Liver Flashcards
(128 cards)
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
Name 3 things that liver function tests measure.
A
- Serum bilirubin.
- Serum albumin.
- Pro-thrombin time.
3
Q
Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease).
A
Alkaline phosphatase.
4
Q
What enzymes increase in the serum in hepatocellular liver disease?
A
Transaminases e.g. AST and ALT.
5
Q
Name a cholestatic enzyme.
A
Alkaline phosphatase.
6
Q
Give 4 causes of hepatitis.
A
- Viral e.g. A, B, C, D, E.
- Drug induced.
- Alcohol induced.
- Autoimmune.
7
Q
Give 2 possible outcomes of acute liver disease.
A
- Recovery.
2. Liver failure.
8
Q
Give 5 causes of acute liver disease.
A
- Viral hepatitis.
- Drug induced hepatitis.
- Alcohol induced hepatitis.
- Vascular.
- Obstruction.
9
Q
Give 3 symptoms of acute liver disease.
A
- Malaise.
- Lethargy.
- Anorexia.
- Jaundice may develop later on.
10
Q
Give 2 possible outcomes of chronic liver disease.
A
- Cirrhosis.
2. Liver failure.
11
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.
12
Q
What is Budd-Chiari syndrome?
A
A vascular disease associated with occlusion of hepatic veins that drain the liver.
13
Q
Give 5 signs of chronic liver disease.
A
- Ascites.
- Oedema.
- Malaise.
- Anorexia.
- Bruising.
- Itching.
- Clubbing.
- Palmar erythema.
- Spider naevi.
14
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?
15
Q
Name a drug that can cause drug induced liver injury.
A
- Co-amoxiclav.
- Flucloxacillin.
- Erythromyocin.
- TB drugs.
16
Q
Name 3 drugs that are not known to cause drug induced liver injury.
A
- Low dose aspirin.
- NSAIDS.
- Beta blockers.
- HRT.
- CCB.
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
Give 3 causes of iron overload.
A
- Genetic disorders e.g. haemochromatosis.
- Multiple blood transfusions.
- Haemolysis.
- Alcoholic liver disease.
20
Q
90% of people with haemochromatosis have a mutation in which gene?
A
HFE.
21
Q
Haemochromatosis is a genetic disorder. How is it inherited?
A
Autosomal recessive inheritance.
22
Q
Describe the pathophysiology of haemochromatosis.
A
Uncontrolled intestinal iron absorption leads to deposition in the liver, heart and pancreas -> fibrosis -> organ failure.
23
Q
What protein is responsible for controlling iron absorption?
A
Hepcidin.
Levels of this protein are decreased in haemochromatosis.
24
Q
How might you diagnose someone with haemochromatosis?
A
- Raised ferritin.
- HFE genotyping.
- Liver biopsy.
25
Name 3 metabolic disorders that can cause liver disease.
1. Haemochromatosis - iron overload.
2. Alpha 1 anti-trypsin deficiency.
3. Wilson's disease - disorder of copper metabolism.
26
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. (+ no protein goes to lungs)
27
What is Wilson's disease?
An autosomal recessive disorder of copper metabolism; there is excessive deposition of copper in the liver. This can lead to fulminant hepatic failure and cirrhosis.
28
What can cause raised unconjugated bilirubin?
A pre-hepatic problem e.g. haemolysis due to sickle cell disease, spherocytosis, hypersplenism etc.
29
Describe the urine and stools in someone with pre-hepatic jaundice?
Urine and stools are normal. There is no itching and the LFT's are normal.
30
What can cause raised conjugated bilirubin?
Raised conjugated bilirubin indicates a cholestatic problem e.g. liver disease (hepatic) or bile-duct obstruction (post-hepatic).
31
Describe the urine and stools in someone with cholestatic jaundice?
Dark urine and pale stools. There may be itching and LFT's are abnormal.
32
Give 3 causes of duct obstruction.
1. Gallstones.
2. Stricture (narrowing) e.g. malignant, inflammatory.
3. Carcinoma.
4. Blocked stent.
33
Give 4 causes of hepatic jaundice.
1. Viral hepatitis.
2. Alcoholic hepatitis.
3. Drugs.
4. Cirrhosis.
34
Give 3 symptoms of jaundice.
1. Biliary pain.
2. Rigors - indicate an obstructive cause.
3. Abdomen swelling.
4. Weight loss.
35
What is ascites?
