1

z
Sistem Respirasi
dr. Nur Syamsi, M.Sc.
 TzU J U A N P E M B E L A J A R A N
2

 Memahami & menjelaskan anatomi sistem pernapasan

 Memahami & menjelaskan fisiologi sistem pernapasan

 Memahami & menjelaskan mekanisme fungsi sistem pernapasan

 Memahami & menjelaskan regulasi fungsi sistem pernapasan

 Memahami & menjelaskan hubungan fungsi sistem pernapasan

dengan sistem lain

 Memahami & menjelaskan patofisiologi gangguan sistem

pernapasan

 Memahami & menjelaskan farmakologi & terapi gangguan sistem

pernapasan

 Memahami & menjelaskan pengkajian fisik sistem pernapasan

3 The Respiratory system consist of :
z
I. Structurally II. Functionally
1. The upper respiratory system 1. The conducting zone
a. Nose a . Nose d. trachea
b. Pharynx ( throat) b. pharynx ( throat) e. bronchi
c. Larynx c. larynx f. bronchioles
2. The lower respiratory system and terminal
a. Trachea bronchioles
b. Bronchi  filter, warm, moisten air and conduct it
c. Lungs into the lungs
2. The respiratory zone
a. respiratory bronchioles
b. alveolar ducts
c. alveoli
 gas exchange between air and blood
4 Overview of the respiratory system
z

Nasal cavity
filters, warms, and moistens air
Pharynx
passageway where pathway
for air and food cross
Upper
Glottis
Respiratory
space between the vocal chords;
Tract
opening to larynx
Larynx
(voice box); produces sound

Trachea
(windpipe); passage of air
to bronchi

Bronchus
passage of air to lungs

Bronchioles
Lower passage of air to alveoli
Respiratory
Tract Lung
contains alveoli (air sacs);
carries out gas exchange

Diaphragm
skeletal muscle; functions
in ventilation

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
5

z
6

z
7

z
 Upper respiratory tract
8

 Nose
sinus
 Pharynx
nasal cavity
sinus
 Larynx
hard tonsil
palate pharynx

nasopharynx
nares
uvula
mouth
tongue oropharynx
tonsils
epiglottis
laryngo-
pharynx
glottis

larynx esophagus

trachea

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
9

HIDUNG

 Bag internal & eksternal

 Bag internal : rongga berlorong yg dipisah mjd rongga hidung ka

& ki o/pembagi vertikal yg sempit  SEPTUM

 Lendir disekresi o/sel2 goblet

 Hidung olfaktorius
10

FARING

 Tuba yg menghub nares & rongga mulut ke laring

 Nasofaring : disebelah posterior hidung & atas palatum mole

 Orofaring : fausial/palatin, tonsil

 Laringofaring : memanjang dr tulang hioid ke kartilago krikoid

 Fungsi faring u/ menyediakan sal pd traktus respiratori & digestif

 Upper respiratory tract
11
Laring
z

 Pria: 5 cm, wanita lebih kecil,

bayi letaknya tinggi. base of
tongue
 Cartilago: Epiglottis
Vocal
 Cartilago thyroidea (Adam’s cords
apple)
 Cricoidea glottis

 Arytenoidea

 Epiglotis © CNRI/ Phototake

 Cavitas laryngis:
 2 plica vestibuli  rima
vestibuli
 2 plica vocalis  rima glotidis
 menghasilkan suara

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
12

 Fungsi utamanya trjd nya vokalisasi

 Laring melindung jln nafas bwh dr obstruksi benda asing & memudahkan batuk

 Epiglotis : menutupi ke arah laring saat menelan

 Glotis : ostium antara pita suara dlm laring

 Kartilago tiroid : kartilago terbesar pd trakea, sbgn membentuk jakun (adam”s

apple)

 Kartilago krikoid : satu2 cincin kartilago yg komplit dlm laring

 Kartilago aritenoid : gerakan pita suara

 Pita suara melekat pd lumen laring

 Lower respiratory tract
13

Trachea
(windpipe); passage of air
to bronchi

Bronchus
passage of air to lungs
Lower
Respiratory
Bronchioles
Tract passage of air to alveoli

Lung
contains alveoli (air sacs);
carries out gas exchange

Diaphragm
skeletal muscle; functions
in ventilation

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
 Lower respiratory tract
14

