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The Patient 20300 > Liver disease > Flashcards

Liver disease Flashcards

1
Q

How serious is the problem of liver disease in the UK.

How many cases are preventable

A

Liver disease is a major, under-recognised cause of preventable morbidity and mortality in the UK

It is the fifth largest cause of premature death in the UK

Only common chronic condition with an increasing death rate

More than 90% of liver disease is preventable

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2
Q

What are the 3 main causes of liver disease

A

Alcohol

Non-alcoholic fatty liver disease (NAFLD)

Viral hepatitis

Account for over 3/4 cases

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3
Q

Give some less comon causes of liver disease

A

Drugs and toxins

Inherited and metabolic disorders
Wilson disease
Glycogen storage disease

Immune disease of the liver

Autoimmune hepatitis
Primary Biliary
Cholangitis (PBC)
Primary Sclerosing Cholangitis (PSC)

Vascular abnormalities
Budd-Chiari syndrome
Veno-occlusive disease (VOD)

Cancer

Biliary tract disorders

Other Infections

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4
Q

Which blood supplies provide the liver with blood

A

Has 2 blood supplies:
Arterial blood – 20% hepatic artery
Venous blood - 80% portal vein

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5
Q

true/false - the liver is the largest single organ and can regenerate itself

A

true

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6
Q

What substances does the liver metabolise

A 
Carbohydrate
Protein
Fat
Steroid hormone
Insulin
Aldosterone
Bilirubin
Drugs!!
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7
Q

What substances does the liver synthesise

A

Proteins
Clotting factors
Fibrinogen
Cholesterol
25-OH of vitamin D
Glucose from fat and protein

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8
Q

What other roles does the liver fulfil (other than synthesis and metabolism)

A 
Production of bile
clearance
homeastasis
stroage
immunological function
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9
Q

Why do we test bilirubin levels to help diagnose liver disease

A

Bilirubin is a product of red blood cell breakdown

Transported to the liver in the serum attached to albumin

Transformed into a water-soluble conjugate which is excreted via the bile into the intestine

Levels increased:
Haemolysis
Hepatocellular damage
Cholestasis

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10
Q

What is jaundice

A

An accumulation of bilirubin which causes skin discolouration

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11
Q

Why do we test for transaminases

A

They are enzymes fund in liver cells. When liver cells break down (as they’re damaged) these enzymes are released
Levels are increased in hepatitis, drugs, sepsis

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12
Q

Where do we find Aspartate transferase and Alanine transferase respectively

A

Aspartate transferase - AST (0-40 iu/L)
Found in liver, heart, skeletal muscle, pancreas, kidney and RBC

Alanine transferase - ALT (5-30 iu/L)
Often termed ‘Liver specific enzyme’

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13
Q

All patients with liver disease will have raised transaminase enzymes – true or false?

A

False, in some cases of severe liver disease there wont be raised transaminase levels as the liver cells are simply too damaged to produce them any more

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14
Q

Where are the alp and ggt enzymes found and what does increased levels of them in the blood show

A

Alkaline Phosphatase – ALP
Usual range 30-120 iu/L
Found in liver, bone, intestine and placenta
Level is increased in cholestasis, damage to biliary tree (bile ducts)

γ-Glutamyltransferase – GGT
Usual range 5-55 iu/L
Found in liver and biliary epithelial cells, pancreas, kidneys, prostate, intestine
Level is increased by enzyme inducers including alcohol, cholestasis, carcinoma of pancreas & GIT

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15
Q

What does a decrease in albumin levels show

A

Decreased level – oedema

Decreased in chronic liver disease - long half life so the problem is chronic

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16
Q

Whyis it often helpful to look at the prothrombin time and international normalised ratio

A 
Prothrombin time (PT) is a blood test that measures how long it takes blood to clot
The international normalised ratio (INR) is a laboratory measurement of how long it takes blood to form a clot. Calculated using prothrombin time

Clotting factors are produced (synthesised) by the liver and have a short half-life (2-3 days).