An accumulation of fluid in the peritoneal cavity that leads to abdominal distension.
36
Give 4 pathophysiological causes of ascites and an example for each.
1. Local inflammation e.g. peritonitis.
2. Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures.
3. Low flow e.g. cirrhosis, thrombosis, cardiac failure.
4. Low protein e.g. hypoalbuminaemia.
37
Describe the pathogenesis of ascites.
1. Increased intra-hepatic resistance leads to portal hypertension -> ascites.
2. Systemic vasodilation (low blood pressure) leads to secretion of RAAS, NAd and ADH -> fluid retention.
4. Low serum albumin also leads to ascites.
38
What are the 3 phases of alcoholic liver disease.
1. Fatty change: hepatocytes contain triglycerides.
2. Alcohol hepatitis.
3. Alcoholic cirrhosis: destruction of liver architecture and fibrosis.
39
What might be seen histologically that indicates a diagnosis of alcoholic liver disease?
Neutrophils and fat accumulation within hepatocytes.
40
What is non alcoholic steato-hepatitis (NASH)?
An advanced form of non-alcoholic fatty liver disease.
41
Give 3 causes of non-alcoholic fatty liver disease.
1. Type 2 diabetes mellitus.
2. Hypertension.
3. Obesity.
4. Hyperlipidaemia.
42
What is cirrhosis?
A chronic disease of the liver resulting from necrosis of liver cells followed by fibrosis. The end result is impairment of hepatocyte function and distortion of liver architecture.
43
Give 3 causes of cirrhosis.
1. Alcohol!
2. Hepatitis B and C.
3. Any chronic liver disease e.g. autoimmune, metabolic, vascular etc.
44
What is the treatment of liver cirrhosis?
1. Deal with the underlying cause e.g. stop drinking alcohol.
2. Screening for HCC.
3. Consider transplant.
45
Approximately what percentage of blood flow to the liver is provided by the portal vein?
75%.
46
Portal hypertension can lead to varices. Explain why.
Obstruction to portal blood flow e.g. cirrhosis leads to portal hypertension. Blood is diverted into collaterals e.g. the gastro-oesophageal junction and so causes varices.
47
Give 3 causes of portal hypertension.
1. Cirrhosis and fibrosis (intra-hepatic causes).
2. Portal vein thrombosis (pre-hepatic).
3. Budd-Chiari (post-hepatic cause).
48
What are the potential consequences of varices?
If they rupture -> haemorrhage.
49
What is the primary treatment for varices?
Endoscopic therapy - banding.
50
What is peritonitis?
Inflammation of the peritoneum often due to infection.
51
What can cause peritonitis?
1. Bacterial infection due to a perforated organ; spontaneous bacterial peritonitis; infection secondary to peritoneal dialysis.
2. Non-infective causes e.g. bile leak; blood from ruptured ecotopic pregnancy.
52
What is the commonest serious infection in those with cirrhosis?
Spontaneous bacterial peritonitis.
It can also affect immunocompromised people and those undergoing peritoneal dialysis.
53
Name a bacteria that can cause spontaneous bacterial peritonitis.
1. E.coli.
| 2. S.pneumoniae.
54
How can spontaneous bacterial peritonitis be diagnosed?
By looking for the presence of neutrophils in ascitic fluid.
55
Give 3 symptoms of peritonitis.
1. Pain.
2. Tenderness.
3. Systemic symptoms e.g. nausea, chills, rigor.
56
Name a cause of pelvic inflammatory disease.
A complication of chlamydial infection.
57
Give 4 reasons why liver patients are vulnerable to infection.
1. They have impaired reticulo-endothelial function.
2. Reduced opsonic activity.
3. Leukocyte function is reduced.
4. Permeable gut wall.
58
What is primary biliary cirrhosis?
An autoimmune disease where there is progressive lymphocyte mediated destruction of intra-hepatic bile ducts -> cholestasis -> cirrhosis.
59
Describe 2 features of the epidemiology of primary biliary cirrhosis.
1. Females affected more than men.
| 2. Familial - 10 fold risk increase.
60
Describe the pathophysiology of primary biliary cirrhosis.
Lymphocyte mediated attack on bile duct epithelia -> destruction of bile ducts -> cholestasis -> cirrhosis.
