Chronic Obstructive Pulmonary Disease BY
Dr Akram Yousuf
Resident Internal Medicine
Liaquat University of Medical Health and Sciences Jamshoro Pakistan
At the end of this lecture student able to:
Define COPD
List causes of COPD
List risk factors of COPD
List signs and symptoms of COPD
List diagnostic measures
Describe treatment of COPD
Identify complications of COPD
Use nursing process
Discuss relevant patient / family education
COPD, EMPHYSEMA, CHRONIC BRONCHITIS,LUNG DISEASE, OBSTRUCTIVE LING DISEASE, PHYSIOLOGY, KINGS COLLEGE,DPT DEPARTMENT ALL necessary information regarding lung disease which you should know
chronic obstructive pulmonary disease and its management
chronic obstructive pulmonary disease is a chronic inflammatory lung disease that causes obstructed airflow from the lungs.
COPD typically has a clear cause and a clear path of prevention, and there are ways to slow the progression of the disease.
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
It contains :
- The new GOLD classification of severity
- The new GOLD treatment guidelines for the treatment of
COPD
Do Not Forget To Visit Our Pages On Facebook on the following Links:
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New technology called Electromagnetic Navigation Bronchoscopy® (ENB) that uses virtual bronchoscopy and real time 3-dimensional CT images that enable me to localize these peripheral lung nodules for diagnosis and treatment. This outpatient procedure is minimally invasive and therefore has a small risk of pneumothorax (2-3%) and its published diagnostic yield rates range from 67% - 86%
At the end of this lecture student able to:
Define COPD
List causes of COPD
List risk factors of COPD
List signs and symptoms of COPD
List diagnostic measures
Describe treatment of COPD
Identify complications of COPD
Use nursing process
Discuss relevant patient / family education
COPD, EMPHYSEMA, CHRONIC BRONCHITIS,LUNG DISEASE, OBSTRUCTIVE LING DISEASE, PHYSIOLOGY, KINGS COLLEGE,DPT DEPARTMENT ALL necessary information regarding lung disease which you should know
chronic obstructive pulmonary disease and its management
chronic obstructive pulmonary disease is a chronic inflammatory lung disease that causes obstructed airflow from the lungs.
COPD typically has a clear cause and a clear path of prevention, and there are ways to slow the progression of the disease.
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
It contains :
- The new GOLD classification of severity
- The new GOLD treatment guidelines for the treatment of
COPD
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/
New technology called Electromagnetic Navigation Bronchoscopy® (ENB) that uses virtual bronchoscopy and real time 3-dimensional CT images that enable me to localize these peripheral lung nodules for diagnosis and treatment. This outpatient procedure is minimally invasive and therefore has a small risk of pneumothorax (2-3%) and its published diagnostic yield rates range from 67% - 86%
Lauren Johnston, MSW, Samantha Buirski and Tim Turnham, PhD present Keeping Our Eyes on a Cure: Patients as Leaders and Advocates at the 2016 CURE OM Patient & Caregiver Symposium.
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Chronic obstructive pulmonary disease..It is one of the most affecting lung disease.. In detailed explanation of disease is there and including its ayurvedic aspect of management is also there...
#Ayurveda#Emphysema#Chronic brochitis
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 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
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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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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
2. The Global Initiative for Chronic Obstructive
Lung Disease (GOLD) guidelines define COPD is a
disease state characterized by airflow limitation
that is not fully reversible, is usually progressive,
and is associated with an abnormal
inflammatory response of the lungs to inhaled
noxious particles or gases.
3.
4.
5.
6.
7.
8. 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.
Difference:
Airflow limitation in emphysema is due to loss of elastic recoil and
decrease in airway tethering, whereas chronic bronchitis leads to
narrowing of airway caliber and increase in airway resistance. Although
some patients predominantly display signs of one of these diseases or
the other, most fall somewhere in the middle of the spectrum between
the 2 conditions.
9.
10.
11.
12.
13.
14.
15.
16. Patient with chronic
bronchitis have dec
alveolar ventilation,
with a low PaO2 and a
high PaCO2. hence
they are cyanosed and
called Blue Bloaters
17.
18.
19.
20.
21.
22. Emphysemetic patients
have inc alveolar
ventilation, a near
normal PaO2 and a
normal or low PaCO2.
