LEC 1 Fix

Study Guide Respiratory System and Disorders
CONTENT
Page
CONTENT …………………………………………………………………………………… 1
PREFACE………………………………………………………………………………..….. 2
GENERAL CURRICULUM RESPIRATORY SYSTEM AND DISORDERS ………….. 3
PLANNERS AND LECTURERS …………………………………………………………... 4
FACILITATORS……………………………………………………………………………... 5
LEARNING ACTIVITY ……………………………………………………………………… 6
STUDENT PROJECT ……………………………………………………………………… 7
ARTICLE REVIEW ASSESSMENT FORM ……………………………………………... 8
ASSESSMENT METHOD …………………………………………………………………. 9
TIME TABLE ………………………………………………………………………………… 10
LEARNING PROGRAMS ………………………………………………………………….. 18
REFERENCES ……………………………………………………………………………… 44
PREFACE
Udayana University, Medical Faclty, DME, 2018 | 1

The medical curriculum has become increasingly vertically integrated, with stronger
basic concept and support by clinical examples and cases to help in the understanding of the
relevance of the underlying basic science. Basic science concepts may help in the
understanding of the pathophysiology and treatment of diseases. Respiratory system and
disorders block has been written to take account of this trend, and to integrate core aspects
of basic science, pathophysiology and treatment into a single, easy to use revision aid.
The respiratory system consists of a pair of lungs within the thoracic cage. Its main
function is gas exchange, but other roles include speech, filtration of microthrombin arriving
from systemic veins and metabolic activities such as conversion of angiotensin I to
angiotensin II and removal or deactivation of serotonin, bradykinin, norepinephrine,
acetylcholine and drugs such as propranolol and chlorpromazine. So this block will discuss
about anatomy, histology, symptom and signs of lung disease and its pathophysiology, major
upper respiratory diseases, major lung diseases, major pediatric lung disease, and basic
principle concept to education, prevention, treatment and rehabilitation in respiratory system
disorder in patient, family and community.
The learning process will be carried out for 4 weeks (20 working days) starts from 20th of
February 2017 as shown in the time table. The final examination will be conducted on 30 th of
March 2017 in the form of MCQ. The learning situation include lecture, individual learning,
small group discussion, plenary session, practice, and clinical skills.
Most of the learning material should be learned independently and discuss in SGD by
the students with the help of facilitator. Lecture is given to emphasize the most important
thing of the material. In small group discussion, the students gave learning task to lead their
discussion.
This simple study guide need more revision in the future, so that the planners kindly invite
readers to give any comments and critics for its completion. Thank you.
Planners
GENERAL CURRICULUM RESPIRATORY SYSTEM AND DISORDERS

Aims:
Comprehend the structure, physiologic, and pathologic of the respiratory system.
Interpret the laboratory and imaging examination of the respiratory system
disorders. Diagnose and treat the patient with common respiratory system
disorders.
Plan education, prevention, management and rehabilitation of respiratory system
disorders to patient, family and community.
Learning outcomes:
Concern about the size of problem and diversity of respiratory disease in the
community.
Able to describe the structure and function of the respiratory system.
Able to interpret the result of examination (physical, laboratory, function test, blood gas
analysis and chest imaging).
Able to explore patients with respiratory problem (runny nose, cough, dyspnea, non
cardiac chest pain, hemoptysis).
Able to manage major upper respiratory diseases (tonsillitis, rhinitis, sinusitis).
Able to manage major lung diseases (TBC, asthma, COPD, lung cancer, pneumonia,
occupational lung disease, pleural disease) on patient, family and community.
Able to manage major pediatric lung disease (bronchiolitis, TB,
asthma). Able to implement DOTS program against TB.
Able to implement the strategy of smoking cessation, especially in patient with
respiratory disease.
Curriculum contents:
Structural and function of the respiratory system.
Physiology of lung in related with oxygen consumption and acid base
balance. Symptoms and signs of lung disease.
Pathophysiology of respiratory system disorders.
Basic physical, laboratory and imaging
examination. Interpretation of examination results.
Drugs that commonly used in respiratory system disorders (decongestant, anti-asthma
& bronchodilators, antitussive, expectorant.
Basic principle concept to education, prevention, treatment and rehabilitation in
respiratory system disorders in patient, family and community.
PLANNERS AND LECTURERS

No Name Department Phone
1 Dr. dr. I Made Muliarta, M.Kes Physiology 081338505350

2 Prof. Dr. dr. Ida Bagus Ngurah Rai, Sp.P Pulmonology 08123804579
3 Prof. dr. I Gst. Md. Aman, Sp.FK Pharmacology 081338770650

4 Dr. dr. Desak Wihandani, M.Kes Biochemistry 081338776244
5 dr. IGK Nyoman Arijana, M.Si.Med Histology 085339644145
6 dr. I Nyoman Gede Wardana, M.Biomed Anatomy 087860405625
7 Dr. dr. Ida Bagus Subanada, Sp.A Paediatric 0812399533
8 dr. Ida Bagus Suta, Sp.P Pulmonology 08123990362
9 dr. Made Bagiada, Sp.PD-KP Pulmonology 08123607874
10 dr. IGN Bagus Artana, Sp.PD Pulmonology 08123994203
11 Dr. dr. Ketut Putu Yasa, Sp.BTKV Surgery 08123843260
12 Dr. dr. Elysanti Martadiani, Sp.Rad Radiology 08123807313
13 dr. Putu Ekawati, M.Repro, Sp.PA Pathology Anatomy 08123958158
14 dr. I Wayan Aryabiantara, Sp.An KIC Anaesthesiology 08123822009
15 dr. Putu Siadi Purniti, Sp.A Paediatric 08123812106
16 dr. Ayu Setyorini, Sp.A Paediatric 081353286780
17 dr. DGA Eka Putra, Sp.THT Otorhinolaryngology 0813387826317
18 dr. Luh Made Ratnawati, Sp.THT(KL) Otorhinolaryngology 08123806108
19 dr. Putu Andrika, Sp.PD-KIC Pulmonology 08123989192
20 dr. Gede Ketut Sajinadiyasa, Sp.PD Pulmonology 085237068670
21 Prof. Dr. dr. Suardana, Sp.THT Otorhinolaryngology 0811385299
FACILITATORS

Regular Class (Class A)
Venue
No Name Group Departement Phone
(3rd floor)
Clinical 3rd floor
1 dr. Ida Ayu Wirawati, SpPK(K) A1 082145723828
Pathology 3.09
dr. Nyoman Suryawati, M.Kes, SpKK, Dermato & 3rd floor
2 A2 0817447279 3.10
FINSDV Venereology
Dr. dr. I Nyoman Bayu Mahendra, 3rd floor
3 A3 Obgyn 081339550423
SpOG(K) 3.11
3rd floor
4 Dr.dr. I Wayan Suranadi, SpAn, KIC A4 Anesthesiology 08123847675 3.12
3rd floor
5 dr. I Gede Budhi Setiawan, SpB(K)Onk A5 Surgery 08123923956 3.13
dr. Wayan Citra Wulan Sucipta Putri, 3rd floor
6 A6 Public Health 087761838141 3.14
MPH
Internal 3rd floor
7 dr. Pande Ketut Kurniari, SpPD A7 082146179796 3.15
Medicine
Dr. dr. Elysanti Dwi Martadiani, SpRad 3rd floor
8 A8 Radiology 081805673099
(K) 3.16
dr. Ida Bagus Rangga Wibhuti, 3rd floor
9 A9 Cardiology 081237287888 3.17
M.Biomed, SpJP(K), FIHA
3rd floor
10 dr. I Made Dwi Ariawan A10 Public Health 081339798632
3.19
EnglishClass (Class B)
Venue
No Name Group Departement Phone (3rd floor)
3rd floor
1 dr. Putu Cintya Denny Yuliyatni, MPH B1 Public Health 081353380666 3.09
3rd floor
2 dr. Ni Nyoman Mahartini , SpPK(K) B2 Clinical Pathology 081337165577
3.10
3rd floor
3 dr. Agus Roy Rusly HH, SpBP-RE(K) B3 Surgery 08123511673 3.11
3rd floor
4 dr. Agung Nova Mahendra, M.Sc B4 Pharmacology 087861030195
3.12
3rd floor
5 dr. Ni Putu Witari, SpS B5 Neurology 081338724040
3.13
Dr. dr. I Gede Ngurah Harry Wijaya 3rd floor
6 B6 Obgyn 0811386935
Surya, SpOG 3.14
dr. IGA Gde Mahendra Wijaya, 3rd floor
7 B7 Radiology 08990179750
SpOnkRad 3.15
Anatomy 3rd floor
8 Dr. dr. Ni Putu Sriwidyani, SpPA B8 081337115012 3.16
Pathology
Dermato & 3rd floor
9 dr. IGAA Dwi Karmila, SpKK B9 08123978446
Venereology 3.17
3rd floor
10 Dr. dr. Tjok GA Senapathi, SpAn, KAR B10 Anesthesiology 081337711220 3.19
LEARNING ACTIVITY

There are several types of learning activity:

1. Lecture
2. Plenary session
3. Independent learning based on the lecture’s
topic Small group discussion to solve the
learning task Practicing
4. Student project
5. Clinical skill and demonstration
6. Self assessment at the end of every topic
Lecture will be held at room 3.02 (3rd floor), while discussion rooms available at 3rd
floor (room A309-A317, A319).
IMPORTANT INFORMATIONS
Meeting of the students’ representative
In the middle of block schedule, a meeting is designed among the student

representatives of every small group discussions, facilitators, and resource persons. The
meeting will discuss the ongoing teaching learning process, quality of lecturers and facilitators
as a feedback to improve the next process. The meeting will be taken based on schedule
from Medical Education Unit.
STUDENT PROJECT

About Topic, Presentation, Rule, Assessment, and Evaluator will be discussed at lecture of
block introduction October, 26th2018
TITLE
(subject/ topic: choose from compentency list)
Name
NIM
Faculty of Medicine, Udayana University

2017
______________
1. Introduction (Pendahuluan)
2. Content (Isi, sesuai topik yang dibahas)
3. Summary (Ringkasan)
4. Refferences: (Daftar Pustaka) Van Couver style
Example:
Journal
Sheetz MJ, King GL. Molecular understanding of hyperglycemia’s adverse effect
for diabetic complications. JAMA. 2002;288:2579-86.
Textbook
Libby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A, Kasper D,
Hoster S, Longo D, Jamason S (eds). Harrison’s principles of internal medicine. 15 th
ed. New York: McGraw Hill; 2001. p. 1977-82.
Internet
WHO. Obesity: preventing and managing the global epidemic. Geneva: WHO 1998.
[cited 2005 July]. Available from:
http://www.who.int/dietphysicalactivity/publications/facts/ obesity/en.
6 – 10 pages, 1.5 space, Times new romance 12
ARTICLE REVIEW ASSESSMENT FORM

Faculty of Medicine, Udayana University

_________________________________________________________________________
__
Block : Respiratory System and Disorders
Name : ________________________________________
Student No. (NIM) : ________________________________________
Facilitator : ________________________________________
Title :
__________________________________________________
__________________________________________________
Time table of consultation
Point of discussion Week Date Tutor sign
1. Title 1
2. Refferences 1
3. Outline of paper 2
4. Content 3
5. Final discussion 4
Assessment
A. Paper structure : 7 8 9 10
B. Content : 7 8 9 10
C. Discussion : 7 8 9 10
Total point : ( A + B + C ) : 3 = _____________
Denpasar, ______________________
Facilitator,
SELF ASSESSMENT

Self assessment of each lecture will be given after each lecture session, and will be
marked. This mark can determine whether the student pass this block or not. Any final mark
between 62 - 64 will be reconsidered with self assessment’s mark to see the student’s status.
Any student with self assessment’s mark 65 or more will pass this block. And for the lower
one will have to attend the remedial examination. It is important to do this self assessment
cautiously, because this activity may be your ticket to pass this block just at first examination.
ASSESSMENT METHOD
Assessment in this theme consists of:
SGD : 5%
Final Exam : 80%
Student Project : 15%
Final mark 65 or more considered to pass this block.
TIME TABLE REGULAR CLASS (CLASS A)
DAY TIME ACTIVITY VENUE PIC

