Chronic Liver Disease & Cirrhosis Quiz
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Questions and Answers

What is the main characteristic of cirrhosis?

  • Fatty liver deposition
  • Irreversible fibrosis of the liver (correct)
  • Increase in liver size
  • Infection in the liver

    • Which mechanism contributes to the development of portal hypertension in cirrhosis?

  • Increased nitric oxide production in the liver
  • Increased endothelin-1 leading to blood vessel constriction (correct)
  • Activation of the hepatic artery
  • Decreased blood flow through the portal vein

    • What does hyperdynamic circulation in cirrhosis result from?

  • Decreased blood flow in the hepatic artery
  • Increased portal vein pressure only
  • Increased blood volume due to water and sodium retention (correct)
  • Increased nitric oxide only in the liver

    • Which complication can arise from portal hypertension?

    <p>Splenomegaly</p> Signup and view all the answers

    What is a significant risk associated with cirrhosis?

    <p>Hepatocellular carcinoma</p> Signup and view all the answers

    What is the primary mechanism causing jaundice in patients with chronic liver disease?

    <p>Impaired conjugation of bilirubin due to hepatocyte damage</p> Signup and view all the answers

    Which of the following is the most common complication of cirrhosis?

    <p>Ascites</p> Signup and view all the answers

    What does fatigue and weakness in chronic liver disease primarily result from?

    <p>Increased energy expenditure from chronic inflammation and malnutrition</p> Signup and view all the answers

    Which symptom of chronic liver disease is associated with excess bilirubin deposited in the skin?

    <p>Pruritis</p> Signup and view all the answers

    Which of the following symptoms is NOT recognized as a cardinal sign of chronic liver disease?

    <p>Diarrhea</p> Signup and view all the answers

    What is the primary reason for administering lactulose to a patient with acute confusion and chronic liver disease?

    <p>To lower ammonia levels</p> Signup and view all the answers

    Which of the following medications is contraindicated as a treatment option for addressing confusion in a patient with hepatic encephalopathy?

    <p>Lorazepam</p> Signup and view all the answers

    What is a common symptom that may indicate progression of hepatic encephalopathy in a patient?

    <p>Acute confusion</p> Signup and view all the answers

    In managing a patient with hepatic encephalopathy, what is the goal for bowel motions when using lactulose?

    <p>3 bowel motions per day</p> Signup and view all the answers

    Which of the following conditions would necessitate the use of paracentesis?

    <p>Ascitic fluid accumulation</p> Signup and view all the answers

    What is the definitive management for end-stage chronic liver disease?

    <p>Liver transplant</p> Signup and view all the answers

    Which statement accurately describes a potential use for rifaximin in a patient with liver disease?

    <p>It lowers ammonia levels</p> Signup and view all the answers

    What does not play a role in reducing ammonia levels in patients with hepatic encephalopathy?

    <p>Senna</p> Signup and view all the answers

    What is chronic liver disease (CLD)?

    <p>A progressive deterioration of liver functions lasting more than six months</p> Signup and view all the answers

    What process leads to the formation of cirrhosis?

    <p>Progressive fibrosis and architectural distortion of the liver</p> Signup and view all the answers

    Which cells initiate the process of fibrosis in chronic liver disease?

    <p>Hepatic stellate cells (HSC)</p> Signup and view all the answers

    What is a distinguishing feature of cirrhosis?

    <p>Formation of widespread nodules and vascular reorganization</p> Signup and view all the answers

    How does fibrosis usually form in chronic liver disease?

    <p>From the deposition of extracellular matrix (ECM) in response to injury</p> Signup and view all the answers

    What role do inflammatory cytokines play in chronic liver disease?

    <p>They make liver cells responsive to further injury and inflammation</p> Signup and view all the answers

    Which condition is NOT a characteristic of chronic liver disease?

