COPD/PPOM

BRONCHITIS
KRONIS atau COPD
type B

Bronkitis kronik adalah inflamasi
kronis saluran nafas yg ditandai dg
udema dan hiperplasi kelenjar sub
mucosal shg terjadi produksi
mukus berlebihan ke batang
bronchial akibatnya terjadi
peningkatan resistensi sal
pernafasaan
secara kronik atau berulang dengan
disertai batuk, yang terjadi hampir
setiap hari selama sekurangnya tiga
bulan dalam 1 tahun selama 2 tahun
berturut turut. .

Etiologi
Faktor lingkungan :
- Merokok
- Pekerjaan
- Polusi udara
-Infeksi berulang

Faktor host :
- usia
- jenis kelamin
- penyakit paru yang
sudah ada
4

5
CHRONIC BRONCHITIS
Chronic bronchitis is defined as "persistent cough with sputum
production for at least 3 months in at least two consecutive
years".

The most important cause of chronic bronchitis is recurrent
irritation of the bronchial mucosa by inhaled substances, as
occurs in cigarette smokers.

The pathological hallmarks of chronic bronchitis are congestion
of the bronchial mucosa and a prominent increase in the
number and size of the bronchial mucus glands. Copious mucus
may be seen within airway lumens. The terminal airways are
most susceptible to obstruction by mucus.


Pathophysiology of chronic bronchitis
Irritants

Hyperplasia and hypertrophy of
mucous secreting cell

Thick mucous
Air trapping
Sticky coating
Air way obstruction
Impaired ciliary function
Edema
Decrease mucous clearance
Bronchial wall thickness and
Lung defense system compromise inflammation

Vulnerable for infection More infection more mucus
VENTILATION COST
In COPD work of breathing is greater for any given
level of ventilation than normal.
VENTILATION
WORK OF
BREATHING
NORMAL COPD
SEVERE COPD
MODERATE COPD
The cost of work at a
given ventilation for
normal and COPD
patients (ACSM,
1998)
Damage to the epithelium impairs the mucociliary
response that clears bacteria and mucus.
Inflammation and secretions provide the
obstructive component of chronic bronchitis.

In contrast to emphysema, chronic bronchitis is
associated with a relatively undamaged
pulmonary capillary bed.
Emphysema or
type A COPD
Definition
Abnormal permanent
enlargement of air spaces
distal to the terminal
bronchioles, accompanied
by the destruction of the
walls and without obvious
fibrosis
Emphysema is characterized
by loss of elasticity of the
lung and abnormal
permanent enlargement of
air spaces with destruction
of the alveolar walls and
capillary beds.

Etiologi
Emphysema
Smoking
the primary risk factor
Long-term smoking is
responsible for 80-90 % of
cases.
Prolonged exposures to
harmful particles and
gases from:
passive smoke,
Industrial smoke,
Chemical gases, vapors,
mists & fumes
Dusts from grains,
minerals & other materials
Alpha 1-antitrypsin
deficiency >>emphysema
Genetics
Bronchitis
Asthma

Pathophysiology
Exposure to inhaled noxious particles & gases
inflammation imbalance of proteinases
and anti-proteinases


Dilatation & destruction
+ mucus secretion
FIG. 1. Inflammatory mechanisms in COPD. Cigarette smoke (and other irritants) activate
macrophages in the respiratory tract that release neutrophil chemotactic factors,
including IL-8 and LTB4. These cells then release proteases that break down connective
tissue in the lung parenchyma, resulting in emphysema, and also stimulate mucus
hypersecretion. These enzymes are normally counteracted by protease inhibitors,
including 1-antitrypsin, SLPI, and TIMP. Cytotoxic T cells (CD8) may also be recruited and
may be involved in alveolar wall destruction. Fibroblasts may be activated by growth
factors releases from macrophages and epithelial cells. CTG, connective tissue growth
factor; COB, chronic obstructive bronchiolitis.
Pathophysiology

Affects alveolar membrane
Destruction of alveolar wall
Loss of elastic recoil
Over distended alveoli

Over distended alveoli
Damage to adjacent
pulmonary capillaries
h dead space
Impaired passive expiration
Impaired gas exchange


Impaired gas exchange
impaired expiration
h CO2
Hypercapnia
Respiratory acidosis

Damaged pulmonary
capillary bed
h pulmonary pressure
h work load for right
ventricle
Right side heart failure (due
to respiratory pressure)
Cor Pulmonale




16
SYMPTOMS
cough
sputum
dyspnea
EXPOSURE TO RISK
FACTORS
tobacco
occupation
indoor/outdoor pollution
SPIROMETRY
Diagnosis of COPD

GAS DARAH ARTERI
LABORATORY TEST
CHEST X-RAY
Spirometry: Normal and COPD
0
5
1
4
2
3
L
i
t
e
r
1
6 5 4
3 2
FVC
FVC
FEV
1
FEV
1
Normal
COPD
3.900
5.200
2.350
4.150 80 %
60 %
Normal
COPD
FVC FEV
1
FVC FEV
1
/
Seconds
Normally, the left side of the
heart produces a higher level of
blood pressure in order to pump
blood to the body; the right side
pumps blood through the lungs
under much lower pressure. Any
condition that leads to prolonged
high blood pressure in the arteries
or veins of the lungs (called
pulmonary hypertension) will be
poorly tolerated by the right
ventricle of the heart. When this
right ventricle fails or is unable to
properly pump against these
abnormally high pressures, this is
called cor pulmonale.
Prognosis ?

