Polytechnic Institute of Guarda HIGHER SCHOOL OF HEALTH GUARD XI Degree in Nursi ng 2nd Year / 2nd Semester Ana Rita

Martins Madureira Ruth Cecile Lopes Sonia Rodrigues GUARD, APRIL 2006 Polytechnic Institute of Guarda HIGHER SCHOOL OF HEALTH GUARD XI Degree in Nursi ng 2nd Year / 2nd Semester Work done by: Ana Rita Martins Madureira Ruth Cecile Lopes Sonia Rodrigues Super vised by: Prof. Paulo Tavares GUARD, APRIL 2006 ACKNOWLEDGEMENT: We thank all those who, directly or indirectly, contributed to this work, particularly to classmates and advisor Professor Paulo Tavares for th eir availability. Thanks INDEX OF FIGURES Sheet FIGURE 1 - Location anatomy of the liver in the human bod y ... ... ... ... ... ... ... .. 8 FIGURE 2 - System of channels of the liver .. . ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 9 FIGURE 3 - l obe liver with the portal system at the vertices and a central vein at its cente r ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... ... 10 FIGURE 4 - Histology of the liver ... ... . .. ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .. 10 FIGURE 5 - Microphotograph of hepatitis A virus ... ... ... ... ... ... ... ... ... ... ... ... .15 FIGURE 6 - Worldwide distribution of hepatitis A ... ... ... ... .. . ... ... ... ... ... ... ... ... ... 16 Figure 7 - Structure of hepatitis B vir us ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 18 Figure 8 - Wor ldwide distribution of hepatitis B ... ... ... ... ... ... ... ... ... ... ... . .. ... ... 19 Figure 9 - Structure of Hepatitis C ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... 22 FIGURE # 10 - Global distribution of hepatitis C ... ... ... ... ... ... ... ... ... ... ... ... ... .23 FIGURE 11 - Schematic and microphotograph of the virion of hepatitis D ... ... ... .. 25 FIGURE # 12 Global distribution of hepatitis D ... ... ... ... ... ... ... ... ... ... ... ... ... .26 FIGURE No. 13 - Micrograph of Hepatitis E ... ... ... ... ... ... .. . ... ... ... ... ... 28 FIGURE No. 14 - World Distribution of Hepatitis E ... . .. ... ... ... ... ... ... ... ... ... ... ... .29 INDEX OF ACRONYMS HAV - hepatitis A virus HBV - Hepatitis B virus HCV - hepatitis C virus HDV - He patitis D HEV - Hepatitis E virus RNA - ribonucleic acid DNA - deoxyribonucleic acid IgM - immunoglobulin Index of abbreviations kg - kilogram ml - milliliters% - Percentage mg / dl - mi lligrams per deciliter nm - nanometer SUMMARY Leaf 0. INTRODUCTION ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .6 1. ANATOMOPATHOLOGICAL LIVER ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 8 2. VIRAL HEPATITI S ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .. . ... ... ... .13 02.01 ACUTE VIRAL HEPATITIS ... ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... ... .. .13 2.1. Hepatitis A ... ... ... ... ... .. . ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 14 2.2

. Hepatitis B ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... 17 2.3. Hepatitis C ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... 20 2.4. Hepati tis D ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .. . ... ... ... ... ... 22 2.5. Hepatitis E ... ... ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... ... ... ... ... ... ... ... 25 2.2 CHRONIC VIRAL H EPATITIS ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .... .. 28 3. NURSING CARE ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... ... .30 4. CONCLUSION ... ... ... ... ... ... ... ... ... ... ... ... ... .. . ... ... ... ... ... ... ... ... ... ... ... ... .. 37 5. REFERENCES ... ... .. . ... ... ... ... ... ... ... ... ... ... ... ... ... .. 39 0. INTRODUCTION This paper entitled, "Hepatitis A, B, C, D and E" comes in the context of Pathol ogy and Medical Nursing taught in 2nd year / 2nd semester of the Eleventh Degree in Nursing, School of Health Guard. The aim of this work to inform one of the d iseases that most affect the public health today, or viral hepatitis, which are an important cause of morbidity and mortality have had a great impact in civiliz ed societies of our time. Hepatitis may have several causes such as virus infect ions, alcohol abuse and certain medications, drugs, hereditary diseases and auto immune diseases, emphasizing that this work will only be described viral hepatit is, since they are the most common and also because are those that fall within t he program of the disciplines of Medical Pathology and Medical Nursing. It is un derstood by hepatitis tables showing a diffuse alteration in the hepatic parench yma with inflammation and alteration of the hepatocyte. This concept has been kn own since the time of Hippocrates,€not been studied in a more scientific until a fter the cases that occurred after the second World War broke two types of viral hepatitis: the epidemic, with a short incubation period and serum with long inc ubation period. Later after the discovery of virus antigen by Blumberg B, and A by Feinstone virus were well-defined two major types of hepatitis. However there were still a large number of hepatitis in which there were none of these viruse s, which is generally called for hepatitis non A and not B. Currently considered to be six types of viruses as those responsible for hepatitis. The hepatitis A virus (HAV) is responsible for disease known two thousand years ago by infectiou s jaundice, hepatitis B virus (HBV) causes the disease now recognized as parente ral transmission and first recorded 100 years ago, in the shipyards Bremen, Germ any at the outbreak of an outbreak of the so-called "catarrhal jaundice" in stev edores who had been vaccinated against smallpox. The third type of hepatitis is the most recent knowledge, as it was in 1977 that the Italian investigator Mario Rizzetto identified the delta agent in patients infected with HBV. In the 80 was described a new variant of hepatitis non A and not B, transmission orofecal, common in Eastern countries caused by the virus de signated E. In 1988, Houghton studied and cloned a new virus was named hepatitis C virus and more recently cloned and found to be another virus with the virus n ame G. Among the viral hepatitis is still possible to distinguish acute hepatiti s from chronic hepatitis, and the latter is represented by an inflammatory proce ss that lasts more than six months, but the chronic infection does not occur in all cases. For the development of this work, to facilitate their understanding i t was divided into two distinct parts. In the first part is a brief reference to the anatomy-physiology of the liver, since this is the major human organ affect ed by hepatitis, but not the only one. In the second part will be reported in de tail viral hepatitis still being made the distinction of acute viral hepatitis i n chronic viral hepatitis. The aim of this work to achieve the following objecti ves: • • • To publicize the anatomo-physiology of the liver; Identify the variou s viral hepatitis; Describe in detail the acute and chronic viral hepatitis taki ng into account the following aspects: a. Definition b. Infectious agent; c. Dis tribution / prevalence / epidemiology; d. Reservoir host / e. Route of transmiss ion; f. Incubation period; g. Symptomatology; h. Diagnosis; i. Medical treatment

