patofisiologi-sist-pernafasan.ppt

8/11/2019 patofisiologi-sist-pernafasan.ppt

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Tujuan dari Respirasiadalah untuk menyediakan oksigen bagi seluruh

jaringan tubuh dan membuang karbon dioksida ke

atmosfer


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Rongga torax Paru adalah organ elastis terletak pada rongga dada/torax.

Paru dilapisi oleh lapisan tipis kontinu yg mengandungkolagen & jar elastis yg disebut PLEURA

Pleura Parietalis melapisi rongga dada sedang Pleuraviseralis melapisi paru .

Rongga pleura: ruangan yg memisahkan pleura parietalis &

viseralis

Cairan pleura: lapisan tipis antara pleura parietalis dg viseralisberfungsi memudahkan kedua permukaan tersebut bergerakselama pernapasan & untuk mencegah pemisahan torax &

paru. Tekanan rongga pleura < tekanan atmosfer: untuk mencegah

kolaps paru.


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Rongga torax

3 faktor yg mempertahankan tekanan negatifintrapleura normal:

1. Jaringan elastis paru memberikan kekuatan kontinu yg

cenderung menarik paru menjauh dr rangka torax.

2. Kekuatan osmotik yg terdapat di seluruh membranpleura.

3. Kekuatan pompa limfatik.

Diafragma: otot berbentuk kubah yg membentuk

dasar rongga torax & memisahkan rongga tersebutdari rongga abdomen.


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Anatomi Saluran Pernapasan


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Anatomi Saluran Pernapasan


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Alveoli

Terdapat 2 tipe sel alveolar: Pneumosit tipe I: lap tipis menyebar & menutupi >

90% daerah permukaan. Pneumosit tipe II: tanggung jawab pada sekresi

surfaktan. Alveolus: suatu gelembung gas yang dikelilingi oleh

jaringan kapiler batas antara cairan & gasmembentuk tegangan muka yang cenderungmencegah pengembangan saat inspirasi & cenderung

kolaps saat ekspirasi. Alveolus dilapisi zat lipoprotein (surfaktan) dapat

mengurangi tengangan permukaan & resistensi saatinspirasi & mencegah kolaps alveolus (expirasi).


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Bronchopulmonary segments

LobulesAlveolar wall cell types

LUNGS 2

terminal

bronchiole

respiratory

bronchiole

pulmonary

artery branch

alveolar sac

simple squamous epithelial cell

macrophage (dust cell)

septal cell (produces surfactant)

Type I alveolar cell

Type II alveolar cell

making surfactant

blood capillary

endothelial cell

macrophage

surfactant

respiratory membrane


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Alveoli

Pembentukan & pengeluaran surfaktan olehpneumosit tipe II disintesis secara cepat dariasam lemak yang diekstraksi dari darah, dgkecepatan pergantian yg cepat. Bila aliran darah

ke paru terganggu (emboli) akibatnya jumlahsurfaktan pada daerah tersebut berkurang. Produksi surfaktan dirangsang oleh ventilasi aktif,

volume tidal yg memadai, hiperventilasi periodik(cepat & dalam) yg dicegah oleh kons O2yang

tinggi (inspirasi). Pemberian O2 kons tinggi jangka lama (pasien dg

ventilasi mekanik) menurunkan produksisurfaktan & menyebabkan kolaps alveolar.


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Pernafasan terdiri dari 4 proses :

1. Ventilasi : Keluar masuknya udara karena adanya selisih

tekanan yang terdapat antara atmosfer dan alveolus

2. Distribusi : Pembagian udara ke cabang -cabang bronkhus

3. Transportasi dan Difusi

- Transport O2dan CO2dalam darah dan cairan tubuh kedan dari sel

- Difusi O2dan CO2antara darah dan alveoli

Pertukaran gas-gas antara alveoli dan kapiler dipengaruhi

oleh tekanan parsial O2& CO2dalam atmosfer

4. Perfusi : Aliran darah yang membawa O2ke jaringan


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JENIS RESPIRASI

1. RESPIRASI EXTERNAL

O2 DIBAWA DARI UDARA

LUAR SAMPAI KE KAPILER2. RESPIRASI INTERNAL

O2DARI KAPILER SAMPAI KE

SEL PADA JARINGAN.


