BABE KE AYURVEDIC MEDICAL

COLLEGE AND HOSPITAL

DAUDHAR (MOGA)

COMPILATION

ON

VIRAL HEPATITIS

DEPTT. OF SWASTHWRITTA
SUBMITTED BY: SUBMITTED TO:
TAMANA SHARMA ASSISTANT PROFESSOR
BATCH 2013 DR. BHAGYASHRI

VIRAL HEPATITIS
Introduction:- Viral hepatitis may be defined as infection of liver caused by half dozen virus.
twenty years ago hepatitis A virus and hepatitis B virus were only known etiological agents of
viral hepatitis. Today in addition to HAV and HBV hepatitis viruses C,D, E & G have also been
identified.1
Hepatitis A
Introduction:-hepatitis A (formely known as “infectious” hepatitis or epidemic jaundice) is an
acute infectious disease caused by hepatitis A virus.1
Hepatitis A virus causing a fecally spread self limiting disease.2
Problem statement
Being enterovirus infection like poliomyelitis, hepatitis A is endemic in most developing
countries.
Areas with high level of infection:-In developing countries with poor sanitary condition
Areas with intermediate level:-Countries with transitional economies
Areas with low level:-In developed countries with good sanitory and hygienic condition.3
Epidemiological determinants
Agent :- Hepatitis A virus ,is an enterovirus of Picornaviridae family. 3,4
Resistance :- Resistant to low pH, heat, chemicals.
Reservoir :- Human cases
Period of infectivity :- 2 weeks before and 1 week after onset of jaundice.
Infective material :- Man’s faeces, blood, serum and other stage of viraemia
Virus excretion:-HAV is excreted in faeces for about 2 weeks before the onset of jaundice.5, 6
Host factor
Age:- More frequent among children than in adults
Sex:- Both sexes
Immunity :- Immunity after attack probably lasts for life.7,8
Environmental factors:- Heavy rainfall, poor sanitation.9,10
Modes of transmission
Major route of transmission :- Direct contact, contaminated water, food, milk, water borne
transmission, faeco oral route, parentral route (rarely occur in viraemia stage)11
Sexual transmission:-Homosexual, oral-anal contact.
Sewage contaminated and inadequate treated water.12
Incubation period
13
10-50 days (14-28) days.
 Clinical features
1.
Nausea
2.
Vomiting
3.
Anorexia
4.
Mild fever14
5.
Headache
6.
Myalgia
7.
Arthralgia,
8.
Vomiting15
Diagnosis
1. ALT
2. Bilrubin
3. Demonstration of HAV in faeces ,blood,bile.16,17,18
Prevention and containment
1.
Control of reservoiur- it is difficult because of low socio economic profile, large
subclinical cases
2.
Control of transmission:- Hand washing before toilet, eating, sanitary disposal
Prevent contamination of food products, control of susceptible population
3.
Vaccines: Formaldehyde inactivated vaccines, Live attenuated vaccines.19
 Hepatitis B
Introduction:- Hepatitis B (serum hepatitis) is an acute systemic infection with major
pathology in liver caused by HBV.20
Hepatitis B virus consists of a core containing DNA and a DNA polymerase
enzyme needed for virus replication .the core of virus surrounded by surface protein..21

Problem statement
Endemic throughout world, developing and tropical regions and in some cases of chronic
liver diseases.23
Epidemiological determinants
Agent:- Hepatitis B virus was discovered by Blumberg in 1963
Reservoir:- Man is only reservoir
Infective material :- Contaminated blood, saliva, vaginal secretions, semen
Resistance: - The virus is quite stable and surviving for at least 7 days.
Period of communicability:- The virus is present in blood during incubation period.24,25

Host factor
Age:-
1. 10% of early childhood
2. 30% less than 5 years
3. 5% after 6 years26
4. 1%antenatal
5. 10%(1-5years of age)27
High risk groups
Homosexuals, Prostitutes, Drug abusers28
Mode of transmission
Parentral route : Through BT, Dialysis, Contaminated syringes & needles, ear piercing,
nose piercing.
Parinatal transmission:-HBV carrier
Sexual transmission:-Particularly homosexuals
Other routes:-Transmission from child – child often called horizontal transmission