j. Nursing interventions; k. Prevention / prophylaxis; Regarding the methodology for the preparation of th is work recorreuse a methodology of investigative nature, in order to gain as mu ch information as possible. 1. ANATOMOPATHOLOGICAL LIVER According to Seeley, (1997 Fig. 1 - Location of anatomical p.842), "The liver is the largest organ in the human body liver. inner body, weighs about 1.36 SOURCE : www.virtual.epm.br kilogram (kg), is located in the upper right quadrant of th e abdomen, resting against the underside of the diaphragm. It consists of two ma jor lobes, the left and right, and two smaller lobes, the caudate and the square . "The various vessels, channels and nerves that enter and leave the liver, flow towards the hepatic hilum (gate), located on the face lower liver. The portal v ein, hepatic artery and a small nerve plexus, penetrate the liver hilum. The lym phatic vessels and the two liver (the right and left lobes), which carry bile ou t of the liver through the hilus. The channels left and right hepatic unite to f orm the common hepatic channel to which will unite the cystic duct, which comes from the gallbladder to form the common bile duct or common bile canal that open s into the duodenum, the large duodenal papilla in together with the pancreatic duct or canal of Wirsung (Figure 2). The gallbladder is a small sac that stores bile and is located on the underside of the liver. FIGURE 2 - System of channels of the liver. SOURCE: Seeley, Red R., Stephens, Trent D.; TATE, Philip, Anatomy and Physiology . Lisbon: Editora Lusodidacta, 1997. ISBN: 972-96610-5-7 Histologically, the liver is covered by a capsule of connective tissue and visce ral peritoneum, except a small area in the face of the diaphragm, in which there is no peritoneum, the uncovered area. In the hilus, the connective tissue capsu le branches, forming a network of septa (walls) towards the interior of the live r constituting its main support. The vessels,€nerves and the channels are distri buted by the liver together with the ramifications of the tissue. The septa of c onnective tissue dividing the liver: in hexagonal lobes each having an apex port al system consists of three vessels: the hepatic portal vein, hepatic artery and hepatic duct (Figure 3) hepatic nerves and lymphatic vessels are also located i n these areas, but are too small to be seen with optical microscopes. FIGURE 3 - hepatic lobe with the portal system at the vertices and a central vei n at its center. SOURCE: Seeley, Red R., Stephens, Trent D.; TATE, Philip, Anato my and Physiology. Lisbon: Editora Lusodidacta, 1997. ISBN: 972-96610-5-7 In the center of each lobe FIGURE 4 - Histology of the liver. There is a central vein. SOURCE: www.hepcentro.com.br unemse central veins to form hepatic veins, leaving the liver in its posterior and superior draining into the inferior vena cava. Central vein of each lobe liver stem strands, arranged as the spokes of a wheel composed of hepatocytes, liver cells functional. The space s between the ridges are liver blood channels, the hepatic sinusoids. The sinuso ids are lined by epithelium desquamation very thin and irregular, composed of tw o types of the endothelial cells, very thin and scattered, and the phagocytic ce lls or Kupffer cells. Among the cells of each string there is a cleft lumen, the bile canaliculus (Figure 4) Physiologically, the liver performs functions that no other organ is capable. This has an important role at the level of digestive and excretory functions, stores and produces nutrients, synthesizes new molecule s and purifies harmful chemicals. The liver produces and secretes approximately 600-1000 ml of bile per day. This plays an important role in digestion, diluting and neutralizing stomach acid and emulsifies fats so that the intestinal lipase

s can act upon them. Storage is another of the functions of the liver, due to th e ability of hepatocytes to withdraw blood sugar and store it in the form of gly cogen. These can also store fat, vitamins (A, B12, D, E and K), copper and iron. Interest however to note that this store is usually temporary, and the amount o f retained products in hepatocytes and the cell size, vary throughout the day. T his happens because the blood coming from the intestine passes through the porta l vein to the liver, where glucose and other substances are removed from blood b y hepatocytes, stored and re-issued when necessary. Thus, the hepatocytes can ma intain blood sugar levels within narrow limits. Another function of the liver is the interconversion of nutrients. Often food is not balanced, proportionate to the needs of the tissues and the liver has the ability to convert some other nut rients. For example, if a person makes a diet extremely rich in protein, can rea ch the liver protein excess and a deficit in carbohydrate and fat. Fractionate t he hepatocytes metabolize amino acids and many of them through metabolic pathway s, so they should be used to produce adenosine triphosphate, lipids and glucose. The hepatocytes also transform substances that can not be used by cells in subst ances more easily usable. Many of the substances ingested are harmful to the bod y's cells, in addition, the body itself produces many metabolites, if accumulate d, are toxic. The liver is one of the first lines of defense against many of the se harmful substances, detoxifies many substances by changing its structure, tor nandoas less toxic or making them easier to remove. For example ammonia, a break down product of amino acid metabolism, is toxic and not easily eliminated from c irculation by the kidneys. The hepatocytes remove it from the bloodstream and co nvert it into urea, which once secreted into the circulation is eliminated by th e kidneys through urine. Phagocytosis is a function of the liver that is perform ed at the level of Kupffer cells, which are located along the walls of hepatic s inusoids. These phagocytose red and white, old and injured, some bacteria and ot her debris that enter the liver through the circulation. The synthesis is the ab ility of the liver has to, by itself, produce new and unique components. Many of the blood proteins: albumin, fibrinogen, globulins, heparin and some coagulatio n factors are produced in the liver and released into the circulation. 2. VIRAL HEPATITIS According to Cotter (2003 p. 42)€hepatitis are diseases of the liver due to mult iple causes (viruses, bacteria, medications, toxic, etc.).. The offending agent causes inflammation and death of liver cells. If the body's response is adequate and can cure hepatitis in this case it is considered that the individual suffer s from an acute hepatitis, but this response is insufficient if the infection pe rsists and becomes chronic. The consequences of viral hepatitis are influenced b y factors such as the following: 1) Virulence of the virus, 2) Extension of pers istent liver injury, 3) individual natural defenses against aggression and liver disease, such as immune status, nutritional status and the general health of th e individual, 4) Supportive care the patient receives. Therefore and because the viral hepatitis is one of the current issues and that more progress has been ex periencing in modern gastroenterology and hepatology, this chapter will be portr ayed the acute and chronic viral hepatitis approaching from the epidemiological aspects to future prospects, through transmission, diagnosis, Clinical, treatmen t, prevention and prognosis, not forgetting some as the current arguments over m oney, sometimes decisive in medicine today. 2.1. ACUTE VIRAL HEPATITIS The hepatitis viral

