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Questions and Answers
What is the function of the common bile duct in the liver's bile drainage system?
What is the function of the common bile duct in the liver's bile drainage system?
In which zone of the acinus is ischaemic/toxic injury most severe?
In which zone of the acinus is ischaemic/toxic injury most severe?
What structures are included in the smallest branches of the portal tracts?
What structures are included in the smallest branches of the portal tracts?
Which statement correctly describes the function of canaliculi in the liver?
Which statement correctly describes the function of canaliculi in the liver?
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What is the acinus in liver histology?
What is the acinus in liver histology?
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What characterizes bridging fibrosis in liver damage?
What characterizes bridging fibrosis in liver damage?
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Which of the following is NOT a characteristic of cirrhosis?
Which of the following is NOT a characteristic of cirrhosis?
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What is the term for chronic passive venous congestion of the liver characterized by a specific gross appearance?
What is the term for chronic passive venous congestion of the liver characterized by a specific gross appearance?
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What is the primary consequence of portal hypertension in cirrhosis?
What is the primary consequence of portal hypertension in cirrhosis?
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What are the consequences of extensive acute liver damage?
What are the consequences of extensive acute liver damage?
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What type of inflammatory cell is predominant in liver disease?
What type of inflammatory cell is predominant in liver disease?
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In the context of liver biopsy, what do grading systems assess?
In the context of liver biopsy, what do grading systems assess?
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In which condition is there an obstruction to venous outflow from the liver?
In which condition is there an obstruction to venous outflow from the liver?
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Which of the following is NOT a liver function?
Which of the following is NOT a liver function?
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What change occurs in sinusoids due to cirrhosis?
What change occurs in sinusoids due to cirrhosis?
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Which factor causes splanchnic vasodilatation in portal hypertension?
Which factor causes splanchnic vasodilatation in portal hypertension?
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What defines chronic liver disease according to duration?
What defines chronic liver disease according to duration?
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What is an essential visual characteristic of liver cirrhosis when using a trichrome stain?
What is an essential visual characteristic of liver cirrhosis when using a trichrome stain?
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Which type of liver injury is characterized by massive hepatic necrosis?
Which type of liver injury is characterized by massive hepatic necrosis?
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What is the likely outcome with ongoing liver insult leading to chronic damage?
What is the likely outcome with ongoing liver insult leading to chronic damage?
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Which liver enzymes are usually elevated in ischaemic liver injury?
Which liver enzymes are usually elevated in ischaemic liver injury?
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What primarily leads to increased pressure in the portal venous system?
What primarily leads to increased pressure in the portal venous system?
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What is a common consequence of portal hypertension in relation to fluid retention?
What is a common consequence of portal hypertension in relation to fluid retention?
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Which of the following best describes compensated cirrhosis?
Which of the following best describes compensated cirrhosis?
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What role does the renin-angiotensin-aldosterone system play in response to portal hypertension?
What role does the renin-angiotensin-aldosterone system play in response to portal hypertension?
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What effect do porto-systemic shunts have on liver function?
What effect do porto-systemic shunts have on liver function?
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What is a potential trigger for decompensating cirrhosis?
What is a potential trigger for decompensating cirrhosis?
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Which condition may indicate decompensated liver cirrhosis?
Which condition may indicate decompensated liver cirrhosis?
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What characteristic is associated with ascites due to portal hypertension?
What characteristic is associated with ascites due to portal hypertension?
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What is the approximate median survival time for a patient with compensated cirrhosis?
What is the approximate median survival time for a patient with compensated cirrhosis?
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Which factor significantly increases the 1-year mortality rate in patients with cirrhosis?
Which factor significantly increases the 1-year mortality rate in patients with cirrhosis?
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What is the median survival time for decompensated cirrhosis?
What is the median survival time for decompensated cirrhosis?
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Which of the following is NOT a complication of decompensated cirrhosis?
Which of the following is NOT a complication of decompensated cirrhosis?
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Which statement best summarizes the prognosis of patients with decompensated cirrhosis?
Which statement best summarizes the prognosis of patients with decompensated cirrhosis?
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What is the reported 1-year mortality rate for patients with decompensated cirrhosis presenting with ascites?
