1. Submitted By :
Mohammed Fazil.K
Final yr BDS ,Part A

2. Definition :
Hepatitis is an acute parenchymal disease
of liver due to variety of causes in which
variable number of hepatocytes undergo
necrosis.
 Depending on the onset and course of liver cell
injury, hepatitis is classified into
 i)Acute Hepatitis
 ii)Chronic Hepatitis

3.  Viral Hepatitis is a systemic disease with
primary inflammation in the liver.
 There are 6 hepatitis viruses-
 Hepatitis A
 Hepatitis B-caused by DNA virus
 Hepatitis C
 Hepatitis D
 Hepatitis E
 Hepatitis G

4.  Dentists are 3-4 times more likely to be exposed
to Hepatitis than with general population.

5.  Acute parenchymal disease of the liver
evolving within hours, days to few weeks is
called Acute hepatitis.
PATHOLOGY
 Mild liver cells injury –Inflammatory damage
or liver cells necrosis
 More severe damage –Subacute bridging
necrosis
 Very severe damage-Massive necrosis , Acute
liver cells atrophy

6.  infective
 Viral-hepatitis A,B,C,D,E,.EBV.cytomegalo virus
 Post viral-reyes syndrome in children
 Non viral- leptospira,toxoplasma
 Non infective
 Drugs-paracetamol,halothane,rifampicin,isoniazid
 Poisons-aflatoxin,carbontetrachloride
 Metabolic-wilsons disease,pregnancy
 Vascular-CHF,shock,budd chiari syndrome

7.  Depending on the type of causative virus,acute
hepatitis is classified as
 Hepatitis A
 HEPATITIS B
 Hepatitis C
 Hepatitis D
 Hepatitis E

8.  Also called as infectious hepatitis
 It is endemic and occurs in person ,lives in poor
conditions-occur mainly in children and young
adults
 Mode of transmission is by faeco-oral route.can
also spread by blood transfusion and homosexual
activity.
 Incubation period is 30 days.
 Period of infectivity is highest during the week
before the onset of clinical symptoms
 Once it occurs it gives life long immunity.

9.  HAV is 27 nm non enveloped single stranded rna-virus
with an icosahedral symmetry
 HAV Belongs to the picornavirus family
CLINICAL FEATURES
2 stages
Prodromal stage/pre icteric and
Icteric stage
Preicteric occur before the development of
jaundice.

10. o Fever,chills,headache.
o Malaise,pains,
o Git symptoms,anorexia,liver tenderness
nausea,vomiting,disturbed smell,dark
coloured urine,clay coloured stools.
o Lasts for few days to 2 weeks and is called
anicteric phase.
o These usually subside with the onset of
jaundice

11.  With clinical onset of jaundice,fever usually
disappears along with other prodormal
symptoms but weight loss persist
 Liver is enlarged,tender and associated with
right hypochondriac pain .
 Associated features of cholestasis[deep
jaundice,dark coloured urine,clay colored
stools,pruritis]
 Splenomegaly usually does not occur in acute
viral hepatitis but has reported in 5-10%cases.

12.  It occur in all cases and takes 2-8 weeks.the
prodormal symptoms disappear and jaundice
starts regressing but liver enlargment and
biochemical abnormalities persist.full recovery
occurs within 1-2 months.

13.  [1] demonstration of virus
 [2]detection of antibody
 [3]biochemical tests
1)DEMONSRATION OF VIRUS
i)Immunoelectron microscopy[IEM]
Virus can be visualised by IEM in faeces.
ii)enzyme-linked immunosorbent assay(ELISA)
Detected in faeces by ELISA
iii)Isolation
Virus has been grown in human and simian cultures but it
is not possible to grow them routinely from faeces of
patients

14. 2)Detection of antibody
Diagnosis depends on demonstration of specific antibody
to HAV in the blood. ELISA kits for detecting igM &
igG antibodies are available
3)Biochemical tests
Liver function test such as alanine aminotransferase
(ALT) and bilirubin supplement the diagnosis
The rise in serum transaminases[SGOT
andSGPT] starts during prodormal phase and
proceeds with rise in bilirubin,the rise is maximum
during icteric phase(400-4000IU),and they fall
during recovery phase.
Rise in enzymes with prodormal symptoms may
be the only clue to diagnose hepatitis during
anicteric phase,which is otherwise difficult.

