CHRONIC OBSTRUCTIVE

PULMONARY DISEASE

Introduction 00:01:50

Global Initiative for chronic Obstructive Lung Disease :

Pocket guide to cOPD diagnosis, management and prevention
FeV proqression over time:

maximal
80.
value
attained
predicted TRI:"LS%
No
COPD
.... TRa : Ia.9%|
% TR3:S.5%cOPD
in 40
FEM

a 30 40 SO 70

Age range under observation

Respiratory unit : Acinus.

Acinus = Respiratory bronchiole+ Alveolar duct +Alveol.
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COPD:
Chronic bronchitis (clinicaD.
enphysema (pathologicab).
Small airuay (<am disease.
space
Active
Patthologjical classitcation of erphysema:
. Centriacinar emphysema (and m):Centre of acinus
(respiratory bronchiole)is involved. more commonls seen
in males, Smokers involving upper lobe.
pedback a. Panacinar emphusemai Entire acinus respiratory
bronchiole, alveolar duct, alveolb is invoved
 a. Paraseptal emphysema,: Commonly seen in young males,
smokers. AsSOciated with spontaneous pneumothorax.
4. Iregular emphysema (mc).
Respiratory -Aveous
bronchiole
Terminal
bronchioles
Aveolar
duct

Normal acinus

Aveolar ducts
Aveolar duct
Respiratory and aveoli
bronchiole
Terminal Septum Terminal
bronchioles bronchioles Septum

Chronic inlammation
Aveoli
Respiratory
bronchiole
and Abrosis

Centriacinar emphsema Paraseptal enmphysema

Paraseptal emphysema

Aveolar ducts
and aveoli Septum
Aveolar duct Alveolus
Termina Terminal
Septum bronchioles
bronchioles

Respiratory
bronchiole
Respiratory
bronchiole

Panacinar emphysema Irregular emphysema

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identity
emphysema 45 yrs.
emphusema without risk facto.
Basilar LL) involvement.
Active
space
Associated with vosculitis/iver disease.
Associated with bronchiectasis.
ASsociated with CAntitrypsin deiciency
This is called non-smoker's emphysema/ Panacinar
emphysema.
 Obstructive
Pulmonary
Pathogenesis of emphysema.! Disease

Triggers Cigarette smoke Genette susceptiblty

eMector cells

macrophages Neutrophils epithelal celsumphocytes

Protease/ Oádart/
eiologjcal pathways Antiprotease Antioxidant Apoptosis ung repair
Key molecules mmP la Neutrophl NF Kappas SOD 3 Rtp 8C Ceramide TEF B ehstin
SeRPNA I elastose NRF a HOAC a

Extracelular Inefective
Pathologjical
resut matrix destruction
Chronic
inlammation
Cell
death repair

upon long term eposure to cigarette smoke in genetically

susceptible a anti trypsin detciencu indivicuais, lung
epithelial cells qTlymphocytes recrit inammatory cels to
the lng
Siologjeal pathuays of protease antiprotease imbalance,
apoptosis and lung repair lead to extracelular matrix
destruction, cell death, chronic infilammation, and inetective
repair. Athough most cf these biological patthways inluence
mutiple pathobiological resw.oy.ngle relationship
between pathways and results is shown.
Asubset of Key molecules related to these bioloqical
pathways is listed

Under a oantitrypsin detciencu, thereare:

m allele :Normal.
Sollele:Some defciercy of aantitrypsin.
2 allele : Severe detciency of a, oantitrypsin.
Null allelei No a, anti trypsin.
Hence, poatients with Pimm is normal. space
Active

P22 is the mc forn of a,antitrypsin deBciency.

Causes risk factors of cOPD:
back usually caused by a signitcant exposure to noxious particles
or gases.
 The main risk Pactor for cOPD is tobacco smoking,
eut other environmental exposures may contribute such as
Puel exposure, air pollution.
COPD Comprises patthological changes in 4different
compartments of the lungs :
" Central airways
Peripheral airways
ung arenchyma.
Pulmonary vasculature.

