SCENARIO

A 40 years old man come to the puskesmas clinic because of a cough that has been
experienced since 4 month ago. This complaint is accompanied by a fever disappear and
sweat at night. He also complained of pain in his entire body especially the chest,
headaches and lack of appetite. Has been known to take drugs that make red urine 3 years
ago. The patients body weight is currently 34 kg and height 160cm.

I. HARD WORD
-

II. KEYWORDS
1. A 40 years old man.
2. Cought complaint since 4 month ago.
3. Intermiten fever and sweat at night.
4. Chest pain, headaches, and lack of appetite.
5. His medication history makes his urine red 3 years ago.
6. Body weight is currently 34 kg and height 160 cm.

III. QUESTION
1. explain the classification and mechanism of cough ?
2. Explain the patomechanism of the symptoms based on the scenario !
3. What are the diagnostic steps based on the scenario ?
4. What are the appropriate diagnostic steps for a case in the scenario?
5. What kind of prevention steps that we could take based on the scenario?
6. What is the islamic perspective that matched with the scenario?
IV. ANSWER

1. Classification and mechanism of cough

- ANATOMY AND PHYSIOLOGY OF RESPIRATION
a. Nasal
Air from outside will enter through the nasal cavity (nasal cavity). The nasal
cavity is covered with mucous membranes, in which there are oil glands (sebaceous
glands) and sweat glands (sudorifera glands). The mucous membrane functions to
catch foreign objects that enter through the respiratory tract. In addition, there are
also short and thick hairs that function to filter dirt particles that enter the air. There
are also konka which have many blood capillaries that function to warm the
incoming air. In the back of the nasal cavity is connected with the nasopharynx
through two holes called choanae. On the surface of the nasal cavity there are fine
hairs and mucous membranes that function to filter the air that enters the nasal
cavity.
b. Pharinx
Air from the nasal cavity enters the pharynx. Pharynx is a 2-channel
branching, namely the respiratory tract (nasofarings) on the front and the digestive
tract (orofarings) on the back. On the back of the pharynx (posterior) there is the
larynx (pharynx) where the vocal cords are located. The entry of air through the
pharynx will cause the vocal cords to vibrate and sound as sound. Eating while
talking can cause food to enter the respiratory tract because the respiratory tract is
currently open. However, our nerves will regulate so that the events of swallowing,
breathing, and speaking do not occur together, causing health problems. The main
function of the pharynx is to provide a channel for the air in and out as well as the
way food and drinks are swallowed, the pharynx also provides a buzzing space
(resonance) for the sound of conversation.
c. Larynx
Larynx is a channel that is surrounded by cartilage. The larynx is between
the oropharynx and trachea, in front of the ranopharynx. One of the cartilage in the
larynx is called epiglottis. Epiglottis is located at the tip of the base of the larynx.
The larynx is covered by a mucous membrane consisting of flat-coated epithelium
that is thick enough so that it is strong to withstand the sound vibrations in the
larynx. The main function of the larynx is to produce sound and also as a place for
air to get in and out. The base of the throat is composed of several cartilages that
form the Adam's apple. The base of the throat can be closed by the valve base of
the throat (epiglottis). When swallowing food, the valve closes the base of the
throat and when breathing, the valve opens. At the base of the throat there is a
sound membrane that will vibrate when there is air from the lungs, for example
when we talk.
d. Trachea
Trachea in the form of a pipe that is ± 10 cm long, is located partly in the
neck and partly in the chest cavity (thorax). The throat wall is thin and stiff,
surrounded by a ring of cartilage, and on the inside of the ciliated cavity. These
cilia function to filter out foreign objects that enter the respiratory tract. Trachea is
located in front of the esophagus. In the chest cavity, the trunk of the throat is
divided into two branches of the throat (bronchi). In the lungs, the throat branches
again branch into very small channels called bronchioles. The tip of the bronchioles
is small bubbles called alveolar bubbles.
e. Bronchus
Windpipe (trachea) branched into two parts, namely the right bronchus and
bronchus left. The structure of the bronchial mucous layer is the same as the
trachea, only the bronchial cartilage is irregular in shape and in the larger part of
the bronchial ring the cartilage encircles the lumen perfectly. The bronchi branch
off again to become bronchioles. The windpipe branched into two bronchi, namely
the left and right bronchi. Both the bronchi go to the lungs, the bronchi branch
again into the bronchioles. The right bronchi (primary bronchi) branch into three
lobar bronchi (secondary bronchi), while the left bronchi branch into two
bronchioles. The smallest branches enter the lung bubble or alveoli. The alveolar
wall contains blood capillaries, through the blood capillaries in the alveoli this
oxygen and air diffuse into the blood. The main function of the bronchi is to
provide a way for air to enter and exit the lungs.
f. Pulmo
 The lungs are located inside the upper thoracic cavity, on the side bounded
by muscles and ribs and at the bottom are limited by strong muscular diaphragms.
There are two parts of the lung, namely the right lung (pulmo dekster) consisting of
3 lobes and the left lung (pulmo sinister) consisting of 2 lobes. The lungs are
covered by two thin membranes, called the pleura. The inner membrane that
immediately surrounds the lungs is called the inner pleura (visceral pleura) and the
membrane that surrounds the chest cavity next to the rib cage is called the outer
pleura (parietal pleura). The lungs are composed of bronchioles, alveoli, elastic
tissue, and blood vessels. The bronchioles do not have cartilage, but the bronchi are
still ciliated and at the ends have ciliated cube-shaped epithelium. Each terminal
bronchioles branch out again into respiratory bronchioles, then become alveolar
ducts. In the walls of the alveolar ducts they contain bubbles called alveoli.

