COPD is characterized by non-reversible airflow limitation caused by an abnormal inflammatory response to noxious particles or gases. The two most common conditions are chronic bronchitis and emphysema. Pharmacological treatments aim to relieve symptoms, prevent disease progression, and improve health outcomes. Therapies include bronchodilators, corticosteroids, vaccines, antibiotics, and supplemental oxygen. Managing exacerbations focuses on reversing acute symptoms and respiratory failure through bronchodilators, corticosteroids, and ventilation support.
Etiopathogenesis and pharmacotherapy of DIPDs
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects).
Etiopathogenesis and pharmacotherapy of DIPDs
a. the pathophysiology of selected disease states and the rationale for drug therapy;
b. the therapeutic approach to management of these diseases;
c. the controversies in drug therapy;
d. the importance of preparation of individualised therapeutic plans based on diagnosis;
e. needs to identify the patient-specific parameters relevant in initiating drug therapy,
and monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects);
f. describe the pathophysiology of selected disease states and explain the rationale for
drug therapy;
g. summarise the therapeutic approach to management of these diseases including
reference to the latest available evidence;
h. discuss the controversies in drug therapy;
i. discuss the preparation of individualised therapeutic plans based on diagnosis; and
j. identify the patient-specific parameters relevant in initiating drug therapy, and
monitoring therapy (including alternatives, time-course of clinical and laboratory
indices of therapeutic response and adverse effects).
Definition and introduction to bronchial asthma - classification of bronchial asthma - pathophysiology and risk factors for bronchial asthma - diagnosis of bronchial asthma - clinical manifestations - investigations - management of bronchial asthma
A basic overview on the management of intra-operative bronchospasm: the risk factors, triggers, diagnosis, prevention and management. Includes a case scenario – discussion.
Definition and introduction to bronchial asthma - classification of bronchial asthma - pathophysiology and risk factors for bronchial asthma - diagnosis of bronchial asthma - clinical manifestations - investigations - management of bronchial asthma
A basic overview on the management of intra-operative bronchospasm: the risk factors, triggers, diagnosis, prevention and management. Includes a case scenario – discussion.
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterized by persistent airflow limitation that is slowly progressive. It is also known as Chronic obstructive lung disease. “(COLD)”
It refers to Chronic Bronchitis and emphysema, a pair of two commonly coexisting disease of the lungs in which the airways become narrowed.
A common, preventable and treatable disease, characterized by persistent respiratory symptoms and airflow limitation that are usually progressive and associated with an enhanced chronic inflammatory response in the airways and/or alveoli due to significant exposure to noxious particles or gases. (Vogelmeier et al., 2017).
I am professionally pharmacist. These slides provide for pharmacy department student. Especially related clinical subject and discussion about disease.
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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.
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
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Copd
1. COPD
Presented by : Anum Abdul Sattar
M.pharm(pharmacy practice)
Ist semester
2. DEFINITION:
(COPD) :-
characterized by non reversible
airflow limitation .
The airflow limitation is usually
progressive and associated with an
abnormal inflammatory response of
the lungs to noxious particles or
gases.
common conditions in COPD :chronic
bronchitis and emphysema.
3. CHRONIC BRONCHITIS:-
chronic / recurrent excess mucus secretion
in bronchial tree with cough occurring mostly
for at least 3 months of the year and at least
2 consecutive years when other causes of
cough have been excluded.
EMPHYSEMA: -
abnormal, permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls, but
without obvious fibrosis.(formation of excess
fibrous connective tissue in organ/tissue as a
reparative process)
8. noxious particles and gases stimulates the activation of
neutrophils,macrophages, and CD8+ lymphocytes,
which release a variety of chemical mediators, including
tumor necrosis factor-α, interleukin-8,and leukotriene
B4. These inflammatory cells and mediators lead to
widespread destructive changes in the airways,
pulmonary vasculature,and lung parenchyma.
oxidative stress ,imbalance between aggressive and
protective defense systems in the lungs (proteases and
antiproteases). Increased oxidants generated by
cigarette smoke react with and damage various proteins
and lipids, leading to cell and tissue damage. Oxidants
also promote inflammation directly and exacerbate the
protease-antiprotease imbalance by inhibiting
antiprotease activity.
9. The protective antiproteaseα1-antitrypsin
(AAT) inhibits several protease enzymes,
including neutrophil elastase. In the presence
of unopposed AAT activity, elastase attacks
elastin, which is a major component of
alveolar walls. A hereditary deficiency of AAT
results in an increased risk for premature
development of emphysema. Activated
inflammatory cells release several other
proteases, including cathepsins and
metalloproteinases. In addition, oxidative
stress reduces antiprotease (or protective)
activity.
13. PULMONARY FUNCTION TEST
Spirometry standard for diagnosing and
monitoring COPD
Establishing of COPD diagnosis: FEV1 (The
forced expiratory volume after 1 second) /
forced vital capacity (FVC) ratio ≤0.7,
demonstrating airflow limitation that is not fully
reversible.
based on SPIROMETRY, severity measured,
assessed
Patients classified by severity of airflow
obstruction (Grades 1–4) then into Group (A,
B, C, or D) based on the impact of symptoms
and risk for future exacerbations.
14. ARTERIAL BLOOD GASES
Patients with severe COPD can have a low arterial
oxygen tension (PaO2 45 to 60 mm Hg) and an
elevated arterial carbon dioxide tension (PaCO2 50 to
60 mm Hg).