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RESPIRASI EXTERNAL


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RESPIRASI INTERNAL


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Active process

Boyles Law

INSPIRATION

FORCED INSPIRATION

Inspiratory muscles

Phrenic nerves (C3-5)Thoracic nerves (T1T11)

thoracic volume

pleural volume

intrapleural pressure

lung volume

intrapulmonic pressure

air flow into the lungs

760 mmHg

760 mmHg

760 mmHg

758 mmHg

BEFORE INSPIRATION DURING INSPIRATION

Process


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Passive process at rest

EXPIRATION

internal intercostals

(11 pairs)

internal intercostals (11 pairs)

rectus abdominis

abdominal obliques

transversus abdominis

Forced expiration

thoracic volume

pleural volume

intrapleural pressurelung volume

intrapulmonic pressure

air flow of the lungs

Process

external abdominal oblique

internal abdominal oblique

transversus abdominis

rectus abdominis

760 mmHg

762 mmHg

elastic recoilsurface tension


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Perubahan diafragma saat inspirasi & ekspirasi


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Otot Pernapasan


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Compliance is the ease with which the lungs and thoracic wall canbe expanded during inspiration.

COMPLIANCE

elasticity

surface tension

Related to two factors:

destroys lung tissue (emphysema)

fills lungs with fluid (pneumonia)

produces surfactant deficiency (premature birth, near-drowning)

interferes with lung expansion (pneumothorax)

Compliance is decreased with any condition that:


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PULMONARY VOLUMES, CAPACITIES, AND RATES

SPIROGRAM

Volumes

tidal volume (500 ml)

anatomical dead space (150 ml)

alveolar ventilation (350 ml)

physiological dead space

inspiratory reserve volume (3000 ml)

expiratory reserve volume (1200 ml)residual volume (1300 ml)

Capacitiestotal lung capacity (TV+IRV+ERV+RV)

vital capacity (TV+IRV+ERV) (4700 ml)

inspiratory capacity (TV+IRV)functional residual capacity (RV+ERV)

Ratesmaximum voluntary ventilation = TV x breaths/minute

alveolar ventilation rate = alveolar ventilation xbreaths/minute

IRV

ERV

TV

RVmaximum

expiration

VC TLC

6000 ml

5000 ml

4000 ml

3000 ml

2000 ml

1000 ml

maximum inspiration


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Kontrol Pernapasan

Otot pernapasan diatur oleh neuron &

reseptor pada pons & medula oblongata.

Faktor utama pengaturan pernapasan: respon

dari pusat kemoreseptor dalam pusat

pernapasan terhadap tekanan persial CO2dan

pH darah arteri


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Kontrol Pernapasan

Persarafan parasimpatis/ kolinergik (mll nervus fagus)

menyebabkan kontraksi otot polos bronkus shg menyebabkanbronkokonstriksi & peningkatan sekresi kel mukosa & selgoblet.

Rangsangan simpatis ditimbulkan epinefrin mll reseptoradrenergik-beta2menyebabkan relaksasi otot polos bronkus,bronkodilatasi, & berkurangnya sekresi bronkus.

Sistem saraf nonkolinergik non adrenergik (NANC): melibatkanberbagai mediator seperti ATP, oksida nitrat, substance P, danVIP (vasoactive intestinal peptide) respon penghambatan,meliputi bronkodilatasi, dan diduga berfungsi sebagaipenyeimbang terhadap fungsi pemicuan oleh sistemkolinergik.


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Kontrol Pernapasan


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Signs and Symptoms of Pulmonary

Disease

Dyspneasubjective sensation ofuncomfortable breathing, feeling short ofbreath

Ranges from mild discomfort after exertion toextreme difficulty breathing at rest.

Usually caused by diffuse and extensive

rather than focal pulmonary disease.

26

j


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Derajat Dyspnea

Tingkat Derajat Kriteria

0 Normal Tidak ada kesulitan bernapss kecuali dengan aktivitasberat.

1 Ringan Terdapat kesulitan bernapas, napas pendek-pendek

ketika terburu-buru atau ketika berjalan menuju

puncak landai.

2 Sedang Berjalan lebih lambat daripada kebanyakan orang

berusia sama karena sulit bernapas atau harus

berhenti berjalan untuk bernapas.3 Berat Berhenti berjalan setelah 90 meter untuk bernapas

atau setelah berjalan beberapa menit.

4 Sangat berat Terlalu sulit bernapas bila meninggalkan rumah atau

sulit bernapas ketika memakai baju atau membuka

baju.


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Dyspnea cont.

Due to:

Airway obstruction

Greater force needed to provide adequate

ventilation

Wheezing sound due to air being forced

through airways narrowed due to constriction

or fluid accumulation Decreased compliance of lung tissue

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Signs of dyspnea:

Flaring nostrils

Use of accessory muscles in breathing

Retraction (pulling back) of intercostal spaces

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BATUK

Batuk merupakan gejala tersering penyakitpernapasan

Batuk merupakan reflex pertahanan yang timbulakibat iritasi percabangan trakeobronkial

Batuk yang berlangsung lebih dari 3 minggu harusdiselidiki untuk memastikan penyebabnya.

