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Questions and Answers
What characterizes acute liver failure in a patient with a previously normal liver?
What characterizes acute liver failure in a patient with a previously normal liver?
Which of the following is a common cause of acute liver failure in the UK?
Which of the following is a common cause of acute liver failure in the UK?
What is a potential histological finding in cases of acute liver failure?
What is a potential histological finding in cases of acute liver failure?
Which of the following conditions is NOT classified as a cause of acute liver failure?
Which of the following conditions is NOT classified as a cause of acute liver failure?
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What does portal hypertension commonly lead to in patients with liver disease?
What does portal hypertension commonly lead to in patients with liver disease?
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Which clinical feature is characteristic of acute liver failure?
Which clinical feature is characteristic of acute liver failure?
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What causes renal impairment in hepatorenal syndrome?
What causes renal impairment in hepatorenal syndrome?
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Which stage of hepatic encephalopathy involves coma?
Which stage of hepatic encephalopathy involves coma?
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Which statement about hepatic encephalopathy is true?
Which statement about hepatic encephalopathy is true?
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Which treatment approach is appropriate for hepatic encephalopathy?
Which treatment approach is appropriate for hepatic encephalopathy?
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What is a potential consequence of increased glutamine in the brain associated with hepatic encephalopathy?
What is a potential consequence of increased glutamine in the brain associated with hepatic encephalopathy?
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Which stage of hepatic encephalopathy is characterized by minimal symptoms that may affect social functions?
Which stage of hepatic encephalopathy is characterized by minimal symptoms that may affect social functions?
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What is the primary mechanism by which ammonia is detoxified in the brain during liver dysfunction?
What is the primary mechanism by which ammonia is detoxified in the brain during liver dysfunction?
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What is the main indication for treating ascitic fluid in patients with a suspected infection?
What is the main indication for treating ascitic fluid in patients with a suspected infection?
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Which liver enzyme is the most sensitive and specific marker for hepatocellular damage?
Which liver enzyme is the most sensitive and specific marker for hepatocellular damage?
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What does an AST/ALT ratio greater than 2 usually indicate?
What does an AST/ALT ratio greater than 2 usually indicate?
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Which laboratory test is least indicative of acute liver damage?
Which laboratory test is least indicative of acute liver damage?
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Which test correlates with elevated alkaline phosphatase to demonstrate liver origin?
Which test correlates with elevated alkaline phosphatase to demonstrate liver origin?
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Why might ALT levels be normal in a patient with chronic liver disease?
Why might ALT levels be normal in a patient with chronic liver disease?
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Which of the following could indicate an extrahepatic source of AST?
Which of the following could indicate an extrahepatic source of AST?
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What is the main source of alkaline phosphatase (ALP) in the liver?
What is the main source of alkaline phosphatase (ALP) in the liver?
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What is the primary mechanism leading to ascites in liver disease?
What is the primary mechanism leading to ascites in liver disease?
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What is the commonest cause of portal hypertension?
What is the commonest cause of portal hypertension?
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Which treatment is considered for primary prevention of variceal bleeding?
Which treatment is considered for primary prevention of variceal bleeding?
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What laboratory finding is important for diagnosing spontaneous bacterial peritonitis (SBP)?
What laboratory finding is important for diagnosing spontaneous bacterial peritonitis (SBP)?
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What is the effect of lactulose in the treatment of hepatic encephalopathy?
What is the effect of lactulose in the treatment of hepatic encephalopathy?
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What condition is characterized by periumbilical collateral veins as a result of portal hypertension?
What condition is characterized by periumbilical collateral veins as a result of portal hypertension?
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Which of the following is a common symptom associated with ascites?
Which of the following is a common symptom associated with ascites?
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Which of the following is considered a contraindication for diuretic use in the management of ascites?
Which of the following is considered a contraindication for diuretic use in the management of ascites?
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What is the primary goal of treating variceal bleeding?
What is the primary goal of treating variceal bleeding?
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What is the recommended approach for managing diuretic-resistant ascites?
What is the recommended approach for managing diuretic-resistant ascites?
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Which of the following conditions can lead to acute liver failure through pregnancy-related mechanisms?
Which of the following conditions can lead to acute liver failure through pregnancy-related mechanisms?
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Which laboratory marker is critical for diagnosing acute liver failure in previously healthy patients?
