This document discusses various types of viral hepatitis. It defines hepatitis as inflammation of the liver and outlines the different causes including viral infections, toxins, genetic factors, and tumors. It then discusses each type of viral hepatitis in more detail, including hepatitis A, B, C, D, and E viruses. For each virus, it covers epidemiology, transmission, clinical presentation, lab markers, treatment, prevention, and other relevant clinical information. It also discusses chronic hepatitis and associated conditions like cirrhosis.
A serious liver infection caused by the hepatitis B virus that's easily preventable by a vaccine.
This disease is most commonly spread by exposure to infected bodily fluids.
Symptoms are variable and include yellowing of the eyes, abdominal pain and dark urine. Some people, particularly children, don't experience any symptoms. In chronic cases, liver failure, cancer or scarring can occur.
The condition often clears up on its own. Chronic cases require medication and possibly a liver transplant.
Hepatitis: inflammation of the liver.
Causes of viral hepatitis:
Common:
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
hepatitis C virus (HCV)
Hepatitis D virus (HDV)
Hepatitis E virus (HEV)
HBV-associated delta agent
A serious liver infection caused by the hepatitis B virus that's easily preventable by a vaccine.
This disease is most commonly spread by exposure to infected bodily fluids.
Symptoms are variable and include yellowing of the eyes, abdominal pain and dark urine. Some people, particularly children, don't experience any symptoms. In chronic cases, liver failure, cancer or scarring can occur.
The condition often clears up on its own. Chronic cases require medication and possibly a liver transplant.
Hepatitis: inflammation of the liver.
Causes of viral hepatitis:
Common:
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
hepatitis C virus (HCV)
Hepatitis D virus (HDV)
Hepatitis E virus (HEV)
HBV-associated delta agent
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
It include the definition , signs and symptoms, types, diagnosis, medical management, Nursing management, preventive measures, complication, Post exposure prophylaxis of Hepatitis.
Presentation by Dr. Mishal Saleem on the topic of Extra hepatic manifestation of hep C, which is a grey area nut very important topic for FCPS Residents.
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
It include the definition , signs and symptoms, types, diagnosis, medical management, Nursing management, preventive measures, complication, Post exposure prophylaxis of Hepatitis.
Presentation by Dr. Mishal Saleem on the topic of Extra hepatic manifestation of hep C, which is a grey area nut very important topic for FCPS Residents.
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2. Outline of presentation
• Hepatitis definitions
• Discussion of each types of viral hepatitis
11/30/2018
3. Hepatitis
• General term: inflammation of liver
• Diseases of the liver
• – Infections (viral)
• – Toxins (alcohol, food, chemical)
• – Genetic (hemochromatosis)
• – Immune (autoimmune hepatitis (AIH),PBC)
• – Neoplasm (hepatocellular carcinoma (HCC)
11/30/2018
4. • Hepatitis: inflammation of liver; presence of inflammatory
cells in organ tissue
• Acute Viral Hepatitis: symptoms last less than 6 months
• Acute Hepatic Failure: Acute liver failure refers to the
development of severe acute liver injury with encephalopathy
and impaired synthetic function (international normalized ratio
[INR] of ≥1.5) in a patient without cirrhosis or preexisting liver
disease in <26weeks.
• Chronic Hepatitis: Inflammation of liver for at least 6 months
• Cirrhosis: Replacement of liver tissue fibrosis, scar tissue
• Fulminant Hepatitis: severe impairment of hepatic functions or
severe necrosis of hepatocytes in the absence of preexisting
liver disease
Clinical Terms
11/30/2018
5. Acute viral hepatitis
• Acute viral hepatitis is a systemic infection affecting the liver
predominantly.
• Almost all cases of acute viral hepatitis are caused by one of five viral
agents:
• Hepatitis A virus (HAV)
• Hepatitis B virus (HBV)
• Hepatitis C virus (HCV)
• HBV-associated delta agent or hepatitis D virus (HDV), and
• Hepatitis E virus (HEV).
11/30/2018
6. Acute viral hepatitis
• All types of viral hepatitis produce clinically similar illnesses.
• These range from asymptomatic and inapparent to fulminant and
fatal acute infections common to all types,
• on the one hand, and from subclinical persistent infections to rapidly
progressive chronic liver disease with cirrhosis and even
hepatocellular carcinoma, common to the blood borne types (HBV,
HCV,and HDV), on the other.
11/30/2018
7. Chronic hepatitis
• Chronic hepatitis represents a series of liver disorders of varying
causes and severity in which hepatic inflammation and necrosis
continue for at least 6 months.