/DATE
1
Friday
BREAK
26 Oct
2018
08.00 – 08.50 Lecture 1: Introduction Class R Dr. dr. Muliarta

09.00 – 09.50 Lecture 2: Ventilation Class R
2 10.00 – 10.50 IL
Monday 11.00 – 11.50 Break
29 Oct 12.00 – 12.50 Lecture 3: Histology of Resp Syst Class R dr. Arijana
2018 13.00 – 13.50 Lecture 4: Gas Exc, Diving, Alti Class R Dr. dr. Muliarta
14.00 – 14.50 IL
15.00 – 15.50 SP
08.00 – 08.50 PRAK1,2: Physio, Histo Lab. Faal& Team
09.00 – 09.50 PRAK1,2: Physio, Histo Lab. Histology
10.00 – 10.50 PRAK1,2: Physio, Histo
3
11.00 – 11.50 Break
Tue
12.00 – 12.50 SGD 1,2 Discussion R Fasilitator
30 Oct
2018
14.00 – 14.50 Pleno1,2 Class R Dr. dr. Muliarta
15.00 – 15.50 Pleno 3,4 Class R dr. Arijana / Dr.
dr. Muliarta
08.00 – 08.50 Lecture 5: Anatomy of Resp Sys1 Class R dr. Wardana
09.00 – 09.50 Lecture 6: Anatomy of Resp Sys2 Class R dr. Wardana
10.00 – 10.50 IL
4
11.00 – 11.50 Break
Wed
12.00 – 12.50 Lecture 7: Functional Char of Pulm Class R Dr. dr. Muliarta
31 Oct
circulation
2018
13.00 – 13.50 Lecture 8: Carriage of O2 dan CO2 Class R Dr. dr. Desak W.
14.00 – 14.50 IL
15.00 – 15.50 SP
5 09.00 – 09.50 SGD 7,8 Discussion R Fasilitator
Thurs 10.00 – 10.50 PRAK3,4: Anatomy, Pathology Lab. Anatomy
1 Nov 11.00 – 11.50 PRAK3,4: Anatomy, Pathology Lab. Pathology
2018 12.00 – 12.50 PRAK3,4: Anatomy, Pathology
13.00 – 13.50 Break
14.00 – 14.50 Pleno 5,6 Class R dr. Wardana
15.00 – 15.50 Pleno 7,8 Class R Dr. dr.
Muliarta/Dr. dr.
Desak W.
08.00 – 08.50 Lecture 9: Control of Acid Base Class R dr. Arya
balance, arterial gas analysis (AGA)
6 09.00 – 09.50 Lecture 10: Control of Resp. Class R Dr. dr. Muliarta
Friday Function
2 Nov 10.00 – 10.50 IL
2018 11.00 – 11.50 Break
12.00 – 12.50 Lecture 11: Pathology of Resp. Tract Class R dr. Ekawati
13.00 – 13.50 Lecture 12: Lung defense Class R dr. Ekawati
Mechanism
14.00 – 14.50 IL
15.00 – 15.50 SP
7 08.00 – 08.50 BCS1: Spirometry, Imaging Skill Lab Dr. dr.
Monday 09.00 – 09.50 BCS1: Spirometry, Imaging Skill Lab Muliarta/dr. Saji
5 Nov 10.00 – 10.50 BCS1: Spirometry, Imaging Skill Lab
2018 11.00 – 11.50 Break


14.00 – 14.50 Pleno 9,10 Class R dr. Arya / Dr. dr.
Muliarta
15.00 – 15.50 Pleno 11,12 Class R dr. Ekawati
8 08.00 – 08.50 Lecture 13: Pharmacological Class R Dr. dr. Satriyasa
Tue concepts of Respiratory medicines
6 Nov 09.00 – 09.50 Lecture 14: Pharmacological and Class R Dr. dr. Satriyasa
2018 nonpharmac Intervention 1
10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 15:Pharmacological and Class R Prof. Aman
nonpharmacological Intervention
13.00 – 13.50 Lecture 16: Resp Imaging Class R Dr. dr. Elysanti
14.00 – 14.50 IL
15.00 – 15.50 SP
08.00 – 08.50 BCS2: Px/ of Children, Imaging Skill Lab dr. Ayu/Dr. dr.
09.00 – 09.50 BCS2: Px/ of Children, Imaging Skill Lab Elysanti
9 10.00 – 10.50 BCS2: Px/ of Children, Imaging Skill Lab
Wed 11.00 – 11.50 Break
7 Nov 12.00 – 12.50 SGD 13,14 Discussion R Fasilitator
14.00 – 14.50 Pleno 13,14 Class R Dr. dr. Satriyasa
15.00 – 15.50 Pleno 15,16 Class R Prof. Aman/Dr.
dr. Elysanti
10 08.00 – 08.50 Lecture 17: Bronchiolitis, asthma in Class R Dr. dr.
Thurs children Subanada
8 Nov 09.00 – 09.50 Lecture 18: Pneumonia, Class R dr. Ayu S.
2018 Bronchopneumonia
10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 19: Aspiration Pneumonia Class R dr. Ayu S.
13.00 – 13.50 Lecture 20: Difteri, Pertusis Class R dr. Siadi
14.00 – 14.50 IL
15.00 – 15.50 SP
11 08.00 – 08.50 BCS3: WSD, Pengambilan cairan Skill Lab Dr. dr. Yasa
Friday pleura, punksi, decomp. jarum
9 Nov 09.00 – 09.50 BCS3: WSD, Pengambilan cairan Skill Lab Dr. dr. Yasa
2018 pleura, punksi, decomp. jarum
10.00 – 10.50 BCS3: WSD, Pengambilan cairan Skill Lab Dr. dr. Yasa
pleura, punksi, decomp. jarum
11.00 – 11.50 Break
Subanada / dr.
Ayu
15.00 – 15.50 Pleno 19,20 Class R dr. Ayu / dr.
Siadi
08.00 – 08.50 Lecture 21: TB in Children Class R dr. Siadi

12 09.00 – 09.50 Lecture 22: Adult Pulmonary TB Class R dr. Suta
Monday 10.00 – 10.50 IL
12 Nov 11.00 – 11.50 Break
2018 12.00 – 12.50 Lecture 23: Extrapulmonary TB Class R dr. Suta
13.00 – 13.50 Lecture 24: TB in the Class R dr. Bagiada
Immunocompromised Host, Abscess
TB
14.00 – 14.50 IL
15.00 – 15.50 SP
13 08.00 – 08.50 BCS4: Nebulisasi and O2 therapi, Skill Lab dr.

Tue Bronchoscopy and provocation test Arya/dr.Artana

13 Nov 09.00 – 09.50 BCS4: : Nebulisasi and O2 therapi, Skill Lab dr.
2018 Bronchoscopy and provocation test Arya/dr.Artana
10.00 – 10.50 BCS4: : Nebulisasi and O2 therapi, Skill Lab dr.
Bronchoscopy and provocation test Arya/dr.Artana
11.00 – 11.50 Break
14.00 – 14.50 Pleno 21,22 Class R dr. Siadi/dr. Suta
dr. Suta/dr.
15.00 – 15.50 Pleno 23,24 Class R Bagiada
08.00 – 08.50 Lecture 25: Asthma, COPD Class R dr. Artana
14 09.00 – 09.50 Lecture 26: Pleural Effusion, Class R dr. Andrika
Wed Emphysema, Lung Edema
14 Nov 10.00 – 10.50 IL
2018 11.00 – 11.50 Break
12.00 – 12.50 Lecture 27: Pneumothorax, Class R Dr. dr. Yasa
Hemothorax
13.00 – 13.50 Lecture 28: Bronchitis, Class R dr. Suta
Bronchiectasis
14.00 – 14.50 IL
15.00 – 15.50 SP
15 08.00 – 08.50 BCS5: CPEP bayi, Rhinoskopi Skill Lab dr. Arya/THT
Thurs posterior
15 Nov 09.00 – 09.50 BCS5: CPEP bayi, Rhinoskopi Skill Lab dr. Arya/THT
2018 posterior
10.00 – 10.50 BCS5: CPEP bayi, Rhinoskopi Skill Lab dr. Arya/THT
posterior
11.00 – 11.50 Break
14.00 – 14.50 Pleno 25,26 Class R dr. Artana/dr.
Andrika
15.00 – 15.50 Pleno 27,28 Class R Dr. dr. Yasa/dr.
Suta
16 08.00 – 08.50 Lecture 29: Lung Ca and Education Class R dr. Saji
Friday of smoking Cessation
16 Nov 09.00 – 09.50 Lecture 30:Disorder of nose, Sinus Class R dr. Ratna
2018 10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 31:Disorder of Pharynx, Class R Prof. Suardana
Disorder of Larynx
13.00 – 13.50 Lecture 32: Nose and Throat Foreign Class R dr. Dewa Eka
Bodies
14.00 – 14.50 IL
15.00 – 15.50 SP
17 08.00 – 08.50 BCS1,2 Skill Lab dr. Saji/Dr.
Monday 09.00 – 09.50 BCS1,2 Skill Lab dr.Muliarta/Dr.
19 Nov 10.00 – 10.50 BCS1,2 Skill Lab Ayu/Dr. dr.
2018 Elysanti
11.00 – 11.50 Break
14.00 – 14.50 Pleno 29,30 Class R dr. Saji/Dr.
Ratna
15.00 – 15.50 Pleno 31,32 Class R Prof.
Suardana/dr.
Dewa Eka
18 BREAK
Tue

20 Nov
2018
19
Wed
EVALUATION
21 Nov
2018

TIME TABLE ENGLISH CLASS (CLASS B)
DAY/DA
TE TIME ACTIVITY VENUE PIC
08.00 – 08.50 Lecture 1: Introduction Class R Dr. dr. Muliarta

1 09.00 – 09.50 Lecture 2: Ventilation Class R
Friday 10.00 – 10.50 IL
26 Oct 11.00 – 11.50 Break
2018 12.00 – 12.50 Lecture 3: Histology of Resp Syst Class R dr. Arijana
13.00 – 13.50 Lecture 4: Gas Exc, Diving, Alti Class R Dr. dr. Muliarta
14.00 – 14.50 IL
15.00 – 15.50 SP
08.00 – 08.50 PRAK1,2: Physio, Histo Lab. Faal& Team
09.00 – 09.50 PRAK1,2: Physio, Histo Lab. Histology
2 10.00 – 10.50 PRAK1,2: Physio, Histo
Monday 11.00 – 11.50 Break
29 Oct 12.00 – 12.50 SGD 1,2 Discussion R Fasilitator
14.00 – 14.50 Pleno 1,2 Class R Dr. dr. Muliarta
15.00 – 15.50 Pleno 3,4 Class R dr. Arijana / Dr.
dr. Muliarta
3 08.00 – 08.50 Lecture 5: Anatomy of Resp Sys1 Class R dr. Wardana
Tue 09.00 – 09.50 Lecture 6: Anatomy of Resp Sys2 Class R dr. Wardana
30 Oct 10.00 – 10.50 IL
2018 11.00 – 11.50 Break
12.00 – 12.50 Lecture 7: Functional Char of Pulm Class R Dr. dr. Muliarta
circulation
13.00 – 13.50 Lecture 8: Carriage of O2 dan CO2 Class R Dr. dr. Desak W.
14.00 – 14.50 IL
15.00 – 15.50 SP
Wed 09.00 – 09.50 SGD 7,8 Discussion R Fasilitator
31 Oct 10.00 – 10.50 PRAK3,4: Anatomy, Pathology Lab. Anatomy
2018 11.00 – 11.50 PRAK3,4: Anatomy, Pathology Lab. Pathology
12.00 – 12.50 PRAK3,4: Anatomy, Pathology
13.00 – 13.50 Break
14.00 – 14.50 Pleno 5,6 Class R dr. Wardana
Muliarta/Dr. dr.
Desak W.
08.00 – 08.50 Lecture 9: Control of Acid Base Class R dr. Arya
5 balance, arterial gas analysis (AGA)
Thurs 09.00 – 09.50 Lecture 10: Control of Resp. Class R Dr. dr. Muliarta
1 Nov Function
2018 10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 11: Pathology of Resp. Tract Class R dr. Ekawati
13.00 – 13.50 Lecture 12: Lung defense Class R dr. Ekawati
Mechanism
14.00 – 14.50 IL
15.00 – 15.50 SP
08.00 – 08.50 BCS1: Spirometry, Imaging Skill Lab Dr. dr.
09.00 – 09.50 BCS1: Spirometry, Imaging Skill Lab Muliarta/dr. Saji
6 10.00 – 10.50 BCS1: Spirometry, Imaging Skill Lab
Friday 11.00 – 11.50 Break
2 Nov 12.00 – 12.50 SGD 9,10 Discussion R Fasilitator
14.00 – 14.50 Pleno 9,10 Class R dr. Arya / Dr. dr.

