LBM 4

Step 1

BTA = AFB (acid fast bacills) is determine the present microbacterium

tuberculosis which after staining the bacteria dont become discoloured by
acid alcohol

Step 2
1.
2.
3.
4.

Why the patient get cough with sputum and sometimes bloody?
Why the friend patient should under go six month treatment?
Why the doctor repeat BTA one more time?
What caused the patient feel decrease appetite, weight lose and
diaphoresis in the night?
5. What the intrepretation in BTA examination in the scenario?
6. Why is there wet ronchi and pulmo apex in auscultation?
7. What is the etiology of the scenario?
8. What is the procedure to BTA test?
9. What is the patogenesis and patophysiology of the scenario?
10.What is the diagnosis and DD?
11.What is the treatment?
12.What is the risk factor of the scenario?
13.What is the additional examination?
14.What is the complication of the scenario?
Step 3
1. Why the patient get cough with sputum and sometimes bloody?

Penderita tbc dengan batuk darah sering karena ulcerasi

walaupun perdarahan yang potensial fatal dapat terjadi

mukosa,
bila suatu

pembuluh darah yang berdekatan dengan suatu lesi cavitas pecah.

Gejala ini banyak ditemukan. Batuk terjadi karena adanya iritasi pada
bronkus. Batuk ini diperlukan untuk membuang produk-produk radang
keluar. Karena terlibatnya bronkus pada setiap penyakit tidak sama,
mungkin saja batuk baru ada setelah penyakit berkembang dalam
jaringan paru yakni setelah berminggu-minggu atau berbulan-bulan
peradangan semula. Sifat batuk dimulai dari batuk kering (nonproduktif) kemudian setelah timbul peradangan menjadi produktif
(menghasilkan sputum). Keadaan yang lanjut adalah berupa batuk
darah karena terdapat pembuluh darah yang pecah. Kebanyakan batuk
darah pada tubrkulosis terjadi pada kavitas, tetapi juga terjadi pada
ulkus dinding bronkus

(IPD FK UI HAL 824)

2. Why the friend patient should under go six month treatment?
3. What caused the patient feel decrease appetite, weight lose and
diaphoresis in the night?
Beberapa infeksi dapat menyebabkan keringat berlebih saat tidur dan yang paling umum
adalahtuberkulosis (TBC). Kemungkinan infeksi lain adalah infeksi bakteri
seperti endocarditis(peradangan di katup jantung), osteomyelitis (peradangan tulang), HIV,
dan berbagai infeksi bakteri lainnya.

(Sumber:Dr.Pasiyan Rachmatullah.1997.Ilmu Penyakit Paru. Semarang:FK

Undip )
Pada hipothalamus (pusat kenyang dan lapar) karena ada infeksi sistemik
karena adanya bakteri merangsang sitokin untuk keluar sitokin
mengeluarkan enzim protease protease memproduksis serotonin
serotonin merangsang pusat kenyang merangsang sensasi kenyang pada
tubuh.
Sumber: Pulmonologi dasar
4. Why is there wet ronchi and pulmo apex in auscultation?
5. What is the diagnosis and DD?

6. What is the classification of the diagnosis?

Primary Disease
Primary pulmonary tuberculosis occurs soon after the initial infection with
tubercle bacilli. In areas of high tuberculosis transmission, this form of