Fewer clotting factors are produced so the PT/INR are ↑ in acute and chronic liver disease (the blood is thinner)

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17
Q

Is there a single test which demonstrates

A

No - Usually at least two will be deranged if liver dysfunction
Trends not isolation

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18
Q

Which criteria do we use to classify liver disease

A

Classified according to both the pattern of damage seen and time course over which damage occurs

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19
Q

What are the names of the two patterns of liver damage and what can they lead to

A

The main patterns of damage can be initially classified as cholestatic or hepatocellular

These are not distinct entities – overlap occurs (most patientd have a combination of both)

Both of these can lead to fibrosis and cirrhosis

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20
Q

Define cholestasis damage

A

Cholestasis
Disruption of bile flow – stagnation of bile in bile ducts
They may be narrowed or damaged

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21
Q

Define hepatocellular damage

A

Hepatocellular
Injury to hepatocytes
Fatty infiltration – steatosis
Inflammation – hepatitis

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22
Q

What is fibrosis and cirrhosis

A

Persistent, extensive hepatocyte damage - active deposition of collagen formation of scar tissue – fibrosis

Disruption of blood flow

Erratic regeneration and nodules can form - cirrhosis

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23
Q

What is the usual cause of acute liver disease

Acute – history of onset of symptoms does not exceed 6 months

A

Most common causes – viral hepatitis and drugs

Acute hepatitis – usually self-limiting with spontaneous recovery

Can go on to acute liver failure or chronic liver disease

24
Q

What is the usual cause of chronic liver disease

A

Progressive and permanent structural

Compensated – the patient still has enough hepatocyte capacity to perform basic functions

Decompensated – do not have enough capacity to perform required liver functions

Commonest causes – alcohol and chronic viral hepatitis

25
Q

What is the childs pugh scoring system used for

A

A scoring system used to asses the severity of liver disease (cirrhosis)

Is used to determine how severe the disease is and how to treat the patient

The tests used to calculate it are the bilirubin, albumin and inr levels

26
Q

What are the general signs and symptoms of liver disease

A

Many patients will be asymptomatic

Can be long time interval between disease occurrence and detection

Initial symptoms may be unspecific:
Fatigue
General malaise
Fever
Nausea and vomiting
27
Q

What are some specific symptoms of liver disease

A

Jaundice – high levels of bilirubin

Pale stools – indicate biliary obstruction. Usually bile excreted into intestine where converted to faecal pigment stercobilin. If obstruction, bile excretion reduced, less pigment produced

Dark urine – obstruction, water soluble conjugated bilirubin can’t be excreted in faeces and therefore body compensates by increasing renal excretion

Pruritus- accumulation of bile salts under skin as not excreted

Spider naevi – vascular changes (accumulation of oestrogen)

Gynaecomastia – enlargement male breast tissue. Due to increased levels of oestrogen (reduced oestrogen degradation in CLD). Suggests impaired metabolic function. Can also get as side-effect of spironolactone (inhibition of testosterone production)

Ascites – presence of excess fluid in peritoneal cavity, leading to swollen abdomen

Varices – abnormally dilated collateral vessels due to increased portal vein pressure (portal hypertension)

Encephalopathy – spectrum of reversible neuropsychiatric changes

Bruising and bleeding (fewer clotting factors)

Liver palms - red hands

Finger clubbing

28
Q

Name 3 complications of liver disease (as a consiquence of cirrosis)

A

Ascites
Encephalopathy
Varices and portal hypertension

29
Q

What is ascites

A

Accumulation of fluid in the peritoneal cavity leading to swollen (or expanded) abdomen – “abdominal distension”

Abdominal distension occurs when substances, such as air (gas) or fluid, accumulate in the abdomen causing its expansion

May also have abdominal (stomach) pain

30
Q

How do we treat ascites (which 2 drugs, why we use these drugs and how we monitor their action)

A

Diuretics
Spironolactone (aldosterone antagonist)
Furosemide (loop diuretic)

Rationale
Diuresis - induces negative fluid balance and reduction in the amount of ascites (free fluid in the abdomen)
Spironolactone (first line) is useful as it is an aldosterone antagonist and liver pts have high circulating levels of aldosterone (because they cant break it down)

Monitor
Daily weight – 0.5 - 1kg/day weight loss

Renal function, urea and electrolytes – especially sodium, potassium and creatinine

31
Q

What non - drug based therapies do we use to treat ascites

A

Fluid/Sodium restriction. Too much salt = water retention

Paracentesis (drain the fluid) for large volume ascites

32
Q

What is Spontaneous Bacterial Peritonitis and how do we diagnose it

A

Spontaneous Bacterial Peritonitis (SBP) is an infection of the ascitic fluid without intra-abdominal source of sepsis (frequent complication)

Patient may have severe pain, raised temperature and raised white-cell count

Diagnosis – take a sample of ascitic fluid. SBP diagnosed if the neutrophil count > 250 cells per mm3 (raised inflammatory markers)

