This document provides an overview of acute and chronic viral hepatitis. It discusses the major agents that cause hepatitis (HAV, HBV, HCV, HDV, HEV), their transmission routes, epidemiology, pathogenesis, clinical presentation, diagnosis, complications, and management. It focuses in more depth on chronic hepatitis B and C, outlining their natural histories, risk factors, progression to cirrhosis and liver cancer over decades, and current treatment options including antiviral drugs and liver transplantation.
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
Introduction to chronic Hepatitis B Infection in Malaysia, epidemiology and common treatment. Phases of chronic Hepatitis B Infection, clinical presentation and complications.
The primary treatment goals for patients with hepatitis B (HBV) infection are to prevent progression of the disease, particularly to cirrhosis, liver failure, and hepatocellular carcinoma (HCC).
Risk factors for progression of chronic HBV include the following :
Persistently elevated levels of HBV DNA and, in some patients, alanine aminotransferase (ALT), as well as the presence of core and precore mutations seen most commonly in HBV genotype C and D infections
Male sex
Older age
Family history of HCC
Alcohol use
Elevated alpha-fetoprotein (AFP)
Coinfection with hepatitis D (delta) virus (HDV), hepatitis C virus (HCV), or human immunodeficiency virus (HIV)
A synergistic approach of suppressing viral load and boosting the patient’s immune response with immunotherapeutic interventions is needed for the best prognosis. The prevention of HCC often includes the use of antiviral treatment using pegylated interferon (PEG-IFN) or nucleos(t)ide analogues.
HBV infection can be self-limited or chronic. No specific therapy is available for persons with acute hepatitis B; treatment is supportive.
La hepatitis se refiere a la inflamación del hígado. Puede ser causada por varios factores, incluidas infecciones virales. Hay varios tipos de hepatitis viral, cada uno causado por un virus diferente. Los tipos más comunes incluyen:
Hepatitis A (VHA): Este tipo de hepatitis suele transmitirse a través de alimentos o agua contaminados. Causa una infección aguda en el hígado, pero la mayoría de las personas se recuperan completamente con el tiempo. Existe una vacuna disponible para la hepatitis A, que se recomienda para los viajeros a áreas con mal saneamiento.
Hepatitis B (VHB): La hepatitis B generalmente se transmite a través del contacto con sangre infectada, fluidos corporales o de madre a hijo durante el parto. Puede causar infecciones agudas y crónicas. Las infecciones crónicas por VHB pueden llevar a complicaciones graves como cirrosis y cáncer de hígado. Existen vacunas disponibles para prevenir la hepatitis B.
Hepatitis C (VHC): La hepatitis C se transmite principalmente a través del contacto con sangre infectada, a menudo compartiendo agujas u otros utensilios de consumo de drogas. También se puede transmitir a través del contacto sexual o de madre a hijo durante el parto. La hepatitis C puede llevar a una enfermedad hepática crónica y, en algunos casos, puede requerir tratamiento antiviral. No hay una vacuna para la hepatitis C, pero ha habido avances significativos en las opciones de tratamiento.
Hepatitis D (VHD): Este tipo de hepatitis solo ocurre en personas que ya están infectadas con hepatitis B. El VHD se considera un virus "auxiliar", ya que requiere la presencia de VHB para replicarse. La infección por VHD puede empeorar mucho la hepatitis B.
Hepatitis E (VHE): Similar a la hepatitis A, la hepatitis E generalmente se transmite a través de agua o alimentos contaminados. Es más común en áreas con saneamiento deficiente y puede causar hepatitis aguda. Aunque existe una vacuna para la hepatitis E, no está ampliamente disponible.
La hepatitis viral puede tener una amplia gama de síntomas, que incluyen fatiga, ictericia (coloración amarillenta de la piel y los ojos), dolor abdominal, náuseas, vómitos y más. Algunas formas de hepatitis viral pueden llevar a enfermedad hepática crónica, cirrosis e incluso cáncer de hígado si no se tratan.
