📚 Lung Diseases | 肺疾病
The human respiratory system is essential for gas exchange, but it is vulnerable to a range of diseases that compromise its function. Lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), lung cancer, tuberculosis, and pulmonary fibrosis can severely impact quality of life and are leading causes of morbidity and mortality worldwide. This article explores the causes, pathophysiology, symptoms, diagnosis, and management of major lung diseases, linking them to the underlying anatomy and physiology covered in A-Level Biology.
人体呼吸系统对气体交换至关重要，但它容易受到一系列疾病的侵害，从而损害其功能。哮喘、慢性阻塞性肺病（COPD）、肺癌、肺结核和肺纤维化等肺部疾病会严重影响生活质量，是全球发病率和死亡率的主要原因。本文探讨主要肺部疾病的病因、病理生理学、症状、诊断和管理，并将其与A-Level生物学所涵盖的基础解剖学和生理学联系起来。
1. Introduction to Lung Structure and Function | 肺结构与功能简介
The lungs consist of branching airways (bronchi and bronchioles) that terminate in alveoli, thin-walled sacs where gas exchange occurs. The alveoli are surrounded by a dense network of capillaries, facilitating the diffusion of oxygen into the blood and carbon dioxide out. The process relies on a large surface area, a short diffusion distance, and a steep concentration gradient maintained by ventilation and blood flow. Any disease that alters these parameters—by thickening the alveolar wall, filling air spaces with fluid or mucus, or destroying alveolar structure—will impair gas exchange.
肺由分支的气道（支气管和细支气管）组成，末端是肺泡，即发生气体交换的薄壁囊。肺泡被密集的毛细血管网络包围，有利于氧气扩散到血液中，二氧化碳扩散出去。这个过程依赖于较大的表面积、较短的扩散距离以及由通气和血流维持的陡峭浓度梯度。任何改变这些参数的疾病——通过增厚肺泡壁、用液体或黏液填充气腔、或破坏肺泡结构——都将损害气体交换。
2. Obstructive vs Restrictive Lung Diseases | 阻塞性与限制性肺疾病概述
Lung diseases are often classified as obstructive or restrictive. Obstructive diseases, such as asthma and COPD, are characterised by airflow limitation caused by airway narrowing, increased resistance, or loss of elastic recoil. Patients typically have difficulty exhaling fully. Restrictive diseases, such as pulmonary fibrosis, involve reduced lung expansion due to stiffness of the lung tissue or chest wall, leading to decreased lung volumes but normal airway resistance.
肺疾病通常分为阻塞性或限制性。阻塞性疾病（如哮喘和COPD）的特征是由气道狭窄、阻力增加或弹性回缩力丧失引起的气流受限。患者通常难以完全呼气。限制性疾病（如肺纤维化）涉及因肺组织或胸壁僵硬导致肺扩张减少，从而导致肺容量下降，但气道阻力正常。
3. Asthma: Causes and Pathophysiology | 哮喘：病因与病理生理
Asthma is a chronic inflammatory disease of the airways, often triggered by allergens (pollen, dust mite faeces), cold air, exercise, or respiratory infections. The inflammation causes bronchoconstriction (tightening of smooth muscle around bronchioles), mucosal oedema, and excessive mucus production. These factors significantly increase airway resistance, making it difficult to breathe, especially during expiration. During an asthma attack, the airways narrow further, and the characteristic wheezing sound is produced as air is forced through constricted passages.
哮喘是一种慢性气道炎症性疾病，通常由过敏原（花粉、尘螨粪便）、冷空气、运动或呼吸道感染触发。炎症导致支气管收缩（细支气管周围平滑肌收紧）、黏膜水肿和黏液分泌过多。这些因素显著增加气道阻力，使呼吸困难，尤其是在呼气时。哮喘发作期间，气道进一步变窄，空气被迫通过狭窄通道时会产生典型的喘鸣音。
From a pathophysiological perspective, mast cells release histamine and leukotrienes, causing immediate bronchoconstriction, while eosinophils and T-lymphocytes drive the chronic inflammatory response. Long-term, airway remodelling can occur, leading to permanent thickening of the basement membrane and persistent obstruction. Spirometry in an asthmatic shows a reduced FEV₁/FVC ratio, which improves after administration of a bronchodilator.
