The document discusses various types of hepatobiliary diseases that can occur during pregnancy including viral hepatitis, drug-induced hepatitis, autoimmune hepatitis, ischemic hepatitis, and viral hepatitis A-E. It notes physiological changes in liver enzymes and function during pregnancy. It provides details on symptoms, transmission, management, and risks for mother and baby associated with each condition.
Pregnancy and viral hepatitis by dr alka mukherjee nagpur m.s. indiaalka mukherjee
Acute viral hepatitis is the most common cause of jaundice in pregnancy. The course of most viral infections is not affected by pregnancy.
Jaundice is a characteristic feature of liver disease. The clinical signs and symptoms are indistinguishable between the various forms of viral hepatitis, thus, the differential diagnosis requires serologic testing for a virus-specific diagnosis, [1, 2] and the diagnosis is by biochemical assessment of liver function.
The differential diagnosis includes other forms of viral hepatitis including mononucleosis and Epstein-Barr virus (EBV) infections, autoimmune disease, and widespread systemic infection with liver failure. Patients presenting with jaundice during pregnancy often require a workup to differentiate obstructive gall bladder or bile duct disease, severe preeclampsia, HELLP (hemolysis, elevated liver enzyme levels, low platelet count), or acute fatty liver of pregnancy from viral hepatitis.
The most useful tests to diagnose hepatitis include laboratory evaluation of urine bilirubin and urobilinogen, total and direct serum bilirubin, alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST), alkaline phosphatase (ALP), prothrombin time (PT), total protein, albumin, complete blood cell (CBC) count, and in severe cases, serum ammonia.
Pregnancy and viral hepatitis by dr alka mukherjee nagpur m.s. indiaalka mukherjee
Acute viral hepatitis is the most common cause of jaundice in pregnancy. The course of most viral infections is not affected by pregnancy.
Jaundice is a characteristic feature of liver disease. The clinical signs and symptoms are indistinguishable between the various forms of viral hepatitis, thus, the differential diagnosis requires serologic testing for a virus-specific diagnosis, [1, 2] and the diagnosis is by biochemical assessment of liver function.
The differential diagnosis includes other forms of viral hepatitis including mononucleosis and Epstein-Barr virus (EBV) infections, autoimmune disease, and widespread systemic infection with liver failure. Patients presenting with jaundice during pregnancy often require a workup to differentiate obstructive gall bladder or bile duct disease, severe preeclampsia, HELLP (hemolysis, elevated liver enzyme levels, low platelet count), or acute fatty liver of pregnancy from viral hepatitis.
The most useful tests to diagnose hepatitis include laboratory evaluation of urine bilirubin and urobilinogen, total and direct serum bilirubin, alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST), alkaline phosphatase (ALP), prothrombin time (PT), total protein, albumin, complete blood cell (CBC) count, and in severe cases, serum ammonia.
Prelabour Rupture of Membrane (PROM) by Sunil Kumar Dahasunil kumar daha
Please find the power point on Prelabour Rupture of Membrane (PROM). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
The increased cardiac output related to pregnancy can lead to heart failure, and the increased heart rate in the third trimester can lead to ischemic events. The potential obstetrical complications include preeclampsia or other hypertensive related disorders, premature birth, and small-for-gestational-age births.
If someone says the word “Herpes”, everyone cringes. Surprisingly, about 2/3 of you reading
this now, may have had HSV 1 (the type that causes cold sores), and about 20% of you may
have had the genital type of Herpes (HSV2).
Prelabour Rupture of Membrane (PROM) by Sunil Kumar Dahasunil kumar daha
Please find the power point on Prelabour Rupture of Membrane (PROM). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
The increased cardiac output related to pregnancy can lead to heart failure, and the increased heart rate in the third trimester can lead to ischemic events. The potential obstetrical complications include preeclampsia or other hypertensive related disorders, premature birth, and small-for-gestational-age births.
If someone says the word “Herpes”, everyone cringes. Surprisingly, about 2/3 of you reading
this now, may have had HSV 1 (the type that causes cold sores), and about 20% of you may
have had the genital type of Herpes (HSV2).