    <p>Acute liver injury with immediate recoverability</p> Signup and view all the answers

    What is the primary event that marks the transition to irreversible fibrosis?

    <p>The transformation of hepatic stellate cells into fibroblasts</p> Signup and view all the answers

    What is a common result of splenomegaly in patients with chronic liver disease?

    <p>Increased platelet consumption</p> Signup and view all the answers

    Which of the following signs is indicative of portal hypertension?

    <p>Ascites</p> Signup and view all the answers

    Which blood test primarily indicates liver synthetic function?

    <p>Coagulation profile</p> Signup and view all the answers

    What is a typical cause of confusion in patients with chronic liver disease?

    <p>Encephalopathy due to reduced ammonia excretion</p> Signup and view all the answers

    Which of the following conditions is specifically noted for causing ascites?

    <p>Reduced albumin synthesis</p> Signup and view all the answers

    Which imaging technique is considered the gold standard for confirming chronic liver disease and cirrhosis?

    <p>Liver Biopsy</p> Signup and view all the answers

    What is NOT a preventative measure for chronic liver disease?

    <p>Use of hepatotoxic medications</p> Signup and view all the answers

    What leads to reduced jaundice in patients with chronic liver disease?

    <p>Improved evacuation of bilirubin</p> Signup and view all the answers

    Which of the following is a pharmacological treatment used for hepatic encephalopathy?

    <p>Rifaximin</p> Signup and view all the answers

    The presence of bruising or petechiae in a patient is primarily an indication of which underlying issue?

    <p>Reduced clotting factor synthesis</p> Signup and view all the answers

    What primary change in nitric oxide and endothelin-1 levels occurs in cirrhosis, contributing to portal hypertension?

    <p>Decreased NO and increased ET-1</p> Signup and view all the answers

    Which anatomical site is most affected by the back pressure resulting from portal hypertension?

    <p>Splenic vein</p> Signup and view all the answers

    How does hyperdynamic circulation in cirrhosis primarily affect blood volume?

    <p>Causes excess water and sodium retention</p> Signup and view all the answers

    What is the consequence of increased portal vein pressure due to cirrhosis?

    <p>Formation of varices in the gastrointestinal tract</p> Signup and view all the answers

    In cirrhosis, which of the following is least likely to be a direct consequence of portal hypertension?

    <p>Renal failure</p> Signup and view all the answers

    What symptom of chronic liver disease is primarily a result of poor gastric emptying and mechanical nausea?

    <p>Nausea and vomiting</p> Signup and view all the answers

    Which symptom in chronic liver disease is caused by excess bilirubin accumulation in the skin?

    <p>Pruritis</p> Signup and view all the answers

    What cardinal sign may point to fluid accumulation in the abdomen due to portal hypertension in a patient with cirrhosis?

    <p>Ascites</p> Signup and view all the answers

    Which sign associated with chronic liver disease may indicate a bleeding tendency due to liver dysfunction?

    <p>Bruising/Petechiae</p> Signup and view all the answers

    What causes the confusion seen in patients with chronic liver disease?

    <p>Accumulation of toxins, including ammonia</p> Signup and view all the answers

    What is the primary action of lactulose in the treatment of a patient with chronic liver disease and acute confusion?

    <p>Lowers ammonia levels in the bloodstream</p> Signup and view all the answers

    Which of the following medications would NOT be appropriate in managing a patient with acute confusion due to hepatic encephalopathy?

    <p>Cefotaxime</p> Signup and view all the answers

    Which procedure is considered definitive management for end-stage chronic liver disease?

    <p>Liver transplant</p> Signup and view all the answers

    What complication might necessitate a paracentesis procedure in a patient with chronic liver disease?

    <p>Presence of ascitic fluid causing discomfort</p> Signup and view all the answers

    Which of the following symptoms is NOT typical of a patient presenting with acute confusion in chronic liver disease?

    <p>Hepatomegaly</p> Signup and view all the answers

    What is the intended outcome of administering lactulose to a patient with hepatic encephalopathy?

