cirrhosis of liver & liver hepatitis.pptx

1. CIRRHOSIS OF LIVER AND HEPATITIS - M.DHIVYA, M.SC NURSING 1 ST YEAR, COLLEGE OF NURSING, MTPG & RIHS .

2. TERMINOLOGIES RELATED TO CIRRHOSIS OF LIVER AND HEPATITIS: Fulminant: The term fulminant refers to a severe and sudden onset of symptoms or disease that progresses rapidly. It describes conditions that develop quickly and with great intensity, often leading to severe outcomes if not treated promptly. Necrosis : Necrosis is the term used to describe the death of cells or tissues in the body due to injury, disease, or lack of blood supply. This cell death occurs in an uncontrolled manner and often leads to the loss of tissue function.

3. Pre necrotic state : The pre-necrotic state refers to the stage before cell death (necrosis) occurs. This stage is characterized by cellular stress and damage that, if not reversed, can lead to irreversible cell injury and necrosis. Understanding and identifying this state is crucial for preventing cell death and mitigating tissue damage. Post-necrotic state : The post-necrotic state refers to the condition of tissues and organs after necrosis has occurred. This state involves the body's response to and repair of the damage caused by cell death.

4. Asterixis : Asterixis is a neurological sign characterized by a sudden, brief, non-rhythmic lapse of sustained posture, typically seen as a "flapping" tremor of the hands when the wrists are extended. This condition is most commonly associated with metabolic encephalopathies, particularly hepatic encephalopathy due to liver failure. Palatable diet: A palatable diet refers to a diet consisting of foods that are appealing and enjoyable to eat. This encompasses factors like taste, texture, aroma, and overall satisfaction that make food pleasant to consume

5. Fibrosis : Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue, typically as a reparative response to injury, inflammation, or chronic damage. It is characterized by the excessive deposition of extracellular matrix components, such as collagen, leading to tissue scarring and functional impairment. Icteric: Icteric is a medical term that refers to jaundice, a condition characterized by the yellowing of the skin, mucous membranes, and whites of the eyes (sclera) due to elevated levels of bilirubin in the blood.

6. Kupffer cells are specialized macrophages located in the liver. They form part of the mononuclear phagocyte system and play a crucial role in the body's immune response .

7. CIRRHOSIS OF LIVER: DEFINITION: Cirrhosis is characterized by fibrosis of liver tissue leading to decreased mass, impaired liver function, and altered blood flow. Cirrhosis was previously thought to be an irreversible condition; now, however, it is recognized that fibrosis may be reversed when the underlying cause is eliminated

8. INCIDENCE: More than 160 million people suffered from cirrhosis in 2017 around the world, and more than 0.8 million patients with cirrhosis died every year. Chronic liver disease affects 1.5 billion people globally and is the 11th leading cause of death worldwide. 1,5 Almost 1.16 million lives are lost worldwide each year due to cirrhosis and its complications, of whom 18.3 % are of Indian origin.

9. CAUSES: Chronic Alcohol Abuse: Alcoholic Liver Disease: Heavy and prolonged alcohol consumption can lead to alcoholic liver disease, which progresses from fatty liver to alcoholic hepatitis and eventually to cirrhosis. Not all heavy drinkers develop cirrhosis, but the risk increases with prolonged alcohol abuse.

10. Chronic Viral Hepatitis: Hepatitis B Virus (HBV): Chronic infection with hepatitis B virus can cause inflammation and damage to liver cells over time, leading to cirrhosis. Hepatitis C Virus (HCV): Chronic infection with hepatitis C virus is a leading cause of cirrhosis globally. HCV infection can lead to chronic liver inflammation and fibrosis, progressing to cirrhosis in a significant proportion of cases.

11. Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH) Autoimmune Hepatitis : An autoimmune condition where the body's immune system attacks liver cells, leading to chronic inflammation and progressive liver damage. If untreated, autoimmune hepatitis can progress to cirrhosis. Genetic Disorders: Hemochromatosis: A genetic disorder where excessive iron is absorbed and deposited in the liver and other organs, leading to liver damage and cirrhosis. Wilson's Disease: A rare genetic disorder where copper accumulates in the liver and other organs, causing liver damage and cirrhosis if untreated.