Las estrategias de prevención incluyen practicar una buena higiene, usar protección durante las actividades sexuales, evitar compartir agujas u objetos personales que puedan estar contaminados con sangre y vacunarse cuando las vacunas estén disponibles (hepatitis A y B).
Si sospechas que tienes hepatitis o has estado expuesto a alguno de los virus, es importante consultar a un profesional médico para obtener un diagnóstico adecuado, tratamiento y orientación.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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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 Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
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
2. WHAT IS VIRAL HEPATITIS ?
A serious disease caused by virus that
attacks the liver . There are various strains
of viral hepatitis which can cause lifelong
infection, cirrhosis ( scarring) of the liver
, liver cancer , liver failure, and death.
24. Serum
bilirubin : 5-20 mg/dl
Direct bil ≥ indirect bil
SGOT/SGPT = 400-4000 IU
ALP : mild elevation
PT is usually normal :
Severe hepatitis prolonged PT
Hypoglycemia
25.
26.
27. Serologic Diagnosis
Ig
M anti-HAV
HBs Ag and Ig M anti-HBc
HCV Ab, HCV RNA PCR
anti-HDV
anti-HEV
36. Chronic hepatitis (CH)
Definition: chronic necroinflammatory injury
characterized
by
liver
cell
necrosis
and
inflammation lasting more than 6 months that
can lead insidiously to liver cirrhosis, end-stage
liver disease and hepatocellular carcinoma.
Prevalence: ~ 2-3% of the population
(Hungary)
37. Major causes of chronic
hepatitis
Chronic hepatitis C (70-80%)
Chronic hepatitis B (10-20%)
Chronic hepatitis D
Chronic autoimmune hepatitis (<10%)
Wilson’s disease
Haemochromatosis
α1-Antitrypsin deficiency
Drug-induced chronic hepatitis
Cryptogenic hepatitis (non-A-E hepatitis)
38. Clinical appearance of CH
mostly asymptomatic
~20%: mild fatique; rarely: mild RUQ pain
discovered by screening lab tests:
- mildly elevated ALT and AST (<10x ULN);
- ALT>AST
- AP and γ-GT: normal or minimally elevated
progression to cirrhosis is slow: years, decades
39. Late symptoms of CH
Marked symptoms only in the stage of
cirrhosis:
marked fatique, muscle weakness and wasting,
poor appetite, nausea, weight loss;
dark urine, jaundice, itching;
abdominal swelling, ascites, edema,
UGI bleeding,
hepatic encephalopathy, etc.
40. Diagnostic tests for chr. hepatitis
Type of CH
Screening test
Confirm. test
CHC
Anti-HCV
HCV RNA
CHB
HBsAg, anti-HBc
HBV DNA,
CHD
Anti-HDV
HDV RNA
Autoimmune
ANA, SMA, anti-LKM Excl. of others,, histology
Wilson’s dis.
Coeruloplasmin
Urine and hep. copper
Haemochromatosis Se iron, TFS
histology, genetic testing
α1-AT def.
Histology
α1-AT
41.
42. Chronic hepatitis C (CHC)
Hepatitis C is a common infection with variable course
170 million infected pts worldwide
CHC can led to liver cirrhosis and hepatocellular
carcinoma (HCC)
2nd or 3rd most common cause of liver cirrhosis and
HCC
No effective vaccine at present
Prevention: avoidandance of high-risk behaviors
43. Risk Factors Associated with
Transmission of HCV
• Illegal injection drug use
• Transfusion or transplant from infected donor
• Occupational exposure to blood
– Mostly needle sticks
• Iatrogenic (unsafe injections)
• Birth to HCV-infected mother
• Sexual/household exposure to anti-HCV
positive contact
• Multiple sex partners
44. Natural history of HCV infection
Acute hepatitis
85%
15%
Recovery and clearance
of HCV-RNA
Persistent infection
60-70%
Chronic hepatitis
20-30%
Liver cirrhosis
~5%
HCC
45. Factors promoting the progression of
CHC
High viral dose, genotype 1, quasispecies
Older age, male sex
Immunodeficiency
Alcohol abuse
Co-infection with HBV, HIV
Iron overload
Environmental contaminants, geography
46.