    <p>Achieve 3 bowel movements per day</p> Signup and view all the answers

    In a patient with chronic liver disease, which treatment should be avoided for managing confusion due to hepatic encephalopathy?

    <p>Lorazepam</p> Signup and view all the answers

    Which antibiotic is used in treating spontaneous bacterial peritonitis in patients with chronic liver disease?

    <p>Cefotaxime</p> Signup and view all the answers

    What is the most defining feature of chronic liver disease (CLD)?

    <p>Progressive deterioration of liver functions over six months</p> Signup and view all the answers

    What process is initiated by hepatic stellate cells (HSC) during chronic liver injury?

    <p>Transformation into fibroblasts</p> Signup and view all the answers

    Which characteristic signifies the transition from reversible to irreversible fibrosis in chronic liver disease?

    <p>Continuous inflammation and injury</p> Signup and view all the answers

    Which statement best describes the vascular changes associated with cirrhosis?

    <p>Formation of neovascular structures</p> Signup and view all the answers

    In chronic liver disease, what primarily causes the accumulation of extracellular matrix (ECM)?

    <p>Upregulation of inflammatory receptors by HSC</p> Signup and view all the answers

    What is a consequence of hepatic architectural distortion in the final stages of chronic liver disease?

    <p>Development of portosystemic shunts</p> Signup and view all the answers

    Which factor is considered essential in driving the progression of fibrosis in chronic liver disease?

    <p>Persistent injury to liver tissue</p> Signup and view all the answers

    What role do inflammatory cytokines play in the development of chronic liver disease?

    <p>They trigger the activation of hepatic stellate cells</p> Signup and view all the answers

    What is the primary reason for fluid retention in chronic liver disease?

    <p>Reduced oncotic pressure due to low albumin</p> Signup and view all the answers

    Which of the following best describes the underlying cause of asterixis in chronic liver disease?

    <p>Liver damage leading to ammonia accumulation</p> Signup and view all the answers

    What is often used to measure the synthetic function of the liver in chronic liver disease?

    <p>Coagulation profile with INR</p> Signup and view all the answers

    Which clinical sign is primarily indicative of hepatic portal hypertension?

    <p>Caput medusae</p> Signup and view all the answers

    What condition may result from the accumulation of toxic metabolites in patients with liver disease?

    <p>Hepatic Encephalopathy</p> Signup and view all the answers

    Which investigation would most accurately evaluate for cirrhosis-related liver changes?

    <p>Liver Biopsy</p> Signup and view all the answers

    What is a notable consequence of reduced bile acid synthesis in chronic liver disease?

    <p>Fat malabsorption</p> Signup and view all the answers

    What factor primarily leads to splenomegaly in patients with chronic liver disease?

    <p>Increased portal venous pressure</p> Signup and view all the answers

    Which dietary change is essential for managing ascites in chronic liver disease?

    <p>Low salt diet to reduce fluid retention</p> Signup and view all the answers

    Which autoimmune condition is associated with liver dysfunction and may present with an elevated anti-mitochondrial antibody?

    <p>Primary Biliary Cholangitis</p> Signup and view all the answers

    Study Notes

    Chronic Liver Disease & Cirrhosis

    • CLD is a progressive deterioration of liver functions for more than six months
    • CLD includes synthesis of clotting factors, other proteins, detoxifying harmful products, and excreting bile.
    • CLD is a continuous progression of inflammation, destruction, and regeneration of liver parenchyma leading to fibrosis and cirrhosis
    • Cirrhosis is the final stage of CLD, resulting in disrupted liver architecture, forming nodules, vascular reorganization, neo-angiogenesis, and ECM deposition

