defense mechanism (ib)
TRANSCRIPT
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CoughOne of the several defense mechanisms of the respiratory tract
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Immune defenses
Defense mechanisms of respiratory tract
Aerodynamic filteringAirways reflexesMucusSecreted substancesCiliaRespiratory epithelium
Non immune defenses
CellularHumoral
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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
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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.
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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
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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
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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
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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
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Terjadinya batuk secara patologik
Inhalasi partikel atau gas polutan atau gas iritatifAspirasi benda asing Mukus berlebihanPeradangan mukosaKelainan mukosa lain
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The Cough reflex
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Penderita datang ke dokter karena ada keluhan
• Keluhan dapat merupakan satu atau kumpulan gejala
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Pencegahan• Menghindari faktor-faktor iritan
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Pengobatan• Prinsip : obati kelainan dasar• Bila perlu simptomatik
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KesimpulanBatuk :• Normal
• Patologis
- Disengaja- Tidak disengaja (refleks)
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The cough receptor could be stimulated by• Inflammatory mediators• Chemical irritants• Osmotic stimuli• Mechanical stimuli
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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
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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)
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Cough receptor to be located in file epithelium• Pharynx• Larynx• Trachea• Bifurcation of major bronchi
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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
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Mekanisme pertahanan saluran
napas• Sistem “Air conditioning”• Sistem “Prossesing”• Sistem “Transporting”• Sistem Imunologik
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60
1-1 2-1 3-1 3E
Temp. in º C
50
40
30
20
10
0
- 10
In the nose In thelung
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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%
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Proses humidifikasi
Rongga hidung Saluran napas bawah33º – 34º C 37º CJenuh Jenuh
Evaporasi : - 75% saluran napas atas- 25% saluran napas bawah
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Rongga mulut Saluran napas bawah
Bernapas lewat mulutEvaporasi : 100% saluran napas bawahlendir kental
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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
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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
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5
Viscous
Watery
Mucus : • Glycoproteins (mucin)• lemak• zat-zat organic• 95% air
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Mencegah akibat invasi nonmikrobial
Protein asing
Histamin releaseIg E
Sc. IgA (-)
Allergic reaction
Normal defense mechanism
Infection
Sc. IgA (-), IgE (+) Chronic respiratory symptom
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Sindroma• Infeksi kronik• Dilatasi/destruksi dinding bronkus• Gejala klinik :
– Batuk kronik– Sputum purulen
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Patogenesis• Pasca infeksi paru (pneumonia)• Infeksi sekunder pada daerah paru yang
kolaps/atelektatik
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Faktor predisposisi• Defek mekanisme pertahanan saluran napas• Alergi• Heriditer
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Klasifikasi• Berdasarkan reversibilitas :
– “Psedobronchiectasis”– “True bronchiectasis”
• Berdasarkan bentuk kelainan :– Fusiform– Silindris– Sakuler
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Diagnosis• Klinik :• Laboratorik• Radiologik :
– Foto Rö polos– Foto Rö dengan kontras– CT-scan
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Pengobatan• Konservatif :
– Fisioterapi– Mencegah jangan sampai dehidrasi– Antibiotika
• Operatif :– Segmentektomi– Lobektomi/pneumektomi
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Komplikasi• “Cor pulmonale”
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Pencegahan• Penting :
identifikasi adanya faktor predisposisi
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• Gejala : Simptomatologi
Patofisiologi
Patologi