Cough

One of the several defense

mechanisms of the respiratory tract
Defense mechanisms of respiratory
tract
Non immune defenses
Aerodynamic filtering
Airways reflexes
Mucus
Secreted substances
Cilia
Respiratory epithelium
Immune defenses
Cellular
Humoral
 Table 1. Pattern recognition receptors involved in the recognition of
microorganisms by airway epithelial cells
Receptor Ligand
TLR1 Tri-acyllipopeptides
Lipoteichoic acid, peptidoglycan, zymosan, microbial lipoproteins and
TLR2
lipopeptides, HSP70 (host)
TLR3 double-stranded RNA
TLR4 LPS, HSP60 and 70 (host), hyaluronic acid fragments (host)
TLR5 Flagellin
TLR6 di-acyl lipopeptides
TLR7 Synthetic compounds
TLR8
TLR9 CpG DNA
TLR10
CD14 LPS
CFTR LPS
LTR : Tool-like receptor; HSP : heat shock protein; CpG : Bacterial deoxyribonucleic acid (DNA)
Containing unmethylated CpG dinulceotides; LPS : lipopolysaccharide; CFTR : cystic fibrosis
Transmembrane conductance regulator
Bals R, Hiemstra PS. Eur Respir J 2004; 23:327-333
Figure 1. The role of the airway epithelium in host’s defence against infection. Overview of secreted
molecules that the play a role in inflammation and host defence. Some of the depicted molecules
appear to be secreted primary to the basolateral side (chemokines), whereas others are secreted
to the apical side (antimicrobial peptides) of the epithelium.

Bals R, Hiemstra PS. Eur Respir J 2004; 23:327-333

 Table 2. Presence of antimicrobial peptides produced by airway epithelial
cells and aiway host defence cells in human lung disease
Component Source Increased levels in lung disease (reference)

-defensins Epithelial cells Pneumonia

inflammatory cells Cystic fibrosis
Panbronchiolitis
ARDS
Chronic bronchitis
Idiopathic pulmonary fibrosis

-defensin (BD) Epithelial cells Pneumonia

hBD-1 Monocytes / Macrophages Cystic fibrosis
hBD-2 Dendritic cells Panbronchiolitis
hBD-3
hBD-4

Cathelicidin Epithelial cells Pneumonia

LL-37/hCAP-18 Neutrophils Sarcoidosis

ARDS : acute respiratory distress syndrome

Bals R, Hiemstra PS. Eur Respir J 2004; 23:327-333

 Komponen refleks batuk
Reseptor Aferen Pusat batuk Eferen Efektor

Laring Cabang nervus

vagus Otot,
Laring, trakea
Trakea
dan bronkus
Bronkus Nervus vagus

Telinga Tersebar merata

di medula dekat pusat
Lambung pernapasan :
di bawah kontrol pusat
Diafragma, otot-otot
yang lebih tinggi Nervus Frenikus,
Hidung Nervus Interkostal,
Interkostal &
Sinus paranasalis trigeminus abdominal
lumbaris
& otot lumbal
Saraf-saraf
Nervus Otot saluran napas
Faring Trigeminus, Fasialis
dan otot bantu napas
glosofaringus Hipoglosus,dll
Perikardium
Nervus frenikus
diafragma
 Zat yang menimbulkan batuk

Larutan osmotik/
Mediator inflamasi Iritan kimia Rendah Cl-
Mekanik

Histamin Nikotin NaCl hipertonik Bronkokonstriksi

Bradikinin Sulfur dioksida Larutan gula Instrumentasi
Prostaglandin E2 Gas klor Larutan urea Aerosol
Prostaglandin F2a Asam sitrat Debu
Asam asetat
Astilkolin
 Refleks batuk dapat gagal
• Tidak mampu bernapas efisien (ada paralisis otot
pernapasan)
• Kegagalan menutup dan membuka glotis
• Kegagalan menggunakan otot pernapasan
• Kegagalan ekspirasi eksplosif
• Anestesi lokal saluran napas atau pemasangan
endotracheal tube
• Depresi susunan saraf pusat
Terjadinya batuk secara patologik

Inhalasi partikel atau gas polutan atau gas

iritatif
Aspirasi benda asing
Mukus berlebihan
Peradangan mukosa
Kelainan mukosa lain
The Cough reflex
Penderita datang ke dokter karena
ada keluhan

• Keluhan dapat merupakan satu atau

kumpulan gejala
 Pencegahan
• Menghindari faktor-faktor iritan
 Pengobatan
• Prinsip : obati kelainan dasar
• Bila perlu simptomatik
 Kesimpulan
Batuk :
• Normal
- Disengaja
- Tidak disengaja (refleks)
• Patologis
The cough receptor could be
stimulated by
• Inflammatory mediators
• Chemical irritants
• Osmotic stimuli
• Mechanical stimuli
Relative size of airborne particles and gases
(microns)
Particles
Pollens 10 - 100
Spores 6 - 60
Fungi 3 - 100
Cotton flax 2 - 100
Grain and wood dust 0.1 - 1000
Algae 0.5
Bacteria 0.3 - 0.5
Viruses 0.15 - 0.45
Tobacco smoke 0.01 - 1
Gases
SO2, CO, NO, NO2, NH4, CO2, O3, Hydrocarbons 0.0001 - 0.0006
 Tussive agents in humans
Inflammatory Chemical Osmotic/low
Mechanical
Mediators irritants Cl- solution
Histamine Capsaicin Bronchoconstriction
Distilled water
Bradykinin Nicotine Hypertonic saline Instrumentation
Prostaglandin E2 Metabisulfite Urea solution Lactose
Prostaglandin F2 Sulfur dioxide Sugar solution Aerosols
Cl gas Dust
Lobiline
Citric acid
Acetid acid
Acetylcholine

