93188048 patofisiologi sist pernafasan

7/27/2019 93188048 Patofisiologi Sist Pernafasan

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Tujuan dari Respirasiadalah untuk menyediakan oksigen bagiseluruh jaringan tubuh dan membuangkarbon dioksida ke atmosfer


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Hidung

Udara masuk disaring,dihangatkan dandilembabkan olehmukosa respirasi.

Partikel kasar disaringoleh rambut hidung.

halus: terjerat dalamlapisan mukus.

Udara masuk faring:bebas debu, suhusebanding suhu tubuh,kelembaban hampir100 %


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Rongga torax Paru adalah organ elastis terletak pada rongga

dada/torax. Paru dilapisi oleh lapisan tipis kontinu ygmengandung kolagen & jar elastis yg disebutPLEURA

Pleura Parietalis melapisi rongga dada sedang

Pleura viseralis melapisi paru . Rongga pleura: ruangan yg memisahkan pleura

parietalis & viseralis

Cairan pleura: lapisan tipis antara pleura parietalis

dg viseralis berfungsi memudahkan keduapermukaan tersebut bergerak selama pernapasan& untuk mencegah pemisahan torax & paru.

Tekanan rongga pleura < tekanan atmosfer: untukmencegah kolaps paru.


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Rongga torax

3 faktor yg mempertahankan tekanannegatif intrapleura normal:

1. Jaringan elastis paru memberikan kekuatankontinu yg cenderung menarik paru menjauh

dr rangka torax.2. Kekuatan osmotik yg terdapat di seluruh

membran pleura.

3. Kekuatan pompa limfatik.

Diafragma: otot berbentuk kubah ygmembentuk dasar rongga torax &memisahkan rongga tersebut darirongga abdomen.


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Anatomi SaluranPernapasan


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Anatomi SaluranPernapasan


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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 yangdikelilingi oleh jaringan kapiler batasantara cairan & gas membentuk teganganmuka yang cenderung mencegah

pengembangan saat inspirasi & cenderungkolaps saat ekspirasi. Alveolus dilapisi zat lipoprotein (surfaktan)

dapat mengurangi tengangan permukaan& resistensi saat inspirasi & mencegah

kolaps alveolus (expirasi).


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Bronchopulmonary segments

LobulesAlveolar wall cell types

LUNGS 2

terminal

bronchiole

respiratory

bronchiole

pulmonaryarterybranch

alveolar

sac

simple squamous epithelial cellmacrophage (dust cell)septal cell (produces surfactant)

Type I alveolarcell

Type II alveolar cellmaking surfactant

bloodcapillary

endothelialcell

macrophage

surfactant

respiratorymembrane


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Alveoli

Pembentukan & pengeluaran surfaktanoleh pneumosit tipe II disintesis secaracepat dari asam lemak yang diekstraksidari darah, dg kecepatan pergantian yg

cepat. Bila aliran darah ke paruterganggu (emboli) akibatnya jumlahsurfaktan pada daerah tersebutberkurang.

Produksi surfaktan dirangsang oleh

ventilasi aktif, volume tidal yg memadai,hiperventilasi periodik (cepat & dalam)yg dicegah oleh kons O2 yang tinggi(inspirasi).

Pemberian O2 kons tinggi jangka lama

(pasien dg ventilasi mekanik)


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Pernafasan terdiri dari 4proses :

