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Module (RESP 1)
Module (RESP 2)

: Respiratory Symptoms
: Pharmacotherapy for The Respiratory System

Module (RESP 3)
Module (RESP 4)
Module (RESP 5)

: Tuberculosis
: Asthma Bronchiale
: Chronic Obstructive Pulmonary Disease

Module (RESP 6)

: Managing Tuberculosis Health Problem in


Module (RESP 7)

: Managing Asthma Bronchiale and Chronic

Obstructive pulmonary Disease in Community

Module (RESP 8)

: Respiratory System Examination

Module (RESP 9)

: Clinical Skill Of Rehabilitation Medic

Module (RESP 10)

: Clinical Skill Of Pharmacotherapy

Module (RESP 11)

: Clinical Skill Of Radiology


Pulmonary and Respiratory Block will be held onsemester V within at
about 6 weeks. In this session , student will learn about







Pulmonary and

pathophysiology, diagnostic problems and management. Therefore skill of history

taking, chest examination, laboratorium finding and treatment are needed.
After working through this nonmodule and integrated module, the student will be
able to :
a. Describe anatomy, histology and physiology aspect connected to pulmonary
and respiratory disease
b. Describe , how to work up patient with pulmonary and respiratory disease
c. Describe management of pulmonary and respiratory disease.



1. Thorax

Overview of thorax
Thoracic apertures
Thoracic wall
a. Vertical lines of thoracic wall
b. Fascia of thoracic wall
c. Skeleton of thoracic wall
d. Muscles of thoracic wall
e. Nerves of thoracic wall
f. Vasculature of thoracic wall
g. Lymphatic drainage
2. Intercostal spaces
- Structure
- Muscles
- Vasculature
- Innervation
3. Movement of thoracic wall & diaphragma




during breathing
Function of the respiratory system
Pulmonary circulation system
Pulmonary ventilation
Volumes and capacities of the lungs
Control of bronchiolar musculature
Gas partial pressures
Transport and gas diffusion capacities
Oxygen intake and uptake during exercise
Oxygen-hemoglobin dissociation curve
The Haldan effect
Respiratory centre
Inspiratory ramp signal
Pneumotaxic centre
The Hering-Beuer reflex
Periodic and the Cheyne-Stokes

17. Regulation of respiration during exercise
18. Sleep apnea
19. Artificial respiration, and
20. Hypoxia.
Normal flora in Respiratory System
Virual infection :

Respiratory syncytial

Others :

Bacterial infection :

Pneumococcal pneumonia
Atypical pneumonia
Others : Klebsiella sp., legionellosis,

Fungal infection :




Pneumocystis pneumonia
Opportunistic mycosis
(Aspergillosis, candidiasis, etc)
Tropical Pulmonary Eosinophillia
Proces of inflamation and malignancy
Acid-base Imbalance
Radiology of thorax
Pharmacologytherapy in Respiratory system


Medical Rehabilitation
Public Health

(Rationale drug use)

Pulmonary Rehabilitation
Managing Tuberculosis, Asthma Bronchiale and
Chronic Obstructive pulmonary Disease in


Thoracic Surgery



Trauma of Thorax
- Respiratory distress syndrome
- Bronchopulmonary Dysplasia
- Apneu in Neonatus
- Pneumothorax in Neonatus
- Aspiration Pneumonia
- Bronchopneumonia
- Bronchiolitis
- Pediatric Tuberculosis
- Pediatric Asthma bronchiale
- Acute Respiratory Distress Syndrome
- Lung Oedem
- Lung Emboli
- Lung Infarct
- Lung cancer,Tumor mediastinum, Pleuritis

Pleural efusion
Acute Bronchitis
Pneumonia ( bacterial, viral)
Cystic Fibrosis

Topics covered in integrated module are:

Module (RESP 1)
Module (RESP 2)

: Respiratory Symptoms
: Pharmacotherapy for The Respiratory System

Module (RESP 3)
Module (RESP 4)
Module (RESP 5)

: Tuberculosis
: Asthma Bronchiale
: Chronic Obstructive Pulmonary Disease

Module (RESP 6)

:Managing Tuberculosis Health Problem in


Module (RESP 7)

: Managing Asthma Bronchiale and Chronic

Obstructive pulmonary Disease in Community

Module (RESP 8)

: Respiratory System Examination

Module (RESP 9)

: Clinical Skill Of Rehabilitation Medic

Module (RESP 10)

: Clinical Skill Of Pharmacotherapy

Module (RESP 11)

: Clinical Skill Of Radiology

Skill related in Respiratory and Pulmonary Block

a. History Taking on Respiratory and Pulmonary Disease
b. Chest Examination
c. Chest X-Ray Description
d. Medical Rehabilitation
e. Pharmacotherapy
a. Self Learning
b. Tutorial
c. Small Class Discussion
d. Student Presentation
e. Lecture
f. Practice
g. Clinical Skill


a. Pharmacology Laboratory
b. Public Health
c. Pulmonology Laboratory
a. Microbiology Laboratory
b. Parasitology Laboratory
c. Anatomy-Pathology Laboratory
d. Clinic-Pathology Laboratory
e. Radiology Laboratory
f. Medical Rehabilitation Laboratory
g. Surgery Laboratory
h. Public Health Laboratory
i. Pediatric Laboratory
j. Pulmonary Laboratory
a. History Taking
b. Chest Examination
c. Skill on Pharmacotherapy

d. Skill on Radiology
e. Skill on Rehabilitations
a. Observational Form
b. Fals and True Topic Examination
c. Multiple Choice Question (MCQ) Examination
d. Check list evaluation

(CODE : RESP 1 )

(For Students)
dr. Triwahju Astuti, MKes,SpP
dr. Iin Noor Chozin, SpP



Course Content : Syndromatology & Symptomatology

Course Topic : Cough, Hemoptysis & Dyspneu
Staff of Pulmonology Department

This module is a part of the elaboration of the area of competence 4 of the

Indonesian Doctor Competencies i.e The Scientific-Base of Medical Sciences
To apply the Concepts and Principles of Symptoms of Respiratory Disease in the
Clinical Practice
Be able to recognize and place the clinical pictures of the most common
diseases related to Cough, Hemoptysis, Dyspneu syndrome and symptoms and
know how to acquire more information on it
a. To address the symptoms of respiratory disease
b. To review the anatomy & pathophysiology, differential diagnosis, pathogenesis,
complication, guidelines for evaluating chronic cough
c. To review the etiology, pathogenesis, differential diagnosis, diagnosis of
b. To review the pathophysiology, differential diagnosis and

guidelines for

evaluating dyspneu
This module is part of Module Symtoms of Respiratory Disease integratedly
designed for medical student of 5thsemester through Teaching-Learning Process
in the 7thBlock both in Lecture and Small Group Discussion. This part of Module
will facilitate the student a basic understanding of the Symptoms in Respiratory
Disease of Cough, Hemoptysis and Dyspneu prior to developing their knowledge
on diseases related to Cough, Hemoptysis and Dyspneu


Texbooks ussually define cough as a deep inspiration followed by a strong
expiration against a closed glottis, which then opens with an expulsive flow of air,
followed by a restorative inspiration; these are the inspiratory, compressive,
expulsive, and recovery phases of cough.
a. Basic term to remind
1) Acute cough: a recent onset of cough lasting < 3 weeks
2) Chronic cough: a cough lasting > 8 weeks
3) Prolonged acute cough
Clearly there is a grey area between acute and chronic cough,
sometimes called subacute cough. An example of such a situation would
be a child with pertussis or postviral cough whose cough may be slowly
resolving over a 38-week period. If a cough is resolving, an additional
period of time may be required to elapse before performing further
investigations. Most acute coughs associated with upper respiratory
infections should be abating in the second and third week. However, if the

cough is not waning by the third week and is becoming more severe in
frequency and intensity (relentlessly progressive), earlier investigations
may be warranted
4) Recurrent cough
A recurrent cough without a cold is taken as repeated (>2/year) cough
episodes, apart from those associated with head colds, that each last
more than 714 days. If the periods of resolution are short, frequently
recurrent cough will be difficult to distinguish from persistent chronic cough.
bAnatomy & Pathophysiology
Experimentally, involuntary coughing appears to be entirely a vagal
phenomenon, which can be initiated only from those structures innervated by
the vagus nerve and its branches. These include the lower part of the
oropharynx, the larynx, and the lower respiratory tract, as well as the tympanic
membrane and the external auditory meatus. Irritation at all these sites can
cause coughing. The one clear exception to vagally mediated coughing is that
caused voluntary. The extremely wide variety of stimuli that can triger cough
points to a similarly wide range of properties of the nerve receptors that are
starting point of the cough reflex.
There are usually three phases involved in the active cough mechanism.
Cough is usually preceded by a deep inspiration (inspiratory phase). This initial
inspiration is important in producing an effective cough by permitting both
expiratory pressure and flow to be maximal during the ensuing expiration. This
high lung volume allows maximum expiratory flow rates. During the second
compressive phase, intrathoracic pressure is raised sufficiently to produce flow
rates necessary for effective cough during the expiratory phase. It is during
this latter phase that the defense mechanism function of cough is carried out;
that is, the removal of undesired material from the lower respiratory tract.
While dynamic changes are taking place in the glottis (eg, while vocal cords
separate and vibrate and the width of the glottis narrows at the aryepiglottic
folds that shake secretions loose from the larynx), the same thoracic and
abdominal muscles that were active during the compressive phase of cough
contract further. The continued shortening of these muscles after the opening
of the vocal cords serves to maintain the rapid flow of air by ensuring a highpressure gradient between intrathoracic airways and the mouth. Numerous
studies have noted that maximum intrathoracic pressures during a cough
occur after the opening of the glottis, attesting to the contribution of the
expiratory muscles in maintaining high pressures, and therefore, high flow.
Along with the larynx and expiratory musculature, the tracheobronchial tree
also undergoes dynamic changes that ensure an effective cough.
c. Differential Diagnosis and Pathogenesis
Cough can be caused by a multiplicity of disorders in a variety of
locations. Because virtually any condition that stimulates cough receptors or

afferent nervous pathways is capable of producing cough. They will be

categorized according to the duration of cough into acute and chronic types.
Acute cough is one that lasts <8 weeks and is most commonly transient and
of minor consequence (eg, the common cold);however, it can occasionally be
potentially life threatening (eg, pulmonary embolism, congestive heart failure,
or pneumonia). Chronic cough lasts 8 weeks and is persistently
troublesome. Because there are patients with respiratory infections (eg,
pertussis) more severe than the common cold who complain of cough for
longer than 3 weeks and have it spontaneously disappear by 8 weeks, some
investigators have chosen to withhold a diagnostic workup for 8 weeks. Last,
because acute cough may become chronic, the categories are not mutually
With respect to the pathogenicity of cough, there are limited data that do
not appear, at this time, to support one common mechanism. For example,
while excessive mucus production may lead to cough by mechanically
stimulating the afferent limb of the cough reflex and extraluminal masses by
compressing/ distorting submucosal airway receptors, an increased sensitivity
of the afferent limb of the cough reflex appears to be an important
pathogenetic mechanism common to patients who have a nonproductive
cough due to variety of diseases (eg,asthma, upper respiratory infection,
gastroesophageal reflux disease [GERD], and angiotensin-converting enzyme
inhibitors [ACEIs]).
d. Complications
During vigorous coughing, intrathoracic pressures up to 300 mm Hg,
expiratory velocities up to 28,000 cm/s or 500 miles per hour (ie, 85% of the
speed of sound), and from 1 to 25 joules of energy can be generated. While
pressures, velocities, and energy of these magnitudes allow coughing to be
an effective means of providing cardiopulmonary resuscitation in the
conscious patient, they also cause a variety of complications. The
complications of cough can affect many organ, Cardiovascular, Neurological,
Gastro Intestinal, Genitourinary, Musculoskeletal, Respiratory, Miscellaneous.
e. Guidelines for Evaluating Chronic Cough
1. Review the patients history and perform a physical examination,
concentrating on the anatomy of the cough reflex and specifically the most
common causes of chronic cough.
2. Order chest radiogram in nearly all patients. It is extremely useful for
initially ranking differential diagnostic possibilities and dirrecting laboratory
3. Do not order additional laboratory test in present smokers or patients
taking an ACEI until the response to cessation of smoking or
discontinuation of the drug for 4 weeks can be assessed.

4. Depending on the results of the initial evaluation, the following may be

obtained : sinus radiographs and allergy evaluation, spirometry, sputum
for mocrobiology and / or cytology.

Hemoptysis is the blood derived from the lungs or bronchial tubes.
Hemoptysis may be scant, producing the appearance of streaks of bright red
blood in the sputum, or profuse, with expectoration of a large volume of blood.
Massive hemoptysis is defined as the expectoration of 600 mL of blood within 24
to 48 hours and may occur in 3 to 10% of all patients with hemoptysis. Gross or
frank hemoptysis produces a quantity smaller than masssive
hemoptysis and greater than blood streaking. Dark red clots may also be
expectorated when blood has been present in the lung for days.
a. Etiology
The more frequent causes of massive hemoptysis are :
- Arteriobronchial fistula
- Congestive heart failure
- Pulmonary arteriovenous fistula
Diffuse intrapulmonary hemorrhage
Diffuse parenchymal disease

Malposition of chest tube

Pulmonary artery rupture
Tracheoartery fistula


Cystic Fibrosis
Lung abscess


Bronchogenic carcinoma
Metastatic cancer

Virtually all causes of hemoptysis may result in massive hemoptysis, but it is
most frequently caused by infection and cancer.
b. Pathogenesis
The bronchial arteries are the chief source of blood for the airways (from
mainstem bronchi to terminal bronchioles), for the supporting framework of the
lung that includes the pleura, intrapulmonary lymphoid tissue, and the large
branches of the pulmonary vessels, and for the nerves in the hilar regions. The

pulmonary arteries supply the pulmonary parenchymal tissue, including the

respiratory bronchioles. Communications between these two blood supplies,
bronchopulmonary arterial and venous anastomoses, occur in the proximity of the
junction of the terminal and respiratory bronchioles. These anastomoses allow the
two blood supplies to complement each other. For instance, if flow through one
system is increased or decreased, a reciprocal change occurs in the amount of
blood supplied by the other system. Arteriographic studies in patients with active
hemoptysis have shown that the systemic circulation is primarily responsible for
the bleeding in about 92% of cases.
The pathogenesis of hemoptysis depends on the type and location of the
disease. In general, if the lesion is endobronchial, the bleeding is from the
bronchial circulation, and if the lesion is parenchymal, the bleeding is from the
pulmonary circulation. Moreover, in chronic diseases, repetitive episodes are
most likely due to increased vascularity in the involved area.
c. Diagnosis
The diagnostic work-up of hemoptysis involves :
History, Physical examination, Complete blood count, Coagulation studies ,
Electrocardiogram, Chest radiograph, Bronchoscopy*
*Although bronchoscopy is not indicated in some conditions (eg, pulmonary
embolism, aortopulmonary fistula, congesrive heart failure), it should routinely be
d. Differential Diagnosis
In evaluating patients with hemoptysis, it is necessary to rule out the causes of
pseudohemoptysis. Unless the cause of pseudohemoptysis is definitively
determined, the spitting up of blood must be assumed to be true hemoptysis. An
upper airway lession must not be assumed to be the cause of the bleeding unless
it is seen bleeding actively at the time of examination.

Dyspnea is a distressing sensation of difficult, labored, or unpleasant breathing.
The word distressing is very important to this definition since labored or difficult
breathing may be encountered by healthy individuals while exercising, but it does
not qualify as dyspnea because it may not be perceived as distressing. The
sensation is often poorly or vaguely described by patients.
1. Pathophysiology
There are multiple stimuli, receptors, nerves, and neural pathways that
mediate the sensation of dyspnea. This multiple neural pathways model of
dyspnea suggests that dyspnea may arise due to abnormalities in the afferent
pathways, the efferent pathways, or the central control centers of the
respiratory system. Since afferent pathways feed back to the central nervous

system from virtually all levels of the efferent pathways, afferent dyspneic
information from virtually all thoracic and upper abdominal organs (including
the pharynx, larynx, airways, lung parenchyma, esophagus, heart, and
stomach) may potentially impact the sensation
The mechanism by which diseases produce dyspnea varies with the disease.
Some affect afferent pathways, others efferent pathways, and others the
central integrative sensory pathways.
2. Differential Diagnosis

Mixed cardiac or pulmonary

Congestive heart failure (right, left or

COPD with pulmonary hypertension and cor



Coronary artery disease


Myocardial infarction (recent or past history)

Chronic pulmonary emboli



Valvular dysfunction

Noncardiac or nonpulmonary

Left ventricular hypertrophy

Metabolic conditions (e.g., acidosis)

Asymmetric septal hypertrophy



Neuromuscular disorders


Otorhinolaryngeal disorders




- Anxiety


- Panic disorders

Restrictive lung disorders

- Hyperventilation

Hereditary lung disorders

COPD=chronic obstructive pulmonary disease.