- COUGH MECHANISM

The bronchi and trachea are very sensitive to light touch, so if there is a
foreign body or other irritant, even in small amounts it will cause a cough reflex.
The larynx and carina (where the trachea branched into the bronchi) are the most
sensitive, and terminal bronchioles and even the alveoli are sensitive to the
stimulation of corrosive chemicals such as sulfur dioxide or chlorine gas. Afferent
impulses originating from the respiratory tract mainly travel through the vagus
nerve to the brain medulla. There, a series of events is automatically moved by the
neuronal trajectory of the medulla, which causes the following effect.
Basically the cough mechanism can be divided into three phases, namely the
inspiration phase, the compression phase and the expiratory phase. Coughing
usually starts from inhalation of a certain amount of air, then the glottis will close
and the pressure in the lungs will increase which is followed by a sudden opening
of the glottis and expiration of a certain amount of air at a certain speed.
The inspiration phase begins with a brief and quick inspiration from a large
amount of air, at this time the reflex glottis is already open. The volume of inspired
air varies greatly in amount, ranging from 200 to 3500 ml above the functional
residual capacity. Other studies mention the amount of air inhaled ranges from 50%
of tidal volume to 50% of vital capacity. There are two main benefits of smoking a
large amount of this volume. First, a large volume will strengthen the expiratory
phase later and can produce expirations faster and stronger. The second benefit, a
large volume will reduce the closed air cavity so that secretion will be easier.
After the air is inspired, then the compression phase begins where the glottis
will close for 0.2 seconds. During this time, pressure in the lungs and abdomen will
increase to 50-100 mmHg. The closure of the glottis is a characteristic of coughing,
which distinguishes it from other forced expiratory maneuvers because it will
produce different forces. The pressure obtained when the glottis is closed is 10 to
100% more
is greater than other methods of forced expiration. On the other hand, coughing can
also occur without glottic closure.
Then, the glottis will actively open and an expiration phase takes place. The
air will come out and vibrate the airway network and the air that is there, making
the coughing sounds that we know. Maximum expiratory air flow will be achieved
within 30-50 seconds after the glottis opens, which is then followed by a steady
stream. The resulting air velocity can reach 16,000 to 24,000 cm per minute, and in
this phase a tracheal diameter reduction of up to 80% can be found.
Cough Classification
 a. Acute Cough
Acute cough is the initial phase of cough and is easy to cure with a period of
less than three weeks. The main causes are upper respiratory tract infections, such
as salesma, acute bacterial sinusitis, pertussis, exacerbation of chronic obstructive
pulmonary disease, allergic rhinitis, and rhinitis due to irritants.
b. Sub-Acute Cough
Sub-acute cough is a transitional phase from acute to chronic which occurs
for 3-8 weeks. The most common causes are cough after infection, bacterial
sinusitis, or asthma.
c. Chronic Cough
Chronic cough is a phase of cough that is difficult to cure because it occurs
in a long period of time that is more than eight weeks. Chronic cough can also be
used as a sign of another disease that is more severe for example; asthma,
tuberculosis (tbc), chronic obstructive pulmonary disease (copd), gastric reflux
disorders, and lung cancer. Based on research, 95% of the causes of chronic cough
are post nasal drip, sinusitis, asthma, gastroesophageal reflux disease (gerd),
chronic bronchitis due to smoking, bronchiectasis, the rest are due to lung cancer,
sarcoidosis, and aspiration due to pharyngeal dysfunction. If for no other reason,
chronic cough can also be caused by psychological factors.[1][2]

2. Pathomechanism of symptoms
a. Intermitten fever

Fever is defined as a form of non-

specific immune system that causes
changes in body temperature regulation
mechanism resulting in an increasing
body temperature above normal as a
result of changes in the center of
thermoregulation located in the anterior
hypothalamus. Normally, body temperature is maintained at changes in enviroment
temperature due to the ability of the thermoregulatory center to regulate the balance
between the heat produced by tissues, specifically muscle and liver with the result
of heat loss. Important heat loss mechanisms are vasodilation and sweating that
indicate the fever is starting to go down.
Mechanism: Fever refers to an increase in body temperature directly related to the
level of pyrogenic cytokines produced to overcome various stimuli. In response to
pyrogenic stimulation, monocytes, macrophages, and kupfer cells secrete cytokines
that act as endogenous pyrogens (IL-1, TNF-α, IL-6, and interferon) acting at the
center of the hypothalamic thermoregulation. In response to these cytokines,
prostaglandin synthesis occurs, especially prostaglandin E2 through the arachidonic
acid metabolism of the cyclooxygenase-2 (COX-2) pathway and cause an increase
in body temperature. The hypothalamus will maintain the temperature according to
the new benchmark and not the normal temperature. Shivering is caused to quickly
increase heat production, while vasoconstriction skin also takes place quickly to
reduce heat dissipation. Thus, the formation of fever in response to pyrogenic
stimulation is something that is experienced and not caused by damage to the
thermoregulatory mechanism.