Muliarta
15.00 – 15.50 Pleno 11,12 Class R dr. Ekawati
7 08.00 – 08.50 Lecture 13: Pharmacological Class R Dr. dr. Satriyasa
Monday concepts of Respiratory medicines
5 Nov 09.00 – 09.50 Lecture 14: Pharmacological and Class R Dr. dr. Satriyasa
2018 nonpharmac Intervention 1
10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 15:Pharmacological and Class R Prof. Aman
nonpharmacological Intervention
13.00 – 13.50 Lecture 16: Resp Imaging Class R Dr. dr. Elysanti
14.00 – 14.50 IL
15.00 – 15.50 SP
8 08.00 – 08.50 BCS2: Px/ of Children, Imaging Skill Lab dr. Ayu/Dr. dr.
Tue 09.00 – 09.50 BCS2: Px/ of Children, Imaging Skill Lab Elysanti
6 Nov 10.00 – 10.50 BCS2: Px/ of Children, Imaging Skill Lab
2018 11.00 – 11.50 Break
14.00 – 14.50 Pleno 13,14 Class R Dr. dr. Satriyasa
15.00 – 15.50 Pleno 15,16 Class R Prof. Aman/Dr.
dr. Elysanti
08.00 – 08.50 Lecture 17: Bronchiolitis, asthma in Class R Dr. dr. Subanada
children dr. Ayu S.
9 09.00 – 09.50 Lecture 18: Pneumonia, Class R
Wed Bronchopneumonia
7 Nov 10.00 – 10.50 IL
2018 11.00 – 11.50 Break dr. Ayu S.
12.00 – 12.50 Lecture 19: Aspiration Pneumonia Class R dr. Siadi
13.00 – 13.50 Lecture 20: Difteri, Pertusis Class R
14.00 – 14.50 IL
15.00 – 15.50 SP
10 08.00 – 08.50 BCS3: WSD, Pengambilan cairan Skill Lab Dr. dr. Yasa
Thurs pleura, punksi, decomp. jarum
8 Nov 09.00 – 09.50 BCS3: WSD, Pengambilan cairan Skill Lab Dr. dr. Yasa
2018 pleura, punksi, decomp. jarum
10.00 – 10.50 BCS3: WSD, Pengambilan cairan Skill Lab Dr. dr. Yasa
pleura, punksi, decomp. jarum
11.00 – 11.50 Break
14.00 – 14.50 Pleno 17,18 Class R Dr. dr. Subanada
/ dr. Ayu
dr. Ayu / dr. Siadi
15.00 – 15.50 Pleno 19,20 Class R
11 08.00 – 08.50 Lecture 21: TB in Children Class R dr. Siadi

Friday 09.00 – 09.50 Lecture 22: Adult Pulmonary TB Class R dr. Suta
9 Nov 10.00 – 10.50 IL
2018 11.00 – 11.50 Break
12.00 – 12.50 Lecture 23: Extrapulmonary TB Class R dr. Suta
13.00 – 13.50 Lecture 24: TB in the Class R dr. Bagiada
Immunocompromised Host,
Abscess TB
14.00 – 14.50 IL
15.00 – 15.50 SP
08.00 – 08.50 BCS4: Nebulisasi and O2 therapi, Skill Lab dr.
12 Bronchoscopy and provocation test Arya/dr.Artana
Monday 09.00 – 09.50 BCS4: Nebulisasi and O2 therapi, Skill Lab dr.
12 Nov Bronchoscopy and provocation test Arya/dr.Artana

2018 10.00 – 10.50 BCS4: Nebulisasi and O2 therapi, Skill Lab dr.
Bronchoscopy and provocation test Arya/dr.Artana
11.00 – 11.50 Break
14.00 – 14.50 Pleno 21,22 Class R dr. Siadi/dr. Suta
15.00 – 15.50 Pleno 23,24 Class R dr. Suta/dr.
Bagiada
13 08.00 – 08.50 Lecture 25: Asthma, COPD Class R dr. Artana
Tue 09.00 – 09.50 Lecture 26: Pleural Effusion, Class R dr. Andrika
13 Nov Emphysema, Lung Edema
2018 10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 27: Pneumothorax, Class R Dr. dr. Yasa
Hemothorax
13.00 – 13.50 Lecture 28: Bronchitis, Class R dr. Suta
Bronchiectasis
14.00 – 14.50 IL
15.00 – 15.50 SP
08.00 – 08.50 BCS5: CPEP bayi, Rhinoskopi Skill Lab dr. Arya/THT
14 posterior
Wed 09.00 – 09.50 BCS5: CPEP bayi, Rhinoskopi Skill Lab dr. Arya/THT
14 Nov posterior
2018 10.00 – 10.50 BCS5: CPEP bayi, Rhinoskopi Skill Lab dr. Arya/THT
posterior
11.00 – 11.50 Break
14.00 – 14.50 Pleno 25,26 Class R dr. Artana/dr.
Andrika
15.00 – 15.50 Pleno 27,28 Class R Dr. dr. Yasa/dr.
Suta
15 08.00 – 08.50 Lecture 29: Lung Ca and Education Class R dr. Saji
Thurs of smoking Cessation
15 Nov 09.00 – 09.50 Lecture 30:Disorder of nose, Sinus Class R dr. Ratna
2018 10.00 – 10.50 IL
11.00 – 11.50 Break
12.00 – 12.50 Lecture 31:Disorder of Pharynx, Class R Prof. Suardana
Disorder of Larynx
13.00 – 13.50 Lecture 32: Nose and Throat Foreign Class R dr. Dewa Eka
Bodies
14.00 – 14.50 IL
15.00 – 15.50 SP
16 08.00 – 08.50 BCS1,2 Skill Lab dr. Saji/Dr.
Friday 09.00 – 09.50 BCS1,2 Skill Lab dr.Muliarta/Dr.
16 Nov 10.00 – 10.50 BCS1,2 Skill Lab Ayu/Dr. dr.
2018 Elysanti
11.00 – 11.50 Break
14.00 – 14.50 Pleno 29,30 Class R dr. Saji/Dr. Ratna
Prof.
15.00 – 15.50 Pleno 31,32 Class R Suardana/dr.
Dewa Eka
17
Monday
BREAK
19 Nov
2018
18 BREAK
Tue

20 Nov
2018
19
Wed
EVALUATION
21 Nov
2018
LEARNING PROGRAMS
LECTURE 1

INTRODUCTION
Dr. dr. I Made Muliarta, M.Kes
Every human being needs oxygen to maintain his survival. Humans can live without
eating and drinking for several days, but do not without oxygen. Humans only live without
oxygen for only a few minutes. The longest breath-resistant record held by a diver with
breathholding for 24 minutes 3.45 seconds at the 17th Mediterranean Dive Show that took
place in Spain on 2016.
Every body cell needs oxygen to metabolize and produce energy and remove carbon
dioxide as a by-product. This is done so that each cell can function optimally. Oxygen and
carbon dioxide in body cells are delivered to and from the pulmonary capillaries by blood
through the work of the heart and blood vessels. The oxygen used by the body comes from
atmospheric air and carbon dioxide from the body is discharged into the atmosphere by the
respiratory system.
The main function of the respiratory system is to provide oxygen for the needs of cells
and remove carbon dioxide produced by body cells. This function can be run through several
processes. The process includes ventilation, oxygen diffusion and carbon dioxide, perfusion,
gas transport, and respiratory regulation.
Learning Task
1. Describe the role of the respiratory system in the body!
2. Describe the internal and external respiration!
3. How does the respiratory system maintain PO2 and PCO2 in the body?
LECTURE 2
PHYSIOLOGY OF RESPIRATORY SYSTEM: VENTILATION

dr. I Made Muliarta, MKes
In living cells aerobic metabolism consumes oxygen and produces carbon dioxide. Gas
exchange requires a large , thin, moist exchange surface, a pump to move air circulatory
system to transport gases to cells. The primary function system are:
Exchange the gases between atmosphere and the
blood. Homeostatic regulation of body pH .
Protection from inhaled pathogens and irritation
substance Vocalization.
In addition to serving these function, the respiratory system also source of significant
losses of water and heat from the lung.
A single respiratory cycle consists of an inspiration and expiration. Relation with
ventilation had to know about compliance, surfactant, lung volume and capacities
Respiratory control resides in a central pattern generator, a net work of neurons in the
pons and medulla oblongata.

Learning Task
1. What is the sequence of event during quiet inspiration (muscle involvement, pressure
changes (intrapulmonary and intrapleura), volume changes)!
2. What is pulmonary ventilation and alveolar ventilation means?
3. Andi, male, 30 years old, has a puncture wound due to car accident in his right chest and
penetrate his pleural cavity. The patient has complained shortness of breathing and
doctor determine that his lung is collapsed.
a. What is this condition called?
b. Describe the mechanism of the lung collapse!
c. What kind respiratory system compensation to anticipate this condition (lung
collapse)?
d. How can he still be alive in this condition?
4. Describe the Boyle’s Law!
LECTURE 3
HISTOLOGY OF RESPIRATORY TRACT
dr. IGK Nyoman Arijana, M.Si.Med
The lower respiratory tract consists of: the lower part of the trachea, the two main
bronchi, lobar, segmental, and smaller bronchi, bronchioles and terminal bronchioles, and last
but not least is the end respiratory unit. These structure make up the tracheobronchial tree.
As for the structure distal to the main bronchi along with a tissue known as the lung
parenchyma.
There are several structure we should also understand, when talking about lower
respiratory tract. Several structures such as thorax, mediastinum, pleurae and pleural cavity,
and lung. Thorax especially thoracic cavity and thoracic wall protect our lung and
mediastinum and also play an important role in respiratory process. The mediastinum, which
has a role in protecting our heart , located between the two lungs, and contains the heart and
great vessels, trachea and esophagus, phrenic and vagus nerves, and lymph nodes.
The pleurae covers the external surface of the lung, and is then reflected to cover the
inner surface of thoracic cavity. Pleurae divided into the visceral (lines the surface of the lung)
and parietal (lines the thoracic wall and diaphragm) one. The space between these two
pleurae called as pleural cavity which contains a thin film fluid to allow the pleurae to slip over
each other during breathing.
The lungs are placed within the thoracic cavity. The lungs contain airways structure,
vessels, lymphatic and lymph nodes, nerves, and supportive connective tissue. The trachea
divides and form the left and right primary bronchi, which in turn divide to form lobar bronchi.
Each lobar bronchi divide again to give segmental bronchi to supply air to bronchopulmonary
segments. The tracheobronchial tree can also be classified into two functional zones: the
conducting zone (proximal to the respiratory bronchioles) which involved in air movement,
and the respiratory zone (distal to the terminal bronchioles) which involved in gaseous
exchange.
The other term to show functional structure of the lower respiratory tract is the acinus.
The acinus defined as the part of the airway that is involved in gaseous exchange. The acinus
consist of respiratory bronchioles, alveolar ducts, and alveoli as the smallest functional

structure of the lung. The areas of lung containing groups of between three to five acini
surrounded by parenchimal tissue are called lung lobules.
The alveolus is an blind-ending terminal sac of respiratory tract. Most gaseous
exchange occurs in the alveoli. The alveoli are lined with type I (structural) and type II
(produce surfactant) of pneumocytes cell. The understanding about histological pattern of
these functional structures of the lung is important in pathophysiology of lung problems.
Learning Tasks
A. Structure of The Upper Respiratory tract
Krishna, a man, 25 years old came to doctor Arjuna clinic with fever, sore throat, sneezing,
runny nose and sometimes blocked nose. He also cannot smell well. The doctor diagnoses
Krishna with acut Rhinopharingitis.
1. Describe the histological structure of the upper respiratory tracts are involved?
2. Describe the histological structure and function of epiglottis!
3. Compare the histological structure and function between vestibular fold and vocal fold!
B. Structure of The Lower Respiratory tract

Radha, a 17 years old beautiful girl, came to doctor Laksmi clinic with shortness of breath,
wheezing and cough with phlegm. The doctor diagnoses Radha with Asthma.
1. Describe the histological structure of the lower respiratory tracts are involved?
2. Compare the histological structure and function between terminal bronchioles and
respiratory bronchioles!
3. Describe the histological structure of the interalveolar septum!
4. Describe the histological structure of blood-air barrier?
5. Describe about the pulmonary surfactant?
LECTURE 4
PHYSIOLOGY OF RESPIRATORY SYSTEM: GAS EXCHANGE, DIVING, ALTITUDE
Gas exchange during external respiration occurs in respiratory membrane. Several

factors may influence gas exchange. Dalton’s law and Henry’s law may apply during gas
exchange.
Some physiologic responses on respiratory system at high altitude and during diving.
Some illnesses/injuries related pressure change may occursat high altitude and during diving.
Learning Task
1. Describe the Dalton’s Law!
2. Describe the factors that influence oxygen diffusion from alveoli into the blood!
3. Predict the response of the pulmonary arterioles and bronchioles when PO2 increase
and PCO2 decrease!
4. Describe some illnesses/ injuries due to high altitude!
5. Describe some illnesses/ injuries due to diving!

