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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

‫مبسحمم ٱرلم ٱلررححمممن ٱلررمحيمم‬

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 writer’s 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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What is the differential diagnose and main diagnose based on the scenario? 4. Headache 3. and respiratory tract. and pulmonary (lung parenchyma) . Runny Nose d. headaches especially in the mornings and lack of appetite. nose outside. Inc. runny nose and sweating at night. Cough b. and larynx. and physiology based on the scenario? 2. the inside of the nose. Answer 1. pharynx. 4 . Fever c.  He also complained of pain in the whole body especially the chest. consisting of the airway. Which includes the main structure of the respiratory system is the respiratory airways. What is the complication based on the scenario? 9. © 2002 by The McGraw-Hill Companies. How about the anatomy. Lack of appetite e. histology. Mention the prevention based on the scenario? 11. Identification the Problems 1. Mention the classification of diagnose based on the scenario? 6. What is the general and supportive examination based on the scenario? 8.) B.  These complaints accompanied by fever. How about the anatomy. histology. and complementary structures (accessory structure).The referred to as upper respiratory airways (airway) is nares. (McGraw-Hill Concise Dictionary of Modern Medicine.  History treatment in public health center does not improve C. Mention the clinical manifestation based on the scenario? 7. Mention the management based on the scenario? 10. and physiology based on the scenario? Anatomy Respiration Structures that make up the respiratory system can be divided into the main structure (principal structure). Explain the etiology and pathomechanism based on the scenario : a. paranasal sinuses. How is the pathomechanism of diagnose based on the scenario? 5. How do you see the case in the view of Islam’s perspective based on the scenario? D. Keywords  A man aged 33 years came to the hospital because the cough he since one month ago.

Bronchus starting from the right and left bronchus principalis (generation 1). the diaphragm. And each lobar bronchus branched into bronchial segmentalis and subsegmental (3-9 generations). and inferior (generation 2) . What is meant by the lung parenchyma is the organ form alveoli groups that surrounds the branches of the bronchial (airway generations 1-24). Then right bronchus principales lobar bronchi branch off into superior. generation respiratory bronchioles 15-18 19-24 alveolar ducts. alveolar sacculus. bronchi. Bronchus principales left lobar bronchi branch off into superior and inferior.whereas the lower respiratory airways (airway) is the trachea. The complementary structure is chest wall consisting of ribs and muscles. medial. respiratory tract generation respiratorius.1 Anatomy Respiration Respiratory Muscles 5 . and pleura. 10-14 airway generation are the terminal bronchioles. and alveoli. the abdominal muscles and other muscles. Figure 1. and bronchioles.

Additional inspiratory muscle (accessory respiratory muscle).The main inspiratory muscle (principal). rectus abdominis • The external oblique abdominis Figure 1. namely: • M. intercostal externa. sternocleidomastoid • Scalenus anterior • Scalenus medius • Scalenus posterior Expiratory muscle (active breathing). namely: • M. intercostal interna • M. interkatiliginus parasternal. interkaliginus parasternal • M.2 Anatomy Respiration Histology Respiration Nose 6 . and • diaphragm muscle. • M. namely: • M.

cartilage. On the nose there is a special epithelium. Sebaceous glands and tiny hairs quasi-layered coated cylindrical epithelium with ciliated mucous glands. 7 . connective tissue. and cartilage (C-shaped). The rear does not have the ring of cartilage (pars membranacea) but filled by muscle fibers.3 Histology of Nose Trachea Consists of a cylindrical epithelium ciliated pseudo-coated (goblet cells). olfactory epithelium. blood vessels. muscles. and connective tissue. serous glands. perikondrium. Figure 1. nerves. Composed of bones.

4 histology of the trachea Larynx Cavity widened.Elastic cartilage: cartilage cuneiform / kornikulata . 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 .A mixture of cartilage: cartilage arichtenoidea • Muscle / ligament: skeletal muscle (3) 8 . irregular shape. between the nasopharynx and trachea. Figure 1.

respiratory epithelium.6 histology of bronchus and bronkhiolus Biochemical Respiration The composition of the respiratory gasAir atmosphere (760 mmHg) has a main composition of gases: 9 .5 histology larynx Bronchus and bronchioles Hyalin consists of cartilage. Figure 1. etc. blood vessels. Figure 1. connective tissue.

10 .3 mmHg Carrier O2 CO2 Hemoglobi 98. It was the Cardinal function of the Lung. . 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.5 % 10 % Plasma (H2CO3). N2 : 79% → P N2: 79% x 760 = 600 mmHg O2 : 21% → P O2: 21% x 760 = 159 mmHg CO2 : 0.04% → P CO2: 0.5 % 30 % n Blood 1. 60 % The presence of water vapor (H2O) with a pressure of 47 mmHg in the alveoli.04% X 760 = 0.

Ventilation lungs. but this work of the heart blood vessels 4. Transport of O2 and CO2 in the blood and body fluids (CES / ECF) to and from cells.7 Anatomy Respiration To achieve this goal. 2. the entry of atmospheric air into the lungs through the alveoli and pulmonary alveoli air discharge into the air / atmosphere again. 3. Diffusion of O2 and CO2 between the pulmonary capillary blood and alveolar air. the respiratory system function: 1. This happens because the continuous ventilation coupled perfusion flow of blood into the alveoli capillaries are also constantly flowing. Perfusion O2 and CO2 that occur between tissue and blood capillaries RESPIRATION MECHANISM INSPIRATION EKSPIRATORY 11 . This point was not included pure respiratory function. Figure 1.

Headache A. Fever c. Explain the etiology and pathology mechanism based on the scenario : a. Cough b. constriction. infiltration. Lack of appetite e. Cough  Etiology  Inhaled irritants (smoke. dust. foreign body. and compression of the airway  Asthma  TBC 12 . smoke.2.) or aspirated (Postnasal drip. Runny Nose d. the stomach contents)  All disorder that causes inflammation. etc.

Afferent pathways including the receptors located on sensory nerve distribution trigemineus.  Fungal infections are generally cause a fever. sepsis. 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.  Viral infections are generally cause fever include viral pneumonia. relaxation of muscle contractions of the diaphragm and the closure of the glottis. B. Fever  Etiology Fever can be caused by infection or non-infectious factors. criptococcosis. As a defense reflex. and others. viruses. and vagus. If the glottis is open. bacterial gastroenteritis. bacteremia. Cough starts with a deep inspiration followed by closure of the glottis. appendicitis. otitis media. among others Coccidioides imitis. glossopharyngeal. pneumonia. the high pressure can help in eliminating mucus and foreign matter. Efferent pathways also include laryngeus nerve and spinal nerves. superior laryngeus. As a result. encephalitis. Fever due to infection can be caused by infection with bacteria. bronchitis. he has afferent and efferent pathways. Lung cancer  interstitial lung disease.  The bacterial infection that generally cause a fever include pneumonia. dengue fever. or parasites. 13 . urinary tract infection. influenza. tuberculosis. cellulitis. chikungunya fever and common viruses such as H1N1. osteomyelitis. a large pressure difference between the atmosphere and accompanied by tracheal narrowing airways produce high levels of air flow rapidly through the trachea. meningitis. fungi. and others. Positive intrathoracic pressure causes constriction of the trachea.

IL-6. ¬ cause difficulty breathing through the nose. autoimmune diseases (arthritis. Air trapped in the pouch of rice.). cutaneous vasoconstriction and mechanisms such as the blankets. or an immune reaction. among others malaria. toxoplasmosis. lymphoma non-Hodgkin's. systemic lupus erythematosus. TNF-α and IFN). Pyrogen exogenous and endogenous pyrogens will stimulate the hypothalamus to form prostaglandin endothelium (Dinarello & Gelfand. vasculitis.). 2005). lymphocytes. the state of teething. inflammatory mediators. Prostaglandins formed later will raise the standard thermostat in hypothalamic thermoregulatory center. White blood cells will release chemicals known as endogenous pyrogen (IL-1. and use of drugs (antibiotics. 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. and helminthiasis  Fever due to non factor infection can be caused by several things. among others shivering. environmental factors (temperature environments externally is too high. among others. causing headache or 14 . etc. difenilhidantoin.). and neutrophils) by exogenous pyrogens in the form of toxins. causing mucus in the pouch of rice reserves. which can not be released and generate pressure. etc. 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. malignancies (Hodgkin's disease. Once the cavity is filled. 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. sinus cavity. leukemia. and antihistamines)  Pathomechanism Fever started from the stimulation of white blood cells (monocytes. etc.  A parasitic infection that usually cause fever. the air flow is blocked.

