 10-15g!
  • High risk patients could be as low as 5g
31
Q

How long after paracetmol overdose does liver failure occur

A

Severe liver damage after 24 hours- unlikely to be reversible
Liver failure 48-96 hours after overdose

32
Q

Paracetamol toxicity

A
33
Q

Paracetamol toxicity - what is a staggered overdose

A
  • Astaggered overdoseinvolves ingestion of a potentially toxic dose ofparacetamolover more than 1 hour, with the possible intention of causing self-harm
  • The MHRA advises that all patients who have ingested a staggered overdose should be treated withacetylcysteinewithout delay.
34
Q

Paracetamol toxicity - therapeutic excess

A

Therapeutic excessis the ingestion of a potentially toxic dose ofparacetamolwith intent to treat pain or fever and without self-harm intent during its clinical use. All patients should be referred to hospital for medical assessment if they meet certain criteria (e.g if they are symptomatic)

Patients with clinical features of hepatic injury such as jaundice or hepatic tenderness should be treated urgently withacetylcysteine.

35
Q

When prescribing to people with liver disease, what should be taken into account?

A
  • Liver disease seriously affects metabolism and duration of action of drugs
  • Prescribing should be kept to a minimum
  • May need to reduce drug doses/change drugs
36
Q

How can hepatic blood flow be reduced in liver disease

A
  • Bioavailability of drugs in drugs going 1st pass metabolism increased
    Drugs that have high extraction via 1st pass may need to have dose adjusted
    E.g. morphine may require dose 10-50% lower

Portosystemic shunting
Reduced 1st pass metabolism

37
Q

Hypoproteinaemia

A

Low Serum Albumin
Albumin main site of drug binding in plasma
Increased concentrations of free drug
Important for drugs that bind strongly to plasma proteins
E.g. Warfarin, phenytoin
Reduced clotting factors
Increased sensitivity to anticoagulants (e.g. warfarin)

Clinical therapeutics 1 (34 decks)

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