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PPOK (Penyakit Paru Obstruksi Kronis)

Definisi
• GOLD (Global Initiative for chronic obstructive
lung disease): COPD adalah suatu penyakit yang
ditandai dengan adanya hambatan aliran napas
yang tidak sepenuhnya refersibel. Hambatan
saluran napas tersebut biasanya bersifat progresif
dan berhubungan dengan respon inflamasi
abnormal paru terhadap partikel atau gas iritan.
Penyebab pembatasan saluran napas
COPD
• Irreversible:

-fibrosis dan penyempitan saluran napas

-hilangnya elastisitas oleh karena alfeoli telah rusak

• Reversible

-akumulasi sel-sel inflamasi, mukus, plasma eksudat pada


bronkus

-kontraksi otot polos sentral maupun perifer

-hiperinflasi dinamis selama exercise


Faktor Resiko
1. Host Faktor
• Genes (alpha1-antitrypsin deficiency)
• Hyperesponsive
• Lung growth (prematur)

2. Exposure
• Asap rokok (90%)
• Debu dan zat kimia di tempat kerja
• Infeksi (streptokokus, S. pneumonia, H. influenza)
• Status sosioekonomi
Yang termasuk dalam COPD
• 1. Bronchitis cronis
• 2. Emphisema
• 3. Bronchitis cronis dan emphisema
Bronchitis Cronis

• Keadaan dengan produksi mukus trakeobronkial yang


berlebihan sehingga menimbulkan batuk kronis berdahak
minimal 3 bulan dalam setahun, sekurang-kurangnya 2
tahun berturut-turut, tidak disebabkan penyakit lainnya.
• Obstruksi saluran napas adalah persistent dan irreversibel.
etiology
• Penyebab utama bronkitis kronis adalah
• asap rokok (90% kasus),
• infeksi saluran napas yang berulang,
• faktor genetik,
• inhalation chemical irritants.
Tanda dan gejala
1. Tanda utama bronkitis chronik adalah batuk
persisten dengan produktif sputum
2. Batuk dan sputum meningkat pada pagi hari
3. Dyspneu pada saat aktivitas
4. Wheezing
5. Tahap akhir: cor pulmonal/heart fail
• edema peripheral
• Distensi vena leher
Pathogenesis
• Faktor inisiasi (asap rokok 90%)

Kerusakan bronkus,
bronkiolus
bronkospasme
Hipersekresi mukus
infeksi

Obstruksi reversibel pada bronkus, bronkiolus

Continued and repeat Continued and repeated infection


injury (smoking)

Chronic inflamasi, Fibrosis mucous membrane,


hyperplasi bronchial mucus gland and goblet
cell, increase mucus production , increase
bronchial wall thickness, increase cilliary
dysfunction

Chronic bronchitis
diagnosis
A. History
1. Lifestyle : smoker
2. Weight : overweight
3. Onset symptom : after age 40 yr
4. Sputum : excessive, purulen
5. Cough : chronic, more severe in
morning
6. Dyspneu : mild to moderate
B. Keluhan pasien

1. Batuk kronis dengan seputum mukopurulen


2. Malaise
3. Nyeri otot
4. Fatigue
5. Insomnia
6. Loss of libido
7. Dyspneu (mild-moderate)
C. Tanda fisik
1. Edema : present
2. Cyanosis : present in advanced disease
3. Use of accesory muscle to breath: absent until end stage
4. Antero posterior chest diameter : normal
5. Auscultation of chest : wheezing, crackles, ronchi,
depend on the severity of disease
6. Percusion : normal
7. Jugular vein distention : present
8. Other : evidence of right-sided heart
failure ( cor pulmonal)
D. General diagnosis test
1. Chest radiografi:
increase bronchial vasculer marking, enlarge
horizontal heart
2. Artery blood gas analisys:
decrease PaO2 ( <65 mm HG, increase Pa
CO2)
3. ECG :
Right axis deviation, right ventriculer
hipertrofi, atrial arytmia
4. Hematocrit: polycitemia
Pasien
Radiology
E. Pulmonary finction test

• Residual folume : increase

• Total lung capacity : normal

• Forced expiratory volume: decrease

• Vital capacity : normal or slight decrease


right-sided heart failure
( cor pulmonal)
Cronic broncitis

Small pulmonary artery related to inflammation in the bronchial wall and


the compensatory spasm of pulmonary blood vessel from hipoxia,

Produce pulmonary hypertension

Right ventricular end diastolic pressure increase

Leading to right ventricular dilation and right sided heart failure


Manifestasi klinik
• Terjadi kelebihan cairan tubuh (edema)
• Jugular vena distensi
• Cyanosis ( stadium akhir)
Emphisema

