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Medicine > Heptites A > Flashcards

Heptites A Flashcards

1
Q

What is etiologic agent of hepatitis A?

A

Hepatitis A Virus (HAV). HAV is highly infectious.

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2
Q

Is HAV infectious?

A

HAV is highly infectious.

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3
Q

What is Reservoir and transmission?

A
  • Humans are the nearly exclusive reservoir of HAV (with rare exceptions of chimpanzees and other
    primates).
  • The virus is extensively shed with feces.
  • Infection is most commonly by the fecal–oral route.
  • Transmission occur from physical contact with an infectious individual or sewage contamination in
    waterborne outbreaks.
  • Sexually transmitted infection that includes oral-anal contact.
  • Transmission through contaminated needles are also possible (the latter mainly in injection drug
    users).
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4
Q

What are risk factors of hav?

A

Risk factors:
- Traveling to endemic areas.
- Close contact with infected individuals (eg, household contacts.)
- Close contact (household or professional) with children attending nursery or preschool.
- Consumption of seafood (shellfish&raquo_space;> raw oysters.) - Sex (especially men who have sex with men [MSM]). - Waste or sewage management, as well as maintenance of equipment used for such purposes.
- Epidemics caused by the consumption of contaminated food and water may also occur.

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5
Q

What is the Incubation and contagious period of ha?

A

Incubation period is usually from 15 to 50 days (on average ~28 days).
- The virus is shed with feces for 1 to 2 weeks before and ~1 week after the onset of signs and
symptoms (the contagious period).
- Patients are no longer contagious 7 days after jaundice occurs.

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6
Q

When patients who have HAV stop being contagious?

A

Patients are no longer contagious 7 days after jaundice occurs.

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7
Q

** HAV does not cause chronic hepatitis.***

A
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8
Q

What is thr clicial features of HAV? ( meet all other Hepatitis acute infection)

A

A non-specific prodromal illness characterized:
1. Headache
2. Myalgia
3. Arthralgia
4. Nausea
5. Anorexia
6. Jaundice.
7. Dark urine and pale stools
8. Vomiting
9. Diarrhea
10. Abdominal discomfort.

• Physical signs:
1. The liver is often tender but only minimally enlarged.
2. Mild splenomegaly
3. Cervical lymphadenopathy

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9
Q

When do we say this is an acute hepatitis?

A

Less than 6 months

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10
Q

What is the investigations needed in acute hepatitis?

A
  1. Liver function test (LFT):
    • A hepatitic pattern of LFTs develops (ALT and AST&raquo_space; ALP and GGT.)
    • Sometime cholestatic pattern develops (HAV) (ALP and GGT&raquo_space; ALT and AST)
    • Serum transaminases typically between 200 and 2000 U/L in an acute infection
    (usually lower and fluctuating in chronic infections).
    • The ALP rarely exceeds twice the upper limit of normal.
    • The plasma bilirubin reflects the degree of liver damage.
    • Prolongation of the PT indicates the severity of the hepatitis but rarely exceeds 25
    seconds, except in rare cases of acute liver failure.
    • The white cell count is usually normal with a relative lymphocytosis.
  2. Serological tests confirm the etiology of the infection
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11
Q

How to diagnose HAV?

A
  1. Serologic tests: - The basis for diagnosis is the finding of positive serum anti-HAV IgM antibodies.
  • The antibodies confirm a recent infection.
  • They may persist for up to 4 to 6 months and are gradually replaced by anti-HAV IgG antibodies, which
    persist for life (indicates immunity.)
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12
Q

How do we know if this patient has immunity to HAV?

A

They may persist for up to 4 to 6 months and are gradually replaced by anti-HAV IgG antibodies, which
persist for life (indicates immunity.)

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13
Q

How to treat HAV?

A

Most individuals do not need hospital care.
• Supportive therapy.

• Drugs such as sedatives and narcotics, which are metabolized in the liver
should be avoided.
• No specific dietary modifications are required. • Elective surgery should be avoided in cases of acute viral hepatitis, as
there is a risk of post-operative liver failure.
• Liver transplantation is very rarely indicated.

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14
Q

What is the prevention of HAV?

