Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
Management Of Chronic Hepatitis B
by Dr S Khan
Courtesy Of Javed iqbal Farooqi
http://www.drkhanblogs.com/2015/05/management-of-chronic-hepatitis-b.html
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
Management Of Chronic Hepatitis B
by Dr S Khan
Courtesy Of Javed iqbal Farooqi
http://www.drkhanblogs.com/2015/05/management-of-chronic-hepatitis-b.html
Primary sclerosing cholangitis (PSC) is a chronic, idiopathic, cholestatic liver disease characterized histologically by peribiliary inflammation and fibrosis.
It can lead to end stage cirrhosis and is a recognized risk factor for hepatobiliary cancers
This lecture is about Extrahepatic Manifestations of HCV presented by Dr. Moustafa El-Tomy, Consultant of Internal Medicine, 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
Primary sclerosing cholangitis (PSC) is a chronic, idiopathic, cholestatic liver disease characterized histologically by peribiliary inflammation and fibrosis.
It can lead to end stage cirrhosis and is a recognized risk factor for hepatobiliary cancers
This lecture is about Extrahepatic Manifestations of HCV presented by Dr. Moustafa El-Tomy, Consultant of Internal Medicine, 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
Systemic treatment in advanced hepatocellular carcinoma (HCC) refers to the use of medications or therapies that are administered throughout the body to target cancer cells beyond the liver. HCC is the most common type of liver cancer and often presents at an advanced stage, making systemic therapies crucial in managing the disease.
One of the main categories of systemic treatment for advanced HCC is targeted therapies. Targeted therapies are designed to selectively inhibit specific molecules or pathways involved in tumor growth, thereby blocking the signals that support cancer cell survival and proliferation. Sorafenib and lenvatinib are examples of targeted therapies that have been approved for the first-line treatment of advanced HCC. They target vascular endothelial growth factor (VEGF) receptors, which play a key role in promoting the growth of new blood vessels necessary for tumor growth. By inhibiting these receptors, these drugs can help slow down tumor growth and improve patient outcomes.
In addition to sorafenib and lenvatinib, other targeted therapies have shown promising results in the treatment of advanced HCC. Regorafenib, for instance, is a multi-kinase inhibitor that targets several pathways involved in tumor angiogenesis, cell proliferation, and survival. Cabozantinib is another multi-kinase inhibitor that has been approved as a second-line treatment option for patients who have progressed on or are intolerant to prior systemic therapy. These targeted therapies have demonstrated efficacy in improving overall survival and delaying disease progression in patients with advanced HCC.
Another significant advancement in systemic treatment for advanced HCC is the use of immune checkpoint inhibitors. Immunotherapy has revolutionized cancer treatment in recent years, including for HCC. Immune checkpoint inhibitors, such as nivolumab and pembrolizumab, work by blocking proteins that act as checkpoints on immune cells, such as programmed cell death protein 1 (PD-1) or its ligand (PD-L1). By doing so, these drugs help restore and enhance the immune system's ability to recognize and eliminate cancer cells. Checkpoint inhibitors have shown promising results, with some patients experiencing durable responses and improved overall survival.
Dr Geethani Galagoda, Consultant Virologist, Medical Research Institute, Colombo. Organized by the Sri Lanka College of Venereologists. Held on world hepatitis day on 28. July 2015 at BMICH
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
- 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
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
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?
Chronic hepatitis b
1. Chronic Hepatitis B (CHB)
Dr. Sayem Bin Latif
MD (Cardiology) Phase A
Chittagong Medical College & Hospital
10 Oct 2018
sayembinlatif@gmail.com
2. HBV
• HBV is a enveloped double stranded DNA virus
• It infects the liver causing hepatocellular inflammation & necrosis
• HBV infection can be either acute or chronic
• Clinical feature varies from asymptomatic to symptomatic,
progressive disease
3.
4.
5.
6.
7.
8.
9. Acute HBV infection
• New-onset hepatitis B infection that may or may not be icteric or
symptomatic
• Diagnosis is based on detection of HBsAg and anti-HBc IgM
• Recovery is accompanied by clearance of HBsAg with seroconversion
to anti-HBs usually within 3 months
10. Chronic HBV infection
• Defined as persistence of hepatitis B surface antigen (HBsAg) for six
months or more after acute infection with HBV
Occult HBV infection
• Persons who have cleared hepatitis B surface antigen, i.e. they are
HBsAg negative but HBV DNA positive, although at very low levels
11.
12.
13.