Which laboratory marker is critical for diagnosing acute liver failure in previously healthy patients?
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Which viral pathogen among the following is primarily associated with acute liver failure?
Which viral pathogen among the following is primarily associated with acute liver failure?
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Which of the following describes a histological finding consistent with acute liver failure?
Which of the following describes a histological finding consistent with acute liver failure?
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What is one potential consequence of severe cholestasis related to liver failure?
What is one potential consequence of severe cholestasis related to liver failure?
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What is a key characteristic of hepatorenal syndrome?
What is a key characteristic of hepatorenal syndrome?
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Which of the following stages of hepatic encephalopathy is characterized by drowsiness?
Which of the following stages of hepatic encephalopathy is characterized by drowsiness?
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Which factor is NOT considered a precipitating cause of hepatic encephalopathy?
Which factor is NOT considered a precipitating cause of hepatic encephalopathy?
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What is the physiological consequence of increased ammonia in the brain?
What is the physiological consequence of increased ammonia in the brain?
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Which classification of hepatic encephalopathy is associated with decompensated liver cirrhosis?
Which classification of hepatic encephalopathy is associated with decompensated liver cirrhosis?
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What is the most significant complication associated with severe hepatic encephalopathy?
What is the most significant complication associated with severe hepatic encephalopathy?
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What distinguishes minimal hepatic encephalopathy from overt hepatic encephalopathy?
What distinguishes minimal hepatic encephalopathy from overt hepatic encephalopathy?
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Why is hepatorenal syndrome often diagnosed as a diagnosis of exclusion?
Why is hepatorenal syndrome often diagnosed as a diagnosis of exclusion?
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What is a significant indicator for initiating treatment in suspected spontaneous bacterial peritonitis (SBP)?
What is a significant indicator for initiating treatment in suspected spontaneous bacterial peritonitis (SBP)?
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Which enzyme is known to leak from hepatocytes due to hepatocellular damage?
Which enzyme is known to leak from hepatocytes due to hepatocellular damage?
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In which situation is an AST/ALT ratio greater than 5 most indicative?
In which situation is an AST/ALT ratio greater than 5 most indicative?
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Which lab test is best correlated with liver obstruction or cholestasis?
Which lab test is best correlated with liver obstruction or cholestasis?
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What does a high alkaline phosphatase (ALP) level indicate?
What does a high alkaline phosphatase (ALP) level indicate?
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What could be a reason for normal AST and ALT levels in a patient with chronic liver disease?
What could be a reason for normal AST and ALT levels in a patient with chronic liver disease?
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What is the typical AST/ALT ratio in patients with alcoholic hepatitis?
What is the typical AST/ALT ratio in patients with alcoholic hepatitis?
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Which of the following tests evaluates the liver's synthetic function?
Which of the following tests evaluates the liver's synthetic function?
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What is a common complication associated with ascites due to liver disease?
What is a common complication associated with ascites due to liver disease?
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What is a therapeutic approach for managing refractory ascites in patients with cirrhosis?
What is a therapeutic approach for managing refractory ascites in patients with cirrhosis?
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Which of the following is NOT a mechanism contributing to ascites development in liver disease?
Which of the following is NOT a mechanism contributing to ascites development in liver disease?
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What is the primary prevention method aimed at reducing the risk of variceal bleeding?
What is the primary prevention method aimed at reducing the risk of variceal bleeding?
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Which type of portal hypertension is characterized by increased resistance to portal blood flow?
Which type of portal hypertension is characterized by increased resistance to portal blood flow?
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What is the most common cause of ascites?
What is the most common cause of ascites?
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What is the recommended action if a variceal bleed does not respond to initial treatments?
What is the recommended action if a variceal bleed does not respond to initial treatments?
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Which finding is indicative of portal hypertension during physical examination?
Which finding is indicative of portal hypertension during physical examination?
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What is the significance of using rifaximin in the management of hepatic encephalopathy?
What is the significance of using rifaximin in the management of hepatic encephalopathy?
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Which of the following conditions is classified under hepatic causes of portal hypertension?
Which of the following conditions is classified under hepatic causes of portal hypertension?