If the color of blood: if unilateral showed a tumor. It was triggered due head injury or injury to the spine. and . Lack of Appetite Neurotransmitters and hormones play an important role. and nasal discharge. For it is known categorization as follows: (1) Substance orexigenic which are substances that trigger hunger. such as: . is usually not due to infection. D. uncontrolled bleeding.Melanocyte Stimulating Hormone (α-MSH) along with Cocaine and Amphetamine-Related Transcript (CART) produced by Neuron pro- opiomelanocortin (POMC) 15 . if the green liquid indicates infection. Secretions from the nose down to the throat known as post nasal drip possibility of the paranasal sinuses. nosebleed.Agouti Related Protein (AGRP) (2) anorexigenic substance that inhibits appetite (in other words. as: . resulting in a sore throat or cough. foreign body. Secretions that is clear like water and polynomial typical for nasal allergies. Rhinorrhea caused nasal infections usually clear up bilateral purulent. However. If bilateral showed granulomatous disorder or diathesis and bleeding. if the running nose constituted by serious traumatic complications. If the sinuses remain blocked. If the mucus continues to flow back toward the tube eustachi. thus affecting the nervous system. full). Excessive mucus that accumulates in the throat or back of the nose causing post-nasal drip. and frequent vomiting.facial nyeripada.Neuropeptide Y (NPY) from the nucleus arcuata released when lower energy savings. Biochemical substance that determines whether to be inhibited appetite (satiety) or triggered (hungry). In children when secretions that there is only one side and smelled likely be a foreign object in the nose. If the fluid is yellow indicates an allergy or infection. can cause ear pain or ear infection. can cause sinusitis. Additional symptoms may include sneezing. symptoms such as fainting. When the yellow-green secretions usually derived from nasal sinusitis If CSF rhinorrhea unilateral indicate a leak or a malignancy.

by contrast inhibition (defects) by AGRP will improve decision foods and reducing energy consumption that can lead to obesity. causing the desire to eat in order to meet calorie needs. receptors primarily on POMC neurons in the arcuate nucleus and paraventricular. While physically. (2) activation of POMC neurons that causes the release of α-MSH and stimulates melanocortin receptors (MCR). POMC activity can also be inhibited by NPY. Conversely. like the NPY and AGRP. this headache arising from the body's reaction to stress. Regulatory caused by temperature: When the body is exposed to a low temperature. lack of sleep. (3) increase production corticotropin releasing hormone (CRH). allegedly can they are due to psychological factors and physical factor. depression and emotional conflict. Leptin stimulation on neurons will result in: (1) a decrease in production stimulator of hunger. Activation of the MCR will reduce retrieval -increase food and energy consumption. certain positions which causes muscle contraction of the head 16 . anxiety. Headache  ETIOLOGY The cause of muscle tension headache is still unknown. the position of the head is settled resulting in muscle contraction head and neck in the long term. Then there is a decrease in metabolic rate so that the fat deposits much in the network. the error in a sleeping position and fatigue can also cause muscle tension headache is. Psychologically. which suppress hunger . Adipocyte tissue produces a hormone called leptin. E. POMC neurons work by releasing α-MSH which binds to the melanocortin receptors (MCR) in the paraventricular nucleus. it is physiologically the body to increase metabolism rate and requires a high amount of fat as an insulator. thereby reducing the activity of MCR and enhances the food. if exposed to high temperatures. In addition. Fitness peregulasi temperature will interact denganpusat satiety-hunger.

the consumption of chocolate. The pain is transmitted by the trigeminal nerve. 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). In addition to the causes mentioned above. X and spinal nerves C-1. there are several triggers that can cause the incidence of this type of headache. C-2 and C-3. The pain is transmitted by the cranial nerves IX. But sometimes it can also root N. Pain stimuli can be caused by the pressure. which is the area occipital.  Pathophysiology Some theories that cause headaches continue to grow until now. activation of trigeminal peripheral. People who used to drink coffee will also experience headaches when the concerned not forget to drink coffee. cortical spreading depression. Has demonstrated the close relationship between the trigeminal nucleus with upper 17 . activation rostral brainstem. 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. If the headache is due to muscle strain psychic influence then it will usually disappear after a period of stress passed. localization and physiology second order trigeminovascular neurons. upper cervical and occipital mayor will menjalarkan pain to the frontal and eye on the ipsilateral side. Such as. the theory of cranial vasodilatation. 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. displacement and chemical process and inflammation of the nociceptors-nociceptors in pain- sensitive structures in head. traction. among others. cheeses and flavoring dishes (MSG). suboccipital and cervical top.

cervical posterior. and several other chemicals" which assists in nerve communication. There is also a said that patients with chronic headaches can be very sensitive to pain general or increased pain to muscle contraction. and shoulders. temporalis.cervical dorsal root segments. and m. m. This is similar to biochemical changes associated with migraine. The muscles are usually involved. m. This may have facial muscle tension and a larger head than people Another cause them more susceptible to headaches after contraction muscle. splenius capitis. levator scapulae. including the spinal trigeminal nuclei and reach cervical motorneuron. sternocleidomastoideus. masseter. m. Trigemino cervical reflex can be demonstrated by way of stimulation n. The study said that people with headache. endorphins. 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. Exteroceptive and nociceptive input from trigemino- cervical reflex polysinaptic transmitted through the route. Given this connection it is clear that the area of the neck pain can perceived or forwarded towards the head and vice versa. trapezius. One of the most popular theories about the causes of headache are contraction of facial muscles. Although it is not known how these chemicals fluctuate. m. Researchers are now starting to believe that the headache may occur as a result of changes of certain chemicals in the brain "serotonin.supraorbitalis and recorded by means of mounting electrodes sternocleidomastoid muscle. On the one hand. among others m. m. These contractions can be triggered by body position long maintained that cause tension in the muscles or wrong sleeping position. neck. the muscle tension in the neck and skin the head can cause headaches in people with impaired chemicals. 18 . there Assuming that this process activates pain pathways to the brain and interfere the brain's ability to suppress pain.

India. Symptoms of this are found. Usually subfebril resemble influenza fever. TB (Tuberculosis)  Etiology : Typically caused by Mycobacterium tuberculosis (sometimes also by Mycobacterium africanum and Mycobacterium bovis).414 million. Coughing is necessary to out an inflammatory products out.000 cases. 3.3. What is the differential diagnose and main diagnose based on the scenario? 1. Coughing occurred because an irritation of the bronchi. These symptoms are rarely found.  Epidemiology : In 1995 approximately 1/3 of the world's population is infected by Mycobacterium tuberculosis. Fever can be cured for a while and can recur. Fever. Chest pain occurs 19 . 1. Among them 75% are in the productive age 20-49 years. 2.617. Chest pain. In 1998 there were 3. Most of these TB cases (95%) and death (98%) occurred in countries that are developing. The nature of the cough begins with a dry cough (non-productive) and then after the onset of inflammation becomes productive (produce sputum). 4.Estimates of the incidence of sputum smear positive in Indonesia is 266 000 1998. 591. the infiltration is already covering half the lungs. Shortness of breath will arise in the disease. Shortness of breath. and Indonesia respectively 1. But sometimes it can reach 40-41◦C body heat. Indonesia is a country with a TB prevalence 3rd highest in the world after China and India.047 cases of TB were recorded around the world.  Clinical manifestation: 1. Usually persistent cough more than 2 weeks. In 1998 an estimated TB in China. Cough / coughing up blood.828 million. Further circumstances are such as coughing up blood because there is a ruptured blood vessel.

the more lean body (BB down). Fever. TB disease is a chronic inflammatory disease. 5. malaise often found to be no appetite. headaches. night sweats. a black shadow on the edge radiolucent lung / pleura (pneumothorax). Pneumonia  Definition of Pneumonia: Pneumonia is a disease of lower respiratory tract (lower respiratory tract (LRT)) acute. At the beginning of the disease when the lesion is still the hotbeds of pneumonia. Malaise. muscle pain. usually caused by infection (Jeremy 2007). when the infiltration of inflammatory cells has reached the pleura. causing pleurisy. 2. Radiological Another frequently accompanies pulmonary tuberculosis is a thickening of the pleura (pleurisy). These lesions are known to tuberculoma.  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). radiology form of patches like a cloud and with indistinct boundaries. The symptoms of this malaise more and more severe and occur irregularly intermittent. When the lesion has been covered with the shadow visible connective tissue in the form of spheres with indistinct boundaries. Symptoms of anorexia. etc. In fact 20 . the mass of liquid in the bottom of the lungs (pleural effusion / empyema). but also on the lower lobe (inferior part) or in the hilum area resembles lung tumors (eg on endobronchial tuberculosis).

with the main source of bacteria. namely bacteria. although the most severe clinical manifestations appear in children. the elderly and people with chronic diseases (Elin. various chemicals and particles. mikroplasma. mushrooms. List of microorganisms that cause pneumonia Bacterial infection Atipical Infection Fungus/Myco Infection 21 .  Etiology: Pneumonia can be caused by a variety of microorganisms. and protozoa. pneumonia is not a single disease. fungi. 2008).1 lists the microorganisms and pathological problems that cause pneumonia (Jeremy 2007). The causes can vary and there are known sources of infection. Table 2. viruses. The disease can occur at any age. viruses.