Indikator: umur dan keparahan
Jika ada hipoksia dan cor pulmonale
prognosis jelek
Dyspnea, obstruksi berat saluran nafas, FEV1 <
0.75 L (20%) angka kematian meningkat,
50% pasien berisiko meninggal dalam waktu 5
tahun
Tujuan Terapi

Memperbaiki keadaan obstruksi saluran nafas
Mencegah dan mengatasi eksaserbasi akut
Menurunkan progresivitas penyakit
Meningkatkan keadaan fisik dan psikis
Menurunkan jumlah hari tidak masuk kerja
Menurunkan lama tinggal di RS
Menurunkan angka kematian
NON FARMAKOLOGI
Menghentikan kebiasaan merokok
Rehabilitasi paru-paru secara komprehensif
dengan OR dan latihan pernafasan
Perbaikan nutrisi
Tidak ada obat yang dapat menunda
memburuknya fungsi paru jika pasien tetap
merokok
Kortikosteroid benefit is very limited, laporan tentang
efektivitasnya masih bervariasi, kecuali jika pasien juga
memiliki riwayat asma
Oksigen untuk pasien hipoksemia, cor pulmonale.
Digunakan jika baseline PaO2 turun sampai < 55 mmHg
Antibiotik digunakan bila ada tanda infeksi, bukan
untuk maintenance therapy
Vaksinasi direkomendasikan untuk high-risk patients:
vaksin pneumococcus (tiap 5-10 th) dan vaksin influenza
(tiap tahun)
1-proteinase inhibitor utk pasien yang defisiensi 1-
antitripsin digunakan per minggu, masih mahal
contoh: Prolastin
Tahap terapi pada PPOK yang stabil

Tahap 1 : Ipratropium bromida (MDI) atau nebulizer, 2-
6 puff 4 x sehari, tunjukkan cara penggunaan yang
tepat, advis pasien ttg pentingnya penggunaan teratur
dan efek samping yg mungkin timbul (mulut kering &
rasa pahit), jika hasil trial : perbaikan FEV1 < 20%
step 2
Tahap 2 : Tambahkan -agonis MDI atau nebulizer,
tunjukkan cara penggunaan yang tepat, advis pasien
ttg pentingnya penggunaan teratur dan efek samping
yg mungkin timbul (takikardi, tremor) jika tidak ada
perkembangan: hentikan -agonis, jika ada perbaikan
tapi kecil step 3
Terapi antibiotika

Berdasarkan evidence terbaru yang tersedia, antibiotika
harus diberikan pada pasien-pasien PPOK yang :
Pasien dengan eksaserbasi akut dengan 3 tanda utama
yaitu : increased dyspnea, increased sputum volume,
increased sputum purulence (Evidence B), atau
Pasien dengan eksaserbasi akut dengan 2 tanda utama,
jika peningkatan purulensi sputum merupakan salah
satunya (Evidence C)
Pasien dengan eksaserbasi parah yang membutuhkan
ventilasi mekanik, baik invasif maupun non-infvasif
(Evidence B)
Tahap 3: Tambah teofilin,mulai dari 400 mg/hari dlm
bentuk sustained released, sesuaikan dosis setiap
interval 3 hari untuk menjaga serum level antara 10-15
g/ml, pantau ESO takikardi, tremor, nervous, efek GI;
jika tidak ada perbaikan hentikan teofilin dan go
to step 4
Tahap 4: Coba dengan kortikosteroid : prednison 30-40
mg/hari selama 2-4 minggu, cek dengan spirometer
(perbaikan 20%), titrasi dosis ke dosis efektif terkecil
(< 10 g sehari), pertimbangkan penggunaan
kortikosteroid inhalasi jika pasien tidak berespon
baik kembali ke steroid oral
Key points
PPOK adalah penyakit yang sebenarnya
secara potensial dapat dicegah stop
smoking
Sekali PPOK terjadi penderita akan
memerlukan terapi yang kompleks yang
efikasinya masih diperdebatkan para ahli
Penyakit ini bersifat progresif dan
ireversibel berbiaya besar baik baik
personal maupun masyarakat
Difference between bronchitis and
emphysema


Productive cough
bronchitis

Classic sign
emphysema

Late in common with
infection
Dyspnea Late in course Common
Wheezing Intermittent Mild
H/O smoking Common Common
Barrel chest Occasionally classic
Prolonged expiration Always present Always present
Cyanosis Common Uncommon
Chronic hypoventilation Common Late in course
Ploycythemia Common Late in course