Mortality rate is approx. 40%

33
Q

How do we treat spontaneous bacterial peritonitis

A

SBP can be caused by gram-positive (or gram-negative) bacteria

Common causative organisms include E. coli and Streptococcus

Initially treat with a broad spectrum intravenous (IV as its such a serious infection) antibiotic e.g.
3rd generation cephalosporins such as ceftazidime 2 grams IV three times a day
Piperacillin with tazobactam 4.5 grams IV three times a day

Treatment for 5 days and review

Norfloxacin/Ciprofloxacin as prophylaxis if the infection is recurrent

34
Q

What is Hepatic Encephalopathy (as a complication of liver disease)

A

Neuropsychiatric changes inc changes in mood & behaviour, confusion, delirium and coma

4 clinical grades dependent on clinical signs

Several theories - accumulation of toxins esp. ammonia crossing into the brain

Precipitants include ↑ protein load, accumulation of ammonia, electrolyte disturbance, drugs, infection

Symptoms similar to hypoglycaemia, alcohol intoxication or withdrawal

35
Q

How do we treat Hepatic Encephalopathy using non - antibiotic methods

A

Strategies aimed at avoiding precipitants + reducing ammonia levels

Laxatives
Lactulose liquid 20-30mls twice to three times a day
Phosphate enema – once or twice daily

Rationale
Inhibits intestinal ammonia production by a number of mechanisms including changing the pH of the gut lumen (reduces absorption of ammonia in to blood stream and also favours growth of non-ammonia producing bacteria) and reducing colonic bacterial load

Monitoring
Aim 2-3 soft stools per day

36
Q

Which antibiotics are used for Hepatic Encephalopathy

A

Antibiotics

Rifaxamin tablets 550mg twice daily
Rationale
low systemic absorption, high levels in faeces. This antibiotic kills gut bacteria to reduce ammonia levels (gut bacteria produce ammonia)

L-ornithine L-aspartate sachets (LOLA) (unlicensed)
Rationale
Increases removal ammonia - naturally occurning amino acids

Dietary protein restriction not recommended

37
Q

What causes portal hypertension and varices

A

Portal hypertension is caused by increased resistance to flow due to:
disruption of hepatic architecture
compression of hepatic venules by regenerating nodules

Collateral vessels form – enable blood to bypass the liver and reduce the pressure on the main vessels. However, they are very weak and liable to burst

38
Q

Which diagnostic tools and treatments do we use in an emergency for portal hypertension and varices

A

Resuscitation – fluids, blood transfusion

Endoscopy – banding, schlerotherapy (glue)

Terlipressin IV 1-2mg bolus then every 4-6 hours
Potent vasoconstriction

Antibiotics – infection is common. IV broad spectrum antibiotic for at least 5 days

Proton-pump inhibitor (PPI) - protects the stomach

39
Q

The likelihood of a second bleed after the fist incidance of portal hypertension and varices is high. Which drugs can we use to lower this risk

A

Propranolol tablets 20-40mg twice daily - reduces the blood pressure around the liver

Non-selective beta-blocker - for areas found outside the heart

Splanchnic vasoconstriction (beta2 blockade)

Cardiac output results in reduced portal pressures (beta1 blockade)

40
Q

How do we treat pruritis in liver disease caused by the build up of bile salts

A

Treatment options include:
Colestyramine (anion-exchange resin) - binds bile acids and prevents reabsorption

Ursodeoxycholic acid (UCDA)
Antihistamines - Chlorpheniramine, Hydroxyzine (sedating), Loratadine, cetirizine (non-sedating
Topical - Calamine lotion,

(Menthol 2% in Aq cream
Ondansetron
Rifampicin
Naltrexone, Naloxone)

41
Q

How common is alcohol related liver disease in the uk

A

Most common cause of liver disease in UK

Increasing incidence in people under 30 and in females

North West of England has one of the highest incidences in the UK

42
Q

What is the reccomended maximum levels of alcohol per week

A

Recommended not to drink more than 14 units/week

nb - Not everyone who drinks excessively will develop liver damage

43
Q

How does alcohol affect the liver

A

Spectrum of liver damage is not uniform. 3 main histological stages, in reality these stages may overlap.