    Pathophysiology: Chronic Liver Disease

    • CLD pathogenesis is a continuous progressive process of hepatic fibrosis, liver tissue distortion, and regeneration nodule formation
    • Fibrosis is the deposition of ECM in response to chronic liver injury
    • Fibrosis is usually irreversible but reversible early on
    • Hepatic stellate cells (HSC), dormant cells found in the space between sinusoids and hepatocytes, transform into fibroblasts and upregulate the expression of inflammatory receptors
    • HSC activation leads to ECM accumulation and progressive fibrosis

    Pathophysiology: Cirrhosis

    • Cirrhosis is the end stage of CLD with irreversible fibrosis
    • Characterized by portal hypertension (increased pressure in the portal vein) and hyperdynamic circulation (increased blood volume in the portal system)
    • Sinusoidal endothelial cells (SECs) which line the hepatic sinusoids produce nitric oxide (NO) - a vasodilator, and endothelin-1 (ET-1) - a vasoconstrictor
    • Increased ET-1 and decreased NO in cirrhosis lead to liver blood vessel constriction and portal hypertension
    • Increased NO in the splanchnic circulation leads to blood vessel dilation, activating the renin-angiotensin-aldosterone system (RAAS), and resulting in water and sodium retention, increasing blood volume and hyperdynamic circulation

    Pathophysiology: Portal Hypertension

    • As resistance to blood flow increases within the portal circulation, the pressure builds up and tries to find alternative routes
    • The pressure can back up into the gastro-oesophageal veins causing esophageal varices, the splenic vein causing splenomegaly, the umbilical veins causing caput medusae, and the rectal viens causing haemorrhoids

    Decompensation

    • Deterioration in liver function in cirrhosis characterized by:
      • Jaundice (impaired bilirubin excretion)
      • Ascites (accumulation of fluid in the abdomen)
      • Hepatic Encephalopathy (neurological symptoms)
      • Variceal Haemorrhage (high mortality)

    Cardinal Symptoms

    • Fatigue and weakness
    • Nausea and vomiting
    • Pruritis
    • Jaundice
    • Bleeding
    • Weight gain
    • Confusion
    • Somnolence
    • Fever/Abdominal pain
    • Upper GI bleeding (haematemesis)

    Cardinal Signs

    • Reduced GCS/Asterixis
    • Jaundice
    • Bruising/Petechiae
    • Raised JVP
    • Ascites
    • Splenomegaly
    • Peripheral Oedema

    Symptoms - Causes

    • Fatigue and weakness: Catabolic state, malnutrition, poor diet of alcohol-related disease (ALD)
    • Nausea and vomiting: Poor gastric emptying, increased acid production, ascites causing mechanical nausea
    • Pruritis: Excess bilirubin deposited in skin
    • Jaundice: Hepatocyte damage, reducing bilirubin conjugation
    • Bleeding: Reduced clotting factors produced, platelets consumed due to splenomegaly
    • Weight gain: Fluid retention and third spacing, given hyperdynamic state, reduced albumin production
    • Confusion: Encephalopathy due to reduced ammonia excretion, vitamin B12 deficiency due to alcohol Wernicke's
    • Fever/Abdominal pain: Subacute bacterial peritonitis due to ascites
    • Upper GI bleed (haematemesis/malaena): Oesophageal Varices due to portal hypertension

    Signs - Causes

    • Reduced GCS/Asterixis: Hepatic Encephalopathy due to reduced excretion of ammonia
    • Jaundice: Hepatocyte damage reducing bilirubin conjugation
    • Bruising/Petechiae: Reduced clotting factor synthesis, consumptive thrombocytopaenia
    • Ascites: Portal hypertension, reduced oncotic pressure due to reduced albumin synthesis
    • Splenomegaly/Caput medusae: Portal hypertension
    • Peripheral oedema: Reduced albumin production
    • Pallor: Anaemia of chronic disease, vitamin B12 deficiency, iron deficiency