Incubation period
29
1. 30-180 days
2. 75 days30
 Clinical picture

Clinical picture are same that of other viral hepatitis31

1. Yellowing of eyes
2. Dark urine
3. Abdominal pain
4. Anorexia
5. Nausea
6. Mild upper quadrant pain or discomfort32
7. Fever
8. Joint pain
9. Loss of appetite
10. Weakness
11. Fatigue33

Prevention and containment

Hepatitis B vaccine:-The recombinant hepatitis B vaccine was introduced In 1986 and

has gradually replaced the plasma derived hepatitis B vaccine 34
Hepatitis B immunoglobulin (HBIG):- For immediate protection HBIG is used for
those acutely exposed to HBsAg positive blood.
For example:-
1. Surgeons
2. Nurses
3. Lab workers
4. Newborn infants of carrier mothers
Passive active immunization:- The simultaneous administration of HBIG and hepatitis
B vaccine is more efficacious than HBIG alone35,36
 Hepatitis C
Introduction:- Hepatitis C is a contagious liver disease that results from infection with
HCV virus37
Hepatitis C is an infection caused by a virus that attacks liver and leads to
inflammation38
Transmission:- Hepatitis C is usually spread when blood from person infected with
hepatitis C virus enters body of non infected person39
Hepatitis C can also be transmitted through sexual contact40

Incubation period
41
2 weeks to 6 months

Clinical features
1. Fever
2. Fatigue
3. Decreased appetite
4. Nausea
5. Vomiting
6. Abdominal pain42
7. Dark urine
8. Grey coloured faeces
9. Joint pain
10. Jaundice43

Diagnosis
1. Serology and virology
2. Molecular analysis
3. Liver function test
4. Liver histology44

Prevention
Primary prevention:-
There is no vaccine for hepatitis C. Risk of infection can be reduced by avoiding:-
1. Unnecessary injections
2. Unsafe blood products
3. Unprotected sex
4. Tattoos
Secondary and tertiary prevention:-
1. Education and counseling
2. Immunization with hepatitis A and B vaccines45
 Hepatitis D
Introduction:- HDV is found throughout the world but with a non uniform distribution.
its highest prevalence has been reported in Italy, middle east, central asia46
With coinfection acute hepatitis D may range from mild to fulminant hepatitis but
fulminant hepatitis is more likely to such simultaneous delta infection. Chronicity rarely
develops in coinfection.
With superinfection (incubation period 30-35days) chronic HBV infection gets
worsened indicated by appearance of severe and fulminant acute attacks, progression of
carrier stage to chronic delta hepatitis or acceleration towards cirrhosis47
The hepatitis D virus is an RNA defective virus which has no independent
existence. It acquires HBV for replication and has same sources and modes of spread48

Investigations
HDV contains a single antigen to which infected individuals make an antibody.
Delta antigen appears in blood only transiently and in practice diagnosing depends on
detecting anti HDV49

Hepatitis E
 The infection caused by hepatitis C virus which was discovered in 1980, is
essentially a water borne disease. Formally termed enterically transmitted hepatitis non
A, non B
HEV is a 29nm to 32nm RNA virus
In addition HEV has a propensity to induce a fulminating form of acute disease
particularly in pregnant woman,upto20% of whom may develop fulminating hepatitis E
with a mortality that may reach about 80% of such cases50,51
Diagnosis is made by level of anti HEV antibodies in serum. No confirmatory
assay is currently available. Anti HEV Igm antibodies have been determined. Hepatitis C
appears to be widespread problem in developing countries52

Hepatitis G
 Hepatitis G virus was discovered in 1996. The prevalence of this infection is still
unknown. Few publications provide information on association of this infection with
blood transmission in india53
A virus distinct from foregoing hepatitis virus has been designated separately as
HGV. HGV infection has been found in blood donor .patients on haemodialysis and as
coinfection with HIV54
Hepatitis G is a newly discovered form of liver inflammation caused by HGV