disease is often seen in children. Because most inspired air is distributed

to the middle and lower lung zones, these areas of the lungs are most
commonly involved in primary tuberculosis. The lesion forming after
infection is usually peripheral and accompanied in more than half of cases
by hilar or paratracheal lymphadenopathy, which may not be detectable on chest
radiography. In the majority of cases, the lesion heals spontaneously and
may later be evident as a small
calcified nodule (Ghon lesion).
In children and in persons with impaired immunity (e.g., those with
malnutrition or HIV infection), primary pulmonary tuberculosis may
progress rapidly to clinical illness.The initial lesion increases in size and
can evolve in different ways. Pleural effusion, which is found
in up to two-thirds of cases, results from the penetration of bacilli into the
pleural space from an adjacent subpleural focus. In severe cases, the
primary site rapidly enlarges, its central portion undergoes necrosis, and
cavitation develops (progressive primary tuberculosis). Tuberculosis in
young children is almost invariably accompanied by hilar or mediastinal
lymphadenopathy due to the spread of bacilli from the lung parenchyma
through lymphatic vessels. Enlarged lymph nodes may compress bronchi,
causing obstruction and subsequent segmental or lobar collapse. Partial
obstruction may cause obstructive emphysema, and bronchiectasis may
also develop. Hematogenous dissemination, which is common and often
asymptomatic,may result in the most severe manifestations of primary M.
tuberculosis infection. Bacilli reach the bloodstream from the pulmonary
lesion or the lymph nodes and disseminate into various organs, where
they may produce granulomatous lesions. Although healing frequently
takes place, immunocompromised persons (e.g., patients with HIV
infection) may develop miliary tuberculosis and/or tuberculous meningitis.
Postprimary Disease
Also called adult-type, reactivation, or secondary tuberculosis,
postprimary disease results from endogenous reactivation of latent
infection and is usually localized to the apical and posterior segments of
the upper lobes, where the substantially higher mean oxygen tension
(compared with that in the lower zones) favors mycobacterial growth. In
addition, the superior segments of the lower lobes are frequently involved.
The extent of lung parenchymal involvement varies greatly, from small
infiltrates to extensive cavitary disease.With cavity formation, liquefied
necrotic contents are ultimately discharged into the airways, resulting in
satellite lesions within the lungs that may in turn undergo
cavitation. Massive involvement of pulmonary segments or lobes, with
coalescence of lesions, produces tuberculous pneumonia. Although up to
one-third of untreated patients reportedly succumb to severe pulmonary
tuberculosis within a few weeks or months
after onset (the classical galloping consumption of the past), others
undergo a process of spontaneous remission or proceed along a chronic,
progressively debilitating course (consumption).Under these

circumstances, some pulmonary lesions become fibrotic and may later

calcify, but cavities persist in other parts of the lungs. Individuals with
such chronic disease continue to discharge tubercle bacilli into the
environment. Most patients respond to treatment, with defervescence,
decreasing cough, weight gain, and a general improvement in well-being
within several weeks.
Early in the course of disease, symptoms and signs are often nonspecific
and insidious, consisting mainly of fever and night sweats, weight loss,
anorexia, general malaise, and weakness. However, in the majority of
cases, cough eventually developsoften initially nonproductive and
subsequently accompanied by the production of purulent sputum,
sometimes with blood streaking. Massive hemoptysis may ensue as a
consequence of the erosion of a blood vessel in the wall of a
cavity.Hemoptysis, however, may also result from rupture of a dilated
vessel in a cavity (Rasmussens aneurysm) or from aspergilloma formation
in an old cavity. Pleuritic chest pain sometimes develops in patients with
subpleural parenchymal lesions. Extensive disease may produce dyspnea
and, in rare
instances, adult respiratory distress syndrome (ARDS).
Physical findings are of limited use in pulmonary tuberculosis. Many
patients have no abnormalities detectable by chest examination, whereas
others have detectable rales in the involved areas during inspiration,
especially after coughing. Occasionally, rhonchi due to partial bronchial
obstruction and classic amphoric breath sounds in areas with large cavities
may be heard. Systemic features include fever (often low-grade and
intermittent) in up to 80% of cases and wasting. Absence of fever,
however, does not exclude tuberculosis. In some cases, pallor and finger
clubbing develop.The most common hematologic findings are
mild anemia and leukocytosis. Hyponatremia due to the syndrome of
inappropriate secretion of antidiuretic hormone (SIADH) has also been
reported.
EXTRAPULMONARY TUBERCULOSIS
Lymph-Node Tuberculosis
(Tuberculous Lymphadenitis)
The most common presentation of extrapulmonary tuberculosis (>40% of
cases in the United States in recent series), lymph-node disease is
particularly frequent among HIV-infected patients. In the United States,
children and women (particularly non-Caucasians) also seem to be
especially susceptible. Once caused mainly by M. bovis, tuberculous
lymphadenitis is today due largely to M. tuberculosis. Lymph-node
tuberculosis presents as painless swelling of the lymph nodes, most
commonly at posterior cervical and supraclavicular sites (a condition
historically referred to as scrofula). Lymph nodes are usually discrete and
nontender in early disease but may be inamed and have a fistulous tract
draining caseous material. Associated pulmonary disease is seen in >40%
of cases. Systemic symptoms are usually limited to HIV-infected patients.
Pleural Tuberculosis

