This document defines COPD and discusses its pathogenesis, risk factors, clinical presentation, investigations, management, and acute exacerbations. COPD is characterized by progressive, partially reversible airflow obstruction caused by noxious particles like cigarette smoke. It is associated with systemic manifestations and comorbidities that worsen its severity. Spirometry is key to diagnosis and severity assessment, showing reduced FEV1 and FEV1/FVC ratio. Management involves smoking cessation, pharmacotherapy including bronchodilators and inhaled corticosteroids, oxygen therapy, and pulmonary rehabilitation. Acute exacerbations are acute worsening of symptoms and may require hospitalization for treatment with systemic corticosteroids and antibiotics.
Lung contusion is when, as a result of chest trauma, there is direct or indirect damage of the parenchyma of the lung that leads to oedema or alveolar haematoma and loss of physiological structure and function of the lung.
Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory form of lung injury that is associated with a variety of etiologies.
Practical approach to interstitial lung diseases Hamdi Turkey
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
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COPD is a chronic respiratory illness that is associated with an abnormal inflammatory response of the lungs to noxious particles and gases. Severe COPD can lead to respiratory failure, repeated hospitalization and death. One of the most important risk factors for COPD is tobacco smoking.
Lung contusion is when, as a result of chest trauma, there is direct or indirect damage of the parenchyma of the lung that leads to oedema or alveolar haematoma and loss of physiological structure and function of the lung.
Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory form of lung injury that is associated with a variety of etiologies.
Practical approach to interstitial lung diseases Hamdi Turkey
These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university
Do Not Forget To Visit Our Pages On Facebook on the following Links:
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AND
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COPD is a chronic respiratory illness that is associated with an abnormal inflammatory response of the lungs to noxious particles and gases. Severe COPD can lead to respiratory failure, repeated hospitalization and death. One of the most important risk factors for COPD is tobacco smoking.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
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.
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
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
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!
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of 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
- 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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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.
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.
Are There Any Natural Remedies To Treat Syphilis.pdf
Chronic obstructive pulmonary disease
1. Chronic Obstructive Pulmonary Disease
*Refer CPG of COPD/Kumar pg 835
Definition preventable andtreatable respiratorydisorder largelycaused by smoking, is characterisedbyprogressive, partially
reversible airflow obstruction andlung hyperinflationwith significant extrapulmonary(systemic)manifestations and
comorbidconditions maycontribute to the severityof the disease in individual patients.
The co-morbidconditions include:(increaseseverityof dz)
a) ischaemic heart disease;
b) hypertension;
c) osteopenia, osteoporosis andbone fractures;
d) cachexia andmalnutrition;
e) normochromic normocytic anaemia;
f) skeletalmusclewasting andperipheralmuscle dysfunction;
g) diabetes mellitus;
h) sleep disorders;
i) cataracts andglaucoma;
j) lung cancer;
k) anxietyand depression both
The chronic airflow limitation - due to a mixture of smallairwaydisease (obstructive bronchiolitis) andlung parenchymal
destruction(emphysema)
Airflowlimitation, associatedwithanabnormal inflammatoryreactionof the lungto noxious particlesor gases, the most
common is cigarette smoke, is usuallyprogressive, especiallyifexposure to the noxious agents persists.
Epidemiology The prevalence ofmoderate to severe COPD in adults aged 30 years or above in the Asia-Pacific regionwas estimatedto
be at approximately6.3% andfor Malaysia at 4.55%.
Mortalityand morbidityratesinthe Asia-Pacific region - higher inmen and increasedwith increasing age
Risk Factor Risk Factor Mechanism
Gene Severe alpha-1 antitrypsin enzyme deficiency causes panlobular emphysema inbothsmokers and
non-smokers (young age).
Most commonlyseeninNorthern European
Alpha-1 Antitrypsin(AAT) – produce byliver, proteinase inhibitor- inhibit neutrophil elastase
(inhibit elastinin alveolar wall and degrade elasticityof lung), secreted into blood and diffuse
into lung
3 mainphenotype: MM(normal), MZ (heterozygous), ZZ (homozygous deficiency)
Normallypt have liver cirrhosis, mayassociatedwithpancreatitis/IBD andetc
Exposure to
particles
A. Tobacco smoke - most common;lessthan10 pack years is uncommon (1 pack year = 20
cigarettes/day/year)
Smoke particles inthe lungs leads to aninflammatoryresponse,increasedmacrophage
and neutrophilinfiltration into the lungs. These immune cells release cytokines,
chemokinesand elastases - degrade elastin, destruction ofalveolar andcapillary.
