LIVER&FRIENDS Flashcards
1
Q
Give 4 functions of the liver.
A
- Glucose and fat metabolism.
- Detoxification and excretion.
- Protein synthesis e.g. albumin, clotting factors.
- Defence against infection.
2
Q
What happens if the liver stops producing albumin?
A
Hypoalbuminaemia -> oedema -> ascites
3
Q
What happens if the liver stops regulating bilirubin?
A
Jaundice, pruritus, light stools & dark urine
4
Q
Give examples of 4 acute liver conditions
A
- Hep A + Hep E
- Drug induced liver injury
- Drug overdose
- Infectious - amoebic liver abscess
5
Q
Name 3 things that liver function tests measure.
A
- Serum bilirubin.
- Serum albumin.
- Pro-thrombin time.
6
Q
Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease).
A
Alkaline phosphatase.
7
Q
What enzymes increase in the serum in hepatocellular liver disease?
A
Transaminases e.g. AST and ALT.
8
Q
Name two hepatocellular enzymes.
A
Alanine transaminase (ALT) Aspartate transaminase (AST)
9
Q
Name a cholestatic enzyme.
A
Alkaline phosphatase
10
Q
Give 4 causes of hepatitis.
A
- Viral e.g. A, B, C, D, E.
- Drug induced.
- Alcohol induced.
- Autoimmune.
11
Q
Give 2 possible outcomes of chronic liver disease.
A
- Cirrhosis.
2. Liver failure.
12
Q
Give 5 causes of chronic liver disease.
A
- ALCOHOL
- NAFLD.
- Viral hepatitis (B, C, E).
- Autoimmune diseases.
- Metabolic e.g. haemochromatosis.
- Vascular e.g. Budd-Chiari.
13
Q
What is Budd-Chiari syndrome?
A
A vascular disease associated with occlusion of hepatic veins that drain the liver.
14
Q
Give 5 signs of chronic liver disease.
A
- Ascites.
- Oedema.
- Malaise.
- Anorexia.
- Bruising.
- Itching.
- Clubbing.
- Palmar erythema.
- Spider naevi.
15
Q
Drug induced liver injury is common. What question should you remember to ask in a patient history?
A
Have you started taking any new medication recently?
16
Q
Name a drug that can cause drug induced liver injury.
A
- Co-amoxiclav.
- Flucloxacillin.
- Erythromyocin.
- TB drugs.
17
Q
What enzyme is responsible for ‘mopping up’ reactive intermediates of paracetamol and so prevents toxicity and liver failure?
A
Glutathione transferase.
18
Q
What are the potential consequences of hepatocyte regeneration in someone with liver cirrhosis?
A
Neoplasia and therefore HCC. Hepatocyte regeneration is liable to errors.
19
Q
What blood test might show that someone has alcoholic liver disease?
A
Serum GGT (gamma-glutamyl transferase) will be elevated.
20
Q
What are the stages of alcoholic liver disease?
A
- Fatty liver
- Alcoholic hepatitis
- Cirrhosis
- Liver failure
21
Q
What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?
A
Mallory bodies
22
Q
What is the pathophysiology of alcoholic liver disease?
A
- Ethanol metabolised in liver by 2 pathways – resulting in an increase in the NADH/NAD ratio.
- Less oxidation of fat -> accumulation of fat in hepatocytes
- Increased ROS damages hepatocytes
- Acetaldehyde damages liver cell membranes
23
Q
What feature seen on liver biopsy is diagnostic of cirrhosis?
A
Nodular regeneration
24
Q
Name the 2 main pathophysiological factors that contribute to the formation of ascites.
A
- High portal venous pressure.
2. Low serum albumin.
25
What type of anaemia do you associate with alcoholic liver disease?
Macrocytic anaemia
26
What is the management for ALD?
1. QUIT ALCOHOL
| 2. thiamine/diazepam to help with withdrawal and malnutrition
27
What are the 3 common metabolic causes of liver failure?
1. Wilsons disease
2. Haemochromatosis
3. alpha 1 anti trypsin deficiency
28
Give 3 causes of iron overload.
1. Genetic disorders e.g. haemochromatosis.
2. Multiple blood transfusions.
3. Haemolysis.
4. Alcoholic liver disease.
29
Haemochromatosis is a genetic disorder. How is it inherited?
Autosomal recessive inheritance.
30
Describe the pathophysiology of haemochromatosis.
Uncontrolled intestinal iron absorption leads to deposition in the liver, heart and pancreas -> fibrosis -> organ failure.
31
How might you diagnose someone with haemochromatosis?
1. Raised ferritin.
2. HFE genotyping.
3. Liver biopsy
32
What is a distinctive presenting feature of haemochromatosis?
Arthralgia from pseudogout
33
What are 2 complications of haemochromatosis?
1. cardiomyopathy
| 2. bronze diabetes
34
How would you manage haemochromatosis?
Desferrioxamine to remove excess iron
35
What is Wilsons disease?
An autosomal recessive disorder which leads to excess copper deposition in liver and CNS
36
What are the key features of Wilsons disease?
1. Kayser-Fleischer rings
| 2. Neurological signs due to copper in CNS
37
What investigation would you carry out in order to confirm the presence of Wilsons disease?
Serum caeruloplasmin
38
How would you manage Wilsons disease?
1. Penicillamine to excrete copper
| 2. Reduce copper intake
39
Describe the mechanism by which alpha 1 anti-trypsin deficiency can lead to chronic liver disease.
Alpha 1 anti-trypsin deficiency results in protein retention in the liver -> eventually cirrhosis.
40
How would you investigate and manage alpha 1 trypsin deficiency?