Mortality: 5-12% of patients were hospitalized. Death for outpatients is less than 1%. The incidence is highest in patients who are very young and elderly. the incidence of this disease is quite high.000 adults.  Classification of Pneumonia 22 . at around 30- 40% (Sajinadiyasa. 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. 2006). 25-50% in ICU patients (Jeremy 2007). In Indonesia alone. and 5-10% were treated in the ICU. about 5-35% with deathreaches 20-50% (Farmacia. 15-45% need hospitalization in (1-4 cases).In the United States. about 10-20% of patients who require hospitalization and mortality among these patients is higher. In developing countries.000 adults. Streptococcus Mycoplasma Aspergillus pneumoniae pneumoniae Histoplasmosis Haemophillus influenza Legionella Candida Klebsiella pneumoniae pneumophillia Nocardia Pseudomonasaeruginosa Coxiella burnetii Gram-negative (E. but mortality in patients hospitalized is high at around 14% (Alberta Medical Association. 2011). the incidence of this disease reached 12 cases per 1. 2002).

Community-acquired pneumonia (community acquired pneumonia. and patients with impaired swallowing reflex (Jeremy 2007). e. the system of phagocytosis carried out by specific cells by eating the particles that reach the surface of the alveoli. Some forms of this mechanism among other forms of anatomical airways. 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. resulting in a healthy person would not have 23 . 2006). d.a. chemotherapy. CAP): pneumonia acquired in the community is that of infection outside the hospital environment. HIV) susceptible to infection by viruses. Aspiration pneumonia / anaerobic: infection by bacteroids and other anaerobic organisms after aspiration of oropharyngeal and gastric juices. LRT infections that occurred within 48 hours after being treated at the hospital in patients who had never been hospitalized for > 14 days b. steroids. Acquired pneumonia of hospital (nosocomial): pneumonia that occur during or more than 48 hours after hospital admission. more than 60% will suffer from pneumonia c. patients who were treated in the ICU. This kind obtained during the patient hospitalized (Farmacia. Opportunistic pneumonia: patients with immune suppression (eg. Lung defense mechanisms Lung trying to remove various microorganisms are inhaled as dust particles and other materials that build up in the lungs. Similarly. coughing reflex. in addition to other bacterial organisms. the infection infectious material can be removed from the respiratory tract. When the function is running well. Pneumonia is the usual type obtained in patients with depressed mental status. mukosilier system. fungi. Nearly 1% of patients treated in the hospital getting pneumonia during treatment. and mycobacteria.

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

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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

Lung abscesses can be classified based on the duration and the likely etiology. A typical lung abscess could be reproduced in animal models via an intratracheal inoculum containing. approximately one third of patients with lung abscess died. or other consequences of chronic pyogenic infections. Although resectional surgery was often considered a treatment option in the past. when one third of the patients died. After penicillins and tetracyclines became available. Acute abscesses are less than 4-6 weeks old. Dr David Smith postulated that aspiration of oral bacteria was the mechanism of infection. obstruction). but 4 microbes. Lung abscess was a devastating disease in the preantibiotic era. bronchiectasis. Prevotellamelaninogenicus. and the remainder developed debilitating illnesses such as recurrent abscesses. spread from an extrapulmonary site. thought to be Fusobacteriumnucleatum. Secondary abscesses are caused by a preexisting condition (eg. sulfonamides did not improve the outcome of patients with lung abscess. a fastidious gram-negative anaerobe. Lung abscesses can be further characterized 27 . He observed that the bacteria found in the walls of the lung abscesses at autopsy resembled the bacteria noted in the gingival crevice. chronic empyema. In the early postantibiotic period. Primary abscesses are infectious in origin. possibly. and. and/or an immunocompromised state. Failure to recognize and treat lung abscess is associated with poor clinical outcome. caused by aspiration or pneumonia in the healthy host. Peptostreptococcus species. the role of surgery has greatly diminished over time because most patients with uncomplicated lung abscess eventually respond to prolonged antibiotic therapy. outcomes improved. bronchiectasis. whereas chronic abscesses are of longer duration. another one third recovered. not 1.pathologic process. In the 1920s.

Epidemiology :  Frequency The frequency of lung abscesses in the general population is not known. by the responsible pathogen.  Sex A male predominance for lung abscess is reported in published case series. anorexia. A lung abscess may be asymptomatic in a small proportion of patients in the early stages. cough with sputum production. Typical symptoms are below. Anaerobic infection in lung abscess Patients often present with indolent symptoms that evolve over a period of weeks to months. night sweats. However.  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. and weight loss. The expectorated 28 . 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. The usual symptoms are fever. such as Staphylococcus lung abscesses and anaerobic abscess or Aspergillus lung abscess.

Abscesses from fungi. In general abscesses are round in shape. Nocardia species. sputum characteristically is foul smelling and bad tasting. Additionally all margins are equally well seen. Cavitation occurs subsequently as parenchymal necrosis ensues. 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. These features are helpful in distinguishing a pulmonary abscess from an empyema 4. and appear similar in both frontal and lateral projections. Radiology: The classical appearance of a pulmonary abscess is a cavity containing an air-fluid level. Bronchiectasis Etiology: Causes of bronchiectasis include the following: 29 . and Mycobacteria species tend to have an indolent course and gradually progressive symptoms. although adjacent consolidation may make assessment of this difficult.

Primary infection 30 . 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.

(ie. 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. It has a propensity to occur in the setting of human immunodeficiency virus (HIV) infection as well as in hosts who are immunocompetent. where antibiotics are used inconsistently. Mycobacterium avium complex (MAC) infection deserves special mention. 31 . 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.

foreign body aspiration). bronchial stenosis from infections. This suggests that Pseudomonas species may promote disease progression. endobronchial tumors. broncholithiasis. 32 . subsequent infection. It results from an abnormal angulation of the lobar bronchus at its origin. and that infection with these species may be related to worsening lung function and increased morbidity and mortality. Sputum smear in these cases is positive for acid-fast bacilli. and tend to voluntarily suppress cough. Bronchial obstruction Focal postobstructive bronchiectasis may occur in a number of clinical settings (eg. and development of bronchiectasis. Right- middle lobe syndrome is a specific type of bronchial obstruction that may result in bronchiectasis. many of these same organisms colonize the damaged bronchi and may cause ongoing damage and episodic infectious exacerbations. encroachment of hilar lymph nodes. predisposing it to obstruction. are older than 60 years. MAC infection has been observed especially in women who are nonsmokers. and CT scan shows small regular nodules and findings of bronchiectasis. Once a patient develops bronchiectasis. Although not a primary cause of bronchiectasis. do not have a known predisposing pulmonary disorder. 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. The organisms found most typically include Haemophilus species (47-55% of patients) and Pseudomonas species (18-26% of patients).

primarily secondary to a defect in the CF transmembrane regulator (CFTR) protein.500 whites and 1 in 17. 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. CF and its variants are the most common cause of bronchiectasis in the United States and other industrialized nations. In was estimated that in 2005. However.Aspiration In adults.000 adults in the United States would have CF.000 blacks in the United States. 10. 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. including food. Patients may also aspirate chewed materials from the stomach. After aspiration. which is an almost universal feature of this disease. comprising 40% of the total CF population. foreign body aspiration often takes place in the setting of altered mental status and involves unchewed food. It may be the sole feature of CF in adults or those 33 . and the risk to patients that have genetic heterozygous mutations remains to be elucidated. Bronchiectasis may also develop in the setting of chronic aspiration. peptic acid. a postobstructive pneumonia may occur. The major pulmonary finding in CF is bronchiectasis. with subsequent development of focal bronchiectasis. and microorganisms. Multiple genetic variants of CF exist. Cystic fibrosis CF is a multisystem disorder that affects the chloride transport system in exocrine tissues. CF is an autosomal recessive disease affecting approximately 1 in 2.