acute it is a infection systemic that affects predominantly the liver. Almost all cases are caused by a five-viral agents: • • • • • The hepatitis A virus (HAV), The hepatitis B virus (HBV), hepatitis C virus (HCV ), delta agent associated with HBV or hepatitis D virus (HDV), hepatitis E virus (HEV). All these are human hepatitis virus RNA (ribonucleic acid) except the hepatitis B virus is a DNA (deoxyribonucleic acid). Although these agents can be distingui shed by their molecular and antigenic properties, all types of viral hepatitis p roduce clinically similar diseases. The 2.1.1.Hepatite Hepatitis A is a FIGURE 5 - Microphotograph of hepatitis A. acute infectious dis ease, SOURCE: www.hepnet.com caused by a small non-enveloped virus that belongs to the genus hepatovirus, family Picornaviridae. This type of hepatitis produce inflammation and necrosis of the liver and can progress to a more severe form. L oss may occur in liver function, putting the patient at risk of life, or does no t develop and remain inactive over the years. As was already mentioned, the infectious agent of hepatitis A is a hepatovirus, consisting of single-stranded RNA. Structurally, it presents a symmetry icosahed ral capsid which is composed of 32 capsómeros, and has 26 mm diameter. The virus enters by the oral route, developing a possible process in the throat, and embe dded in the intestinal mucosa. From this produces a phase of viremia, and is tra nsported to the liver where it replicates, the portal circulation, observing the formation of cytoplasmic vesicles. Subsequently leaves the liver and is excrete d with the feces. The mechanism of action is produced, so in two steps, one with high viral replication without hepatocellular necrosis and bile elimination of the virus, and a second, with decreased viral production, disappearance of HAV i n the stools, appearance of antibodies in serum and cell injury. After an incuba tion period ranging between 10 and 50 days, with an average of about 28 days, th e picture begins abruptly with a range of symptoms common to all viral hepatitis , both of nonspecific nature, such as liver-specific amendment. The disease has three typical phases: • • • State pre-icteric (with symptoms such as fever, mala ise, nausea ,...); jaundiced (can be kept at a mean of one to three weeks) conva lescence that remains until there is normalization of serum enzymes. Infection with hepatitis A virus has global distribution and can be characterize d in geographical areas by the prevalence of antibodies against HAV (anti-HAV), which indicates prior infection in the general population. Thus hepatitis A is u sually more common in less developed countries, due to the precariousness of bas ic sanitation. It focuses mainly on children and adolescents, usually few sympto ms at this age. On the other hand, are estimated to occur in adults, 30 deaths i

n 1,000 patients. However it is estimated that over 90% of the population above 30 years have developed natural immunity to this virus. FIGURE 6 - Worldwide dis tribution of hepatitis A. SOURCE: www.hepnet.com The only reservoir hosts or the VHA is the man but can chimpanzees and some moll usks serve as carriers and transmit the infection, although not proven this poin t.€Usually the diagnosis of acute HAV infection is made based on the presence or absence of immunoglobulins - IgM antibodies against the virus (IgM anti-HAV). T his diagnosis is performed through sampling and subsequent blood test looks for antibodies that fight the virus may be from this, to differentiate between a cur rent infection and an old, whereas a high number of IgM anti-HAV antibodies indi cate a recent exposure. There are also blood tests that measure the degree of de struction of the liver, however did not indicate what caused the destruction. Ho wever, another type of diagnostic for determining the disease: physical examinat ion, clinical examination, serological tests by searching for specific antibodie s against the virus and also the virological tests aimed at virus isolation by i noculation in cell cultures. Because HAV infection is self-limiting, this does n ot become chronic however, treatment in general can not be specific because ther e is no medical treatment for this pathology. Thus, the preferred treatment is conservative so this is to support measures related symptoms, and patients in th e acute phase: • • Avoid taking any medications or eating something that is hepa totoxic or is metabolized in the liver, such as paracetamol or alcohol; Maintain a balanced diet preferably low-fat and high in carbohydrates. In the near futur e, the market introduction of a bivalent combination vaccine against hepatitis v iruses A and B, could be a first step towards the eradication of infection with hepatitis A virus worldwide and probably will for universal immunization of chil dren . At the same time it becomes mandatory in order to improve the general san itary conditions of the people and act completely objective from the vaccine in the area of prevention. In short one can say that hepatitis A is a benign, selflimited and with a good prognosis, which over the years has been undergoing majo r epidemiological changes that are first and foremost related to the improvement of hygiene- health of populations. 2.1.2.Hepatite BA Hepatitis B is a disease defined as inflammation of the liver caused by HBV virus DNA, family Hepdnaviridae. The infectious viral particle, co nsists of an internal structure and external envelope (surface antigen), with 42 nm in diameter, possessing inside the virus genome - DNA, which has a partially double stranded and an enzyme - polymerase. FIGURE 7 - Structure of HBV. SOURCE: www.museum-grenoble.fr The process of HBV infection includes entering the hepatocyte, the exclusion of its genetic material into the cellular compartment where the first phase replica tion takes place, the replication of the same material and its transcription and translation, and finally meeting the various components of virion particles in the new "daughter" and its export from the infected cells. Thus, the virus genom e is converted into a closed circular chain of DNA with covalent bonds. Usually the incubation period for HBV is long, ranging from six weeks to four months. Thus a first step there is a phase of viremia with a high degree of replication and liver enzyme abnormalities, which under normal conditions, has a positive ev olution, ie the replication stops. Regarding the epidemiology of hepatitis B car e say that this is one of the most common infectious diseases worldwide. There a re about one million deaths annually by acute or chronic liver disease associate d with HBV. The prevalence of hepatitis B is highly variable among different are as of the world, with a variation in the rate of carrier status from 0.1 to 20%. This variation is related to differences in the predominant mode of transmissio