• Milder forms are non progressive or only slowly progressive, while
more severe forms may be associated with scarring and architectural
reorganization, which, when advanced, lead ultimately to cirrhosis.
11/30/2018
9. Chronic viral hepatitis
• Both the enterically transmitted forms of viral hepatitis, hepatitis A
and E, are self-limited and do not cause chronic hepatitis .
• In contrast, the entire clinicopathologic spectrum of chronic hepatitis
occurs in patients with chronic viral hepatitis B and C as well as in
patients with chronic hepatitis D superimposed on chronic hepatitis
B.
11/30/2018
10. Viral Hepatitis-types
Virus Source Transmission Chronicity Prevention
A Stool Feco-oral No Immunoglobulin
Vaccination
B Parentral Percutanous
per mucosal
Yes Immunoglobulin
Vaccination
Immunoglobulin
Vaccination
C Parentral Percutanous
per mucosal
Yes Blood donor screening
Risk behavior
modification
D Parentral Percutanous
per mucosal
Yes HBV Prevention
E Stool Feco-oral No Safe water cleaning
11/30/2018
11. 1.Hepatitis A Virus: HAV
• 27nm RNA picornavirus
• 4 capsid proteins; 1 serotype
• Virus not cytopathic to hepatocytes; causes liver injury by stimulating
both cellular and humoral immune responses
11/30/2018
12. Hepatitis A Virus: HAV
• Epidemiology: fecal-oral viral transmission
• • Associated with
• – Poor hand washing
• – Poor personal hygiene habits
• – Inadequate sanitation
• – Day-care centers
• – Institutionalized populations
• – Endemic areas of world
11/30/2018
13. Hepatitis A Virus: HAV
• Symptoms
• – Onset usually abrupt, lasting 1-2 weeks
• – Acute disease, self-limiting, most recover fully
• More commonly seen in children and adolescents
• More virulent in middle age and older
• – Diagnosis may be missed: under-reporting
• Rarely complications (0.4%)
11/30/2018
14. • Symptoms
• Vague: flu-like complaints, onset abrupt
• Abdominal pain, diarrhea, fatigue, fever, headache,
• malaise, anorexia, myalgia, arthralgia,
• nausea/vomiting, sore throat, hepatomegaly,
• hepatic tenderness
• Jaundice: adults ~50-80%; rare in children so usually not clinically
detected
• Urine: amber color, ‘dark’
11/30/2018
15. Serological markers:hav
• – Virus present in blood briefly (shed in stool)
• – By the time symptoms appear, antibody in serum HAVAB – present
4 weeks after infection
• IgM - acute disease (1-8 weeks after onset of symptoms)
• IgG – immunity after 2 months, continuing for years
11/30/2018
16. Laboratory:for HAV
• – Test for presence of HAV antibody = HAVAB
• • HAVAB-IgM (acute infection)
• • HAVAB-total (IgM and IgG: past infection)
• – Monitor disease with liver enzymes and bilirubin
• • AST, ALT >3XULN (~500-1000 U/L)
• • Total bilirubin: increased (~1.1-9.0 mg/dl)
• • Urine bilirubin: positive
11/30/2018
18. Complications of HAV
• Relapsing hepatitis
• cholestatic hepatitis
• 85% of HAV infected individuals have full clinical and biochemical
recovery with in 3 months and nearly all have complete recovery
by six months.
11/30/2018
20. Prevention
. Infected individuals are contagious during the incubation period
and remains so for about a week after jaundice appears.
. Sanitary practices
. Hand washing
11/30/2018
21. prevention
• Pre- and post exposure
• Passive immunization : serum immune globulin
• Active immunization: inactivated whole HAV vaccine
11/30/2018
22. 2.Hepatitis B Virus: HBV
• 42 nm DNA enveloped hepadnavirus virus
• with several surface markers
11/30/2018
24. hepatitis B surface antigen (HBsAg)
• The envelope protein expressed on the outer surface of the virion
• spherical and tubular structures
• the product of the S gene of HBV
• Indicate on going infection
• Antibody :anti-HBs
• Anti-HBs effective in neutralizing virus only when HBV is extracellular
11/30/2018
25. The C gene
• has two initiation codons
a precore
a core region
• precore region: HBeAg the protein product
• the core region: HBcAg is the protein product
11/30/2018
26. hepatitis B core antigen (HBcAg)
• 27-nm nucleocapsid core particle
• Inner core HBV
• Not secreted in serum but is expressed in on the hepatocyte surface
• Nucleocapsid proteins are coded for by the C gene
• antibody : anti-HBc
- marker of HBV infection(recent/current infection)
11/30/2018
27. hepatitis B e antigen (HBeAg),
• is a product of the C gene: precore regine
• The secreted nucleocapsid protein
• HBeAg provides qualitative marker of HBV replication and relative
infectivity.
