COPD is a common preventable disease characterized by persistent airflow limitation associated with chronic inflammation in the airways and lungs due to noxious particles. The severity of COPD is assessed using symptoms, spirometry results, exacerbation risk, and comorbidities. Treatment involves smoking cessation, pharmacotherapy including bronchodilators and inhaled corticosteroids, rehabilitation, vaccination, and management of exacerbations with oxygen therapy, bronchodilators, corticosteroids, and antibiotics.
Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function.
Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function.
Pulmonary medicine- Scope and Future by Dr. Jebin Abraham, MD.Jebin Abraham
Pulmonary Medicine is a branch of medicine that deals with respiratory diseases, chest wall diseases, sleep disorders, allergy and much more. This presentation describes this specialty branch in detail with scope and current perspectives being emphasized. It will help in PG aspirant medicos, academicians and undergraduate students to know about Pulmonary Medicine in detail.
Pulmonary medicine- Scope and Future by Dr. Jebin Abraham, MD.Jebin Abraham
Pulmonary Medicine is a branch of medicine that deals with respiratory diseases, chest wall diseases, sleep disorders, allergy and much more. This presentation describes this specialty branch in detail with scope and current perspectives being emphasized. It will help in PG aspirant medicos, academicians and undergraduate students to know about Pulmonary Medicine in detail.
Chronic Obstructive Pulmonary Disease (COPD) by Dr Kemi DeleKemi Dele-Ijagbulu
Presentation on definition and general overview of COPD, how to differentiate COPD from Asthma, how to make diagnosis of COPD, simple tools for assessment of COPD; available therapeutic options; as well as management of stable COPD, COPD exacerbations and comorbidities
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.
Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by persistent respiratory symptoms and airflow limitation. The main symptoms include dyspnea, cough, and sputum production. COPD is caused by exposure to inhaled irritants, most often cigarette smoke, leading to chronic inflammation and structural changes in the lungs.
The predominant form of COPD is chronic bronchitis, which involves chronic cough and sputum production for at least 3 months per year for 2 consecutive years. This is associated with inflammation and eventual thickening of the bronchial tubes. Emphysema is another form of COPD characterized by permanent enlargement of airspaces and destruction of lung parenchyma.
The airflow limitation in COPD is due to a combination of parenchymal destruction (emphysema) and small airways disease (chronic bronchitis). The obstruction is generally progressive and irreversible. Diagnosis is based on symptoms, exposure history, and spirometry showing irreversible airflow limitation.
COPD treatment aims to reduce symptoms, improve exercise tolerance, prevent exacerbations, and slow disease progression. Smoking cessation is essential. Medications used include bronchodilators and inhaled steroids. Supplemental oxygen may be required in advanced disease. Exacerbations are treated with antibiotics, oral steroids, and other supportive therapies. Patients often have decreased quality of life and COPD is a leading cause of mortality worldwide.
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).
Etiopathogenesis and pharmacotherapy of COPD
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).
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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
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.
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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.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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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
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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.
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
2. Definition
• As per GOLD guidelines ( Jan. 2015 ), it is defined
as :
• “COPD is a common preventable and treatable
disease, characterized by persistant airflow
limitation, that is usually progressive,
• and associated with chronic inflammatory
response in the airways and lungs to noxious
particles and gases “
• Exacerbations and comorbity contribute to the
overall severity in the individual.
3. • COPD is said to be an independent entity and previously
included conditions like emphysema and chronic broncitis are
not included in the current definition.
• However the basic pathophysioloic mechanism may have
features of both the diseases ,i.e., chronic inflammation (
chronic bronchitis) or parenchyma destruction ( emphysema ).
4. Burden of COPD
• Leading cause of morbidity and moratlity
worldwide – economic and social burden
• The prevalence related primarily to tobacco
smoking , also biomass fuel, indoor and outdoor
pollution.
• The global burden of disesase study projected
that COPD may become 3rd leading cause of
death by the year 2030
• It is a major economic burden and healthcare
costs.
