home
about the project
Medical news
For authors
Licensed books on medicine
<< Previous Next >>

viral hepatitis B (clinic, diagnosis, treatment)

Etiology: hepatitis B virus (HBV, HBV) - DNA-based hepatadavirus. The viral envelope protein is represented by the surface antigen (HBsAg) - the “Australian” AG, the nucleocapsid contains the core antigen (HBcAg), infectious (HBeAg), HBxAg, DNA and enzymes (polymerase and protein kinase). Each of the HBV antigens causes a humoral immune response, manifested by the production of the corresponding antibodies (anti-HBs, anti-HBc, anti-HBe).

Epidemiology: source - patients with both manifest and asymptomatic forms of acute and chronic hepatitis B. The mechanism of infection: parenteral; transmission methods: natural (from mother to child - vertical and perinatal; through sexual contact with an infected person - sexual; during other contacts with an infected person - horizontal) and artificial (in violation of the integrity of the skin and mucous membranes).

Pathogenesis: the virus does not have a direct damaging effect on hepatocytes, their cytolysis is carried out immuno-indirectly due to a reaction from cellular immunity through cytotoxic T-lymphocytes.

Clinic:

a) the incubation period from 42 to 180 days, an average of 60-120 days.

b) the initial (preicteric) period - 7-14 days; the disease begins with signs of a mixed variant of the preicteric period without a significant increase in body temperature. Symptoms of intoxication and dyspeptic manifestations are moderate, in a third of patients an arthralgic variant of the initial period (increased pain in large joints at night and in the morning). The initial period of the disease lasts 7-14 days or more, however, with infections associated with blood transfusion, it can be shorter.

c) the icteric period - 3-4 weeks, more pronounced and prolonged pain, sometimes sharp pains in the right hypochondrium. Weakness persists, loss of appetite comes to anorexia. Nausea and even vomiting are frequent. Often itchy skin. The liver is always enlarged, on palpation it is smooth, with a slightly densified texture, an increase in the spleen is noted. Gallbladder symptoms may be positive. In peripheral blood, leukopenia with lympho- and monocytosis, sometimes with a plasma reaction. ESR is reduced to 2-4 mm / h, in the convalescence period it can accelerate to 18-24 mm / h with subsequent normalization in the absence of complications. Hyperbilirubinemia is more pronounced and persistent than with GA, especially in the 2-3rd week of the icteric period; there is an increase in the activity of aminotransferases in blood serum with a decrease in the sublimate test and prothrombin index. Serological blood tests show HBsAg, anti-HBc IgM.

In severe cases - signs of an increase in liver failure and progression of necrotic processes in the liver - increased general muscle weakness, dizziness, apathy, anorexia, nausea, increased vomiting, the appearance of unmotivated excitement, memory impairment; progressive increase in icteric color of the skin; a decrease in the size of the liver, increased soreness of its edge; the appearance of hemorrhagic syndrome (petechial rash on the skin, nosebleeds, hemorrhage at the injection site, “tarry” stool, vomiting with an admixture of blood); the appearance of edematous ascites syndrome (edema on the feet and lower third of the legs, ascites); the occurrence of fever, tachycardia, neutrophilic leukocytosis; an increase in the content of total bilirubin in blood serum with an increase in its indirect fraction; a decrease in cholesterol below 2.6 mmol / L.

d) the period of convalescence — normalization of the activity of aminotransferases by the 30-35th day of the disease with a mild form, with moderate form — by the 40-50th day, with severe form - by the 60-65th day.


Diagnosis: medical history (blood transfusion, surgery, etc.), clinic (gradual onset of the disease, prolonged icteric period, allergic skin rashes, lack of well-being or worsening with the appearance of jaundice, prolonged icteric period with a slow disappearance of the disease’s symptoms in the period of convalescence), serological reactions (early detection of HBsAg, HBeAg, anti-HBc IgM, and HBV DNA in the blood, with a favorable course - rapid disappearance of HBeAg first with the appearance of anti-HBe, HBV DNA, then HBsAg with the appearance Anti-HBs; replaced early anti-HBc IgM appear later anti-HBc IgG).

Long-term circulation (more than 3 months) in the blood of HBeAg, HBV DNA, as well as anti-HBc IgM and HBsAg in a stably high titer indicate a prolonged course of the infection process and a high probability of chronicity. The possible development of chronic hepatitis should also be considered when detecting HBsAg in a stable titer for 6 months. and more from the onset of the disease, even in the absence of markers of active viral replication (HBeAg, anti-HBc IgM, HBV DNA), clinical symptoms, and normal biochemical parameters.

For the diagnosis of chronic HBV - a puncture biopsy.

In this case, only the results of analyzes of puncture biopsy samples of the liver help to establish the correct diagnosis.

Treatment:

1. Therapy - as with HAV (see question 9.1.)

2. Antiviral - alpha-interferon (recombinant: intron A, roferon A, realdiron and native: wellferon, human leukocyte interferon) with a threat of chronicity or a gradient course, synthetic nucleosides - famciclovir (famvir), lamivudine (epivir, azidothymidine, thymoside), protease inhibitors - saquinavir (invirase), indinavir (crixivan), interferon inducers - neovir (cycloferon), amixin, immunomodulators - leukinferon, interleukin-1 (betaleukin), interleukin-2 (roncoleukin). It is indicated for severe hepatitis B (in the presence of markers of active viral replication) with the risk of developing acute liver failure, especially with signs of hepatic encephalopathy, as well as with the threat of chronicity.

