ACUTE PARENCHYMAL LIVER

DISEASE
VIRAL HEPATITIS
 CAUSE
• 5 ESTABLISHED HUMAN HEPATITIS VIRUSES.
• A ,B ,C, D, E,
• EXISTENCE OF G , & T T VIRUSES FOUND
• VIRAL HEPATITIS IS COMON CAUSE OF
JAUNDICE
• THESE VIRUSES CAUSE ILLNESSES WITH
SIMILAR CLINICAL & PATHOLOGICAL
FEATURES.
 HEPATITIS A
• ACUTE SELFLIMITED NECROINFLAMATORY
DISEASE
• INFECTION OF HEPATOCYTES BY H A V
• SMALL POSITIVE STRAND R N A VIRUS.
• RELATED TO PICONAVIRDIE.
• LIVER INJURYDUE TO IMMUNE CELLULAR
RESPONSE TO VIRAL ANTIGENS EXPRESSED IN
HEPATOCYTES.
 CLINICAL FEATURES
• ROUTE OF INFECTION --- FECAL ORAL
• OCCURS SPORADICALLY OR IN EPIDEMIC
FORMS.
• OVERCROWDING ,POOR HYGEINE ,&
SANITATION
• 5---14 AGEGROUP MOST COMMON
• ADULTS INFECTED OFTEN BY SPREAD FROM
CHILDREN.
 CLINICAL FEATURES CONTD.
• INFECTION IN YOUNG CHILDREN
ASYMPTOMATIC OR UNRECOGNISED.
• INFECTION IN ADULTS SYMPTOMATIC
• ASSOCIATED WITH ACUTE ICTERIC HEPATITIS.
• SEVERE DISEASE MORE COMMON AFTER 40
• ONLY A SINGLE SEROTYPE OF H A V
• NO ANTIGENIC DIFFERENCE IN STRAINS.
 CLINICAL FEATURES CONTD
• INCUBATION PERIOD----15 TO 30 DAYS
• INFECTIVITY OF HOST 14 TO 21 DAYS BEFORE
ONSET OF JAUNDICE &7—8 DAYS AFTER.
• SERUM &SALIVA MUCH LESS INFECTIOUS
• URINE &SEMEN NOT INFECTIOUS.
• EXPLOSIVE WATER & FOOD BORNE EPIDEMICS
DESCRIBED.
 PRODROMAL SYMPTOMS
• FATIGUE ,WEAKNESS ,ANOREXIA,NAUSEA,
VOMITING,ABDOMINAL PAIN.
• LESS COMMONLY FEVER ,HEADACHE,
ARTHRALGIA,MYALGIA,DIARRHOEA.
• IN 90% CASES JAUNDICE &DARK COLOURED
URINE AFTER 1---2 WEEKS OF PRODROMAL
SYMPTOMS
• ANICTERIC CASES 3.5 TIMES>THAN ICTERIC
MAINLY IN CHILDREN
 CLINICAL FEATURES CONTD
WITH APPEARANCE OF JAUNDICE –PRURITIS &
EXTRAHEPATIC MANIFESTATIONS SEEN.
-MILD ENLARGED TENDER LIVER—85 %
-SPLENOMEGALY---- 15%.
-POSTERIOR CERVICAL LYMPHADENOPATHY-15%
SEVERITY AGE DEPENDENT >50 YRS MOST
SERIOUS.
IN PREGNANCY NO ^RISK (FETAL OR MATERNAL)
 CLINICAL COURSE
• USUAL COURSE ---
DURATION OF JAUNDICE < 2WKS IN MAJORITY
• COMPLETE CLINICAL & BIOCHEMICAL
RECOVERY IN 2 MONTHS IN 60%. CASES.
• IN SIX MONTHS IN 100% CASES.
• TWO ATYPICAL COURSES OF ACUTE
INFECTION.
• A)PROLONGED CHOLESTATIC &b) RELAPSING.
 ATYPICAL COURSES
• A)PROLONGED CHOLESTATIC
• DURATION OF JAUNDICE > 12 WKS.
• PRURITIS FATIGUE,LOOSE STOOLS,WT LOSS,
• ALT <500 IU/L DURING CHOLESTASIS.
• SPONTANEOUS RECOVERY.
• B)RELAPSING OR POLYPHASIC 6—12% CASES.
• INITIAL PHASE FOLLOWED BY REMISSION.4 TO15
WEEKS.WITH RELAPSE thereafter.
• ALT NORMAL IN REMISSION &>1000IU/L RELAPSE
 PROGNOSIS
• OVERALL PROGNOSIS---EXCELLENT
• CHRONIC HEPATITIS DOES NOT OCCUR.
• DIAGNOSIS
• ANTI H A V IgM PEAKS DURING ACUTE PHASE
& DURING CONVALESCENCE.PERSISTS
THROUGHOUT COURSE OF DISEASE.
• DECLINE TO UNDETECTABLE LEVEL 3-4 MTHS
• IN 25% CASES PERSISTS FOR 6 MONTHS.
 DIAGNOSIS CONTINUED
• H A V IgG APPEARS IN EARLY CONVALSCENCE.
• REMAINS DETECTABLE FOR
DECADES.INDICATES PREVIOUS EXPOSURE
&IMMUNITY.
• RISING TITRES OF IgM INDICATE RECENT
EXPOSURE.
• BOTH ELISA & R I A METHODS ARE SENSITIVE.
• VIRAL R N A IN SERUM & BODY FLUIDS BY PCR.
 EXTRAHEPATIC MANIFESTATIONS
• EVANESCENT RASH 14 %
• ARTHRALGIA 11%
• LESS COMMONLY—LEUCOCYTOPLASTIC
VASCULITIS
.GLOMERULONEPHRITIS,ARTHRITIS
• IMMUNE COMPLEX DISEASE PLAY
AETIOLOGICAL ROLE.
 COMPLICATIONS