The diagnosis of acute respiratory failure in COPD is
made on the basis of an acute drop in PaO2 of 10 to 15
mm Hg / acute increase in PaCO2 that decreases
serum pH 7.3 /less.
If acute respiratory distress develops (e.g.pneumonia
/COPD exacerbation) the PaCO2 may rise sharply
resulting in an uncompensated respiratory acidosis
Respiratory acidosis is a condition that occurs when the
lungs can't remove enough of the carbon dioxide (CO2)
produced by the body. Excess CO2 causes the pH of blood
and other bodily fluids to decrease, making them too acidic.
15. TREATMENT
Prevent disease progression
Relieve symptoms
Improve exercise tolerance
Improve health status
Prevent and treat exacerbations
Reduce mortality
16. THERAPEUTIC PLAN
Approaches to treatment:
1. Pharmacotherapy
2. Non pharmacological therapy
3. Surgical management
4. Managing exacerbations
Improving outcomes
18. PHARMACOTHERAPY
The current pharmacological treatment of COPD
is symptomatic
1. it is mainly based on:
I. bronchodilators : selective β2-adrenergic agonists
(short- and long-acting)
II. Anticholinergics
III. Methyl xanthines
IV. combination of these drugs.
V. Corticosteroids
2. other types of medication (vaccines,
antibiotics,α1- anti trypsin augmentation
therapy, mucolytic agents, antioxidants,
immunoregulators, antitussives and
vasodilators).
19. Treat symptoms of low risk for exacerbations(Group A) :
short-acting inhaled bronchodilators .
more persistent symptoms(Group B):long-acting inhaled
bronchodilators .
For high risk for exacerbations (Groups C and D):
inhaled corticosteroids.
Short-acting inhaled bronchodilators (β2-agonists or
anticholinergics) :initial therapy for patients with
intermittent symptoms;
relieve symptoms and increase exercise tolerance.
Long-acting inhaled bronchodilators (β2-agonists
[LABA] or anticholinergics) : moderate to severe COPD
when symptoms occur on a regular basis or when
short-acting agents provide inadequate relief.
They relieve symptoms , reduce exacerbation frequency, and
improve quality of life and health status.
26. 2.OTHER THERAPIES
vaccines
antibiotics
α1- anti trypsin augmentation therapy:
◦ Not recommended for patients with COPD
that is unrelated to genetic deficiency.
mucolytic agents:
◦ Patients with viscous sputum may benefit
from mucolytics , overall benefits are small
Immuno regulators
Vasodilators:
◦ Nitric oxide is contraindicated in stable
COPD. The use of endothelium modulated
agents for treatment of pulmonary
hypertension associated with COPD is not
recommended
27. Expectorants and mucolytics
◦ use of saturated solutions of potassium iodide, ammonium
chloride, acetylcysteine, and guaifenesin.
Respiratory stimulants
◦ no role in long-term management
◦ some utility in the acute setting include almitrine and
doxapram.
Narcotics
◦ Systemic (oral/parenteral)opioids(morphine), can relieve
dyspnoea for patients with end-stage COPD.
Dietary supplements
◦ antioxidants (vit E ,C , β-carotene),reduce frequency of
exacerbations .may be beneficial in COPD as a result of an
imbalance between oxidants and antioxidants
Surgical interventions
◦ bullectomy,
◦ lung volume reduction surgery
◦ (LVRS), and lung transplantation.
Suppressive Anti microbial agents (to treat colonized
28.
29. α1- ANTI TRYPSIN
AUGMENTATION THERAPY
Used as an augmentation therapy in
patient with inherited AAT deficiency.
To maintain the serum concentrations
above the protective threshold.
Consists of weekly infusion of pooled
human AAT plasma level.
30.
31.
32.
33.
34. COPD EXACERBATION
An exacerbation of COPD is defined as “an event
in the natural course of the disease characterized
by a change in the patient's baseline dyspnoea,
cough, and/or sputum and beyond normal day-to-
day variations, that is acute in onset and may
warrant a change in regular medication in a patient
with underlying COPD
TREATMENT:
The goals are to
◦ 1) prevent hospitalization or reduce length of
◦ hospital stay
◦ 2) prevent acute respiratory failure and death
◦ 3) resolve symptoms
◦ 4) return to baseline clinical status and quality of life.
35.
36. MANAGING EXACERBATION:
NON PHARMACOLOGICAL
THERAPY:
oxygen therapy( for patients
with hypoxemia.)
Non invasive positive
pressure ventilation:
◦ ventilatory support with
oxygen and pressurized
airflow using a face or
nasal mask without
endotracheal intubation.
PHARMACOLOGICAL
THERAPY:
i)Bronchodilators ii)
corticosteroids iii) anti
microbial therapy
37. COMPLICATIONS
Cor Pulmonale
◦ condition that causes the right side of the heart to fail.
◦ Long-term high blood pressure in the arteries of the lung
and right ventricle of the heart lead to cor pulmonale.
◦ High blood pressure in the arteries of the lungs is
called pulmonary hypertension.
Treatment:
◦ Long-term oxygen therapy and diuretics
◦ Other pharmacologic agents:
hydralazine,
calcium channel blockers,
angiotensin-converting enzyme inhibitors,
angiotensin II antagonists.
38. POLYCYTHEMIA
Condition
where hematocrit (the
volume
percentage of red
blood cells in
the blood) is
>55% due to an
increase in the RBC
number/decrease in
the volume of plasma
treatment:
◦ phlebotomy (removal of
blood from the
circulation).
◦ oxygen therapy