Involvement of the pleura, which accounts for 20% of extrapulmonary

cases in the United States, is common in primary tuberculosis and may
result from either contiguous spread of parenchymal inammation or, as in
many cases of pleurisy accompanying postprimary disease, actual
penetration by tubercle bacilli into the pleural space.
Tuberculosis of the Upper Airways
Nearly always a complication of advanced cavitary pulmonary
tuberculosis, tuberculosis of the upper airways may involve the larynx,
pharynx, and epiglottis. Symptoms include hoarseness, dysphonia, and
dysphagia in addition to chronic productive cough. Findings depend on the
site of involvement, and ulcerations may be seen on laryngoscopy. Acidfast smear of the sputum is often positive, but biopsy may be necessary in
some cases to establish the diagnosis. Carcinoma of the larynx may have
similar features but is usually painless.
Genitourinary Tuberculosis
Genitourinary tuberculosis, which accounts for 15% of all
extrapulmonary cases in the United States,may involve any portion of the
genitourinary tract. Local symptoms predominate, and up to one-third of
patients may concomitantly have pulmonary disease. Urinary frequency,
dysuria, nocturia, hematuria, and ank or abdominal pain
are common presentations. However, patients may be asymptomatic and
the disease discovered only after severe destructive lesions of the kidneys
have developed. Urinalysis gives abnormal results in 90% of cases,
revealing pyuria and hematuria.
Skeletal Tuberculosis
In the United States, tuberculosis of the bones and joints is responsible for
10% of extrapulmonary cases. In bone and joint disease, pathogenesis is
related to reactivation of
hematogenous foci or to spread from adjacent paravertebral lymph nodes.
Weight-bearing joints (the spine in 40% of cases, the hips in 13%, and the
knees in 10%) are most commonly affected. Spinal tuberculosis (Potts
disease or tuberculous spondylitis) often involves
two or more adjacent vertebral bodies. Although the upper thoracic spine
is the most common site of spinal tuberculosis in children, the lower
thoracic and upper lumbar vertebrae are usually affected in adults. From
the anterior superior or inferior angle of the vertebral body, the lesion
slowly reaches the adjacent body, later affecting the intervertebral
disk.With advanced disease, collapse of vertebral bodies results in
kyphosis (gibbus).

Harrison manual of medicine 17th edition, Fauci Braunwald kasper Hauser Longo
Jameson Loscalzo, International Edition
7. What is the etiology of the scenario?
Mycobacteria belong to the family Mycobacteriaceae and the order
Actinomycetales.Of the pathogenic species belonging to the M.
tuberculosis complex, the most common and important agent of human
disease is M. tuberculosis.The complex includes M. bovis (the bovine
tubercle bacilluscharacteristically resistant to pyrazinamide, once an

important cause of tuberculosis transmitted by unpasteurized milk, and

currently the cause of a small percentage of cases worldwide), M. caprae
(related to M. bovis),M. africanum (isolated from cases in West, Central,
and East Africa),M. microti (the vole bacillus, a less virulent and rarely
encountered organism), M. Pinnipedii (a bacillus infecting seals and sea
lions in the southern hemisphere and recently isolated from humans), and
M. canettii (a rare isolate from East African cases that produces unusual
smooth colonies on solid media and is considered closely related to a
supposed progenitor type). M. tuberculosis is a rod-shaped, nonsporeforming, thin aerobic bacterium measuring 0.5 m by 3 m.
Mycobacteria, including M. tuberculosis, are often neutral on Grams
staining. However, once stained, the bacilli cannot be decolorized by acid
alcohol; this characteristic justifies their classification as acid-fast bacilli
(AFB;).Acid fastness is due mainly to the organismshigh content of
mycolic acids, long-chain cross-linked fatty acids, and other cell-wall lipids.

Harrison manual of medicine 17th edition, Fauci Braunwald kasper Hauser Longo
Jameson Loscalzo, International Edition
8.

What is the patogenesis and patophysiology of the scenario?

