Liver cirrhosis Flashcards
1
Q
what lobes are the liver made out of
A
- right and left lobes
2
Q
What is the blood supply of the liver
A
- Hepatic artery 25%
- portal vein 75%
- hepatic venous drainage
3
Q
What two veins form the hepatic portal vein
A
splenic and superior mesenteric vein
4
Q
describe the venous drainage of the liver
A
- left hepatic vein
- right hepatic vein
- middle hepatic vein
5
Q
What do the kupffer cells do
A
- immune function of the liver
6
Q
Where are the stellate cells
A
between blood vessels and the sinusoids
7
Q
How do the stellate cells act towards inflammation and cause hepatic portal hypertension
A
- when there is inflammation and scarring cause collagen formation
- smooth surface gets disrupted
- this leads to liver cell failure
- this leads to distortion of the morphology of the liver and makes the liver hard
- this causes a problem in the flow of the portal vein that bathes the hepatocytes
- causes the pressure to rise which leads to portal hypertension
8
Q
How does acute liver failure happen
A
- liver cells if there is a toxic insult collapse and this leads to a shrinkage of the volume of the liver
9
Q
What are the functions of the liver
A
Protein synthesis: Albumin, Clotting Factors and lots
Carbohydrate metabolism
Glycogen storage
Gluconeogenesis
Lipid metabolism
Bile production
Immunological function
Reticuloendothelial system
Hormone & drug metabolism/excretion
Detoxification
10
Q
what are the clinical features of acute liver failure (haemodynamic and hepatocellular dysfunction)
A
Hepatocellular dysfunction
- coagulopathy
- jaundice
- encephalopathy
- increased sepsis risk
Haemodynamic consequences
- cerebral edema
- renal failure
11
Q
What are the clinical features of chronic liver disease (haemodynamic and hepatocellular dysfunction)
A
Hepatocellular dysfunction
- Jaundice
- encephalopathy
- coagulopathy
- increased sepsis risk
Haemodynamic consequences Portal hypertension - splenomegaly - varices - ascites - hepatic encephalopathy
12
Q
What is the difference between onset in acute and chronic liver disease
A
- Acute = liver prior to onset of injury is normal
- chronic = liver abnormal before hand just asymptomatic and becomes symptomatic
13
Q
describe how the scarred liver causes portal hypertension
A
- once the liver becomes scarred
- the portal system struggles to enter the scarred liver
- due to the increased pressure
- this causes an increase pressure in the portal vein
- ## this causes portal hypertension
14
Q
What pressure causes porto-systemic capsules to open
A
12 mmHg
- causes a back pressure
- this opens collaterals which allows the portal vein to empty into systemic circulation
15
Q
What are the clinical features of portal hypertension
A
Splenomegaly
- pancytopenia
Varices
- oesophageal
- gastric
- rectal
Ascites
Hepatic encephalopathy
16
Q
How does encephalopathy happen
A
- ammonia does not get converted into urea
- leaks into the systemic circulation
- travels up to the brain
- gives rise to hepatic encephalopathy
17
Q
What are the sites of varices in portal hypertension
A
- oesophageal
- gastric
- rectal
18
Q
How does a patient with chronic liver disease present
A
Asymptomatic
Cholestatic
- jaundice
- pruritus
- pale stools/dark urine
systemic
- weight loss
- muscle loss
- fatigue
Decompensation
- jaundice
- fluid retention: abdominal distension and swelling feet
- drowsiness/confusion
- GI bleed
- infection (sepsis)
19
Q
What is decompensated cirrhosis
A
- phase in cirrhosis when symptoms of liver disease manifest
20
Q
What are the symptoms of decompensated liver cirrhosis
A
Ascites Jaundice Hepatic Encephalopathy Coagulopathy Hepato Renal syndrome (HRS) Recurrent infections / sepsis (SBP)
21
Q
What are the triggers for decompensation
A
GI bleed Infection Drugs (Diuretics) & Alcohol abuse Constipation Progression of liver disease Hepatocellular carcinoma Portal Vein Thrombosis
22
Q
What does the history of liver disease include
A
Risk factors:
Alcohol history
Intravenous drug use
Past History of liver disease: jaundice Medications /Over the Counter/Herbal Social History Sexual & Travel History Occupation Family history of liver disease Co-morbidity: Obesity, Diabetes
23
Q
What are the signs of compensated liver diseae
A
- xanthelasamas
- parotid enlargement
- spider naevi
- gynecomastia
- liver (small or large)
- splenomegaly
- scratch marks
- testicular atrophy
- purpura pigmented ulcers
- palmar erythema
24
Q
What are the complications of liver cirrhosis
A
Variceal Bleed Ascites Spontaneous Bacterial peritonitis Hepatorenal Syndrome Jaundice
25
How do you treat variceal bleed
```
Treatment
