1.

ANATOMY OF LUNGS
 pyramid-shaped, paired organs that are
connected to the trachea by the right and left
bronchi
 on the inferior surface, the lungs are bordered
by the diaphragm. The diaphragm is the flat,
dome-shaped muscle located at the base of
the lungs and thoracic cavity.
 enclosed by the pleurae, which are attached to
the mediastinum
 The right lung (3 lobus) is shorter and wider
than the left lung (2 lobus), and the left lung
occupies a smaller volume than the right
 Cardiac notch is an indentation/ lekukan on the
surface of the left lung, and it allows space for
the heart 
 The apex of the lung is the superior region
 Base is the opposite region near the
diaphragm
 The costal surface of the lung borders the
ribs. The mediastinal surface faces the
midline.
 Each lung is composed of smaller units called
lobes. Fissures separate these lobes from
each other
 The right lung consists of three lobes: the
superior, middle, and inferior lobes.
 The left lung consists of two lobes: the
superior and inferior lobes
 A bronchopulmonary segment is a division of
a lobe, and each lobe houses multiple
bronchopulmonary segments. Three on the
right, two on the left.
 An interlobular septum is a wall, composed of

connective tissue, which separates lobules

from one another.
 Mulut/ hidung -> oropharynx/ nasopharynx ->
 Portion of the lung involved gas exchange and
larynx -> trachea -> bronchi -> bronchioles ->
constitute the terminal respiratory unit or
alveolar
acinus. Acinus includes respiratory bronchioles,
 Trachea divides at the carina into right anf left
alveolar ducts and alveoli (alveolar sacs).
mainstem bronchi.
 Alveolar efficient mechanism for O2 and CO2
 Mainstem bronchi which branch into lobar
transfer between alveolar spaces and pulmonary
bronchi (three on the right, two on the left),
capillary blood.
segmental bronchi, and extensive system of
subsegmental and smaller bronchi.
BLOOD SUPPLY OF LUNGS
 plays an important role in gas exchange and
serves as a transport system for gases
throughout the body.  glands, and blood vessels.
 This blood supply contains deoxygenated
blood and travels to the lungs where
erythrocytes, also known as red blood cells,
pick up oxygen to be transported to tissues
throughout the body.
 The pulmonary artery is an artery that arises
from the pulmonary trunk and carries
deoxygenated, arterial blood to the alveoli.
 Pulmonary artery : One arteriole and an
accompanying venule supply and drain one
pulmonary lobule
 As they near the alveoli, the pulmonary arteries
become the pulmonary capillary network.
 The pulmonary capillary network consists of tiny
vessels with very thin walls that lack smooth
muscle fibers.
 The capillary wall meets the alveolar wall,
creating the respiratory membrane
 Once the blood is oxygenated, it drains from the
alveoli by way of multiple pulmonary veins,
which exit the lungs through the hilum.
NERVOUS INNERVATION OF LUNGS
 Dilation and constriction of the airway are
achieved through nervous control by the
parasympathetic and sympathetic nervous
systems. 
 The parasympathetic system
causes bronchoconstriction, whereas the
sympathetic nervous system
stimulates bronchodilation. 
 Reflexes such as coughing, and the ability of
the lungs to regulate oxygen and carbon
dioxide levels, also result from this autonomic
nervous system control. 
 Sensory nerve fibers arise from the vagus
nerve, and from the second to fifth thoracic
ganglia.
 The pulmonary plexus is a region on the lung
root formed by the entrance of the nerves at
the hilum. The nerves then follow the bronchi in
the lungs and branch to innervate muscle fibers,
PLEURAL OF THE LUNGS
 The pleura (plural = pleurae) is a serous
membrane that surrounds the lung.
 The pleurae consist of two layers : visceral and
parietal
 The visceral pleura is the layer that is superficial
to the lungs, and extends into and lines the lung
fissures 
 Parietal pleura is the outer layer that connects to
the thoracic wall, the mediastinum, and the
diaphragm.
 The visceral and parietal pleurae connect to
each other at the hilum.
 The pleural cavity is the space between the
visceral and parietal layers.
 Two major functions: They produce pleural fluid
and create cavities that separate the major
organs
 Pleural fluid is secreted by mesothelial cells
from both pleural layers and acts to lubricate their
surfaces. This lubrication reduces friction
between the two layers to prevent trauma
during breathing, and creates surface tension
that helps maintain the position of the lungs
against the thoracic wall. 
 Adhesive characteristic of the pleural fluid
causes the lungs to enlarge when the thoracic
wall expands during ventilation, allowing the
lungs to fill with air.
2. DESCRIBE THE MECHANISM OF CONTROL
OF BREATHING
 Respirasi di kontrol oleh Medulary Respiratory
Centers (made of ventral & dorsal groups)
 Ventral : responsible for the rythmicity of
breathing
 Dorsal : responsible for inspiration of
diaphragm
 Pontime Respiratory Center : berinteraksi
dengan medula untuk smooth respiratory
rythm.
 Pontime akan mengirim sinyal ke medula
respiratory center -> ventral dan dorsal akan
bekerja sama, lalu mereka akan mengirim sinyal
untuk inspirasi dan ekspirasi.
stimulate/ supress the medullary respiratory
center & respiration
b. PERIPHERAL CHEMORECEPTOR -> berlokasi di
carotid dan aortic bodies -> detect chemical
changes in blood.
Contoh : kalau ia mendeteksi decrease oxygen di
blood pH (O2 ↓, Ph ↓, H+ ↑, CO2 ↑) -> aortic dan
carotic bodies akan stimulate/ trigger the
chemoreceptor -> lalu chemoreceptor ini akan
menstimulate respiratory center -> quicker
respiratory rate -> quicker the breath in (more
oxygen in) and out (more carbon dioxide out).
c. CENTRAL CHEMORECEPTOR -> berlokasi di
medula -> kerjanya sama yaitu detect changes in
Ph -> lalu chemoreceptor ini akan menstimulate
respiratory center -> can breath faster, breathing
out more carbon dioxide and inhaling more oxygen.
d. RECEPTOR IN MUSCLE AND JOINTS ->
distimulasi ketika excercise, lalu receptor ini akan
mesntimulasi respiratory center -> can breathe
quicker (important when excercise, karena need
more oxygen) -> take more oxygen and blow out all
the acid that has built up