3. Guidelines for evaluating dyspnea

Acute dyspnea
A clinical approach is recommended for evaluating acute dyspnea. It consists
of performing history and physical examination and performinglaboratory
test , considering potensial life-threatening conditions first (eg,acute asthma,
pulmonary embolism, pulmonary oedema states, pneumonia)
Chronic dyspnea
The following systematic, diagnostic approach has been validated in patients
with chronic dyspnea who were evaluated in a university hospital, out patient
pulmonary clinic.
1. Review the patients history and perform a physical examination,
concentrating on the anatomy of the potential origins of the dyspnea
sensation and spesifically, the most common causes of dyspnea : COPD,







respiratory diseases, and the hyperventilation syndrome.

2. Order a chest radiograph in nearly all patients
3. Depending on the results of the initial evaluation and chest radiographs,

the following may be obtained

Pulmonary function testing

Noninvasive cardiac studies to include ECG, echocardiography, and

stress testing.
Chest CT scan
Comprehensive ETT
Other more invasive test such as cardiac catheterization and lung

4. Whenever posible, the final determination of the cause of dyspnea is made by
observing which specific therapy eliminates dyspnea as a complaint. Since
dyspnea may be simultaneously due to more than one condition, do not stop
therapy that appears to be partially successful; rather, sequentially add to it.

First thoughts about chest pain almost invariably turn to the pain of
myocardial ischemia. However, cardiac pain is often distinguishable from
other types of chest pain because of its viselike nature; its characteristic
radiation to the left arm, shoulder or neck; and its lack of relation to breathing.
Extracardiac painful sensations can arise from various sites within the thorax,
most often from the pleura, the lungs and the chest wall. Pain may also be
referred to the thorax as a result of GERD.
Pleuritic Pain
The most characteristic pain associated with the respiratory apparatus is
pleural pain. It originates in the parietal pleura and endothoracic fascia; the
visceral pleura is insensitive to pain. In contrast to the deep, oppressive
substernal pain of myocardial infarction, pleuritic pain is identified by the
patient as being close to the thoracic cage. It is predominantly an inspiratory
pain reflecting the stretching of inflamed parietal pleura during movement of
the thorax; coughing or laughing is exceedingly distressing; the patient often
clutches the chest to minimize its excursion. The pain is usually local, but
sometimes it spreads along the course of the intercostals nerves that supply
the affected area. Irritation of the diaphragmatic pleura by an inflammatory
process either below or above the diaphragm often causes ipsilateral
shoulder pain when the central portion of the diaphragm is involved;
sometimes the pain is reffered to the abdomen when the outer diaphragmatic
pleura is irritated.
As a rule, pleural pain is part of a syndrome of pleural inflammation that
includes malaise and fever; an important exception to this generalization is
the pleural pain of pulmonary infraction, which is often unassociated with any
premonitory signs. In addition to inflammation and malignant etiologies,
pleuritic pain occurs with pneumothorax.
Pulmonary Pain
A second distinctive type of respiratory chest pain accompanies a
tracheitis or tracheobronchitis. The pain is searing and is most pronounced

after cough. Invariably this central chest pain is associated with evidence of
upper respiratory infection.
In uncommon type of chest pain is associated with pulmonary hypertension. It
is usually absent at rest and appears during exertion. The pain is substernal
and is invariably associated with dyspnea; it subsides promptly when exercise
stops. It is often mistaken for left heart angina until the presence of pulmonary
hypertension is uncovered. It may be due to right ventricular strain and
Chest Wall Pain
Pain in the chest is a common clinical problem. It may arise from within
the thorax (the heart, pericardium, lungs, pleura, chest wall) or be referred
from elsewhere (e.g., from below the diaphragm). Characteristic patterns and
associations may help to clarify the source of the pain.
Pleural pain is generally associated with fever or dyspnea. Most often it is
abrupt in onset, unilateral, and incapacitating. As a rule, it affects the lower
part of the chest, but occasionally it is referred to the shoulder or

abdomen. Almost invariably, pleural pain is aggravated by deep breathing

or coughing. The patient tends to splint the chest on the affected side.
Tachypnea and shallow tidal volumes are a consistent pattern.
Musculoskeletal pain arising in the chest that is also aggravated by breathing
may be confused with pleuritic pain. It is rarely severe and incapacitating, is
often bilateral, and generally is intensified by changes in body position or
flexing the thorax. The affected muscles are often tender to gentle pressure. A
fractured rib is often identified as the source of pain by a history of a fall,
injury, or trauma. Additional clues are point tenderness and crepitus of the
affected area, reproduction of the pain upon manual compression of the
chest, or radiographic evidence of the broken rib.
Pain arising from the large airways is usually burning in nature and
retrosternal in location and is disturbing rather than incapacitating. It is
aggravated by cough and is commonly accompanied by evidence of a
bronchitis. Cold air may be intolerable.
The pain of a pulmonary sulcus tumor (Fig. 27-19) is quite distinctive. This
unusual location of a carcinoma of the lung was originally described by
Pancoast in 1932 as characterized by pain along the distribution of the eighth
cervical and the first and second thoracic nerves, Horners syndrome, local
destruction of bone by the tumor, and atrophy of hand muscles. The chest
radiograph is distinctive in showing a small, sharply defined shadow at one
apex. Destruction of one or more of the upper three ribs posteriorly and of
their adjacent transverse processes may also be observed

Figure 24-19 Pulmonary sulcus tumor. A..Chest radiopraph , B. Relationships

of apex of lung to adjacent bony structures. C. Lateral view of area occupied
by apex of lung, showing proximity not only to nerves of brachial plexus but
also to sympathetic chain and to blood vessels. A mass that grows posteriorly
and laterally can encounter sympathetic chain and bony structures; superiorly,
the axillary vessels, branchial plexus, and bony structures; anteriorly, the
subclavian vein and its tributaries.
Miscellaneous Pain
Other structures in the mediastinum can be the source of chest pain.
Noteworthy are the types of pain arising from the esophagus (peptic
esophagitis) and dissection of the aorta. Their patterns and intensity help to
distinguish them from respiratory pain. Esophageal disease is typically
accompanied by a burning pain, frequently after eating. Acid reflux may
worsen with recumbency. Aortic dissection is often described with a sharp,
teraing sensation of acute onset with radiation to the shoulder; these are often
signs of impending cardiovascular collapse.
Arthritis of the cervical spine is a common cause of thoracic pain. Usually
the cause is quite clear because of the chacarteristic distribution of the pain.
Cervical spondylosis occasionally causes severe pain in the chest and arms,
but it is more apt to mimic myocardial infarction than is respiratory pain. A
metastatic tumor the thoracic spine often causes bilateral symmetric pain;
there is often discomfort to palpation over the affected area. Unilateral pain,
along the distribution of an intercostals nerce, is characteristic of herpes
zoster before the appearance of the skin eruption and is often described as
an intense burning sensation.
Anxiety can produce or intensify chest pain. Usually, pain related to
anxiety is accompanied by dyspnea and hyperventilation. Manifestations of
vasomotor instability, such as excessive palmar sweating, flushing, and
tachycardia, may accompany the complaint of chest pain due to anxiety.
Rarely does the pain conform to acharacteristic or consistent pattern. Anxiety

also interferes with the quantification of pain originating in a somatic lesion

and with its management.
8. Module Task
Find out your answer to the following tasks by yourself after discuss it with
your group or after reading the suggested references below.
1. Explain the questions that should be addressed in cough evaluation
2. Describe the cough resulted from lung tuberculosis.
3. Explain complication of the cough in pulmonary organ.
4. Explain the causes of acute cough and chronic cough
5. What do you know about hemoptysis, explain the possible source of
6. Describe the schema of pathophysiology of dyspnea.
7. Explain the questions that should be addressed in dyspnea evaluation
9. References
1. Irwin, Richard S. (2003). Symptoms of Respiratory Disease. ACCP
Pulmonary Board Review. Dundee Road. Northbrook Illinois. p. 327-360.
2. Mason, Robert J; Murray, John F; Broaddus, V. Courtney; Nadel, Jay A.
(2005). Textbook of Respiratory Medicine. Elsevier Saunders Philadelphia,
Pennsylvania. p. 815-847.
3. MD Shields, A Bush, ML Everard, S McKenzie, R Primhak (2008).
Recommendations for the assessment and management of cough in children.
Thorax, 63:1-15
4. Morgan WC, Hodge HL (1998). Diagnostic evaluation of dyspnea. American
Family Physician.
10. Teaching Learning Process
This Module should be used as Teaching-Learning Process Media prior to lecture
and or Class Discussion


(For Students)


DR.dr. Setyawati S. Karyono,MKes



Learning Objectives
By the end of this session, students should be able to:
1. Describe the special problems associated with chemotherapy of mycobacterium
infections (properties of mycobacteria, resistance of mycobacteria and adverse effects)
2. Describe the pharmacodynamic and pharmacokinetic properties of the first-line drugs
used in tuberculosis (isoniazid, ethambutol, pyrazinamide, rifampin, and streptomycin).

3. Describe the adverse effects of the first-line drugs used in tuberculosis (isoniazid,
ethambutol, pyrazinamide, rifampin, and streptomycin).
Mycobacteria are intrinsically resistant to most antibiotics. Because they grow slowly compared
with other bacteria, antibiotics that are most active against growing cells are relatively
ineffective. Mycobacterial cells can also be dormant and thus completely resistant to many
drugs or killed only very slowly. The lipid-rich mycobacterial cell wall is impermeable to many
agents. Mycobacterial species are intracellular pathogens, and organisms residing within
macrophages are inaccessible to drugs that penetrate these cells poorly. Finally, mycobacteria
are notorious for their ability to develop resistance. Combinations of two or more drugs are
required to overcome these obstacles and to prevent emergence of resistance during the
course of therapy. The response of mycobacterial infections to chemotherapy is slow, and
treatment must be administered for months to years, depending on which drugs are used.
Drug used in tuberculosis:
Isoniazid (INH), rifampin, pyrazinamide, ethambutol, and streptomycin are the five first- line
agents for treatment of tuberculosis. Table of the drug combinations tuberculosis therapy listed




Paduan obat yang dianjurkan

TB paru BTA +

2 RHZE / 4 RH atau

BTA -, lesi luas

2 RHZE / 6 HE


*2RHZE / 4R3H3




TB paru putus

TB paru BTA

RHZES / 1RHZE/ sesuai hasil uji resistensi

atau 2RHZES / 1RHZE / 5 RHE
3-6 kanamisin, ofloksasin, etionamid,
sikloserin/15-18 ofloksasin, etionamid,
sikloserin atau 2RHZES/ 1RHZE / 5RHE

alergi, dapat

Sesuai lama pengobatan sebelumnya, lama berhenti

minum obat dan keadaan klinis, bakteriologi dan
radiologi saat ini atau * 2RHZES / 1RHZE /
2 RHZE /4 RH atau 6RHE atau * 2RHZE / 4 R3H3

lesi minimal


RHZE / sesuai hasil uji resistensi (minimal OAT yang

sensitif) + obat lini 2 (pengobatan minimal 18 bulan)



Sesuai uji resistensi + OAT lini 2 atau H seumur


H = isoniazid

R= rifampin

Z= pirazinamid

E= etambutol

1. Describe the pharmacokinetic of isoniazid (INH), rifampin, pyrazinamide, ethambutol,
and streptomycin.

2. Describe the pharmacodynamic (mechanism of action) isoniazid (INH), rifampin,

pyrazinamide, ethambutol, and streptomycin.
3. Describe the mechanism of resistance of isoniazid (INH), rifampin, pyrazinamide,
ethambutol, and streptomycin to mycobacteria.
4. Describe the adverse effects of isoniazid (INH), rifampin, pyrazinamide, ethambutol,
and streptomycin.


Setyawati S Karyono
Pharmacology Department of Medical Faculty Brawijaya Universty
Learning Objectives
By the end of this session, the students should be able to:
1. Explain the pharmacodynamic and pharmacokinetic properties of bronchodilator drugs.
2. Explain the pharmacodynamic and pharmacokinetic properties of anti-inflammatory
agent in asthma bronchial.
3. Describe the side effects and toxicity of drugs used in asthma bronchial
4. Manage pharmacotherapy of asthma bronchial

The clinical hallmarks of asthma are recurrent, episodic bouts of coughing, shortness of breath,
chest tightness, and wheezing. In mild asthma, symptoms occur only occasionally, e.g., on
exposure to allergens or certain pollutants, on exercise, or after a viral upper respiratory
infection. More severe forms of asthma are associated with frequent attacks of wheezing
dyspnea, especially at night, and even chronic limitation of activity. Asthma is the most common
chronic disabling disease of childhood, but it affects all age groups.
Asthma is physiologically characterized by increased responsiveness of the trachea and bronchi
to various stimuli and by widespread narrowing of the airways that changes in severity either
spontaneously or as a result of therapy. Its pathologic features are contraction of airway smooth
muscle, mucosal thickening from edema and cellular infiltration, and inspissations in the airway
lumen of abnormally thick, viscid plugs of mucus.
Asthma is associated with inflammation of the airway wall. Increased numbers of various types
of inflammatory cells, most notably eosinophils but also basophiles, mast cells, macrophages,
and certain types of lymphocytes, can be found in airway wall biopsies and in bronchoalveolar
lavage fluid from asthmatic patients. Inflammatory mediators and various cytokines also are
increased in the airways of asthmatic subjects compared with healthy control subjects.
The mechanisms underlying bronchial hyperreactivity are somehow related to inflammation of
the airway mucosa. The agents that increase bronchial reactivity, such as ozone exposure,
allergen inhalation, and infection with respiratory viruses, also cause airway inflammation.
Asthma therapies are thus sometimes divided into two categories: "short-term relievers" and
"long-term controllers." Short-term relief is most effectively achieved with bronchodilators,
agents that increase airway caliber by relaxing airway smooth muscle, and of these the adrenoceptor stimulants are the most widely used. Theophylline, a methylxanthine drug, and
antimuscarinic agents are also used for reversal of airway constriction. Long-term control is
most often achieved with an anti-inflammatory agent such as an inhaled corticosteroid, with a
leukotriene antagonist, or with an inhibitor of mast cell degranulation, eg, cromolyn or

The adrenoceptor agonists have several pharmacologic actions important in the treatment of
asthma. They relax airway smooth muscle and inhibit release of some bronchoconstricting
substances from mast cells. They may also inhibit microvascular leakage and increase
mucociliary transport by increasing ciliary activity or by affecting the composition of mucous
secretions. As in other tissues, the agonists stimulate adenylyl cyclase and increase the
formation of cAMP in the airway tissues.

Bronchodilation is promoted
by cAMP. Intracellular levels
of cAMP can be increased
by -adrenoceptor agonists,
which increase the rate of
its synthesis by adenylyl





inhibitors such as theophylline, which slow the rate of its degradation.

Bronchoconstriction can be inhibited by muscarinic antagonists and possibly by adenosine
antagonists (theophylline).
Glucocorticoids do not directly relax airway smooth muscle and thus have little effect on acute
bronchoconstriction. By contrast, these agents are singularly effective in inhibiting airway
inflammation. Very few mechanisms of inflammation escape the inhibitory effects of these
drugs. The antiinflammatory effects of glucocorticoids in asthma include modulation of cytokine
and chemokine production; inhibition of eicosanoid synthesis; marked inhibition of accumulation
of basophils, eosinophils, and other leukocytes in lung tissue; and decreased vascular


Describe the pharmacotherapy of asthma bronchial based on the pathophysiology.

Explain the mechanism of action of each bronchodilator.
Describe the pharmacokinetics of bronchodilators, especially theophylline.
Explain the diseases and drugs that influence theophylline metabolism.
Explain the mechanism of action of steroid anti-inflammatory drug in asthma

6. Describe the adverse effects of steroid anti-inflammatory drug and how to reduce it.

Suggested Reading
1. Goodman & Gilman's The Pharmacological Basis Of Therapeutics - 11th Ed. (2006) :
Chapter 27.
2. Katzung Basic & Clinical Pharmacology -8th Ed; Chapter 19.