Diagnosis
Only method of detecting HGV is a complex and costly DNA test is not widely
available55

dkeyk ( Kamala)
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jäihr'k—Uew=ks Hksdo.kksZ grsfUæ;%AA…‡AA
nkgkfoikdnkscZY;lnuk:fpdf"kZr%A
dkeyk cgqfiÙkS"kk dks"B'kk[kkJ;k erkAA…ˆAA
dkykUrjkr~ [kjhHkwrk —PNªk L;kr~ dqEHkdkeykA
—".kihr'k—Uew=ks Hk`'ka 'ku'p ekuo%AA…‰AA
ljäkf{keq[kPNfnZfo.ew=ks ;'p rkE;frA
nkgk:fpr`"kkukgrUækeksglefUor%AA…ŠAA
u"VkfXulaK% f{kça fg dkeykoku foi|rsA ¼ p‐fp‐ 16 ½

Samprapti
The patient of panduroga who takes pitta aggravating things excessively, his
pitta burns blood and flesh and thus gives rise to disorder. His eyes, skin, nails and face
become deep yellow and he looks like a frog. His senses and organs lose their functions
and he is associated with burning sensation , indigestion , debility, malaise, anorexia.
This is known as kamala. It is due to aggravation of pitta and is known as located in
koshtha or shakha. kumbhakamala being established firmly due to chronicity becomes
curable with difficulty.

Sadhya-Asadhyatav
The patient of jaundice succumbs soon to disease if faeces and urine become
black yellow, there are excessive swelling, blood in eyes and mouth, vomiting faeces and
urine, fainting, burning sensation, anorexia, thirst, hardness in bowel, drowsiness,
confusion, loss of power of digestion and consciousness56,57
Pathogenesis in due course of time, when kamala become chronic, it is known as
kumbha kamala and is curable with difficulty58,59

Nidana
By taking pitta aggravating things.

Chikitsa

Dadimadhya ghritta -10 gm with cow milk

Katukadhya ghritta – 10 gm with cow milk
Lauh bhasm – 2mg
Haritaki churna – 3-6 gm
Haridra churna – 4 mg
References
1. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 190
2. Text book of pathology : Harsh Mohan, 7th edition Pg. No. 605
3. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 191
4. Text book of pathology : Harsh Mohan, 7th edition Pg. No. 606
5. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 191
6. www.who.int>mediacentre>factsheets
7. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 191
8. www.ncbi.nlrm.nin.gov.
9. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 191
10. www.ncbi.nlrm.nin.gov.
11. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 191
12. www.who.int>mediacentre>factsheets
13. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 191
14. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 192
15. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 948
16. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 192
17. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 948
18. Text book of pathology : Harsh Mohan, 7th edition Pg. No. 606
19. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 193
20. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 193
21. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 948
22. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 193
23. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 948
24. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 193
25. www.who.int>mediacentre>factsheets
26. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 194
27. www.ncbi.nlrm.nin.gov.
28. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 194
29. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 195
30. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 948
31. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 195
32. emedicine.medscope.com
33. www.mayoclinic.org
34. www.m.webmd.com
35. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 196
36. www.m.webmd.com
37. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 197
38. www.who.int
39. www.cdc.gov
40. www.healthline.com
41. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 197
42. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 197
43. www.cdc.gov
44. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 953
45. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 197
46. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 199
47. Text book of pathology : Harsh Mohan, 7th edition Pg. No. 607
48. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 952
49. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 952
50. Text book principle and practice of Davidson's medicine, 21st edition. Pg. 954
51. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 198
52. https://en.m.wikipedia.org
53. Text book of preventive & social medicine: K. Park, 11th edition Pg. No. 199
54. Text book of pathology : Harsh Mohan, 7th edition Pg. No. 607
55. medical-dictionary.thefreedictionary.com
56. Madhava Nidana
57. Charaka Samhita Chikitsa Sthana 16th chapter
58. Madhava Nidana
59. Charaka Samhita Chikitsa Sthana 16th chapter