LECTURE 5
ANATOMY OF UPPER RESPIRATORY TRACT
dr. I Nyoman Gede Wardana, M.Biomed
The respiratory system consists of conducting zone and respiratory zone. Conducting
zone, whose walls are too thick to permit exchange of gases between the air in the tube and
the blood stream. The nostrils (nares), nasal cavity, pharynx, larynx, trachea, bronchi, and
terminal bronchioles are included in this zone. Respiratory zone, whose walls are thin enough
to permit exchange of gases between tube and blood capillaries surrounding them. Air travels
to the lungs through that zone. The right lung divided into three lobes: superior, middle, and
inferior. The left lung divided into two lobes: superior and inferior. Each lung cover by a
membrane that called pleura. Both lungs are inside the thoracic cage. The thoracic cage is
formed by the vertebral column behind, the ribs, and intercostal spaces on other side and the
sternum and costal cartilages in front. Below it separated from the abdominal cavity by
diaphragm
Learning Task
Vignette 1:
Kesawa, 32 years old, was seen in the clinic ten days ago, was diagnosed with rhinitis and
sent home with instructions for increased fluids, decongestants, and rest. Kesawa presents
today with worsened symptoms of malaise, low-grade temperature, nasal discharge, night
time coughing, mouth breathing, early morning pain over sinuses, and congestion. The doctor
diagnose he is suffering sinusitis.
1. Describe the boundaries of the nasal cavity and its blood supply!
2. Describe the paranasal sinuses and its opening at nasal cavity!
Vignette 2:
Gotawa, a singer-18 years old came to clinic with complain a hoarse voice for 3 days. She
also suffers sore throat, nose block, and fever. She was diagnosed laryngitis
1. Describe the structure of larynx and location of vocal cord!
2. Describe the intrinsic and extrinsic muscle of larynx!
LECTURE 6
ANATOMY OF LOWER RESPIRATORY TRACT
dr. I Nyoman Gede Wardana, M.Biomed
Vignette 3:
Mande, 30 years old male came to clinic with chief complaint difficulty to breath start from this
morning. He also suffers cough, runny nose and fever. He has history bronchial asthma when
he was 2 years old. The doctor diagnose he is suffering bronchial asthma.
1. Describe the structure of trachea!
2. Describe the different between right and left main bronchus!
3. Describe the principal different between trachea, bronchi, and bronchioles!

Vignette 4:
A 57-year-old male is admitted to the hospital with a chief complaint of shortness of breath for
2 weeks. The radiology examination shows a large left-side pleural effusion.
1. Describe the different between right lung and left lung!
2. Describe the structure of pleura!
3. Describe the structure of thoracic wall!
LECTURE 7
FUNCTIONAL CHARACTERISTIC OF PULMONARY CIRCULATION
Physiology
LECTURE 8
CARRIAGE OF OXYGEN AND CARBON DIOXIDE
Dr. dr. Desak Wihandani, M.Kes
The supply of oxygen to the tissues is our most immediate physical need. We take in
about 250 ml of oxygen gas per minute and this is our most pressing physical need. If our
oxygen supply is interrupted for more than a few minutes, irreversible damage is done to
some tissues, notably the brain. Oxygen is abundantly available in the air around us but
cannot diffuse into our tissues at sufficient rate to meet our needs. It must be transported from
the lung, the specialized organ for gas exchange, by the blood to all the other tissue.
While oxygen has to be transported from lungs to tissues, carbon dioxide must be
transported from the tissues for excretion by the lungs. Carbon dioxide has physicochemical
properties that make its transport less difficult then transport of oxygen. Carbon dioxide can
be transported in the blood in three ways: in simple solution, by reversible conversion to
bicarbonate and by reversible combination with haemoglobin to form carbamino
haemoglobin.
Learning Task:
1. Describe the structure and function of hemoglobin!
2. Describe the mechanism of oxygen binding to hemoglobin!
3. Describe the differences between hemoglobin and myoglobin!
4. Describe the mechanism of oxygen binding to myoglobin!
5. Describe conformational differences between deoxygenated and oxygenated Hb!
6. Summarize the processes by which carbondioxide is transported from peripheral
tissues to the lungs!

LECTURE 9
CONTROL OF ACID BASE BALANCE, ARTERIAL GAS ANALYSIS (AGA)
dr. Arya Biantara, Sp.An
Acid-Base Balance
There is large daily flux of oxygen, carbon dioxide and hydrogen ion through the human body.
Carbon dioxide generated in tissues dissolves in H2O to form carbonic acid, which in turn
dissociates releasing hydrogen ion. The blood concentration of hydrogen ion is constant, it
remains between 36 and 46 nmol/L (pH 7,36-7,46). Changes in pH will affect the activity of
many enzyme and tissue oxygenation. Problems with gas exchange and acid-base balance
underlie many diseases of respiratory system.
Blood Gases
Blood gas measurement is an important first-line investigation performed whenever there is a
suspicion of respiratory failure or acid-base disorders. In respiratory failure, the results of
such measurements are also an essential guide to oxygen therapy and assisted ventilation.
The key clinically used parameters are pH, pCO 2 and pO2, the bicarbonate concentration is
calculated from pH and pCO2 values.
Learning Task:
1. Describe organs in our body involved in acid-base balance, and how they work!
2. Describe acid-base balance disorders! What is mean by :
a. Respiratory alkalosis,
b. metabolic alkalosis,
c. respiratory acidosis, and
d. metabolic acidosis?
3. In which condition respiratory acidosis and respiratory alkalosis occurs?
4. What is the importance of blood gas measurement. To perform measurement where
are the blood sample taken from? What kind of measurements are done?
LECTURE 10
CONTROL OF RESPIRATORY FUNCTION
When considering contol of breathing, the main control variable is PaCO2 (we try to
control this value near to 40 mmHg). This can be carried out by adjusting the respiratory rate,
the tidal volume, or both. By controlling PaCO2 we are effectively controlling alveolar
ventilation (see Ch.3) and thus PACO2. Although PaCO2 is the main control variable, PaO2 is
also controlled, but normally to a much lesser extent than PaCO2. However, the PaO2 control
system can take over and become the main controlling system when the PaO2 drops below
50 mmHg. Control can seem to be brought about by:
1. Metabolic demands of the body (metabolic control)-tissue oxygen demand and acid-
base balance.
2. Behavioural demands of the body (behavioral control) – singing, coughing, laughing
(i.e.control is voluntary).
These are essentially feedback and feed-forward control systems, respectively. The
behavioural control of breathing overalys the metabolic control. Its control is derived from
higher centres of the brain. The axons of neurons whose cell bodies are situated in the
cerebral cortex bypass the respiratory centres in the brainstem and synapse directly with
lower motor neurons that control respiratory muscles. This system will not be dealt with in this
next;we shall deal only with the the metabolic control of respiration.
Learning Tasks
1. Discuss the central control of breathing with reference to the pontine respiratory group
and the dorsal-ventral respiratory groups of medulla spinalis!
2. List the different types of receptors involved in controlling the respiratory system!
3. Describe factors that stimulate central and peripheral chemoreceptor!
4. Outline the response of the respiratory system to change in carbon dioxide
concentration, oxygen concentration and pH!
5. Discuss the mechanism thought to influence the control of ventilation in exercise!
6. Discuss the changes that occur in response to high altitude!
LECTURE 11
PATHOLOGY OF UPPER AND LOWER URINARY TRACT
dr. Ni Putu Ekawati, Sp.PA, M.Repro
The term “upper airways” is used here to include the nose, pharynx, and larynx and
their related parts. Disorders of these structures are among the most common afflictions of
humans, but fortunately the overwhelming majority are more nuisances than threats.
Inflammatory diseases are the most common disorders of the upper respiratory tract, i.e.
rhinitis, sinusitis, pharyngitis, tonsillitis and laryngitis. It may occur as the sole manifestation of
allergic, viral, bacterial or chemical insult. Although most infections are self-limited, they may
at times be serious, especially laryngitis in infancy or childhood, when mucosal congestion,
exudation, or edema may cause laryngeal obstruction. Tumors in these locations are
infrequent but include the entire category of mesenchymal and epithelial neoplasms. Some
distinctive types are nasopharyngeal angiofibroma, Sinonasal (Schneiderian) Papilloma,
Olfactory Neuroblastoma and Nasopharyngeal Carcinoma.
Classification of lower respiratory tract (lung) diseases can be made based on the result
of lung function test, although some authors prefer etiology and pathogenesis background.
Some important diseases are obstructive lung disease (asthma, COPD, bronchiectasis) and
restrictive lung disease (ARDS), and also infections, diseases of vascular origin and tumors.
Pleura as protective structure of the lungs, are sometimes involved as secondary
complication of some underlying disease, but in rare case, can be primary.
Because of the complexity of respiratory disease, it is important to understand their

pathogenesis, supported by recognizing their morphologic changes.
LEARNING TASK
Case 1
A male patient, 16 year old, came to a doctor with chief complaint difficulties in breathing. It
has occurred since 1 month ago. This patient suffers from rhinitis alergica since he was 3
year old. On physical examination, a pedunculated nodule in right nasal cavity was found. It
was whitish in color, 1.5 cm in diameter occluding the nasal cavity.
1. Based on clinical finding, what is the most possible diagnosis?
2. What are the DDs?
3. Describe the morphological appearance (macroscopy and microscopy) that supposed

to be found to confirm your diagnosis!
4. Explain the pathogenesis of this diasease!
Case 2
A male patient, 65 year old, has suffered from dyspnea and productive cough since 1 year
ago. Lung function test showed increased of FEV1 with normal FVC (confirm an obstructive
lung disease). He is a heavy smoker since he was 25 year old. No history of atopy. No
evidence of cardiac disorders.
1. Mention 4 diseases including in the spectrum of obstructive lung disease!
2. Explain their pathogenesis!
3. Distinguish their morphology!
Case 3
A female patient, 50 year old, has suffered from tumor of right lung with pleural effusion. As
the first step to confirm the diagnosis, doctor asked the patient to do cytology test.
1. Mention some cytology test can be choose for this patient!
2. Among the test mention above (A), which one is the most simple and non-invasive?
3. And, discuss how to collect the specimen!