• POST HEPATITIC SYNDROME-PROLONGED

MALAISE,^ LIVER ENZYMES,PERSISTENCE OF
IgM ANTIBODIES.
• TYPE 1 AUTOIMMUNE HEPATITIS.
• FULMINANT LIVER FAILURE IS RARE.
• PREVENTION
• PREVENTIVE BETTER HYGEINE SANITATION.
• (CONTD)
 PASSIVE IMMUNIZATION
• THOSE AT RISK,TRAVELLERS,HOUSEHOLDCTS.
• I S I S(IMMUNE SERUM IMMUNOGLOBULIN
• BEFORE EXPOSURE 85 -95% PROTECTION.
• 1—2 WKS OF EXPOSURE-PREVENT
/ATTENUATE INFECTION.
• BEYOND 2 WEEKS-NO EFFECT.
• DOSE 0.02ml/Kg 2 MONTHS PROTECTION.
• 0.05ml/Kg—4—6 MONTHS PROTECTION.
 ACTIVE IMMUNIZATION
• INACTIVATED VIRUS VACCINE
• ADULT DOSE 1 ml SINGLE DOSE
• BOOSTER 6—12 MONTHS LATER

• TREATMENT
• ONLY SUPPORTIVE MEASURES.
• WITH SEVERE CHOLESTASIS SHORT COURSE
PREDNISOLONE 30 mg/DAY TAPERING.
ACUTE PARENCHYMAL LIVER
DISEASE
HEPATITIS B
 HEPATITIS B VIRUS
• DOUBLE STRANDED D N A VIRUS
• HEPATITIS B VIRON
• CONSIST OF 1) SURFACE 2) CORE
• CORE—C gene 1)HBeAg –pre C region –soluble
secreted protein 2) HBcAg-after precore region- not
secreted remains in hepatocytes exported after
encapsidation by HBSAg envelope. Contain HBV DNA.
P GENE codes for DNA POLYMERASE. X GENE –HBxAg
transactivation transcription of cellular & viral genes.
• SURFACE S gene codes for surface protein-HBsAg
• Excess OF HBsAg ,SPHRES & TUBULES ARE FREE IN
SERUM.
 VIRON