The trachea Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or
display.
cilia goblet cell
 A tube, often called the
windpipe, that
connects the larynx
with the 1° bronchi

 Made of connective
tissue, smooth muscle
and cartilaginous rings

 Lined with cilia and

2,865
mucus that help to © Dr. Kessel & Dr. Kardon/Tissues & Organs/Visuals Unlimited
X
keep the lungs clean
15
16

BRONCHUS
 Cab dr trachea (bronchus dextra & sinistra)

 Bronchus dextra > pendek drpd sinistra

 Bronchus bronchiolus vestibulum atrium2 alveoli

PARU-PARU
17

 Paru-paru (pulmo):
 Pulmo dexter  3 lobus
 Pulmo sinister  2 lobus
 Apex pulmonis
 Basis pulmonis
 Hilus pulmonalis
 Tempat keluar masuknya
bronchi, vasa darah, vasa
lymphatica dan nervi
 Terdapat alveoli
18
SELAPUT PARU
z

 Pleura parietale
 Pleura viscerale
19

z
Pertukaran Gas (Respirasi)
Fungsi utama dari sistem pernapasan  mengambil oksigen dan megeluarkan karbon
dioksida. Pertukaran gas ini disebut respirasi dan terjadi antara atmosfer, darah, dan sel
dalam fase yang berbeda :

 Ventilasi pulmonari  pernapasan

 Udara dihirup ke dalam paru-paru dan kemudian dikelurkan dari paru-paru

 Respirasi eksternal (respirasi pulmonari)

 Pertukaran gas antara paru-paru dan darah  darah mengambil O2 dan melepaskan CO2

 Respirasi internal (respirasi jaringan).

 Pertukaran gas antara darah dan sel jaringan  darah melepaskan O2 dan mengikat CO2

 Respirasi seluler (oksidasi) adalah reaksi metabolik yang terjadi dalam sel.
 menggunakan oksigen dan glukosa  menghasilkan energi dalam bentuk ATP + CO2
20

Olfaction (penciuman/penghidu)

 hidung  reseptor penciuman

Produksi suara.

 Getaran partikel udara menghasilkan suara. Ketika manusia

mengeluarkan udara ke luar, udara melewati laring (kotak suara) dimana
terdapat membran khusus yang disebut pita suara. Udara menyebabkan
pita suara bergetar dan menghasilkan bunyi yang kemudian diubah
menjadi kata oleh otot faring, muka, lidah, dan bibir. Faring, rongga
hidung, dan sinus paranasal juga bertindak sebagai tempat resonansi
untuk suara.
 21
Komponen z Fungsi
Lubang hidung memungkinkan udara untuk masuk dan keluar rongga hidung; filter rongga
Hidung
hidung, menghangatkan, dan melembabkan udara yang dihirup
Membawa udara antara rongga hidung dan laring; filter, menghangatkan, dan melembabkan
udara yang dihirup; berfungsi sebagai jalan terusan untuk makanan dari mulut ke
Faring
kerongkongan; menyetarakan tekanan udara dengan telinga tengah melalui tabung
pendengaran
Membawa udara antara faring dan trakea; mengandung pita suara untuk menghasilkan suara
Laring
dalam vokalisasi; mencegah obyek masuk trakea

Membawa udara antara laring dan bronkus; filter, menghangatkan, dan melembabkan udara
Trakea
yang dihirup

Membawa udara antara trakea dan bronkiolus; filter, menghangatkan, dan melembabkan udara
Bronkus
yang dihirup

Bronkiolus Mengatur laju aliran udara melalui bronkokonstriksi dan bronkodilatasi

Alveoli Memungkinkan pertukaran gas antara udara di alveoli dan darah dalam kapiler sekitarnya
Tabel. Komponen respirasi dan fungsinya
22

MEKANISME PERNAPASAN
 Inspirasi (menarik napas)
 otot-otot interkostal eksternal menggerakkan tulang rusuk ke atas dan keluar.
 otot diafragma berkontraksi dan membentuk kubah yang datar
 meningkatkan ruang di paru-paru dan menyebabkan udara secara otomatis ditarik
ke dalam paru-paru