B. Organic dust and chemical-Ammonia, hydrogen sulphide, inorganic dust and organic dust
(livestockfarmer)
C. Indoor air pollution(heating and cooking)- biomassand coal
D. Outdoor air pollution- motor vehichles
Lung growth and
development
Anyfactor affects lung growth during gestationandchildhood has potential for increasing risk.
Oxidative stress Results fromanimbalance betweenoxidants (generated byphagocytes during mitochondrial
electron transport, air pollutants, cigarette smoke, etc.) andantioxidants, directlyinjures the lungs
and initiates lung inflammation
Gender Women are more susceptible to the effects oftobaccosmoke thanmen
Infection
Chronic IV drug
user/
socioeconomic
status
IV drug users ofcocaine, methadone and heroinare at higher risk;this is attributedto the vascular
damage induced bythe insoluble filler (cornstarch, cellulose, talc, fiber etc)
2. Pathology/
Pathogenesis
Increase in the numbers of neutrophils(in the airwaylumen), macrophages(inthe airwaylumen, airwaywall, and
parenchyma), andCD8+ lymphocytes (inthe airwaywall andparenchyma)
Emphysema: The inflammatoryresponse, mediatedbyneutrophils, macrophagesand CD8+ T-cells, release inflammatory
mediators and enzymes that damage the lungparenchyma. Proteaseslike elastase andmatrix metalloproteinases (MMPs)
released bythese inflammatorycells break downthe connective tissue of the alveolar walls andthe septae. A lossof
elastic recoil leads to diminished expiratoryflowrates, air trappingandairwaycollapsing.
Chronic bronchitis: Mucous glandenlargement, goblet cellhyperplasiaandmucociliary dysfunctionoccur in larger airways,
causing excessive mucus productionandbuild-upreducingthe airwaylumen. Althoughthese pathological changes inthe
large airways, it appears that the major site of increasedairwayresistance is the small airways (≤
2mm). Fibrosis andsmoothmuscle hypertrophy mayoccur alongwith excess mucus production andcellular infiltration in
the peripheral airways.
Pathophysiolog
y
Emphysema Chronic Bronchitis
Parenchymal destruction: Recurrent damage to the alveoli
eventuallyleads to septal destructionalongwith the
capillarybedalso.
Matched V/Q (ventilation/perfusion ratio) defect: Since
both the terminal bronchioles andalveolialong withthe
capillarybedhave been destroyed, areas oflow ventilation
also have poor perfusion.
Mild hypoxia: Hyperventilation develops andcardiac
output (CO) drops whichleads to areasof poor blood flow
in relativelywell oxygenatedareas. Due to thispoor CO,
the rest of the bodysuffers fromtissue hypoxia.
Cachexia: At the pulmonarylevel, the low CO leads to
pulmonarycachexia;which induces weight loss andmuscle
wasting. This gives these patients the characteristic “pink-
puffer” appearance.
Small airway inflammation: Mechanisms discussedabove
lead to inflammationinthe smaller bronchioles andmucus
secretions further narrowthe airwaylumen. Despite this, the
parenchyma are relativelyless damaged.
V/Q mismatch: The physiologic response leads to a dropin
ventilationandcompensation withthe rise inCO. Increased
perfusion inthe areasof poor ventilationtakes place
eventuallycausing hypoxia andsecondarypolycythemia.
Severe hypoxia and hypercarbia: Chronic V/Q mismatch
leads to decreased oxygenation/deoxygenationof the blood
resulting inhypoxemia andincreased CO2 retention
(respiratoryacidosis ensues).
Pulmonary hypertension and cor pulmonale: Chronic
hypercapnia andrespiratoryacidosis leadto arterial
vasoconstrictioninthe lungs. With the retrograde pressure
build-up, the right ventricular pressures continue to rise and
eventuallycausing RV failure. Otherwise, knownas cor
pulmonale.
