REPORT OF PBL

MODUL 2 BREATHLESS
RESPIRATORY SYSTEM

TUTOR : dr. Yani Sodiqah

GROUP 14:
NURUL SALSABILAH MUSTAJAR

: 110 2014 0035

MUHAMMAD ALGHIFARI SULKAF : 110 2014 0063

INDAH KURNIA RAMADHANI. M

: 110 2014 0079

MUHAMMAD ZUHAL DARWIS

: 110 2014 0085

ADE NOVITA SAM

: 110 2014 0093

NUR AZIZAH ALFIYAH. A

: 110 2014 0094

FENNY PUTRIANA SALIM

: 110 2014 0106

WIDYA KEMALASARI

: 110 2014 0119

SITTI MUTMAINNAH

: 110 2014 0134

SESARIH FATIMAH NUR.B

: 110 2014 0143

MEDICAL FACULTY
MUSLIM UNIVERSITY OF INDONESIA
MAKASSAR
2015

Case 2

A 7 years old girl was taken to the hospital emergency room by her parents
complaining of shortness of breath since 4 hours ago. That child had been suffering from
shortness of breath 2 years ago. This complaint is sometimes accompanied by a cough and
fever. On physical examination the child looks cyanosis, respiratory rate 40 times with chest
wall retraction. The same history in both parents is denied.

Difficult Words :
1. Cyanosis : is a bluish skin due to excessive amount of deoxyHb in blood vessels of skin,
especially capillaries
2. Retraction : withdrawal lower chest wall when breathing in conjunction with increased
Respiratory rate
3. Shortness of breath : Dyspnea is subjective symptoms such as people with a desire to
Increase efforts to obtain breathing air
Keywords :
7 years old girl
Shortness of breath since 4 hours ago
Accompanied by cough & fever
Had been suffering from shortness of breath 2 years ago
Looks cyanosis, respiratory rate 40 time with chest wall retraction
Same history in both parents denied
Questions :
1. What is the patophysiology of dyspneu based on scenario?
2. What is the relation between dyspneu and fever?
3. What is the Anatomy of Respiratory Tract?
4. Why the child looks cyanosis?
5. Why the respiratory rate is 40 time on physical examination?
6. Why is the chest wall retraction on physical examination?
7. What is the most cause of dyspneu in children?
8. What is the differential diagnosis of the case?
9. What is the way to diagnose?
10. What is the therapy based on the differential diagnose in the case?
Answers :
1. What is the patophysiology of dyspneu based on scenario?
Mechanism of dyspnea
Similarly, reflex chemostimulation by CO2 causes dyspnea, even in the presence of
respiratory muscle paralysis or cord transection, indicating that reflex chemoreceptor
3

stimulation per se is dyspnogenic. Sensory afferents in the vagus nerves have been considered
to be closely associated with dyspnea.1
Dyspnea is associated with activation of the limbic system, especially the insular area.
These findings permit a clearer understanding of the mechanisms of dyspnea: Afferent
information from reflex stimulation of the peripheral sensors (chemoreceptors and/or vagal C
fibers) is processed centrally in the limbic system and sensorimotor cortex and results in
increased neural output to the respiratory muscles. A perturbation in the ventilatory response
due to weakness, paralysis, or increased mechanical load generates afferent information from
vagal receptors in the lungs (and possibly mechanoreceptors in the respiratory muscles) to the
sensorimotor cortex and results in the sensation of dyspnea. 1

2. What is the relation between dyspneu and fever ?

 Fever : Microoganism runs to the blood and will be phagocyte by macrphages and
lymphocyte with granular and removed after that IL-1 will be realesed PGL e2
work in hipothalamus fever reaction
Hypersecretion of mucous gland acumulated in respiratory tract( Goblet cell) The
ariway become obstruction
Allergens Release (Bradikinin,ECF-A, NC2F-A, PAF, Prostaglandin, proteoglycan)
AMP decrease and GMP Increase Inrease of bronchial muscle tone
obstruction dyspnea
Acute infection Need more oxygen due to an icreased of metabolism. Temperature
of the body increased because pirogen reaction oxygen requirement increase
Dyspnea.5
3. The anatomy of respiratory system ?

