PENYAKIT PARU OBTRUKTIF

KRONIK (PPOK)
Bronkitis kronis
Batuk + dahak kumat2-an lebih dari 2
tahun oleh karena merokok atau polusi
Emfisema
Sesak nafas + batuk kumat2an lebih dari 2
tahun oleh karena merokok atau polusi
 EMFISEMA
• Klinis: dyspnea keadaan istirahat, dada
cembung (tong chest), hipersonor, sianotik,
jari tabuh.
• CXR: hiperlusen, diafragma datar
• Kelainan utama pada cabang bronkus
terminal yg. berhubungan dengan alveoli
• Septa alveoli rusak  luas alveoli  
inefisiensi pertukaran gas
• Kerusakan septa o.k. elastase yang
dihasilkan netrofil lebih tinggi dari alfa-1
antitripsin yg melindungi integritas alveoli
• Kerusakan bersifat irreversibel
Emphysema. PA Chest radiography in a patient with
severe emphysema secondary to alpha-1 antitrypsin
deficiency
Emphysema. Graphic depiction of centrilobular versus
panlobular emphysema
Pathology …. 13 (normal parenchyma)
Pathology …. 14 (emphysema)
Pathology …. 15
Pathology …. 16 (normal small airway)
Pathology …. 17
 “Small Airways Dysfunction”

Expiratory flow
limitation
On forced
exhalation
F
l
o
w During exercise

At rest
Volume
 Wall thickening
– inflammation -
- mucus gland
hypertrophy

↑ Secretions
Bronchus
Wall thickening
– inflammation
– repair
-- remodeling
Loss of alveolar
Bronchiole attachments

Wall thinning -
inflammation -
elastolysis

Coalescence ↓
Elasticity
Alveoli
 COPD and the
Distribution of Airway
Resistance

Silent Zone

Large airway

Airway Normal Central Air Small Air-

Resistance way Obst. way Obst.
Central 80 160 80
Peripheral 20 20 40
Small airway R total 100 180 120
COPD Pathology and Abnormal
Breathing Mechanics
• ↑ Airway resistance
• ↓ Elastic recoil
• Expir. flow limitation
• Air trapping and
dynamic hyperinflation
• ↑ Work of breathing
• Dyspnea, cough and
other respiratory ssx
• ↓ Quality of life
Pathology of Breathing Peripheral Lung Zone

• Airways open
and not prone
to collapse 
low resistance
• Lung recoil
strong enough
to drive tidal
expiration
(passive)
• Work of
breathing is
minimal
Pathology:Altered Lung Mechanics

• Airway wall
thickened and
collapsing 
high resistance
• Alveoli thinned
out  poor
elastic recoil
• Expiratory flow
limitation
• Residual volume
increased
 Thin-section CT scan of a
Smoker

End-inspiration End-expiration
Pathology …..
Pathology …..
Pathology …..
 PPOK
Eksaserbasi Akut
1. Batuk + dahak berlebihan
2. Dahak berubah warna 
kuning,hijau,bau
3. Demam  tanda infeksi
4. Sesak nafas memberat (emfisema)
 PPOK Eksaserbasi Akut
Manajemen:
1. Istirahat + O2  2-3 liter/menit
2. Diet tinggi kalori,tinggi protein, rendah karbohidrat
3. Antibiotika: makrolid, kuinolon, penisilin
4. Steroid oral: metil prednisolon, prednison 40-60
mg/hari  7-10 hari
5. Steroid inhalasi: budesonid/flutikason 1-2 mg/hari
6. Bronkodilator inhalasi: salbutamol/terbutalin 600-
1200 mcg/hari+Ipatrium bromid (Combivent)
7. Aminofilin lepas lambat 200-400 mg  2x/hari
8. Mukolitik: N asetil sistein, ambroksol, OBH, GG
 SUMMARY
• OXYDATIVE STRESS  INFLAMATION
• INCREASE CYTOKINE + CHEMOKINE
• IMBALANCE PROTEASE-ANTIPROTEASE
• MUCOUS SECRETION
• REMODELLING SMALL AIRWAY
• PARTIALLY IRREVERSIBLE  IRREVERSIBLE
• OBSTRUCTION  AIRTRAPPING
• DESTRUCTION PARENCHYMA  EMPHYSEMA