Faculty Of Medicine Makassar, 12 November 2016

Universitas Muslim Indonesia

Tutorial Report
Modul Cough

Written by Group 14 :

ANY MUSTAFA 110 2015 0027

ZIHAN AYU PRATIWI 110 2015 0036
MAFTUHATUL AFIAH 110 2015 0061
A. ST. ZURAIDHA P.A 110 2015 0081
DESI TRIUTAMI SALEH 110 2015 0068
SITI ANNISAH 110 2015 0111
ULFA DINARIANI 110 2015 0122
RIFQI ADITYA 110 2015 0078
A.MUH. YASSER MUKTI 110 2015 0022
ANDI AISYA ZEALAND HALIZA 110 2015 0051
Tutor:
dr. Hasta Handayani Idrus, M.Kes
Medical Faculty
Muslim University Of Indonesia
2016
 PREFACE

Praise is merely to the Almighty Allah SWT for the gracious mercy and
tremendeous blessing that enable writer for finishing the Modul assignment
entitled Cough. The writer also wish to express his deep and sincere gratitude
for those who have guided in completing this assignment, especially to dr. Hasta
Handayani Idrus, M.Kes writers tutor. In completing this paper, the writer faced
many problems, but with the help of many people, all the problems could be
passed. May Allah SWT give the blessing for them. The writer realizes that this
paper is far from perfect in the arrangement or in the content of the paper. The
writer hopes that the suggestions from the reader can be a support to make
her better in the next paper project.

Finally, the writer expects that it can be a medium for the reader to deepen
the knowledge about the figure of speech and its application.

Makassar, November 2016

Group 14

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 Scenario 1

A man aged 33 years came to the hospital because the cough he experienced
since one month ago. These complaints accompanied by fever, runny nose and
sweating at night. He also complained of pain in the whole body especially the
chest, headaches especially in the mornings and lack of appetite. History treatment
in public health center does not improve.

A. Difficult Word Clarification

- Cough : A voluntary or involuntary explosive expulsion of air from the

lungs verb To explosively expulse air from the lungs after
(McGraw-Hill Concise Dictionary of Modern Medicine. 2002 by The
McGraw-Hill Companies, Inc)
- Fever : Elevation of body temperature above about 37 C, taken in the
mouth. Fever is due to a resetting of the body's thermostat at a higher level
so that heat production, mainly by shivering, is induced. The resetting is
caused by the cytokine interleukin-1 produced by white cells under the
influence of bacteria, cancer, coronary thrombosis, stroke, crushing injury
and other conditions. Fever inhibits the growth of bacteria and causes an
increase in antibody production. The recognition of these advantages has
led to a general abandonment of the former practice of routinely trying to
reduce moderate fever.
(Collins Dictionary of Medicine Robert M. Youngson 2004, 2005)
- Runny nose : The production of extra mucus by the nose. Rhinorrhea is
the medical term for this common problem. The nose makes extra mucus
whenever something that is in the nose, such as pollen or dust, needs to be
removed. Mucus formation is also part of the histamine reaction to
allergies and of the body's defenses during respiratory infections.
(McGraw-Hill Concise Dictionary of Modern Medicine. 2002 by The
McGraw-Hill Companies, Inc.)
- Lack of appetite : A decreased appetite is when your desire to eat is
reduced. The medical term for a loss of appetite is anorexia.

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 (McGraw-Hill Concise Dictionary of Modern Medicine. 2002 by The
McGraw-Hill Companies, Inc.)

B. Keywords
A man aged 33 years came to the hospital because the cough he since one
month ago.
These complaints accompanied by fever, runny nose and sweating at night.
He also complained of pain in the whole body especially the chest,
headaches especially in the mornings and lack of appetite.
History treatment in public health center does not improve

C. Identification the Problems

1. How about the anatomy, histology, and physiology based on the scenario?
2. Explain the etiology and pathomechanism based on the scenario :
a. Cough b. Fever c. Runny Nose d. Lack of appetite e.
Headache
3. What is the differential diagnose and main diagnose based on the scenario?
4. How is the pathomechanism of diagnose based on the scenario?
5. Mention the classification of diagnose based on the scenario?
6. Mention the clinical manifestation based on the scenario?
7. What is the general and supportive examination based on the scenario?
8. What is the complication based on the scenario?
9. Mention the management based on the scenario?
10. Mention the prevention based on the scenario?
11. How do you see the case in the view of Islams perspective based on the
scenario?

D. Answer
1. How about the anatomy, histology, and physiology based on the
scenario?

Anatomy Respiration

Structures that make up the respiratory system can be divided into the
main structure (principal structure), and complementary structures (accessory
structure). Which includes the main structure of the respiratory system is the
respiratory airways, consisting of the airway, and respiratory tract, and pulmonary
(lung parenchyma) .The referred to as upper respiratory airways (airway) is nares,
nose outside, the inside of the nose, paranasal sinuses, pharynx, and larynx,

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whereas the lower respiratory airways (airway) is the trachea, bronchi, and
bronchioles.

What is meant by the lung parenchyma is the organ form alveoli groups
that surrounds the branches of the bronchial (airway generations 1-24). Bronchus
starting from the right and left bronchus principalis (generation 1). Then right
bronchus principales lobar bronchi branch off into superior, medial, and inferior
(generation 2) . Bronchus principales left lobar bronchi branch off into superior
and inferior. And each lobar bronchus branched into bronchial segmentalis and
subsegmental (3-9 generations). 10-14 airway generation are the terminal
bronchioles, respiratory tract generation respiratorius. generation respiratory
bronchioles 15-18 19-24 alveolar ducts, alveolar sacculus, and alveoli.
The complementary structure is chest wall consisting of ribs and muscles, the
abdominal muscles and other muscles, the diaphragm, and pleura.

Figure 1.1 Anatomy Respiration

Respiratory Muscles

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The main inspiratory muscle (principal), namely:
M. intercostal externa,
M. interkatiliginus parasternal, and
diaphragm muscle.

Additional inspiratory muscle (accessory respiratory muscle), namely:

M. sternocleidomastoid
Scalenus anterior
Scalenus medius
Scalenus posterior

Expiratory muscle (active breathing), namely:

M. intercostal interna
M. interkaliginus parasternal
M. rectus abdominis
The external oblique abdominis

Figure 1.2 Anatomy Respiration

Histology Respiration

Nose

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 Composed of bones, cartilage, muscles, nerves, blood vessels, olfactory
epithelium, and connective tissue. Sebaceous glands and tiny hairs quasi-layered
coated cylindrical epithelium with ciliated mucous glands. On the nose there is a
special epithelium.

Figure 1.3 Histology of Nose

Trachea

Consists of a cylindrical epithelium ciliated pseudo-coated (goblet cells),

serous glands, connective tissue, perikondrium, and cartilage (C-shaped). The rear
does not have the ring of cartilage (pars membranacea) but filled by muscle fibers.

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 Figure
1.4

histology of the trachea

Larynx
Cavity widened, irregular shape, between the nasopharynx and trachea.
1. Microscopic :

Mucosa: ciliated epithelium and stratified epithelium stratified squamous non-

horned
The lamina propria: Woven connective and glandular rare

Cartilage :

- Hyaline cartilage: k thyroid / cricoid

- Elastic cartilage: cartilage cuneiform / kornikulata

- A mixture of cartilage: cartilage arichtenoidea

Muscle / ligament: skeletal muscle (3)

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 Figure 1.5 histology larynx

Bronchus and bronchioles

Hyalin consists of cartilage, blood vessels, respiratory epithelium, connective

tissue, etc.

Figure 1.6 histology of bronchus and bronkhiolus

Biochemical Respiration

The composition of the respiratory gasAir atmosphere (760 mmHg) has a

main composition of gases:

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 N2 : 79% P N2: 79% x 760 = 600 mmHg
O2 : 21% P O2: 21% x 760 = 159 mmHg
CO2 : 0.04% P CO2: 0.04% X 760 = 0.3 mmHg

Carrier O2 CO2
Hemoglobi 98.5 % 30 %
n
Blood 1.5 % 10 %
Plasma
(H2CO3)- - 60 %

The presence of water vapor (H2O) with a pressure of 47 mmHg in the

alveoli, the composition of oxygen and carbon dioxide gas is different:
H2O: the partial pressure of 47 mmHg

O2: the partial pressure of 104 mmHg

CO2: the partial pressure of 40 MMH

Physiology Respiration

The purpose of breathing is to provide oxygen / O2 for all body tissues and
dispose of the carbon dioxide / CO2 into the atmosphere. It was the Cardinal
function of the Lung.