5. Risk factors for COPD
• Genes – α1 AT deficiency
• Exposure to particles - Tobacco smoke, Occupational
Indoor and Outdoor air pollution
• Lung growth and development : factors affecting normal
lung growth can increase individual risk.
• Gender – M >F, but prevalence changing.
• Age – association unclear. Indicates cumulative exposure.
• Respiratory infections – severe childhood respiratory
infection, TB, HIV : Independent risk factors
• Socioeconomic status – poverty is a risk factor
• Asthma/Bronchial hyperreactivity - a risk factor. 12 – 20%
asthmatics may progress on to chronic airflow limitation
• Chronic Bronchitis – increased likelihood in people with
mucus hypersecretion, reduced FEV 1 and those who
continue to smoke
6. Pathology
• Changes found in :
Parenchyma
Vasculature
And airways
The salient changes are :
• Chronic inflammation
• Parenchymal / airspace destruction
7. Pathogenesis
• Oxidative stress
Oxidents generated in cigarrette smoke and inflammatory cells
Reduced endogenous oxidents : reduction in transcription factor
nrf2
Biomarkers found in exhaled breath : hydrogen peroxide, 8-
isoprostane
• Protease-antiprotease imbalance
Protease mediated destruction of elastin- major cause of
emphysema
• Inflammatory cells
Increase in CD8+ T lymphocytes
Increased macrophages and neutrophils
• Inflammatory mediators
• Chemotactic factors – recruit inflammatory cells
• Proinflammatory chemokines – amplify inflammation
• Growth factors – amplify remodelling
8. Pathophysiology
• Airflow limitation and air trapping
Progressive hyperinflation and air trapping – reduction in
FEV1/FVC and FEV1
Hyperinflation – dyspnea and effort limitation
Up regulation of pro- inflammatory cytokines ( IL 8, TNF α )
• Gas exchange abnormalities
Gas exchange worsens as disease progresses
Reduced ventilatory drive – reduced ventilation
V : Q mismatch
• Mucus hypersecretion
Increase in Goblet cells and submucosal glands – increased
mucus production
9. • Pulmonary hypertension
Develops late in course
Chronic hypoxic vasoconstriction and vascular remodelling
May lead to right heart hypertrophy and failure
• Exacerbations
Triggered by pollutants, infections or unknown factors
Increased hyperinflation and gas trapping, expiratory flow limitation
V:Q mismatch is worsened
• Systemic features
Inflammatory mediators – cachexia, muscle wasting
IHD, heart failure
Osteoporosis
Anemia of chronic disease,
DM, metabolic syndrome
Major depression
10. Assessment
The goals are to :
• Determine the severity of the disease,
• its impact on the patient’s health status
• and the risk of future events ( exacerbations)
• to guide therapy.
Assess :
symptoms
degree of airflow limitation using spirometry
risk of exacerbations
comorbidities
11. Assessment : History taking
• Exposure to risk factors : cigarette smoke, biomass
fuels, occupational exposure
• Medical history – bronchial asthma, allergy , sinusitis,
nasal polyps, childhood resp. infection
• Family history of COPD
• History of exacerbations or previous hospitalizations
• Presence of comorbidities
• Social and family support available
• Possibilities of reducing risk factors : smoking cessation
12. Assessment : Symptoms
• The characteristic symptoms of COPD are chronic
and progressive dyspnea, cough, and sputum
production that can be variable from day-to-day.
• Dyspnea: Progressive, persistent and
characteristically worse with exercise.
• Chronic cough: May be intermittent and may be
unproductive.
• Chronic sputum production: COPD patients
commonly cough up sputum.
13. • Quantitative measurement of symptoms:
• COPD Assessment Test (CAT): An 8-item
measure of health status impairment in
COPD(http://catestonline.org).
• Clinical COPD Questionnaire (CCQ): Self-
administered questionnaire developed to
measure clinical control in patients with COPD
(http://www.ccq.nl).