 Ekspirasi (mengeluarkan napas)

 otot-otot interkostal eksternal berelaksasi dan tulang rusuk kembali ke posisi
istirahat.
 Diafragma berelaksasi, kembali ke bentuk kubah aslinya.
 menyebabkan ruang di paru-paru menjadi lebih kecil, memaksa udara keluar dari
paru-paru
23

Gbr. Mekanisme pernapasan

z
Gas Exchange in Lungs & Tissues
Regulation of hydrogen ion concentration by the
z Respiratory System
z
z
28

MASALAH PERNAPASAN
1. Hipoksia (anoksia)
 @ defisiensi oksigen, kondisi berkurangnya kadar oksigen di badingkan
kadar normalnya secara fisiologis dalam jaringan dan organ.

 terjadi akibat insufisiensi oksigen dalam atmosfer ; anemia (insufisiensi sel

darah merah); gangguan sirkulasi darah ; penyakit paru; yang mengganggu
ventilasi pulmonary ; atau keberadaan zat toksik seperti karbonmonoksida
atau sianida di dalam tubuh.
29

MASALAH PERNAPASAN
2. Hiperkapnia
 @ peningkatan kadar CO2 dalam cairan tubuh dan sering disertai hipoksia. CO2
berlebih meingkatkan respirasi dan konsentrasi yang hidrogen, yang akan
menyebabkan asidosis (kadar asam berlebih)

3. Hipokapnia
 @ penurunan kadar CO2 dalam darah, biasanya terjadi akibat hiperventilasi
(pernapasan cepat) dan pengeluaran CO2 >>>  menyebabkan terjadinya
alkalosis (jumlah bikarbonat berlebih) dalam cairan tubuh.

4. Asfisia atau Sufokasi

 @ suatu kondisi hipoksia atau hiperkapnia akibat ketidakcukupan ventilasi
pulmonary
30

z
Setelah udara masuk ke dalam alveoli terjadi pertukaran gas:

 Bikarbonat (HCO3-) masuk ke dalam eritrosit, bertukar dengan keluarnya

ion Cl.

 Segera setelah oksigen (O2) terikat dengan hemoglobin, HCO3-

membentuk asam karbonat. Karena adanya enzim karbonat-anhidrase
CO2 dikeluarkan ke dalam alveoli.

Di dalam jaringan terjadi hal sebaliknya

 CO2 hasil metabolisme masuk ke dalam eritrosit.

 Hemoglobin merupakan buffer utama terhadap H+

 Dengan adanya enzim karbonat-anhidrase CO2 berikatan dengan air

(H2O) membentuk asam karbonat (H2CO3), tetapi segera berdisosiasi
menjadi H+ dan HCO3-.
31

CO2 + H2O H2CO3 H ++HCO3-

z
32

Acid Base imbalance

33

z
Acid-base disturbance
I. Respiratory acidosis II. Respiratory alkalosis

Common Cause : Common Cause :

 Respiratory depression (drugs,  Hyperventilation (emotions, pain,
central nervous system trauma) respiratory overventilation)

 Pulmonary disease (pneumonia, Mode of compensation

chronic obstructive pulmonary
disease, respiratory  Kidneys will excrete increased
underventilation) amounts of HCO3 to lower pH

Mode of compensation
 Kidneys will retain increased
amounts of HCO3 to increase pH
34

III. Metabolic acidosis IV. Metabolic alkalosis

Common Cause : Common Cause :

 Diabetes, shock, renal failure,
intestinal fistula
Mode of compensation
 Lungs "blow off" CO2 to raise pH
 Sodium bicarbonate overdose,
prolonged vomiting, nasogastric
drainage
 Hypokalemia- K & H change
 Hypochloremia- HCO3 cation
Balance
 Excessive streoids- Increases
Renal clearance

Mode of compensation
 Lungs retain CO2 to lower pH
35

z
 Respiratory Regulation

 When breathing is increased,

the blood carbon dioxide level
decreases and the blood
becomes more Base
 When breathing is decreased,
the blood carbon dioxide level
increases and the blood becomes more Acidic
 By adjusting the speed and depth of
breathing, the respiratory control centers
and lungs are able to regulate the blood pH
minute by minute
36