LECTURE 12
LUNG DEFENCE MECHANISM
dr. Ni Putu Ekawati, Sp.PA, M.Repro
Respiratory tract is an organ that constantly exposed by contaminated air. It is there

fore a small miracle that the normal lung parenchyma remains sterile. Fortunately, a plethora
of immune and non immune defense mechanisms exist in the respiratory system, extending
from the nasopharynx all the way into alveolar airspaces.
The major categories of defense mechanisms to be discussed include : (1) physical or

anatomic factors related to deposition and clearance of inhaled materials, (2) antimicrobial
peptides, (3) phagocytic and inflammatory cells that interact with inhaled materials, (4)
adaptive immune response, which depends on prior exposure to recognize the foreign
materials. Each components appears to have a distinct role, but a tremendous degree of
redundancy and interaction exists among different components.
Any condition breaks down the lung defense mechanism may result in lung injury and
respiratory tract infections
Learning Tasks
1. Defense mechanism of the lung and respiratory tract ca be divided into four major
categories. Mention them, their components and explain how each of them acts
against foreign materials!
2. Explain about diseases or conditions that break the lung defense mechanism down
which result in increase susceptibility to respiratory tract infections!
LECTURE 13
PHARMACOLOGICAL CONCEPTS OF RESPIRATORY MEDICINES
Dr. dr. Bagus Komang Satriyasa, M.Repro
LECTURE 14
PHARMACOLOGICAL AND NON PHARMACOLOGICAL INTERVENSION I
Prof. dr. GM Aman
Drugs for cough, rhinitis, asthma bronchiale

Cough is a protective reflex mechanism that removes foreign material and secretions
from the bronchi and bronchioles. It can be inappropriately stimulated by inflammation in the
respiratory system or by neoplasia. In these cases, antitussive (cough suppressant) drugs
are sometimes used. It should be understood that these drugs merely suppress the
symptom without influencing the underlying condition. In cough associated with
bronchiectasis or chronic bronchitis, antitussive drugs can cause harmful sputum thickening
and retention. They should not be for the cough associated with asthma.
Most drugs used in rhinitis are effectively relief the symptom of rhinitis, not affect the
underlying disease. No drug can relief symptom completely. Drugs are more effective for
allergic rhinitis than non allergic rhinitis, and acute form of allergy respond more favorable
than chronic form of allergy. The most common drugs used for rhinitis are antihistamine,
nasal disodium cromoglycate, nasal decongestant, anticholinergic, intranasal corticosteroid.
Bronchial Asthma is a disease characterized by airway inflammation, edema and
reversible bronchospasm. Bronchodilator and anti-inflammatory are the most useful drugs
used in asthma. B2 selective agonists, muscarinic antagonists, aminophylline and
leukotriene
eceptor blockers are the most effective bronchodilator. Anti-inflamatory drugs such as
corticosteroid, mast cell stabilizers, leucotriene antagonists, and an anti IgE antibody are
widely used. Short acting B2 agonist are the most widely used for acute asthma attack, by
relaxing airway smooth muscle. Theophylline, aminophylline and antimuscarinic agent are
also used for acute asthma attack. Long term control can be achieved with an anti-
inflammatory agent such as corticosteroid (systemic or inhaled), with leucotriene antagonist,
mast cell stabilizers (cromolyn or nedocromil). Long acting B2 agonists such as Salmeterol
and Formeterol, are effectively in improving asthma control, when taken regularly.
Learning Tasks
The patient complained about a sore throat and a nasty cough. It started two weeks ago with
a cold. The cold was over within a week, but he continued coughing, especially at night. He
is a heavy smoker. After physical examination you diagnosed a dry, tickling cough.
Task 1
1) Differentiate between Antitussive, Expectorant, Mucolytic!
2) Differentiate the effects of Codeine, Dextromethorphan and Diphenhydramine!
3) List the side effects of Codeine!
4) In this patient, what kind of anti cough you give best?
Task 2
If the patient also has sneezing, rhinorrhea and congested nose and then you diagnosed as
rhinitis.
1) List the group of drugs used for Rhinitis!
2) List the drugs used as oral nasal decongestant, and describe the important side
effects!
3) List the side effects of intranasal decongestant!
4) What is the drug of choice for patient suffer from Rhinitis Medicamentosa?
LECTURE 15
PHARMACOLOGICAL AND NON PHARMACOLOGICAL INTERVENSION II
Prof. dr. GM Aman
Learning Task
If the patient come with cough, breathless, and in your examination, you found wheezing.
After physical examination you diagnosed Acute attack of bronchial asthma.
1. Chose the drug of first choice for this patient!
2. List the side effects of this drug!
3. Compare the effect of this drug with Salmeterol!
4. Theophyllin is a bronchodilator, but has a narrow safety margin. List the side effects &
toxic effect of Theophyllin!
5. Ipratropium not as effective as Salbutamol in treating bronchial asthma. What is the
main use of Ipratropium?
6. Cromolyn and Nedocromil are often used for Asthma bronchial. Describe the
mechanism of action of Cromolyn (Disodium Cromoglycate)!
7. To decrease the side effet of Corticosteroid in asthma patient, Corticosteroid often
use as inhaled Corticosteroid. What are the side effect of inhaled Corticosteroid?
8. List the anticough that are contraindicated in acute asthma attack!
9. If you need anticough, what drug you give best?
LECTURE 16
RESPIRATORY IMAGING
dr. Elysanti, Sp.Rad
The imaging investigations of the chest may be considered under the following heading:
1. Simple X- ray (conventional X-ray).
2. Chest screening.
3. Tomography.
4. Bronchography.
5. Pulmonary angiography.
6. Isotope scanning.
7. Computed tomography(CT-scan).
8. MRI.
9. Needle biopsy.
The conventional Chest X-ray has to diagnose the anatomical disorders of the chest for
example:
1. Lungs disease-----pneumonia, mass, atelectasis etc.

2. Pleural disease----pleural effuse, pneumothorax etc.
3. Cardiac disease----cardiomegali.
4. Bone disorders-----fracture.
5. Soft tissue disease—emphysema cutis.
Sometimes conventional X-ray diagnostic can not enough for diagnostic of the chest
disorders, for this the CT scan, MRI, bronchography, and arteriography can be help.
Learning Tasks
A male patient, 68 years old, with chronic cough and hemoptoe.
1. What is the imaging choice for establish the diagnosis ?
2. What kind of diagnosis you will consider if the imaging revealed some consolidation
at the apex of the right lung accompanied by rib destruction?
A 1- month old female patient is suffered from fever and dyspneu.
1. What kind of abnormality you hope to see on the chect X ray film?
2. What do you thing about the diagnosis of the disease?
LECTURE 17
BRONCHIOLITIS AND ASTHMA IN CHILD
dr. IB Subanada, SpA
Bronchiolitis is an acute inflammatory disease of the lower respiratory tract

(bronchioles) caused predominantly by respiratory syncytial virus (RSV). The inflammation
response characterized by bronchiolar epithelial necrosis, bronchiolar occlusion, and
peribronchiolar collection of lymphocytes. Bronchiolus become edematous and obstructed
with mucus and celluler debris, which may lead to partial or complete collapse of the
bronchioles. By the age 2 years nearly all children have been infected, with severe disease
more common among infants aged 1-3 months.
The clinical manifestation, initially upper respiratory signs and symptoms and followed
by obstructed bronchioles signs and symptoms.
The white blood cell and differential counts are usually normal. Chest x-ray reveals
hyperinflation, peribronchial cuffing, and atelectasis.
The mainstay of therapy is supplemented oxygen with close monitoring and supportive
care.
There are higher incidence of wheezing and asthma in children with history of
bronchiolitis. Pooled hyperimmune RSV intravenous immunoglobulin (RSV-IVIG) and
palivizumab intramuscular are effective to preventing severe RSV disease in high risk
infants. The case fatality rate is less than 1%.
Learning Tasks
A 6-months old male infant came to Outpatient Clinic, Department of Child Health,
Medical School, Udayana University, Sanglah Hospital, Denpasar with the chief complaint of
difficult to breath since yesterday. According to his mother, three days before, he suffered
from coryza, cough, and low grade fever. On physical examination, fast breathing, wheezing
and a prolonged expiratory phase were found. Please discuss his mother the disease of the
infant!
Learning Tasks
1. Explain the pathological concept of asthma in child!
2. Explain the clinical manifestations of asthma in child!
3. Explain the diagnosis principles of asthma in child!
4. Determine the severity of asthma and the degree of asthma attack in child!
5. Construct management plans for asthma attack in child (reliever) and determine the
need for controller management!
6. Identify the need for referral!
LECTURE 18
PNEUMONIA AND BRONCHOPNEUMONIA
dr. Ayu Setyorini, Sp.PA(K)
LECTURE 19
ASPIRATION PNEUMONIA
dr. Ayu Setyorini, Sp.PA(K)
LECTURE 20
DIPHTHERIA, PERTUSIS
dr. Siadi, Sp.PA(K)
LECTURE 21
ASTHMA AND COPD
Dr. Artana, Sp.PD