3. History clerking Dyspnoea (hallmark)
Progressive over months or years and is persistent. As lung functiondeteriorates, the breathlessness interferes with
patients’ dailyactivities.
Cough
Initiallyintermittent but later present daily, oftenwithchronic sputum production
Extrapulmonarymanifestation and comorbidities
Wheezinng and chest tightness
Exposure to risk factor
i) Smoking history:
Quantificationof tobaccoconsumption:total pack-years = (number of cigarettes smoked per day÷ 20) x
number of years of smoking
ii) Occupationalandenvironmental exposures to other lung irritants
Impact ofdisease on psychosocial well being
PMH- Exacerbationandadmissionfor resp illness
FHx of resp dz
Presence of comorbidities
Current medicaltherapyandits appopriateness
Social andfamilysupport available for pt
Physical
Examination
A. General Examination
Tachypnoea
Long term O2 therapy
Hand- Warmpalm, finger clubbing, nicotine stained finger, asterixis (flapping tremor) ,boundingradialpulse
Neck- Increase JVP(cor pulmonale), Use acessorymusclesof breathing
Face- central cyanosis (nasolabial), polycythemia (like red eyes), pursed lip
B. Respiratory(chest)Examination
a) Inspection
Barrel chest (anterior posterior diameter increase- seen inchronic hyperinflation:asthma, COPD)
Scars (previous surgicaland chest drains)
Others- dilatedveins, skindiscoloration, visible pulsation, radiotherapyskin changes(erythema andskin
thickening)
b) Palpation
Chest expansion
lung shouldexpandsymmetricallybyat least 5 cm
DLCO (diffusing capacity of
lung): extentto which
oxygen passes from theair
sacs ofthelungs into the
blood
4. Reduce expansion side= lesionside
Unilateral/ bilateral (chronic airflow limitation- bilateral)
Apex beat
Vocal fremitus-repeat “nenek-nenek”, compare bothside-upper, middle, lower (increase= consolidationfibrosis
and above pleural effusion;decrease= pleural effusionor collapse)
c) Percussion-hyperresonance
d) Auscultation- ronchi (airwayobstruction,CA, cardiac failure), loudS2 (pulmonaryHTN), prolongedexpiration,
reducedbreathsound)
C. Loss ofcardiac andliver dullness
D. Leg- ankle edema (cor pulmonale)
Investigation 1. Lung fx test (spirometry/ peakflow meter)
Spirometryis performed inpeople withexposure to risk factors whohave chronic coughand sputum productioneven
without dyspnoea as it mayhelpidentifypatients earlier inthe course of the disease
Criteria to interpret
FEV1 Volume expiredinthe first secondof a forcedmaximal expiration
Initiatedafter maximalinspiration;measure ofhowquicklyfulllungs empty
FVC Maximumvolume ofair whichcanbe expired withmaximal force (after a maximal inspiration)duringa forced
manoeuvre
FEV1/FVC
Or FER
Show index of airflowlimitation
PEF Maximal expiratoryflow rate achievedduring the forcedexpiratorymanoeuvre (L/s)
5. Use the FEV1 /FVCratioto detect obstruction – Use FEV1 as % predictedto grade severityof obstruction
Use FVC(or VC) to assess restriction – Low FVC(VC) inpresence ofsignificant obstruction does not
necessarilyindicate restriction – Need to confirmandquantifyrestriction withmeasurement of TLC
Peak flowmeasurements detect airflow limitation but has poor specificity. The relationshipbetweenpeak expiratory
flow andFEV1 is poor inCOPD
2. Bronchodlator reversibilitytest
Response to a bronchodilator is considered significant ifthe change inFEV1 is both at least 200 mL and 12% above
the pre-bronchodilator FEV1
3. CXR: presence ofhyperinflation(flatteneddiaphragmandincreasedlung volume), bullae andhyperlucencyof the lungs
4. ABG:performedinpatients withFEV1 < 40% predictedif theyhave lowarterial oxygen saturation (less than92% on pulse
oximetry) or with clinical signs ofrespiratoryfailure or cor pulmonale as these patients maybenefit fromlong term oxygen
therapyat home
5. FBC:anemia ofchronic dz/polycythemia for chronic hypoxaemia
6. ECG: pulmonaryHTN
7. Alpha-1 Antitrypsindefeciencyscreening:performed inyoungCOPD patients (< 45 years old) or those whohave a strong
familyhistoryof the disease.