11/30/2018
28. "gap" or "window" period
• Time gap b/n disappearance of HBsAg and the appearance of anti-
HBs
• During this period anti-HBc may represent the only serologic
evidence of current or recent HBV infection
11/30/2018
29. Anti-HBc
• isolated anti-HBc does not necessarily indicate active virus replication
• isolated anti-HBc represent hepatitis B infection
• Persist indefinitely
11/30/2018
30. Viral markers
• HBsAg: HBV infection
• HBsAg + IgM anti-HBc: acute HBV hepatitis
• IGM anti-HBc: acute HBV hepatitis during window period
• HBsAg + IgG anti-HBc: chronic HBV hepatitis
• HBeAg: high replication and infectivity
• Anti-Hbe: low replication and infectivity
• Anti-HBs: recovery from HBV infection or vaccination for HBV
11/30/2018
31. CON
• Absence of Hbe in the presence of HBV DNA indicate precore mutant
HBV
• HBV carrier: HBs Ag+ anti-Hbe+ normal LFT
11/30/2018
33. Transmissions of Hepatitis B
• Percutaneous inoculation a major route of hepatitis B
transmission(Blood & Blood products)
• semen and saliva
• Oral
• sexual contact
• perinatal transmission
• sub-Saharan Africa, intimate contact among toddlers
• All Body fluids
11/30/2018
34. HBV
• Incubation period from 30–180 days
• Prodromal syndrome
serum sickness–5-10% pts with fever,arthralgia,rash angeoedema
,nephritis
• Clinical jaundice:-- acute viral hepatitis
- fulminant hepatitis
• chronic hepatitis:--cirrosis
- hepatoma
- nephrotic syndrome
- polyarthritis nodosa
11/30/2018
36. Natural history
• 90% of adult HBV compelete recovery
• Case fatality rate 0.1%
• Risk of chronicity depending on the age of acquisition of HBV
-New born 90%
-Early childhood 20-50%
-Adult<5%
-Adult and immunocompromized>50%
11/30/2018
38. chronic HBV infection
HBsAg remains detectable beyond 6 months
anti-HBc is primarily of the IgG class
11/30/2018
39. Treatment for HBV
• IFN - should be avoided b/c of increased risk of hepatic
necroinflammation.
options
. Lamivudine
. Adefovir
. Tenofovir
. Entecavir
.Treament can be stopped after confirmation that the patient has cleared
HBSAg.
11/30/2018
41. HBV-- immunization
• hepatitis B immune globulin (HBIG), reducing the frequency of clinical
illness, not in preventing infection
• Active immunazation with three IM (deltoid, not gluteal) injections of
hepatitis B vaccine
• recommended at 0, 1, and 6 months
• Pregnancy is not a contraindication to vaccination
11/30/2018
44. 3.Hepatitis D
• The delta hepatitis agent HDV
• is a defective RNA virus that coinfects with and requires the helper
function of HBV for its replication and expression.
• The delta core is "encapsidated" by an outer envelope of HBsAg,
indistinguishable from that of HBV
• complete hepatitis D virions and liver injury require the cooperative
helper function of HBV
• intracellular replication of HDV RNA can occur without HBV.
11/30/2018
45. Coinfection Vs superinfection
• HDV simultaneously with HBV (co-infection)
• HDV infect a person already infected with HBV (superinfection)
11/30/2018
47. 4.Hepatitis C Virus: HCV
• Single stranded enveloped RNA flavivirus
• Cause of majority of cases previously known as non-A, non-B hepatitis
• First recognized in 1989
11/30/2018
48. Hepatitis C Virus: HCV
• Most common cause of chronic hepatitis in North America, Europe
and Japan
• High prevalence in general population:
• ~ 200 million worldwide
• ~ 4.5 million infected in US
• ~ 230,000 new cases per year in US
• ~ 8,000-10,000 deaths per year in US
11/30/2018
49. Natural history after acute HCV
• 15% cure
• 85 %chronic hepatitis
• have intermittent elevations in serum liver enzymes such as alanine
aminotransferase ( ALT)
• after 10 to 20 years, 2 to 20 per cent develop cirrhosis
• 20 per cent of those who develop cirrhosis will have a life-
threatening complication
ascites, variceal bleeding, hepatic encephalopathy hepatocellular
carcinoma.
