Hepatitis C is a liver inflammation caused by the Hepatitis C virus (HCV). It is the most common cause of non-A, non-B hepatitis worldwide and a major cause of chronic liver disease. HCV is a positive-sense RNA virus of the Flaviviridae family with 6 genotypes. It infects hepatocytes and lymphocytes. Chronic HCV can lead to serious liver problems like cirrhosis or liver cancer over many years. Diagnosis involves liver tests, HCV antibody and RNA detection. There is no vaccine but treatment with antiviral drugs can cure most cases of HCV infection.
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
This lecture is about Spectrum of HCV infection presented by Dr. Muhammad Mostafa Abdel Ghaffar, Head of Tropical Medicine Department, Ahmed Maher Teaching Hospital.
The lecture was presented in the scientific meeting of Internal and Tropical Medicine departments, Ahmed Maher Teaching Hospital titled (Towards Eradication of HCV in Egypt) in celebration of World Hepatitis Day on July 28, 2016.
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http://www.no4c.com
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
This lecture is about Spectrum of HCV infection presented by Dr. Muhammad Mostafa Abdel Ghaffar, Head of Tropical Medicine Department, Ahmed Maher Teaching Hospital.
The lecture was presented in the scientific meeting of Internal and Tropical Medicine departments, Ahmed Maher Teaching Hospital titled (Towards Eradication of HCV in Egypt) in celebration of World Hepatitis Day on July 28, 2016.
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This lecture is about Virology of HCV presented by Dr. Mahmoud Elzalabany, Internal Medicine Resident, Ahmed Maher Teaching Hospital.
The lecture was presented in the scientific meeting of Internal and Tropical Medicine departments, Ahmed Maher Teaching Hospital titled (Towards Eradication of HCV in Egypt) in celebration of World Hepatitis Day on July 28, 2016.
https://www.facebook.com/AMTH.IM
https://www.facebook.com/events/1072758396145209/
http://www.no4c.com
BCC4: Pierre Janin on 4 Newer Agents for Hepatitis CSMACC Conference
Janin speaks on the dawn of a revolution for treating Hepatitis C. This was recorded at Bedside Critical Care Conference 4. Full postings can be found at www.intensivecarenetwork.com
Hepatitis b virus (hbv) infection a silent epidemicAung Zayar Paing
Myanmar is one of the countries with high HBV prevalence. Compared to other diseases like TB, HIV and malaria, HBV received less attention than it should to be educated, tested, vaccinated and treated.
A number of new hepatitis viruses (G, TT, SEN) were discovered late in the past century. We review the data available in the literature and our own findings suggesting that the new hepatitis G virus (HGV), disclosed in the late 1990s
OBI is a complex entity that comprises many conditions and different situations. Patients who have recovered from acute hepatitis B can carry HBV genomes for a long time,
and the virus might aggravate the course of their liver disease, when other causes of liver damage are present.The availability of highly sensitive molecular methods
has made it possible to unveil several virological features of OBI, to show its worldwide diffusion, and to reveal its possible involvement in different clinical settings. Relevant evidence indicates that HBV persistence as an OBI represents an important risk factor for HCC development.
Transmission risk factors, symptoms, diagnosis and treatment of hepatitis B. This is a deliberate presentation made to be easily understood by lay persons to appreciate the thinking of the doctors when it comes to treatment for hepatitis B
La disponibilidad de un sistema de multiplicación del virus de la hepatitis C (VHC) infeccioso en cultivos celulares está permitiendo investigar nuevos factores de respuesta a tratamientos antivíricos en condiciones controladas. Se presentará evidencia de que el fitness vírico puede ser un factor de multiresistencia a inhibidores y quese pueden obtener eficientes reducciones de carga viral empleando diseños secuenciales de administración de inhibidores que incluyan ribavirina. Se discutirán posibilidades de aplicación clínica.