 Things in the lungs that can regulate the repiratory

center and they can influence the respiratory center
in brain stem :
a. Irritant receptor : protective the lungs, membantu
dalam memblow up irritant. Ketika receptor ini
berstimulasi, dia akan mensupress respiratory
center untuk slow down the respiration.
b. Stretch receptor : cause protective reflex di
inisiasi by extreme over inflation of the lungs ->
they will supres the respiration -> slow down the

 Lalu sinyal itu dapat melakukan inspirasi dan

ekspirasi di thorax dimana tempat lungs berada.
Otot yang berperan penting dalam respirasi
yaitu otot diafragma dan otot intercostal
(diantara ribs).
 Sinyal akan mengirim impuls ke muscle of lungs
untuk mentrigger inspirasi atau ekspirasi.
 Contoh : impuls dikirim via neuron ke intercostal
muscle saat inspirasi -> tulang rusuk nya akan
terangkat. Lalu impuls juga dikirim ke
diaphragm saat inspirasi -> diaphragm
descend/ turun.
 Semakin cepat impulsnya maka semakin cepat
breathing nya, semakin lambat impulsnya
makan semakin lama breathingnya.
 Yang mempengaruhi kerjanya respiratory respiratory rate.
center:
a. HIGHER CENTERS OF THE BRAIN : 3. ETIOLOGY OF PULMONARY TB
voluntary control, pain, emotion,  Infection of Mycobacterium Tuberculosis
temperature.  Patients infected with M tuberculosis who
Faktor ini dapat mempengaruhi respiratory
have no clinical, bacteriologic, or
rate dengan cara : pertama, faktor ini
mensupress pontine respiratory center ->
 radiographic evidence of active TB are
said to have latent TB infection.  primary TB). Lesi expansion tuberkel sampe ke lug
 Active TB may occur from reactivation of
previously latent infection or from
progression of primary infection.
 Transmission of TB occurs from individuals
infected with pulmonary (and rarely
laryngeal) disease. Infection results from
the inhalation of aerosolized droplets
containing the bacterium from cough or
sneeze.
 transmission depends on the infectivity of
the source case (e.g., smear status and
extent of cavitation on CXR), the degree of
exposure to the case (e.g., proximity,
ventilation, and the length of exposure), and
susceptibility of the person in contact
with an infected case.
 HIV-infected individuals are at greater risk
of reactivation as well as progression to
primary TB
 Increased risk for the development of active
TB include :
- persons with recent tuberculin skin test
(TST) conversion
- the homeless
- injection drug users
- cigarette smokers
- immunocompromised individuals (e.g.,
people with diabetes, prolonged
corticosteroid therapy, end-stage renal
disease (ESRD), malnutrition, or
hematologic malignancies).  berhubungan dengan reactivation disease atau
4. PATHOPHYSIOLOGY OF PULMONARY
TUBERCULOSIS
PRIMARY TB
Pertama bakteri masuk melalui inhalation of
droplet nuclei. Lalu bakteri akan masuk sampai ke
alveoli. Di alveoli bakteri bakal dimakan oleh
alveolar macrofag supaya bakterinya mati. Ada
bakteri yang mati, ada juga bakteri yang dapat
bertahan di macrofag akan bermultiplikasi di dalam
macrofag. Bakteri yang bermultipkikasi akan
membunuh macrofag sehingga menghasilkan
respons dari sistem imun (monosit, other alveolar
macrophage, neutrofil -> semua ini berasal dari
nodular granulomatous struktur yang disebut
sebagai tubercle). Imun sistem ini akan
merespons dengan bakteri M.tuberculosisnya
dimatikan/ dibersihkan, menjadi latent infection,
dan progression to primary disease.
Kalau bakterinya bermultiplikasi uncontrolled
dapat menyebabkan tuberclenya enlarge dan
bakteri akan masuk ke lymph nodes ->
lymphadenopathy (clinical manifestation of
parenkim + lymph node = GHON COMPLEX.
Bakteri akan terus berproliferasi sampai
CELLULAR IMMUNE SYSTEM efektif (2-6 minggu
setelah kena infeksi), di mediasi oleh sel T
HELPER (TH1). Sel T dan macrofag akan
membentuk granuloma. Dimana pusatnya
