HIV AIDS Lecture Presented by me in my Community Dentistry Class, BIBI ASIFA DENTAL COLLEGE, SHAHEED MOHTARMA BENAZIR BHUTTO MEDICAL UNIVERSITY LARKANA, SINDH, PAKISTAN.
Blood stream infections- clinical microbiologySijo A
Blood stream infections (BSI) refers to the presence of organisms in blood which are threat to every organ in the body.
It causes shock, multiple organ failure and DIC (Disseminated Intravascular Coagulation).
The presence of bacteria in blood is called Bacteremia.
The bacteria circulate and actively multiply in the blood stream is called Septicemia.
The presence of virus in blood is called Viremia.
The presence of parasite in blood is called Parasitemia.
The presence of fungi in blood is called Fungemia.
HIV AIDS Lecture Presented by me in my Community Dentistry Class, BIBI ASIFA DENTAL COLLEGE, SHAHEED MOHTARMA BENAZIR BHUTTO MEDICAL UNIVERSITY LARKANA, SINDH, PAKISTAN.
Blood stream infections- clinical microbiologySijo A
Blood stream infections (BSI) refers to the presence of organisms in blood which are threat to every organ in the body.
It causes shock, multiple organ failure and DIC (Disseminated Intravascular Coagulation).
The presence of bacteria in blood is called Bacteremia.
The bacteria circulate and actively multiply in the blood stream is called Septicemia.
The presence of virus in blood is called Viremia.
The presence of parasite in blood is called Parasitemia.
The presence of fungi in blood is called Fungemia.
What are the precautionary measures for Human Immunodeficiency Virus?Lal PathLabs
A virus that attacks the immune system, the natural defense system of our body is what we consider as Human Immunodeficiency Virus. This is the one which kills the cells of the body. Here we will have a complete analysis of what this disease and also the reasons for spreading of the disease and how adversely this affects our body, along with all its possible precautions.
This slide contains information regarding HIV, ARV. This can be helpful for proficiency level and bachelor level nursing students. Your feedback is highly appreciated. Thank you!
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.
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
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
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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HIV AIDS
1. AIDS
Acquired Immune Deficiency Syndrome
Dr. Sudha Tiwari,
Asst. Professor,
PSS Central Institute of Vocational
Education, NCERT, Bhopal
2. What is HIV/AIDS
• HIV stands for human immunodeficiency virus,
which is the virus that causes HIV infection.
• AIDS stands for acquired immunodeficiency
syndrome. AIDS is the most advanced stage of HIV
infection.
• HIV attacks and destroys the infection-fighting CD4
cells of the immune system. The loss of CD4 cells
makes it difficult for the body to fight off infections
and certain cancers. Without treatment, HIV can
gradually destroy the immune system and advance to
AIDS.
3. Epidemiology of HIV/AIDS in India
• In India in 2017 (Source-unaids.org)
•2 100 000 people were living with HIV out of
which((41.9%) were women
•HIV incidence per 1000 uninfected—the number of
new HIV infections among the uninfected population
over one year—among all people of all ages was 0.1.
•HIV prevalence—the percentage of people living with
HIV—among adults (15–49 years) was 0.2%.
•88 000 people were newly infected with HIV.
•69 000 people died from an AIDS-related illness.
4. What are the symptoms of HIV/AIDS?
• Within 2 to 4 weeks after infection with HIV, some
people may have flu-like symptoms, such as fever,
chills, or rash, swollen glands, chills, weakness, and
weight loss.
• The symptoms may last for a few days to several weeks.
• During this earliest stage of HIV infection, the virus
multiplies rapidly.
• Opportunistic infections occur more frequently or are
more severe in people with weakened immune systems
than in people with healthy immune systems.
• HIV destroys vital cells required for the functioning of
the immune system.
5.
6. HIV progress through three stages:
Stage 1: Acute stage, the first few weeks after transmission
• Early symptoms are flu-like.
