Liver Diseases PDF

Liver Diseases Sunday 02-05-2021 Functions of liver • Biosynthesis: albumin, globuins, lipoproteins, etc. • Metabolic regulation: plays a major role in carbohydrates, lipids and protein metabolism. • Detoxification: endogenous and exogenous compounds. • Secretion: water soluble end products, bile...

Liver Diseases Sunday 02-05-2021 Functions of liver • Biosynthesis: albumin, globuins, lipoproteins, etc. • Metabolic regulation: plays a major role in carbohydrates, lipids and protein metabolism. • Detoxification: endogenous and exogenous compounds. • Secretion: water soluble end products, bile salts, etc. • Storage: fat soluble vitamins and water soluble as B12. HEPATITIS • Hepatitis is inflammation of the liver. • Infectious causes are viral hepatitis, infectious mononucleosis, secondary syphilis, and tuberculosis. • Noninfectious hepatitis causes: drugs (i.e., acetaminophen, halothane, ketoconazole, methyldopa, and methotrexate) or, more commonly, alcohol. Viral hepatitis • Five distinctive types of hepatitis viruses; A, B, C, D and E, they all target the liver. • The clinical manifestations of the five forms of viral hepatitis are quite similar. • Hepatitis A virus (HAV) and hepatitis E virus (HEV) are forms of infectious hepatitis; they are spread largely by the fecal–oral route are associated with poor sanitary conditions, are highly contagious, occur in outbreaks as well as sporadically, and cause self-limited hepatitis only. • Hepatitis B virus (H BV), hepatitis C virus (HCV), and hepatitis D virus (HDV) are forms of serum hepatitis, are spread largely by parenteral routes and less commonly by intimate or sexual exposure, and are not highly contagious. They are capable of leading to chronic infection and, ultimately, to cirrhosis and hepatocellular carcinoma Pathophysiology and Complications • The hepatocyte injury in viral hepatitis suggest that IMMUNE RESPONSES T-cell responses to viral antigens expressed may be the major effectors of injury. Other proinflammatory cytokines, natural killer cell activity, and antibody dependent cellular cytotoxicity also may play roles in cell injury and inflammation during acute hepatitis virus infection. Hepatitis B (Serum hepatitis) Hepatitis B virus (HBV) is a DNA virus with a nuclear capsule enveloped by an outer lipid layer containing hepatitis B surface antigen (HBsAg). The nuclear capsule contains other viral components, including the hepatitis B core antigen (HBcAg), the e antigen (HBeAg), DNA, and DNA polymerase An important consideration among dental professionals is the risk of percutaneous transmission through punctures or cuts with instruments infected from HBV-positive patients, or absorption through the mucosal surfaces (eyes, oral cavity). Transmission through saliva can occur as a result of absorption from mucosal surfaces . HBsAg (infectious) Indicates currently infectious (appears 2-10 weeks after exposure &In acute cases, this antigen is undetectable after 4–6 months. Persistence of HBsAg indicates carrier state (The presence of the HBsAg for longer than 6 months is indicative of chronic hepatitis B infection). Anti-BsAg (recovery or successful immunization) Anti-HBc (IgM antibody to HBc antigen acute,Persistently infected, or previously infected nonprotective) HBeAg (infectious) Anti-HBeAg (clearing/cleared infection) HEPATITIS B OCCUPATIONAL TRANSMISSION HBV is highly infectious when compared with HIV even minute traces of infected bloo d as little as 0.0001 ml can transmit infection. After percutaneous or other sharps injury in health care workers involving exposure to contaminated blood, the risk of contracting HBV infection is reported to range from 6% to 30%, with potential infectiousness correlating with presence of HBeAg in the serum (i.e., serum with HBeAg and HBsAg may be 10 times more infectious than serum with HBsAg alone). HBV can survive for at least 1 week in dried blood on environmental surfaces and contaminated needles and instruments. HBV vaccination HBV vaccine is given in three doses over a six month period and produces an effective antibody response in the majority of individuals. When the vaccine is given according to the protocol of 0, 1, and 6 months: 30–50% protection occurs after the first dose. After the second dose 50–75% protection occurs, and after the third dose 90% protection occurs. Hepatitis C (Posttransfusion hepatitis non-A non-B) Hepatitis C is caused by the hepatitis C virus (HCV). HCV is an enveloped virus, with a single-stranded RNA genome contained in a capsid. Flavivirus 6 major genotypes (40 related subtypes). • Transmission: mainly percutaneous. Very low risk with sexual transmission • Incubation: 2weeks-6months (average 3 months). • Risk groups • mainly IV drug users, and blood transfusion prior to 1992 • Risk of infection with needle stick injury 2-8% • 80-90% risk of becoming chronic carrier. Prevention of Hepatitis C • At present, there are no means of prevention of hepatitis C other than avoidance of high-risk behaviors and appropriate use of standard precautions. • Accidental needle-stick exposure is perhaps the most frequent issue in prevention of transmission. At present, neither immune globulin nor preemptive therapy with antiviral agents or interferon is recommended in this situation. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • Patients classically exhibit three phases of acute illness. • The prodromal (preicteric) phase, ➢ which usually precedes the onset of jaundice by 1 or 2 weeks, ➢ consists of — abdominal pain, — anorexia, — intermittent nausea, — vomiting, — fatigue, — myalgia, — malaise, and — fever. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • The icteric phase ➢onset of clinical jaundice, ➢Many nonspecific prodromal symptoms may subside, but gastrointestinal symptoms (e.g., anorexia, nausea, vomiting, right upper quadrant pain) may increase, especially early in the phase. ➢Hepatomegaly and splenomegaly frequently are seen. ➢This phase lasts 2 to 8 weeks. Hepatitis: CLINICAL PRESENTATION Signs and Symptoms • During the convalescent or recovery (posticteric) phase, ➢symptoms disappear, but hepatomegaly and abnormal liver function values may persist for a variable period. ➢ This phase can last for weeks or months, and recovery time for hepatitis B and C is generally longer. TREATMENT • As with many viral diseases, therapy basically is palliative and supportive. Bedrest and fluids may be prescribed, especially during the acute phase. A nutritious and high calorie diet is advised. • Alcohol and drugs metabolized by the liver are not to be ingested. • Viral antigen and ALT levels should be monitored for 6 months to determine whether the hepatitis is resolving. • Chronic hepatitis is treated by administration of interferon (alfa-2b) (3–10 million units given three times weekly for 6 months to 1 year). • Corticosteroids usually are reserved for patients with fulminant hepatitis. • Liver transplantation is a last resort for patients who develop cirrhosis. Dental management 1. Identification of potential or actual carriers of HBV, HCV and HDV is very difficult through history. 2. All patients with viral hepatitis must be managed as though they are potentially infectious, so standard precautions for infection control should be implemented. 3. It is recommended that all dental health care workers should receive vaccination against HBV and implement standard precautions during the care of all dental patients. 4. Patients with active hepatitis: • Should be referred for medical treatment, only urgent dental treatment should be provided with strict adherence to standard precautions of infection control and preferably in isolated operatory. • Aerosols should be minimized. • Drugs that are metabolized in liver should be avoided. • If surgery is necessary prothrombin time (PT) and bleeding time should be obtained. 5. Patients with history of hepatitis: • Since most patients are unaware that they have had hepatitis, identification of carriers is very difficult, and requesting screening tests for every patient is not practical.The only method for providing protection is to adopt a strict program of clinical asepsis for all patients. • If knowing the type of hepatitis virus through history is not possible, screening test can be ordered for the presence of HBsAg or Anti-HCV. 6. Patients at high risk of HBV or HCV infection: • Screening is recommended for HBsAg and Anti-HCV. • Patients who are carriers might have chronic active hepatitis leading to bleeding problems or metabolism problems that require treatment modification. • If accidental needle stick occurs, knowing if the patient is HBsAg positive or HCV positive is very important to determine the need for immunoglobulin, vaccine and follow up medical care. 7. Patients who are hepatitis carriers: • Standard precautions of infection control should be followed. • Such patients may have chronic active hepatitis with compromise liver function. Liver function tests can be ordered and consultation with physician may be needed. 8. Patients with signs and symptoms of hepatitis • Only emergency dental care should be provided in isolated operatory with adherence to the standard precautions of infection control. • Routine dental care should be postponed and the patient referred to the physician. 9. Dentists who are hepatitis virus carriers: • If the dentist is found to be positive for blood transmissible virus, exposure-prone procedures should not be performed, or strict adherence to aseptic technique should be followed to prevent transmission. • Periodic retesting is necessary. 10. Postexposure protocols for percutaneous or permucosal exposures to blood.: • In case of percutaneous or permucosal exposure through needle stick or puncture wound contaminated with blood from an individual who is HBsAg, the risk of infection may approach 30%. ❖ If the exposed is vaccinated; a test to evaluate Anti-HBsAg should be done: • If inadequate levels (< 10 mIU/mL )→ HB immunoglobulin + vaccine booster should be administered. • If adequate levels (> 10 mIU/mL )→ nothing further is required. ❖ If the exposed is not vaccinated→ HB immunoglobulin + initiation of vaccination is recommended. • For HCV; no postexposure protocol or vaccine is available. 