Airway Tract
-

Cavum nasi
Pharynx
Larynx
Trachea
Cavitas thoracis
Pulmo
Bronchus6

Respiratory Muscles
Inspiration

Diaphragma

Intercostal externa

Pectoralis major

Scaleneus

Sternocleidomastoideus

Serratus anterior

Expiration

Intercostal interna

Rectus abdominis

Transversus abdominis

Obliqus abdominis int et ext6

4. Why the child looks cyanosis?

Cyanosis term means bluish skin. Cyanosis is a physical sign of the characteristics of
the mucous membranes, nail beds, and blue skin. The cause is hemoglobin that does not
contain excessive amounts of oxygen in the blood vessels of the skin, especially in the
capillaries. oxygenated hemoglobin that does not have a dark blue-purple color that is visible
through the skin. in general, cyanosis appears when the arterial blood contains more than 5
grams of hemoglobin that contains no oxygen in every 100 ml of blood.7
Patients with dyspnea is one of the causes of respiratory gas abnormality in body fluids,
especially hypercapnia and hypoxia. Too little of oxygen in the air and too little hemoglobin
that caused by hipoksia makes the child looks cyanosis.7

5. Why the respiratory rate is 40 time on physical examination?

In general shortness of breath occurs due to inflammation of the respiratory tract
caused by infection or irritation of the respiratory tract. Shortness of breath may occur from a
variety of mechanisms such as if the space physiology increases will be causes the disruption
in exchange between O2 and CO2 causing ventilation requirement increased. Causing
shortness of breath in normal people dead space these are few and not very important, but in
people in a state of pathological tract respiratory the dead space will increase.2

Similarly, if an increase in the exchange of prisonerd airway will also be affected and
may also cause shortness.2
Tightness may also occur in people who declined to pulmonary compliance, the lower
the ability of the lung compliance, the greater the transmural pressure gradient which can
curve for inspiration to produce normal lung development. Causes of decline in lung
compliance can vary one of which was the replacement of lung tissue with fibrous connected
tissued due to inhalation of irritants asbston or similar.2

6. Why is the chest wall retraction on physical examination?

On physical examination of the asthma bronchial, there are not generally abnormalities
when patients do not experience an attack. When the attack, can be found shortness of breath,
chest hyperinflation, chest indrawing (retraction), expiration lengthwise with audible wheeze.
Retraction indicate a forced breathing. Increasing breathing work in asthmatics resulted in the
neck and intercostals muscles (chest wall retraction).3,4

7. What is the most cause of dyspneu in children?

The cause of dispnea on child.
- Exposure to environmental conditions for certain medication:
1.) Allergen, such as pollen, fungus or chemicals resulting in a complaint form
bronchospasm with shortness of breath.
2.) Dust, smoke, cigarette smoke, and other chemical can cause irritations of the airway
that cause of bronchospasm.
3.) Drugs consumption/injection can cause hypersensitivity.8

8. What is the differential diagnosis of the case?

Symptoms

Dyspneu Cough

Fever

Wheezin Retra

Cyanos

Lab

Rad

ction
+

is
+

GBA

X-Ray

Leucocyte

X-Ray

Asthma

+/-

g
+

Bronchial
Bronchitis

+/-

Chronic

Bronchial asthma
Bronchial asthma is an inflammatory airway disorder that involves a lot of
inflammatory cells and mediators . Asthma can be mild and do not interfere with the activity ,
but there is also the nature of the heavy and disruptive activity .9
Asthma is known by history of respiratory symptoms such as wheezing , shortness of
breath , chest distress and cough that vary over time and in intensity , along with expiratory
airflow limitation .9
Clinical symptoms
1. coughing up phlegm worsened in the morning and evening.
2. shortness
3. wheezing on auscultation
4. at heavy attack used a breathing muscles ( retractions supraclavicula , intercostal , and
epigastric )
The properties of typical symptoms of asthma
1. symptoms occur repeatedly ( episodic )
2. embossed time / particular season ( periodic )
3. heavy-light different symptoms ( variable )
4. can recover / disappear spontaneously or with medication ( reversible )
5. there is a history of asthma / allergy others ( atopy ) in patients or their families
9

6. there are various factors ( trigger)

Precipitating factors
1. allergens ( house dust , animal dander )
2. food ( spices , flavorings , preservatives )
3. Respiratory tract infections
4. Changes in the weather
5. Chemicals and pharmaceuticals
6. excessive activity
7. irritants
8. The smell that stimulates
9. emotion9

Bronchitis chronic is a respiratory disease that is often acquired in the community.