12. Biliary Tract Disorders: Primary Biliary Cholangitis (PBC): An autoimmune disease affecting the bile ducts inside the liver, leading to inflammation, scarring (fibrosis), and eventually cirrhosis. Primary Sclerosing Cholangitis (PSC) : A chronic inflammatory disease of the bile ducts outside the liver, which can lead to liver cirrhosis over time.

13. Toxic Exposures: Toxic Hepatitis: Exposure to certain chemicals, drugs, or toxins can cause acute or chronic liver damage, leading to cirrhosis in severe cases. Other Causes : Cryptogenic Cirrhosis: Cirrhosis where the underlying cause is unknown, despite extensive evaluation. Chronic Heart Failure: Long-standing congestive heart failure can lead to liver congestion and fibrosis, sometimes progressing to cirrhosis (cardiac cirrhosis).

14. TYPES OF CIRRHOSIS: Alcoholic Cirrhosis Posthepatic Cirrhosis Biliary Cirrhosis

15. PATHOPHYSIOLOGY: In cirrhosis, functional liver tissue is gradually destroyed and replaced by fibrous scar tissue. As hepatocytes and liver lobules are destroyed, the metabolic functions of the liver are lost. Structurally abnormal nodules encircled by connective tissue develop. This fibrous connective tissue forms constrictive bands that disrupt blood and bile flow within liver lobules. Blood no longer flows freely through the liver to the inferior vena cava. This restricted blood flow leads to portal hypertension, increased pressure in the portal venous system.

16. MULTI SYSTEM EFFECTS OF CIRRHOSIS OF LIVER:

17.   Neurologic: Portal systemic encephalopathy (agitation lethargy stupor coma) Paresthesias Sensory disturbances Asterixis (“liver flap”) Cardiovascular: Bounding pulse Pulmonary hypertension Portal hypertension Dysrhythmias Hematologic: clotting factors Thrombocytopenia Anemia

18. Potential Complication: Disseminated intravascular coagulation Reproductive: Oligomenorrhea (female) Testicular atrophy (male) Integumentary: Jaundice (skin, sclera of eyes) Erythema of palms Spider angioma Decreased body hair Pruritis Ecchymoses Caput medusae (dilated veins around the umbilicus)

19. Endocrine: Gynecomastia in males Potential Complication Diabetes mellitus Respiratory Dyspnea Gastrointestinal: Esophageal : Esophageal varices Stomach/intestines: Abdominal pain Anorexia Ascites Nausea Clay- colored stools Peptic ulcers GI bleeding Hemorrhoids

20. Hepatic: Atrophic, nodular liver Splenomegaly Potential Complication: Liver cancer Immune System: Leukocytopenia Susceptibilityto infections Metabolic Processes: Fluid and electrolyte imbalances Hypoalbuminemia Hypokalemia Hypocalcemia Malnutrition Muscle wasting

21. NORMAL LIVER:

22. FATTY LIVER:

23. DIAGNOSTIC EVALUATION: Liver function studies include ALT, AST, and ALP CBC with platelets Coagulation studies Serum electrolytes Bilirubin levels Serum albumin levels Serum ammonia Serum glucose and cholesterol levels

24. Abdominal ultrasound Esophagoscopy Liver biopsy

25. MANAGEMENT: MEDICAL MANAGEMENT: Diuretics reduce fluid retention and ascites. Spironolactone (Aldactone) is frequently the drug of first choice because it addresses one of the causes of ascites—increased aldosterone levels. If additional diuresis is necessary, a loop diuretic such as furosemide (Lasix) may be added to the regimen.

26. Diuretics - to treat ascites . Drug of choice: spironolactone ( Aldactone) and if necessary a loop diuretics (furosemide) can be added Antibiotics - to treat infection and to reduce nitrogenous load and ammonia levels. Drug of choice: neomycin, metronidazole and rifaximin. Lactulose - reduces the number of ammonia forming organism in the bowel and increases the acidity of colon contents, converting ammonia into ammonium ions. Beta blockers- nadolol or propranolol to reduce portal hypertension and prevent bleeding to esophageal varices

27. Ferrous sulphate and folic acid to treat anemia and vitamin K to reduce risk of bleeding. Blood transfusion: RBC , platelets and plasma to achieve hemostasis . Antacids Benzodiazepines - oxazepam (not metabolized by liver) can be administered to relieve anxiety