What is the reported 1-year mortality rate for patients with decompensated cirrhosis presenting with ascites?
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In terms of prognosis, how does the development of complications in cirrhosis affect mortality?
In terms of prognosis, how does the development of complications in cirrhosis affect mortality?
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Which of the following conditions is associated with a highest mortality risk exceeding 50% in decompensated cirrhosis?
Which of the following conditions is associated with a highest mortality risk exceeding 50% in decompensated cirrhosis?
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What outcome is likely if liver damage is extensive and leads to acute liver failure?
What outcome is likely if liver damage is extensive and leads to acute liver failure?
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Which type of cell injury is characterized by the death of small groups of liver cells?
Which type of cell injury is characterized by the death of small groups of liver cells?
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Which condition involves obstruction to venous outflow from the liver, leading to liver injury?
Which condition involves obstruction to venous outflow from the liver, leading to liver injury?
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In chronic passive venous congestion of the liver, what is the characteristic gross appearance known as?
In chronic passive venous congestion of the liver, what is the characteristic gross appearance known as?
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What typically marks the initial phase of ischaemic liver injury?
What typically marks the initial phase of ischaemic liver injury?
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What is a possible consequence of ongoing liver injury that results in chronic damage?
What is a possible consequence of ongoing liver injury that results in chronic damage?
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Which of the following provides the liver with its primary blood supply?
Which of the following provides the liver with its primary blood supply?
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Which statement best describes ischaemic hepatitis?
Which statement best describes ischaemic hepatitis?
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What characteristic feature is shared by both compensated and decompensated cirrhosis?
What characteristic feature is shared by both compensated and decompensated cirrhosis?
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What is a primary consequence of chronic biliary disease on liver function?
What is a primary consequence of chronic biliary disease on liver function?
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What characterizes the inflammation assessment of liver damage?
What characterizes the inflammation assessment of liver damage?
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Which of the following conditions is most likely to cause portal hypertension?
Which of the following conditions is most likely to cause portal hypertension?
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How does ascites develop in the context of liver disease?
How does ascites develop in the context of liver disease?
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What cellular changes occur in the liver during prolonged injury?
What cellular changes occur in the liver during prolonged injury?
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Which of the following metabolic dysfunctions is frequently associated with non-alcoholic fatty liver disease?
Which of the following metabolic dysfunctions is frequently associated with non-alcoholic fatty liver disease?
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What important role do hepatic stellate cells play in liver pathology?
What important role do hepatic stellate cells play in liver pathology?
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What histological feature is indicative of cirrhosis as observed under H&E staining?
What histological feature is indicative of cirrhosis as observed under H&E staining?
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Which of the following best describes the changes in hepatic venous pressure gradient (HVPG) associated with cirrhosis?
Which of the following best describes the changes in hepatic venous pressure gradient (HVPG) associated with cirrhosis?
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In which specific pattern does portal fibrosis typically manifest in cases of alcohol-related liver disease?
In which specific pattern does portal fibrosis typically manifest in cases of alcohol-related liver disease?
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What is a physiological consequence of portal hypertension resulting from cirrhosis?
What is a physiological consequence of portal hypertension resulting from cirrhosis?
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Which of the following describes the stage of liver damage characterized by bridging fibrosis?
Which of the following describes the stage of liver damage characterized by bridging fibrosis?
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What is a critical risk factor associated with cirrhosis that significantly impacts patient survival?
What is a critical risk factor associated with cirrhosis that significantly impacts patient survival?
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What vascular alteration is associated with advanced cirrhosis?
What vascular alteration is associated with advanced cirrhosis?
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What histological staining technique is commonly used to visualize fibrous tissue in liver biopsy samples?
What histological staining technique is commonly used to visualize fibrous tissue in liver biopsy samples?
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What is the approximate median survival time for a patient with decompensated cirrhosis?
What is the approximate median survival time for a patient with decompensated cirrhosis?
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Which complication is most likely to occur with decompensated cirrhosis?
Which complication is most likely to occur with decompensated cirrhosis?
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What is the 1-year mortality rate for a patient with compensated cirrhosis with varices?
