Cirrhosis Flashcards
Liver cirrhosis
Result of chronic inflammation and damage to liver cells
Cells replaced with scar tissue and nodules
Causes
Alcohol
NAFLD
Viral hepatitis (B and C)
Rarer causes
Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (amiodarone, methotrexate, sodium valproate)
Signs
Jaundice
Hepatomegaly
Splenomegaly
Spider naevi
Palmar erythema
Gynaecomastia and testicular atrophy
Bruising
Ascites
Caput medusae
Asterixis
Bloods
LFTs often normal but deranged if decompensated
Albumin decreases
Prothrombin time increases
Hyponatraemia indicates fluid retention
Urea and creatinine deranged in hepatorenal syndrome
Viral markers and autoantibodies to find cause
Alpha-fetoprotein raised in hepatocellular carcinoma
Albumin and prothrombin time markers of
Synthetic function
Enhanced liver fibrosis test
First line recommended investigation for NAFLD (not available in many areas)
Measures HA, PIIINP and TIMP-1
<7.7 none to mild fibrosis
>7.7-9.8 moderate fibrosis
>9.8 severe fibrosis
Ultrasound
Nodularity of the surface of the liver
Corkscrew appearance of arteries with increased flow as compensating for reduced portal flow
Ascites
Splenomegaly
US patients with HCC every 6 months
Fibroscan
Checks elasticity of liver by sending high frequency waves
Endoscopy
To assess for and treat oesophageal varices when portal hypertension suspected
CT and MRI scans
To look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessels and ascites
Child-Pugh score
Indicates severity
Bilirubin
Albumin
INR
Ascites
Encephalopathy
General management
US and aFP every 6 months for HCC
Endoscopy every 3 years in patients without known varices
High protein, low sodium diet
MELD score every 6 months
Consideration of liver transplant
Managing complications
MELD score
Takes into account bilirubin, creatinine, INR and sodium when requiring dialysis
Gives percentage estimated 3 month mortality and helps guide referral for liver transplant
Complications
Malnutrition
Portal hypertension, varices and variceal bleeding
Ascites and spontaneous bacterial peritonitis
Hepato-renal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma
Malnutrition
Increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth
Affects metabolism of proteins in the liver and reduces the amount of protein produced
Disrupts livers ability to store glucose as glycogen and release it when required
Results in body using muscle tissue as fuel leading to muscle wasting and weight loss
Management of malnutrition
Regular meals (every 2-3 hours)
Low sodium (to minimise fluid retention)
High protein and high calorie
Avoid alcohol
Portal vein comes from
Superior mesenteric vein and splenic vein
Portal hypertension
Cirrhosis increases resistance of blood flow in liver
Increased back-pressure into the portal system
Causes vessels at sites where portal system anastomoses with systemic venous system to become swollen and tortuous
Sites that varices occur
Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)
Treatment of stable varices
Propanolol reduces portal hypertension
Elastic band ligation
Injection of sclerosant
Transjugular intra-hepatic portosystemic shunt
TIPS
Interventional radiologist inserts wire into jugular vein, down vena cava and inter liver via hepatic vein
Make connection through liver tissue between hepatic vein and portal vein and put stent in place
Allows blood to flow directly from portal vein to hepatic vein and relieves pressure in portal system and varices
Management of bleeding oesophageal varices
Rescusitation
- vasopressin analogues cause vasoconstriction
- correct coagulopathy with vitamin K and fresh frozen plasma
- prophylactic broad spectrum antibiotics
- consider intubation and ICU if life threatening bleed
Urgent endoscopy
- inject sclerosant to cause inflammatory obliteration of the vessel
- elastic band ligation
Sengstaken-Blakemore tube
Sengstaken-Blakemore tube
Inflatable tube inserted into oesophagus to tamponade bleeding varices
Used when endoscopy fails
Ascites
Increased pressure in portal system causes fluid to leak out of capillaries in liver and bowel into peritoneal cavity
Drop in circulating pressure causes reduction on BP entering kidneys
Kidneys sense lower pressure and release renin, leads to increased aldosterone
Cirrhosis causes transudative (low protein) content
Spontaneous bacterial peritonitis
Infection developing in ascitis fluid and peritoneal lining without any clear cause
Presentation of SBP
Can be asymptomatic
Fever
Abdominal pain
Deranged bloods (raised WCC, CRP, creatinine or metabolic acidosis)
Ileus
Hypotension
Most common organisms of SBP
Escherichia coli
Klebsiella pneumoniae
Gram positive cocci (staph and enterococcus)
Management of SBP
Take an ascitic culture prior to giving antibiotics
Usually treated with IV cephalosporin
Hepatorenal syndrome
Hypertension in portal system leads to dilation of portal blood vessels
Leads to loss of blood volume in kidneys
Leads to hypotension in kidneys and activation of RAAS
Causes renal vasoconstrction leading to starved kidneys
Leads to rapid deterioration of kidney function
Fatal within a week unless liver transplant performed
Hepatic encephalopathy
Build up of toxin, particularly ammonia, in the brain
Reduced consciousness and confusion
More chronically presents with changes to personality, memory and mood
Precipitating factors of hepatic encephalopathy
Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (sedatives)
Management of hepatic encephalopathy
Laxatives promote excretion of ammonia
Antibiotics (rifaxmin) reduces number of intestinal bacteria producing ammonia
Nutritional support (may need NG tube)