This lecture is about Virology of HCV presented by Dr. Mahmoud Elzalabany, Internal Medicine Resident, Ahmed Maher Teaching Hospital.
The lecture was presented in the scientific meeting of Internal and Tropical Medicine departments, Ahmed Maher Teaching Hospital titled (Towards Eradication of HCV in Egypt) in celebration of World Hepatitis Day on July 28, 2016.
https://www.facebook.com/AMTH.IM
https://www.facebook.com/events/1072758396145209/
http://www.no4c.com
BCC4: Pierre Janin on 4 Newer Agents for Hepatitis CSMACC Conference
Janin speaks on the dawn of a revolution for treating Hepatitis C. This was recorded at Bedside Critical Care Conference 4. Full postings can be found at www.intensivecarenetwork.com
Hepatitis b virus (hbv) infection a silent epidemicAung Zayar Paing
Myanmar is one of the countries with high HBV prevalence. Compared to other diseases like TB, HIV and malaria, HBV received less attention than it should to be educated, tested, vaccinated and treated.
A number of new hepatitis viruses (G, TT, SEN) were discovered late in the past century. We review the data available in the literature and our own findings suggesting that the new hepatitis G virus (HGV), disclosed in the late 1990s
OBI is a complex entity that comprises many conditions and different situations. Patients who have recovered from acute hepatitis B can carry HBV genomes for a long time,
and the virus might aggravate the course of their liver disease, when other causes of liver damage are present.The availability of highly sensitive molecular methods
has made it possible to unveil several virological features of OBI, to show its worldwide diffusion, and to reveal its possible involvement in different clinical settings. Relevant evidence indicates that HBV persistence as an OBI represents an important risk factor for HCC development.
Transmission risk factors, symptoms, diagnosis and treatment of hepatitis B. This is a deliberate presentation made to be easily understood by lay persons to appreciate the thinking of the doctors when it comes to treatment for hepatitis B
La disponibilidad de un sistema de multiplicación del virus de la hepatitis C (VHC) infeccioso en cultivos celulares está permitiendo investigar nuevos factores de respuesta a tratamientos antivíricos en condiciones controladas. Se presentará evidencia de que el fitness vírico puede ser un factor de multiresistencia a inhibidores y quese pueden obtener eficientes reducciones de carga viral empleando diseños secuenciales de administración de inhibidores que incluyan ribavirina. Se discutirán posibilidades de aplicación clínica.
what you need to know about the liver ?
What is Hepatitis ?
Types of hepatitis
Hepatitis C virus
History & Statics
Causes
Prevention
Concequences
Symptoms
Analysis
Behaving with infected people
vaccine
Genotypes
Treatments
Management
Summary
Epidemiology of Hepatitis C Virus in Egypt; an overviewMahmoud Elzalabany
This lecture is about Epidemiology of HCV in Egypt presented by Prof. DeWolfe Miller, Professor of Epidemiology, Hawaii University.
The lecture was presented in the scientific meeting of Internal and Tropical Medicine departments, Ahmed Maher Teaching Hospital titled (Towards Eradication of HCV in Egypt) in celebration of World Hepatitis Day on July 28, 2016.
https://www.facebook.com/AMTH.IM
https://www.facebook.com/events/1072758396145209/
http://www.no4c.com
Research Paper presentation on "Antiviral activity of Acacia nilotica agains...Zohaib HUSSAIN
Presented by: : Zohaib HUSSAIN
Hepatitis C virus (HCV) belonging to the family Flaviviridae has infected 3% of the population worldwide and 6% of the population in Pakistan.
Pegylated INF-α plus ribavirin only treatment available
Thirteen medicinal plants were collected from different areas of Pakistan on the basis of undocumented antiviral reports against different viral infections.