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.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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 Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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ASA GUIDELINE
NYSORA Guideline
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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
2.
Pregnancy is associated with many physiological changes
that must be considered in the diagnosis of hepatobiliary
diseases:
Outside pregnancy, the liver receives up to 25–35% of the
cardiac output and this does not change significantly
during pregnancy.
Spider angiomas and palmar erythema, which are
classically associated with chronic liver disease, are also
common during pregnancy and usually disappear after
delivery
physiological changes
3.
Because of hemodilution, serum albumin levels
decrease.
The most significant changes are the decreased liver
transaminases levels to 25% pre-pregnancy levels by
the third trimester.
Alkaline phosphatase levels can increase up to four
times due to placental alkaline phosphatase and
increased maternal bone turnover.
4.
Bilirubin levels usually unchanged or slightly
decreased
Total bile acid concentrations not significantly
different.
5.
is inflammation of the liver.
Viral infection is the most common cause of hepatitis
in the world
other causes are drug-induced , autoimmune,
alcoholic and ischemic hepatitis.
Hepatitis
6.
halothane, acetaminophen, phenytoin, methyldopa,
isoniazid, and diclofenac are the most common
causes
Mgm by stopping the offending drug and follow up
by serial biochemical measurements
Recovery should be expected in the majority of
patients after discontinuing the drug. However,
acute liver failure caused by an idiosyncratic drug
reaction has a mortality rate of over 80 percent
without liver transplantation
Drug induced hepatitis
7.
bilirubin greater than two times the upper limit of
normal in the setting of an ALT greater than three
times the upper limit of normal) following
introduction of a drug potentially portends a poor
prognosis and should also prompt immediate
referral for hepatologist.
N-acetylcysteine for acetaminophen toxicity and L-
carnitine for cases of valproic acid overdose
improves the outcome.
8.
Autoimmune hepatitis is a chronic hepatitis that occurs
women of childbearing age.
It has a heterogeneous and fluctuating nature, leading to
marked variability in its clinical manifestations from
asymptomatic patients to debilitating disease with acute
liver failure.
The disease activity is usually attenuated during
pregnancy, and dosages of medication can be decreased
Nonetheless, flares have occurred in 11% of patients
during gestation and up to 25% in the postpartum period
Autoimmune hepatitis
10.
One clue to diagnose autoimmune hepatitis the
coexistence of other diseases with autoimmune
features(hemolytic anemia, idiopathic
thrombocytopenic purpura, type 1 diabetes mellitus,
thyroiditis)
11.
pregnancy in women with AIH has been associated with
an increased risk of prematurity, low birth weight and
fetal loss.
The presence of anti-Ro/SSA,anti-La/SSB and
anticardiolipin antibodies was associated with adverse
pregnancy outcome.
Patients need to be monitored carefully during pregnancy
and several months post-partum because of the risk of
flares in disease activity(In women with abnormal liver
function tests, also measure the prothrombin time and a
blood glucose level. A full blood count may reveal
thrombocytopenia in women with hyperslenism
12.
Usual therapy consists of glucocorticoids and/or
azathioprine, both of which are safe during pregnancy.
Doctors caring for women with AIH should also consider
increasing the dose of immunosuppressive therapy in the
third trimester or immediately after delivery.
women with uncomplicated disease who have not had a
flare should be able to have a normal labor and delivery.
If a woman with AIH has portal hypertension, it is
advisable to avoid pushing in the second stage of labor.
13.
Issues related to medications and lactation
Azathioprine and prednisolone/prednisone enter
breast milk in low concentrations and should be
continued during lactation
Contraceptive recommendations
In well-controlled disease, any form of contraception
can be used.
If hepatic impairment is present, estrogen-containing
contraceptives are usually discouraged
14.
refers to diffuse hepatic injury resulting from acute hypo
perfusion.
The term hepatitis is somewhat a misnomer since the
injury is not mediated by an inflammatory process.