1. Ventilasi : Keluar masuknya udara karenaadanya selisih tekanan yang terdapatantara atmosfer dan alveolus

2. Distribusi : Pembagian udara ke cabang-cabang bronkhus

3. Transportasi dan Difusi

- Transport O2 dan CO2 dalam darah dan cairan tubuh kedan dari sel

- Difusi O2 dan CO2 antara darah dan alveoli

Pertukaran gas-gas antara alveoli dankapiler dipengaruhi oleh tekanan parsial O2

& CO2 dalam atmosfer

4. Perfusi : Aliran darah yang membawa O2 ke


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JENIS RESPIRASI

1. RESPIRASI EXTERNAL

O2 DIBAWA DARI UDARA

LUAR SAMPAI KEKAPILER

2. RESPIRASI INTERNAL

O2 DARI KAPILER SAMPAIKE 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 (T1 T11)

thoracic volumepleural volumeintrapleural pressurelung volumeintrapulmonic 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

internalintercostals(11 pairs)

internal intercostals (11 pairs)rectus abdominisabdominal obliquestransversus abdominis

Forced expiration

thoracic volumepleural volume

intrapleural pressurelung volumeintrapulmonic pressure

air flow of the lungs

Process

external abdominalobliqueinternal abdominalobliquetransversus abdominis

rectus abdominis

760 mmHg

762 mmHg

elastic recoilsurface tension


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Perubahan diafragma saatinspirasi & ekspirasi


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Otot Pernapasan


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Compliance is the ease with which the lungs andthoracic wall can be expanded during inspiration.

COMPLIANCE

elasticitysurface 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, ANDRATES

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/minutealveolar ventilation rate = alveolar ventilation x breaths/minute

IRV

ERV

TV

RVmaximum

expiration

VC TLC

6000 ml

5000 ml

4000 ml

3000 ml

2000 ml

1000 ml

maximuminspiration


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Kontrol Pernapasan

Persarafan parasimpatis/ kolinergik (mll nervus

fagus) menyebabkan kontraksi otot polos bronkusshg menyebabkan bronkokonstriksi & peningkatansekresi kel mukosa & sel goblet.

Rangsangan simpatis ditimbulkan epinefrin mllreseptor adrenergik-beta2 menyebabkan relaksasi

otot polos bronkus, bronkodilatasi, &berkurangnya sekresi bronkus.

Sistem saraf nonkolinergik non adrenergik (NANC):melibatkan berbagai mediator seperti ATP, oksidanitrat, substance P, dan VIP (vasoactive intestinalpeptide) respon penghambatan, meliputi

bronkodilatasi, dan diduga berfungsi sebagaien eimban terhada fun si emicuan oleh


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Kontrol Pernapasan


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Signs and Symptoms ofPulmonary Disease

Dyspnea subjective sensation ofuncomfortable breathing, feelingshort of breath

Ranges from mild discomfort afterexertion to extreme difficultybreathing at rest.

Usually caused by diffuse andextensive rather than focalpulmonary disease.

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D j t D


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Derajat DyspneaTingkat Derajat Kriteria

0 Normal Tidak ada kesulitan bernapss kecuali denganaktivitas berat.

1 Ringan Terdapat kesulitan bernapas, napas pendek-pendek ketika terburu-buru atau ketikaberjalan menuju puncak landai.

2 Sedang Berjalan lebih lambat daripada kebanyakanorang berusia sama karena sulit bernapasatau harus berhenti berjalan untuk bernapas.

3 Berat Berhenti berjalan setelah 90 meter untukbernapas atau setelah berjalan beberapamenit.

4 Sangat berat Terlalu sulit bernapas bila meninggalkanrumah atau sulit bernapas ketika memakaibaju 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 beingforced 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 inbreathing

Retraction (pulling back) ofintercostal spaces

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BATUK

Batuk merupakan gejala terseringpenyakit pernapasan

Batuk merupakan reflex pertahanan yang

timbul akibat iritasi percabangantrakeobronkial

Batuk yang berlangsung lebih dari 3minggu harus diselidiki untuk

memastikan penyebabnya. Bronkhitis kronik, asma, tubercolosis danpneomonia merupakan penyakit yangsecara tipikal memiliki batuk sebagai

gejala yang mencolok


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Cough may result from:

Inflammation of lung tissue Increased secretion in response to

mucosal irritation

Inhalation of irritants Intrinsic source of mucosal disruption such as tumor invasion of bronchial wall

Excessive blood hydrostatic pressure

in pulmonary capillaries Pulmonary edema excess fluid passesinto airways

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When cough can raise fluid intopharynx, the cough is described as a

productive cough, and the fluid issputum.