Pathogenesis
The pathogenesis of tuberculosis in a previously unexposed
immunocompetent person is centered on the development of a cellmediated immune response that confers resistance
to the organism and development of tissue hypersensitivity to the
tubercular antigens.
The destructive features of the disease, such as caseating necrosis and
cavitation, result from a cell-mediated hypersensitivity response rather
than the destructive capabilities of the tubercle bacillus.
Macrophages are the primary cell infected with M. tuberculosis. Inhaled
droplet nuclei pass down the bronchial tree without settling on the
epithelium and are deposited in the alveoli. Soon after entering the lung,
the bacilli are phagocytosed by alveolar macrophages but resist killing.
Although the macrophages that first ingest M. tuberculosis cannot kill the
organisms, they initiate a cell-mediated immune response that eventually
contains the infection. As the tubercle bacilli multiply, the infected
macrophages degrade the mycobacteria and present their antigens to
helper (CD4) T lymphocytes. The sensitized helper T cells, in turn,
stimulate the macrophages to increase their concentration of lytic
enzymes and ability to kill the mycobacteria. When released, these lytic
enzymes also damage lung tissue. The development of a population of
activated cytotoxic (CD8) T cells and macrophages capable of ingesting
and destroying the bacilli constitutes the cell-mediated immune response,
a
process that takes about 3 to 6 weeks to become effective.
In persons with intact cell-mediated immunity, the cell-mediated immune
response results in the development of a gray-white, circumscribed
granulomatous lesion, called a Ghon focus, that contains the tubercle
bacilli, modified macrophages, and other immune
cells.

It is usually located in the subpleural area of the upper segments of the

lower lobes or in the lower segments of the upper lobe. When the number
of organisms is high, the hypersensitivity reaction produces significant
tissue necrosis, causing the central portion of the Ghon focus to undergo
soft, caseous (cheeselike) necrosis. During this same period, tubercle
bacilli, free or inside macrophages, drain along the lymph channels to the
tracheobronchial lymph nodes of the affected lung and there evoke the
formation of caseous granulomas. The combination of the primary lung
lesion and lymph node granulomas is called a Ghon complex . The Ghon
complex eventually heals, undergoing shrinkage, fibrous scarring, and
calcification, the latter being visible radiographically. However, small
numbers of organisms may remain viable for years. Later, if immune
mechanisms decline or fail, latent tuberculosis infection has the potential
to develop into secondary tuberculosis.

Essentials of Pathophysiology
CONCEPTS OF ALTERED HEALTH STATES
3 EDITION 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.
9. What is the risk factor of the scenario?

Harrison manual of medicine 17th edition, Fauci Braunwald kasper Hauser Longo
Jameson Loscalzo, International Edition
10.What is the complication of the scenario?
11.What is the procedure to BTA test?

Tata Cara Pemeriksaan Dahak. Perlu dilakukan pemeriksaan

dahak 3 kali untuk memastikan seseorang menderita TBC atau
tidak. Waktu pemeriksaan dahak adalah sebagai berikut :
1. Sewaktu (S); dahak diambil di unit pelayanan kesehatan
pada waktu kunjungan pertama kali
2. Pagi (P) ; dahak diambil pagi hari berikutnya dirumah
segera setelah bangun tidur pagi kemudian dibawa dan
diperiksa di unit pelayanan kesehatan ,

3. Sewaktu (S); dahak diambil diunit pelayanan kesehatan

pada saat menyerahkan dahak pagi.
http://puskesmasbamban.wordpress.com/2009/04/05/24maret-hari-tb-sedunia/
Pelaporan
IUATLD
(Internasional
Tuberculosis Lung Disease) SPS

Union

Against

Jumlah basil

Hasil yang dilaporkan

(-) BTA/ 100 LP

0 (negatif)

1-9 BTA/ 100LP

1-9 BTA/ 100LP (tulis

jumlah)

10-99 BTA/ LP

1+

1-10 BTA/LP

2+

> 10 BTA/ LP

3+

12.Why the doctor repeat BTA one more time?

13.What the intrepretation in BTA examination in the scenario?
14.What is the additional examination?
15.What is the treatment?

Harrison manual of medicine 17th edition, Fauci Braunwald kasper Hauser Longo
Jameson Loscalzo, International Edition