(For Student)
dr. Triwahju Astuti, MKes,SpP
dr. Iin Noor Chozin, SpP





In this module, medical student will learn epidemiology,

how TB disease

develops in the body (pathogenesis), clinical manifestation, diagnosis and

treatment of active TB disease. As a public health worker, you should understand
these concepts so that you can educate the patients you serve.

This module is a part of the elaboration of the area of competence 4 of the
Indonesian Doctor Competencies in Pulmonary and Respiratory Disease.


a. To become familiar with the epidemiology of tuberculosis.
b. To review the pathogenesis and clinical presentation of tuberculosis.
c. To address issues concerning the prevention of tuberculosis, including the
diagnosis and treatment of tuberculosis infection.
d. To review issues concerning the diagnosis and treatment of tuberculosis


This module is part of Respiratory Module, integratedly designed for medical
students of 5th semester through Teaching-Learning Process in the 14 Bloc both
in Lecture and Small Group Discussion. This part of module will facilitate the
student a Pulmonary and Respiratory Disease in the Clinical Practice.


ACCP Pulmonary Board Review, (2003).Dundee Road. Northbrook

Illinois. p.417- 425.

Rom WN, Garay SM, Tuberculosis, 2nd edition, Lippincot Williams &

Wilkins, Philadelphia
Mason, Robert J; Murray, John F; Broaddus, V. Courtney; Nadel, Jay A.
(2005). Textbook of Respiratory Medicine. Elsevier Saunders Philadelphia,

Kementerian Kesehatan





Penyakit dan Penyehatan Lingkungan (2011), Pedoman Nasional

Pengendalian Tuberkulosis.


This Module should be used as Teaching-Learning Process Media prior to lecture
and or Class Discussion


At the turn of the 20th century, tuberculosis (TB) was one of the leading
causes of death in the United States. After the discovery of effective
chemotherapy, the rate of TB significantly declined an average of 8% per year
between 1953 and 1983. From 1985 to 1992, however, TB unexpectedly
increased by approximately 20%. Factors associated with the resurgence
included the HIV epidemic, increased immigration of foreign born persons from
high-incidence areas, an increased number of medically underserved persons

(eg, homeless individuals, drug abusers), and probably most importantly, the
deterioration of the public health infrastructure for the control of TB. Associated
with the increased incidence was an increased number of drug-resistant TB
Worldwide, TB has not declined as in the United States. According to
themost recent statistics from the World Health Organization, the number of new
disease cases of Tb in 2000 was approximately 8.4 million worldwide, added to
the existing 16.2 million cases. Ninety-five percent of TB cases occur in
developing countries (especially in Africa and Asia) where HIV infection is
common and resources are scarce and unavailable to ensure proper TB
treatment. It is estimated that 1.87 million people died of the disease, with a
fatality rate as high as 50% in some countries with high rates of HIV coinfection.
In addition, approximately one third of the world, or 1.86 billion people, are
infected with Mycobacterium tuberculosis (MTB). To make matters worse, the
incidence of drug-resistant TB worldwide is increasing. During the 1990s, an
estimated 30 million people died as a result of TB, making a strong argument for
its being the most important pathogen in the world today.
Causative Agent of TB
TB is caused by a group of five closely related mycobacteria (M
tuberculosis,ycobacterium bovis, Mycobacterium africanum, Mycobacterium
microti, and Mycobaterium canettii) which form the M tuberculosis complex. The
MTB organism is responsible for the majority of cases of TB in the world. Risk
factors for acquiring TB infection, a prerequisite for the development of disease,
are related to having contact with a source case. In the United States, important
risk factors for infection are: close contact to a TB case; immigration from an
endemic area (eg, Africa, Asia, or Latin America); exposure to untreated TB
cases in congregate living facilities (eg, homeless shelters, correctional facilities,
nursing homes, or other health care facilities); age; and residence in highincidence location (eg, inner cities, travel to foreign endemic areas).

After inhalation, the droplet nucleus is carried down the bronchial tree to a
respiratory bronchiole or alveolus, where it is phagocytized by resident alveolar
macrophages. The nuclei are able to survive at this primary site of infection;
bacilli multiply initially within the macrophages and within 2 weeks are






secondary sites. The

development of an immune response, heralded by the development of delayedtype hypersensitivity over the next 4 weeks, leads to granuloma formation with a
subsequent decrease in bacillary numbers. This stage of disease is called latent

TB infection (LTBI), detected by a reaction to the tuberculin skin test. Patients

with TB infection are asymptomatic, but they have the potential to progress to
active disease later. For most individuals with normal immune function,
proliferation of MTB is arrested once cell-mediate immunity develops, though
small numbers of viable bacilli may remain within the granuloma. Although a
primary complex can sometimes be seen on chest radiograph, the majority of
pulmonary TB infections are clinically and radiographically inapparent. Most
commonly, a positive tuberculin skin test result in the only indication that infection
has taken place. Individuals with LTBI but not active disease are not infectious
and thus cannot transmit the organism.
Once infected with TB, 3 to 5% of immunocompetent individuals develop
active disease within 2 years (defined as progressive with a large inoculation or
immunosuppression) and an additional 3 to 5% develop TB during the remainder
of their lifetime. Most infected individuals are able to mount an effective immune
response that encapsulates these organism, usually for the rest of the hosts life,
thus preventing the progression from infection to disease. Years after the initial
infection and in a small proportion of patients (approximately 5%), the immune
system may not be able to contain these lantent organisms, so reactivation of
TB disease develops. Most cases of TB were thought to be due to reactivation
from remote infection (about 90% of cases), but studies utilizing DNA
fingerprinting indicate that recent transmission (especially among HIV-positive
individuals) probably accounts for as much as 40% of cases of TB.
The partnership between HIV and TB has augmented the deadly
potentials of each disease. By destroying the CD4 cells of the hosts immune
system, HIV allows dormant TB to activate and rapidly cause disease. In
response to the reactivation of TB, CD4 cells become stimulated and begin to
replicate. This activation further renders the CD4 cells vulnerable to invasion by
HIV and allows the virus to further replicate within these cells. This leads to a
vicious cycle of increasing viral load, which causes a further deterioration of the
hosts immune system. Studies have shown that the 1-year mortality rate for
treated, HIV-related TB ranges from 20 to 35% with little variation between
cohorts from industrialized and developing countries.
Clinical Manifestations, Diagnosis, and Treatment of Active TB Disease
Active TB remains primarily a disease of the pulmonary system; however,
in HIV-infected individuals, up to 60% of patients with TB will have
extrapulmonary involvement alone (approximately 30%) or in addition to
pulmonary disease (about 33%), as opposed to 15% in individuals not infected
with HIV. TB can occur in almost any organ, but the most common sites of
extrapulmonary involvement include the pleura, lymph nodes (particularly
cervical and hilar), the CNS (as meningitis or tuberculoma), genitourinary system,
blood, and bone marrow.

The key element to the diagnosis of TB is to have a high degree of

suspicion, especially in those groups at high risk. Early recognition of the disease
is essential to stop further transmission, but no single clinical, radiographic or
laboratory tool is sensitive or specific enough to be diagnostic so astute clinical
assessment is required.
A careful history to elicit the most common symptoms of pulmonary TB (ie,
fever, productive cough, weigh loss, wasting, night sweats, shortness of breath,
and occasionally hemoptysis) should be obtained. The systemic nature of many
of these symptoms is due to the cytokine release associated with the
inflammatory response by the host to the organism. These symptoms are usually
present for a prolonged period, characteristically weeks to months. A history of
possible TB exposure risk (eg, previous exposure, history of homelessness or
prolonged stay in a correctional or other congregate setting, drug abuse history,
migration from an endemic area, prior PPD test) should also be elicited. Physical
examination generally is not helpful in establishing the diagnosis.
Patients with prolonged symptoms, especially those at high risk for TB,
should undergo a chest radiograph immediately (Table 3). Pulmonary TB in
immunocompetent hosts nearly always causes abnormalities on the chest film,
although an endobronchial lesion may not be associated with a radiographic
finding. In primary TB occurring as a result of recent infection, the process is
generally seen as a middle or lower lung zone infiltrate, often associated with
ipsilateral hilar adenopathy. In primary pulmonary pleuritis, a unilateral pleural
effusion may be present. The PPD results initially may be negative in these
cases. Pleural fluid findings are usually predominated by lymphocytes, negative
for acid-fast bacilli (AFB) and positive on culture in only 50 to 60% of cases. The
addition of pleural biopsy for histologic studies and culture increases the yield to
approximately 80%.
Pulmonary TB that develops as a result of endogenous reactivation of
latent infection in immunocompetent hosts usually causes abnormalities in the
upper lobes of one or both lungs. Cavitation is common in this form of TB. The
most frequent sites are the apical and posterior segments of the lung, with the
right lung affected slightly more often than the left. Healing of the tuberculous
lesions usually results in a scar, with loss of lung parenchymal volume and often
calcification. In the immunocompetent adult with TB intrathoracic adenophaty is
uncommon but may occur, especially with primary infection. As TB progresses,
infected material may be spread via the airways into otherparts of the lungs,
causing a patchy bronchopneumonia. Erosion of a parenchymal focus of TB into
blood or lymph vessel may lead to dissemination of the organism and a miliarly
pattern (evenly distributed small nodules) on the chest film.
General indications for Chest Radiograph to Detect TB*
Unexplained cough (> 3 wk)
Unexplained cough with fever (> 3 d)

Unexplained pleuritic chest pain, hemoptysis, and / or dyspnea

Unexplained fever, night sweats, weight loss
*From Pitchenik AE, Brooks R. the most common clinical mistakes prevention,
diagnosis and therapy of tuberculosis. In: Tuberculosis in Florida: the clinicians desktop
reference. Florida TB Conrol Coalition, 1999.
The foundation of rapid, accurate microbiological diagnosis of TB is proper
specimen collection and rapid transport to the laboratory. At least three sputum
specimens should be sent for AFB smear, culture, and (in some cases) nucleic acid
amplification, to attempt to establish the diagnosis microbiologically. A quality sputum
specimen should a content a volume of 5 to 10 mL. If the patient is unable to produce
an adequate specimen, sputum induction and/or bronchoscopy should be considered
(with proper infection control precautions used).
Sputum smears, the time-honored test for the diagnosis of TB, are only positive
in approximately 50% of active cases. The advantage of the smear is that it is both rapid
and cheap. The reason for its low sensitivity is the need for 10,000 to 100,000
organisms in a milliliter of specimen. In addition, the smear is not specific, as other
mycobacteria also may have similar appearance. Patients with smear positive sputa are
more likely to transmit infection to contacts compared to those with smear negative
studies, although this latter group has clearly been shown to transmit infection.
Culture results are positive in approximately 80% of cases, but unfortunately take
a prolonged time to grow: up to 8 weeks for solid median and 1 to 3 weeks for liquid
media. A positive culture requires a result of at least 500 organisms per milliliter.
Susceptibility testing (which should be performed on all initial isolates) may take another
1 to 3 weeks.










microbiologically and are considered to be culture-negative or clinical TB. In these

patients, the diagnosis is based on the presence of symptoms, positive tuberculin skin
test, a radiographic appearance compatible with TB, and an improvement in clinical
status after treatment with antituberculous therapy, despite negative microbiological
studies and no other etiology accounting for the illness. This is found more often in
children and individuals from whom quality specimens are difficult to obtain.
Bronchoscopic studies using BAL and transbronchial biopsy, done with appropriate
infection control precautions, may help establish the diagnosis and rule out other
etiologies when the diagnosis is in question. When TB is strongly suspected, initiation of
presumptive antituberculous therapy is appropriate while awaiting microbiological
Since the advent and utilization of effective chemotherapy against TB in the 1950s,
95% of all individuals with pansusceptible TB who complete therapy are now cured. In
those individuals with multidrug-resistant strains (resistant to at least INH and rifampin),
over 40% of cases may fail to respond to traditional chemotherapy.

The ATS and the CDC recommended that four-drug therapy with INH, rifampin, PZA,
and either ethambutol or streptomycin be started initially in patients from areas where
INH resistance exceeds 4%, until susceptibility test results are available. In areas with
<4% INH resistance, the fourth drug may be omitted from the initial regimen. Once the
results reveal susceptibility to INH, rifampin, and PZA, the ethambutol or streptomycin
should be discontinued. After 2 months of therapy, PZA is stopped, and INH and
rifampin are continued for an additional 4 months for a total o 6 months of treatment. If
cultures are not negative after 2 months of therapy, then treatment should be extended
for at least 4 months after negative results are achieved. The regimen can be given
effectively either daily or intermittently, utilizing directly observed therapy (DOT). It may
also be used for those individuals infected with HIV, as well as patients with
extrapulmonary disease (except for children with milliary TB, bone / joint TB, or
tubeculous meningitis, who should receive a minimum of 12 months of therapy). If PZA
cannot be given for the first 2 months, a reasonable alternative is INH and rifampin
administered for 9 months. A 4-months regimen of INH and rifampin is acceptable
therapy for adults who have active TB and who have negative smears and cultures
(culture negative or clinical TB).
The need to treat with multiple drugs for a prolonged period leads to the major obstacle
facing the control of TB: adherence to therapy. If patients do not take their medications
as prescribed for the entire period, treatment failure and resistance may develop. Once
medications are begun, adherence needs to be assured. The recent decline of TB in the
United States has been attributed in large part to the implementation and utilization of
DOT, which has been shown to significantly improve the completion rates of TB therapy,
as well as impede the development of resistant strains. Through DOT, representatives
of health care facilities (usually from the public health system) go into the community to
observe and assure thet patients take their medications. Numerous studies have
demonstrated that there is no reliable way to predict which patient will be adherent to
therapy; therefore, all patients with active TB disease should be considered for DOT.
Those not started on DOT should be given combination pills (pills containing INH,
rifampin and PZA together) to avoid monotherapy and the subsequent development of
Patients must be monitored for effectiveness of treatment and toxicity. Soon after
starting therapy, patients should experience an improvement in symptoms (such as
cough, fevers, night sweats) and weight gain. Those who do not experience an
symptom improvement or who fail to convert their cultures to negative within 2 months
of treatment initiation should be evaluated for treatment failure. More than 90% of
patients on appropriate therapy have negative culture results after 2 months of
Potential reasons for treatment failure include: (1) resistance to prescribed medications
or the use of an inadequate combination of drugs, resulting in increased drug
resistance; (2) inadequate medication levels caused by malabsorption, food or drug
interactions, or concurrent medical conditions; and (3) noncompliance with prescribed
treatment regimens. Of these, the latter is by far the most common cause of treatment

failure. It is important to seek the advice of a TB expert when patients have resistant
disease, a complicating concurrent medical conditions, or lack of expected response to
Adverse reactions are not uncommon in the treatment of TB. INH, best known for its
hepatotoxicity, also causes peripheral neuropathy for which vitamin B6 (pyridoxine) is
prescribed as prophylaxis. Rifampin may cause hepatotoxicity in addition to muscle and
joint stiffness and pain. Baseline liver function tests should be performed for all patients
beginning treatment, and monthly monitoring is recommended for anyone with baseline
abnormalities or concomitant liver disease. Clinical monitoring by eliciting symptoms of
toxicity, is recommended for all other patients. If transaminase levels become elevated
and symptoms resolve or improve, medications should be discontinued. Once signs and
symptoms resolve or improve, medications should be reintroduced sequentially and the
patient should be monitored for recurrence of hepatitis. PZA can also cause
hepatotoxicity as well as high uric acid levels resulting in gout-like symptoms.
Ethambutol is associated with optic neuritis, especially in doses > 20 mg / kg / d and in
patients with renal insufficiency. Monthly assessment of visual acuity and color
discrimination is recommended to identify patients who may be experiencing this
Drug resistance has been increasing in the United States as well as worldwide. The
most common reasons for the development of drug resistance are patient non
adherence and physician mistakes (eg, adding a single drug to failing regimen),
multidrug-resistant TB is defined as strains resistant to at least INH and rifampin.
Outbreaks of such strains have been well documented, resulting in significant morbidity
and mortality, especially among HIV-infected populations. Control and prevention of
such outbreaks have required the expenditure of significant efforts and resources by
hospital and TB control programs. Treatment of multidrug-resistant TB is frequently
unsuccessfull, requiring the use of more toxic, expensive drugs, in addition to possible
surgery; thus, emphasis is on prevention. In patients with suspected drug-resistant TB,
treatment should be started with the recommended four drugs plus at least two
additional agents to which the patients organism is thought to be susceptible. In
patients with confirmed multidrug-resistant disease, therapy with three drugs to which
the isolate is susceptible is recommended for at least 12 months after documented
conversion of the cultures to negative. Most expert recommend 18 to 24 months of total
therapy. Patients with rifampin-resistant TB should be treated with isoniazid, PZA, and
ethambutol for at least 12 months after cultures convert to negative. Consultation with a
TB expert is recommended for the management of drug-resistant TB.
Patients with HIV have a response to therapy similar to that of individuals without HIV
infection; however, the treatment of HIV has altered TB therapy. Protease inhibitors
(PIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs), two of the most
potent agents available to control HIV, interfere with rifampin, the most important drug
available in TB treatment. Rifampin is a potent inducer of the hepatic p450 system. This
induction enhances the metabolism of the PIs and NNRTIs, causing reduced serum
levels and leading to ineffective viral suppression, as well as the development of