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Study Notes
Acute Liver Failure
- Acute liver injury with encephalopathy and deranged coagulation (INR > 1.5) in a patient with a previously normal liver
- Rare but life-threatening syndrome
- Most common causes vary worldwide, but usually involve viral hepatitis (especially in the UK, paracetamol overdose is common)
- Histologically, there is necrosis of liver acini, involving a substantial part of the liver
- Severe fatty change may be seen in some cases, examples include pregnancy, Reye syndrome, or after intravenous tetracycline
Causes of Acute Hepatic Failure
- Viral hepatitis (e.g., Hepatitis A, Hepatitis B, cytomegalovirus, hemorrhagic fever virus)
- Drugs (e.g., paracetamol, antibiotics, antidepressants, salicylate [Reye syndrome], NSAID, herbal medicines)
- Toxins, organic solvents, mushroom toxin
- Hepatic failure in pregnancy (e.g., acute fatty liver of pregnancy, HELLP syndrome)
- Vascular causes (e.g., Budd-Chiari syndrome, portal vein thrombosis)
- Alpha-1 antitrypsin deficiency
- Wilson disease
- Malignancy (e.g., extensive metastases)
- Heatstroke
Clinical Features of Acute Liver Failure
- Jaundice
- Hepatic encephalopathy
- Fever, vomiting, low blood pressure, low blood glucose
- Cerebral edema (in 80% of patients)
- Impaired gluconeogenesis
- Kidney injury (e.g., hepatorenal syndrome and acute tubular necrosis)
Hepatorenal Syndrome
- Renal impairment secondary to liver disease
- Haemodynamic effects of portal hypertension reduce renal perfusion, typically associated with ascites
- Diagnosis of exclusion – no other kidney pathology
- Poor prognosis
Hepatic Encephalopathy
- Spectrum of neuro-psychiatric abnormalities seen in liver dysfunction and/or porto-systemic shunting
- Functional disturbance of the brain, potentially reversible
- If severe, associated with cerebral edema and cerebral hypoperfusion
- Types:
- Type A: acute liver failure
- Type B: porto-systemic shunting with normal liver
- Type C: cirrhosis (= decompensation)
- Episodic (may be recurrent) HE +/- persistent HE
Stages of Hepatic Encephalopathy
- Stages 1-4: Confusion, Drowsiness, Somnolence, Coma
- Minimal HE may be revealed by psychometric testing
- Minimal HE can affect social function, work life, behavior, and fitness to drive
- Minimal HE + stage 1 HE = covert HE, stages 2 to 4 = overt HE
Hepatic Encephalopathy: Pathogenesis
- Reduced detoxification in the liver
- Portosystemic shunting allows more ammonia to enter the systemic circulation, bypassing the liver
- Detoxification of ammonia occurs more in skeletal muscle/kidney and converted to glutamate (NOT UREA as in the liver)
- Astrocytes in the brain also detoxify ammonia via glutamine synthetase
- Increased glutamine in the brain brings more water into astrocytes → swelling of astrocytes → cerebral edema & intracranial hypertension
Hepatic Encephalopathy: Treatment
- Identify and correct precipitating factors (e.g., infection, bleeding, dehydration, drugs)
- Reduce ammonia production and absorption (e.g., lactulose [oral or enema], non-absorbable antibiotics [e.g., rifaximin], fluids, stop diuretic therapy)
Portal Hypertension
- Classified by level/site of origin of portal hypertension
- Commonest cause is cirrhosis
- Pathogenesis in cirrhosis:
- Initiated: increased resistance to portal blood flow
- Augmented: increased portal blood flow
- Classification of causes of portal hypertension:
- Pre-hepatic: portal vein thrombosis
- Hepatic:
- Cirrhosis
- Non-cirrhotic (e.g., portal tract fibrosis due to schistosomiasis)
- Post-hepatic: obstruction of venous outflow from the liver (rare)
Consequences of Portal Hypertension
- Porto-systemic collaterals:
- Extrahepatic: portal venous and systemic venous circulations anastomose:
- Varices (esophageal and gastric, risk of bleed)
- Rectal, periumbilical (‘caput medusae’)
- Extrahepatic: portal venous and systemic venous circulations anastomose:
- Shunting of portal venous blood (reduced liver function)
- Haemodynamic alterations:
- Ascites and hepatorenal syndrome
- Splenomegaly (congestive)
- Secondary hypersplenism
Esophageal and Gastric Varices
- 30% of patients with esophageal varices will have a bleed
- Mortality is high, high rate of recurrence
- Heavy alcohol users are at increased risk
- Remember: not all upper GI bleeds are varices
Esophageal and Gastric Varices: Prevention and Treatment
- Primary Prevention: Screen to identify and treat moderate to severe varices before a first bleed, endoscopic band ligation and/or non-selective beta blockers.
