Hepatitis is inflammation of the liver tissue. Some people or animals with hepatitis have no symptoms, whereas others develop yellow discoloration of the skin and whites of the eyes (jaundice), poor appetite, vomiting, tiredness, abdominal pain, and diarrhea. Hepatitis is acute if it resolves within six months, and chronic if it lasts longer than six months.

1. HEPATITIS
Presented by:
Sonam Yadav
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5. .
PHYSIOLOGY
OF LIVER
Protein and
glucose
metabolism
Amino
conversion
Drug and fat
metabolism
Bile
formation
Formation of
clotting
factors
Bilirubin
excretion
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6. HEPATITIS
■ Hepatitis is defined as the
inflammation of the liver.
■ According to WHO, 325 million
people globally live with a hepatitis
infection.
■ Viral hepatitis B infection in the
world is among 257 million people.
■ Hepatitis C infection is among 71
million people globally.
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7. .
■ Nearly 96,000 people die annually in India due to Hepatitis C, which has
become a hidden epidemic according to WHO report.
■ India has an estimated number of 40 million chronic Hepatitis B Virus
(HBV) infected people throughout the country, constituting about 11
percent of the estimated global Hepatitis-B burden.
■ The prevalence rate of Chronic Hepatitis B Virus (HBV) infection in India
is around 3 to 4 percent.
■ The prevalence of HCV infection in India is 1 per cent.
■ Men are more prone as compared to women.
EPIDEMIOLOGY
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8. Types Of Hepatitis (Based On Duration)
ACUTE HEPATITIS
Duration more than 6 months
Duration less than 6 months
CHRONIC HEPATITIS
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9. TYPES OF HEPATITIS (cause based)
VIRAL HEPATITIS NON VIRAL
HEPATITIS
Drug Induced Hepatitis
Toxic Hepatitis
OTHER TYPES
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Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Autoimmune Hepatitis
Alcoholic Hepatitis
Non Alcoholic
Steatohepatitis (NASH)

10. Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
VIRAL HEPATITIS
Hepatitis G
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HEPATITIS A HEPATITIS B HEPATITIS C HEPATITIS E
TYPE OF VIRUS RNA DNA RNA RNA
ROUTE OF
TRANSMISSION
Feaco-oral route Parenteral Parenteral Feaco-oral route
SEVERITY OF
ILLNESS
Mild Severe Mild Mild
CHRONICITY
OF DISEASE
None 10% 50-60% None

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13. .
■ Formerly as Infectious hepatitis.
■ Accounts for 20-25% of cases of clinical hepatitis.
Hepatitis A
Causative organism:
Hepatitis A virus
Incubation period:
15- 50 days
(average: 28 days)
Mode of transmission:
Fecal oral route
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Etiological factors
Invasion of virus into liver cells and
replication
Cytotoxic cytokines and NK cells
release to attack virus
Lysis of infected hepatocytes
Scar tissue forms around dead and
infected liver cells
Liver damage and improper function
cirrhosis
Reduces blood flow to the liver
Permanent Shrinking and hardening of
liver
Chronic infection
Dormant and reactivation
PATHOPHYSIOLOGY

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1. Prodromal Symptoms

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Icteric Phase
2. Icteric Phase

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3. Convalescent Phase

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19. Assessment and Diagnostic findings
 The liver and spleen are often moderately enlarged for a few days after
onset; otherwise, apart from jaundice, there are few physical signs.
 Hepatitis A antigen may be found in the stool a week to 10 days before
illness and for 2 to 3 weeks after symptoms appear.
■ HAV antibodies are detectable in the serum, but usually not until
symptoms appear: done through ELISA.
 Biochemical test may reveal abnormal levels of bilirubin, alanine
aminotransferase, and protein.
 Blood tests: 2 kind of antibodies – IgM (shows acute infection) and IgG
(previous infection).
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• To diagnose jaundice and assess the severity of jaundice
Bilirubin
• To assess for hemolysis
Unconjugated bilirubin
• To diagnose cholestasis
Alkaline phosphatase
• To diagnose hepatocellular carcinoma and to assess disease progression
SGOT/AST
• ALT lower than AST is found in person’s with alcoholism
SGPT/ALT
• To diagnose autoimmune hepatitis
Gamma globulin