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 Figure 1.7 Anatomy Respiration

To achieve this goal, the respiratory system function:

1. Ventilation lungs, the entry of atmospheric air into the lungs

through the alveoli and pulmonary alveoli air discharge into the
air / atmosphere again.
2. Diffusion of O2 and CO2 between the pulmonary capillary blood
and alveolar air. This happens because the continuous ventilation
coupled perfusion flow of blood into the alveoli capillaries are also
constantly flowing.
3. Transport of O2 and CO2 in the blood and body fluids (CES /
ECF) to and from cells. This point was not included pure
respiratory function, but this work of the heart blood vessels
4. Perfusion O2 and CO2 that occur between tissue and blood
capillaries

RESPIRATION MECHANISM INSPIRATION EKSPIRATORY

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2. Explain the etiology and pathology mechanism based on the scenario :
a. Cough
b. Fever
c. Runny Nose
d. Lack of appetite
e. Headache

A. Cough

Etiology
Inhaled irritants (smoke, smoke, dust, etc.) or aspirated
(Postnasal drip, foreign body, the stomach contents)
All disorder that causes inflammation, constriction, infiltration,
and compression of the airway
Asthma
TBC

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 Lung cancer
interstitial lung disease, pneumonia, and lung abscess
Congestive heart failure
The use of angiotensin-converting enzyme (ACE) inhibitors (5 to 20% of
patients taking these agents)
Pathomechanism
According to Weinberger (2005) cough could be initiated together
there voluntarily or reflexively. As a defense reflex, he has afferent and
efferent pathways. Afferent pathways including the receptors located on
sensory nerve distribution trigemineus, glossopharyngeal, superior
laryngeus, and vagus. Efferent pathways also include laryngeus nerve and
spinal nerves. Cough starts with a deep inspiration followed by closure of
the glottis, relaxation of muscle contractions of the diaphragm and the
closure of the glottis. Positive intrathoracic pressure causes constriction of
the trachea. If the glottis is open, a large pressure difference between the
atmosphere and accompanied by tracheal narrowing airways produce high
levels of air flow rapidly through the trachea. As a result, the high pressure
can help in eliminating mucus and foreign matter.
B. Fever
Etiology
Fever can be caused by infection or non-infectious factors. Fever due to
infection can be caused by infection with bacteria, viruses, fungi, or
parasites.
The bacterial infection that generally cause a fever include pneumonia,
bronchitis, osteomyelitis, appendicitis, tuberculosis, bacteremia, sepsis,
bacterial gastroenteritis, meningitis, encephalitis, cellulitis, otitis media,
urinary tract infection, and others.
Viral infections are generally cause fever include viral pneumonia,
influenza, dengue fever, chikungunya fever and common viruses such as
H1N1.
Fungal infections are generally cause a fever, among others Coccidioides
imitis, criptococcosis, and others.

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 A parasitic infection that usually cause fever, among others malaria,
toxoplasmosis, and helminthiasis
Fever due to non factor infection can be caused by several things, among
others, environmental factors (temperature environments externally is too
high, the state of teething, etc.), autoimmune diseases (arthritis, systemic
lupus erythematosus, vasculitis, etc.), malignancies (Hodgkin's disease,
lymphoma non-Hodgkin's, leukemia, etc.), and use of drugs (antibiotics,
difenilhidantoin, and antihistamines)

Pathomechanism
Fever started from the stimulation of white blood cells (monocytes,
lymphocytes, and neutrophils) by exogenous pyrogens in the form of
toxins, inflammatory mediators, or an immune reaction. White blood cells
will release chemicals known as endogenous pyrogen (IL-1, IL-6, TNF-
and IFN). Pyrogen exogenous and endogenous pyrogens will stimulate the
hypothalamus to form prostaglandin endothelium (Dinarello & Gelfand,
2005). Prostaglandins formed later will raise the standard thermostat in
hypothalamic thermoregulatory center. The hypothalamus will assume the
current temperature is lower than the temperature of the new benchmark so
that it triggers mechanisms in order to increase the heat, among others
shivering, cutaneous vasoconstriction and mechanisms such as the
blankets. So that there will be an increase in heat production and decreased
heat reduction that will eventually cause the body temperature rises to the
new benchmark

C. Runny Nose
Rhinorrhea or Runny Nose characterized by an excessive amount of
mucus produced by the mucous membrane of the nasal cavity. mucous
membranes to produce mucus mucus faster than the process itself, causing mucus
in the pouch of rice reserves. Once the cavity is filled, the air flow is blocked,
cause difficulty breathing through the nose. Air trapped in the pouch of rice, sinus
cavity, which can not be released and generate pressure, causing headache or

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facial nyeripada. If the sinuses remain blocked, can cause sinusitis. If the mucus
continues to flow back toward the tube eustachi, can cause ear pain or ear
infection. Excessive mucus that accumulates in the throat or back of the nose
causing post-nasal drip, resulting in a sore throat or cough. Additional symptoms
may include sneezing, nosebleed, and nasal discharge. Rhinorrhea caused nasal
infections usually clear up bilateral purulent. Secretions that is clear like water and
polynomial typical for nasal allergies, is usually not due to infection. If the fluid is
yellow indicates an allergy or infection, if the green liquid indicates infection.
When the yellow-green secretions usually derived from nasal sinusitis If CSF
rhinorrhea unilateral indicate a leak or a malignancy. If the color of blood: if
unilateral showed a tumor, foreign body; If bilateral showed granulomatous
disorder or diathesis and bleeding. Secretions from the nose down to the throat
known as post nasal drip possibility of the paranasal sinuses. In children when
secretions that there is only one side and smelled likely be a foreign object in the
nose. However, if the running nose constituted by serious traumatic
complications, symptoms such as fainting, uncontrolled bleeding, and frequent
vomiting. It was triggered due head injury or injury to the spine, thus affecting
the nervous system.

D. Lack of Appetite
Neurotransmitters and hormones play an important role. Biochemical
substance that determines whether to be inhibited appetite (satiety) or triggered
(hungry). For it is known categorization as follows:
(1) Substance orexigenic which are substances that trigger hunger, such as:
- Neuropeptide Y (NPY) from the nucleus arcuata released when lower energy
savings, and
- Agouti Related Protein (AGRP)
(2) anorexigenic substance that inhibits appetite (in other words, full). as:
- Melanocyte Stimulating Hormone (-MSH) along with Cocaine and
Amphetamine-Related Transcript (CART) produced by Neuron pro-
opiomelanocortin (POMC)

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 POMC neurons work by releasing -MSH which binds to the
melanocortin receptors (MCR) in the paraventricular nucleus. Activation of the
MCR will reduce retrieval -increase food and energy consumption, by contrast
inhibition (defects) by AGRP will improve decision foods and reducing energy
consumption that can lead to obesity. POMC activity can also be inhibited by
NPY, thereby reducing the activity of MCR and enhances the food.

Regulatory caused by temperature:

When the body is exposed to a low temperature, it is physiologically
the body to increase metabolism rate and requires a high amount of fat as an
insulator. Fitness peregulasi temperature will interact denganpusat satiety-hunger,
causing the desire to eat in order to meet calorie needs. Conversely, if exposed to
high temperatures. Then there is a decrease in metabolic rate so that the fat
deposits much in the network. Adipocyte tissue produces a hormone called leptin,
receptors primarily on POMC neurons in the arcuate nucleus and paraventricular.
Leptin stimulation on neurons will result in:
(1) a decrease in production stimulator of hunger, like the NPY and AGRP, (2)
activation of POMC neurons that causes the release of -MSH and stimulates
melanocortin receptors (MCR), (3) increase production corticotropin releasing
hormone (CRH), which suppress hunger ,
E. Headache
ETIOLOGY

The cause of muscle tension headache is still unknown. allegedly can they
are due to psychological factors and physical factor. Psychologically, this
headache arising from the body's reaction to stress, anxiety, depression and
emotional conflict.

While physically, the position of the head is settled resulting in muscle

contraction head and neck in the long term, lack of sleep, the error in a
sleeping position and fatigue can also cause muscle tension headache is. In
addition, certain positions which causes muscle contraction of the head

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 and neck is performed in conjunction with activities that require increased
eye function in the long term such as reading can also cause this type of
headache.

In addition to the causes mentioned above, there are several triggers that
can cause the incidence of this type of headache, among others, the
consumption of chocolate, cheeses and flavoring dishes (MSG). People
who used to drink coffee will also experience headaches when the
concerned not forget to drink coffee. If the headache is due to muscle
strain psychic influence then it will usually disappear after a period of
stress passed.

Pathophysiology

Some theories that cause headaches continue to grow until now. Such as,
the theory of cranial vasodilatation, activation of trigeminal peripheral,
localization and physiology second order trigeminovascular neurons,
cortical spreading depression, activation rostral brainstem.

Pain stimuli can be caused by the pressure, traction, displacement and

chemical process and inflammation of the nociceptors-nociceptors in pain-
sensitive structures in head. If these structures are located at or even above the
tentorium serebelli stimulated the pain will arise noticeably spread to the area in
front of the boundary line vertical drawn from both left and right ear over the top
of the head (the area frontotemporal and parietal anterior). The pain is transmitted
by the trigeminal nerve.

While the stimulation of structures sensitive to pain under tentorium (at

the posterior cranial fossa) roots with the upper cervical nerve branches peripheral
will cause pain in the back of the line, which is the area occipital, suboccipital and
cervical top. The pain is transmitted by the cranial nerves IX, X and spinal nerves
C-1, C-2 and C-3. But sometimes it can also root N. upper cervical and occipital
mayor will menjalarkan pain to the frontal and eye on the ipsilateral side. Has
demonstrated the close relationship between the trigeminal nucleus with upper

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cervical dorsal root segments. Trigemino cervical reflex can be demonstrated by
way of stimulation n.supraorbitalis and recorded by means of mounting electrodes
sternocleidomastoid muscle. Exteroceptive and nociceptive input from trigemino-
cervical reflex polysinaptic transmitted through the route, including the spinal
trigeminal nuclei and reach cervical motorneuron. Given this connection it is clear
that the area of the neck pain can perceived or forwarded towards the head and
vice versa.