Bronkhitis kronik, asma, tubercolosis dan

pneomonia merupakan penyakit yang secara tipikalmemiliki batuk sebagai gejala yang mencolok


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Cough may result from:

Inflammation of lung tissue

Increased secretion in response to mucosalirritation

Inhalation of irritants Intrinsic source of mucosal disruptionsuch as

tumor invasion of bronchial wall

Excessive blood hydrostatic pressure in

pulmonary capillaries Pulmonary edemaexcess fluid passes into

airways

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When cough can raise fluid into pharynx, the

cough is described as a productive cough, and

the fluid issputum. Production of bloody sputum is called hemoptysis

Usually involves only a small amount of blood

loss

Not threatening, but can indicate a serious

pulmonary disease

Tuberculosis, lung abscess, cancer,

pulmonary infarction.

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Cough that does not produce sputum is called

a dry, nonproductiveor hacking cough.

Acute cough is one that resolves in 2-3 weeksfrom onset of illness or treatment of

underlying condition.

Us. caused by URT infections, allergic rhinitis,acute bronchitis, pneumonia, congestive heart

failure, pulmonary embolus, or aspiration.

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A chronic cough is one that persists for more

than 3 weeks.

In nonsmokers, almost always due to

postnasal drainage syndrome, asthma, or

gastroesophageal reflux disease

In smokers, chronic bronchitis is the mostcommon cause, although lung cancer should

be considered.

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SPUTUM Pembentukan sputum:

Orang dewasa normal mukus sekitar 100ml dalam saluran napas tiap hari Mukusdiangkut menuju faring dengan gerakan

pembersihan silia yang melapisi saluranpernapasan bila mukus berlebihanproses pembersihan tidak efektif

mukus tertimbun membran mukosaakan terangsang mukus dibatukkankeluar sebagai sputum.


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SPUTUM

Sputum yang berwarna kekuning-kuninganmenunjukkan infeksi.

Sputum yang berwarna hijau merupakanpetunjuk penimbunan nanah timbul karenaadanya verdoperoksidase yang dihasilkan olehpolimorfonuklear (PMN).

Sputum yang berwarna merah muda dan berbusamerupakan tanda edema paru akut.

Sputum yang berlendir lekat dan warna abu-abu

atau putih merupakan tanda bronkhitis kronik.Sedangkan sputum yang berbau busukmerupakan tanda abses paru atau bronkiektasis.


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Cyanosis

When blood contains a large amount ofunoxygenated hemoglobin, it has a dark red-bluecolor which gives skin a characteristic bluishappearance.

Most cases arise as a result of peripheralvasoconstrictionresult is reduced blood flow,which allows hemoglobin to give up more of its

oxygen to tissues- peripheral cyanosis. Best seen in nail beds

Due to cold environment, anxiety, etc.

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Central cyanosiscan be due to :

Abnormalities of the respiratory membrane

Mismatch between air flow and blood flow

Expressed as a ratio of change in ventilation (V) to

perfusion (Q) : V/Q ratio

Pulmonary thromboembolus - reduced bloodflow

Airway obstructionreduced ventilation

In persons with dark skin can be seen inthe whites of the eyes and mucous

membranes.

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Jari Tabuh

Jari tabuh adalah perubahan bentuknormal falang distal dan kuku tangan dankaki serta ditandai dengan

1. Kehilangan sudut kuku yangnormalnya 160 derajat.

2. Rasa halus berongga pada dasarkuku.

3. Ujung jari menjadi besar.

jari tabuh berhubungan dengan peyakitparu (TB, abses paru, atau kanker

paru). Penyakit kardiovaskuler(tetralogi fallot atau endokarditisinfektif) atau penyakit hati kronik

Next


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Next

2. Hipoksia (O2yang tidak adekuat dalam tingkat jaringan) dan

Hipoksemia (PaO2 dibawah normal normal 80-100 mmhg).

Tanda dan gejala hipoksemia dan hipoksia tidak spesifik dan

mencakup takipnea, dispnea, sakit kepala, pikiran yang

bingung, takikardi, dan sianosis.

3. Hipokapnia dan hiperkapniaHipokapnia didefinisikan sebagai menurunnya PaCO2 45 mmhg. Penyebab langsung adalah selalu

hipoventilasi alveolar (kegagalan dalam mengeliminasi CO2secepat produksinya).


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Pain

Originates in pleurae, airways or chest wall

Inflammation of the parietal pleura causessharp or stabbing pain when pleura stretches

during inspiration Usually localized to an area of the chest wall,

where a pleural friction rubcan be heard

Laughing or coughing makes pain worse

Common with pulmonary infarction due toembolism

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Inflammation of trachea or bronchi produce a

central chest pain that is pronounced after

coughing Must be differentiated from cardiac pain

High blood pressure in the pulmonary

circulation can cause pain during exercise thatoften mistaken for cardiac pain (angina

pectoris)

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Respiratory Disorders

Respiratory disorder can be classified into differentgroup

Respiratory tract infection

Common cold,Influenza,Pneumonias,T.B

Disorder of lung inflation

Pleural pain and pleural effusion

Obstructive air way disorders

Bronchial asthma, COPD, Emphysema, Bronchitis

Pulmonary vascular disorder

Lung cancer


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INFLUENZA

Penyakit yang disebabkan oleh virus influenza.