• Emphisema adalah kelainan pada paru yang


ditandai dengan pembesaran abnormal yang
permanen pada rongga udara distal bronkial
terminal, disertai dengan kerusakan dinding
alveolus , tanpa adanya fibrosis
Etiology

Cigarette smoking (>70 pack-year)

Air polution

Occupation ( working with or near asbeston)

A1-antytripsin
• Emphisema cenderung berkembang dalam waktu
yang lama, dan sering terjadi pada seseorang dg
usia >50 th

• Merokok dg jumlah >70 bungkus / tahun


merupakan faktor resiko tinggi terjadi PPOK
• proses penuaan normal, mulai sekitar usia 30,,
mencerminkan perubahan serupa dengan
yang terlihat pada emfisema :

Loss of alveoli

Increase in the size of alveolar duct

Loss of gas exchanging surface area (4% per


decade), and decrease bronchial muscle
• Ketika emphisema terjadi pada usia muda-
dewasa, atau usia <50 th pada perokok

Deficiency A1-antitrypsin

Penyakit herediter yang ditandai dengan


penurunan jumlah A1 antitrypsin pada serum (25-
50 mg/dl)

<2% pasien emphisema


• A1-antitrypsin adalah suatu enzim yang berfungsi
sebagai pelindung jaringan alveolus dari kerusakan
yang disebabkan oleh zat proteolisis (protease)
dari ( neutrophil, macrofagh ).
Type emphisema
1. Centriacinar ( centrilobuler emphisema)
• Dilatasi pada respiratory bronkhiolus
• Terjadi pada perokok berat dan berhubungan
dengan bronkitis kronis
2. Panacinar (Panlobuler) emphisema
• Dilatasi pada bagian peripheral ( duktus alveolus
dan alveolus)
• Berhubungan dengan A1 antitripsin deficiency
3. Paraseptal emphisema ( dilatasi distal acinus)
4. Irreguler emphisema (irreguler pd acinus karena
terbentuk scar)
Panacinar emphisema Centriasinar emphisema
patogenesis
•Destruction of alveolar tissue
and septa
•Increased mucus secretion
•Inflammation in the
bronchiolus
•Impaired in air way clearence
•Loss of radial traction with
collapse of bronchial leading to
air trapping
Manifestasi klinis
1. Dyspneu is usually the first symptom
2. Weight loss
3. Barrel chest
4. Prolong expiration
5. Sits forward in a hunched-over position
6. Breathes trough purs lips
7. Pink puffer
Pink puffer
Barrel chest
diagnosis
A.History
1. Lifestyle : smoker
2. Weight : weight loss
3. Onset symptom : after age 50 yr
4. Sputum : mild, mucoid
5. Cough : minimal or absent
6. Dyspneu : progresif exertion dyspneu
Patient complain
• Dyspneu on exertion,
• fatigue (kelelahan) ,
• insomnia
C. Tanda fisik
1. Edema : absent

2. Cyanosis : absent

3. Use of accesory muscle to breath: present

4. Antero posterior chest diameter : barrel chest

5. Auscultation of chest : decrease breath sound,

heart sound, prolong expiration

6. Percusion : hyperersonance

7. Jugular vein distention : absent

8. Other : purs lips breathing


D. General diagnosis test
1. Chest radiografi:
hyperinflation, flat, low diafragma, normal or
small vertical heart
2. Artery blood gas analisys:
decrease PaO2 ( 60-80 mm HG), normal or
increase Pa CO2 (increase with advancing
disease)
3. ECG :
normal or tall symmetrical P wave,
tachycardi if hypocix
4. Hematocrit: normal
E. Pulmonary finction test

• Residual folume : increase

• Total lung capacity : increase

• Forced expiratory volume: decrease

• Vital capacity : decrease


Derajat PPOK
1. Pasien beresiko
• chronic symptom : batuk, sputum/dyspneu
• Exsposure to risk factor: merokok, polusi
• Normal spirometry:
FEV1/FVC pasca bronchodilator >70%
FEV1 ≥80%
2. PPOK RINGAN
• FEV1/FVC < 70%
• FEV1 ≥80%
• WITH OR WITHOUT SYMPTOMS

