Liver Cirrhosis Flashcards
(56 cards)
1
Q
Why does liver cirrhosis occur?
A
- it is the result of chronic inflammation that damages the liver cells
- damaged liver cells are replaced with scar tissue (fibrosis)
- nodules of scar tissue form within the liver
2
Q
Why does portal hypertension occur in cirrhosis?
A
- fibrosis affects the structure and blood flow through the liver
- there is increased resistance in the vessels leading to the liver
- this results in an increased pressure in the portal system
3
Q
What are the most common causes of cirrhosis?
A
- hepatitis B
- hepatitis C
- alcoholic liver disease
- non alcoholic fatty liver disease
4
Q
What are some of the rarer causes of cirrhosis?
A
- autoimmune hepatitis
- primary biliary cirrhosis
- haemochromatosis
- Wilsons disease
- alpha-1 antitrypsin deficiency
- cystic fibrosis
- drugs
it is important to consider these as some of them are potentially reversible
5
Q
Which drugs can potentially cause cirrhosis?
A
- S - sodium valproate
- A - amiodarone
- M - methotrexate
remember - SAM
6
Q
What are the signs of cirrhosis?
A
- jaundice (raised bilirubin)
- caput medusae (portal HTN)
- palmar erythema (hyperdynamic circulation)
- gynaecomastia / testicular atrophy (endocrine dysfunction)
- bruising (abnormal clotting)
- ascites
- spider naevi
- hepatomegaly (but liver then shrinks as it becomes more cirrhotic)
- splenomegaly (portal HTN)
- asterixis (in decompensated disease)
7
Q
What are spider naevi?
A
telangiectasia with a central arteriole and small vessels radiating away
telangiectasia (“spider veins”) - dilated / broken blood vessels near the surface of the skin
8
Q
What blood tests are performed in cirrhosis?
A
LFTs:
* usually normal
- all markers become deranged in decompensated disease (ALP, AST, ALT + bilirubin)
albumin + prothrombin time:
- markers of synthetic function
- low albumin and raised PTT is seen
U&Es:
- hyponatraemia indicates fluid retention in severe disease
urea + creatinine:
- deranged in hepatorenal syndrome
alpha-fetoprotein:
- tumour marker for HCC
9
Q
Why is alpha-fetoprotein (AFP) measured in cirrhosis?
A
- it is a tumour marker for hepatocellular carcinoma
- it should be checked every 6 months with USS
- this is a screening test for HCC
10
Q
What is the enhanced liver fibrosis (ELF) blood test?
When is it used?
A
- first line investigation for assessing fibrosis in NAFLD
- cannot be used for diagnosing cirrhosis of other causes
it is currently not available in many areas
11
Q
How can the ELF score be used to determine whether fibrosis is present?
A
- a score < 7.7 indicates no or mild fibrosis
- a score 7.7 - 9.8 indicates moderate fibrosis
- a score of 9.8 or higher indicates severe fibrosis
it measures 3 markers - HA, PIIINP and TIMP-1
12
Q
What may be seen on ultrasound in cirrhosis?
A
- nodularity of the surface of the liver
- “corkscrew” appearance of arteries with increased flow
- enlarged portal vein with reduced flow
- ascites
- splenomegaly
13
Q
When is a patient with cirrhosis offered an USS?
A
- NICE recommend AFP + USS every 6 months in patients with cirrhosis
- this screens for HCC
14
Q
What is FibroScan and what does it test for?
A
- it checks the elasticity of the liver by sending high frequency sound waves into it
- this assesses the degree of cirrhosis
it is called “transient elastography”
15
Q
How frequently should a FibroScan be performed?
A
- it should be performed every 2 years in patients at risk of cirrhosis
- hepatitis C
- heavy alcohol drinkers
- NAFLD + evidence of fibrosis on ELF test
- alcoholic liver disease
- it should be performed yearly in chronic hepatitis B
heavy alcohol drinkers = > 50 units for men and > 35 units for women per week
16
Q
When is endoscopy performed in cirrhosis?
A
to assess for and treat oesophageal varices if portal hypertension is suspected
17
Q
When may CT and MRI scans be performed in cirrhosis?
A
to look for:
- hepatocellular carcinoma
- hepatosplenomegaly
- ascites
- abnormal blood vessel changes
18
Q
What test is needed to make a definitive diagnosis of cirrhosis?
