Viral hepatitis is caused by viral infection of the liver which leads to hepatic inflammation and jaundice. There are several types of hepatitis viruses including hepatitis A, B, C, D, and E. These viruses are transmitted differently, with some spread through food/water (hepatitis A/E) and others through blood or bodily fluids (hepatitis B/C/D). Laboratory tests are used to diagnose viral hepatitis by detecting elevated liver enzymes, viral antigens, antibodies, or viral genomes in the blood or stool.
Benign Biliary Stricture is a common condition which we encounter during gastro practice. Here we discuss in detail about its diagnosis and management.
Benign Biliary Stricture is a common condition which we encounter during gastro practice. Here we discuss in detail about its diagnosis and management.
Viral hepatitis is a systemic disease primarily involving the liver.
Hepatotropic viruses : liver is the target organ and the main site of virus replication
Hepatitis A virus (HAV)
hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV, delta virus)
Hepatitis E virus (HEV).
Enterically:
virus is spread from person-to-person by putting something in the mouth that has been contaminated with the stool of a person with hepatitis E. This type of transmission is called "fecal-oral." For this reason, the virus is more easily spread in areas where there are poor sanitary conditions
The hepatitis B virion (Dane particle):
outer lipid envelope with the surface antigen (HBsAg).
an electron-dense core (nucleocapsid): ds circular DNA and polymerase surrounded by the core antigen (HBcAg).
The HBsAg is produced in excess by the infected hepatocytes and is secreted in the form of spherical
and filamentous particles.
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.
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
The POPPY STUDY (Preconception to post-partum cardiovascular function in prim...
HEPATITIS.ppt
1. Viral hepatitis is viral infection
of the liver that causes hepatic
inflammation which is followed
by the classic icteric symptoms
of jaundice and the release of
liver enzymes
2. Periods and clinical symptoms of hepatitis
Hepatitis B, C or D also cause:
- Skin rash
- Arthralgia
- Weight loss
1. Incubation period.
2. Preicteric period. 3. Icteric period.
4. Recovery.
4. Jaundice/Icterus
• Elevated levels of bilirubin in blood is
associated with “dark colored” urine.
• Obstructive jaundice causes impairment of
excretion into the small intestine.
• This results in the loss of the “normal
yellowing” of the stool.
• The stool are “white or achrolic”.
5. Classification of Hepatitis Viruses
Virus Family Nucleic acid Envelope
HAV Picornaviridae ss +RNA No
HBV Hepadnaviridae Incomplete circular ds –DNA Yes
HCV Flaviviridae ss +RNA Yes
HGV Flaviviridae ss +RNA Yes
HDV Genus Deltavirus ss –RNA Yes
HEV Hepeviridae ss +RNA No
TTV Circinoviridae ss –DNA No
SEN virus Circoviridae ss –DNA No
6. Viral hepatitis
Transmission
FOOD & WATER BORN BLOOD BORN
Incubation period
Hepatitis A: 2-6 weeks Hepatitis B: 2-6 months
Hepatitis E: 2-9 weeks Hepatitis C: 2-26 weeks
Hepatitis D: unlimited
Type of hepatitis
Acute Acute, chronic
10. Hepatitis A (infectious hepatitis)
• 1) is spread:
– by the fecal-oral route by ingestion of
contaminated food and water;
– through close physical contact.
• 2) contagious period extends 2-3 weeks
before and 8-10 days after onset of jaundice.
Virus may cause asymptomatic shedding.
• 3) does not cause chronic liver disease.
• 4) immunity is life-long.
11. Spread of HAV within the body
HAV enters the body by ingestion and intestinal infection. Then it
spreads by the bloodstream, to the liver, a target organ. Large
numbers of virus particles are detectable in feces during the
incubation period, beginning as early as 10-14 days after exposure.
Pathological changes appear exclusively in the liver.
12. Outcomes of Infection with Hepatitis A Virus
Outcome Children Adults
Inapparent
(subclinical)
infection
80–95% 10–25%
Icteric disease 5–20% 75–90%
Complete recovery > 98% > 98%
Chronic disease None None
Mortality rate 0.1% 0.3–2.1%
13.
14. Laboratory diagnosis of hepatitis A
• Biochemical tests to study liver function:
- The Bilirubin.
- Alanine aminotransferase (ALT).
- Aspartate aminotransferase (AST).
• Serology: ELISA
– Acute infection: IgM.
– Past Infection i.e. immunity: IgG.
• Direct demonstration:
– ELISA (detection of antigen in stool),
– RT-PCR of faeces.
17. Epidemiology of HEV infection
• Contagious period extends from before to
after symptoms.
• Transmission - via fecal-orale route by
ingestion of contaminated food and water.
• It causes only acute disease.
• Life long immunity.
• HEV infection is especially
serious in pregnant women
(mortality rate about 20 %).