There are several types of fever, one of which is intermittent fever. Intermittent
fever is where the body temperature drops to normal levels for several hours in a
day, or is often said to be fever-arising. The mechanism of these fever occurs due
to infection of each virus, bacteria, parasite has a different time for one life cycle.
In response to the entry of microbes into the body, certain phagocytic cells
(macrophages) release endogenous pyrogens that act on the hypothalamus. The
hypothalamus, as the center of integration of body thermoregulation, receives
afferent information about temperatures in various parts of the body and triggers
highly complex and coordinated adjustments in the mechanism of heat reception
and heat dissipation. The hypothalamus can respond to changes in blood
temperature as small as 0.01 C.[3][4][5]
b. Lack of apetite
The hypothalamus is the part of the brain that plays an important role in
regulating the processes of homeostasis, including regulating behavior and appetite.
The arcuate nucleus, which is located around the base of the ventricles III, has two
different populations of neurons to regulate food intake. Neurons that produce
neuropeptides Y (NPY) act as accelerators that work to stimulate food. Whereas
other nearby neuron populations that produce pro-opiomelanocortin (POMC) work
in the same brain area as the NPY area to cause food inhibition. When one of the
neurons is activated, the other population is inhibited. For example, when NPY
neurons are activated by a decrease in leptin levels, the secreted NPY will bind to
its receptors in POMC neurons (Y1 receptors) and cause inhibition of the activity
of these POMC neurons. Neurons that produce NPY also produce agouti related
peptides (AgRP) which can block MC4R receptors (receptors for α-MSH).
Activation of neurons that express NPY / AgRP when the energy balance is
negative, can stimulate eating in two ways, namely by releasing NPY appetite
stimulants and by reducing the work of melanocortin / POMC appetite suppressor.
NPY will then bind to Y1 and Y5 receptors in the lateral hypothalamus (LHA)
area. Binding with Y1 and Y5 receptors in LHA causes activation of melano-
concentrating hormone (MCH) and orexin neurons (as second-order neurons).
Activation of MCH and orexin neurons will result in increased appetite through
higher central regulation of behavior, namely the median and insular prefrontal
cortex. The hypothalamus receives input neural, endocrine and metabolic signals,
then integrates them and uses various effector pathways to generate behavioral,
autonomic or endocrine responses.[6]

c. Headache
Pain begins with stimulation of pain receptors by pain stimulus that is divided
into three (mechanical, thermal, and chemical). In mechanical pain, muscle spasm
is a common cause of pain because it can cause obstruction of blood flow to the
tissue, increase tissue metabolism and direct stimulation to mechanical sensitive
pain receptors. In thermal pain, the pain is caused by temperature that does not
correlate with the amount of damage that occurs but correlates with the speed of
tissue damage that arises such as infection, ischemic tissue, bruising, etc. In
chemical pain, there are several substances that stimulate pain such as bradykinin,
serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes.
Pain can be divided into two such as fast pain and slow pain. Fast pain or acute
pain, is pain that is felt within 0.1 s after the stimulus is given. This pain is caused
by mechanical and thermal stimuli. This pain signal is transmitted from the
peripheral nerve to the spinal cord through fiber A with speeds reaching 6-30 m / s.
The neurotransmitter that might be used is glutamate which is also an excitatory
neurotransmitter that is widely used on CNS. Glutamate generally only has a work
duration of several milliseconds.

Slow pain, chronic pain, is pain that is felt within more than 1 second after a
stimulus is given. This pain can be caused by mechanical, chemical and thermal
stimuli but the most frequent stimulus is a chemical stimulus. This pain signal is
transmitted from the peripheral nerve to the spinal cord via C fiber with speeds
reaching 0.5-2 m / s. The neurotramitter that may be used is the substance P.
Although all pain receptors are free nerve endings, the pathway taken can be
divided into two pathways, namely the fast-sharp pain pathway and the slow-
chronic pain pathway. After reaching the spinal cord through the dorsal spinal cord,
this pain fiber will end up in the neuron relay on the dorsal horn and will then be
divided into two tracts which will then lead to the brain. The tract is a
neospinotalamicus for fast pain and paleospinotalamicus for slow pain.[7]

d. Sweat at night
When TB-causing bacteria enter the body, the body will carry out defense
mechanisms to fight these bacteria. One way is to increase the formation of
macrophages derived from monocytes. This macrophage is a type of white blood
cell that works, it will produce a chemical molecule called TNF-alpha (Tumor
Necrosis Factor - alpha). These molecules then give signals to the brain to increase
the set point thermoregulator in the hypothalamus. Due to the increase in the
thermoregulator set point, the body will be triggered to increase body temperature
by reducing the diameter of blood vessels (vasoconstriction) to prevent excessive
heat loss and to signal a shivering response. After this set point is reached, the body
will try to release excess body heat, one of which is by sweating.[8]

e. Chest pain
Pleural disease usually manifests with mild to severe pleuritic chest pain, which
can be accompanied by dispnoe. Other symptoms include fever, night sweats, and
weight loss. Disease can be in acute or chronic form and often causes effusion and
often leads to smooth effusion. unilateral and accompany active parenchymal
disease in 70% of patients. Pleural TB will develop several stages of the disease but
often appears as a manifestation of the primary disease and appears for 6 months
after TB infection. These symptoms are rarely found, usually found in patients who
have complaints of dry cough (non productive) and this pain will increase. if the
patient coughs, this symptom arises when infiltration of inflammation has reached
the pleura, causing pleurisy. It will be felt if there is friction between the two pleura
when the patient inhales / releases his breath.[9]

f. Pain throughout the body

The occurrence of infection by the bacterium Tuberculosis (Mycobacterium
tuberculosis), namely aerobic bacteria that can live mainly in the lungs because it
has a high oxygen partial pressure. When a person with active pulmonary TB
coughs, bacteria can be released into the air and can infect others. This occurs when
there is a Mycobacterium Tuberculosis bacteria sandwiched in the alveoli. The TB
which has been infected with blood flow and circulates throughout the body is
known as TB miliaria, which is a very serious form of this disease. Miliaria TB
generally occurs in children and people with immune systems weak body. TB
germs spread through the lymphatic ducts to the regional lymph glands, the lymph
glands which have lymphatic ducts to the primary focus location. During the early
weeks of the infection process, TB germ growth occurs so that the body's tissues,
which have not been sensitized to tuberculin initially, develop sensitivity. At the
time of the formation of this primary complex, primary TB infection is declared to
have occurred. During the incubation period, before the formation of cellular
immunity, lymphogenic and hematogenous spread can occur. miliary spread
through blood vessels (haematogenous) .Military spread causes TB throughout the
lungs, bones, meningen, etc. On hematogenous spread, TB germs enter the blood
circulation and spread throughout the body. causing TB is called a systemic
disease. Lung tuberculosis is a chronic inflammation (active TB) so that there can
be discomfort, aches, fever, decreased appetite, weight loss, headaches, fatigue.
These symptoms are getting heavier and disappear and occur irregularly.[10]