Nevertheless, the profound elevation in
aminotransferases is similar to that seen in acute viral and
toxic hepatitis
Ischemic hepatitis is usually first detected because of
elevations in liver biochemical tests following a
hypotensive episode.
Occasional patients have symptoms suggesting acute
hepatitis, including nausea, vomiting, anorexia, malaise,
and right upper quadrant pain
Ischemic hepatitis
15.
rapid rise in serum aminotransferase levels associated
with an early massive rise in lactate dehydrogenase
(LDH) levels. Peak aminotransferase levels are typically
25 to 250 times the upper limit of normal and are reached
within one to three days of the hemodynamic insult.
aminotransferase levels subsequently decline steadily,
usually returning to normal within 7 to 10 days. The
serum bilirubin level rarely rises above four times the
upper limit of normal, usually beginning its rise after
aminotransferase levels have begun to decline.
Hepatic synthetic function usually remains normal or is
only mildly impaired.
16.
features may suggest an ischemic rather
than a viral cause of liver injury.
An early rapid rise in the serum LDH level is unusual in viral
hepatitis.
A ratio of serum alanine aminotransferase to LDH of less than
1.5 early in the course of acute hepatitis may be more likely to
suggest ischemic hepatitis.
A rapid fall in serum aminotransferase levels after the initial
rise is characteristic of ischemic liver injury and atypical for
other causes of hepatitis.
Ischemic hepatitis is often accompanied by additional evidence
of end-organ hypo perfusion, especially acute tubular necrosis
of the kidney.
17.
Management of ischemic hepatitis should be aimed
at restoring cardiac output and reversing the
underlying cause of hemodynamic instability.
Limited data suggest that intravenous
administration of dopamine, at either "renal" or
"cardiac" doses, leads to preservation, and perhaps
augmentation, of hepatic blood flow,
treatment with intravenous N-acetylcysteine was
described in a case report. The mechanism of benefit
may have been due to a cytoprotective effect.
18.
The commonest cause of hepatic dysfunction in
pregnancy.
Caused by:
1. hepatitis virus A,B,C,Dor E
2. CMV
3. HSV
4. EBV
With exception of hepatitis E,HSV infection the
clinical features don't differ from non pregnant
female.
Viral hepatitis
19.
Some people with hepatitis have no symptoms and
When symptoms occur, they can include:
1. jaundice
2. abdominal pain
3. loss of appetite
4. nausea and vomiting
5. diarrhea
6. fever
Acute hepatitis
20.
Symptoms of chronic hepatitis can include:
1. feeling unusually tired all the time
2. depression
3. jaundice
4. a general sense of feeling unwell
Both hepatitis A&E don't cause chronic disease
Chronic hepatitis
21.
The course of hepatitis A during pregnancy is
generally similar to that in non pregnant patients.
severe illness during the third trimester may be
associated with an increased risk for premature labor
and premature rupture of membranes
It is not an important cause of maternal or neonatal
morbidity, yet it can be transmitted from mother to
child.
Hepatitis A
22.
Pathogenesis of mother-to-child transmission
it is very rare.
Only two cases of intrauterine transmission following
maternal infection in the first trimester have been
reported and resulted in fetal meconium peritonitis.
Maternal infection in the third trimester may result in
asymptomatic neonatal infection and/or self-limited
neonatal cholestasis
Breastfeeding is not implicated in transmission
23.
Around 90% of pregnant female with acute infection
transmit infection to infant while only 10-20% in
chronic cases and this risk is high, if the infection is
acquired during the third trimester or if the infected
mother is positive for (eAg) and the viral DNA count
is elevated
90% of Infected newborn will be chronic carrier
&upto25% will develop cirrhosis or HCC if not
receive vaccine& immunoglobulin
Hepatitis B
24.
Hepatitis C virus has the particular ability to
establish chronic infections, leading to cirrhosis and
hepatocellular carcinoma.
The predominant mechanism of MTCT has
traditionally been thought to be intrapartum
&debate exists about whether a greater proportion
happens in utero
Hepatitis C
25.
The highest incidence of HEV infection is in Africa,
Middle East, and Central America
HEV is the second most common cause of sporadic
hepatitis in North Africa and the Middle East.