What is the 1-year mortality rate for a patient with compensated cirrhosis with varices?
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How does the presence of ascites affect the prognosis of a patient with cirrhosis?
How does the presence of ascites affect the prognosis of a patient with cirrhosis?
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What is the median survival time for all patients diagnosed with cirrhosis?
What is the median survival time for all patients diagnosed with cirrhosis?
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In terms of prognosis, what is indicated by the development of other complications in decompensated cirrhosis?
In terms of prognosis, what is indicated by the development of other complications in decompensated cirrhosis?
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What effect does compensated cirrhosis have on a patient's 1-year mortality rate?
What effect does compensated cirrhosis have on a patient's 1-year mortality rate?
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Which of the following statements regarding the prognosis of decompensated cirrhosis is accurate?
Which of the following statements regarding the prognosis of decompensated cirrhosis is accurate?
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What physiological change leads to higher mean hydrostatic pressure in portal hypertension?
What physiological change leads to higher mean hydrostatic pressure in portal hypertension?
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Which of the following is a consequence of sodium and water retention associated with portal hypertension?
Which of the following is a consequence of sodium and water retention associated with portal hypertension?
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Which mechanism describes the body's response to counteract widespread vasodilatation in portal hypertension?
Which mechanism describes the body's response to counteract widespread vasodilatation in portal hypertension?
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What condition can lead to further reduction in liver perfusion and worsened liver damage in portal hypertension?
What condition can lead to further reduction in liver perfusion and worsened liver damage in portal hypertension?
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How is ascites primarily caused in patients with portal hypertension?
How is ascites primarily caused in patients with portal hypertension?
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Which complication is commonly associated with decompensated cirrhosis?
Which complication is commonly associated with decompensated cirrhosis?
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What is a primary effect of reflex renal vasoconstriction in the context of portal hypertension?
What is a primary effect of reflex renal vasoconstriction in the context of portal hypertension?
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Which factor could trigger decompensation in a compensated cirrhosis state?
Which factor could trigger decompensation in a compensated cirrhosis state?
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Study Notes
Liver Structure
- The liver is made up of plates of hepatocytes.
- Sinusoids are located between the plates of hepatocytes.
- Sinusoids drain into central hepatic vein branches.
- Portal tracts consist of the smallest branches of the:
- Portal vein
- Hepatic artery
- Bile duct
- There is a sharp interface between the portal tract and the surrounding parenchyma.
Bile Drainage
- Bile is formed by hepatocytes.
- Bile is secreted into canaliculi between hepatocytes.
- Small ductules form from canaliculi, which join to form small ducts in portal tracts.
- The left and right hepatic ducts join to form the common hepatic duct.
- The common hepatic duct joins the cystic duct to form the common bile duct.
- 75% of the time, the common bile duct and pancreatic duct join at the ampulla.
- The gallbladder is only responsible for bile storage.
Acinus
- The acinus is the favoured concept for understanding liver structure.
- The center of the acinus is the portal tract, which serves as the focal point for blood supply.
- The acinus refers to the hepatocytes and sinusoids from two adjacent lobules supplied by one portal tract.
- This concept helps explain patterns of damage: ischemic/toxic injury is most severe in zone 3.
Vascular Injury to the Liver
- Chronic (passive) venous congestion of the liver is associated with right heart failure (e.g., cor pulmonale, mitral stenosis).
- It is most marked in rare cases of tricuspid incompetence and constrictive pericarditis.
- Mild elevation of liver blood tests (ALT, AST) is common.
- Obstruction to venous outflow from the liver (hepatic vein/IVC) is known as Budd-Chiari syndrome.
- Infarction of the liver is extremely unusual.
- Ischemic injury to the liver ("ischemic hepatitis," "shock liver") is associated with hypoperfusion, hypotension/shock/circulatory failure.
- Marked elevation of liver blood tests (ALT, AST) is seen.
- Outcome depends on the underlying cause.
- Susceptibility is increased by passive venous congestion or cirrhosis.
Liver Function
- Synthesis of most plasma proteins, including clotting factors.
- Bile formation:
- Bilirubin excretion.