resistance. Conversely, the PIs and NNRTIs interfere with the metabolism of the
rifamycins, causing high serum levels and potential toxicity.
With the use of antiretroviral therapy and the subsequent improvement in the
hosts immune response, patients with TB disease may actually exhibit a paradoxical
worsening of their clinical condition, thought due to an inflammatory response from the
immune reactivation. These patient may experience the development of new ascites,
lymphadenopathy, fever, pleural effusions or cerebral lesions. These may be lifethreatening conditions, depending on the site and size of the lesion. Clinicians treating
TB patients with HIV must be aware of this phenomenon and rule out other etiologies
that maybe responsible for development of the lesions and / or clinical worsening. If no
other etiology can be found, continued treatment for HIV and TB usually results in an










immunomodulators (eg, steroids) may be indicated to slow the progression of this


1. Name five factors that contributed to the increase in the number of TB
cases between 1985 and 1992.
2. Please explain the epidemiology of Tuberculosis in Indonesia
3. Explain the mode of transmission of Tuberculosis
4. After the tubercle bacilli reach the small air sacs of the lung (the alveoli),
what happens to them?
5. How does being infected with both M. tuberculosis and HIV affect the risk
for TB disease?
6. A 30-year-old man visits the health department for a TST because he is
required to have one before starting his new job as a health care worker. He
has an 18mm positive reaction to the TST. He has no symptoms of TB, and
his chest x-ray findings are normal.
a. Should this be considered a case of TB?
b. Should this man be considered infectious?
7. Why must TB disease be treated for at least 6 months?
8. Which four drugs are recommended for the initial treatment of TB disease?
9. Why should at least two drugs be used to treat TB disease?
Name two factors that can lead to drug resistance.
10. Mention the definition of Multi Drug Resistant (MDR)Tuberculosis
Explain the Programmatic Management of Drug resistant Tuberculosis
11. In what special situations should treatment for TB disease last longer than
the usual course of treatment?
12. Explain the TB-HIV Collaboration
13. Name the drug or drugs that may cause each of the following symptoms or
adverse reactions.
14. How often should patients be monitored for adverse reactions to TB
15. You are assigned to deliver medications to TB patients as part of the
directly observed therapy program where you work. When you visit Mr. Xs
house, you ask him how he is feeling. He tells you that he was up all night
What are the possible causes?

16. Ms. A, a patient who started treatment for TB disease last week, calls the
TB clinic to complain that her urine has changed to a funny color.
Name two possible causes, and explain how each would affect the color of
the urine.
17. Mr. B was diagnosed with smear-positive pulmonary TB in January. He was
treated with isoniazid, rifampin, and pyrazinamide by his private physician.
He visited his physician again in March. His drug susceptibility test results
were not available at the time of this appointment. Nevertheless, the
physician discontinued his prescription of pyrazinamide and gave him
refills of isoniazid and rifampin. Mr. B visited his physician again in April.
He had a persistent cough, and his sputum smear was found to be positive.
What should be done next?
18. Name four ways by which clinicians can assess whether a patient is
adhering to treatment.
19. What is the best way to ensure that a patient adheres to treatment?
20. Explain the implementation of Directly Observed Treatment Short-course
(DOTS) strategy in Indonesia.
21. How can clinicians determine whether a patient is responding to
22. Under what circumstances should patients be reevaluated?


(For Student)

dr. Triwahju Astuti, MKes,SpP
dr. Iin Noor Chozin, SpP




The guidelines define asthma as a chronic inflammatory disease of the airways in

which many cells play a role. In particular, mast cells, eosinophils, and T-lymphocytes.
In susceptible individuals this inflammation causes recurrent episodes of wheezing,
breathlessness, chest tightness, and cough, particularly at night and/or in the early
morning. These symptoms are usually associated with widespread but variable airflow
limitation that is at least partially reversible either spontaneously or with treatment. This
inflammation also causes an associated increase in airway hyperresponsivness to a
variety of stimuli.
The typical triad of symptoms of asthma is wheezing, shortness of breath, and
cough with or without sputum production. These symptoms are not specific for asthma
and can be seen in other acute and chronic airway diseass. For example, an acute viral
tracheobronchitis associated with or following typical URI symptoms can cause the
asthma triadof symptoms and can be associated with bronchial hyperresponsiveness
for upto 6 wks. Unlike asthma, these symptoms usually resolve completely over time.
There are both short and long term therapeutic objectives for every asthmatic
patient. Short term objectives are the control of immediate symptomps and response to
falling peak flow rate measurements. Long term objectives are those directed to disease
prevention, since there are now well proven strategies to avoid serious exacerbations of

acute bronchospasm which often lead to emergency room visits or hospitalization. In

order to meet these therapeutic objectives, four components of asthma care should be
First, optimal treatment of asthma depends on a

careful assessment of the

patients symptoms as well as objective monitoring by office spirometry and

home PEFR measurements.

Second, treatment of asthma with bronchodilator and anti-inflammatory
medication is tailored to the patients needs and relies on a staging system that is

based on the symptoms and objective measures of lung function.

Third, measures should be taken to avoid respiratory allergens and irritants that
can cause worsening of symptoms. This includes avoidance of outdoor allergens
such as ragweed, grass, pollens, and molds, and indoor allergens such as
animal dander, house-dust mites, and cockroach antigen. When exposure cannot
be avoided, allergen immunotherapy should be considered, although this
modality is somewhat controversial. Indoor irritants such as smoke from
cigarettes and wood-burning stoves, strong odors, and cleaning solutions are

particularly troublesome.
Fourth, patient education can be a powerful tool in asthma control. Family
members also can be helpful, especially with children and elderly adults. Active
participation by a patient in monitoring lung function, avoidance of provocative
agents, and decisions regarding medications provide asthma management skills
that give that patient the confidence to control their own disease.


This module is a part of the elaboration of the area of competence 4 of the
Indonesian Doctor Competencies in The Pulmonary and Respiratory Disease.

1. To understand the epidemiology of asthma and the contributions of


predisposition and environmental factors.

2. To learn the pathology and pathophysiology of asthma and impotance of
inflammatory mechanisms of this disease.
3. To appreciate the risk factors for asthma and the causes of exacerbation of
4. To be able to objectively and accurately diagnose this disease.
5. To learn the strategies of treating asthma based on the GINA Guidelines.
This module is part of Integrated Module Respiratory, designed for medical students
of 5th semester through Teaching-Learning Process in the 14th Bloc both in Lecture

Small Group Discussion. This part of Module will facilitate the student a

Pulmonary and Respiratory Disease in the Clinical Practice.

ACCP Pulmonary Board Review, (2003).Dundee Road. Northbrook Illinois.

Global initiative for Asthma, 2006, 2009

Mason, Robert J; Murray, John F; Broaddus, V. Courtney; Nadel, Jay A.

(2005). Textbook of Respiratory Medicine. Elsevier Saunders Philadelphia,


This Module should be used as Teaching-Learning Process Media prior to lecture
and or Class Discussion
1. Explain the epidemiology oh Asthma Bronchiale
2. Explain the pathophysiology of Asthma Bronchiale.
3. Give details about histhologic findings that occured in Asthma Bronchiale
4. There is neurogenic influences in physiologic mechanisms of respiratory
system. Give details about abnormality of neural control of the airway in
Asthma Bronchiale.
5. Explain the bronchial hyperresponsiveness in Asthma Bronchiale.
6. Explain about airflow limitation and list the cause of airflow limitation.
7. Explain about atopic Asthma.
8. Explain about Nonatopic Asthma.
9. Give details about risk factors for Asthma
10. Explain about clinical features of Asthma.
11. Explain about treatment oh Asthma.
12. Explain about guidelines of treatment protocols for asthma based on
severity of disease and asthma control level.
13. Explain the severity and treatment of asthma exacerbations


(For Student)

dr. Triwahju Astuti, MKes,SpP
dr. Iin Noor Chozin, SpP





Internationally accepted opinion defines COPD as a disease state
characterized by chronic airflow limitation due to chronic bronchitis and
emphysema. Chronic bronchitis has been defined in clinical terms: the presence
of chronic productive cough for at least three consecutive months in two
consecutive years. Other causes of chronic productive cough must been ruled
out. Emphysema, on the other hand, has been defined by its pathologic
description: an abnormal enlargement of the air spaces distal to the terminal
bronchioles accompanied by destruction of their walls and without obvious
fibrosis. Contrary to this traditional view, recent data have shown that this
destructive process is accompanied by a net increase in the amount of collagen
suggesting there is indeed active fibrosis associated with the breakdown of the
elastic frame-work of the lung.
Over the past decade three has been increasing interest in the
pathogenesis and management of COPD as it became recognized that the
disease was having a major worldwide impact. It has been calculated that COPD
ranks as the 12th largest disease burden in the world with projections that it will
rank number 5 by year 2020. In the United States at present, estimates from
national interviews taken by the National Center for Health Statistics show that
more than 16 million people are afflicted with COPD; about 14 million are thought
to have chronic bronchitis while 2 million have emphysema. It is likely that these
statistics underestimate the prevalence of COPD by as much as 50%, as many
patients underreport their symptoms and remain undiagnosed. In the National
Health and Nutrition Examination survey (NHANES) III, using surveys, physical
exams and pulmonary function testing, prevalence estimates using World Health
Organization definitions show that 23.6 million adults (13.9% of the adult
population) have COPD. The average number of days of restricted activities
reported by patients with COPD is very high, ranking this condition among the
highest chronic conditions for this measure of morbidity in the nation. In 1996,
COPD was listed as the 8th leading cause of disability-adjusted life years (DALYs)
in men and the 7th leading cause of hospitalizations in the United States. In 1998,
nearly 2% af all hospitalizations were attributed to COPD and 7% had COPD as
a contributing cause of hospitalization. More striking are COPD statistics

regarding the elderly. Nearly 20% af all hospitalizations in patients over the age
of 65% had COPD as a primary or contributing cause.
Perhaps even more striking and ominous are the magnitude and trend of
the mortality rates for COPD. Over the past few decades the mortality rates
associated with other common disease such as cardiovascular disease and
stroke were declining. During the same time period, the mortality rate for COPD
was rising at an alarming rate. For example, the U.S. death rate for COPD rose
almost 33% during the years 1979 to 1991, resulting in COPD becoming the 4 th
leading cause of death in this country. While the death rate for men has reached
a plateau in recent years, among it has continued to rise. In 1998, 54,615 men
and 51,377 women died from COPD. From 1995 to 1998 the death rate for
COPD increased 9% for U.S women.

This module is a part of the elaboration of the area of competence 4 of the
Indonesian Doctor Competencies in The Pulmonary and Respiratory Disease.


a. To review the current definition of COPD and describe how this definition
may be inadequate based on our current understanding of the disease.
b. To explore the impact of COPD including morbidity and mortality.
c. To review the risk factors for COPD.
d. To explore the natural history of COPD from its earlier asymptomatic stages
to the late stages associated with morbidity and mortality.
e. To explore the current understanding of the pathophysiology of COPD
trough an understanding of the pathologic changes that occur.
f. To review the current state of therapy for COPD including preventive
measures such as smoking cessation.


This module is part of Integrated Module Respiratory, designed for medical
students of 5th semester through Teaching-Learning Process in the 14th Bloc
both in Lecture and Small Group Discussion. This part of Module will facilitate
the student a Pulmonary and Respiratory Disease in the Clinical Practice.


ACCP Pulmonary Board Review, (2003).Dundee Road. Northbrook

Illinois. p.59 75
Global Initiative for Chronic Obstructive Lung Disease, 2006, 2011
Mason, Robert J; Murray, John F; Broaddus, V. Courtney; Nadel, Jay A.
(2005). Textbook of Respiratory Medicine. Elsevier Saunders Philadelphia,



This Module should be used as Teaching-Learning Process Media prior to lecture
and or Class Discussion


1. Explain about risk factor for Chronic Obstructive Pulmonary Disease
2. There is a Genetic influence in Risk Factors for COPD, please explain
3. Explain about pathology of Chronic Obstructive Pulmonary Disease .
4. Chronic Bronchitis is one of type COPD, give details about these
5. Emphysema is one of type COPD, give details about these pathology .
6. Explain about pathophysiology of Chronic Obstructive Pulmonary
7. Give details about Clinical Aspects of Chronic Obstructive Pulmonary
Disease. (Symptoms, Physical Exam and Laboratory Tests )
8. Give details about Management of Chronic Obstructive Pulmonary
9. Explain about Acute Exacerbation of Chronic Obstructive Pulmonary
10. Explain about Diagnostic and Therapeutic Approaches of COPD acute



(For Students)





A Comprehensive and Continuum Care for Tuberculosis
Tuberculosis is one of top ranking public health problem in the world. Indonesia is ranked
as having the third highest TB burden in the world, with 244 prevalent (active) TB cases
per 100 000 population, which, in 2008, equated to an estimated 565 614 people living
with TB. The prevalence of infection with the human immunodeficiency virus (HIV)
among the adult population nationally is estimated at 0.16%, and HIV infection is
characterized as a concentrated epidemic; however, in Indonesias Papua province, the
prevalence is 2.5%, which is considered a generalized epidemic. Twelve provinces have
been identified as priority areas for HIV interventions, and an estimated 193 000 people
are living with HIV in Indonesia. Among incident (new) TB cases, the estimated
prevalence of HIV is 3.0% nationally. Multidrug-resistant TB (MDR-TB) is estimated to
account for 2.2% of all TB cases nationally; this is lower than the estimated South Asian
regional average of 4.0%. Given the high burden of TB in Indonesia, the 2.2% represents
12 209 MDR-TB cases emerging every year.
The long term treatment duration, and the impact of incomplete treatment regiment along
with its spreading mechanism resulted in global burden of Tuberculosis. Specific
attention and program and worldwide collaboration has been developed since the first
identification of Tuberculosis infection. While a significance prevalence reduction has
been achieved in year 2009 by half halted the TBC cases, poor adherence, multiple drug
resistant, burdenof disease in vulnerable population, and TB-HIV infection problem
remain .
The STOP TB strategie was launched as an expansion of DOT strategy in companion
with ISTC. In responds to the global agreement of TB management, the Indonesian
government has launch National Strategy and Guide for Managing Tuberculosis. As a
part of health care provider physician an important and strong responsibility to manage
the Tuberculosis according to the national health system and standar for TB
This module was developed as an integrated part of other TB module in Respiratory
Block with the focus on appliying preventive medicine and community approcah and
responsibility. A thorough understanding of other TB module is needed to work with the
tasks in this module.
Learning Objective
1. Distinguish the different type and classification of Tuberculosis cases as a base for
further intervention program
2. Describe and explain the meaning of Tuberculosis program monitoring and evaluation
3. Identify the application of preventive medicine in managing Tuberculosis cases.

4. Identify the physician action and responsibility in managing Tuberculosis patient

based on DOTS ISTC
5. Assess the patient behaviour that might influence treatment adherence and propose a
strategy to overcome the problem
Reading Matterial

Stop TB Stratergy : DOT and ISTC

Strategi Nasional Pengendalian Tuberkulosis
Pedoman Nasional Penanggulangan Tuberkulosis
Improving Patient Adherence

Module Task 1: Identifying the patient diagnosis, type, and classification (TB Form)
Understanding the patient case type and classification is important for monitoring and
evaluating the TB program. The patient type and classification also serve as a guide for
determining patient treatment regimen. Patient confirming diagnosis is important to
determine the appropriate examination, treatment and referral decision. Every health
care provider need to understand the implementation of TBC diagnosis, examination and
treatment guideline and reporting mechanism.
For the following cases, identify the type and classification of each case for completing
TB form

Mr Mamad is suffering from productive cough since a few months, with shorthnes of
breath, chest paint and loss body weight up to 3 kg. The sputum examination a week

ago show Neg/Neg/Neg.

