The document discusses the Global Initiative for Chronic Obstructive Lung Disease (GOLD) which provides guidelines for the management and treatment of COPD. GOLD was launched in 1997 with the objectives of recommending effective COPD prevention and management strategies worldwide and increasing awareness of COPD as a public health issue. The document defines COPD as a chronic lung disease characterized by persistent airflow limitation that is usually progressive. It also discusses factors that influence COPD development and progression, pathophysiology, diagnosis and assessment, therapeutic options including pharmacologic therapies, and the roles of bronchodilators in symptom management.
Asthma vs COPD - A quick summary of the differences between themLGM Pharma
Asthma is a lung disease that affects almost 20 million Americans. COPD, or chronic obstructive pulmonary disease is a chronic lung disease that afflicts 24 million patients in the U.S. COPD is mainly caused by smoking or secondhand smoke, while asthma can by caused by exposure to allergens, dust and air pollutants. Innovative treatments are needed to combat both asthma and COPD, and LGM Pharma provides quality API's for the R&D needs of clients seeking treatments for these lung diseases.
Asthma is a serious public health problem throughout the world, affecting people of all ages. When uncontrolled, asthma can place severe limits on daily life, and is sometimes fatal.
Asthma vs COPD - A quick summary of the differences between themLGM Pharma
Asthma is a lung disease that affects almost 20 million Americans. COPD, or chronic obstructive pulmonary disease is a chronic lung disease that afflicts 24 million patients in the U.S. COPD is mainly caused by smoking or secondhand smoke, while asthma can by caused by exposure to allergens, dust and air pollutants. Innovative treatments are needed to combat both asthma and COPD, and LGM Pharma provides quality API's for the R&D needs of clients seeking treatments for these lung diseases.
Asthma is a serious public health problem throughout the world, affecting people of all ages. When uncontrolled, asthma can place severe limits on daily life, and is sometimes fatal.
In this section We describe drugs used in Asthma and COPD and Most of the slides are prescribed from Lippincott's Pharmacology. Other references include:
1. Kd triphati Pharmacology
2. Basic Pharmacology
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
Do Not Forget To Visit Our Pages On Facebook on the following Links:
https://www.facebook.com/groups/569435236444761/
AND
https://www.facebook.com/groups/690331650977113/
In this section We describe drugs used in Asthma and COPD and Most of the slides are prescribed from Lippincott's Pharmacology. Other references include:
1. Kd triphati Pharmacology
2. Basic Pharmacology
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
Do Not Forget To Visit Our Pages On Facebook on the following Links:
https://www.facebook.com/groups/569435236444761/
AND
https://www.facebook.com/groups/690331650977113/
Chronic obstructive pulmonary disorders COPD is a [preventable and treatable disease with some significant extra pulmonary effects that may contribute to the severity in individual clients.
It is characterized by airflow limitation that is not completely reversible.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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
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.
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
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.
1. GOLD16 – MANAGEMENT
AND TREATMENT OF COPD
Raphael Northoff-PTA (pharmaceutical & technical assistant)
Intern with Clinica Universidad de La Sabana
2. About GOLD
lounched in
1997
Health care
professionals
from over 50
different nations
Initial virsion of
guidelines in
2001
In collaboration
with NIH and
WHO
Updates
prepaered every
year
World COPD
Day
Relationships
with profit-
making
organizations
3. GOLD objectives
Recommend effective COPD management and prevention strategies for use in all
countries.
Increase awareness of the medical community, public health officials and the general
public that COPD is a public health problem.
Decrease morbidity and mortality from COPD through implementation and
evaluation of effective programs for diagnosis and management.
Promote study into reasons for increasing prevalence of COPD including relationship
with environment.
Implement effective programs to prevent COPD.
4. The GOLD definition of COPD
Chronic Obstructive Pulmonary Disease (COPD), a common preventable and
treatable disease, is characterized by persistent airflow limitation that is
usually progressive and associated with an enhanced chronic inflammatory
response in the airways and the lung to noxious particles or gases.
Exacerbations and comorbidities contribute to the overall severity in
individual patients.
5. is a leading cause of morbidity and mortality worldwide and results in an
economic and social burden that is both substantial and increasing
Inhaled cigarette smoke and other noxious particles such as smoke from
biomass fuels cause lung inflammation, a normal response that appears to be
modified in patients who develop COPD
may induce parenchymal tissue destruction (resulting in emphysema), and
disrupt normal repair and defense mechanisms (resulting in small airway
fibrosis). These pathological changes lead to air trapping and progressive
airflow limitation and in turn to breathlessness and other characteristic symptoms
of COPD
COPD
6. FACTORS THAT INFLUENCE DISEASE
DEVELOPMENT AND PROGRESSION
COPD
GENS
AGE &
GENDER
LUNG GROWTH
AND
DEVELOPMENT
SOCIOECO-
NOMIC
SATTUS
EXPOSURE
TO
PARTICLES
ASTHMA,
BRONCHIAL
HYPERACTIVIT
Y
CHRONIC
BRONCHITIS
alpha-1 antitrypsin
Men ≈ women
Duration of exposure?
