TABLE OF CONTENTS
Page
Table of Contens 1
Introduction 2
Curriculum 3
Planner team & Lecturers 4
Facilitators 6
General Time Table 7
Important Informations 8
Meeting of the students’ representative 8
Self Assessment 8
Assessment Method 8
Time Table (Regular Class) 9
Time Table (English Class) 14
INTRODUCTION
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 6 weeks (27 working days) starts from 22nd of February 2016 as shown in the time table. The final examination will be conducted on 4th of April 2016 in the form of MCQ. The learning situation include lecture, individual learning, small group discussion, plenary session, practice, and clinical skill.
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.
CURRICULUM
RESPIRATORY SYSTEM AND DISORDER
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
PLANNER TEAM
LECTURERS
No
Name
Department
Phone
1 Prof. Dr.dr.IB Ngr Rai Sp.P (K) Pulmonology 08123804579 2 dr.I GN Sri Wiryawan,M.Repro Histology 08123925104 3 dr.Gede Wardana, M.Biomed Anatomy 0361-7864957 4 Dr.dr.Dsk Made Wihandani,
M.Kes
Biochemistry 081338776244 5 dr.Ida Bagus Subanada, Sp.A Paediatric Dept. 0812399533 6 dr.Dewa Artika, Sp.P Pulmonology 08123875075 7 dr.Ida Bagus Suta, Sp.P Pulmonology 08123990362 8 dr. Made Bagiada, Sp.PD-KP Pulmonology 08123607874
18 dr. Luh Made Ratnawati, Sp.THT(KL)
Otorhinolaryngology 08123806108 18 dr. Putu Andrika, Sp.PD-KIC Pulmonology 08123989192 19 dr. Gede Ketut Sajinadiyasa,
Sp.PD
~ FACILITATORS ~ Regular Class (Class A)
No Name Group Departement Phone (2&3 Venue rd floor)
1 dr. Gde Somayana, Sp.PD A1 Interna 081345136913 2nd floor:R.2.09
2 dr. Ida Bagus Wirakusuma, MOH A2 Public Health 08124696647 2nd floor:R.2.10
3 dr. I Gusti Ngurah Pramesemara , M.Biomed,
Repro A3 Andrology 081338605087
2nd floor: R.2.11
4 Dr.dr. Tjok G A Senapathi, Sp.An. KAR A4 Anasthesi 081337711220 2nd floor:R.2.12
5 Dr. dr. I Dewa Made Sukrama, MSi, Sp.MK(K) A5 Microbiology 081338291965 2nd floor:R.2.13
6 Dr.dr. Ketut Sudartana, Sp.B-KBD A6 Surgery 0811398996 2nd floor:R.2.14
7 dr. I Kadek Swastika , M Kes A7 Parasitologi 08124649002 2nd floor:R.2.15
8 dr. Made Widhi Asih, Sp.Rad (K) A8 Radiologi 081916442626 2nd floor:R.2.16
9 dr. Ketut Sudiasa, Sp.B (K) Trauma A9 Surgery 08123811106 2nd floor:R.2.23
10 dr. I Made Oka Negara, FIAS A10 Andrology 085935054964 3nd floor:R.3.21
11 dr. Ida Ayu Sri Wijayanti, M.Biomed, Sp.S A11 Neurology 081337667939 3nd floor:R.3.22
12 dr. I Gusti Ayu Agung Elis Indira , Sp.KK A12 Dermatology 081338718384 3nd floor:R.3.23
English Class (Class B)
No Name Group Departement Phone (2&3Venue rd floor)
1 Dr. dr. Desak Made Wihandani, M.Kes B1 Biochemistry 081338776244 2nd floor:R.2.09
2 dr. I Gusti Ayu Sri Darmayani, Sp.OG B2 DME 081338644411 2nd floor:R.2.10
3 Dr. dr. Made Ratna Saraswati, Sp.PD-KEMD-FINASIM B3 Interna 08123814688 2nd floor:R.2.11
4 dr. I Gusti Ayu Artini, M.Sc B4 Pharmacology 08123650481 2nd floor:R.2.12
5 dr. Ni Ketut Sri Diniari, Sp.KJ B5 Psychiatry 081338748051 2nd floor:R.2.13
7 Dr. dr. Anak Agung Wiradewi Lestari , Sp.PK B7 PathologyClinical 08155237937 2nd floor:R.2.15
8 Dr.dr. Susy Purnawati, MKK B8 Fisiology 08123989891 2nd floor:R.2.16
9 Dr.dr. Ni Made Linawati, M.Si B9 Histology 081337222567 2nd floor:R.2.23
10 Dr.dr. Elysanti Dwi Martadiani, Sp.Rad B10 Radiology 081805673099 3nd floor:R.3.21
11 dr.Kumara Tini, Sp.S B11 Neurology 081238701081 3nd floor:R.3.22
