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8/7/2019 Update in Airway Diseases for Internal Medicine Resident 2010
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Update in Airway Diseasesfor Internal Medicine ResidentCOPD/ Asthma
F
F F
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Pathogenesis of asthma
Diagnosis of asthma Guideline for asthma management
Asthma in special situationOccupational asthmaExercise induced bronchoconstrictionAsthma and pregnancy, GERD, AR
Interesting Topics in Asthma
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A chronic inflammatory disorder of the airways
Many cells and cellular elements play a role Chronic inflammation leads to an increase inairway hyper-responsiveness with recurrentepisodes of wheezing, coughing and shortnessof breath, particularly at night and earlymorning
Widespread, variable and often reversibleairflow limitation
GINA guidelines, 2006.
Definition of asthma
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Inducers
Allergens, Chemical sensitisers,Air pollutants, Virus infections
Inflammation
TriggersAllergens,Exercise
Cold Air, SO2
Particulates
Symptoms
Cough WheezeChest tightness
Dyspnoea
Airway
HyperresponsivenessAirflow Limitation
Barnes PJ
Host FactorsGenetics predisposing
Prevention of smoking exposure
(both in utero and after birth) mayprevent asthma development
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Asthma vs. COPD
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Th2 in allergic disease
IL-4,IL-5,IL-13
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Question
Cells induced sputum F
asthma A. Eosinophils
B. NeutrophilsC. Alveolar macrophage
D. LymphocyteE. Epithelial cells
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Inflammations in asthma
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Most abundant cells in induced sputum ofhealthy subjects and asthma is neutrophils
Asthma with sputum eosinophilia (>3% of cells) Thickening of basement membrane
More likely responsive to corticosteroids Asthma with sputum neutrophilia (>60-65%) In non-allergic asthma
In patients with acute exacerbation More severe obstruction/ severity of asthma Less likely to response to corticosteriods
Inflammations in asthma
Proc Am Thorac Soc Vol 6. pp 256259, 2009
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Asthma diagnosis
iagnosis of
sthmaF asthma
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CXR chronic infection, lung cancer
To support the diagnosis of reversible airwayobstruction
1. Spirometry (pre-post bronchodilator)2. PER3. Bronchial provocative test4. Methacholine or histamine challenge
Investigation for diagnosis of asthma
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Asthma diagnosis
iagnosis of
sthma
History
PT/ PE
Bronchialprovocative
test
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Peak flow measurementPeak flow measurement eak low eter
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Asthma diagnosis
eak low
ariation or diagnosis of asthma by peak flow variability
assessmentpeak flow variability =PEReveningPERmorning x 100
1/2(PERevening + PERmorning) > 20% suggest asthma (variable obstruction)
In diagnosed asthma cases, peak flow can be used forself monitoring and self management plans, assessseverity.
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Asthma diagnosis
eak low
ariability
310/700:44%
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Asthma diagnosis
ronchial
hallengesl (bronchial
hyperresponsiveness)lF methacholine or histamine
lPC20 FF methacholine FEV1 20% baseline F
lF PC20 lFFF asthma PT
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Asthma diagnosis
ronchial
hallenge
Positive bronchial challenge = asthma
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Late/ short onset of wheezing
Localizing wheezingNot respond to corticosteroids/LABA
May be position relatedNo history of previous allergic diseasePrevious historyo f TB
Clues from CXR or PT
Large airway obstruction
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er r
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10
8
6
4
2
0
-2
-4
-6
0 1 2 3 4 5 6
Flow
(L/s)
Volume (L)
Identify discordance between FEV1 and PEF
F 48 yrs 1.64 m
FVC 3.03 L, FEV1 2.63 L,FEV1% = 87%, PEF = 3.97 L/s
F/P = 11.0
FEV1 in mls > 10 UAOUAO
PEF in L/min
Empey D. Br Med J 1972; 3: 503-505.
Miller MR et al. Q J Med 1990; 74: 177-188.
low Volume LoopSimple approach for interpreting PTPE curves pper irway
bstruction
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Cough Variant Asthma
In a subgroup of asthmatic patients cough isthe predominant or sole symptom.Thiscondition has been termed cough variantasthma (CVA).
Patients with CVA comprise a distinctsubgroup of individuals with asthma, ratherthan simply being asthmatic patients who
cough. Patients with CVA have a significantly moresensitive cough reflex. But with a lesser
degree of bronchial hyperresponsiveness
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Cough Variant Asthma
In patient with CVA, bronchoprovocationtesting with inhaled methacholine should beused to document the presence of bronchialhyperresponsiveness and, therefore, thediagnosis of asthma.
The presence of bronchialhyperresponsiveness in a patient with chronic
cough is consistent with, but is not diagnosticof, CVA. A definitive diagnosis of CVA canonly be made after the documented resolution
of cough with specific treatment of asthma.