and. ultimately. encompassed the clinical triad of situsinversus.000 population. they do not display the other findings of CF. However. 34 . sinusitis. bronchiectasis. Young syndrome Young syndrome is clinically similar to CF and may represent a genetic variant of CF. A variant of this condition. Allergic bronchopulmonaryaspergillosis Allergic bronchopulmonaryaspergillosis (ABPA) is a hypersensitivity reaction to inhaled Aspergillus antigen that is characterized by bronchospasm. and obstructive azoospermia. It is most often observed in middle-aged men in North America and is a leading cause of male infertility. It is manifested by immotile or dyskinetic cilia and/or sperm. Primary ciliary dyskinesia Primary ciliary dyskinesia is a group of inherited disorders that may affect 1 in 15. and bronchiectasis in the setting of immotile cilia of the respiratory tract. especially with mucoidP aeruginosa. Bronchiectasis associated with CF is believed to occur secondary to mucous plugging of proximal airways and chronic pulmonary infection.with genetic variations of the disease. Patients with Young syndrome have bronchiectasis (often predominant in the lower lobes). nasal polyps or sinusitis. The criterion standard for diagnosis of Young syndrome is electron microscopic analysis of the structure of the cilia. The pathogenesis of bronchiectasis in these patients is believed to be similar to that of bronchiectasis in CF. initially described by Kartagener. This may lead to poor mucociliary clearance.000-30. recurrent pulmonary infections.

and dramatic responses to therapeutic corticosteroids. CT scanning of the chest demonstrates central airway bronchiectasis. differentiating this condition from other causes of bronchiectasis. Bronchiectasis is believed to be secondary to airway plugging by viscid secretions containing hyphae of Aspergillus species. 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. 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. Immunodeficiency states Immunodeficiency states may be congenital or acquired. The most common congenital conditions (albeit rare) involve B-lymphocyte functions. elevated immunoglobulin E (IgE) levels. although the disorder has been diagnosed 35 .bronchiectasis. The resulting bronchiectasis is thin-walled and affects the central and medium-sized airways. Other features of ABPA include eosinophilia.

Swyer-James syndrome (unilateral hyperlucent lung) likely is a developmental disturbance that leads to unilateral bronchiolitis. in some cases. It results in exudative pleural effusions. Congenital anatomic defects Bronchiectasis can result from a variety of congenital anatomic defects. 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.in adults who did not have a history of repeated infections. Williams-Campbell syndrome (congenital cartilage deficiency) is the absence of cartilage from lobar to first. 36 . Mounier-Kuhn syndrome (tracheobronchomegaly) is a rare disorder characterized by dilation of the trachea and segmental bronchi (central bronchiectasis). with resultant acquired immunodeficiency syndrome (AIDS). bronchiectasis. hyperinflation. HIV disease. Establishing the diagnosis is important because gammaglobulin replacement may reduce the number of infections and resultant lung injury.to second-generation segmental airways that results in extensive peripheral bronchiectasis. and. 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. Yellow-nail syndrome is rare. Bronchopulmonary sequestration is a congenital abnormality classified as either intralobar or extralobar and results in chronic lower respiratory tract infections that lead to bronchiectasis.

but it is believed that the AAT abnormalities make patients more susceptible to respiratory tract infections and subsequent bronchial damage. wheezing. 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. 37 . Less specific symptoms include dyspnea. The pathogenesis of bronchiectasis in this setting is unclear. A rare variant known as dry bronchiectasis manifests as episodic hemoptysis with little-to-no sputum production. Clinical Presentation: The classic clinical manifestations of bronchiectasis are cough and daily mucopurulent sputum production. fever. Blood-streaked sputum or hemoptysis may result from airway damage associated with acute infection. both in patients with true AAT deficiency and in patients with heterozygous phenotypes. Epidemiology: Currently no systematic data are available on the incidence or prevalence of bronchiectasis. Bronchiectasis remains a major cause of morbidity in less- developed countries. weakness.Alpha1-antitrypsin (AAT) deficiency Bronchiectasis has been noted to occur in this rare condition. with significantly lower prevalence in areas where immunizations and antibiotics are readily available. Dry bronchiectasis is usually a sequela of tuberculosis and is found in the upper lobes. especially in countries with limited access to medical care and antibiotic therapy. and weight loss. The best data available suggest that the prevalence of bronchiectasis mirrors the socioeconomic conditions of the population under study. often lasting months to years. pleuritic chest pain.

such as fatigue and malaise. often in childhood. or Mycoplasma infection. Although patients may report repetitive pulmonary infections that require antibiotics over several years. Sputum is typically produced on a daily basis in greater than 70% of patients. Patients may experience an increase in generalized constitutional symptoms. or severe bacterial pneumonia. Some patients produce sputum 38 . a single episode of a severe infection. findings of obstruction on spirometry testing. With secondary infection or poorly treated pneumonia. or pleuritic pain. All children underwent chest multi-detector CT (MDCT) scans. 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. Rarely. These include tuberculosis. low-grade fever may occur. a foul odor of the sputum. Chronic wet cough may also be an indicator of bronchiectasis. CF is the most common cause of bronchiectasis in children and young adults. and. shortness of breath. may result in bronchiectasis.occurring in up to 98% of patients. most patients relate a history of childhood infections that may include tuberculosis. Of the 144 children. However. Most individuals have never smoked (55%) or have smoked too little to account for their degree of cough. Today. wheezing. occasionally. pertussis. as well as increased dyspnea. 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. the discrete pathogens are often unknown. In a retrospective study of 144 Australian children with a chronic wet cough. pertussis. and daily sputum production. Chronic productive cough is prominent. with one study reporting production in 96% of patients. 106 exhibited evidence of bronchiectasis on their MDCT scan.

Similar to dyspnea. massive hemoptysis may occur but is rarely a cause of death. Hemoptysis occurs in 56-92% of patients with bronchiectasis. a 2006 review reported a rate of 62%.only with acute upper respiratory tract infections. however. Weight loss often occurs in patients with severe bronchiectasis. This is often the factor that leads patients to consult a physician. It is most commonly secondary to chronic coughing but also occurs in the setting of acute exacerbation. Hemoptysis is generally mild and manifested by blood flecks in the patient's usual purulent sputum. Therefore. it may also be secondary to concomitant conditions such as asthma. Pleuritic chest pain is an intermittent finding. sputum becomes purulent and may develop an offensive odor.Dyspnea typically occurs in patients with extensive bronchiectasis observed on chest radiographs. Bleeding usually originates from dilated bronchial arteries. which contain blood at systemic (rather than pulmonary) pressures. Sputum is typically mucoid and relatively odorless. occurring in 19-46% of patients. During infectious exacerbations. but otherwise they have quiescent disease. Hemoptysis is more commonly observed in dry bronchiectasis. Wheezing is commonly reported and may be due to airflow obstruction following destruction of the bronchial tree. Dyspnea may occur in as many as 72% of patients. Fatigue is commonly reported (73% of patients). Marked dyspnea is more likely to be secondary to a concomitant illness. such as chronic bronchitis or emphysema. This is believed to be secondary to increased caloric requirements associated with the increased work of coughing 39 .

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. There are more than 60 different toxins in tobacco smoke that can cause cancer and these are referred to as carcinogens. Weight loss suggests advanced disease but is not diagnostic of bronchiectasis. chewing tobacco and snuff 40 . Radiology: Chest x-rays are usually abnormal. Overall there appears to be an increase in bronchovascular markings. other tobacco products such as pipe tobacco. Smoking is the cause of lung cancer in more than 90% of cases and is the single biggest risk factor for lung cancer. thought to represent peribronchovascular fibrosis 5. Pulmonary vasculature appears ill-defined. although non-smokers can also develop the condition. Smoking and other risk factors for lung cancer are described below. Tram- track opacities are seen in cylindrical bronchiectasis. Although tobacco smoking is the main risk factor for lung cancer.and clearing secretions. and bronchi seen end on may appear as ring shadows. Fever may occur in the setting of acute infectious exacerbations. and air-fluid levels may be seen in cystic bronchiectasis. cigars. but are inadequate in the diagnosis or quantification of bronchiectasis.

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 .

low. In severe pneumonia. After a few days. are relatively virulent so that only a small inoculum is required to result in a pneumonia.000 to 600.5-7 Aspiration pneumonia is the most common cause of death in patients with dysphagia due to neurologic disorders. 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.  Symptoms The signs and symptoms of aspiration pneumonia vary.Haemophilus influenza. Staphylococcus aureus. The inoculum in what was traditionally recognized as aspiration pneumonia was larger and typically apparent. several studies in. Pneumonia Aspiration  Epidemiology Nevertheless.  Radiology 42 . the patient expectorates mucoid or mucopurulent sputum. aspiration pneumonia referred to an infection caused by less virulent bacteria. primarily oral pharyngeal anaerobes. The predominant symptoms may be headache. and gram- negative bacteria. myalgia. such as Streptococcus pneumoniae. The aspiration episode is often subtle.acquired pneumonia are aspiration pneumonia. rash. pleuritic pain. The micro-organisms that commonly cause these pneumonias.000 people each year in the United States.  Etiology Aspiration pneumonia is caused by bacteria that normally reside in the oral and nasal pharynx.grade fever. a condition that affects approximately300. the patient’s cheeks are flushed and central cyanosis affects the lips and nail beds. Historically.tis. a late sign of poor oxygenation (hypoxemia).6. and pharyngi.dicate that 5 to 15 percent of cases of community.