12 dr. Nyoman Suryawati , M.Kes, Sp.KK B12 Dermatology 0817447279 3nd floor:R.3.23
GENERAL TIME TABLE
FOR A AND B CLESSES
CLASS A
CLASS B
TIME
ACTIVITIES
TIME
ACTIVITIES
08.00-09.00 Lecture 09.00-10.00 Lecture
09.00-10.30 Independent learning 10.00-11.30 Student project 10.30-12.00 SGD 11.30-12.00 Break
12.00-12.30 Break 12.00-13.30 Independent learning 12.30-14.00 Student project 13.30-15.00 SGD
14.00-15.00 Plenary session 15.00-16.00 Plenary session
There are several types of learning activity:
Lecture
independent learning based on the lecture’s topic Small group discussion to solve the learning task Practice
Student project
Clinical skill and demonstration
Self assessment at the end of every topic Plenary session
Lecture will be held at room 401, while discussion rooms available at 2
ndand
3
rdfloor (room A209-A216, A223, A321, A322, A323)
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.
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 65 to 69 will be reconsidered with self assessment’s mark to see the student’s status. Any student with self assessment’s mark more than 70 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.
ASSESSMENT METHOD
Assessment in this theme consists of:
SGD : 5%
Final Exam : 80% Student Project : 15%
Final mark more than 70 considered to pass this block. Certain conditions applied for those with final mark between 65 – 69. These students will be analyzed using their self assessment’s mark. Students with final mark 65 – 69 and self assessment’s mark equal or more than 70 will also considered pass this block.
TIME TABLE
REGULAR
CLASS
1
Monday
Feb 22,
2016
08.00-08.15
Introduction
Class room Prof.I.B. Rai 08.15-09.00Lecture 1
Anatomy of
Respiratory System
Class room dr.Wardana
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr.Wardana
2
Tuesday
Feb 23,
2016
08.00-09.00Lecture2
Histology of
Respiratory System
Class room dr. Sri Wiryawan
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr. Sri Wiryawan
3
Wednesday
Feb 24,
2016
08.00-09.00
Lecture 3
Physiology of
Respiratory System:
Ventilation
Class room
dr. Muliarta
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr. Muliarta
4
Thursday
Feb 25,
2016
08.00-09.00
Lecture 4
Physiology of
Respiratory System:
Gas Exchange,
diving, altitude
Class room dr. Muliarta
09.00-15.00
Independent learning
Practice : Anatomy, Histology
Anatomy: 1st floor
dr. Wardana
Histology: 4th
floor dr. Sri Wiryawan
5
Friday
Feb 26,
2016
08.00-09.00
Lecture 5
Carriage of oxygen
and Carbon dioxide
Class room dr. Desak Wihandani
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
6
Monday
Feb 29, 2016
08.00-09.00
Lecture 6
Control of acid base
balance, Arterial Gas
Analysis (AGA)
Class room dr. Desak Wihandani
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr. Desak Wihandani
7
Tuesday
March 1,
2016
08.00-09.00
Lecture 7
Control of
Respiratory Function
and Blood Gas
Analyzes
Class room Prof. Wiryana
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room Prof. Wiryana
8
Wednesday
March 2,
2016
08.00-09.00
Lecture 8
Pathology of
Respiratory Tract
Class room dr. Winarti
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project Hospital Visit
14.00-15.00 Plenary session Class room dr. Winarti
9
Thursday
March 3,
2016
08.00-09.00
Lecture 9
Lung Defense
Mechanism
Class room dr. Winarti
09.00-15.00
Independent learning
Practice : Physiology, Pathology Anatomy (PA)