8. 6 Minutes WalkTest
Measures the distance coveredduring six minutes
Arterial oxygendesaturationcanbe measured witha pulse oximeter duringwalking.
9. Others: to detect other commonco-morbidities
fasting plasma glucose
serum albumin
6. serum fastinglipids
Differential dx
(Mnemonic:
ABCDVT)
a) Asthma
b) Bronchoectasis
c) Congestive Heart Failure
d) Diffuse parenchymal lungdz
e) PulmonaryVascular dz
f) Tuberculosis
Severity
Follow up Evaluationof the following:
Exposure to riskfactor:askabt smokingandwillingnessto stop
Current sx andnew or worseningsx;consider comorbidities
P/E and checkfor:
a) BMI, weight-nutritional status
b) Respiratoryfailure/ cor pulmonale
c) Anyconcomittant dz
Spirometrymeasurement
Medication effectivenessand compliance (MDI correct use?)
Exacerbation hx:
Causes, frequencyandseverityof exacerbation
Increase needof bronchodilator and systemic glucocorticoid- access severity
Hospitalization shouldbe documented(duration, invasive + non-invasive ventilation)
Pt education
7. Management
Pharmacotherapy
Short Acting
1) Short Acting B2 Agonists – MDI salbutamol 200mcg, Fenoterol 200mcg ,
Terbutaline 500mcg PRN
2) Short acting Anti Cholinergics – MDI Ipratropium Bromide 40mcg QID
Long Acting
1) LABA – MDI Salmeterol 50mcg BD, Formoterol 9mcg BD
2) LAAC – Tiotropium 18mcg OD
InhaledCorticosteroids (ICS)
1) MDI Budesonide 400mcg BD
2) MDI Fluticasone 500mcg BD
Combinations
a) MDI Combivent = Salbutamol + IpratropiumBromide (SABA + SAAC)
b) MDI Seretide = fluticasone propionate/salmeterol (ICS + LABA)
Methyxanthines– Theophylline 125-300mg BD
Corticosteroids
1) IV hydrocortisone 100mg QID1/7
2) T Prednisolone 30mg OD 5/7
LTOT (long term oxygentherapy)
Indications
1) PaO2 <55mmHg or Sa O2
<88%, with/without
hypercapnia
2) Pa O2 55-60mmHg, SaO2
89% + pulm hpt, peripheral
edema (CHF), polycythemia
Surgical intervention
1) Lung volume reductionsurgery
2) Bullectomy
3) Lung transplantation
8.
9. Acute exacerbation of COPD
Definition Natural course of the disease characterisedbya sustained (lasting 48 hours or more) worsening ofthe patient’s baseline
dyspnoea, cough, and/or sputum that is beyondnormal day-to-dayvariations, is acute in onset, and maywarrant a change in
regular medication
Causes a) Cigarette smoking
b) Bacterial/viralinfection
Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydophila
pneumoniae, Klebsiellapneumoniae, Pseudomonas aeruginosa, Acinetobacter baumannii andStaphylococcus aureus
c) Enviromentalfactor
d) Unknownetiology
e) Other precipitating factors include congestive heart failure, coldair andpulmonaryembolism
Clinical
features
Dyspnoea, cough and productionof sputum, confusion, lethargy
Physical exam
1) Vital signs – T, RR, PR, BP
2) Poor prognosis – confusion, reducedconscious level, cachexia, respirator distress, cyanosis
3) Co morbids – CVS, DM, lung CA, neurovascular dz
Investigation 1) ABG
2) Sputum C&S
3) CXR
4) ECG
5) FBC, LFT, RP
Differential
DX
(ABCDEFP)
Asthma (mayco-exist withCOPD)
Bronchiectasis
Lung cancer
Diffuse parenchymal lungdisease
Pulmonaryembolism
Heart failure.
Pneumothorax
Managemen
t