Medicinal plants were air dried, extracted and screened out against HCV by infecting HCV inoculums of 3a genotype in liver cells
RT-PCR results demonstrate that acetonic and methanolic extract of Acacia nilotica(AN) showed more than 50% reduction at non toxic concentration
A serious liver infection caused by the hepatitis B virus that's easily preventable by a vaccine.
This disease is most commonly spread by exposure to infected bodily fluids.
Symptoms are variable and include yellowing of the eyes, abdominal pain and dark urine. Some people, particularly children, don't experience any symptoms. In chronic cases, liver failure, cancer or scarring can occur.
The condition often clears up on its own. Chronic cases require medication and possibly a liver transplant.
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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.
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
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.
2. • It is the inflammation of liver caused by
Hepatitis C virus.
• It is the most common cause of non A non B
hepatitis.
• It is a major cause of chronic liver disease in
the world.
3. Hepatitis C virus
• Part of Flaviviridae family of viruses
– Associated with both human and animal disease
– 3 genera: pestiviruses (cattle, pigs), flaviviruses
(dengue, yellow fever), hepaciviruses (HCV)
• It is an enveloped, icosahedral virus having single
stranded positive sense RNA.
• 6 genotypes worldwide, many subtypes and
isolates based on nucleotide diversity
• Quasispecies within individual
• In vivo replication in liver and lymphocytes
4.
5. HCV Genome
• 9.6 kb positive strand RNA genome
• Open reading frame encoding polyprotein of
~3010 amino acids
• 3 highly conserved areas:
–5’ UTR: initiating translation
–Core: codes for capsid protein monomer
–3’ UTR: essential for RNA synthesis &
packaging
8. Mode of Transmission
6015
10
4 11
Injecting drug use
Sexual trnsmission
Transfusion before
screening
Occupational
Others
Incubation period: 2 to 26 weeks; Mean 6-12
weeks
9. Immune response
• Patterns of viraemia
1. Drop after peak successful control
2. Drop followed by rebound chronic
infection
3. Consistent HCV chronic infection
11. Viral resistance
• NS 5A & E2 can interfere with PKR
• The core protein can inhibit the JAK-STAT
pathway by which IFN signals
• NS3/4A can block the accumulation of
phosphorylated IRF3 which inhibitrs
expression of type 1 interferons and IFN
stimulated genes.
12. Cell mediated immunity
• More vigorous CD8+ and CD4+ T cell
responses in all individuals that controlled
infection
• Chronic infections occur when
–unable to mount HCV-specific T cell
responses
–strong response that results in viral RNA
clearance, followed by contraction in
CD8+/CD4+ and rebound in viremia
13. Antibodies
• Role of antibodies unclear and poorly studied
• Virus can be cleared in absence of detectable
antibody responses
• Neutralizing antibodies target E2, which is
highly variable and able to evade
14. Immune-mediated liver injury
• Host immune response and not viral
replication
• HCV infects only 1-10% of hepatocytes
• IFN-γ and TNF-α from CD8+ destroy nearby
non-infected hepatocytes (“bystander killing”)
• HCC occurs mainly
due to high turnover
rate in hepatocytes
15. Clinical features
Acute
• Usually
asymptomatic
• Constitutional
symptoms
• Jaundice
• Right upper quadrant
pain
Chronic
• When there is persistent
RNA for more than 6
months
• Fatigue is the most
common symptom
• Jaundice is rare
• Immune complex
mediated diseases
18. Patients with risk to progression to
chronic hepatitis
• Older age
• Longer duration of
infection
• Advanced histologic
stage and grade
• Genotype 1
• More complex
quasispecies variety
• Increased hepatic iron
• Concominant other liver
disease
Alcoholic liver disease
Hemochromatosis
α₁ antitrypsin deficiency
Steatohepatitis
• HIV Infection
• Obesity
19. Diagnosis
Liver function test
Parameters Acute Chronic
Bilirubin (both conj
& unconj)
Raised Raised
ALT/AST Increased (400-1000
IU/L)
Episodic rise
Alkaline
phosphatase
Normal to ˂3 times
normal elevation
Normal to ˂3 times
normal elevation
Albumin Normal Decreased
Prothrombin time Usually normal Increased
20. Anti HCV antibody
First
generation
Against C100-
3 (NS4)
Appear 1-3
weeks after
infection
Second
generation
Against C200
& C33c (NS3)
Appear 9-10
weeks After
infection
Third
generation
Against C22-3
(core) & NS5
Appear 7-9
weeks after
infection
21.