 Kidney Regulation

 Excess acid is excreted

by the kidneys, largely in
the form of ammonia
 The kidneys have some
ability to alter the
amount of acid or base
that is excreted, but this
generally takes several
days
37

z
GANGGUAN PADA SISTEM RESPIRASI
z

Batuk
 proses eksipirasi eksplosif yg memberikan
mekanisme proteksi normal u/
membersihkan saluran pernafasan dari
sekresi a/ benda asing bukan penyakit 
gejala atau tanda adanya gangguan pada
saluran pernafasan
z
Patofisiologi Batuk

 Melibatkan kompleks rangkaian refleks yang bermula dari

stimulasi terhadap reseptor iritan
z

OBAT BATUK
Antitusif
Ekspektoran
Mukolitik
 z
ANTITUSIF
Codein, Dextromethorphan, Benzonatate, Difenhidramin
Hcl
 Menekan batuk kering

 sentral (pusat batuk/medula) 

meningkatkan ambang batas respon pusat menurunkan
batuk frekuensi dan

 perifer (tr. respiratorius)  blokade intensitas

reseptor sensorik  menghambat batuk
peregangan paru
z
Codein

Pharmacodynamics

 bekerja dgn cara menekan pusat batuk (medula)  menghambat

impuls batuk

Pharmacokinetics

 Absorption
 gastrointestinal tract  oral

 Distribution
 tersebar luas pd jaringan tubuh, melewati placenta & jg tdpt di ASI.
Ikatan dgn prot. plasma 7% - 25%.
z
Codein

 Metabolisme
 di hepar, 70% - 80% conjugation with glucuronic acid  codeine-
6-glucuronide (C6G) ; 5% – 10% by O-demethylation 
morphine ; 10% N-demethylation to norcodeine

 Excretion
 ± 90% of the total dose of codeine is excreted through the kidneys

 t½ codein dan metabolitnya  ± 3jam.

z
Codein

 Side Effects
 Constipation, Drowsiness, Nausea/vomiting, Addictive potential

 Cough suppression by opioids may allow accumulation of

secretions and lead to airway obstruction

 Dosis
 Adult: 15-30 mg 3-4 times daily.

 Child : 2-5 yr 3 mg; 6-12 yr 7.5-15 mg. Doses to be taken 3-4

times daily
z
Codein

 Contraindication
 Acute or severe bronchial asthma
 Significant respiratory depression
 use of MAOIs within the last 14 days
 Known or suspected gastrointestinal obstruction, including paralytic
ileus
 Hypersensitivity to codeine

 Interaction
 Drugs interaction : MAO inhibitors
 Food interaction : Alcohol
z
DMP

Pharmacodynamics

 bekerja dgn cara menekan pusat batuk (medula) 

menghambat impuls batuk

Pharmacokinetics

 Absorption : GI tract.

 Distribution : Terdistribusi luas pd jaringan tubuh

 Metabolism : di hepar  demetilasi mjd dextrorphan (active)

 Excretion : >>> urine

z
DMP

 Contraindications:
 penggunaan MAO inhibitor selama 2mgu  dpt me↑kan
serotonergic effect of Dextromethorphan. This may cause
serotonin syndrome.
 ≠ u/ mengobati batuk yg disebabkan o/ merokok, asthma, or
emphysema

 Side Effects:
 severe dizziness, anxiety, restless feeling, or nervousness;
 confusion, hallucinations; or
 slow breathing
z
Benzonatate

 Pharmacodynamics

 menganestesi stretch receptors yg terdapat

pada tr. respiratorius,

 Pharmacokinetics:

 Taken orally as a softgel capsule.

 act 15 - 20 min’ and effect lasts for 3 - 8 hours.

z
EKSPEKTORAN

 Sebenarnya tidak lebih baik dari plasebo (IONI, 2017)

 Contoh :

 Glyseril Guaiacolate (Guaifenesin)

 Succus liquairitiae

 Ammonium klorida
z
Glyseril Guaiacolate

Pharmacodynamics

 increasing sputum volume and reducing the viscosity

of bronchial secretions, guaifenesin facilitates
expectoration of retained secretions

 helps loosen phlegm (mucus) and thin bronchial

secretions, make coughs more productive
z
Glyseril Guaiacolate

 Pharmacokinetics
 Absorption: Well absorbed from the GI tract.