The disease is a public health problem because it is chronic, persistent and progressive.
Respiratory infections are a common clinical problem in patients with chronic bronchitis
which may aggravate the disease. Acute exacerbation of chronic bronchitis infections which
may aggravate the disease. Exacerbation of acute infection will accelerate the damage that
has occurred, in addition to the germs that cause exacerbation also affects the morbidity of
this disease. The illness lasts longer than acute bronchitis, which lasts for one year with a
frequency of productive cough frequency 3 months for 2 years in a row.10

A. Ethiolgy
Smoking or exposure to pollution is a major cause chronic of bronchitis. Patients with
chronic bronchitis are more susceptible to recurrence of lower respiratory tract infection. The
range of viral infections, bacteria, and broad mikroplasma can cause episodes of acute

10

bronchitis. Exacerbation of chronic bronchitis is almost certainly the case during the winter.
Breathing cold air can cause bronchospasm for the vulnerable.11
There are several factors that the etiology of chronic bronchitis, namely:
1. Cigarettes
There is a close relationship between smoking and a decrease in VEP (forced expiratory
volume) in one second. Cigarette pathologically associated with bronchial mucus gland
hyperplasia and metaplasia inhibition activity of the vibrating hair cells, alveolar
macrophages and surfactants.
2.

Infection

Upper respiratory tract infection in someone with chronic bronchitis is almost always caused
lung infection bottom, and cause lung damage increases. Exacerbations of bronchitis is most
often begins with a suspected viral infection, which then lead to secondary infection by
bacteria. The bacteria are most often Haemophilus influenzae and streptococcus pneumonia.
3.

Pollution

Pollution is not so great influence as factors that cause bronchitis, but when added smoke,
factors will be higher.
4. Heredity
Unknown clear whether heredity plays a role or not, except in patients with deficiency of
alpha-1 anti-trypsin which is a protein. Work of this protein is neutralizing proteolytic
enzymes that damage tissue, so the deficiency of alpha-1 anti-trypsin cause tissue damage.
5. Old Age
With increasing age, the immune system will decline, so that the man who since the
beginning of smoking would be more susceptible to this disease.
B. Pathofisiology
The smoke irritates the airway causing hypersecretion of of mucus and inflammation.
Due to this constant irritation, the glands that secrete mucous and goblet cells increase in

11

number, the function of cilia decreases, and more mucus is produced. As a result, the
bronchioles become narrowed and clogged.12
Structural changes in the lungs causing physiological changes which are
characteristics of chronic bronchitis like chronic cough, sputum production, airway
obstruction,disruption of gas exchange, pulmonary hypertension and cor-pulmonale.12
Due to the changeof bronchial and alveolar an interruption occurs in gas exchange.
causing two serious problems, namely:
1.

Blood flow and air flow to the walls of the alveoli that not appropriate
(mismatched).Most places (alveoli) there is adequate blood flow but very

2.

little flow
air and partly elsewhere instead. Performance is declining from the pump
respiration especially the muscles of respiration resulting in overinflasi and
narrowing of the airway, causing hypoventilation and insufficient air to the
alveoli causing blood CO2increase and O2 in the blood decrease.12

9. What is the way to diagnose?

Step to diagnose

History Taking

Physical Examination

Laboratory

Radiology

Others13

Anamnesis
1. Location. Where is it? Does it radiate?
2. Quality. What is it like?
3. Quantity or severity. How bad is it? (For pain, ask for a rating on a scale of 1 to 10)
12