- Bile salts for digestion of fats and fat-soluble vitamins (ADEK).
- Detoxification of endogenous and exogenous compounds.
- Intermediary metabolism (alteration and storage).
- Immune function, acting as a buffer between the gut and the rest of the body.
- Storage of normal and abnormal substances.
- Hematopoiesis (in fetal and infant stages).
Damage to the Liver
- The liver has reserve and regenerative capacity.
- Outcomes of acute damage depend on:
- The degree of damage.
- The risk of acute liver failure if damage is extensive.
- Recovery with transient damage and no acute liver failure.
- Chronic damage if the insult is ongoing or repeated.
- Chronic liver disease is defined as lasting more than 6 months.
- Ongoing insult leads to chronic disease, characterized by:
- Fibrosis, increasing in degree with progression to cirrhosis.
- Different causes may co-exist, be superimposed, or potentiate each other.
Patterns of Cell Damage/Death
- Different types of cell injury can be reversible or irreversible.
- Different triggers for injury:
- Direct cytopathic, cytotoxic, or ischemic effects.
- Damage to hepatocytes rendering them antigenic (e.g., HBV).
- Damage to cells perceived as antigenic (e.g., autoimmune hepatitis).
- Different degrees of injury:
- Single cell death (apoptosis).
- Small groups of cells die (spotty necrosis).
- Large, confluent groups of cells die (bridging necrosis).
- Massive hepatic necrosis.
Assessment of Liver Damage
- Inflammation +/- necrosis: extent is "grade."
- Inflammation can be portal/periportal or lobular (parenchymal).
- Interface inflammation is known as "piecemeal necrosis."
- Necrosis can be present in single cells, as spotty necrosis, or bridging necrosis.
- Predominant inflammatory cell type depends on the etiology, not the duration of the disease.
Fibrosis
- Degree/extent of fibrosis is "stage."
- Fibrosis can be portal, periportal, bridging, or cirrhosis.
- Portal fibrosis connects portal tracts to each other.
- Periportal fibrosis connects portal tracts to central veins.
- Bridging fibrosis connects portal tracts to portal tracts or portal tracts to central veins.
- Cirrhosis is the most advanced stage of fibrosis.
Stages of Liver Fibrosis
- Stages of liver fibrosis are assessed using a trichrome stain.
- Fibrous tissue is stained blue by the trichrome stain.
Definition of Cirrhosis
- Cirrhosis is a diffuse distortion of the liver architecture with:
- Fibrous bands/septa surrounded by regenerative nodules.
- Distorted vascular relationships.
- Cirrhosis causes portal hypertension.
- It reduces the functional capacity of the liver.
- There is an increased risk of hepatocellular carcinoma in cirrhosis.
Cirrhosis (Continued)
- Cirrhosis is a structural endpoint of chronic liver disease due to ongoing damage.
- It represents a state of diminished liver reserve.
- Vascular changes due to cirrhosis include:
- Obliteration/thrombosis of veins within the liver.
- Collateral channels/shunts forming within the liver.
- Sinusoids becoming "capillarized" (loss of fenestrations).
- Rising hepatic venous pressure gradient (HVPG).
Portal Hypertension in Cirrhosis
- Initiated by increased hepatic resistance to portal blood flow, leading to elevated HVPG.
- Augmented by splanchnic vasodilatation (via.NO), increasing portal blood flow.
- Splanchnic vasodilatation lowers total peripheral resistance (TPR) and blood pressure (BP).
- A compensatory increase in cardiac output leads to a hyperdynamic circulation in cirrhosis.
- Splanchnic vasodilatation triggers compensatory mechanisms.
Simplified View of Portal Hypertension
- Increased blood supply to the intestines (splanchnic vasodilatation) leads to increased blood flow in the portal system.
- With a blocked liver, the portal venous system experiences increased pressure.
Portal Hypertension, Ascites & HRS
- Compensatory mechanisms for widespread vasodilatation include:
- Activation of the renin-angiotensin-aldosterone system.
- Stimulation of ADH secretion.
- Sodium and water retention.
- Reflex renal vasoconstriction, reducing perfusion and glomerular filtration rate (GFR).