 Distribution :

 Metabolism: di hepar (oksidasi & demetilasi)

 Excretion: Via urine. Elimination half-life: ±1 hr.

z
Glyseril Guaiacolate

 Contraindication
 Hypersensitivity

 Side effects
 Significant  Abdominal pain, nausea, vomiting, diarrhoea.
 Rare  Nervous: Dizziness, drowsiness,
headache.Genitourinary: Nephrolithiasis. Endocrine: Hypouricaemia. Dermatologic: Ra
sh.

 Dosis
 Adult: As conventional preparation 200-400 mg 4 hrly as needed. As extended-release
tab: 600-1,200 mg 12 hrly as needed. Max: 2,400 mg/daily.
 Child: 4-<6 yr 50-100 mg 4 hrly as needed. Max: 600 mg daily; 6-<12 yr 100-200 mg 4
hrly as needed. Max: 1,200 mg daily; ≥12 yr Same as adult dose
z
MUKOLITIK

 untuk batuk berdahak, mempercepat ekspektorasi dan

mengurangi viskositas sputum

 Contoh

 Bromhexin

 Ambroxol

 Erdosistein

 Karbosistein

 Mesistein
z
BROMHEXIN

Pharmacodynamics

 acts on the mucus at the formative stages in the glands,

within the mucus-secreting cells  disrupts the structure
of acid mucopolysaccharide fibres in mucoid sputum and
produces a less viscous mucus, which is easier to
expectorate.

 enhances mucus transport by reducing mucus viscosity

and by activating the ciliated epithelium (mucociliary
clearance)
z

Pharmacokinetics

 Absorption: Rapidly absorbed from the GI tract. Bioavailability:

Approx 20%. Time to peak plasma concentration: Approx 1 hr.

 Distribution: Widely distributed to body tissues. Crosses blood

brain-barrier and placenta (small amounts). Plasma protein
binding: >90%.

 Metabolism: Extensive hepatic first-pass metabolism.

 Excretion: Via urine (approx 85-90%, mainly as metabolites).

Terminal elimination half-life: 13-40 hr
z

 Adverse Reactions
 GI side effects; headache, dizziness, sweating,
skin rashes.
Inhalation: Cough or bronchospasm.
 Bromhexine and Pregnancy
 Category A: increase the frequency of
malformations or other direct or indirect harmful
effects on the foetus having been observed.
z
BROMHEXIN

 Kontraindikasi:

 Hipersensitivitas.

 Dosis:

 Adult: 8-16 mg

 Child: 2-5 yr 8 mg daily in 2-3 divided doses; 6-11

yr 4-8 mg; ≥12 yr Same as adult dose.
z
AMBROXOL

Pharmacodynamics:

 active metabolite of bromhexine

 causes an increase in secretion in the respiratory tract

 promotes surfactant production and stimulates ciliary activity

 assist the flow of mucus and its removal (mucociliary clearance)

 significant reduction in cytokine release, both in the blood and in

mononuclear and polynuclear cells
z

Pharmacokinetics:
 Absorption: GI tract. Peak plasma levels are attained after 0.5-3
hrs.
 Distribution: Plasma protein-binding is around 90%. After oral, IV
and IM administration, ambroxol is distributed rapidly and
extensively from the blood into the tissues. The highest active
ingredient concentrations are measured in the lung.
 Metabolism: in the liver mainly by conjugation.
 Elimination: Around 30% of an oral dose is eliminated via the
first-pass effect. The terminal half-life (t½) is 10 hrs.
z
AMBROXOL

 Dosis
 Dewasa: kapsul lepas lambat 1 kali sehari 75 mg, sesudah makan. Dewasa dan anak di atas
12 tahun:1 tablet (30 mg) 2-3 kali sehari; Anak 6-12 tahun: 1/2 tablet 2-3 kali sehari. Sirup
tetes (drops): 15 mg/ml drops (1 mL= 20 tetes): Anak s/d 2 tahun: 0,5 mL (10 tetes) 2 kali
sehari; Ambroksol drops dapat dicampur bersama dengan sari buah, susu atau air.Sirup 15
mg/5 mL (1 sendok takar = 5 mL): Anak usia 6-12 tahun: 2-3 kali sehari 1 sendok takar; 2-6
tahun: 3 kali sehari 1/2 sendok takar; di bawah 2 tahun: 2 kali sehari 1/2 sendok takar.

 ADR
 Mild GI effects and allergic reactions.

