Contrary to common belief, hepatitis-B, if acquired in adult stage, can be fully cured. Even a chronic one acquired in infancy can be easily mitigated. Hepatitis-B is an oft-forgotten and very much prevalent in the population.
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.
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.
Case study of a 22 year old male patient admitted under medics with an unknown disease process, likely infectious with unknown causative agent. Extensive investigation revealed leptospirosis. Presented at hospital lunchtime medical meeting. These slides have been altered to ensure patient anonymity, and to better display information without a presenter.
Sources for all imagery and sources listed in references section where possible. I do not claim ownership of any images or graphics. Slides for educational purposes only, and should not replace clinical judgement. No monetary gain was made for this work.
world hepatitis day awareness presentation july 2022.pptxanjalatchi
World Hepatitis Day (WHD) is recognized annually on July 28th, the birthday of Dr. Baruch Blumberg (1925–2011). Dr. Blumberg discovered the hepatitis B virus in 1967, and 2 years later he developed the first hepatitis B vaccine
Case study of a 22 year old male patient admitted under medics with an unknown disease process, likely infectious with unknown causative agent. Extensive investigation revealed leptospirosis. Presented at hospital lunchtime medical meeting. These slides have been altered to ensure patient anonymity, and to better display information without a presenter.
Sources for all imagery and sources listed in references section where possible. I do not claim ownership of any images or graphics. Slides for educational purposes only, and should not replace clinical judgement. No monetary gain was made for this work.
world hepatitis day awareness presentation july 2022.pptxanjalatchi
World Hepatitis Day (WHD) is recognized annually on July 28th, the birthday of Dr. Baruch Blumberg (1925–2011). Dr. Blumberg discovered the hepatitis B virus in 1967, and 2 years later he developed the first hepatitis B vaccine
Author: Dr Christa Maria Joel
Module: Principles of Infection and Disease Control
Supervisor: Dr William Mackay Gordie and Ms Fiona Hernandez
University of the West of Scotland
Spread the Awareness about #Hepatitis with us on this World Hepatitis Day!
#28July #WorldHepatitisDay
*Free Shipping on all US Orders - Coupon Code "FS99"
www.OffshoreCheapMeds.co
World Hepatitis Day (WHD) is observed every year on 28th July.
On this day efforts are made to raise awareness of the different types of viral hepatitis under one theme.
This day aims at making significant change in the healthcare field by uniting patient organizations, medical professionals, governments and general public and spread awareness of viral hepatitis.
So, On this DAY, is an opportunity to boost the efforts of WHO’s strategy to help countries eliminate hepatitis.
On this day, it is the birthday of Nobel –Prize winning scientist Dr. Baruch Blumberg, who discovered hepatitis B virus (HBV) and developed a diagnostic test and vaccine for the virus.
In India, 40 million people are chronically infected with hepatitis B;
6 to 12 million people are chronically infected with hepatitis C.
HEV is the most important cause of epidemic hepatitis,
HAV is more common among children. Most acute liver failures diagnosed are attributable to HEV.
Hepatitis B and Hepatitis C are the major cause of chronic liver disease and liver cancer in the world.
Hepatitis B is a vaccine-preventable disease. Although federal public health officials recommend that all new borns, children, and at-risk adults receive the vaccine, about 46,000 new acute cases of the HBV infection emerge each year, including 1,000 in infants who acquire the infection during birth from their HBV-positive mothers.
Unfortunately, there is no vaccine for hepatitis C, which is transmitted by direct exposure to infectious blood.
The burden of infection is highest in the WHO Western Pacific Region and the WHO African Region, where 116 million and 81 million people, respectively, are chronically infected.
India falls under the category of intermediate endemicity zone (average of 4%).
A balanced Diet;
Be careful with vitamins, herbals and minerals use;
Light Daily Exercise;
Vaccination, particularly for HBV, and where appropriate HAV and HEV (a HEV vaccine has been developed and licensed in China, but is not yet widely available);
Injection, blood and surgical safety and universal precautions;
Prevention of mother-to-child transmission of HBV.
Each Year, more than a million lives are lost to hepatitis- We aren't waiting to change that, we’re fighting to making it happen.
Join the movement and make your voice heard
We aren't waiting
I Pledge to end Hepatitis
Thus, Hepatitis Day is an ideal opportunity for us to come together and raise awareness about viral hepatitis among people.
Viral hepatitis is the leading cause of liver cancer and the most common reason for liver transplantation
In the United States, an estimated 1.2 million Americans are living with chronic Hepatitis B and 3.2 are living with chronic Hepatitis C
Many do not know they are infected
Each year an estimated 21,000 persons become infected with Hepatitis A; 35,000 with Hepatitis B, and 17,000 with Hepatitis C
Hepatitis A – fecal/oral, contaminated food, vaccine available
Hepatitis B – blood, semen, vertical (mother-child), vaccine available
Hepatitis C – blood (IV drug use, transfusion, organ donation, unsterile injecting equipment, sexual intercourse)
Hepatitis D – survives only in cells co-infected with hepatitis B
Hepatitis E* – contaminated food or water, fecal/oral
*causes short-term disease and is not a chronic carrier state
Hepatitis B is a viral infection affecting the liver. The disease goes through different phases, which can be diagnosed by serology. Diagnostic testing comprises the three most important parameters: HBs antigen, anti-HBs antibody, and anti-HBc antibody. These three parameters can be used to identify active infection, previous infection, and status after vaccination. In addition, anti-HBc IgM antibody can be used to confirm acute infection. Hepatitis B virus (HBV) is a small DNA virus which is capable of integrating into the host genome and causes various liver diseases most notably liver cirrhosis and liver cancer.