- Ascites develops due to:
- Sodium and water retention associated with portal hypertension.
- Preferential accumulation of fluid in the peritoneal cavity.
- Leakage from peritoneal vessels.
- Higher mean hydrostatic pressure due to portal hypertension.
- Lower oncotic pressure (due to low albumin).
Portal Hypertension & Shunts
- Shunts develop to attempt to decompress portal hypertension:
- Intrahepatic porto-systemic shunts/collaterals.
- Extrahepatic porto-systemic anastomoses dilate.
- Therapeutic insertion of transjugular intrahepatic porto-systemic shunt (TIPS).
- Shunted blood bypasses the liver:
- Further reduces liver function (increases risk of hepatic encephalopathy).
- Exacerbated by "capillarisation" of sinusoids.
- Reduces liver perfusion, worsening damage.
Compensated vs Decompensated Cirrhosis
- Compensated ("silent") cirrhosis:
- May or may not have biochemical/radiological abnormality.
- May or may not have signs of chronic liver disease/portal hypertension.
- May or may not have varices on esophagogastroduodenoscopy (OGD).
- Potentially unstable state:
- Further injury may trigger decompensation:
- Infection, bleeding, hypotension, alcohol, medications, dehydration, trauma, surgery.
- Further injury may trigger decompensation:
Decompensated Cirrhosis
- Decompensated cirrhosis is characterized by:
- Ascites (may become refractory to treatment).
- Hepatic encephalopathy.
- Variceal hemorrhage.
- Hepatorenal syndrome (HRS).
- Jaundice.
- Infection (esp. spontaneous bacterial peritonitis).
- Hepatocellular carcinoma.
Prognosis of Cirrhosis
- Decompensation significantly affects prognosis (rate of progression).
- Prognosis is poor:
- One-year mortality is 1% for compensated cirrhosis.
- One-year mortality is 4% for compensated cirrhosis with varices.
- One-year mortality is 20% for decompensated cirrhosis with ascites.
- One-year mortality is >50% for decompensated cirrhosis with other features.
Natural History of Chronic Liver Disease
- Development of compensated cirrhosis can progress to decompensated cirrhosis, leading to death.
- Median survival is approximately 9 years for patients with compensated cirrhosis.
- Median survival is approximately 1.6 years for patients with decompensated cirrhosis.
- Orthotopic Liver Transplant (OLT) represents a treatment option.
Survival Times in Cirrhosis
- Survival times in cirrhosis are influenced by the stage of the disease.
- Median survival for all patients with cirrhosis is approximately 9 years.
- Median survival for patients with decompensated cirrhosis is approximately 1.6 years.
Overview of Liver Disease
- Liver disease is a significant cause of morbidity and mortality globally.
- Liver disease is less common than heart disease, cancer, and stroke.
- Gastroenterologists manage liver disease, sometimes specialising as hepatologists.
- Surgeons manage gallstones, pancreatitis, and extrahepatic biliary tract disease.
- GPs manage abnormal liver blood tests.
- Common aetiologies are:
- Cirrhosis: alcohol versus chronic viral disease (HBV)
- Tumours: liver metastases and pancreatic cancer versus primary hepatocellular carcinoma
- Disease patterns vary depending on the geographical location.
Causes of Liver Damage
- Liver damage can be caused by a variety of factors including:
- Alcohol abuse
- Non-alcoholic fatty liver disease (NAFLD)
- Associated with metabolic syndrome (type 2 DM, obesity etc.).
- Viruses:
- Acute infections: Hep A, E
- Chronic infections: Hep B, C
- Drugs
- Autoimmune diseases
- Inherited metabolic disorders: HFE, Wilson's disease, A1AT deficiency
- Vascular disorders: congestion or ischemia
- Chronic biliary disease: injury to the liver due to retained bile salts
Liver Structure
- The liver is a large organ (~1.5 kg).
- The liver has a large functional reserve.
- The liver has a stable cell population meaning it is capable of regeneration.
- The liver has a limited repertoire of responses to acute and chronic injury.
- It is important to consider the history, examination and test results when assessing liver disease as different causes of injury can interact.