15.  Serum albumin levels are normal.
 Prothrombin time may be normal in mild disease but gets
prolonged in severe cases.
 Serum alkaline phosphatase levels are normal except in
cholestatic phase.
 Urine urobilinogen is increased in early phase of disease,it
dissapears if intrahepatic cholestasis develops.
 During cholestatic phase ,bile salts and bile pigments appear
in urine.
 During recovery phase ,urobilinogen reappears and bile
salts and bile pigments dissapear.
 Ultrasound of the liver shows an enlarged liver with normal
echotexture.

16.  As the cases are highly infectious ,hence barrier
nursing care should be enforced with proper disposal
of urine and faeces.
 1)BED REST-enforced in patients with severe hepatitis
till the signs and symptoms dissapear and liver
functions start returning towards normal.Bed rest is
usually adviced to ill patients,pregnant women.
 2)DIET-due to anorexia these persons usually do not
accept solid diet ,hence light diet in the form of fruit
juice,soft drinks and glucose is acceptable,normal diet
of 3000kcal should be advised as apetite returns.
 Good amount of protiens and high carbohydrate intake
should be encouraged.

17. PROPHYLAXIS
General prophylaxis
 Improved sanitary practices.
 Prevention of fecal contamination of food and
water.
 Isolation and proper disposal of faeces and urine
Specific passive prophylaxis
 Immune serum globulins(anti-HAV) have been
employed in close contacts,pregnant women.
 Vaccine for hepatitis A is available

18. HEPATITIS B VIRUS (HBV) (SERUM
HEPATITIS)
Caused by hepadna virus,the virus only
replicates in liver.
Its route of transmission is mostly through
infected blood and blood products,hence also
called as TRANSFUSION HEPATITIS
MORPHOLOGY
 HBV is a complex 42 nm double shelled
Particle.
 The outer surface or envelope of virus
contains hepatitis B surface antigen (HBs Ag).
 It encloses an inner icosahedral 27 nm
nucleocapsid (core), which contains hepatitis B
core antigen (HBc Ag).
 lnside the core is the genome, a circular
double stranded DNA and a DNA polymerase

20.  Blumberg and coworkers (1965):described
a protein antigen in serum of an
Australian aborigine, which gave a positive
Precipitation reaction with sera from two
Haemophiliacs who had received multiple
transfusions. This antigen was named
Australia antigen. It was subsequently
established to be the surface component of
hepatitis B virus (HBsAg).

21.  ELECTRON MICROSCOPY of sera of hepatitis B
patients shows three types of particles.
The most abundant form is a spherical particle (22nm in
diameter
second type is tubular (22 nm in diameter)particle of
varying length.
These two types are antigenically identical and are the
surface subunits of hepatitis B virus (HBsAg).
The third type is a double shelled spherical structure (42
nm in diameter).
 This particle is the complete hepatitis B virus or
Dane particle.

22. ANTIGENIC STRUCTURE
1.HBsAg- Surface antigens (envelope protein)
2. HBcAg- It is the core (nucleocapsid) antigen of the
virus. It is not detectable in patients blood.
3. HBeAg- It is the hidden antigenic component of
core.