• Breathlessness Measurement using the
Modified British Medical Research Council
(mMRC) Questionnaire: relates well to other
measures of health status and predicts future
mortality risk.
14. Assessment : degree of airflow limitation
• Spirometry should be performed after the
administration of an adequate dose of a short-
acting inhaled bronchodilator to minimize
variability.
• A post-bronchodilator FEV1/FVC < 0.70
confirms the presence of airflow limitation.
• Where possible, values should be compared to
age-related normal values to avoid over
diagnosis of COPD in the elderly.
15.
16.
17. Classification of severity
There is however a weak correlation between FEV1, symptoms and patient’s QOL.
WITHIN ANY CATEGORY PATIENT MAY HAVE QOL VARYING FROM WELL PRESERVED
TO POOR HEALTH STATUS.
Thus, formal symptomatic assessment is also required.
18. Assessment : risk of exacerbations
To assess risk of exacerbations use history of
exacerbations and spirometry:
• 2 or more exacerbations within the last year
or an FEV1 < 50 % of predicted value are
indicators of high risk.
• 1 or more hospitalizations for COPD
exacerbation should be considered high risk.
19.
20. Assessment : comorbidities
COPD patients are at increased risk for:
• Cardiovascular diseases
• Osteoporosis
• Respiratory infections
• Anxiety and Depression
• Diabetes
• Lung cancer
• Bronchiectasis
These comorbid conditions may influence mortality
and hospitalizations and should be looked for
routinely, and treated appropriately
21. Other investigations
• Chest X-ray: Seldom diagnostic but valuable to exclude alternative
diagnoses and establish presence of significant comorbidities.
• CT chest : not routinely recommended. Done only when there is
doubt in diagnosing COPD or to rule out other D.D.
• Lung Volumes and Diffusing Capacity: Help to characterize severity,
but not essential to patient management.
Typically there is decresed FEV1, FEV1/FVC ; increased RV , RV/TLC ;
DlCo may reduce in emphysema
• Oximetry and Arterial Blood Gases: Pulse oximetry can be used to
evaluate a patient’s oxygen saturation and need for supplemental
oxygen therapy.
SpO2 < 92% warrants ABG analysis.
• Alpha-1 Antitrypsin Deficiency Screening: Perform when COPD
develops in patients of Caucasian descent under 45 years or with a
strong family history of COPD and /or lower lobe emphysema.
Values 15 -20% of normal suggest homozygous deficiency
22. • Exercise Testing: Objectively measured exercise
impairment, is a powerful indicator of health
status impairment and predictor of prognosis.
6MWT
Ergometry ( cycle / treadmill )
CPET
• Composite Scores: Several variables (FEV1,
exercise tolerance assessed by walking distance
or peak oxygen consumption, weight loss and
reduction in the arterial oxygen tension) identify
patients at increased risk for mortality.
23. BODE index
It is a composite tool for predicting severity. Its utility is still under
investigation.
26. Key points ( stable COPD )
• Smoking cessation has the greatest capacity to influence the natural
history of COPD. Health care providers should encourage all
patients who smoke to quit.
• Pharmacotherapy and nicotine replacement : reliably increase long-
term smoking abstinence rates.
• regular physical activity and should repeatedly be encouraged to
remain active
• Appropriate pharmacologic therapy : can reduce COPD symptoms,
reduce the frequency and severity of exacerbations, and improve
health status and exercise tolerance.
• None of the existing medications for COPD has been shown
conclusively to modify the long-term decline in lung function.
• Influenza and pneumococcal vaccination should be offered
depending on local guidelines.
28. Overview of treatment of stable COPD
• Identification and reduction of exposure to risk
factors are important steps in prevention and
treatment.
• Individualized assessment of symptoms, airflow
limitation, and future risk of exacerbations should
be incorporated into the management strategy.
• rehabilitation and maintenance of physical
activity.
• Pharmacologic therapy is used to reduce
symptoms, reduce frequency and severity of
exacerbations, and improve health status and
exercise tolerance
29. • Long-acting formulations of beta2-agonists and
anticholinergics are preferred over short-acting
formulations.