granuloma mengandung bahan necrosis (caseous
center), bakteri TB, peripheral granulation tissue
yang terdiri dari makrofag dan limfosit.
Granuloma berfungsi untuk mencegah
pertumbuhan lebih lanjut dan penyebaran
bakteri TB. Biasanya pasien yg mengalami hal ini
tidak menular dan memiliki infeksi lantent, lalu pada
pemeriksaan fisiknya pasien ini memiliki CXR
normal dan test tuberkulinya positif.
Kalau bakterinya tidak tekendali, bakteri nya
dapat tersebar melalui hematogen. Penyebaran
bakteri ini disebut Miliary TB ditandai dengan
millet seeds.
SECONDARY TB
REACTIVATION
Old granulomanya akan aktif kembali karena
resistensi pasiennya melemah. Contohnya pada
pasien cancer, chemotherapy, AIDS, old age.
Develops after primary infection.
REINFECTION
Terpapar bakteri baru yang memiliki high dose
virulent bacilli. Biasanya di daerah endemic.
PATHOPHYSIOLOGY OF PLEURAL
TUBERCULOSIS
Efusi pleura TB dapat terjadi karena
tuberkulosis primer. Pada orang dewasa, paling
sering terjadi karena penyakit reaktivasi dan pada
anak-anak, paling sering mereka terjadi dalam
pengaturan penyakit primer.
Pengembangan efusi pleura TB terjadi paling
sering sebagai akibat dari reaksi hipersensitivitas
tertunda terhadap mycobacteria atau
mycobacterial antigen di ruang pleura/ tuberculous
pleural effusion develops when a subpleural focus
of disease ruptures into the pleural space.
Penyakit pleura dapat berkembang melalui
penyebaran hematogen setelah infeksi primer.
5. CHEMOTHERAPY OF TB
First Line Drugs :
- Isoniazide (INH/ H)
- Rifampicin
- Pyrazinamide (Z)
- Ethambutol (E)
- Streptomycin (S)
 Second Line Drugs: - Less effective than INH or rifampin
- MOA : inhibit of protein synthesis
- Thiacetazone - Dose : 15 mg/ kg BB, atau
- Paraaminosalicylic acid (PAS) BB > 60 kg : 1000 mg
- Ethionamide BB 40 -60 kg : 750 mg
- Cyclosporin BB <40 kg : sesuai BB
- Kanamycin
- Amikacin GOAL OF ANTITUBERCULAR CHEMOTHERAPY:
- Capreomycin - Kill dividing bacilli
- Kuinolon - Kill persisting bacilli
- Prevent emergence of resistence
ISONIAZIDE
- Kombinasi two or more drugs
- Tuberculocidal Mechanism of action -> - INH dan R most effectious drugs duration of
destroying tubercle bacilli therapy is shortened from >12 months to 9
- Menginhibit sintesis dari mycolic acid months.
- Dosis : 5 mg/ kg BB, maximal 300, 10mg / - Addition of Z for initial 2 months futher
kg BB 3 x seminggu, atau 15mg / kg BB 2 x reduce
seminggu, atau 300mg/hari untuk dewasa, - Durasi pengobatan dari kena infeksi sampai
intermitten : 600 mg/kali 6 bulan
- Single daily dose of all first line drug is
RIFAMPICIN prefered
- 2-3 bulan awal untuk bunuh bakteri TB
- Derivative of rifamycin B - 4-6 bulan remaining bacilli are eleminated,
- Bactericidal -> membunuh bakteri sehingga tidak kambuh lagi
- MOA : Inhibits DNA depent RNA synthesis
- Dosis : 10 mg/ kg BB, maximal 600 mg 2- 6. BCG (Bacillus Calmette-Guérin) RESPONSE TO
3x / minggu atau BB>60 KG : 600mg, BB MYCOBACTERIUM TB
40-60kg : 450 mg  BCG stimulates antibodies and creates a
resistance without damaging the organism. T
PYRAZINAMIDE
 he BCG vaccine recruits CD4 and CD8 T cells
- Weakly tuberculocidal as a response to protective mycobacterial
- MOA : inhibits mycolic acid synthesis, but by antigens .
interacting with a different fatty acid  After recruiting these cells, the new cells are
synthase encoding gene. exposed to the macrophage product
- Dose : interleukin 12 which calls for T cells to
Fase intensif : 25 mg/ kg BB, 35 mg/ kg BB secrete interferon y .
3 x seminggu, 50 mg/ kg BB 2 x seminggu,  When Mycobacterium tuberculosis enters the
atau : cell, interferon y reduces the pH in the
BB > 60 kg : 1500 mg phagosomal membrane and produces
BB 40 -60 kg : 1000 mg superoxide and nitric oxide, which can
BB <40 kg : 750 mg destroyMycobacterium tuberculosis

