Types of Liver Disease and Ways To Prevent Them
1. Chronic Liver Disease
Chronic liver disease (CLD) is characterized by a steady decline in liver activities over a period of more than six months. These processes include the production of clotting factors and other proteins, the detoxification of toxic metabolic byproducts, and the excretion of bile. Cirrhosis and fibrosis are the results of CLD, which is a chronic process of inflammation, liver parenchymal damage, and regeneration.
Chronic liver disease has a wide range of etiologies, including toxins, long-term alcohol consumption, infection, autoimmune diseases, genetic abnormalities, and metabolic problems. In the last stage of chronic liver disease called cirrhosis, the architecture of the liver is disrupted, there are numerous nodules that form, the blood vessels are reorganized, there is neo-angiogenesis, and an extracellular matrix is deposited. The focus is on the common etiologies, clinical symptoms, and therapy of chronic liver disease because it is such a prevalent clinical condition.
One of the most common causes of death, particularly in underdeveloped countries, is chronic liver disease. Recently, it has been shown that chronic liver disease is becoming more common. Alcoholic liver disease, chronic viral hepatitis, including hepatitis B and C, non-alcoholic fatty liver disease (NAFLD), and hemochromatosis make up the bulk of chronic liver illnesses in the developed world. (1)
How To Prevent Chronic Liver Disease
- Avoid various types of alcohol (wine, liquor, mixed drinks, beer).
- Regular screening for hepatitis B and hepatitis C
- Vaccination against hepatitis A and B
- Avoid iron supplementation unless there is an iron deficiency.
- Avoid over-the-counter painkillers (aspirin, acetaminophen) and other hepatotoxic drugs.
- Maintain a good lipid profile to avoid metabolic syndrome.
Chronic Liver Disease Treatment
The aim of treatment is to halt the spread of the illness and its complications, and this calls for a multidisciplinary strategy. The major management tenets are the elimination of underlying causes, control of portal hypertension, and individualized therapy for each condition.
Esophageal varices: One of the fatal side effects of varices is bleeding, which can be treated with vigorous fluid resuscitation, vasopressors, and endoscopy. In an emergency, endoscopic band ligation and injectable sclerotherapy are the typical treatments for variceal bleed. Early transjugular intrahepatic portosystemic shunt (TIPS) may improve survival in some patients. For both primary and secondary esophageal varices prevention, propranolol is utilized. Treatment options for ascites must include sodium restriction and diuretics. Therapeutic paracentesis is performed for tight ascites. Another option is albumin infusion. SBP is often treated with broad-spectrum antibiotics at first, followed by specialized antibiotics following a culture.
Hepatic encephalopathy: Hepatic encephalopathy patients typically get well when the precipitating factor is treated, combined with rifaximin and lactulose. Lactulose reduces the absorption of ammonia from the digestive system by converting it to ammonium ions. Through its osmotic impact, lactulose also improves constipation, which helps to lessen the symptoms of hepatic encephalopathy. Rifaximin is used to reduce gut flora’s generation of ammonia. Hepatorenal syndrome patients may benefit from a liver transplant.
Hepatorenal syndrome: Two categories for HRS based on severity. When compared to HRS 2, HRS 1 is more serious. The intensity and location of the patient influence the treatment options. Norepinephrine, terlipressin, midodrine, and octreotide with albumin infusion are all possible treatment options. When all other treatments fail to work for a patient, liver transplantation is the only option left. In some patients, the TIPS operation may be helpful.
2. Acute Liver Failure
Acute liver failure (ALF) is a complex clinical condition defined by increased liver biochemistry, coagulopathy, and hepatic encephalopathy. The most popular categorization is, which separates liver failure into three categories hyperacute liver failure (within 7 days), acute (between 1 and 4 weeks), and subacute (5 to 12 weeks). (2)
Patients frequently pass away from the complications of acute liver failure, which is a complicated condition. Patient management in the intensive care unit is required before moving them to a facility with liver transplant capabilities. Along with the diagnostic process, treatment should start as soon as possible.
Acute Liver Failure Prevention and Treatment
Supportive care, prevention and control of complications, specialized treatment when the exact etiology is established, and diagnosis of prognosis and the need for liver support, including possible liver transplantation, are all part of ALF management. Acute liver failure caused by a non-acetaminophen has also been helped by N-acetylcysteine (NAC). Regardless of the cause, preventing cerebral edoema is the cornerstone of ALF treatment. To do this, one can use head elevation, mannitol, hyperventilation, and cerebroprotective techniques.
Here are 7 ways to prevent and control acute liver failure:
- Access hemodynamic stability and the requirement for intravenous fluids, as well as the maintenance of normal acid-base levels and electrolytes. To guarantee adequate renal and cerebral perfusion, vasopressors should be used to maintain a mean arterial pressure of 75 mm Hg or above.
- Because the patients have coagulopathy and poor platelet functioning, keep an eye on their hematocrit. Platelets and fresh frozen plasma are only used to treat coagulopathy in individuals who are actively bleeding or before an invasive operation. Patients should be started on proton pump inhibitors on an empirical basis to prevent gastrointestinal bleeding.
- Consider a fever workup that includes blood and urine cultures, and begin empirical antibiotics as needed.
- Monitor hepatic encephalopathy and protect the airway (aspiration risk) if the patient’s encephalopathy worsens. To avoid cerebral edoema, these patients should be intubated and placed on a regimen.