ABCDE
Antibiotics - variceal bleed increases risk of sepsis which can increases hepatic portal tension which leads to more bleeding in varices
Terlipressin
Endoscopic therapy
- Banding
- Glue Injection
TIPSS
```
26
What are the primary and secondary prophylaxis for variceal bleeding
- Beta blockers: Carvedilol
| - banding to obliterate
27
How do you diagnose ascites
- Clinical examination
- peripheral oedema
- liver ultrasound and doppler
- ascitic tap - to remove the risk of spontaneous bacterial peritonitis (SBP)
28
How can a liver ultrasound and doppler investigate liver cirrhosis and portal hypertension
normal flow in portal vein is towards the liver, once the liver is scarred the portal vein struggles to put blood towards the liver and there is retrograde flow which will show up on the ultrasound
29
How do you diagnose spontaneous bacterial peritonitis (SBP)
Ascitic tap
WCC > 250 mm3
Neutrophils (>80%)
Gram - rods ( + enterococcus)
30
What are you at risk of developing if you have ascites
spontaneous bacterial peritonitis (SBP)
31
describe the pathophysiology of ascities
- increase in portal hypertension
- this leads to splanchnic vasodilation
- this leads to a decreased effective circulatory volume
- this leads to activation of renin-angiotensin-aldosterone system
- renal sodium avidity leads to ascites
- renal vasoconstriction can cause hepatorenal syndrome
- excess of ADH causes increase serum hyponatremia
32
who do you see hyponatraemia in patients with decompensated liver failure
- RAAS system is activated
- leads to an excess of ADH
- this causes serum hyponatraemia
33
Why does hyponatraemia make it difficult to deal with ascites
- because it effects the ability to use diuretics in the treatment of ascites
34
How do you treat ascites
- Fluid restriction
• Low Na diet
Diuretics
• Spironolactone
• Furosemide - if response to spironlactone is poor
* Paracentesis - drainage of ascites - done over a period of 6 hours
* TIPSS
* Liver Transplantation
35
How do you treat spontaneous bacterial peritonitis (SBP)
IV antibiotics - e.g. Piperacillin and Tazobactam 2.4g/8hours for 5 days or until sensitivities known
Human albumin solution (HAS)
- Give prophylaxis or high risk patients( low albumin, high PT/INR, low ascitic albumin) or those who have had a previous episode e.g. Ciprofloxacin 500mg PO daily
36
What is spontaneous bacterial peritonitis (SBP) often associated with
Encephalopathy, Jaundice and
| Renal Failure (Hepatorenal syndrome)
37
What is hepatorenal syndrome
- renal failure in a setting of cirrhosis
| - worsening renal function with a urinary sodium excretion of less than 10
38
What are the types of hepatorenal syndrome
- HRS type 1
| - HRS type 2
39
What is the difference between the two hepatorenal syndrome
- HRS type 1 = precipitant e.g. SBP, alcoholic hepatitis
| - HRS type 2 = progressive
40
How do you treat hepatorenal syndrome
Human Albumin Solution(HAS)
Terlipressin
Liver Transplantation
41
How is hepatic encephalopathy graded
- Mild confusion to coma - grade I to IV
42
What defines the grades of hepatic encephalopathy
Grade 1
- slight change in behaviour and alteration of sleep pattern with nightime insomnia and sleeping during the daytime
Grade 2
- presence of hepatic flap
- patient is confused but you can have a conversation with them
Grade 3
- presence of hepatic flap
- Patient is too confused to have a conversation
Grade 4
- coma
43
What can cause hepatic encephalopathy to develop
Constipation
Sepsis
GI Bleeding
Drugs
- Opioids
- Benzodiazepines
- Diuretics
Dehydration
Portal Vein Thrombosis
44
How do you diagnose hepatic encephalopathy
Clinical
- Hepatic Flap
EEG
Serum ammonia
45
How do you treat hepatic encephalopathy
Treat precipitants factors
Lactulose
Rifaximin
Liver transplantation
46
describe how bilirubin is broken down
- bilirubin binds to the albumin and becomes unconjugated bilirubin
- goes to the liver and binds to glucoronic acid - becomes conjugated bilirubin
- goes to the small intestine and is broken down by bacteria
47
what are the types of jaundice
- pre-hepatic
- hepatic
- cholestatic
48
What happens to the colour of the urine in pre hepatic bilirubin
urine does not become yellow
| - skin and sclera may become yellow
49
What happens to the urine in hepatic bilirubin
the urine is dark yellow
50
What happens to the skin and sclera in cholestatic jaundice
yellowing of the sclera
itching
dark urine
clay colour stools
51
What causes pre hepatic jaundice
- haemolysis
52
What causes hepatic jaundice
- Gillberts
- hepatitis - viral
- drug
- alcohol
- cirrhosis
53
What can cause cholestatic jaundice
- sex hormones