Large airway changesin COPD:

-Neutrophils in sputum
mucus hypersecretion

Squamous metaplasia of
epitheliumn
No basement membrane
Goblet cell
hyperplasia.
thickenin9
tmacrophages
‘co8+ cels
mucus gland hyperplasia
Litte increase in airuay
Smooth musle

Smal airwauy changes in COfD:

-inlamnatory
exudate in men
5c0a9804c98a9f4bf802667a

-Disrupted alveolar
attachments

Thickened wall witth

Active
space inlammatory cell,
macrophages, cD8t cells,
Abroblasts

-Peribronchial Abrosis

ymphoid folicle
 Smal airuay changes: Disease
" LOSS ot alveolor attachments ’ Fall in elastic recoil
Bc0a9804c98a914bf802667a

pressure hyperinated lungs).

Inammatory esaudate.
" Thickened wal.

Lung pareehymal changes in COPD:

-Alveolar wall
destruction

-LoSs of eloasticity
Destruction of pumonary
capllary bed
inlammatory cells,
macrophages, co8+
ymphocytes

Chronic bronchitis severely affects the lung parenchyma

while emphysema is a airway disease minimal parenchymal
involvement).
Chronic bronchitis Hypoxia thypercarbia, -* Type l
Respiratory Pailure.
Lung parenchymal changes in COPD:
" Alveolar wall destruction.
Pulmonary capillary bed destruction.

Pulmonary hypertension in COPD 00:18:27

Chronic hypoxia
Pulmonary vasoconstriction mascularization

Intinal hyperplasia space

Active
Pulmonary hypertension Fibrosis
obliteration

Cor pulmonale edema

Feedback

Death
 Large small airway changes are more common in
emphysema.
Lung parenchymal i pulmonary vasculature involvemernt are
more common in chronic bronchitis,

emphysema (pink butfer):

only mid to moderate hypoxemia (ao, is usualy o5 mm
Hg.
In addition, these patients maintain normal or even
slightly reduced Paco,
These patients tend to be thin, to experience
hyperinHation at total lung capacity, and to be ree ot
signs o right heart foailure.

cChronic bronchitis (blue bloater):

Patients with the tupe Bpattern are characterized by
marked hypoxemia and peripheral edema resuting rom
right heart failure.
They have frequent respiratory tract infections,
experience chronic carbon dioxide retention Paco, 45
mmHa, and have recurrent episodes of cor pulmonale.
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Chronic bronchitis
tmphysema
Detnition Clinical. Pathological.
Sumptom Cough with sputum. Duspnoea.
Signs Cyanosis. Cachectic.
Cor puirmonale. HOOver sign.
Hyper resonance.
Pursed lip.
PFT TLC normal. TLC RV high.
DLCO normal. DCO low.
Fev/FVC deereasedFev/ Fvc decreased.
CXR Normal. AP diameter inereased.
Active
space
Respiratory faiure Type il uith hypoia i Type i(witth hypoxia).
|hypercarbia).
 ClassiAcation of airlow limitation severity in COfD: Disease

Based on post bronchodilator FeV, j in patients with Fev/FVC< 0.7

GOLDI mild Fey 2 80% predicted
GOLD a moderate SO% S Fev< 80% predicted
GOLD 3 Severe 30% S FEV < S0% predicted
GoLD 4 Very severe FEV< 30% predicted

Management of COPD 00:27:26

Reqular treatment with ICS (nhaled corticosteroids) increases

the risk of pneumonia especially in those with severe COPD :
Evidence A.
Long term use of oral qlucocorticoids has numerous side
eects with no evidence of benets : "evidence A?.

GOLD-a09 quidelines introduced blood eosinophils count with

a cut of of IO0cells/microliter as a biomarker Por estimating
the eficacy of cs for the prevention of exacerbations.