28. NUTRITION AND FLUID MANAGEMENT: Sodium intake – 2grams/day and fluid restriction – 1500ml/day Palatable diet with adequate calories and proteins , parenteral nutrition can be administered when food intake is limited Vitamin and mineral supplements- thiamine, folate and B12 and fat soluble vitamins A, D, E and K

29. SURGICAL MANAGEMENT: Liver transplantation : Liver transplantation is indicated for some patients with irreversible, progressive cirrhosis. A decline in functional status, increasing bilirubin levels, falling albumin levels, and increasing problems with complications that respond poorly to treatment are indications for liver transplantation. Malignancy, active alcohol or drug abuse, and poor surgical risk are contraindications for the surgery.

30. MELD SCORE FOR LIVER TRANSPLANTATION:

31. MANAGEMENT OF COMPLICATIONS: ASCITES: Paracentesis, aspiration of fluid from the peritoneal cavity, may be a diagnostic or a therapeutic procedure. It may be done therapeutically to relieve severe ascites that does not respond to diuretic therapy. The goal of paracentesis is to relieve respiratory distress caused by excess fluid in the abdomen. Ascites fluid may be withdrawn in moderate amounts of 500 mL to 1 L daily to reduce the risk of fluid and electrolyte imbalances. Large-volume paracentesis, withdrawal of 4 to 6 L of fluid at one time, may be used. Albumin is often administered intravenously during large-volume paracentesis to maintain intravascular volume as the pressure of the ascites fluid in the abdomen is relieved.

32. ESOPHAGEAL VARICES: In variceal ligation or banding, small rubber bands are placed on varices to occlude blood flow. Endoscopic sclerosis involves injecting a sclerosing agent directly into the varices to induce inflammation and clotting. Balloon tamponade of bleeding varices may be used if bleeding cannot be controlled through vasoconstriction or if endoscopy is unavailable or contraindicated by the patient’s condition.

33. PORTAL HYPERTENSION: Transjugular intrahepatic portosystemic shunt (TIPS) may be used as an emergency measure to relieve portal hypertension and its complications of esophageal varices and ascites. A channel is created through the liver tissue using a needle inserted transcutaneously . An expandable metal stent is inserted into this channel to allow blood to flow directly from the portal vein into the hepatic vein, bypassing the cirrhotic liver.M

34. HEPATITIS: Hepatitis is inflammation of the liver. It is usually caused by a virus, although it may result from exposure to alcohol, drugs and toxins, or other pathogens. Hepatitis may be acute or chronic in nature. Chronic hepatitis also increases the risk for developing liver cancer.

35. INCIDENCE: An estimated 354 million people worldwide live with hepatitis B or C, and for most, testing and treatment remain beyond reach. Some types of hepatitis are preventable through vaccination. A WHO study found that an estimated 4.5 million premature deaths could be prevented in low- and middle-income countries by 2030 through vaccination, diagnostic tests, medicines and education campaigns. WHO’s global hepatitis strategy, endorsed by all WHO Member States, aims to reduce new hepatitis infections by 90% and deaths by 65% between 2016 and 2030.

36. TYPES: Hepatitis A virus (HAV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), The Hepatitis B-associated delta virus (HDV), and Hepatitis E virus (HEV). Fulminant Hepatitis Autoimmune Hepatitis

37. PATHOPHYSIOLOGY : The inflammatory process of hepatitis, whether caused by a virus, toxin, or other mechanism, damages hepatic cells and disrupts liver function. Cell-mediated immune responses damage hepatocytes and Kupffer cells, leading to hyperplasia, necrosis, and cellular regeneration. The flow of bile through bile canaliculi and into the biliary system can be impaired by the inflammatory process, leading to jaundice.

38. When the inflammatory process is mild (e.g., hepatitis A), the liver parenchyma is not significantly damaged. The inflammatory processes associated with hepatitis B and hepatitis C, however, can lead to severe liver damage. The metabolism of nutrients, drugs, alcohol, and toxins and the process of bile elimination are disrupted by the inflammation of hepatitis A

39. Hepatitis viruses replicate in the liver, indirectly damaging liver cells (hepatocytes). The viruses provoke an immune response that causes inflammation and necrosis of hepatocytes, leading to the clinical presentation of acute disease. Although the extent of damage and the immune response vary among the different hepatitis viruses, the disease itself usually follows a predictable pattern. No manifestations are present during the incubation period after exposure to the virus.

