Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by persistent respiratory symptoms and limited airflow. The document defines COPD and its components of chronic bronchitis and emphysema. It describes the respiratory anatomy and physiology. Risk factors for COPD include cigarette smoking, occupational exposures, and genetic factors. The diagnosis is made through spirometry and imaging. Treatment focuses on smoking cessation, bronchodilators, pulmonary rehabilitation, and managing exacerbations.
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).
These slides offer a comprehensive overview of Chronic Obstructive Pulmonary Disease (COPD), a progressive lung disorder characterized by airflow limitation and persistent respiratory symptoms. Delve into the pathophysiology of COPD, understanding the role of smoking, environmental factors, and genetic predisposition in its development. Learn about the clinical manifestations, including chronic bronchitis and emphysema, and how they contribute to the disease's progression. The presentation explores diagnostic methods such as spirometry and imaging techniques, as well as the GOLD guidelines that aid in disease staging and management. Discover the multifaceted treatment approaches, including bronchodilators, inhaled corticosteroids, pulmonary rehabilitation, and lifestyle modifications. These slides provide a comprehensive resource for grasping the complexities of COPD and its management.
Chronic Obstructive Pulmonary Disease BY
Dr Akram Yousuf
Resident Internal Medicine
Liaquat University of Medical Health and Sciences Jamshoro Pakistan
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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).
These slides offer a comprehensive overview of Chronic Obstructive Pulmonary Disease (COPD), a progressive lung disorder characterized by airflow limitation and persistent respiratory symptoms. Delve into the pathophysiology of COPD, understanding the role of smoking, environmental factors, and genetic predisposition in its development. Learn about the clinical manifestations, including chronic bronchitis and emphysema, and how they contribute to the disease's progression. The presentation explores diagnostic methods such as spirometry and imaging techniques, as well as the GOLD guidelines that aid in disease staging and management. Discover the multifaceted treatment approaches, including bronchodilators, inhaled corticosteroids, pulmonary rehabilitation, and lifestyle modifications. These slides provide a comprehensive resource for grasping the complexities of COPD and its management.
Chronic Obstructive Pulmonary Disease BY
Dr Akram Yousuf
Resident Internal Medicine
Liaquat University of Medical Health and Sciences Jamshoro Pakistan
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
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
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
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
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.
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.
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.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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
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
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
Follow us on: Pinterest
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
3. DEFINITION
• Chronic obstructive pulmonary disease (COPD) is defined as a disease
state characterized by persistent progressive respiratory symptoms
and airflow limitation that is not fully reversible
• includes emphysema
• chronic bronchitis
4. DEFINITION
• Chronic bronchitis is defined clinically as the presence of a
chronic productive cough for 3 months during each of 2 consecutive
years (other causes of cough being excluded).
• Emphysema is defined pathologically as an abnormal, permanent
enlargement of the air spaces distal to the terminal bronchioles,
accompanied by destruction of their walls and without obvious
fibrosis.
5. RESPIRATORY ANATOMY
• Upper Respiratory Tract: Nasal cavity, Pharynx. Larynx, Upper part of trachea.
• Lower Resoiratory Tract: Lower part of the trachea, Bronchial tree, Lungs
• Functionally, the respiratory system can be divided into a conducting zone and a
respiratory zone
Conducting Zone- route for incoming and outgoing air, remove debris and
pathogens from the incoming air, and warm and humidify the incoming air
– nasal cavity, Pharynx. Larynx, trachea bronchial tree.
• bronchi have walls consisting of cartilage and smooth muscle, epithelial lining with
Cilia and goblet cells, submucosal mucus secreting glands, endocrine cells
6. RESPIRATORY ANATOMY
Respiratory Zone- structures directly involved in gas exchange.
• begins where the terminal bronchioles join a respiratory bronchiole, the
smallest type of bronchiole, which then leads to an alveolar duct, opening
into a cluster of alveoli.
7.
8. RESPIRATORY PHYSIOLOGY- RESPIRATORY
VOLUMES AND CAPACITIES
• Tidal volume (TV) – amount of air moving in and out of the lungs with each
breath (about 500ml on average)
• Inspiratory reserve volume (IRV) – amount of air that can be taken in forcibly
over the tidal volume
• Expiratory reserve volume (ERV) – amount of air that can be forcibly exhaled
over tidal volume
• Residual volume – amount of air that always remains in the lungs; it cannot
be exhaled.