21. Two-dose vaccine be given to adults
18 years of age or older, with the
second dose 6 to 12 months after the
first.
PREVENTION
Children and adolescents 2 to 18 years
of age receive three doses, with the
second dose 1 month after the first and
the third dose 6 to 12 months later.
Vaccination: Havrix & Vaqta
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22. Travelers to developing countries
Settings with poor or uncertain sanitation conditions
Recommended for:
Other high-risk groups (homosexual men, injection/intravenous drug
users, staff of day care centers, and health care personnel).
Immune globulin: for household members and sexual contacts of people with hep. A,
Day care center and restaurant workers with exposure to or infected with hepatitis A
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23. Good personal hygiene and
proper sanitation
Twinrix (combined
Hep. A and B vaccine )
is available for
vaccination of people 18
years of age and older
with indications for hep.
A and B vaccination. (3
doses-0,1,6 months)
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25. Medical Management
 Supportive treatment
 Bed rest during the acute stage.
 During the period of anorexia, the patient should receive frequent small
feedings, supplemented, if necessary, by IV fluids with glucose.
 Optimal food and fluid levels are necessary to counteract weight loss and
slow recovery.
 Gradual but progressive ambulation seems to hasten recovery, provided
the patient rests after activity and does not participate in activities to the
point of fatigue.
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26. Nursing Management
■ Assist the patient and family in coping with the temporary disability
and fatigue that are common in hepatitis.
■ Specific guidelines about diet, rest, follow-up blood work.
■ The importance of avoiding alcohol.
■ Sanitation and hygiene measures (particularly hand washing) to prevent
spread of the disease.
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27. .
Hepatitis B
Causative organism:
Hepatitis B virus
Incubation period:
60-150 days
(average 90 days)
Mode of transmission:
percutaneous and per
mucosal routes
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28. Risk factors
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31. Assessment And Diagnostic Finding
Hepatitis B virus is a DNA virus composed
of the following antigenic particles:
 HBcAg- hepatitis B core antigen
 HBsAg- hepatitis B surface antigen
(antigenic material on the viral surface, a
marker of active replication and infection)
 HBeAg- an independent protein
circulating in the blood.
 HBxAg- gene product of X gene of HBV
DNA
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32. .
 Anti-HBc-antibody, persists during the active phase
of illness, may indicated continuing HBV in the liver.
 Anti-HBs-antibody, detected during late
convalescence, usually indicates recovery and
development of immunity.
 Anti-HBe-antibody, signifies reduced infectivity.
 Anti-HBxAg-antibody, may indicate ongoing
replication of HBV.
■ HBsAg appears in the circulation in 80-90% of
infected patients 1 to 10 weeks after exposure to HBV
and 2 to 8 weeks before the onset of symptoms or an
increase in transferase levels.
■ Liver ultrasound or transient elastography can show
the amount of liver damage.
■ liver biopsy, and fibro tests
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33. Continued screening of
blood donors
Wearing Gloves while handling
blood, body fluids and sample
of HBsAg positive specimen
Maintaining good
personal hygiene
Use of disposable syringe, needle
and lancets
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Prevention