It causes a self-limited acute infection, although
fulminant hepatitis can develop.
Chronic hepatitis does not develop after acute HEV
infection.
Hepatitis E
26. For reasons that are not understood, fulminant hepatic
failure occurs more frequently during pregnancy,
resulting in high mortality rate of 15 to 25 percent.
primarily in women in the third trimester , resembling
liver failure from acute fatty liver of pregnancy, hepatic
infarction in (HELLP), or herpes simplex hepatitis
Trans placental transmission of HEV has been
documented by specific HEV IgM in cord blood and virus
isolation by PCR, in up to 33% of neonates born to women
infected in the third trimester ,resulting in neonatal
massive hepatic necrosis and death. Nonetheless, other
infants have recovered from in utero infection
27.
Affected patients may have a prodrome of fever and
upper respiratory tract symptoms. Usually more
severe when occurring in the third trimester.
A vesicular eruption, if present, should suggest the
diagnosis.
Despite marked abnormalities in serum
aminotransferases and the prothrombin time, they
are usually anicteric at presentation.
delivery is usually unnecessary and therapy with
acyclovir is often successful.
Herpes simplex
28.
Hepatitis A is transmitted predominantly by the fecal-
oral route.
Prevention can be aided by adherence to sanitary
practices such as hand washing, heating foods
appropriately, and avoidance of water and foods in
endemic areas.
Hospitalized patients with HAV do not require isolation
or contact precautions unless incontinent. Frequent hand
washing should be enough to prevent spread in the hospital
setting.
prevention
29.
INDICATIONS FOR VACCINATION :
1. Persons with clotting-factor disorders or chronic liver disease.
2. Persons traveling to countries with high or intermediate endemicity(one
dose of HAV vaccine at least 2 weeks before traveling, and a booster dose
6–12 months after the initial vaccination).
3. Persons with HIV infection.
4. Close family contacts of index cases.
5. Persons with recent exposure for post-exposure prophylaxis.
Prevention of maternal illness after a known exposure to
HAV:
Passive immunization with immunoglobulin within 2 weeks of
exposure & HAV vaccination is effective in preventing 80–90% of HAV cases
30.
Hepatitis B
All pregnant women should be routinely screened
for HBsAg and HBsAb, regardless of previous
testing or vaccination.
If vaccination is indicated in pregnancy, it is safe and
effective
Indication for vaccination:
Household contacts of patients with hepatitis B
Intravenous drug users
31.
Healthcare workers
Patients on chronic hemodialysis
patients requiring repeated blood or blood product
transfusion
Patients with chronic liver disease
All unvaccinated persons traveling to areas with
intermediate to high levels of endemic HBV infection
Both hepatitis A,B vaccines &immunoglobulin are safe
during pregnancy.
32.
should receive both HBV vaccination and HBV
immunoglobulin (HBIG 400 IU IM), preferably
within 24 hours of exposure but can be administered
up to 72 hours post exposure.
Hepatitis D
The mainstay of prevention of HDV infection is
vaccination against its helper virus
WOMEN EXPOSED TO HBV DURING
PREGNANCY
33.
Hepatitis E is a water-borne pathogen transmitted
by the fecal-oral route.
To reduce the risk of contracting HEV while
traveling to endemic areas, it is important to
maintain hygienic practices such as hand washing
with safe water, particularly before handling food,
avoiding drinking water and avoiding eating
unpeeled fruits and vegetables.
Currently there is no vaccine available
34.
Pregnancy is generally well tolerated by women
with chronic hepatitis who don't have advanced ds.
Reactivation of the virus and exacerbation of the
disease during or after gestation are uncommon.
Preconception
35.
Mild liver ds& will achieve
pregnancy soon
Elect to finish ttt before
pregnancy
Pt got pregnant on
antiviral ttt(discuss
risk/benefit of
discontinuation
• Defer ttt till complete
family
• PG/INF
(48mo)+contraception
• Change drug category C to
B
• Can discontinue if no
cirrhosis
Options for HBV ttt in CBP
36.
treatment be considered in patients with HBeAg
positive or HBeAg negative chronic hepatitis.