• Transmission through placenta results in death of
fetus.
18.
19. Family Hepadnaviridae. Hepatitis B virus
The hepatitis B virion (Dane particle):
- outer lipid envelope with the surface antigen (HBsAg).
- an electron-dense core (nucleocapsid): ds circular DNA
and polymerase surrounded by the core antigen (HBcAg).
The HBsAg is produced in excess by the infected
hepatocytes and is secreted in the form of spherical
and filamentous particles.
HBeAg is the soluble
component of the core, with is
released during active
infection.
HBxAg is a transactivator of
viral transcription that appears
to contribute to HCC by
altering patterns of host gene
expression.
20. Pathway for the replication of HBV
1. Attachment to the cell surface receptor,
fusion and releasing the core into
the cytoplasm.
2.The core proteins dissociate from the DNA.
3. Completion of ds DNA by DNA polymerase
and entering the nucleus.
4. Formation of a circular episome.
5. Transcription of mRNAs.
6. Translation.
7. RNA is encapsidated by core proteins.
8. Inside the core, the RNA is transcribed to
minus strand DNA by polymerase called
reverse transcriptase.
9.Transcription the minus strand DNA into a
plus strand DNA.
10. Budding the virus through the
endoplasmic reticulum and/or Golgi Body
membranes from which it acquires HBsAg.
11. Shedding of viruses embedded in a lipid
bilayer and empty envelopes from HBsAg.
• 1011 new virions are produced every
day during acute infection
21. Characteristics of HBV
• Stable to:
– Acid at pH 2,3
– UV radiation
– Phenol
– Temperature:
• 1000 C for 5 minutes retains infectious activity
• 200 C for 3 months
• 40 C (in a refrigerator) for 6 months
– Survival:
• in dried blood for 4-5 months,
• in frozen plasma for 15-20 years,
• the presence of gross amounts of blood may interfere with the germicidal
action of disinfectants.
• Inactivated by:
– Autoclaving (1200 C for 20 min).
– Boiling for 60 minutes.
– Chloramine 1-2% for 2 hours.
– Ethanol 70-80% for 2 min.
– Formalin 1,5 % for 2 min.
– Hydrogen peroxide
23. Hepatitis B (serum hepatitis)
• 1) Transmission:
–parenterally,
–sexually,
–vertically (from mother to fetus),
–close contact (hemocontact).
• 2) chronic hepatitis in 10% to 15% of adult
patients, 30-90% of young patients
• 3) is causally associated with primary
hepatocellular carcinoma and cirrhosis.
24.
25. Epidemiology of HBV infection
• Virus is shed during both symptomatic
and asymptomatic periods.
• Transmission:
- In blood, semen, and vaginal
secretions, saliva and mother’s milk.
- Via transfusion, needle stick injury,
injecting drug use, sex, child-birth, and
breast-feeding.
Infective dose is 0.000001 ml of blood.
26. High Moderate
Low/Not
Detectable
blood semen urine
serum vaginal fluid feces
wound exudates saliva sweat
tears
breast milk
Concentration of hepatitis B virus in body fluids
Concentration HBV in the blood 109 virions per 1 ml
30. HBV can multiply in monocytes, T- and B-lymphocytes, NK.
Extrahepatic manifestation: glomerulonephritis, vasculitis and
ARTHRITIS-DERMATITIS (a serum sickness-like syndrome).
These patients experience rash, petechiae, purpura, arthralgia
and arthritis.
It involves mostly small joints of hands and knees and occurs in
the prodrome period, before jaundice appears and resolves
within a week.
32. CLINICAL OUTCOMES OF HEPATITIS B
Principal considerations:
Asymptomatic carrier: the carrier
patient never develops antibodies
against HBsAg and harbors the virus
without liver injury.
Chronic persistent hepatitis: the patient
has a low-grade hepatitis
Chronic active hepatitis: the patient has
an acute hepatitis state that continues
without the normal recovery (last longer
than 6-12 months).
Fulminant hepatitis: severe acute
hepatitis with rapid destruction of the
liver.
33.
34. Hepatocellular carcinoma
A section of a liver removed
at liver transplantation
showing a massive HCC (in
white) and multiple satellite
nodules
35. Pathology
Symptoms are immune-
mediated, resulting from
inflammation and cell-mediated
(cytotoxic T cell) responses to
HBsAg on the surface of
hepatocytes. These resolve the
disease.
If the cell-mediated
immune response is weak,
symptoms are mild but the
infection does not resolve and
chronic hepatitis ensues.
Chronic hepatitis leads to
cirrhosis and hepatocellular
carcinoma. Both of these are fatal
in the absence of a liver transplant
36.
37. HBsAg window
• “HBsAg window” - the period from about 6 to 8 months when
neither free HBsAg nor its antibody can be detected.