One of the most popular theories about the causes of headache are
contraction of facial muscles, neck, and shoulders. The muscles are usually
involved, among others m. splenius capitis, m. temporalis, m. masseter, m.
sternocleidomastoideus, m. trapezius, m. cervical posterior, and m. levator
scapulae. The study said that people with headache. This may have facial muscle
tension and a larger head than people Another cause them more susceptible to
headaches after contraction muscle. These contractions can be triggered by body
position long maintained that cause tension in the muscles or wrong sleeping
position. There is also a said that patients with chronic headaches can be very
sensitive to pain general or increased pain to muscle contraction. A theory also
said the strain or stress which produces contractions the muscles around the skull
causes vasoconstriction of blood vessels that flow reduced blood oxygen and
causing delays accumulated results metabolism which will eventually cause pain.

Researchers are now starting to believe that the headache may occur as a result
of changes of certain chemicals in the brain "serotonin, endorphins, and several
other chemicals" which assists in nerve communication. This is similar to
biochemical changes associated with migraine. Although it is not known how
these chemicals fluctuate, there Assuming that this process activates pain
pathways to the brain and interfere the brain's ability to suppress pain. On the one
hand, the muscle tension in the neck and skin the head can cause headaches in
people with impaired chemicals.

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3. What is the differential diagnose and main diagnose based on the
scenario?
1. TB (Tuberculosis)
Etiology :
Typically caused by Mycobacterium tuberculosis (sometimes also by
Mycobacterium africanum and Mycobacterium bovis).

Epidemiology :
In 1995 approximately 1/3 of the world's population is infected by
Mycobacterium tuberculosis. In 1998 there were 3,617,047 cases of TB
were recorded around the world. Most of these TB cases (95%) and death
(98%) occurred in countries that are developing. Among them 75% are in
the productive age 20-49 years. Indonesia is a country with a TB
prevalence 3rd highest in the world after China and India. In 1998 an
estimated TB in China, India, and Indonesia respectively 1.828 million,
1.414 million, 591,000 cases.Estimates of the incidence of sputum smear
positive in Indonesia is 266 000 1998.

Clinical manifestation:
1. Fever. Usually subfebril resemble influenza fever. But sometimes it
can reach 40-41C body heat. Fever can be cured for a while and
can recur.
2. Cough / coughing up blood. Symptoms of this are found.
Coughing occurred because an irritation of the bronchi. Coughing
is necessary to out an inflammatory products out. The nature of the
cough begins with a dry cough (non-productive) and then after the
onset of inflammation becomes productive (produce sputum).
Further circumstances are such as coughing up blood because there
is a ruptured blood vessel. Usually persistent cough more than 2
weeks.

3. Shortness of breath. Shortness of breath will arise in the disease,

the infiltration is already covering half the lungs.
4. Chest pain. These symptoms are rarely found. Chest pain occurs

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 when the infiltration of inflammatory cells has reached the pleura,
causing pleurisy.
5. Malaise. TB disease is a chronic inflammatory disease.
Symptoms of anorexia, malaise often found to be no appetite, the
more lean body (BB down), headaches. Fever, muscle pain, night
sweats, etc. The symptoms of this malaise more and more severe
and occur irregularly intermittent.

Radiologically:

TB lesion location generally at the apex of the lung (apical segment of

the upper lobes or the apical segment of the lower lobe), but also on the
lower lobe (inferior part) or in the hilum area resembles lung tumors (eg
on endobronchial tuberculosis). At the beginning of the disease when the
lesion is still the hotbeds of pneumonia, radiology form of patches like a
cloud and with indistinct boundaries. When the lesion has been covered
with the shadow visible connective tissue in the form of spheres with
indistinct boundaries. These lesions are known to tuberculoma.
Radiological Another frequently accompanies pulmonary tuberculosis is a
thickening of the pleura (pleurisy), the mass of liquid in the bottom of the
lungs (pleural effusion / empyema), a black shadow on the edge
radiolucent lung / pleura (pneumothorax).
2. Pneumonia
Definition of Pneumonia:

Pneumonia is a disease of lower respiratory tract (lower respiratory tract

(LRT)) acute, usually caused by infection (Jeremy 2007). In fact

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 pneumonia is not a single disease. The causes can vary and there are
known sources of infection, with the main source of bacteria, viruses,
mikroplasma, mushrooms, various chemicals and particles. The disease
can occur at any age, although the most severe clinical manifestations
appear in children, the elderly and people with chronic diseases (Elin,
2008).

Etiology:
Pneumonia can be caused by a variety of microorganisms, namely
bacteria, viruses, fungi, and protozoa. Table 2.1 lists the microorganisms
and pathological problems that cause pneumonia (Jeremy 2007).

List of microorganisms that cause pneumonia

Bacterial infection Atipical Infection Fungus/Myco

Infection

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 Streptococcus Mycoplasma Aspergillus
pneumoniae pneumoniae Histoplasmosis
Haemophillus influenza Legionella Candida
Klebsiella pneumoniae pneumophillia Nocardia
Pseudomonasaeruginosa Coxiella burnetii
Gram-negative (E. Coli) Chlamydia psittaci

Viral infection Protozoa Other causes

infection

Influenza Pneumocytis Aspirasi

Coxsackie carinii Pneumonia lipoid
Adenovirus Toksoplasmosis Bronkiektasis
Sinsitial respiratori Amebiasis Fibrosis kistik

Epidemiology:

Annual incidence: 5-11 cases per 1,000 adults; 15-45% need

hospitalization in (1-4 cases), and 5-10% were treated in the ICU. The
incidence is highest in patients who are very young and elderly. Mortality:
5-12% of patients were hospitalized; 25-50% in ICU patients (Jeremy
2007).In the United States, the incidence of this disease reached 12 cases
per 1,000 adults. Death for outpatients is less than 1%, but mortality in
patients hospitalized is high at around 14% (Alberta Medical Association,
2002). In developing countries, about 10-20% of patients who require
hospitalization and mortality among these patients is higher, at around 30-
40% (Sajinadiyasa, 2011). In Indonesia alone, the incidence of this disease
is quite high, about 5-35% with deathreaches 20-50% (Farmacia, 2006).

Classification of Pneumonia

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a. Community-acquired pneumonia (community acquired pneumonia, CAP):
pneumonia acquired in the community is that of infection outside the hospital
environment. LRT infections that occurred within 48 hours after being treated
at the hospital in patients who had never been hospitalized for > 14 days
b. Acquired pneumonia of hospital (nosocomial): pneumonia that occur during
or more than 48 hours after hospital admission. This kind obtained during the
patient hospitalized (Farmacia, 2006). Nearly 1% of patients treated in the
hospital getting pneumonia during treatment. Similarly, patients who were
treated in the ICU, more than 60% will suffer from pneumonia
c. Aspiration pneumonia / anaerobic: infection by bacteroids and other
anaerobic organisms after aspiration of oropharyngeal and gastric juices.
Pneumonia is the usual type obtained in patients with depressed mental status,
and patients with impaired swallowing reflex (Jeremy 2007).
d. Opportunistic pneumonia: patients with immune suppression (eg, steroids,
chemotherapy, HIV) susceptible to infection by viruses, fungi, and
mycobacteria, in addition to other bacterial organisms.
e. Recurrent pneumonia: results and aneorob aerobic organisms that occur in
cystic fibrosis and bronchietacsis

Factors Affecting Occurrence of pneumonia known several factors

that influence the occurrence of pneumonia are:
a. Lung defense mechanisms
Lung trying to remove various microorganisms are inhaled as dust
particles and other materials that build up in the lungs. Some forms of this
mechanism among other forms of anatomical airways, coughing reflex,
mukosilier system, the system of phagocytosis carried out by specific cells
by eating the particles that reach the surface of the alveoli. When the
function is running well, the infection infectious material can be removed
from the respiratory tract, resulting in a healthy person would not have

23
 happened a serious infection .. Recurrent respiratory infections caused by
various components of pulmonary defense system that does not work well.
b. Colonization of bacteria in the respiratory tract
In the airway or quite a lot of bacteria that are komnesal. When their
number is increasing and reaches a concentration sufficient, the bacteria
then enter the lower respiratory tract and lungs, and failure mechanisms of
airway clearance, this situation manifests as disease. Microorganisms that
does not stick to the mucosal surface anaps channel will join with
respiratory secretions and carried along with the cleaning mechanism, so
there is no colonization.

c. Cleaning the airways of the lower respiratory tract infectious materials

and lungs repeatedly penetrated by various microorganisms of the upper
airways, but does not cause pain, it indicates the presence of a lung
defense mechanism is so efficient that can be swept clean of
microorganisms before they multiply and cause disease. Lung defense
against hazardous materials and infectious form of reflex cough, airway
constriction, also aided by the humoral immune response (Supandi, 1992).

Anamnesis:
The main complaint that often occurs in patients with pneumonia are
shortness
breathing, increased body temperature, and cough. In patients with
pneumonia,
cough usually occurs suddenly and does not decrease after taking a cough
medicine that is usually available in the market. Initially the cough is
nonproductive, but will further develop into a productive cough with
purulent mucus yellowish, greenish, and often malodorous. Patients
usually complain of high fever and chills. Their complaints of chest pain,
shortness of breath, increased respiratory rate, fatigue, and headaches
(Supandi, 1992; Jeremy, 2007; Alberta Medical Association, 2011).

