The Syndrome of Cirrhosis Flashcards
Liver cells that lay down fibrosis?
Hepatic stellate cells
2 main problems in liver cirrhosis?
Loss of functions due to there not being enough hepatocytes
Disruption of normal blood flow to and from the liver
Which veins drain into the portal system?
Superior mesenteric
Splenic vein
Gastric vein
Part from the inferior mesenteric
How does blood flow through the liver?
Oxygenated blood from hepatic artery + nutrient-rich, deoxygenated blood from the hepatic vein
Meet at the liver sinusoids
Goes into the:
Central vein
Hepatic vein
IVC
How does blood flow from the hepatic portal vein to the IVC?
There is a very low pressure in the hepatic vein (5-3 mmHg) with only a small gradient across the liver to the hepatic vein, which returns the blood to the IVC
What are the 4 anastomoses between the portal venous system and the systemic venous system?
Oesophageal and gastric venous plexus
Umbilical vein from the left portal vein to the epigastric venous system
Retroperitoneal collateral vessels
Hemorrhoidal venous plexus
Effects of portal hypertension on the anastamoses between the portal venous system and systemic venous system?
May become engorged, dilated or varicosed
Leads to rupture
ADD PICTURE 2
What is portal hypertension?
Pressure above the normal range of 5-8 mmHg
OR
A gradient of greater than 5 mmHg between the portal and hepatic veins
This represents an increase in hydrostatic P within the portal vein
2 causes of portal hypertension?
- Increased resistance to portal flow (R)
- Increased portal venous inflow (Q)
The change in pressure is equal to Q x R
How does cirrhosis affect the vasculature?
Leads to impaired hepatocellular and sinusoidal hypertension and portal-systemic shunting
Response is release of vasodilators; this decreases resistance (splanchnic and peripheral vasculature) also decreases blood volume
There is an increase in RAAS, sympathetc and ADH activity
Sodium and water retention leads to ASCITES
Classification of portal hypertension causes?
- Prehepatic - block of the portal vein before liver
- Intrahepatic - due to distortion of the liver architecture; this is either:
Pre-sinusoidal
OR
Post-sinusoidal, e.g: cirrhosis, alcoholic hepatitis
Also, budd-chiari syndrome
Pathway of hepatic carcinogenesis?
Recurrent hepatocyte death leads to regeneration that is recurrent and a mitogenic environment
Inflammation leads to deregulation of cell cycle control and DNA damage, from reaction oxygen and nitrogen species, etc
There may be other reasons, e.g: integration of Hep B viral DNA into self cells
When does hepatic carcinogenesis mostly occur?
When there is liver cirrhosis, for one reason or another
2 types of liver cirrhosis?
Compensated cirrhosis
Decompensated cirrhosis
Describe the presentation and diagnosis of compensated cirrhosis
Clinically, they are normal and it is usually and incidental finding
Portal hypertension may also be present
Describe the two presentations of decompensated cirrhosis
Liver failure:
Acute on chronic (can be pushed over the threshold by an acute event, e.g: infection, insult)
End stage liver disease - eventually, there will be insufficient hepatocytes
Signs of compensated cirrhosis?
Spider naevi (press in centre; positive test if all of the spider legs blanch) Palmar erythema Finger clubbing Gynaecomastia Hepatomegaly Splenomegaly
May be no signs
Signs of decompensated cirrhosis?
Jaundice Ascites Encephalopathy Bruising Leukonycia (extended white of nails)
Complication of cirrhosis?
Ascites (appearance of this is a marker of poor prognosis)
Encephalopathy
Variceal bleeding
Liver failure
General principles of treating decompensated cirrhosis?
Remove/treat the underlying cause
Look for and treat infection
Avoid NaCl retention (they are already retaining Na+)
Low threshold to switch to gluconeogenesis and lipolysis and catabolism
Nutritional recommendations in decompensated cirrhosis?
Small frequent meals and snacks to reduce fasting gluconeogenesis and muscle catabolism; beware fasting over night
Common complications of decompensated liver cirrhosis, and there causal diseases, and how to prevent this?
Osteoporosis and osteomalacia are common - supplement with calcium and vitamin D
Vitamin B supplementation (thiamine) is required in excess alcohol intake
In Primary Sclerosing Cholangitis and in Primary Biliary Cirrhosis, they may develop a vitamin deficiency in fat-soluble vitamins, so monitor and supplement
Diagnosing ascites?
Shifting dullness when lying on back and side
Ascites on ultrasound
Treatment of ascites?
Improve underlying liver disease and look for and treat infection, e.g: spontaneous bacterial peritonitis
Drugs; ensure they are not taking NSAIDs and think of the Na+ load if they are on IV
Give diuretics, but spironolactone first
Reduce salt intake but maintain nutrition; no added sodium diet
Paracentesis
TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt) - an aritificial vein connects the portal vein to the hepatic vein
Transplantation
Does abstaining from alcohol improve alcohol-related cirrhosis with ascites?
Yes; abstinence means 3/4 survive at 3 years
Describe sodium balance
Input (from diet) - output (urine + insensible)
Why is spironolactone used before diuretics in liver cirrhosis, but not in heart failure)
There is more aldosterone released in liver cirrhosis
Treating patients with spironolactone for ascites?
In new ascites - escalate spironolactone
In recurrent ascites - increments of spironolactone and loop diuretic
Monitor U&E frequently
Problems with ascities paracentesis?
Risk of infection
Encephalopathy
Hypovolaemia
What is hepatic encephalopathy?
Confusion/altered level of consciousness due to toxin build-up, e.g: ammonia generated in the intestine, from nitrogenous compounds, is shunted past the liver into the systemic circualtion
Diagnosed by looking for flap confusion, any neurological symptoms and alcohol withdrawal
Treatment of hepatic encephalopathy?
Look for cause, e.g: infection, metabolic, drugs, liver failure, and treat the cause
Lactulose (Rifaxamin) clears the gut and reduces transit time
Maintain nutritional status with small, frequents meals
If it was spontaneous, consider transplantation
What is Spontaneous Bacterial Peritonitis (SBP) and how is it diagnosed?
Translocated bacterial infection of ascites
Percuss all ascites
Neutrophil count > 250 cells/mm3
Treatment of SBP?
Urgent:
Antibiotics
Vascular-instability terlipressin (vasoconstrictive and improve renal perfusion)
Maintain renal perfusion
What is varices oesophageal?
Bleeding as a consequence of portal hypertension and can also occur in other anastamoses
Pathophysiology of variceal bleeding?
Portal hypertension causes an increase in varix size and decreased wall thickness, leading to increased variceal wall tension
Prophylaxis of variceal bleeds?
Using endoscopy, check for varices; if the patient has them:
Non-selective β-blockers, like propranolol and carvidelol
Variceal ligation sometimes
If they are bleeding, give terlipressin
Endoscopic therapies available for varices?
Sclerotherapy (injection that hardens tissue)
Variceal ligation - this is banding that has quicker eradication; if this does not work, balloon tamponade can be used
Complications of balloon tamponade?
Aspiration
Perforation
TIPSS (stops bleeding by shunting blood from the portal to the hepatic vein)
Secondary prevention of variceal bleeding?
β-blockers
Variceal band ligation
When to consider liver transplantation?
If patient has significant risk and if UKLED score is over 49 (takes into account INR, creatinine, bilirubin and Na+)
Which patients is UKELD not useful for?
Those with variant syndrome, e.g: chronic hepatic encephalopathy, polycystic liver disease, primary hyperlipidaemia, etc - have a bad prognosis but the score is not high enough
Hepatic cellular carcinoma