4. Timing. When did (does) it start? How long did (does) it last? How often did (does) it
come?
5. Setting in which it occurs. Include environmental factors, personal activities,
emotional reactions, or other circumstances that may have contributed to the illness.
6. Remitting or exacerbating factors. Does anything make it better or worse?
7. Associated manifestations. Have you noticed anything else that accompanies it?13

Physical Examination
INSPECTION :
- Shape and Size Thoracic, if theres any deformity or not. Deformity of chest wall can
cause problem of breathing
- Surface chest
Interpretation :
Increase Volume : emfisema, efusi, pneumotorax
Decrease Volume : atelectasis,fiborocis, Schwarte
- Respiratory mucle help, means we did force inspiration
- Costae and Intercostae, if theres any fracture or not
- Fossa Jugularis, Intra & Supra clavicularis, to see involvement of heart in problem of
breathing
- Type and frequency of respiratory, to see if its tacypneu or dyspneu
PALPATION
- Position of mediastinum: trachea, ictus. Deviation of mediastinum can be a marker to

identify the disease

Deviation to a healthy side : fluid, air, massa
Deviation to contralateral side : fibrosis, schwarte, atelectasis
Throbbing vibration, Lump, edema, crepitus
Tenderness
Vocal fremitus, could be decrease or increase. Increase happen in pneumonia, while
decreasing happen in atelectasis, or pleuras effusion

PERCUSSION
In thorax area, in normal condition will be heard sonor sound in the lung
AUSCULTATION

13

Breath Sound
Ronchi : is a short discontinue sound that heard when inspiration. Ex : obstruction
Wheezing: is a sound that heard when theres a narrowing of respiratory tract. Ex :
asthma, bronchitis
Stridor : is a pathology sound that occur when theres obstruction in laryng or trachea
Bronchovesiculer : is a normal breathsound that heard if we put sthetoscop near the

hillus of the thorax

Whispering Sound
Normal : if heard in laryng
Pathology : Consolidation, atelectasis

Additional Examination
Spirometry
Clinical indications
-

To evaluate symptoms, signs or abnormal test results.

Provide objective, quantifiable measures of lung function.
Evaluate and monitor disease.
Assess effects of environmental/occupational/drug exposures both adverse (e.g.

amiodarone) and beneficial (e.g. bronchodilators).

Pre-operative assessment.
Employment/insurance assessment.
Early detection of bronchiolitis obliterans in lung transplant patients.13

Patient preparation
1. Explain what the test involves. Most respiratory technicians demonstrate technique to
ensure maximal effort and cooperation of patient.
2. Patient must fully inhale before test.
3. Exhale into breathing tube. Must be maximal effort with no hesitation.
4. No cough/glottal closure in the first second.
5. Test must last at least 6s (up to 15s with obstruction).
6. No evidence of airflow leak/obstruction of mouthpiece.13

Interpretation
At least three acceptable tracings should be obtained. Examine each tracing to ensure
adequate effort made by patient, that it is reproducible, and that there are no artefacts.
FEV/FVC ratio: Index of the presence/absence of airflow limitation.
Young and middle aged healthy non-smokers rate >75%.
14

Older normal patients ratio 7075%.

FEV/FVC Decreased: Obstructive.
Classify severity using FEV, expressed as % of predicted value, e.g.
COPD, asthma.
FEV/FVC flat or increased : Restrictive but need reduced TLC to confirm, e.g. lung fibrosis,
chest wall problems, pulmonary effusion and oedema.13
Sputum microscopy & culture/sputum cytology
Clinical indications
Microbiology:
Productive cough with sputum.
Infective exacerbations of any chronic lung disease.
Pneumonia.
Cytology:
Suspected lung cancer, especially in elderly/frail patients.
Patient preparation
-

Explain need for the sputum sample.

Provide suitable sputum pots.
Early morning samples are best.
Consider induced sputumuse ultrasonically nebulised hypertonic saline to facilitate
sputum production in association with chest physiotherapy.