23. VIRAL GENES AND ANTIGENS
 The viral genome consists of two linear
strands of DNA held in a circular
configuration.Associated with one strand of
DNA is a viral DNA polymerase .
 This polymerase can repair the gap in the
incomplete (the plus strand) strand and
render the genome fully double stranded
MODES OF TRANSMISSION
There are three important modes of
transmission of HBV infection:
1. Parenteral
2. Perinatal
3. Sexual

24. 1) Parenteral Transmission
 Transmission of infection may result from
accidental inoculation of minute amounts of
blood, blood products or fluid containing HBV
during medical, surgical or dental Procedures.
2) Perinatal transmission -occurs when carrier
mother's blood contaminates the mucous
membranes of the newborn during birth.
That is occurs primarily in infants born to HbsAg
carrier mothers or mothers suffering from acute
infection.

25. 3) sexual Transmission
 HBV is present in body fluids such as semen and
vaginal secretions, hence it can be transmitted by sexual
contact.
CLINICAL FEATURES
 Onset is slow, usually insidious but more severe.
 from 6weeks to 6 months.
 The course of acute HBV infection can be divided into
three phases:
 Preicteric phase
 Icteric phase
 Convalescent phase

26. 1) Preicteric Phase
 Patient develops malaise, anorexia,
weakness,myalgia, nausea and vomiting.
2) lcteric Phase
 Patient develops jaundice, pale stools and dark
urine (bilirubinuria).
3) Convalescent Phase
 This phase is long and drawn out with malaise
and fatigue,

27. Hepatitis B Carriers
There are two types of hepatitis B carriers
 1.super carriers
 2.simple carriers
1.Super carriers: They have HBe Ag in blood and
are highly infectious. Very minute amount of serum
or blood can transmit the infection. These are called
super carriers.
2. Simple carriers: They are more common type of
carriers who have no HBeAg and a low level of HBs
Ag in blood. They transmit the infection only
when large volumes of blood or serum are
transferred, as in blood transfusion. These are
named simple carriers.

28. L.D--------1)DETECTION OF VIRAL MARKERS
(i) HBsAg
 HBsAg is recognised as a specific marker for HBV infection.
 It is the first marker to appear in blood after infection.
 HBsAg disappears with recovery from clinical disease in
most patients, however it persists for years in carriers.
 Antibody to HBsAg appears within weeks after the
disappearance of HBsAg and persists for very long periods.
 Anti-HBs is the protective antibody

30. (ii) HBeAg
 Sera containing HBeAg are believed to be highly
infectious and those with anti-HBe of little
infectivity
 The presence of HBeAg is thought to be an
adverse prognostic sign.
 The disappearance of HBeAg is followed by
appearance of anti-HBe.

31. (iii) HBcAg
 It is not detectable in the serum but can be
demonstrated in liver cells by
immunofluorescence.
 Anti-HBc antibody usually appears in serum a
week or two after the appearance of HBsAg.
 It remains lifelong and thus serves as a useful
indicator of prior infection with HBV, even
after all the othermarkers become
undetectable.

33. 2) Viral DNA Polymerase
It appears transiently in serum during pre-icteric phase.
3) Polymerase Chain Reaction (PCR)
HBV DNA level can be detected in serum by PCR. It is a
highly sensitive test.

34. Prophylaxis
1. General Preventive Measures
 health education,improvement of personal hygiene and
strictattention to sterility.
 An important preventive measure is the screening for HBsAg
and HBeAg in blood donors.
 Use of unsterile needles,syringes and other material must be
avoided to prevent hepatitis B infection.

35. 2. Immunization
i)Passive immunisation
Passive immunisation may be employed
following any accidental exposure to
hepatitis B infection.
 Hepatitis B immunoglobulin(HBIG) is
prepared from donors with high titres
of anti-HBs.
It can be given in doses of 300-500 IU
intramuscularly
It may not prevent infection but protects
against illness and the development of
carrier state.

36. (ii) Active immunisation
 Following vaccines are available.
(a) Plasma derived vaccine:
 Vaccine is prepared by purifying 22 nm
particle of HBs Ag from the plasma of
healthy carriers.
 The particles are inactivated with
formaldehyde.
 The vaccine is immunogenic and safe.