11. Drug consideration: • No special drug considerations are required for a patient who has completely recovered from viral hepatitis. • However, if a patient has chronic active hepatitis or is a carrier of HBsAg or HCV and has impaired liver function, the dosage of drugs metabolized by the liver should be decreased, or these drugs should be avoided, if possible ((Aspirin, Acetaminophen, Lidocaine, Ibuprofen, Ampicillin, Tetracycline, Metronidazol) • A quantity of three cartridges of 2% lidocaine (120 mg) is considered a relatively limited amount of drug. Hepatitis: Oral Manifestations and Complications • Abnormal bleeding is associated with hepatitis and significant liver damage. • This may result from ✓ abnormal synthesis of blood clotting factors, ✓ abnormal polymerization of fibrin, ✓ inadequate fibrin stabilization, ✓ excessive fibrinolysis, or ✓ thrombocytopenia associated with splenomegaly that accompanies chronic liver disease. Hepatitis: Oral Manifestations and Complications cont.... • Before any surgery is performed, the platelet count should be obtained, and it should be confirmed that the international normalized ratio (INR) is lower than 3.5. • If the INR is 3.5 or greater, the potential for severe postoperative bleeding exists. • In this case, extensive surgical procedures should be postponed. • If surgery is necessary, an injection of vitamin K usually corrects the problem and should be discussed with the physician. • Chronic viral hepatitis increases the risk for hepatocellular carcinoma. This malignancy rarely metastasizes to the jaw (fewer cases in the jaw were reported ). • Oral metastases primarily present as hemorrhagic expanding masses located in the premolar and ramus regions of the mandible. Alcoholic liver disease • alcohol is hepatotoxic and its metabolite, acetylaldehyde, is fibrinogenic. • Chemokines also are implicated in the pathogenesis of alcoholic liver disease. Alcohol-induced influx of endotoxin (lipopolysaccharides) from the gut into the portal circulation can activate Kupffer cells, which leads to enhanced chemokine release. Chemokines, in turn, directly and indirectly damage liver hepatocytes. • An alcoholic is a man who drinks regularly 30 units/week or a woman who drinks 20 units/week. Clinical presentation Pathophysiology and Complications The pathologic effects of alcohol on the liver are expressed as one of three disease entities. These conditions may exist alone but commonly appear in combination. 1. Fatty liver (Steatosis): no visible manifestations except liver enlargement; it is considered completely reversible, 2. Alcoholic hepatitis : alcoholic hepatitis is considered a reversible condition. The clinical presentation of alcoholic hepatitis often is nonspecific and may include features such as nausea, vomiting, anorexia, malaise, weight loss, and fever. More specific findings include hepatomegaly, splenomegaly, jaundice, ascites, ankle edema, and spider angiomas. 3. Cirrhosis most serious form of alcoholic liver disease, which generally is considered an irreversible condition characterized by progressive fibrosis. It may remain asymptomatic for many years until sufficient destruction of the liver parenchyma has occurred to produce clinical evidence of hepatic failure. Ascites, spider angiomas, ankle edema, and jaundice may be the earliest manifestations, but frequently hemorrhage from esophageal varices is the initial sign. Spider nevi caput medusae Dental management 1. Detection of such patients by: • History; the patient should be asked about the type, quantity, frequency, pattern and consequences of alcohol use, also family history of alcoholism. • Clinical examination for signs and symptoms of alcoholic liver disease. • Alcohol odor on breath. • Information from family members or friends. 2. A patient with untreated alcoholic liver disease is not a candidate for elective, outpatient dental care and should be referred to a physician. 3. In patients with history of alcohol liver disease or alcohol abuse, a physician should be consulted to verify the patient's current status, medications, laboratory values (if present) and contraindications for medications and surgery. 4. If signs and symptoms of alcoholic liver disease are present the dentist can request some screening tests before surgical procedures; complete blood count (CBC) with differential, AST, ALT, platelet count, thrombin time, PT and INR. Abnormal results should be discussed with the physician. 5. Treatment considerations; 3 major dental treatment considerations apply for patients with alcoholic liver disease: • Bleeding tendencies; can be managed with the assistance of physician, this may entail the use of local hemostatic agents, fresh frozen plasma, vitamin K, platelets and antifibrinolytic agents. • The unpredictable metabolism of drugs; In mild to moderate liver disease, enzymatic induction is likely to have occurred leading to increased tolerance to LA, sedatives, hypnotics and GA, thus larger doses may be needed to attain the desirable effects of these drugs. In cirrhosis or alcoholic hepatitis avoid drugs that are metabolized in the liver or using half dose particularly if aminotransferases level (AST and ALT) is 4 times more than normal, serum bilirubin is more than 2mg/dl, serum albumin lower than 35g/L, with signs of ascites and encephalopathy or malnutrition. • The risk of infection or spread of infection; because these patients have reduced reticuloendothelial capacity and altered cell mediated immune function, but antibiotic prophylaxis is not needed unless there is an ongoing infection. Consultation with the physician regarding the use of antibiotic may be considered especially in patients with moderate or severe liver disease. Oral complications and manifestations 1. Poor oral hygiene and caries which is due to neglect. 2. Impaired gustatory function. 3. Nutritional deficiency can result in anemia causing glossitis, loss of papillae, angular and labial cheilitis. 4. Bleeding tendencies cause spontaneous gingival bleeding, mucosal ecchymoses and petechiae. 5. Alcohol breath odor. 6. Jaundiced mucosal tissues