Stage 2: Clinical latency or chronic stage
• Non-specific symptoms observed like headaches and other
aches and pains, swollen lymph nodes, recurrent fevers,
night sweats, fatigue, nausea, vomiting, diarrhea, weight
loss
Stage 3: AIDS
• Symptoms are recurrent fever, chronic swollen lymph
glands, chronic fatigue, night sweats, skin lesions,
recurrent or chronic diarrhea, rapid weight loss, neurologic
problems, anxiety and depression.
8. How HIV Transmit?
• The spread of HIV from person to person is called HIV
Transmission. HIV is spread only in certain body fluids
from a person who has HIV. These body fluids include:-
Blood
Semen
Pre-seminal fluid
Vaginal fluids
Rectal fluids
Breast milk
• Unprotected sex with HIV infected person
• Sharing injection drug equipment (works), such as
needles, with someone who has HIV
10. You can’t get HIV by :-
• shaking hands or hugging a person who has HIV.
• from contact with objects such as dishes, toilet seats,
or doorknobs used by a person with HIV.
• sharing food or drinks, including drinking fountains
• saliva, tears, or sweat (unless mixed with the blood of
a person with HIV)
• HIV is not spread through the air or in water or by
mosquitoes, ticks, or other blood-sucking insects.
11. How is AIDS diagnosed?
• Diagnosis of AIDS is based on the following criteria:-
A drop in CD4 count to less than 200 cells/mm3. A
CD4 count measures the number of CD4 cells in a
sample of blood. OR
The presence of certain opportunistic infections.
• No HIV test can detect HIV immediately after infection.
• The first HIV protein (antigen) that can be measured is
p24 (from 1 to 8 weeks after exposure).
• In general, nucleic acid tests (NAT) can detect HIV the
soonest, followed by combination or fourth generation tests,
and then antibody tests.
• Fourth-generation test looks for both HIV antibodies
and antigens.
13. HIV/AIDS Tests
• Nucleic acid test (NAT)-it detects the amount
of virus(viral load) in blood of people who have
early symptoms of HIV.
• Fourth Generation -Antibody/antigen tests-
check the blood for antibodies and antigens.
ELISA for screening &
Western Blot for confirmation
14.
15. 1.ELISA- detect HIV antibody
• The blood sample added to a cassette/well that
contains the viral protein, called antigen.
• If the blood contains antibodies in response to HIV,
it will bind with the antigen and cause the cassette's
contents to change colour.
16. 2. Western Blot- detect HIV antibodies
• It separates the blood proteins and detects the HIV
specific proteins (HIV antibodies)
• It confirm a positive ELISA, and the combined tests are
99.9% accurate.
17. Timeline for HIV infection, immune responses and
window period for tests
18. Window Period
• The window period is time between HIV
infection and the point when the test will give
an accurate result.
• During the window period a person can have HIV
and be very infectious but still test HIV negative.
• The window period for a 4th generation
antigen/antibody test is about four weeks. By
this time 95% of infections will be detected .
• There is a three month window period after
exposure, for the confirmatory result to detect
more than 99.9% of infections.
19. What is the treatment for HIV?
• Antiretroviral therapy (ART) is the use of HIV medicines
to treat HIV infection.
• ART prevents HIV from multiplying, which reduces the
amount of HIV in the body (called the viral load) .
• Having less HIV in the body protects the immune system
and prevents HIV infection from advancing to AIDS.
• ART can’t cure HIV, but HIV medicines help people with
HIV live longer, healthier lives.
• ART also reduces the risk of HIV transmission. A main
goal of ART is to reduce a person’s viral load to an
undetectable level.
20.
21.
22. Anti-Retroviral Treatment
• Antiretroviral (ARV) HIV drugs are divided into seven drug
classes based on how each drug interferes with the HIV
life cycle.
• These seven classes include:-
• nucleoside reverse transcriptase inhibitors (NRTIs),
• non-nucleoside reverse transcriptase inhibitors
(NNRTIs), protease inhibitors (PIs),
• fusion inhibitors,
• CCR5 antagonists,
• post-attachment inhibitors, and
• integrase strand transfer inhibitors (INSTIs).