Khusnul Mar'iyah, Zulkarnain Zulkarnain

Patofisiologi penyakit infeksi tuberkulosis

Introduction

Patofisiologi penyakit infeksi tuberkulosis. Pelajari patofisiologi tuberkulosis (TBC), infeksi paru menular oleh bakteri Mycobacterium tuberculosis. Pahami transmisi, respons imun, pembentukan granuloma, dan gejala khas TBC.

Abstract

Tuberkulosis merupakan penyakit infeksi menular yang disebabkan oleh agen infeksi bakteri Gram positif Mycobacterium tuberculosis yang bersifat aerob obligat yang umumnya menyerang organ paru pada manusia. Penyakit ini ditularkan oleh penderita BTA positif yang menyebar melalui droplet nuclei yang keluar saat penderita batuk atupun bersin. Patofisiologi penyakit tuberkulosis dimulai dari masuknya bakteri ke dalam alveoli lalu Sistem imun dan sistem kekebalan tubuh akan merespon dengan cara melakukan reaksi inflamasi. Fagosit menekan bakteri, dan limfosit spesifik tuberculosis menghancurkan bakteri dan jaringan normal. Reaksi tersebut menimbulkan penumpukan eksudat di dalam alveoli yang bisa mengakibatkan bronchopneumonia. Selanjutnya terbentuk granulomas yang diubah menjadi fibrosa, Bagian sentral dari massa tersebut disebut ghon tuberculosis dan menjadi nekrotik membentuk massa seperti keju dan membentuk jaringan kolagen kemudian bakteri menjadi dorman. Penularan tuberkulosis dipengaruhi oleh faktor umur, jenis kelamin, kebiasan merokok, pekerjaan, status ekonomi dan lingkungan. Penderita tuberkulosis umumnya akan mengalami gejala seperti batuk lebih dari dua minggu, sesak nafas, mudah lelah, nafsu makan turun, dahak bercampur darah, demam, dan berat badan menurun.

Review

The abstract, titled "Patofisiologi penyakit infeksi tuberkulosis," offers a foundational overview of the infectious disease tuberculosis, primarily focusing on its underlying biological mechanisms. The chosen topic is highly relevant, given that tuberculosis remains a significant global health challenge. The abstract effectively introduces the causative agent, *Mycobacterium tuberculosis*, its Gram-positive and obligate aerobic nature, and its primary target organ (lungs), while also clearly delineating the mode of transmission via droplet nuclei from smear-positive individuals. The abstract's strength lies in its concise description of the initial stages of infection, from bacterial entry into the alveoli to the immune system's response, including inflammatory reactions, phagocytosis, and the involvement of specific lymphocytes. It accurately describes the formation of granulomas, their transformation into fibrotic tissue, and the subsequent caseous necrosis leading to a Ghon focus, ultimately resulting in bacterial dormancy. However, some aspects could benefit from further precision or elaboration. The statement "limfosit spesifik tuberculosis menghancurkan bakteri dan jaringan normal" could be more nuanced; while immune-mediated tissue damage is central to TB pathology, the exact mechanisms (e.g., delayed-type hypersensitivity leading to caseation) could be detailed. Furthermore, while risk factors (age, gender, smoking, occupation, socioeconomic status, environment) and clinical symptoms are listed, their mechanistic link to the *pathophysiology* of disease progression or reactivation is not explored, making them seem somewhat detached from the core pathological narrative. A critical missing component for a comprehensive pathophysiology review is the mechanism of disease reactivation from dormancy, which accounts for a substantial portion of active TB cases. In conclusion, the abstract offers a solid introductory summary of TB pathophysiology, suitable for a general audience or as an initial educational resource. It covers the essential progression from infection to dormancy effectively. For a deeper academic contribution, a full paper based on this abstract would benefit from expanding on the precise cellular and molecular mechanisms of immune-mediated tissue damage, elaborating on the processes leading to latency and, crucially, detailing the factors and pathways involved in the reactivation of dormant bacilli into active disease. Integrating the listed risk factors and symptoms more deeply into the pathological narrative would also strengthen its contribution as a "patofisiologi" focused piece.

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