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?

Splenomegaly Signup and view all the answers

What is a significant risk associated with cirrhosis?

Hepatocellular carcinoma Signup and view all the answers

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

Impaired conjugation of bilirubin due to hepatocyte damage Signup and view all the answers

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

Ascites Signup and view all the answers

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

Increased energy expenditure from chronic inflammation and malnutrition Signup and view all the answers

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

Pruritis Signup and view all the answers

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

Diarrhea Signup and view all the answers

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

To lower ammonia levels 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?

Lorazepam Signup and view all the answers

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

Acute confusion Signup and view all the answers

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

3 bowel motions per day Signup and view all the answers

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

Ascitic fluid accumulation Signup and view all the answers

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

Liver transplant Signup and view all the answers

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

It lowers ammonia levels Signup and view all the answers

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

Senna Signup and view all the answers

What is chronic liver disease (CLD)?

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

What process leads to the formation of cirrhosis?

Progressive fibrosis and architectural distortion of the liver Signup and view all the answers

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

Hepatic stellate cells (HSC) Signup and view all the answers

What is a distinguishing feature of cirrhosis?

Formation of widespread nodules and vascular reorganization Signup and view all the answers

How does fibrosis usually form in chronic liver disease?

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

What role do inflammatory cytokines play in chronic liver disease?

They make liver cells responsive to further injury and inflammation Signup and view all the answers

Which condition is NOT a characteristic of chronic liver disease?

Acute liver injury with immediate recoverability Signup and view all the answers

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

The transformation of hepatic stellate cells into fibroblasts Signup and view all the answers

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

Increased platelet consumption Signup and view all the answers

Which of the following signs is indicative of portal hypertension?

Ascites Signup and view all the answers

Which blood test primarily indicates liver synthetic function?

Coagulation profile Signup and view all the answers

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

Encephalopathy due to reduced ammonia excretion Signup and view all the answers

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

Reduced albumin synthesis Signup and view all the answers

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

Liver Biopsy Signup and view all the answers

What is NOT a preventative measure for chronic liver disease?

Use of hepatotoxic medications Signup and view all the answers

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

Improved evacuation of bilirubin Signup and view all the answers

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

Rifaximin Signup and view all the answers

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

Reduced clotting factor synthesis Signup and view all the answers

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

Decreased NO and increased ET-1 Signup and view all the answers

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

Splenic vein Signup and view all the answers

How does hyperdynamic circulation in cirrhosis primarily affect blood volume?

Causes excess water and sodium retention Signup and view all the answers

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

Formation of varices in the gastrointestinal tract Signup and view all the answers

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

Renal failure Signup and view all the answers

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

Nausea and vomiting Signup and view all the answers

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

Pruritis 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?

Ascites Signup and view all the answers

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

Bruising/Petechiae Signup and view all the answers

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

Accumulation of toxins, including ammonia 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?

Lowers ammonia levels in the bloodstream 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?

Cefotaxime Signup and view all the answers

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

Liver transplant Signup and view all the answers

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

Presence of ascitic fluid causing discomfort 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?

Hepatomegaly Signup and view all the answers

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

Achieve 3 bowel movements per day 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?

Lorazepam Signup and view all the answers

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

Cefotaxime Signup and view all the answers

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

Progressive deterioration of liver functions over six months Signup and view all the answers

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

Transformation into fibroblasts Signup and view all the answers

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

Continuous inflammation and injury Signup and view all the answers

Which statement best describes the vascular changes associated with cirrhosis?

Formation of neovascular structures Signup and view all the answers

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

Upregulation of inflammatory receptors by HSC Signup and view all the answers

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

Development of portosystemic shunts Signup and view all the answers

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

Persistent injury to liver tissue Signup and view all the answers

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

They trigger the activation of hepatic stellate cells Signup and view all the answers

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

Reduced oncotic pressure due to low albumin Signup and view all the answers

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

Liver damage leading to ammonia accumulation Signup and view all the answers

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

Coagulation profile with INR Signup and view all the answers

Which clinical sign is primarily indicative of hepatic portal hypertension?

Caput medusae Signup and view all the answers

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

Hepatic Encephalopathy Signup and view all the answers

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

Liver Biopsy Signup and view all the answers

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

Fat malabsorption Signup and view all the answers

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

Increased portal venous pressure Signup and view all the answers

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

Low salt diet to reduce fluid retention Signup and view all the answers

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

Primary Biliary Cholangitis 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.