g. Red urine
Red urine is caused by the influence of the drug. One of the drugs that gives the
side effect of red urine is Anti Tuberculosis (OAT) drug, rifampicin. Rifampin is
one of the most effective OAT, along with isoniazid, is the basic regimen of
tuberculosis treatment. it is active against fast-growing and slow-growing bacteria.
1. Work Mechanism
Rifampicin can easily diffuse across the cell membrane because of its
lipophilic characteristics. The bactericidal activity of this drug depends on the
ability of this drug to inhibit the transcription of ribonucleotide acid (RNA).
The mechanism of action of this drug is by binding to the beta subunit of RNA
Polymerase (RNAP) which depends on DNA thus inhibits RNA transcription.
This complex of enzyme bonds and drugs inhibits the initiation of RNA chain
formation and its elongation.
2. Drug metabolism
The bioavailability of rifampicin is estimated to reach 90-95% because of its
readiness to be absorbed through the gastrointestinal tract. The highest plasma
 levels of rifampicin are reached after 2-4 hours of oral entry. Consumption with
food will slow down but not reduce absorption of the drug. The half-life of
rifampicin is 1.5-5 hours and extends to liver damage. About 60-90% of the
drug binds to plasma protein and is distributed to organs and body fluids such
as the lungs, liver, bile, and urine. And as much as 60-80% of the drug is
metabolized in the liver. A small portion of this drug is metabolized to
formilrifampin which has a bactericidal effect of 10%. About 15-30% of the
drug is excreted through the kidneys and only 7% of this drug is discharged
through urine in its original form. About 60-65% of the drug is discharged
through bile and feces.
3. Side effects
Side effects of rifampicin use are gastrointestinal disorders (anorexia,
diarrhea, nausea and vomiting), blood disorders (thrombocytopenia,
eosinophilia, leukopenia and anemia), neurological disorders (headaches),
edema and discoloration of urine, feces, sweat, water, water saliva, sputum,
tears and other bodily fluids turn orange to red.[11]

3. Diagnostic steps for the case

ANAMNESIS
1. Say bismillahirrahmanirrahim.
2. Show a friendly attitude, say hello
3. Maintain a relaxed and relaxed atmosphere, speak with clear pronunciation
using language that can be understood and mention the patient's name.
4. Ask about the patient's general data:
5. name: unknown
6. gender: male
7. age: 35 years old
8. address: unknown
9. marital status: unknown
10. occupation: unknown
11. Ask the main complaint and explore the history of the present disease (RPS)
12. Main complaint: coughing up with blood
13. Onset and duration of cough complaints: experienced since 3 days
14. Other complaints that accompany: decreased appetite and weight and night
sweats.
15. Already treated or not: unknown
16. Past disease history (RPD): the patient has coughed during the past 2 months.
17. History of allergies, psychosocial history, family history of illness: unknown
18. Asking other physiological functions, if there is interference continue the
history based on the complaint.
19. End the history by repeating the results of the interview / cross check. end the
conversation with thanks and will continue with the physical examination and
other supporting examinations.

PHYSICAL EXAMINATION
Preparation :
1. Provide information to the patient about the examination to be performed and
request permission to carry out the examination
2. Patients are asked to take off clothes
3. Allow sitting / lying down
4. The examiner stands to the right of the patient
INSPECTION:
1. Conduct initial inspection by paying attention
- Hair (looks dry or not, easily falls out or not)
- Eyes (conjunctiva seen anemic or not, sclera visible jaundice or not)
- Nose (secretions, blood clots, masses or lumps)
- Mouth (lip cyanosis / no, mucosa, tonsils, pharynx, secretions, lobe
breathing)
- Neck (Trachea in the middle or not, enlarged KGB)
 - Skin: former herpes (post herpetic neuralgia), venous dilation (superior
cava syndrome, cirrhosis of the liver)
- Extremities: fingers (cyanosis / not, clubbing fingers)
- Level of awareness
2. Pay attention to the shape of the chest
- Symmetrical or not
- Concave or convex in one side or both
- Does the patient use additional muscles for breathing
- Look for prominent areas or local retractions
- Is there a deformity of the chest cavity
- Calculate breathing frequency
- Posterior: location of vertebrae, gibus, deformity
PALPASI
1. By using both hands to check whether there is supraclavicular
lymphadenopathy and neck, tumor metastasis
2. Check the position of the trachea with the index finger if it is normal, deviation
to the right or left
3. Palpate the chest wall, using both hands to make sure - Is there local tenderness
- Is there mass or crepitation - Ensuring chest movement (1/3 upper, middle and
lower 1/3)
4. Assessing vocal remitus, place both sides of the medial palm on the wall / side
of the chest
5. Assess the widening of the right and left ribs respectively
6. Allow to take a deep breath
7. Please say the words "nine nine" or "iii iii iii"
8. Determine the difference in left and right vocal fremitus (tactile fremitus)
PERKUSI
1. 11. Perform percussion from the top down on the front chest evenly throughout
the chest 12. Conduct chronig isthmus examination
2. 13. Compare the same places on both the right and left sides
3. 14. Determine the limits of sonor change to deaf
4. 15. Give a sign for the act of punksi experiment (if found suspicious areas
pleural effusion suspicious)
AUSKULTASI
1. 16. The stethoscope is placed anterior, lateral and posterior to the chest
systematically 17. The sufferer is asked to take a deep breath
2. 18. Auscultate systematically and compare the sounds that are heard on each
side
3. Determine the type of respiratory sounds * Vesicular * Bronchovesicular *
Bronchial
4. Determine the type of additional breath sounds: wheezing, ronchie, stridor
5. Determine the location of changes from vesicular sound to disappear
6. Repeat inspection inspection, palpation, percussion and auscultation of the
posterior part of the body
SUPPORTING INVESTIGATION
1. Microscopic examination of sputum
Sputum examination serves to establish the diagnosis, assess the success of
treatment and determine the potential for transmission. This examination
collected 3 consecutive spasms every morning (SPS) 9.
 S (when): Sputum is collected when suspect tuberculosis comes for its first
visit. On returning home, suspects brought a sputum pot to collect phlegm on
the second morning.
 P (morning): Phlegm is collected at home on the second morning,
immediately after waking up. The pot was brought and handed over to the
officers themselves.