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 Diagnosis:
The goal is to diagnose, identify complications, assess severity, and
determine the classification to help select antibiotics (Jeremy 2007).
Diagnosis is based principally on clinical pneumonia, whereas the chest x-
ray examination needs to be done to support the diagnosis, diamping to see
the extent of pathological abnormalities more accurately (Supandi, 1992).
Clinical Features:
Clinical features are usually preceded by acute respiratory infections parts
on for several days, followed by fever, chills, body temperature sometimes
exceeding 40oC, sore throat, muscle pain, and joint pain. Also
accompanied by a cough, with purulent sputum, sometimes bloody
(Supandi, 1992). In young or old patients and atypical pneumonia (eg
Mycoplasma), picture nonrespirasi (eg, confusion, rash, diarrhea) can
stand out (Jeremy,
2007).
Supporting investigation :
In laboratory tests a routine blood test found an increase in white
blood cells (White blood Cells, WBC) WBC count is usually obtained
15000-40000 / mm3, if it is caused by a virus or mikoplasme WBC count
may be normal or decreased (Supandi, 1992; Jeremy, 2007). In the state of
leukopenia erythrocyte sedimentation rate (ESR) is usually increased to
100 / mm3, and C-reactive protein to confirm a bacterial infection. Blood
gas identify respiratory failure (Jeremy 2007). Positive blood culture can
be 20-25% of untreated patients, Sometimes found elevated levels of
blood urea, creatinine but still within normal limits (Supandi, 1992).
Radiological pneumonia can not show significant differences between
viral infection by the bacteria. Pneumonia virus generally showed
interstitial infiltrates picture and hyperinflation. Pneumonia caused by the
bacteria Pseudomonas often show their bilateral infiltrates or
bronchopneumonia.
Management
a. Antibiotic therapy beginning: Describe the best guesses based on the

25
 classification of pneumonia and possible organism, because the results of
microbiological unavailable for 12-72 hours. But adjusted if there are
results and antibiotic sensitivity (Jeremy 2007).
b. Supportive measures: includes oxygen to maintain PaO2> 8 kPa (SaO2
<90%) and intravenous fluid resuscitation to ensure hemodynamic
stability. Assisted ventilation: ventilasinon invasive (eg, continuous
positive airway pressure (continuous positive airway pressure), or
mechanical ventilation may be required in respiratory failure.
Physiotherapy and bronchoscopy help sputum clearance (Jeremy 2007).

3. Lun
g

Abscess

Etiology:

Lung abscess is defined as necrosis of the pulmonary tissue and

formation of cavities containing necrotic debris or fluid caused by
microbial infection. The formation of multiple small (<2 cm) abscesses is
occasionally referred to as necrotizing pneumonia or lung gangrene. Both
lung abscess and necrotizing pneumonia are manifestations of a similar

26
pathologic process. Failure to recognize and treat lung abscess is
associated with poor clinical outcome.

In the 1920s, approximately one third of patients with lung abscess

died. Dr David Smith postulated that aspiration of oral bacteria was the
mechanism of infection. He observed that the bacteria found in the walls
of the lung abscesses at autopsy resembled the bacteria noted in the
gingival crevice. A typical lung abscess could be reproduced in animal
models via an intratracheal inoculum containing, not 1, but 4 microbes,
thought to be Fusobacteriumnucleatum, Peptostreptococcus species, a
fastidious gram-negative anaerobe, and, possibly,
Prevotellamelaninogenicus.

Lung abscess was a devastating disease in the preantibiotic era,

when one third of the patients died, another one third recovered, and the
remainder developed debilitating illnesses such as recurrent abscesses,
chronic empyema, bronchiectasis, or other consequences of chronic
pyogenic infections. In the early postantibiotic period, sulfonamides did
not improve the outcome of patients with lung abscess. After penicillins
and tetracyclines became available, outcomes improved. Although
resectional surgery was often considered a treatment option in the past, the
role of surgery has greatly diminished over time because most patients
with uncomplicated lung abscess eventually respond to prolonged
antibiotic therapy.

Lung abscesses can be classified based on the duration and the

likely etiology. Acute abscesses are less than 4-6 weeks old, whereas
chronic abscesses are of longer duration. Primary abscesses are infectious
in origin, caused by aspiration or pneumonia in the healthy host.
Secondary abscesses are caused by a preexisting condition (eg,
obstruction), spread from an extrapulmonary site, bronchiectasis, and/or an
immunocompromised state. Lung abscesses can be further characterized

27
 by the responsible pathogen, such as Staphylococcus lung abscesses and
anaerobic abscess or Aspergillus lung abscess.

Epidemiology :

Frequency

The frequency of lung abscesses in the general population is not known.

Sex
A male predominance for lung abscess is reported in published case series.
Age
Lung abscesses likely occur more commonly in elderly patients because of
the increased incidence of periodontal disease and the increased
prevalence of dysphagia and aspiration. However, a case series from an
urban center with high prevalence of alcoholism reported a mean age of 41
years
Clinical Presentation

Symptoms depend on whether the abscess is caused by anaerobic or other

bacterial infection. A lung abscess may be asymptomatic in a small
proportion of patients in the early stages. Typical symptoms are below.

Anaerobic infection in lung abscess

Patients often present with indolent symptoms that evolve over a period of
weeks to months. The usual symptoms are fever, cough with sputum
production, night sweats, anorexia, and weight loss. The expectorated

28
 sputum characteristically is foul smelling and bad tasting. Patients may
develop hemoptysis or pleurisy

Other pathogens in lung abscess

These patients generally present with conditions that are more acute in
nature and are usually treated while they have bacterial pneumonia.
Cavitation occurs subsequently as parenchymal necrosis ensues. Abscesses
from fungi, Nocardia species, and Mycobacteria species tend to have an
indolent course and gradually progressive symptoms.

Radiology:

The classical appearance of a

pulmonary abscess is a cavity
containing an air-fluid level. In
general abscesses are round in
shape, and appear similar in both
frontal and lateral projections.
Additionally all margins are
equally well seen, although
adjacent consolidation may make
assessment of this difficult. These features are helpful in distinguishing a
pulmonary abscess from an empyema

4. Bronchiectasis

Etiology:

Causes of bronchiectasis include the following:

29
 Primary infections

Bronchial obstruction

Aspiration

Cystic fibrosis

Primary ciliary dyskinesia

Allergic bronchopulmonaryaspergillosis

Immunodeficiency states

Congenital anatomic defects

Connective-tissue disorders

Alpha1-antitrypsin (AAT) deficiency

Autoimmune diseases

Idiopathic inflammatory disorders

Autosomal dominant polycystic kidney disease

Traction from other processes

Toxic gas exposure

Primary infections

Bronchiectasis may be the sequela of a variety of necrotizing infections

that are either inadequately treated or not treated at all. Primary infection

30
 (ie, in the absence of intrinsic defects or noninfectious extrinsic insults)
was a particularly common cause of bronchiectasis in developed countries
prior to the widespread use of antibioticsand it remains important in
developing countries, where antibiotics are used inconsistently.

Typical offending organisms that have been known to cause bronchiectasis

include the following:

Klebsiella species

Staphylococcus aureus

Mycobacterium tuberculosis

Mycoplasma pneumoniae

Nontuberculous mycobacteria

Measles virus

Pertussis virus

Influenza virus

Herpes simplex virus

Certain types of adenovirus

Infection with respiratory syncytial virus in childhood may also result in

bronchiectasis.

Mycobacterium avium complex (MAC) infection deserves special

mention. It has a propensity to occur in the setting of human immunodeficiency
virus (HIV) infection as well as in hosts who are immunocompetent.

31
 MAC infection has been observed especially in women who are
nonsmokers; are older than 60 years; do not have a known predisposing
pulmonary disorder; and tend to voluntarily suppress cough. Sputum smear in
these cases is positive for acid-fast bacilli, and CT scan shows small regular
nodules and findings of bronchiectasis.

Once a patient develops bronchiectasis, many of these same organisms

colonize the damaged bronchi and may cause ongoing damage and episodic
infectious exacerbations. The organisms found most typically include
Haemophilus species (47-55% of patients) and Pseudomonas species (18-26% of
patients).

Although not a primary cause of bronchiectasis, P aeruginosa often causes

chronic bronchial infection in patients with non-CF bronchiectasis via a
mechanism involving biofilm formation and the release of virulence factors. This
suggests that Pseudomonas species may promote disease progression, and that
infection with these species may be related to worsening lung function and
increased morbidity and mortality.

Bronchial obstruction

Focal postobstructive bronchiectasis may occur in a number of clinical

settings (eg, endobronchial tumors, broncholithiasis, bronchial stenosis from
infections, encroachment of hilar lymph nodes, foreign body aspiration). Right-
middle lobe syndrome is a specific type of bronchial obstruction that may result in
bronchiectasis. It results from an abnormal angulation of the lobar bronchus at its
origin, predisposing it to obstruction, subsequent infection, and development of
bronchiectasis.

32
Aspiration

In adults, foreign body aspiration often takes place in the setting of altered
mental status and involves unchewed food. Patients may also aspirate chewed
materials from the stomach, including food, peptic acid, and microorganisms.

After aspiration, a postobstructive pneumonia may occur, with subsequent

development of focal bronchiectasis. Bronchiectasis may also develop in the
setting of chronic aspiration. Further recognized is that a history of
gastroesophageal reflux is a risk factor for aspiration and that the organism
Helicobacter pylori may play a role in the development of bronchiectasis in this
group of patients.

Cystic fibrosis

CF is a multisystem disorder that affects the chloride transport system in

exocrine tissues, primarily secondary to a defect in the CF transmembrane
regulator (CFTR) protein. CF and its variants are the most common cause of
bronchiectasis in the United States and other industrialized nations.

