This document discusses viral hepatitis, caused by hepatitis viruses A, B, C, D, E, and G. It provides information on the structure, transmission, clinical features, diagnosis, and prevention of each type of viral hepatitis. Hepatitis A virus is enterically transmitted while hepatitis B, C, and D are typically transmitted parenterally. Hepatitis B and C can cause chronic infection and lead to cirrhosis or liver cancer, while hepatitis A and E do not typically cause chronic infection. Diagnosis involves testing for viral markers and antibodies. Prevention strategies include vaccination, blood donor screening, and risk behavior modification.
Types of hepatitis
HEPATITIS - symptoms
How To Diagnose Hepatitis?
Treatment
Main Prevention Measures for Hepatitis B and C
Hepatitis in Pregnant Women
Oral Manifestations of Hepatitis
Management of patients with hepatitis B and C infection in dental office
Types of hepatitis
HEPATITIS - symptoms
How To Diagnose Hepatitis?
Treatment
Main Prevention Measures for Hepatitis B and C
Hepatitis in Pregnant Women
Oral Manifestations of Hepatitis
Management of patients with hepatitis B and C infection in dental office
HEPATITIS IS THE INFLAMMATION OF THE LIVER, CAUSED BY VIRUSES, TOXINS, OR CHEMICALS (INCLUDING DRUGS).
1.
VIRAL HEPATITIS
2.
TOXIC HEPATITIS
3.
CHRONIC HEPATITIS
4.
ALCOHOLIC HEPATITIS
The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
Viral hepatitis is inflammation of the liver caused by a virus. Several different viruses, named the hepatitis A, B, C, D, and E viruses, cause viral hepatitis.
All of these viruses cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong. Chronic hepatitis can lead to cirrhosis, liver failure, and liver cancer.
Researchers are looking for other viruses that may cause hepatitis, but none have been identified with certainty. Other viruses that less often affect the liver include cytomegalovirus; Epstein-Barr virus, also called infectious mononucleosis; herpesvirus; parvovirus; and adenovirus.
National Institute of Diabetes and Digestive and Kidney Diseases:
HEPATITIS IS THE INFLAMMATION OF THE LIVER, CAUSED BY VIRUSES, TOXINS, OR CHEMICALS (INCLUDING DRUGS).
1.
VIRAL HEPATITIS
2.
TOXIC HEPATITIS
3.
CHRONIC HEPATITIS
4.
ALCOHOLIC HEPATITIS
The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
Viral hepatitis is inflammation of the liver caused by a virus. Several different viruses, named the hepatitis A, B, C, D, and E viruses, cause viral hepatitis.
All of these viruses cause acute, or short-term, viral hepatitis. The hepatitis B, C, and D viruses can also cause chronic hepatitis, in which the infection is prolonged, sometimes lifelong. Chronic hepatitis can lead to cirrhosis, liver failure, and liver cancer.
Researchers are looking for other viruses that may cause hepatitis, but none have been identified with certainty. Other viruses that less often affect the liver include cytomegalovirus; Epstein-Barr virus, also called infectious mononucleosis; herpesvirus; parvovirus; and adenovirus.
National Institute of Diabetes and Digestive and Kidney Diseases:
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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
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
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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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
3. Viral hepatitis is a systemic disease with primary
inflammation in the liver.
Caused by Hepatitis viruses A,B,C,D,E,G
Infection caused by hepatitis B – most severe
Hepatitis B & C viruses also responsible for many cases of
primary hepatocellular carcinoma.
Hepatitis B is a DNA virus while others(A,C,D,E,G)
contain RNA genome.
5. Viral Hepatitis - Historical Perspective
A“Infectious”
“Serum”
Viral hepatitis
Enterically
transmitted
Parenterally
transmitted
F, G,
? other
E
NANB
B D C
Source: CDC
6. Features HAV HBV HCV HDV HEV HGV
Genome RNA DNA RNA RNA RNA RNA
Nomenclat
ure
Picrornavi
ridae
hepadnavir
idae
Flavivirida
e
Deltavirus Calcivirida
e
Flavivirida
e
Mode of
transmissi
on
Enteric Parenteral
Sexual
Perinatal
Parenteral
Sexual
Parenteral enteric Parenteral
Sexual
Perinatal
Ag in
blood
HAV HBsAg,
HBeAg
HCV HDAg HEV ?