ETHAMBUTOL
- Tuberculostatic
- MOA : inhibit arabinogalactan synthesis &
mycolic acid incorporation in mycobacterial
cell wall
- Dose :
Fase intensif : 20 mg/ kg BB
Fase lanjutan : 15 mg/ kg BB, 30 mg/ kg BB
3 x seminggu, 45 mg/ kg BB 2 x seminggu,
atau :
BB > 60 kg : 1500 mg
BB 40 -60 kg : 1000 mg
BB <40 kg : 750 mg
Dosis intermiten : 40 mg/ kg BB/ kali
STREPTOMYCIN
- Tuberculocidal
 - Tuberculosis Emphyema
Rupture of Tuberculosis lesion in pleural
cavity → purulent fluid in pleural cavity
(Empyema)
- Pneumothorax : rupture of sub. Pleural
tuberculosis lesion
- Atelectasis : Diminished volume affecting all or
part of a lung (alveoli collapse)/ alveoli don’t fill
with air
- Gagal nafas
- Heart failure

9. HYPOXEMIA :  condition where arterial

oxygen tension or partial pressure of oxygen
(PaO2) is below normal (normal value is
between 80 and 100 mmHg).
HYPOXIA : reduction of oxygen supply at the
tissue level, which is not measured directly by
a laboratory value.

