Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

The Patient > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What are some of the causes of liver disease?

A

Alcohol (approx. 50-70% of cirrhosis is alcohol related)
Non-alcoholic fatty liver disease (NAFLD)
Viral hepatitis
Drugs and toxins
Inherited and metabolic disorders (e.g. Wilsons disease)
Immune disease of the liver (e.g. autoimmune hepatitis)
Vascular abnormalities (e.g. Budd-Chiari syndrome)
Cancer
Biliary tract disorders
Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The liver is the _ single organ excluding _.

A

Largest

The skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is the liver supplied with blood?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The liver has a remarkable ability for _.

A

Regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some of the functions of the liver?

A

Metabolism including carbohydrate, protein, fat, steroid hormone, insulin, aldosterone, bilirubin and drugs
Synthesis including proteins, clotting factors, fibrinogen, cholesterol, 25-OH of vitamin D and glucose from fat and protein
Immunological through Kupffer cells
Storage including fat soluble vitamins, A, D, K B12 and folic acid
Homeostasis through glucose control
Production of bile, secretion of bile salts and enterohepatic circulation
Clearance including bilirubin, drugs and toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can we diagnose liver disease?

A

Using liver blood tests (previously called LFT’s but renamed as they don’t exactly reflect the function of the liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do liver blood tests cover?

A 
Bilirubin 
Transaminases 
ALP and γ-GT
Albumin
PT/INR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the usual range for bilirubin?

A

5-20 micromol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is bilirubin?

A

Product of RBC breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does bilirubin reach the liver and what happens once it does?

A

Transported to the liver in the serum attached to albumin

Once in the liver, transformed into a water-soluble conjugate which is then excreted via the bile into the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do raised bilirubin levels suggest?

A

Haemolysis
Hepatocellular damage
Cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What level does a patients bilirubin have to be for them to be clinically jaundice?

A

> 50 micromol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the transaminases relevant to liver blood tests?

A 
Aspartate transferase (AST)
Alanine transferase (ALT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the usual range for AST and ALT?

A

AST 0-40 iu/L

ALT 5-30 iu/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where are AST and ALT found?

A

AST is found in the liver, heart, skeletal muscle, pancreases, kidney and RBC’s
ALT is found primarily in the liver, often termed ‘liver specific enzyme’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do raised AST and ALT levels suggest?

A

Hepatitis (inflammation)
Drugs
Sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Do all patients with liver disease have raised transaminase enzymes?

A

No
Patients with severe liver disease may not have raised levels of transaminases as their cells are so damaged they can no longer produce transaminases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is ALP?

A

Alkaline phosphatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the usual range for ALP?

A

30-120 iu/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where can ALP be found?

A

In the liver, bone, intestine and placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What do raised ALP levels suggest?

A

Cholestasis

Damage to biliary tree

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is γ-GT?

A

γ-Glutamyltransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the usual range for γ-GT?

A

5-55 iu/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where can γ-GT be found?

A

In the liver and biliary epithelial cells, pancreas, kidneys, prostate and intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What do raised γ-GT levels suggest?

A

Cholestasis
Carcinoma of pancreas and GIT
Presence of enzyme inducers such as alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is albumin a marker of?

A

How well the liver is functioning as it is one of the proteins synthesised by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the usual range for albumin?

A

35-50 g/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the half-life of albumin?

A

20-26 days (long)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What do decreased albumin levels suggest?

A

Oedema

Chronic liver disease (albumin has a long half life and so won’t be decreased straight away)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is PT?

A

Prothrombin time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is INR?

A

International Normalised Ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the usual ranges for PT and INR?

A

PT <16 secs

INR <1.2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why are PT and INR indicators of liver function?

A

Because clotting factors are synthesised in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the half-life of prothrombin?

A

2-3 days (short)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What do raised PT/INR levels suggest?

A

Acute and chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

When are liver blood tests considered ‘abnormal’?

A

If the level is 2x the upper limit of what is considered normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What needs to be taken into account when interpreting liver blood tests?

A

They are fairly non-specific
Need to look at trends amongst the results rather than look at them in isolation
Usually at least 2 will be deranged if there is liver dysfunction
Always check reference ranges and units
Blood tests are not always abnormal and similarly abnormal liver blood tests are not necessarily because of liver dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is liver disease classified?

A

According to both the pattern of disease seen and the time course over which the damage occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

When is liver disease considered acute?

A

Onset of symptoms does not exceed 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

When is liver disease considered chronic?

A

Symptoms exceed 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The main patterns of damage can be initially classified as…

A

Cholestatic or hepatocellular
These are not distinct entities, overlap occurs
Both can lead to fibrosis or cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is cholestasis?