They are not Cynosed
and called Pink Puffers .
23. Blue Bloaters have dec alveolar ventilation, with a low PaO2 and
a high PaCO2. They are cyanosed but not breathless and may go
on to develop cor pulmonale. Their respiratory centres are
relatively insensitive to CO2 and they rely on hypoxic drive to
maintain respiratory effort —supplemental oxygen should be
given with care
Pink Puffers have inc alveolar ventilation, a near normal PaO2
and a normal or low PaCO2. They are breathless but are not
cyanosed. They may progress to type 1 respiratory failure
Blue Bloaters V/S Pink Puffers
24.
25.
26.
27.
28.
29.
30. • Occupational exposures, such as coal, silica and cadmium
• Low Birth Weight Baby
• Childhood Infections or Maternal Smoking
• Recurrent Infections
• Low socioeconomic status
• Cannabis smoking
31.
32. • Most patients with chronic obstructive pulmonary disease
(COPD) seek medical attention late in the course of their
disease.
• Patients often ignore the symptoms because they start
gradually and progress over the course of years.
• Patients typically present with a combination of signs and
symptoms of chronic bronchitis, emphysema, and reactive
airway disease.
33. The common symptoms includes,
• Cough (The cough usually is worse in the mornings and
produces a small amount of colorless sputum)
• Worsening Dyspnea (Breathlessness is the most significant
symptom, but it usually does not occur until the 4th to 6th
decade of life. By the time the FEV1 has fallen to 50% of
predicted, the patient is usually breathless upon minimal
exertion)
• Wheezing (Wheezing may occur in some patients, particularly
during exertion and exacerbations)
35. Some important clinical differences may help distinguish between
the types of COPD:
• Classic findings for patients with chronic bronchitis include
productive cough with gradual progression to intermittent
dyspnea; frequent and recurrent pulmonary infections and
progressive cardiac/respiratory failure with edema and weight
gain.
• Classic findings for patients with emphysema include a long
history of progressive dyspnea with late onset of nonproductive
cough; occasional mucopurulent relapses; and eventual
cachexia and respiratory failure.
36.
37. • The sensitivity of a physical examination in detecting mild to
moderate COPD is relatively poor.
• Patients with severe disease experience tachypnea and
respiratory distress with simple activities.
• The respiratory rate increases in proportion to disease severity.
• Use of accessory respiratory muscles and paradoxical indrawing
of lower intercostal spaces is evident (known as the Hoover
sign).
• In advanced disease, cyanosis, elevated jugular venous pulse
(JVP), and peripheral edema can be observed.
38. On Inspection:
• The patient is dyspnoeic with pursuing of lips and resp rate of
>30 br/mins.
• The chest is barrel shaped.
• Indrawing of lower intercostal space on inspiration due to low
flat diaphragm.
• Suprasternal and Supraclavicular Excavation.
• Prominent accessory muscles of respiration may be seen.
39. On Percussion:
• Increased resonance in both lung fields.
• Obliteration of liver and cardiac dullness (liver dllness may be
lower down)
On Auscultaion:
• Breath sounds may be diminished but vesicular with prolong
expiration
• Rhonchi may be present if associated with chronic bronchitis
40.
41. Chronic bronchitis Emphysema
• 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
• 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
• Overall appearance is more like
classic COPD exacerbation
42.
43.
44.
45.
46. • Pulmonary function tests are essential for the diagnosis and
assessment of the severity of disease, and they are helpful in
following its progress.
• If post bronchodilators shows FEV1/FVC <70% of predicted, it
may indicates the obstructive pattern of lung disease.
47.
48. Arterial Blood Gas Analysis
• provides the best clues as to acuteness and severity of disease
exacerbation.
• Patients with mild COPD have mild to moderate hypoxemia
without hypercapnia. As the disease progresses, hypoxemia
worsens and hypercapnia may develop
Serum Electrolytes
• Patients with COPD tend to retain sodium. In addition, serum
potassium should be monitored carefully, because diuretics, beta-
adrenergic agonists, and theophylline act to lower potassium
levels.
• Chronic respiratory acidosis leads to compensatory metabolic
alkalosis. In the absence of blood gas measurements, bicarbonate
levels are useful for following disease progression
49. Sputum DR
• In persons with stable chronic bronchitis, the sputum is
mucoid and macrophages are the predominant cells.
