The Slide covers for the- Hepatitis B Virus and Infection. INTRODUCTION, MODES OF TRANSMISSION, HIGH RISK GROUPS, PATHOGENESIS, CLINICAL MANIFESTATION, DIAGNOSIS, PROPHYLAXIS, PREVENTION.
The Slide covers for the- Hepatitis B Virus and Infection. INTRODUCTION, MODES OF TRANSMISSION, HIGH RISK GROUPS, PATHOGENESIS, CLINICAL MANIFESTATION, DIAGNOSIS, PROPHYLAXIS, PREVENTION.
Viral hepatitis is a systemic disease primarily involving the liver.
Hepatotropic viruses : liver is the target organ and the main site of virus replication
Hepatitis A virus (HAV)
hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV, delta virus)
Hepatitis E virus (HEV).
Enterically:
virus is spread from person-to-person by putting something in the mouth that has been contaminated with the stool of a person with hepatitis E. This type of transmission is called "fecal-oral." For this reason, the virus is more easily spread in areas where there are poor sanitary conditions
Hepatitis" means inflammation of the liver and also refers to a group of viral infections that affect the liver .
The most common types are Hepatitis A, Hepatitis B, and Hepatitis C.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation.
An estimated 4.4 million Americans are living with chronic hepatitis; most do not know they are infected
Hepatitis B virus HBV infection in detailsHassn Aljubory
Presentation
serological markers
Laboratory test
vaccinations
Chronic hepatitis B
Approach
Harrison
Davidsons
Step up medicine
Mksap
Notes & notes
Gastrointestinal disease
Hepatology
Risk group
Management
Hepatitis in pregnancy
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Pharma Pcd Franchise in Jharkhand - Yodley Lifesciences
Hepatitis B In children by Dr. kaniz fathema, resident, paediatric Gastroenterology, BSMMU,Bangladesh
1. Presented by
Dr. Kaniz Fathema
Resident, Phase- B (year 4)
Paediatric Gastroenterology & Nutrition
B S M M U
Hepatitis B virus infection
in children and adolescents
6. Pathogenesis
HBV is a predominantly noncytopathogenic virus that
causes injury mostly by immune-mediated processes.
most complete immune response being associated with the
greatest likelihood of viral clearance but also the most severe
injury to hepatocytes.
infection of hepatocytes by HBV, resulting in expression of viral
antigens (nucleocapsid antigens—HBcAg and HBeAg) on the
cell surface.
These antigens, in combination with class I major
histocompatibility proteins, make the cell a target for cytotoxic
T-cell lysis.
Circulating immune complexes containing HBsAg can result in
extrahepatic manifestation
Fulminant HBV due to hyper-vigorous immune response
7. Routes of transmission
Hepatitis B virus can be transmitted via body fluids, either through mother-to-
infant transmission (70 – 80%) or horizontally through blood transfusion,
injection, sexual exposure, or close contact in the family or with caretakers.
Intrauterine HBV infection occurs rarely, in <5% of the infants of HBeAg- and
HBsAg-positive mothers.
most perinatal HBV transmission occurs at or near the time of birth, 90 percent of
these infants will acquire acute HBV infection if no preventive measures are
taken.
High infectivity : 0.0002 ml of infected blood is sufficient
Stable in environment for 7 days
8. High Intermediate Low
Carrier rate ≥8% 2 to 7% ≤1%
Predominant age
at infection
Perinatal and
early childhood
Early childhood Adult
Predominant
mode of infection
Mother to child;
percutaneous
Percutaneous;
sexual
Percutaneous;
sexual
Epidemiology and modes of transmission of
9. Age of infection Rate of persistent infection
Perinatal period
Mother HBeAg(+), HBsAg(+) >90%
Mother HBeAg(-),
HBsAg(+)
<5%, but with risk of acute or
fulminant hepatitis
Preschool age 23%
Young adults 2.7~10%
10. Risk of chronic hepatitis B virus carriage by age of infection
11. Why perinatal infection become chonic
The relatively high maternal viral load transmitted to the
neonate with a physiologically immature immune system
during perinatal period .