A

Elevated levels of substances usually excreted via bile, this leads to symptoms such as jaundice, pruritus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does cholestasis affect?

A

Absorption of fat soluble drugs and vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is cholestasis caused by?

A

Disruption of bile blow e.g. stagnation of bile in bile ducts
Intrahepatic causes such as problems with biliary ductiles caused by primary biliary cholangitis (PBC), drugs, inflammation
Extrahepatic causes such as mechanical obstruction caused by inflammation of bile ducts, strictures or gall stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does cholestasis affect liver blood tests?

A

Increase in bilirubin, ALP, γ-GT (linked to biliary tree)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is hepatocellular damage?

A

Injury to hepatocytes (liver) cells e.g. by toxins, viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What can hepatocellular damage lead to?

A

Steatosis (fat inside or outside liver cells)

Hepatits (inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hepatocellular damage can be…

A

Acute or chronic

Small or widespread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does hepatocellular damage affect liver blood tests?

A

Increase in transaminase enzymes, γ-GT, bilirubin (later)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is fibrosis?

A

Persistent, extensive hepatocyte damage

Active deposition of collagen formation of scar tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is cirrhosis?

A

When erratic regeneration occurs and nodules can form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which comes first, fibrosis or cirrhosis?

A

Fibrosis

53
Q

The spectrum of liver damage is…

A

Not uniform

There are 3 main histological stages, in reality these stages may overlap

54
Q

What are the 2 main routes of alcohol metabolism?

A

Alcohol metabolised (by oxidation) to acetylaldehyde
Acetylaldehyde is then metabolised to acetate by aldehyde dehydrogenase
Acetate is then further metabolised to water, fatty acids and carbon dioxide
The ‘microsomal ethanol oxidising system’ is activated when high quantities of alcohol are taken in, this produces unstable free radicals

55
Q

_ _ will increase metabolism of alcohol and drugs metabolised via this route.

A

NB 2E1 induction

56
Q

What scoring system in cirrhosis?

A

Child’s Pugh Scoring System
Gives you an indication of how severe the patients cirrhosis is and classifies it into 3 classes, A, B and C, dependent on score, with C being the most advanced

57
Q

What are the most common causes of acute liver disease?

A

Viral hepatitis and drugs

58
Q

Does acute liver disease always progress?

A

Not always, but can go on to acute liver failure or chronic liver disease

59
Q

What is meant by the term ‘compensated’?

A

Enough hepatocyte capacity to perform functions

60
Q

What is meant by the term ‘decompensated’?

A

Do not have enough capacity to perform required liver functions

61
Q

What are the most common causes of chronic liver disease?

A

Alcohol and chronic viral hepatitis

62
Q

How can we manage chronic liver disease?

A

Treat the underlying condition where possible
Treat symptoms and complications
Surveillance for hepatocellular carcinoma (HCC)
Transplant may be the only option for some patients

63
Q

Where are complications most commonly seen?

A

In chronic liver disease

64
Q

How does complication management vary based on the cause of liver disease?

A

Management of complications remains the same regardless of the cause of liver disease

65
Q

Do all patients with liver disease have symptoms?

A

No, many patients will be asymptomatic

Can be a long time interval between disease occurrence and detection as a result

66
Q

What are some of the initial, unspecific symptoms of liver disease?

A

Fatigue
General malaise
Fever
N&V

67
Q

What are some of the later, more specific symptoms of liver disease?

A 
Jaundice 
Pale stools
Dark urine
Pruritus 
Spider naevi 
Bruising and bleeding 
Gynaecomastia 
Liver palms 
Finger clubbing 
Ascites 
Varices 
Encephalopathy 
(Last 3 generally seen in end stage liver disease)
68
Q

What is jaundice caused by?

A

High levels of bilirubin

69
Q

What do pale stools indicate?

A

Biliary obstruction
Usually bile is excreted into the intestine where it is converted to the faecal pigment stercobilin
If there is obstruction, bile excretion is reduced, and so less pigment is produced

70
Q

What does dark urine indicate?

A

Obstruction
Water soluble conjugated bilirubin can’t be excreted in faces and therefore body compensates by increasing renal excretion

71
Q

What are ‘spider naevi’?

A

Vascular changes

72
Q

What is gynaecomastia?

A

Enlargement of the male breast tissue

73
Q

What does gynaecomastia indicate?

A

Impaired metabolic function

Increased levels of oestrogen as reduced oestrogen degradation in chronic liver disease

74
Q

What is gynaecomastia also a side effect of?

A

Spironolactone

Inhibition of testosterone production

75
Q

What is ascites?

A

Presence of excess fluid in the peritoneal cavity leading to a swollen abdomen

76
Q

What does ascites cause?

A

An excess of sodium in the body

77
Q

How can ascites be treated?