3. PPOK SEDANG
• FEV1/FVC < 70%
• 50%≤FEV1<80%
• WITH OR WITHOUT SYMPTOMS
4. PPOK BERAT
• FEV1/FVC < 70%
• 30%≤FEV1<50%
• WITH OR WITHOUT SYMPTOMS

5. PPOK SANGAT BERAT


• FEV1/FVC < 70%
• FEV1<30% OR FEV1<50%
• Predicted plus chronic respiratory failure
DIAGNOSA BANDING

1. Asma bronchial

2. Bronkiektasis

3. Tuberculosis

4. CHF (Congestive Heart Failure )


1. Asma bronchial

• Adalah penyakit inflamasi kronis pada saluran


nafas yang menyebabkan gejala berulang yi:
wheezing, sesak nafas, dada terasa sesak, dan
batuk, terutama pada malam hari, atau pada
pagi hari.
• Gejala tersebut berhubungan dengan
bronchokontriksi dan airflow limitation
(pembatasan saluran nafas) yg bersifat
reversibel (spontan atau dg treatment)
Type asthma
1. Atopic asthma
 Begin in childhood
 A positive family history
 Asthmatic attack are often preceded by
allergy rinitis, urticaria
 Trigger by environmental antigent : dust,
pollen, food.
allergen
pathogenesis
macrophage

CD4 sell

TH2 cell

B sell IGE Mast sell


eosinophil

mediator mediator

Bronchospasme neutrophil
Monosit Damage
Increase vascular permiability
Limphosit ephitelium
Mucus production
Basofil
Immediate phase
Late phase ( 4-8 hours)
(minutes)
2. Nonatopic asthma
Trigger by respiratory tract infection
Virus ( Rhinovirus, parainfluenza Virus),
bacteri.
A positive family history is uncommon
Serum IGE normal
No other associated allergies
Skin test are negative
• 3. drug induce asthma

aspirin-inhibiting COX pathway of asam


arachidonat-without affecting
lipoxygenase route- leukotrin-
bronchokontriksi
Tanda Klinis
• sesak nafas,
• wheezing, tachicardi, tachypneu
• dada terasa sesak,
• Batuk dan peningkatan sputum ( thick/kental,
scant/sedikit, sticky/lengket)
• ( beberapa pasien dg batuk kering dan yg lainnya dg
batuk produktif.)

 serangan asthma berlangsung hingga beberapa jam dan


diikuti oleh batuk yang berkepanjangan.
diagnosis
1. Pemeriksaan fisik
• Sesak napas, wheezing, tachicardi, tacipneu, batuk.
2. Pemeriksaan sputum
• Charcot-leyden cristal (eosinophil membrane),
eosinophil.
3. Spirometri
• Airflow obstruction is indicate by FEV1/FVC <75%
4. Pemeriksaan darah: peningkatan sell darah putih,
eosinophil.
5. Radiographi
• Normal atau hyperinflasi dg diafragma mendatar
pada progresif disease.
Bronchiektasis
Bronkiektasis adalah dilatasi dari bronchi
Anak anak mempunyai resiko tinggi
bronchiktasis karena faktor anatomi saluran
nafas: small (kecil), soft (lunak,lemah), elastic
bronchi.
Bronchi pd anak anak sangat mudah
mengalami kerusakan : overinflasi dan distensi
karena inflamasi dan inveksi
patogenesis
Inflamasi dan infeksi berulang ( H. Influenza)
Inflamasi menyebabkan kerusakan dinding
central bronchi dan perifer bronchi dan
bronchiolus = persistent dilation of the
medium-size bronchi and bronchiolus
Kerusakan ephitel cillia, squamous cell
metaplasia, pembentukan pus,
Menyebabkan obstruksi saluran nafas
Manifestasi klinik
• Child ussualy present:
1. Chronic productive cough
2. Copious amount of purulent
3. Foul-smelling
4. Green or yellow sputum
5. Other clinic feature: hemoptysis, ronchi, bad
breath, skin pallor.
Diagnosis
1. History of chronic productive cough
2. Produce copious amounts of foul-smelling,
purulen sputum
3. Radiografi: increase bronchial marking,
thickening of bronchial walls
4. Pulmonary function test: decrease airflow
and vital capacyti in advanced cases
5. Arteri blood gas: hypoxemia (decrease PaO2),
hypercapnea (increase PaCO2).
CHF (Congestive Heart Failure )