 P (morning): Phlegm is collected at home on the second morning,

immediately after waking up. The pot was brought and handed over to the
officers themselves.
  S (when): Phlegm is collected on the second day, when submitting sputum in
the morning.
2. Blood tests
The results of routine blood tests show less specific indicators for pulmonary Tb.
Blood sediment rate (LED) the first hour and second hour are required. This data
can be used as an indicator of the state of stability of the patient's equilibrium
value, so that it can be used for one response to the treatment of patients as well
as the possibility of detecting the patient's cure rate.
3. Radiological examination
Standard inspection is a PA chest radiograph. Other checks on indications are
lateral photo, lordotic top, oblique, CT-Scan. In cases where the SPS sputum is
positive, a chest X-ray is not required
Radiological features of inactive pulmonary tuberculosis:
a. Fibrotic, especially in the apical and / or posterior segment of the upper lobe
and / or superior segment of the lower lobe.
b. Calcification.
c. Pleural thickening.[12]

4. The differential diagnosis

1. TUBERCULOSIS
Introduction
Tuberculosis (TB) is an ancient human disease caused by Mycobacterium
tuberculosis which mainly affects the lungs, making pulmonary disease the
most common presentation.
Etiology
M. tuberculosis causes tuberculosis. M. tuberculosis is an alcohol and acid-
fast bacillus. It is part of a group of organisms classified as the M. tuberculosis
complex.
Epidemiology
 Tuberculosis is present globally. However; developing countries account for
a disproportionate share of tuberculosis disease burden. In addition to the six
countries listed above, several countries in Asia, Africa, Eastern Europe, and
Latin and Central America continue to have an unacceptably high burden of
tuberculosis.
In more advanced countries, high burden tuberculosis is seen among recent
arrivals from tuberculosis-endemic zones, health care workers, and HIV-
positive individuals. Use of immunosuppressive agents such as long-term
corticosteroid therapy has also been associated with an increased risk.
Pathophysiology
Although, usually a lung infection, tuberculosis is a multi-system disease
with protean manifestation. The principal mode of spread is through inhalation
of infected aerosolized droplets. The body's ability to effectively limit or
eliminate the infective inoculum is determined by the immune status of the
individual, genetic factors and whether it is a primary or secondary exposure to
the organism. Additionally, M. tuberculosis possesses several virulence factors
that make it difficult for alveolar macrophages to eliminate the organism from
an infected individual. The virulence factors include the high mycolic acid
content of the bacteria outer capsule, which makes phagocytosis to be more
difficult for alveolar macrophages. Furthermore, some of the other constituents
of the cell wall such the cord factor may directly damage alveolar macrophages.
Several studies have shown that mycobacteria tuberculosis prevents the
formation of an effective phagolysosome, hence, preventing or limiting the
elimination of the organisms.
The first contact of the Mycobacterium organism with a host leads to
manifestations known as primary tuberculosis. This primary TB is usually
localized to the middle portion of the lungs, and this is known as the Ghon
focus of primary TB. In most infected individuals, the Ghon focus enters a state
of latency. This state is known as latent tuberculosis.
History and Physical
 A chronic cough, hemoptysis, weight loss, low-grade fever, and night sweats
are some of the most common physical findings in pulmonary tuberculosis.
Secondary tuberculosis differs in clinical presentation from the primary
progressive disease. In secondary disease, the tissue reaction and
hypersensitivity is more severe, and patients usually form cavities in the upper
portion of the lungs.
Treatment / Management
Latent Tuberculosis
Drug of choice is isoniazid. It is usually given with vitamin B6, pyridoxine
(to prevent nerve damage). Isoniazid is recommended for Mantoux or
quantiferon positive individuals and should be continued for 6 or 9 months.
Treatment of confirmed TB requires a combination of drugs. Combination
therapy is always indicated, and monotherapy should never be used for
tuberculosis. The most common regimen for TB includes the following anti-
TB medications:
First-Line Medications, Group 1
- Isoniazid
- Rifampicin
- Rifabutin
- Rifapentine
- Pyrazinamide
- Ethambutol
Isoniazid and Rifampicin follow a 4-drug regimen (usually including Isoniazid,
Rifampicin, Ethambutol, and Pyrazinamide) for 2 months or six months.
Vitamin B6 is always given with Isoniazid to prevent neural damage
(neuropathies).[13]