2. Mr Wawan , 39 years old, with productive cough for their rest two months. A month
ago he was suffering from high fever and was diagnose as typhoid fever. At the recent
visit, he was asked to take sputum examination in three consecutive time, and all the
result show positive finding. From the anamnesis it was identified that Mr Wawan
never have TB treatment regimen.
3. Mr Rifki, 65 years old is a TB patient under OAT first category and adhere to reguler
visit in outpatient department. A month before complete regimen, the laboratorium
examination show BTA (+).
4. Mr Hari, 50 years old, complaining of feeling weakness, reducing appetite, chest pain
in upper right, pain increase while cough (bloody). At the hospital, Mr Hari was
performing three time sputum examination (SPS) with all positive result. According to

Mr Hari, he has been cured from TB a year ago.

Cici six years old child, daughter of Mr and MRs Khalid. She is suffering with fever,
cough for more than 3 weeks, reducing appetite wih unclear cause for more than 2
weeks. She already take paracetamol, but no definitive outcome. Cici grand mother,
who live at the same home was die three month ago due to TB. Cici was further refer
to the Pediatric Clinic at Provincial hospital. From the examination the doctor found
multiple lymphonodi enlargement (size >1cm) at axilla

and neck. Cici was also

suffering from severe malnutrition (BW/Age <60%), BW=15 kg, with positive TB scar.
She never get TB treatment.
Module Task 2: Measuring the indicator for TB program and describe its meaning

For the following indicator, explain: a) the meaning and objective of the indicator, b)what
are the data needed and from which TB form the data should be available, c)what is the
target performance in each indicator

Case detection rate

Case notification rate
Conversion rate
Cure rate
Error rate

Module Task 3: The Doctor responsibility in managing Tuberculosis (Understanding DOT)

A component of case management that helps to ensure that patients adhere to treatment
is directly observed therapy (DOT). DOT is the most effective strategy for making sure
patients take their medicines. DOT means that a health care worker


physician) or other designated individual (kader kesehatan or voluntary health care

worker) watches the patient swallow every dose of the prescribed drugs (PMO=
pengawas minum obat). DOT should be considered for all patients because it is difficult
to reliably predict which patients will be adherent. Even patients who intend to take their
medicine might have trouble remembering to take their pills every time. All DOT activities
in each visits should be documented.

Reading Questions:

Who should be considered for DOT?

List and explain four tasks that are part of the DOT encounter.
Name at least five places where DOT can be given.
What are four advantages of DOT?
What are the public health responsibilities as a physician in managing TBC
according to ISTC

Case study 1
You are assigned to deliver DOT to Mrs. Wignjo, a 76-year-old woman who lives alone in
the house. She and her husband bought the house many years ago. Mrs. Wignjo was
recently discharged from a hospital. Upon discharge from the hospital, she received
education about TB and about the need to take medications until she completes the
treatment. She was told that she would be started on DOT and a health care worker
would visit her at her home to help her take her medication. Mrs. Wignjo is elated to have
some company. She happily offers you cookies and wants to talk awhile before she
takes her medication.
1. What are the tasks that should be completed when you deliver DOT to Mrs. Wignjo?
Case study 2
Bram is a 27-year-old single unemployed male. He has been in and out of rehabilitation
clinics for crack use. He picks up odd jobs in the warehouses and diners on the
waterfront. He lives in a single room boarding house. Four weeks ago he was brought by
the police to the emergency room of General Hospital for treatment of stab wounds to the
right arm resulting from a drug deal gone bad. Upon admission he was intoxicated,
appeared poorly nourished and underweight, and had a productive cough. His smears
were positive for AFB and he was started on appropriate therapy. He remained in the
hospital for 5 days. Against medical advice, Bram then insisted on leaving the hospital.
On the day of discharge, the responsible nurse telephoned a report to the district heath
office, and instructed Bram to go to the nearest primary health care (Puskesmas) the
next morning for evaluation and a supply of medicine. He failed to keep his appointment.
The next week a health cadre (kader kesehatan) was assigned to locate Bram and
persuade him to come to the Puskesmas. The cadre found him lying on a park bench
near the hotel where he lives. The health care worker convinced Bram to go to the clinic
for follow-up tests. At the clinic, Bram reluctantly agrees to take his medication, although
he does not want DOT. He says he is not a baby and can take the medication on his

1. What is the prevention level applied in this case? Describe the prevention strategy
plan applied in this case (who are the target group, objectives, how?)
2. How would the health cadre help Bram adhere to his treatment regimen?
3. What can the health cadre say about DOT to convince Bram of its importance
Module Task 4: Managing patient adherence to TB treatment plan
Patient adherence is the core problem in assuring complete and continuum of
tuberculosis care. Incomplete core or treatment drop out is the main causes for multiple
drug resistant, relaps and un-detected new case development. Every health provider

need to assess the patient behavior or adherence barrier and plan the intervention to
overcome the barrier.
1. If a health care worker conducts a behavioral diagnosis, what methods can the health
care worker use to help a patient whose adherence problem is:
a. Forgetfulness?
b. Lack of motivation?
c. A complex regimen?
d. Poor relationship with the health care worker?
2. Describe how cultural, religious, or other personal beliefs can affect the treatment for
3. Name eight specific things the health care worker can do to form an effective
partnership with his or her patient.
4. Who can provide support to a patient and help the patient remember to take
5. What are two things the health care worker can do to tailor the regimen to the
patients lifestyle?
6. What is a formal adherence agreement?
7. What three methods can be used to help patients keep their appointments?
Case Study 3
Mr. Sugeng is a recent transmigran from Pacitan who is working on two different jobs to
support his wife and three children. He has been on DOT for 2 months and his TB
symptoms have greatly improved. Mr. Sugeng has kept daily DOT appointments with the
health care worker, but recently has missed two appointments and skipped his last clinic
1. Why Mr. Sugeng become nonadherent?
2. What steps can the health care worker take to help Mr. Sugeng keep his
appointments and adhere to therapy?
Case study 4
Ms. Johan is a 68-year-old widow with active TB disease. She has several other health
problems, including obesity, osteoarthritis, and poorly controlled diabetes. She needs a
cane to help her walk and often becomes anxious when she leaves her apartment
(rumah susun). She lives in a low-income housing block 3 miles from the TB clinic and
does not have transportation. Ms. Johnsons two children live outside the city and visit
1. Conduct a behavioral diagnosis of Ms. Johnsons potential barriers to completing her
TB treatment and the methods that can be used to overcome the barriers.





The respiratory history
Presenting symptoms
Cough is a common presenting respiratory symptom. It occurs when deep inspiration is followed by
explosive expiration. Flow rates of air in the trachea approach the speed of sound during a forceful cough.
Coughing enables the airways to be cleared of secretions and foreign bodies. The duration of a cough is
important. A cough of recent origin, particulary if associated with fever and other symptoms of respiratory
tract infection, may be due to acute bronchitis or pneumonia. A chronic cough associated with wheezing
may be due to asthma; sometimes asthma can present with just cough alone. An irritating chronic dry
cough can result from oesophageal reflux and acid irritation of the lungs. A similar cough is not
uncommonly associated with the use of the angiotensin-converting enzyme (ACE) inhibitors. These are
drugs used in the treatment of hypertension and cardiac failure. A chronic cough which is productive of
large volumes of purulent sputum may indicate the development of a new and serious underlying problem
(e.g infection or lung cancer).
The patients description of his or her cough may be helpful. A cough associated with inflammation of the
epiglotis may have a barking quality. Cough caused by tracheal compression by a tumour may be loud and
brassy. Cough associated with recurrent laryngeal nerve palsy has a hollow sound because the vocal cords
unable to close completely; this has been described as a bovine cough. A cough that is worse at night is
suggestive of asthma of heart failure, while coughing that comes on immediately after eating or drinking
may be due to a tracheo-oesophageal fistula or oesophageal reflux.
It is an important though, perhaps, a somewhat unpleasant task to inquire about the type of sputum
produced. Be warned that some patients have more interest in their sputum than others and may go into
more detail than you really want. A large volume of purulent (yellow or green) sputum suggests the
diagnosis or bronchiectasis or lobar pneumonia. Foul-smelling dark-coloured sputum may indicate the
presence of a lung abscess with anaerobic organisms. Pink frothy secretions from the trachea, which
occur in pulmonary oedema, should not be confused with sputum. Haemoptysis (coughing up of blood) can
be a sinister sign of lung disease and must always be investigated. It is best to rely on the patients

assessment of the taste of the sputum which is, not unexpectedly, foul in conditions like bronchiectasis or
lung abscess.
The awareness that an abnormal amount of work is required for breathing is called dyspnoea. It can be due
to respiratory or cardiac disease. Careful question-ing about the timing of onset, severity and pattern of
dysponea is helpful in making the diagnosis. The patient may be aware of this only on heavy exertions or
have much more limited exercise tolerance. Dyspnoea can be graded from I to IV based on the New York
Heart Association classification:

Class I disease present but no dyspnoea or dyspnoea only on heavy exertion

Class II - dyspnoea on moderate exertion
Class III dyspnoea on minimal exertion
Class IV dyspnoea at rest

It is more useful, however, to determine the amount of exertion that actually causes dyspnoea, i.e. the
distance walked, or the number of steps climbed. The association of dyspnoea with wheeze suggests
airways disease, which may be due to asthma or chronic airflow limitation. The duration and variability of
the dyspnoea are important. Dyspnoea that worsens progressively over a period of weeks, months or years
may be due to pulmonary fibrosis. Dyspnoea of more rapid onset may be due to an acute respiratory
infection (including bronchopneumonia or lobar pneumonia) or to pneumonitis (which may be infective or
secondary to a hypersensitivity reaction). Dyspnoea that varies from day to day or even from hour to hour
suggests a diagnosis of asthma. Dyspnoea of very rapid onset associated with sharp chest pain suggest a
pneumothorax. Dyspnoea, described by the patient as inability to take a breath big enough to fill the lungs
and associated with sighing, suggests anxiety. Dyspnoea on moderate exertion may be due to the
combination of obesity and a lack of physical fitness (a not uncommon combination)


A number of conditions can cause continuous whistling noise during breathing. These include asthma or
chronic airflow limitation, and airways obstruction by a foreign body or tumour. Wheeze is usually maximal
during expiration and is accompanied by prolonged expiration.
Chest pain due to respiratory disease is usually different from that associated with myocardial ischaemia.
The pleura and central airways have pain fibres and may be the source of respiratory pain. Pleural pain is
characteristically pleuritic in nature, i.e. sharp and made worse by deep inspiration and coughing. It is
typically localized to one area of the chest. It may be of sudden onset in patients with lobar pneumonia,
pulmonary infraction or pneumothorax and is often associated with dyspnoea.
Patients may occasionally with episodes of fever at night. Tuberculosis, pneumonia and mesothelioma
ahould always be considered in these cases. Occasionally patients with tuberculosis present with episodes
of drenching sweating at night. Hoarseness may sometimes be considered a respiratory system symptom.
It can be due to transient inflammation of the vocal cords (laryngitis), vocal cord tumour or recurrent
laryngeal nerve palsy
Sleep apnoea is an abnormal increase in the periodic cessation of breathing during sleep. Patients
with obsructive sleep abnoea (where airflow stops during sleep for periods of at least 10 seconds and
sometimes for over 2 minutes, despite persistent respiratory efforts) typically present with daytime
somnolence, chronic fatigue, morning headaches and personality disturbances. Very loud snoring may be
reported by anyone within earshot. These patients are often obese and hypertensive. Patients with
centralsleepapnoea (where there is cessation of inspiratory muscle activity) may also present with
somnolence but do not snore excessively.
Some patients respond to anxiety by increasing the rate and depth of their breathing. This is called
hyperventilation. The result is an increase in CO 2 excretion and the development of alkalosis - a rise in the
pH of the blood. These patients may complain of variable dyspnoea; they have more difficulty breathing in
than out. The alkalosis results in paraesthesiae of the fingers and around the mouth, lightheadedness,
chest pain and a feeling of impending collapse.

It is important to find out what drugs the patient is using, how often they are taken and whether they are
inhaled or swallowed. The patients previous and current medications may give a clue to the current
diagnosis. Bronchodilators and inhaled steroids are prescribed for chronic airflow limitation, asthma and
bronchiectasis. Chronic respiratory disease including sarcoidosis, hypersensitivity pneumonias and asthma
may have been treated with oral steroids. Oral steroid use may predispose to tuberculosis. Patients with
chronic lung conditions like cystic fibrosis or bronchiectasis will often be very knowledgeable about their
treatment and can describe the various forms of physiotherapy that are essential for keeping their airways
Almost every class of drug can produce lung toxicity. Examples include pulmonary embolism from
use of the oral contraceptive pill, interstitial lung disease from cytotoxic agents (e.g. methotrexate,
cyclophosphamide, bleomycin), bronchospasm from beta-blockers or non-steroidal anti-inflammatory drugs
and cough from ACE inhibitors. Some medications known to cause lung disease may not be mentioned by
the patient because they are illegal (e.g.cocaine), are used sporadically (e.g. taken orally (e.g timolol eye
drops). The clinician therefore needs to ask about these types of drug specifically.
Past history
One should always ask about previous respiratory illness including pneumonia, tuberculosis or chronic
bronchitis , or abnormalities of the chest X-ray which have been previously reported to the patient. Patients
with the acquired immunodeficiency syndrome (AIDS) have a high risk of developing Pneumocystis carinii
pneumonia and indeed other chest infections including tuberculosis. The commonest pathogens in these
patients are still S.pneumoniae and H. Influenzae.
Occupational history
In no system are the patients present and previous occupations of more importance. A detailed
occupational history is essential. One must ask about exposure to dusts in mining industries and factories
(e.g. asbestos, coal, silica, iron oxide, tin oxide, cotton, beryllium, titanium oxide, silver, nitrogen, dioxide,
anhydrides). Working or household exposure to animals, including birds, is also relevant (e.g. Q fever or

psittacosis). Exposure to mouldy hay, humidifiers or air conditioners may also result in lung disease (e.g.
allergic alveolitis). The patient may be unaware that his or her occupation involved exposure to dangerous
substances; for example, factories making insulating cables and boards very often used asbestos until 20
years ago. Asbestos exposure can result in the development of asbestosis, mesothelioma or carcinoma of
the lung up to 30 years later. Relatives of people working with asbestos may be exposed when handing
work clothes.
It is most important to find out the patient actually does when at work, the duration of any exposure,
use of protective devices and whether other workers have become ill. An improvement in symptoms over
the weekend is a valuable clue to the presence of occupational lung disease, particularly occupational
asthma. This can occur as a result of exposure to spray paints or plastic or soldering fumes.
Social history
A smoking history should be routine, as it is the major cause of chronic airflow limitation and lung cancer. It
is also increases the risk of spontaneous pneumothorax and of Goodpastures syndrome. It is necessary to
ask how many packers of cigarettes a day a patient has smoked and how many years the patients has
smoked. An estimate should be made of the number of packet years of smoking. Remember that this is
based on 20-cigarette packets and that packets of cigarettes are getting larger; curiously, most
manufacturers now make packets of 30 or 35. More recenthly, giant packets of 50 have appeared. These
are too large to fit into pockets and must be carried in the hands as a constant reminder to the patient of his
or her addiction. Occupation may further affect cigarette smokers; for example, asbestos workers who
smoke are at an especially high risk of lung cancer. Passive smoking is now regarded as a significant risk,
and exposure to other peoples cigarette smoke at home and at work should be asked about.
Many respiratory conditions are chronic and may interfere with the ability to work. Housing
conditions may be inappropriate for a person with a limited exercise tolerance or an infectious disease. An
inquiry about the patients alcohol consumption is important. The drinking of large amounts of alcohol in
binges can sometimes result in aspiration pneumonia, and alcoholics are more likely to develop
pneumococcal or Klebsiellapneumonia. Such information may influence the decision about whether to
advise treatment at home or in hospital.