A
liver biopsy
19
Q
What score is used to indicate the severity of cirrhosis?
A
Child-Pugh score
indicates severity of cirrhosis and prognosis
20
Q
What parameters are used to calculate the Child-Pugh score?
A
- encephalopathy
- INR
- bilirubin
- albumin
- ascites
- each parameter is given a score of 1, 2 or 3
(remember parameters as EIBAA)
21
Q
What is the MELD score and when is it used?
A
- it is used every 6 months in patients with compensated cirrhosis
- it assesses whether they require dialysis
- it gives a 3-month estimated mortality which helps guide referral for liver transplant
22
Q
What parameters are included in the MELD score?
A
- bilirubin
- INR
- creatinine
- sodium
remember parameters as BICS
23
Q
What stages are involved in the general management of cirrhosis?
A
- USS + AFP every 6 months to assess for HCC
- MELD score every 6 months
- high protein and low sodium diet
- endoscopy every 3 years (in patients without known varices)
- consider liver transplant
- manage complications
24
Q
How is the prognosis of cirrhosis estimated?
A
- through use of the Child-Pugh and MELD scores
- disease course is variable
- 5-year survival is around 50%
25
What are the potential complications of cirrhosis?
* malnutrition
* hepatorenal syndrome
* ascites + spontaneous bacterial peritonitis
* hepatic encephalopathy
* hepatocellular carcinoma
* portal hypertension, varices + bleeding
26
Why is a liver biopsy no longer recommended by NICE as a diagnostic tool for cirrhosis?
* the procedure is associated with **adverse effects**, such as bleeding and pain
* FibroScan and imaging are used instead
* ELF score is used in NAFLD
27
Why does malnutrition occur in cirrhosis and what are the consequences of this?
* cirrhosis affects **metabolism of proteins** in the liver, reducing the amount of protein produced
* it affects the ability to **store glucose as glycogen**, leading to use of muscle tissue as fuel
* this leads to **muscle wasting + weight loss**
28
How is malnutrition as a result of cirrhosis managed?
* regular meals (every 2-3 hours)
* **low sodium diet** (to minimise fluid retention)
* **high protein** + high calorie diet
* avoid alcohol
29
What is the portal vein formed from?
What happens in portal hypertension?
* the portal vein is formed from the **superior mesenteric vein** and **splenic vein**
* in cirrhosis there is **increased resistance** to blood flow in the liver
* this leads to **increased back-pressure** in the portal system
30
How does portal hypertension result in varices?
* there is increased back-pressure in the portal system
* this causes the vessels to become **swollen / tortuous** at the sites where the **portal system anastomoses with the systemic venous system**
* varices are swollen, tortuous vessels
31
At which sites do varices develop?
* gastro-oesophageal junction
* ileocaecal junction
* rectum
* anterior abdominal wall via the umbilical vein (caput medusae)
32
What are the symptoms associated with varices?
* varices do not produce symptoms **until they start bleeding**
* there is a high blood flow through varices
* patients can **exsanguinate** (bleed out) **very quicky**
33
What are the 3 main options for the treatment of stable varices?
**propanolol:**
* acts as a non-selective beta blocker to reduce portal HTN
**elastic band ligation**
**injection of sclerosant:**
* less effective than band ligation
34
What is involved in the transjugular intra-hepatic portosystemic shunt (TIPS) procedure?
* a wire is inserted under XR guidance
* the wire passes through the jugular vein, down the vena cava and into the liver via the hepatic vein
* a **connection is made** between the **hepatic vein** and **portal vein**
* a **stent** is put into place
* this allows blood to flow directly from the portal vein into the hepatic vein to **relieve the pressure in the portal system + varices**
35
When is a TIPS procedure performed?
* if medical and endoscopic treatment of varices fails
OR
* there are bleeding varices that cannot be controlled in other ways
36
What are the 4 stages involved in resuscitation when there are bleeding oesophageal varices?
**terlipressin:**
* or other vasopressin analogue
* causes vasoconstriction and slows bleeding
**correct coagulopathy:**
* with vitamin K and FFP
**broad spectrum abx:**
* prophylactic abx reduces mortality
**intubation / ICU:**
* consider ICU as patients can become life-threateningly unwell
## Footnote
FFP = fresh frozen plasma which contains many clotting factors
37
What is required urgently when oesophageal varices are bleeding?