2. PNEUMONIA
Introduction
 Pneumonia has been defined as an infection of the lung parenchyma. Rather
than looking at it as a single disease, health care professionals must remember
that pneumonia is an umbrella term for a group of syndromes caused by a
variety of organisms resulting in varied manifestations and sequelae.
Etiology
- Bacterial causes
They have been classically studied under the subheadings "typical" and
"atypical" organisms in terms of ease of culture positivity. Common typical
organisms include Pneumococcus, Haemophilus influenzae, Moraxella
catarrhalis, Group A Streptococcus, and other aerobic and anaerobic gram-
negative organisms. Atypical organisms commonly seen in clinical practice
include Legionella, Mycoplasma, Chlamydia, among others.[7] In the United
States, the most common bacterial causes of CAP include Streptococcus
pneumoniae, Staphylococcus aureus, Mycoplasma pneumoniae, and gram-
negative enteric bacilli.
- Viral causes
It is often observed that viral species colonize nasopharynx of patients with
CAP. Whether they are the primary cause or contribute to the pathogenesis by
secondary bacterial causes is still being investigated. However, some of the
most frequent viral agents implicated in CAP in the United States include
influenza virus followed by respiratory syncytial virus, parainfluenza virus, and
adenoviruses.
- Fungal causes
Fungal infections are usually implicated in patients with certain predisposing
immunocompromised states like HIV and organ transplant recipients, among
others. However, often overlooked, some fungal species can cause pneumonia
in immunocompetent individuals which results in a delay in diagnosis and leads
to unfavorable outcomes. The 3 commonest ones in North America include
Histoplasma, Blastomyces, and Coccidioides.
History and Physical
 Historically, the chief complaints in case of pneumonia include systemic
signs like fever with chills, malaise, loss of appetite, and myalgias. These
findings are more common in viral pneumonia as compared to bacterial
pneumonia. A small fraction of patients may have an altered mental status,
abdominal pain, chest pain, and other systemic findings. Pulmonary findings
include cough with or without sputum production. Bacterial pneumonia is
associated with purulent or rarely blood-tinged sputum. Viral pneumonia is
associated with watery or occasionally mucopurulent sputum production. There
may be an associated pleuritic chest pain with the concomitant involvement of
the pleura. Dyspnea and a diffuse heaviness of the chest are also seen
occasionally.
Common findings on physical examination include:
- Tachypnea
- Tachycardia
- Fever with or without chills
- Decreased or bronchial breath sounds
- Egophony and tactile fremitus, both suggestive of a consolidative
process
- Crackles on auscultation of the affected regions of the lung
- Dullness on percussion
Epidemiology
Pneumonia is a fairly prevalent disease and carries a heavy burden in all
populations. A study carried out by the US Centers for Disease Control and
Prevention (CDC) aimed at estimating its burden in North America found that
CAP accounted for the eighth leading cause of mortality in the United States
and the seventh leading cause of mortality in Canda after adjusting for various
gender and age differences.
Pathophysiology
There is an intricate balance between the organisms residing in the lower
respiratory tract and the local and systemic defense mechanisms (both innate
and acquired) which when disturbed gives rise to inflammation of the lung
parenchyma, i.e., pneumonia. Common defense mechanisms that are
compromised in the pathogenesis of pneumonia include:
Systemic defense mechanisms like humoral and complement-mediated
immunity that is compromised in diseases like common variable
immunodeficiency (CVID), X-linked agammaglobulinemia (inherited), and
functional asplenia (acquired). Impaired cell-mediated immunity predisposes
individuals to infection by intracellular organisms like viruses and organisms of
low virulence like Pneumocystis pneumonia (PJP), fungal causes, among others
The mucociliary clearance that is often impaired in cigarette smokers, post-viral
state, Kartergerner syndrome, and other related conditions Impaired cough
reflex seen in comatose patients, certain substances of abuse Accumulation of
secretions as seen in cystic fibrosis or bronchial obstruction The resident
macrophages serve to protect the lung from foreign pathogens. Ironically, the
inflammatory reaction triggered by these very macrophages is what is
responsible for the histopathological and clinical findings seen in pneumonia.
The macrophages engulf these pathogens and trigger signal molecules or
cytokines like TNF-a, IL-8, and IL-1 that recruit inflammatory cells like
neutrophils to the site of infection. They also serve to present these antigens to
the T cells that trigger both cellular and humoral defense mechanisms, activate
complement and form antibodies against these organisms. This, in turn, causes
inflammation of the lung parenchyma and makes the lining capillaries "leaky,"
which leads to exudative congestion and underlines the pathogenesis of
pneumonia.
Treatment / Management
Management of CAP involves initial risk stratification of the patient and to
decide whether to manage the patient on an outpatient basis, in a general
medicine ward, or in an intensive care unit (ICU) setting. The "CURB-65" scale
has been used extensively for this purpose. The components of this scale
include confusion, uremia (BUN greater than 20 mg/dl), a respiratory rate
 greater than 30 per minute, blood pressure less than 90 mm Hg systolic or less
than 60 mm Hg diastolic, and age greater than 65. One point is awarded for
every positive criterion that the patient meets. Patient disposition is decided as
follows.
- A score of 0 to 1: Outpatient management. These patients are treated
empirically using Fluoroquinolones or Beta-lactams+ Macrolides if
adverse comorbidities are present and with Macrolides or Doxycycline
if no comorbidities are present.
- A score of 2 to 3 indicates admission and management in a general
medicine ward. The first line of treatment is a choice between
fluoroquinolones or macrolides plus beta-lactams.
- A score of 4 or more warrants management in an ICU. The empiric
regimen, in this case, is a choice between a combination of a beta-
lactam plus fluoroquinolones or beta-lactams plus macrolides.[14]