CF is an autosomal recessive disease affecting approximately 1 in 2,500

whites and 1 in 17,000 blacks in the United States. In was estimated that in 2005,
10,000 adults in the United States would have CF, comprising 40% of the total CF
population.

Multiple genetic variants of CF exist, and the risk to patients that have
genetic heterozygous mutations remains to be elucidated. However, a reasonable
assumption is that patients with CF can be divided into 2 groups: (1) those with
classic disease that is readily diagnosed based on clinical and laboratory data and
(2) those with less severe disease that manifests later in life and who have
ambiguous genetic testing results.

The major pulmonary finding in CF is bronchiectasis, which is an almost

universal feature of this disease. It may be the sole feature of CF in adults or those

33
with genetic variations of the disease. Bronchiectasis associated with CF is
believed to occur secondary to mucous plugging of proximal airways and chronic
pulmonary infection, especially with mucoidP aeruginosa.

Young syndrome

Young syndrome is clinically similar to CF and may represent a genetic

variant of CF. It is most often observed in middle-aged men in North America and
is a leading cause of male infertility.

Patients with Young syndrome have bronchiectasis (often predominant in

the lower lobes), sinusitis, and obstructive azoospermia. However, they do not
display the other findings of CF. The pathogenesis of bronchiectasis in these
patients is believed to be similar to that of bronchiectasis in CF. The criterion
standard for diagnosis of Young syndrome is electron microscopic analysis of the
structure of the cilia.

Primary ciliary dyskinesia

Primary ciliary dyskinesia is a group of inherited disorders that may affect

1 in 15,000-30,000 population. It is manifested by immotile or dyskinetic cilia
and/or sperm. This may lead to poor mucociliary clearance, recurrent pulmonary
infections, and, ultimately, bronchiectasis.

A variant of this condition, initially described by Kartagener, encompassed

the clinical triad of situsinversus, nasal polyps or sinusitis, and bronchiectasis in
the setting of immotile cilia of the respiratory tract.

Allergic bronchopulmonaryaspergillosis

Allergic bronchopulmonaryaspergillosis (ABPA) is a hypersensitivity

reaction to inhaled Aspergillus antigen that is characterized by bronchospasm,
34
bronchiectasis, and immunologic evidence of a reaction to
AspergillusspeciesABPA should be suspected in patients with a productive cough
who also have a long history of asthma-type symptoms that do not respond to
conventional therapy.

Bronchiectasis is believed to be secondary to airway plugging by viscid

secretions containing hyphae of Aspergillus species. The resulting bronchiectasis
is thin-walled and affects the central and medium-sized airways.

CT scanning of the chest demonstrates central airway bronchiectasis,

differentiating this condition from other causes of bronchiectasis. Other features
of ABPA include eosinophilia, elevated immunoglobulin E (IgE) levels, and
dramatic responses to therapeutic corticosteroids.

Immunodeficiency states

Immunodeficiency states may be congenital or acquired. The most common

congenital conditions (albeit rare) involve B-lymphocyte functions.
Hypogammaglobulinemia in these cases may take one of the following forms] :

Immunoglobulin G (IgG) subclass deficiency

X-linked agammaglobulinemia

Immunoglobulin A (IgA) deficiency

Immunoglobulin M (IgM) deficiency

Immunoglobulin E (IgE) deficiency

Patients with hypogammaglobulinemia usually present in childhood with

repeated sinus or pulmonary infections, although the disorder has been diagnosed

35
in adults who did not have a history of repeated infections. Establishing the
diagnosis is important because gammaglobulin replacement may reduce the
number of infections and resultant lung injury.

HIV disease, with resultant acquired immunodeficiency syndrome (AIDS),

has been implicated in the development of bronchiectasis and demonstrates the
accelerated bronchial damage that may occur from repeated infections in patients
who are immunosuppressed. Bronchiectasis in HIV infection has occurred with
and without obvious preceding pulmonary infection and may occur secondary to
immunologic dysfunction from the HIV disease itself.

Congenital anatomic defects

Bronchiectasis can result from a variety of congenital anatomic defects.

Bronchopulmonary sequestration is a congenital abnormality classified as either
intralobar or extralobar and results in chronic lower respiratory tract infections
that lead to bronchiectasis.

Williams-Campbell syndrome (congenital cartilage deficiency) is the

absence of cartilage from lobar to first- to second-generation segmental airways
that results in extensive peripheral bronchiectasis.

Mounier-Kuhn syndrome (tracheobronchomegaly) is a rare disorder

characterized by dilation of the trachea and segmental bronchi (central
bronchiectasis).

Swyer-James syndrome (unilateral hyperlucent lung) likely is a

developmental disturbance that leads to unilateral bronchiolitis, hyperinflation,
and, in some cases, bronchiectasis.

Yellow-nail syndrome is rare. It results in exudative pleural effusions.

36
Alpha1-antitrypsin (AAT) deficiency

Bronchiectasis has been noted to occur in this rare condition, both in

patients with true AAT deficiency and in patients with heterozygous phenotypes.

The pathogenesis of bronchiectasis in this setting is unclear, but it is

believed that the AAT abnormalities make patients more susceptible to respiratory
tract infections and subsequent bronchial damage.

Epidemiology:

Currently no systematic data are available on the incidence or prevalence

of bronchiectasis. A general theory is that the emergence of vaccines and
antibiotics in the 20th century resulted in a decline in the rate of bronchiectasis in
developed countries.

The best data available suggest that the prevalence of bronchiectasis

mirrors the socioeconomic conditions of the population under study, with
significantly lower prevalence in areas where immunizations and antibiotics are
readily available. Bronchiectasis remains a major cause of morbidity in less-
developed countries, especially in countries with limited access to medical care
and antibiotic therapy.

Clinical Presentation:

The classic clinical manifestations of bronchiectasis are cough and daily

mucopurulent sputum production, often lasting months to years. Blood-streaked
sputum or hemoptysis may result from airway damage associated with acute
infection. Less specific symptoms include dyspnea, pleuritic chest pain, wheezing,
fever, weakness, and weight loss.

A rare variant known as dry bronchiectasis manifests as episodic

hemoptysis with little-to-no sputum production. Dry bronchiectasis is usually a
sequela of tuberculosis and is found in the upper lobes.

37
 Although patients may report repetitive pulmonary infections that require
antibiotics over several years, a single episode of a severe infection, often in
childhood, may result in bronchiectasis. These include tuberculosis, pertussis, or
severe bacterial pneumonia. Today, CF is the most common cause of
bronchiectasis in children and young adults.

Chronic wet cough may also be an indicator of bronchiectasis. In a

retrospective study of 144 Australian children with a chronic wet cough, Goyal
and colleagues found that those whose cough did not resolve after 4 weeks of
treatment with oral antibiotics were 20 times more likely to have bronchiectasis.
All children underwent chest multi-detector CT (MDCT) scans. Of the 144
children, 106 exhibited evidence of bronchiectasis on their MDCT scan.

Exacerbations of bronchiectasis that are caused by acute bacterial

infections are often heralded by the onset of increased sputum production over
baseline, increased viscidity of sputum, and, occasionally, a foul odor of the
sputum. Rarely, low-grade fever may occur. Patients may experience an increase
in generalized constitutional symptoms, such as fatigue and malaise, as well as
increased dyspnea, shortness of breath, wheezing, or pleuritic pain.

With secondary infection or poorly treated pneumonia, the discrete

pathogens are often unknown. However, most patients relate a history of
childhood infections that may include tuberculosis, pertussis, or Mycoplasma
infection.

Most individuals have never smoked (55%) or have smoked too little to
account for their degree of cough, findings of obstruction on spirometry testing,
and daily sputum production.

Chronic productive cough is prominent,occurring in up to 98% of patients.

Sputum is typically produced on a daily basis in greater than 70% of patients, with
one study reporting production in 96% of patients. Some patients produce sputum

38
only with acute upper respiratory tract infections, but otherwise they have
quiescent disease.

Sputum is typically mucoid and relatively odorless. During infectious

exacerbations, however, sputum becomes purulent and may develop an offensive
odor.

Hemoptysis occurs in 56-92% of patients with bronchiectasis. Hemoptysis

is more commonly observed in dry bronchiectasis. Hemoptysis is generally mild
and manifested by blood flecks in the patient's usual purulent sputum. This is
often the factor that leads patients to consult a physician. Bleeding usually
originates from dilated bronchial arteries, which contain blood at systemic (rather
than pulmonary) pressures. Therefore, massive hemoptysis may occur but is rarely
a cause of death.

Dyspnea may occur in as many as 72% of patients; a 2006 review reported

a rate of 62%.Dyspnea typically occurs in patients with extensive bronchiectasis
observed on chest radiographs. Marked dyspnea is more likely to be secondary to
a concomitant illness, such as chronic bronchitis or emphysema.

Wheezing is commonly reported and may be due to airflow obstruction

following destruction of the bronchial tree. Similar to dyspnea, it may also be
secondary to concomitant conditions such as asthma.

Pleuritic chest pain is an intermittent finding, occurring in 19-46% of

patients. It is most commonly secondary to chronic coughing but also occurs in
the setting of acute exacerbation.

Fatigue is commonly reported (73% of patients). Weight loss often occurs

in patients with severe bronchiectasis. This is believed to be secondary to
increased caloric requirements associated with the increased work of coughing

39
and clearing secretions. Weight loss suggests advanced disease but is not
diagnostic of bronchiectasis.

Fever may occur in the setting of acute infectious exacerbations.

