Lec.1 INTRODUCTION FOR RESPIRATORY DISEASES

Lec:1 Dr. Mohammed Alhamdany
INTRODUCTION FOR RESPIRATORY DISEASES
FUNCTIONAL ANATOMY AND PHYSIOLOGY
During breathing, free movement of the lung surface relative to the chest wall is facilitated by sliding contact between the parietal and visceral pleura, which cover the inner surface of the chest wall and the lung. Inspiration involves downward contraction of the dome-shaped diaphragm (innervated by the phrenic nerves) and upward, outward movement of the ribs on the costovertebral joints, caused by contraction of the external intercostal muscles (innervated by intercostal nerves). Expiration is largely passive, driven by elastic recoil of the lungs.
The acinus is the gas exchange unit of the lung and comprises branching respiratory bronchioles and clusters of alveoli. Here the air makes close contact with the blood in the pulmonary capillaries, and oxygen uptake and CO2 excretion occur. The alveoli are lined with flattened epithelial cells (type I pneumocytes) and a few, more cuboidal, type II pneumocytes. The latter produce surfactant, which is a mixture of phospholipids that reduces surface tension and counteracts the tendency of alveoli to collapse under surface tension. Type II pneumocytes can divide to reconstitute type I pneumocytes after lung injury.

Control of breathing
The respiratory motor neurons in the posterior medulla oblongata are the origin of the respiratory cycle. Their activity is modulated by multiple external inputs :
• Central chemoreceptors in the medulla sense the pH of the cerebrospinal fluid (CSF) and are indirectly stimulated by a rise in arterial PCO2.
• The carotid bodies sense hypoxaemia but are mainly activated by arterial PO2 values below 8 KPa (60 mmHg).
• Muscle spindles in the respiratory muscles sense changes in mechanical load.
• Cortical (volitional) and limbic (emotional) influences can override the automatic control of breathing.

Ventilation/perfusion matching and the pulmonary circulation
The process of respiration depend on 4 factors:
1-the ventilation which can affect by disease such as COPD
2-ventilation-perfusion match which can affect in asthma
3-diffusion which can affect in pulmonary fibrosis
4-perfusion which can affect in pulmonary hypertension
The defect in each one factor can result in hypoxia, while hypercapnea can result in only disease affect ventilation, or in severe ventilation-perfusion mismatch; that because the hypercapnea can compensate by wash out of CO2 in healthy area , while O2 can’t be compensate due to the limit of hemoglobin.

To achieve optimal gas exchange within the lungs, the regional distribution of ventilation and perfusion must be matched. At segmental and subsegmental level, hypoxia constricts pulmonary arterioles and airway CO2 dilates bronchi, helping to maintain good regional matching of ventilation and perfusion. Lung disease may create regions of relative underventilation or underperfusion, which disturb this regional matching, causing respiratory failure. In addition to causing ventilation–perfusion mismatch, diseases that destroy capillaries or thicken the alveolar capillary membrane (e.g. emphysema or fibrosis) can impair gas diffusion directly.
Pulmonary hypertension occurs when vessels are destroyed by emphysema, obstructed by thrombus, involved in interstitial inflammation or thickened by pulmonary vascular disease. The right ventricle responds by hypertrophy, with right axis deviation and P pulmonale on the ECG. Pulmonary hypertension with hypoxia and hypercapnia is associated with generalised salt and water retention (‘cor pulmonale’), with elevation of the jugular venous pressure (JVP) and peripheral oedema. This is thought to result mainly from a failure of the hypoxic and hypercapnic kidney to excrete sufficient salt and water.
Lung defences
Upper airway defences
Large airborne particles are trapped by nasal hairs, and smaller particles settling on the mucosa are cleared towards the oropharynx by the columnar ciliated epithelium.
During cough, expiratory muscle effort against a closed glottis results in high intrathoracic pressure, which is then released explosively.
Lower airway defences
The sterility, structure and function of the lower airways are maintained by close cooperation between the innate and adaptive immune responses.
The innate response in the lungs is characterized by a number of non-specific defence mechanisms. Inhaled particulate matter is trapped in airway mucus and cleared by the mucociliary escalator. Cigarette smoke increases mucus secretion but reduces mucociliary clearance and predisposes towards lower respiratory
tract infections, including pneumonia.
Defective mucociliary transport is also a feature of several rare diseases, including Kartagener’s syndrome, Young’s syndrome and ciliary dysmotility syndrome, which are characterized by repeated sino pulmonary infections and bronchiectasis.
Airway secretions contain an array of antimicrobial. In particular, alpha1- antiproteinase (A1Pi) regulates neutrophil elastase, and deficiency of this may be associated with premature emphysema. Macrophages engulf microbes, organic dusts and other particulate matter. They are unable to digest inorganic agents, such as asbestos or silica, which lead to their death and the release of powerful proteolytic enzymes that cause parenchymal damage.
Adaptive immunity is characterised by the specificity of the response and the development of memory. Lung dendritic cells facilitate antigen presentation to T and B lymphocytes.
INVESTIGATION OF RESPIRATORY DISEASE
Imaging
The ‘plain’ chest X-ray
This is performed on the majority of patients suspected of having chest disease. A postero-anterior (PA) film provides information on the lung fields, heart, mediastinum, vascular structures and thoracic cage .Additional information may be obtained from a lateral film, particularly if pathology is suspected behind the heart shadow.