44
Q

How do we metabolise alcohol

A

2 main routes alcohol metabolism:

  1. Alcohol metabolised (oxidation) to acetylaldehyde. Acetylaldehyde metabolised acetate by aldehyde dehydrogenase. Further metabolised to water, fatty acids and CO2.
  2. Activated when higher quantities alcohol intake – microsomal ethanol oxidizing system. Produces unstable free radicals

NB 2E1 induction will increase metabolism of alcohol and drugs metabolised via this route

45
Q

How do we manage alcohol withdrawal in hospital (and why do we do it)

A

Treatment of acute alcohol withdrawal is with a combination sedatives and vitamin supplementation – Chlordiazepoxide + Pabrinex IV or oral vitamin B co strong and thiamine

Withdrawal symptoms can range from mild – severe (delirium tremens)
Delirium, marked tremor
Fear and delusions, restlessness and agitation
Fever
Rapid pulse
Dehydration
Seizures

46
Q

How do benzodiazepines work to treat alcohol withdrawal (and which one is commonly used)

A

Main drug used - Chlordiazepoxide because it has a long half-life and slower onset action – less abuse potential. It also has a low potency

Rationale
Chlordiazepoxide
prevents withdrawal symptoms such as agitation and alcohol withdrawal seizures (sedative and anti-convulsant properties)

Mechansim
Benzodiazepines are cross-tolerant with alcohol and modulate anxiolysis by stimulating GABA-A receptors. During withdrawal from one agent, the other may serve as a substitute

47
Q

Why do we use a detoxification regime for patients on benzodiazapines

A

We prescribe oral reducing regimen + as required dosing – known as detoxification regime which helps to reduce the dose over 5 days to manage their symptoms

48
Q

Which vitamins are provided to patients who are coming off alcohol and why do we use them

A

Pabrinex given intravenously (IV) – 1-3 pairs twice – three times a day
Thiamine and vitamin B co-strong orally

Indication
Treat potential thiamine deficiency
Prevent development Wernicke’s encephalopathy (complication of alcohol withdrawal - confusion)

Rationale
Likely to be vitamin deficient:
Poor diet (high in carbohydrate, low in protein, vitamins and minerals) 
Alcohol prevents thiamine absorption - causes malabsorption in the intestinal mucosa
49
Q

What is viral hepatitis

A

Viral infections that specifically target the liver

Theres at least five viruses that cause hepatitis (liver inflammation) without significant damage to other organs
Acute hepatitis or chronic hepatitis

50
Q

How is hepA transmitted and what is the prognosis of a patient who has it

A

Hepatitis A (HAV)
Commonest form infective hepatitis
Primarily enterically transmitted - faecal-oral route
Often mild
Doesn’t progress to chronic liver disease or carrier status

51
Q

What is HEPB and what is the prognosis of a patient who has it

A

Enveloped DNA virus (hepadnavirus) so is very difficult to eradicate.
Number of subtypes (genotypes)

Highly contagious - present in blood, saliva, urine, semen, vaginal fluids

Clinical course – dependent on age of infection

Progression of HBV – child doesn’t usually show signs of disease but most will go on to develop chronic infection with a sig proportion then going on to develop cirrhosis
Adult – show some signs of infection – increase transaminase and jaundice. Self-limiting for most but small proportion adults will get chronic infection

Treatment dependent on number of factors including age, extent of liver damage, virology and HBV DNA level

52
Q

How do we treat chronic hepB

A

Chronic Hepatitis B Treatment

Oral antivirals – entecavir or tenofovir

Pegylated Interferon for some patients (short course)

Aiming for “functional cure” - virus level isnt replicating and causing further liver damage. Eradication is almost impossible

Treatment with oral antivirals is long-term for majority of patients

Treatment supported by NICE guidelines

Vaccination is available

53
Q

What is HEPD and how is it related to hepB

A

Also known as delta virus

Can only replicate in presence of Hepatitis B virus

Can get HDV at same time as HBV (co-infection) or at a later date (superinfection)

Acquired in same way

Combination of HBV and HDV increase risk of progression to chronic hepatitis and cirrhosis

54
Q

Is HEPE as severe as HEPB

A

No - Similar clinical course to HAV
Enterically transmitted - faecal-oral route
Often mild
Doesn’t progress to chronic liver disease or carrier status

55
Q

What type of virus is HEPC, how do we diagnose it and is it curable

A

Single stranded RNA virus - Flaviviridae family

Blood-borne virus

Six major genotypes identified (1-6)

Diagnosis – include testing for Hepatitis C antibodies, HCV RNA and genotype

Majority of those infected are undiagnosed – asymptomatic

Slow (20 year infection!), progressive disease – “silent killer”

Hepatitis C is curable (aim of treatment is eradication)

56
Q

What are the aims of the treatments of HEPC

A

A sustained virological response (SVR) – viral eradication

Number of different treatments available –8-12wk courses

Choice and duration dependent on genotype, extent of liver damage and treatment history

WHO target – eliminate HCV as public health threat by 2030

The Patient 20300 (24 decks)

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