    Differential Diagnosis

    • Alcohol related liver disease
    • Non-alcoholic fatty liver disease
    • Viral Hepatitis (Hepatitis B, C)
    • Autoimmune Hepatitis
    • Primary Sclerosing Cholangitis
    • Primary Biliary cholangitis
    • Medication related (Methotrexate, amiodarone)
    • Hereditary (Haemochromatosis, Wilson's disease, Alpha-1 Antitrypsin deficiency)
    • CHF/Nephrotic syndrome (for oedema)

    Investigations: Bloods

    • Liver function tests (LFTs): Raised ALT/AST (hepatocyte damage), raised GGT/ALP (biliary tree injury), raised bilirubin (jaundice)
    • Coagulation profile: Raised INR, reduced coagulation factor production (measure of liver synthetic function)
    • Albumin: Reduced (measure of synthetic function)
    • Full blood count (FBC): Low platelets, anemia
    • Viral Hepatitis screen: Hepatitis A, B, C, EBV, CMV, VZV, HIV
    • Autoantibody screen: Anti Liver Kidney Ab (AIH), Anti Smooth muscle Ab (PSC), Anti Mitochondrial Ab (PBC)
    • Iron studies and ferritin: Raised Ferritin, Fe, and T sat, low TIBC (HFE)
    • Caeruloplasmin and serum copper: Reduced in Wilson's
    • Serum A1AT Level: Reduced A1AT deficiency

    Investigations: Imaging

    • Liver Ultrasound: Evaluate liver morphology for nodularity or coarse texture of cirrhosis, evaluate for ascites, hepatomegaly/splenomegaly, hepatocellular carcinoma (HCC)
    • MRI Liver/MRCP: MRI Liver - higher quality image to evaluate for liver tumour/morphology, MRCP to evaluate biliary tree (PSC/PBC)
    • Oesophagogastroduodenoscopy (OGD): To screen/surveillance for oesophageal varices

    Investigations: Special Tests

    • Liver elastography: Can give a score to evaluate hepatic steatosis and fibrosis
    • Liver Biopsy: Gold standard but invasive, may not be required if other investigations suggest CLD/Cirrhosis

    Management

    • Prevention: Alcohol cessation, avoid hepatotoxic medications, weight loss and diet management, diabetes mellitus optimisation for hepatic steatosis, hepatitis A and B vaccination
    • Pharmacological: Beta blockers for varices, lactulose for encephalopathy (increases bacterial uptake of ammonia), rifaximin for encephalopathy, diuretics and low salt diet for ascites and oedema management
    • Procedures: Paracentesis to drain ascitic fluid, OGD banding of varices, trans-jugular intrahepatic portosystemic shunt
    • Surgical: Liver transplant definitive management
    • Palliative care: Can be involved early for optimisation of symptoms and advanced care planning

    Case Presentation

    • A 65-year-old man presents with acute confusion and behavioural disturbance
    • He has haemochromatosis and chronic liver disease
    • Physical exam shows: asterixis, distended abdomen with shifting dullness, caput medusae
    • The appropriate treatment for his confusion is Lactulose.
    • Lactulose lowers ammonia levels and is indicated for the treatment of hepatic encephalopathy
    • Rifaxamin is also indicated in addition to lactulose
    • Lorazepam sedation does not address the underlying cause
    • Cefotaxime is used for spontaneous bacterial peritonitis

    Chronic Liver Disease

    • Chronic Liver Disease (CLD) is the progressive deterioration of liver function for more than six months
    • CLD includes reduced ability to:
      • Synthesize clotting factors
      • Synthesis of other proteins
      • Detoxification of harmful metabolic products
      • Excretion of bile
    • CLD is a continuous process of inflammation, destruction, and regeneration of liver parenchyma, leading to fibrosis and cirrhosis

    Cirrhosis

    • Cirrhosis is the end stage of CLD
    • Cirrhosis results in disruption of liver architecture, the formation of widespread nodules, vascular reorganization, neo-angiogenesis, and extracellular matrix deposition