14. Initial assessment of subjects with chronic
HBV infection
• The initial evaluation of a subject with chronic HBV infection should
include –
Complete history
Physical examination
Assessment of liver disease activity and severity and
Markers of HBV infection (HBsAg, HBeAg/anti-HBe & HBV DNA)
15. • In addition, all first degree relatives and sexual partners of subjects
with chronic HBV infection should be advised –
To be tested for HBV serological markers (HBsAg, anti-HBs, anti-HBc)
To be vaccinated if they are negative for these markers
16. The assessment of the severity of liver
disease
• To identify patients for treatment and HCC surveillance
• Based on a physical examination and biochemical parameters (AST,
ALT, GGT, alkaline phosphatase, bilirubin, and serum albumin and
gamma globulins, full blood count and prothrombin time)
• An abdominal hepatic ultrasound is recommended in all patients
17. • A liver biopsy or a non-invasive test should be performed to
determine disease activity in cases where biochemical and HBV
markers reveal inconclusive results
• Of the non-invasive methods, transient elastography (FibroScan®)
has been mostly studied and seems to offer a higher diagnostic
accuracy for the detection of cirrhosis
18. • HBeAg and anti-HBe detection are essential for the determination of
the phase of chronic HBV infection
• Measurement of HBV DNA serum level is essential for the diagnosis,
establishment of the phase of the infection, the decision to treat and
subsequent monitoring of patients
• Serum HBsAg quantification can be useful, particularly in HBeAg-
negative chronic HBV infection and in patients to be treated with
interferon-alfa (IFNa)
19. • HBV genotype is not necessary in the initial evaluation, although it
may be useful for selecting patients to be treated with IFNa offerering
prognostic information for the probability of response to IFNa therapy
and the risk of HCC
• Co-morbidities, including alcoholic, autoimmune, metabolic liver
disease with steatosis or steatohepatitis and other causes of chronic
liver disease should be systematically excluded including co-infections
with hepatitis D virus (HDV), hepatitis C virus (HCV) and HIV
• Testing for antibodies against hepatitis A virus (anti-HAV) should be
performed, and patients with negative anti-HAV should be advised to
be vaccinated against HAV
20.
21. Indications for treatment
• All patients with HBeAg positive or negative chronic hepatitis B,
defined by HBV DNA > 2,000 IU/ml, ALT > ULN and/or at least
moderate liver necroinflammation or fibrosis, should be treated
• Patients with compensated or decompensated cirrhosis need
treatment, with any detectable HBV DNA level and regardless of ALT
levels
22. • Patients with HBV DNA >20,000 IU/ml and ALT >2xULN should start
treatment regardless of the degree of fibrosis
• Patients with HBeAg-positive chronic HBV infection, defined by
persistently normal ALT and high HBV DNA levels, may be treated if
they are older than 30 years regardless of the severity of liver
histological lesions
• Patients with HBeAg-positive or HBeAg-negative chronic HBV
infection and family history of HCC or cirrhosis and extrahepatic
manifestations can be treated even if typical treatment indications
are not fulfilled
23. • Patients who are not candidates for antiviral therapy should be
monitored with periodical assessments of –
Serum ALT
HBV DNA level
Assessment of liver fibrosis severity by non-invasive markers
24. Treatment strategies
Currently, there are two main treatment options for CHB patients -
Nucleoside/nucleotide analogues (NA) or
IFNa, currently pegylated (PegIFNa)
25.
26. Classification of NA
Low barrier against HBV
resistance
• Lamivudine (LAM)
• Adefovir dipivoxil (ADV)
• Telbivudine (TBV)
High barrier against HBV
resistance
• Entecavir (ETV)
• Tenofovir disoproxil fumarate
(TDF)
• Tenofovir alafenamide (TAF)
27.
28.