-Introduction to Hepatitis
– Viral Hepatitis Transmission
– Symptoms & acute vs. chronic
5:35 - Laboratory Tests and Councilman Bodies
– Hep B Serology (HBsAg & Anti-HBs)
– Treatment of Viral Hepatitis
- Vaccines
The rate of deaths due to liver cancer is increasing faster than any other type of cancer. Hepatitis B and C are major contributing factors to liver cancer. At this seminar, learn the critical importance of hepatitis prevention and treatment.
Outbreak of hepatitis b, epidemiology, and transmission in provinces of pakistanshahzebkhanshaz
hepatitis is much serious problem throughout the world the work presenting the epidemiology and transmission and risk factors are involved in spreading of disease
all information about
it include :-
1- DEFINITION
2- SIGNS AND SYMPTOMS
3- MECHANISM
4- RISK FACTOR
5- COMPLICATIONS
6- PRECAUTION
7- PREVENTION
8- EPIDEMIOLOGY
9- TREATMENT
and finally video about the mechanism of action
if you van not open it
hit this link
https://www.youtube.com/watch?v=ZuUfGeoN_cw
i hope it meet what you want
Coronaviruses & the Chromosomal Mutations of Sars Cov-2Lashhkaraa
This short document covers all the types of coronaviruses that exist in nature, the specific one that has caused the epidemic and the mutations that being caused in its genome.
A commentary on the lives of two children around the world who are met with their first experience of discrimination of their communities and a discussion on the life-long scar such an ordeal leaves.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...
Hepatitis-B: A Case Study
1. H E P A T I T I S B
detailed research on one of the most fatal diseases
witnessed by the humankind
A B I O L O G Y P R O J E C T R E P O R T
E F F O R T S B Y : - S A U M Y A P A N W A R , S 6 B
S U B M I T T E D T O : - M S R I C H A B H A T I A
2. 2
T A B L E O F C O N T E N T S
S.no. Topic Pages
1. Acknowledgments 3
2. Introduction 5
3. Natural History of Hepatitis-B 8
4. Modes of Transmission 13
5. Signs & Symptoms 15
6. Diagnosis 16
7. Prognosis 23
8. Treatment 24
9. Prevention 26
10. Case Studies 29
11. Bibliography 33
3. 3
A C K N O W L E D G E M E N T S
I would like to express my heartfelt gratitude towards my Biology teacher Ms.
Richa Bhatia for giving me an opportunity to dig deeper into the science of
diseases by assigning us a task to create a project on one such disease. It indeed
turned out to be a rollercoaster of knowledge for me, debunking some of the
myths that even I believed in.
I would also take this opportunity to thank my loving parents who, since my
formative years, have tried inculcating my interest in science; these efforts have
presumably borne fruits. Mamma has played a vital role in the culmination of
this report by lending her vast knowledge about the subject, assisting me in
finding material and motivating me to put my best foot forward.
I am obliged beyond measure to all the well-known scientists and medical
professionals and unknown alike, for putting heart and soul into their
respective fields and working obstinately; it is only because of their painstaking
labors that we have achieved milestones in research and medicine and are now
aware of the various aspects of our being.
Lastly, I am grateful to Krishnji for always making me listen to my heart and
guiding me to do the right thing with the sweet sound of his flute!
4. 4
To Srish,
From the beautiful abode, that she is keeping an eye on me,
I am sure she will be proud. I love you…
5. 5
I N T R O D U C T I O N
iral hepatitis is a potentially life-threatening infection of the liver
caused by any of the half dozen viruses: hepatitis A virus (HAV),
hepatitis B virus (HBV), it was originally known as "serum hepatitis",
hepatitis C virus (HCV), hepatitis D virus (the delta agent) and
hepatitis E virus (HEV). Hepatitis G virus has been newly discovered and
resembles HCV, but more closely, the flaviviruses; the virus and its effects are
under study and though it is known to infect humans, but is not known to
cause human diseases. It is known that many other viruses may be implicated
to cause hepatitis such as cytomegalovirus, Epstein-Barr virus, yellow fever
virus, and rubella virus. Disease caused by non-hepatitis viruses is called
hepatitis A-E. Viruses of herpes simplex, varicella and adenoviruses can also
cause hepatitis in immunocompromised individuals, but these cases are rare.
However, this report shall be focusing primarily on hepatitis B.
The Problem Statement
Human beings are the only reservoir of this virus and it is highly fatal when not
diagnosed earlier and not treated on time. Chronic hepatitis B can cause liver
damage which can lead to many lethal outcomes like chronic hepatic
insufficiency, cirrhosis, hepatocellular carcinoma, and even death.