• Vital capacity – maximum amount of air that can be forcefully exchanged; VC
= TV+IRV+ERV
• Total lung capacity = VC+RV
9.
10. EPIDEMIOLOGY
• COPD is a disease of increasing public health importance around the
world.
• COPD is the third most common cause of death worldwide with
2.5million deaths per year(6%) and 4th most common cause of death in
low income countries (WHO)
• COPD affects >10 million persons in the United States.
• In Africa, the estimated prevalence is 13.4% (Finney et al, 2012)
• The prevalence of COPD in sub-Saharan Africa has been poorly
studied. A meta-analysis of nine crosssectional studies (5 from
11. RISK FACTORS
• Cigarette smoking (>10 packs per year)
• Passive or second-hand smoking
exposure
• Extremes of age
• Lower socio-economic group
• Male gender
• Increased airway responsiveness
• Respiratory infections
• Occupational exposures, -coal, gold,
dust, and cotton.
• Ambient air pollution
• Alpha 1 antitrypsin deficiency
12. PATHOPHYSIOLOGY
• Pathologic changes in chronic obstructive pulmonary disease (COPD)
occur in the large (central) airways, the small (peripheral)
bronchioles, and the lung parenchyma.
• Most cases of COPD are the result of exposure to noxious stimuli,
most often cigarette smoke. The normal inflammatory response is
amplified in persons prone to COPD development.
• Small airways may become narrowed by cells (hyperplasia and
accumulation), mucus, and fibrosis, and extensive small airway
destruction has been demonstrated to be a hallmark of advanced COPD.
13. EMPHYSEMA PATHOGENESIS
• comprises a series of four interrelated events:
• (1) Chronic exposure to cigarette smoke in genetically susceptible individuals
triggers inflammatory and immune cell recruitment within large and small airways
and in the terminal air spaces of the lung.
• (2) Inflammatory cells release proteinases that damage the extracellular matrix
supporting gas exchange surfaces of the lung.
• (3) Structural cell death occurs through oxidant-induced damage, loss of cellular-
matrix attachments leading to alveolar destruction.
• (4) Disordered repair of elastin and other extracellular matrix components
contributes to air space enlargement and emphysema.
15. EMPHYSEMA PATHOGENESIS
• Furthermore, loss of alveoli leads to airflow limitation by 2
mechanisms.
• First, loss of the alveolar walls results in a decrease in
elastic recoil, which leads to airflow limitation.
• Second, loss of the alveolar supporting structure leads to airway
narrowing, which further limits airflow.
17. EMPHYSEMA PATHOGENESIS
• Centriacinar emphysema - focal destruction limited to the respiratory
bronchioles and the central portions of the acini. associated with
cigarette smoking and typically most severe in the upper lobes.
• Panacinar emphysema - entire alveolus distal to the terminal
bronchiole. The panacinar type is typically most severe in the lower
lung zones. generally develops in patients with homozygous alpha1-
antitrypsin (AAT) deficiency.
• Distal acinar emphysema, or paraseptal emphysema.- least common form
and involves distal airway structures, alveolar ducts, and sacs. This
form of emphysema is localized to fibrous septa or to the pleura and
18. CHRONIC BRONCHITIS PATHOGENESIS-FIXING
• Damage to the endothelium impairs the mucociliary response that clears
bacteria and mucus.
• Inflammation and secretions provide the obstructive component of chronic
bronchitis.
• Neutrophilia develops in the airway lumen, and neutrophilic infiltrates
accumulate in the submucosa.
• The respiratory bronchioles display a mononuclear inflammatory process, lumen
occlusion by mucus plugging, goblet cell metaplasia, smooth muscle
hyperplasia, and distortion due to fibrosis.
• These changes, combined with loss of supporting alveolar attachments, cause
airflow limitation by allowing airway walls to deform and narrow the airway
lumen.
19. CHRONIC BRONCHITIS PATHOGENESIS
In contrast to emphysema, chronic bronchitis is associated with a relatively
undamaged pulmonary capillary bed.
• The body responds by decreasing ventilation and increasing cardiac output.
• This V/Q mismatch results in rapid circulation in a poorly ventilated lung,
leading to hypoxemia and polycythemia.
• Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary
artery vasoconstriction and cor pulmonale.