Gejala yang ditimbulkan antara lain pilek,

hidung tersumbat, bersin- bersin, dan tenggorokan

terasa gatal. Perlu diketahui virus iniselalu hanya bisa menembus saluran pernafasan

atas saja , sehingga bisa disimpulkan

saluran respirasi yang lebih dalam sangat resistenimmun terhadap virus ini.


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Asthma

is a chronic inflammatorydisorder of the airways inwhichmany cellsandcellular elements play arole

In susceptible individuals,this inflammation causesrecurrent episodes ofwheezing, breathlessness,chest tightnessandcoughing, particular ly atnight or in the ear lymorning..

eosinophils

epithelial cells

neutrophils

Macropha-

ges

T lympho-

cytes

mast cells

Cells


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Causes and Triggers

oAllergies such as to pollens, mold spores, pet

dander, and dust mites

oInfections (colds, viruses, flu, sinus infection)

oExercise

oAspirin or nonsteroidal anti-inflammatory drug

(NSAID) hypersensitivity, sulfite sensitivity

oUse of beta-adrenergic receptor blockers (including

ophthalmic preparations)

Cont


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oIrritants such as strong odors from perfumes or

cleaning solutions, air pollution, and tobacco smokeoWeather (changes in temperature and/or humidity, cold

air)

oStrong emotions such as anxiety, laughter, crying, and

stress

oIndustrial triggers (wood, grain dust, cotton dust,

isocyanate containing paints, aluminum, hair spray,

penicillins)

oBeta blockers even in form of eye drops


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oGastroesophageal reflux disease

oChronic sinusitis or rhinitisoOSA (obstructive sleep apnoe)

oObesity

oAlergy bronchopulmonaryaspergilosis

COMORBID CONDITION


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ASMA

Asma ekstrinsik (alergik)(alergen, spt: debu,blu halus, serbuk)

intrinsik (idiopatik)

(fak nonspesifik spt flu, latihan fisik, emosi dapatmemicu serangan asma)

campuran

(Komponen asma instrinsik+Ekstrinsik)


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Two main pathophysiologic types of

asthma

Extrinsic asthma;common in children,

associated with a genetic predispositionand is precipitated by a known

allergens. It is related to the formation

of antibody IgE in the body

I l i l M h i i


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Immunological Mechanisms in

Respiratory Diseases

fi i l i


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Patofisiologi Asma


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Intrinsic asthma;tend to develop in

adulthood, and symptoms are triggered by non-allergic factors such as;

1. Viral infection, irritants which cause

epithelial damage and mucosal inflammation

2. Emotional upset which mediates excess

parasympathetic input3. Exercise which causes water ad heat loss

from the airways


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Pathophysiology


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Pathophysiology

Release of inflammatory mediator producebronchial smooth muscle spasm Vascular congestion Increase vascular permeability

Edema formation Production of thick tenacious mucus Impair mucociliary function Thickening of air way wall

Increase response of bronchial smooth muscle Damage epithelium produce hyper

responsiveness and obstruction

gambar


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Faktor2 yang mengakibatkan obstruksi ekspirasi pada asma bronkial. A.

Potongan melintang dari bronkiolus yang mengalami oklusi akibat spasme

otot, mukosa yang membengkak, dan mukus dalam lumen, B . Potongan

memanjang dari bronkiolus

gambar


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The mechanism of inflammation in

asthma can beAcute; early recruitment of cells to the airways

Subacute; resident and recruited cells are activated to causea more persistent pattern of inflammation

Chronic; cells damage is persistent and subject to ongoing repair,permanent change in the airway may occur with airway remodelling

G b kli ik


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Gambaran klinik

Batuk yang memburuk pada malam hari

Sesak nafas

Mengi atau Wheezing(a high-pitched whistlingsound that occurs when exhaling) due to turbulentairflow through a narrowed airway

nafas pendek tersengal-sengal.

Produksi sputum meningkat, sulit tidur

Hambatan pernafasanan reversibel

Adanya peningkatan gejala pada saat olahraga,infeksi virus, eksposur terhadap alergen danperubahan musim.

Terbangun di malam hari krn gejala seperti di atas .