Hepatitis B is endemic throughout the world, especially in tropical and
developing countries and also in some regions of Europe. It has no seasonal
nature. Its prevalence varies from country to country depending on a complex
V
Figure 1: (Left) a healthy liver, (right) a cirrhotic liver
6. 6
mix of behavioral, environmental and host
factors. In general, it is lowest in countries
with high standards of living (e.g.: Australia,
North America, North Europe) and highest
in countries or area where socio-economic
levels are lower (e.g.: China, South-east
Asia, South America).
About a third of the world population has
been infected by hepatitis B at one point in
their lives, including 343 million who have
chronic infections. The Global Burden of
Disease study estimated that there were
686,000 deaths caused by hepatitis B in
2013 and a 5.9 per 100,000 age-
standardized death rates globally, 4 of
which 300,000 deaths were attributed to
liver cancer and 317,400 deaths to cirrhosis
of the liver secondary to hepatitis B. In
India, as per latest estimates, 40 million
people are chronically infected with
hepatitis B, making our country second in
the globe only to China. However, since
many episodes go unreported or
unrecognized, the actual number of
hepatitis B cases would be anybody’s guess.
Every year, nearly 10,000 patients die from HBV infection in India. HBV was
also implicated in a major epidemic outbreak in Ahmedabad (Gujarat) in 1984.
Deaths due to viral hepatitis are much more than due to AIDS and tuberculosis
according to a publication by WHO. This is because hepatitis B is 50-100 times
more infectious than HIV. Yet, while people are by and large aware of HIV,
there is little awareness about hepatitis. It has been a global health concern and
the WHO’s 2015 Agenda for Sustainable Development commits to combating
viral hepatitis to its elimination. A plethora of socio-economic factors have led
7. 7
to an increase in the burden of hepatitis, despite being preventable by
vaccination since 1982, which are as follows:
1. Poverty & illiteracy
2. Social stigma
3. Cultural, traditional practices
4. Ignorance about vaccination
5. Availability of authentic medication
6. Lack of awareness, myths, and inaccurate information, etc.
Due to poverty and illiteracy, people prefer quackery instead of medical advice
for prompt and cheap treatment. In many such cases, people with mild
problems, which can be addressed even without treatment end up with other
viral diseases by reusing injections. This transmission becomes problematic if
this viral disease is lethal and incurable or patients cannot afford the cost of
treatment. Apart from the increased chances of liver cancer, it is important to
remember that patients with hepatitis B may develop anemia as a result of
autoimmune hemolytic anemia and rarely aplastic anemia.
Figure 2: People belonging to lower income strata are neither able to get tested for hepatitis, nor afford patented
medicnes or the expensive treatment. Reuse of syringes is a more common practice in poorer regions.
8. 8
N A T U R A L H I S T O R Y O F
H E P A T I T I S B
Incubation period
The incubation period is from 45-180 days (2-6 months). Lower doses of the
virus often result in longer incubation periods. The median incubation period is
said to be lower than 100 days.
Agent factors
a) AGENT: Hepatitis B virus was discovered by Blumberg in 1963. It is a
complex, 42 nm, double-shelled DNA virus, originally known as the
“Dane particle”. It replicates in the
liver cells. It has 3 distinct antigens – a
surface antigen, also known as the
“Australian antigen” (HBsAg – envelope
glycoprotein), a core antigen (HBcAg – a
nucleocapsid “core” protein) and an “e”
antigen (HBeAg – a longer polypeptide
transcript with a pre-core and core region).
They stimulate the production of the
respective antibodies e.g., surface antibody
Figure 3: An artist's impression of the hepatitis virus
9. 9
(anti-HBs), core antibody (anti-HBc) and “e” antibody (anti HBe). The
antibodies and their antigens act as useful markers of HBV infection. It
has enzyme DNA polymerase that exhibits reverse transcriptase activity
and genomic replication occurs through an intermediate RNA template.
b) RESERVOIR OF INFECTION: Human is the only reservoir of the
infection which can be spread either through carriers or from cases. The
continued survival of
infection is due to a large
number of individuals who
are carriers of the virus,
estimated to be above 257
million. Cases may range
from symptomatic to
unapparent. The risk of an
adult becoming a carrier
following acute infection is 5-
15%; in infants, it may
exceed 50%.
c) INFECTIVE MATERIAL: Contaminated blood is the main source of
infection, although the virus has been found in body secretions like
mother’s milk, vaginal secretions, semen, and saliva (rare) of infected
persons.
d) RESISTANCE: The virus is quite stable and capable of surviving on
environmental surfaces for days. It can be readily destroyed by sodium
hypochlorite, as is by heat sterilization in an autoclave for 30-60 minutes.
e) PERIOD OF COMMUNICABILITY: The virus is present in the blood
during the incubation period (for a month before jaundice) and the acute
phase of the disease. Period of communicability is usually several
months (occasionally years in chronic carriers) or until the disappearance
of HBsAg and appearance of surface antibody.
Figure 4: Data suggests that the earlier a child acquires
hepatitis B infection, more is the probability of it becoming
severe in adulthood.