3. BRONCHIETASIS
Introduction
Initially, bronchiectasis was described in the early 19th century by Laennec.
Bronchiectasis is a chronic condition characterized by permanent and
irreversible dilatation of the bronchial airways and impairment of mucociliary
transport mechanism due to repeated infection leading to colonization of
organism and pooling of the mucus in the bronchial tree.
Etiology
Historically, the most common cause of bronchiectasis was thought to be an
antecedent respiratory infection, often during childhood. The causes are
idiopathic, acquired, or infection-related.
Bacterial Infections
• Mycobacterium: Tuberculosis and atypical
• Haemophilus influenzae
• Pseudomonas aeruginosa
• Staphylococcus aureus
• Mycoplasma and HIV
Viral Infections
• Respiratory syncytial virus and measles
Fungal Infections
Bronchial obstruction
• Foreign body
• Mucus plug
• Tumors
• Hilar lymphadenopathy (right middle lobe syndrome: extrinsic compression
from postinfectious adenopathy)
Postinflammatory pneumonitis
• Chronic aspiration/gastroesophageal reflux disorder
• Chronic sinusitis
• Inhalational injury
Congenital/Genetic
• Cystic fibrosis
• Young syndrome
• PCD: primary ciliary dyskinesia (Kartenger Syndrome)
• immunodeficiency (hypogammaglobulinemia)
• Alpha1-antitrypsin deficiency (AAT)
• Mounier-Kuhn syndrome
Inflammatory diseases
• Ulcerative colitis
• Rheumatoid arthritis
• Sjögren syndrome
Pulmonary Diseases
• Asthma
• Bronchomalacia
• Cronic-obstructive pulmonary disease (COPD) (reported in up to 50% of
patients with moderate-to-severe COPD)
• Diffuse panbronchiolitis
• Idiopathic pulmonary fibrosis (traction bronchiectasis)
Altered immune response
• Allergic Bronchopulmonary Aspergillosis
• Hypersensitivity pneumonitis
Epidemiology
The prevalence of bronchiectasis is not precisely known. International data
show an increase in the prevalence of bronchiectasis over recent years. It occurs
in every age group and, in the pre-antibiotic era, it most often began in
childhood.[4]Recent evidence shows that bronchiectasis disproportionately
affects women and older individuals, and may be contributing to an increasing
healthcare burden.
Pathophysiology
The three most important mechanisms that contribute to the pathogenesis of
bronchiectasis are an infection, airway obstruction, and peribronchial
fibrosis.Neutrophils dominate airway inflammation in bronchiectasis, driven by
high concentrations of neutrophil chemo-attractants such as interleukin-8
(CXCL-8), and leukotriene B4. Airway bacterial colonization occurs because of
impaired mucociliary clearance and because of failure of neutrophil
opsonophagocytic killing. Other mechanisms of immune dysfunction include
failure of clearance of apoptotic cells and T-cell infiltration, with recent
evidence pointing to an important role of Th17 cells.
Treatment / Management
Bronchiectasis is treatable but rarely curable.
Treatment Goals:
• Identifying and treating the underlying cause
• Improve tracheobronchial clearance
• Control infection
• Reverse airflow obstruction
General Management
Identifying and treating the underlying cause: Immunoglobulin replacement,
steroids, and antifungals for ABPA, treatment for NTM, and of CF all represent
opportunities to treat the underlying cause specifically, and systematic testing
of all patients is recommended in consensus guidelines.[9][10][11]
Improve tracheobronchial clearance: Most physicians recommend mucus
clearance as the mainstay of therapy in bronchiectasis, Postural drainage
consists of adopting a position in which the lobe to be drained is uppermost,
and should be performed for a minimum of 5 to 10 minutes twice a day.
Efficiently performed, this is of great value both in reducing the amount of a
cough and sputum and in preventing recurrent episodes of bronchopulmonary
infection.
Deep breathing followed by forced expiratory maneuvers (the "active cycle of
breathing" technique) is of help in allowing secretions in the dilated bronchi to
gravitate towards the trachea, from which vigorous coughing can clear them.
"Percussion" of the chest wall with cupped hands may help to dislodge sputum,
and a number of mechanical devices are available which cause the chest wall to
oscillate, thus achieving the same effect.
Control infection: Choice of antibiotic should primarily be based on the results
of culture and sensitivity. When no specific pathogen is identified, and the
patient is not seriously ill, an oral agent like amoxicillin, co-amoxiclav, or
macrolides for 2 weeks is sufficient.
Use a higher dose of oral amoxicillin 1 gm twice per day for 2 weeks,
especially if colonized with H. influenza, if pseudomonas-colonized then a 2-
week course of ciprofloxacin 750 mg twice per day (with cautious use in the
elderly) is reasonable.
For patients with moderate-to-severe symptoms, parenteral antibiotics, such
as an aminoglycoside (gentamicin, tobramycin) and an antipseudomonal
synthetic penicillin, a third-generation cephalosporin, or a fluoroquinolone,
may be indicated.
Treatment for Pseudomonas isolates 2 weeks of intravenous (IV)
antipseudomonal antibiotics, nebulized colistin for 3 months, or nebulized
colistin for 3 months with an additional 4 weeks of oral ciprofloxacin.
Maintenance therapy with intermittent antibiotics is not used routinely in
patients with non-CF bronchiectasis, and the decision to use long-term
antibiotics should be individualized.
Inhaled aminoglycosides can be of benefit in chronic non-CF bronchiectasis;
however, the treatment needs to be of a sustained duration.
Reverse airflow obstruction:
• In patients with airflow obstruction, inhaled bronchodilators and
corticosteroids should be used to enhance airway patency.
General management: As with other respiratory diseases, patients with
bronchiectasis should be encouraged to stop smoking. Vaccination against
influenza and pneumococcal disease is also recommended.
Adjunctive Surgical Treatment:
• Surgery is only indicated in a small proportion of cases. These are usually
young patients in whom the bronchiectasis is unilateral and confined to a single
lobe or segment as demonstrated by CT.
• Surgery is an important adjunct to therapy in some patients with advanced or
complicated disease.
• Single- or double-lung transplantation has been used as a treatment of severe
bronchiectasis, predominantly when related to CF. In general, consider patients
with CF and bronchiectasis for lung transplantation when FEV falls below 30%
of the predicted value. Female patients and younger patients may need to be
considered sooner.
• Massive hemoptysis: Bronchial artery embolization and/or surgery is first-
line therapy for the management of massive hemoptysis.[15][16]
5. Disease prevention
a. Stay at home. Don't go to work or school or sleep in a room with someone
else during the first few weeks of treatment for active TB
b. Ventilate the room. TB germs spread more easily in a closed room where the
air does not move. If the ventilation is still lacking, open the window and
use the fan to release the air inside the room to the outside.
c. Close your mouth using a mask. Use a mask to close your mouth whenever
this is an effective step to replace TB. Don't forget to dispose of the mask
regularly.
d. Spit coming in certain places that have been given disinfectants (soap
water).
e. BCG immunization is given to infants given 3-14 months
f. Avoid cold air.
g. Try to get enough sunlight and fresh air into the bed.
h. Dry the mattress, pillows and main bed in the morning.
i. All items used by sufferers must also wash them and cannot be used by
others.
j. Foods must be high in calories and high in protein.[17]

