Cirrhosis: Etiology, Features, and Complications

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Questions and Answers

Which of the following best describes the pathophysiology linking portal hypertension to the development of ascites?

  • Reduced hepatic synthesis of albumin leads to decreased oncotic pressure, promoting fluid extravasation into the peritoneal space, exacerbated by increased portal venous pressure. (correct)
  • Portal hypertension causes increased lymphatic drainage from the liver, overwhelming the lymphatic system's capacity to return fluid to the systemic circulation.
  • Increased portal pressure directly forces fluid into the peritoneal cavity due to disruption of the liver capsule.
  • Elevated portal venous pressure stimulates the kidneys to retain sodium and water, leading to increased intravascular volume and subsequent ascites formation.

A patient with cirrhosis and known oesophageal varices is admitted with haematemesis. After initial resuscitation, which intervention has the highest priority in the acute management?

  • Urgent abdominal paracentesis to relieve potential ascites-related pressure on varices.
  • Administration of intravenous Vitamin K to correct coagulopathy.
  • Endoscopic variceal ligation to directly control the source of bleeding. (correct)
  • Commencement of a high-protein diet to promote liver regeneration.

In a patient with portal hypertension secondary to cirrhosis, which laboratory finding would be LEAST expected?

  • Elevated alanine transaminase (ALT) and aspartate transaminase (AST).
  • Elevated serum albumin. (correct)
  • Prolonged prothrombin time.
  • Reduced platelet count.

A patient with portal hypertension and cirrhosis develops hepatic encephalopathy. What is the primary mechanism by which lactulose improves this condition?

<p>Lactulose acidifies the colon, converting ammonia ($NH_3$) to ammonium ($NH_4^+$), which is then excreted in the faeces, reducing ammonia absorption. (A)</p> Signup and view all the answers

Which statement best explains the rationale for restricting dietary sodium in a patient with portal hypertension and ascites?

<p>Decreased sodium intake reduces intravascular volume by decreasing water retention, which subsequently minimizes fluid extravasation into the peritoneal cavity. (C)</p> Signup and view all the answers

A cirrhotic patient with portal hypertension develops spontaneous bacterial peritonitis (SBP). Besides antibiotics, which of the following is MOST likely to improve survival in this patient population?

<p>Administration of intravenous albumin. (C)</p> Signup and view all the answers

Which of the following mechanisms most directly contributes to the formation of ascites in patients with liver cirrhosis?

<p>Visceral venodilation causing pooling of blood in the abdominal cavity, compounded by reduced serum albumin leading to decreased blood osmotic pressure. (B)</p> Signup and view all the answers

A patient with cirrhosis develops hepatic encephalopathy. What is the underlying mechanism for this condition?

<p>The liver's impaired ability to detoxify nitrogenous waste products, leading to elevated ammonia levels that affect brain function. (A)</p> Signup and view all the answers

What is the most likely reason for a patient with cirrhosis and portal hypertension to develop thrombocytopenia?

<p>Sequestration of platelets in the enlarged spleen (hypersplenism) secondary to portal hypertension. (B)</p> Signup and view all the answers

A patient with known cirrhosis and portal hypertension presents with sudden altered mental status. After ruling out other causes, hepatic encephalopathy is suspected. Which medication would be LEAST appropriate to manage this patient's acute condition?

<p>Furosemide. (D)</p> Signup and view all the answers

Hepatorenal syndrome (HRS) is a severe complication of cirrhosis. Which pathophysiological process is most directly implicated in the development of HRS?

<p>Venodilation in the portal circulation leading to blood pooling, distributive shock, and subsequent renal hypoperfusion. (D)</p> Signup and view all the answers

In a patient with cirrhosis, what is the most significant consequence of impaired prothrombin synthesis by the liver?

<p>Increased risk of bleeding due to impaired blood coagulation. (B)</p> Signup and view all the answers

Why does portal vein obstruction lead to the formation of collateral venous channels in patients with portal hypertension?

<p>To bypass the obstructed portal vein, allowing blood from the digestive tract and spleen to return to the systemic circulation. (B)</p> Signup and view all the answers

What is the primary reason behind the development of spider naevi in individuals with liver cirrhosis?

<p>Hormonal imbalances due to impaired liver metabolism, leading to increased estrogen levels and dilation of cutaneous arterioles. (B)</p> Signup and view all the answers

Which of the following best explains why patients with cirrhosis are at an increased risk of developing hepatocellular carcinoma?

<p>Chronic liver inflammation and regeneration, increasing the likelihood of mutations and uncontrolled cell growth. (B)</p> Signup and view all the answers

Why is the formation of oesophageal varices a significant concern in patients with portal hypertension?

<p>They can rupture and cause life-threatening gastrointestinal bleeding. (C)</p> Signup and view all the answers

Flashcards

Portal Hypertension

Obstruction of the portal vein leading to increased pressure.

Main Cause of Portal Hypertension

Cirrhosis is the most common.

Complications of Portal Hypertension

Bleeding varices, splenomegaly, ascites, and edema.

Serum Bilirubin Test

Evaluates liver damage and predicts outcomes.

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Diet for Portal Hypertension

High carbohydrate, low protein, low sodium.

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Vitamin K Use

To correct prolonged clotting and prevent bleeding.

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Treating Bleeding Varices

Endoscopic variceal ligation (banding) is safer.

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Lactulose

Used to reduce ammonia levels in hepatic encephalopathy.