10. 10
Host factors
a) AGE: In countries in which infection with HBV is relatively uncommon,
the highest prevalence is found in the 20-40-year age group. In countries
where the
infection is
common, much
infection occurs
perinatally or
during early
childhood. The
younger an
individual is
when they
contract acute
HBV, the
higher the likelihood that they will develop the chronic form. This is
visualized in the graph alongside which reflects the percentage of
individuals who become chronic HBV carriers in relation to the age at
which they were acutely infected. Older age at diagnosis appears to be
an important determinant
of progression to cirrhosis
and increased mortality.
This may be because the
aging immune system
cannot contain the disease
process or simply because
of the longer duration of
infection.
b) GENDER: The
likelihood of Hepatitis B
persistence is 1.3 times
higher among males.
Fibrosis appears to
progress more slowly in
11. 11
females than in males with chronic hepatitis B, suggesting that estrogens
have a protective effect on fibrogenesis.
c) HIGH-RISK GROUPS: Certain groups carry higher risk. For example,
i) Tribal: The high endemicity of HBV infection in the tribal
populations has been attributed to inbreeding, poor hygienic living
conditions, close person-to-person contact and certain socio-culture
practices that may facilitate the transmission of HBV.
ii) Children: Chronic HBV infection in India is acquired in childhood,
presumably before 5 years of age, through horizontal transmission. In
South Asia, the age of acquisition of HBV is an important
determinant of outcome; the earlier the age, the higher the likelihood
of chronicity. The risk of chronicity in HBV infection acquired at
different ages ranges from >90% in newborns, 30% in children aged
2–5 years and
<5% in adults.
iii) Sexually
promiscuous:
There is a
significant excess
of serologic evidence of hepatitis type B infection in two high-
promiscuity populations: patients with venereal diseases and their
unrelated sexual contacts (15% to 18%) and male, but not
female, homosexuals (37% to 51%).
iv) Health Care Workers: The risk
of contracting HBV by Health
Care Workers (HCWs) is four-
times greater than that of the
general adult population. The
highest rates are seen among dentists,
physicians, laboratory workers, dialysis
workers, cleaning service employees, and
Figure 5: Pie chart representing the transmission risk
in HCWs
12. 12
nurses.
v) Drug abusers: India has an estimated 1.1 million injection drug users.
Outbreaks of viral hepatitis B in this group have been linked to the
usage of inadequately sterilized needles and syringes for the intake of
narcotics.
External factors
a) Chronic alcoholism plays a major role in increasing the rate of
progression to both cirrhosis and Hepatocellular Carcinoma (HCC).
Among patients with chronic hepatitis B, those with a history of heavy
drinking have a 6-fold higher risk of progression to cirrhosis.
b) Additional external factors that may increase the risk of liver cancer and
induce the development of carcinoma include tobacco smoking and
dietary carcinogens such as aflatoxins which contaminate food stored in
humid conditions.
c) Patients suffering from immunodeficiency syndromes are at a very high
risk of developing a fatal hepatitis infection. The prevalence of HBV
infection in HIV-infected persons has ranged between 2.25 and 29.7%.
Figure 6: Study shows that people who had been hospitalized for alcoholic hepatitis only had a 31.8% chance of living
for five or more years.
13. 13
M O D E S O F
T R A N S M I S S I O N
Transmission of HBV infection can happen mainly through 2 routes: (1)
Vertical, i.e. from the mother to the neonatal and (2) Horizontal, i.e. by other
routes like sexual contact, transmission through blood and other body fluids,
etc.
i. Perinatal/vertical route
Spread of HBV from carrier mothers to infants
appears to be an important factor for
the high prevalence of hepatitis B
infection in some regions, particularly
China and Southeast Asia. The risk of
infection varies from country to
country and may reach 40%. The
mechanism of perinatal infection is
uncertain. Although HBV can infect
the fetus in utero, this rarely happens and
infection usually occurs at the time of birth, as a result of
a leak of maternal blood into the baby’s circulation, or ingestion or accidental
inoculation of blood. Infection of the baby is usually anicteric and is recognized
by the appearance of surface antigen between 600-120 days of birth.
ii. Horizontal route
a. Parenteral route
14. 14
Hepatitis B is essentially a blood-
borne infection. It is transmitted by
infected blood and blood products
through transfusions, dialysis,
contaminated syringes, needles,
pricks if skin, handling of infected
blood, accidental inoculation of
minute quantities of blood such as during surgical and dental procedures,
immunization, traditional tattooing, body piercings, ritual circumcision,
acupuncture, etc. Accidental percutaneous inoculations by shared razors and
toothbrushes have been implicated as an occasional cause of hepatitis B. Close
living quarters/playground play as a toddler is also a source of HBV infection
(may contribute to high rate of horizontal transmission in Africa).
b. Sexual
transmission
There is ample evidence
for the spread of
infection by intimate
contact or by sexual
route. The sexually
promiscuous, particularly
male homosexuals, are at
a very high risk of
infection with hepatitis
B.
iii. Other routes
Transmission by blood-sucking arthropods (e.g.: mosquitoes, bed bugs) is
suspected but there is no convincing evidence to support this suggestion.