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Early vs late onset asthma
Early onset asthma: since childhood (
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Exercise induced asthma
Exercise is the most common trigger factor of
broncho-spasm in asthmatic patient Exercise induced bronchospasm also occursin 10% of non-atopic, no asthma patients
Usually indicate poor control asthma Can be prevented by adequate asthma
control or using bronchoditor prior to exercise Anti-leuketriene can also prevent exerciseinduced bronchospasm
a uati th a
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GINA guidelines, 2006.
ontrol
guidelineCharacteristic Controlled
(All of the following)Partly Controlled(Any measurepresent in any week)
Uncontrolled
Daytime symptoms None(twice or less/wk) More than twice/week Three or morefeatures of partlycontrolled asthmapresent in any weekLimitations ofactivities
None Any
Nocturnal symptoms None AnyNeed for reliever/rescue medication
None(twice or less/ week)
More than twice/week
Lung function (PE orEV1)
Normal
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ACT= asthma control testCut off 19 from 25 (5 )
Associated conditions that can
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Allergic rhinitis/ post nasal drip
GERD Drugs ( beta-blocker, ACEI)
Sinusitis
Associated conditions that can
aggravate asthma
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Aspirin induced asthma
Triads: asthma, ASA intolerance, sinusitiswith nasal polyps
Asthma is usually severe and poorly respondto inhaled corticosteriods
Rhinorrhea and nasal congestion usuallyproceed asthma+ASA intolerance for 1-5 yrs Patient usually has asthma attack wiht rhinitis
and conjunctival injection within 3 hours afteringestion of ASA or NSAIDS
Antileukotriene can be use to controlsymptoms
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REDUCE INCREASE
Asthma education
Environmental controlAs-needed rapid-
acting 2-agonistAs-needed rapid-acting 2-agonist
Controller
options
Select oneSelect one Select oneSelect one Add one or moreAdd one or more Add one or bothAdd one or both
Low-dose inhaled
ICS
Low-dose ICS pluslong-acting
2-agonist
Medium-or high-dose ICS plus long-
acting 2-agonist
Oralglucocorticosteroid
(lowest dose)
Leukotriene
modifier
Medium-or high-
dose ICS
Leukotriene
modifierAnti-IgE treatment
Low-dose ICS plusleukotriene modifier
Sustained releasetheophylline
Low-dose ICS plus
sustained release
theophylline
Treatmentsteps
Step 1 Step 2 Step 3 Step 4 Step 5
GINA Report 2007 (www.ginasthma.org)
Budesonide
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NEJM 1994;331:700-705
1200 mcg/day
Budesonide 400
mcg/day
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Step down of Controller
If symptom is stable for3 months can try
step down If on moderate to high dose ICS, reduce doseto 50%
If on low dose ICS, may try once daily If low dose ICS and controlled for one year
may consider stop medication
If ICS+ LABA, try reduce ICS 50%
If ICS + other controller, try reduce ICS 50%
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Asthma control
Symptoms based
A th T t t St t i
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Sont JK et al, Am J Respir Crit Care Med 1999
Asthma Treatment Strategies
Asthma Treatment Strategies
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Pre Post
Reference-strategy
4
6
8
10
12
ReticularLayer
Thickness
(m)
Pre Post
AHR-strategy
Sont JK et al, Am J Respir Crit Care Med 1999
p = 0.3 p = 0.005
p = 0.03
Asthma Treatment Strategies
Anti IgE in Asthma
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B-cellB-cell
IgE
omalizumab complexes
with free IgE
XolairMast cell
Allergen-drivenB-cell secretes IgE
FcRI
Anti IgE in Asthma
Anti IgE in Asthma
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Add-on therapy to improve asthma control in adults andadolescents (12 years) with severe persistent allergicasthma positive skin test or serum IgE to a perennialaeroallergen or high IgE level 30 and 700 IU andwho have reduced lung function (EV1
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Total dose (mg) per 28 days
Body weight (kg)BaselineIgE (IU/mL) 2025 >2530 >3040 >4050 >5060 >6070 >7080 >8090 >90125 >125150
30100 75 75 75 150 150 150 150 150 300 300
>100200 150 150 150 300 300 300 300 300 450 600
>200300 150 150 225 300 300 450 450 450 600 750
>300400 225 225 300 450 450 450 600 600
>400500 225 300 450 450 600 600 750 750
>500600 300 300 450 600 600 750 DO NOT ADMINISTER
>600700 300 450 450 600 750
Q4 wks
Q2 wks
BW X IgE level X 0.016 (not more than 750 mg/ 4 week)if dose < 300mg 4 wks > 300 mg 2 wks
Anti IgE in Asthma
Clinical eatures of NA
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Clinical eatures of NA
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x
in acute severes
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Asthma diagnosis
x c asthma
agnesium
agnesium ebuli ed
ddinganticholinergic
vs nebuli er
same
Interesting Topics in COPD
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Smoking cessation
Pathogenesis of COPD Diagnosis of asthmaPT Management of COPDStable COPDAcute exacerbation
Interesting Topics in COPD
COPD Definition 2010
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COPD Definition 2010
COPD is a preventable and treatable
disease with some significant extra-pulmonary effects that may
contribute to the severity in individualpatients.