Possible results
Induced sputum results in successful sputum production in >70% of normal
and asthmatic subjects who cannot produce sputum spontaneously.
Gram stain

Gram +ve or ve organisms

ZN stain

AAFB

Microscopy

Differential cell count

Eosinophils in asthma

Cytology

Malignant cells
Small cell, squamous cell, adenocarcinoma cells

Interpretation
- Commensal organisms common.
- Streptococcus pneumoniae and Haemophilus influenzae likely pathogens in COPD.
- Streptococcus pneumoniae commonest organism in community-acquired pneumonia.
15

- Staphylococcus aureus and Pseudomonas likely in bronchiectasis.

- Nosocomial infections:
Staphylococcus aureus.
Pseudomonas.
Klebsiella.
Bacteroides.
Gram ve enterobacteria.
- Adenocarcinoma and small cell lung cancer diagnostic.
- Squamous cell carcinoma on cytology can reflect premalignant change.13

Radiology Examination
We can use X-ray or CT-Scan to identify the disease, especially in respiratory disease.
Plain film
Findings of chronic bronchitis on chest radiography are nonspecific and include
increased bronchovascular markings and cardiomegaly.

Emphysema manifests as lung

hyperinflation with flattened hemidiaphragms, a small heart, and possible bullous changes.
On the lateral radiograph, a "barrel chest" with widened anterior-posterior diameter may be
visualized. The "saber-sheath trachea" sign refers to marked coronal narrowing of the
intrathoracic trachea (frontal view) with concomitant sagittal widening (lateral view).
CT
Findings of COPD may be seen in a variety of CT studies, e.g. contrast enhanced CT,
CTPA, staging CT chest, HRCT.
In chronic bronchitis, bronchial wall thickening may be seen in addition to enlarged
vessels. Repeated inflammation can lead to scarring with bronchovascular irregularity
and fibrosis.

10. What is the therapy based on the differential diagnose in the case?
A. ASTHMA BRONKIAL
16

Treatment of severe asthma. In cases of inadequate asthma control, an increased ICS dose
of up to 800 lg BDP equivalent (201) can be used at the discretion of the prescribing
physician. Patients requiring higher doses should be referred to a specialist. The
efficacy/safety ratio of routine oral steroids vs high-dose ICS generally favors ICS. Severe
asthma may require regular treatment with an oral corticosteroid (i.e. daily or every other
day). Prior to treatment, national guidelines on age-related indications should be reviewed.
Asthma control and maintenance therapy must be assessed regularly and specialist care
should be sought when low-dose ICS plus add-on medication (or doubling of dose of
standard ICS) are not adequate. Triple therapy with ICS, LTRAs and LABA can also be
attempted before resorting to oral corticosteroids (202). If good control has been achieved
and maintained, consideration should be given to gradually reducing maintenance therapy.
Regular reassessments are necessary to ensure that adequate control is maintained and the
minimum therapy needed to maintain acceptable asthma control is established. Severe asthma
in children is uncommon and its presence should prompt careful consideration of the
differential diagnostic possibilities as well as the potential for lack of adherence to prescribed
treatment regimens. Management of children aged 02 years. The 02 year age group is the
most difficult to diagnose and treat because the evidence base in this age group is limited.
(See Box 1 for stepwise treatment procedure in this age group). Persistent asthma begins in
the preschool years and alterations in lung structure and function that are present at this time
may determine asthma status and lung function throughout childhood and adolescence.
It is not clear how frequent the child_s obstructive episodes should be before continuous
ICS or LTRA therapy is
instituted according to the atopic or nonatopic phenotype. Although a Cochrane review
reported no clear evidence of the benefit of b2-agonist therapy in the management of
recurrent wheeze in this age group (203), the evidence is conflicting and some studies have
reported benefit (204206). LTRAs have reduced asthmatic episodes in children aged 25
years (158), and there is some evidence that they may be beneficial in the 02 age group
(156). However, it is debatable whether a reduction from 2.34 to 1.60 episodes per year, as
seen in this large study, justifies the use of LTRAs. In smaller, double-blind, randomized
controlled trials, infants characterized as having mild persistent (207) or severe (208) asthma
and treated with nebulized corticosteroids (i.e. budesonide) had less day- and night-time
asthma symptoms and fewer exacerbations. In a study of young children with severe,
corticosteroid-dependent asthma, nebulized budesonide reduced day- and nighttime asthma
symptoms while concurrently reducing oral corticosteroid requirement (209). However,
17

several studies have reported that use of inhaled corticosteroids in early infancy has no effect
on the natural history of asthma or development of wheeze later in childhood.
Asthma treatment in children aged 02 years