从病理生理学角度看，肥大细胞释放组胺和白三烯，引起即时支气管收缩，而嗜酸性粒细胞和T淋巴细胞驱动慢性炎症反应。长期来看，可能发生气道重塑，导致基底膜永久增厚和持续性阻塞。哮喘患者的肺活量测定显示FEV₁/FVC比率降低，在给予支气管扩张剂后会改善。
4. Chronic Obstructive Pulmonary Disease (COPD) | 慢性阻塞性肺疾病（COPD）
COPD is a progressive, largely preventable lung disease characterised by persistent airflow limitation. It is most commonly caused by long-term exposure to cigarette smoke, but biomass fuel smoke and industrial pollutants also contribute. COPD encompasses two main conditions: chronic bronchitis and emphysema, which often coexist.
COPD是一种进行性、大体可预防的肺疾病，特征为持续性气流受限。最常见的原因是长期接触香烟烟雾，但生物质燃料烟雾和工业污染物也有影响。COPD包括两种主要病症：慢性支气管炎和肺气肿，两者常同时存在。
5. Chronic Bronchitis | 慢性支气管炎
Chronic bronchitis is defined clinically as a productive cough with sputum production for at least three months per year over two consecutive years. Inhaled irritants cause hypertrophy and hyperplasia of the mucus-secreting glands in the bronchi, leading to excessive, thick mucus. This mucus obstructs the airways, and the impaired ciliary function (due to toxins like those in tobacco smoke) reduces clearance. The airway walls become inflamed and oedematous, further narrowing the lumen. Patients suffer from persistent coughing, wheezing, and recurrent respiratory infections.
慢性支气管炎的临床定义为连续两年中每年至少有三个月出现伴有咳痰的咳嗽。吸入的刺激物导致支气管中分泌黏液的腺体肥大和增生，产生过多、黏稠的黏液。这些黏液阻塞气道，而毒素（如烟草烟雾中的）导致的纤毛功能受损降低了清除能力。气道壁发炎并水肿，进一步收窄管腔。患者会出现持续性咳嗽、喘鸣和反复呼吸道感染。
The hallmark of chronic bronchitis is obstruction due to mucus plugging and inflammation, not primarily alveolar destruction. On spirometry, FEV₁ is reduced, and the FEV₁/FVC ratio is < 0.7, similar to other COPD components. Hypoxaemia and hypercapnia can develop as the disease progresses, sometimes leading to cyanosis ("blue bloaters").
慢性支气管炎的标志是由于黏液堵塞和炎症导致的阻塞，而非主要是肺泡破坏。在肺活量测定中，FEV₁降低，FEV₁/FVC比率<0.7，与其他COPD组分相似。随着疾病进展，可能出现低氧血症和高碳酸血症，有时导致发绀（"蓝色臃肿型"）。
6. Emphysema | 肺气肿
Emphysema involves the permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by destruction of alveolar walls. The primary cause is an imbalance between proteases (such as elastase, released by neutrophils and macrophages) and antiproteases (such as α₁-antitrypsin). Cigarette smoke inactivates α₁-antitrypsin and stimulates inflammatory cells to release elastase, which digests elastin in alveolar walls. This destruction reduces the total surface area for gas exchange and the elastic recoil of the lungs. Consequently, the airways collapse during expiration, trapping air in the lungs. Patients become breathless, often with a barrel-shaped chest, and use accessory muscles to breathe. They are sometimes called "pink puffers" because they maintain oxygenation through hyperventilation but exhibit prolonged expiratory phases.
肺气肿涉及终末细支气管远端气腔的永久性扩大，伴有肺泡壁的破坏。主要原因是蛋白酶（如弹性蛋白酶，由中性粒细胞和巨噬细胞释放）和抗蛋白酶（如α₁-抗胰蛋白酶）之间的失衡。香烟烟雾使α₁-抗胰蛋白酶失活，并刺激炎症细胞释放弹性蛋白酶，
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