Respiratory Essay - Grade: 1st PDF

Preview

Summary

practice essay for exams...

Description

RESPIRATORY ESSAY Obstructive lung disease Obstructive lung disease are diseases where there is a decreased exhaled airflow caused by narrowing or block of the airways. Eg. Asthma, emphysema, chronic bronchitis. The obstruction of airway or increased resistance to air flow can be caused by conditions inside the 1) lumen, 2) in the wall of the airway and in the 3) peribronchial region.   

Excessive secretions Reduced airway diameter Loss of radial traction

Chronic Obstructive Pulmonary Disease COPD is a functional category designating a chronic condition of persistent obstruction of airflow. Chronic bronchitis and chronic pulmonary emphysema are the disease associated with this condition. It is the 2nd most common cause of hospital admissions and the fifth most common cause of death. Cigarette smoking is the most important factor assoc. with COPD. Mortality rate is higher in men, although female mortality is steadily rising. Early symptoms of COPD include mild shortness of breath on exertion, smoker’s cough as the body tries to get rid of harmful things that cant be cleared by immunological processes alone. At later stages, dyspnoea, weakness and cough get worse. There is difficulty in breathing out, cough is more productive with thick tenacious mucous. COPD has a sliding scale of both emphysema and chronic bronchitis, and ~10%of patients will have bronchial hyperresponsiveness.

Chronic bronchitis – Pathology •

Obstruction

– due to reduced airway diameter from the inflammation and oedema -

From the excessive mucous secretions and decreased clearance

• The obstruction leads to a ventilation-perfusion mismatch, increased PaCO2 (causing acidosis) and hypoxaemia and cyanosis. •

Hypoxaemia causes two things:

Hypoxic blood circulates through kidneys, causing the kidneys to release erythropoietin which stimulates increased production of RBC, in attempt to compensate by increasing the oxygen carrying capacity, however this makes the blood more viscous Hypoxaemia can also lead to pulmonary vasoconstriction, wherein bloodflow is reduced in underventilated areas of the lungs. This causes pulmonary hypertension, and ultimately, cor pulmonale.

1

Cor pulmonale is a right-sided heart failure caused by alteration in the structure and function of the right ventricle due to the chronic overpumping of the RV to compensate for the increased vascular resistance.

Chronic bronchitis – histology The hallmark of disease is hypertrophy and hyperplasia of mucous glands in the large bronchi, leading to overproduction of mucous and formation of semisolid plugs. Thick mucous creates perfect breeding ground for a variety of bacteria. There is a loss of cilia, therefore there is a reduction in effective mucus clearance. The chronic inflammation caused by persisting insult or exposure to irritants leads to hypertrophy of the airway smooth muscle and thickening of the basement membrane.

Long term consequences of chronic bronchitis Airway obstruction -> hypoxaemia, cyanosis -> pulmonary vasocontriction -> hypertension -> increased EPO -> polycythaemia -> increased blood viscosity

Emphysema      

Characterised by abnormal, permanent enlargement of the airspaces due to the breakdown of bronchi and bronchioles, as well as the blood vessels that supply them. The bronchial mucosa becomes oedematous and cilia are destroyed. Mucus producing glands hypertrophy, and there is also a difficulty in the removal of mucus due to destruction of cilia, therefore there is an increased obstruction of airway passages. The loss of capillaries serving the alveoli means exchange of oxygen and CO 2 is decreased. The inhalation of cigarette smoke then causes inflammation in the small airways leading to fibrosis, smooth muscle hyperplasia, squamous metaplasia and other chronic changes. The inflammatory cells involved are neutrophils and macrophages in the lumen and epithelium. In the mucosa, macrophages and T-lymphocytes are involved.

Emphysema – pathology  

  

Partly due to the destruction of the pulmonary vascular bed and partly due to hypoxic pulmonary vasoconstriction, the pulmonary artery pressures rise resulting in cor pulmonale. Normal elasticity of the lungs, which allows for normal expansion and return to normal of the lungs while breathing is severely impaired – expiration requires effort instead of being passive. This extra work requires more oxygen. Air trapping and chronic hyperinflation occur because of abnormal expiration – the amount of new air that can be inspired is reduced. Lack of structural support means bronchi collapse during expiration – leading to more obstruction, and hyperinflation due to air being trapped behind collapsed airways. There is now unequal flow to the lung – some area are overventilated whilst some are underventilated.

2

Even early-stage changes are irreversible. Changes can be in a gross level and can sometimes be seen with the naked eye (bullae). About a third of the lung is destroyed before symptoms are seen. 1030% of smokers susceptible to COPD. 2% IV drug users develop emphysema – pulmonary vascular injury from embolization of cornflour, cellulose, talc etc. There is no cure to emphysema.

Aetiology Cigarettes may stimulate macrophages to release neutrophil chemoattractants, leading to an excessive number of neutrophils in the lungs. These neutrophils release excessive amounts of elastase, a proteolytic enzyme. The elastase inhibitors are overwhelmed, resulting in the destruction of elastin. While neutrophils predominate, macrophages and CD8+ T lymphocytes are increased in various parts of the lungs. Several mediators – leukotriene B4, IL-8 and TNF contribute to the inflammatory process. Cigarettes reduce the activity of elastase inhibitors, as well as induce uncontrolled activity of elastase. Resynthesis of elastin is also inhibited by cigarette – triple insult. Repeated bouts of coughing from the smoke inhalation may also directly rupture alveolar septa.