In short, transmission occurs in a wide variety of epidemiological settings. It
can spread either from carriers or from people with no apparent infection, or
during the incubation period, illness or early convalescence.
15. 15
S I G N S & S Y M P T O M S
Signs and symptoms of hepatitis B range from mild to severe. They usually
appear about one to four months after
you've been infected, although you
could see them as early as two weeks
post-infection. Some people, usually
young children, may not have any
symptoms.
Hepatitis B signs and symptoms
may include:
Abdominal pain
Dark urine
Fever
Joint pain
Loss of appetite
Nausea and vomiting
Weakness and fatigue
Jaundice (Yellowing of skin and
the whites of eyes)
16. 16
D I A G N O S I S
CLINICAL OBSERVATION:
Peculiar symptoms in one’s body may develop into a number of clinical
syndromes after exposure to hepatitis B virus, which are as follows:-
1. Carrier state: without clinically apparent disease or with chronic hepatitis
2. Asymptomatic infection: serologic evidence only
3. Acute hepatitis: anicteric or icteric
4. Chronic hepatitis: with or without progression to cirrhosis
5. Fulminant hepatitis: sub-massive or massive hepatic necrosis
Carrier State
A “carrier” is an individual
without manifest symptoms
who harbors and therefore can
transmit an organism. With
hepatotropic viruses, there are
(1) those who harbor one of the
viruses but are suffering little or
no adverse effects (a “healthy”
carrier) and (2) those who have
chronic liver disease but are
essentially free of symptoms or
disability. Both constitute
reservoirs of infection.
Infection in the early years, particularly through vertical transmission during
childbirth, produces a carrier state 90-95% of the times. In contrast, only 1-
17. 17
10% of adult infections yield a carrier state. Individuals with impaired immunity
are particularly likely to become carriers.
Asymptomatic Infection
Not surprisingly, patients in this group are identified incidentally on the basis of
minimally elevated serum transaminases or after the fact by the presence of
antiviral antibodies.
Acute Viral Hepatitis
This disease can be divided majorly into four phases: (1) an incubation period,
(2) asymptomatic preicteric period, (3) asymptomatic icteric phase, (4)
convalescence. Peak infectivity occurs during the last asymptomatic days of the
incubation period and the early days of acute symptoms.
The preicteric period is marked by non-specific, constitutional symptoms.
Malaise is followed in a few days by general fatigability, nausea, and anorexia.
Weight loss, low-grade fever, headaches, osteoporosis, shaking chills, pain, and
diarrhea are inconstant symptoms. Physical examination reveals a mildly
enlarged and tender liver.
Remarkably, as jaundice appears and the patient enters the icteric phase, other
symptoms begin to abate. The jaundice is caused predominantly by increased
bilirubin levels in the blood and hence is accompanied by dark-colored urine
and light-colored stools. Retention of bile salts results in distressing skin itching
(pruritus).
Figure 7: Symptoms of the preicteric phase of acute hepatitis B
18. 18
The icteric phase is absent in about half of hepatitis B patients. In a few weeks
to perhaps several months, jaundice and most of the other systemic symptoms
clear as convalescence begins.
Chronic Viral Hepatitis
The initial physical examination
should document the presence or
lack of signs of chronic liver
disease. For most patients with
chronic hepatitis B, the physical
examination is normal. The
clinical features of chronic
hepatitis are extremely variable and are not predictive of outcome. In some
patients, the only signs of chronic disease are persistent elevations of serum
transaminases, hence the misleading designation, “transaminitis”. The most
common symptoms are fatigue; less commonly, there are malaise, anorexia, and
occasional bouts of mild jaundice. Physical findings are few, most common
being spider angiomas, palmar erythema, mild hepatomegaly, hepatic
tenderness, mild splenomegaly. These symptoms are indicative of an advanced
disease.
Fulminant Hepatitis
When hepatic insufficiency progresses from the onset of symptoms to hepatic
encephalopathy within 2-3 weeks, it is termed as fulminant hepatic failure,
which is most often induced my hepatic viruses.
LABORATORY FINDINGS:
Serological testing
There are six serological markers used in hepatitis B panel of blood tests that
are essentially three different tests (HBsAg, Anti-HBs, & Anti-HBc) to detect
Figure 8: Symptoms of chronic viral hepatitis
19. 19
the presence of different antigens and antibodies in our blood serum. These are
as follows:-
1. Hepatitis B surface antigen (HBsAg)
This is a protein on the surface of the HBV; it is detected in acute or
chronic hepatitis infection and is hence, used to detect if the patient has
hepatitis or not. This antigen is also used in making hepatitis B vaccines.
2. Hepatitis B e antigen (HBeAg)
A product of the nucleocapsid (envelope) gene of the hepatitis B virus, this
antigen is found in serum during acute and chronic hepatitis B infection. Its
presence indicates that the virus is replicating and the infected person has
high levels of HBV. However, patients that are HBeAg negative may also
have high levels of HBV.
3. Total hepatitis B core antibody (anti-HBc)
It appears at the onset of symptoms in acute hepatitis B infection and
persists for life. The presence of anti-HBc indicates previous or ongoing
infection with HBV.