A

Vaccination is the key method of primary prevention (People travelling to endemic area, close
contacts of HAV-infected patients, individuals with chronic hepatitis B or C infections.)
- Strict hand hygiene

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15
Q

What do you know about HB antigens?

A
  1. Hepatitis B surface antigen (HBsAg): is an indicator of active infection.
  2. Hepatitis B core antigen (HBcAg):
    - Not found in the blood, but antibody to it (anti-HBc) appears early in the illness which subside
    gradually but then persists: - Two types of anti-HBc : IgM (acute infection) and IgG (chronic infection)
    - Anti-HBc is initially of IgM type, with IgG antibody appearing later.
    - Anti-HBc (IgM) can sometimes reveal an acute HBV infection when the HBsAg has disappeared and
    before anti-HBs has developed (Window period).
  3. Hepatitis B e antigen (HBeAg) is an indicator of active viral replication.
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16
Q

What etiologic agent of HBV?

A

Etiologic agents: Hepatitis B virus (HBV.)

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17
Q

What is Reservoir and transmission of HBV?

A
  • The only HBV reservoir is individuals with active disease or carriers.
  • Routes of transmission include parenteral* (contact with infected blood and blood-contaminated
    instruments), sexual, and perinatal transmission
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18
Q

What is the Incubation and contagious period of HBV?

A
  • The incubation period is from 28 to 160 days (average, 70-80 days).
  • Patients with positive serum HBeAg tend to be more contagious because of the presence of high
    levels of HBV DNA in the blood.
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19
Q

What is the risk factor of HBV?

A
  • Close contact with a person with HBV infection (household contacts, sexual contacts)
  • Treatment with blood products, hemodialysis, multiple sexual partners,
  • IV drug use
  • Occupational exposure to blood and body fluids (health-care professionals),
  • Being a prison inmate.

• The risk of vertical mother-to-child transmission without interventions:
- ~90% for HBeAg-positive mothers
- ~10% for HBeAg-negative HBsAg-positive mothers

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20
Q

What is the clinical symptoms and signs of acute HBV?

A

A non-specific prodromal illness characterized:
1. Headache
2. Myalgia
3. Arthralgia
4. Nausea
5. Anorexia
6. Jaundice.
7. Dark urine and pale stools
8. Vomiting
9. Diarrhea
10. Abdominal discomfort.

• Physical signs:
1. The liver is often tender but only minimally enlarged.
2. Mild splenomegaly
3. Cervical lymphadenopathy

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21
Q

How to diagnose acute HBV?

A
  1. Virologic tests: Measurements of serum HBV DNA levels.
  2. Serologic tests:
    - HBV antigens (HBsAg, HBeAg)
    - specific antibodies (anti-HBc IgM and IgG, anti-HBe, anti-HBs)
    • Anti-HBc IgM positivity being an important marker of acute hepatitis B
    in the “window period” (the period between disappearance of HBsAg
    and appearance of anti-HBs antibodies).
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22
Q

There is a pic for HEPATITIS B VIRUS

A
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23
Q

What is the complications of acute HBV?

A
  1. Acute liver failure: (rapid development of encephalopathy and impaired liver synthetic function)
    - The most serious complication (~1% of patients)
    - More frequently in young women and in 30%-40% of patients with hepatitis D virus [HDV] coinfection.
  • The risk is also higher in patients with preexisting hepatitis C virus [HCV] infection.
  1. Extrahepatic complication (caused by immune complexes) include:
    - Systemic vasculitides (eg, polyarteritis nodosa), polymyalgia rheumatica, erythema nodosum,
    glomerulonephritis and nephritic syndrome (more common in children),
    - Mixed cryoglobulinemia (abnormal proteins that thicken and clump together at cold temperatures) ?
    - Myocarditis.
    - Guillain-Barré syndrome.
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24
Q

How to treat patients with acute HBV?

A

Supportive therapy.
High rates of spontaneous HBV clearance in adult.

25
Q

What is the prognosis of acute HBV?

A

Acute hepatitis B may progress to chronic hepatitis B in:
- 90% of neonates and infants .
- 30% of children aged 1 to 5 years .
- 2% to 5% of older children and adults.
• Risk factors for progression to chronic disease include perinatal or early childhood
infection, high exposure to the virus, male sex, advanced age, immunosuppression, and use of glucocorticoids.
• Mortality is <1% and is mainly due to fulminant liver failure.
The course is more severe in patients with HCV or HDV coinfection

26
Q

How to prevent acute HBV?