Family history
A family history of asthma, cystic fibrosis or emphysema should be sought. Alpha 1 antitrypsin deficiency,
for example, is an inherited disease, and carries are extremely susceptible to the development of
emphysema. A Family history or infection with tuberculosis is also important.
The Trachea
The position of the trachea is most important, and time should be spent establishing it accurately. Form in
front of the patient the forefinger of the right hands is pushed up and backwards from the suprasternal
notch until the trachea is felt. If the trachea is displaced to one side its edge rather than is middle will be felt
and a larger space will be present on one side than the other. Slight displacement to the right is fairly
common in normal people. This examination is uncomfortable for the patient, so one must be gentle.
Significant displacement of the trachea suggests, but is not specific for, disease of the upper lobes
of the lung.
Tracheal tug is demonstrated when the finger resting on the trachea feels it move inferiorly with
each inspiration. This is a sign of gross overexpansion of the chest because of airflow obstruction.
If the patient appears dyspnoeic and use of the accessory muscles of respiration is suspected, the
examiners fingers should be placed in the supraclavicular fossae. When the scalene muscles are recruited
they can be felt to contract under the fingers. Even more severe dyspnoea will result in use of the
sternomastoid muscles. Their contraction is also easily felt with inspiration. Use of these muscles for long
periods is exhausting and a sign if impending respiratory failure.
The Chest
The chest should be examined anteriorly and posteriorly by inspection, palpation, percussion and
auscultation.Compare the right and left sides during each part of the examination.
Shape and symmetry of the chest. When the anteroposterior (AP) diameter is increased compared with the
lateral diameter. The chest is described as barrel-shaped. An increase in the AP diameter indicates

hyperinflation and is seen often in patients with severe asthma or emphysema. It is not always a reliable
guide to the severity of the underlying lung disease.
A pigeon chest (pectus carinatum) is a localisedprominence(an outward bowing of the sternum
and costal cartilages). It may be a manifestation of chronic childhood respiratory illness, in which case it is
thought to result from repeated strong contractions of the diaphragm while the thorax is still pliable. It also
occurs in rickets.
A funnel chest (pectus excavatum)is adevelopmental defect involving is usually an aesthetic one
but in severe cases lung capacity may be restricted.
Harrisons* sulcus is a linear depression of the lower ribs just above the costal margins at the site
of attachment of the diaphragm. It can result from severe asthma in childhood, or rickets.
Kyphosis refers to an exaggerated forward curvature of the spine, while scoliosis is lateral bowing.
Kyphoscoliosis may be idiopathic (80%), secondary to poliomyelitis, or associated with Marfans
syndrome. Severe thoracic kyphoscoliosis may reduce the lung capacity and increase the work of
Lesions of the chest wall may be obvious. Look for scars from previous thoracic operation, or
from chest drains for a previous pneumothorax or pleural effusion. Thoracoplasty causes severe chest
deformity: this operation was performed for tuberculosis and involved removal of a large number of ribs on
one side of the chest to achieve permanent collapse of the affected lung. It is no longer performed because
of the availability of effective antituberculosis chemotherapy. Radiotherapy may cause erythema and
thickening of the skin over the irradiated area. There is sharp demarcation between abnormal and normal
skin. There may small tattoo marks indicating the limits of the irradiated area. Signs of radiotherapy usually
indicate that the patient has been treated for carcinoma of the lung, breast or, less often, for lymphoma.
Subcutaneous emphysema is a crackling sensation felt on palpating the skin of the chest or neck.
On inspection, there is often diffuse swelling of the chest wall and neck. It is caused by air tracking from the
lungs and is usually due to a pneumothorax; less commonly it can follow rupture of the oesophagus or a
pneumomediastinum (air in the mediastinal space).
Prominent veins may be seen in patients with superior vena caval obstruction. It is important to
determine the direction of blood flow .

Movement of the chest wall should be noted. Look for asymmetry of chest wall movement
anteriorly and posteriorly. Assesment of expansion of the upper lobes is best achieved by inspection from
behind the patients, looking down at the clavicles during moderate respiration. Diminished movement
indicates underlying lung disease. The affected side will show delayed or decreased movement. For
assessment of lower lobe expansion, the chest should be inspected posteriorly.
Reduced chest wall movement on one side may be due to localized pulmonary fibrosis,
consolidation, collapse, pleural effusion or pneumothorax. Bilateral reduction of chest wall movement
indicates a diffuse abnormality such as chronic airflow limitation or diffuse pulmonary fibrosis.
Look for paradoxical inward motion of the abdomen during inspiration when the patient is supine
(indicating diaphragmatic paralysis).
Chest expansion. Place the hands firmly on the chest wall with the fingers extending around the sides of
the chest. The thumbs should almost meet in the middle line and should be lifted slightly off the chest so
that they are free to move with respiration. As the patient takes a big breath in, the thumbs should move
symmetrically apart at least 5cm. Reduced expansion on one side indicates a lesion on that side. The
causes have been discussed above.
Lower lobe expansion is assessed from the back in this way. Some idea of upper and middle lobe
expansion is possible when the manoeuvre is repeated on the front of the chest, but this is better gauged
by inspection.
Apex beat, When the patient is lying down, establishing the position of the apex beat may be
helpful, as displacement towards the side of the lesion can be caused by collapse of the lower lobe or by
localized pulmonary fibrosis. Movement of the apex beat away from the side of the lung lesion can be
caused by pleural effusion or tension pneumothorax. The apex beat is often impalpable in a chest which is
hyperexpanded secondary to chronic airflow limitation.
Vocal fremitus.. Palpate the chest wall with the palm of the hand while the patient repeats ninety-nine. The
front and back of the chest are each palpated in two comparable positions with the palm of one hand on
each side of the chest. In this way differences in vibration on the chest wall can be detected. This can be a

difficult sign to interpret. It depends on the recognition of changes in vibration conducted to the examiners
hands while the patient speaks. Practice is needed to appreciate the difference between normal and
abnormal but comparing one side with the other is often helpful. The causes of change in vocal fremitus are
the same as those for vocal resonance.
Ribs. Gently compress the chest wall anteroposteriorly and laterally. Localized pain suggest a rib facture,
which may be secondary to trauma, or may be spontaneous as a result of tumour deposition, bone disease
or sometimes the result of severe and prolonged coughing.
With the left hand on the chest wall and the fingers slightly separated and aligned with the ribs, the middle
finger is pressed firmly against the chest. Then the pad of the right middle finger is used to strike firmly the
middle phalanx of the middle finger of the left hand. The percussing finger is quickly removed so that the
note generated is not dampened. The percussing finger must be held partly flexed and a loose swinging
movement should come from the wrist and not from the forearm. Medical students will soon learn to keep
the right middle fingernail short. Percussion of symmetrical areas of the anterior, posterior and axilarry
regions is necessary. Percussion in the supraclavicular fossa over the apex of the lung should not be
forgotten. Percuss the clavicle directly with the percussing finger. On percussion posteriorly the scapulae
should be moved out of the way by asking the patient to move the elbows forward across the front of the
chest; this rotates the scapulae anteriorly.
The feel of the percussion note is as important as its sound. The note is affected by the thickness
of the chest wall, as well as by underlying structures. Percussion over a solid structure, such as the liver or
a consolidated area of lung, produces a dull note. Percussion over a fluid-filled area, such as a plaural
effusion, produces an extremely dull (stony dull) note. Percussion over the normal lung produces a
resonant note and percussion over hollow structures, such as the bowel a pneumothorax, produces a
hyperresonant note.
Considerable practice is required before expert percussion can be performed, particularly in front of
an audience. The ability to percuss well is usually obvious in clinical examination and counts in a students
favour, as it indicates a reasonable amount of experience in the wards.

Liver dullness. The upper level of liver dullness is determined by percussing down the anterior chest in the
mid-clavicular line. Normally, the upper level of the liver dullness is the fifth rib in the right mid-clavicular
line. If the chest is resonant below this level it is a sign of hyperinflation, usually due to emphysema or
Breath sounds. Using the diaghragm of the stethoscope one should listen to the breath sound in the some
areas.It is important to compare each side with the other. Remember to listen high up into the axillae and,
using the bell of the stethoscope applied above the clavicles, to listen to the lung apices.
A number of observations must be made while auscultating and, as with auscultation of the heart different
parts of the cycle must be considered. Listen for the quality of the breath sounds; the intensity of the breath
sounds; and the presence of additional (adventitiour) sounds.
Quality of breath sounds: normal breath sound are heard with the stethoscope over all parts of
the chest. The patients should be asked to breathe through the mouth so that added sounds from the
nasopharynx do not interfere. These sounds are produced in the airways rather than the alveoli. They had
once been thought to arise in the alveoli (vesicles) of the lungs and are therefore called vesicular sounds.
They have rather fancifully been a compared to the sound of wind rustling in leaves. Their intensity is
related to total airflow at the mouth and to regional airflow. Normal (vesicular) breath sounds are louder and
longer on inspiration than on expiration and there is no gap between the inspiratory and expiratory sounds.
They are due to the transmission of air turbulence in the large airways filtered through the normal lung to
the chest wall.
Bronchial breath sounds here turbulence in the large airways is heard without being filtered by the
alveoli, producing a different quality. Bronchial breath sounds have a hollow, blowing quality. They are
audible throughout expiration and there is often a gap between inspiration and expiration. The expiratory
sound has a higher intensity and pitch than the inspiratory sound. Bronchial breath sounds are more easily
remembered than described. They are heard over areas of consolidation, as solid lung conducts the sound
of turbulence in main shown in .

Occasionally breath sounds over a large cavity have an exaggerated bronchial quality. They very
hollow or amphoric sound has been likened to that heard when air passes over the top of a hollow jar
(Greek amphoreus).
Intensity of the breath sounds : it is better to describe breath sounds as being of normal or
reduced intensity than to speak about air entry. The entry of air into paints of the lung cannot be directly
gauged from the breath sounds.
Causes of reduced breath sounds include chronic airflow limitation (especially emphysema),
pleural effusion, pneumothorax, pneumonia, a lrge neoplasm, and pulmonary collapse.
Added (adventitious) sounds: there are two types of added sounds: continous (wheezes) and
interrupted (crackles)
Continous sounds are called wheezes. They are abnormal findings and have a musical quality. The
wheezes must be timed in relation to the repiratory cycle. They may be heard in expiration or inspiration or
both.Wheezes are due to continousoscilation of opposing airway walls and imply significant airway
narrowing. Wheezes tend to be louder on expiration. This is because the airways normally dilate during
inspiration and are narrower during expiration. An inspiratory wheeze implies severe airway narrowing.
The pitch (frequency) of wheezes varies. It is determined only by the velocity of the air jet and is
not related to the length of the airway. High pitched wheezes are produced in the smaller bronchial and
have a whistling quality, whereas low pitched wheezes arise from the larger bronchi.
Wheezes are usualy the result of acute or chronic airflow obstruction due to asthma (often high
pitched) or chronic airflow limitation (often low pitched). Here a combination of bronchial muscle spasm,
mucosal oedema and excessive secretions results in airflow limitation. Wheezes are a poor guide to the
severity of airflow obstruction. In severe airways obstruction wheeze can be absent because ventilation is
so reduced that the velocity of the air jet is reduced below a critical level necessary to produce the sound.
A fixed bronchial obstruction, usually due to carcinoma of the lung, tends to cause a localized
wheeze, which has a single musical note (monophonic) and does not clear with coughing.
Interrupted non-musical sounds are best called crackles. There is a lot of confusion about the
naming of these sounds, perhaps as a result of mistranslation of lannec. Some authors describe low
pitched crackles as rales and high pitched ones as crepitations, but others do not make this distinction. The
simplest approach is to call all these sounds crackles, but also to describe their timing and pitch.

Crackles are probably the result of loss of stability of peripheral airways which collapse on
expiration. With high inspiratory pressures, there is rapid air entry into the distal airways. This causes the
abrupt opening of alveoli and of small-or medium-sized bronchi containing secretions in regions of the lung
deflated to residual volume. More compliant (distensible) areas open up first followed by the increasingly
stiff areas. Fine and medium pitched crackles are not caused by air moving through secretions as was once
thought but by the opening and closing of small airways.
Late or pan-inspiratory crackles suggest disease confined to the alveoli. They may be fine, medium
or coarse in quality. Fine crackles have been likened to the sound of hair rubbed between the fingers or to
the sound Velero makes when being unstrapped they are typically caused by pulmonary fibrosis. As fibrosis
becomes more severe the crackles extend earlier into inspiration and are heard further up the chest.
Medium crackles are usually due to left ventricular failure. Here the presence of alveolar fluid disrupts the
function of the normally secreted surfactant. Course crackles are characteristic of pools of retained
secretion and have an unpleasant gurgling quality. They tend to change with coughing, Which also has an
unpleasant gurgling quality. Bronchiectasis is a common cause, but any disease that leads to retention of
secretions may produce these features.
Pleural friction rub: when thickened, roughened pleural surfaces rub together as the lungs expand
and contract, and a continous or intermitten grating sound may be audible.
A pleural rub indicates pleurisy, which may be secondary to pulmonary infarction or pneumonia.
Rately, malignant involvement of the pleura, a spontaneous pneumothorax or pleurodynia may cause a rub.
Vocal resonance. Auscultation over the chest while a patient speaks gives further information
about the lungs ability to transmit sounds. Over normal lung the low pitched components of speech are
heard with a booming quality and high pitched components are attenuated. Consolidation lung, however,
tends to transmit high frequencies so that specch heard throught the stethoscope takes on bleathing quality
(called aegophony Greek alx goat, phone voice). When a patient with aegophony says e as in been it
sounds like a as in bay.
Ask the patient to say ninety-nine while you listen over each part of the chest. Over consolidated
lung the numbers will become clearly audible, while over normal lung the sound is muffled. If vocal
resonance is present, bronchial breathing is likely to be heard. Sometimes vocal resonance is increased to
such an extent that whispered speech is distinctly heard: this is called whispering pectoriloquy.

If a very localized abnormality is found at auscultation, try to determine the lobe and approximately
which segment or segments are involved.

History Taking (Respirasi)









Jenis kegiatan
Menyapa pasien dan mempersilahkannya duduk dengan pengaturan yang
Memperkenalkan diri kepada pasien
Menanyakan kembali identitas pasien: nama, usia, tempat tinggal, pekerjaan,
status keluarga
Menjelaskan tujuan wawancara
Menanyakan keluhan utama pasien
Menggali keluhan riwayat penyakit saat ini (History of present illness) : cough,
sputum production ( amount, colour, frequency, hemoptysis), chest pain,
wheezing / stridor, dyspnea, hoarseness.
Mengidentifikasi keluhan secara lengkap dengan menanyakan tentang:
Onset ( saat )
Location ( tempat )
Duration ( lama berlangsung
Character ( sifat )
Mengidentifikasi permasalahan kesehatan masa lalu (Past History)
Permasalahan medis kronis, Penyakit sewaktu masa kecil
infeksi paru
Riwayat ginekologis
Pernah mondok di RS Pemeriksaan kesehatan rutin
(prolonged hospital stay)
Riwayat pembedahan
Riwayat trauma
Mengidentifikasi pemakaian obat-obatan
Nama obat
Efek samping
Apakah memakai resep dokter?
Rute pemberian
Mengidentifikasi penyakit yang diderita oleh keluarga pasien ( asthma, kanker,
penyakit di usia muda, tuberkulosis paru)
Mengidentifikasi kehidupan pribadi dan sosial pasien:
Status pernikahan
Kebiasaan merokok, jumlah
batang per hari, lama kebiasaan
Pekerjaan (debu, asbestos,
Binatang peliharaan

Faktor resiko HIV-AIDS ( IDU,

tatto, free sex)
Menanyakan beberapa keluhan sistematik yang mungkin dirasakan pasien:


Sistem saraf pusat: pusing, Sistem genito-urinari: sulit

visus, vertigo, tinitus, ...
miksi, hematuri, nyeri sewaktu
menstruasi, disfungsi ereksi.
Kardiovaskular-respirasi: sesak

Sistem lokomotor: nyeri dan

nafas, pembengkakan tungkai,
palpitasi, nyeri dada,..
kaku sendi, ...
Sistem pencernakan: nafsu
penurunan berat badan, nyeri
13. Merangkum hasil wawancara
14. Memberi kesempatan kepada pasien untuk mengungkapkan apa yang belum jelas
15. Menutup pertemuan
Jumlah nilai

= tidak dikerjakan

= dikerjakan tetapi kurang sesuai/benar

= dikerjakan dengan benar

Jumlah nilai

Nilai akhir = -------------------------- x 100 =

Catatan: Mahasiswa/peserta dinyatakan LULUS apabila nilai akhir mencapai 80

Latar Belakang

Pemeriksaan fisik merupakan salah satu bagian yang sangat penting dalam menegakkan
diagnosis. Diperkirakan > 70% diagnosis dapat ditegakkan dari anamnesis yang baik.
Dengan anamnesis yang baik ditambah dengan pemeriksaan fisik yang baik pula, maka
akan dapat ditegakkan diagnosis yang lebih akurat lagi.
Seorang dokter seharusnya sudah mempunyai data pendahuluan dari pasien sebelum
melakukan pemeriksaan fisik melalui anamnesa yang telah dilakukan sebelumnya,
melihat data cataan medik yang sudah ada sebelumnya. Selama pemeriksaan
hendaknya dokter pemeriksa berkomunikasi dengan pasien agar merasa lebih nyaman

Tujuan Pembelajaran

sehingga diperoleh hasil pemeriksaan yang tepat dan efisien.