18). 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. For the majority of individuals with normal immune function. bones. In persons with intact cell-mediated immunity. The organisms grow for 2 to 12 week. the droplet nucleus is carried down the bronchial tree and implants in a respiratory bronchiole or alveolus. until they reach 103 to 104 in number.4. Mention the pathogenesis of diagnose based on the scenario? After inhalation. 43 . dividing approximately every 25 to 32 hours within the macrophage. The bone marrow. collections of activated T cells and macrophages form granulomas that limit multiplication and spread of the organism. tuberculosis is arrested once cell-mediated immunity develops. which is sufficient to elicit a cellular immune response that can be detected by a reaction to the tuberculin skin test. Organisms deposited in the upper lung zones. Certain organs and tissues are notably resistant to subsequent multiplication of these bacilli. but uncontrolled multiplication of the bacteria in these sites is exceptional. which is often necrotic. Before the development of cellular immunity. and spleen are almost always seeded with mycobacteria. If the bacillus is able to survive initial defenses. proliferation of M. and brain may find environments that favor their growth. it can multiply within the alveolar macrophage. liver. kidneys. The organisms tend to be localized in the center of the granuloma. tuberculosis are formed but do not appear to be protective. even though small numbers of viable bacilli may remain within the granuloma. and numerous bacterial divisions may occur before specific cellular immunity develops and limits multiplication. Antibodies against M. there is no immediate host response to infection. The tubercle bacillus grows slowly. Mycobacterium tuberculosis has no known endotoxins or exotoxins. therefore. tubercle bacilli spread via the lymphatics to the hilar lymph nodes and thence through the bloodstream to more distant sites.

tuberculosis has taken place. the response to infection with the tubercle bacillus provides protection against reinfection. especially those with low CD4 1 cell counts. previously infected person. HIV-infected persons. Most commonly.. HIV infection. tuberculosis. e. a positive tuberculin skin test result is the only indication that infection with M. the majority of pulmonary tuberculosis infections are clinically and radiographically inapparent.g. tuberculosis. In a person with intact cell-mediated immunity. any 44 . Conversely. develop tuberculosis disease rapidly after becoming infected with M. It is estimated that approximately 10% of individuals who acquire tuberculosis infection and are not given preventive therapy will develop active tuberculosis. an individual who has a prior latent infection with M. Individuals with latent tuberculosis infection but not active disease are not infectious and thus cannot transmit the organism. as well as by corticosteroids and other immunosuppressive drugs. The risk of developing tuberculosis also appears to be greater during the first 2-yr of life. the intensity of such exposure. The likelihood of reinfection is a function of the risk of reexposure. Furthermore. The ability of the host to respond to the organism may be reduced by certain diseases such as silicosis. and diseases associated with immunosuppression. up to 50% of such persons may do so in the first 2 yr after infection with M. In these circumstances. tuberculosis (not treated) and then acquires HIV infection will develop tuberculosis disease at an approximate rate of 5– 10% per year. when half the cases will occur. in an otherwise healthy. In the United States the risk of reexposure to an infectious case is low. and the integrity of the host’s immune system. diabetes mellitus. the likelihood of developing tuberculosisdisease is greater.Although a primary complex can sometimes be seen on chest radiograph. The risk is highest in the first 2 year after infection.

5. lymph nodes. meninges. pleura. but in immunocompetent individuals.  Extrapulmonary tuberculosis (EPTB) refers to any bacteriologically confirmed or clinically diagnosed case of TB involving organs other than the lungs. skin. without radiographic abnormalities in the lungs. constitutes a case of extrapulmonary TB. clinical and laboratory evidence indicates that disease produced by the inhalation of a second infecting strain is uncommon. 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 . Miliary TB is classified as PTB because there are lesions in the lungs. organisms that are deposited in the alveoli are likely to be killed by the cell-mediated immune response. Exceptions may occur. Tuberculous intra-thoracic lymphadenopathy (mediastinal and/or hilar) or tuberculous pleural effusion. genitourinary tract.g. A patient with both pulmonary and extrapulmonary TB should be classified as a case of PTB. joints and bones. e. reinfection has been documented to occur both in persons without recognized immune compromise and in persons with advanced HIV infection. abdomen. 2. However. 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.

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. Previously treated patients have received 1 month or more of anti-TB drugs in the past. .New patients have never been treated for TB or have taken anti-TB drugs for less than 1 month. New and relapse cases of TB are incident TB cases. and are now diagnosed with a recurrent episode of TB (either a true relapse or a new episode of TB caused byreinfection). 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 . 3. They are further classified by the outcome of their most recent course of treatment as follows: . . were declared cured or treatment completed at the end of their most recent course of treatment. 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. Relapse patients have previously been treated for TB.resistant tuberculosis. of disease.) . 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. 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. (These were previously known as treatment after defaultpatients. Patients with unknown previous TB treatment history do not fit into any of the categories listed above.

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. Extensive drug resistance: resistance to any fluoroquinolone and to at least one of three second-line . tuberculosis: . whether 47 . in addition to multidrug resistance. If the patient’s HIV status is subsequently determined. injectable drugs (capreomycin. Rifampicin resistance:1 resistance to rifampicin detected using phenotypic or genotypic methods. Any HIV-negative TB patient subsequently found to be HIV-positive should be reclassified accordingly. Classification based on drug resistance Cases are classified in categories based on drug susceptibility testing (DST) of clinical isolates confirmed to be M.conducted at the time of TB diagnosis or other documented evidence of enrolment in HIV care. . kanamycin and amikacin). such as enrolment in the pre-ART register or in the ART register once ART has been started. . . Monoresistance: resistance to one first-line anti-TB drug only. . 4. Multidrug resistance: resistance to at least both isoniazid and rifampicin. he or she 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. Polydrug resistance: resistance to more than one first-line anti-TB drug (other than both isoniazid and rifampicin). with or without resistance to other anti-TB drugs. It includes any resistance to rifampicin.

weakness Special symptoms: •Wheezing 48 . so it is quite difficult to diagnose in clinic. future drug regimens may make it important to classify patients by their strain resistance patterns to fluoroquinolones. multidrug-resistant TB (MDR-TB) and extensively drug-resistant TB (XDR-TB) are also included. Sometimes. fever attack present but occur intermittent such as. While it has been the practice until now to limit the definitions of monoresistance and polydrug resistance to first-line drugs only. can be accompanied by blood (hemoptysis) • Fever is not too high that lasts longer. second-line injectable agents and any other anti-TB drug for which reliable DST becomes available. When enumerating rifampicin-resistant TB (RR-TB). 6. usually felt at night and accompanied with night sweats. Clinical picture is not too distinctive or not specific. 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. monoresistance. These categories are not all mutually exclusive. for instance. influenza •Loss of appetite and weight loss • feeling unwell (malaise). Systemic symptoms / general: • Coughing for more than 3 weeks. polydrug resistance or extensive drug resistance. multidrug resistance.

Bone tuberculosis When the bone is infected. 49 . Tuberculosis show no typical symptoms. there will be symptoms such as bone infection where the surface of the skin excrete pus. Approximately 30-50% of children contact with adult pulmonary tuberculosis patients give positive tuberculin test results. where tuberculosis can be detected if there is history of contacts with adult with tuberculosis.5 years who live with pulmonary tuberculosis patients adults with positive smear. This is cause by the compression by enlarged lymph nodes. reported that 30% of them being infected. In children aged 3 months . In pediatric patients. •Chest pain If there is fluid in the pleural cavity(cavum pleura). Wheezing sound is weakened voice accompanied by shortness of breath. the loss of consciousness and convulsions. •Extra PulmonalTuberculosis -. can be accompanied with complaints of chest pain. detected by serology and blood examination. --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. In the case of blockage of bronchi. it would create “wheezing” sound.

50 .

51 . 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). Mention the general and supportive examination based on the scenario? TB is a disease caused by Mycobacterium tuberculosis. symptoms will depend on the area affected. 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). 7.

ethnic or racial group. Also. tuberculosis. Test for TB Infection The Mantoux tuberculin skin test (TST) or the TB blood test can be used to test for M. 3. infection. occupation) that may increase the patient’s risk for exposure to TB or to drug- resistant TB. Additional tests are required to confirm TB disease. who looks for a reaction (induration) on the arm. 52 . tuberculosis infection. country of origin. It is also important to consider demographic factors (e. age.g. clinicians should determine whether the patient has medical conditions. but cannot be used to definitively diagnose TB. The TB blood test measures the patient’s immune system reaction to M. especially HIV infection. or disease. 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.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 patient’s history of TB exposure. 2. 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. However. Chest Radiograph A posterior-anterior chest radiograph is used to detect chest abnormalities. and cavitation. These abnormalities may suggest TB. such as HIV infection or other illnesses. 4. The test is read within 48 to 72 hours by a trained health care worker. density. Physical Examination A physical exam can provide valuable information about the patient’s overall condition and other factors that may affect how TB is treated. Lesions may appear anywhere in the lungs and may differ in size. that increase the risk of latent TB infection progressing to TB disease. shape..