34. .
A yeast-recombinant hepatitis B vaccine is
used to provide active immunity and has
shown rates of protection greater than 90%
in healthy people
Active Immunization
Nurses and health care professionals exposed
to blood and blood products
All unvaccinated people being evaluated for
a STI, history of STI, people with multiple
sex partners, people who have sex with IV or
injection drug users, or sexually active men
with other men.
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35. Passive Immunity: Hepatitis B Immune Globulin
Hepatitis B immune globulin (HBIG) provides
passive immunity to hepatitis B and is indicated for
people exposed to HBV who have never had hepatitis
B and have never received hepatitis B vaccine.
Specific indications for postexposure vaccine with
HBIG include:
(1) Inadvertent exposure to HBAg-positive blood
through percutaneous (needlestick) or transmucosal
(splashes in contact with mucous membrane) routes
(2) sexual contact with people positive for HBAg
(3) Perinatal exposure.
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36. Medical Management
 Treatment of acute hepatitis B is indicated only in patients with severe
hepatitis and liver failure.
 Nucleoside and nucleotide analog such as tenofovir, adenofovir, lamivudine.
 Interferon: standard interferon (intron A), pegylated interferon (peglntron):
Alpha interferon as the single modality of therapy: regimen of 5 million units
daily or 10 million units three times weekly for 4 to 6 months.
 Liver transplant
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37. Dietary management
 Recommend small, frequent meals, minimize periods without food intake.
 Provide intake of 25-30 kcal/day.
 Provide protein intake of 1-1.5 g/kg/day.
 Carefully monitor fluid balance.
 Be aware that that enteral feedings may be necessary if anorexia, nausea,
and vomiting persist.
 Instruct patient to abstain from alcohol during acute illness and for at least
6 months after recovery.
■ Advise patients to avoid substances (medications, herbs, illicit drugs, and
toxins) that may affect liver function.
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38. 11-06-2021 38
Types of hepatitis on the basis of duration?
Types of hepatitis on the basis of cause?
Name of the vaccine for hepatitis A prevention?
Stages of symptoms development in hepatitis?
What are the four antigenic particles of hepatitis B DNA virus?
Dose, route and frequency of hepatitis B vaccine?
Route of transmission for hepatitis A and hepatitis C?

39. Hepatitis C
Incubation period:
14-182 days
(average: 14-84 days)
Mode of transmission:
Direct percutaneous or
mucous membrane
exposure
Causative organism
Hepatitis C virus
Non-A, Non-B hepatitis,
or NANB hepatitis
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40. Risk factors
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41. Assessment and diagnostic findings
■ HCV antibody: ELISA: It takes at least 4 weeks after infection before
antibody appears.
■ HCV-RNA: PCR is done to diagnose HCV infection in acute phase,
however its main use is in monitoring the response to antiviral therapy.
■ Liver ultrasound
■ Biochemical studies
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42. Management:
 Combination of two antiviral agents, peginterferon and ribavirin (Rebetol),
is effective in producing improvement in patients with Hepatitis C and in
treating relapse.
 Peginterferon (pegasys)
 Ribavirin must be used cautiously in women of
childbearing age.
 The triple therapy of protease inhibitor, peginterferon,
and ribavirin is recommended as standard of treatment for Hepatitis C by
American Association for the study of liver disease.
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43. Prevention
 Advise avoidance of high-risk behaviors such as IV drug use.
■ Use needless IV and injection systems in health care
 Use barrier precautions in situation of contact with blood or body fluids.
 Monitor cleaning, disinfection and sterilization of reusable devices in
patient care settings.
 Avoid multidose vials in patient care settings.
 Use standard precautions in clinical care.
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44. Hepatitis D
The virus requires hepatitis
B surface antigen for its
replication, only
individuals with hepatitis B
are at risk for hepatitis D.
Incubation period:
21-140 days
Causative organism
Hepatitis D virus
Mode of
transmission:
Same as hepatitis B
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Coinfection &
superinfection

45. .
Diagnosis
■ Anti-delta antibodies on testing confirm the diagnosis.
■ Sexual contact with those having hepatitis B is considered to be an
important mode of transmission B and D.
Management
■ Treatment is similar to that of other forms of hepatitis.
■ Interferon alpha is the only licensed drug for the treatment of hepatitis
D.
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46. Hepatitis E
Incubation period:
15 to 65 days
Causative organism
Hepatitis E virus
Mode of
transmission:
Fecal oral route
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Resembles
Hepatitis A
Jaundice is nearly
always present
Diagnosis:
Anti HEV
IgM and Ig G
HEV RNA quantification

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Hepatitis G or GB virus-C
NA NB NC
Hepatitis
Incubation period:
14 to 145 days
Causative organism
Hepatitis G virus &
GB virus-C
Strong significance in
HIV coinfection.
Mode of
transmission:
Parenteral or sexual