The e antigen is a small viral secretory protein that can cross
the placenta barrier. As both HBeAg and HBcAg are highly
cross-reactive in terms of helper T-cell recognition,
transplacental HBeAg may induce a specific unresponsiveness
of helper T-cells to HBeAg and HBcAg in the neonates born to
HBeAg-positive, HBsAg positive mothers .
the coreprotein or major histocompatibility class I protein
might not be recognized, the cytotoxic lymphocytes might not
be activated.
12. Spectrum of clinical illness
Acute :
1. Sub clinical or an-icteric hepatitis
2. Icteric hepatitis
3. Fulminant hepatitis
Chronic :
1. Asypmtomatic HBsAg carrier state
2. Chronic hepatitis
3. Cirrhosis
4. Hepatocellular carcinoma
16. Interpretation of the hepatitis B serologic panel
HBsAg anti-HBc anti-HBs Interpretation
N N N Susceptible
N Positive Positive Immune due to
natural infection
Negative Negative Positive Immune due to
hepatitis B
vaccination
Positive Positive
anti-HBc
IgM
Negative Acutely infected
Positive anti-HBc
Positive
Positive Chronically infected
IgM anti-
HBc
Negative
Negative Positive Negative Four interpretations
possible
17. Four interpretations:
1. Might be recovering from acute HBV infection.
2. Might be distantly immune and test not sensitive enough to
detect very low level of anti-HBs in serum.
3. Might be susceptible with a false positive anti-HBc.
4. Might be undetectable level of HBsAg present in the
serum, and the person is actually chronically infected.
18. Acute HBV infection
The incubation period lasts one to four months.
A serum sickness-like syndrome may develop during the
prodromal period, followed by mostly mild constitutional
symptoms, anorexia, nausea, jaundice, and right upper
quadrant discomfort.
The symptoms and jaundice generally disappear after one to
three months, but some patients have prolonged fatigue even
after normalization of serum aminotransferase concentrations.
20. Acute hepatitis
HBsAg +ve
AntiHBc
IgM +ve
Acute Hep B
No Rx
>90% will recover.
and clear HBsAg
5-10% will
progress to CHB
Anti HBcIgM -ve
Chronic Hepatitis B
Follow up child , if
HBsAg positive after
6 months - Chronic
22. MANAGEMENT OF ACUTE HBV
supportive management alone.
severe acute hepatitis, treatment with a nucleoside/tide
analog might be considered.
fulminant hepatitis caused by HBV, liver transplant may
be necessary.
23. Chronic HBV infection
Asymptomatic and grow and develop normal
vague right upper quadrant discomfort and fatigue.
Extrahepatic manifestations.
chronic HBV infection is characterized by persistently
positive HBsAg > 6 month.
In contrast with acute HBV, total anti-HBc is usually
positive (because of the immunoglobulin G [IgG]
component), while IgM anti-HBc is negative (unless during
a flare of chronic HBV).
24. Rates of spontaneous seroconversion (loss of HBeAg) are
less than 2 percent per year in children younger than three
years of age, and increase to about 8 percent per year during
puberty and young adulthood.
25. History
risk factors for coinfection with HCV and/or HIV, use
of alcohol, and family history of HBV infection, liver
disease, and liver cancer.
physical examination
assess for growth parameters and for signs of chronic
liver disease
26. Laboratory testing
Initial evaluation:
Complete blood count with platelets, albumin, and prothrombin time-----
normal in children with chronic HBV.
Liver biochemical tests (ALT,AST, total bilirubin,ALP)
tests for HBV replication HBeAg, HBeAb, and HBV DNA.