4. IgM antibody to hepatitis B core antigen (IgM anti-HBc)
Its presence
indicates the
presence of
acute (>6
months) and
not chronic
hepatitis B
infection. It is
also found
during viral
reactivations
of chronic
hepatitis.
20. 20
5. Hepatitis B surface antibody (anti-HBs)
The presence of the antibody to the surface antigen indicates recovery and
immunity from HBV infection. Anti-HBs also develops in a person who has
been successfully vaccinated against hepatitis B.
6. Hepatitis B e antibody (HBeAb or anti-HBe)
Spontaneous conversion from e antigen to e antibody (a change known as
“e” seroconversion) is a predictor of long-term clearance of HBV in
patients undergoing antiviral therapy and indicates lower levels of HBV.
Seroconversion also occurs in natural infection.
The interpretation of the test results to create a diagnosis that can be done
in the following ways:
21. 21
Liver-related tests
The hepatitis B virus specifically attacks the liver, so health care providers will
order blood tests to monitor the health of your liver. Some of the most
common liver-related blood tests are described below.
1. ALT (alanine aminotransferase) is found almost exclusively in the liver
and is monitored most closely in a chronic hepatitis B infection. This test
is useful in deciding whether a patient would benefit from treatment or
for evaluating how well a person is responding to therapy. The upper
limits of normal for ALT in healthy adults is 35 U/L for men and 25
U/L for women.
2. AST (aspartate aminotransferase) is found in the liver, heart, and muscle
so is less accurate than the ALT in measuring liver damage. However,
this enzyme is often ordered to help monitor potential liver damage
from the hepatitis B virus.
(ALT & AST are two enzymes the levels of which are checked in
liver function test or LFT)
3. AFP (Alpha-FetoProtein) - This is a normal protein produced in the
developing fetus, thus, pregnant women will have elevated AFP. Other
adults, however, should not have elevated AFP in their blood. This test
is used to screen for primary liver cancer patients with chronic hepatitis
B. Patients should have their AFP levels monitored at every visit since
hepatitis B is the leading cause of liver cancer. If the AFP level is high,
the health care provider will order more blood tests and imaging studies.
4. Ferritin - Iron is stored in the liver in the form of ferritin. Increased
levels of ferritin indicate that a high level of iron is being stored. This
could result from an increased iron intake in the diet (vitamin
supplements, food cooked in iron pots, etc.). For people living with
chronic hepatitis B, a high level can indicate liver damage since ferritin is
leaked into the bloodstream as liver cells are injured by the virus.
22. 22
Liver imaging
Non-invasive imaging
procedures may be used
to monitor the health of
the patient’s liver. An
abdominal ultrasound is a
swift, painless procedure
that can be used to detect
abnormalities in the liver,
such as cancer. Some
people with chronic
hepatitis B require regular
(6 monthly) liver
ultrasounds because they have been assessed as having a high risk of
developing serious liver disease. Ultrasound is useful for detecting tumors
and can potentially detect cirrhosis. If the ultrasound test reveals a tumor,
the doctor may want the patient to have a CT scan or an MRI done. The
CT scan (computed tomography or CAT scan) is a specialized X-ray that
produces a picture of the liver. MRI (magnetic resonance imaging) also
takes a picture, but it uses a magnetic field and radio wave pulses.
Liver Biopsy
A biopsy is a minor surgical procedure done in the hospital that allows experts
to examine tissue taken from the liver and determine how healthy the liver is.
Liver biopsy is more reliable than both ALT and HBV DNA levels in the
decision to treat patients with HBeAg-negative chronic HBV.
Figure 9: A sample liver ultrasound sonograph
Figure 10: Images of sample liver biopsy reports
23. 23
P R O G N O S I S
Prognosis can be variable for different types of hepatitis B. The hepatitis B
virus causing acute hepatitis usually only stays in the system for around one to
three months. The infection usually resolves without treatment and most adults
recover completely. However, in around 1 in 20 affected adults, the infection is
chronic and stays in the body for six months or more. This chronic form of
hepatitis B is very common in young infants and children. About 90% of
infants who are infected as newborns and 20% of young children affected go
on to develop chronic infection. Even if these children do not have symptoms,
they can still
pass the
infection onto
other people.
Children who
get the infection
from carrier
mothers have a
40% lifetime risk
of death from
cirrhosis or
hepatocellular carcinoma. Cirrhosis of the liver can take up to 20 years to
develop and may not cause any symptoms initially. Eventually, the liver damage
can lead to symptoms such as those mentioned above.
Fulminant hepatitis is a rare complication of acute hepatitis B where the
immune system attacks the liver and causes severe damage. The condition
affects around 1 in 100 adults who have chronic hepatitis B, but children are
affected much more rarely. Some of the symptoms of fulminant hepatitis B
include confusion, jaundice, and ascites. The most important factors for
predicting survival in FHF are the degree of encephalopathy and the patient's
age.
Figure 11: Possible courses of complications a chronic hepatitis infection can take, altering
the prognosis of the condition
24. 24
T R E A T M E N T
Once a patient is diagnosed with hepatitis
B, they are usually referred to a liver
specialist called a hepatologist. There are
decisions patients have to make to
protect their livers such as avoiding
alcohol and tobacco and eating healthy foods.
