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

TLR2

Lipoteichoic acid, peptidoglycan, zymosan, microbial lipoproteins and

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 hosts 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

-defensins

Epithelial cells
inflammatory cells

Increased levels in lung disease (reference)

Pneumonia
Cystic fibrosis
Panbronchiolitis
ARDS
Chronic bronchitis
Idiopathic pulmonary fibrosis

-defensin (BD)
hBD-1
hBD-2
hBD-3
hBD-4

Epithelial cells
Monocytes / Macrophages
Dendritic cells

Cathelicidin
LL-37/hCAP-18

Epithelial cells
Neutrophils

Pneumonia
Cystic fibrosis
Panbronchiolitis

Pneumonia
Sarcoidosis

ARDS : acute respiratory distress syndrome

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

Komponen refleks batuk

Reseptor

Aferen

Laring

Cabang nervus
vagus

Pusat batuk

Eferen

Otot,

Laring, trakea
dan bronkus

Trakea
Bronkus

Efektor

Nervus vagus

Telinga
Lambung
Hidung
Sinus paranasalis

Nervus
trigeminus

Faring

Nervus
glosofaringus

Perikardium
diafragma

Nervus frenikus

Tersebar merata
di medula dekat pusat
pernapasan :
di bawah kontrol pusat
Diafragma, otot-otot
Nervus Frenikus,
yang lebih tinggi
Interkostal &
lumbaris

Interkostal,
abdominal
& otot lumbal

Saraf-saraf
Trigeminus, Fasialis
Hipoglosus,dll

Otot saluran napas

dan otot bantu napas

Zat yang menimbulkan

batuk
Mediator inflamasi

Iritan kimia

Larutan osmotik/
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
Asam asetat
Astilkolin

Debu

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

In the nose

Temp. in C
60

In the
lung

50
40
30
20
10
0
- 10

1-1

2-1

3-1

3E

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
Mediators

Chemical
irritants

Histamine

Capsaicin

Bradykinin
Prostaglandin E2
Prostaglandin F2

Nicotine
Metabisulfite
Sulfur dioxide
Cl gas
Lobiline
Citric acid
Acetid acid
Acetylcholine

Osmotic/low
Cl- solution

Mechanical

Bronchoconstriction
Hypertonic saline Instrumentation
Urea solution
Lactose
Sugar solution
Aerosols
Dust
Distilled water

(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
Crowding
Larger families

TH1

Better hygiene
Better homes
ventilation
Indoor allergens
Smaller families
Pollution
e.g. diesel particulates
environmental tobacco smoke

Infections

ISS-ODN
e.g. TB
Viruses
e.g. measles

ISS-ODN
e.g. GIT bacteria
? antibiotic
Viruses
e.g. RSV, PIV3
Parasites

TH2

INTRAUTERINE
ENVIRONMENT

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

Water vapour content

Of the air g/m3
40

30

20

10
5
0

Relative hygrometry
of surrounding air
%
97.1
%
73.4
%
36.4
%
23.3

%
13.1

In the nose

In the
lung

Proses
humidifikasi

Rongga hidung Saluran napas bawah

33 34 C37 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

IMPACTION

> 10

SEDIMENTATION

5-10

Nasal cavity

Trachea
Primary bronchus

2-5
SEDIMENTATION
+
DIFFUSION
DIFFUSION

Secondary bronchus

Terminal bronchus

<2

<2

Respiratory
bronchiole
Alveoli

Alveolar
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
FOG

0.80

AUTOMOBILE EXHAUST PARTICULATES

POLLEN &
FUNGAL SPORES

TOBACCO SMOKE
VIRUS

0.60

BACTERIA

L
TA
TO

DEPOSITION FRACTION

SMOG

0.40

0.20

PU
LM
ON
AR
Y

DUSTS

FUMES

TRA
CH
EO
BR
ON
CH
IAL

0
0.05

0.1

0.2

0.5

1.0

2.0

5.0

AERODYNAMIC DIAMETER m (Microns)

10.0

20.0

50.0

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 R polos
Foto R 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