Radiology:
Chest x-rays are usually abnormal, but
are inadequate in the diagnosis or
quantification of bronchiectasis. Tram-
track opacities are seen in cylindrical
bronchiectasis, and air-fluid levels may
be seen in cystic bronchiectasis.
Overall there appears to be an increase
in bronchovascular markings, and
bronchi seen end on may appear as
ring shadows. Pulmonary vasculature
appears ill-defined, thought to represent peribronchovascular fibrosis

5. Lung Cancer
Epidemiology
The reported prevalence of pain in patients with lung cancer is 28%-51%

Etiology
The main cause of lung cancer is smoking, although non-smokers can also
develop the condition. Smoking and other risk factors for lung cancer are
described below.
Smoking is the cause of lung cancer in more than 90% of cases and is the
single biggest risk factor for lung cancer. There are more than 60 different
toxins in tobacco smoke that can cause cancer and these are referred to as
carcinogens.
Although tobacco smoking is the main risk factor for lung cancer, other
tobacco products such as pipe tobacco, cigars, chewing tobacco and snuff

40
 can also raise the risk of lung cancer and other forms of cancer such as
mouth cancer and esophageal cancer.

Symptoms
Cough
Dyspnea
Hoarseness
Chest pain
Wheezing
Hemoptysis
Nausea/Vomiting
Swelling of face and arms
Anorexia
Weight Loss
Fatigue
Bone pain
Clubbing
Headache
Seizures

Radiology

41
6. Pneumonia Aspiration
Epidemiology

Nevertheless, several studies in- dicate that 5 to 15 percent of cases of

community- acquired pneumonia are aspiration pneumonia.5-7 Aspiration
pneumonia is the most common cause of death in patients with dysphagia
due to neurologic disorders, a condition that affects approximately300,000
to 600,000 people each year in the United States.

Etiology

Aspiration pneumonia is caused by bacteria that normally reside in the oral

and nasal pharynx. Historically, aspiration pneumonia referred to an
infection caused by less virulent bacteria, primarily oral pharyngeal
anaerobes. It is now recognized that the many common community-
acquired and hospital-acquired pneumonias result from the aspiration of
pathogens from the oral cavity or nasopharynx. The micro-organisms that
commonly cause these pneumonias, such as Streptococcus
pneumoniae,Haemophilus influenza, Staphylococcus aureus, and gram-
negative bacteria, are relatively virulent so that only a small inoculum is
required to result in a pneumonia. The aspiration episode is often subtle.
The inoculum in what was traditionally recognized as aspiration
pneumonia was larger and typically apparent.

Symptoms

The signs and symptoms of aspiration pneumonia vary. The predominant

symptoms may be headache, low- grade fever, pleuritic pain, myalgia,
rash, and pharyngi- tis. After a few days, the patient expectorates mucoid
or mucopurulent sputum. In severe pneumonia, the patients cheeks are
flushed and central cyanosis affects the lips and nail beds, a late sign of
poor oxygenation (hypoxemia).

Radiology

42
4. Mention the pathogenesis of diagnose based on the scenario?

After inhalation, the droplet nucleus is carried down the bronchial

tree and implants in a respiratory bronchiole or alveolus. Whether or not
an inhaled tubercle bacillus establishes an infection in the lung depends on
both the bacterial virulence and the inherent microbicidal ability of the
alveolar macrophage that ingests it (4, 18). If the bacillus is able to survive
initial defenses, it can multiply within the alveolar macrophage. The
tubercle bacillus grows slowly, dividing approximately every 25 to 32
hours within the macrophage. Mycobacterium tuberculosis has no known
endotoxins or exotoxins; therefore, there is no immediate host response to
infection. The organisms grow for 2 to 12 week, until they reach 103 to
104 in number, which is sufficient to elicit a cellular immune response that
can be detected by a reaction to the tuberculin skin test.

Before the development of cellular immunity, tubercle bacilli

spread via the lymphatics to the hilar lymph nodes and thence through the
bloodstream to more distant sites. Certain organs and tissues are notably
resistant to subsequent multiplication of these bacilli. The bone marrow,
liver, and spleen are almost always seeded with mycobacteria, but
uncontrolled multiplication of the bacteria in these sites is exceptional.
Organisms deposited in the upper lung zones, kidneys, bones, and brain
may find environments that favor their growth, and numerous bacterial
divisions may occur before specific cellular immunity develops and limits
multiplication. In persons with intact cell-mediated immunity, collections
of activated T cells and macrophages form granulomas that limit
multiplication and spread of the organism. Antibodies against M.
tuberculosis are formed but do not appear to be protective. The organisms
tend to be localized in the center of the granuloma, which is often necrotic.
For the majority of individuals with normal immune function, proliferation
of M. tuberculosis is arrested once cell-mediated immunity develops, even
though small numbers of viable bacilli may remain within the granuloma.

43
Although a primary complex can sometimes be seen on chest radiograph,
the majority of pulmonary tuberculosis infections are clinically and
radiographically inapparent. Most commonly, a positive tuberculin skin
test result is the only indication that infection with M. tuberculosis has
taken place. Individuals with latent tuberculosis infection but not active
disease are not infectious and thus cannot transmit the organism. It is
estimated that approximately 10% of individuals who acquire tuberculosis
infection and are not given preventive therapy will develop active
tuberculosis.

The risk is highest in the first 2 year after infection, when half the
cases will occur. The ability of the host to respond to the organism may be
reduced by certain diseases such as silicosis, diabetes mellitus, and
diseases associated with immunosuppression, e.g., HIV infection, as well
as by corticosteroids and other immunosuppressive drugs. In these
circumstances, the likelihood of developing tuberculosisdisease is greater.
The risk of developing tuberculosis also appears to be greater during the
first 2-yr of life.

HIV-infected persons, especially those with low CD4 1 cell counts,

develop tuberculosis disease rapidly after becoming infected with M.
tuberculosis; up to 50% of such persons may do so in the first 2 yr after
infection with M. tuberculosis. Conversely, an individual who has a prior
latent infection with M. tuberculosis (not treated) and then acquires HIV
infection will develop tuberculosis disease at an approximate rate of 5
10% per year.

In a person with intact cell-mediated immunity, the response to

infection with the tubercle bacillus provides protection against reinfection.
The likelihood of reinfection is a function of the risk of reexposure, the
intensity of such exposure, and the integrity of the hosts immune system.
In the United States the risk of reexposure to an infectious case is low.
Furthermore, in an otherwise healthy, previously infected person, any

44
 organisms that are deposited in the alveoli are likely to be killed by the
cell-mediated immune response. Exceptions may occur, but in
immunocompetent individuals, clinical and laboratory evidence indicates
that disease produced by the inhalation of a second infecting strain is
uncommon. However, reinfection has been documented to occur both in
persons without recognized immune compromise and in persons with
advanced HIV infection.

5. Mention the classification of diagnose based on the scenario?

1 Classification based on anatomical site of disease

Pulmonary tuberculosis (PTB) refers to any bacteriologically confirmed

or clinically diagnosed case of TB involving the lung parenchyma or the
tracheobronchial tree. Miliary TB is classified as PTB because there are
lesions in the lungs. Tuberculous intra-thoracic lymphadenopathy
(mediastinal and/or hilar) or tuberculous pleural effusion, without
radiographic abnormalities in the lungs, constitutes a case of
extrapulmonary TB. A patient with both pulmonary and extrapulmonary
TB should be classified as a case of PTB.

Extrapulmonary tuberculosis (EPTB) refers to any bacteriologically

confirmed or clinically diagnosed case of TB involving organs other than
the lungs, e.g. pleura, lymph nodes, abdomen, genitourinary tract, skin,
joints and bones, meninges.

2. Classification based on history of previous TB treatment

(patient registration group)

Classifications based on history of previous TB treatment are slightly

different from those previously published.They focus only on history of
previous treatment and are independent of bacteriological confirmation or site

45
 of disease. Note also that the registration groups for DR-TB are slightly
different and are described in the Companion handbook to the WHO guidelines
for the programmatic management of drug- resistant tuberculosis.New patients
have never been treated for TB or have taken anti-TB drugs for less than 1
month.

Previously treated patients have received 1 month or more of anti-TB

drugs in the past. They are further classified by the outcome of their most recent
course of treatment as follows:

- Relapse patients have previously been treated for TB, were declared
cured or treatment completed at the end of their most recent course
of treatment, and are now diagnosed with a recurrent episode of TB
(either a true relapse or a new episode of TB caused byreinfection).

- Treatment after failure patients are those who have previously

been treated for TB and whosetreatment failed at the end of their
most recent course of treatment.

- Treatment after loss to follow-up patients have previously been

treated for TB and were declared lost to follow-up at the end of their
most recent course of treatment. (These were previously known as
treatment after defaultpatients.)

- Other previously treated patients are those who have previously been
treated for TB but whose outcome after their most recent course of
treatment is unknown or undocumented.

Patients with unknown previous TB treatment history do not fit into any
of the categories listed above. New and relapse cases of TB are incident TB
cases.

3. Classification based on HIV status

HIV-positive TB patient refers to any bacteriologically confirmed or

clinically diagnosed case of TB who has a positive result from HIV testing

46
conducted at the time of TB diagnosis or other documented evidence of
enrolment in HIV care, such as enrolment in the pre-ART register or in the ART
register once ART has been started.

HIV-negativeTB patient refers to any bacteriologically confirmed or

clinically diagnosed case of TB who has a negative result from HIV testing
conducted at the time of TB diagnosis. Any HIV-negative TB patient
subsequently found to be HIV-positive should be reclassified accordingly.