Consider a diagnosis of asthma if >3 episodes of reversible bronchial obstruction

have been documented within the previous 6 months

Intermittent b2 agonists are first choice (inhaled, jet nebulizers in the US and oral in

Europe) despite conflicting evidence

LTRA daily controller therapy for viral wheezing (long- or short-term treatment)
Nebulized or inhaled (metered-dose inhaler and spacer) corticosteroids as daily
controller therapy for persistent asthma, especially if severe or requiring frequent oral

corticosteroid therapy
Evidence of atopy/allergy lowers the threshold for use of ICS and they may be used

as first-line treatment in such cases

Use oral corticosteroids (e.g. 12 mg/kg prednisone) for 35 days during acute and
frequently recurrent obstructive episodes.

Management of children aged 35 years. First-line treatments in this group include ICS
and LTRA in children with intermittent or persistent disease. See Box 2 for stepwise
treatment procedure in this age group. Management of acute asthma episodes. Note that
airway obstruction in children with acute asthma improves faster on oral rather than ICS.
Management of exercise-induced asthma. Exerciseinduced asthma is a common clinical
presentation of asthma that occurs in 7080% of children with asthma who do not receive
anti-inflammatory treatment. Most children with exercise-induced asthma are allergic and
allergen-specific treatment should be part of their management. Exercise-induced asthma
without other manifestations of asthma can usually be controlled by short-acting inhaled b2
agonists taken 1015 min before exercise. When combined with other asthma symptoms,
exercise-induced asthma is best controlled with ICS either alone or in combination with
reliever treatment. Recent evidence suggests that LTRAs may be an alternative option to ICS
in exercise induced asthma, since they have a quick, consistent, and long-lasting effect in
preventing the fall in FEV1 after exercise challenge. Regular use did not induce tolerance
against their protective effects.
If full control is not achieved with ICS, add:
(a) inhaled short-acting b2 agonist before exercise,
(b) LTRA in addition to ICS,
18

(c) inhaled LABA in addition to ICS.

There is a possibility of developing tolerance to inhaled b2 agonists used on a regular basis
(217). In some patients, the combination of ICS, LTRA and inhaled LABA may be needed to
prevent exercise-related symptoms. Ipratropium bromide may be tried after individual
assessment, but is usually added to other treatments. In certain circumstances (i.e. in
asthmatic athletes with obvious exercise-induced asthma, but not satisfying the requirements
set up by World Anti-Doping Agency and/ or International Olympic Committee medical
commission
for using inhaled steroids) LTRA alone may be tried, but should be clearly followed up for
assessment of treatment effect. Note that lack of response to treatment may indicate
misdiagnosis of exercise-induced asthma and patients may require reassessment.
Asthma treatment in children aged 35 years

ICS are the first choice, budesonide 100200 lg 2 or fluticasone 50125 lg 2 by

MDI
Short-acting b2 agonists, salbutamol 0.1 mg/dose or terbutaline 0.25 mg/dose 12

puffs at 4-h intervals as needed

LTRA can be used as monotherapy instead of ICS if symptoms are intermittent or

mild persistent
If full control is not achieved with ICS, add LTRA montelukast 4 mg granules or 4
mg
chewing tablet

If control still not achieved consider the following (nonsequential) options:

o Add LABA at least intermittently (although note lack of published evidence
o

supporting use in this age group)

Increase ICS dose

Add theophylline
B. bronkhitis

Outcome

Without complications such as bacterial superinfection, acute bronchitis will heal by itself, so
the goal management only provides comfort patients, therapy dehydration and pulmonary
disorders caused. But on chronic bronchitis there are two therapeutic purposes: first, reducing
then a second malignancy eliminate symptoms and exacerbations to achieve an infection-free
interval panjang.28
19

Main therapy

Antibiotic therapy in acute bronchitis is not recommended unless accompanied by fever and a
cough that lasts more than 6 days, suspicion the involvement of respiratory tract bacteria such
as S. pneumoniae, H. Influenzae For persistent cough> 10 days suspected
Mycobacterium pneumoniae involvement so that the use of antibiotics recommended. For
children with cough> 4 weeks should undergo further examination of the possibility of
tuberculosis, pertussis or sinusitis.