• With an exacerbation, sputum becomes purulent because of
the presence of neutrophils
• A mixture of organisms often is visible with Gram stain.The
pathogens cultured most frequently during exacerbations are
Streptococcus pneumoniae, Haemophilus influenzae, Moraxella
catarrhalis and Pseudomonas aeruginosa.
Alpha 1 Anti Trypsin :
• Measure alpha1-antitrypsin (AAT) in all patients younger than 40
years or in those with a family history of emphysema at an early
age. The diagnosis of severe AAT deficiency is confirmed when the
serum level falls below the protective threshold value of 11
mmol/L (ie, in the range of 3-7 mmol/L)
50. Pulse Oximeter
• when combined with clinical observation, this test can be a
powerful tool for instant feedback on a patient's status
Blood C.P
• Chronic hypoxemia may lead polycythemia.
• A hematocrit greater than 52% in men or 47% in women is
indicative of polycythemia.
• Correction of hypoxemia should reduce secondary
polycythemia in patients who have quit smoking
51. Echocardiography:
• Many patients with long-standing COPD develop secondary
pulmonary hypertension from chronic hypoxemia and
vascular remodeling.
• This may result in eventual right-sided heart failure (cor
pulmonale)
right-sided heart catheterization
• may be performed to measure pulmonary artery pressures
directly and to gauge the response to vasodilators.
52.
53. Modified British Medical Research Council (mMRC) is used to
assess the degree of Breathlessness in the patient of COPD.
54. GOLD criteria for assessing the severity of airflow obstruction
(based on the percent predicted postbronchodilator FEV1 when
the FEV1/FVC is < 70%) are as follows:
• Stage I (mild) - FEV 1 80% or greater of predicted
• Stage II (moderate) - FEV 1 50-79% of predicted
• Stage III (severe) - FEV 1 30-49% of predicted
• Stage IV (very severe) - FEV 1 less than 30% of predicted or FEV 1
less than 50% and chronic respiratory failure
55.
56.
57.
58.
59.
60.
61.
62.
63. Once the diagnosis of COPD is
established, it is important to
educate the patient about the
disease and to encourage his or
her active participation in
therapy.
64.
65.
66.
67.
68.
69.
70. • Smoking cessation continues
to be the most important
therapeutic intervention for
COPD
71. • Smoking cessation continues
to be the most important
therapeutic intervention for
COPD
• Studies have shown that
brief (3 mins) counseling
to urge a smoker to quit
results in smoking quit rate
of 5 – 10%.
72. • Smoking cessation continues
to be the most important
therapeutic intervention for
COPD
• Studies have shown that
brief (3 mins) counseling
to urge a smoker to quit
results in smoking quit rate
of 5 – 10%.
• Nicotine replacement
therapy (nicotine gum,
nasal spray, transdermal
patch, sublingual tablet) as
well as pharmacotherapy
with Bupropion or
nortriptyline reliably
increases long term
smoking abstinence rate.
80. Oxygen therapy for COPD
• Oxygen is usually given via a facemask or nasal cannulae.
• Titrate the amount guided by the SaO2 (aim for 94–98% (or 88–92% if, or at
risk of hypercapnia)
• Humidification is only required for longer-term delivery of O2 at high flow
rates and tracheostomies.
Nasal cannulae: preferred by patients, but O2 delivery is relatively imprecise
and may cause nasal soreness. The flow rate (1–4L/min) roughly defines the
concentration of O2 (24–40%). May be used to maintain SaO2 when
nebulizers need to be run using air.
Venturi mask: provides a precise percentage of O2 (FiO2) at high flow rates.
Colour codes:
24% BLUE
28% WHITE
35% YELLOW
40% RED
60% GREEN
Start at 24–28% in COPD
81. Indication of Long term Oxygen
Therapy in COPD
When PaO2 is <55mmHg or SaO2 <88% irrespective of PaCO2.
When PaO2 is 55-60 mmHg associated with
• Pulmonary Hypertension
• Peripheral Edema suggesting CCF
• Nocturnal Hypoxemia
• Secondary Polycythemia (Hematocrit > 55%)
• Carboxyhemoglobin <3% (in patient who have stopped
smoking)
82.
83.
84.
85.