37. (b) Recombinant yeast hepatitis B vaccine:
 It is produced by a recombinant DNA in
yeasts in which a plasmid containing the
gene of HBs Ag has been incorporated.
 HBsAg particles produced are extracted and
purified for use as vaccine.
 The vaccine is as immunogenic as plasma-derived
vaccine.
 It is safe and free from side effects.

38.  Both vaccines are adsorbed with aluminum
hydroxide as adjuvant, stored in cold but not
frozen.
 Three doses at O, 1 and 6 months are
administered intramuscularly into deltoid muscle.

39. HEPATITIS C VIRUS (HCV)
 It is a 50-60 nm virus with a linear single
stranded RNA.
Modes of infection
 It is transmitted by needle stick injuries,
use of contaminated needles and
syringes,transfusion of infected blood and
blood products, and sexual intercourse.
 Maternal-neonatal transmission has also
been reported.

40. Clinical Features
 Clinical infection with hepatitis C is
generally less
severe, with milder symptoms, absent or less
marked
jaundice.

41. Laboratory Diagnosis
It can be established by
 detection of anti-HCV (antibody) by
ELISA.
 Viral genome(HCV RNA) can be
detected by polymerase chain
reaction (PCR) and by
immunofluorescence

42. Prophylaxis
 general prophylaxis
 blood or blood products screening is
possible.

43. HEPATITIS D VIRUS (HDV)(DELTA
ANTIGIEN) .
 The HDV is a defective virus as it is
dependent on the helper function of HBV for
its replication and expression.
 It belongs to genus Delta virus
 It is spherical, 36-38 nm diameter RNA
particle surrounded by HBsAg enveIope .
 The genome is a single stranded small
circular molecule of RNA.
 It encodes its own nucleoprotein, the delta
antigen or HDAg , but the outer envelope
(HBs Ag) of HDV is encoded by the genome
of HBV coinfecting the same cell.
 HBV is necessary for the production of HDV
virions.

44. clinical features
 HDV infection can occur in presence of
HBV under two situation :
(i) Simultaneous infection with both HDV and
HBV (coinfection)
(ii) Super infection of an HBsAg carrier by
HDV.
Transmission occurs parenterally
Coinfection with HBV and HDV results in
hepatitis of increased severity than the disease
caused by HBV alone.

45. Laboratory Diagnosis
 Diagnosis can be made by detecting the
IgM anti-delta antibody in serum.
 ELISA and RIA kit are commercially
available for detection of antibodies to
HDV.
 HDAg (Delta antigen)is primarily
expressed in liver cell nuclei,where it can
be detected by immuno-fluorescence.
 It is occasionally present in serum.
 HDVRNA can be detected by
hybridisation using a radiolabelled probe.

46. Prophylaxis
 No specific prophylaxis exists, but
immunization with the hepatitis B
vaccine is effective because delta antigen
cannot infect Persons immune to HBV.
 Screening of blood donors for HBsAg
will also limit blood borne HDV
infection.

47. HEPATITIS E virus (HEV)
Belongs to family calciviridae
 They are spherical,nonenveloped and 27-38 nm in
diameter.
 They possess single stranded RNA genome, which
is surrounded by icosahedral capsid
Pathogenesis
 Hepatitis E has been shown to occur in epidemic,
endemic and sporadic forms almost exclusively in
developing countries.
 It isprimarily associated with ingestion of faecally
contaminated drinking water.
 Clinically the disease resembles that of hepatitis A.
 The disease is generally mild and self limited.

48. Laboratory Diagnosis
1) Exclusion Of hepatitis A and hepatitis B
 Hepatitis A can be excluded by lgM serology
and hepatitis B by absence of HBs Ag and
anti HBc-igM
2) lmmunoelectron microscopy
 Faeces is examined by electron microscopy of
aggregated calcivirus-like particles using
monoclonal antibodies.