Gestation, birth,
childhood
“Childhood infections”
“Childhood
disadvantages'”
Poverty inversely related to risk
of developing COPD
Smoke, organic/ inorganic
dusts, chemical agents and
fumes, (indoor) air pollution,
occupational exp.
May be risk factor,
clinically separating
may not be easy
hypersecretion of
mucus decline FEV1,
young + smoking +
chronical bronchitis ↑
developing COPD
11. Inflammatory aspect asthma - COPD
Both are associated with chronic inflammation of respiratory tract
BUT
Differences in the involved inflammatory cells and mediators
for instance
COPD asthma
CD8+ (cytotoxic) Tc1 lymphocytes eosinophils, leukotriens, IL5
present only in smokers, neutrophilic
Differences in pathological pathway, symptoms and response to therapy
Some patients with COPD have features consistent with asthma and may have a
mixed inflammatory pattern with increased eosinophils
12. Pathophysiology - Comorbidities
COPD often coexists with other diseases that may havea significant impact prognosis!
Cardiovascular disease Depression Osteoporosis
Lung cancer Metabolic Syndrome & Diabetes GERD
13. Process of managing COPD
Diagnose
& Assess
Adjust
treatment
Review
response
Diagnose
Identify & reduce exposure to risk
factors
Inhaler technique & adherence
COPD medications
Non-pharmacologic treatment
Symptoms
Exacerbations
Side effects
Patient satisfaction
Lung function
Hospitalization
discharge and
follow up
ICU
Palliative
care
14. Diagnosis and Assessment
Consider clinical diagnosis of COPD if patient has:
dyspnea, chronic cough or sputum production, and a history of exposure to risk factors for
the disease
Spirometry is required to make the diagnosis in this clinical context
presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent
airflow limitation and thus of COPD
Comorbidities occur frequently in COPD patients
cardiovascular disease, skeletal muscle dysfunction, metabolic syndrome, osteoporosis,
depression and lung cancer
can occur in patients with mild, moderate and severe airflow limitation and influence the
prognosis
comorbidities should be actively looked for and treated appropriately if present
Goals of COPD assessment:
determine the severity of the disease (including severity of airflow limitation), the impact on
the patient’s health status, and the risk of future events (exacerbations, hospital admissions
and death) guide therapy
16. Assessment of COPD
Symptoms
• CAT¹
• CCQ²
• mMRC³ (only
assessment of
breathlessness)
Airflow
limitation
• Based on post-
bronchodilator
FEV1 (GOLD
Classification 1-
4)
Risk of
Exacerbation
• Frequency and
hospitalization
Comorbiditis
• May influaence
mortlity and
hospitalization
• Look for routinely
and treat
appropiatly
¹ CAT COPD Assessment Test
² CCQ Clinical COPD Questionaire
³ mMRC modified British Medical Research Council
18. Therapeutic options
Smoking cessation!
Greatest capacity to influence COPD !
if effective resources and time are dedicated to
smoking cessation, 25% long term quit rates can
be achieved
PREVENTION COUNCELING
NICOTINE
REPLEACEMENT
THERAPY
Programs with clear,
consistent and repeated
nonsmoking messages
Smoke-free schools..
Even short counseling
results quit rates of
5-10%
Nicotine gum, inhaler or
spray, transdermal patch,
sublingual tablet etc.
Varenicline ?
Bupropion ?
Nortriptiyline ?
19. Therapeutic options
Occupational Exposure
Elimination or reduction of exposures in the workplace
Surveillance and early detection
Indoor and Outdoor Air Pollution
Reduce or avoid burning biomass for cooking and heating in
poorly ventilated dwellings
Advice patient to monitor public anouncements of air quality
Physical Activity
Remain activ!
All COPD patients benefit from regular physical activity
21. Pharmacological therapies for stable
COPD
Improve health status and
exercise tolerance
Reduce symptoms/
frequency and severity of
exacerbations/ mortality
To date, none of the existing medications for COPD has been
conclusively shown to modify the long-term decline in lung function
when this is tested as a primary or secondary outcome in clinical trials
22. Care of the health!
It is crucial for patients with COPD to understand the nature of their disease!
education!