A

Vaccination is the key method of
primary prophylaxis.

•Passive immunoprophylaxis with
hepatitis B immunoglobulin (HBIG) is used mostly to prevent vertical transmission to the newborn.

27
Q

What is chronic HBV?

A

• Chronic hepatitis B is a chronic (>6 months) liver disease that is characterized by
necroinflammatory lesions
• HBV DNA can integrate into the host’s genome of hepatocytes and other cells.

• Signs and symptoms: Most patients have no symptoms for a long time.

28
Q

What is the complications of chronic HBV?

A

a) Cirrhosis
b) HCC
b) Extrahepatic complications caused by immune complexes: Polyarteritis nodosa, leukocytoclastic vasculitis, glomerulonephritis, and polymyalgia rheumatica.

Chronic HBV infection can cause hepatocellular carcinoma (HCC) with or without cirrhosis.

29
Q

How to manage a patient with chronic HVB?

A

Treatments are still limited, as no drug is consistently able to eradicate hepatitis B infection completely.

• The goals of treatment are HBeAg seroconversion, reduction in HBV-DNA and
normalization of the LFTs.

• The indication for treatment is a high viral load in the presence of active hepatitis, as
demonstrated by elevated serum transaminases and/or histological evidence of inflammation and fibrosis. (see next slide)

30
Q

There are Two different types of drugs are used to treat chronic hepatitis B:

A
  1. Direct-acting nucleoside/nucleotide analogues (Lamivudine, Entecavir and tenofovir)
  2. Pegylated interferon-alfa.
31
Q

When the treatment of chronic HBV indicated?

A

Treatment is indicated in
1-immune reactive &
2-HBeAg-negative chronic hepatitis B

There is a pic in photos.

32
Q

What is importanat in follow up patients with chronic HBV?

A

• Monitoring for HCC is usually done every 6 months.
• Screening modality: Abdominal ultrasonography +/- Alpha-fetoprotein (AFP) every
6 months remains the standard.

• In patients not currently meeting the criteria for therapy, monitoring of liver function
tests and liver enzymes (ALT) should be performed every 3 to 6 months and HBV DNA every 6 months.

• Ideally, evaluation of liver fibrosis should be updated every 1 to 3 years, depending on
the HBeAg status and HBV DNA.

33
Q

is Acute HCV often ? And what is its etiologic agent?

A

Acute symptomatic infection with hepatitis C is rare .

Etiologic agent: Hepatitis C virus (HCV).

34
Q

What is Reservoir and transmission?x

A
  • The only HCV reservoir is patients with hepatitis C.
  • The routes of transmission include contact with blood, blood products, nonsterile medical
    instruments or nonmedical equipment, such as razor blades, needles and syringes in injection
    drug users, toothbrushes).
  • The risk of HCV transmission to a sexual partner is uncommon.
35
Q

Is it common to have sexual transmission of HCV?

A
  • The risk of HCV transmission to a sexual partner is uncommon.
36
Q

What are the risk factors of HCV?

A

Injection drug use.
- The risk of neonatal infection from a seropositive mother is ~2%.

  • 4% to 7% in the case of mothers with positive serum HCV RNA on the day of delivery.
  • 15% in mothers with HIV coinfection.
37
Q

What is the incubation and contagious period of HCV ?

A
  • The incubation period is 15 to 160 days (average, 50 days).
  • Patients are contagious starting ≥1 week before the onset of symptoms and remain
    contagious as long as HCV RNA is positive.
  • HCV particles are contagious on environmental surfaces for up to 6 weeks.
38
Q

Clinical features and natural history of HVC?

A
  • Most patients with HCV infection are asymptomatic.
  • HCV clearance in acute hepatitis C is observed in 15% to 20% of patients.
  • The remaining patients develop chronic hepatitis C, out of which 5% to 20% may progress to
    liver cirrhosis within 20 to 25 years.
39
Q

How to diagnose a HCV patient?