Asthma
Airway hyper responsiveness is known as the denominator underlying all form of
asthma. The basis of this abnormal bronchial response is not fully understood. Most current
evidence suggests that bronchial inflammation is the substrate for this hyper
responsiveness, manifested by the presence of inflammatory cells and by damage of
bronchial epithelium. In extrinsic (allergic) asthma, bronchial inflammation is caused by type I
hypersensitivity reactions, but in intrinsic asthma, the cause is less clear. Incriminated in
such cases are viral infections of the respiratory tract and inhaled air pollutant such as sulfur
dioxide, ozone and nitrogen dioxide.
General Objektif:
1. Mampu menjelaskan penegakan diagnosis asma.
2. Mampu menyusun program pengobatan jangka panjang asma.
3. Mampu mengidentifikasi pasien dengan serangan asma akut.
4. Mampu memberikan pengobatan awal pasien dengan serangan asma akut.
5. Mampu mengidentifikasi pasien asma akut yang perlu perawatan inap di rumah sakit,
dan merujuknya.
Triger
Anda sebagai seorang dokter yang bekerja di sebuah Puskesmas kota, datang seorang
pasien wanita, usia 36 tahun. Dia menyampaikan bahwa telah menderita asma sejak usia
remaja. Dalam 3 bulan terakhir ini, dia mengalami serangan asma hampir setiap 3 hari ,
termasuk serangan di malam hari. Untungnya, kata pasien, serangan asmanya dapat diatasi
dengan obat semprot yang dia miliki. Pasien menginginkan agar terbebas dari penyakitnya
ini.
Learning Task
1. Jelaskan bagaimana saudara memastikan bahwa pasien tersebut memang
menderita asma!
2. Apakah asma pasien tersebut dalam keadaan terkontrol? Jelaskan!
3. Apakah inhaler yang dipergunakan oleh pasien tersebut termasuk ke dalam
kelompok pelega (reliever)? Jelaskan perbedaan fungsi antara reliever dan
controller, dan sebutkan obat-obat dari kedua kelompok tersebut!
4. Susun rencana penatalaksanaan jangka panjang pasien tersebut!
5. Apabila suatu saat pasien tersebut mengalami suatu serangan asma akut, terapi apa
yang akan saudara berikan?
6. Jelaskan kreteria serangan asma akut berat!
COPD
Chronic Obstructive Pulmonary Disease (COPD) is a disease state characterized by
airflow limitation that is not fully reversible. COPD is the fourth leading cause of death in the
world and the number of patients is projected to increase worldwide in the future. Tobacco
accounts for an estimate of 90% to the risk of developing COPD. Patient with COPD first
complaining chronic cough with sputum and followed by dyspnea. This condition worsening
progressively until the patient unable to do his daily activities.
Treatment aim for COPD is to decrease symptom, without stopping the progression of
this disease. Prevention is more important in this condition, such as by smoking cessation
program.
General Objektif:
1. Mampu menjelaskan penegakan diagnosis PPOK serta penilaian kombinasi pasien.
2. Mampu menyusun rencana pengobatan pada kasus PPOK stabil.
3. Mampu menangani factor risiko pasien PPOK.
4. Mampu menentukan eksaserbasi akut dari PPOK.
5. Mampu menjelaskan manajemen gawat darurat pasien dengan PPOK eksaserbasi
akut.
Triger
Seorang pasien laki-laki usia 70 tahun datang bersama anaknya kepoliklinik paru Rumah
Sakit Daerah tempat anda bertugas dengan mengeluh sesak nafas. Sesak nafas dirasakan
sangat berat, berpakaian pun pasien mengaku sesak. Sebelumnya pasien memang
merokok sejak usia 20 tahun sebanyak 2 pak sehari. Pasien juga mengatakan sering
opname di rumah sakit karena serangan sesak nafas yang sangat berat. Pasien dan
keluarganya ingin mengetahui dengan pasti mengenai penyakitnya serta tindak lanjut
penanganannya.
Learning Task
1. Jelaskan bagaimana penegakan diagnosis pasien tersebut!
2. Bagaimanakan kombinasi penilaian pasien ini? Data apa saja yang saudara perlukan
untuk melengkapi kombinasi penilaian tersebut?
3. Sebutkan dan jelaskan obat-obat yang dapat digunakan untuk menangani kasus
PPOK stabil!
4. Bagaimana anda menyusun rencana penatalaksanaan pasien ini secara
komprehensif?
5. Bagaimana penatalaksanaan pasien ini apabila mengalaami PPOK eksaserbasi
akut?
LECTURE 22, 23
PULMONARY TB AND EXTRAPULMONARY TB
dr. IB Sutha, SpP
WHO estimates that about 9.27 million new cases in 2007 compared with 2.24 million
cases in 2006, with 44% or 4.1 million cases of the infectious cases (sputum smear new
cases with positive). TB problem in Indonesia is a national problem, the case is increasing
and increasingly concerned with the increasing HIV infection and AIDS are rapidly growing
emergence of multi-drug resistance TB problem.
Tuberculosis is an infectious disease directly caused by the bacteria Mycobacterium
tuberculosis that primarily attacks the lungs. TB bacteria are rod-shaped, aerobic with a
complex cell wall structure, it was mainly composed of fatty acids that are acid resistant and
can survive in a dormant form.
TB germs enter through inhalation of the bacteria will reach the alveoli and catched by
alveolar macrophages, the bacteria will die. If the germs stay alive it will proliferate to form
primary apex (Primer Apex) and will limphogen or hematogenous spread. Primary apex
surround by limphogen spreading form the "primary complex of Ghon" and formed specific
cellular immunity is characterized by a positive tuberculin test. If the immunity is low,
complex primary complications, the patient became ill and the symptoms and clinical signs
of disease. M. tuberculosis may attack any organ of the body and most importantly the
lungs.
Clinical symptoms involve respiratory symptoms and prodromal symptoms, whereas
clinical signs obtained at once with the examination depends on the type and extent of
lesions in the lungs and surrounding organs. Radiological examination of the thorax will get
the infiltrates, fibrosis and kaverna. Bacteriological examination by smear and culture of
sputum smear examination.
TB treatment follow national treatment program. Tuberculosis control which refers to
the eradication of TB WHO guideline.
General Objectives
1. Knowing the microbiology, epidemiology and pathogenesis of tuberculosis.
2. Knowing the clinical symptoms, clinical and radiological signs of pulmonary TB and
extra-pulmonary TB.
3. Able to clasify Tuberculosis.
4. Able to explain treatment program of tuberculosis and side effect.
5. Able to describe the prevention of tuberculosis and MDR TB.
Triger
A male patient aged 25 years came to a health center with complaints of bloody cough every
time since one month ago. That was not originally phlegm but since two weeks ago a
yellowish productive cough. The coughing did not disappear with anti-cough medicine.
Shortness of breath and chest pain is absent. Patients feel the slightly fever and night
sweating and also weakness, no appetite. Patients had never been sick before, enough
food, smoking and family sometimes there is no similar illness. Physical examination has
been found: look thin, alert state, blood pressure 110/70 mmHg; pulse rate 108 x/mnt;
Respiration rate 24 breaths/mntT.aksila 370C. Lymph nodes enlargement on the right neck.
On chest examination: symmetrical right-left chest, normal heart, vesicular breath sounds in
the chest and rhales on the third upright.
Learning Tasks:
1. What should you do to ensure the diagnosis of this patient?
2. What should you do for this patient with enlargement of gland in the neck?
3. If the sputum smear examination results - / +2 / -, what is diagnosis?
4. Explain the treatment program appropriate to this patient!
5. Explain about patient monitoring and Communication-Information-and Education for
this patient and his family?
LECTURE 24
TB IN THE IMMUNOCOMPROMISED HOST
dr. Made Bagiada, SpPD-KP
Sebagai seorang dokter yang bekerja di tingkat pelayanan primer, pemahaman

tentang diagnosis dan penatalaksanaan TB pada imunokompromais sangatlah penting.
Kejadian TB lebih tinggi pada imunokompromais dibanding dengan non-imunokompromais.
Penyakit infeksi kronik ini bila tidak ditangani dengan baik menyebabkan morbiditas dan
mortalitas yang tinggi. Di Indonesia dengan beban TB tinggi (nomor 5 di dunia) akan lebih
tinggi lagi dengan meningkatnya prevalensi penderita HIV/AIDS.
TB adalah penyakit infeksi kronis yang disebabkan oleh M.tuberculosis. Tempat masuk
dan target organ terbanyak adalah paru. Orang yang terinfeksi M.tuberculosis hanya
sebagian kecil yang menjadi sakit TB dan sebagian besar tidak menjadi sakit (latensi).
Orang yang tidak sakit (latensi) akan menjadi sakit (reaktivasi) atau TB aktif bila terjadi
penurunan daya tahan tubuh atau imunitas (imunokompromais). Secara umum klinis TB
ditandai dengan batuk-batuk produktif lebih dari 2 – 3 minggu disertai dengan gejala-gejala
respiratorik lainnya dan gejala non-respiratorik. Namun, manifestasi klinis dari TB pada
individu imunokompromais terletak pada derajat beratnya penurunan imunitas. Sering tanda
dan gejala TB atipikal, sering terjadi kesalahan diagnosis, sehingga prognosis menjadi lebih
buruk.
Imunokompromais adalah suatu kondisi dimana sistem kekebalan tubuh seseorang
melemah atau tidak ada. Individu yang imunokompromais kurang mampu melawan atau
memerangi infeksi karena respon imun yang berfungsi tidak benar. Contoh orang
imunokompromais adalah mereka yang terinfeksi HIV atau AIDS, wanita hamil, atau sedang
menjalani kemoterapi atau terapi radiasi untuk kanker. Kondisi lain dengan
imunokompromais, seperti kanker tertentu dan kelainan genetik, diabetes mellitus, dan
penderita yang mendapatkan terapi TNF-α. Individu immunocompromised kadang-kadang
lebih rentan terhadap infeksi serius dan /atau komplikasi dibanding orang sehat. Mereka
juga lebih rentan untuk mendapatkan infeksi oportunistik, yaitu infeksi yang biasanya tidak
mengenai orang yang sehat.
Dalam keadaan penderita dengan imunokompromais, seorang dokter harus dapat

mengenali penyakit TB aktif. Diagnosis TB pada imunokompromais adalah dengan
menemukan kuman BTA pada sputum baik dengan pemeriksaan langsung BTA maupun
kultur. Pengobatan TB penderita imunokompromais sama dengan pada non-
imunokompromais dan pengobatan TB-nya diutamakan. Dokter harus mampu
mengidentifikasi penderita TB pada imunokompromais yang tidak respon (resisten) dengan
obat TB, sehingga dapat melakukan tindakan lebih dini untuk menurunkan perburukan
prognosis (kematian).
General Objektif
1. Mampu menjelaskan penegakan diagnosis TB pada imunokompromais.
2. Mampu menyusun program pengobatan jangka panjang penderita TB pada
imunokompromais.
3. Mampu mengidentifikasi kemungkinan gagal respon pengobatan (resisten) penderita
TB pada imunokompromais.
4. Mampu menyusun pengobatan utama pada penderita TB dengan imunokompromais.
5. Mampu mengidentifikasi penderita TB dengan imunokompromais yang perlu rujukan
lebih lanjut.
Trigger
Anda sebagai seorang dokter yang bekerja di sebuah Puskemas, datang seorang pasien
laki-laki, usia 28 tahun. Dia mengeluhkan panas badan sejak lebih kurang 2 minggu.
Demam tidak begitu tinggi dan tidak sampai menggigil. Disamping demam juga ada batuk-
batuk ringan tanpa disertai dahak yang dialami lebih dari 1 minggu. Penderita sudah minum
obat penurun panas dan obat batuk yang dibeli di warung tapi tidak ada kesembuhan. Berat
badan penderita dirasakan menurun drastis belakangan ini. Napsu makan berkurang
sehingga badan penderita dirasakan semakin kurus. Penderita adalah seorang sopir
pengangkut barang jawa – bali, sudah menikah dan mempunyai anak wanita usia 4 tahun.
Sesekali penderita minum bir. Penderita mempunyai tattoo di badannya yang dibuat sewaktu
penderita klas 1 SMA.
Learning Task
1. Jelaskan bagaimana saudara memastikan bahwa pasien tersebut memang
menderita TB dan imunokompromais!
2. Mengapa TB laten menjadi reaktivasi (TB aktif)?
3. Bagaimana saudara mengenali pasien TB imunokompromais mengalami
ImmuneReconstitution Inflammatory Syndrome (IRIS)?
4. Jika ternyata pasien tersebut menderita TB dengan imunokompromais bagaimana
cara menyusun pengobatan penderita?
5. Bagaimana cara menilai respon pengobatan TB pada pasien dengan
imunokompromais?
6. Jelaskan kriteria TB pada imunokompromais!
LECTURE 25
TB IN CHILD
dr. Ni Putu Siadi Purniti, SpA
Tuberculosis (TB) is systemic infection cause by Mycobacterium tuberculosis

complex : M tuberculosis, M. Bovis, M. africanum, M. microti, and M. canetti. Tuberculosis
infection occurs after inhalation of infective droplet nuclei containing M. tuberculosis. A
reactive tuberculin skin test and the absence of clinical and radiographic manifestations are
the hallmark of this stage. Tuberculosis disease occurs when sign and symptoms or
radiographic changes becaome apparent. In the year 2001 prevalens rate of TB is
5,6/100.000 population, of these, 931 (6 % ) cases occurred in children < 15 year of age
(rate 1,5/100.000 population). Transmission of M tuberculosis is person to person, usually by
airborne mucus droplet nuclei, particles 1-5 µm in diameter that contain M tuberculosis. In
the United States, most children are infected with M. tuberculosis in their home by adult
patient tuberculosis close to them. The tubercle bacilli multiply initially within alveoli and
alveolar duct. Most of bacilli are killed, but some survive within nonactivated macrophages,
which carry them through lymphatic vessels to the regional lymph nodes. When the primary
infection is the lung, the hilar lymph nodes ussualy are involved. The primary complex of
tuberculosis includes local infection at the portal of entry ( primary focus) and the regional
lymph nodes that drain the area. During the development of the primary complex, tubercle
bacilli are carried to most tissues of the the body through the blood and lymphatic
vessels.Pulmonary tuberculosis that occurs more than a year4 after the primary infection is
usually caused by endogenous regrowth of bacilli persisting in partially encapsulated lesions.
The majority of children with tuberculosis infection develop no signs or symptoms at any
time. Occasionally, infection is marked by low grade fever and mild cough, and rarely by high
fever, cough, malaise, and flu like symptoms. Several drugs are used to effect a relatively
rapid cure and prevent the emergence of secondary drug resistance during therapy. The
standard therapy of intrathoracic tuberculosis (pulmonary disease and/or hilar
lymphadenopathy) in children, recommended by the CDC and AAP, is 6 month regiment of
isoniazid (INH), rifampin (RIF) supplemented in the first 2 month of treatment by
pyrazinamide (PZA).
Learning Tasks
In Outpatient Clinic Department of Pediatric, the baby 10 month of age carried by the
mother with the chief complaint is loss of weight since 3 month, suffered low grade fever,
chronic cough, malaise and flu like symptoms. The grandfather whom was diagnosed
pulmonary tuberculosis and she has been in recent closed contact. In physical examination
found that there were enlargement of neck lymph nodes.
Learning Resources
Nelson Textbook of Pediatrics Ed. 17 th 2004: pp 958-972
LECTURE 26
PLEURAL EFFUSION, EMPHYSEMA, LUNG EDEMA
dr. Putu Andrika, SpPD-KIC
Membran tipis pleura terdiri dari dua lapisan yaitu pleura visceralis dan pleura
parietalis. Penumpukan cairan melebihi jumlah fisiologis 10-20 ml disebut efusi pleura,
akibat dari peningkatan produksi yaang melebihi kemampuan absorpsi.
Penting untuk menegakkan diagnosis berdasarkan anamnesis yang baik dan
pemeriksaan fisik yang teliti, pemeriksaan radiologi torak serta melakukan pungsi pleura.
Analisis cairan pleura akan sangat berguna untuk menuntun kearah penyebab efusi pleura.
Dibedakan cairan efusi yang transudat dan eksudat.
Volume efusi pleura yang banyak akan menimbulkan gangguan fungsi respirasi yang
memerlukan pengeluaran cairan efusi melalui aspirasi cairan pleura (torako sentesis) atau
melalui pemasangan chest cube (Water Seal Drainage).
Dalam mengelola pasien dengan efusi selain menangani keluhan akibat
menumpuknya cairan efusi juga harus menangani penyebab terjadinya efusi tersebut.
General Objektif:
1. Mampu menjelaskan penegakan diagnosis efusi pleura.
2. Mampu menilai analisis cairan pleura.
3. Mampu merencanakan pemeriksaan penunjang untuk mendapatkan penyebab
terjadinya efusi pleura.
4. Mampu mengidentifikasi kasus yang memerlukan penanganan segara dan kasus
yang harus dirujuk ke rumah sakit.
Triger:
Seorang wanita muda datang dengan keluhan sesak nafas yang semakin memberat sejak
seminggu. Pada pemeriksaan fisik didapatkan frekwensi nafas 24 x/mnt, suhu tubuh 37,5 o
C, pemeriksaan torak asimetris, kanan tertinggal, perkusi redup dan suara nafas melemah di
bagian kanan bawah. Penderita juga mengeluh batuk batuk sejak 3 bulan yang lalu dan
pernah batuk berisi darah segar sedikit, juga nampak semakin kurus.
Learning Task
1. Apakah kemungkinan penyebab keluhan pasien tersebut?
2. Pemeriksaan penunjang apa yang diperlukan?
3. Perlukah melakukan parasentesis? Jelaskan!
4. Perlukah pemasangan WSD? Apa alasannya?
LECTURE 27
PNEUMOTHORAX, HEMOTHORAX
Dr. dr. Yasa, Sp.BTKV
Pneumotoraks merupakan salah satu kegawatdaruratan di bidang paru yang berarti