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51. NON VIRAL HEPATITIS
.
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52.  Carbon tetrachloride,
 Vinyl chloride,
 Herbicides,
 phosphorus,
 chloroform,
 gold compounds, and
 Industrial chemicals known as polychlorinated biphenyls.
Toxic hepatitis resembles viral hepatitis in onset.
 Obtaining a history of exposure to hepatotoxic chemicals, medications, or other
agents assists in early treatment and removal of the offending agent.
TOXIC HEPATITIS
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53. . Symptoms:
 Anorexia, nausea, and vomiting, jaundice and hepatomegaly.
 Symptoms are more intense for the more severely toxic patient.
 Recovery from acute toxic hepatitis is rapid if the hepatotoxin is identified
early and removed.
• Recovery is unlikely if there is a prolonged period between exposure and
onset of symptoms. There are no effective antidotes.
• Vomiting may be persistent, with the emesis containing blood. Clotting
abnormalities may be severe, and hemorrhages may appear under the skin.
• Delirium, coma, and seizures develop, and within a few days the patient
may die of fulminant hepatic failure.
• Therapy is directed toward restoring and maintaining fluid and electrolyte
balance, blood replacement, and comfort and supportive measures.
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54. .
 Acetaminophen,
 Isoniazid,
 Halothane,
 Certain antibiotics,
 Antimetabolites,
 Medications used to treat rheumatic and musculoskeletal disease,
 Antidepressants, psychotropic medications, anticonvulsants, and
 Inhalational agents of the halothane family are metabolized by the liver and excreted in
bile. These volatile anaesthetics may also decrease hepatic blood flow. Halothane
hepatitis is a dreaded but rare complication of halothane administration
 Isoflurane is considered the anaesthetic agent of choice in patients with liver disease.
DRUG INDUCED HEPATITIS
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More than 900
drugs, toxins and
herbs

55. .
Risk factors:
■ Females
■ Old Age
■ Alcoholic or Liver disease
■ Comorbidities such as AIDS, TB, ARF, DM, etc.
Symptoms:
 Usually the onset is abrupt, with chills, fever, rash, pruritus, arthralgia, anorexia, and nausea.
 Later, there may be jaundice and dark urine and an enlarged and tender liver.
 When the offending medication is withdrawn, symptoms may gradually subside.
 However, reactions may be severe and even fatal, even though the medication is stopped.
 If fever, rash, or pruritus occurs from any medication, its use should be stopped immediately.
 A short course of high-dose corticosteroids may be used in patients with severe hypersensitivity.
 Liver transplantation
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56. AUTOIMMUNE HEPATITIS
.
■ It is a chronic inflammation of the liver of unknown cause
■ Majority of patients are women.
■ It is characterized by the presence of autoantibodies.
■ There is an autoimmune reaction against normal hepatocytes.
■ Type 1 and type 2 are the two types of autoimmune hepatitis.
Diagnosis:
■ serological markers such as antinuclear antibodies, anti-DNA antibodies.
Treatment:
■ Prednisone, and azathioprine
■ Patient who does not respond to prednisone and azathioprine, cyclosporine,
budesonide, methotrexate are used.
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57. .
■ Alcoholic hepatitis is a disease, inflammatory condition of the liver caused
by heavy alcohol consumption over an extended period of time.
Diagnosis:
■ CBC, LFT, USG, CT scan, blood clotting test, liver biopsy.
Treatment:
■ Patients needs to stop drinking.
ALCOHOLIC HEPATITIS
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58. .
■ It is a part of non-alcoholic fatty liver disease (NAFLD)
■ It is a condition where fat builds up in the liver not due to alcohol
consumption.
■ It is the inflammation and liver cell damage along with fat in liver.
■ It is a serious condition that results in cirrhosis, hepatocellular cancer, liver
failure.
Risk factors
 Obesity
 DM
 HTN
 Hyperlipidemia
NON ALCOHOLIC STEATOHEPATITIS (NASH)
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59. .
Clinical findings
 Elevated liver enzymes, Liver biopsy, liver scan, CT scan, and USG.
Treatment :
 There is no definitive treatment and therapy is directed at reduction of risk
factors
 Treat diabetes, weight reduction and management of hyperlipidemia.
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60. PREVENTION