A

1- Virologic tests:
- HCV RNA can be detected in serum as early as 1 to 3 weeks from infection (because it is
detectable intermittently, HCV infection cannot be excluded on the basis of a single test result
and repeat testing is necessary).

  1. Serologic tests:
    - Anti-HCV antibodies are detected 4 to 10 weeks from infection (average, 7 weeks).
    - At the onset of symptoms, anti-HCV are detectable in 50% to 70% of patients, and at
    3 months, in >90%.
  • The results may be negative in patients who are immunocompromised or treated with
    hemodialysis.
40
Q

How to treat HCV virus?

A
  1. Antiviral treatment:
    - Was previously recommended after 24 weeks of diagnosis and the regimen was similar
    to chronic hepatitis C. (see slide 37).
    - However, the 2017 guidelines from the European Association for the Study of the
    Liver (EASL) recommend treatment at the time of diagnosis with a direct-acting
    antiviral (DAA) regimen that is similar to that used in chronic hepatitis .. (slide 37)
41
Q

Follow up of HCV?

A

• Perform follow-up virologic studies (HCV RNA levels) at 6 months to exclude chronic
hepatitis even if ALT levels are normal.
• Patients should be tested for hepatitis B virus, HIV, and other sexually transmitted
infections, if appropriate.
• Provide education and counseling regarding prevention of further transmission,
especially avoiding blood donation and avoiding sharing needles in IV drug users.
• Encourage vaccination against hepatitis A and B if the patient is not immune.

42
Q

What are the complications and prognosis of HCV?

A

• Complications:
1. Acute liver failure (<1% of patients).
2. Complications caused by immune complexes: Glomerulonephritis, mixed
cryoglobulinemia (more frequent in patients with chronic hepatitis C).
3. Progression to chronic hepatitis C.

• Prognosis:
- Mortality is low and mainly due to the rare fulminant hepatitis (primarily in
patients with HCV and hepatitis virus A or B coinfection).

43
Q

How to prevent HCV ?

A

.No specific vaccines or immunoglobulins are available.
• The key prevention method is adherence to the general rules of prevention of blood-
borne infections.
• Instruct the patient how to reduce the risk of infecting others by preventing contact with the patient’s personal belongings that may be contaminated with blood (eg,
toothbrushes, razors, needles, syringes).
• Patients should adhere to safe-sex practices.
• HCV-positive women may continue breastfeeding.

44
Q

• HCV-positive women may continue breastfeeding.

A
45
Q

What do we know about CHRONIC HCV?

A

• Chronic hepatitis C is a chronic (>6 months) disease characterized by hepatic
necroinflammatory changes.

46
Q

What are the complication of chronic HCV if left untreated?

A

a) Cirrhosis.(Risk factors for progression from chronic hepatitis to cirrhosis include male gender,
immunosuppression (such as co-infection with HIV), prothrombotic states and heavy alcohol misuse.
)

b) HCC (HCC without liver cirrhosis is rare).

c) Extrahepatic complications caused by immune complexes: Polyarteritis nodosa, vasculitis, glomerulonephritis, and polymyalgia rheumatica.

47
Q

How to treat chronic HCV?

A

• The aim of treatment is to eradicate infection • The viral clearance achieved 6 months after finishing treatment (termed sustained virological
response, SVR) have risen from less than 40% a decade ago to levels approaching 100%.
• The infection is cured in more than 99% of patients who achieve an SVR.

48
Q

What medication used to treat chronic HCV?

A

Medications: A combination of direct-acting antiviral (DAA) agents is the current standard
of therapy (+/- ribavirin). (see next slide)
• DAA monotherapy is unacceptable due to the risk of selection of resistant strains.
• pegylated interferon-alfa were used treat HCV in the past but anymore.

• Response to treatment: Negative serum HCV RNA levels

49
Q

What is etiologic factor of HDV( delta virus)?

A
  • Hepatitis D (delta) virus (HDV)
  • RNA virus that is capable of replication only in the presence of hepatitis B virus (HBV).
  • Acute hepatitis D may be a result of coinfection (simultaneous infection with HBV and
    HDV) or HDV superinfection in an HBV carrier.
  • The virus is present worldwide, affecting about 5% of all HBV patients.
  • The reservoir, route of transmission, and risk factors are as in hepatitis B.
50
Q

What is he incubation of HDV?