47. Epidemiology of HBV
HBV is a common cause of viral hepatitis
400 million carriers worldwide
Prevalence in the population of developed countries:
carriers: 1%, anti-HBsAg +: 10 %;
incidence: 35 per 100 000 in a year;
in the 3rd world (Far/Middle East):
carriers: 8%; anti-HBsAg +: 50 %
48. Transmission of HBV
HBV is present in all body fluids and secretions!
Highly contagious! Blood cc. may be as high as 1013/ml
Vertical transmission: in the perinatal period; > 90%
Horizontal transmission:
by blood, blood products, surgery
injection-drug abuse, needle-stick injury
sexual activity,
occupational exposure
household contact
tattooing, shaving, etc.
49. Natural history of HBV infection
1%
Acute hepatitis
10%
Persistent infection
Fulminant hepatitis
90%
Recovery and clearance
of HBV-DNA
2-3%
Chronic active hepatitis
1%
Liver cirrhosis
Carrier state
100-fold risk
HCC
50. Natural History of Chronic HBV
Infection
Resolution
Acute
Infection
Stabilisation
Chronic
Hepatitis
Chronic
Carrier
Compensated
Cirrhosis
Cirrhosis
Liver
Cancer
Progression Decompensated
Cirrhosis
(Death)
30–50 Years
Adapted from Feitelson, Lab Invest 1994
Death
52. Diagnosis of CHC
Screening for liver disease
elevated se ALT (<10x UNL)
Screening for HCV infection
se anti-HCV (enzyme immunoassay)
Confirmation: detection of viremia
se HCV RNA (rtPCR)
53. Diagnosis of CHB
Follow-up of patients with acute HBV infection
Screening for liver disease (elevated se ALT)
Screening for HBV infection
se HBsAg (enzyme immunoassay)
Confirmation: detailed serology;
detection of viremia se HBV-DNA (PCR)
55. Evaluation of patients with CHB
and C
Clinical: signs and symptoms of chronic hepatitis;
evaluation of coexisting diseases
Laboratory: se
ALT, bilirubin, albumin, prothrombin
(se AP, GGT , Fe, transferrin
saturation, ferritin, renal function tests, autoimmune
markers)
Virological:
HBV: serology, se HBV-DNA; anti-HDV
HCV: se HCV-RNA, viral titer, genotype
Histological: liver biopsy histology
56. CHC: current therapies
Interferon-α: may eradicate HCV infection;
antiviral, immunoregulator, anti-inflammatory;
may inhibit fibro- and carcinogenesis;
costly, unpleasant (injection!); 5-20% efficacy
Interferon-α + ribavirin
doubled efficacy in HCV clearance
Iron reduction (venesections)
biochemical but not virological improvement;
improved responsiveness to IFNα
57. CHB: current therapies
Interferon-α: may eradicate HBV infection;
antiviral, immunoregulator, anti-inflammatory;
may inhibit fibro- and carcinogenesis;
costly, unpleasant, 20-30% efficacy
Lamivudine, adefovir, entecavir (virostatic drugs):
advantages: oral administration; well tolerable;
less contraindications
disadv.: relapse after discontinuation; escape;
long-term (>12 mo) treatment
58. Side effects of therapy
Interferon-alpha:
Early: flu-like illnes, fatique, cytopenias
Late: depression with suicidal
risk, psychosis, anorexia, weight loss, sepsis, thyroid
dysfunction, deteoriation of liver disease, hair-loss
Ribavirin:
• Dose-dependent, mild, reversible hemolytic anemia
59. Therapy of end-stage CHB and C:
liver transplantation
CHC is the leading indication for OLT
Antiviral pretreatment is advised
Recurrence of the infection is universal;
a great problem in hepatitis B infection;
survival rate is less affected by HCV
Therapy with IFN, ribavirin or lamivudine is
possible