HIV status unknown TB patient refers to any bacteriologically

confirmed or clinically diagnosed case of TB who has no result of HIV testing
and no other documented evidence of enrolment in HIV care. If the patients
HIV status is subsequently determined, he or she should be reclassified
accordingly.

4. Classification based on drug resistance

Cases are classified in categories based on drug susceptibility

testing (DST) of clinical isolates confirmed to be M. tuberculosis:

- Monoresistance: resistance to one first-line anti-TB drug only.

- Polydrug resistance: resistance to more than one first-line anti-TB
drug (other than both isoniazid and rifampicin).
- Multidrug resistance: resistance to at least both isoniazid and
rifampicin.
- Extensive drug resistance: resistance to any fluoroquinolone and to at
least one of three second-line
- injectable drugs (capreomycin, kanamycin and amikacin), in addition
to multidrug resistance.
- Rifampicin resistance:1 resistance to rifampicin detected using
phenotypic or genotypic methods, with or without resistance to other
anti-TB drugs. It includes any resistance to rifampicin, whether

47
 monoresistance, multidrug resistance, polydrug resistance or
extensive drug resistance.
These categories are not all mutually exclusive. When enumerating
rifampicin-resistant TB (RR-TB), for instance, multidrug-resistant TB
(MDR-TB) and extensively drug-resistant TB (XDR-TB) are also
included.

While it has been the practice until now to limit the definitions of
monoresistance and polydrug resistance to first-line drugs only, future
drug regimens may make it important to classify patients by their strain
resistance patterns to fluoroquinolones, second-line injectable agents and
any other anti-TB drug for which reliable DST becomes available.

6. Mention the clinical manifestation based on the scenario?

Symptoms of Tuberculosis disease can be divided into general symptoms and

specific symptoms that arise according to the organ involved. Clinical picture is
not too distinctive or not specific, so it is quite difficult to diagnose in clinic.

Systemic symptoms / general:

Coughing for more than 3 weeks, can be accompanied by blood (hemoptysis)

Fever is not too high that lasts longer, usually felt at night and accompanied with
night sweats. Sometimes, fever attack present but occur intermittent such as,
influenza

Loss of appetite and weight loss

feeling unwell (malaise), weakness

Special symptoms:

Wheezing

48
 In the case of blockage of bronchi, it would create wheezing sound. This
is cause by the compression by enlarged lymph nodes. Wheezing sound is
weakened voice accompanied by shortness of breath.

Chest pain

If there is fluid in the pleural cavity(cavum pleura), can be accompanied with

complaints of chest pain.

Extra PulmonalTuberculosis

-- Bone tuberculosis

When the bone is infected, there will be symptoms such as bone infection
where the surface of the skin excrete pus.
--Meningitis TuberculosisTuberculosis can affect the brain (especially on the layer
that surround the brain) referred to as meningitis (inflammation of the lining of
the brain), the symptoms are high fever, the loss of consciousness and
convulsions.

In pediatric patients, Tuberculosis show no typical symptoms, where

tuberculosis can be detected if there is history of contacts with adult with
tuberculosis. Approximately 30-50% of children contact with adult pulmonary
tuberculosis patients give positive tuberculin test results. In children aged 3
months - 5 years who live with pulmonary tuberculosis patients adults with
positive smear, reported that 30% of them being infected, detected by serology
and blood examination.

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50
 7. Mention the general and supportive examination based on the scenario?

TB is a disease caused by Mycobacterium tuberculosis. TB disease should be

suspected in persons who have the following symptoms:

Unexplained weight loss

Loss of appetite

Night sweats

Fever

Fatigue

If TB disease is in the lungs (pulmonary), symptoms may include:

Coughing for longer than 3 weeks

Hemoptysis (coughing up blood)

Chest pain

If TB disease is in other parts of the body (extrapulmonary), symptoms will depend

on the area affected.

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How Do You Evaluate Persons Suspected of Having TB Disease?

A complete medical evaluation for TB includes the following:

1. Medical History

Clinicians should ask about the patients history of TB exposure, infection, or disease.
It is also important to consider demographic factors (e.g., country of origin, age, ethnic or
racial group, occupation) that may increase the patients risk for exposure to TB or to drug-
resistant TB. Also, clinicians should determine whether the patient has medical conditions,
especially HIV infection, that increase the risk of latent TB infection progressing to TB
disease.

2. Physical Examination

A physical exam can provide valuable information about the patients overall
condition and other factors that may affect how TB is treated, such as HIV infection or other
illnesses.

3. Test for TB Infection

The Mantoux tuberculin skin test (TST) or the TB blood test can be used to test
for M. tuberculosis infection. Additional tests are required to confirm TB disease. The
Mantoux tuberculin skin test is performed by injecting a small amount of fluid called
tuberculin into the skin in the lower part of the arm. The test is read within 48 to 72 hours by
a trained health care worker, who looks for a reaction (induration) on the arm.

The TB blood test measures the patients immune system reaction to M. tuberculosis.

4. Chest Radiograph

A posterior-anterior chest radiograph is used to detect chest abnormalities. Lesions

may appear anywhere in the lungs and may differ in size, shape, density, and cavitation.
These abnormalities may suggest TB, but cannot be used to definitively diagnose TB.
However, a chest radiograph may be used to rule out the possibility of pulmonary TB in a
person who has had a positive reaction to a TST or TB blood test and no symptoms of
disease.

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5. Diagnostic Microbiology

The presence of acid-fast-bacilli (AFB) on a sputum smear or other specimen often

indicates TB disease. Acid-fast microscopy is easy and quick, but it does not confirm a
diagnosis of TB because some acid-fast-bacilli are not M. tuberculosis. Therefore,
a culture is done on all initial samples to confirm the diagnosis. (However, a positive culture
is not always necessary to begin or continue treatment for TB.) A positive culture for M.
tuberculosisconfirms the diagnosis of TB disease. Culture examinations should be completed
on all specimens, regardless of AFB smear results. Laboratories should report positive results
on smears and cultures within 24 hours by telephone or fax to the primary health care
provider and to the state or local TB control program, as required by law.

6. Drug Resistance

For all patients, the initial M. tuberculosis isolate should be tested for drug resistance.
It is crucial to identify drug resistance as early as possible to ensure effective treatment. Drug
susceptibility patterns should be repeated for patients who do not respond adequately to
treatment or who have positive culture results despite 3 months of therapy. Susceptibility
results from laboratories should be promptly reported to the primary health care provider and
the state or local TB control program.

8. Mention the complication based on the scenario?

Pulmonary tuberculosis, if not handled properly will cause complications. The

complications that occur in patients with pulmonary tuberculosis can be divided into two,
namely:

1. Early complications: pleurisy, pleural effusion, empyema, laryngitis, intestines.

2. Complications at an advanced stage:

The complications are common in patients with advanced stage are:

a. Massive hemoptysis (bleeding from the lower respiratory tract) that can cause death
due to airway obstruction or hypovolemic shock

b. Lobar collapse due to blockage of the duct

c. Bronkietaksis (local bronchial dilation) and fibrosis (formation of connective tissue

in the recovery process or reactive) in the lungs

53
 d. Pnemotoraks spontaneously, that collapse spontaneously because the bull / blep
broken

e. The spread of infection to other organs such as the brain, bones, joints, kidneys, etc.

9. Mention the management based on the scenario?

TB treatment is aimed at;

a. Curing patients and restore the quality of life and productivity.

b. Preventing death.

c. Prevent recurrence.

d. Reduce transmission.

e. Preventing drug resistance

Treatment of tuberculosis carried by the principle - the principle as following:

OAT must be given in the form of a combination of several types of drugs, in sufficient
quantities and appropriate doses according to the category of treatment. Do not use OAT
alone (monotherapy). usage OAT Combination Fixed Dose (OAT-KDT) more profitable
and highly recommended.

To ensure patient compliance swallowing the drug, do direct supervision (DOT =

Directly Observed Treatment) by a Supervisory Swallowing Drugs (PMO)

TB treatment is given in two stages, namely intensive and continuation phases.

1. Early Stage (Intensive)

54
 In the intensive phase (early) patients received the drug every day and need directly
supervised to prevent the development of drug resistance. When The intensive phase of
treatment given correctly, usually infectious patients become non-infectious within 2
weeks.

Most patients with sputum smear positive TB negative (conversion) within 2 months.

2. Secondary Phase

In the advanced stages patients received fewer types of drugs, but in a longer period
of time. Advanced stages it is important to kill germs persistent so as to prevent the
occurrence of recurrence.

OAT alloys used in Indonesia, namely:

a. Category I

- Pulmonary tuberculosis (new cases), smear positive or lesions on chest radiograph

contained large.

- Alloy drugs recommended is 2 RHZE / 4 RH or 2 RHZE / 6HE or 2 RHZE / 4R3H3.

b. Category II

- Pulmonary tuberculosis relapse cases.

Alloy drugs recommended is 2 RHZES / 1 RHZE before No resistance test results. If the
test of resistance have been there, give according to the drug resistance test results.

- Pulmonary TB treatment failure cases

Alloy drugs recommended are the second-line drugs before there are results resistance
test (example: 3-6 months kanamycin, ofloxacin, ethionamide, cycloserine followed 15-
18 months ofloxacin, ethionamide, cycloserine).

Under no circumstances do not allow the initial phase can be given 2 RHZES / 1 RHZE.

continuation phase in accordance with the results of resistance testing.