Testing for coinfectio--- HCV, HAV, HDV, HIV
Additional evaluation :
other causes of liver disease in children with signs and symptoms that are
atypical for HBV
Screening for HCC
Liver biopsy for patients who are being considered for treatment of
chronic HBV infection
Testing for HBV genotype is not necessary at the time of diagnosis
27. Chronic HBV infection (HBsAg-positive for >6 months with positive (total) anti-HBc, and negative IgM anti-HBc.)
+ + + - - +++
(Serum HBV typically >1
million international
units/mL) (HBV DNA
>20,000 international
units/mL or 105 copies/mL)
Normal or mildly
elevated(ALT <2
times the upper
limit of normal)
Immune-tolerant phaseΔ
+ + + - - +++
(Serum HBV >20,000
international units/mLor
105 copies/mL) )
Persistently
elevated(ALT >1.5
to 2 times the
upper limit of
normal)
Immune-active HBeAg-
positive / immune
clearance (HBeAg-
positive chronic hepatitis)
+ - + - + ++
(Serum HBV >2000
international units/mL)
Elevatednormal or Immune-active, HBeAg-
negative OR reactivation
OR HBeAg-negative
chronic HBV or HBeAg-
negative replicative phase
HBeAg-negative chronic
hepatitis
+ - + + - to ++
(Serum HBV ≤2000
international units/mL)
Normal or mildly
elevated
Inactive chronic HBV OR
latent, nonreplicative or
inactive carrier
- - ±(ge
neral
± ± + in liver; - to + in serum Normal Occult HBV
H
Bs
A
g
H
Be
Ag
Ig
M
anti
-Bc
Total
anti-
HBc*
Ant
i-
HB
s
Anti
-
HBe
HBV DNA ALT¶ Interpretation
31. screened for HBV regardless of their vaccination
history
Individuals born in areas with high (≥8%) or
intermediate (≥2%) prevalence rates for HBV.
Pregnant women
Those requiring immunosuppressive therapy
Donors of blood, plasma, organs, tissues, or semen
Infants born to HBV-infected mothers
32. screened if they were not vaccinated or were
vaccinated but did not have screening prior to
vaccination
infants whose parents were born in regions with high HBV
endemicity (≥8%)
Household and sexual contacts of HBsAg-positive persons
Persons who have ever injected drugs
Persons with multiple sexual partners and/or history of
sexually transmitted diseases
Men who have sex with men
Inmates of correctional facilities
Individuals with chronic liver disease
Individuals with HIV infection
Individuals infected with HCV
Patients with end-stage renal disease.
34. VACCINE FORMULATIONS
TYPE: Single antigen vaccines , Combination vaccines
Storage : between 36 and 46°F (2 and 8°C) .
Efficacy : >90% in preventing HBV infection
Vaccine-induced immunity : long lasting .
Routine booster doses are not necessary for children and
adolescents with normal immune status.
Route : intramuscularly (IM)
Site: anterolateral thigh (for children <3 years) or deltoid (for
children ≥3 years).
35. Inappropriate administration
Intervals that were too short (eg, <4 weeks between the first
and second dose; <8 weeks between the second and third
dose; or <16 weeks between the first and third dose); doses
administered four or fewer days less than these intervals are
considered valid
Receipt of the final dose of the primary infant series at <24
weeks of age;
Administration by a route other than intramuscular
Administration at a site other than the anterolateral thigh or
deltoid
36. Catch-up hepatitis B (HepB) vaccine
●unvaccinated or incompletely vaccinated against HBV
●unknown or uncertain vaccination status
●received doses of HepB vaccine that were administered
inappropriately, unless serologic testing (if performed)
indicates that they responded adequately.
HepB vaccine series does not need to be restarted if it
was interrupted
37. POSTEXPOSURE IMMUNIZATION
with or without adjunctive hepatitis B immune globulin
is recommended for unvaccinated or incompletely
vaccinated children and adolescents with exposure to
blood or infectious secretions (eg, bite, needlestick,
sexual assault).
38. prevaccination serology
not routinely necessary.
The risk of adverse effects is not increased in
persons who are immune to HBV because of past
infection or immunization .
39. Single antigen
vaccines Age group Volume
(mL)
Dose
HBsAg
(mcg)
Recombivax HB
Pediatric/adolesce
nt formulation
Birth through
17 years
0.5 5
Adult formulation 11 through 15
years
1 10
Engerix B¶ Birth through
17 years
0.5 10
Recommended doses of formulations of hepatitis B
40. Maternal
HBsAg
status
Single antigen* plus
combination vaccine
Dose Age
Positive 1 Birth (≤12 hours)*
HBIG Birth (≤12 hours)
2 2 months
3 4 months
4 6 months
Unknown 1 Birth (≤12 hours)*
2 2 months
3 4 months
4 6 months
Negative 1 Birth (≤24 hours)*
2 2 months
3 4 months
4 6 months
hepatitis B immunoprophylaxis for term and preterm infants
with birth weight ≥2 kg
If mother find as HBsAg-positive or status remains unknown HBIG 0.5 mL should be given by one
week of age.