Patients with compensated cirrhosis and HBV DNA
>2,000 IU/mL and those with decompensated
cirrhosis and detectable HBV DNA by PCR assay
should be considered for antiviral therapy,
regardless of the serum ALT level.
WHO SHOULD BE
TREATED
37.
Patients in whom therapy is indicated: acute liver
failure, clinical complications of cirrhosis, cirrhosis
or advanced fibrosis with high serum HBV DNA, or
reactivation of chronic HBV after chemotherapy or
immunosuppression.
Patients for whom therapy may be indicated:
patients in the immune-active phase who do not
have advanced fibrosis or cirrhosis (HBeAg-positive
or HBeAg-negative chronic hepatitis).
criteria for treatment were suggested in a 2008
consensus conference from the United States
National Institutes of Health
38.
Patients for whom immediate therapy is not
routinely indicated: (1) Patients with chronic HBV in
the immune tolerant phase (with high levels of
serum HBV DNA but normal serum ALT levels or
little activity on liver biopsy); (2) Patients in the
inactive carrier or low replicative phase (with low
levels of or no detectable HBV DNA in serum and
normal serum ALT levels); (3) Patients who have
latent HBV infection (HBV DNA without HBsAg)
43.
Counseling both male and female patients about the risks
of pregnancy while on RBV therapy, and for six months
after discontinuing treatment, is critically important.
RBV cause limb abnormalities, craniofacial defects,
anencephay& anophthalmia.
any woman that becomes pregnant on RBV should
immediately notify their physician, and receive
appropriate counseling about teratogenicity and the
option for therapeutic abortion.
So advise all patients on RBV to practice at least two
forms of contraception
Chronic hepatitis C
44.
All pregnant women should be offered screening for
HBV,HCV,HIV at the booking visit.
All women who exhibit ‘high risk’ behaviors for
contracting blood-borne viruses should be
rescreened for HBV and HCV and HIV in the third
trimester
Antenatal care
45.
For Women positive for hepatitis B or C:
Liver function tests (transaminases, albumin,
bilirubin and INR) should be performed every 3
months till 6 months postpartum(rare risk of flare).
Hepatitis A virus immunity (HAV IgG)
As There is evidence that patients with any
acute/chronic HBV or HCV are at increased risk for
adverse outcomes if they acquire HAV. It is
recommended that if they are not immune to HAV, to
be vaccinated
46.
woman test positive to antibodies for HCV then a
blood test for HCV RNA Polymerase Chain Reaction
(PCR) should be ordered to detect the presence or
absence of the virus in the blood, the viral load, and
the genotype
woman with HBsAg positive HBeAg , anti-HBe and
HBV DNA levels should be measured.
47.
Women positive for hepatitis B or C, particularly
those with a high viral load, should be counseled
about the potential risk of transmission with invasive
procedures. Non-invasive prenatal testing may be
an option for some women. In those requiring
invasive procedures, amniocentesis is probably safer
than CVS, and transplacental amniocentesis is best
avoided, if possible
Invasive procedure
48.
At 26-28 wk perform HBV DNA level to determine
need for ttt as number of studies have shown
lamivudine and recently telbivudine therapy used
during the third trimester of pregnancy in HBsAg-
positive women to be safe and to reduce the risk of
intra-uterine and perinatal transmission of HBV if
given in addition to passive and active vaccination.
Antiviral therapy
50.
1. Conflicting data of increased DM risk in chronic
HBV infection
2. No evidence of change management in case of
PPROM.
3. HCV ab positive female at higher risk of obstetric
cholestasis which occur at earlier gestation.
Effect of disease on pregnancy
51. HBV HCV
HBsAg +ve & HBe Ag –ve & DNA –
ve ==2-15%
HCV Ab +ve& HCV RNA –ve
=<1%
HBsAg +ve & HBe Ag +ve & DNA
+ve==80-95%
HCV Ab +ve& HCV RNA +ve
=11%
HCV Ab +ve& HCV RNA +ve
&HIV Ab +ve =16%
4-Risk for perinatal transmission
52.