If there is no resistance test results, can be given 5 RHE.

55
3. Pulmonary TB withdrawing treatment.

1. Treated 4 months

- BTA is currently negative. Clinical and radiological inactive or no repair the OAT
treatment is stopped. when the picture radiology active, perform further analysis to ensure
TB diagnosis by also considering the possibility of another lung disease. If confirmed TB,
the treatment begins from the start with a stronger regimen and run longer treatment time
(2 RHZES / 1 RHZE / 5R3H3E3).

- BTA is currently positive. Treatment starts from the beginning with alloy stronger
medication and treatment period longer.

2. Treated 4 months

- When the smear-positive, treatment starts from the beginning with alloys stronger
medication and long treatment times long (2 RHZES / 1 RHZE / 5 R3H3E3).

- When the smear negative, positive chest X-ray picture of active TB,treatment continued.

c. Category III

- Pulmonary tuberculosis (new cases), smear negative or lesions on chest radiograph

contained minimal.

- Alloy drug administered is 2RHZE / 4 R3H3.

d. Category IV

- Chronic pulmonary tuberculosis cases. Regimen is recommended when there is no

resistance test results, give RHZES. If there has been a resistance test results, provide
appropriate resistance test results (minimum OAT sensitive plus second-line drugs
(medication at least 18 months).

e. Category V

- MDR TB, the recommended treatment regimen in accordance with the resistance test
plus OAT lines 2 or H lifetime.

56
TB drugs have side effects including:

1. Isoniazid can cause liver damage which would cause nausea, vomiting, and jaundice.
sometimes can cause numbness in the limbs.

2. Rifampicin can cause liver damage, discoloration of water eyes, sweat, and urine
orange.

3. Pyrazinamide can cause liver damage and gout.

4. Ethambutol can cause blurred vision and impaired color vision because the drug affects
the optic nerve

5. Streptomycin can cause dizziness and hearing loss due to nerve damage in the ear.

Treatment Results

The end result of treatment of smear positive pulmonary tuberculosis patientsand

negative. Categorized as follows:

a. Heal the outcome of patients with sputum smear or culture-positive before treatment,
and the results of sputum smear or culture negative at the end of treatment and at least
one inspection previous sputum negative and the chest X-ray, radiology picture serial
(minimum 2 months) remains the same / repair.

b. Detailed treatment of a patient who has completed treatment but did not have the
results of the examination of sputum or culture at the end of treatment.

c. Died of a patient who died with any cause during the treatment.

d. Failing a patient with sputum or culture-positive results in or more in the fifth month of
treatment.

e. Default / drop-out is lost in the treatment of patients with two consecutive months or
more.

f. Moving a patient who moved into unit (recording and reportingdifferent and the final
outcome of treatment is unknown.

57
10. Mention the prevention based on the scenario?

The best way to prevent tuberculosis is the treatment of patients with TB infection so
that the chain of transmission was interrupted.

1. Protection against TB exposure

Early diagnosis and management is the best way to reduce exposure to TB.
The risk exposure contained in TB wards and wards, where the medical staff and
other patients receive repeated exposure of patients who are exposed to TB. There are
several factors that may affect the transmission among others :

a. How to cough

Patients should use a handkerchief to cover your mouth and nose when
coughing or sneezing so that no transmission occurs through the air.

b. Lowering the concentration of bacteria

- Sunlight and Ventilation

Sunlight can kill the TB germs and good ventilation can prevent the
transmission of TB germs in the room.

- Filtration

Air filtration depending on the facilities and resources available.

- UV radiation bactericidal M. tuberculosis is highly sensitive to UV radiation

bactericidal.

This radiation methods should be used in rooms inhabited infectious TB

patients and the room where the action is induced sputum or bronchoscopy.

c. Mask

Use of masks regularly will reduce the spread of germs through the air. If
possible, TB patients with uncontrolled cough are advised to use a mask at all times.

58
The medical staff also recommended to use a mask when exposure to respiratory
secretions can not be avoided.

d. Recommended NTP (National TB Prevention) against TB exposure:

- Immediate hospitalization of patients with pulmonary TB BTA (+) for the intensive
phase of treatment, if needed.

- Patients should be isolated to reduce the risk of TB exposure to other patients.

- Patients are isolated should not leave the room without wearing a mask.

- Patients with suspected or confirmed infected with TB should not be placed in

rooms occupied by patients who are immunocompromised, such as HIV patients,
transplantation, or oncology.

2. Vaccination BCG (Bacillus Calmette Guerin)

BCG is a live vaccine derived from M.bovis. BCG function is to protect

children against disseminated TB and extra-pulmonary TB weight (TB meningitis and
miliary TB). BCG does not have the effect of lowering cases of pulmonary
tuberculosis in adults. BCG given intradermally to the uninfected population.

a. tuberculin test

Neonates and infants up to 3 months old with no history of contact with TB,
can be given the BCG vaccination without prior tuberculin test.

b. Routine Vaccination

In countries with high TB prevalence, WHO recommends BCG vaccination as

early as possible, especially newborns.

3. Prevention Therapy

The purpose of preventive therapy is to prevent TB infection to disease,

because TB disease can occur in 10% of people who have TB infection.
Chemoprophylaxis may be given when there is a history of contact with a positive
tuberculin skin test but no symptoms or radiological evidence of TB. The drugs used
are usually isoniazid (5 mg / kg) for 6 months. If possible, do with

59
 direct observation.

The group receiving prophylaxis, namely:

- Infants with pulmonary tuberculosis-infected mothers

Babies who are breast-feeding mothers with pulmonary TB, should receive
isoniazid for 3 months. After 3 months, carried out the tuberculin test. If the result is
negative then be vaccinated, if positive then continued isoniazid for 3 months again. If
there is evidence of disease, it is necessary to be given the full treatment.

- Children with a history of contacts, tuberculin negative, apparently healthy,

no history of BCG, the same as the above.

- Children with a history of contacts, positive tuberculin (without a history of BCG).

Children without symptoms should be given a 6-month isoniazid prophylaxis.

Children with symptoms and examination showed tuberculosis TB treatment is

given.

Children with symptoms, but the examination did not show TB, isoniazid
prophylaxis (Wieslaw et al, 2001).

11. How do you see the case in the view of Islams perspective based on the scenario?

AL QURAN

2 (QS. An Nisaa:9)

Dan hendaklah takut kepada Allah orang-orang yang seandainya meninggalkan
dibelakang mereka anak-anak yang lemah, yang mereka khawatir terhadap
(kesejahteraan) mereka. Oleh sebab itu hendaklah mereka bertakwa kepada Allah dan
hendaklah mereka mengucapkan perkataan yang benar

3 (QS. Yusuf: 87)

60





Hai anak-anakku, pergilah kamu, maka carilah berita tentang Yusuf dan saudaranya
dan jangan kamu berputus asa dari rahmat Allah. Sesungguhnya tiada berputus asa
"dari rahmat Allah, melainkan kaum yang kafir

)4 (QS. Ali Imran: 104

Dan hendaklah ada di antara kamu segolongan umat yang menyeru kepada kebajikan,
menyuruh kepada yang maruf dan mencegah dari yang munkar; merekalah orang-
orang yang beruntung

5 )(QS. Al-Hujurat: 13

61









Hai manusia, sesungguhnya Kami menciptakan kamu dari seorang laki-laki dan
seorang perempuan dan menjadikan kamu berbangsa-bangsa dan bersuku-suku
supaya kamu saling kenal-mengenal. Sesungguhnya orang yang paling mulia diantara
kamu disisi Allah ialah orang yang paling takwa diantara kamu. Sesungguhnya Allah
Maha Mengetahui lagi Maha Mengenal.

)6 (QS. Al-Maidah: 2

Hai orang-orang yang beriman, janganlah kamu melanggar syiar-syiar Allah, dan
jangan melanggar kehormatan bulan-bulan haram, jangan (mengganggu) binatang-

62
 binatang had-ya, dan binatang-binatang qalaa-id, dan jangan (pula) mengganggu
orang-orang yang mengunjungi Baitullah sedang mereka mencari kurnia dan
keridhaan dari Tuhannya dan apabila kamu telah menyelesaikan ibadah haji, maka
bolehlah berburu. Dan janganlah sekali-kali kebencian(mu) kepada sesuatu kaum
karena mereka menghalang-halangi kamu dari Masjidilharam, mendorongmu berbuat
aniaya (kepada mereka). Dan tolong-menolonglah kamu dalam (mengerjakan)
kebajikan dan takwa, dan jangan tolong-menolong dalam berbuat dosa dan
pelanggaran. Dan bertakwalah kamu kepada Allah, sesungguhnya Allah amat berat
siksa-Nya

SUNNAH

1

Orang mukmin yang kuat lebih baik dan lebih disenangi di mata Allah dari pada
orang mukmin yang lemah. (HR. Muslim)

2
Dan Allah selalu menolong seorang hamba selagi hamba-Nya mau menolong
saudaranya. (HR. Muttafaq alaih)

Sabda Rasulullah, Sesungguhnya Allah SWT menciptakan penyakit dan obat, maka
berobatlah tetapi janganlah kalianberobatdengan yang haram

63
4

Sebaik-baik manusia adalah yang bermanfaat bagi orang lain. (Al-Hadits)

Islam itu bersih maka peliharalah kebersihan karena sesungguhnya tidak masuk
surga kecuali orang-orang yang bersih. (Al-Hadis)

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