Current treatments for hepatitis B fall into two general
categories:
Immune modulator Drugs – These are interferon-type drugs (drugs that
are proteins which are produced by host cells infected with viruses) that
boost the immune system to help get rid of the hepatitis B virus. They are
given as a shot (similar to how insulin is given to people with diabetes) over
6 months to 1 year.
Antiviral Drugs – These are drugs that stop or slow down the hepatitis B
virus from reproducing, which reduces the inflammation and damage of
your liver. These are taken as a pill once a day for at least 1 year and usually
longer.
The majority of people with acute infection completely recover within a
couple of months and never go on to develop chronic hepatitis. There is no
specific treatment for short-term (acute) hepatitis B and unless symptoms are
severe, patients can generally manage these at home. Doctors usually advise
paracetamol for pain due to acute infection and strong painkillers like codeine
if severe pain is reported. Any nausea or vomiting symptoms can often be
relieved with medications such as metoclopramide (anti-emetic). Once
symptoms improve, patients need a further blood test to check they are free of
the virus and that chronic hepatitis B has not developed.
For chronic HBV infection, the World Health Organization (WHO)
recommend treating the individual with an antiviral medication. This is not a
cure, but it can stop the virus from replicating and prevent its progression into
25. 25
an advanced liver disease because a person with chronic HBV infection can
develop cirrhosis or liver cancer quickly and without warning. In low-income
settings, liver cancer can be fatal within months of diagnosis. Blood tests,
ultrasound scans and perhaps liver biopsy may also be required to check the
state of the liver and how much damage has been done.
The medications chosen to manage chronic hepatitis B depends on whether the
virus is causing persistent liver damage
because the immune system is sometimes able
to suppress the virus without any liver damage
being caused. For patients with a fairly healthy
liver function, the first treatment approach is
often a drug called peginterferon alfa 2-a
(immune modulator). If this therapy fails,
antiviral drugs such as entecavir and tenofovir
may be prescribed which are safe, highly effective and
recommended by the WHO.
In some cases, the medication is successful at
enabling the immune system to control the
virus and the treatment may no longer be
required.
There is no surgical treatment for hepatitis B. If
liver damage is severe enough that the liver starts
to fail, the only treatment that will help is a liver transplant. Liver transplant is a
major undertaking with an extended recovery period. It also depends on the
availability of a matching donor liver. If a liver transplant becomes a possibility
for the patient, the health care provider will discuss the risks and benefits with
him/her.
26. 26
P R E V E N T I O N
Since there is no specific treatment, prevention has been the major aim in
managing viral hepatitis B. The following measures are available –
a. Hepatitis B vaccine
i. Plasma-derived vaccine: This is based on the surface antigen
(HBsAg) which is harvested and purified from the plasma of human
carrier of HBV. The final vaccine is a formalin-inactivated sub-unit viral
vaccine for intramuscular
injection. Each 1 ml dose of
vaccine contains 20 µg of
hepatitis surface antigen
formulated in an alum
adjuvant. The vaccine is
given in 3 doses at 0, 1 and 6
months. An effective
antibody response is generally
attained after 3 doses in 95%
of vaccinees. Immunity
continues at protective levels
for approximately 3-5 years. Booster doses may be given after 3-5 years.
Both pre-exposure and post-exposure administration has been
recommended. Classical examples of post-exposure prophylaxis are the
protection of newborn infants born to HBV carrier mothers, and
individuals accidentally exposed to parenterally to HBV infection
through cuts, injuries, transfusions, and needlesticks. It is advisable but
not mandatory to give specific anti-HBs immunoglobin with or before
the vaccine dose in post-exposure cases.
Post-exposure prophylaxis is indicated in countries with a high
prevalence rate of HBV infection. In these countries, hepatitis B vaccine
27. 27
must be classified and
used in the same
category as DPT and
polio. Unfortunately,
the high cost of
vaccine preludes its
use in those parts of
the world where it is
most needed.
The vaccine has no effect on HBsAg carriers and is unnecessary in
persons with surface antibody from the previous infection.
ii. RDNA-yeast derived vaccine: An
alternate vaccine against hepatitis B was
licensed for the first time in the USA
in 1987. The recombinant DNA
vaccine was elaborated from the
cultures of yeast cloned with HBsAg
s-gene. Several field trials have shown that this vaccine is as
immunogenic, safe and effective as the plasma-derived vaccine and is
more cost-effective than the latter. The fact that this vaccine does
not depend on the scarce plasma resource is an added advantage.
b. Hepatitis immunoglobin (HBIG)
For immediate protection, HBIG is used for those acutely exposed to
HBsAg positive blood, for example, (a) surgeons, nurses or laboratory
workers, (b) newborn infants or carrier mothers, (c) sexual contacts of
acute hepatitis B patients. The HBIG should be given as soon as
possible after accidental inoculation (ideally before 6 hours and
preferably not later than 48 hours). At the same time, the victim’s blood
is drawn for HBsAg testing. If the test is negative, vaccination should be
started immediately and a full course be given. If the test is positive for
surface antibody, no further action is needed.