• With the ensuing hypoxemia, polycythemia, and increased CO2 retention, these
patients have signs of right heart failure and are known as "blue bloaters."
20.
21. SYMPTOMS
• Patients typically present with a combination of signs and symptoms
of chronic bronchitis, emphysema, and reactive airway disease.
Symptoms include the following:
• Cough, usually worse in the mornings and productive of a small
amount of colorless sputum
• Breathlessness: The most significant symptom, but usually does not
occur until the sixth decade of life
• Wheezing: May occur in some patients, particularly during exertion
and exacerbations
22. PHYSICAL EXAMINATION
Relatively poor sensitivity in mild-to-moderate COPD
• In severe COPD:
• Cyanosis, visible in the lips and nail beds
• Peripheral edema
• Tachypnea and respiratory distress with simple activities
• Use of accessory respiratory muscles and paradoxical indrawing of lower
intercostal spaces (Hoover sign)
• Sitting in the characteristic “tripod” position to facilitate the actions of the
sternocleidomastoid, scalene, and intercostal muscles for a prolonged expiratory
phase.
• Elevated jugular venous pulse (JVP)
23. PHYSICAL EXAMINATION
• Thoracic examination reveals the following:
• Hyperinflation (barrel chest)
• Wheezing – Frequently heard on forced and unforced expiration
• Diffusely decreased breath sounds
• Hyperresonance on percussion
• Prolonged expiration
• Coarse crackles beginning with inspiration in some cases
24. PHYSICAL EXAMINATION- PREDOMINANT CHRONIC BRONCHITIS (BLUE
BLOATERS)
• Patients may be obese
• Frequent cough and expectoration are typical
• Use of accessory muscles of respiration is common
• Coarse rhonchi and wheezing may be heard on auscultation
• Patients may have signs of right heart failure (ie, cor pulmonale), such as edema
and cyanosis
25. PHYSICAL EXAMINATION- PREDOMINANT EMPHYSEMA (PINK PUFFERS)
• Patients may be very thin with a barrel chest
• Patients typically have little or no cough or expectoration
• Breathing may be assisted by pursed lips and use of accessory respiratory muscles;
patients may adopt the tripod sitting position
• The chest may be hyperresonant, and wheezing may be heard
• Heart sounds are very distant
26.
27. • current evidence demonstrates that most patients have elements of
both chronic bronchitis and emphysema and that the physical
examination does not reliably differentiate the two entities.
28. INVESTIGATIONS
• Post-bronchodilator spirometry- FEV1/FVC < 70%, with normal TLC.
• The diffusing capacity may be reduced
• Arterial blood gases and oximetry may demonstrate resting or
exertional hypoxemia.
• Elevated hematocrit suggests the presence of chronic hypoxemia,
• α1AT assay
29. INVESTIGATIONS
• Chest X Ray
–Obvious bullae, paucity of parenchymal markings, or hyperlucency on suggests
the presence of emphysema.
–Increased lung volumes and flattening of the diaphragm suggest hyperinflation
• Chest computed tomography (CT) scan
–current definitive test for establishing the presence or absence of emphysema,
the pattern of emphysema, and the presence of significant disease involving
medium and large airways
–It also enables the discovery of coexisting interstitial lung disease and
bronchiectasis,
–help determine the possible value of surgical therapy
30. INVESTIGATIONS-OTHERS
• Hematocrit – Patients with polycythemia (hematocrit greater than 52% in men or
47% in women)
• Serum potassium – Diuretics, beta-adrenergic agonists, and theophylline
• Measure AAT in all patients younger than 40 years, in those with a family history
of emphysema at an early age, or with emphysematous changes in a nonsmoker
• Sputum evaluation will show a transformation from mucoid in stable chronic
bronchitis to purulent in acute exacerbations
• Pulse oximetry.
• Electrocardiography can help establish that hypoxia is not resulting in cardiac
ischemia and that the underlying cause of respiratory difficulty is not cardiac in
nature
• Right-sided heart catheterization can confirm pulmonary artery hypertension and
31. COPD SEVERITY ASSESSMENT
• GOLD Spirometric calculation-population based method.
COPD severity categories based on respiratory symptoms.
• Modified Medical Research Council Dyspnea Scale (mMRC ) or COPD
Assessment Test (CAT) and annual frequency of COPD exacerbations.