Explain the COPD risk factors for its progression and their role in achieving optimal
health outcomes
Ongoing monitoring including continuous evaluation of exposure to risk factors and
monitoring of disease progression
general advice on healthy living, including diet and the fact that physical exercise is safe
and encouraged
23. evidence for the effectiveness of
pharmacologic treatments is not available
for patients with
FEV1 > 80% predicted
No evidence to recommend one
class of long-acting
bronchodilators over another for
initial treatment
Consider Combination of 2 long-
term bronchodilators if severe
breathlessness
Combination with PDE 4 inhibitor
may be considered if chronic
bronchitis
Unfortunately there is only one
study directly comparing ICS/ long-
acting beta agonist or long-acting
anticholinergic, which makes
differentiation difficult
First choice: inhaled corticosteroid
plus long-acting beta2-agonist or long-
acting anticholinergic, although there
are conflicting findings concerning this
treatment
second choice: combination of all
three classes of drugs (inhaled
corticosteroids/long-acting beta2-
agonist/long-acting anticholinergic)
“other possible treatments” if recommended first -
or alternative choice are unavailable or
unaffordable
24. Bronchodilators
are central to symptom management in COPD
increase the FEV1 or change other spirometric variables
usually widening of the airways (smooth muscles) rather than changes in lung
elastic recoil
improve emptying of the lungs
tend to reduce dynamic hyperinflation at rest and during exercise
The extent of these changes, especially in severe and very severe patients, is not
easily predictable from the improvement in FEV1
Dose – response : highly Increasing the dose of beta2-agonist/ anticholinergic
(especially nebulizers) subjective benefit in acute episodes but not necessarily
helpful in stable disease
25. Bronchodilators
are central to symptom management in COPD
Inhaled therapy is preferred
The choice between different bronchodilators depends on availability and
individual response symptoms relief and side effects?
beta2-agonists
Anticholinergics
Theophylline
Long acting bronchodilators
convenient/ more effective at producing maintained symptom relief than short acting
bronchodilators
Reduce exacerbations and related hospitalizations
Combining may improve efficacy and decrease the risk of side effects compared to
increasing the dose of an single bronchodilator
Short acting Long acting
are prescribed on as-needed or on a regular basis
26. beta 2-agonists (SABA/ LABA)
Selective stimulation of adrenergic receptors bronchial musculature
Effect:
Spasmolytic in bronchial tubes
Bronchodilator effect
short onset of action 1 - 5 min and relief for 3 - 6 hours
Fenoterol, Salbutamol, Terbutaline ect.
long slow onset and duration of 12 to 24 hours
Formoterol (rapid onset), Salmoterol ect.
27. Anticholinergics
inhibition of muscarinic Ach-receptors
Bronchodilator effect by inhaling anticholinergic
prevent wheezing, shortness of breath, coughing and chest tightness as b2-
agonist do
Tiotropium
Blocks selectively M1 and M3 for more than 24 hours
reduces exacerbations and related hospitalizations, improves symptoms
and health status and improves the effectiveness of pulmonary rehabilitation
28. Combination of Bronchodilators
may increase the degree of bronchodilation or lesser side effects!
long-acting beta2-agonist + long-acting anticholinergic
significant increase in lung function whereas outcomes is still limited
beta2-agonist + anticholinergic or theophylline
may produce additional improvements in lung function and health status compared to
either medication alone
Short-term formoterol and tiotropium has been shown to have a bigger impact on FEV1
than the single components
short-acting beta2-agonist + anticholinergic
greater and more sustained improvements in FEV1 than either drug alone
(does not produce evidence of tachyphylaxis over 90 days of treatment)
29. Methylxanthines
Controversy remains of the exact effect f xanthine derivatives
Unspecific adenosine-receptor agonist, antagonizing equally A1, A2, A3
A2b (A3) responsible for release of inflammatory mediators
Unspecific Inhibition of phosphodiesterase (PDE)
in so doing also bronchodilatating effect
Theophylline
metabolized by cytochrome P450/ Clearance declines with age
many other physiological variables and drugs modify theophylline
All studies that have shown efficacy of theophylline in COPD were performed with slow-release
preparations
Theophylline is less effective and less well tolerated than inhaled long-acting bronchodilators
30. Corticosteroids
Inhaled Corticosteroids (ICS)
only as combination therapy
dose-response relationships and long-term safety of ICS in COPD are not known
their role in the management of stable COPD is limited to specific indications
if FEV1 < 60% predicted regular treatment with ICS improves symptoms, lung function, and
quality of life, and reduces the frequency of exacerbations
Only moderate to high doses have been used in long-term clinical trials
Oral Corticosteroids (OCS)
Long-term treatment is not recommended (numerous side-effects)
for treating acute exacerbations improve symptoms, lung function, reduce rate of treatment
failure, and shorten length of hospital stay
preventing a subsequent exacerbation
31. Combination ICS/ Bronchodilator
ICS + long-acting beta2-agonist
more effective than the individual components in improving lung function and health
status and reducing exacerbations in moderate to very severe COPD
addition of a long-acting beta2-agonist/ ICS combination to tiotropium
improves lung function, quality of life and may reduce exacerbations (more studies of
triple therapy are needed
is associated with an increased risk of pneumonia
32. Phosphodiesterase inhibitors
(PDE – inhibitors)
Oral administration once daily
principal action is to reduce inflammation by inhibiting of the breakdown of
intracellular cyclic AMP
no direct bronchodilator activity
improve FEV1 in patients treated with salmeterol or tiotropium
May be helpful for patients with chronic bronchitis
should always be used in combination with at least one long-acting bronchodilator!