terisinya rongga pleura oleh udara. Pneumotoraks ini perlu mendapatkan perhatian serius,
karena dengan penanganan yang cepat dan tepat akan sangat mengurangi angka
kematiannya. Sebagai seorang dokter yang ada di fasilitas kesehatan primer, sangat
diperlukan pengetahuan mengenai keadaan ini.
Diagnosis pneumotoraks dapat ditegakkan dari anamnesis, pemeriksaan fisik dan foto
polos dada. Pneumotoraks dapat dibagi berdasarkan berbagai kriteria, tetapi yang paling
sering adalah dibagi menurut terjadinya (pneumotoraks artifisial, traumatic, serta spontan)
serta berdasarkan jenis fistelnya (pneumotoraks terbuka, tertutup, dan ventil).
Beberapa kondisi pneumotoraks akan sangat mengancam nyawa, sehingga
memerlukan penanganan yang tepat dan segera. Penatalaksanaan pneumotoraks pada
prinsipnya adalah mengeluarkan udara yang ada di rongga pleura tersebut, terapi
penyebabnya, serta edukasi untuk mencegah berulangnya pneumotoraks pada pasien yang
memiliki risiko.
General Objektif:
1. Mampu menjelaskan penegakan diagnosis pneumotoraks.
2. Mampu menyebutkan beberapa penyebab pneumotoraks yang sering dijumpai.
3. Mampu menjelaskan beberapa pembagian jenis pneumotoraks.
4. Mampu menyusun rencana penatalaksanaan pasien dengan pneumotoraks.
Triger
Seorang pasien laki-laki usia 30 tahun datang kePuskesmas tempat anda bertugas dengan
mengeluh sesak nafas tiba-tiba dan sangat berat. Pasien sebelumnya dengan riwayat
menderita penyakit TB paru dan sudah berobat dengan lengkap. Sebelumnya pasien
sempat terbatuk-batuk, kemudian tiba-tiba sesak nafas. Pasien ini tampak sesak dan
sianosis.
Learning Task
1. Jelaskan temuan fisik dan foto polos dada yang kemungkinan ditemukan pada
pasien pneumotoraks tersebut!
2. Sebutkan beberapa penyebab pneumotoraks yang anda ketahui!
3. Bagaimana penatalaksanaan kasus dengan pneumotoraks tersebut?
LECTURE 28
BRONCHITIS AND BRONCHIECTASIS
dr. IB Sutha, SpP
Untuk menentukan suatu Bronkitis dan Bronkiektasis tidaklah terlalu sulit, tapi
diperlukan suatu pemahaman untuk mendiagnosis dan penatalaksanaan Bronkitis dan
Bronkiektasis dengan baik dan benar. Disamping prevalensinya cukup tinggi, penyakit ini
bila tidak ditangani dengan baik, akan berlanjut menjadi lebih parah.
Bronkitis adalah inflamasi saluran napas sentral yang mengenai mukosa ditandai oleh
batuk dengan dahak, sering disertai dengan panas dan sesak.Bronkiektasis adalah kelainan
pada dinding bronkus besar dan sedang berupa kelemahan otot sehingga terjadi pelebaran
lumen, karena proses infeksi transmural dan pelepasan mediator.
Diagnosis Bronkitis berdasarkan pada anamnesa, pemeriksaan fisik dan foto toraks,
sedang bronkiektasis ditegakkan dengan anamnesa, pemeriksaan fisik, foto toraks, CT
Scan, dan kultur sputum.
Prinsip penatalaksanaan Bronkitis dan Bronkiektasis adalah dengan menghilangkan
batuk dan produksi dahak. Bila disertai tanda infeksi dapat ditambahkan antibiotika. Pada
Bronkiektasis perlu dilakukan Chest Fisioterapi atau bronkoskopi untuk mempermudah
pengeluaran sputum. Pada keadaan eksaserbasi sering disebabkan oleh infeksi apakah
viral atau bakteri.
General Obyektif
1. Mampu menjelaskan penegakan diagnosis bronkitis dan bronkiektasis.
2. Mampu menyususn program pengobatan jangka panjang.
3. Mampu mengidentifikasi pasien dengan keadaan eksaserbasi.
4. Mampu memberikan pengobatan awal pasien dengan serangan akut.
5. Mampu mengidentifikasi pasien eksaserbasi yang perlu rawat inap dan merujuknya.
Triger
Seorang penderita laki umur 35 th datang dengan keluhan : batuk berdahak sejak 3 bulan
dan memberat sejak 5 hari yang lalu dan disertai dengan panas badan. Bila diperhatikan
dahaknya ada 3 lapis yaitu dari atas sampai bawah mulai dari yang bening sampai keruh
dan batuknya terutama pagi hari. Dikatakan pula setahun lalu pernah menderita sakit seperti
ini dan kadang disertai sesak napas, bila dahaknya sulit dikeluarkan.
Learning Task
1. Jelaskan bagaimana saudara memastikan bahwa pasien tersebut menderita
bronchitis!
2. Bagaimana sdr membedakan dengan bronkiektasis?
3. Apakah penderita tsb dalam keadaan eksaserbasi? Jelaskan!
4. Jelaskan prinsip pengobatan pasien dg bronkitis dan bronkiektasis!
5. Obat-obat apa saja yang diperlukan pada pasien tsb diatas?
6. Apa yang dikerjakan bila sputum pasien tsb diatas sulit dikeluarkan?
LECTURE 29
KANKER PARU (LUNG CANCER) AND EDUCATION OF SMOKING CESSATION
dr. Gede Ketut Sajinadiyasa, SpPD
Kanker Paru merupakan penyebab kematian tersering diantara kematian oleh karena
kanker di seluruh dunia baik pada laki-laki ataupun perempuan. Insiden kanker paru di dunia
diperkirakan 1,3 juta kasus per tahunnya. Kanker paru terjadi sebagai akibat proses yang
komplek antara paparan karsinogen dan kerentanan genetik. Faktor kebiasaan dan
lingkungan berhubungan dengan terjadinya kanker paru dan merokok merupakan faktor
risiko utama. Jenis histologi kanker paru sebagian besar adalah Small Cell Lung Cancer
(SCLC) dan Non Small Cell Lung Cancer(NSCLC) . NSCLC terdiri atas squamus cell
carcinoma, adeno carcinoma dan large cell carcinoma. Manifestasi klinis dari kanker paru
dapat asimtomatik pada stadium awal dan baru bergejal pada stadium lanjut. Pasien
biasanya datang dengan keluhan batuk, batuk darah, sesak, nyeri dada dan suar serak.
Sering juga dijumpai tanda-tanda syndrome paraneoplastik dan gejala umum seperti
anoreksia, asthenia dan berat badan yang menurun.
Diagnosis kanker paru dapat ditegaknya dengan anamnesis, pemeriksaan fisik dan
pemeriksaan penunjang. Pemeriksaan penunjang yang umum dikerjakan seperti sitologi
sputum, rontgen dada, ct scan toraks, Biopsi(FNAB/TTB), bronkoskopi, PET scan dan
lainnya. Setelah diagnosis ditegakkan dan sebelum memulai pengobatan ditentukan stadium
penyakit dan status performan. Dengan diketahuinya jenis histology dan stadium penyakit
kemudian ditentukan modalitas terapi. Modalitas terapi pada pasien kanker paru diantaranya
adalah pembedahan, kemoterapi, radiasi dan target terapi.
General Objektif
1. Mengetahui patogenesis, faktor risiko, dan usaha preventif kanker paru.
2. Dapat mengetahui klasifikasi kanker paru.
3. Mengetahui proses penegakan diagnosis dan stadium kanker paru.
4. Mengetahui modalitas penunjang dalam penegakan diagnosis.
5. Mengetahui modalitas terapi kanker paru dan merujuk.
Triger
Seorang pasien laki-laki umur 65 tahun datang ketempat pratek saudara sendirian dengan
keluhan batuk berdarah. Satu minggu yang lalu pasien sempat menjalani cek up didapatkan
pada foto rontgen dada, tumor dengan ukuran diameter 2,5 cm pada hilus kiri menempel di
pinggang jantung kiri. Pada pemeriksaan USG abdomen didapatkan tumor multiple ukuran
diameter sekitar 1-1,5 cm pada hati, sedang pemeriksaan yang lain dalam batas normal.
Pasien memiliki kebiasaan merokok sejak umur 20 tahun dengan jumlah 1-2 bungkus per-
harinya.
Learning Task
1. Apa yang saudara lakukan untuk memastikan diagnosis pasien ini?
2. Kalau diperlukan tindakan invasive, prioritas tindakan yang saudara usulkan?
Jelaskan alasannya!
3. Bila ini kanker paru, apa kemungkinan klasifikasi histologinya?
4. Tentukan stadium pasien ini dan status performannya serta alasannya!
5. Tentukan modalitas terapinya
LECTURE 30
DISORDERS OF NOSE AND SINUS
dr. Ratna, SpTHT
References
1. Textbook Diseases of the Ear, Nose and Throat edited by Martin Burton CHURCHILL
LIVINGSTQNE 15TH ED 2000: Section 5 The Larynx, Pharynx and Oesophagus. Pp
165-206
LECTURE 31
DISORDERS OF PHARYNX AND LARYNX
Prof. Suardana
The Adenoids (pharyngeal tonsils) are a triangular mass of lymphoid tissue located on
the posterior aspect of the boxlike nasopharynx. The nasopharynx serves as a conduit for
Inspired air and Sinonasal Sections that drain from the nasal cavity into the oropharynx. a
resonance box for for speech and a drainage area for the Eustachian tube — middle ear
mastoid complex.
Adenoid have three types of Surface epithelium ciliated pseudostratified squamous,
and transitional.
The Adenoids and tonsils, like all lymphoid tissue, enlarge when infected. Although
lymphoid tissue does act to fight infection. Some time bacteria and viruses can lodge within it
and survive. Group A B—hemolytic streptococcus (GABHS) is classically described as the
only bacterium implicated frequently in acute Adenoiditis or tonsilitis.
Chronic infection, either viral or bacterial, can keep the pad of adenoids enlarged for
years, even into adulthood. Some viruses, Such as the Epstein Barr virus, can cause
dramatic enlargement of lymphoid tissue.
Clinical classification of the adenoid : Acute adenoiditis, recurrent Acute Adenoiditis,
chronic adenoiditis and obstructive Adenoid Hyperplasia. Clinical classification of the tonsils:
acute tonsillitis, recurrent acute tonsillitis, chronic tonsillitis, and obstructive tonsilar
hyperplasia.
The main symptoms of adenoid diseases is Rhinorhea, chronic nasal obstruction
(associated with Snoring and obligate mouth breathing), malodorous, cough, post nasal drip,
sinusitis, otitis media and a hyponasal voice. The main symptomsof tonsils diseases are:
sore throat, dysphagia, fever, halithosis, muffled voices, snoring, and other symptomsof
sleep disturbance and tender cervical adenopathy.
Adenoiditis is best diagnosed by clinical history, physical examination,
nasopharyngoscopy, and radiography. The physical examination should include both anterior
and posterior rhinoscopy. A lateral neck radiograph and sinus radiography taken to show soft
tissue density, can show the adenoids and sinus. Tonsilitis is diagnosed by clinical history,
physical examination, throat culture, and flexible laryngoscope.
Management of diseases of the adenoids and tonsils: antimicrobial, intranasal steroids
and adenoidectomy. Indications for tonsillectomy and adenoidectomy are obstruction,
infection and Neoplasia.
The anatomy of the larynx consist of cart.Haginous framework bound together by
ligaments and covered with muscle and mucous membrane. The most important cartilage is
the arytenoid cartilages which is can rotate and slide on the cricoid cartilage and thus play
an important role in the movement of the vocal cords. The epiglottis is a leaf-shape cartilage
of the larynx which is attached to the base of the tongue by the glossoepiglottic ligament and
inner part of thyroid cartilage. The thyroid cartilage is that which makes the prominence upon
the front of the neck known as ‘Adam’s apple, particularly visible in man. Interior of the larynx
can looking down by laryngoscopy indirect or direct. The function of the larynx includes
protection of lower respiratory tract and phonation. The protection of respiratory tract acting
by the epiglottis, sensory nerve supply which is produce cough and vocal cords. Voices or
phonation is produce by vocal cords function consist adduction and abduction movement
and vibration of the vocal cords.
Patient with a foreign body in his/her pharynx, or oesophagus, usually knows what has
happened and is usually right. It can stick in his tonsils, his vallecula, his pyriform fossa, or in
his postcricoid region. Most fish bones stick in accessible regions, usually the back of the
tongue or tonsils. Foreign bodies seldom stick in the larynx itself, except when an affluent,
elderly, and often intoxicated diner gets a piece of steak caught in his larynx, as a result of
which he gasps and collapses. Treat him immediately.\
Throat
Normal Vocal cord and disorders
The symptoms of laryngeal disorders are hoarseness, dysphonia and stridor.