Setelah selesai mengikuti pelatihan, peserta mampu melakukan :
1. Inspeksi dada saat istirahat (statis)
2. Inspeksi saat respirasi (dinamis)
3. Palpasi ekspansi pernafasan
4. Palpasi tactile fremitus
5. Palpasi apex jantung
6. Perkusi paru

Metoda Pembelajaran

7. Auskultasi paru
- Kuliah singkat
- Video session
- Demonstrasi dengan model anatomik

Alat Bantu

- Berlatih mandiri dengan sesama teman

- Model anatomik (manekin) 2 buah lengkap alat pemeriksaan
- Stetoskop 5 buah

- Audio visual 1 set

Daftar Instruktur

- Kapas alkohol 10 sachet

4 X 50 menit
- dr. Yani Jane Sugiri SpP
- dr. Susanthy Dj, SpP
- dr. Putu P. Putra, SpP
- dr Triwahju Astuti, SpP
- dr. Suryanti Dwi Pratiwi, SpP


- dr. Iin Noor Chozin, SpP

Check list
1. Talley N J, OConnor S, 2003. Clinical Examination, A Systemic Guide To Physical
Diagnosis, 4th Edition. APAC Publishers Singapore
2. Berg D; Worzala K, 2006. Atlas of Adult Physical Diagnosis. Lippincott Williams &
3. Delp MH; Manning RT, 1981. Majors Physical Diagnosis An Introduction to the
Clinical Process. 9th Edition. WB. Saunders Company. Philadelphia.
4. Burnside JW, 1981. Physical Diagnosis 16 th Edition. William & Wilkins Baltimore /
5. Handono Kalim, 1996. Pedoman Diagnostik Fisik Ilmu Penyakit Dalam. Laboratorium
Ilmu Penyakit Dalam Fakultas Kedokteran Universitas Brawijaya Malang.





Have the patient undress to the waist, ideally sitting on the edge of the bed.


Wash your hands and cleanse your stethoscope with alcohol wipe.
(a) Chest wall deformities: Are there any chest wall deformities? (e.g. pectus
excavatum / pectus carinatum) Does the chest appear over expanded? (i.e. Barrel
shaped chest ) Is there any Kyphosis present? Scoliosis?

Pectus excavatus
(b) Scars: Is there any evidence of scars from previous surgery?
(c) Respiratory rate: Consider this opportunity to measure the patients respiratory
rate. Often when you tell a patient that you are measuring their respiratory rate they
often tend to breath slower or faster. Therefore respiratory rate is often measured
surreptitiously by observing the respiratory movements of the chest wall, while
placing you fingers over the patient's radial pulse and telling them that you are
Taking their pulse where as in fact you are measuring their respiratory rate! The
normal respiratory rate in an adult is 12 breaths per minute. A raised respiratory rate

is called tachypnoea
(a) Apex beat : Feel for the patients apex beat. The apex beat is often impalpable
in a chest which is hyper-expanded secondary to chronic airflow obstruction.
Movement of the apex beat from one side to the other may be caused by several
conditions including pleural effusion, tension pneumothorax

(b) Chest expansion : By assessing chest expansion the examiner aims to assess
the range and symmetry of chest wall movements. Place your hands firmly on the
chest wall, with your thumbs slightly lifted off the chest so that they are free to move
with respiration (placing your thumbs up provides the examiner with a visible marker
to assess the range and symmetry of chest wall movements). Ask the patient to take
a deep breath in and observer the range and symmetry of movement. Reduced
expansion on one side indicates a lesion on that side. This should be performed on
the front and the back of the patients chest.

Assessment of anterior and posterior chest wall expansion


(a) Place you hand on the patients chest wall with the fingers slightly separated and
aligned with the ribs and pressing the middle finger firmly again the chest.

(b) With the other hand (usually the middle finger) strike firmly the middle phalanx of
the middle finger that is on the patients chest wall.

(c) The percussing finger is removed quickly therefore not to dampen the
generated noise. The percussing finger should be held partly flexed and a loose
swinging motion should come form the wrist


(a) Breath sounds : Normal breath sounds are called vesicular. The intensity of the
sounds increase during inspiration and then fade away during the first third of
expiration. Bronchial breath sounds, heard in inspiration and expiration, result from
enhanced transmission of higher frequency sounds through solid lung tissue as in
consolidation or fibrosis.
(b) Intensity of the breath sounds :Usually described as being normal, reduced or
absent. It is important to compare air entry in all areas of the chest. For example
breath sounds may be absent locally over a pneumothorax or a pleural effusion.
(c) Added sounds : Wheeze, rhonchi, crepitations (crackles), pleural rub




0 1 2

1. Menempatkan pasien dlm posisi duduk ditepi tempat tidur pemeriksaan
2. Mengamati dan melaporkan abnormalitas yang ditemukan
3. Melihat adakah simetri/asimetri dan melaporkan abnormalitas yang ditemukan
4. Memeriksa ekspansi dada muka dan belakang dan melaporkan hasilnya
5. Memeriksa stem fremitus dan melaporkan hasilnya
6. Melakukan perkusi dada bagian depan pada tempat yang telah ditentukan dan
melaporkan hasilnya
Melakukan perkusi dada bagian belakang pada tempat yang telah ditentukan


dan melaporkan hasilnya

8. Memeriksa suara nafas dan melaporkan hasilnya
9. Memeriksa ada tidaknya perubahan intensitas suara nafas dan melaporkan

Memeriksa ada tidaknya suara nafas tambahan (ronchi, wheezing, dll) dan
melaporkan hasilnya



= tidak dikerjakan

= dikerjakan tetapi kurang sesuai/benar

= dikerjakan dengan benar

Jumlah nilai
Nilai akhir = -------------------------- x 100 =

Catatan: Mahasiswa/peserta dinyatakan LULUS apabila nilai akhir mencapai 80




Chest Physical Therapy

Lab. Ilmu Kedokteran Fisik dan Rehabilitasi
FK Unibraw Malang /RSU Dr. Saiful Anwar
Chest Physical Therapy :

Yaitu penggunaan metoda fisik untuk perawatan pernafasan pada penderita dengan penyakit paru.
Bila penderita berbaring terlentang, maka gerakan otot diafragma dan intercostal menurun, pernafasan
menjadi lebih dangkal. Juga terjadi pengumpulan sekret di bagian bawah dan pengeluaran sekret lebih
sukar karena gerakan cilia yang kurang efektif disamping posisi terlentang tersebut. Maka akan terjadi
mikro atelektasis. Batuk juga lebih sukar dilakukan dalam posisi terlentang tersebut.
Keadaan-keadaan tersebut diatas disertai dengan kelemahan otot abdomen menyebabkan
penderita mudah terkena infeksi saluran nafas bagian atas dan pneumonia hipostatik. Itulah sebabnya
penderita perlu turning setiap waktu tertentu (2 jam) untuk mencegah hal-hal tersebut di atas, juga
mencegah komplikasi lain seperti : dekubitus, tromboplebitis dll.
Tujuan :
o meningkatkan efisiensi ventilasi
o meningkatkan toleransi latihan
Chest Physical Therapy t.a. :

Teknik Relaksasi


Breathing Control


Breathing Exercise


Postural Drainage


Teknik Manual

Teknik Manual :
a. Perkusi
b. Shaking
c. Vibrasi
Indikasi Chest P.T. :

PPOM : asma, bronkhitis khronis, emfisema


Post OP. thoraks, sistem kardiovaskular


Berbaring lama


Penyakit neuromuskular dengan refleks batuk menurun


Yang tergantung alat ventilasi

Penderita Post Operasi : perlu diberikan latihan sebelum operasi, karena bila setelah operasi maka

penderita sulit kooperatif karena rasa nyeri disamping pengaruh analgesik.

Teknik Relaksasi :
Tujuan :
1. me < tegangan otot-otot pernafasan tambahan
2. me < kecemasan karena dyspnea
3. merangsang sense of well being

Terdiri dari :
1. Posisi optimal untuk latihan pernafasan diafragma :



2. gentle repetitive movements : dengan peregangan manual, pasif, gentle dan shaking
technique oleh terapis pada leher, bahu dan lengan sehingga mengurangi tegangan.

II. Breathing Control (gentle breathing) :

Yaitu pernafasan :

Memakai bagian bawah dada

Membutuhkan sedikit tenaga

Mengurangi sesak nafas

Otot-otot yang dipakai : intercostal, scalenus, diafragma dan abdomen.

Manfaat :
1. Mengurangi kerja pernafasan
2. Mengurangi sesak nafas
3. Membantu pernafasan ke pola normal
4. Perbaiki ventilasi bagian basal paru
Cara :

Posisi : duduk / miring

Dinding abdomen relaks, lutut sedikit fleksi

Tangan pada bagian ant.costal margin

Bernafas tenang lewat hidung

Bahu dan dada atas relaks

Gerakkan iga-iga bawah ke bawah dan medial

Merasakan gerakan dada bagian bawah

Penting :bernafas dengan usaha minimal dan lewat hidung.

Hindari :
1. forced expiration karena ekspirasi harus pasif
2. Ekspirasi yang memanjang yang menyebabkan pola nafas tak teratur dan tak efisien
3. Gerakan otot-otot abdomen yang akan mengganggu pernafasan
4. Gerakan dada bagian atas dan otot-otot pernafasan yang bekerja berlebihan
III. Breathing Exercise :

Penderita aktif pada waktu fase inspirasi dan ekspirasi sesuai kebutuhan.
Tujuan :
Mencapai fungsi paru yang optimal
Manfaat :
1. Melepaskan perlekatan sekret bronkhus
2. Membantu pengeluaran sekret
3. Membantu pengembangan jar.paru (re-expansion)
4. Mobilisasi dinding thoraks
5. Perbaiki hubungan ventilasi-perfusi
6. Melatih otot-otot pernafasan
7. Melatih mengatasi dyspnea

Macam-macamnya :
1. Thoracic Expansion Exercises :
a. Unilateral Lower Thoracic Expansion
b. Bilateral Lower Thoracic Expansion
c. Apical Thoracic Expansion
d. Posterior Lower Expansion
2. The Forced Expiration Technique

1. Thoracic Expansion Exercises

Merupakan latihan inspirasi untuk memperbaiki gerakan dinding dada. Dengan inspirasi,
volume paru meningkat, aliran udara masuk melalui saluran ventilasi kolateral meningkat dan
membantu melepaskan perlekatan sekret ketika melalui bronkhus yang mengandung sekret. Juga
alveoli yang kolaps akan berkembang. Waktu inspirasi penuh, tahan 3 detik, dan ini merupakan
metoda efektif untuk mengurangi terjadinya atelektasis. Metoda ini menggunakan gerakan dinding
dada pada daerah tertentu.
a. Unilateral Lower Thoracic Expansion

Penderita duduk / setengah duduk

Taruh telapak tangan (ipsilateral / kontralateral) pada garis mid axiliar iga ke 7, 8, 9

Penderita relaks, bernafas sambil merasakan iga bawah bergerak ke bawah dan dalam

Pada akhir espirasi, tangan menekan untuk memberi rangsangan proprioseptif

Pada inspirasi penuh, ditahan 2-3 detik, lalu lepaskan tekanan tangan

Waktu menaruh telapak tangan, jangan angkat bahu

Inspirasi : aktif, ekspirasi : pasif

b. Bilateral Lower Thoracic Expansion


Posisi seperti di atas

Tekanan pada kedua sisi garis mid axiliar bagian bawah dada dengan telapak tangan /
punggung tangan

Teknik bernafas seperti di atas

Tak dipakai untuk dada bagian atas karena sulit untuk relaksasi sendi bahu adekuat

Dilakukan terutama setelah operasi

c. Apical Thoracic Expansion


Berguna bila ada gerakan terbatas dinding dada bagian atas, misal :

gross pleural effusion

pengembangan tak sempurna jaringan paru, terutama apical pneumothoraks, misal

setelah lobektomi

Tekanan dengan ujung jari-jari di sebelah bawah clavicula

Tarik nafas, kembangkan dada ke depan dan ke atas melawan tekanan tersebut

Bahu harus relaks

Pengembangan dinding dada ditahan selama 2-3 detik

Bila latihan ini sulit, disarankan tahan nafas sebentar pada saat inspirasi penuh, lalu
mendengus 2-3 kali sebelum ekspirasi

d. Posterior Lower Expansion


Duduk bersandar ke depan, punggung lurus

Tekanan oleh fisioterapis atau sendiri pada bagian posterior unilatral bagian bawah iga

Bisa memakai belt selebar 5-7 cm, panjang 2 m, penderita duduk di kursi karena lebih

Belt diletakkan setinggi ziphisternum, dipegang oleh tangan kontra lateral lalu dililitkan ke
dinding dada

1 ujung dipegang tangan kontra lateral setinggi ziphisternum, sisi lain dilibatkan ke paha
dan ujungnya dipegang dengan tangan kontra lateral.

2. The Forced Expiration Technique

Yaitu cara untuk membantu membuang / mengeluarkan sekresi bronkhus yang berlebihan
dari jalan nafas yanpa menyebabkan spasme bronkhus. Terdiri atas 1 atau 2 forced expiration,
diikuti periode relaksasi dan breaking control. Bila sekret mencapai saluran nafas yang besar,
dibuang dengan dibatukkan dengan high lung volume. Periode breaking control perlu
mencegah terjadinya bronkhospasme. Dengan teknik ini terjadi kompresi dan pengecilan jalan
nafas pada daerah tertentu. Misal : pada high lung volume, daerah tersebut terletak pada trakhea
dan bronkhus utama. Bila volume paru menurun, daerah tersebut akan turun ke distal dan diikuti
gerakan bergetar dari daerah bronkhus.
Pada penderita dengan obstruksi jalan nafas, penyempitan lebih jelas dan tersebar tak
merata. Supaya batuk, perlu usaha expirasi yang besar dengan cara menutup glottis sehingga
tekanan intra thoracic meningkat, lalu dibuka tiba-tiba, terjadi perbedaan tekanan yang besar
antara tekanan alveolar dan tekanan trakheal atas.
Tekanan intra thoracic meningkat, menekan membran posterior trakhea dan mengecilkan
sampai 1/6 nya. Dengan aliran cepat dan penyempitan tersebut maka mukus dan pertikel-pertikel
asing terdorong ke trakhea dan dapat dibatukkan.

Batuk yang efektif :

Tarik nafas dalam batuk sambil kontraksikan otot-otot abdomen.
Kemudian diikutibreaking control.
IV. Postural Drainage :

Penderita diberi posisi sedemikian agar gaya gravitasi membantu drainase sekret dari daerah
tertentu paru. Posisi berdasarkan anatomi bronkhial.
Tujuan :
Membersihkan sekret seefektif mungkin tanpa menyebabkan kelelahan
Lama : 10-20 menit
1-5 x sehari
Perlu partisipasi aktif disertai :
1. Thoracic Expansion Exercise : untuk membantu melepaskan sekret bronkhus
2. Breathing Control untuk mencegah hiperventilasi dan lelah
3. The Forced Expiration Technique : untuk membersihkan sekret dan mencegah
kemungkinan peningkatan obstruksi saluran nafas
4. Teknik Manual
Penderita dimiringkan 10o atau 15 o atau diganjal bantal.
Kontra indikasi Postural Drainage :
1. Bentuk darah
2. Hipertensi berat
3. Edema Serebri
4. Aneurisma Aorta dan Serebral
5. Aritmia jantung
6. Edema paru
7. Kelainan esofagus atau diafragma (terjadi gastric reflux)

Terapi Tambahan :
1. Bronkhodilator
2. Humidifikasi
3. Obat Mukolitik
4. IPPB (Intermittent Positive Pressure Breathing)

5. PEP (Positive Expiratory Pressure)

Asma akut dan emfisema berat : dispneu meningkat dengan postural drainage, jadi posisi harus
dimodifikasi. Penderita osteoporosis dan deposit metastatik pada iga / tulang belakang, maka
clapping / shaking harus dengan gentle.
Penderita dengan penyakit paru unilateral :
Pertukaran gas akan meningkat dengan posisi berbaring pada paru yang sehat, lalu diberikan
perkusi dan vibrasi.
Penderita dengan penyakit paru bilateral :
Berbaring pada sisi kanan, mungkin karena tekanan jantung pada paru kiri atau karena volume
paru kiri yang kurang, lalu diberikan perkusi dan vibrasi.
Pursed Lip Breathing
Yaitu mengeluarkan nafas melalui mulut yang sedikit terbuka sehingga menimbulkan obstruksi dan
mengurangi kecepatan aliran udara, meningkatkan tekanan dalam mulut. Akibatya :
1. Tekanan pada trakheobronkhial meningkat, saluran nafas tetap terbuka untuk periode lebih
lama pada waktu ekspirasi, mengurangi tekanan saluran nafas dan air trapping.
2. Mengurangi dispneu.
3. Sirkulasi pada capillary bed paru meningkat sehingga mencegah merembesnya serum ke
dalam alveoli.

