chronic active virus hepatitis Flashcards
etiology
Viral Hepatitis B commonly associated with Viral Hep D.
pathogenesis
Aggressive hepatitis
- ↓ metabolic activity, ↓ synthetic function, ↓detoxification functn
- Acute attack of virus → stay long time in organism (in DNA) → virus disturb funct of m‘brane → cell dystrophy (direct degradation & necrotic changes) → virus activated by DNA polymerase → replication of virus → affected cells secreting special Ag (liver specific lipoproteins) → organism produce Ab → delayed hypersensitivity → macrophages infiltrate into lobule → produce enz → cell affectd
- Later if hyperactivity of lymphocytes → affection of whole liver
- Cell damage is due to infiltration & autoAb causes necrotic changes → free spaces occupied by collagenic tissues → liver fibrosis → Imbalance btw parenchyma & fibrotic tissues → sclerosis
clinical picture
- Dull pain, arthralgia, LOW, xanthomas, vasculitis, hyperpigmttn
- hepatomegaly, splenomegaly, Hypersplenism, red nose, club fingers (AV shunt)
- small liver syndrome, hemangioma (small red spots)
- Red lips, jaundice, spider nevi, palmar erythema, gynecomastia, raspberry tongue.
- Cytolysis, immunoinflmtory, Cholestasis, Hepatodepression, Hemorrhagic syndromes
- Mesenchymal inflammation – arthralgia, myalgia, enlarged lymph nodes, vasculitis, fever, dysproteinemia, ↓ albumins
- nausea, anorexia, urine dark and stools pale
symptoms and signs
- 3-5 yrs after acute viral infection
- Hepatomegaly, jaundice
- Pain – boring, aching, intensive, increased after physical exertion
- Ascites, edema
- Fatigue, weakness, bad mood, dyspepsia
- hepatodepression, cytolysis, Hemorrhagic syndrome, mesenchymal inflmtn
- hypersplenism – pancytopenia
- hepatic signs – stars erythema
- progressive period (virus replicatn): nephritis, carditis, ↑AST & ALT, Liver failure, Death
investigation
- Liver biopsy –bridging necrosis, infl infiltrate, fibrosis
- US – hepatomegaly & splenomegaly
- Lab: +ve serological test for respective virus, ↓prothrombin, ↓cholinesterase, ↓cholesterol, ↓fibrinogen, ↑toxins, ↑ALT, AST, conjugated bilirubin
- liver biochemistry – bilirubinuria and increased urinary urobilinogen. Increased AST and ALT
- Haematological tests – leucopenia with lymphocytosis.
- Viral markers: antibodies to HAV
etiological diagnostics
Hep B immunological Dx (viral serological markers Abs to virus B, C, D)
- HBsAg & HBV DNA with HBE Ag found in serum
- HBs Ag – may be seen as ground glass, appearance in cytoplasm on H & E stain
- HBc Ag seen in hepatocytes by immunohistochem staining
- Hepatitis B – HbsAg, IgG anti-HBc, HBeAg, HBV DNA
- Hepatitis C – anti-HCV, HCV RNA
- Hepatitis D – anti-HDV, HDV RNA, HBsAg, IgG anti-HBc
treatment
- Diet No. 5 – no fatty food, spices, alcohol, rest, balanced diet
- Etiological Tx
Antiviral drugs - interferon, acyclotin, virocides, Lamivudine, Adeforvir, Dipivoxil, Interferogens, Exogenous interferons (interferon-α) - Pathogenetic Tx
- Hepatoprotectors – Riboxin, acid glutaminic acid, Vipamic, Legalon, lipoic acid, phospholipids
- Glucocorticoids - Symptomatic Tx
- Diuretics – for ascites
- Liver funct improvemt: vitamins B, C & PP
- prednisolone, contra-cholerectics & cholekines
prognosis
- prognosis is excellent with complete recovery.
- Prognosis is usually poor w liver cirrhosis development in last stages within 10 years after infection.
- complications associated w cirrhosis such as acsites, esophageal varices, encephalopathy
- Prognosis is worse if Hep B + D