* following resuscitation, **urgent endoscopy** is required
* there may be **injection of sclerosant** into the varices to cause "inflammatory obliteration"
* or **elastic band ligation** of varices
38
What is done if endoscopy fails to control bleeding varices?
**Sengstaken-Blakemore tube**
* an inflatable tube inserted into the oesophagus to tamponade the bleeding varices
39
Why does ascites occur as a result of cirrhosis?
* increased pressure in the portal system causes **fluid to leak out of the capillaries** in the liver / bowel
* fluid enters the **peritoneal cavity**
40
How does ascites affect the kidneys?
* there is a **drop in circulating volume** as fluid is lost into the peritoneal space
* kidneys secrete **renin** as a result of lower BP
* renin leads to increased **aldosterone** secretion
* there is increased **reabsorption of fluid + sodium** in the kidneys
41
What type of ascites is caused by cirrhosis?
transudative ascites
| i.e. low protein content
42
What is involved in the management of ascites?
* **low sodium diet**
* anti-aldosterone diuretics (**spironolactone**)
* **paracentesis** (ascitic tap / drain)
* consider TIPS procedure / transplantation in refractory ascites
* **prophylactic antibiotics**
43
Why are prophylactic antibiotics given in ascites?
What antibiotics are given?
* to reduce the risk of spontaneous bacterial peritonitis (SBP)
* **ciprofloxacin** or **norfloxacin** are given
* given to all patients with **< 15g/L protein** in the ascitic fluid
44
When does ascites become clinically detectable?
it is not detectable until there is at least **500ml fluid** present
45
What are the clinical features of ascites?
* abdominal distension / discomfort
* weight gain
* reduced appetite
* **shortness of breath** (due to diaphragmatic splinting in large volume ascites)
46
How is a sample of ascitic fluid obtained?
What colour would this be in cirrhosis?
* a sample is obtained using a neddle and syringe
* this is called "ascitic tap" or "paracentesis"
* fluid is **clear / straw coloured** in cirrhosis
47
What is spontaneous bacterial peritonitis (SBP)?
an **infection** developing in the ascitic fluid + peritoneal lining **without any clear cause**
| (e.g. not secondary to ascitic drain / bowel perforation)
## Footnote
occurs in around 10% of patients with ascites secondary to cirrhosis
48
How does SBP present?
* it can be **asymptomatic**
* fever
* abdominal pain
* deranged bloods (raised WCC, CRP, creatinine / metabolic acidosis)
* ileus
* hypotension
## Footnote
as it can be asymptomatic, there should be a low threshold for ascitic fluid culture
49
What are the most common causative organisms of SBP?
* ***Escherichia coli***
* ***Klebsiella pneumoniae***
* Gram positive cocci (staphylococcus / enterococcus)
50
What is involved in the management of SBP?
* take an **ascitic culture** prior to giving antibiotics
* usually treated with **IV cephalosporin** - e.g. **cefotaxime**
51
What is hepatorenal syndrome and why does it occur?
* hypertension in the portal system leads to **dilation of portal blood vessels**
* blood pools in the portal vessels
* there is a **loss of blood volume** in other areas of circulation
* there is **activation of the RAAS** due to reduced kidney BP
* this results in renal **vasoconstriction**
* renal vasoconstriction and low circulatory volume starves the kidneys of blood
* there is **rapidly deteriorating kidney function**
52
What is the treatment for hepatorenal syndrome?
liver transplant
## Footnote
hepatorenal syndrome is fatal within 1 week if transplant is not performed
53
What causes hepatic encephalopathy?
* a **build up of toxins** in the blood - particularly **ammonia**
* ammonia is produced by intestinal bacteria when they break down proteins and is absorbed in the gut
54
Why does ammonia build up in the blood in cirrhosis?
* functional impairment of hepatocytes **prevents metabolism of ammonia** into harmless waste products
* **collateral vessels** between the portal / systemic circulation means **ammonia can bypass the liver** and directly enter the systemic circulation
55
How does hepatic encephalopathy present?
**acute presentation:**
* reduced consciousness
* confusion
**chronic presentation:**
* changes to personality / mood
* memory disturbances
56
What are the precipitating factors for hepatic encephalopathy?
* constipation
* electrolyte disturbances
* infection
* GI bleeding
* high protein diet
* medications (sedatives)