6. Islamic perspective for the case

According to Mustamir, there are 4 things that become the mechanism of the
Qur'an in treating physical ailments, including:[18]
- The Qur'an teaches how to breathe well,
- The letters of the Qur'an when read can train the muscles in the nose, mouth,
throat, even the muscles of the chest and stomach.
- Good recitation of the Qur'an can act as music therapy.
- Fourth, with the concept of religiopsikoneoruimunologi (art of healing by
combining spiritual, psychological, and physical dimensions.
Allah ta'ala has confirmed that the Qur'an is syifa ', not merely laughter'. This is in
accordance with the words of Allah Sawt listed in one of the letters, namely:
‫ارا‬
ً ‫س‬ َّ ‫آن َما ه َُو ِّشفَا ٌء َو َرحْ َمةٌ ِّل ْل ُمؤْ ِّمنِّينَ ۙ َو ََل يَ ِّزيد ُ ال‬
َ ‫ظا ِّل ِّمينَ إِّ ََّل َخ‬ ِّ ‫َونُن َِّز ُل ِّمنَ ْالقُ ْر‬
"And We have brought down from the Qur'an a shaykh 'and mercy to those who
believe, and it does not add to those who do wrong besides loss" (QS. Al Isra'
82).[19]
 REFERENCES

1. Aditama, Tjandra Yoga. Patofisiologi Batuk. Bagian Pulmonologi Fakultas Kedokteran

Universitas Indonesia.
2. Fernandez, Gregory James. 2018. Sistem Pernapasan. Bagian Ilmu Penyakit Dalam
Fakultas Kedokteran Universitas Udayana.
3. Ganong, W. F. 2009. Buku Ajar Fisiologi Kedokteran. Edisi 22. Jakarta: EGC.
4. Dalal S., Zhukovsky, D. S., 2006.Patophysiology and Management of Fever. Article
ReviewJournal of Surgical Oncology:Vol 4
5. Aru W.Sudoyono, Setiyohadi Bambang. Buku Ajar Ilmu Penyakit Dalam. Jilid III.
Edisi IV. 2006. Pusat Penerbitan Departemen Ilmu Penyakit Dalam Fakultas
Kedokteran Universitas Indonesia. Jakarta. Hal 1703
6. Guyton, A.C.,Hall.J.E. 2014. Buku Ajar Fisiologi Kedokteran. Edisi 12. Jakarta : EGC
7. Sudoyo, Aru W., Setiyo Hadi Bambang, dkk. 2009. Buku Ajar Ilmu Penyakit Dalam.
Jilid III. Edisi V. Jakarta : internapublishing
8. Oliviera, Ivona. 2016. PolaKejadianPenyakitKomorbid Dan EfekSamping OAT Pada
PasienTuberkulosis Di Rsup Dr. Kariadi.FakultasKedokteranUniversitasDiponegoro.
9. Retno Asti Werdhani. 2005. Patofisiologi, Diagnosis, dan
KlafisikasiTuberkulosis.DepartemenIlmuKedokteranKomunitas, Okupasi, dan
Keluarga. Jakarta: FK UI.
10. Sudoyono,A., Setiyohadi, B., Alwi, I., Simadibtara, M., Setiadi, S., 2010. Buku Ajar
IlmuPenyakitDalam.Interna Publishing. Jakarta.
11. Depkes RI. 2009. KeputusanMenteriKesehatanRepublik Indonesia
TentangPedomanPenanggulanganTuberkulosis (TB). Jakarta.
12. (referensi langkah diagnosis ???)
13. Rotimi Adigun; Rahulkumar Singh.Tuberculosis.2019.StatPearls Publishing LLC.
14. Vardhmaan Jain; Abhishek Bhardwaj.Pneumonia Phatalogy.2019. StatPearls
Publishing LLC.
15. Ho T, Cusack RP, Chaudhary N, Satia I, Kurmi OP. Under- and over-diagnosis of
COPD: a global perspective. Breathe (Sheff). 2019 Mar;15(1):24-35. [PMC free
article] [PubMed]
16. Ferri S, Crimi C, Heffler E, Campisi R, Noto A, Crimi N. Vitamin D and disease
severity in bronchiectasis. Respir Med. 2019 Mar;148:1-5. [PubMed]
17. (referensi pencegahan ???)
18. Mustamir.sembuh dan sehat dengan mukjizat Al-quran.2007.lingkaran.h-84.
19. Mushaf Al-quran.surah al-isra.ayat 84.juz 15.Penerbit:Sabiq.