- Sufficient nutrition should be provided, with 1.0 to 1.5 grams of protein per kg per day.
- Keep an eye out for hypoglycemia and keep your blood glucose levels between 160 and 200.
- Discontinue all home medications except those that we determine must be kept.
3. Drug-Induced Liver Injury
One of the most common causes of liver dysfunction is drug-induced liver injury (DILI), which can produce a wide range of symptoms such as asymptomatic transaminitis, acute hepatitis, chronic hepatitis, cholestasis, and liver failure. It can be caused by a variety of prescription medicines, herbal and nutritional supplements.
Nonsteroidal anti-inflammatory medications (NSAIDs), anti-infective drugs (anti-tubercular drugs), anti-cancer drugs, hormone drugs, immunosuppressive agents, sedatives, and neuropsychiatric pharmaceuticals are among the numerous kinds of drugs that cause drug-induced liver impairment. Acetaminophen is the most commonly implicated medication in drug-induced liver damage. Antibiotics are the most common class of medications that cause liver damage, and amoxicillin-clavulanate is the most common antibiotic in this class. Herbal supplements also induce a variety of symptoms, but their use is underreported.
Drug-Induced Liver Injury Treatment
The initial step in treating drug-induced liver impairment is stopping the implicated substance. The treatment for acetaminophen intoxication is N-acetylcysteine. However, it has been demonstrated that intravenous N-acetylcysteine increases survival in patients with acute liver failure unrelated to acetaminophen. Valproate damage has been treated with carnitine. Although they have not been well researched, steroids have been suggested as a possible treatment for liver damage. Currently, immune-mediated drug-induced liver damage is treated with glucocorticoids. However, the effectiveness of silymarin alone or in combination with benzylpenicillin has not yet been thoroughly investigated. Ursodeoxycholic acid may be tested in cholestasis patients.
4. Alcohol Liver Disease
Alcoholic cirrhosis, the most severe and irreversible form of liver damage brought on by alcohol consumption, is the culmination of a spectrum of illnesses that start with fatty liver, proceed occasionally to alcoholic hepatitis, and end with alcoholic liver disease.
Alcoholic liver disease has three phases:
- Alcoholic Fatty Liver, is a condition in which fat builds up in the liver parenchyma.
- Alcoholic hepatitis: At this stage, the liver cells become inflamed; the prognosis relies on how severe the damage is. Alcoholic hepatitis can be treated with abstinence from alcohol, nutrition support, infection treatment, and prednisolone therapy in severe instances, although more severe cases result in liver failure.
- Alcoholic cirrhosis: Liver damage at this stage is permanent and results in portal hypertension and cirrhosis complications.
Alcohol Liver Disease Treatment
Control of alcohol The severity of liver disease varies on the disease.
- Abstinence from alcohol and involvement in program for detoxification
- nutritional assistance
- screening for esophageal varices in people with cirrhosis and for hepatocellular cancer with ultrasonography every six months
- Acetaminophen dosage should not exceed 2000 mg per day since chronic alcoholics are more likely to develop hepatotoxicity from it. The typical person has a daily acetaminophen tolerance of up to 4000 mg.
- Treatment of liver illnesses that coexist, such as viral infections that cause hepatitis B and C
5. Non-Alcoholic Fatty Liver Disease
In the absence of heavy alcohol consumption, macrovesicular alterations without inflammation (steatosis) and lobular inflammation are referred to as non-alcoholic fatty liver disease (NAFLD) or “Fatty Liver.” It can be separated into two subgroups: NASH and NAFL (Non-Alcoholic Fatty Liver) (Non-Alcoholic Steatohepatitis). Hepatic steatosis without any signs of hepatocellular damage, such as inflating hepatocytes, is referred to as NAFL.
Fat builds up in the liver for a number of reasons. It most frequently entails increased transport of free fatty acids (FFAs) to the liver, increased fatty acid synthesis in the liver, decreased FFA oxidation, or decreased very-low-density lipoprotein production or secretion (VLDL).  
Additional elements that could cause fatty liver include:
- The using of drugs (e.g., tamoxifen, amiodarone, methotrexate)
- Hypermetabolic conditions (e.g., glycogen storage disorders, homocystinuria)
- Dietary status (e.g., total parenteral nutrition, severe malnutrition, over nutrition, or a starvation diet)
- Other medical conditions, such as celiac sprue and Wilson disease.
Non-Alcoholic Fatty Liver Disease Treatment
The foundations of the therapy are dietary changes and weight loss. Glycemic and lipid management are also part of the treatment. Gastric bypass or other weight loss surgical modalities should be taken into consideration for patients who are severely obese. Hepatic steatosis is known to be decreased by weight loss. According to the available research, losing three to five percent of one’s body weight is required to see a change in steatosis, but up to ten percent of one’s body weight is needed to see a change in necroinflammation.
Pharmacological options include Metformin, Vitamin E, fish oil, Orlistat (an inhibitor of gastric and pancreatic lipase), and Sibutramine. It is only advised to use metformin if there is another indication for it because studies have revealed that it has no discernible impact on liver histology. Currently, only non-diabetic patients with biopsy-proven NASH are advised to take vitamin E. Although the long-term consequences of pioglitazone are unknown, it can be used to treat patients with biopsy-proven steatohepatitis.
Recommended For You