Diafragmatic Breathing
Yaitu pernafasan memakai otot pernafasan utama diafragma, posisi semi fowler / side lying. 1 tangan
pada bagian atas abdomen, tangan lain pada thoraks atas. Kontraksikan diafragma, mka ia akan
bergerak ke bawah, abdomen menonjol dan bagian bawah dada melebar, tekanan pleura menurun dan
udara masuk ke paru.

Guna :
1. Untuk penderita yang bernafas dengan otot-otot nafas tambahan dan sedikit gerakan
2. Untuk meningkatkan tidal colume dan menurunkan RR.
3. Untuk memperbaiki gas darah.
Abdominal Breathing
Yaitu pernafasan dengan mengontraksikan otot-otot abdomen untuk membantu ekspirasi dan
memperbaiki posisi diafragma untuk inspirasi berikutnya. Pernafasan ini mengurangi kadar CO 2 .
V. Teknik Manual :
1. Perkusi :
Dinding dada digetarkan, maka saluran nafas akan juga bergetar sehingga mukus terlepas dan hal
ini akan lebih efektif bila disertai dengan Thoracic Expansion Exercises.
o Clapping :
Dengan tangan dalam posisi seperti mangkuk, lalu dengan cepat ditepukkan pada dinding
dada dengan gerakan fleksi-ekstensi pergelangan tangan. Kulit ditutupi pakaian / handuk
supaya tidak luka.
o Gentle Clapping :
Merangsang batuk pada infant dan anak-anak.
o Tapping :
Dengan ujung jari-jari tangan (ke II / III) terutama untuk small infant.

2. Shaking :
Yaitu gerakan ritmis ke bawah pada dinding dengan tekanan gentle memakai tangan terapis.
Dilakukan waktu ekspirasi. Hal ini berguna untuk memperbaiki aerasi pada area khusus.
3. Vibrasi :
Yaitu gerakan getaran halus pada dinding dada dengan tekanan ringan oleh tangan fisioterapis.
Sangat efisien untuk membersihkan sekret dan dapat dipakai bila daerah tersebut terasa nyeri.
Pada bronkhospasme berat, perlu bronkhodilator, dan bila efeknya kurang maka clapping sangat
bermanfaat (60x / m). Mechanical Percussor misalnya : High Frequency Oscillator.
Kontra Indikasi Teknik Manual
1. Batuk darah.
2. Nyeri pleuritik akut.
3. TBC paru aktif.
Posisi Postural Drainage

Upper Lobus

Apical Bronchus : duduk tegak dengan sedikit variasi tergantung letak lesi, bisa bersandar ke
depan, belakang dan samping.


Posterior Bronchus :

Kanan : tidur pada sisi kiri horizontal, kemudian berputar 45 o ke arah wajah, istirahat
pada bantal dan kepala diganjal.


Kiri : tidur pada sisi kanan, berputar 45 o ke arah wajah dengan 3 bantal mengganjal
bahu (30 cm) dari kasur.


Anterior Brochus : tidur terlentang dengan lutut sedikit fleksi.



Superior Bronchus : tidur terlentang dengan tubuh bagian berputar ke kanan, diganjal
bantal pada bagian kiri bahu sampai paha. Kaki tempat tidur ditinggikan 35 cm, dada
dinaikkan sampai 15 o.


Inferior Bronchus : idem.


Lobus Medialis

Lateral Bronchus : tidur terlentang dengan tubuh bagian berputar ke kiri, diganjal bantal
pada bagian kanan bahu sampai paha. Kaki tempat tidur ditinggikan 35 cm, dada dinaikkan
sampai 15 o.


Medial Bronchus : idem.


Lower Lobe

Apical Bronchus : tidur tengkurap dengan bantal dibawah perut.


Medial Basal Bronchus : tidur pada bagian kanan dengan bantal pada paha, kaki tempat
tidur ditinggikan 45 cm, dada dinaikkan 20 o.


Anterior Basal Bronchus : tidur terlentang dengan pantat diganjal bantal dan lutut fleksi, kaki
tempat tidur ditinggikan 45 cm, dada dinaikkan 20 o.


Lateral Basal Bronchus : tidur pada sisi berlawanan dengan bantal dibawah paha, kaki
tempat tidur ditinggikan 45 cm, dada dinaikkan 20 o.


Posterior Basal Bronchus : tidur tengkurap dengan bantal dibawah paha, kaki tempat tidur
ditinggikan 45 cm, dada dinaikkan 20 o.

Batuk yang efektif diperlukan untuk menghilangkan obstruksi saluran pernapasan dan memelihara paruparu tetap bersih. Batuk merupakan bagian penting pada pengobatan pasien pada kondisi penyakit paru
akut maupun kronis.
Mekanisme terjadinya batuk :
1. Terjadi inspirasi dalam
2. Glottis menutup dan corda vocalis mengeras
3. Otot-otot abdomen kontraksi dan diaphragma elevasi sehingga tekanan intrathoracal dan
abdominal meningkat
4. Glottis membuka
5. Terjadi letupan udara expirasi
Daftar Kepustakaan

Haas F, Axen K : Pulmonary Therapy and


Rehabilitation : In Principles and Practice, Baltimore, Williams & Wilkins Co, 1979, p. 123 134.
Helmholz HF, Stonmington HH : Rehabilitation for
Respiratory Dysfunction : In Kotte FJ, Lehmann JF : Krusens Handbook of Physical Medicine and


Rehabilitation, 4 Ed, Philadelphia, WB Sauders, 1990, p. 858 873.

Rondinelli RD, Hill NS : Rehabilitation of the
Patient with Pulmonary Disease, In Delisa : Rehabilitation Medicine, Principles and Pratice ,
Philadelphia, JB Lippincott, 1988, p. 696 -697.
Webber BA : The Brompton Hospital Guide to


Chest Physiotherapy, Oxford, Blackwell Scientific Publication, 1988, p. 15 -36.



: ____________________________________________


: ____________________________________________


: ____________________________________________


: ____________________________________________





Mencuci tangan
Pemeriksa memperkenalkan diri dan menjelaskan tentang tujuan pemeriksaan
Menempatkan diri di sebelah didepan pasien
Posisi pasien semifowler, comfortable, relax menghadap kedepan / tidur terlentang
Menginstruksikan pasien untuk tarik napas dalam ( inspirasi ) melalui hidung dan mulut

tertutup, gerakan dada kedepan dan terangkat keatas.

Kemudian mengistruksikan pasien megeluarkan udara pelan pelan melalui mulut dengan




bibir mencucu dalam waktu 2 kali waktu inspirasi

Mengulang point 6 dan 7 minimal 10 kali
Posisikan pasien sesuai dengan area sputum yang paling banyak diatas
Lakukan teknik manual (clapping, tapping ) pada area sputum yang paling banyak (10 15

menit )
1 Pasien diinstruksikan napas pelan dan dalam dengan menggunakan diaphragma
2 Pasien menahan napas 2 detik
3 Lakukan batuk 2 kali dengan mulut sedikit terbuka
4 Pause / berhenti
5 Tarik napas pelan
6. Istirahat
Total tindakan benar.
Prosentase ****

* : Diisi dengan tanda check () jika dilakukan dengan benar dan tanda (-) jika tidak dilakukan atau
dilakukan tetapi salah.

** : Setiap mahasiswa diberi kesempatan 3 kali. Nomor 1,2,3 merupakan nomor kesempatan
pemeriksaan, jika dalam satu atau dua kali kesempatan pemeriksaan telah dapat dilakukan
dengan benar maka kolom berikutnya tidak perlu diisi.

*** = (total tindakan benar / 12) x 100 %





Pemilihan terapi baik obat dan non obat merupakan proses akademik dan pengalaman..

Pemilihan obat

dan penulisan resep memerlukan pemahaman patofisiologi penyakit, farmakologi dasar ( al

farmakodinamik, faramakokinetik obat ) dan sosiobudaya pasien perlu dipertimbangkan. Selain itu respon
terhadap obat sangat individual sehingga pemilihan obat terhadap pasien sangat individual.

Pemilihan obat berdasar konsep rational drug used merupakan hak dokter, tetapi penentuan terapi / obat
adalah hak pasien. Untuk itu perlu komunikasi yang cukup antara dokter pasien sebelum resep ditulis
dan pelaksanaan pengobatan dimulai

(a.l informasi tentang efek obat, efek samping, instruksi

penggunaan, larangan selama pengunaan obat dan hal lain yang kontekstual).Pengobatan belum
dianggap selesai tanpa diakhiri dengan monitoring dan evaluasi hasil pengobatan.
Untuk mencapai kemampuan pemilihan obat atau ketrampilan terapi dengan menggunakan konsep
farmakoterapi berbasis rational drug used diperlukan pelatihan berulang dan tidak melakukan kesalahan
yang sama pada proses pelatihan berikutnya. Latihan awal sampai akhir merupakan satu kesatuan yang
tidak terpisahkan. Aplikasi sesungguhnya terhadap pasien akan Saudara terapkan pada saat kepaniteraan
dan program internship dokter. Dengan kemampuan ketrampilan terapi diharapkan tidak terjadi pemilihan
obat hanya menyalin resep dari senior, tetapi kemampuan yang berdasar pada penggunaan obat yang

Selamat bekerja,

Ka Lab Farmakologi FKUB

Ketrampilan terapi meliputi kemampuan melakukan proses terapi dengan mengikuti 6 langkah
berikut : 1. Menentukan problem pasien, 2. Menentukan tujuan terapi, 3. Menentukan intervensi terapi, 3.
Memulai terapi dengan menulis resep, 5. Memberikan komunikasi tentang obat dan 6. Kemampuan
melakukan monitoring dan evaluasi hasil terapi.

Pada pelatihan ketrampilan terapi untuk sistem pernafasan, kardiovaskular dan urinarius akan
diberikan kasus yang sesuai dengan masing-masing sistem. Untuk setiap kasus kerjakan sesuai 6 langkah
proses terapi.
Kerjakan kasus-kasus berikut sesuai dengan 6 langkah proses terapi :
Kasus sistem pernafasan
Seorang anak 4 th, dibawa kedokter dengan keluhan panas sudah 3 hari ini. Sudah diberi parasetamol,
panas turun sebentar kemudian naik lagi. Pagi ini anak tersebut batuk-batuk, tanpa diikuti pilek. Anak
tersebut masih mau bermain. Pada pemeriksaan didapatkan BB=20 kg, suhu tubuh=38,5 o C, pharynx
tampak merah, sekret (+) kental warna kekuningan. Pemeriksaan fisik yang lain dalam batas normal
Seorang pasien wanita 30 th, datang dg serangan asma akut yang kemungkinan dipicu oleh infeksi virus
di tenggorokan. Wheezing (+), batuk khususnya malam hari, suhu 37,5 0C. Sebelumnya tidak sakit infeksi
tenggorokan dan tidak minum obat.
Kasus kardiovaskular
Laki-laki bernama P.Umar 45 th memeriksakan diri ke dokter karena merasa kepala terasa berat. Dari
pemeriksaan didapatkan tekanan darah 150/100 mm Hg. Penderita sudah diberi advis rendah garam,
tetapi tekanan darah belum turun. Pasien adalah penderita asma bronkhiale dan sudah biasa
menggunakan salbutamol inhaler kalau sesak nafas. Sekarang tidak ada keluhan sesak.
Laki-laki berusia 60 th, tanpa riwayat penyakit lain sebelumnya. Pada akhir bulan ini dia merasakan
beberapakali nyeri dada seperti tercekik yang membuat lemas. Nyeri dada timbul pada saat aktivitas fisik
dan segera hilang setelah aktivitas dihentikan. Pasien ini sudah berhenti merokok selama 4 th. Dari riwayat
keluarga didapatkan, bapak dan saudaranya meninggal karena serangan jantung. Pasien tidak minum
obat, hanya kadang-kadang minum parasetamol. Dari pemeriksaan auskultasi didapatkan mur-mur pada
arteri karotis dan arteri femoralis kanan. Tekanan darah 130/85 mm Hg, nadi 78 x/menit teratur dan BB
Kasus Traktus Urinarius

Bu Ati (38 th), 3 hari ini mengeluh sering kencing, sedikit-sedikit. Setiap kencing dirasakan tidak tuntas dan
diakhir kencing terasa sakit dan panas di daerah keluarnya kencing. Warna kencing kuning bening. Badan
terasa demam dan tidak ada keluhan lain. Pemeriksaan fisik lain dalam batas normal
Pak Amat (65 th), datang ke UGD puskesmas, pada jam 7 pagi dengan keluhan tidak bisa kencing.
Penderita merasa mulai jam 9 tadi malam kencingnya hanya sedikit-sedikit dan sakit. Mulai jam 12 tengah
malam sampai datang di puskesmas tidak bisa kencing sama sekali, padahal rasanya ingin kencing.
Sekarang perutnya di bagian bawah terasa sangat nyeri. Pada pemeriksaan didapatkan pembesaran
kelenjar prostat.
Modul Lab Farmakologi Untuk PANUM
Guide to good Prescribing, WHO









Jenis kegiatan
Menyapa pasien dan mempersilahkannya duduk dengan pengaturan yang
Memperkenalkan diri kepada pasien
Menanyakan kembali identitas pasien: nama, usia, tempat tinggal, pekerjaan,
status keluarga
Menetapkan problem / diagnosa pasien
Menentukan tujuan terapi
Menentukan P-treatment (Advis, non drug)
Menentukan pemilihan obat (P-drug) dengan mempertimbangkan ;
Mengidentifikasi obat yang dipilih meliputi :
Nama obat
Bentuk obat
Lama pengobatan
Menulis resep lengkap
Nama & alamat
Nama generik obat
Bentuk obat
Cara pemberian
Nama & alamat pasien
Memberikan informasi, instruksi dan perhatian yang meliputi :
Efek obat (efeknya apa, kapan efek muncul, berapa lama efeknya)
Efek samping (berupa apa, apa yang akan dilakukan)
Instruksi (cara minum/penggunaan obat, dosis, interval, berapa lama, apa
yang harus diperhatikan)
Perhatian (dosis maksimum, interaksi, efek yang tidak dikehendaki,
penghentian obat)
Menyampaikan kapan kontrol untuk monitoring & evaluasi pengobatan
Catatan : Komunikasi yang disampaikan untuk no 9 dan 10 harus :
- Jelas dan dapat dimengerti
- Struktur pembicaraan runtut

0 1 2

- Beri kesempatan pasien (atau keluarga yang mengantar) untuk

mengekspresikan dirinya atau memberikan pertanyaan ke dokter
- Pastikan pasien (keluarganya) mengerti instruksi yang diberikan. Pasien
(keluarganya)diminta untuk mengulangi instruksi
Penilaian dimulai dari no urut 4 10 (jumlah soal 7)


0 = tidak dikerjakan

1 = dikerjakan tetapi kurang sesuai/benar


2 = dikerjakan dengan benar

Jumlah nilai
Nilai akhir = -------------------------- x 100 =

Catatan: Mahasiswa/peserta dinyatakan LULUS apabila nilai akhir mencapai 90



Tujuan Pembelajaran :


Mahasiswa mampu membuat permintaan pemeriksaan radiologi sesuai dengan indikasi dan kontra
indikasi dari klinis pasien.


Mahasiswa mampu menunjukkan radioanatomi thorax

Soft Tissue
Costa, Scapula, Clavicula, Vertebra thoracalis

: - Parenchym paru
- A. pulmonalis dan cabang-cabangnya
- Trachea dan cabang-cabangnya


Mahasiswa memahami dan mampu menunjukkan radioanatomi dari foto thorax PA dan lateral pada
kasus foto thorax normal, infiltrat, cavitas, bronchiectasis, tumor paru primer dan metastase.


Memahami dasar menegakkan diagnosa dari foto thorax


1. X - Foto Thorax PA Normal


Soft tissue
Costa, Scapula, Clavicula, Vertebra
Parenchym paru
A. pulmonalis dan cabang-cabangnya
Trachea dan cabang-cabangnya

2. X- Foto Infiltrat
3. X- Foto Cavitas
4. X- Foto Bronchiectasis
5. X- Foto Tumor Paru Primer
6. X- Foto Tumor Paru Metastase

(dr. ... )