Lecture notes

CTB 9: Respiratory and cardiovascular diseases

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Module
Cardiovascular and thoracic biology

Institution
Imperial College London (ICL)

Lecture notes from Imperial College London, Medical Biosciences BSc, 2nd year, cardiovascular and thoracic biology (CTB) module. Lecture 9 on respiratory and cardiovascular diseases: investigate what happens when homeostatic processes break down, thereby leading to disease. We will be looking at...

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Uploaded on September 27, 2023
Number of pages 7
Written in 2022/2023
Type Lecture notes
Professor(s) Duncan rogers
Contains All classes

cardiology
cardiovascular
thoracic
cardiothoracic
respiratory
diseases
homeostasis
asthma
copd
atherosclerosis
hypertension
pulmonary
heart
lungs
airways
treatment
drugs

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Cardiovascular and Thoracic biology Imperial College London

£ 71.91 £ 42.49 9 items

1. Lecture notes - Ctb 10: step into the future
2. Lecture notes - Ctb 8: anaphylaxis: a cardiovascular-respiratory problem
3. Lecture notes - Ctb 2: mechanical and electrical properties of the heart
4. Lecture notes - Cbt 4:blood pressure and flow
5. Lecture notes - Ctb 6: cell biology of the respiratory tract
6. Lecture notes - Cbt 7: cell biology of the cardiovascular system
7. Lecture notes - Ctb 5: assessing performance of the cardiopulmonary system
8. Lecture notes - Ctb 3: ventilation and gas transport
9. Lecture notes - Ctb 9: respiratory and cardiovascular diseases
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Respiratory & cardiovascular diseases
- when homeostatic processes break down

Asthma
- common lung condition causing intermittent breathing difficulties => poor quality of life/ death
- clinical features: wheezing, shortness of breath (bronchoconstriction), cough, sputum (all reversible)
=>
- intrapulmonary bronchus occluded by a plug
of mucus, plasma exudate, inflammatory cells

pathophysiological features:
- ‘mucus’ plug in airway lumen
=>
- epithelium fragility (areas missing)
- more mucus-producing goblet cells (hyperplasia)
- thicker basement membrane
- smooth muscle hypertrophy
- blood congestion + angiogenesis
- inflammatory cells infiltration

=>
- smooth muscle contraction: bronchoconstriction
=> airway epithelium into folds
- lumen occluded by mucus (mucus hypersecretion)
=> complete airway blockage

- pathophysiology: inflammatory cells (mast cells, T-helper TH2) infiltration
=> release cytokines recruiting eosinophils
=> release chemokines recruiting inflammatory mediators
=> bronchoconstriction, mucus secretion, plasma exudation, vasodilation
=> epithelial damage: expose sensory nerve endings => activated by mediators (bradykinin)
=> cholinergic reflex to bronchoconstriction & mucus secretion

, => release of growth factors: fibroblasts activation
=> laying down of connective tissue, basement membrane thickening, smooth muscle
hypertrophy, increased number of goblet cells...

NO bronchiolar fibrosis !

- treatment: bronchodilators (prevent bronchoconstriction), anti-inflammatory glucocorticosteroids
(inhibit transcription of inflammatory mediators)
=> effective if compliance to treatment (except for ‘severe’ asthma)

COPD
- clinical features: shortness of breath (fibrosis), cough, sputum, poor quality of life (all constant)
=> can’t breath out quickly => can’t exercise, laugh...
=> caused by inhalation of noxious materials (tobacco, cooking/ heating/ lighting, pollution...)
=> 3 processes: - chronic bronchitis: damaged lung airways (bronchi inflammation) => mucus
hypersecretion => cough + cough up sputum (mucus)
increase alveolar
- emphysema: damaged lung tissue (alveoli broken down => holes in lungs => air
dead space =>
gets trapped => can’t exhale down normally)
higher pulmonary
- small airways disease (chronic bronchiolitis): fibrosis of the bronchioli => lungs
ventilation
can’t take up O2 => heart has to work harder

lat not lot
of sputum ,
a
of
sputum

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