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Investigations

Pulmonary function testing (spirometry)Forced expiratory volume (FEV)

Methacholine or histamine challenge testingExercise testing

Peak expiratory flow rate monitoring

i ( )


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Forced expiratory volume (FEV)

Volume(litres)

Time (second)

1 2 3 4

Asthma patient

Normal subject

FEV1

FVC

Component Classification of Asthma Severity (>12 yrs)

P i t t


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of

SeverityIntermittent

Persistent

Mild Moderate Severe

Symptoms 2 d/wk

but not daily

DailyThroughout the

dayNighttimeawakening

1x/wk but not

nightlyOften 7x/wk

SABA use 2 d/wk

but not daily &

not >1x on any day

DailySeveral times

per day

Interferencewith activity

NONE Minor limitation Some limitation Extremelylimited

Lung function

Normal FEV1between

exacerbations

FEV1:>80%

predicted

FEV1/FVC:

normal

FEV1 : >80%

predicted

FEV1/FVC: normal

FEV1: >60% but


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Leukotriene receptor antagonists Direct antagonist

of mediators responsible for airway inflammation in asthma

Bronchodilators Provide symptomatic relief ofbronchospasm due to acute asthma exacerbation (short-actingagents) or long-term control of symptoms (long-acting agents)

Drug categories

CorticosteroidsHighly potent agents that are the primary

choice for treatment of chronic asthma and prevention of acuteasthma exacerbations. Numerous inhaled corticosteroids are used for

asthma and include beclomethasone (Beclovent, Vanceril),

budesonide (Pulmicort Turbuhaler), flunisolide (AeroBid),

fluticasone (Flovent), and triamcinolone (Azmacort).


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5-L ipoxygenase inhibitors Inhibit the formation ofleukotrienes. Leukotrienes activate receptors that may be

responsible for events leading to the pathophysiology of asthma,

including airway edema, smooth muscle constriction, and alteredcellular activity associated with inflammatory reactions

Mast cell stabil izers Prevent the release of mediators frommast cells, which results in airway inflammation and bronchospasm.

Indicated for maintenance therapy of mild-to-moderate asthma or

prophylaxis for EIA


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Three Steps of Asthma Treatment

Step 1- Control bronchospasm with short- acting b2 agonists or

long-acting salmeterol

Step 2- Control inflammation with inhaled corticosteroids or

leukotriene antagonist

Step 3- Control severe exacerbation with oral corticosteroids

St 1


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Step 1

Is to control bronchospasm with inhaled b2

agonists. Short-acting b2agonists are appropriatefor patients with mild, intermittent asthma who donot require daily maintenance therapy.

Inhaled b2 agonists are effective, work quicklywithin 2 to 3 minutes and provide acute relief forup to 4 to 6 hours

Remember thatshort-acting b2 agonists areindicated for use as rescue bronchodilators duringacute attacks of bronchospasm.


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When daily maintenance therapy is needed for

more persistent symptoms, the long-acting b2

agonist salmeterol is an excellent and effectivechoice in treatment

Salmeterol can be taken once or twice a day as an

inhaled bronchodilator

The bronchodilating action of salmeterol is

delayed in onset (20-30 minutes) but frequently

lasts 8 to 12 hours when taken properly.


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Step 2

Is to control inflammation when there is evidenceof persistent or frequently recurring symptoms

with inhaled corticosteroids or leukotriene

antagonists, or the non-steroidal anti-

inflammatory agents cromolyn sodium or

nedocromil sodium

This is maintenance anti-inflammatory therapywithout any direct bronchodilator effect.

I h l d ti t id d l ti t id d t t l


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Inhaled corticosteroidsand oral corticosteroidsare used to control

inflammation in asthma

Corticosteroids prevent the migration of inflammatory cells and

increase the responsiveness of airway b2 receptors

Corticosteroids have been shown to reduce acute bronchial

hyperresponsiveness to irritants and may chronically blunt the early

airway response to irritants with continued useThe new inhaled corticosteroid, fluticasone propionate, appears to

possess a higher potency than other inhaled corticosteroids.

Like other inhaled corticosteroids, fluticasone is indicated for the

maintenance treatment of asthma as prophylactic therapy

Recent studies have shown that it can reduce oral prednisone use

while improving asthma control.