Abs in
blood
Anti HAV Anti HBs
Anti HBe
Anti HBc
Anti-HCV Anti-HDV Anti-HEV Anti-HGV
envelope
Chronic
carrier
state
No Yes Yes Yes No ?
Hepatic Ca No Yes Yes No No No
7. Features Hepatitis A Hepatitis B
Virus
Diameter 27nm 42nm
Genome RNA DNA
Symmetry Icosahedral Icosahedral
Envelope Non-enveloped Enveloped
Stability 60° C x 60 mnts Survives Survives
100° C x 5 mnts Inactivated Inactivated
usual mode of infection Faeco-oral Pareneral
Clinical features
IP 2-6 wks 2-6 mnths
Onset Usually acute Insidious
Fever < 38° C Usual Rare
Chronicity Rare Common
Age incidence Children & young adults All ages
Seasonal distribution Post monsoon in India
Autumn, winter
All year around
8. Features Hepatitis A Hepatitis B
Lab diagnosis
HBs Ag Absent Present
Raised serum IgM Common Rare
Raised serum transaminase For few days For many weeks
Virus in faeces Present early Absent
Mortality 0.1% 1-10%
Carrier state
Blood Upto 8 mnths Upto 5 yrs
Faeces Upto 1-3 mnths Not known
9. Viral Hepatitis - Overview
A B C D E
Source of
virus
feces blood/
blood-derived
body fluids
blood/
blood-derived
body fluids
blood/
blood-derived
body fluids
feces
Route of
transmission
fecal-oral percutaneous
permucosal
percutaneous
permucosal
percutaneous
permucosal
fecal-oral
Chronic
infection
no yes yes yes no
Prevention pre/post-
exposure
immunization
pre/post-
exposure
immunization
blood donor
screening;
risk behavior
modification
pre/post-
exposure
immunization;
risk behavior
modification
ensure safe
drinking
water
Type of Hepatitis
Source: CDC
10.
11. Family- Hepadnaviridae
Genus- Orthohepadnavirus
Morphology
• Complex 42nm double shelled particle.
• Outer surface/envelope of virus contains
hepatitis B surface antigen(HBsAg).
• It encloses an icosahedral 27nm nucleocapsid
(core),which contains hepatitis B core antigen(HBcAg)
12.
13. Inside the core is genome, a circular double stranded DNA
and a DNA polymerase.
Australia antigen- surface component of hepatitis B
virus(HBsAg)
Electron microscopy – shows 3 types of particles.
Most abundant –spherical particle (22nm in diameter)
Tubular(22nm diameter) particle of varying length
Double shelled spherical structure(42nm) – this particle is the
complete hepatitis B virus or Dane particle.
14. HBsAg – surface antigens (envelope protein)
HBcAg - core (nucleocapsid) antigen of the virus.
It contains group specific protein & is not detectable in
patient’s blood
HBeAg – appears in serum along with HBsAg but
disappears within a few weeks. it is the hidden
antigenic component of core.
HBcAg & HBeAg though immunologically distinct
are coded by the same gene.
15. HBsAg carries group specific antigen ‘a’ and two
types of specific antigens ,d or y and w or r.
4 antigenic types of HBsAg – adw, adr, ayw and ayr.
Type adw is predominant in Europe and USA
Type adr in Asia.
Type ayw is predominant in Africa, Russia and India.
Additional surface antigens of HBV (q,x,f,t,j,n,g) are
described,but they have not been characterized
16. Consists of two linear strands of DNA held in a circular
configuration.
One of the strands (plus strand) is incomplete while other is
complete.
This gives the appearance of partially double strand and
partially single stranded DNA.
Associated with the plus strand is a viral DNA polymerase.
It can repair the gap in the incomplete (plus strand) and
render the genome fully double stranded.
17. Genome has four genes (with different regions ) coding for
different antigens.
S gene encodes major HBsAg, consists of S region & 2 pre S
regions
C gene encodes HBcAg & HBe protein, has 2 regions C &
pre C
P gene is largest & codes for DNA polymerase
X codes for non particulate protein HBxAg.