n and the age at which infection is acquired. So since 1993 we are witnessing a decline in the number of reported cases of acute hepatitis B, with a prevalence of infection in males and in the age group 15 to 35 years, suggesting that the i nitial contact with the hepatitis B virus occurs, more frequently in adolescents and young adults, the associandose risk behaviors. The incidence of hepatitis B has declined not only due to the vaccine, available since 1981 but also due to changes in risk behaviors that have led to reduced transmission. FIGURE 8 - Worl dwide distribution of hepatitis B. SOURCE: www.fiocruz.br The diagnosis relies on the notion of contagion, the notion of risk groups in th e determination of aminotransferases and simple serological investigations.€Here the simplest means of diagnosis is re-evaluating the presence or absence of IgM in the blood of the individual antiVHB suspected infected. Bilirubin has genera lly modest elevations (50-10 mg / dl), but the best indicator of prognosis of pa tients with acute hepatitis is the prothrombin time, is also important to the va lue of serum albumin. Treatment of acute hepatitis B usually valued three aspect s: physical activity, diet and drug therapy. For physical activity, the determin ation of this depends on the welfare of the patient, so there is no evidence tha t bed rest in bed or restrictions on physical activity alter the course of the d isease. With regard to diet this can be changed at the onset due to nausea and v omiting, so it may be necessary to administer glucose sera to supplement caloric intake and restore hydration. The readjustment electrolyte with potassium may a lso be necessary. After control of vomiting and, as the appetite is restored, th e diet can be divided into 5-6 meals a day getting the foods dependent on the pa tient's appetite. No need for vitamin supplements except vitamin K in some situa tions where there are changes in the values of prothrombin time. During the acut e phase should be avoided drinking alcohol. After the recovery phase there is no evidence it can be more harmful for these patients than for the general populat ion. Drug therapy is the treatment of choice for individuals with HBV, so that w e can use anti-emetics, to control the vomiting. In acute cholestatic-intensive use of Cholestyramine is indicated for the control of pruritus. Usually given th e full recovery of these individuals do not need the administration of antiviral s. Looking ahead, the eradication of HBV infection in the world is of paramount importance, therefore all efforts should go for prevention preventing new infect ions and for the effective treatment of hepatitis chronic, in order to eradicate the human agent of shells that are approximately 400 million worldwide. 2.1.3.Hepatite CO hepatitis C virus is an RNA virus of the Flaviviridae family a nd was identified in 1989, because hepatitis C previously was part of so-called hepatitis non A non B. FIGURE 9 - Structure of hepatitis C. SOURCE: www.museum-g renoble.fr The HCV virion is a spherical particle of 30-60 nm in diameter consisting of a c asing within which the viral genome is composed of a single strand of RNA. It is not clear the mechanism by which the virus is able to replicating. It is only known enzyme involved - the RNA polymerase. The viral re plication of HCV can be detected shortly after exposure. Peak viremia occurs dur ing the pre-icteric and progression to chronic hepatitis is not possible to pred ict. From the standpoint of epidemiology, prevalence by age group shows two dist inct patterns: a steady increase with age from 0.3% to 1% per year in countries like Japan and Taiwan, or a peak between 30-40 years as Australia, North America and even Western Europe. There is also a higher prevalence in men and a lower i ncidence in Western Europe and the United States. One can see that the general f ramework of epidemiology can be achieved first by defining risk groups, and seco ndly by establishing the mode of transmission of HCV. Thereby addicts and hemodi alysis are two populations of patients not transfused in which the prevalence of HCV is clearly increased. FIGURE 10 - Worldwide distribution of hepatitis C. SO

URCE: www.fiocruz.br . Hepatitis C is considered a silent disease because 75% of cases progress asympto matically making it extremely treacherous if you think that 85% of cases progres s to chronicity. Infection with hepatitis C begins as a flu after an incubation period of between two weeks to more than 1 year, although the average is 6-8 wee ks. A similar evolution is slow to hepatitis B, unfortunately produced antibodie s are not neutralizing and do not confer immunity in most cases. Generally, the reservoir of hepatitis C virus is the human patient or carrier and chimpanzees. For the diagnosis, the initial phase, the anti-HCV may be negative because their appearance may occur only at around 2-3 months after onset of clinical manifest ations.€Where there are difficulties in diagnosing acute hepatitis C and when th e suspicion is strong can be important to investigate the presence of HCV RNA wh ich appears frequently before the anti-HCV. Several studies have demonstrated a direct relationship between viral replication and levels of iron, there are indi cations that high levels of iron favor viral replication, so this may be informa tion that will reinforce the diagnosis. Other parameters that can be changed and should be evaluated: alkaline phosphatase, bilirubin, albumin, platelet count a nd prothrombin time. The virological response is assessed by viral load and the presence of viral RNA in the circulation. The count of the viral load is importa nt for monitoring response to treatment. The histological response is examined b y liver biopsy, unfortunately not well accepted by patients. Besides the orienta tion towards change in lifestyle, eradicating alcohol and improving eating habit s drug therapy is the use of Ribavirin and Interferon. Interferon is used for ge notypes 2 and 3 for a period of six months with a cure rate between 60-70%, unfo rtunately the most common genotype in our midst is the genotype 1, these cases m ust be made use of interferon by an years to get a cure rate between 30-40%. It is believed that interferon inhibits virus replication and enhances the protecti ve action of the immune system. Many patients, however, can not terminate treatment due to side effects. Among the contraindications to interfer on are: decompensated chronic diseases (epilepsy, diabetes, hypertension, corona ry heart disease), depression, autoimmune diseases, pregnancy and patients over 65 years. As contraindications to ribavirin are: anemia, hemolysis, renal failur e, coronary disease, cerebrovascular disease. The evaluation of treatment of hep atitis C is made by biochemical response, virological and histological evaluatio n. In biochemical evaluation to monitor the dosages of alanine aminotransferase. A good nutritional status and a balanced diet are also important because they a im to stimulate the immune and liver protection. 2.1.4.Hepatite D Hepatitis D is a disease caused by an incomplete virus that depends on the hepat itis B virus to replicate. The HDV or Delta is the infectious agent called the h epatitis D, is 36-43 nm belongs to the family of Viróides1 containing a nucleo i nside diameter of 19 nm. This consists of circular RNA genome of a single chain and a single structural protein, the hepatitis delta antigen (AgHD), both encaps ulated by HBsAg. The VHD presents itself, organically, as the sole agent and sat ellite subviral human depends exclusively on the help given by the DNA of the he patitis B virus (HBV DNA) and its respective envelope proteins to complete its l ife cycle. It is unique in its kind in human pathology and one can not only mult iply in the presence of hepatitis B. 1 Viroids - small infectious agents composed of small RNA, circular, they do not r eflect any protein. It has the capsid that are not viruses. FIGURE 11 - Schematic and microphotograph of the virion of hepatitis D. SOURCE:

www.hepnet.com Upon entry, the genome and the associated delta antigen is transported to the ce ll nucleus where replication begins. The HDV genome is transcribed and replicate d by DNA polymerase II of the host cell. After the replication of HDV RNA, this requires structural proteins of HBV can lead to a viable viral progeny. The defe ctive nature and the need to have the VHD Equipment enzymatic HBV cause for an i ndividual becomes infected, have to necessarily be infected with HBV. This infec tion can occur simultaneously by two viruses - co-infection, or may appear in an individual previously infected with a virus B superinfection. The main host and reservoir of VHD is the man and the chimpanzee HBV carrier, and the incubation period lasts between 15-45 days and their presence in blood is prolonged and may forever remain in the body, which can lead to forms severe liver disease. Regarding the epidemiology hepatitis D, this has increased in endemic areas wher e we observe a high prevalence of hepatitis B. In Northern Europe and the United States, where the VHD is not endemic, infection is mainly confined to drug addi cts. In areas endemic for HDV, as in the Brazilian Amazon and Venezuela, inappar ent exposure is responsible for many cases of transmission of HDV is by the pare nteral or mucous membranes. In the last decade there was€a change in the epidemi ological pattern, as it noted a decline in the prevalence of acute hepatitis and chronic HDV in the Mediterranean area. South America, especially the sub-tropic al area, it remains an important reservoir for new outbreaks of HDV infection. C onversely, the prevalence of HDV is low in Asian countries with high prevalence of HBV carriers. FIGURE 12 - Worldwide distribution of hepatitis D. SOURCE: www. hepnet.com The diagnostic methods may be direct or indirect. As direct methods exist: • • A ssessment of levels of C-Reactive Protein, Enzyme Immunoassays. As indirect method exists: • Detection of serum antibodies against AgHD The conclusions are only possible to remove with some reliability, having been m ade serological tests, including evaluation of serum levels of C-Reactive Protei n. In case this is a possible co-infection, the diagnosis is made based on the a ppearance of antigens and antibodies in blood during the incubation or already a t the dawn of the disease. The anti-HDV develop later in the acute phase, and us ually subside after infection. In superinfection, HBV is found in the body befor e the acute phase, there are antibodies to HDV IgM and IgG, with the latter pers ist indefinitely. You can also search the blood Delta antigen and RNA of HDV. In case of contact blood treatment after the individual is vaccination with the va ccine against HBV, but also must take an injection of immunoglobulin HB soon as possible after exposure to the disease. And 2.1.5.Hepatite Hepatitis E is an acute infectious liver disease virulent in nature, caused by t he hepatitis E virus (HEV) which causes inflammation and necrosis of the liver. This virus is composed entirely of viral RNA and protein, with a diameter of 2734 nm. The HEV has icosahedral symmetry with 32 depressions and extensions, like spines, is also worth noting that this belongs to the Calicivirus family. Figure 13 - Micrograph of hepatitis E. SOURCE: www.hepnet.com Hepatitis E is considered a public health problem in parts of the world, affecti ng a large population, especially young adults. The virus is transmitted by orof ecal mainly by contaminated water and disease outbreaks have occurred in Asia, A frica and America (particularly in Central America). These areas are known for t heir poor socio-economic conditions, with inadequate health infrastructure and h ygiene. HEVs can present itself in two forms: acute sporadic hepatitis, which ca