49. 3) ELISA test and western blot assay
These are used for detection of lgM and lgG
antibodies.
4) Polymerase chain reaction (PCR)
HEV RNA can be detected in faeces or acute
phase sera of patients.

50. Prophylaxis
 Hepatitis E can be prevented by
1. improved standards of sanitation
2. chlorinated water

51. HEPATITIS G VIRUS- (HGV)
 In 1996, this virus was first isolated from a
patient with chronic hepatitis, this has been
called hepatitis G virus.
 HGV RNA has been found in patients with
acute, chronic and fulminant hepatitis,
haemophiliacs, patients with multiple
transfusions, blood donors and intravenous
drug addicts.
 Its role in hepatitis is not clear

52.  The genome of HGV consists of single
stranded RNA.
 HGV replicates in peripheral blood cells.
 The virus is transmitted parenterally,
sexually and from mother to child.
 A significant proportion of HIV-infected
individuals are also HGV-co infected ,there is
no evidence of a relationship between HGV
infection and hepatic carcinoma.
 HGV infection subsides after several years
and anti-hepatitis G envelope antibody
develops

53. PROPHYLAXIS.
 HGV infection can be prevented by
employing the general prophylactic
measures used for HBV and HCV.

54. NON-A, NON-B (NANB) HEPATITIS
 It refers to viral hepatitis resembling type A or type B
clinically and epidemiologically but not caused by
either of these virus.
 Now 4 types (hepatitis C,D,E,G) of NANB virus are
known.
 The diagnosis is possible with serological test.

55. CLINICAL MANIFESTATIONS
• HCV virus DNA has been detected in the saliva of
patients with chronic Hepatitis C infection and it has been
demonstrated that the saliva of HCV carriers is infectious.
• A number of reports suggesting association between HCV
and Sjogren’s syndrome.
• Extrahepatic manifestations including salivary gland
enlargement.
• Patients may report xerostomia along with chronic major
salivary gland enlargement.

56. • Females with chronic HCV infection had greater
tendency for sialadenitis.
• HCV infected patients do not commonly experience dry
eyes along with xerostomia.
• There is greater prevalence of HCV infection in dialysis
patients and are encouraged to undergo periodic testing
for HCV infectivity.

57. • Disease manifestation include jaundice,
malaise, fever, anorexia, nausea, abdominal
pain, dark “stormy” “foamy” urine, chalky
grey stools, rash and arthritis.
• Many chronic hepatitis carriers are also at
higher risk of hepatocellular carcinoma

58.  Modes of transmission of HCV in
health care settings
• Accidental needlesticks
• Blood splashes into eyes
• Blood transfusion
• Contaminated immunoglobulins
• Organ transplantation
• Infected cardiac surgeons to patients
• Patient to patient via colonoscope

59.  Prolonged course of therapy with interferon-alpha
have beneficial effects
 A daily regimen of interferon alpha-2b plus ribavirin
for 6 to 12 months provide more promising results
than interferon monotherapy
 An effective vaccine for hepatitis C is not commercially
available

60.  Acute fulminant hepatitis is said to be present
when a previously healthy person develops
acute hepatitis and goes in to hepatic
encepholapathy within 8 weeks of illness .
 Cases that evolve at a slower pace are called
sub acute or subfulminant hepatitis or hepatic
failure.
 It is a life threatening syndrome characterised
by fever,jaundice and mental
features(confusion, precoma and coma)

61.  1)Acute viral hepatitis all types,but rare with
hepatitis A.
 2)Drugs- all hepatotoxic drugs
 3)Pregnancy with hepatitis
 4)Wilsons disease
 5)Poisons-ccl4,phosphorus.
 6)Reyes syndrome(fatty liver with
encephalopathy in children).