Physiology:
2nd floor dr. Muliarta PA: Joint Lab
(4th floor) dr. Winarti
10
Friday
March 4,
2016
BKFK
11
08.00-09.00
Lecture 10
Pharmacological and
non pharmacological
interventions
Class room Prof. Aman
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
Monday
March 7,
2016
14.00-15.00 Plenary session Class room Prof. Aman
12
Friday
March 11,
2016
08.00-09.00
Lecture 11
Pharmacological and
non pharmacological
interventions
Class room Prof. Aman
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project Hospital Visit
14.00-15.00 Plenary session Class room Prof. Aman
13
Monday
March 14,
2016
08.00-09.00
Lecture 12
Respiratory Imaging
Class room dr. Elysanti
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr. Elysanti
14
Tuesday
March 15,
2016
08.00-09.00
Lecture 13
Bronchiolitis, asthma
in children,
Pneumonia
Class room dr. IB Subanada
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project Hospital Visit
14.00-15.00 Plenary session Class room dr. IB Subanada
15
Wednesday
March 16,
2016
08.00-09.00
Lecture 14
TB in children, Difteri,
Pertusis
Class room dr. Siadi Purniti
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr. Siadi Purniti
16
Thursday
March 17,
2016
08.00-09.00
Lecture 15
Pulmonary TB and
Extrapulmonary TB,
TB in the
Immunocompromised
Host, Abses TB
Class room dr. Sutha,
dr. Bagiada
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project Hospital Visit
14.00-15.00 Plenary session Class room dr. Sutha, dr. Bagiada
17
08.00-09.00Lecture 16
Asthma,
COPD
Class room
Friday
March 18,
2016
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room Prof. IB Rai, dr. Artana
18
Monday
March 21,
2016
08.00-09.00
Lecture 17
Pleural effusion,
Pneumothorax,
Hematothorax
Class room dr. Andrika, dr, Yasa09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project Hospital Visit
14.00-15.00 Plenary session Class room dr. Andrika, dr, Yasa
19
Tuesday
March 22,
2016
08.00-09.00
Lecture 18
Bronchitis and
Bronchiectasis,
Lung Ca and
Smoking Cessation
Class room
dr.Dewa Artika,
dr. Saji
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
14.00-15.00 Plenary session Class room dr.Dewa Artika, dr. Saji
20
Wednesday
March 23,
2016
08.00-08.30 08.30-09.00Lecture 19
Disorder of nose,
sinus
Class room dr. Ratna, Sp.THT
09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project Hospital Visit
14.00-15.00 Plenary session Class room dr. Ratna, Sp.THT
21
Thursday
March 24,
2016
08.00-09.00
Lecture 20
Disorder of larynx,
Disorder of Pharynx
Class room Prof. Suardana, dr. Dewa Artha Eka Putra, Sp.THT 09.00-10.30 Independent learning
10.30-12.00 SGD Disc room Facilitator
12.00-12.30 Break
12.30-14.00 Student project
22
Monday
March 28,
2016
08.00-15.00 BCS: SpirometryBCS: WSD, Radio Imaging (Pre-test, lecture, demo Practice, discussion)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor)
Anatomy (1st floor)
dr. Muliarta dr. Yasa dr. Elysanti
23
Tuesday
March 29,
2016
08.00-15.00BCS: Physical Diagnostic of Thorax
BCS: Bronchoscopy BCS: THT
(Pre-test, Lecture, practice, demo)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor) Anatomy (1st floor) dr. Saji dr. Sutha dr. Lely
24
Wednesday
March 30,
2016
08.00-15.00 BCS: SpirometryBCS: Physical Diagnostic of Thorax
(Pre-test, lecture, practice, demo)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor) Anatomy (1st floor) dr. Muliarta dr. Saji
25
Monday