Production of bloody sputum is calledhemoptysis

Usually involves only a small amountof blood loss

Not threatening, but can indicate a

serious pulmonary diseaseTuberculosis, lung abscess, cancer,

pulmonary infarction.

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Jari Tabuh

Jari tabuh adalah perubahanbentuk normal falang distal dankuku tangan dan kaki sertaditandai dengan

1.Kehilangan sudut kuku yang

normalnya 160 derajat.2.Rasa halus berongga padadasar kuku.

3.Ujung jari menjadi besar.

jari tabuh berhubungan dengan

peyakit paru (TB, abses paru,atau kanker paru). Penyakitkardiovaskuler (tetralogi fallotatau endokarditis infektif) ataupenyakit hati kronik


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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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Asthma

is a chronic inflammatorydisorder of the airways inwhichmany cells andcellular elements play arole

In susceptible individuals,this inflammation causesrecurrent episodes ofwheezing, breathlessness,chest tightness and

coughing,particularly atnight or in the earlymorning..

eosinophils

epithelial cells

neutrophils

Macrophages

T lymphocytes

mast cells

Cells


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Causes and Triggers

oAllergies such as to pollens, mold spores, petdander, 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)


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oGastroesophageal reflux disease

oChronic sinusitis or rhinitisoOSA (obstructive sleep apnoe)

oObesity

oAlergy bronchopulmonary

aspergilosis

COMORBID CONDITION


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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


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P fi i l i A


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Patofisiologi Asma


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gambar


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Faktor2 yang mengakibatkan obstruksi ekspirasi pada asmabronkial. A. Potongan melintang dari bronkiolus yangmengalami oklusi akibat spasme otot, mukosa yangmembengkak, 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 cause amore persistent pattern of inflammation

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


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Forced expiratory volume (FEV)

Volum

e(litres

(

Time (second

1 1 1 1

Asthma

patient

Normal subject

FEV1

FVC

Component

of

Classification of Asthma Severity (>12 yrs)Intermittent Pe sistent


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of

Severity

Intermittent Persistent

Mild Moderate Severe

Symptoms 2 d/wk

but not daily

Daily Throughout theday

Nighttimeawakening

1x/wk but not

nightly

Often 7x/wk

SABA use 2 d/wk

but not daily &

not >1x on any day

Daily Several times per

day

Interferencewith activity

NONE Minor limitation Some limitation Extremely limited

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 antagonistsDirect antagonistof mediators responsible for airway inflammation in asthma

Bronchodilators Provide symptomatic relief ofbronchospasm due to acute asthma exacerbation (short-acting agents)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 acute asthmaexacerbations. 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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Three Steps of Asthma Treatment

Step 1 - Control bronchospasm with short- acting b2 agonists orlong-acting salmeterol

Step 2- Control inflammation with inhaled corticosteroids orleukotriene antagonist

Step 3 - Control severe exacerbation with oral corticosteroids


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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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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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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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FAKTOR RISIKO


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Host:

- Genetik: Defisiensialpha 1 anti tripsinatau antiprotease

(menghambat aksi dari(menghambat aksi dari

enzym protease)enzym protease)

- Hipereaktivitasbronkus

Lingkungan: Asap rokok (faktor

risiko utama - sigaret) Partikel debu & bahan

kimia perindustrian Polusi udara Indoor air pollution from

heating and cooking withbiomass in poorly

ventilated dwellings Infeksi Status sosial

PATOGENESA


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PATOGENESA

Inflamasi /Keradangan kronis pd sal.napas, parenkim paru, sistemvaskuler paru pe makrofag,limfosit T (CD8+), netrofil releasemediator LB4, IL8, TNF

Imbalance proteinase anti

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 interplayThe 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.