61. Complications
■ Fibrosis
■ Liver cancer
■ Hepatitis coinfection
■ Fulminant hepatitis
■ Liver cirrhosis
■ Hepatic encephalopathy
■ Kidney related problems
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62. Nursing assessment
 Assess for systemic and liver related symptoms
 Obtain history such as IV drug use, sexual activity, travel and ingestion of
possible contaminated food or water to assess for any mode of transmission
of the virus
 Assess size and texture of liver to detect enlargement or characteristics of
cirrhosis
 Obtain vital signs.
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63. 1. Imbalanced nutrition less than body requirements related
to the effects of liver dysfunction
 Encourage small frequent feedings of high calorie, low fat diet.
 Avoid large quantities of protein during acute phase of illness
 Encourage taking pleasing meals in an environment with minimal noxious
stimuli
 Administer or teach self-administration of antiemetics as prescribed.
 Encourage eating meals in a sitting position to decrease pressure on the
liver.
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64. 2. Deficient fluid volume related to nausea and vomiting
 Monitor intake and output
 Provide frequent oral fluids as tolerated.
 Administer IV fluids for patients with inability to maintain oral fluids
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65. 3. Activity intolerance related to anorexia and liver
dysfunction
 Promotes periods of rest during symptom producing phase
 provide emotional support and diversional activities
 encourage gradual resumption of activities and mild exercise during
convalescent period
 promote comfort by administering analgesics and prescribed.
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66. 4. risk for injury related to coagulopathy because of impaired
liver function
 Monitor and teach patient to monitor and report sign of bleeding
 Monitor PT and administer Vitamin K as ordered.
 Avoid trauma that may cause bruising.
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67. 5. Risk of disease transmission related to unhygienic
practices
 Stress importance of proper public and home sanitation and proper
preparation of foods
 Encourage specific protection for close contacts such as immune globulin
as soon as possible to household contact of HAV
 HBIG as soon as possible to blood or body fluids contact of HBV patients,
followed by HBV vaccine series
 Explain precautions to patient and family about transmission and
prevention of transmission
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68. 6. Disturbed thought process related to complication such as
hepatic encephalopathy
 Monitor for signs of encephalopathy
 Monitor for worsening of condition from stupor to coma
 Maintain calm, quite environment and reorient patient as needed.
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69. .
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SUMMARY

70. .
■ As discussed throughout the presentation, hepatitis is defined as the
inflammation of liver. Hepatitis can be further classified as viral and
non-viral hepatitis. Viral hepatitis includes hepatitis A, B, C, D, E and G
and non-viral hepatitis that are caused due to medications include toxic
hepatitis and drug induced hepatitis.
■ Nurses can also counsel the patients and their family for various options
available in treatment for hepatitis.
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CONCLUSION

72. .
 Brunner & Suddarth’s. Textbook of Medical Surgical. 13th edition Volume-2. New
Delhi: Wolters Kluwer;2015; Page no. 1349-1353
 Lewis’s. Textbook of Medical-SurgicalNursing.11thEditionVolum 2. Chintamani
Mani;2010
 Joyce M. Black and Jane Hokanson; medical surgical nursing; volume 2, 8th edition,
reed Elsevier, India pvt.
 [Internet]. Cdc.gov. 2021 [cited 11 April 2021]. Available from:
https://www.cdc.gov/hepatitis/resources/professionals/pdfs/abctable.pdf
 Hepatitis [Internet]. Slideshare.net. 2021 [cited 11 April 2021]. Available from:
https://www.slideshare.net/NikhilVaishnav3/hepatitis-128140979
 Hepatitis - Wikipedia [Internet]. En.wikipedia.org. 2021 [cited 11 April 2021].
Available from: https://en.wikipedia.org/wiki/Hepatitis
■ Hepatitis: Types, Symptoms, and Treatment [Internet]. Healthline. 2021 [cited 11 April
2021]. Available from: https://www.healthline.com/health/hepatitis#treatment
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References

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