 Precaution : 1st trimester of pregnancy

 Interaksi : Pemberian bersamaan dengan antibiotik (amoksisilin sefuroksim, eritromisin,

doksisiklin) menyebabkan peningkatan penerimaan antibiotik kedalam jaringan paru-paru.
 Patogenesis Asma
z

Medscape, 2017
Patofisiologi Asma
z is also an inflammatory disease of the lungs
Chronic
characterized by: obstructive pulmonary
disease
 Progressive emphysema (alveolar destruction)
 Bronchiolar fibrosis / chronic bronchitis .

 Loss of bronchiolar elasticity leads to closure of

smaller air tubes during expiration.
 The airway obstruction is accentuated during
exercise causing shortness of breath.
 Bronchodilators prevent closure of peripheral air
tubes during expiration and afford symptomatic relief
in COPD patients, but improvement is generally
<15%.
 z
Bronchodilators
Leukotriene Mast cell Corticosteroi Anti-IgE
antagonists stabilizers ds antibody

β2 Agonis:

Beclomethasone,
Sodium cromoglycate, Ketotifen
Salbutamol,

Budesonide,
Fluticasone

Inhalation:
Terbutaline,

Montelukast, Zafirlukast
Salmeterol,
Formoterol

Omalizumab
Methylxanthines:
Teofilin,
Aminofilin

Prednisolone and
Hydrocortisone,
Systemic:
others
Anticholinergics:
Ipratropium
bromide,
Tiotropium
bromide
 z
Β2 - Agonis
Salbutamol, Terbutaline, Salmeterol, Formoterol
Adrenergic drugs cause bronchodilatation through β2
receptor stimulation → relaxation.

Adrenergic drugs are the mainstay of treatment of

reversible airway obstruction.

They are the most effective and fastest acting

bronchodilators when inhaled.
 β2 - Agonis
z

Short acting (4–6 hours) :

• Salbutamol
• Terbutaline

Indication

• relief of bronchospasm in asthma

Long lasting (12 hours):

• Salmeterol
• Formoterol

Indication :

• for prevention of asthma symptoms

• not for use in relieving an asthma attack (not be used to treat acute
symptoms)
• should be used with a corticosteroid
z

COPD
• Long-acting β2 agonists are superior to short-acting
ones, and equivalent to inhaled anticholinergics in
COPD.
• They reduce breathlessness by preventing expiratory
closure of peripheral airways and abolishing the
reversible component of airway obstruction.
 Methylxantine
z Teofilin, Aminofilin

 Theophylline and its compounds have been extensively used in

asthma, but are not considered first line drugs any more.
 They are used more often in COPD.
 MoA : menghambat aktivitas enzim fosfodiesterase
 Methylxantine
z

ES :
 Narrow margin of safety
 Rapid injection menyebabkan syncope, precordial pain,
bahkan ke†an
 Anticholinergics
z Ipratropium, Tiotropium

 Atropinic drugs  bronkodilatasi  menghambat reseptor M2

• Pelepasan Ach  bronkokonstriksi

& me↑kan sekresi mukus
• Penghambatan Ach oleh
antikolinergic  bronkodilatasi &
me↓kan sekresi mukus
• Kurang efektif dibanding agonis B2
pada asma bronkial
• Merupakan bronkodilator pilihan
utk COPD

 ADR : mulut kering, mual, konstipasi, sakit kepala

 Interaksi : derivat xantin, adrenoseptor beta, β-blockers, MAO inhibitors, antidepresan
trisiklik
 Anticholinergics
z

Ipratropium bromide Tiotropium bromide

• short acting • long acting
• Dosis : 1 dosis, 3-4 • Dosis : 1 kali sehari
kali sehari. satu kapsul u/ inhalasi
(22,5 mcg tiotropium
• Penderita COPD yang bromide setara
memiliki kebiasaan dengan18 mcg
merokok, dianjurkan tiotropium)
konseling dokter u/
penentuan dosis • ≠ ditelan, ≠ lebih dari 1
kali sehari.