Inhaled nonsteroidal anti inflammatory drugs like


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Inhaled nonsteroidal anti-inflammatory drugs like

cromolyn or nedocromil may reduce symptoms in

patients with mild to moderate asthmaThey are frequently prescribed in children and in

adults with allergic asthma

They inhibit the activation of mast cells and

eosinophils, block inhaled neurogenic stimuli, and

may reduce airway temperature changes that can

trigger an asthma attack

Nedocromil may allow the reduction of

corticosteroid use in selected patients


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Step 3

Is to control severe exacerbations with systemicoral corticosteroids, i.e. prednisone 1 mg/kg or 40

to 60 mg daily for 1 to 2 weeks

Many patients are steroid-dependent and

frequently develop cushingnoid features such as

hyperglycemia, fluid retention, weight gain with

moon facies, and easy bruisability


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Anticholingeric drugslike ipratropiummay have an adjunctive role in asthma therapy

They block vagal pathways and produce

bronchodilation by decreasing airway vagal tone

They are less potent than b2 agonists and have aslow onset of action

While they may reduce mucus secretion, there is no

evidence that they modulate the inflammatory

response

Oral theophyllineand intravenous


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Oral theophyllineand intravenousaminophylline were once the mainstay of

asthma treatment, especially nocturnal asthma

Originally thought to act as a

phosphodiesterase inhibitor to increase cAMP,

these methylxanthines are now though toantagonize adenosine, a mediator of acute

inflammation

Theophyllines reverse bronchospasm, enhancemucociliary clearance, and increase

diaphragmatic contraction


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However, theophylline is probably useful as an

adjunct to b2 agonists and anti-inflammatory drugs

Any benefit may be diminished somewhat by a

narrow therapeutic range (5 to 15 g/ml) which can

lead to serious and toxic consequences, e. g. seizures,

tachyarrhythmias when exceeded

Its use in the emergency treatment of asthma is not

recommended but recent evidence suggest it maymodulate chronic asthma symptoms more effectively

than is generally perceived.


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The use of cytotoxic agents, e. g.methotrexate, cyclosporine can not berecommended unless standard therapywith b2 agonists and anti-inflammatory

drugs have failed


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leukotriene receptor antagonists,

Specifically, LTD4 receptor antagonist and 5-

lipoxygenase inhibitors can completely block the

acute phase response and block part of the

delayed phase response

Blocking the generation of leukotrienes or

blocking their actions on cells may be helpful incontrol of asthma and treatment of asthma attacks


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DEFINISI PPOM/COPD

Penyakit obstruksi saluran nafas kronis

dan progresif yg ditandai oleh hambatan

aliran udara yg bersifat non reversibel

atau reversibel sebagian bersifat

progresif & berhubungan dg respons

inflamasi abnormal paru thd partikel atau

gas beracun.

Bronkitis kronik& emfisema


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Bronkitis kronik& emfisema

Meskipun bronkitis kronik dan emfisema

merupakan 2 proses yg berbeda, tp penyakit

ini sering ditemukan bersama2 pada penderita

COPD.

Merupakan penyebab kematian terbanyak

COPD mnyerang pria 2x lebih banyak dari

wanita karena faktor perokok

Faktor etiologi utama adalah merokok dan

polusi udara

FAKTOR RISIKO


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Host:

- Genetik: Defisiensi alpha 1

anti tripsin atau

antiprotease (menghambat

aksi dari enzym protease)

- Hipereaktivitas bronkus

Lingkungan:

Asap rokok (faktor risikoutama - sigaret)

Partikel debu & bahan kimia

perindustrian Polusi udara

Indoor air pollution fromheating and cooking withbiomass in poorly

ventilated dwellings Infeksi

Status sosial

PATOGENESA


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PATOGENESA

Inflamasi /Keradangan kronis pd sal. napas,

parenkim paru, sistem vaskuler paru pe

makrofag, limfosit T (CD8+), netrofil release

mediator LB4, IL8, TNF Imbalance proteinaseanti proteinase

Stres oksidatif

Ketiga faktor diatas akan merusak struktur

paru.

i th t thi i fl t hi h


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The theory of interplay

is that this inflammatory process whichincludes alveolar macrophages in some wayreleases neutrophil chemotactic factorsknown as (IL-8 ) causing neutrophils toemigrate from the blood space into theairspace to release elastase .

In normal circumstances alpha-1-antitrypsinbinds to the elastase and prevents it frombinding to elastin thus destroying thestructure of the lungs.

i th bl d d i l ti


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Neutrophils

in the blood and air space release more activeoxygen species in smokers, than in non smokers,these together with the 1017 oxidants in inhaled

cigarette smoke inactivate the alpha-1-antitrypsinat its active site.

This reduces the ability of alpha-1-antitrypsin tobind to elastase by a factor of approximately 2000allowing active ealstase to bind to elastin andcause the enlargement of the airspace that is seen

in emphysema P-Selectin , L-seletin adhesionsare important for the transport of inflammatorycells in the systemic circulation .