n occur in both endemic as in non-endemic and large epidemics affecting thousand s of people in a short space of time, which are often caused by fecal contaminat ion of water drinking. HEV infection is associated with significant morbidity an d mortality, particularly in pregnant women. During the last decade, at least 30 epidemics or outbreaks were reported in 17 countries. Sporadic cases have also been referred to Europe among the individuals recently returned from countries w here infection is endemic. It should be noted that epidemics usually occur associated with rainy seasons or monsoons leading to flooding and consequently t he mixing of rainwater with water for domestic consumption and feces contaminate d with HEV occurring thus spreading the virus. FIGURE 14 - Worldwide distributio n of hepatitis E. SOURCE: www.hepnet.com The human appears to be the natural host and reservoir of HEV, yet there is evid ence to suggest the existence of other animal reservoirs of HEV, including roden ts, pigs, monkeys and chickens, which will give the nature of this infection a z oonosis. The diagnosis of hepatitis E relies primarily on laboratory tests of li ver function biochemical nature, and that these tests include the detection of a nti-HEV. Evaluation of serum C-reactive protein for detection of HEV RNA in seru m and stool tests are more sensitive and specific, yet are still under investiga tion. With regard to medical treatment, hepatitis E has no specific treatment. General ly, therapeutic measures aimed at reducing the intensity of symptoms, however, t he initial period of illness is indicated relative rest and the return to activi ties should be gradual. Alcoholic beverages should be abolished and the food sho uld be eaten according to appetite and acceptance of the patient, with no need f or special diets. 2.2.€Chronic viral hepatitis Hepatitis is a chronic condition characterized by n ecro-inflammatory liver lesions that remain for a period exceeding six months ma y, however, have other causes such as alcoholic liver disease, autoimmune hepati tis, primary biliary cirrhosis, cholangitis primary sclerosing, primary biliary cirrhosis, Wilson disease, primary hemochromatosis, deficit of α - 1 - ntitryps in, induced hep titis nd hep titis non- lcoholic. Although much less common th n cute hep titis, chronic hep titis m y persist for ye rs or even dec des. Typi c lly, milder forms re not progressive or progressing only slowly so some symp tom tic, le ding to cirrhosis nd liver f ilure. Usu lly the virus of hep titis A nd E do not c use chronic hep titis. For the hep titis C virus th t is comm on c use of chronic hep titis, where s bout 75% of c ses of hep titis C chronic course. The hep titis B virus, sometimes with the hep titis D c uses sm ller percent ge of chronic infections. In m ny individu ls with chronic hep titis, no obvious c use c n be detected, so this in the first inst nce it m y be symptom tic. Approxim tely one third of c ses of chronic hep titis occurs fter n epis ode of cute vir l hep titis. The rem inder develops gr du lly, with no prior di se se course. Symptoms of chronic hep titis, the most common include: • Feeling of gener l discomfort; • • • • • • • • Appetite, f tigue, low fever, discomfort in the upper bdomen, j undice, chronic liver dise ses; Splenomeg ly (enl rgement of the spleen), net retention. The di gnosis of chronic vir l hep titis b sed on the combin tion of five elemen ts: 1. Clinici n, who here h s minor or lmost null bec use p tients re usu lly present without symptoms. 2. Biochemist. If the ALT (SGPT, ALT) re elev ted fo r period exceeding six months then the p tient h s clinic l picture of chron ic hep titis. 3. Serologic l s the etiologic gent involved, there must be po sitive for vir l m rkers, 4. Virologic l determin tion of nucleic cids of the r espective virus s this llows us to ev lu te the vir l replic tion 5. Liver bio

 

 

 

 

 

 

 

   

 

 

     

 

 

   

 

 

   

 

 

 

 

 

   

 

   

   

 

 

   

 

   

 

 

 

 

 

   

 

   

 

     

   

 

 

 

 

 

     

   

   

 

 

 

   

 

 

 

 

 

 

 

 

 

 

 

       

 

 

 

 

 

 

 

       

 

 

 

psy - its ccomplishment is lw ys indic ted in p tients whose incre se in ALTS is more th n six months. Besides being ble to ssess necrosis, infl mm tory inf iltr tion, fibrosis, presence or bsence of cirrhosis, m y be c rried out more s tudies. However only the serologic l ev lu tion, complemented by the study virol ogic l nd in some c ses for biopsy, will m ke specific di gnosis s ccur te s possible. To tre t chronic hep titis usu lly resorts to ntivir l ther py wit h interferon, which is t present the most effective drug. 3. NURSING CARE Nursing c re to h ve with vir l hep titis re directly linked with the symptoms, tr nsmission routes, nursing interventions nd prevention. Thus on the symptoms nd it is lmost lw ys the s me in ll vir l hep titis. Thus the most common s ymptoms include: • • • • • • • • • • • • • • • • • • • • M l ise, f tigue, l ck of ppetite, flu-like symptoms, fever, joint p in, j undice the skin nd eyes, d rk urine, p le stools; Chills; Dyspepsi ; lymph denop thy, bdomin l p in from the right fl nk, n use , vomiting, di rrhe , menstru l cycle ch nges, he d che, itching, cholest sis; • • • • • • Prostr tion; In ppetence; Astheni , intoler nce to ler nce by tob cco smoking; Hemop tomeg li ; lcohol nd f tty foods, into

The ctivities of nursing in the c se of hep titis focus m inly on gener l suppo rtive c re to promote rest, fluid nd electrolyte b l nce, injury prevention, pr evention of spre d of the dise se, knowledge nd dequ te nutrition, comfort, pr evention of ch nge in skin integrity nd preventing soci l isol tion. • • Promot e rest periods th t llow the p tient to rel x nd doze; Incre sed exercise tole r nce; the Te ch the p tient to slowly nd gr du lly incre se your toler nce to the ctivity; o Provide proper diet to incre sed ctivity, the limiting ctivi ty whether physic l ctivity fter the resumption of the liver enzyme levels inc re se, • M inten nce of fluid int ke nd nutrition l st tus; o Provide dequ te fluid int ke t le st 3000 ml / d y of fluids, the fluids m y be dministered or lly if n use nd vomiting re not serious, otherwise, people re given intr ve nously, the d ily ssess the w ter b l nce nd weight to determine if the p tien t ingests the proper mount, to encour ge the p tient to drink fluids such s ju ices fruit nd soft drinks, which provide in terms of both qu ntity nd nutrient s; o Provide well b l nced diet in terms of nutrients nd c lories, nd these must be b sed on body surf ce nd ge of the p tient, the Pl n with the p tient e ch diet it is ple s nt; Encour ge the p tient to m ke sm ll, frequent me ls, b ec use they gener lly re better toler ted th n l rger me ls; Restrict the f ts; Promote the proper or l hygiene c n be n id to stimul te th e ppetite, the Administer nti-emetics bout h lf n hour before me ls, the Avo id lcoholic bever ges bec use they re met bolized in the liver; • Prevention s pre d of infection, the proper h nd w shing by p tients nd by he lth profession ls to use gloves when h ndling feces / urine, blood nd other bodily fluids Usi

 