- Secondary Prevention: Treat to prevent recurrent bleeding, endoscopic band ligation and/or non-selective beta blockers.
- Variceal Bleed: Resuscitate, drugs to reduce portal blood flow, prevent/treat complications (aspiration, infection, HE), endoscopic treatment of varices by band ligation, endoscopic sclerotherapy not favoured (complications), if above fail: TIPS placement or surgery.
Ascites in Liver Disease
- Sodium retention by the kidneys → increases the volume of extracellular fluid → ascites and edema
- Increased hydrostatic pressure due to portal hypertension
- Lower oncotic pressure (to keep fluid in) due to low albumin
- Clinical Presentation:
- Abdominal distension
- Shifting dullness on percussion
Ascites
- Cirrhosis is the commonest cause (>80%)
- Other causes: malignancy, non-cirrhotic portal hypertension, heart failure, pancreatitis, TB
Ascites Management
- Paracentesis = tap of ascites fluid
- Diagnostic tap – do cell count, microbiology (blood culture bottles), albumin, cytology
- Therapeutic tap - diuretic-resistant ascites in cirrhosis
- Treatment:
- Na+ restriction, diuretics (spironolactone)
- Avoid NSAID (risk of acute renal failure and hyponatremia, lowers effect of diuretics)
- High index of suspicion for infection (low threshold for paracentesis)
- Diuretic-resistant = refractory ascites
Spontaneous Bacterial Peritonitis (SBP)
- Infection of ascites fluid without evidence of surgically-treatable intra-abdominal cause
- Infection associated with cirrhosis (E.coli, Klebsiella)
- Early diagnosis and prompt treatment give better outcome
- Subtle/silent presentation
- Low threshold for paracentesis of ascites fluid
- Suspect: Fever, abdominal pain/tenderness, altered mental state
- Treat if ascites fluid cell count >250 polys/mm3
- Antibiotic prophylaxis if high risk (e.g., previous SBP or bleed)
Liver Blood Tests
-
Hepatocellular Damage:
- Transaminases (ALT, AST)
-
Obstruction to Bile Flow (Cholestasis):
- Alkaline phosphatase (ALP), Gamma-glutamyl transferase (GGT)
- Bilirubin
-
Liver Function:
- Bilirubin – abnormality not liver or biliary tract specific
- Albumin (long half life, indicator of chronic damage)
- Coagulation function (PT/INR) (clotting factors have short half life– better indicator of acute damage)
Hepatocellular Damage: Liver Enzymes
- Alanine transaminase (ALT): sensitive/specific marker for hepatocellular damage
- Aspartate transaminase (AST): less specific, also in muscle, myocardium, kidney
- Both leak from damaged hepatocytes
- Level of rise is poorly correlated with severity/prognosis
- Very high in acute hepatocellular damage
- May be only mildly elevated or normal despite chronic liver disease
- AST/ALT ratio can be informative
- Usually >2 suggests alcohol-related damage
AST/ALT Ratio
- Ratio of AST to ALT made by hepatocytes is approximately 2.5:1. AST is removed from serum by the liver sinusoidal cells twice as quickly, so resulting serum levels are about equal in healthy individuals.
- BUT in conditions with chronic, constant hepatocyte damage (e.g., alcoholic hepatitis, hepatocellular carcinoma) and during early-stage acute liver damage (e.g. viral hepatitis) the serum levels of AST and ALT reflect levels closer to background in hepatocytes.
- An AST/ALT ratio >5 indicates an extrahepatic source of AST.
Obstructive (Cholestatic) Liver Enzymes
-
Alkaline Phosphatase (ALP):
- Situated on the hepatocyte border of bile canaliculi
- Hepatocytes react to obstruction to bile flow by leaking alkaline phosphatase
- Other sources: bone, placenta
-
Gamma-glutamyl transferase (GGT):
- Very sensitive but not specific
- Good for correlating with elevated alkaline phosphatase to demonstrate that ALP is of liver origin
- Also induced by alcohol, drugs.