K l h t k b t k d h k


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KLINIS

Keluhan utama: sesak napas, batuk, dahak

Sesak timbul progresif sp mengganggu aktivitas,

men-dadak memberat bila tjd eksaserbasi

Batuk kronis, memberat pagi hari, dahak mukoid

purulen bila eksaserbasi

Suara mengi (wheezing)

Batuk darah blood-streaked purulen sputum (eksa-serbasi)

Nyeri dada (pleuritis, pneumotoraks, emboli paru)

Anoreksi & BB menurun progresif jelek

Noxious particles


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Noxious particles

and gases

Lung inflammation

Host factors

COPD pathology

ProteinasesOxidative stress

Anti-proteinasesAnti-oxidants

Repair mechanisms

PATOLOGI


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Saluran napas besarHipertrofi kelenjar & pe jumlah sel Goblethipersekresi mukus

Saluran napas kecil

Recycled injury & repair dinding sal. napasremodeling (pe kolagen & jar. ikat) penyempitanlumen & obstruksi sal. napas

Parenkim paru

Destruksi parenkim emfisema sentrilobuler Vaskulerpulmonal, Penebalan dd pembuluh darah


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Pathophysiology


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p y gy

The different pathogenic mechanisms produce thepathological changes which, in turn, give rise tothe physiological abnormalities in COPD:

mucous hypersecretion and ciliary dysfunction,

airflow limitation and hyperinflation,

gas exchange abnormalities,

pulmonary hypertension,

systemic effects.

Pathophysiology of COPD


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A di t GINA


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According to GINA

What is the difference between asthma andCOPD (chronic obstructive lung disease)?

COPD is a collective name for chronicbronchitis and emphysema, two diseases

that are almost always caused by smoking.Many of the symptoms of COPD are similar to

those of asthma (e.g. breathlessness,wheezing, production of too much mucus,

coughing).


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COPD/PPOM


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COPD/PPOM

BRONCHITISKRONIS atau COPD

B


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type B

Bronkitis kronik adalah inflamasi

kronis saluran nafas yg ditandai dg

udema dan hiperplasi kelenjar sub

mucosal shg terjadi produksi

mukus berlebihan ke batang

bronchial akibatnya terjadi

peningkatan resistensi salpernafasaan

secara kronik atau berulang dengan

disertai batuk, yang terjadi hampir

setiap hari selama sekurangnya tiga

bulan dalam 1 tahun selama 2 tahunberturut turut..

Eti l i


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Etiologi

Faktor lingkungan :- Merokok

- Pekerjaan

- Polusi udara

-Infeksi berulang

Faktor host :

- usia

- jenis kelamin

- penyakit paru yang

sudah ada

CHRONIC BRONCHITIS


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Chronic bronchitis is defined as "persistent cough with sputumproduction for at least 3 months in at least two consecutiveyears".

The most important cause of chronic bronchitis is recurrent

irritation of the bronchial mucosa by inhaled substances, asoccurs in cigarette smokers.

The pathological hallmarks of chronic bronchitis are congestion

of the bronchial mucosa and a prominent increase in thenumber and size of the bronchial mucus glands. Copious mucusmay be seen within airway lumens. The terminal airways are

most susceptible to obstruction by mucus.

Pathophysiology of chronic bronchitis


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Irritants

Hyperplasia and hypertrophy ofmucous secreting cell

Thick mucous

Air trapping

Sticky coating Air way obstruction

Impaired ciliary function

Edema

Decrease mucous clearance

Bronchial wall thickness and

Lung defense system compromise inflammation

Vulnerable for infection More infection more mucus


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CHANGES IN LUNG VOLUMES

VENTILATION COST


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In COPD work of breathing is greater for any givenlevel of ventilation than normal.

VENTILATION

WORK OF

BREATHING

NORMAL COPD

SEVERE COPD

MODERATE COPDThe cost of work at a

given ventilation fornormal and COPD

patients (ACSM,

1998)


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Emphysema or

type A COPD


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type A COPD

Definition

Abnormal permanentenlargement of air spacesdistal to the terminalbronchioles, accompaniedby the destruction of the

walls and without obviousfibrosis

Emphysema is characterizedby loss of elasticity of thelung and abnormalpermanent enlargement ofair spaces with destructionof the alveolar walls andcapillary beds.

Eti l i


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EtiologiEmphysema

Smokingthe primary risk factorLong-term smoking isresponsible for 80-90 % ofcases.Prolonged exposures toharmful particles andgasesfrom:

passive smoke,Industrial smoke,Chemical gases, vapors,mists & fumesDusts from grains,minerals & other materials

Alpha 1-antitrypsindeficiency>>emphysemaGeneticsBronchitisAsthma

Pathophysiology


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Pathophysiology

Exposure to inhaled noxious particles & gasesinflammation imbalance of proteinases

and anti-proteinases

Dilatation & destruction

+ mucus secretion


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FIG. 1. Inflammatory mechanisms in COPD. Cigarette smoke (and other irritants) activate

macrophages in the respiratory tract that release neutrophil chemotactic factors,

including IL-8 and LTB4. These cells then release proteases that break down connective

tissue in the lung parenchyma, resulting in emphysema, and also stimulate mucus

hypersecretion. These enzymes are normally counteracted by protease inhibitors,

including 1-antitrypsin, SLPI, and TIMP. Cytotoxic T cells (CD8) may also be recruited and

may be involved in alveolar wall destruction. Fibroblasts may be activated by growth

factors releases from macrophages and epithelial cells. CTG, connective tissue growth

factor; COB, chronic obstructive bronchiolitis.