• CAT is an 8-item COPD health status measure with Likert scale
responses for questions about cough, phlegm, chest tightness,
dyspnea on one flight of stairs, limitation in home activities,
confidence in leaving the home, sleep and energy. Range of total
score is 0–40.
36. TREATMENT- STABLE PHASE COPD
• TREATMENT GOALS
–Provide symptomatic relief
–Reduce future risk
–Improve exercise tolerance, overall health status
–Prevent and treat exacerbation AND complications
–Reduce morbidity and mortality
• Response to therapy should be assessed, and decisions should be made
whether or not to continue or alter treatment.
37. TREATMENT- STABLE PHASE COPD
• Some interventions have been demonstrated to improve survival of
patients with COPD
Smoking cessation.
Oxygen therapy in chronically hypoxemic patients.
Lung volume reduction surgery (LVRS) in selected patients with
emphysema.
Use of triple therapy significantly lowers mortality compared with
dual bronchodilation
38. PHARMACOTHERAPY
• General management:
• smoking cessation
–nicotine replacement therapy available as gum, transdermal patch,
lozenge, inhaler, and nasal spray;
–bupropion; and
–varenicline, a nicotinic acid receptor agonist/antagonist.
• Annual influenza vaccination
• One-off pneumococcal vaccination every 5 years.
39. PHARMACOTHERAPY
• Bronchodilator therapy:
Short-acting Beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA)
is first-line treatment.
For patients who remain breathless or have exacerbations despite using short-
acting bronchodilators the next step is determined by the FEV1.
• FEV1 > 50% (Stage I & II):
Long-acting beta2-agonist (LABA), for example salmeterol, or: Long-acting
muscarinic antagonist (LAMA), for example tiotropium.
• FEV1 < 50% (Stage III & IV):
LABA + high-dose inhaled corticosteroid (ICS) in a combination inhaler, or:
LAMA.
40.
41.
42.
43.
44. LTOT
• Patients who receive LTOT should breathe supplementary oxygen for at least 15
hours a day. Oxygen concentrators are used to provide a fixed supply for LTOT.
• Assess patients for LTOT if any of the following:
• Oxygen saturations less than or equal to 92% on room air
• Very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be
'considered' for patients with severe airflow obstruction (FEV1 30-49% predicted).
• Patients with a PaO2 of less than 55 mm Hg, a PaO2 of less than 59 mm Hg with
evidence of polycythemia, or cor pulmonale.
• Reevaluate these patients 1-3 months after initiating therapy.
47. EXACERBATIONS OF COPD
• Exacerbations are a prominent feature of the natural history of
COPD.
• Exacerbations are episodic acute worsening of respiratory symptoms,
including increased dyspnea, cough, wheezing, and/ or change in the
amount and character of sputum.
• The three cardinal symptoms of COPD exacerbation include
–increases in dyspnea,
–Increase in sputum volume, and
–Increase in sputum purulence.
48. EXACERBATIONS OF COPD
• Though symptoms of COPD exacerbations usually last for about 7 to 10 days,
the patient may not fully recover for several weeks to months.
• Patients with severe (FEV1 <50% predicted) or very severe airflow
obstruction (FEV1 <30% predicted) on average have 1–3 episodes per year.
49. EXACERBATIONS OF COPD- RISK FACTORS
• The strongest single predictor of exacerbations is a history of a previous
exacerbation
• Duration of COPD,
• History of antibiotic or theophylline use,
• Advanced age,
• Increased ratio of pulmonary artery to aorta cross-sectional dimension,
• Comorbid conditions (e.g., chronic heart failure, diabetes mellitus, GORD
etc.).
• Patients with increased sputum production, productive cough, and an
elevated blood eosinophil count (>0.34 x 109 cells/L)
50. EXACERBATIONS OF COPD- RISK FACTORS
• Environmental pollution, temperature, and pulmonary embolism are also
known exacerbation triggers.
• Chest Infections
–Bacteria frequently implicated include Haemophilus influenzae(most
common), Streptococcus pneumoniae and Moraxella catarrhalis. In
addition, Mycoplasma pneumoniae or Chlamydia pneumoniae are found in
5–10% of exacerbations.
–Viral respiratory infections are present in approximately one-third of
COPD exacerbations. rhinovirus being the most important pathogen.
• In 20–35%, no specific precipitant can be identified.