6.) A positive culture for M. the initial M. regardless of AFB smear results. if not handled properly will cause complications. Diagnostic Microbiology The presence of acid-fast-bacilli (AFB) on a sputum smear or other specimen often indicates TB disease.5. tuberculosisconfirms the diagnosis of TB disease. a positive culture is not always necessary to begin or continue treatment for TB. Drug Resistance For all patients. It is crucial to identify drug resistance as early as possible to ensure effective treatment. 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. The complications that occur in patients with pulmonary tuberculosis can be divided into two. Massive hemoptysis (bleeding from the lower respiratory tract) that can cause death due to airway obstruction or hypovolemic shock b. a culture is done on all initial samples to confirm the diagnosis. Susceptibility results from laboratories should be promptly reported to the primary health care provider and the state or local TB control program. intestines. 8. Mention the complication based on the scenario? Pulmonary tuberculosis. tuberculosis isolate should be tested for drug resistance. Therefore. namely: 1. Culture examinations should be completed on all specimens. Acid-fast microscopy is easy and quick. tuberculosis. Complications at an advanced stage: The complications are common in patients with advanced stage are: a. pleural effusion. laryngitis. 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. (However. empyema. but it does not confirm a diagnosis of TB because some acid-fast-bacilli are not M. 2. Early complications: pleurisy. Lobar collapse due to blockage of the duct c. as required by law. Bronkietaksis (local bronchial dilation) and fibrosis (formation of connective tissue in the recovery process or reactive) in the lungs 53 .

Curing patients and restore the quality of life and productivity. a. d. • To ensure patient compliance swallowing the drug. b. e. Reduce transmission. bones. usage OAT Combination Fixed Dose (OAT-KDT) more profitable and highly recommended. Preventing drug resistance Treatment of tuberculosis carried by the principle . c. that collapse spontaneously because the bull / blep broken e. in sufficient quantities and appropriate doses according to the category of treatment. 1. Pnemotoraks spontaneously. Mention the management based on the scenario? TB treatment is aimed at. Do not use OAT alone (monotherapy). 9.the principle as following: • OAT must be given in the form of a combination of several types of drugs. Prevent recurrence. do direct supervision (DOT = Directly Observed Treatment) by a Supervisory Swallowing Drugs (PMO) TB treatment is given in two stages. kidneys. joints. d. etc. The spread of infection to other organs such as the brain. Preventing death. Early Stage (Intensive) 54 . namely intensive and continuation phases.

Most patients with sputum smear positive TB negative (conversion) within 2 months. usually infectious patients become non-infectious within 2 weeks. cycloserine followed 15- 18 months ofloxacin. • If there is no resistance test results. 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. ethionamide. namely: a. 2. Category II . ofloxacin. smear positive or lesions on chest radiograph contained large. Advanced stages it is important to kill germs persistent so as to prevent the occurrence of recurrence. Category I . • Alloy drugs recommended is 2 RHZES / 1 RHZE before No resistance test results. Secondary Phase In the advanced stages patients received fewer types of drugs. When The intensive phase of treatment given correctly. ethionamide. • Under no circumstances do not allow the initial phase can be given 2 RHZES / 1 RHZE. If the test of resistance have been there. • continuation phase in accordance with the results of resistance testing. b.Pulmonary tuberculosis relapse cases. . 55 . can be given 5 RHE.Pulmonary tuberculosis (new cases).Alloy drugs recommended is 2 RHZE / 4 RH or 2 RHZE / 6HE or 2 RHZE / 4R3H3. . OAT alloys used in Indonesia. In the intensive phase (early) patients received the drug every day and need directly supervised to prevent the development of drug resistance. but in a longer period of time. cycloserine).

give RHZES. Treated ≤ 4 months .MDR TB. Category V .treatment continued.3. treatment starts from the beginning with alloys stronger medication and long treatment times long (2 RHZES / 1 RHZE / 5 R3H3E3). the recommended treatment regimen in accordance with the resistance test plus OAT lines 2 or H lifetime. 56 . e. perform further analysis to ensure TB diagnosis by also considering the possibility of another lung disease.Alloy drug administered is 2RHZE / 4 R3H3. when the picture radiology active. provide appropriate resistance test results (minimum OAT sensitive plus second-line drugs (medication at least 18 months). d. If there has been a resistance test results. Treatment starts from the beginning with alloy stronger medication and treatment period longer. . If confirmed TB.When the smear negative. smear negative or lesions on chest radiograph contained minimal. Regimen is recommended when there is no resistance test results.Chronic pulmonary tuberculosis cases. 1. Clinical and radiological inactive or no repair the OAT treatment is stopped. Treated ≥ 4 months . 2. Category III . the treatment begins from the start with a stronger regimen and run longer treatment time (2 RHZES / 1 RHZE / 5R3H3E3). positive chest X-ray picture of active TB. Category IV .BTA is currently positive. Pulmonary TB withdrawing treatment. . c.When the smear-positive.Pulmonary tuberculosis (new cases).BTA is currently negative. .

Heal the outcome of patients with sputum smear or culture-positive before treatment. vomiting. d. f. Categorized as follows: a. and jaundice. sometimes can cause numbness in the limbs. Streptomycin can cause dizziness and hearing loss due to nerve damage in the ear. Moving a patient who moved into unit (recording and reportingdifferent and the final outcome of treatment is unknown. Ethambutol can cause blurred vision and impaired color vision because the drug affects the optic nerve 5. 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.TB drugs have side effects including: 1. Rifampicin can cause liver damage. Isoniazid can cause liver damage which would cause nausea. • Treatment Results The end result of treatment of smear positive pulmonary tuberculosis patientsand negative. Failing a patient with sputum or culture-positive results in or more in the fifth month of treatment. b. Default / drop-out is lost in the treatment of patients with two consecutive months or more. e. 4. Died of a patient who died with any cause during the 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. c. 2. discoloration of water eyes. sweat. 3. 57 . Pyrazinamide can cause liver damage and gout. and urine orange. radiology picture serial (minimum 2 months) remains the same / repair.

58 .Sunlight and Ventilation Sunlight can kill the TB germs and good ventilation can prevent the transmission of TB germs in the room. If possible. 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. . Protection against TB exposure Early diagnosis and management is the best way to reduce exposure to TB. 1. Lowering the concentration of bacteria .10. Mask Use of masks regularly will reduce the spread of germs through the air. where the medical staff and other patients receive repeated exposure of patients who are exposed to TB. This radiation methods should be used in rooms inhabited infectious TB patients and the room where the action is induced sputum or bronchoscopy. c. tuberculosis is highly sensitive to UV radiation bactericidal. 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. The risk exposure contained in TB wards and wards. There are several factors that may affect the transmission among others : a. TB patients with uncontrolled cough are advised to use a mask at all times.Filtration Air filtration depending on the facilities and resources available. b. .UV radiation bactericidal M.

Patients with suspected or confirmed infected with TB should not be placed in rooms occupied by patients who are immunocompromised. if needed. can be given the BCG vaccination without prior tuberculin test. If possible.Patients are isolated should not leave the room without wearing a mask. Vaccination BCG (Bacillus Calmette Guerin) BCG is a live vaccine derived from M. tuberculin test Neonates and infants up to 3 months old with no history of contact with TB. BCG function is to protect children against disseminated TB and extra-pulmonary TB weight (TB meningitis and miliary TB). d. b.The medical staff also recommended to use a mask when exposure to respiratory secretions can not be avoided. BCG given intradermally to the uninfected population. or oncology. Routine Vaccination In countries with high TB prevalence. . 2.bovis. The drugs used are usually isoniazid (5 mg / kg) for 6 months. . a.Immediate hospitalization of patients with pulmonary TB BTA (+) for the intensive phase of treatment. BCG does not have the effect of lowering cases of pulmonary tuberculosis in adults. 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. WHO recommends BCG vaccination as early as possible. do with 59 . transplantation. Recommended NTP (National TB Prevention) against TB exposure: . Prevention Therapy The purpose of preventive therapy is to prevent TB infection to disease. 3. such as HIV patients.Patients should be isolated to reduce the risk of TB exposure to other patients. especially newborns. because TB disease can occur in 10% of people who have TB infection. .