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Pathophysiology of COPDPathophysiology of COPD


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According to GINA


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According to GINA

What is the difference betweenasthma and COPD (chronicobstructive lung disease)?

COPD is a collective name for

chronic bronchitis andemphysema, two diseases thatare almost always caused by

smoking. Many of the symptoms

of COPD are similar to those ofasthma (e.g. breathlessness,wheezing, production of too

much mucus, coughing).


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COPD/PPOM


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COPD/PPOM


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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


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Pathophysiology of chronic bronchitisPathophysiology of chronic bronchitis


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IrritantsIrritants

Hyperplasia and hypertrophy ofHyperplasia and hypertrophy ofmucous secreting cellmucous secreting cell

Thick mucousThick mucous

Air trappingAir trapping

Sticky coating Sticky coating Air way obstructionAir way obstruction

Impaired ciliary function Impaired ciliary function

EdemaEdema

Decrease mucous clearance Decrease mucous clearance

Bronchial wall thickness andBronchial wall thickness and

Lung defense system compromise inflammationLung defense system compromise inflammation

Vulnerable for infection More infection more mucusVulnerable for infection More infection more mucus


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VENTILATION COST


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In COPD work of breathing is greater forany given level of ventilation than normal.

VENTILATIONVENTILATION

WORK OFWORK OF

BREATHINGBREATHING

NORMAL COPDNORMAL COPD

SEVERE COPDSEVERE COPD

MODERATE COPDMODERATE COPDThe cost of work at aThe cost of work at a

given ventilation forgiven ventilation fornormal and COPDnormal and COPD

patients (ACSM,patients (ACSM,

1998)1998)


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Damage to the epithelium impairsthe mucociliary response that clearsbacteria and mucus. Inflammation

and secretions provide the

obstructive component of chronicbronchitis.

In contrast to emphysema, chronicbronchitis is associated with arelatively undamaged pulmonary

capillary bed.

or type ACOPD


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COPD

DefinitionDefinition Abnormal permanentAbnormal permanent

enlargement of airenlargement of airspaces distal to thespaces distal to theterminal bronchioles,terminal bronchioles,accompanied by theaccompanied by the

destruction of the wallsdestruction of the wallsand without obviousand without obviousfibrosisfibrosis

Emphysema isEmphysema ischaracterized by losscharacterized by lossof elasticity of the lungof elasticity of the lungand abnormaland abnormalpermanentpermanentenlargement of airenlargement of airspaces withspaces withdestruction of thedestruction of the

alveolar walls andalveolar walls and

Eti l i


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EtiologiEmphysema

Smokingthe primary riskfactorLong-term smoking isresponsible for 80-90% of cases.Prolonged

exposures toharmful particlesand gases from:

passive smoke,Industrial smoke,Chemical gases,vapors, mists &fumes

Dusts from grains,minerals & othermaterials

Alpha 1-antitrypsindeficiency>>emphysemaGenetics

Bronchitis

Pathophysiology


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Pathophysiology

Exposure to inhaled noxious particles &gases inflammationimbalance of proteinases and anti-

proteinases

Dilatation & destruction

1mucus secretion


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FIG. 1. Inflammatory mechanisms in COPD. Cigarette smoke (and otherirritants) activate macrophages in the respiratory tract that releaseneutrophil chemotactic factors, including IL-8 and LTB4. These cells thenrelease proteases that break down connective tissue in the lungparenchyma, resulting in emphysema, and also stimulate mucushypersecretion. These enzymes are normally counteracted by proteaseinhibitors, 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 growthfactors releases from macrophages and epithelial cells. CTG, connective

tissue growth factor; COB, chronic obstructive bronchiolitis.