62.  a)cerebral features-disturbed concentration,poor
alertness,disorientation,slurred speech.
 b)jaundice
 c)fetor hepaticus-ammoniacal odour in breath due
to methyl mercaptans.
 d)flapping tremors
 e)liver dullness
 f)Bleeding diathesis
 g)cerebral oedema-nuerological manifestations
 h)signs of portal hypertension

63.  Bilirubin-it is raised both conjugated and
unconjugated
 Serum transaminases are raised,they may fall with
progression of the disease.
 Serum albumin is usually normal to low.
 Prothrombin time may be prolonged in severe
form of the disease.
 Leucocytosis may occur
 EEG is done to grade the hepatic encephalopathy
 Serum ammonia levels are usually high
 Reduced liver size with normal echotexture

64.  No sedation is given unless the patient is violent.if
necessary a small dose of phenobarbitone or 5mg
of IV Diazepam may be given
 Care of comatosed patients .care of back,
bowel,bladder,skin,respiration,pulse,BP
 Intravenous 5-10% glucose drip to give nutrition
and to prevent hypoglycemia
 Intravenous vitamin K,10 mg daily for 3 days with
IV vitamin C 500 mg daily in the drip to prevent
bleeding.
 Intravenous H2 blockers,ranitidine 50 mg twice a
day,may be given to prevent gastrointestinal
bleeding.

65.  It is defined as any hepatitis lasting 6 months
or longer
 AETIOLOGY
 1)infective-hepatitis B,C,D.
 2)Toxic-Drugs(alpha methyldopa,isoniazid)
 3)Metabolic-Wilsons
disease,heamochromatosis.
 Unknown-autoimmune hepatitis

66.  This type occurs commonly in men over 30 years
 It may also come to physicians attention in a
patient who is being treated for viral
hepatitis,which fails to resolve within 12 weeks.
 In these patients HbcAg and HBV DNA persist
with low levels of IgM anti-HBc (HbcAg positive
Hepatitis B)
 In some cases spontaneous mutation of core
promoter region of HBV genome may result in
chronic Hepatitis called HbeAg-negative hepatitis
B

67.  Non specific features include ill health , fatigue,
weakness.
 Clinical relapses occur , sometimes super conversion of
HbeAg to anti-Hbe and vice versa.
 The physical signs include tender hepatomegaly.
 Jaundice may be mild or absent.Splenomegaly occurs in
25% cases .
 Some patients may have spider telangiectasia
 INVESTIGATIONS
o Moderate increase in serum bilirubin and serum
transaminases
o Hypoalbuminaemia is present if the disease is advanced.
o Viral markers of hepatitis B (HbsAg, Hbv DNA and Hbc
Ag)are present.
o Liver Biopsy shows histological changes-GROUND
GLASS appearance inside the cytoplasm of hepatocytes.

68.  INTERFERON-alpha 2a(180microgram per week
for 48 weeks)or recombinant human interferon
alpha(5 million daily or 10 million units thrice a
week IM for 4-6 months.
 Nucleoside and analogs are better tolerated and
more effective than interferon
 Lamivudine100 mg daily suppreses HBV DNA in
serum and improves liver histology in 60% cases
and normalises enzyme levels in 40% cases after 1
year treatment .
 Adefovir is also effective in Hbc-positive and
HbcAg negative patients.

69.  Risk to dental professionel-hepatitis B,C and other types can
be transmitted to the dentist by blood contaminated needles
or instrument stick from an infected patient in acute phase
of disease.
 Clotting factors assesment- if surgery is necessary , obtain
preoperative prothrombin time and bleeding time , as in
liver diseases deficiency of clotting factor may be present.
 Universal infection precaution-dental personnel may act as a
source of infection to patient . Dentists who are carriers of
HBV and who do not practice universal infection control
precautions can transmit the infection to patient . At the
same time it is required to avoid infection from patient to be
transmitted to dental personnel.
 Strict aseptic procedure-use of masks , gloves for all persons
is a must.
 Minimize aerosol production-by using a slow speed hand
piece and using air syringe.