Tr nsmission of hep titis: Hep titis A nd E c n be tr nsmitted from person to p erson or by fec l-or l route, s the gent of infection is found in feces. The m ost common forms of tr nsmission nd most frequently reported re: • • Cont min tion from the ingestion of cont min ted w ter nd food; tr nsmission by tr nsfus ion of blood components obt ined from donors in the incub tion period. The tr ns mission of hep titis B, C nd D is prim rily p renter lly, nd c n lso be found in blood, semen nd s liv . Cont ct with the virus c n est blish itself in seve r l w ys: • • • • • • • • Blood tr nsfusion; Addiction; Sting ccident l t ttoos , cupuncture, dent l tre tments; Vi sexu l Vi perin t l - Mother nd child du ring pregn ncy through p ss ge through the birth c n l or through bre stfeeding; Nursing interventions:

 

 

 

 

 

   

   

     

 

 

 

 

 

 

 

 

     

 

 

 

 

           

 

 

   

 

 

 

 

       

 

 

 

   

   

   

   

 

 

 

   

 

 

 

 

 

 

 

       

   

 

 

 

       

   

 

 

 

   

 

   

 

           

 

 

   

 

 

         

 

 

 

 

 

 

 

   

 

                                       

   

     

 

 

 

 

 

 

 

 

 

 

 

         

               

 

 

     

 

   

 

 

 

 

 

   

     

     

   

 

 

 

 

   

 

 

 

 

       

   

 

         

   

                       

 

 

 

 

 

 

 

 

 

 

 

 

 

 

   

 

 

     

 

 

             

 

 

 

 

     

 

 

 

 

 

 

 

 

       

B ths rel x tion; B ck M ss ge; fresh sheets on the bed, quiet, d rk environment , o Provide the p tient during the icteric st ge of the dise se, comfort me sures designed to relieve the itching: Use fresh clothes, light, nd not void we ri ng tight clothing or wool bl nkets; Use of bed linen soft, dry nd cle n; Perform immersion b ths with w rm w ter but not hot; Applying skin cre ms n d lotions, emollients; Use so p superf tted; Avoid ctivities th t stimul te the swe t nd incre se body temper ture; M int in cool environment, dminis ter nti- ntihist mines ccording to the prescription; Diversify ctivities suc h s re ding, television nd r dio to reduce the perception of the p tient in pr uritus; • Cut the fingern ils of the p tient to void the itching nd skin les ions; M inten nce Support He lth; o Provide n open nd honest environment where nurses nd p tients c n communic te without hesit tions nd prejudices; The nur se should discuss the risk of contr cting vir l hep titis through multiple sexu l p rtners, sh ring of intr venous drug m teri l, mong other • Improving the So ci l Inter ction;

The nurse must expl in to the p tient nd the f mily of the import nce nd need for isol tion but emph sizes th t this does not prohibit soci l inter ction nd visits, • Injury Prevention; ev lu te the signs of bleeding: Survey of blood in the urine nd feces; Assessing the existence of recurrent bleeding due to n y incision;€ Se rch for the presence of petechi e on the skin; Bec use of petechi e, ssess vit l signs, including hypotension, ev lu te the prothrombin time, hem tocrit nd hemoglobin, the T ke the following prec utions to void ble eding: Pl n so th t the blood s mples throughout the s mple is t ken t once t o void multiple punctures; Avoid intr muscul r injections nd subcut neous; Lobby, t the sites of venous puncture for 5 minutes fter the procedure; Use toothbrushes gentle to void tr um of the gums nd c use bleeding; Avoid the use of dent l floss; Use the m chine electric r zor inste d of bl des; dmi nister vit min K if the prothrombin time is incre sed. Prevention / prophyl xis: for the prevention nd prophyl xis th t includes m inly the he lth educ tion of the p tient's f mily but lso the community, nd one of nurse's prim ry objectives should be the correction nd er dic tion of infectiou s foci. So with reg rd to prophyl xis nd prevention should be t ken the followi ng me sures: • Notific tion of outbre ks - to notify uthorities immedi tely of epidemiologic l surveill nce municip l, region l or centr l, th t it would promp t the investig tion of the common sources nd tr nsmission control through preve ntive me sures m inly educ tion l me sures. • Educ tion of the popul tion lw ys w sh h nds thoroughly with so p nd w ter before touching food or before e ting nd fter using the b throom or ch nging di pers, protects g inst hep titis n d other dise ses • Me sures of s nit tion System of tre ted w ter nd sewer re essenti l to reduce the virus circul tion, prevent the cont min tion of drinking

     

ng the gown, goggles nd / or m sk when it is likely th t blood or fluid sprinkl e org nic, the Cle n d ily nd promote priv te house-to-b th; Isol te the p ti ent if other p tients if possible, the Proper cle ning, introduction into b gs nd l beling of cont min ted items such s sheets nd bedp ns, the Disc rd instru ments cont min ted such s rect l thermometers, the Proper cle ning, introductio n into b gs nd l beling equipment nd bedding cont min ted Correct the destruct ion of ny instruments or needles exposed to blood or body fluids of the p tient , properly l bel the blood s mples to protect of who h ndles the Avoid cont min tion of bre ks in mucous membr nes with blood or body fluids of the p tient, the Expl in to p tients who should void sexu l cont ct until the results of liver function norm lized, the Inform the p tient th t c n never be blood donor; • P romotion of comfort me sures nd promotion of skin integrity; o Provide the p ti ent during the e rly st ge of the dise se, gener l comfort me sures such s:

 

 

           

     

 

   

 

   

 

 

 

 

   

 

 

 

 

   

 

   

 

 

 

       

 

 

 

           

 

 

 

 

 

 

 

 

 

 

 

 

 

       

 

 

 

     

     

 

 

   

 

 

 

 

 

 

 

     

 

 

 

 

             

 

 

 

 

   

 

 

   

 

 

 

 

 

 

 

 

     

 

 

 

 

 

   

 

 

 

 

       

 

 

     

 

       

 

 

 

     

 

       

 

 

 

 

 

 

   

   

   

 

 

   

           

                                   

 

 

 

 

 

 

 

 

       

   

   

   

 

 

 

 

 

 

   

 

       

   

   

   

 

 

   

         

 

 

       

 

   

 

 

   

 