March 31,
2016
08.00-15.00BCS: Physical Diagnostic of Thorax
BCS: Provocation test BCS: THT
(Pre-test, lecture, demo)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor) Anatomy (1st floor) dr. Saji dr Artana dr. Lely
26
Friday
April 1
,
2016
08.00-15.00
BCS: Physical Diagnostic of Thorax, Provocation test, Spirometry, WSD, Bronchoscopy, Radio Imaging, THT (Practice, post-test) Class Room Physiology Dept. (2nd floor
TIME TABLE
ENGLISH
CLASS
DAY/DATE
TIME
VENUE
PIC
1
Monday
Feb 22,
2016
09.00-09.15
Introduction
Class room Prof.I.B. Rai 09.15-10.00Lecture 1
Anatomy of
Respiratory System
Class room dr.Wardana
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr.Wardana
2
Tuesday
Feb 23,
2016
09.00-10.00Lecture2
Histology of
Respiratory System
Class room dr. Sri Wiryawan
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr. Sri Wiryawan
3
Wednesday
Feb 24,
2016
09.00-10.00
Lecture 3
Physiology of
Respiratory System:
Ventilation
Class room
dr. Muliarta
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr. Muliarta
4
Thursday
Feb 25,
2016
09.00-10.00
Lecture 4
Physiology of
Respiratory System:
Gas Exchange,
diving, altitude
Class room dr. Muliarta
10.00-16.00
Independent learning
Practice : Anatomy, Histology
Anatomy: 1st floor
dr. Wardana
Histology: 4th
floor dr. Sri Wiryawan
5
Friday
Feb 26,
2016
09.00-10.00
Lecture 5
Carriage of oxygen
and Carbon dioxide
Class room dr. Desak Wihandani
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
6
Monday
Feb 29, 2016
09.00-10.00
Lecture 6
Control of acid base
balance, Arterial Gas
Analysis (AGA)
Class room dr. Desak Wihandani
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr. Desak Wihandani
7
Tuesday
March 1,
2016
09.00-10.00
Lecture 7
Control of
Respiratory Function
and Blood Gas
Analyzes
Class room Prof. Wiryana
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room Prof. Wiryana
8
Wednesday
March 2,
2016
09.00-10.00
Lecture 8
Pathology of
Respiratory Tract
Class room dr. Winarti
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project Hospital Visit
15.00-16.00 Plenary session Class room dr. Winarti
9
Thursday
March 3,
2016
09.00-10.00
Lecture 9
Lung Defense
Mechanism
Class room dr. Winarti
10.00-16.00 Independent learning Practice : Physiology, Pathology Anatomy (PA)
Physiology: 2nd floor
dr. Muliarta
PA: Joint Lab
(4th floor) dr. Winarti
10
Friday
March 4,
2016
BKFK
11
Monday
March 7,
2016
09.00-10.00
Lecture 10
Pharmacological and
non pharmacological
interventions
Class room Prof. Aman
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room Prof. Aman
12
Friday
March 11,
2016
09.00-10.00
Lecture 11
Pharmacological and
non pharmacological
interventions
Class room Prof. Aman
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project Hospital Visit
15.00-16.00
Plenary session
Class room Prof. Aman13
Monday
March 14,
2016
09.00-10.00
Lecture 12
Respiratory Imaging
Class room dr. Elysanti
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr. Elysanti
14
Tuesday
March 15,
2016
09.00-10.00
Lecture 13
Bronchiolitis, asthma
in children,
Pneumonia
Class room dr. IB Subanada
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project Hospital Visit
15.00-16.00 Plenary session Class room dr. IB Subanada
15
Wednesday
March 16,
2016
09.00-10.00
Lecture 14
TB in children, Difteri,
Pertusis
Class room dr. Siadi Purniti
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr. Siadi Purniti