Computed tomography
Computed tomography (CT) provides detailed images of the pulmonary parenchyma, mediastinum, pleura and bony structures. Sophisticated software facilitates three dimensional reconstructions of the thorax and virtual bronchoscopy.
CT is superior to chest radiography in determining the position and size of a pulmonary lesion and whether calcification or cavitation is present. It is now routinely used in the assessment of patients with suspected lung cancer and facilitates guided percutaneous needle biopsy. Information on tumour stage may be gained by examining the mediastinum, liver and adrenal glands.
High-resolution CT (HRCT) uses thin sections to provide detailed images of the pulmonary parenchyma and is particularly useful in assessing diffuse parenchymal lung disease, identifying bronchiectasis, and assessing type and extent of emphysema.
Assessment of the pulmonary circulation
CT pulmonary angiography (CTPA) has become the investigation of choice in the diagnosis of pulmonary thromboembolism, when it may either confirm the suspected embolism or highlight an alternative diagnosis.
Positron emission tomography
Positron emission tomography (PET) scanners depend on the ability of malignant tissue to absorb and metabolise glucose rapidly. The radiotracer 18F fluorodeoxyglucose (FDG) is infused and rapidly taken up by malignant tissue. It is then phosphorylated but cannot be metabolized further, becoming ‘trapped’ in the cell. PET is useful in the investigation of pulmonary nodules, and in staging mediastinal lymph nodes and distal metastatic disease in patients with lung cancer.
Co-registration of PET and CT (PET-CT) enhances localization of the mass.
Future advances will see the combination of PET and magnetic resonance
imaging (MRI).
Endoscopic examination
Bronchoscopy
The trachea and the first 3–4 generations of bronchi may be inspected using a flexible bronchoscope. Flexible bronchoscopy is usually performed under local anaesthesia with sedation, on an outpatient basis. Abnormal tissue in the bronchial lumen or wall can be biopsied, and bronchial brushings, washings or aspirates can be taken for cytological or bacteriological examination.
Rigid bronchoscopy requires general anaesthesia and is reserved for specific situations, such as massive haemoptysis or removal of foreign bodies. Endobronchial laser therapy and endobronchial stenting may be easier with rigid bronchoscopy.


Respiratory function testing
Respiratory function tests are used to aid diagnosis, assess functional impairment, and monitor treatment or progression of disease.
Airway narrowing is assessed by asking patients to blow out as hard and as fast as they can into a peak flow meter or a spirometer. Peak flow meters are cheap and convenient for home monitoring of peak expiratory flow (PEF) in the detection and monitoring of asthma, but results are effort-dependent. More accurate and reproducible measures are obtained by inhaling fully, then exhaling at maximum effort into a spirometer. The forced expired volume in 1 second (FEV1) is the volume exhaled in the first second, and the forced vital capacity (FVC) is the total volume exhaled. FEV1 is disproportionately reduced in airflow obstruction, resulting in FEV1/FVC ratios of less than 70% (while the ratio more than 70% in restrictive air way disease). For obstructive pattern, spirometry should be repeated following inhaled salbutamol; a large improvement in FEV1 (over 400 mL) and variability in peak flow over time are features of asthma.
To distinguish large airway narrowing (e.g. tracheal stenosis or compression) from small airway narrowing, flow/volume loops are recorded using spirometry.
These display flow in relation to lung volume (rather than time) during maximum expiration and inspiration, and the pattern of flow reveals the site of airflow obstruction.











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