Different Types Of Liver Diseases – This presentation is an excerpt from the AlF Poster Competition 2021. The competition features posters and short videos created by early career researchers from around the country on six academic focus areas: fatty liver disease, liver cancer, liver transplantation, pediatric liver disease, rare liver diseases and infections virus. Participants are tasked with translating complex medical information into paper that can be easily understood by patients or the general public. Posters are reviewed by a panel of judges made up of members of the Medical Advisory Board, Board Members and friends of ALF to select a winner in each category.
Liver cancer is the 4th leading cause of cancer-related death worldwide and is the second deadliest cancer. While treatments and survival rates for various types of cancer have improved over the past few decades, the prognosis for liver cancer remains poor and deadly. In fact, the death toll in the US has increased by more than 40% in the past two decades.
Different Types Of Liver Diseases
There are several types of liver cancer, but today I will focus on hepatocellular carcinoma (or HCC), which is a primary cancer that originates from liver cells and accounts for 90% of liver cancers. Most HCC occurs in patients with liver disease. There are many contributing factors, including genetic predisposition, family history, environmental exposure, and age and more, but the bottom line is that HCC often develops from a damaged liver. It includes viral hepatitis, such as hepatitis B, hepatitis C; alcoholism, fatty liver disease, and now the increasing prevalence of obesity and diabetes which increases the risk of liver disease and thus increases the risk of cancer.
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The pathogenesis of liver disease into HCC is a complex process with many steps. When the liver is injured, the liver tries to regenerate and replace damaged cells. This repair process involves the production of collagen which is a fiber that stiffens the cells.
Chronic liver disease causes the continued maintenance of this repair process. It will make the liver bigger and harder, and all the collagen will replace healthy cells. This is what we usually call liver scarring, or fibrosis. If left untreated, this scarring can lead to severe scarring of the liver, which we call cirrhosis.
Cirrhotic livers tend to accumulate DNA mutations. These changes affect the cell cycle (such as growth and cell division) and cells instead of regenerating properly, cluster together to form nodules. This is called a dysplastic and precancerous nodule.
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Increased damage and chronic inflammation provide this abnormal cell proliferation, invasiveness, and good survival. including evading the body’s immune system, having its own vascular supply to grow unblocked, and become immortal cancer cells. Progressively, dysplastic nodules turn into eventually hepatocellular carcinoma.albumin, protein transport, lipids, carbohydrate metabolism, lipid metabolism, bile acid metabolism, Bilirubin metabolism, Hormone inactivation, Drug inactivation and excretion, Function maintenance.
3 Types of liver disease Cholestasis: bile duct damage from stones or tumors, Primary biliary cirrhosis Infections: hepatitis A, B, C, EBV, CMV Chemical damage: drugs and alcohol Heredity: Wilsons disease, hemochromatosis Vascular damage: Budd-Chiari Autoimmunity: hepatitis autoimmune, primary sclerosing cholangitis Congenital anomalies: biliary atresia, Caroli’s disease Metabolic diseases: galactosemia, fatty liver disease.
Non-alcoholic fatty liver disease (NAFLD) Alcohol Autoimmune – autoimmune hepatitis, PBC (Primary Biliary Cirrhosis), PSC (Primary Sclerosing Cholangitis) Haemochromatosis Drugs (MTX, amiodarone) Cystic fibrosis, a1antitryptin deficiency, Port Liver Cirrhosis) Other Cryptogenic: sarcoidosis, amyloid, schistosomiasis
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5 Liver function tests A non-invasive way to diagnose the presence of liver dysfunction A laboratory test abnormality allows to identify the most severe type of disease. to the treatment, and adjust the treatment if necessary
Participates in gluconeogenesis, transferring amino groups from aspartate or alanine to ketoglutaric acid to form oxaloacetate or pyruvate. AST is present in cytosol and mitochondria in liver, cardiac muscle, skeletal muscle, kidney, brain, pancreas, lung, WBC and RBC. AST is the first sign of liver damage cytosolic enzyme ALT, the most abundant in the liver, so the liver is special but its half-life is long.
AST mild elevation (10 times UNL) acute viral hepatitis Alcoholic liver disease autoimmune hepatitis and toxic and drug-induced liver necrosis Shock or ischemia to the liver. ALT level 1 in alcoholic liver disease, drug addiction, malignancy, cirrhosis.