16
Thursday
March 17,
2016
09.00-10.00
Lecture 15
Pulmonary TB and
Extrapulmonary TB,
TB in the
Immunocompromised
Host, Abses TB
Class room dr. Sutha,
dr. Bagiada
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project Hospital Visit
15.00-16.00 Plenary session Class room dr. Sutha, dr. Bagiada 09.00-10.00
Lecture 16
Asthma,
COPD
Class room
17
Friday
March 18,
2016
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room Prof. IB Rai, dr. Artana
18
Monday
March 21,
2016
09.00-09.00
Lecture 17
Pleural effusion,
Pneumothorax,
Hematothorax
Class room dr. Andrika, dr, Yasa12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project Hospital Visit
15.00-16.00 Plenary session Class room dr. Andrika, dr, Yasa
19
Tuesday
March 22,
2016
08.00-09.00
Lecture 18
Bronchitis and
Bronchiectasis,
Lung Ca and
Smoking Cessation
Class room
dr.Dewa Artika,
dr. Saji
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project
15.00-16.00 Plenary session Class room dr.Dewa Artika, dr. Saji
20
Wednesday
March 23,
2016
09.00-09.30 09.30-10.00Lecture 19
Disorder of nose, sinus Class room dr. Ratna, Sp.THT
12.00-13.30 Independent learning
13.30-15.00 SGD Disc room Facilitator
11.30-12.00 Break
10.00-11.30 Student project Hospital Visit
15.00-16.00 Plenary session Class room dr. Ratna, Sp.THT
22
Monday
March 28,
2016
08.00-15.00 BCS: SpirometryBCS: WSD, Radio Imaging (Pre-test, lecture, demo Practice, discussion)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor)
Anatomy (1st floor)
dr. Muliarta dr. Yasa dr. Elysanti
23
Tuesday
March 29,
2016
08.00-15.00BCS: Physical Diagnostic of Thorax
BCS: Bronchoscopy BCS: THT
(Pre-test, Lecture, practice, demo)
Class Room Physiology Dept. (2nd floor
24
Wednesday
March 30,
2016
08.00-15.00
BCS: Spirometry
BCS: Physical Diagnostic of Thorax
(Pre-test, lecture, practice, demo)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor)
Anatomy (1st floor)
dr. Muliarta dr. Saji
25
Monday
March 31,
2016
08.00-15.00
BCS: Physical Diagnostic of Thorax
BCS: Provocation test BCS: THT
(Pre-test, lecture, demo)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor)
Anatomy (1st floor)
dr. Saji dr Artana dr. Lely
26
Friday
April 1
,
2016
08.00-15.00
BCS: Physical Diagnostic of Thorax, Provocation test, Spirometry, WSD, Bronchoscopy, Radio Imaging, THT
(Practice, post-test)
Class Room Physiology Dept. (2nd floor
Joint Lab (4th Floor)
Anatomy (1st floor)
dr. Saji dr Artana dr. Sutha dr. Muliarta dr. Yasa dr. Elysanti dr. Lely
27
Monday
April 5,
2016
LEARNING PROGRAMS
LECTURE 1
ANATOMY OF RESPIRATORY TRACT
Abstract
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 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
LECTURE 2
HISTOLOGY OF RESPIRATORY TRACT
dr. Sri Wiryawan, MRepro
Abstract
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
I. 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 !
II. Structure of The Lower Respiratory tract
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 3
PHYSIOLOGY OF RESPIRATORY SYSTEM: VENTILATION
dr. I Made Muliarta, MKes
Abstract
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
LEARNING TASK
dr. Muliarta, MKes
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 4
PHYSIOLOGY OF RESPIRATORY SYSTEM: GAS EXCHANGE, DIVING,
ALTITUDE
dr. I Made Muliarta, MKes
Abstract
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 occurs at high altitude and during diving.