Penyebab utama CHF adalah ischemic


cardiomiopathy dan hypertensi

Manifestasi klinis, CHF dibagi 2:

Left-sided heart failure

Rigth-sided heart failure


Left-sided heart failure
Disebabkan oleh:
1. Left ventrikel infarction
2. Cardiomiopaty
3. Aortic
4. Systemic hypertension
patofisiology
Left Ventricular Failure

Backward effect Forward effect

Decrease ejection fraction Decrease cardiac output

Increase left ventricel preload

Increasi left atrium pressure Decrease tissue


RAS
perfusion
activation
Increase pulmonary pressure

Fluid
Increase right ventriculer after load Pulmonary retention
congestion

Right ventricular
hypertrophi
Backward effect Forward effect
1.Dyspneu on exertion 1. Fatigue (kelelahan)
2.Orthopneu 2. Oliguria
3.Cough 3. Increase heart rate
4.Paroxysmal nocturnal 4. Restlessness (gelisah)
dyspneu 5. Confusion
5.Cyanosis 6. anxiety
6.Basilar crackles
Right ventricular failure
• Penyebab:
1. Infark ventrikel kanan
2. Penyakit paru
3. Semua penyebab gagal ventrikel kiri
Patogenesis
Right Ventricular Failure

Backward effect Forward effect

Decrease ejection fraction Decrease output to left ventricle

Increase right ventricel preload


Decrease left ventricle
Increasi right atrium pressure Cardiac output

Sistemic congestion
RAS Decrease tissue
actifation perfusion

hepar splen gastroin Ren Lower Fluid retention


testinal extremitas
Backward effect Forward effect
1.Hepatomegali 1. Fatigue
2.Ascites 2. Oliguria
3.Splenomegali 3. Increase heart rate
4.Anorexia 4. Restlessness (gelisah)
5.Subcutan edema 5. Confusion
6.Vena jugular distensi 6. anxiety
TBC (Tuberculosis)
• Kuman penyebab :
mycobakterium tb (bakteri aerob, bentuk
batang, tahan asam).
• Cara penularan :
Kuman masuk secara inhalasi (<5mikrometer)
pada saat pasien batuk, bersin, bicara.
pathogenesis
M.Tuberculosis

Jaringan Paru

Fagosit alveolar
macrofagh

dindingM. TBC
( arabinomanan)

Menghambat aktifasi
macrofagh

Sel T CD4 Melisiskan


Multiplikasi M.TBC
sel terinfeksi
dimacrofagh
TNF Peningkatan
Ghon tubercle macrofagh
Manifestasi klinis
Batuk kronis >14-21 hari
( batuk kering- berminggu minggu/ berbulan
bulan Purulent sputum- batuk darah )
 demam subfebris (demam influenza)
Berkeringat pada malam hari
 malaise (anoreksia, BB turun, sakit kepala,
nyeri otot)
Sesak nafas ( penyakit yg sudah lanjut)
TB Suspects

Sputum AFB Microscopy

Two or three Only one Three


smears + smear + smears -
Non anti TB
antibiotic
X-ray and Repeat
medical officer’s AFB No improve improve
judgment

One or more All


smears + smears -

X-ray and
medical officer’s
judgment

No TB
YES TB
Management of COPD
1. Farmakology
A. Bronchodilator
anticholinergic,β2-adrenergic reseptor agonist,
methylxanthin
B. Cortichosteroid
C. Antibiotic
2. Non-farmacology
Reducing risk factors, pulmonary
rehabilitation, oxygen terapy,
3. Surgical therapy
Bronchodilator
A. Inhaled Anticholinergics
 Effect: decrease bronchoconstriction and
glandular mucus
 Short-acting inhaled anticholinergic
-such as : ipratropium
-maximum bronchodilation in 1-2H, maintained
approximately 4H
 Long-acting inhaled anticholinergic
-such as: tiotropium
-result in prolonged bronchodilation for 24H or
more
-dose: once-daily dosing regiment
COMBIVENT® GENERIC
Ipratropium Ipratropium and Ipratropium
Albuterol

• Open airways by relaxing tight muscles POSSIBLESIDEEFFECTS


around them. • Coughing
• Always inhaled. • Dry mouth
• Available as metered-dose inhalers, dry • Nausea
powder inhaler, or as a liquid for nebulization. • Headache
• Most often used together with short-acting
or long-acting beta2-agonists.