Pathophysiology


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Affects alveolarmembrane Destruction of alveolar

wall Loss of elastic recoil Over distended alveoli

Over distendedalveoli Damage to adjacent

pulmonary capillaries dead space Impaired passive

expiration

Impaired gasexchange

Impaired gasexchange impaired expiration

CO2 Hypercapnia Respiratory acidosis

Damaged pulmonarycapillary bed pulmonary pressure

work load for rightventricle

Right side heart failure(due to respiratorypressure)

Cor Pulmonale

Gas Exchange is poor


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because

Loss of alveolar structure basethereby causing decreased gasexchange surface area

Mechanically, elastance is lost due tothe constant stretching of distalairways

Consequently, these patients arevery compliant, because the naturaltendency for the lung to collapse is

inadvertently lost


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This V/Q mismatch results inrelatively limited blood flowthrough a fairly well oxygenatedlung with normal blood gasesand pressures in the lung, incontrast to the situation in bluebloaters. Because of low cardiac

output, however, the rest of thebody suffers from tissue hypoxiaand pulmonary cachexia.Eventually, these patients

develo muscle wastin and


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Spirometry: Normal and COPDSpirometry: Normal and COPDSpirometry: Normal and COPDSpirometry: Normal and COPD


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Spirometry: Normal and COPDSpirometry: Normal and COPDSpirometry: Normal and COPDSpirometry: Normal and COPD

Liter

FVC

FVC

FEV

FEV

Normal

COPD

.

.

.

. %

%

Normal

COPD

FVCFEV FVCFEV/

Seconds

Normally, the left side of


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y,the heart produces ahigher level of blood

pressure in order to pumpblood to the body; the rightside pumps blood throughthe lungs under muchlower pressure. Anycondition that leads toprolonged high bloodpressure in the arteries orveins of the lungs (calledpulmonary hypertension)will be poorly tolerated by

the right ventricle of theheart. When this rightventricle fails or is unableto

properly pump against

these abnormally high

Prognosis ?


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Indikator: umur dan keparahan Jika ada hipoksia dan cor pulmonale

prognosis jelek

Dyspnea, obstruksi berat salurannafas, FEV1 Pneumonia, TBC,

Pancreatitis

- Limphosit > TBC, limphoma,

keganasan- Eosinophil > Emboli , Parasit,Jamur

- Eritrosit 5 10 ribu/mm3

Pneumoni,Keganasan

- Eritrosit 100 ribu / mm3 Keganasan, Trauma,

Gambaran Radiologi EfusiPleura


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Pleura

< 300 CC : Secara fisik tak adaperubahan.

Foto PA: sinus masih nampak lancip.

Foto Lat: sinus nampak mulai tumpul> 500 cc : Gerak dada/ fremitus

suara/fremitus raba menurun,suara

ketok redup> 1000 cc: dada cembung, egofoni

positip

> 2000 cc: mediastinum terdorong

Foto Thorax


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Foto Thoraks:Perselubungan Padahemitoraks

Dextra dengan sinus frenicuscostalis kanan tumpul

Penatalaksanaan EfusiPleura


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Pleura

- Evakuasi cairan pleura /torakosentesis

volume pengambilan maksimal

1000 ccsetiap kali pengambilan

- Pemasangan WSD

# Efusi Pleura massive# Efusi Pleura haemorhagic

# Hematotoraks, Empyema

# Chylotoraks Chiliform

FARMAKOLOGI


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Antikolinergik inhalasi first line therapy, dosisharus cukup tinggi : 2 puff 4 6x/day; jika sulit,gunakan nebulizer 0.5 mg setiap 4-6 jam prn,exp: ipratropium or oxytropium bromide

Simpatomimetik second line therapy :

terbutalin, salbutamol Kombinasi antikolinergik dan simpatomimetikuntuk meningkatkan efektifitas

Metil ksantin banyak ADR, dipakai jika yanglain tidak mempan

Mukolitik membantu pengenceran dahak,namun tidak

93188048 patofisiologi sist pernafasan

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