Its pulmonary component ischaracterized by airflow limitation
that is not fully reversible.
COPD Definition 2010
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COPD Definition 2010
The airflow limitation is usually both
progressive and associated with anabnormal inflammatory response of
the lungs to noxious particles orgases.
COPD Definition
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COPD Definition
Susceptible
patient
Noxious stimuli
Other factors:Infections
:Environmentetc.
Airflow limitationbnormal inflammation
i
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essation 5l Ask
l Advise/Educate
l Assessment l Assist
l Arrange ollow-up
FF
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1 regnant smoker
2 actating
3 mokelesscigarette
4 dolescent
5 moke 10
tt
COPD Diagnostic/staging
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COPD Diagnostic/staging
COPD
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Breathlessness
InactivityDeconditioningDeconditioningReduced exercise capacity
ExacerbationsExacerbations
Expiratory flow limitationsAir trapping/
hyperinflation
HRQL
Extrapulmonary manifestations
DisabilityDisability MortalityProgressive loss of lung
function
Systemic Inflammations in COPD
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Systemic Inflammations in COPD
Consequences of systemic
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The systemic inflammation is probably related to
several systemic effects of COPD:
1) involuntary weight loss;
2) muscle wasting;
3) reduced functional capacity and health
status;
4) increased cardiovascular morbidityand mortality;5) Impaired bone metabolism.
q y
inflammation in COPD
COPD staging
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g g
Severity Post BDFEV1
MILD 80%
MODERATE 50%FEV1
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1. Airways inflammation
2. Airway obstruction and air trapping3. Respiratory impairment and
deconditioning/ lung functiondecline
4. requent exacerbations5. Multisystem (extrapulmonary)
involvement
Stop smoking/ noxious stimuli
Bronchodilator: shortand long acting
Anti-inflammation: ICS
Rehabilitation+ Rx co-existing diseaseVaccination
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Treatment: Stage 2
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Regular SABA
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Meptin
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Components of pulmonary
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rehabilitation in chronic lung disease
Treatment: Stage 3
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Stage 3/4 Stage 2
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Long acting bronchodilator 1-2
SABA 1-2 + theophylline + rehab.
LABA + inhaled corticosteroids
Inhaled corticosteroids alone
> 1 Severe exacerbation in past 12 months
LABA: salmeterol, formoterol LAMA: tiotropium
Treatment: Stage 1
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Treatment: Stage 4
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COPD
Long Term Oxygen Therapy
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>15 hr/day
PaO2 < 55 . SaO2 < 88%
PaO2 55-60 . SaO2 89-90%
cor pulmonale pulmonary hypertension erythrocytosis (Hct > 55%)
Prevention of AECB
Prevention of COPD exacerbation
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Sapey E. Thorax 2006;61:250-258
Influenza vaccination
Pulmonary rehabilitationStop smokingLong acting bronchodilator
Inhaled corticosteroids (EV1
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Wood-Baker RR. Cochrane Database Syst Rev 2005; (1): CD001288Ten randomised trials comparing parenteral or oral corticostersoid
with placebo Date of last search August 2004 ewer treatment failure within 30 days, OR 0.84 (95%CI, 0.34 to 0.68) Necessary to treat 9 patients (95%CI, 6 to 14) with systemic
corticosteroids to avoid one treatment failure Early EV1, up to 72 hr. showed significant treatment
benefit (EV1 140 ml) Significant improvement breathlessness and blood gases
6-72 hr. after treatmentRisk of hyperglycemia was significantly increased, OR 5.48; 95% CI 1.58
to 18.96
Exacerbation: ClassificationPrevention of AECB
Classification Exacerbation
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Anthonisen NR et al Ann Intern Med 1987 ;106:196-204
Increase in:Dyspnea
Sputum volumeSputum purulence
Type IAll three present,antibiotic
recommended
Type IITwo of three present,antibiotic
recommendedif includes purulence
Type IIIOne of threepresent,
antibiotic notrecommended
in
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l F NPVV COPD AR ,
F( several multicenter, randomizedcontrolled trials)l
success rate 58-93%l first-line intervention in eligibleCOPD with AR
l combination of CPAP and IPVV is preferred.l COPD CH Pneumonia FF
COPD with acute exacerbation.
in
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Noninvasive positive pressure ventilation (NPPV)should be offered to patients with exacerbations
when, after optimal medical therapy andoxygenation, respiratory acidosis (pH
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Ventilator Management
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Large endotracheal tube (oral route)
Adequate sedationShort I-time, prolong expiratory time
Increase inspiratory flow, decreaserespiratory rate, sedationPermissive hypercapnea
Accept high peak airway pressure (keepplateau pressure < 35 cmH2O)
VC may be preferable to PC
Ventilator Management
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Monitor for air trapping/ auto-PEEP
Aggressive bronchodilator via MDI ornebulizerConsider PEEP to counter act auto-
PEEP ( trigger F)
May require bronchoscopic for mucousremoval