28. 28
c. Passive-active immunization
The simultaneous administration of HBIG and hepatitis B vaccine is
more efficacious than HBIG alone. HBIG does not interfere with
antibody response to the hepatitis B vaccine. This combined procedure
is ideal both for prophylaxis of person accidentally exposed to blood
known to contain HBV and for prevention of the carrier state in the
newborn babies of the carrier mothers. HBIG should be given as soon
as possible, preferably before 24 hours. Hepatitis B vaccine should be
given intramuscularly within 7 of exposure and second and third doses
given one and six months respectively, after the first dose.
d. Other measures
All blood donors should be screened for HBV infection, and those
positive for Australia antigen should be
rejected. Voluntary
blood donation should
be encouraged because
purchased blood has
shown a greater risk of
post-transfusion
hepatitis. Health
personnel should be
alerted about the importance of
adequate sterilization of all
instruments and to practice
simple hygienic procedures.
Carriers should be told not to
share razors or toothbrushes and use barrier
methods of contraception; they should not donate
blood.
29. 29
C A S E S T U D I E S
C A S E - 1
Name : Mr. Sunil Kumar, s/o Mr. Banwari Lal (Name changed)
Sex : Male
Age : 37 years
Civil status : Unmarried
Date admitted : 01/06/2018
Complaints : General weakness, headache, restlessness, loss of sleep
History of
present illness :
Mild headaches, restlessness, and loss of sleep started
occurring 6 months ago; general weakness began 3 weeks
ago; intensity of headaches increased since then; no
additional symptoms
Personal
history :
No previous hospitalizations; no records of substance abuse,
alcoholism, or tobacco; currently not under any medication
except the occasional use of ibuprofen for headaches (1-2
times a day); sexually active with several partners
Family history :
No history of cancer; no cases of hepatitis B, uterine fibroid,
heart diseases from the mother’s side
Examination
findings :
Appetite is mildly diminished; rounded
tender abdomen; patient sleeps for 2
hours a night; yellowish
eyes; dark urine
Blood test
reports :
ALT – 1520 IU/ml, AST – 1230 IU/ml; HBsAg +ve,
HBsAb –ve, HBeAg +ve, Anti-HBc IgM +ve
30. 30
Ultrasound
findings :
Hepatomegaly, no
splenomegaly, marginal
ascites, thickened GB wall,
normal bile ducts
Diagnosis : Acute hepatitis B (non-severe)
Treatment :
Rest recommended, proper nutrition, consumption of fluids,
replace ibuprofen with paracetamol
Follow-up after every six weeks with fresh serum test reports, additional
appointments necessary till HBV has been completely eliminated and reports
become normal
C A S E - 2
Name :
Late Mrs. Bimla Devi w/o Mr. Santosh Singh (Name
changed)
Sex : Female
Age : 44 years
Civil status : Married
Date admitted : 17/10/2018
Complaints : Diffuse abdominal pain, subjective fever, and jaundice
History of Brought to the hospital after four days of overpowering sore
31. 31
present illness : abdomen, continuous fever and yellowing of skin and eyes
Personal
history :
No history of alcoholism; no mention of ingestion of toxic
substances, homeopathic medicines or excessive use of
acetaminophen
Examination
findings :
Jaundice, painful epigastric palpation, painful right upper
quadrant palpation, no peritoneal irritation, no signs of
chronic liver disease, no signs of neurological distress and no
encephalopathy
Blood test
reports :
ALT – 6.315 mg/dl, AST – 8.947 mg/dl (worsened in the
next 3 days); HBsAg +ve,; HBsAb, HBeAg, Anti-HBc IgM
results requested
Ultrasound
findings :
Liver necrosis; starry night
appearance (acute edema,
necrosis); hyperechoic areas
Diagnosis : Prodromal period of hepatic failure
Treatment : Admitted for clinical observation; 0.5 mg doses of entecavir
started daily; patient was referred for liver transplantation
On the fourth day, the patient suffered overall
deterioration to grade II hepatic encephalopathy.
Applicable medicines to counter encephalopathy and
to manage liver disease were begun. The patient was
moved to the ICU for progression to hepatic
encephalopathy grade III and hemodynamic
deterioration requiring vasopressor support. She did
not respond favorably, and on the 5th day, she
developed grade IV hepatic encephalopathy. A CT
scan of her brain was taken that appeared to be
32. 32
normal. There was no clinical improvement. She had also developed upper
gastrointestinal bleeding for which infusion of omeprazole was initiated. She
was transfused with 15 cc/kg of plasma plus vitamin K. The patient progressed
to cardiac arrest. She was unresponsive to advanced maneuvers and died 5 days
after admission to the institution and nine days after onset of symptoms. The
cause of death was determined to be fulminant liver failure secondary to
hepatitis B.
33. 33
B I B L I O G R A P H Y
Park’s Textbook of Preventive and Social Medicine by K Park
Davidson’s Principles & Practice of Medicine by Sir Stanley Davidson
Robbins Pathologic Basis of Disease by Cortan, Kumar & Collins
www.mayoclinic.org
www.ncbi.nlm.nih.gov
www.hepb.org
www.news-medical.net
www.hepmag.com
www.wikipedia.org