. The group receiving prophylaxis.Children with a history of contacts. should receive isoniazid for 3 months. If the result is negative then be vaccinated. • Children with symptoms. apparently healthy. . but the examination did not show TB. direct observation. An Nisaa’:9) ‫خاففوا ا ع لل ليحههمح‬ ‫فا ل‬ ‫ضععل ف‬ ‫فهه حم ذ فرري ي ة‬ ‫ة ه‬ ‫خلح ه‬ ‫كوا ا ه‬ ‫منح ل‬ ‫ن ل لوح ت للر ف‬ ‫ذي ل‬‫ش ٱل ي ه‬ ‫وللحي لخح ل‬ ٩ ‫دا‬ ‫دي ف‬ ‫س ه‬‫قوفلوا ا قلوحةل ل‬ ‫قوا ا ٱلل ي ل‬ ‫ه وللحي ل ف‬ ‫فللحي لت ي ف‬ Dan hendaklah takut kepada Allah orang-orang yang seandainya meninggalkan dibelakang mereka anak-anak yang lemah.Children with a history of contacts. Yusuf: 87) 60 . • Children with symptoms and examination showed tuberculosis TB treatment is given. the same as the above. positive tuberculin (without a history of BCG). Oleh sebab itu hendaklah mereka bertakwa kepada Allah dan hendaklah mereka mengucapkan perkataan yang benar 3 (QS. tuberculin negative. 11. How do you see the case in the view of Islam’s perspective based on the scenario? AL QURAN 2 (QS. it is necessary to be given the full treatment. namely: . no history of BCG. 2001). isoniazid prophylaxis (Wieslaw et al. yang mereka khawatir terhadap (kesejahteraan) mereka. carried out the tuberculin test. if positive then continued isoniazid for 3 months again.Infants with pulmonary tuberculosis-infected mothers Babies who are breast-feeding mothers with pulmonary TB. After 3 months. • Children without symptoms should be given a 6-month isoniazid prophylaxis. If there is evidence of disease.

maka carilah berita tentang Yusuf dan saudaranya‬‬ ‫‪dan jangan kamu berputus asa dari rahmat Allah.‬‬ ‫‪menyuruh kepada yang ma´ruf dan mencegah dari yang munkar. melainkan kaum yang kafir‬‬ ‫)‪4 (QS. Al-Hujurat: 13‬‬ ‫‪61‬‬ .‫ح‬ ‫سوا ا ه‬ ‫من يروح ه‬ ‫خيهه وللل ت لا ايح‍م‍ ف‬ ‫ف ولأ ل ه‬ ‫س ل‬ ‫من فيو ف‬ ‫سوا ا ه‬ ‫س ف‬‫ح ي‬‫ي ٱذحهلفبوا ا فلت ل ل‬ ‫ي علب لن ه ي‬ ‫ن ‪٨٧‬‬‫ففرو ل‬ ‫م ٱلحك عل ه‬‫قوح ف‬‫من يروحهح ٱلل يهه إ هيل ٱلح ل‬‫س ه‬‫هۥ لل ي لا ايح‍م‍ ف‬ ‫ٱلل ي ههه إ هن ي ف‬ ‫‪“Hai anak-anakku. Sesungguhnya tiada berputus asa‬‬ ‫"‪dari rahmat Allah. Ali Imran: 104‬‬ ‫سب لتح ولع لل ليحلها ل‬ ‫ما‬ ‫ما ك ل ل‬‫سا إ هيل وفسحعلهلاا ل للها ل‬ ‫ف ٱلل ي ف‬ ‫ه ن لفح ف‬ ‫لل ي فك لل ر ف‬ ‫ل ل‬ ‫سيلنا أوح أخحط لأحن لاا لرب يلنا وللل ت لحح ه‬ ‫ملح‬ ‫خذحلنا هإن ن ي ه‬ ‫سب لتحت لرب يلنا لل ت ف ل‬ ‫ؤا ه‬ ‫ٱكحت ل ل‬ ‫ملحلنا‬ ‫ح ر‬ ‫من قلبحل هن لاا لرب يلنا وللل ت ف ل‬‫ن ه‬ ‫ذي ل‬‫هۥ ع لللى ٱل ي ه‬ ‫ملحت ل ف‬ ‫ح ل‬ ‫ما ل‬ ‫ع لل ليحلنا إ هصحةرا ك ل ل‬ ‫موحل لى علنا‬ ‫ل‬ ‫ت ل‬ ‫فرح ل للنا ولٱرح ل‬ ‫حمحن لاا أن ل‬ ‫ف ع لينا ولٱغح ه‬ ‫ة ل للنا ب هههۦه ولٱعح ف‬ ‫طاقل ل‬ ‫ما لل ل‬ ‫ل‬ ‫خل لقحن عل ف‬ ‫ل‬ ‫صرحلنا ع لللى ٱلح ل‬ ‫كم‬ ‫س إ هينا ل‬‫ن ‪ ٢٨٦‬ي يلعأي يلها ٱلينا ف‬ ‫ري ل‬ ‫قوحم ه ٱلحك عل ه‬ ‫ف ه‬ ‫فلٱن ف‬ ‫مك فمح‬ ‫ل ل هتعارففوا ا إ ل‬ ‫جعللحن علك فمح ف‬ ‫من ذ لك لر و ف‬ ‫ن أكحلر ل‬ ‫شفعوةبا ولقللبائ ه ل ل ل ل ي ه ي‬ ‫ى ول ل‬ ‫ع‬ ‫ل‬ ‫ث‬ ‫أن‬ ‫ر ل‬ ‫ر‬ ‫خهبيرر ‪١٣‬‬ ‫م ل‬ ‫ه ع لهلي م‬ ‫ن ٱلل ي ل‬ ‫قى عك فمحا إ ه ي‬ ‫عند ل ٱلل يهه أ لتح ل‬ ‫ه‬ ‫‪Dan hendaklah ada di antara kamu segolongan umat yang menyeru kepada kebajikan. pergilah kamu. merekalah orang-‬‬ ‫‪orang yang beruntung‬‬ ‫‪5‬‬ ‫)‪(QS.

dan‬‬ ‫‪jangan melanggar kehormatan bulan-bulan haram. Sesungguhnya Allah‬‬ ‫‪Maha Mengetahui lagi Maha Mengenal. Sesungguhnya orang yang paling mulia diantara‬‬ ‫‪kamu disisi Allah ialah orang yang paling takwa diantara kamu. sesungguhnya Kami menciptakan kamu dari seorang laki-laki dan‬‬ ‫‪seorang perempuan dan menjadikan kamu berbangsa-bangsa dan bersuku-suku‬‬ ‫‪supaya kamu saling kenal-mengenal. ‫جعللحن علك فمح ف‬ ‫ف‬ ‫خل لقحن عل ف‬ ‫ل‬ ‫شفعوةبا‬ ‫ى ول ل‬ ‫من ذ لك لرر ولأنث ل ع‬‫كم ر‬ ‫س إ هينا ل‬ ‫ي يلعأي يلها ٱلينا ف‬ ‫م‬ ‫ن ٱلل ي ل‬ ‫ه ع لهلي م‬ ‫عند ل ٱلل يهه أ لتح ل‬ ‫قى عك فمحا إ ه ي‬ ‫مك فمح ه‬ ‫ل ل هتعارففوا ا إ ل‬ ‫ن أكحلر ل‬ ‫ولقللبائ ه ل ل ل ل ي ه ي‬ ‫خهبيرر ‪١٣‬‬ ‫ل‬ ‫‪Hai manusia.‬‬ ‫)‪6 (QS. jangan (mengganggu) binatang-‬‬ ‫‪62‬‬ . janganlah kamu melanggar syi´ar-syi´ar Allah. Al-Maidah: 2‬‬ ‫م وللل‬ ‫شعيلعئ هلر ٱلل يهه وللل ٱل ي‬‫حيلوا ا ل‬ ‫ل‬ ‫حلرا ل‬ ‫شهحلر ٱلح ل‬ ‫مفنوا ا لل ت ف ه‬ ‫ن لءا ل‬ ‫ذي ل‬‫ي يلعأي يلها ٱل ي ه‬ ‫من‬ ‫ن فلضحةل ر‬ ‫م ي لبحت لفغو ل‬ ‫حلرا ل‬ ‫ت ٱلح ل‬ ‫ن ٱلحب ليح ل‬ ‫قل يلعئ هد ل وللل لءا ر‬ ‫مي ل‬ ‫ٱلحهلدحيل وللل ٱلح ل‬ ‫ن قلوحم م‬ ‫شن ‍لا ف‬ ‫طافدوا ا وللل ي لجحره ل‬ ‫من يك فمح ل‬ ‫حل للحت فمح فلٱصح ل‬ ‫ذا ل‬ ‫يرب رههمح ولرهضحوعلن ةاا ولإ ه ل‬ ‫دوا ا ولت للعاولفنوا ا ع لللى ٱلحب هرر‬ ‫ل‬ ‫ل‬ ‫حلرام ه أن ت لعحت ل ف‬ ‫جد ه ٱلح ل‬ ‫مسح ه‬ ‫ن ٱلح ل‬ ‫دوك فمح ع ل ه‬ ‫ص ي‬‫أن ل‬ ‫ن ٱل ل ي ل‬ ‫ه‬ ‫قوا ا ٱلل ي مهه إ ه ي‬ ‫ولٱلت يقحول مىه وللل ت للعاولفنوا ا ع لللى ٱلحإ هثحم ه ولٱلحعفدحولع هنا ولٱت ي ف‬ ‫ب‪٢‬‬ ‫قا ه‬ ‫ديد ف ٱلحعه ل‬‫ش ه‬‫ل‬ ‫‪Hai orang-orang yang beriman.