• Anti-HBsAg are undetectable because they are complexed with the large
amount of the antigen that is shed from infected cells.
• The best tool for diagnosis of an acute HBV infection during the
window is
the presence of
anti-HBcIgM
38.
39. Laboratory markers for HBV infection and their interpretation
• HBsAg – present in acute or chronic infection. It is detectable
in the blood from 1 to 6 months after infection.
• anti-HBs – marker of recovery and/or immunity to HBV
infection (from about 8 months after infection).
• anti-HBc IgM - marker of recent acute infection (≤6 months).
• anti-HBc IgG - past or chronic infection.
• HBeAg - indicates active replication of virus and therefore
infectiveness (from 2 to 6 months after infection).
• anti-HBe - virus no longer replicating. However, the patient can
still be positive for HBsAg which is made by integrated HBV
(from about 4 months after infection).
• DNA - indicates active replication of virus.
41. Hepatitis D virus (HDV) - delta agent
ss, circular (-) RNA virus similar to certain
plant viroids. It has delta antigen.
- HDV is coated with HBsAg which is needed
for release from the host hepatocyte and for
entry in the next round of infection.
- 3 genotypes.
43. Epidemiology of HDV infection
• HDV infects children and adults with underlying
HBV infection.
• Transmission:
- parenterally and sexually;
- vertically (rarely).
- In blood, semen, and vaginal secretions;
- Unsterilized equipment and infusion.
Intravenous drug abusers, transfusion and organ
recipients, and hemophiliacs are at highest risk for
infection.
44. Consequences of delta virus infection
• Co-infection by HDV and HBV exacerbates the acute disease
(90%) and fulminant hepatitis (2-4%) is more likely than with
HBV alone.
• Superinfection of a person already infected with HBV causes
a more rapid, severe progression than co-infection because
super-infection requires HBV replication before HDV replication
can occur.
– about half of the patients exhibit acute hepatitis that resolves
– about 10-40% get chronic persistent hepatitis
– 7-10% get fulminant hepatitis.
45. Laboratory markers for HDV infection
• In an HBV-HDV co-infection:
– HDV antigen is detected in about ¼ of patients.
HDV antigen disappears when HBsAg appears,
– anti-HDV IgG and IgM are usually seen,
– anti-HDV decline as the symptoms resolve and,
unlike anti-HBs, there are no antibodies to show
that the patient was once HDV-infected,
– anti-HBs IgG rises.
• In a super-infection by HDV:
– HBsAg and HDV RNA remain because super-
infection usually leads to chronic infection.
– anti-HDV IgG rises.
46.
47.
48. Family Flaviviridae.
Hepatitis C and G viruses
Enveloped ss+RNA viruses, 55-65 nm diameter.
14 genotypes of HCV.
5 genotypes of HGV.
Electron micrograph of
the hepatitis C viruses
49. HCV life cycle
• a) Virus binding and internalization,
• b) cytoplasmic release and uncoating,
• c) translation,
• d) RNA replication,
• e) packaging and assembly,
• f) virion maturation and release.
51. Epidemiology of HCV and HGV infection
• 85-90% patients will develop chronic disease.
• About 50% of chronic carriers of HCV progress to cirrhosis or liver cancer in 10-40 years.
• Transmission:
- parenterally (through sharing
drug-injection equipment or
from transfusion of unscreened
blood or untreated clotting factors),
- sexually,
- perinatally.
- In blood, semen, and vaginal secretions.
- Contagious period extends 2-3 weeks before and 10 weeks
after onset of symptoms.
53. Risk factors of hepatitis C
• Blood-to-blood contact (mainly transfusion):it is estimated that 90% of persons
with chronic HCV infection were infected through transfusion of unscreened blood
or blood products.
• Unsterilized injection equipment and infusion: considered to be the primary
sources of HCV infection.
• Sexual intercourse: although this is rare, and usually only occurs when HIV is also
present and makes blood contact more likely.
• Dental equipment: People can be exposed to HCV via inadequately or improperly
sterilized medical or dental equipment including needles or syringes, oral hygiene
instruments, and jet air guns, etc.
• Hemodialysis: The basic problem is that proper sterilization methods are not
followed.
• Occupational exposure to blood: Medical and dental personnel, first responders
(e.g. surgeons, nurses and emergency medical technicians) can be exposed to
HCV through needle sticks or blood spatter to the eyes or open wounds.
• Tattoos: Tattooing dyes, ink pots, piercing implements can transmit HCV-infected
blood from one person to another if proper sterilization techniques are not followed.
• Shared personal care items: Such as razors, toothbrushes, cuticle scissors, and
other manicuring or pedicure equipment can easily be contaminated with blood
carrying the virus, and take care that HCV can live on dried blood for 15 days.
• Vertical transmission: refers to the transmission of a communicable disease from
an infected mother to her child during delivery.