Normal Liver - Blood Supply
- The liver receives blood from two sources:
- Hepatic artery
- Portal vein
- Blood flows into sinusoids.
- Sinusoids are blood spaces separating plates of hepatocytes.
- Sinusoids are lined by fenestrated endothelium and macrophages (Kupffer cells).
- The space of Disse, the area between sinusoids and hepatocytes contains hepatic stellate cells.
- Venous drainage occurs via the hepatic vein to the IVC to the right ventricle.
Vascular Injury to the Liver
- Liver infarction is extremely unusual.
- Ischemic injury can occur causing:
- "Ischemic hepatitis" or "shock liver"
- Associated with hypoperfusion, hypotension/shock/ circulatory failure
- Marked elevation in liver blood tests (ALT, AST)
- Outcome depends on the cause.
- Susceptibility is increased by passive venous congestion and cirrhosis.
Liver Function
- The liver performs many essential functions in the body, including:
- Synthesis of most plasma proteins
- Clotting factors
- Bile formation:
- Bilirubin: excretion
- Bile Salts: digestion - fat/fat-soluble vitamins ADEK
- Detoxification of endogenous and exogenous compounds
- Intermediary metabolism: alteration and/or storage of nutrients
- Immune function:
- Acts as a buffer between the gut and the rest of the body
- Storage of normal and abnormal compounds
- Haematopoiesis: in fetal/infant stages
Damage to the Liver
-
Acute Damage:
- The liver has significant reserve and regenerative capacity.
- Outcomes depend on the degree of damage.
- Very extensive damage can result in acute liver failure.
- Transient damage can result in recovery with no acute liver failure.
- On-going/repeated insults can cause chronic damage.
-
Chronic Damage:
- Ongoing insult can lead to chronic liver disease (>6 months).
- Fibrosis develops over time in varying degrees, leading to:
- Cirrhosis
- Different causes of liver injury can co-exist, be superimposed and/or potentiate each other.
Assessment of Liver Damage
-
Grade: Refers to:
- Extent of inflammation and/or necrosis
- Whether inflammation is portal/periportal or lobular (parenchymal)
- The amount of portal/periportal and/or lobular inflammation present
- Interface inflammation (piecemeal necrosis)
- Specific patterns of portal/periportal damage
- If necrosis is present, whether it involves single cells, spotty necrosis, or bridging necrosis.
- Predominant inflammatory cell type:
- Depends on etiology, not whether the disease is of acute or chronic duration.
-
Stage: Refers to:
- Degree/extent of fibrosis:
- Portal fibrosis
- Periportal fibrosis (sometimes perivenular/perisinusoidal pattern in alcohol/NAFLD)
- Bridging fibrosis: portal to portal tract or portal to central vein
- Cirrhosis
- Degree/extent of fibrosis:
- Liver biopsy:
- Complex scoring systems assess grade and stage independently.
Definition of Cirrhosis
- Cirrhosis is the end-stage of chronic liver disease due to ongoing chronic damage.
- Cirrhosis is characterized by:
- Diffuse distortion of liver architecture
- Fibrous bands/septa
- Regenerative nodules
- Distorted vascular relationships
- Cirrhosis causes portal hypertension.
- Cirrhosis reduces the functional capacity of the liver.
- Cirrhosis increases the risk of hepatocellular carcinoma.
Cirrhosis - Vascular Changes
- Vascular changes occur within the liver during cirrhosis:
- Obliteration/thrombosis of veins within the liver
- Collateral channels/shunts form within the liver
- Sinusoids become "capillarised" (lose fenestrations)
- Hepatic venous pressure gradient (HVPG) rises
Portal Hypertension in Cirrhosis
- Portal hypertension is initiated by increased hepatic resistance to portal blood flow leading to a rise in HVPG.
- Splanchnic vasodilation (via NO) increases portal blood flow, augmenting portal hypertension.
- Splanchnic vasodilatation lowers TPR and BP.
- Compensatory increase in cardiac output leads to a hyperdynamic circulation of cirrhosis.