HBxAg & its antibody are found to be present in patients with
severe chronic hepatitis & hepatocellular carcinoma.
20. HBV has not been cultivated in the laboratory.
Limited production of the virus and its proteins can be
obtained from cell lines transfected with HBV DNA.
HBV proteins have been cloned in yeast and bacteria.
The virus survives heating of 60 C for 60 min but gets
inactivated at 100 C for 5min.
Inactivated by formaldehyde (1:4000) and 2% gluteraldehyde.
21. Parenteral transmission – result from accidental
inoculation of minute amounts of blood, blood products
or fluid containing HBV during medical,surgical or
dental procedures.
Perinatal transmission – occurs when carrier mother’s
blood contaminates the mucus membranes of the
newborn during birth.
Sexual transmission – HBV is present in body fluids i.e.
semen & vaginal secretions, hence can be transmitted by
sexual contact. Male homosexuals are at higher risk of
acquiring infection.
22. Slow onset
IP -6weeks-6months
Pre-icteric phase-malaise, anorexia, weakness, myalgia,
nausea & vomiting.
Few patients develop arthralgia, serum sickness, polyarteritis
nodosa and glomerulonephritis.
Icteric phase-jaundice, pale stools & dark urine
(bilirubinemia).
Convalescent phase- long. The duration of uncomplicated
hepatitis is usually 8-10 weeks, but mild symptoms may
persist for more than one year.
23. Super carriers – have HBeAg in blood & are highly
infectious. their blood contains high titre of HBsAg
and DNA polymerase.
HBV may also be demonstrable in blood.
Very minute amount of serum/blood can transmit the
infection.
Simple carriers – more common.
Have no HBeAg and a low level of HBsAg in blood.
HBV and DNA polymerase are absent.
They transmit the infection only when large volumes
of blood/serum are transferred ,as in blood transfusion.
24. Humoral response
Antibody to HBsAg –associated with resistance to
infection.
useful indication of past infection or recent immunity.
Antibody to HBcAg-rises rapidly following infection.
Not protective. Appears to be related to the amount and
duration of replication of the virus. The highest titre of
anti-HBc are found in persistent HBsAg carriers.
Antibody to HBeAg-seen in sera of patients with low
infectivity.
Cell mediated immunity
Defective function of T-cell may favor development of
chronic liver damage.
25. Detection of viral markers
HBsAg-specific marker for HBV infection.
First marker to appear in blood after infection.
Peak levels- in pre icteric phase
Remains in circulation throughout the icteric or
symptomatic course of the disease.
HBsAg disappears with recovery from clinical disease in
most patients, however,it persists for years in carriers.
Antibody to HBsAg appears within weeks after the
disappearance of HBsAg and persists for very long periods.
Anti HBs is the protective antibody
26. Appears in serum at the same time as HBsAg, but
disappears within a few weeks.
Sera containing HBeAg – highly infectious.
Indicator of active intra-hepatic viral replication and
presence in blood of HBV DNA, virions & DNA
polymerase.
Disappearance of HBeAg is followed by appearance
of anti-HBe.
27. Not detectable in serum.
Can be demonstrable in liver cells by mmunoflorescence
Anti –HBc antibody usually appears in serum a week or
two after the appearance of HBsAg.
Earliest antibody to appear in blood.
Remains lifelong-useful indicator of prior infection
28.
29. Clinical condition
HBsAg HBE
Ag
Anti
HBs
Anti
Hbe
Anti HBc
IgM IgG
Late IP or early hepatitis + + _ _ _ _
Acute hepatitis + + _ _ + _
Late or Chronic HBV infection + +/_ _ _ _ +
Simple carrier + _ _ _ _ +
Super carrier + + _ _ _ +
Past infection _ _ + + _ +
Immunity following vaccination _ _ + _ _ _
30.
31. Viral DNA polymerase
Appears transiently in serum during preicteric phase
Polymerase chain reaction
HBV DNA detected by PCR
HBV DNA is indicator of viral replication in liver and so
helps to assess the progress of patients under antiviral
chemotherapy.
Biochemical tests
Acute viral hepatitis –transaminases b/w 500-2000 units.