86.
87.
88.
89.
90.
91. An exacerbation of COPD is:
“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.”
92. The most common causes of COPD exacerbations are viral
upper respiratory tract infections and infection of the
tracheobronchial tree.
Diagnosis relies exclusively on the clinical presentation of the
patient complaining of an acute change of symptoms that is
beyond normal day-to-day variation.
The goal of treatment is to minimize the impact of the current
exacerbation and to prevent the development of subsequent
exacerbations.
93. Short-acting inhaled beta2-agonists with or without short-
acting anticholinergics are usually the preferred
bronchodilators for treatment of an exacerbation.
Systemic corticosteroids and antibiotics can 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.
COPD exacerbations can often be prevented.
94. Short-acting inhaled beta2-agonists with or without short-
acting anticholinergics are usually the preferred
bronchodilators for treatment of an exacerbation.
Systemic corticosteroids and antibiotics can 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.
COPD exacerbations can often be prevented.
95.
96.
97. Indications of Hospitalization
Marked increase in the symptoms.
Severe underlying COPD
Failure to respond to initial Outpatient management
Presence of serious comorbidities
Older age
Insufficient home support
Editor's Notes
COPD is an umbrella term use to describe group of repiratory disease, the most common being C.Brochitis and emphsema. ,any people living with copd may have both c.b and emphysema, afew people have both asthma and copd
COPD is an umbrella term use to describe group of repiratory disease, the most common being C.Brochitis and emphsema. ,any people living with copd may have both c.b and emphysema, afew people have both asthma and copd
COPD is an umbrella term use to describe group of repiratory disease, the most common being C.Brochitis and emphsema. ,any people living with copd may have both c.b and emphysema, afew people have both asthma and copd
COPD is an umbrella term use to describe group of repiratory disease, the most common being C.Brochitis and emphsema. ,any people living with copd may have both c.b and emphysema, afew people have both asthma and copd
COPD is an umbrella term use to describe group of repiratory disease, the most common being C.Brochitis and emphsema. ,any people living with copd may have both c.b and emphysema, afew people have both asthma and copd
In normal functioning lungs when air is inhaled, it travels down to trachea and bronchial tube.
From where air reach the terminal bronchioles that are rich with blood supply,
Normally the walls of air sacs are elastic
From where air reach the terminal bronchioles that are rich with blood supply,
Normally the walls of air sacs are elastic
Inhalling air causes each air sac filled with air, exhalling causes air sacs to deflate
Efficient uptake of air in alveoli provides oxygen to the blood which is then carried to all parts of the body
In Copd however specially in chronic bronchitis
In Copd however specially in chronic bronchitis
Airways becomes thick and inflamed and they produce more mucous than usual due to hypertrophy of goblet cells.
Excessive mucous can block the airways and makes it hard to breath.
Due to blockage in the airways in chronic bronchitis.
In emphysema the walls of the airsacs are damaged and loose their elastic quality,
The air sacs becomes broken and lose their shape
As the air space get largers the air is trapped inside it and there are fewer air sacs to supply oxygen to the body
Because air is trapped inside airsacs, it becomes difficult for lung to deflate
Trapped air makes it harder to get fresh air into the lungs and makes breathing more difficult.
Cigrette smoking is the leading cause of copd, long term exposure to second hand smoking and irritants like etc can also lead to copd. An uncommon genetic disorder called alpha 1 antitrypsin deficiency can also sometimes leads to copd
Cigrette smoking is the leading cause of copd, long term exposure to second hand smoking and irritants like etc can also lead to copd. An uncommon genetic disorder called alpha 1 antitrypsin deficiency can also sometimes leads to copd
Cigrette smoking is the leading cause of copd, long term exposure to second hand smoking and irritants like etc can also lead to copd. An uncommon genetic disorder called alpha 1 antitrypsin deficiency can also sometimes leads to copd
Cigrette smoking is the leading cause of copd, long term exposure to second hand smoking and irritants like etc can also lead to copd. An uncommon genetic disorder called alpha 1 antitrypsin deficiency can also sometimes leads to copd
Cigrette smoking is the leading cause of copd, long term exposure to second hand smoking and irritants like etc can also lead to copd. An uncommon genetic disorder called alpha 1 antitrypsin deficiency can also sometimes leads to copd