CIRRHOSIS Flashcards
Asterixis (liver flap), confusion and coma in a patient with liver cirrhosis is caused by what?
Hyperammonaemia
Liver normally converts ammonia into urea, this does not happen in liver damage
How does lactulose work to lower hyperammonaemia?
- Synthetic disaccharide broken down in colon by bacteria to fatty acids
- This lowers colonic pH which favours formation of NH4+ over NH3
- NH4+ not absorbed → trapped in colon
- Result ⇒ lower plasma ammonia concentrations
Explain why people with liver cirrhosis get the following symptoms:
- Jaundice
- Hypoglycaemia
- Coagulopathy
- Ascites/oedema
- Jaundice: loss of bilirubin metabolism
- Hypoglycaemia: loss of gluconeogenesis
- Coagulopathy: loss of clotting factors
- Ascites/oedema: loss of production of albumin
Which two forces control movement of fluid out of capillaries and into tissues?
- Hydrostatic pressure: drives fluid out of capillaries
- Oncotic pressure: proteins pull water into capillaries
Oestrogen levels rise in liver cirrhosis. Explain why and list three symptoms this would cause
Oestrogen is normally removed by the liver
- Gynaecomastia in men
- Spider naevi
- Palmar erythema
What does cirrhosis of the liver cause to blood flow through it? What condition will this cause?
Obstructed blood flow through liver → increased pressure in portal vein → portal hypertension
In liver disease which normally constitutively expressed vasodilator is produced in large amounts?
► this causes which hallmark sign seen in cirrhosis?
Nitric oxide (NO)
Reduced systemic vascular resistance → reduced blood pressure
Patients with cirrhosis but without portal hypertension will not develop which condition?
Ascites
Define ascites. How would you diagnose?
how is it treated?
Abnormal buildup of fluid in peritoneal cavity
- Diagnosis → physical exam, history, bloods, USS / CT, paracentesis
- Paracentesis → needle inserted through abdominal wall and fluid removed
Which blood vessels are responsible for many of the side-effects caused by portal hypertension? Explain why. Give 4 clinical consequences of this condition
Venous collaterals → Portosystemic collaterals (varices) develop spontaneously via engorgment of pre-existing normally collapsed anastomoses between portal and systemic venous systems. Shunt blood away from liver to systemic system, to reduce portal pressure. Not sufficient for normalising pressure.
- Umbilicus: caput medusa
- Oesophagus: varicose, upper GI bleed
- Stomach: upper GI bleed
- Rectum: haemorrhoids
Where is most oesophageal venous blood drained? Where is the rest drained? How does this relate to formation of varices in portal hypertension?
- Most drain into oesophageal veins → superior vena cava
- Small amount drains to left gastric vein (AKA coronary vein) → portal vein
♦ There are normally small collapsed collaterals between oesophageal veins and left gastric vein. In portal HTN these become engorged.
How does portal hypertension cause gastric varices? Which blood vessels are involved?
Small and normally collapsed collateral vessels between left gastric vein and splenic vein become engorged in portal hypertension
Which veins are involved in the collaterals causing this condition?
Caput Medusa
paraumbilical and epigastric veins: collaterals become engorged in portal hypertension
What are haemorrhoids? Where do internal haemorrhoids occur? Which vessels are involved when they are caused by portal hypertension?
- Vascular cushions
- Help maintain faecal continence and ensure no liquid escapes through sphincter
- If they become swollen → pathological
- Seen in constipation, straining, raised intra-abdominal pressure (pregnancy, ascites)
Internal: Above dentate line
Vessels involved in haemorrhoids in portal HTN: superior rectal vein and middle/inferior rectal veins
Why do you many patients with liver cirrhosis have low platelets? 2 points
Hypersplenism caused by engorgement of spleen as a result of portal hypertension → splenic sequestration
Depressed thrombopoietin levels
A patient with acute onset abdominal pain, splenomegaly, all the symptoms of portal hypertension but a normal liver biopsy is likely to have which condition?
Portal vein thrombosis
Give two reasons for new/worsening ascites in liver disease. How can you differentiate?
- Portal hypertension
- Malignancy causing leaky vasculature
► Sample ascitic fluid via paracentesis and work out difference between serum albumin and albumin in ascites
Serum albumin - ascites albumin = SAAG (serum ascites albumin gradient)
What is the treatment for ascites?
- Sodium restriction
- Spironolactone (drug of choice), loops 2nd line
- Paracentesis
- TIPS: transjugular intrahepatic portosystemic shunt
What infection are people with ascities more likely to get?
Which bacteria is normally implicated?
What symptoms would you expect to see?
How would you treat?
- Spontaneous bacterial peritonitis: ascitic fluid infection
- Gut bacteria → E. coli or klebsiella
- Fever, abdominal pain, tenderness
- Third-generation cephalosporin: achieves good levels in ascitic fluid
Describe some of the ways liver cirrhosis is diagnosed
- Gold standard: biopsy. Not if diagnosis clear from history, done only when it will change management
- Imaging: may show small, nodular liver but not sensitive or specific
- Clinical: ascites, low platelet, spider angiomata
Which cells are activated in liver disease and proliferate to produce fibrous tissue? What do they normally do in the liver?
- Stellate cells
- Perisinusoidal cells, normally storage site for retinoids (vit A metabolites)
- High yield fact: major contributor to liver cirrhosis