22.
23. HCV RNA
• In acute infection detected within 2 weeks.
• Decreases after antibody production.
• Detected by
1. PCR
2. Branched DNA technique.
• HCV antigen: an EIA for hcv antigen is
available but less sensitive than HCV RNA.
24. Prognostic test
• 1.Genotyping:
Detected by : DNA sequencing, PCR
hybridization
Genotype 1&4 have worst prognosis.
Genotype 2&3 have better prognosis.
• 2. Viral load: high viral load→ poor response
to therapy.
25. Liver biopsy
• It is done in chronic hepatitis
To know the etiology ,
For grading and staging of the disease
To monitor the treatment.
26. Liver biopsy finding in
chronic hepatitis C
• 1.Portal tracts: Inflammation may confine to portal
tracts or may spill into adjacent parenchyma, with
necrosis of hepatocytes (interface hepatitis);there may
be bridging inflammation and necrosis. The portal
infiltrate is rich in lymphocytes, often forming
lymphoid aggregates and even a follicle with prominent
germinal centres.
• 2. Bile duct lesion: swelling and polystratifications of
bile duct lining cell, infiltration by lymphocytes and
larger macrophages and preservation of the basement
membrane of the bile duct.
27. Liver biopsy finding in
chronic hepatitis C
• 3. Lobular lesion:
• There may be loss of architecture. Hepatocytes show
balloning degeneration and necrosis.There may be
bridging necrosis.
May comprise a striking number of acidophil bodies
Cholestasis may be there.(canalicular bile plugs)
Mild to moderate steatosis, usually macrovesicular
type( more common in genotype 3).
Increased amount of hepatic iron even in absence of
blood transfusion.
28. Liver biopsy finding in
chronic hepatitis C
Periportal hepatocytes may contain Mallory Denk body
like coarse clumps of eosinophilic cytoplasm.
The lymphocytic infiltration in the lobules form rows
along the sinusoids.
Fibrosis is progressive in chronic hepatitis C. Portal
deposition→ Portal and periportal deposition→
Formation of bridging fibrous septa.
Angiogenesis occurs in CHC in the portal tract, fibrous
septa and periportal zone.
Continued loss of hepatocytes and fibrosis results in
cirrhosis,with fibrous septae and hepatocyte
regenerative nodule.
HCV RNA can be detected by in-situ hybridization.
29.
30. Chronic hepatitis C
showing portal tract expansion with inflammatory cells and fibrous tissue and
interface hepatitis with spillover of inflammation into the adjacent parenchyma. A
lymphoid aggregate is present.
31. Scheuer system of grading and staging
Grading
Grade 1 no or minimal
inflammation
Grade 2 Portal inflammation or
lobular inflammation,
no necrosis.
Grade 3 Mild piecemeal
necrosis or focal
hepatocellular necrosis.
Grade 4 Moderate piecemeal
necrosis or severe focal
damage.
Grade 5 Severe piecemeal
necrosis or bridging
necrosis.
Staging
Stage 0 No fibrosis.
Stage 1 Enlarged fibrotic
portal tract.
Stage 2 Periportal or
occasional portal
to portal septa.
Stage 3 Bridging necrosis
with
architectural
distortion, no
obvious
cirrhosis.
Stage 4 cirrhosis
32.
33. Prevention
• Never share drug equipments
• Practice safer sex
• Always use new sterilized
equipments
• Don’t touch dirty needles