3. For complications associated with encephalopathy: stopping the psychomotor agitation of sodium with oxybutyrate, sedux-sen; gastric lavage (via a nasogastric tube) and high or siphon enemas to reduce auto-toxicity; oral administration of poorly absorbed antibiotics (kanamycin 0.5 g 4 times a day), enterosorbents; fractional enteral nutrition in combination with parenteral; GCS (not less than 180-240 mg of prednisolone) parenterally; infusion therapy; with hemorrhagic manifestations - protease and fibrinolysis inhibitors (epsilon-aminocaproic acid, contracal, gordox).
<< Previous Next >>
= Skip to textbook content =

viral hepatitis B (clinic, diagnosis, treatment)

  1. viral hepatitis A (clinic, laboratory diagnostics, treatment)
    Etiology: HAV (picornavirus family). Epidemiology: the source of infection is a patient with all forms of acute infectious process (patients with anicteric and asymptomatic forms are of particular importance). Transmission mechanism: fecal-oral, infection occurs with the use of infected water and food, sometimes by contact and household. The greatest susceptibility to hepatitis A is characteristic of children.
  2. . viral hepatitis C, D, E (clinic, diagnosis, treatment)
    HCV is a disease similar in epidemiological characteristics to hepatitis B, but proceeding more easily and differing in icteric forms with a relatively rapid reverse development of the disease. Anicteric, subclinical, and inapparent forms of HS are more common, which are transferred without inpatient treatment, but in 80-90% of cases they pass into chronic hepatitis and in 20-30% of patients into cirrhosis
  3. LECTURE No. 17. Bronchial obstructive syndrome. Clinic, diagnosis, treatment. Respiratory failure. Clinic, diagnosis, treatment
    Bronchial obstructive syndrome is a clinical symptom complex observed in patients with generalized obstruction of bronchial patency, its leading manifestation is expiratory dyspnea, asthma attacks. Diseases accompanied by airway obstruction. The main causes of airway obstruction in children. 1. Obstruction of the upper respiratory tract: 1) acquired: a)
  4. LECTURE No. 19. Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment, prevention
    LECTURE No. 19. Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment,
  5. Question 14 Viral hepatitis
    - inflammation of the liver tissue caused by viruses. Hepatitis viruses belong to different taxa and differ in biochemical and molecular characteristics, but all these viruses are united by the fact that they cause hepatitis in humans. Chronic liver diseases, including viral hepatitis B and C, are among the ten leading causes of death in the world. Currently, a large number of viruses are known.
  6. clinic, diagnosis, treatment
    A. Ornithosis (psittacosis) is an acute infectious disease from the group of zoonoses with natural foci. It is characterized by fever, general intoxication, lung damage, central nervous system, enlarged liver and spleen. Etiology: Chlamydia psittaci. Epidemiology: reservoir and source of infection - domestic and wild birds. In most cases, infection occurs aerogenic (by inhalation of dust containing
  7. clinic, diagnosis, treatment
    Adenoviral infections are acute viral diseases occurring with a predominant lesion of the respiratory system, eyes and lymph nodes. Etiology: DNA Adenovirus. Epidemiology: the source of infection is patients with clinically expressed or erased forms of the disease, the route of infection is airborne, alimentary is not excluded. Pathogenesis: gates of infection - predominantly
  8. clinic, diagnosis, treatment
    Tick-borne encephalitis (spring-summer, taiga, Russian, Far Eastern) is a natural focal transmissible (tick-borne) virus infection characterized by a primary lesion of the central nervous system. The disease is characterized by polymorphism of clinical manifestations and severity of the course (from mild erased forms to severe progredient forms). Etiology: tick-borne encephalitis virus. Epidemiology:
  9. clinic, diagnosis, treatment
    Clinic: incubation period from 1 to 6 days. Clinical polymorphism is characteristic. The disease begins acutely without a prodrome. Chills, headache, malaise, weakness, pain in muscles and joints, insomnia, sore throat, loss of appetite appear. Body temperature is low-grade, sometimes up to 38-40 ° С. Along with symptoms of general intoxication, often signs of gastrointestinal damage come to the fore
  10. Clinic, diagnosis and treatment.
    To differentiate each of the purulent forms of the process is practically impossible and inexpedient, since their treatment is fundamentally the same. This is due to the variety of damaging agents and factors, the initial characteristics of the body, with a change in the biological properties of pathogens and the emergence of new methods of exposure (antibiotics, chemotherapeutic drugs, etc.). However, it is always based on
  11. clinic, diagnosis, treatment
    Rabies is a viral disease that occurs with a severe lesion of the National Assembly and usually ends in death. Etiology: rabies virus Neuroryctes rabid Epidemiology: source of infection - infected animals (foxes, wolves, dogs, cats, bats, rodents, horses, small and cattle), the route of infection is contact, occurs when the animal bites or saliva
Medical portal "MedguideBook" © 2014-2019
info@medicine-guidebook.com