7. CRITERIA OF SUCCESSFUL TREATMENT ON TB

8. COMPLICATION OF TB
- Hemoptysis/ batuk berdarah
- Pleurisy & Pleural Effusion
Hypersensitivity reaction to tub proteins with a
few month of prior tuberculosis in young children.
10. RESPIRATION GAS EXCHANGE
Setelah tissue used the oxygen, deocygenated Di paru terdpaat alveoli, dimana alveoli terdapat
blood akan balik melalui venules -> vein -> vena cava pulmonary arteri dan pulmonary vein.
superior/inferior -> jantung. Dari jantung deoxygenated
blood akan di pompa ke paru melalui pulmonary artery.
Di paru, darahnya akan mengeluarkan CO2 dan paru
akan reoxygenated the blood dengan mengambil
banyak O2 ke darah. Oxygenated bloodnya akan balik
ke jantung melalui pulmonary vein. Lalu oxygenated
blood akan di pompa dari aorta-> arteri ->arteriol ->
seluruh tubuh.
Oxygen di tubuh di transport oleh RBC dan plasma :

Proses bagaimana CO2 balik ke alveolus :

- CO2 yang ada di plasma langsung masuk ke
alveolus
- Bikarbonat dan hidrogen yang ada di plasma
akan membentuk karbondioksida dan water.
(HCO3- + H+ -> CO2 + H2O) PROSES LAMBAT.
Lalu CO2 nya masuk ke alveolus
- Oxygen di dalam RBC berikatan dengan - Bikarbonat yang ada di plasma bisa masuk ke
Hemoglobin (Hb) = HbO2 -> Hb + O2. O2 nya bisa RBC melalui transporter , lalu Cl - bakal keluar.
masuk ke interstitial fluid, lalu O2 nya dapat Bikarbonat yang masuk akan berikatan dengan
digunakan oleh tissue. hidrogen. Dengan bantuan enzyme Carbonic
- Lalu, O2 yang melalui plasma juga dapat masuk Anhydrase yang berfungsi untuk mempercepat
ke intersitial fluid dan digunakan oleh tissue. proses HCO3- + H+ -> CO2 + H2O. Lalu CO2 nya
Setelah O2 digunakan, tissue akan membentuk CO2 : akan keluar dari RBC dan masuk ke alveolus
- Dalam jumlah yang sedikit CO2 dapat langsung - Carboamino Hb yang ada di RBC (HbCO 2) akan
masuk ke darah melalui plasma. pecah menjadi Hb + CO2. Lalu CO2 nya akan
- CO2 ditransport ke darah melalui plasma lalu keluar dari RBC dan masuk ke alveolus.
berikatan dengan air = CO2 + H2O -> HCO3- + H+
(Bicarbonate dan hidrogen) PROSES NYA LEBIH Proses bagaimana O2 dari alveolus masuk ke darah :
LAMBAT
- Sebagian kecil O2 langsung masuk ke plasma
- Sebagian besar CO2 akan masuk ke RBC lagi
- Kebanyakan O2 akan masuk ke RBC dan
dan berikatan dengan air = CO2 + H2O . Dengan
berikatan dengan hydrogen hemoglobin
bantuan enzyme Carbonic Anhydrase yang
membrentuk oxyhemoglobin dan hidrogen (O2 +
berfungsi untuk mempercepat proses CO 2 + H2O
HHb -> HbO2 + H+) . HIdrogennya akan
-> HCO3- + H+ (Bicarbonate dan hidrogen)
mensupply bicarbonat
PROSESNYA LEBIH CEPAT. Bikarbonat akan
berusaha untuk keluar dari RBC melalui
Oxygen transport :
transporter, saat bikarbonat keluar maka Cl - akan
a. dissolve in plasma (<2%)
masuk ke RBC. Hidrogennya akan bereaksi
b. bind to hemoglobin (98%)
dengan Hb dan membentuk hydrogen hemoglobin
(H+ + Hb -> HHb)
Oxygen Saturation : concentration oxygen in the blood
- CO2 masuk ke dalam RBC dan berikatan dengan
( normal : 95-100%)
Hb dan membentuk carbo amino hemoglobin
(CO2 + Hb -> HbCO2):
Carbon dioxide transport :
a. dissolve in plasma (~10%)
b. Carboamino Hb (20%)
c. bicarbonate plasma (70%)
Carbon dioxide & pH :
a. ↑ CO2 , ↓ pH = blood acidic
b. ↓ CO2 , ↑ pH = blood Alkaline
.