Cirrhosis

Gastroenterology (12%) Core Clinical Conditions

1B The Physician Associate is able to identify the condition as a possible diagnosis: may not have the knowledge/resources to confirm the diagnosis or to manage the condition safely, but can take measures to avoid immediate deterioration and refer appropriately.

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Definition Aetiology Pathophysiology Sign and Symptoms Investigations Management

Cirrhosis is a chronic, progressive liver disease characterised by the irreversible scarring and damage of liver tissue. It occurs as a result of long-term liver injury and inflammation, which leads to the replacement of healthy liver cells with fibrous scar tissue. This scarring disrupts the normal structure of the liver, impairing its ability to function efficiently.

1. Chronic Alcohol Abuse: Chronic and excessive alcohol consumption remains one of the leading causes of cirrhosis. Prolonged alcohol abuse leads to the accumulation of toxic metabolites in the liver, causing inflammation, cell injury, and eventually, fibrosis. Over time, this fibrotic scarring disrupts the liver's normal structure, impairing its function and leading to cirrhosis.
2. Viral Hepatitis: Viral hepatitis, particularly hepatitis B and C, is a significant cause of cirrhosis worldwide. These viruses primarily target liver cells, leading to chronic inflammation and subsequent scarring. Hepatitis B and C can be transmitted through blood, sexual contact, or intravenous drug use. Timely identification and treatment of viral hepatitis are crucial in preventing the progression to cirrhosis.
3. Non-Alcoholic Fatty Liver Disease (NAFLD): NAFLD, characterised by the accumulation of fat in the liver, is becoming increasingly prevalent and is closely associated with metabolic disorders such as obesity, type 2 diabetes, and dyslipidemia. In some individuals, NAFLD can progress to non-alcoholic steatohepatitis (NASH), a condition where liver inflammation and fibrosis occur, eventually leading to cirrhosis.
4. Autoimmune Hepatitis: Autoimmune hepatitis is a chronic inflammatory liver disease in which the immune system mistakenly attacks and damages liver cells. Over time, this persistent inflammation can cause cirrhosis. The exact triggers for autoimmune hepatitis remain unknown, but genetic and environmental factors likely play a role.
5. Genetic Disorders: Certain genetic disorders and inherited conditions can predispose individuals to cirrhosis. Examples include hemochromatosis, a condition causing excess iron accumulation in the liver, leading to tissue damage; Wilson disease, which results in copper accumulation; and alpha-1 antitrypsin deficiency, impairing liver enzyme production, among others. These genetic factors highlight the importance of understanding an individual's family history and screening for specific disorders.
6. Toxic Exposures: Exposure to toxins such as certain medications, chemicals, and industrial solvents can cause liver damage and eventually cirrhosis. Long-term exposure to these substances, either occupationally or through environmental factors, can progressively impair liver function and structure.

The most common cause of cirrhosis worldwide is chronic alcohol abuse, although other factors such as viral hepatitis, non-alcoholic fatty liver disease (NAFLD), autoimmune diseases, and genetic disorders can also contribute to its development.

The pathophysiology of cirrhosis involves a complex interplay of several mechanisms. Initially, hepatocellular injury occurs due to the inciting factors. In the case of alcohol abuse, this injury is primarily the result of toxic effects on hepatocytes and the generation of free radicals. In viral hepatitis, direct viral invasion leads to hepatocyte destruction and subsequent inflammation. Over time, these insults lead to chronic inflammation, hepatocyte death, and activation of the wound healing process.

As the liver tries to repair the damaged tissue, it initiates a cascade of events that involve the activation and proliferation of hepatic stellate cells (HSCs) and the deposition of extracellular matrix (ECM) proteins, particularly collagen. HSCs play a critical role in fibrogenesis and the subsequent development of fibrous scar tissue. They transform into myofibroblasts, which actively produce collagen and other ECM components, resulting in the formation of fibrous septa within the liver parenchyma.

The excessive accumulation of ECM disrupts the organised architecture of the liver. It leads to the distortion of hepatic lobules and the formation of regenerative nodules, which are islands of regenerating hepatocytes surrounded by fibrous tissue. This nodular regeneration further contributes to the development of cirrhosis by impeding blood flow through the liver, resulting in portal hypertension.

As cirrhosis progresses, the liver's ability to carry out its essential functions is compromised. Hepatocytes become dysfunctional, impairing the synthesis of proteins such as albumin and clotting factors. The reduced production of these proteins contributes to hypoalbuminemia and a predisposition to bleeding disorders. Additionally, impaired liver function leads to the accumulation of toxins, such as ammonia, in the bloodstream, causing hepatic encephalopathy.

Portal hypertension, a hallmark of cirrhosis, occurs due to increased resistance to blood flow within the liver. The fibrous septa disrupt the normal vasculature, leading to increased pressure within the portal vein. This elevated pressure causes collateral circulation to develop, leading to the formation of varices in the oesophagus, stomach, and rectum. These varices are prone to rupture, resulting in life-threatening bleeding.

Moreover, the liver's ability to metabolise and detoxify substances is compromised in cirrhosis. Hepatic clearance of medications, hormones, toxins, and waste products is reduced, leading to potential drug toxicity and accumulation of harmful metabolites in the body. The liver's role in regulating glucose metabolism, lipid metabolism, and bile production is also compromised, contributing to metabolic disturbances often observed in cirrhosis patients.