61
Give 3 diseases associated with primary biliary cirrhosis.
1. Thyroiditis.
2. RA.
3. Coeliac disease.
4. Lung disease.
(Other autoimmune diseases).
62
Give 5 symptoms of primary biliary cirrhosis.
1. Itching.
2. Fatigue.
3. Dry eyes,
4. Joint pains.
5. Variceal bleeding.
63
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.
64
Give 4 risk factors for gallstone development.
1. Female.
2. Obese (fat).
3. Fertile.
4. Age (forty)
- The 4 Fs!
65
How can gallstones be removed from the gall bladder?
Laproscopic cholecystectomy.
66
Give 4 potential complications of gallstones in the bile duct.
1. Biliary pain.
2. Obstructive jaundice.
3. Cholangitis (infection of the biliary tract).
4. Pancreatitis.
67
What is ascending cholangitis?
Obstruction of biliary tract causing bacterial infection. Regarded as a medical emergency.
68
Name the triad that describes 3 common symptoms of ascending cholangitis.
Charcot's triad:
1. Fever.
2. RUQ pain.
3. JAUNDICE (cholestatic)!
69
What is charcot's triad?
It describes 3 common symptoms of ascending cholangitis:
1. Fever.
2. RUQ pain.
3. Jaundice (cholestatic)!
70
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.
(endoscopic retrograde cholangiopancreatography)
71
Describe the management of ascending cholangitis.
- IV fluid.
- IV antibiotics e.g. cefotaxime and metronidazole.
- ERCP to remove stone.
- Stenting.
72
What is the difference between ascending cholangitis and acute cholecystitis?
A patient with acute cholecystitis would not have signs of jaundice!
73
What is acute cholecystitis?
Inflammation of the gall bladder caused by blockage of the bile duct -> obstruction to bile emptying.
74
Give 3 symptoms of acute cholecystitis.
1. RUQ pain.
2. Fever.
3. Raised inflammatory markers.
- NO JAUNDICE!
75
Give 2 risk factors for acute cholecystitis.
1. Obesity.
| 2. Diabetes.
76
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.
77
Give 3 symptoms of primary sclerorsing cholangitis.
1. Itching.
2. Rigor.
3. Pain.
4. Jaundice.
75% also have IBD.
78
What is biliary colic?
Gallbladder attack - RUQ pain due to a gall stone blocking the bile duct.
79
What can trigger biliary colic?
Eating a heavy meal especially one that is high in fat.
80
What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important.
It is important to do an ascitic tap so you can rule out spontaneous bacterial peritonitis asap.
81
What would be raised in the blood tests taken from someone with primary biliary cirrhosis?
1. Raised IgM.
2. Raised ALP.
3. Positive AMA.
82
What 4 features would you expect to see in the blood test results taken from someone who has overdosed on paracetamol.
1. Metabolic acidosis.
2. Prolonged prothrombin time (due to coagulability).
3. Raised creatinine (renal failure).
4. Raised ALT.
83
What 3 symptoms make up the triad of Wernicke's encephalopathy?
1. Ataxia.
2. Opthalmoplegia.
3. Confusion.
84
How can Wernicke's encephalopathy be reversed?
Give IV thiamine.
85
What histological stain can be used for haemochromatosis?
Perl's stain.
86
Name 4 fat soluble vitamins.
ADEK.
87
What is the main difference between biliary colic and acute cholecystitis?
Acute cholecystitis has an inflammatory component.
88
What is the treatment for acute cholecystitis?
Laparoscopic cholecystectomy.
89
Why might someone with primary biliary cirrhosis experience itching as a symptom?
Because there is a build up of bilirubin.
90
Give 3 components of gallstones.
1. Cholesterol.
2. Bile pigment.
3. Phospholipid.
91
What investigations might you do in someone who you suspect has gallstones?
Ultrasound and ERCP.
92
Are most liver cancers primary or secondary?
Secondary (metastasised from somewhere).
93
Where have most secondary liver cancers arisen from?
1. GI tract.
2. Breast.
3. Bronchus.
94
Describe the aetiology of HCC.
Most HCC is in patients with cirrhosis. This is often due to HBV/HCV and alcohol.
95
Give 5 symptoms of HCC.
1. Weight loss.
2. Anorexia.
3. Fever.
4. Malaise.
5. Ascites.
96
What investigations might you do on someone who you suspect has HCC?