A

Restrict fluid/sodium intake
Diuretics e.g. spironolactone, furosemide
Paracentesis for large volumes (involves inserting a drain and draining off ~8-10L of liquid)

78
Q

Why is spironolactone 1st line for diuretics in the liver patients?

A

It is an aldosterone antagonist and liver patients will have higher levels of aldosterone

79
Q

How should patients suffering from ascites be monitored?

A

Weight (aim for 0.5-1kg weight loss/day)

Daily U&E’s especially Na, K, Cr (you’re using high doses of diuretics, electrolytes will be affected)

80
Q

What is spontaneous bacterial peritonitis?

A

Infection of the ascitic fluid without intra-abdominal source of sepsis
A frequent complication of ascites

81
Q

How is spontaneous bacterial peritonitis diagnosed?

A

Neutrophil count >250 cells per mm3

82
Q

How is spontaneous bacterial peritonitis treated?

A

With a broad spectrum IV antibiotic e.g. 3rd generation cephalosporins, co-amoxiclav, tazocin

83
Q

What can be given for spontaneous bacterial peritonitis prophylaxis?

A

Norfloxacin

Ciprofloxacin

84
Q

What is hepatic encephalopathy?

A

Neuropsychiatric changes including changes in mood and behaviour, confusion, delirium and coma
4 different grades dependent on clinical signs

85
Q

What causes hepatic encephalopathy?

A

Accumulation of toxins especially ammonia (this is why a lot of treatments are targeting at reducing ammonia levels)

86
Q

What are some precipitants of hepatic encephalopathy?

A 
Increased protein load
Accumulation of ammonia 
Electrolyte disturbance
Drugs 
Infection
87
Q

Symptoms of hepatic encephalopathy are similar to?

A

Hypoglycaemia

Alcohol intoxication or withdrawal

88
Q

How is hepatic encephalopathy treated?

A

Want to avoid precipitants and reduce ammonia levels
Laxatives are the mainstay of treatment (aim for 2-3 soft stools per day) e.g. lactulose liquid, phosphate enema
Antibiotics e.g. Rifaxamin
L-ornithine L-aspartate sachets

89
Q

Why is Rifaxamin used in hepatic encephalopathy treatment?

A

It has low systemic absorption meaning high levels in faeces, it kills gut bacteria to reduce amino levels (gut bacteria produce ammonia)

90
Q

Why is L-ornithine L-aspartate used in hepatic encephalopathy treatment?

A

Part of the urea cycle

Increases removal of ammonia

91
Q

What is portal hypertension and what is it caused by?

A

An increase in pressure in the portal vein
This is caused by increased resistance to flow due to,
Disruption of hepatic architecture
Compression of hepatic venules by regenerating nodules

92
Q

How does the body respond to portal hypertension?

A

Forms collateral vessels, enables blood to bypass the liver
Works temporarily, but eventually as the liver condition worsens, and pressure rises, these weak blood vessels burst and bleed out (bleeding varices)

93
Q

How can portal hypertension/ bleeding varices be treated?

A

Resuscitation with fluids and blood transfusion
Endoscopy to perform banding (putting tiny elastic bands on vessels) or sclerotherapy (glueing the collateral vessels)
Terlipressin can be used as a temporary fix, a potent vasoconstrictor (reduces pressure around the liver)
Antibiotics as infection is common in liver patients, IV broad spectrum
PPI

94
Q

What can be given as secondary prophylaxis for portal hypertension/ bleeding varices?

A

Propanolol tablets 20-40mg BD
A non-selective beta blocker
Works in GI system to lower pressure around the liver
Low doses given as propranolol is extensively first pass metabolised and this will not happen as effectively

95
Q

What causes pruritus?

A

Accumulation of bile salts under the skin as they are not excreted

96
Q

How can pruritus be treated?

A

Colestyramine (binds bile acids and prevents reabsorption, anion-exchange resin)
Ursodeoxycholic acid (works on how bile acids are broken down)
Antihistamines e.g. chlorpheniramine
Topical treatments e.g calamine lotion
Ondansetron, Rifampicin, Naltrexone, Naloxone (not usually associated with treating itching but have been found to help in some patients)

97
Q

What are some of the symptoms of alcohol withdrawal?

A 
Delirium
Marked terror 
Fear and delusions
Restlessness and agitation
Fever
Rapid pulse
Dehydration 
Seizures
98
Q

How are symptoms of alcohol withdrawal treated?

A

Treated with a combination of sedatives and vitamin supplementation e.g. Chlordiazepoxide and Pabrinex IV or oral vitamin B co strong and thiamine

99
Q

Why is Chlordiazepoxide used in the treatment of alcohol withdrawal?