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Liver Cirrhosis

Chronic liver injury leading to regeneration, fibrosis, and liver failure.

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Common Causes of Cirrhosis

Excess alcohol and chronic hepatitis C are the most common causes.

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Clinical Signs of Cirrhosis

Gynaecomastia, testicular atrophy, spider naevi, palmar erythema, finger clubbing, amenorrhoea.

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Portal Hypertension in Cirrhosis

Compression of portal venous vessels in the liver by scar tissue.

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Ascites in Cirrhosis

Visceral venodilation and low serum albumin.

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Hepatic Encephalopathy

Impaired liver detoxification leads to confusion, tremor, and coma.

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Portal Vein Function

Portal vein carries blood from digestive tract/spleen to liver.

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Porto-Systemic Shunt Locations

Esophageal varices, anorectal varices, caput medusae, retroperitoneal anastomoses.

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Study Notes

  • Cirrhosis of the liver results from chronic hepatic injury
  • The healing process involves regeneration and fibrosis
  • Cirrhosis can progress to liver failure

Aetiology

  • Common causes include excess alcohol and chronic hepatitis C
  • Schistosomiasis (bilharziasis) is the most common cause in Egypt

Clinical Features

  • Gynaecomastia (enlargement of breast tissue in men)
  • Testicular atrophy
  • Amenorrhoea (absence of menstruation)
  • Spider naevi (small, spider-like blood vessels visible on the skin)
  • Finger clubbing (enlargement of the fingertips and changes to the nail angle)
  • Palmar erythema (redness of the palms)

Complications

  • Impaired metabolism of carbohydrates, proteins, and lipids
  • Impaired metabolism of bilirubin causes jaundice
  • Impaired synthesis of albumin and prothrombin
  • Portal hypertension results from compression of portal venous vessels by scarred liver tissue
  • Visceral venodilation outside the liver can be caused by portal hypertension
  • Ascites is caused by visceral venodilation and low serum albumin levels
  • Low serum albumin levels are also responsible for blood osmotic pressure
  • Hepatic encephalopathy presents as confusion, flapping tremor, and hepatic coma
  • It results from the liver's inability to detoxify nitrogenous waste products, leading to ammonia conversion to urea
  • Hepatorenal failure involves venodilation of portal circulation, leading to blood pooling and distributive shock
  • Hepatorenal failure results in renal hypoperfusion and high mortality
  • Malignant change can result in hepatocellular carcinoma

Portal Hypertension

Portal Circulation

  • The liver receives blood from the hepatic artery and the portal vein
  • The portal vein returns blood from the digestive tract and spleen to the liver
  • In the liver, nutrients are metabolized, and toxins are detoxified and filtered before blood returns to the heart

Collateral Porto-Systemic Venous Channels

  • Portal obstruction leads to collateral channels development between portal and systemic venous circulations
  • Sites of these channels:
  • Lower oesophagus: forming oesophageal varices (most important)
  • Lower rectum: forming anorectal varices (second important)
  • Around the umbilicus: forming caput medusae
  • Retroperitoneal and diaphragmatic anastomoses

Aetiology

  • Portal hypertension results from obstruction to portal vein
  • Normal portal vein pressure is between 5 and 10 mmHg
  • Cirrhosis is the most common cause of portal hypertension

Complications

  • Bleeding oesophageal, anorectal varices, or duodenal ulcers due to development of collateral porto-systemic venous channels
  • Splenomegaly: progressive spleen enlargement caused by portal congestion. Often associated with anaemia, leucopenia, and thrombocytopenia
  • Ascites: Fluid accumulation in the peritoneal cavity
  • Leg and foot oedema: Fluid accumulation in subcutaneous tissues causes swelling

Preparation of a patient with portal hypertension

Preoperative Investigations

  • Serum bilirubin: Jaundice severity is an important indicator
  • Direct bilirubin type rises primarily, followed by the indirect type in biliary obstruction cases
  • Liver enzyme tests: Increased alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase
  • Prolonged prothrombin time
  • Low serum albumin
  • Abdominal CT or MR scan: Provides best assessment of focal liver lesions and splenomegaly
  • Ultrasound: Assess focal liver lesions and splenomegaly
  • Upper GIT endoscopy: Detect varices
  • Liver biopsy: Determine the cause of cirrhosis
  • Portal Vein pressure measurement: Above 11 mmHg is diagnostic (using special catheter)

Preoperative Management

  • Rehydration: Intravenous fluids for good rehydration
  • Diet: High carbohydrates with low protein and sodium
  • Albumin: Administer albumin for hypo-albuminaemia
  • Blood/Platelets: Administer blood for anaemia and platelets for thrombocytopaenia
  • Vitamin K: Administer to correct prolonged prothrombin time
  • Diuretics: Spironolactone for ascites; abdominal paracentesis for severe ascites
  • Dialysis: Provide for patients with underlying renal failure
  • Bleeding Oesophageal Varices: Endoscopic variceal ligation is safer and more effective than sclerotherapy
  • Lactulose: Especially for hepatic encephalopathy; 50 ml t.d.s. to produce osmotic diarrhoea, remove protein and blood, and prevent proliferation of ammonia-producing organisms
  • Non-selective B-blockers: Propranolol and nadolol are treatments to cause visceral venoconstriction and should be continuous
  • Antibiotics: Cephalosporin or ciprofloxacin as prophylaxis against infection
  • Avoidance: Avoid hepatotoxic and nephrotoxic medications: morphine, halothane, acetaminophen, gentamycin etc

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