Clinical Conditions

Patogen

Early Therapy

Bronkhitis acute

commonly virus

Lini I: without antibiotika

Lini II:Amoksisilin,amoksi-klav,
makrolida

Bronkhitis Kronik

Bronkhitis

Kronik

H.influenzae,

Lini I: Amoksisilin

Moraxella catarrhalis,

Lini II: Amoksi-klav,

S. pneumoniae

azitromisin, kotrimoksazol

with s.d.a,K. Pneumoniae,

complications

Lini I: Ceftazidime, Cefepime

P. aeruginosa, Gram
(-) batang lain

Bronkhitis

kronik

with s.d.a.

Lini I: Meropenem atau

bacteri infections

Ceftazidime/Cefepime+Ciprofloks
asin oral.

Antibiotics that can be used see table 5.1, with long therapy 5- 14 days whereas chronic
bronchitis optimal for 14 days Giving antiviral amantadine may impact shorten
long illness if given within 48 hours after infection with influenza virus A.

Supporting Therapy
20

 Stop smoking, because smoking can thwart mechanism the body's defenses
Bronkhodilasi using salbutamol, albuterol.
analgesics or antipyretics using paracetamol,NSAIDs.
Antitusiv, codeine or dextrometorfan to suppress cough.
Vaporizer

DAFTAR PUSTAKA

1. Nausherwan K. Burki, MD, PhD, FCCP and Lu-Yuan Lee, PhD. Mechanisme of
dyspnea. 2010. www.ncbi.nlm.nih.gov
2. Elizabeth. J. corwin. Buku Saku Patofisiologi. Edisi revisi 3. Jakarta:EGC. 2009.
Halaman 541 544
3. Tanto chris et al. Kapita Selekta Kedokteran Ed 4. Jilid 1. Jakarta: Media Aesculapius
2014. Page 164.
4. W. Sudoyo Aru et al. Buku Ajar Ilmu Penyakit Dalam. Jilid III. Ed V. 2009. Jakarta:
Interna Publishing. Page 2190.
5. Price, Sylvia, Lorraine M. Wilson. 2006 Patofisiologi Konsep Klinis Proses Penyakit,
Vol. 2, Ed. 6, pp. 783-792: Penerbit Buku Kedokteran EGC, Jakarta
6. Sherwood, Lauralee. Human Phisiology. Cell to system Ed.8 . EGC. Jakarta. Page 488
7. Guyton and hall. Buku ajar fisiologi kedokteran. Singapore : Elsevier. Ed. XII. hal
558
8. W. Sudoyo Aru et all. Buku Ajar Ilmu Penyakit Dalam. Jilid III. Ed V. 2009. Jakarta:
Interna Publishing. Page 2189.
9. Buku Ajar Ilmu Penyakit Dalam. EGC : Jakarta.
10. Anzueto AR, Schaberg T. Acute exacerbation of Chronic bronchitis. London. Science
Press Ltd. 2003
11. Pillette C, Quadrhiri Y, Godding V, Vaerman JP, Sibille Y. Lung Mucosal Immunity :
Immunoglobulin-A revisited. Eur Respir J 2001; 18 : 571-88
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12. NHLBI. Pathogenesis, Pathology and Pathophysiology. Global Initiative for Chronic
Obstructive Lung Disease. Global strategy for the diagnosis, management and
Prevention of COPD. NHLBI/WHO Report. NHLBI. 2001
13. Provan, Drew. 2002. Oxford Handbook Of Clinical and Laboratory Investigation

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