dan jangan tolong-menolong dalam berbuat dosa dan pelanggaran. Dan bertakwalah kamu kepada Allah. maka berobatlah tetapi janganlah kalianberobatdengan yang haram” 63 . Muttafaq ‘alaih) 3 ‫ أوأجأعأل ِهعلدكلل أدامء أدأواءء أفأتأداأويوا أوأل أتأداأويوا ِهبأحأرامم‬، ‫إِهدن ادلأ أأينأزأل اعلدداأء أواعلددأواأء‬ Sabda Rasulullah. Dan janganlah sekali-kali kebencian(mu) kepada sesuatu kaum karena mereka menghalang-halangi kamu dari Masjidilharam. mendorongmu berbuat aniaya (kepada mereka). dan binatang-binatang qalaa-id. maka bolehlah berburu. Muslim) 2 ‫أو الد فِهى أعيوِهن ياعلأعيبِهد أمنا أكناأن ياعلأعيبدد فِهى أعيوِهن أأِهخييِهه‬ “Dan Allah selalu menolong seorang hamba selagi hamba-Nya mau menolong saudaranya”. sesungguhnya Allah amat berat siksa-Nya SUNNAH ‫ل‬ 1 ‫خرـايرـمر‬ ‫ي ف‬ ‫كرـ ل‬ ‫ل ل‬ ‫ف ولهفرـ ا‬ ‫ضعهي ا ه‬ ‫ن ال ي‬ ‫م ه‬ ‫ن االرـ ف‬ ‫مؤ ا ه‬ ‫ب إ هللرـى اللهه ه‬ ‫م ل‬ ‫ح ي‬ ‫خرـي امر ولأ ل‬ ‫ن ال ا ل‬ ‫قرـوهيي ل‬ ‫م ف‬ ‫ا لالرـ ف‬ ‫مؤ ا ه‬ “Orang mukmin yang kuat lebih baik dan lebih disenangi di mata Allah dari pada orang mukmin yang lemah”. binatang had-ya. (HR. dan jangan (pula) mengganggu orang-orang yang mengunjungi Baitullah sedang mereka mencari kurnia dan keridhaan dari Tuhannya dan apabila kamu telah menyelesaikan ibadah haji. Dan tolong-menolonglah kamu dalam (mengerjakan) kebajikan dan takwa. (HR. “Sesungguhnya Allah SWT menciptakan penyakit dan obat.

Weinberger. In: Kliegman. University of Texas Health Science Center at San Antonio. ed. Sherwood. Netter. 2010. R. L.. D..nlm. Davis. Jakarta: EGC) Guyton. 6.emedicinehealth. 205-206. E.. R. 2007. John E. N.B. Infectious Disease: Fever without a focus. A.. and Baltimore. & Hall. J. S. Fisiologi Manusia dari Sel ke Sistem.. 5.P. L.M.. USA: McGraw Hill. R. Edisi 11. Harrison’s Principles of Internal Medicine.. New York: Elsevier. S. Jakarta: EGC 3. Available from: http://emedicine. Marcdante. Kaneshiro. K. H. Available from: http://www. Fever.htm. University of Washington. 7. D. Arthur C. L. Nelson Essentials of Pediatrics.. Fever in Adults.J.. Braunwald.. and Behrman. Jenson. 2007. (Al-Hadis) REFERENCE 1. D.4 ‫أخيدر اعلنناِهس أأينأفدعدهيم ِهعلنلنناِهس‬ Sebaik-baik manusia adalah yang bermanfaat bagi orang lain.B. S.asp?articlekey=58831. 2010.. 16 th ed..S.com/article/801598-overview.E. C.com/script/main/art.. J.medscape. and Zieve. Lauralee. Buku Ajar Fisiologi Kedokteran. Available from: http://www. Chicago College of Osteopathic Medicine of Midwestern University. H. In: Kasper.. L.gov/medlineplus/ency/article/000980. (Al-Hadits) 5 ‫ص صعين صابييبه صعبن اللنبيي صصللا ى ا ل‬ ‫ل‬ ‫صعين صسيعبديببن صاببا ى صولقٍصا ص‬ ‫ل صطيفب ليبحبب اللطيصب صنبظيفف ليبحبب اللنصظٍصاصفصة‬ ‫صعصلييبه صوصسلصم بالن ا ص‬ ‫صكبريفم ليبحبب ايلصكصرصم صجصوافدليبحبب ايلصجصواصدصفصنيظلفيواصايفصنيصتلكيم‬ “Islam itu bersih maka peliharalah kebersihan karena sesungguhnya tidak masuk surga kecuali orang-orang yang bersih”. 2009.K. 5th ed. Hauser. Graneto.W.. Atlas Anatomi. 64 . E.nih. 2011.. Jenson. Pediatric Fever. 2005. 459-461.. e-book 2. 4. Jameson. Fauci. Cough and Hemoptysis. Longo.

Perhimpunan Dokter Paru Indonesia.. 2010. J.TB Elimination : Tuberculin Skin Testing.Jakarta : Balai Penerbit FK UI 1996 .Tuberkulosis: Pedoman Diagnosis dan Penatalaksanaan di Indonesia. diagnosis dan klasifikasi Tuberkulosis by Retno Asti Werdhani. 2012. I. Kinik. TB Manual National Tuberculosis ProgrammeGuidelines.Jun 06. 2010.Departemen Kesehatan Republik Indonesia. Pedoman Nasional Penanggulangan Tuberkulosis.T. 2007. Buku Ajar Ilmu Kesehatan THT. STD. 2009. and Kanra. Departemen Ilmu Kedokteran Komunitas. 2006. F. Definitions and reporting framework for tuberculosis – 2013 revision. Obesity and Paediatric Migraine. G. Perhimpunan Dokter Paru Indonesia.. L.A.. Rhinorrhea Definition. K.2012.. Migraine Headache. 16.International Headache Society. A.euro. Alehan.8. ed. M.. Nardell. dan Setiati. FKUI. I.H. Wieslaw. Edisi 5. I. 45: 936-8 14.Aspiration Pneumonia: New Insights for the Healthcare Professional. Leary. 11.. Causes. 2016 17. Buku Ajar Ilmu Penyakit Dalam Jilid 2. Buku Ajar Ilmu Penyakit Dalam Jilid III. Ed 6. Lantsberg.Scholaryedition 19. Elise K. dkk.. MD.Lung Cancer: A Multidisciplinary Approach. Okupasi. National Center for HIV/AIDS. 2014. R. Demam: Tipe dan Pendekatan. Elizabeth A et al.gov/tb 22. N. 15. A.int/__data/assets/. WHO. 26.. 10.html 24. http://cdc.. 2007. 2001. 2006. 25. Jakarta: Interna Publishing. A.. 2008.. 2767-2768 9.Availablefrom : www.who. Headache. Jakarta: Balai Penerbit FKUI. and TB Prevention. E. dan keluarga. Alwi.2012. Nelwan. George. Ethan E Emmons.com/home/infections/tuberculosis_and_leprosy /tuberculosis. DepkesRI. Edisi 2. Available from: http://www.O. Ashton Acton. 2010. Symptoms. VII : 915-918: 23. Erol. Wirguin.pdf 65 . Journal of Bronchiectasis. Alison.. S. Persatuan Ahli Penyakit Dalam. National Institute of Health 13. Horev. S.W.R. Hidayah.. Patofisiologi.. Viral Hepatitis... Dalam: Sudoyo. Willey Blackwell 18. Cetakan I. Diagnosis and Treatment.merckmanuals. Management of allergic and non-allergic rhinitis: a primary care summary of the BSACI guideline.et al.Setiyohadi.2011. Pneumonia. Ifergane. Medan : Institutional Repository USU. Cephalalgia 30: 105. The Prime Health. Simadibrata./E75464.Pg 5-6 21. Tuberculosis. Switzherland 20. A High Incidence of Migraine with Aura among Morbidly Obese Women. 12. B.

66 .