• • • • • • • Avoid excessive use of lcohol, drugs; Avoid swimming in re s with cont min ted w ter nd the use of disinfect nts in swimming pools; Use immunoglobulin when i n cont ct with virus th t does not h ve v ccine, void cont ct with blood or s ecretions of infected persons; disinfect wounds in the body nd cover them with b nd ges nd dressings, s nit ry g rb ge should be properly tre ted nd sep r te d; M king educ tion to p tients to refr in from h ving sex with others while the liver function tests re not norm l. 4. CONCLUSION After this work, entitled Hep titis within the discipline of p thology nd nursi ng c re is possible to conclude th t ll types of hep titis th t re known t pr esent m jor public he lth problems. Considered emerging dise ses, nd ccordin g to Cotter (2003), re dise ses of the liver due to multiple c uses (viruses, b cteri , medic tions, toxic, etc.).. The offending gent c uses infl mm tion nd de th of liver cells, emph sizing th t these m y be second ry to other dise ses . Vir l hep titis c n be cl ssified into cute (A, B, C, D nd E) nd chronic (B , C nd D). The cute vir l hep titis is systemic infection th t predomin ntly ffects the liver. The chronic hep titis is liver infl mm tion th t persists fo r t le st six months. They h ve high prev lence worldwide nd Europe n. As l re dy identified sever l f ctors th t re ssoci ted with more r pid evolution o f these dise ses, yet the buse of lcohol nd vir l co-infections (HIV) h ve gre ter imp ct on their n tur l history. Much h s been evolved by the di gnosis nd tre tment of which is simil r in ll dise ses, prevention nd control, howev er, v ry consider bly. E ch of hep titis is c used by different virus, dependi ng on the c us tive gent of dise se differs s to the mode of tr nsmission nd the immunologic l ch r cteristics, p thologic l nd clinic l. It is lso worth s ying th t the m in role of the nurse is to prevent through educ tion it provide s to p tients, f milies nd communities.€Thus the nurse must inculc te cert in ttitudes in these people, c re nd beh vior so s to minimize the symptoms nd t he inherent risk of hep titis tr nsmission. So the nurse should direct the p tie nt tow rds this: • • • Perform Drinking dequ te rest nd proper nutrients to yo ur situ tion to identify possible clinic l signs nd symptoms of bleeding • • M int ining n dequ te insul tion without le ve to soci lize, while t king into ccount cert in risk beh viors to detect nd report ch nges indic tive of worse ning of their situ tion (eg incre sed f tigue, n use nd vomiting uncontroll bl y. St rt of bleeding, worsening of discomfort the right hypochondrium nd w ter retention) • Underst nd th t it m y t ke sever l months or more for their medic l condition i s restored nd this should be ev lu ted frequently to check the v lues of blood tests nd others th t llow ssessment of its evolution

 

w ter • Guid nce d yc re nd preschool institutions nd schools closed for the est blishment of strict me sures of hygiene, to minimize tr nsmission fec l-or l route. • • V ccin tion g inst hep titis A nd B The he lth profession ls shoul d we r gloves, goggles nd m sk whenever there is possibility of cont ct (or s pl sh) of blood or secretions cont min ted with hep titis B or C or with mucous skin lesions. • • • • • Use of tre ted w ter or boiled W sh veget bles, fruits nd veget bles; not sh re syringes nd needles, toothbrushes, r zors, scissors or other objects for person l use, use of condoms during sexu l intercourse; Monit oring pre- Christm s for ppropri te counseling nd prevention of tr nsmission;

 

     

   

 

 

 

 

 

     

 

 

 

 

 

 

 

 

         

 

 

 

 

             

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

   

 

   

   

     

   

 

   

   

 

 

   

   

         

 

 

 

 

         

 

 

 

 

 

 

   

 

   

 

   

 

   

 

 

 

 

     

 

   

   

 

 

 

   

     

     

 

 

 

 

 

 

   

 

 

 

 

 

 

 

 

                                                                                       

 

 

     

 

 

 

 

   

       

 

 

 

 

 

 

   

 

 

 

 

 

 

 

 

 

 

 

 

   

 

 

 

   

     

               

 

   

     

• And their f milies re t ught bout proper pre nd post exposure prophyl xis, n d this educ tion should include methods to prevent tr nsmission of infection. It is concluded th t despite the dec des of evolution th t h s been h ppening in t his re , nd the iscovered. • dv nces m de t ll levels, the notion th t m n h s still to be d

5. REFERENCES • • • • • Cotter, Joseph - vir l hep titis, G stroenterology Cente r Of District Hospit ls, June, 2003. FONSECA, John - hep titis: recent dv nces g inst complex virus. "Super Interess nte" No. 23. M rch (2000) p.76-81. JULE S, L. [Et l] - Acute Vir l Hep titis. In HARRISON - Intern l Medicine. Rio de J neiro: Gu n b r Koog n, 1992, ch. 295, 12th ed. 2 vol. ISBN 85-86804-26-6 JULE S, L. [Et l] - Chronic Hep titis. In HARRISON - Intern l Medicine. Rio de J nei ro: Gu n b r Koog n, 1992, ch. 297. 12th ed. 2 vol. ISBN 85-86804-26-6 THOMAS, deber - Intervention in People with Problems of the Hep tic System. In PHIPPS, Wilm - Medic l-Surgic l Nursing. Lisbon: Editor Lusodid ct , 2003. Sec. 37. 6t h ed. Vol III. ISBN: 972-8383-65-7 • • • • REBELO, L. - Viruses on the loose in Portug l. "Gr nde Report gem" No. 112. July (2000) 52-64. SAGNELLI E.; STROFFOLI NI. T. - Decre se in HBV endemic in It ly. "Journ l of Hep tology. It ly (1997) Seeley, Red R., [et l] - An tomy nd Physiology. Lisbon: Editor Lusodid ct , 1 997. ISBN: 972-96610-5-7 VELA, M. [Et l] - Virus de l s hep titis. "Gener l Med ic l Microbiology." 557 578 WebGr f: • • • • • www.msd-br zil.com; www.hepnet.co m; www.museum-grenoble.fr; www.fiocruz.com; www.virtu l.epm; • www.hepcentro.com.br;