Viral Hepatitis Flashcards
Pan-genotypic HCV regimens
GLE/PIB
SOF/VEL
Hawthorne Effect
Hawthorne Effect: Intervention group is more likely to improve because it is aware of being observed. 1. More likely to occur when the baseline data are collected retrospectively and intervention data are collected prospectively
Acute presentation of viral hepatitis
All viral hepatitis infections cause an acute infection. Depending on the viral pathogen, the individual’s immune system may be able to fight off the infection, resulting in self-limited acute infection, but the proportion of patients developing chronic infection varies by age, infectious agent, and other patient characteristics.
There are no differentiating symptoms between the different types of viral hepatitis (A–E). In many cases, acute symptoms are mild or go unnoticed
When present, possible signs and symptoms include:
a. Fever
b. Fatigue
c. Loss of appetite
d. Nausea or vomiting
e. Abdominal pain
f. Dark urine
g. Clay-colored bowel movements
h. Joint pain
i. Jaundice
Signs of decompensated cirrhosis
Decompensated cirrhosis i. Decompensated cirrhosis is defined as presence of: (a) Bleeding varices (b) Ascites (c) Spontaneous bacterial peritonitis (d) Hepatic encephalopathy (e) Hepatorenal syndrome (f) Hepatocellular carcinoma (g) Jaundice
Child-Pugh components
Bilirubin, albumin, INR, ascites, encephalopathy
Natural history of HAV
Average incubation period for HAV is 28 days (range 15–50 days)
Peak infectivity can be present 2 weeks before and 1 week after symptoms begin.
HAV causes an acute viral hepatitis only and does not cause a chronic infection. 2. Up to 70% of children younger than 6 years are asymptomatic. More than 70% of older children and adults will have jaundice. 3. When present, symptoms usually last less than 2 months. Around 10% of symptomatic individuals have prolonged or relapsing disease for up to 6 months.
Diagnosis of HAV
HAV cannot be diagnosed on the basis of clinical presentation only. Laboratory evaluation is necessary to distinguish HAV from other types of viral hepatitis.
Elevated anti-HAV (IgM antibodies) can distinguish acute HAV infection from other types of hepatitis. IgM antibodies are detected 5–10 days postexposure
HAV vaccine recommendations
Recommended groups for vaccination include: (a) All children at age 1 year
(1) Travelers to high- or intermediate-risk countries
(2) Men who have sex with men
(3) People who inject drugs
(4) Individuals with potential for occupational exposure
(5) Household members of newly adopted children from countries with high endemicity
(c) Individuals at risk of complications from HAV infection
(1) Chronic liver disease, including those awaiting or who have received liver
transplantation
(2) Clotting factor disord
Post exposure prophylaxis for HAV exposure
Previously unvaccinated individuals recently exposed to HAV should receive a single dose of
single-antigen HAV vaccine or immunoglobulin (0.02 mL/kg) as soon as possible and within
2 weeks of exposure.
b. Close personal contacts of individuals with confirmed HAV infection on the basis of anti-HAV
IgM should receive postexposure prophylaxis, including:
i. Household contacts
ii. Sexual partners
iii. Individuals who have shared illicit drugs with an infected source patient
iv. Child care center staff, attendees, and attendees’ household members when:
(a) One or more HAV cases are confirmed in children or employees
(b) Two or more HAV cases are confirmed in households of center attendees
v. Restaurant staff who directly handle food if infected person was also a food handler
HBV natural history
. 4. Mean incubation period for onset of symptoms is 90 days (range 60–150 days) after exposure
Acute HBV 1. Most adults (more than 95%) with acute HBV infection recover spontaneously without treatment
Around 30% of patients with chronic HBV develop cirrhosis, 23% of whom decompensate within 5 years.
HBV infection Phase I characteristics
Phase 1: HBeAg-positive chronic HBV infection, which corresponds to “immune-tolerant” phase, is characterized by presence of HBeAg, very high concentrations of HBV DNA, and persistently normal ALT (less than 40 IU/mL). In the liver, there is minimal or no necroinflam- mation or fibrosis.
Phase 2 HBV infection
Phase 2: HBeAg-positive chronic HBV infection, which corresponds to “immune-tolerant” phase, is characterized by presence of HBeAg, high concentrations of HBV DNA, and ele- vated ALT (greater than 40 IU/mL). In the liver, there is moderate or severe necroinflamma- tion and accelerated progression of fibrosis.
Phase 3 HBV infection
Phase 3: HBeAg-negative chronic HBV infection, previously termed inactive carrier phase, is characterized by presence of antibodies to HBeAg (anti-HBe), undetectable or low HBV DNA concentrations, and ALT concentrations less than 40 IU/mL. Some patients can have elevated HBV DNA, but usually, these correspond with less than 20,000 IU/mL. These patients have minimal necroinflammatory activity and low fibrosis and are generally at low risk of progress- ing to cirrhosis or hepatocellular carcinoma if they remain in this phase. HBsAg loss and/or seroconversion can occur spontaneously in 1%–3% of cases per year.
Phase 4 HBV infection
Phase 4: HBeAg-negative chronic HBV is characterized by negative HBeAg, usually with detectable anti-HBe and persistent or fluctuating concentrations of serum HBV DNA at mod- erate/high concentrations. These patients also have persistently elevated or fluctuating ALT concentrations. Liver histology reveals necroinflammation and fibrosis. Spontaneous disease remission rates are low.
Phase 5 HBV infection
Phase 5: HBsAg-negative phase is characterized by undetectable HBsAg and positive anti- bodies to HBcAg (anti-HBc), with or without detectable antibodies to HBsAg (anti-HBs). This phase is analogous to “occult HBV infection” in prior nomenclature. These patients have nor- mal ALT values and usually have undetectable HBV DNA. Immunosuppression can lead to HBV reactivation (HBVr) in these patients.