Portal Hypertension, Ascites, and Hepatorenal Syndrome (HRS)
- Compensation for widespread vasodilation:
- Activation of the renin-angiotensin-aldosterone system
- Stimulation of ADH secretion
- Sodium and water retention
- Reflex renal vasoconstriction, reducing perfusion and GFR, increasing the risk of hepatorenal syndrome (HRS)
-
Ascites:
- Accumulation of fluid in the peritoneal cavity due to:
- Sodium and water retention associated with portal hypertension
- Leakage from peritoneal vessels
- Higher mean hydrostatic pressure due to portal hypertension
- Lower oncotic pressure due to low albumin
- Accumulation of fluid in the peritoneal cavity due to:
-
Hepatorenal Syndrome (HRS):
- A progressive, life-threatening renal dysfunction in patients with cirrhosis.
- Characterized by:
- Severe vasoconstriction of the renal arteries
- Decreased renal blood flow
- Oliguria (decreased urine output)
- Increasing creatinine levels
- Associated with high mortality rates
Compensated vs Decompensated Cirrhosis
-
Compensated Cirrhosis (silent):
- May or may not have biochemical or radiological abnormality
- May or may not have signs of chronic liver disease or portal hypertension
- May or may not have varices on OGD (gastroscopy).
- Potentially unstable state.
- Further injury can trigger decompensation:
- Infection
- Bleeding
- Hypotension
- Alcohol
- Medications
- Dehydration
- Trauma
- Surgery
-
Decompensated Cirrhosis:
- Characterized by:
- Ascites (may become refractory to treatment)
- Hepatic encephalopathy
- Variceal haemorrhage
- Hepatorenal syndrome (HRS)
- Jaundice
- Infection (especially spontaneous bacterial peritonitis)
- Hepatocellular carcinoma
- Characterized by:
-
Prognostic Impact:
- Decompensation significantly affects prognosis (rate of progression).
- One-year mortality:
- Compensated: 1%
- Compensated with varices: 4%
- Decompensated, ascites: 20%
- Decompensated, other features: >50%
Survival Times in Cirrhosis
- Decompensation significantly affects survival.
- Median survival:
- Patients with cirrhosis: ~9 years
- Patients with decompensated cirrhosis: ~1.6 years
Treatment Options
- Treatment options for cirrhosis depend on the severity of the disease and the presence of specific complications.
- Potential treatments include:
- Medications to manage complications like ascites, encephalopathy, and variceal bleeding.
- Liver transplantation: a definitive treatment option for end-stage liver disease, particularly for decompensated cirrhosis with specific complications.
- Transjugular Intrahepatic Portosystemic Shunt (TIPS): a procedure to reduce pressure in the portal vein by creating a shunt between the portal vein and the hepatic vein, offering temporary relief for complications like ascites and variceal bleeding.
Preventative Measures
- Preventative measures can help reduce the risk of liver disease and complications:
- Avoiding excessive alcohol consumption
- Maintaining a healthy weight
- Getting vaccinated against hepatitis A and B
- Screening for hepatitis C infection
- Managing underlying conditions like diabetes and obesity
- Avoiding potentially hepatotoxic drugs
Factors Affecting Prognosis
- Several factors influence the prognosis of patients with cirrhosis, including:
- Severity of liver disease
- Presence and severity of complications
- Age of the patient
- Overall health status
- Response to treatment
- Lifestyle adjustments
Importance of Early Diagnosis and Management
- Early diagnosis and appropriate management of liver disease are crucial to improve patient outcomes and prevent serious complications.
- Regular screening for liver disease is particularly important for individuals who have risk factors like excessive alcohol consumption, obesity, diabetes, or exposure to hepatitis viruses.
Areas of Further Research
- Significant research continues to focus on:
- Developing new treatments to slow or reverse liver damage
- Improving strategies to manage complications like ascites, encephalopathy, and variceal haemorrhage
- Identifying novel biomarkers for early detection and disease monitoring
- Understanding the complex pathogenesis of cirrhosis and developing targeted interventions
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Description
Test your knowledge on the intricate structure of the liver, including the arrangement of hepatocytes and the role of sinusoids. Explore the journey of bile from its formation to drainage, and discover the essential features of liver anatomy such as the acinus and portal tracts.