z
Ipratropium bromide
• Absorption: 10-30% of a dose is
deposited in the lungs, small
amount reaches systemic
circulation. Poorly absorbed from
the GI tract.
• Distribution: Plasma protein
binding: ≤9% (oral inhalation);
<20% (nasal).
• Metabolism: hepar,via ester
hydrolysis (41%) and conjugation
(36%).
• Excretion: urine and faeces. Half-
life: 2 hr (oral inhalation); 1.6 hr
(nasal).
Anticholinergics
Tiotropium bromide
• Absorption: Systemically
absorbed from the lungs. Time to
peak plasma concentration: 5 min
(dry powd inhalation); 5-7 min
(inhalation soln).
• Distribution: Volume of
distribution: 32 L/kg. Plasma
protein binding: Approx 72%.
• Metabolism: hepar, by non-
enzymatic cleavage and by
CYP2D6 and CYP3A4 isoenzymes.
• Excretion: urine as unchanged
drug. Half-life: 5-6 days (dry powd
inhalation).
z
Leukotriene Antagonists
Montelukast, Zafirlukast
MoA  hampir sama
• Menghambat cys-leukotrienes C4, D4, dan E4 (LTC4,
LTD4, LTE4)
Indikasi
• Terapi profilaksis untuk asma ringan – sedang & asma
kronis
• ≠ pd asma berat
ADR
• sakit kepala, rashes, eosinofilia, neuropati perifer,
komplikasi jantung  minimal
Dosis :
• Montelukast : 10mg 1x sehari (malam hari)
• Zafirlukast : 20 mg 2x sehari, anak < 12th tdk dianjurkan
 z
Leukotriene Antagonists

Interaksi
• Montelukast : Fenobarbital, fenitoin, & rifampisin
me↓kan kadar montelukas dalam plasma. Gemfibrozil
me↑kan paparan sistemik montelukas
• Zafirlukast : asetosal me↑kan konsentrasi plasma
zafirlukast, zafirlukast me↑kan efek antikoagulan
warfarin & kumarin
Mechanism of action Leukotriene Antagonists
z
Mast Cell Stabilizers
Ketotifen, Sodium Kromoglikat, Nedokromil Natrium

 Menghambat degranulasi sel mast dengan cara

memicu stimulus dan menghambat pelepasan
histamin, LTs, PAF, interleukins, dsb dari sel mast.
Penghambatan pelepasan mediator dilakukan melalui
blokade influx kalsium ke dalam sel mast.
 Terapi jangka panjang akan menurunkan respon
inflamasi sel.
 tidak efektif digunakan pada serangan asma akut.
z
Mast Cell Stabilizers

Ketotifen

 Interaksi  drugs : May potentiate effects of sedatives, hypnotics and

antihistamines.
Potentially Fatal: Reduced platelet count with oral antidiabetics. Food : May
potentiate effects of alcohol

 Pharmacokinetics:
Absorption: Completely absorbed from the GI tract (oral). Minimally absorbed
(ophth). Bioavailablity: Approx 50%. Time to peak plasma concentration: 2-4 hr.
Distribution: Plasma protein binding: 75%. Enters breast milk.
Metabolism: Undergoes hepatic first-pass metabolism; converted to inactive
ketotifen-N-glucuronide metabolite.
Excretion: Mainly via urine (60-70% as metabolites, 1% as unchanged drug).
Elimination half-life: Biphasic: 3-5 hr (initial); approx 21 hr (terminal).
 Mast Cell Stabilizers
z

Sodium kromoglikat
•Absorption: Oral: Poorly absorbed from the GIT with only 1% bioavailability.
Inhalation: 8-10% of a dose of fine powd is deposited and rapidly absorbed
from the lungs
•Asthma prophylaxis
Adult: 20 mg four times daily as dry powder/nebulised soln or 10 mg four times
daily as aerosol, increased to 6-8 times daily if necessary, reduced to 5 mg four
times daily once asthma has been stabilised. Additional doses may be taken
before exercise.
 Mast Cell Stabilizers
z

Nedokromil sodium

 Chronic asthma. Not for use in acute asthma attacks; acute bronchospasm

 Duration: Inhalation: 2 hr.

Pharmacokinetics:
Absorption: Poorly absorbed. Bioavailability: 2-17% (inhalation); <4%
(ophthalmic).
Distribution: Protein-binding: 89%.
Excretion: Via urine 70% and via faeces (30%) as unchanged drug.
Elimination half-life: 1.5-3.3 hr.