A 
Sedative and anti-convulsant properties 
Long half-life (5-30 hours)
Extensively protein bound (96%)
Low potency 
Slower onset of action (less abuse potential)
Long acting
100
Q

How should Chlordiazepoxide be prescribed?

A

With an oral reducing regimen and given as needed by patient in a detoxification regimen

101
Q

Why do people experiencing alcohol withdrawal need vitamin supplementation?

A

To treat a potential thiamine deficiency
Thiamine deficiency can cause Wernicke’s encephalopathy (irreversible)
Alcohol prevents thiamine absorption (causes malabsorption in the intestine mucosa)
Alcoholics are also often vitamin deficient due to a poor diet (high in carbohydrate, low in protein, vitamins and minerals)

102
Q

Viral hepatitis can be…

A

Acute or chronic

103
Q

Viral hepatitis is caused by…

A

Hepatitis A, B, C, D or E virus

104
Q

What is the commonest form of infective hepatitis?

A

Hepatitis A

105
Q

How is hepatitis A transmitted?

A

Primarily enterically transmitted (faecal-oral route)

106
Q

Is hepatitis A serious and how does it progress?

A

Usually mild and does not progress to chronic liver disease or carrier status

107
Q

For which types of viral hepatitis is there a vaccine?

A

A, B

108
Q

What is the structure of the hepatitis B virus and how does it infect cells?

A

An enveloped DNA virus (hepadnavirus)

Incorporates itself into cells making it difficult to treat (very similar to HIV)

109
Q

Is hepatitis B contagious?

A

Highly

Present in blood, saliva, urine, semen and vaginal fluids

110
Q

How is hepatitis B treated?

A

Clinical course is dependent on age of infection but it is usually difficult to eradicate and treatment revolves around trying to reduce levels
Also depends on age, extent of liver damage, virology and HBV DNA level
Oral antivirals e.g. Entecavir or Tenofovir are used (this is often long term for the majority of patients)
Pegylated interferon

111
Q

What is the leading cause of hepatocellular carcinoma (HCC)?

A

Hepatitis B

112
Q

What is hepatitis D also known as?

A

Delta virus

113
Q

Hepatitis D can only replicate in the presence of…

A

Hepatitis B virus

114
Q

What is the relationship between hepatitis D and B?

A

Acquired in the same way
Can get HDV at the same time as HBV (co-infection) or at a later date (superinfection)
Combination of the two increases the risk of progression to chronic hepatitis and cirrhosis
Treatments for HDV very similar to HBV

115
Q

Hepatitis E has a similar clinical course to which other hepatitis virus?

A

HAV

116
Q

How is hepatitis E transmitted?

A

Faecal-oral route

117
Q

Is hepatitis E serious and how does it progress?

A

Usually mild and does not progress to chronic liver disease or carrier status

118
Q

What is the structure of the hepatitis C virus?

A

Single stranded RNA virus of the Flavivirdae family (means it can be eradicated?

119
Q

Hepatitis C is a…

A

Blood borne virus

120
Q

How many major genotypes of hepatitis C have been identified?

A

6

121
Q

How is hepatitis C diagnosed?

A

Testing for hepatitis C antibodies, HCV RNA and genotype

Majority of those infected are undiagnosed as it is largely asymptomatic

122
Q

Hepatitis is C is known as the…

A

‘Silent killer’, a slow progressive disease

123
Q

Is hepatitis C curable?

A

Yes

124
Q

How is hepatitis C treatment selected?

A

Finite courses

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

125
Q

WHO aims to?

A

Eliminate HCV as a public health threat by 2030

126
Q

In drug induced liver disease, does discontinuation of the drug result in resolution?

A

Generally, yes but not always the case

127
Q

What is an intrinsic reaction (type A)?

A

Predictable
Reproducible
Would happen to everybody
Dose dependent
Tend to occur rapidly e.g. within hours
Tend to have necrosis, acute liver failure
An example of intrinsic/type A reaction is a paracetamol overdose

128
Q

What is an idiosyncratic reaction (type B)?

A

Tends to be the vast majority of drugs
Not predictable
Not reproducible
Not dose dependent
Take longer to occur e.g. weeks to months
Can result from metabolism idiosyncrasy or immunoallergic reaction
Can cause any type of liver injury e.g. increased LFT’s, jaundice, fever, rash, eosinophilia
An example of an idiosyncratic/type B reaction is warfarin causing cholestasis

129
Q

What is the role of the pharmacist in liver disease?

A

Ensure regular monitoring of LFT’s
Ensure patients and prescribers are aware of side-effects and warning signs
Take a full drug history including herbal, OTC
Be aware of drugs commonly implicated and how to manage this
Advise on management including supportive therapy

The Patient (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions