Liver cirrhosis increases resistance to blood flow and leads to higher pressure in the portal venous system, resulting in portal hypertension. Effects of portal hypertension include:

- Splenomegaly (increase in size of the spleen) is found in 35% to 50% of patients.

- Esophageal varices result from collateral portal blood flow through vessels in the stomach and esophagus (a process called portacaval anastomosis). When these blood vessels become enlarged, they are called varices and are more likely to rupture. Variceal rupture often leads to severe bleeding, which can be fatal.

- Caput medusa are dilated periumbilical collateral veins due to portal hypertension. Blood from the portal venous system may be shunted through the periumbilical veins and ultimately to the abdominal wall veins, manifesting as a pattern that may resemble the head of Medusa.

- Cruveilhier-Baumgarten murmur is a venous hum heard in the epigastric region (on examination by stethoscope) due to collateral connections forming between the portal system and the periumbilical veins as a result of portal hypertension.

There are some changes seen in cirrhosis whose causes are not clearly known. They may also be a sign of other non-liver related causes.

- Nail changes.

- Muehrcke's lines – paired horizontal bands separated by normal color resulting from hypoalbuminemia (inadequate production of albumin). It is not specific for cirrhosis.

- Terry's nails (double nails) – proximal two-thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia

- Clubbing – angle between the nail plate and proximal nail fold > 180 degrees. It is not specific for cirrhosis and can therefore can be due to a number of conditions

- Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain. It is not specific for cirrhosis.

- Dupuytren's contracture. Thickening and shortening of palmar fascia (tissue on the palm of the hands) that leads to flexion deformities of the fingers. Caused by fibroblastic proliferation (increased growth) and disorderly collagen deposition. It is relatively common (33% of patients).

- Other. Weakness, fatigue, anorexia, weight loss.

Embryogenically, congenital hepatic fibrosis is due to malformation of the duct plate, a round structure appearing in the eighth week of gestation that is formed by primitive hepatocytes, which differentiate into cholangiocytes. Congenital hepatic fibrosis usually presents in adolescent or young adulthood, but onset of signs and symptoms can range from early childhood through mid-life. Clinical features may vary but commonly include Cholangitis, hepatomegaly and signs of portal hypertension.

Chronic liver failure usually occurs in the context of cirrhosis, itself potentially the result of many possible causes, such as excessive alcohol intake, hepatitis B or C, autoimmune, hereditary and metabolic causes (such as iron or copper overload, steatohepatitis or non-alcoholic fatty liver disease).

Acute liver failure is defined as "the rapid development of hepatocellular dysfunction, specifically coagulopathy and mental status changes (encephalopathy) in a patient without known prior liver disease".

The disease process is associated with the development of a coagulopathy of liver aetiology, and clinically apparent altered level of consciousness due to hepatic encephalopathy. Several important measures are immediately necessary when the patient presents for medical attention. The diagnosis of acute liver failure is based on physical exam, laboratory findings, patient history, and past medical history to establish mental status changes, coagulopathy, rapidity of onset, and absence of known prior liver disease respectively.

The exact definition of "rapid" is somewhat questionable, and different sub-divisions exist which are based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms. This is sub-divided into "fulminant hepatic failure", which requires onset of encephalopathy within 8 weeks, and "subfulminant", which describes onset of encephalopathy after 8 weeks but before 26 weeks. Another scheme defines "hyperacute" as onset within 7 days, "acute" as onset between 7 and 28 days, and "subacute" as onset between 28 days and 24 weeks.

The main features of acute liver failure are rapid-onset jaundice, weakness, and eventually, changes in mental status that can begin as mild confusion but progress to coma.

Coagulopathy is another cardinal feature of ALF. The liver has the central role in the synthesis of almost all coagulation factors and some inhibitors of coagulation and fibrinolysis. Hepatocellular necrosis leads to impaired synthesis of many coagulation factors and their inhibitors. The former produces a prolongation in prothrombin time which is widely used to monitor the severity of hepatic injury. There is significant platelet dysfunction (with both quantitative and qualitative platelet defects). Progressive thrombocytopenia with the loss of larger and more active platelets is almost universal. Thrombocytopenia with or without DIC increases risk of intracerebral bleeding.

The condition is usually congenital, but sporadic cases have also been reported. It may be associated with other congenital defects, commonly with autosomal recessive polycystic kidney disease, the most severe form of PKD. Some suggest that these two conditions are one disorder with different presentation.

The acute syndrome presents with rapidly progressive severe upper abdominal pain, yellow discoloration of the skin and whites of the eyes, liver enlargement, enlargement of the spleen, fluid accumulation within the peritoneal cavity, elevated liver enzymes, and eventually encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Liver cell death and severe lactic acidosis may be present as well. Caudate lobe enlargement is often present. The majority of patients have a slower-onset form of Budd–Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a "spider's web". Patients may progress to cirrhosis and show the signs of liver failure.

On the other hand, incidental finding of a silent, asymptomatic form may not be a cause for concern.

Fatty liver is a reversible condition wherein large vacuoles of triglyceride fat accumulate in liver cells via the process of steatosis (i.e., abnormal retention of lipids within a cell). Despite having multiple causes, fatty liver can be considered a single disease that occurs worldwide in those with excessive alcohol intake and the obese (with or without effects of insulin resistance). The condition is also associated with other diseases that influence fat metabolism. When this process of fat metabolism is disrupted, the fat can accumulate in the liver in excessive amounts, thus resulting in a fatty liver. It is difficult to distinguish alcoholic FLD, which is part of alcoholic liver disease, from nonalcoholic FLD (NAFLD), and both show microvesicular and macrovesicular fatty changes at different stages.

The accumulation of fat in alcoholic or non-alcoholic steatosis may also be accompanied by a progressive inflammation of the liver (hepatitis), called steatohepatitis. This more severe condition may be termed either alcoholic steatohepatitis or non-alcoholic steatohepatitis (NASH).

This may cause fatty liver, hepatitis, fibrosis and sclerosis leading to cirrhosis and finally liver failure.

This large, atypical haemangioma of the liver may present with abdominal pain or fullness due to haemorrhage, thrombosis or mass effect. It may also lead to left ventricular volume overload and heart failure due to the increase in cardiac output which it causes. Further complications are Kasabach-Merritt syndrome, a form of consumptive coagulopathy due to thrombocytopaenia, and rupture.

Fatty liver (FL) is commonly associated with alcohol or metabolic syndrome (diabetes, hypertension, obesity, and dyslipidemia), but can also be due to any one of many causes:

- Metabolic: abetalipoproteinemia, glycogen storage diseases, Weber–Christian disease, acute fatty liver of pregnancy, lipodystrophy

- Nutritional:malnutrition, total parenteral nutrition, severe weight loss, refeeding syndrome, jejunoileal bypass, gastric bypass, jejunal diverticulosis with bacterial overgrowth

- Drugs and toxins: amiodarone, methotrexate, diltiazem, expired tetracycline, highly active antiretroviral therapy, glucocorticoids, tamoxifen, environmental hepatotoxins (e.g., phosphorus, mushroom poisoning)

- Alcohol: Alcoholism is one of the major causes of fatty liver due to production of toxic metabolites like aldehydes during metabolism of alcohol in the liver. This phenomenon most commonly occurs with chronic alcoholism.

- Other: celiac disease, inflammatory bowel disease, HIV, hepatitis C (especially genotype 3), and alpha 1-antitrypsin deficiency

Features of VOD include weight gain, tender hepatomegaly, ascites, and jaundice; it often is associated with renal failure.

Liver haemangiomas are typically hyperechoic on ultrasound though may occasionally be hypoechoic; ultrasound is not diagnostic. Computed tomography (CT), magnetic resonance imaging (MRI) or single-photon emission computed tomography (SPECT) using autologous labelled Red Blood Cells (RBC) with Tc-99m is diagnostic. Biopsy is avoided due to the risk of haemorrhage.

Hepatic haemangiomas can occur as part of a clinical syndrome, for example Klippel-Trenaunay-Weber syndrome, Osler–Weber–Rendu syndrome and Von Hippel-Lindau syndrome.

Hepato-biliary diseases include liver diseases and biliary diseases. Their study is known as hepatology.

Liver disease (also called hepatic disease) is a type of damage to or disease of the liver.

Hepatic veno-occlusive disease or veno-occlusive disease (VOD) is a condition in which some of the small veins in the liver are obstructed. It is a complication of high-dose chemotherapy given before a bone marrow transplant (BMT) and is marked by weight gain due to fluid retention, increased liver size, and raised levels of bilirubin in the blood. The name sinusoidal obstruction syndrome is now preferred if VOD happens as a result of chemotherapy or bone marrow transplantation.

Apart from chemotherapy, VOD may also occur after ingestion of certain plant alkaloids such as pyrrolizidine alkaloids (in some herbal teas), and has been described as part of a rare hereditary disease called "hepatic venoocclusive disease with immunodeficiency" (which results from mutations in the gene coding for a protein called SP110).

People who develop ischemic hepatitis may have weakness, fatigue, mental confusion, and low urine production (oliguria). A small percentage of affected people may develop hepatic coma. Jaundice can occur, but is rare and transient, as is actual loss of function of the liver.