 Dosis : Adult: As sodium: 4 mg inhaled 4 times daily; reduce to bid once

desired clinical response is observed.
Child: ≥6 yr: As sodium: 4 mg inhaled 4 times daily; reduce to bid once
desired clinical response is observed.
z

 Absorption: Completely absorbed from the GI tract (oral).

Minimally absorbed (ophth). Bioavailablity: Approx 50%. Time to
peak plasma concentration: 2-4 hr.
Distribution: Plasma protein binding: 75%. Enters breast milk.
Metabolism: Undergoes hepatic first-pass metabolism;
converted to inactive ketotifen-N-glucuronide metabolite.
Excretion: Mainly via urine (60-70% as metabolites, 1% as
unchanged drug). Elimination half-life: Biphasic: 3-5 hr (initial);
approx 21 hr (terminal).
z
Corticosteroids
Beklometasone, Budesonid, Dexametason

 Sbg controller

 me↓kan inflamasi

 Indikasi
 Pd penggunaan β2 agonis 3x/mgu a/ lebih

 asma yg mengganggu tidur > 1x/mgu

 Eksaserbasi 2thn terakhir + kortikosteroid sistemik a/ nebu

bronkodilator
z

 ES KS
 Kepadatan mineral me↓  osteoporosis

 pe↑ risiko glaukoma & katarak  inhalasi jgka panjang dosis tinggi

 Retardasi pertumbuhan  KS oral

 kandidiasis
z

 Precaution

 Hipertensi

 Diabetes

 Anak2 & ibu hamil

 z
Anti IgE antibody
Omalizumab
Indikasi : pengobatan tambahan u/ kontrol asma alergik persisten
berat pd pasien dewasa & anak (usia > 6 tahun), ekserbasi asma
berat yg tidak tertangani dengan inhalasi kortikosteroid dosis tinggi
bersama dengan agonis beta-2, pasien dengan asma termediasi Ig-E

ADR : sakit kepala; reaksi suntikan seperti nyeri, eritema, pruritus dan
bengkak; nyeri perut; demam

Injeksi subkutan, dewasa dan remaja > 12 tahun didasarkan oleh

jumlah IgE (IU/mL) dan berat badan
IONI, 2017
IONI, 2017
z
Tuberkulosis

 Etiologi : Mycobacterium tuberculosis

 Bakteri aerob, gram positif, dinding sel mengandung komplek

lipida-glikolipida serta lilin (wax) yg sulit ditembus bahan kimia

 Cepat † dgn matahari, bertahan hidup pada t4 gelap & lembab

 Dapat memperbanyak diri dalam sel2 fagosit

 Penyebaran melalui droplet

 Gejala : demam, batuk, BB ↓, malaise, sesak, nyeri dada

 OAT
z

Obat Anti Tuberkulosis

z

 prinsip-prinsip yang dipakai adalah :

 Menghindari penggunaan monoterapi

 OAT diberikan dalam bentuk kombinasi dari beberapa jenis obat,

dalam jumlah cukup dan dosis tepat sesuai dengan kategori
pengobatan  mencegah timbulnya kekebalan terhadap OAT

 Untuk menjamin kepatuhan penderita dalam menelan obat, dilakukan

dengan pengawasan langsung (DOT = Directly Observed Treatment)
oleh seorang Pengawas Menelan Obat (PMO)

 Pengobatan TB diberikan dalam 2 tahap, yaitu tahap intensif dan

lanjutan
z

Mekanisme kerja OAT

• Aktivitas bakterisidal, untuk bakteri yang
membelah cepat
• Aktivitas bakteriostatis, obat-obatan yang
mempunyai aktivitas bakteriostatis terhadap
bakteri tahan asam.
• Aktivitas sterilisasi, terhadap bakteri
semidormant
z

Primer :

• paling efektif
• paling rendah toksisitasnya
• resistensi cepat bila digunakan sebagai
obat tunggal  kombinasi 3-4 obat
• INH (Isoniazid), Rifampisin ,
Pirazinamida, Streptomisin, Etambutol
z

Sekunder

• aktivitas antibakterinya lebih lemah

• lebih toksik
• hanya digunakan bila terdapat resistensi
atau intoleransi terhadap obat primer
• kanamisin, etionamid, levofluoxacin,
asam aminosalisilat, sikloserin
WHO, 2006
WHO, 2006
WHO, 2006