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It is found in almost all tissues – isoenzymes It is found in the microvilli of the bile ducts in the liver It is also found in the bones, intestines, placenta, kidneys and wbc The increase can be physical or pathological Physiological In the tissue that stimulates. Metabolism The third trimester of pregnancy Puberty.
Found in hepatocytes and biliary epithelial cells Sensitive to hepatobiliary disease but Ltd by lack of cleanliness. or more suggestive AlD medication may cause mild elevation Normal range 0 to 30 IU/L
The spectrum of abnormalities is similar to the specific SAP of hepatobiliary disease. It can be used to confirm the hepatic origin of high SAP.
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Lactate dehydrogenase (LDH) is often elevated in hepatocellular dysfunction.
17 Serum Bilirubin The breakdown product of heme (hemoglobin component in red blood cells) Hepatocytes take bilirubin, mix it so it dissolves in water and place it in the bile duct to be excreted through the intestine. Red cells break down (undigested) Hepatic: unable to metabolize bilirubin (conjugated) Decreased concentration Fails to produce bilirubin Post-hepatic: blocks bile flow (conjugated)
Up to 1.5 X ULN Repeat if also in 3 months > 1.5 X ULN Try the unattached part. Unconjugated > 70% in patients with normal LFTs, CBC and TSH = probable Gilberts Syndrome > 3.0 X ULN Unconjugated > 70% consider hemolysis Conjugated > 50% consider ultrasound
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Blocking factor: prothrombin (PT) – specific for liver dysfunction / liver dysfunction Albumin: low in chronic liver disease Glucose: hypoglycemia indicates liver dysfunction.
Decreased chronic and severe liver disease Other causes of hypoalbinemia: protein-losing enteropathy Urinary loss: malnutrition nephrotic syndrome.
Serum globulin is often increased in the absence of cirrhosis alpha1-Antitrypsin: – neonatal jaundice and – cirrhosis in children and adults.
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Alpha-fetoprotein: – moderate levels are found, for example; during viral infection, – the most important findings in hepatocellular carcinoma.
Antinuclear Ab and muscle Antiismooth Ab: in autoimmune hepatitis type 1 Anti-LKM1 antibody in type 2 AIH Antibody for soluble liver antigen in type 3 AIH
Hepatic detoxification of urea Increased serum levels due to decreased detoxification by the liver and due to portal-systemic shunting.
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Cholesterol increases in liver disease, especially cholestatic disease with a low percentage of esterification. Abnormal lipoprotein X in biliary cirrhosis. Triglyceride levels increase due to decreased accumulation of liver cells
EBV, Toxo, CMV, Leptospirosis Ferritin and fasting transferrin saturation, genetics Hemochromatosis Caeruloplasmin and copper (serum), 24 hour urine copper Autoantibodies: ANA, ASMA, AMA, Celiac Immunoglobulins: IgG, IgA, IgM Cholesterol, triglyceride a1antitriglyceride + – fetoprotein ( cirrhosis only)
31 Chronic hepatitis B % of infants and children affected by hepatitis develop chronic hepatitis B, but <5% of adults. Chronic hepatitis B carriers have a ~25% risk of liver damage, cirrhosis, liver failure and liver cancer. LFTs should be checked at least 6 times a month. Hepatitis B virus testing, using HBsAg, is recommended for all unvaccinated individuals.
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HBsAg Negative Positive No evidence of Hepatitis B infection If positive for 6 months, it is consistent with Hepatitis B infection.
Anti-HBs Matches previous infection or vaccination No evidence of previous infection or vaccination See footnote (b) Anti-HBs Negative Positive Anti-HBs has documented immunity, the patient can be considered protected for a long time unless he is not immune. . If in doubt, go back and retest the anti-HBs in three weeks. A small number of patients may be positive for anti-HBc from previous HBV infection in the absence of anti-HBs. If there is a strong suspicion of previous infection or high risk, then order anti-HBc.
34 Chronic Hepatitis C – Most people will have no symptoms during the acute infection but about 70% will remain infected. – Chronic diseases carry a high risk of liver damage, cirrhosis and liver cancer. – Blood test for Anti HCV-Ab for all people at risk, for example: recipients of blood / parts.
Stages Of Liver Damage Chart Poster Hepatitis Cirrhosisi
Anti HCV Ab No evidence of chronic Hepatitis C disease See footnote (a) Indicates current, past or chronic Hepatitis C infection See footnote (b) Negative Positive A negative test excludes infection in the past 8 weeks. Anti-HCV positive followed by HCV RNA test. Keep LFTs normal and
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