Serum bilirubin –may rise upto 25 fold
32. General preventive measures
Health education, improvement of personal hygiene and sterility.
Screening of HBsAg & HBeAg in blood donors.
Avoid unsterile needles, syringes
Immunisation
1. Passive immunisation
Employed following any accidental exposure to HBV infection.
HBIG prepared from donors with high titres of anti HBs.
Dose-300-500 IU i/m
Administered preferably within 48 hrs
2nd dose usually given at interval of 4 weeks after the 1st dose.
33. 2. Active immunisation
Plasma derived vaccine - Prepared by purifying 22nm particle
of HBsAg from plasma of healthy carriers.
Separated by ultracentrifugation & inactivated with
formaldehyde.
Recombinant yeast hepatitis B vaccine - Produced by
recommbinant DNA in yeasts in which a plasmid containing
the gene of HBsAg has been incorporated
Doses – 0 – 1- 6 months I/M into deltoid muscle
Recombinant Chinese hamster ovary cell hepatitis B vaccine
Synthetic peptide vaccine – under experimental stage
34. IFN α alone or in combination with antiviral like
lamivudine & famcyclovir has been beneficial in
some hepatitis cases
47. Screening test: highly sensitive enzyme-linked
immunoassay (EIA)
Confirmation can be with recombinant
immunoblot assay (RIBA), but HCV RNA
confirms presence of infection & that it is active
49. Indications for tx: based on liver biopsy, not liver
enzyme abnormalities or quantitative HCV levels
HCV genotypes vary in their response to tx
Pegylated INF + ribavirin is current most effective tx
strategy
Tx in collaboration with GI specialist
50.
51. Etiology: defective RNA virus; uses HBsAg so can
only occur with acute or chronic HBV
Mode of transmission: blood
Incidence: localized outbreaks among IDU
Spectrum of illness: acute hepatitis, can be
fulminant, chronic hepatitis with usual sequelae
52. Potential for chronicity: more than 70% of super-
infections of chronic HBV lead to chronic HDV
Diagnosis: HDVab, HDV RNA, HBVsAg
Treatment: supportive care
Prevention: prevention of HBV, treatment of HBV
53.
54.
55. Etiology: RNA virus
Non-enveloped
Mode of transmission: fecal-oral
Spectrum of illness: acute hepatitis, mild to fulminant
Potential for chronicity: none
Treatment: supportive care
Prevention: pre-exposure (immunization), post-
exposure (immune globulin)
58. Prevalent worldwide
Childhood infection less common in U.S.
Only 15-25% of U.S. adults immune → large
susceptible population
Oral-fecal spread, including contaminated food &
water, makes avoidance difficult
59. Compatible clinical syndrome
Total HAV antibody (HAVAB) tests for both IgG &
IgM; does not distinguish between acute & prior
Hepatitis A
+ HAVAB, - HAV IgM → prior infection
+ HAVAB, + HAV IgM → acute infection
60. Havrix (GlaxoSmithKline)
Vaqta (Merck)
Both: two shots 6-12 mo apart
Twinrix (GlaxoSmithKline) contains both HAV &
HBV vaccines; given in series of 3 shots at 0, 1 mo,
& 6 mo
61. Recommended those at risk of infection & for
those wishing to obtain immunity
U.S. moving toward universal childhood
immunization
62. Children living in US areas with incidence >
20/100,000
Travel/residence in incidence country
Men who have sex with men
Injection drug users
People with clotting disorders
Occupational risk
Chronic liver disease
63. Follows recognition of active case
Immune globulin: 0.02 ml/kg IM
Give ASAP & within 2 weeks
Target those with close contact (household &
sexual), Day Care staff & attendees, common-source
exposures (e.g. food handler)
64.
65. FAMILY CALCIVIRIDAE
27-38nm-nonenveloped ssRNA
ICOSAHEDRAL-surface-depressions
Etiology: RNA virus
Mode of transmission: Fecal-oral
Spectrum of illness: acute, self-limited hepatitis;
mortality in pregnant women
66. MOI –contaminated water
IP -2-8wks
Mild selflimiting,epidemics
No cirrhosis,chronic hepatitis