There are more than a hundred different kinds of liver disease. Symptoms may include jaundice and weight loss. These are some of the most common:

- Fascioliasis, a parasitic infection of liver caused by a Liver fluke of the "Fasciola" genus, mostly the "Fasciola hepatica".

- Hepatitis, inflammation of the liver, is caused by various viruses (viral hepatitis) also by some liver toxins (e.g. alcoholic hepatitis), autoimmunity (autoimmune hepatitis) or hereditary conditions.

- Alcoholic liver disease is a hepatic manifestation of alcohol overconsumption, including fatty liver disease, alcoholic hepatitis, and cirrhosis. Analogous terms such as "drug-induced" or "toxic" liver disease are also used to refer to disorders caused by various drugs.

- Fatty liver disease (hepatic steatosis) is a reversible condition where large vacuoles of triglyceride fat accumulate in liver cells. Non-alcoholic fatty liver disease is a spectrum of disease associated with obesity and metabolic syndrome.

- Hereditary diseases that cause damage to the liver include hemochromatosis, involving accumulation of iron in the body, and Wilson's disease. Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency and glycogen storage disease type II.

- In transthyretin-related hereditary amyloidosis, the liver produces a mutated transthyretin protein which has severe neurodegenerative and/or cardiopathic effects. Liver transplantation can give a curative treatment option.

- Gilbert's syndrome, a genetic disorder of bilirubin metabolism found in a small percent of the population, can cause mild jaundice.

- Cirrhosis is the formation of fibrous tissue (fibrosis) in the place of liver cells that have died due to a variety of causes, including viral hepatitis, alcohol overconsumption, and other forms of liver toxicity. Cirrhosis causes chronic liver failure.

- Primary liver cancer most commonly manifests as hepatocellular carcinoma and/or cholangiocarcinoma; rarer forms include angiosarcoma and hemangiosarcoma of the liver. (Many liver malignancies are secondary lesions that have metastasized from primary cancers in the gastrointestinal tract and other organs, such as the kidneys, lungs.)

- Primary biliary cirrhosis is a serious autoimmune disease of the bile capillaries.

- Primary sclerosing cholangitis is a serious chronic inflammatory disease of the bile duct, which is believed to be autoimmune in origin.

- Budd–Chiari syndrome is the clinical picture caused by occlusion of the hepatic vein.

The first symptoms typically include fever, intermittent abdominal pain, and hepatomegaly. Occasionally, jaundice occurs.

Morbidity is common and is caused by complications of cholangitis, sepsis, choledocholithiasis, and cholangiocarcinoma. These morbid conditions often prompt the diagnosis. Portal hypertension may be present, resulting in other conditions including splenomegaly, hematemesis, and melena. These problems can severely affect the patient's quality of life. In a 10-year period between 1995 and 2005, only 10 patients were surgically treated for Caroli disease, with an average patient age of 45.8 years.

After reviewing 46 cases of Caroli disease before 1990, 21.7% of the cases were the result of an intraheptic cyst or nonobstructive biliary tree dilation, 34.7% were linked with congenital hepatic fibrosis, 13% were isolated choledochal cystic dilation, and the remaining 24.6% had a combination of all three.

Budd–Chiari syndrome is a very rare condition, affecting 1 in a million adults. The condition is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement. The formation of a blood clot within the hepatic veins can lead to Budd–Chiari syndrome. The syndrome can be fulminant, acute, chronic, or asymptomatic.

Peliosis hepatis is an uncommon vascular condition characterised by multiple, randomly distributed, blood-filled cavities throughout the liver. The size of the cavities usually ranges between a few millimetres and 3 cm in diameter. In the past, it was a mere histological curiosity occasionally found at autopsies, but has been increasingly recognised with wide-ranging conditions from AIDS to the use of anabolic steroids. It also occasionally affects spleen, lymph nodes, lungs, kidneys, adrenal glands, bone marrow, and other parts of gastrointestinal tract.

Peliosis hepatis is often erroneously written "peliosis hepati"ti"s", despite its not being one of the hepatitides. The correct term arises from the Greek "pelios", i.e. discoloured by extravasated blood, livid, and the Latinized genitive case (hepatis) of the Greek "hepar", liver.

Signs and symptoms depend largely upon the primary lesions giving rise to the condition. In addition to the heart or lung symptoms, there will be a sense of fullness and tenderness in the right hypochondriac region. Gastrointestinal catarrh is usually present, and vomiting of blood may occur. There is usually more or less jaundice. Owing to portal obstruction, ascites occurs, followed later by generalised oedema. The stools are light or clay-colored, and the urine is colored by bile. On palpation, the liver is found enlarged and tender, sometimes extending several inches below the costal margin of the ribs.

Symptoms having to do with hepatomegaly can include several, among them the individual may experience some weight loss, poor appetite and lethargy (jaundice and bruising may also be present)