51. SEVERITY OF EXARCEBATION
SEVERITY OF
EXARCEBATION
TYPE OF EXARCEBATION CHARACTERISTICS
SEVERE TYPE 1 Increased dyspnea, sputum
volume and sputum purulence
MODERATE TYPE 2 Any 2 of the above 3 cardinal
symptoms
MILD TYPE 3 Any 1 of the above 3 cardinal
symptoms and 1 or more of the
following minor symptoms or
signs
- Cough
- Wheezing
- Fever without an obvious
source - Upper respiratory
tract infection in the past 5 days
- Respiratory rate increase
>20% over baseline
- Heart rate increase >20% over
baseline
52. TREATMENT - COPD EXARCEBATION
• The goal of therapy when treating a COPD exacerbation are
– The recovery to baseline clinical status.
– Prevention of future exarcebations.
– Prevention of hospitalization or reduction in hospital stay,
– Prevention of acute respiratory failure and death,
53. INDICATIONS FOR ADMISSION FOR ACUTE EXARCEBATION.
• Failure of outpatient treatment
• Marked increase in dyspnea
• Altered mental status
• Increase in hypoxemia or hypercapnia
• Onset of new physical signs (eg cyanosis, periphaeral edema)
• Presence of serious comorbidities (eg heart failure or new onset
arrhythmias))
• Freque nt exarcebations
• Older age
• Inability to tolerate oral medications such as antibiotics or steroids
54. INDICATIONS FOR ICU ADMISSION
• Severe dyspnea that responds inadequately to initial emergency therapy.
• Changes in mental status.(confusion, lethargy, coma)
• Persistent or worsening hypoxemia (PaO2 <5.3Kpa, 4OmmHg) and
severe/worsening resiratory acidosis (PH <7.25) despite supplemental
oxygen and noninvasive ventilation.
• Need for invasive Mechanical ventilation.
• Hemodynamic instability-need for vasopressors.
55. TREATMENT - COPD EXARCEBATION
• Bronchodilators
Mild exacerbations- use of short-acting beta2-agonists (SABA), with or
without short-acting anticholinergics
Moderate-to-severe exacerbations- SABA+ systemic corticosteroid.
Continued use of long-acting bronchodilators throughout the
exacerbation or start as soon as possible before discharge.
• Controlled oxygen therapy.
Start at 24-28%. AIM: 88-92%. Adjust according to ABG: AIM: PaO2 8kpa with rise of
PaCo2 <1.5kpa
56. TREATMENT - COPD EXARCEBATION
• Steroids
Give prednisolone 30 mg daily for 7-14 days. Prolonged courses offer no
additional benefit.
• Antibiotics
Give antibiotics only if sputum is purulent or there are clinical signs of
pneumonia.
Improves FEV1, shortens duration of hospitalization and recovery time, reduce
the risk of early relapse.
• NIV should be considered within the first 60 minutes of hospital arrival in all
patients with an acute exacerbation of COPD in whom a respiratory acidosis
57.
58. REFERENCES
• Adeloye D, Basquill C, Papana A, et al. An estimate of the prevalence of COPD in
Africa: a systematic analysis. COPD 2015;12:71-81. 10.3109/15412555.2014.908834
• Ozoh OB, Awokola T, Bust SA. Medical student’s knowledge about the management of COPD
in Nigeria. Int J Tuber Lung Dis 2014; 18: 117–21.
• American Journal of Respiratory and Critical Care Medicine 2012;185:A6029 Chronic
Obstructive Pulmonary Disease In Sub Saharan Africa: A Systematic Review Lydia J.
Finney , Johanna Feary , Stephen B. Gordon , Jo Leonardi Bee , Kevin Mortimer ,
https://doi.org/10.1164/ajrccm-conference.2012.185.1_MeetingAbstracts.A6029
• Oxford handbook of clinical Medicine. 10th edition P184-187; P160;P812-814
• Summarizing the 2021 Updated GOLD Guidelines for COPD, US Pharmacist. US Pharm.
2021;46(7):30-35.
59. • venturi masks
• examples of drugs and classes
• HYPOXEAMIA DEFINITION
• nasal prongs non rebreayhable
• side eefect of steroids
• NORMAL PAO2 PCO2 AND OTHERS
• COR PULMONALE SX. Cyanosis
• Polycythaemia
• Peripheral oedema
• Raised jugular venous pressure
• ASTHMA VS COPD
• RELEVANT ANATOMY
• read oxford
• when is theophylline indicated and other drugs
• respiratory failure types
• ARACHIDIONIC ACID PATHWAY FOR BROCHOCONSTRICTION
60.