Anticholinergics – Short-Acting and Long-Acting


B. Inhal β2-adrenergic reseptor agonist
 Effect : induce bronchodilation

 Short-acting B2-adrenergic receptor agonis SABAs


-such as: terbutalin&albuterol
-as needed basis to relieve symptoms because a rapid
onset of action.
-provide effect bronchodilation 4-6H
Albuterol Albuterol and Ipratropium

Open airways by relaxing tight muscles around POSSIBLESIDEEFFECTS


them. • Rapid heartbeat
• Usually inhaled, although occasionally taken • Nervousness
as tablets. • Tremors and shakiness
• Available as metered-dose inhaler, dry • Nausea
powder inhaler, or as a liquid for nebulization. • Dry mouth and throat
• Carry the inhaler with you wherever you go • Increased blood pressure
for quick relief from sudden shortness • Muscle weakness
of breath. • Decreased blood potassium level

Beta2-Agonists – Short-Acting
 Long-acting β2-adrenergic receptor agonists (LABAs)
- formoterol and salmeterol
- maintenance therapies for the long-term prevention and
reduction of COPD-related symptoms
-effect >12H
Open airways by relaxing tight muscles around
them.
• Often dry powdered inhalers, although they
are occasionally taken as tablets.
• The inhaled medicines are only taken twice a
Salmeterol day.
Formoterol • Not to be used for quick relief of shortness of
breath.

POSSIBLESIDEEFFECTS
(Very uncommon)
• Racing heart
• Tremors (shaking)
• Nervousness (gelisah)

LONG-ACTING BETA2 AGONISTS


C. Methylxanthines.
 such as : aminophylline and theophylline
 use of these agents is considered controversial because: third-line
treatment option after inhaled β2-agonists and anticholinergic agents
because wide range of dose-related toxic effect & its limited clinical
efficacy.
 Adverse events associated with methylxanthine treatment include
possible fatal atrial and ventricular arrhythmias, convulsions,
headaches, insomnia, nausea and heartburn.
 theophylline continues to be used in the treatment of COPD
primarily because of its low cost
Bronchodilator Combination Therapy
 Combined treatment with a β2-adrenergic receptor agonist, an
anticholinergic agent, and/or theophylline have been shown to provide
additional improvements in lung function and health status compared with
single-agent therapy for COPD.

 Results of a study conducted by van Noord et al.demonstrated that


combination therapy with formoterol plus tiotropium improved
pulmonary function, as assessed by several lung function parameters (e.g.
FVC and FEV1), more than improvements achieved with either component
alone.
Stage III to stage IV COPD

• Oral corticosteroids (OCS) and ICS are used as add-on therapy in very specific
situations in the management of stable COPD.

• The 2006 GOLD guidelines recommend ICS therapy with agents such as
beclomethasone dipropionate, budesonide, fluticasone propionate, mometasone
furoate and triamcinolone acetonide for the treatment of patients with advanced
COPD (FEV1<50% predicted) who experience repeated exacerbations.
PULMICORT Beclomethasone
Fluticasone
budesonid®

Reduce inflammation and swelling of the


airways.
• Because they are inhaled, they generally only
affect your lung and airways,
not your entire body.

Inhaled Steroids
influenza vaccination
• The influenza vaccine has been shown to reduce serious illness
for patients with COPD by as much as 50%.

• Pneumococcal vaccine is also recommended for patients


>65years old = to reduce pneumococcal pneumonia in
patients with COPD
Non-pharmacologic Therapy for COPD
A. Reducing Risk Factors

• Smoking cessation
• Reducing and eliminating occupational exposures to
airborne pollutants
• Consistent and persistent patient education and
counselling

B. Pulmonary Rehabilitation

• exercise training, nutritional counselling, and patient


education
• Exercise training should include aerobic and resistance
exercises to improve aerobic capacity and muscle
strength
Oxygen Therapy
• Oxygen therapy decrease pulmonary hypertension, increases
exercise capacity and lung function, improves the mental and
emotional states of patients.

• Surgical Options

• Lung volume reduction surgery (LVRS), Lung transplantation


Managing COPD Exacerbations

• Patients who experience acute exacerbations


commonly present with increased breathlessness,
wheezing, tightness in the chest, increased cough
sputum production, change in colour and tenacity of
sputum, and fever.

• associated with infections (S.Pneumonia, H.influenza)


of the tracheobronchial tree and with air pollution.