A

21 to 140 days (average, 35 days).

51
Q

What is Clinical features and natural history?

A

The course of HBV/HDV coinfection is similar to that of hepatitis B.
• HDV superinfection in a patient with chronic HBV infection leads to exacerbation of the
disease, resulting in progression to acute liver failure (particularly in asymptomatic HBV carriers).
• HDV can cause chronic hepatitis.
• Chronic HDV infection develops in 70% to 90% of patients with superinfection.

52
Q

Haw to diagnose HDV patient?

A

• Hepatitis delta antigen [HDAg]) is present in the blood only in the first few days of disease.
• The diagnosis of HBV/HDV coinfection is made in patients with high serum anti-HBc IgM and anti-HDV IgM levels.
• Anti-HDV IgM persist for ~6 weeks (in exceptional cases for 12 weeks) and are then
replaced by anti-HDV IgG.
• Levels of HBsAg are low or undetectable (due to suppression by HDV; often this also
affects anti-HBc IgM).
• In the case of HDV superinfection in an HBV-infected patient, anti-HDV IgM are
detected, which are subsequently replaced by anti-HDV IgG; for some time both antibody classes can be detected in serum.

*Anti-HBc IgM are not detected.

53
Q

How to treat in patients with HDV?

A

• There are no guidelines for the treatment of acute HDV infection.
• In patients with chronic HDV infection, the recommended treatment is pegylated
interferon alpha-2a administered for 48 weeks.

• In those with HBV DNA, nucleoside analogue (NA) therapy may be of benefit. • The prognosis is worse in individuals with HBV-HDV coinfection compared with HBV
infection alone in terms of rapid progression to cirrhosis and development of hepatocellular carcinoma.

54
Q

How to prevent HDV?

A

hepatitis B vaccination

55
Q

What is the etiologic agent for HEV?

A

Etiologic agent: Hepatitis E virus (HEV).
Eight genotypes are known in this group.
- Genotypes 1 and 2 cause human infections only.
- Transmitted in contaminated water sources by the fecal-oral route.
- Outbreaks tend to occur in areas with poor hygiene.
- Genotypes 3 and 4 are zoonotic, most commonly found in pigs (true primary host).
- Humans become infected when they consume infected meat.
- Pathogenesis is not fully known. The primary site of viral replication is probably the
gastrointestinal tract.

56
Q

What is Clinical features, natural history, and prognosis?

A
  • In the majority of patients (up to 80%) HEV infection is asymptomatic.
  • Manifestations of symptomatic HEV infection are as in other types of acute viral hepatitis.
57
Q

Mortality rates in HEV?

A

• Estimated mortality rates:
- 0.2% to 4% in young adults
- Up to ~10% in children <2 years
- 10%-25% in pregnant women due to obstetric complications and fulminant liver failure).
- In middle-aged and elderly men rarely fatal.
• The antibodies that develop after HEV clearance are nonprotective and reinfections can occur.
• Chronic infections (only in the case of HEV genotype 3) may occur, particularly in
immunosuppressed patients.

58
Q

How to diagnose HEV?

A

• Laboratory test results are the same as in other types of acute viral hepatitis.
• Diagnosis is usually based on the detection of serum anti-HEV antibodies (IgM antibodies
appear in the prodromal period and are then replaced by IgG antibodies).
• The most reliable finding for hepatitis E is a positive serum HEV RNA test result. • Chronic infection is diagnosed in patients with serum HEV RNA persisting >3 months.

59
Q

How to treat and prevent HEV patients?

A

• Most cases of acute HEV infection are self-limiting and do not require antiviral therapy.
• In patients with severe acute HEV or acute-on-chronic liver failure, the use of ribavirin may be
considered for 3 months.
• In addition, patients with primary liver disease infected with HEV genotype 3 and those receiving
immunosuppressive drugs in doses that cannot be reduced or in whom dose reduction is ineffective
may consider ribavirin 600 to 800 mg/d for ≥3 months as monotherapy or in combination with
peginterferon alpha.

• Prevention:
- In endemic regions improvement of hygiene standards, including water supply, is necessary.
- Hepatitis E vaccine against genotype 4 HEV is approved in China but does not provide immunity.

Medicine (13 decks)

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