    Pathophysiology of CLD

    • CLD is a progressive process of hepatic fibrosis, liver tissue architectural distortion, and regeneration nodule formation
    • Fibrosis is ECM deposition in response to chronic liver injury
    • Hepatic stellate cells (HSC) are usually dormant cells found between sinusoids and hepatocytes
    • HSC are activated in response to chronic liver injury, transforming into fibroblasts and upregulating inflammatory receptors
    • This leads to ongoing HSC activation, resulting in ECM accumulation and progressive fibrosis

    Pathophysiology of Cirrhosis

    • Cirrhosis is the end stage of CLD with irreversible fibrosis
    • Cirrhosis is characterized by portal hypertension and hyperdynamic circulation
    • Sinusoidal endothelial cells (SECs) produce nitric oxide (NO) and endothelin-1 (ET-1)
    • In cirrhosis, increased ET-1 and decreased NO lead to liver blood vessel constriction, initiating portal hypertension
    • In splanchnic circulation, increased NO leads to blood vessel dilation, activating the renin-angiotensin-aldosterone system (RAAS), resulting in water and sodium retention, increasing blood volume, and creating hyperdynamic circulation
    • Cirrhosis is a risk factor for Hepatocellular Carcinoma

    Portal Hypertension

    • Portal hypertension is increased pressure in the portal vein
    • Portal hypertension occurs due to increased resistance to blood flow within the portal circulation
    • Portal vein pressure backs up and tries to find alternative routes around the obstruction
    • This pressure can back up into:
      • Gastro-oesophageal veins: oesophageal varices
      • Splenic vein: splenomegaly
      • Umbilical veins: caput medusae
      • Rectal veins: haemorrhoids

    Decompensation

    • Decompensation is an acute deterioration in liver function in a patient with cirrhosis
    • Decompensation is characterised by the development of:
      • Jaundice
      • Ascites
      • Hepatic Encephalopathy
      • Variceal Haemorrhage

    Cardinal Symptoms of CLD & Cirrhosis

    • Fatigue and weakness
    • Nausea and vomiting
    • Pruritis
    • Jaundice
    • Bleeding
    • Weight gain
    • Confusion
    • Somnolence
    • Fever/Abdominal pain
    • Upper GI bleeding: Haematemesis

    Cardinal Signs of CLD & Cirrhosis

    • Reduced GCS/Asterixis
    • Jaundice
    • Bruising/Petechiae
    • Raised JVP
    • Ascites
    • Splenomegaly
    • Peripheral Oedema

    Causes of Symptoms in CLD & Cirrhosis

    • Fatigue and weakness: Catabolic state, malnutrition, poor diet
    • Nausea and vomiting: Poor gastric emptying, increased acid production, ascites causing mechanical nausea
    • Pruritis: Excess bilirubin deposited in skin
    • Jaundice: Hepatocyte damage, reducing conjugation of bilirubin
    • Bleeding: Reduced clotting factor production, platelets consumed due to splenomegaly
    • Weight gain: Fluid retention and third spacing, reduced albumin production
    • Confusion: Encephalopathy due to reduced ammonia excretion, B12 deficiency due to alcohol Wernicke's
    • Fever/Abdominal pain: Subacute bacterial peritonitis due to ascites
    • Upper GI Bleed: Haematemesis, malaena: Oesophageal Varices due to portal hypertension

    Causes of Signs in CLD & Cirrhosis

    • Reduced GCS/Asterixis: Hepatic Encephalopathy due to reduced excretion of ammonia
    • Jaundice: Hepatocyte damage reducing conjugation of bilirubin
    • Bruising/Petechiae: Reduced clotting factor synthesis, consumptive thrombocytopaenia
    • Ascites: Due to portal hypertension, reduced oncotic pressure due to reduced albumin synthesis
    • Splenomegaly/Caput medusae: Portal hypertension
    • Peripheral oedema: Reduced albumin production
    • Pallor: Anaemia of chronic disease, B12 deficiency, iron deficiency