• cytoplasm
• HBSAg--------- surface HBSAg
• HBSAg-
• -.core
• Pgene
• CORE ---- DNA DNA Polymerase
• C gene - HBcAg ,HBeAg , X gene-HBxAg
 Clinical course
ACUTE---a)SUBCLINICAL
b) ICTERIC
C) FULMINANT
CHRONIC__inactive carrier state
__chronic hepatitis
__cirrhosis
___hepatocellular carcinoma
 MODE OF TANSMISSION
• HORIZONTAl
• _injection drug use
• _infected unscreened blood/blood products
• _tattoos/acupunture needles.
• Dental extraction
• Sexual---homosexual & heterosexual.
• VERTICAL-----HBsAg POSITIVE MOTHER
 CLINICAL MANIFESTATIONS
• INCUBATION PERIOD 1 TO 4 MONTHS
• PRODROMAL PHASE ABRUPT/INSIDIOUS
• MALAISE,ARTHRALGIA,EASY FATIGUABILITY
• UPPER RESPIRATORY SYMPTOMS,ANOREXIA
• DISTASTE FOR SMOKING,NAUSEA,VOMJTTING
• DIARRHOEA/CONTIPATION
• SOMETIMES SERUM SICKNESS---fever,skin rash
• Polyarthralgia&arthritis,polyartritis nodosa
• glomerulonephritis
 Clinical manifestations contd
• Prodromal contd
• Fever low grade,
• Mild constant right upper quadrant/epigastric
pain,
• ICTERIC PHASE after 5—10 days
• Worsening of symptoms,fall in pulse rate with
appearance of jaundice,
• Progressive improvement follows.
 Clinical manifestations contd
• Convalscent phase
• In 2—3 wks acute illness subsides
• Sense of well being,return of
appetite,disappearance of jaundice,etc
• Complete clinical &biochemical recovery may
take 16 weeks
• Signs hepatomegaly 50%,splenomegaly 15%
• Aplastic anaemia rare
 Clinical course
• Fulminant course in first 4 wks
• Another hepatitis superimposed on
SYMPTOMLESS hepatitis carrier may
precipitate fulminant course , encephalopathy
/coma.
• SUBACUTE HEPATIC NECROSIS increasing
severe disease evolving over 1 to 3 months
• CHRONIC HEPATITIS DEVELOP INSIDIOUSLY
 INVESTIGATIONS
• LAB, FEATURES- AST, ALT ^Prodromal phase
precede rise in Bilirubin,^s Bilirubin ^P. T
• INTERPRETATION HBsAg IgM IgG Ige Anti-
HBs
• Incubation period + + - - -
• Acute hepatitis
• Early + + - - -
• Established + + + + -
• convalescence+ - +- + - +-
• 6 months 1 yr - - + - +
 prevention
• Behavior modification
• Passive immunoprophylaxis
• Active immunization
• Passive immunization************
• Neonates born to HBsAg +ve mothers
• After needle stick exposure
• After sexual intercourse
• After liver transplant of pts who were HBsAg +ve
before implant.
 prevention
• Passive 0.13ml/kg anti HBIG immediately after delivery
or within1 2 hrs of birth with recombinant vaccine
• Sexual/ needle prick-ANTI HBIG 0.5—0.7 ml/kg as soon
as possible –no more than 7 days after.
• ACTIVE IMMUNIZATION
• PREVENTION OF PRIMARY INFECTION
• High risk group,health care workers,parenteral drug
users,infants of infected mothers
• Recombitant vaccine
• engerixB10mico gm recombivax 20 micogm in adults
 TREATMENT
• FOR ACUTE INFECTION SUPPORTIVE
• Antiviral therapy not indicated
• Chronic
• Lamuvidine interferon alfa