1. Fatigue and Weakness: Feeling exhausted and experiencing a constant lack of energy is a common complaint among cirrhosis patients. The liver's compromised ability to convert nutrients into energy contributes to fatigue and weakness.

2. Jaundice: Cirrhosis can cause a yellowing of the skin and the whites of the eyes, known as jaundice. This occurs due to the liver's inability to process bilirubin, a yellowish pigment produced by the breakdown of red blood cells.

3. Abdominal Pain: As cirrhosis progresses, individuals often experience discomfort or pain in the upper right portion of the abdomen. This can be due to an enlarged, swollen liver causing pressure on surrounding organs.

4. Fluid Retention: When the liver is unable to produce sufficient amounts of a protein called albumin, fluid accumulation in the abdomen (ascites) and legs (oedema) can occur. This leads to noticeable swelling and increased weight.

5. Easy Bruising and Bleeding: The liver plays a crucial role in producing blood clotting factors. In cirrhosis, decreased liver function can impair the clotting process, resulting in a tendency to bruise easily and prolonged bleeding from minor injuries.

6. Digestive Issues: Cirrhosis can lead to digestive problems such as nausea, vomiting, decreased appetite, and unintentional weight loss. The compromised liver function affects the body's ability to metabolise and absorb nutrients.

7. Changes in Mental Functioning: Hepatic encephalopathy is a condition that can arise from cirrhosis. It affects brain function and can cause mental confusion, forgetfulness, personality changes, and even coma in severe cases.

8. Spider Angiomas: These are small, spider-like blood vessels that appear on the skin's surface, particularly on the chest, face, and arms. They are caused by increased pressure in the vessels due to liver damage.

9. Gynecomastia: In cirrhosis, hormonal imbalances can occur, leading to the development of breast tissue in males (gynecomastia). This is due to the compromised liver's reduced ability to break down oestrogen.

10. Increased Sensitivity to Medications: Cirrhosis affects the liver's ability to metabolise medications, making individuals more susceptible to the side effects of various drugs.

Blood Tests:

A full blood count (FBC) allows evaluation of red and white blood cell counts and platelet levels, which can be affected by liver dysfunction. Liver function tests provide information about liver enzymes, bilirubin levels, and protein synthesis capabilities. Abnormalities in these values may suggest liver damage and the presence of cirrhosis.

Imaging Studies:

• Abdominal ultrasound is a non-invasive method used to visualise the liver, detect abnormal liver tissue, examine the blood flow within the liver, and identify any associated complications like liver tumours or ascites (fluid accumulation in the abdomen).

• Computerised tomography (CT) scans and magnetic resonance imaging (MRI) can provide detailed images of the liver and confirm the presence of cirrhosis.

• A liver biopsy may be necessary to definitively establish the diagnosis of cirrhosis when other methods are inconclusive or if the underlying cause needs to be identified.

Medical Interventions:

1. Identifying and treating underlying causes: It is crucial to identify and address the underlying cause of cirrhosis. Common causes include alcohol abuse, viral hepatitis, fatty liver disease, autoimmune disorders, and certain medications. Treating or managing these causes is essential in preventing further liver damage.

2. Symptom management: Cirrhosis can present with various symptoms such as fatigue, jaundice, itching, and fluid accumulation. Medications may be prescribed to manage these symptoms, including diuretics to reduce fluid retention and laxatives for constipation. Additionally, nutritional support may be provided to combat malnutrition and fatigue.

3. Preventing complications: Cirrhosis increases the risk of complications like portal hypertension, ascites, hepatic encephalopathy, and hepatocellular carcinoma. Medications may be prescribed to prevent or manage these complications, such as beta-blockers to reduce portal hypertension or lactulose to treat hepatic encephalopathy. Regular screening for liver cancer may also be advised.

Lifestyle Modifications:

1. Dietary changes: Cirrhosis patients should follow a balanced diet that includes adequate protein intake while limiting sodium and fluid intake to manage fluid retention. In advanced cases, a low-protein diet may be recommended to reduce the load on the liver. It is essential to avoid alcohol completely as it can worsen liver damage.

2. Weight management: Maintaining a healthy weight is crucial for cirrhosis patients. Obesity and excess weight can worsen liver function and lead to fatty liver disease. A physician or dietitian can provide guidance on achieving and maintaining a healthy weight.

3. Physical activity: Regular exercise within one's capacity can help improve overall well-being, reduce fatigue, and manage weight. Patients should consult with their healthcare provider to determine the appropriate level of physical activity for their condition.

Ongoing Monitoring and Support:

1. Medical follow-up: Regular check-ups and monitoring are essential for cirrhosis patients. This is often done by the gastroenterologist.

2. Support groups and counselling: Cirrhosis can have a significant impact on a person's mental and emotional well-being. Engaging with support groups or seeking counselling can provide emotional support and help manage the associated stresses and challenges.

3. Vaccinations and lifestyle precautions: Vaccinations for hepatitis A and B should be considered for cirrhosis patients who are not already immune. It is important to practise good hygiene, including handwashing, and to avoid risky behaviours such as intravenous drug use to prevent infections that can further damage the liver.

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