• inhaled bronchodilators are preferred over oral
bronchodilators.
• Long-term treatment with inhaled corticosteroids
added to long-acting bronchodilators is recommended
for patients with high risk of exacerbations
• Long-term monotherapy with oral or inhaled
corticosteroids is not recommended in COPD.
• The phospodiesterase-4 inhibitor roflumilast may be
useful to reduce exacerbations for patients with FEV1 <
50% of predicted, chronic bronchitis, and frequent
exacerbations
30. MANAGEMENT OF ACUTE EXACERBATION
• DEFINITION ( GOLD, jan 2015)
“an acute event characterized by a worsening of the
patient’s respiratory symptoms that is beyond normal
day-to-day variations and leads to a change in
medication.”
There is notable change in :
• Baseline dyspnea
• Cough
• Sputum production
32. ASSESSMENT OF AE
• SIGNS OF SEVERITY ARE :
Use of accessory muscles of respiration
Paradoxical chest wall movements
Worsening or new onset central cyanosis
Development of peripheral edema
Hemodynamic instability
Deterioration of mental status
33. Investigations to be sent
• Arterial blood gas measurements (in hospital): PaO2 < 8.0 kPa with
or without PaCO2 > 6.7 kPa when breathing room air indicates
respiratory failure.
• Chest radiographs: useful to exclude alternative diagnoses.
• ECG: may aid in the diagnosis of coexisting cardiac problems.
• Whole blood count: identify polycythemia, anemia or bleeding.
• Purulent sputum during an exacerbation: indication to begin
empirical antibiotic treatment.
• Biochemical tests: detect electrolyte disturbances, diabetes, and
poor nutrition.
• Spirometric tests: not recommended during an exacerbation
37. Oxygen therapy
• low-flow intranasal cannulae / 24–35% Venturi mask - titrated to SpO2 of
88–92% .
• Excessive oxygen therapy is the cause of increased hypercapnia
• ABGs should be repeated 1 hour
• If the rise in PaCO2 is excessive (>10¯mmHg ), then FiO2 should be
reduced, titrating SpO2 to 2–3% below the previous value, and arterial
blood gases should be repeated.
• If no PaCO2 rise occurs with oxygen therapy, then a higher SpO2 may be
targeted with repeat ABG.
• Inadequate reversal of hypoxia (e.g. SpO2 < 85%) is suggestive of an
additional problem such as pneumonia, pulmonary oedema or embolus,
or a pneumothorax.
• Although high levels of O2 should be avoided, reversal of hypoxia is
important and O2 should not be withheld in the presence of hypercapnia,
or withdrawn if it worsens.
38. PHARMACOTHERAPY
• Bronchodilators:
Short-acting inhaled beta2-agonists with or without short-acting
anticholinergics are preferred ( no controlled trials).
No significant difference between MDI vs nebulizers
No studies done to evaluate long acting bronchodilators ( beta 2
agonists/ anticholinergics ) with or without inhaled steroids in AE.
IV methylxanthines ( amino, theophylline) : considered 2nd line
therapy. Used in selected patients when insufficient response to
short acting bronchodilators.
NEBULIZED MAGNESIUM AS AN ADJUVANT TO SALBUTAMOL HAS NO
EFFECT ON IMPROVING FEV1
39. • Systemic Corticosteroids:
Shorten recovery time,
improve lung function (FEV1) and arterial hypoxemia
(PaO2), and
reduce the risk of early relapse, treatment failure, and
length of hospital stay.
• A dose of 40 mg prednisone per day for 5 days is
recommended
• Methylprednisolone 0.5 mg/kg every 6 hrly for 72 hrs. also
has been tried
• Nebulized budesonide may be alternative to oral steroids.
• LONG TERM ORAL OR NEBULIZED STEROIDS ARE NOT
RECOMMENDED.