40. CLINICAL MANIFESTATIONS: PREICTERIC PHASE: “Flulike” symptoms: malaise, fatigue, fever Gastrointestinal: anorexia, nausea, vomiting, diarrhea , constipation Muscle aches, polyarthritis Mild right upper abdominal pain and tenderness ICTERIC PHASE: Jaundice Pruritus Clay- colored stools Brown urine Decrease in preicteric phase symptoms (e.g., appetite improves; no fever)

41. POSTICTERIC/CONVALESCENT PHASE: Serum bilirubin and enzymes return to normal levels Energy level increases Pain subsides Gastrointestinal: minimal to absent

42. DIAGNOSIS EVALUATION: Liver function tests Alanine aminotransferase (ALT) l evels may exceed 1000 U/L or more in acute hepatitis. Aspartate aminotransferase (AST) blood levels may be 20 to 100 times normal values. ■ Alkaline phosphatase (ALP) Serum ALP levels often are elevated in hepatitis, and may remain elevated after ALT and AST levels have returned to normal ranges.

43. Serum bilirubin levels , including conjugated and unconjugated, are elevated in viral hepatitis due to impaired bilirubin metabolism and obstruction of the hepatobiliary ducts by inflammation and edema . The bilirubin level decreases as inflammation and edema subside. Laboratory tests for viral antigens and their specific antibodies Ultrasound used to visualize the liver more accurately including blood vessels, inflammation and any other pathological changes. Liver biopsy Metabolic tests

44. MEDICAL MANAGEMENT: Severe cases of acute hepatitis B may be treated with an antiretroviral drug such as lamivudine ( Epiver , Heptovir ), adefovir ( Hepsera ), entecavir ( Baraclude ), tenofovir ( Viread ) or telbivudine ( Tyzeka ). Acute hepatitis C generally is treated with interferon alpha , an antiviral agent, to reduce the risk of chronic hepatitis C. While single drug treatment with interferon is common, a long-acting interferon (peginterferon or Pegasys ) may be combined with the antiviral drug ribavirin ( Rebetol , Virazole ). Combination therapy with peginterferon and ribavirin is the treatment of choice for chronic hepatitis C.

45. Interferon alpha interferes with viral replication, reducing the viral load. It is given by intramuscular or subcutaneous injection. Virtually all patients treated with interferon develop a flulike syndrome with fever, fatigue, muscle aches, headache, and chills. Acetaminophen helps alleviate some of these adverse effects, which tend to decrease over time. Depression also is a common adverse effect of this drug. Instruct patients to contact their physician if suicidal thoughts or manifestations of depression develop.

46. In addition to interferon alpha or peginterferon, options for treating chronic hepatitis B include antiviral drugs such as lamivudine or adefovir. Using an antiviral drug in combination with an interferon reduces liver inflammation and fibrosis.

47. Entecavir is the most potent of the HBV antivirals and may be used as an alternate to lamivudine or adefovir. Treatment of acute hepatitis also includes as-needed bed rest, adequate nutrition as tolerated, and avoidance of strenuous activity, alcohol, and agents that are toxic to the liver. In most cases, clinical recovery takes 3 to 16 weeks.

48. COMPLEMENTARY THERAPIES: Milk thistle, with its active ingredient silymarin, has been used by herbalists to treat liver disease for over 2000 years. Clinical studies have demonstrated that treatment with silymarin promotes quality of life and reduces symptoms in patients with hepatitis C. Herbalists also may use licorice root to treat hepatitis. It has both antiviral and anti-inflammatory effects.

49. Long-term use of lico rice root, however, can lead to hypertension and affect fluid and electrolyte balance. Herbal preparations also may be used to relieve the adverse effects of interferon alpha. Ginger can help relieve nausea, and St. John’s wort is used for the depression associated with interferon alpha.

50. COMPLICATIONS: Chronic Hepatitis Cirrhosis Liver Failure Liver Cancer Portal Hypertension Hepatic Encephalopathy Coagulopathy Jaundice Kidney Problems Other Organ Involvement Extrahepatic Manifestations