Cause of death    

Death occurs from lack of enough functional tissue to sustain life. Could also occur from a superimposed pulmonary infection (pneumonia). Leads to respiratory failure – acidosis, hypoxia, coma. Could also cause cor pulmonale.

Emphysema from alpha1 antitrypsin deficiency This is emphysema not related to cigarettes, but due to a natural deficiency. Alpha1 antitrypsin is a serum protein which inactivates proteolytic enzymes such as trypsin, fibrinolysins and leukocyte enzymes, eg. Elastase. The concentration of the enzyme is genetically determined – severe deficiency may develop an aggressive pulmonary emphysema that manifests in adolescence or early adulthood. There are no other effects associating with inhaling noxious substances, eg. no associated chronic bronchitis and cough or excess sputum production.

3

Lung function tests Dynamic results compared to predicted:   

FEV1 down FVC down FEV1/FVC% down

Means obstructive disease. Bronchodilator challenge: Improvement in FEV1 compared to predicted: No response 25%. Reversibility suggests asthma (0.5l/s change in asthma)

In obstructive disease:     

Residual Volume >120% And/ or RV/TLC% >120% Air-trapping evident (mucus) TLC >120% Hyperinflation present (emphysema)

TLCO/KCO down in obstructive disease Emphysema

FEV1 FEV1: Forced expiratory volume in 1 second – the volume that can be expired in the first second of a maximal FVC (forced expiration). FEV is affected by the airway resistance during forced expiration. Any increase in resistance reflects any disease that cause structural changes (eg. In chronic bronchitis), bronchoconstriction (eg. In asthma), obstruction in the airway (eg. Inhaled foreign body or excessive mucus secretions) or destruction of the lung parenchyma which interferes with the radial traction that normally holds the airway open. This then results to a lower FEV 1/FVC ratio.

VC and FVC VC: Vital capacity or slow VC – total volume of gas that can be exhaled comfortably after a full inspiration. FVC: Forced vital capacity – volume of the lungs that can be expired with maximal force following a full inhalation. The vital capacity or forced vital capacity is a measure of the lung capacity, hence a reduction in FVC reflects any disease that will affect the ventilatory capacity of the lungs, ie. the restrictive diseases

4

such as pulmonary fibrosis which affects the distensibility of lungs, or space occupying lesions such as cysts. This will then result to a normal or higher FEV1/FVC ratio. In obstructive disease, the rate at which FVC is obtained is slower, as narrowed airways mean that the rate air is expired is slower - ~5-20s, normal is about 6s. However they might not be capable of exhaling all this air so might present as low FVC.

STATIC VOLUME TESTS 

Residual volume - determined by anatomical mechanics of the chest wall. This typically occurs at 25% of TLC. With increasing age or disease that cause airtrapping due to collapsed airways, RV increases, as air cannot get out.



Total lung capacity - Total lung capacity can give a big hint between emphysema and chronic bronchitis. In progressed emphysema, we will see bubbles outside of lung (bullae). This increases total lung capacity. So: -

RV/TLC% > 120% = air trapping present TLC > 120% = hyperinflation present. An increase of TLC below 20% = no hyperinflation

Treatment of COPD Corticosteroids are very useful in ~10% of patients. The frequency of acute exacerbations may be reduced with inhaled corticosteroids. Combined inhalers with B2 agonists plus corticosteroids exist – budenoside plus fomoterol or fluticasone plus salmeterol, beclometason plus formoterol. They are used in patients with severe COPD (FEV 1 > 50%) with a history of repeated exacerbations and symptoms despite use of long acting bronchodilators. Two weeks of oral steroids in acute exacerbations was shown to decrease fatality and hospitalisation rate, but they do not alter the progressive decline in lung function seen in disease – there is no slowing of the reduction in FEV1. Mucolytics Secretions in COPD consist of mucus-derived glycoproteins and leukocyte-derived DNA. Nacetylcysteine reduces mucus viscosity. Anticholinergics reduce mucus secretion via muscarinic receptors in mucus glands.

Other treatments Low flow oxygen can be used with care – mechanical ventilation may be necessary. Lung transplant may be used in emphysema. Surgery can be done to remove bullae (bullectomy) and fo lung volume reduction.

5

Oxygen toxicity High concentrations of O2 over long periods damage the lung. It can lead to swollen epithelium and increased capillary permeability leading to interstitial and alveolar oedema. Epithelium may become denuded, replaced by type 2 epithelial cells and eventually interstitial fibrosis occurs. Normal subjects complain of discomfort after 24hrs of 100% O 2. >50% O2 for 2 days probably produces toxicity.

CO2 retention due to O2 therapy. Chronic elevation of PaCO 2 means central chemoreceptors no longer act as 1 o breathing stimulus. Peripheral chemoreceptors take over and are sensitive to hypoxia – oxygen levels become the main ventilatory stimulus. Oxygen therapy relieves the hypoxia and therefore depresses ventilation.

6...