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. Why the patient get cough with sputum and sometimes bloody?2. Why the friend patient should under go six month treatment?3. Why the doctor repeat BTA one more time?4. 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 mukosa, walaupun perdarahan yang potensial fatal dapat terjadi 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 (non-produktif) 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 DiseasePrimary 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 para-tracheal 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 smallcalcified 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 foundin 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 DiseaseAlso 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 undergocavitation. 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 monthsafter 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 develops—often 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 (Rasmussen’s 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 rareinstances, 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 aremild anemia and leukocytosis. Hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) has also been reported.

EXTRAPULMONARY TUBERCULOSISLymph-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 inflamed 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 TuberculosisInvolvement 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 inflammation or, as in many cases of pleurisy accompanying postprimary disease, actual penetration by tubercle bacilli into the pleural space.Tuberculosis of the Upper AirwaysNearly 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. Acid-fast 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 flank or abdominal painare 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 TuberculosisIn 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 ofhematogenous 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 (Pott’s disease or tuberculous spondylitis) often involvestwo 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 bacillus—characteristically 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, non–spore-forming, thin aerobic bacterium measuring 0.5 µm by 3 µm. Mycobacteria, including M. tuberculosis, are often neutral on Gram’s 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 organisms’high 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 cell-mediated immune response that confers resistanceto 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, aprocess 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 immunecells.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/2009/04/05/24-maret-hari-

tb-sedunia/

Pelaporan IUATLD (Internasional Union Against Tuberculosis Lung Disease) SPS

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