29. NAs for naïve CHB patients recommendations
• The long-term administration of a potent NA with high barrier to
resistance is the treatment of choice regardless of the severity of liver
disease (Grade 1 recommendation)
• The preferred regimens are ETV, TDF and TAF as monotherapies
• LAM, ADV and TBV are not recommended in the treatment of CHB
30. PegIFNa monotherapy for CHB patients
• PegIFNa can be considered as an initial treatment option for patients
with mild to moderate HBeAg positive or negative CHB (Grade 2
recommendation)
• The standard duration of PegIFNa therapy is 48 weeks
• The extension of the duration of PegIFNa therapy beyond week 48
may be beneficial in selected HBeAgnegative CHB patients
31. Monitoring of patients treated with ETV, TDF
or TAF
• All patients treated with NA should be followed with periodical
assessments including –
ALT (every 3–4 months during the first year and every six months
thereafter) and
HBV DNA (every 3– 4 months during the first year and every 6–
12 months thereafter)
32. • Patients at risk of renal disease treated with any NA and all patients
regardless of renal risk treated with TDF should undergo periodical
renal monitoring including at least –
eGFR
Serum phosphate
33. Treatment of patients with decompensated
cirrhosis
• Patients with decompensated cirrhosis should be immediately treated
with a NA with high barrier to resistance, irrespective of the level of
HBV replication, and should be assessed for liver transplantation
• PegIFNa is contraindicated in patients with decompensated cirrhosis
• Patients should be closely monitored for tolerability of the drugs and
the development of rare side effects like lactic acidosis or kidney
dysfunction
34. Endpoints of therapy
• The induction of long-term suppression of HBV DNA levels represents
the main endpoint of all current treatment strategies
• The induction of HBeAg loss, with or without anti-HBe
seroconversion, in HBeAg-positive CHB patients is a valuable
endpoint, as it often represents a partial immune control of the
chronic HBV infection
35. • A biochemical response defined as ALT normalisation should be
considered as an additional endpoint, which is achieved in most
patients with long-term suppression of HBV replication
• HBsAg loss, with or without anti-HBs seroconversion, is an optimal
endpoint, as it indicates profound suppression of HBV replication and
viral protein expression
37. HIV co-infected patients
• All HIV-positive patients with HBV co-infection should start
antiretroviral therapy (ART) irrespective of CD4 cell count
• HIV-HBV co-infected patients should be treated with a TDF- or TAF-
based ART regimen
38. HDV co-infected patients
• PegIFNa for at least 48 weeks is the current treatment of choice in
HDV-HBV co-infected patients with compensated liver disease
• In HDV-HBV co-infected patients with ongoing HBV DNA replication,
NA therapy should be considered
• PegIFNa treatment can be continued until week 48 irrespective of on-
treatment response pattern if well tolerated
39. Acute hepatitis B
• More than 95% of adults with acute HBV hepatitis do not require
specific treatment, because they will fully recover spontaneously
40. • Only patients with severe acute hepatitis B, characterised by –
• Coagulopathy (INR > 1.5) or
• Protracted course (persistent symptoms or marked jaundice for >
4 weeks)
• Signs of acute liver failure
should be treated with NA and considered for liver
transplantation
41. Goals of antiviral treatment in acute viral
hepatitis-B
• Preventing the risk of acute or subacute liver failure is the main
treatment goal
• Improving quality of life by shortening the disease associated
symptoms
• Lowering the risk of chronicity (if NA treatment was initiated within 8
weeks of acute hepatitis B presentation in genotype A infected
individuals)
42. • Early antiviral therapy with highly potent NAs can prevent progression
to acute liver failure and subsequently liver transplantation or
mortality
• This effect, however, is not seen if antiviral therapy is initiated late in
the course of severe acute hepatitis B in patients with already
manifested acute liver failure and advanced hepatic encephalopathy
• The use of glucocorticoids in acute severe hepatitis B is supported by
older studies, but these studies in most cases did not include current
antiviral drugs
43. Healthcare workers
• HBV infection alone should not disqualify infected persons from the
practice or study of surgery, dentistry, medicine, or allied health fields
• Healthcare workers performing exposure prone procedures with
serum HBV DNA >200 IU/ml may be treated with NA to reduce
transmission risk
44. Pregnancy Recommendations
• Screening for HBsAg in the first trimester of pregnancy is strongly
recommended
• In a woman of childbearing age without advanced fibrosis who plans
a pregnancy in the near future, it may be prudent to delay therapy
until the child is born
• Pregnant women with CHB and advanced fibrosis or cirrhosis, therapy
with TDF is recommended
45. • In pregnant women already on NA therapy, TDF should be continued
while ETV or other NA should be switched to TDF
• In all pregnant women with high HBV DNA levels >200,000 IU/ml or
HBsAg levels >4 log10 IU/ml, antiviral prophylaxis with TDF should
start at week 24–28 of gestation and continue for up to 12 weeks
after delivery
46. •Breast feeding is not contraindicated in HBsAg-
positive untreated women or on TDF-based
treatment or prophylaxis
47. Patients undergoing immunosuppressive
therapy or chemotherapy
• All candidates for chemotherapy and immunosuppressive therapy
should be tested for HBV markers prior to immunosuppression
• All HBsAg-positive patients should receive ETV or TDF or TAF as
treatment or prophylaxis
• HBsAg-negative, anti-HBc positive subjects should receive anti-HBV
prophylaxis if they are at high risk of HBV reactivation
48. Dialysis and renal transplant patients
• All dialysis and renal transplant recipients should be screened for HBV
markers
• HBsAg-positive dialysis patients who require treatment should receive
ETV or TAF
• All HBsAg-positive renal transplant recipients should receive ETV or
TAF as prophylaxis or treatment
• HBsAg-negative, anti-HBc positive subjects should be monitored for
HBV infection after renal transplantation
49. New biomarkers of HBV infection
• Viral cccDNA
• Hepatitis B core-related antigen (HBcrAg)
• Circulating HBV RNA
50. Reference
• EASL 2017 Clinical Practice Guideline for Chronic Hepatitis B
• WHO Guideline for Chronic Hepatitis B, 2015