40. • Antibiotics should be given to patients with 3 cardinal
symptoms:
increased dyspnea,
increased sputum volume,
and increased sputum purulence,
Who require mechanical ventilation
• Recommended duration : 5 -10 days
• Drug choice based on local resistance pattern. Usually
empirical treatment is with aminopenicillin with or
without BLI, macrolide or tetracycline.
• Improvement in dyspnea and sputum purulence
indicates clinical success.
42. • The goal of NIV is:
to unload respiratory muscles and augment
ventilation and oxygenation
reduce CO2 and correct acidosis until the
underlying problem can be reversed
when applied intermittently, to offset the
adverse effects of sleep- or position-induced
adverse changes to ventilation, increased upper
airway resistance and lung volume.
Reduce VAP
Reduce ICU LOS
44. • The goals of IMV in COPD are:
to support ventilation while reversible
components improve,
to allow respiratory muscle to rest and recover
whilst preventing wasting from total inactivity
to minimise dynamic hyperinflation.
45. INVASIVE VENTILATION TECHNIQUE
• MODE : Volume A/C
• INITIAL Tv : 5 -8 ml/kg IBW
• TARGET PEAK PRESSURE : below 40 – 45
cmH2O
• RR : < 14/ min
• I : E RATIO – 1:3 to 1:4
• FiO2 : < 0.5 ( depending on PaO2 )
46. PEEP
• e PEEP is beneficial as :
It reduces gas trapping
Stents open the airways
Reduces work of breathing to trigger
inspiratory flow.
• As e PEEP is applied , the Tv will increase
without an increase in airway pressure until :
e PEEP exceeds i PEEP.
47. Weaning
• The simple criterion of patient respiration rate/tidal volume <100
breaths/min per litre had the best predictive value for weaning
• Other indications to extubate include :
• FiO2<40%;
• PaO2/FiO2>200,
• PEEP 5cmH2O,
• Cardiovascular stability,
• afebrile,
• pH > 7.35, PaCO2<50mmHg
• GCS >10 and,
• static compliance >25mL/cmH2O.
• Some patients unable to achieve these criteria may require weaning with
PaCO2 50–65mmHg with a bicarbonate level of >30¯mmol/L allowed or
encouraged to reduce the work of breathing and achieve a less abnormal
pH.
• Following extubation, weaning can be continued with immediate
placement upon NIV
48. Adjunctive therapy
1. ANTICOAGULANTS
• Subcutaneous heparin (e.g. 5000 units b.d.) is recommended as a prophylactic measure
against venous thromboembolism. There is no evidence for warfarinisation in COPD patients
with pulmonary hypertension.
2. ELECTROLYTE CORRECTION
• Electrolyte correction is important. Hypophosphataemia,hypomagnesaemia,hypocalcaemia
and hypokalaemia may impair respiratory muscle function.
• Hyponatraemia may occur with inappropriate antidiuretic hormone release or with excess
use of diuretics and inappropriate intravenous fluids.
3. NUTRITION
• Nutrition is important, as patients with severe COPD are often undernourished – a subnormal
BMI is a risk factor for mortality in COPD.
• Excessive carbohydrate calories should be avoided as this increases CO2 production (by
>15%) and may worsen respiratory failure.
• Low-carbohydrate/high-fat combinations are preferred in ARF during spontaneous
ventilation.
49. 4. CHEST PHYSIOTHERAPY
• Chest physiotherapy should be initiated and regularly
repeated as both a curative and preventive measure.
• Encouragement of coughing and deep breathing are the
two most important factors.
• ‘Bubble positive expiratory pressure (PEP)’ is an
inexpensive method of assisting sputum clearance in
patients with retained secretions or those having difficulty
expectorating.
5. NEBULISED MUCOLYTIC AGENTS
• Nebulised mucolytic agents, such as N-acetylcysteine,
continue to be proposed, although their benefit hasnever
been established in acute exacerbations of COPD.
• Oral mucolytics have been shown to reduce cough
frequency and severity in stable COPD