Pathophysiology


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Affects alveolar membrane Destruction of alveolar wall

Loss of elastic recoil

Over distended alveoli

Over distended alveoli Damage to adjacent

pulmonary capillaries

hdead space

Impaired passive expiration

Impaired gas exchange

Impaired gas exchange impaired expiration

hCO2

Hypercapnia

Respiratory acidosis

Damaged pulmonarycapillary bed hpulmonary pressure

hwork load for rightventricle

Right side heart failure (dueto respiratory pressure)

Cor Pulmonale

Gas Exchange is poor because


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Gas Exchange is poor because

Loss of alveolar structure base therebycausing decreased gas exchange surface area

Mechanically, elastanceis lost due to the

constant stretching of distal airways

Consequently, these patients are very

compliant, because the natural tendency for

the lung to collapse is inadvertently lost


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This V/Q mismatch results in relativelylimited blood flow through a fairly welloxygenated lung with normal blood gasesand pressures in the lung, in contrast to thesituation in blue bloaters. Because of lowcardiac output, however, the rest of the bodysuffers from tissue hypoxia and pulmonary

cachexia. Eventually, these patients developmuscle wasting and weight loss and areidentified as "pink puffers."

Di i f COPD


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109

SYMPTOMS

cough

sputumdyspnea

EXPOSURE TO RISKFACTORS

tobacco

occupation

indoor/outdoor pollution

SPIROMETRY

Diagnosis of COPD

GAS DARAH ARTERI

LABORATORY TEST

CHEST X-RAY

Spirometry: Normal and COPD


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Spirometry: Normal and COPD

0

5

1

4

2

3

Liter

1 65432

FVC

FVC

FEV1

FEV1

Normal

COPD

3.900

5.200

2.350

4.150 80 %

60 %

Normal

COPD

FVCFEV1 FVCFEV1/

Seconds

Normally, the left side of the


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heart produces a higher level of

blood pressure in order to pump

blood to the body; the right sidepumps blood through the lungs

under much lower pressure. Any

condition that leads to prolonged

high blood pressure in the arteries

or veins of the lungs (called

pulmonary hypertension) will be

poorly tolerated by the right

ventricle of the heart. When this

right ventricle fails or is unable to

properly pump against these

abnormally high pressures, this is

called cor pulmonale.

Prognosis ?


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Indikator: umur dan keparahan

Jika ada hipoksia dan cor pulmonale

prognosis jelek

Dyspnea, obstruksi berat saluran nafas, FEV1 25.000 / mm3 Empyema

- Netrophil > Pneumonia, TBC, Pancreatitis- Limphosit > TBC, limphoma, keganasan

- Eosinophil > Emboli , Parasit, Jamur

- Eritrosit 510 ribu/mm3 Pneumoni,

Keganasan

- Eritrosit 100 ribu / mm3 Keganasan,Trauma,

Infark Paru- Sel ganas ditemukan pada 5060 %

Keganasan

Gambaran Radiologi Efusi Pleura


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< 300 CC : Secara fisik tak ada perubahan.

Foto PA: sinus masih nampak lancip.

Foto Lat: sinus nampak mulai tumpul

> 500 cc : Gerak dada/ fremitus suara/fremitusraba menurun,suara ketok redup

> 1000 cc: dada cembung, egofoni positip

> 2000 cc: mediastinum terdorong


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Penatalaksanaan Efusi Pleura


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- Evakuasi cairan pleura / torakosentesisvolume pengambilan maksimal 1000 cc

setiap kali pengambilan

- Pemasangan WSD# Efusi Pleura massive

# Efusi Pleura haemorhagic

# Hematotoraks, Empyema# Chylotoraks, Chiliform

FARMAKOLOGI


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Antikolinergik inhalasi first line therapy, dosis harus cukuptinggi : 2 puff 46x/day; jika sulit, gunakan nebulizer 0.5mg setiap 4-6 jam prn, exp: ipratropium or oxytropiumbromide

Simpatomimetik second line therapy : terbutalin,

salbutamol Kombinasi antikolinergik dan simpatomimetik untuk

meningkatkan efektifitas

Metil ksantin banyak ADR, dipakai jika yang lain tidakmempan

Mukolitik membantu pengenceran dahak, namun tidak memperbaiki aliran udara masih kontroversi, apakah

patofisiologi-sist-pernafasan.ppt

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