(Adapted from Fuller RW. Cough. In Crystal RG, West JB, Barnes PJ et al (eds).
The lung. Scientific Foundation. New York, Raven Press, 1991, with permission)
Cough receptor to be located in file
epithelium
• Pharynx
• Larynx
• Trachea
• Bifurcation of major bronchi
 IMMUNE RESPONSE DEVELOPMENT
TH1 : TH2 BALANCE

Environment
• Poor sanitation • “Better” hygiene
• Crowding • “Better” homes
• Larger families ventilation
Indoor allergens
• Smaller families
TH1 • Pollution
e.g. diesel particulates
environmental tobacco smoke

Infections TH2
INTRAUTERINE
• ISS-ODN • ISS-ODN
ENVIRONMENT
e.g. TB e.g. GIT bacteria
• Viruses ? antibiotic
e.g. measles • Viruses
e.g. RSV, PIV3
• Parasites

Genetic predisposition provides a large heritable component to atop and asthma. With the intrauterine
environment predisposing infants to a TH2-like phenotype the impact of the external environment
 Mekanisme pertahanan
saluran napas
• Sistem “Air conditioning”
• Sistem “Prossesing”
• Sistem “Transporting”
• Sistem Imunologik
 In the nose In the
Temp. in º C lung
60

50

40

30

20

10

- 10
1-1 2-1 3-1 3E
 Water vapour content In the nose In the
Of the air g/m3 lung

40

30
Relative hygrometry
of surrounding air
%
97.1
20
%
73.4
%
36.4
10 %
23.3
%
13.1
5

0
 Proses humidifikasi
Rongga hidung Saluran napas bawah
33º – 34º C37º C
Jenuh Jenuh

Evaporasi : - 75% saluran napas atas

- 25% saluran napas bawah
Rongga mulut Saluran napas bawah

Bernapas lewat mulut

Evaporasi : 100% saluran napas bawah
lendir kental
 PARTICLE SIZE
Nasal cavity
IMPACTION > 10 

SEDIMENTATION 5-10  Trachea

Primary bronchus

2-5  Secondary bronchus

SEDIMENTATION Terminal bronchus

+
DIFFUSION <2 Respiratory
bronchiole
DIFFUSION <2 Alveolar
Alveoli Ducts & Sacs
Particles penetrate the respiratory tract to different degrees according to their size.
This diagram also depicts the mechanisms that operate to clear particles from
the Respiratory tract according to size
 DIFFUSION SEDIMENTATION INERTIAL IMPACTION
1.00

SMOG FOG

0.80 AUTOMOBILE EXHAUST PARTICULATES

DEPOSITION FRACTION

POLLEN &
FUNGAL SPORES
TOBACCO SMOKE

0.60 VIRUS
BACTERIA
TO
TA
L

PU
0.40 LM FUMES DUSTS
ON
AR
Y

0.20 TRA
CH
EO
BR
ON
CH
IAL

0
0.05 0.1 0.2 0.5 1.0 2.0 5.0 10.0 20.0 50.0

AERODYNAMIC DIAMETER m (Microns)

 Viscous

5
Watery

Mucus : • Glycoproteins (mucin)

• lemak
• zat-zat organic
• 95% air
 Mencegah akibat invasi nonmikrobial
Protein asing

Sc. IgA (-) Histamin release

Ig E
Allergic reaction

Normal defense mechanism

Infection

 Sc. IgA (-), IgE (+) Chronic respiratory symptom

Sindroma
• Infeksi kronik
• Dilatasi/destruksi dinding bronkus
• Gejala klinik :
– Batuk kronik
– Sputum purulen
Patogenesis
• Pasca infeksi paru (pneumonia)
• Infeksi sekunder pada daerah paru yang
kolaps/atelektatik
Faktor predisposisi
• Defek mekanisme pertahanan saluran napas
• Alergi
• Heriditer
Klasifikasi
• Berdasarkan reversibilitas :
– “Psedobronchiectasis”
– “True bronchiectasis”
• Berdasarkan bentuk kelainan :
– Fusiform
– Silindris
– Sakuler
Diagnosis
• Klinik :
• Laboratorik
• Radiologik :
– Foto Rö polos
– Foto Rö dengan kontras
– CT-scan
Pengobatan
• Konservatif :
– Fisioterapi
– Mencegah jangan sampai dehidrasi
– Antibiotika
• Operatif :
– Segmentektomi
– Lobektomi/pneumektomi
Komplikasi
• “Cor pulmonale”
Pencegahan
• Penting :
identifikasi adanya faktor predisposisi
• Gejala : Simptomatologi

Patofisiologi

Patologi