1. Blood serum alpha-fetoprotein may be raised.
2. US or CT to identify lesions.
3. MRI.
4. Biopsy if diagnostic doubt.
97
Describe the treatment for HCC.
1. Surgical resection of solitary tumours.
2. Liver transplant.
3. Percutaneous ablation. (using radio waves through skin)
98
Give 3 symptoms of haemochromatosis.
1. Hepatomegaly.
2. Cardiomegaly.
3. Diabetes.
4. Hyperpigmentation of the skin.
5. Lethargy.
99
Name 3 diseases that lead to heamolytic anaemia and so a raised unconjugated bilirubin and pre-hepatic jaundice.
1. Sickle cell disease.
2. Hhereditary spherocytosis/elliptocytosis.
3. GP6D deficiency.
4. Hypersplenism.
100
Give 3 causes of liver failure.
1. Infection e.g. viral hepatitis B, C.
2. Induced e.g. alcohol, drug toxicity.
3. Inherited e.g. autoimmune.
101
Hepatic encephalopathy is a complication of liver failure. Describe the pathophysiological mechanism behind this.
The liver can't get rid of ammonia and so ammonia crosses the BBB -> cerebral oedema.
102
Give 4 complications of liver failure.
1. Hepatic encephalopathy.
2. Abnormal bleeding.
3. Jaundice.
4. Ascites.
103
Describe the treatment for liver failure.
1. Nutrition.
2. Supplements.
3. Treat complications.
4. Liver transplant.
104
You do an ascitic tap in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?
Spontaneous bacterial peritonitis.
105
Describe the treatment for spontaneous bacterial peritonitis.
Cefotaxime and metronidazole.
106
Give 5 symptoms of ruptured varices.
1. Haematemesis.
2. Melaena.(dark sticky faeces with partly digested blood)
3. Abdo pain.
4. Dysphagia.
5. Anaemia.
107
What type of anaemia do you associate with alcoholic liver disease?
Macrocytic anaemia.
108
Name a protozoa that can cause amoebic liver abscess?
Entemoeba histolytica.
109
What are the symptoms of entemoeba histolytica?
- RUQ pain.
- Bloody diarrhoea.
- Fever and malaise.
Often the patient has a history of foreign/rural travel.
110
What is the treatment for entemoeba histolytica?
Metronidazole.
111
What drug would you give to someone that has overdosed on paracetamol?
IV N-Acetyl-Cysteine.
112
With which disease would you associate Reynold's pentad?
Ascending cholangitis.
113
Describe Reynold's pentad.
- Charcot's triad (fever, RUQ pain and jaundice).
- + hypotension.
- + altered mental state.
114
What blood test might show that someone has alcoholic liver disease?
Serum GGT (gamma glutamyl transferase) will be elevated.
115
What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?
Mallory bodies. (damaged intermediate fillaments in hepatocytes).
116
What feature seen on liver biopsy is diagnostic of cirrhosis?
Nodular regeneration.
117
A man has his ascites drained and is advised to restrict his diet. Which non-hormonal substance will promote re-accumulation of the ascites?
Salt.
118
What is the treatment for Wilson's disease.
Lifetime treatment with penicillamine.
119
Name the 2 main pathophysiological factors that contribute to the formation of ascites.
1. High portal venous pressure.
| 2. Low serum albumin.
120
State two pathological changes that occur in the liver with continued consumption of excessive amounts of alcohol.
1. Fatty liver.
2. Alcoholic hepatitis.
3. Cirrhosis.
121
A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.
Hypoalbuminaemia.
122
What 2 products does haem break down into?
Fe2+ and biliverdin.
123
What enzyme converts biliverdin to unconjugated bilirubin?
Biliverdin reductase.
124
What is the function of glucuronosyltransferase?
It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.
125
What protein does unconjugated bilirubin bind to and why?
Albumin.
It isn't H2O soluble therefore it binds to albumin so it can travel in the blood to the liver.
126
What does conjugated bilirubin form?
Urobilinogen.
127
What is responsible for the conversion of conjugated bilirubin into urobilinogen?
Intestinal bacteria.
128
What are the 3 possible pathways of urobiliogen?
1. It can go back to the liver via the enterohepatic system.
2. It can go to the kidneys forming urinary urobilin.
3. It can form stercobilin which is excreted in the faeces.