11/30/2018
50. Hepatitis C Virus: HCV
• 80-90% of HCV infections related to blood
• – Hemodialysis from years ago
• – Tattoo parlors
• – Health care workers
• – IV drug users make up the largest percentage
• – Blood transfusions prior to 1990 when ARC began screening for HCV
antibody
• Vertical and sexual transmission inefficient
11/30/2018
51. Hepatitis C Virus: HCV
• No vaccine available
• • No completely effective treatment
• • Liver transplant
11/30/2018
52. Hepatitis C Virus: HCV
• Symptoms
• – Majority of infected patients are asymptomatic
• – Vague flu-like symptoms often go unnoticed
• – Jaundice ~25%
11/30/2018
53. HCV
• acute hepatitis C recovery is rare
• progression to chronic hepatitis is the rule
11/30/2018
54. Hepatitis C Virus: HCV
• Serological marker:
• HCV antibody detected in
• – 50-70% patients at onset of symptoms
• – 80% patients at 5-6 weeks post initial infection
• – 90% patients at 3 months post initial infection
• – Not protective: no immunity
11/30/2018
55. Hepatitis C Virus: HCV
• Laboratory:
• HCV antibody Used to diagnose
• – Indicates active infection with HCV
• – Patient considered to be infective
• Present in acute and chronic infection
• – Current assays can detect AB 9 weeks post exposure (method dependent)
11/30/2018
56. Hepatitis C Virus: HCV
• HCV RNA: tests for the RNA genomic fingerprint(1,2,3 & 4)
• AST and ALT
• Levels fluctuate widely after infection
• – Normal in ~33% of chronic HCV patients
• HCV-antibody is not protective: patients are considered to be
infective
11/30/2018
58. EXTRAHEPATIC MANIFESTATIONS OF HBV
&HCV
• a serum sickness–like syndrome in 5-10% of HBV
• Glomerulonephritis with the nephrotic syndrome
• Generalized vasculitis (polyarteritis nodosa)
• mixed cryoglobulinemia(EMC)
• HCV infection may be complicated by hepatic
steatosis,hypercholesterolemia, insulin resistance (and other
manifestations of the metabolic syndrome), and type 2 diabetes
mellitus.
11/30/2018
60. 5.Hepatitis E
• RNA virus
• cases occur after contamination of water
• An epidemiologic feature that distinguishes HEV from other enteric
agents is the rarity of secondary person-to-person spread from
infected persons to their close contacts
• HEV is the most common cause of acute hepatitis; one-third of the
global population appears to have been infected
• zoonotic reservoir for HEV in swine
11/30/2018
61. HEV
• Incubation period 14-60 ,mean40 days
• Onset : acute
• No chronic case
• Age preference: young adult(20-40)
• Transmission: feco oral
• Fulminent hepatitis 1-2%
10-20% pregnant
• No carrier
11/30/2018
62. HEV
• No risk hepatoma
• Prognosis good
• Diagnosis :anti-HEV,HEV RNA
• Prophylaxis : vaccine
• Therapy: none
11/30/2018
Editor's Notes
Acute liver failure is characterized by acute liver injury, hepatic encephalopathy, and an elevated prothrombin time/international normalized ratio (INR). It has also been referred to as fulminant hepatic failure, acute hepatic necrosis, fulminant hepatic necrosis, and fulminant hepatitis
Both the enterically transmitted forms of viral hepatitis, hepatitis A and E, are self-limited and do not cause chronic hepatitis (rare reports notwithstanding in which acute hepatitis A serves as a trigger for the onset of autoimmune hepatitis in genetically susceptible patients or in which hepatitis E can cause chronic liver disease in immunosuppressed hosts, e.g., after liver transplantation).
After acute illness, anti-HAV of the IgG class remains detectable indefinitely, and patients with serum anti-HAV
are immune to reinfection.
A detectable hepatitis C virus (HCV) RNA by polymerase chain reaction (PCR) in the setting of undetectable anti-HCV antibodies that subsequently become detectable within 12 weeks is generally considered definitive proof of acute HCV infection
HCV RNA can be detected within a few days of exposure to HCV—well before the appearance of
anti-HCV—and tends to persist for the duration of HCV infection
The most sensitive indicator of HCV infection is the presence of HCV RNA,