Representing drug: Roflumilast
33.
34.
35. Mucolytics and Antioxidant Agents
a few patients with viscous sputum may benefit from mucolytics, benefits seem to
be very small
widespread use of these agents cannot be recommended at present
In most common use:
N-acteylcystein, also an antioxidative agent
could maybe have a role in the treatment of patients with recurrent exacerbation
Cystein
36. Other pharmacological treatments
Vaccines
• Influenza vaccination can reduce serious
illness(lower respiratory tract infections) requiring
hospitalization up to death in COPD patients
• Pneumococcal polysaccharide vaccine
recommended for COPD patients ≥ 65 years
younger patients with significant comorbid conditions
Alpha-1 Antitrypsin Augmentation
• only young patients with severe hereditary alpha-1
antitrypsin deficiency and established emphysema
may be candidates
• very expensive, is not available in most countries
Antibiotics
• Not recommended,
except for treatment of
infectious exacerbations/
other bacterial infections
Vasodilators
• nitric oxide is
contraindicated in stable
COPD
Antitussives
• Cough has a significant
protective role
37. Other treatments
Oxygen therapy
• increase survival in patients with severe
resting hypoxemia
• Indicated for PaO2 ≤ 8.0 kPa/ SaO2 ≤ 88%,
pulmonary hypertension, congestive
cardiac failure, polycythemia ?
Ventilatory support
• Non-invasive ventilation (NIV) is
increasingly used in patients with stable
very severe COPD
• contradictory results regarding the clinical
benefits of long-term NIV
NIV + long-term O2 may
be of some use in a
selected subset of
patients
It may improve survival
but does not improve
quality of life
patients with COPD and
obstructive sleep apnea
benefit from continuous
positive airway pressure
(CPAP) in survival and
risk of hospital
admission
38. Surgical treatments
Lung Volume Reduction Surgery (LVRS)
parts of the lung are resected
reduce hyperinflation making respiratory muscles more effective pressure generators by
improving their mechanical efficiency In addition LVRS increases the elastic recoil pressure of
the lung and thus improves expiratory flow rates and reduces exacerbations
advantage of surgery over medical therapy more significant among patients with
predominantly upper-lobe emphysema and low exercise capacity prior to treatment
Lung Transplantation
appropriately selected patients with very severe COPD improve quality of life and functional
capacity
post-operative mortality, acute rejection, fungal or bacterial infections etc.
limited by the shortage of donor organs and costs
39. Treatment of Exacerbations
exacerbation of COPD
acute event
worsening of the patient’s respiratory symptoms beyond normal day-today variations
change in medication
most common precipitating factors
viral upper respiratory tract infections
infection of the tracheobronchial tree
diagnosis of an exacerbation
clinical presentation of the patient complaining of an acute change of symptoms (baseline dyspnea,
cough and/ or sputum production), beyond day-to-day variations
goal of treatment in COPD exacerbation
minimize the impact of the current exacerbation
prevent the development of subsequent exacerbations
40. Exacerbation – severity assessment
Arterial blood gases measurements
Pa02 < 8.0 kPa with or without PaCO2 > 6.7 kPa respiratory failure
Chest radiographs to exclude alternative diagnoses
ECG – coexisting of cardiac problems ?
Other laboratory tests
Whole blood count polycythemia or bleeding ?
Purulent sputum empirical antibiotic treatment ?
Biochemical tests electrolyte disturbances, diabetes, poor nutrition ?
41. Exacerbation - Treatment options
Oxygen
key component of hospital treatment of an exacerbation.
titrated to a target saturation of 88-92%
Bronchodilators
short-acting inhaled beta2-agonists with or without short-acting anticholinergics
Intravenous methylxanthines (theophylline/ aminophylline) may be considered as
second-line therapy if insufficient response to short-acting bronchodilators
Systemic corticosteroids
shorten recovery time, improve lung function, arterial hypoxemia reduce the risk of early
relapse, treatment failure, and length of hospital stay
42. Exacerbation - Treatment options
Antibiotics
infectious agents in COPD exacerbations can be viral or bacterial
use remains controversial
Antibiotics should be given to patients:
with increased dyspnea, increased sputum purulence (+ sputum volume)
Who require mechanical ventilation
antibiotics for only moderately or severely ill patients with COPD exacerbations with
increased cough and sputum purulence