Recommendations of GOLDaOi9 for combination

bronchodilotor therapy :
LCombining bronchodilators with different mechanisms
and durations of action may inerease the degree ot
bronchodilation with air lower risk of side efects,
compared to increasing the dose of a sinale
bronchodilator.
a. Treatment witth Formoterol (Formohale) and Tiotropium
in separate inhalers 007justcool@gmail.com
hasa bigqer impact on FEv than
either component alone.
Pharmacoloqical treatment or cOPD:
space
Active
2a moderate Group D: LAMA LAMA +
exacerbotions or 21
Group C: LABA* or lCS + LABA**
LAMA
leading to hospitalization
Group 8:A ong acting
|Oto Imoderate Group A: bronchodilator. (LAeA OR
exacerbations (not A bronchodilator
Feedback LAMA
|leadingto hospital mmRC O-1,CAT mmRC a, CAT I0
admission
 *Consider if highly symptomatic (eg CAT >a0).007justcool@gmail.com
**consider if eos 300.

Eos Blood eosinophil cournt in cel/micro.

mmRC: modified medical research counci duspnoea. questionnaire.
CAT COPD assesSment test.

ICS/LAeA Combination decreases exacerbations to a qreater

extent than a LABA LAMA combination ot higher blood
eosinophilic concentrations.

Group Ci
Initial therapy should consist of a single
long acting bronchodilator. In tuwo head
to head comparisons the tested LAMA was superior to the
LABA regarding exacerbation prevention therefore we
recommend starting therapy witth a LAMA in this qroup.
f there is no response even on a drugs

Combination of LABA + LAmA + 1CS.

still noresponse.

1 Fev, <s0% : Oral PDEA inhibitor (Rolumilast) or Azithromycin.

Follow up pharmacoloqical treatment:

I. f the response to initial treatrment is appropriate,
maintain it.
a. f not:
Consider the predominant treatable trait to target
(dyspnea or exacerbations).
use exacerbation pathway if
both exacerbation and
Active
space
dyspnea need to be tarqeted.
Place patient in box
corresponding to current Inhaler

treatment Pollow indications.

ASsess response, adjust review
 Pulmonary
These recommendations donoy Disease

respond on the Aeco

assessment at diagnosis.
Dyspnea Exacerbations

LAOA or LAMA LABA or LAMA

LAA + LAMA LABA + ICS LABA + LAMA LABA + \CS

Consider Consider i
eos > Io0 eos 300
Consider |LABA + LAMA LAGA + LAMA
switching + CS + 1CS
inholer device
or molecules.

Inwestigate In former smokers

(and treat) Rofumilast FEV SO
otner causes of Chronic bronchitis Azithromyein
dyspnea.

80s : Blood eosinophil count (cellsuL).

Consider it eos 2300 or eos ZI00 and 2a moderate
exacerbations/ihospitoalizotion.
Consider de-escalation of ICS or suwitch pneumonia,
inappropr iate oriqinal indication or lack of response to iCS.

e0DE index : em/obstructive ventilatory detect/ duyspnoea

severity/exercise capacity
" LABA or LAMA are the foundation of treatment.
Long term oxygen therapy required mandator ily f
Pao, <S5 mmH or Pao, Ss to 60 mmHq with RHF Por
atleast Is to 18 hrs/day
Lung volume reduction surqery is contraindicated when
FEV < aO%.
space
Active

Follow up pharamacoloagical treatnent

Dyspnoea :
For potients with persistent breathlessness or exercise5c0a9804c98a 9f4bf802667a
eedback
Iinitation on long acting bronchodilator monotherapy the
use of two bronchodilators is recommended
" For potients witth persistent breathlessness or exercise
288 Respiratory 38
System
limitation on LABA/IcS treatment, LAMA can be added to
escalate to triple therapy
Aternatively, suwitching from LABACs to LABA/LAmMA should be
considered # the original indication for iCS was incappropriate.
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Oxygen concentrators

Preseription of suppleental oxygen to cOPD patients:

Arterial hypoxemia deined as :
<S5 mmHa (7.3 KPa) or Sa0a <88%
pa, Or

Pao, 55 but <oo mmHg (13 but <8 KPa)

with RHF or eytrocytosis.

Preseribe Supplemental O and titrate to Keep Sao > 90%

Recheck in o0-90 daus to asSess :

supplemental O, is still indicated.
Active
space
H
prescribed supplemental O, is effective.