Acute Liver Failure
- Acute liver failure is a rare but life-threatening syndrome characterized by encephalopathy and impaired coagulation (INR > 1.5) in a patient with a previously normal liver.
- The most common causes of acute liver failure vary globally, but often involve viral hepatitis or paracetamol overdose.
- Histologically, acute liver failure is characterized by necrosis of liver cell clusters (acini) affecting a significant portion of the liver.
- Severe fatty changes in the liver can be observed in cases of pregnancy, Reye syndrome, or after intravenous tetracycline use.
Causes of Acute Hepatic Failure
- Viral: hepatitis A, hepatitis B, cytomegalovirus, hemorrhagic fever viruses
- Drugs: paracetamol, antibiotics, antidepressants, salicylates (Reye syndrome), NSAIDs, herbal medicines
- Toxins & Solvents: organic solvents, mushroom toxin
- Pregnancy: acute fatty liver of pregnancy, HELLP syndrome
- Vascular: Budd-Chiari syndrome, portal vein thrombosis
- Genetic: alpha-1 antitrypsin deficiency, Wilson disease
- Malignancy: extensive metastases
- Heatstroke
Clinical Features of Acute Liver Failure
- Jaundice
- Hepatic encephalopathy
- Fever, vomiting, low blood pressure, low blood glucose
- Cerebral edema (80% of patients)
- Impaired gluconeogenesis
- Kidney injury (hepatorenal syndrome)
- Acute tubular necrosis
Hepatorenal Syndrome
- Renal impairment secondary to liver disease.
- Haemodynamic effects of portal hypertension impair renal perfusion, often associated with ascites.
- Diagnosis of exclusion - other kidney pathologies are ruled out such as:
- Hypovolemia/shock
- Acute tubular necrosis
- Associated with a poor prognosis.
Hepatic Encephalopathy
- Spectrum of neuro-psychiatric abnormalities seen in liver dysfunction and/or porto-systemic shunting.
- Represents a functional disturbance of the brain, potentially reversible.
- Severe cases can lead to cerebral edema and cerebral hypoperfusion.
- Classified into four types:
- Type A: acute liver failure
- Type B: porto-systemic shunting with a normal liver
- Type C: cirrhosis (decompensation)
- Episodic (may be recurrent) HE +/- persistent HE
Stages of Hepatic Encephalopathy
- Stage 1: Confusion
- Stage 2: Drowsiness
- Stage 3: Somnolence
- Stage 4: Coma
Hepatic Encephalopathy: Pathogenesis
- Reduced detoxification in the liver.
- Portosystemic shunting allows ammonia to enter the systemic circulation, bypassing the liver.
- Ammonia detoxification shifts from the liver to skeletal muscle and kidney, leading to the conversion of ammonia to glutamate.
- Astrocytes in the brain detoxify ammonia via glutamine synthetase.
- Increased glutamine in the brain causes water influx into astrocytes, leading to brain swelling, cerebral edema, and intracranial hypertension.
Hepatic Encephalopathy: Treatment
- Identify and correct precipitating factors:
- Infection
- Bleeding
- Dehydration
- Drug use (sedatives, alcohol)
- Reduce ammonia production and absorption:
- Lactulose (oral or enema): acidifies the gut
- Non-absorbable antibiotics (e.g., Rifaximin): reduce urease-producing bacteria
- Fluids: prevent dehydration
- Discontinue diuretic therapy
Portal Hypertension
- Classified by the level/site of origin of portal hypertension.
- The most common cause is cirrhosis.
- Pathogenesis in cirrhosis:
- Increased resistance to portal blood flow
- Increased portal blood flow
- Classification of causes of portal hypertension:
- Pre-hepatic: portal vein thrombosis
-
Hepatic:
- Cirrhosis
- Non-cirrhotic (e.g., portal tract fibrosis due to schistosomiasis)
- Post-hepatic: obstruction of venous outflow from the liver (rare)
Consequences of Portal Hypertension
-
Porto-systemic collaterals:
- Extrahepatic anastomoses between portal venous and systemic venous circulations:
- Varices (esophageal and gastric, risk of bleeding)
- Rectal varices
- Periumbilical varices (“caput medusae”)
- Extrahepatic anastomoses between portal venous and systemic venous circulations:
- Shunting of portal venous blood: reduced liver function
-
Haemodynamic alterations:
- Ascites and hepatorenal syndrome
- Splenomegaly: congestive, secondary hypersplenism
Esophageal and Gastric Varices
- 30% of patients with esophageal varices will experience a bleed, which carries a high mortality rate and recurrence risk.