Usually cases with advanced cirrhosis infertile due
to anovulation. But pregnancy can occur in early
cases of cirrhosis which increases the risk of:
1. FGR
2. PTB
3. IUFD
4. Gestational HTN
5. Placental Abruption
6. Peripartum hemorrhage
5-complications associated with cirrhosis
53.
Management don't differ in pregnancy
Endoscopy for variceal screening safe during
pregnancy
Banding & sclerotherapy is mgm of active bleeding
Beta blocker used with caution
Octreotide not used due to risk of uterine ischemia
54.
CS does not appear to reduce the risk of transmission
Avoid procedures that may increase risk of vertical
transmission :
• fetal blood sampling
• fetal scalp electrode use
• early artificial rupture of membranes should be avoided
where possible
• Prolonged rupture of membranes (>6 hours) may increase the
risk of transmission, so it is recommended that the second
stage of labor be kept short
• if assisted delivery is required the use of soft cup vacuum
extraction or forceps is preferred over a metal cup which poses
increased risk for scalp injury
Intra partum
55.
The neonate should be bathed to remove maternal
body secretions prior to administering intramuscular
injections
56.
Prevention of neonatal infection:
1=hepatitis A:
Immunoglobulin at a dose of 0.02 mg/kg is
recommended to prevent neonatal infection if
maternal illness develops 2 weeks before or 1 week
following delivery
2= hepatitis B:
all newborn infants receive a monovalent hepatitis B
vaccine at birth (within 24 hours). Followed by 3
doses at 2, 4 and 6 months of age
Postpartum
57.
If an infant has not received a birth dose within the 1st 7 days
of life, a primary 3-dose course of vaccine should be given, at 2,
4 and 6 months of age; catch-up of the birth dose is not
necessary.
In addition infants should receive passive immunization with
HBIG at birth (preferably within 12 hours and certainly within
48 hours).
This regimen has an overall efficacy of 95%but the efficacy is
lower for mothers with very high HBV viral load
Anti-HBs antibody and HBsAg levels should be measured in
infants born to mothers with chronic hepatitis B infection 3 to
12 months after completing the primary vaccine course.
Referral to a pediatrician with expertise in viral hepatitis is
recommended if HBsAg positive
59.
Although breast milk from chronically HBV-infected
mothers is known to contain the virus. breastfeeding
does not seem to increase the risk of transmission to
the neonate above that already posed by pregnancy
and delivery .
In addition, appropriate neonatal active and passive
immunization has been shown to eliminate any
theoretical risk of transmission through this route
However, some advise temporary suspension of
breastfeeding if a woman develops cracked nipples
or mastitis.
60.
3= hepatitis C
HCV infection acquired from perinatal transmission
progresses to chronic HCV in 80% of cases, with very
few children clearing it spontaneously.
Cord blood testing of HCV is not recommended as it
can yield false-positive or false-negative results
child at risk of perinatal transmission exposure to
HCV should be tested for HCV antibodies at 18
months of age. Testing prior to this time is limited
due to passive transfer of maternal antibodies
61.
if diagnosis of vertical transmission necessary prior
to 18 months of age (e.g. parental request) then
testing of infant serum HCV RNA can be obtained
when the infant is 2 and 6 months of age.
Hepatitis B virus (HBV) vaccination is recommended
within 12 hours of birth as these neonates are at
higher risk of infection, and if a child is infected with
HCV they may be more prone to severe infection if
they contract HBV
62.
ACOG&AAP support breast feeding in HCV Ab positive
female.
studies have shown that HCV RNA has been detected at low
levels in breast milk, but that the virus is likely to becomes
inactive in the neonatal digestive tract
• risk for transmission is higher if the woman has damaged,
cracked or bleeding nipples. Advise the mother to express and
discard breast milk until the nipples are healed, and to
artificially feed until then.
If one breast/nipple is undamaged she may be able to feed the
neonate from that side and provide top-ups as required until
healing occurs.