61. • Features suggesting a diagnosis of COPD
• • Persistent dyspnoea on effort with cough and wheeze
• • History of smoking or exposure to other risk factors
• • Slow progression
• • Abnormal post bronchodilator spirometry
• Features that suggest the presence of asthma
• • Young age at onset
• • Diurnal or day-to-day variability and seasonal variation
• • Presence of atopy and/or allergic rhinitis
• • Significant bronchodilator responsiveness
• Additional considerations in the diagnosis of asthma and COPD
• • Asthma and COPD may co-exist, and distinguishing them may be difficult
• • Asthmatics who smoke may have an accelerated decline in lung function
• • COPD patients may have a raised eosinophil count and bronchodilator responsiveness
62. • AIRFLOW OBSTRUCTION
• Airflow limitation, also known as airflow obstruction, is typically determined for
clinical purposes by spirometry, which involves forced expiratory maneuvers after the
subject has inhaled to total lung capacity. Key parameters obtained from spirometry
include the volume of air exhaled within the first second of the forced expiratory
maneuver (FEV1) and the total volume of air exhaled during the entire spirometric
maneuver (forced vital capacity [FVC]). Patients with airflow obstruction related to
COPD have a chronically reduced ratio of FEV1/FVC. In contrast to asthma, the reduced
FEV1 in COPD seldom shows large responses to inhaled bronchodilators, although
improvements up to 15% are common.
63. • HYPERINFLATION
• In COPD there is often “air trapping” (increased residual volume
and increased ratio of residual volume to total lung capacity) and
progressive hyperinflation (increased total lung capacity) late in
the disease
64. • hyperinflation can push the diaphragm into a flattened position with a number of
adverse effects.
– First, by decreasing the zone of apposition between the diaphragm and the abdominal
wall, positive abdominal pressure during inspiration is not applied as effectively
to the chest wall, impairing inspiration.
– Second, because the muscle fibers of the flattened diaphragm are shorter than those
of a more noRmally curved diaphragm, they are less capable of generating
inspiratory pressures than normal.
– Third, the flattened diaphragm must generate greater tension to develop the
transpulmonary pressure required to produce tidal breathing.
– Fourth, the thoracic cage is distended beyond its normal resting volume, the
inspiratory muscles must do work to further inflate as recoil function is lost.
65. GAS EXCHANGE
• The partial pressure of oxygen in arterial blood Pao2 usually
remains near normal until the FEV1 is decreased to ~50% of
predicted, and even much lower FEV1 values can be associated with a
normal Pao2, at least at rest.
• PaCO2 is usually elevated when FEV1 is <25% of predicted.
• Non-uniform ventilation and ventilation-perfusion mismatching are
characteristic of COPD, reflecting the heterogeneous nature of the
disease process within the airways and lung parenchyma.
66. • Lung volume reduction surgery in selected patients:
–If PCO2 ≥ 7.4
–Severe limitation of exercise capacity despite
maximal therapy.
–Predominant upper lobe emphysema.
– Persistent symptoms despite a period of
pulmonary rehabilitation
Editor's Notes
The conducting zone of the respiratory system includes the organs and structures not directly involved in gas exchange. The gas exchange occurs in the respiratory zone.
Bronchial Tree
Primary bronchi – right and left branches of the trachea that enter the lungs
Secondary bronchi – branches of the primary that enter each lobe of the lungs
Tertiary bronchi – more branches of the secondary bronchi
Bronchioles – smallest branches within the lungs
Alveolar ducts – microscopic branches of the bronchioles
Alveoli – terminal air sacs where gas exchange takes place (anatomy resembles a bunch of grapes)
Surfactant – mixture of lipoproteins that reduces the attraction between water molecules in the alveoli; it prevents collapse of the alveoli
Increase frequency of bronchodilator use and consider giving via a nebuliser(Salbutamol 5mg/4h and Ipratropium 500mcg/6h)
Acutely ill patients: 94-98%.
Patients at risk of hypercapnia (e.g. COPD patients): 88-92%.
Oxygen should be reduced in stable patients with satisfactory oxygen saturation.