    Differential Diagnosis for CLD & Cirrhosis

    • Alcohol related liver disease
    • Non-alcoholic fatty liver disease
    • Viral Hepatitis- Hepatitis B, C
    • Autoimmune Hepatitis
    • Primary Sclerosing Cholangitis
    • Primary Biliary cholangitis
    • Medication related: Methotrexate, amiodarone
    • Hereditary: Haemochromatosis, Wilson's Disease, Alpha 1 Antitrypsin Deficiency
    • CHF/Nephrotic syndrome (for oedema)

    Investigations for CLD & Cirrhosis

    • Bloods:

      • LFTs: Raised ALT/AST hepatocyte damage, raised GGT/ALP biliary tree injury, raised bilirubin: Jaundice
      • Coagulation profile: Raised INR, reduced coagulation factor production
      • Albumin: Reduced - measure of synthetic function
      • FBC: Low platelets, Anaemia
      • Viral Hepatitis Screen: Hep A, B, C, EBV, CMV, VZV, HIV
      • Autoantibody screen: Anti Liver Kidney Ab- AIH, Anti Smooth muscle Ab- PSC, Anti Mitochondrial Ab-PBC
      • Iron studies and ferritin: Raised Ferritin, Fe, and T sat, low TIBC- HFE
      • Caeruloplasmin and serum copper: Reduced in Wilson's
      • Serum A1AT Level: Reduced A1AT deficiency

    • Imaging:

      • Liver Ultrasound: Evaluate liver morphology for nodularity or coarse texture of cirrhosis, evaluate for ascites, hepatomegaly/splenomegaly, HCC
      • MRI Liver/ MRCP: MRI Liver - higher quality image to evaluate for liver tumour/morphology, MRCP to evaluate the biliary tree- PSC/PBC
      • OGD: To screen/surveillance of oesophageal varices

    • Special Tests:

      • Liver elastography: Can give a score to evaluate for hepatic steatosis and fibrosis
      • Liver Biopsy: Gold standard but invasive, may not be required if other investigations suggest CLD/Cirrhosis

    Management of CLD & Cirrhosis

    Prevention

    • Alcohol cessation
    • Avoid hepatotoxic medications
    • Weight loss and diet management
    • DM optimisation for hepatic steatosis
    • Hep A and B vaccination

    Pharmacological

    • B Blockers for varices
    • Lactulose for encephalopathy
    • Rifaxamin for encephalopathy
    • Diuretics and low salt diet for ascites and oedema management

    Procedures

    • Paracentesis to drain ascitic fluid
    • OGD banding of varices
    • Trans-jugular Intrahepatic Portosystemic Shunt

    Surgical

    • Liver transplant: definitive management

    Palliative Care

    • Involved early for optimization of symptoms and advanced care planning

    Case Presentation

    • 65 year old gentleman presents to the ED with acute confusion and behavioural disturbance
    • Past medical history includes haemochromatosis and chronic liver disease
    • Physical examination demonstrates asterixis, distended abdomen with shifting dullness, caput medusae
    • The appropriate treatment for his confusion is lactulose
    • Lactulose lowers ammonia levels and therefore is indicated for the treatment of hepatic encephalopathy
    • Rifaxamin is also indicated for hepatic encephalopathy
    • Senna is a stimulant laxative and has no role in ammonia reduction
    • Lorazepam sedation will not address the underlying cause
    • Cefotaxime is an antibiotic used for treatment of spontaneous bacterial peritonitis

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    Description

    Test your knowledge on Chronic Liver Disease (CLD) and its progression to cirrhosis. This quiz covers the pathophysiology, mechanisms of liver damage, and the roles of the hepatic stellate cells in fibrosis. Understand the intricacies of liver function and disease management.

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