41. Maternal
HBsAg status
Single antigen plus combination
vaccine*
Dose Age
Positive¶ 1 Birth (≤12 hours)
HBIG Birth (≤12 hours)
2 2 months
3 4 months
4 6 months
Unknown 1 Birth (≤12 hours)
HBIG Birth (≤12 hours)
2 2 months
3 4 months
4 6 months
Negative 1 Hospital discharge or
age 1 month
2 2 months
3 4 months
4 6 months
hepatitis B immuno-prophylaxis for preterm infants
with birth weight <2 kg
42. Single-antigen vaccines should be used for the birth dose.
Combination vaccines (eg, Pediarix) cannot be administered at
birth or before age 6 weeks.
Infants born to HBsAg-positive mothers should receive
immunoprophylaxis as recommended whether or not their mother
received antiviral therapy during the third trimester.
The final dose in the vaccine series should not be administered
before age 24 weeks (164 days).
Some Consideration…..
43. POSTVACCINATION SEROLOGY
usually is not necessary for immunocompetent children and
adolescents Except
●Women who are HBsAg-positive
●Women whose prenatal HBsAg results were not available at
the time of delivery but who have other evidence suggestive of
chronic hepatitis B infection
●Women whose HBsAg-status cannot be determined
Test : both HBsAg and anti-HBs]should be obtained after
receiving ≥3 doses of HepB vaccine, usually at 9 to 12 months of
age or one to two months after the last dose of HepB vaccine
44. Hemodialysis patients and Immune-
compromised patients
anti-HBs one to two months after administration of
the last dose of the primary HepB vaccine series
annual anti-HBs testing for hemodialysis patients
and administer a booster dose of HepB vaccine
when the anti-HBs concentration is <10 mIU/mL,
45. Contraindications and precautions for hepatitis B vaccines
ADVERSE REACTIONS :
• ususlly safe. Pain, erythema at the injection and fever
>37.7°C (99°F)
Contraindications
Severe allergic reaction (eg, anaphylaxis) after a previous
dose or to a vaccine component (eg, yeast)
Precautions
Infant weighing <2 kg (4.4 pounds)
Moderate or severe illness with or without fever (ie, illness
more severe than upper respiratory infection, otitis media,
gastroenteritis)
46. incorrectly perceived as contraindications or precautions to hepatitis B
vaccine
Pregnancy
Autoimmune disease (eg, systemic lupus erythematosus, rheumatoid arthritis)
Mild acute illness with or without fever (eg, upper respiratory infection,
otitis media, gastroenteritis)
Mild-to-moderate local reaction (eg, swelling, redness, soreness) after
previous dose
Low-grade or moderate fever after previous dose
Current antibacterial therapy (except for oral typhoid vaccine)
Convalescent phase of illness
Recent exposure to infectious disease
History of penicillin allergy, other nonvaccine allergies, relatives with
allergies, or receiving allergen extract immunotherapy
History of Guillain-Barré syndrome
48. COUNSELING
Household members of children with chronic HBV should be
screnned and vaccinated
risk of transmission to others, including perinatal transmission
and risk of environmental exposure from blood
Household members should not share toothbrushes or razors
no special measures in sharing of eating utensils
to participate in all regular activities (school and sports)
universal precautions in daycare centers, schools, sports
clubs, and camps
49. MONITORING
ALT HBeAg HBeAb USG For
HCC
Immune
tolerant
phase
every 6 to
12 months
every 12
months
every 12
months
2 to 3
yearly
Immune
active, HB
eAg-
positive
phase
ALT becomes elevated (>40
international units/L), biochemical
tests and serologies should be
measured more frequently (eg,
every three to six months).