LEARNING TASK
dr. Muliarta, MKes
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
CARRIAGE OF OXYGEN AND CARBON DIOXIDE
dr. Desak Wihandani
Abstract Gas Transport
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.
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 6
CONTROL OF ACID BASE BALANCE, ARTERIAL GAS ANALYSIS (AGA)
dr. Desak Wihandani
Abstract
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, pCO2 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 ?
LECTURE 7
CONTROL OF RESPIRATORY FUNCTION
Prof. Dr. dr. Wiryana, SpAn
Abstract
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 8
PATHOLOGY OF UPPER AND LOWER URINARY TRACT
dr. Ni Wayan Winarti, SpPA
ABSTRACT
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.
A. Mention 4 diseases including in the spectrum of obstructive lung disease! B. Explain their pathogenesis!
C. 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.
A. Mention some cytology test can be choose for this patient!
B. Among the test mention above (A), which one is the most simple and non-invasive? And, discuss how to collect the specimen
LECTURE 9
LUNG DEFENCE MECHANISM
dr. Ni Wayan Winarti, SpPA
Abstract
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.
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 10
PHARMACOLOGICAL AND NON PHARMACOLOGICAL INTERVENSION I
Prof. dr. GM Aman
Abstract
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 leucotriene receptor 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 Day 10
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 11
PHARMACOLOGICAL AND NON PHARMACOLOGICAL INTERVENSION II
Prof. dr. GM Aman
Task Day 11
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
1. List the anticough that are contraindicated in acute asthma attack. 2. If you need anticough, what drug you give best
LECTURE 12
RESPIRATORY IMAGING
dr. Elysanti, Sp.Rad
Abstract
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.
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. What is the imaging choice for establish the diagnosis ?
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
What kind of abnormality you hope to see on the chect X ray film? What do you thing about the diagnosis of the disease?
LECTURE 13
BRONCHIOLITIS AND
ASTHMA IN CHILD
Dr. IB Subanada, SpA
Abstract
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.
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. abl to identify the need for referral
LECTURE 14
TB IN CHILD
dr. Ni Putu Siadi Purniti, SpA
Abstract
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
LECTURE 15
PULMONARY TB AND EXTRAPULMONARY TB
TB IN THE IMMUNOCOMPROMISED HOST
dr. IB Sutha, SpP and dr. Bagiada, SpPD
PULMONARY TB AND EXTRAPULMONARY TB
dr. IB Sutha, SpP
Abstract
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.
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
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?
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.
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.
Tugas
Diskusikan!
1. Jelaskan bagaimana Sdr memastikan bahwa pasien tersebut memang menderita TB dan imunokompromais!
2. Mengapa TB laten menjadi reaktivasi (TB aktif)?
3. Bagaimana Sdr mengenali pasien TB imunokompromais mengalami Immune
Reconstitution 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 16
ASTHMA
Prof. IB Rai
Abstract
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.
Tugas:
Diskusikan!
1. Jelaskan bagaimana Sdr. 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 Sdr. berikan?
6. Jelaskan kreteria serangan asma akut berat!
LECTURE 16
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
dr. IGN Bagus Artana, SpPD
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.
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 eksaserbasiakut
Kasus:
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.
Tugas:
Diskusikanlah mengenai:
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 17
PLEURAL EFFUSION
dr. Putu Andrika, SpPD-KIC
PNEUMOTHORAX
dr. Yasa, SpBTKV
PLEURAL EFFUSION
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.
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:
Tugas: Diskusikan
1. Apakah kemungkinan penyebab keluhan pasien tersebut? 2. Pemeriksaan penunjang apa yang diperlukan?
3. Perlukah melakukan parasentesis? (jelaskan) 4. Perlukah pemasangan WSD, apa alasannya? PNEUMOTORAKS
dr. Yasa, SpBTKV
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. 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 Kasus:
Seorang pasien laki-laki usia 30 tahun datang kePuskesmas tempat anda bertugas dengan mengeluh se
