Obstructive Pulmonary Disorders (physiology) Flashcards
what are three obstructive airway diseases?
asthma, chronic bronchitis, emphysema
what are chronic bronchitis and emphysema known as ?
COPD
what is normal FEV1 volume?
3.5L-4L
What is normal FVC volume?
5L
what are spirometry values predicted upon?
age sex and height
how does peak expiratory flow work?
the first time a peak expiratory flow is done, a baseline is established. Consecutive readings are then compared to the baseline:
80-100% baseline= normal
<50%= airway obstruction
What does a peak expiratory flow allow a patient to do?
allows patient to measure respiratory rate at home
what is a normal peak expiratory flow range?
400-600litres/min
what is the clinical definition of chronic bronchitis?
cough productive of sputum most days for at least 3 consecutive months for 2 or more consecutive years
what may chronic bronchitis be confused with due to the similar presentation?
bronchial asthma - difficult to differentiate by history alone so investigations essential
when is ‘complicated’ chronic bronchitis?
- acute infective exacerbation i.e. bronchopneumonia
- FEV1 falls
what are the 4 main characteristics of chronic bronchitis?
- mucous hyper secretion (occludes lumen)
- fibrosis of BRONCHIOLAR WALLS
- airway oedema
- bronchoconstriction
what are the morphological changes in chronic bronchitis in large airways?
- increase in number and size (hyper plastic) of mucous glands and goblet cells
- inflammation and fibrosis is a minor component
what are the morphological changes in chronic bronchitis in small airways?
- goblet cells appear - normally none
- respiratory epithelium changes its character to produce more mucous (protective mechanism to chronic irritation)
what do all processes in chronic bronchitis lead to?
narrowing airway & hence airflow limitation
What is Emphysema?
Increase beyond normal in the size of airspaces distal to the terminal bronchiole arising from either dilatation or destruction of alveolar wall and without obvious fibrosis –> have hyper inflated lungs
what airway is the last one to have respiratory epithelium?
terminal bronchiole
what does the loss of alveolar walls in emphysema account for?
bigger spaces
where may this loss of alveolar wall occur within the acinus?
- Centriacinar
- Panacinar
- Periacinar
- Scar (irregular)
what is an acinus
terminal + respiratory bronchiole
alveolar duct
alveolar sac
describe centriacinar emphysema
This is the most important- mostly related to smoke particles (causes inflammation)
These are the alveolar walls immediately surrounding the terminal and respiratory bronchioles
In this region that most material inhaled into lung and deposited therefore inflammation & irritation at its maximum - result is hole in middle of acinus
where is centriacinar maximal?
In apex of lung / whole upper lobe -because clearance mechanisms to get rid of particles inhaled into lungs are worse at apex and more efficient at base due to better perfusion
describe panacinar emphsyema
massive destruction of entire acini - end up with huge areas of destroyed lung –> all gas exchange tissue disappears
mostly due to alpha-1-antitrypsin deficiency
where is panacinar emphysema maximal?
lower regions of lung
describe periacinar emphysema
loss of tissue at edge of acinus, particularly in acini against pleura
Don’t cause problems until they burst - in which case may cause a spontaneous pneumothorax, leak of air into pleural space –> bulla/bleb (air that escapes into surrounding tissue and forms a bubble in the lung)
What is scar ‘irregular’ emphysema?
emphysematous spaces around scar tissue in lungs
what is the pathogenesis of emphysema?
- smoking –> which leads to alpha-1-antitrypsin deficiency
- ageing
- alpha-1-antitrypsin deficiency
How does alpha-1-antiryspin deficiency lead to emphysema?
In normal people, inflammation results in the release of elastase and protease enzymes which destroy foreign material & bacteria, however these enzymes could also potentially start to dissolve own tissue. This process is kept in check by anti-elastases and anti-protease enzymes. In absence of alpha-1-antitrypsin, this process is no longer regulated and results in tissue destruction and emphysema
how does smoking lead to alpha-1-antitrypsin deficiency?
chemicals in smoking which damage function of these protective enzymes
is there a reversible component in COPD and if so, how?
Yes there is, using asthma drugs to target certain mechanisms of airflow obstruction, however most obstruction cannot be overcome
what are the ways of airflow obstruction which can be targeted by pharmacological intervention?
inflammation & smooth muscle tone aka bronchoconstriction
what contributes to airflow obstruction in small airways?
- smooth muscle tone
- inflammation
- fibrosis
- partial collapse of airway wall on expiration
- loss of alveolar attachments most important
how does small airway stay open & not collapse especially on expiration when pressure is high?
because of attachments to alveolar walls - radial pull of alveolar wall around airway
what happens to alveoli if they lose their wall?
they collapse & will not stay open long enough for normal breathing
Where is air flow laminar ?
lower airways
where is air flow turbulent?
upper airways
what are the normal values of Normal PaO2 in kPa
10.5 - 13.5 kPa
what are the normal values of normal PaCO2 in kPa
4.8-6.0 kPa
what characterises type 1 respiratory failure?
Pa02 < 8kPa (PaCO2 normal or low)
what characterises type 2 respiratory failure?
Pa02 < 8kPa AND PaCO2 >6.5kPa (Pa02 usually low)
what are 4 abnormal states associated with hypoxaemia ?
- low V/Q ratio
- diffusion impairment
- alveolar hypoventilation
- Shunt
what is commonest cause of hypoxaemia encountered clinically?
V/Q mismatch
what does hypoxaemia due to low V/Q respond well to?
even a small increase in FIO2
what do diseases which affect gas diffusion usually not affect?
CO2 levels since co2 diffuses 20 times faster than oxygen
do shunts respond well or poorly to an increase in FIO2?
poorly - no ventilation in shunt so oxygen wont help
what is chronic (hypoxic) Cor Pulmonale?
RHF in isolation- Hypertrophy of the RV resulting from a disease affecting the function and or structure of the lung, expected when this is due to a disease affecting the left side of the heart
what are some features of Cor Pulmonale?
- pulmonary vasoconstriction
- RV has to work harder
- RH fails due to hypoxaemia
why is there hypertension in cor pulmonale?
pulmonary vasoconstriction
what else happens in a state of chronic hypoxia such as in COPD?
decreased oxygenation of lungs–> chronic hypoxaemia –> bone marrow produces more RBC (polycythaemia)–> increases viscosity of blood –> have to pump thicker blood through thinner vessels
who does COPD lead to cor pulmonale?
hypoxic alveoli cause pulmonary arterioles to vasoconstrict –> since most alveoli in lung hypoxic, vasoconstriction occurs across entire lung –> increase BP in vasculature –> pulmonary hypertension –> RH has to work harder –> RV hypertrophy –> cor pulmonale
