T8-L1: Benign Lung Pathology Flashcards
How can inflammation affect the lungs?
- Narrowing of the tube lumens due to swelling
- Vasodilation and oedema causing leaking into the intestitum
- Thick walls by scarring reducing gas exchange
- Acute inflammatory cells like neutrophils release chemicals such as proteases and active oxygen species to kill microorganisms. They damage normal local tissues triggering destruction and inflammation.
- Scarring/Loss of tissue impacting the functioning of the lung tissue
- Increased resistance for the heart to pump against due to leaky capillary beds
What is the pathogenesis and pathophysiology of asthma?
Asthma is the reversible intermittent narrowing of the conducting airways.
It is due to sensitisation and re-exposure leading to narrowing.
The pathophysiology shows thickening of the walls, inflammation causing oedema and swelling. This inflammation causes hyperplasia of muscles and glands, reversible bronchospasm and mucus production.
Clinically this can present with cough, wheeze, SOB and tight chest.
A 65 year old man dies and at autopsy the lungs show enlarged airspaces with reduced alveolar walls especially around the bronchioles. What clinical syndrome is likely to accompany this?
The patient shows Emphysema - alveolar walls are lacking and will collapse in exhalation. There is less surface are for gas exchange.
Accompanying Emphysema is Bronchitis as the patient has COPD.
The wall are thickened by inflammation obstructing airflow. Persistent mucus may predispose to is infection if it is not cleared properly. The wall with inflammation and recurrent infection may lead to airway scarring and bronchiectasis
Give the pathogenesis of Bronchiectasis.
Bronchiectasis is results mainly due to obstruction of the airways e.g. by a tumour, thick much or an infection.
In the case of mucus in the lumen, there is damage to the lung tissue. Persistent mucus and pus damages the integrity of the wall, causing dilation due to the lack of support.
Due to the weakened wall, the walls collapse of exhalation and so leading to obstructive ventilatory defects. It can also present with a productive cough, haemoptysis and repeated infections. Morphologically we see dilated inflamed airway walls.
Give definitions of 4 forms of chronic interstitial disease.
Idiopathic Pulmonary Fibrosis (IPF): This is a condition of fibrosis of the interstitum. The fibrosis leads to reduced/absent gas exchange. It is especially in the lower zones of the lungs and is fatal. Seen in older men, mostly over 60.
Pneumoconiosis: Patients breath in particulates, mostly dust, triggering fibrosis. There is loss of diffusion surface and narrowing of the vascular bed and alveolar walls.
Sarcoid: Following granulomas there is scarring. Sarcoid is a multi system granulomatous disease that mostly affects mediastinal lymph nodes and the lungs. The granulomatous inflammation leads to scarring.
Hypersensitivity Pneumonitis: Hypersensitivity response to antigen in wall of bronchioles. Inflammation then triggers fibrosis if antigen is not removed. There are lots of inflammatory cells widening the interstitium reducing gas exchange. Usually centred around conducting airways as this is where the trigger is concentrated. It is and inflammatory and fibrotic bronchiolar response to inhaled antigens. Triggers include mould, animal faeces, paint fumes etc.
How can fibrosis affect the lungs?
In fibrosis, in there is narrowing of the vascular bed and alveolar walls. Just like in emphysema and Pneumoconiosis, fibrosis leads to is increased resistance on the right heart.
A 14 year old boy has had repeated episodes of chest infections as well as problems with malabsorption worsening since birth. What is the most likely diagnose?
Cystic Fibrosis