Investigate: Serum alpha-1-antitrypsin
Mx:
1. Manage COPD
2. Liver transplant is a cure
41
When would you see raised ALP? (alkaline phosphatase)
Anything to do with biliary tree damage
| Note: also raised in bone resorption eg mets
42
When would you see raised AST/ALT? (Aspartate transaminase/ alanine aminotransferase)
Raised in liver damage
43
How long does hepatitis persist for to be deemed chronic?
6 months
44
Give 3 infective causes of acute hepatitis.
1. Hepatitis A to E infection.
2. EBV.
3. CMV.
4. Toxoplasmosis.
45
Give 3 non-infective causes of acute and chronic hepatitis.
1. Alcohol.
2. Drugs.
3. Toxins.
4. Autoimmune.
46
Give 3 symptoms of acute hepatitis.
1. General malaise.
2. Myalgia.
3. GI upset.
4. Abdominal pain.
5. Raised AST, ALT.
6. +/- jaundice.
47
Give 3 infective causes of chronic hepatitis.
1. Hepatitis B (+/-D).
2. Hepatits C.
3. Hepatitis E.
48
What are the potential complications of chronic hepatitis?
Uncontrolled inflammation -> fibrosis -> cirrhosis -> HCC.
49
Which hepatitis viruses are made up of RNA?
Hepatitis A, C, D, E (Hep B is DNA)
50
Which forms of hepatitis are transmitted faeco-orally?
Hep A (abroad) + Hep E (England)
51
Which forms of hepatitis have readily available vaccines ?
Hep A and B
52
How do you treat Hep A and Hep E?
1. Supportively
2. Monitor liver function
3. Manage close contacts
(they are self - limiting)
53
Describe two treatment options for chronic HBV infection.
1. Alpha interferon (Pegylated interferon-α 2a = pegasys (stimulates immune response)
2. Antivirals e.g. tenofovir. They inhibit viral replications.
54
How do you treat Hep C?
Antiviral: Velpatasvir/sofosbuvir
55
How do you detect viral hepatitis?
Viral serology - anti Hep * IgM then IgG
56
What is primary biliary cirrhosis?
An autoimmune disease where there is progressive lymphocyte mediated destruction of intra-hepatic bile ducts -> cholestasis -> cirrhosis.
57
Describe 2 features of the epidemiology of primary biliary cirrhosis.
1. Females affected more than men.
| 2. Familial - 10 fold risk increase.
58
Give 3 diseases associated with primary biliary cirrhosis.
1. Thyroiditis.
2. RA.
3. Coeliac disease.
4. Lung disease.
(Other autoimmune diseases).
59
Which immunoglobulins are raised in AIH/PBC/PSC?
```
AIH = IgG
PBC = IgM
PSC = variable
```
60
Give 5 symptoms of primary biliary cirrhosis.
1. Itching.
2. FATIGUE.
3. Dry eyes,
4. Joint pains.
5. Variceal bleeding.
61
What is the treatment for primary biliary cirrhosis?
Ursodeoxycholic acid;
| improves liver enzymes; reduces inflammation and portal pressure and therefore the rate of variceal development.
62
What is ascending cholangitis?
Obstruction of biliary tract causing bacterial infection. Regarded as a medical emergency.
63
Name the triad that describes 3 common symptoms of ascending cholangitis.
Charcot's triad:
1. Fever.
2. RUQ pain.
3. JAUNDICE (cholestatic)!
64
What investigations might you do in someone who you suspect might have ascending cholangitis?
1. Ultrasound.
2. Blood tests - LFT's.
3. ERCP - definitive investigation.
65
Describe the management of ascending cholangitis.
- IV fluid.
- IV antibiotics e.g. cefotaxime and metronidazole.
- ERCP to remove stone.
- Stenting.
66
What is the difference between ascending cholangitis and acute cholecystitis?
A patient with acute cholecystitis would not have signs of jaundice!
67
What is acute cholecystitis?
Inflammation of the gall bladder caused by blockage of the bile duct -> obstruction to bile emptying.
68
Give 3 symptoms of acute cholecystitis.
1. RUQ pain.
2. Fever.
3. Raised inflammatory markers.
4. MURPHYS SIGN
- NO JAUNDICE!
69
Give 2 risk factors for acute cholecystitis.
1. Obesity.
| 2. Diabetes.
70
Describe the pathophysiology of primary sclerosing cholangitis.
Inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure.
71
Give 3 symptoms of primary sclerorsing cholangitis.
1. Itching.
2. Rigor.
3. Pain.
4. Jaundice.
75% also have IBD!!!
72
What is biliary colic?
Gallbladder attack - RUQ pain due to a gall stone blocking the bile duct.
73
What can trigger biliary colic?
Eating a heavy meal especially one that is high in fat.
74
Give 5 signs of PBC/PSC.
Bile:
Pruritus
Jaundice
```
Cholesterol:
Xanthelasma
Hyperpigmentation
Xeropthalmia
Corneal arcus
```
75
What is PSC also associated with?
1. Complication of cholangiocarcinoma
| 2. Correlation with ulcerative colitis
76
What vitamin supplementation would patients with PBC/PSC need?
Vit ADEK
77
What is a complication of having gallstones?
Acute cholecystitis
78
What drug would you give to someone that has overdosed on paracetamol?
IV N - acetyl - cysteine
79
With which disease would you associate Reynold's pentad?
Ascending cholangitis.
80
Describe Reynold's pentad.
- Charcot's triad (fever, RUQ pain and jaundice).
+ hypotension.
+ altered mental state.
81
Describe the epidemiology for developing gallstones
1. Fat
2. Female
3. Forty
4. Fertile
82
Which bugs are most likely to cause ascending cholangitis?
E. coli, klebsiella, enterococcus (group D strep)