Hoarseness is caused by an abnormal flow of air past the vocal cords. The voice is harsh
when turbulence is created by the irregularity of the vocal cords. The irregularity of the vocal
cord caused by vocal nodule, edema of the vocal cord and laryngitis. Dysphonia is
weakness of the voice caused by paresis or paralysis of the vocal cords. And aphonia is loss
of voice. Stridor is a high pitch sound, is produce by lesion that narrowing the airway. If
narrowing of the airway upper the vocal cord produce inspiratory stidor, and if narrowing the
airway below the vocal cord will produce inspiratory and expiratory stridor.
Some lesion will be discussed are vocal cord nodule, vocal cord paralysis, laryngeal
palillomas and gastrolaryngopharyngeal reflux disease. Vocal nodule or Singer’s nodes is
benign lesion in the vocal cord particularly at the site of the junction of the anterior third and
posterior two-thirds of the cord (halfway along the membranous cord). This condition is
caused by misuse of the voice or overuse as well as singers, teachers, priest, actors who
have not undergone formal voice training. Misuse of the voice also happen in the
schoolchildren, sometime call by screamer’s node.
Vocal cord paralysis causes of dysphonia symptom, define as weakness or even
though temporary loss of the voice (aphonia). A vocal cord may paralysed by mechanical
fixation of the arytenoids or vocalis muscle or by nerve paralysis. Paralysis may be unilateral
or bilateral and the cords paralysed in abduction or adduction. Abduction paralysis causes
loss of the voice because the cord can not move to the midline position and adduction
paralysis, the cords can not move to the lateral position and cause severe stridor.
Laryngeal papilloma is a benign lesion single or multiple, non keratinizing papilloma in
characteristic is due by infection of human papilloma virus type 6 and 11. Papillomatosis
present more frequently in children than in adult, the peak incidence occurring between 2
and 5 years of age, and very common of high recurrent. Relaps or recurrent may be
precipitated by trauma or immunosuppressive condition.
Gastrolaryngeal reflux is very common condition to causes hoarseness. The pathology
of gastro-esophageal-laryngeal reflux disease may be a result of direct effect of gastric acid,
bile salts or enzymes on mucosa of the larynx.
Learning Tasks
1. Describe and discuss of specific symptoms of the larynx disease & disorders!
2. Describe and discuss etiology and patophysiology of hoarseness, dysphonia and
stridor with its clinical implication!
3. Manage and provide initial management or refer patient with certain larynx disease
and disordes!
Learning Tasks
1. Describe and discuss of etiology of adenoid diseases!
2. Explain pathogenesis of adenoid diseases!
3. Describe and discuss of clinical classification of diseases in the adenoids!
4. Describe clinical evaluation to support diagnosis of the adenoid diseases!
5. Manage and provide initial management or refer patient with certain adenoid
diseases!
6. Explain indications for adenoidectomy!
7. Describe complications of adenoid diseases and adenoidectomy!
Learning Resources
1. Textbook Diseases of the Ear, Nose and Throat edited by Martin Burton CHURCHILL
LIVINGSTQNE 15TH ED 2000: Section 5 The Larynx, Pharynx and Oesophagus. Pp
165-206.
2. Textbook Current Medical Diagnosis & Treatment Edited by Lawrence M.Tierney,Jr.
Stephen J.Mc Phee, Maxine A.Papadakis 45 Ed 2006: Diseases of the Larynx p209-
213.
3. Linda Brodsky. Christhopher Poje. Tonsilitis, Tonsillectomy and Adenoidectomy. In BaiIe
BJ Editor. Head and Neck Surgery-Otolaryngologv 3 ed. Philadelphia Lippincort
Williams and Willkins; 2001 p 979— 991.
LECTURE 32
NOSE FOREIGN BODIES, THROAT FOREIGN BODIES
SpTHTdr. Dewa Artha Eka Putra, SpTHT
Nasal foreign bodies are commonly encountered in emergency departments. Although

more frequently seen in the pediatric, they can also occur in adult. Children’s interests in
exploring their bodies make them more prone to lodging foreign bodies in their nasal
cavities.
References
Textbook Diseases of the Ear, Nose and Throat edited by Martin Burton CHURCHILL
LIVINGSTQNE 15TH ED 2000
REFERENCES
1. Essential Clinical Anatomy, 2nd ed, Keith L. Moore and Anne M.R.Agur, Lippincott
William & Willems, Philadhelpia, 2002.
2. Bloom & Fawcett’s Concise Histology, 2nd ed, Fawcett D.N., Jensh, R.P, London,
2002.
3. Textbook of Medical Physiology, 10th ed, A.C. Guyton, Hall, Philadelphia, WB
Saunders Co, 2000.
4. Medical Biochemistry, Baynes J and Dominiczak, London, 1999.
5. Katzung & Trevor’s Pharmacology, Examination & Board Review, 6th ed. A.J. Trevor,
B.G. Katzung, Susan B Masters.
6. Robbins Basic Pathology, 7th ed, Kumar V, Cotran RS, Robbins SL. WB Saunders,
Philadelphia, 2003.
7. Textbook of disorder and injuries of the musculoskeletal system, Robert B. Salter MD
Apley’s system Orthopaedics and Fractures. Apley, Solomon.
8. Harrison’s, 16th ed. 2005.
ADDITIONAL TEXTBOOK
9. Review of Medical Physiology, 10thed, W.F. Ganong, California : LANGE

MedicalPublications.
10. Human Physiology – An Integrated Approach. 2nded. Silverthorn, 2001 New
Jersey :Prentice-Hall Inc.
11. Pocket Companion to Textbook of Medical Physiology, 10thed, A.C. Guyton,
Hall,Philadelphia, WB Saunders Co, 2000, pp. 52 – 95

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Study Guide Respiratory System and Disorders

Udayana University, Medical Faclty, DME, 2018 | 1

GENERAL CURRICULUM RESPIRATORY SYSTEM AND DISORDERS

Udayana University, Medical Faclty, DME, 2018 | 2

PLANNERS AND LECTURERS

Udayana University, Medical Faclty, DME, 2018 | 3

No Name Department Phone

1 Dr. dr. I Made Muliarta, M.Kes Physiology 081338505350

3 Prof. dr. I Gst. Md. Aman, Sp.FK Pharmacology 081338770650

Udayana University, Medical Faclty, DME, 2018 | 4

Regular Class (Class A)

Udayana University, Medical Faclty, DME, 2018 | 5

There are several types of learning activity:

In the middle of block schedule, a meeting is designed among the student

Udayana University, Medical Faclty, DME, 2018 | 6

Faculty of Medicine, Udayana University

ARTICLE REVIEW ASSESSMENT FORM

Udayana University, Medical Faclty, DME, 2018 | 7

Block : Respiratory System and Disorders

Student No. (NIM) : ________________________________________

Time table of consultation

Point of discussion Week Date Tutor sign

Total point : ( A + B + C ) : 3 = _____________

Udayana University, Medical Faclty, DME, 2018 | 8

Assessment in this theme consists of:

Final mark 65 or more considered to pass this block.

TIME TABLE REGULAR CLASS (CLASS A)

DAY TIME ACTIVITY VENUE PIC

Udayana University, Medical Faclty, DME, 2018 | 9

08.00 – 08.50 Lecture 1: Introduction Class R Dr. dr. Muliarta

Udayana University, Medical Faclty, DME, 2018 | 10

13.00 – 13.50 SGD 11,12 Discussion R Fasilitator

08.00 – 08.50 Lecture 21: TB in Children Class R dr. Siadi

Udayana University, Medical Faclty, DME, 2018 | 11

Tue Bronchoscopy and provocation test Arya/dr.Artana

Udayana University, Medical Faclty, DME, 2018 | 12

Udayana University, Medical Faclty, DME, 2018 | 13

TIME TABLE ENGLISH CLASS (CLASS B)

08.00 – 08.50 Lecture 1: Introduction Class R Dr. dr. Muliarta

Udayana University, Medical Faclty, DME, 2018 | 14

11 08.00 – 08.50 Lecture 21: TB in Children Class R dr. Siadi

Udayana University, Medical Faclty, DME, 2018 | 15

Udayana University, Medical Faclty, DME, 2018 | 16

Udayana University, Medical Faclty, DME, 2018 | 17

Udayana University, Medical Faclty, DME, 2018 | 18

dr. I Made Muliarta, MKes

Udayana University, Medical Faclty, DME, 2018 | 19

dr. IGK Nyoman Arijana, M.Si.Med

Udayana University, Medical Faclty, DME, 2018 | 20

B. Structure of The Lower Respiratory tract

Dr. dr. I Made Muliarta, M.Kes

Gas exchange during external respiration occurs in respiratory membrane. Several

Udayana University, Medical Faclty, DME, 2018 | 21

dr. I Nyoman Gede Wardana, M.Biomed

dr. I Nyoman Gede Wardana, M.Biomed

Udayana University, Medical Faclty, DME, 2018 | 22

Dr. dr. Desak Wihandani, M.Kes

Udayana University, Medical Faclty, DME, 2018 | 23

dr. Arya Biantara, Sp.An

Dr. dr. I Made Muliarta, M.Kes

dr. Ni Putu Ekawati, Sp.PA, M.Repro

Because of the complexity of respiratory disease, it is important to understand their

2. What are the DDs?