54. Pathogenesis of HCV infection
• Hepatocytes are target cells for HCV.
• CPE – lysis of hepatocytes.
• Sensitive cells: monocytes, macrophages, B-
lymphocytes, neutrophiles, cells of bone marrow.
• HCV can reproduce in cells of pancreas, adrenal
glands, thyroid glands, spleen.
• Immunomediated extrahepatic manifestations:
– vasculitis (malaise, arthralgia, purpura);
– glomerulonephritis;
– altered nervous system (peripheral nerves, brain).
58. Laboratory diagnosis of viral hepatitis
• Biochemical methods: Detection of the level of
bilirubin and enzymes ALT, AST in serum.
• Serology:
ELISA - Detection of the Ag
and antibodies
• Detection of a viral genome: PCR
• Rapid immunochromatographic test
59. Rapid test
• A direct test for the visual detection of hepatitis viruses antigenes or
antibodies in serum.
• It is based on the principle of sandwich chromatographic immunoassay.
• Its result appears within 15-30 minutes.
60. • The test sample is applied to a thin
strip of nitrocellulose held in a
plastic frame.
• The nitrocellulose is impregnated
with antibodies directed against the
assayed antigen. These antibodies
are labeled with colored gold
spheres to permit visual readout of
the assay.
• The same antibody, minus the
colored spheres, is bound along a
line further down the strip.
• When the clinical sample is applied
to the strip, it migrates by capillary
action towards the opposite end. An antigen that reacts with the
labeled antibodies will also be bound
by the immobilized antibodies as the
complex moves down the strip. The
result is a visible colored line on the
filter indicating that antigen is present
in the sample.
61. Vaccines
• Against Hepatitis A
Havrix (inactivated)
• Against Hepatitis B (recombinant)
- Monovaccines (HBsAg – genetic engineering):
Engerix B
H-B-Vax
Recombivax B
- Divaccines:
Twinrix (inactivated HAV + HBsAg)
64. Treatment
• Anti-HBV immune globulin is effective soon after exposure. It
can also be given neonatally to children of HBsAg-positive
mothers. Ideally, the immune globulin should be administered
within 24 hours of birth or exposure and is probably not
effective after one week from exposure.
• Interferon - for HBeAg +ve carriers with chronic active hepatitis.
Response rate is 30 to 40%.
• Lamivudine - a nucleoside analogue reverse transcriptase
inhibitor. Well tolerated, most patients will respond favorably.
However, tendency to relapse on cessation of treatment.
Another problem is the rapid emergence of drug resistance.
• Adefovir – less likely to develop resistance than Lamivudine
and may be used to treat Lamivudine resistance HBV. However
more expensive and toxic
• Entecavir – most powerful antiviral known, similar to Adefovir
• Successful response to treatment will result in the
disappearance of HBsAg, HBV-DNA, and seroconversion to
anti-HBeAg.
65. Familly Circinoviridae.
Transfusion Transmitted Virus (TTV)
Non-enveloped circular ss (-) DNA virus.
16 genotypes.
• The virus has been found worldwide with an extraordinarily
high prevalence of chronic viremia in apparently healthy
people, up to nearly 100% in some countries.
• TTV-DNA was detected:
– in 47% of patients with fulminant hepatitis,
– In 46% of patients with chronic liver,
– in patients with liver cirrhosis,
– and hepatocellular carcinoma.
• Virus DNA is not integrated in tumour cells, which
may suggest that the virus is a passenger rather
that causative of the tumour.
66. Transfusion Transmitted Virus
• Transmission:
- by parenteral exposure to blood,
- sexually,
- enterally (fecal-oral),
- from mother to child.
• The detection of TTV in saliva, nasopharyngeal
secretions, skin and hair might imply that household
contact transmission is also possible.
• The highest detection rates amongst:
– polytransfused,
– thalassemic,
– long-term hemodialysis patients,
– hemophiliacs treated with the nonvirally inactivated clotting-
factor concentrates,
– intravenous drug abusers.
67. Family Circoviridae. Hepatitis SEN virus
Non-enveloped circular ss (-) DNA virus.
8 genotypes.
Transmission:
• via blood-product transfusion,
• via parenteral drug use,
• via iatrogenic means in a hospital setting,
• sexually,
• perinatally, or by other means.
68. Hepatitis SEN virus
• The majority of patients who acquire de novo
transfusion-associated SEN-V infection appear to
clear the virus with time.
– In the National Institute of Health (NIH) study, 77% of
post-transfusion infected patients cleared the virus, in
the majority within a 6-month period after infection.
• Nonetheless, a few patients did not clear the virus
for years, and 13% appeared to have chronic
SEN-V infection.
– It is unknown whether these chronically-infected patients
would eventually clear the virus if followed over many
years (i.e., decades).