Liver cirrhosis : Etiology , Pathology , Clinical manifestations , Diagnosis , Treatment

Liver Cirrhosis

Definition and development

Cirrhosis is a diffuse, usually irreversible process in which ongoing liver injury causes inflammation, cell damage, fibrosis, and regenerative nodules. The resulting distortion of normal liver structure impairs liver function and blood flow through the organ.

Causes

The video identifies the most common causes as:

• Hepatitis C
• Alcohol-related liver disease
• Non-alcoholic fatty liver disease
• Hepatitis B

Less common causes include autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, and drug-induced liver injury.

Pathology

Cirrhosis was historically described by the size of its nodules:

• Micronodular: Nodules smaller than 3 mm; associated in the video with alcohol, hemochromatosis, cholestatic disease, and impaired hepatic venous outflow.
• Macronodular: Nodules larger than 3 mm and of varying sizes; associated with chronic viral hepatitis.

The liver’s appearance may change as disease progresses, with micronodular cirrhosis sometimes progressing to a macronodular pattern.

Clinical features

Compensated cirrhosis may cause nonspecific symptoms such as reduced appetite, weight loss, weakness, and fatigue.

Decompensated cirrhosis may cause more distinct symptoms, including confusion, ascites, edema, vomiting blood, itching, and black stools.

Physical findings described include:

• Jaundice, dark urine, and palmar redness
• Spider angiomas, often on the trunk, face, and upper limbs
• Ascites, which may produce abdominal distension, a fluid wave, and flank dullness
• Hepatic encephalopathy and asterixis
• Gynecomastia and reduced gonadal function
• Caput medusae
• An enlarged, normal-sized, or small liver; when palpable, it may feel firm and nodular
• Enlarged parotid glands, particularly in alcohol-related liver disease
• Fetor hepaticus: a sweet, pungent breath odor that may suggest severe portal-systemic shunting

Muscle cramps can occur and may be severe. Women may develop chronic anovulation and absent or irregular menstrual bleeding. Men may develop hypogonadism, with impotence, infertility, reduced sexual drive, or testicular atrophy. As cirrhosis progresses, mean arterial pressure may fall, contributing to hepatorenal syndrome and serving as a predictor of survival.

Child–Pugh severity classification

The Child–Pugh score assesses liver disease severity using five measures. For coagulation, the video gives either prothrombin-time prolongation or INR thresholds.

Measure 1 point 2 points 3 points Ascites Absent Slight Moderate Bilirubin <2 mg/dL (<34.2 µmol/L) 2–3 mg/dL (34.2–51.3 µmol/L) >3 mg/dL (>51.3 µmol/L) Albumin >3.5 g/dL (>35 g/L) 2.8–3.5 g/dL (28–35 g/L) <2.8 g/dL (<28 g/L) Coagulation: PT prolongation over control <4 seconds 4–6 seconds >6 seconds Or coagulation: INR <1.7 1.7–2.3 >2.3 Encephalopathy None Grade 1–2 Grade 3–4

• Class A: 5–6 points — well-compensated disease
• Class B: 7–9 points — significant functional compromise
• Class C: 10–15 points — decompensated disease

The video gives approximate one- and two-year survival rates of 85–100% for Class A, 60–80% for Class B, and 35–45% for Class C.

Diagnosis

Liver biopsy is described as the gold standard, but it may not be necessary when clinical, laboratory, and imaging findings strongly suggest cirrhosis.

• Ultrasound is the most commonly used imaging test in the video. It can assess liver contour, blood flow, and abdominal fluid.
• Other imaging mentioned includes abdominal CT and MRI. Chest and kidney–ureter–bladder radiographs may be used to assess secondary complications.
• Laboratory assessment may include bilirubin, AST, ALT, gamma-glutamyl transpeptidase, prothrombin time, platelet count, and electrolytes. The video notes prolonged prothrombin time, low platelet count, and low sodium as possible findings.

Complications

Portal hypertension is presented as the underlying cause of many complications. Increased pressure can cause blood to back up into esophageal and gastric veins, producing varices, and can contribute to ascites.

Complications include:

• Ascites and spontaneous bacterial peritonitis
• Variceal bleeding
• Portal vein thrombosis
• Cardiomyopathy
• Hepatopulmonary syndrome
• Hepatorenal syndrome
• Hepatic encephalopathy

Treatment

Treatment focuses on addressing the underlying liver disease, managing harmful exposures, and preventing or treating complications.

• Beta blockers help lower pressure in patients with esophageal or gastric varices.
• Lactulose is used during acute hepatic encephalopathy. It helps prevent ammonia absorption. The video explains that ammonia and other neurotoxic substances may build up in the blood and enter the brain when liver function fails.
• Transjugular intrahepatic portosystemic shunt (TIPS) may be performed for severe portal hypertension, creating an alternate route for blood through the damaged liver.
• Liver transplantation is described as the only cure for a cirrhotic liver. The patient’s prognosis may be assessed with the Child–Pugh classification or the Model for End-Stage Liver Disease (MELD) score.

Speakers and sources featured

• One unnamed narrator/presenter delivers the educational module.
• No additional speakers or external sources are identified in the subtitles.
• The video is associated with the Dr. G. Bhanu Prakash Animated Medical Videos channel.