CoughOne of the several defense mechanisms of the respiratory tract

Immune defenses

Defense mechanisms of respiratory tract

Aerodynamic filteringAirways reflexesMucusSecreted substancesCiliaRespiratory epithelium

Non immune defenses

CellularHumoral

Table 1. Pattern recognition receptors involved in the recognition of microorganisms by airway epithelial cellsReceptor 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 LPSLTR : 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

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.

Table 2. Presence of antimicrobial peptides produced by airway epithelial cells and aiway host defence cells in

human lung disease

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

Component Source Increased levels in lung disease (reference)

-defensins Epithelial cells inflammatory cells

PneumoniaCystic fibrosis

PanbronchiolitisARDSChronic bronchitisIdiopathic pulmonary fibrosis

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

Epithelial cells Monocytes / Macrophages

Dendritic cells

PneumoniaCystic fibrosisPanbronchiolitis

Cathelicidin LL-37/hCAP-18

Epithelial cellsNeutrophils

PneumoniaSarcoidosis

ARDS : acute respiratory distress syndrome

Komponen refleks batukReseptor Aferen Pusat batuk Eferen Efektor

Cabang nervus vagus

Nervus vagus

Otot,Laring, trakeadan bronkus

Laring

Trakea

Bronkus

Telinga

Lambung

Tersebar meratadi medula dekat pusat

pernapasan :di bawah kontrol pusat

yang lebih tinggiHidungSinus paranasalis

Nervustrigeminus

Nervus Frenikus,Interkostal &

lumbaris

Diafragma, otot-ototInterkostal, abdominal

& otot lumbal

Faring Nervusglosofaringus

Saraf-saraf Trigeminus, Fasialis

Hipoglosus,dll

Otot saluran napasdan otot bantu napas

Perikardiumdiafragma Nervus frenikus

Zat yang menimbulkan batuk

Mediator inflamasi Iritan kimia Larutan osmotik/Rendah Cl- Mekanik

NaCl hipertonik

Larutan gula

Larutan urea

Histamin

Bradikinin

Prostaglandin E2

Prostaglandin F2a

Bronkokonstriksi

Instrumentasi

Aerosol

Debu

Nikotin

Sulfur dioksida

Gas klor

Asam sitrat

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 iritatifAspirasi benda asing Mukus berlebihanPeradangan mukosaKelainan 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

KesimpulanBatuk :• Normal

• Patologis

- Disengaja- Tidak disengaja (refleks)

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 - 100Spores 6 - 60Fungi 3 - 100Cotton flax 2 - 100Grain and wood dust 0.1 - 1000Algae 0.5Bacteria 0.3 - 0.5Viruses 0.15 - 0.45Tobacco smoke0.01 - 1

GasesSO2, CO, NO, NO2, NH4, CO2, O3, Hydrocarbons 0.0001 - 0.0006

Tussive agents in humansInflammatory

MediatorsChemicalirritants

Osmotic/lowCl- solution Mechanical

Histamine Capsaicin Distilled water BronchoconstrictionBradykinin Nicotine Hypertonic saline Instrumentation

Prostaglandin E2 Metabisulfite Urea solution LactoseProstaglandin F2 Sulfur dioxide Sugar solution Aerosols

Cl gas DustLobiline

Citric acidAcetid 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

TH1

TH2INTRAUTERINEENVIRONMENT

Genetic predisposition provides a large heritable component to atop and asthma. With the intrauterineenvironment predisposing infants to a TH2-like phenotype the impact of the external environment

IMMUNE RESPONSE DEVELOPMENTTH1 : TH2 BALANCE

Environment• Poor sanitation• Crowding• Larger families

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

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

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

Mekanisme pertahanan saluran

napas• Sistem “Air conditioning”• Sistem “Prossesing”• Sistem “Transporting”• Sistem Imunologik

60

1-1 2-1 3-1 3E

Temp. in º C

50

40

30

20

10

0

- 10

In the nose In thelung

1-1 2-1 3-1 3E

Relative hygrometry of surrounding air

In the noseWater vapour contentOf the air g/m3

In thelung

40

30

20

10

5

0

73.4%

36.4%

13.1%23.3%

97.1%

Proses humidifikasi

Rongga hidung Saluran napas bawah33º – 34º C 37º CJenuh Jenuh

Evaporasi : - 75% saluran napas atas- 25% saluran napas bawah

Rongga mulut Saluran napas bawah

Bernapas lewat mulutEvaporasi : 100% saluran napas bawahlendir kental

Particles penetrate the respiratory tract to different degrees according to their size.

This diagram also depicts the mechanisms that operate to clear particles fromthe Respiratory tract according to size

AlveolarDucts & Sacs

Respiratorybronchiole

Terminal bronchus

Secondary bronchus

Primary bronchus

Trachea

Nasal cavity

5-10

> 10

2-5

< 2 < 2 Alveoli

SEDIMENTATION +

DIFFUSION

DIFFUSION

SEDIMENTATION

IMPACTION

PARTICLE SIZE

DIFFUSION SEDIMENTATION INERTIAL IMPACTION

SMOG FOG

AUTOMOBILE EXHAUST PARTICULATES

TOBACCO SMOKE

VIRUSBACTERIA

DUSTS

POLLEN &FUNGAL SPORES

TRACHEOBRONCHIAL

50.020.010.02.0 5.00.2 0.50.1 1.00.05

0.20

0

0.40

0.60

0.80

1.00

DEP

OSI

TIO

N F

RA

CTI

ON

TOTAL

PULMONARY

AERODYNAMIC DIAMETER m (Microns)

FUMES

5

Viscous

Watery

Mucus : • Glycoproteins (mucin)• lemak• zat-zat organic• 95% air

Mencegah akibat invasi nonmikrobial

Protein asing

Histamin releaseIg E

Sc. IgA (-)

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