- promazines
- cancer of the bile duct
- gallstones
- cancer of the head of the pancreas
54
How do you assess jaundice
```
History: obstructive Versus non obstructive jaundice
UrineColour
PaleStools
Itching
AbdominalPain
```
Onset, Duration
Weight loss, anorexia, fever
Causes & Risk factors of Liver Disease
55
How do you treat jaundice
Pre Hepatic: haemolysis/Drugs
Hepatic: Hepatitis/cirrhosis
Post Hepatic: Biliary
56
What is the care bundle for patients with decompensated liver cirrhosis
- FBC
- U AND E
- Ascitic tap
- take an alcohol history
- important to do an infection screen
- screen for acute kidney injury
- management of GI bled
- encephalopathy
57
Why do we have a care bundle for patients with decompensated liver cirrhosis
■Reduce variations in outcomes: mortality for non elective liver admissions in non specialist acute hospitals varies 15% to 35%
■To ensure evidence based treatments delivered within first 24 hours of hospital admission and to commence within 6 hours of admission
58
name three common causes of cirrhosis
- alcohol (most common cause in the west)
- hepatitis B and C (most common cause worldwide)
- NAFLD (Increasingly more common in the west)
59
Name uncommon causes of cirrhosis
- primary biliary cholangitis
- secondary biliary cholangitis
- autoimmune hepatitis
- hereditary haemochromatosis
- hepatic venous congestion
- budd-chiari syndorme
- Wilson's disease
- drugs
- idiopathy
- glycogen storage disease
- cystic fibrosis
60
What histologically does cirrhosis look like
loss of normal hepatic architecture with bridging fibrosis and nodular regeneration
61
Name three types of complication of cirrhosis
- hepatic failure
- portal hypertension
- hepatocellular carcinoma
62
Name the complications resulting from hepatic failure
- coaguloapthy
- encephalopathy
- hypoalbuminaemia
- sepsis
- spontaneous bacteria peritonitis (SBP)
- Hypoglycaemia
63
Name the complications resulting from portal hypertension
- ascites
- splenomegaly
- portosystemic shunt including oesophageal varices
- caput medusae
64
name the investigations that you would carry out in suspected cirrhosis
- Blood – LFTs,
- Liver US and doppler MRI – show a small liver or hepatomegaly, splenomegaly, focal liver lesions, reversed flow in portal vein or the presence of ascites
- MRI – increase caudate lobe size
- Ascitic tap – SBP presence
- Liver biopsy – confirms the clinical diagnosis
65
What would the blood show if you had cirrhosis
- normal or raised bilirubin
- raised AST, ALT, ALP, Gamma GT
- loss of albumin
- raised PT/INR
- WCC and platelets decreased
66
What would a liver US and Doppler show in cirrhosis
- hepatomegaly or small liver
- splenomegaly
- focal liver lesions
- hepatic vein thrombus
- reversed flow in the portal vein
- ascites
67
What would and MRI show in cirrhosis
- increased in caudate lobe size
- smaller islands of regenerating nodules
- presence of right posterior hepatic notch
68
What would and ascitic tap indicate in cirrhosis
- neutrophils >250mm3 indicates SBP
| - should be performed and fluid sent for MC&S
69
what is the general management of cirrhosis
- good nutrition
- alcohol abstinence
- avoid NSAIDs, sedatives and opiates
- pruritus - colestyramine 4g/12hr PO, 1 hour after other drugs
- consider Ultrasound and alpha fetoprotein every 6 months to screen for HCC
70
what organisms cause SBP
- E.coli
- Klebsiella
- streptococci
71
What are the types of acute liver induced failure
- paracetamol induced liver failure
| - non paracetamol liver failure
72
What is the defintion of paracetamol causing liver failure
- arterial pH <7.3 24 hour after ingestion
or all of the following:
- PT>100s
- creatine >300umol/L
- grade III or IV encephalopathy
73
What is the definition of non paracetamol liver failure
PT>100s
or 3 out of 5 of the following:
- drug-induced liver failure
- age <10 or >40 years old
- >1 week from 1st jaundice to encephalopathy
- PT >50s
- bilirubin >300umol/L
74
what is prioritisation for liver transplant based upon
- UK end-stage liver disease score
Calculated from
- sodium
- creatinine
- bilirubin
- INR
75
what are the contraindications to liver transplant
- extra hepatic malignancy
- severe cardiorespiratory disease
- systemic sepsis
- expected non-compliance with drug therapy
- ongoing alcohol consumption (in those with alcohol-related cirrhosis)
76
what are the complications of liver cirrhosis
Hepatic failure
- Coagulopathy
- Encephalopathy
- hypalbuminaemia
- SBP
- Hypoglycaemia
Portal hypertension
- Ascites
- Splenomegaly
- Portosystemic shunt including oesophageal varices
Increased risk of hepatocellular carcinoma