6 monthly
Inactive
chronic
HBV
every 6 to
12 months
every 12
months
every 12
months
needed
50. SELECTION OF PATIENTS FOR ANTIVIRAL
TREATMENT
goal of treatment
reduce the risks of progression to cirrhosis and of
hepatocellular carcinoma (HCC).
efficacy of treatment measured through intermediate
outcomes such as changes in short-term virologic,
biochemical, and histologic parameters.
51. Treatment of Phase of chronic HBV
Immune
tolerant
NOT as chance
development
of drug
resistance,
Exception : cirrhosis or other signs of severe liver
disease even if the ALT levels are normal
Immune
active, HBsAg-
positive
(clearance)
phase –
markedly elevated ALT values (>10 times the ULN), observation for
several months then Testing at least every three months
There are three possible outcomes :
Spontaneous seroconversion to inactive chronic HBV ("carrier" state)
: no treatment
Persistent immune active phase : treatment is indicated.
Spontaneous resolution of the HBV infection: monitored for
reactivation of infection and for HCC
Inactive
chronic HBV
should not be
treated
HBV DNA should be measured if ALT becomes
elevated
Immune
active, HBeAg-
negative
(reactivation)
close monitoring and Antiviral therapy is indicated to minimize liver
damage
Adults with this condition are typically treated indefinitely.
53. Immune active, HBsAg-positive (clearance) phase treatment
for patients who have persistently abnormal ALT (>2 times
the ULN or >60 units/L, whichever is lower) and HBV DNA
>20,000 international units/mL or 105 copies/mL for at least
four to six months either HBeAg-positive or HBeAg is
negative treatment should be given.
If there is evidence of hepatic decompensation, treatment
should be initiated earlier
54. who will be undergoing immunosuppression –
Treatment is appropriate in all phases
a nucleos(t)ide is often used in an effort to prevent reactivation;
drugs may be discontinued after the immunosuppressive therapy
is complete and if HBV DNA remains <20,000 units/mL and ALT is
normal.
56. Pegylated
IFNα
Entecavir* Tenofovir
Duration of
treatment
1 year >1 year¶ >1 year¶
Age group
(FDA approval)
≥3 years ≥2 years ≥2 years
Route Subcutaneous Oral Oral
Side effects Many Negligible
Potential
nephrotoxicity, reduced
bone mineral density (
Drug
resistanceΔ
None
∼1% up to year
6
None, up to year 8
57. Entecavir, Tenofovir:
without cirrhosis treatment should continue for
at least 12 months after seroconversion from
HBeAg to anti-Hbe or treatment indefinitely
unless the patient clears HBsAg.
with cirrhosis continued indefinitely unless they
clear HBsAg.
patients are at risk for exacerbations of
hepatitis B after discontinuation ofall
nucleos(t)ide .
58. New biomarkers of HBV infection
Hepatitis B core-related antigen (HBcrAg)
composite bio- marker comprising several antigens expressed from the
precore/- core gene: HBcAg, HBeAg, and prec22 precursor protein.
concerning the translational activity of the HBV infection beyond HBsAg
quantification.
partly reflect the amount of intrahepatic DNA and cccDNA in
hepatocytes especially in HBeAg-positive patients.
defining the phase of chronic HBV infection, especially in HBe- negative
patients,
predicting the long-term HCC risk.
to monitor NA or PegIFNa based treatments and pre- dicting therapeutic
efficacy including the risk of relapse after stopping NAs.
59. Circulating HBV RNA
HBV RNA can be released into the serum in the form of
enveloped pregenomic RNA containing virions .
interesting marker to study cccDNA transcrip- tional activity.
correlation between quantitative serum HBV RNA dynamics
and HBeAg loss in both NA and PegIFNa treated patients
demonstrated by using a new rapid amplification of cDNA-
ends with polymerase chain reaction (RACE-PCR)
new marker for monitoring NA therapy.
in predicting viral rebound after discontinuation of NAs.
60. Take home messages….
Management is difficult
Treatment is costly
Treatment outcome guarded
Prevention is better than cure
Health education and vaccination at birth
are the logical and practical approach.