- Heavy alcohol users are particularly susceptible.
Esophageal and Gastric Varices: Management
-
Primary prevention:
- Screen for and treat moderate to severe varices before their first bleed.
- Endoscopic band ligation and/or non-selective beta blockers.
-
Secondary prevention:
- Treatment to prevent recurrent bleeding.
- Endoscopic band ligation and/or non-selective beta blockers.
-
Variceal bleed:
- Resuscitate the patient.
- Medications to reduce portal blood flow.
- Prevent/treat complications (aspiration, infection, HE).
- Endoscopic treatment of varices by band ligation.
- Placement of a Transjugular Intrahepatic Portosystemic Shunt (TIPS) or surgery if other methods fail.
Ascites in Liver Disease
- Ascites results from increased fluid volume in the extracellular space due to:
- Sodium retention by the kidneys
- Increased hydrostatic pressure due to portal hypertension
- Reduced oncotic pressure (albumin levels)
- Clinical presentation: abdominal distention, shifting dullness on percussion.
Ascites
- Cirrhosis is the most common cause (>80%).
- Other causes:
- Malignancy
- Non-cirrhotic portal hypertension
- Heart failure, pancreatitis, tuberculosis
Ascites: Management
-
Paracentesis:
- Diagnostic: analyze ascites fluid for cell count, microbiology, albumin, and cytology.
- Therapeutic: for diuretic-resistant ascites in cirrhosis.
-
Medical management:
- Sodium restriction
- Diuretics (spironolactone)
- Avoid NSAIDs
- High index of suspicion for infection
- Diuretic-resistant ascites = refractory ascites
Spontaneous Bacterial Peritonitis (SBP)
- Infection of ascitic fluid without surgically-treatable causes.
- Most commonly associated with cirrhosis (E.coli, Klebsiella).
- Early diagnosis and treatment lead to better outcomes.
- Often presents subtly or silently.
- A low threshold for paracentesis should be used.
- Suspect SBP with: fever, abdominal pain/tenderness, altered mental state.
- Treat if ascitic polymorphonuclear cell count > 250 cells/mm3.
- Implement antibiotic prophylaxis for high-risk individuals (e.g., previous SBP or bleed).
Liver Blood Tests
-
Hepatocellular damage:
- Transaminases (ALT, AST)
-
Obstruction to bile flow (cholestasis):
- Alkaline phosphatase (ALP) , Gamma-glutamyl transferase (GGT)
- Bilirubin
-
Liver function:
- Bilirubin
- Albumin
- Coagulation function (PT/INR)
Hepatocellular Damage: Liver Enzymes
- Alanine transaminase (ALT): sensitive and specific marker for hepatocellular damage.
- Aspartate transaminase (AST): less specific, also present in muscle, myocardium, and kidney.
- Both enzymes leak from damaged hepatocytes.
- The level of enzyme elevation does not correlate well with severity or prognosis.
- AST and ALT are very high in acute hepatocellular damage.
- They may be mildly elevated or normal despite chronic liver disease.
AST/ALT Ratio
- In healthy individuals, the AST/ALT ratio is approximately 2.5:1.
- In conditions with chronic or recent hepatocyte damage (e.g., alcoholic hepatitis, hepatocellular carcinoma), the AST/ALT ratio may be closer to 1.
- An AST/ALT ratio >5 suggests an extrahepatic source of AST.
Obstructive (Cholestatic) Liver Enzymes
-
Alkaline phosphatase (ALP):
- Present on the border of bile canaliculi in hepatocytes.
- Elevation indicates obstruction to bile flow.
- Other sources: bone, placenta
-
Gamma-glutamyl transferase (GGT):
- Very sensitive but not specific.
- Helps confirm that elevated ALP is of liver origin.
- Also induced by alcohol and drugs.
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Description
This quiz explores the critical aspects of acute liver failure, focusing on its causes, symptoms, and histological features. It emphasizes the importance of recognizing this rare but life-threatening condition, especially in relation to viral hepatitis and drug overdoses. Test your knowledge and understanding of this significant medical syndrome.
