Obstructive airway diseases Flashcards
what characteristic is shared by lung cancer, other tumours, inhaled foreign bodies, chronic scarring diseases like bronchiectasis and secondary tuberculosis associated with obstruction of large airway?
they are localised obstruction of the airways (most likely the large airways)
is it possible to have generalised obstruction of the airways? which part of the airway do they affect?
yes, but they are rare, they affect the small airways (bronchiolar)
what is the most component of chronic bronchitis, emphysema and asthma?
the most important component is airway obstruction
do chronic bronchitis, emphysema, asthma have the same mechanism for obstruction?
no
what 2 test can be used to demonstrate obstructive lung disease?
spirometry and peak flow
what is the normal value for FEV1?
3,5-4L
what is the normal value for FVC?
5L
what is the normal value for FEV1/FVC?
0,7-0,8
what factors does a predicted FVC rely on?
predicted FVC is based on age, sex, height
what is the normal value for a peak flow?
400-600L/min
what is the normal range for peak expiratory flow rate (PEFR)?
80-100% of best value
what is the value of a moderate fall for peak expiratory flow rate (PEFR)?
50-80% of best value
what is the value of a marked fall for peak expiratory flow rate (PEFR)?
<50% of best value
what are the main feature of obstructive lung disease?
airflow limitation, PEFR reduced, FEV1 reduced, FVC possibly reduced, FEV1 less than 70% of FVC
what are chronic bronchitis and emphysema better known as?
Chronic Obstructive Pulmonary Disease - COPD (COAD or COLD)
what is the main reason for bronchial asthma?
type 1 hypersensitivity in the airways
why would the mast cells degranulate and cause the inflammation?
because of specific IgE, drugs, chemicals, ‘stress’, cold
how are asthma airways and chronic asthma airways different?
chronic asthma airways have mucus, plasma exudation, epithelial shedding/damage, more inflammation, all of which makes it even more difficult for the air to pass
is bronchial asthma a reversible airway obstruction?
yes
how can bronchial asthma be reversed?
by drugs, medical intervention or spontaneously (bronchial smooth muscle contraction and inflammation can be modified by drugs)
what is the common aetiology of chronic bronchitis and emphysema?
smoking, atmospheric pollution, dust, effect of age and susceptibility, prevalence (men > women but.. increasing in developing countries)
which deficiency is an extremely rare cause of emphysema?
alpha-1-antiprotease (antitrypsin)
what is the clinical definition of chronic bronchitis?
cough productive sputum most days in at least 3 consecutive months for 2 or more consecutive years
what does chronic bronchitis diagnosis exclude?
TB, bronchiectasis
what may chronic bronchitis diagnosis may be confused with?
asthma
what is a ‘complicated’ chronic bronchitis?
when mucopurulent (acute infective exacerbation) or FEV1 falls
what morphological changes are there in large airways?
mucous gland hyperplasia, Goblet cell hyperplasia, (inflammation and fibrosis is a minor component)
what morphological changes are there in small airways? (when chronic bronchitis takes place)
Goblet cells appear, inflammation and fibrosis in long standing disease
what is the pathological definition of emphysema?
increase beyond the normal in the size of airspaces distal to the terminal bronchial arising either from dilatation or from destruction of their walls and without obvious fibrosis
what are the different forms of emphysema?
centriacinar, panacinar, periacinar - scar (irregular, bullous emphysema)
what are the steps of centri-acinar emphysema?
begins with bronchiolar dilatation, then alveolar tissue is lost
what are the characteristics of centri-acinar?
bigger airways, loss of alveolar tissue
what are the characteristics of pan-acinar?
loss of alveolar tissue (less alveoli)
what is a periacinar/ scar emphysema/ bullous emphysema?
emphysematous space greater than 1cm
what does smoking cause?
protease-antiprotease imbalance (lack of anti-elastase, production of elastase, production of neutrophils and macrophages, lack of repair mechanisms and elastin synthesis)
which protein is no longer produced in case of alpha-1-antitrypsin deficiency?
anti-elastase
what happens when there is too much neutrophils and macrophages?
too much elastase is produced
what happens when there is too much elastase, no anti-elastase to regulate it, too little repair mechanisms and too much elastin synthesis ?
tissue destruction and therefore emphysema
is airway obstruction in chronic bronchitis and emphysema reversible?
traditional considered as no, there actually may be a reversible component
does emphysema pathogenesis include partial collapse of airway wall on expiration?
yes, the loss of alveolar attachment (alveolar to main small airway) is most important and causes the airway wall to collapse (as it is held by the alveoli like a tent, the alveoli being it’s pegs)
what is the normal value of PO2?
10,5-13,5kPa
what is the normal value of PCO2?
4,8-6,0kPa
what is the value of PO2 for a type 1 respiratory failure?
PO2 < 8 kPa (PCO2 usually normal or low)
what is the value of PCO2 for a type 2 respiratory failure?
PCO2 > 6,5 kPa (PO2 usually low)
what is hypoxaemia?
low concentration of oxygen in the blood
what four abnormal states are associated with hypoxaemia?
ventilation/perfusion imbalance, diffusion impairment, alveolar hypoventilation, shunt
why do you get hypoxaemia during COPD?
because all four abnormal states are present:
- airway obstruction causes VENTILATION AND PERFUSION ABNORMALITY (MISMATCH)
- reduced respiratory drive causes ALVEOLAR HYPOVENTILATION
- loss of alveolar surface area causes DIFFUSION IMPAIRMENT
- only during acute infective exacerbating causes SHUNT
why do you get hypoxaemia in pneumonia?
2 abnormal states are present:
- bronchitis/ bronchopneumonia cause MISMATCH (some ventilation of abnormal alveoli, just not enough)
- severe bronchopneumonia and lobar pattern with large areas of consolidation cause SHUNT (no ventilation of abnormal alveoli)
what is the normal volume of air breathed in during a minute?
4L/min
what is the normal cardiac output?
5L/min
what is the normal V/Q?
4/5 or 0,8
what does low V/Q translate as?
hypoxaemia (low V/Q is the commonest cause of it)
how could there be low V/Q in just some alveoli?
due to local alveolar hypoventilation or some focal disease
how do you that hyoxaemia due to low V/Q?
slightly increase the fraction of inspired O2 (FIO2), the fraction of O2 which comes from an oxygen device
what is a shunt?
blood passing from right to left side of the heart without contacting ventilated alveoli
what is the percentage of shunt blood?
2-4%
when can there be a pathological shunt?
when there is alveolar malformations, congenital heart disease and pulmonary disease
how well do large shunts respond to increases in FIO2?
poorly, the blood leaving normal lung is already 98% saturated
how are falls in PO2 due to hypoventilation corrected?
raise in FIO2
why is shunt a protective mechanism?
the body does not want to send blood to alveoli short of oxygen
how does the pulmonary circulation react to hypoxia? when is this localised? when does this concern all vessels?
vasoconstriction, can be localised except when there is hypoxaemia (then all vessels constrict)
what disease results in hypertrophy of the right ventricle? what does this disease affect?
chronic (hypoxic) cor pulmonale, affects the function and/or the structure of the lung
when is cor pulmonale not responsible for hypertrophy of the right ventricle?
when pulmonary alterations are the result of diseases primarily affecting the left side of the heart or congenital heart disease
how much does the normal ‘free’ right ventricle weigh?
<70g
how much does the hypertrophied ‘free’ right ventricle weigh?
more (ex: 165g)
why is hypoxic cor pulmonale linked to pulmonary hypertension?
because there is pulmonary vasoconstriction, hypertrophy in pulmonary arterioles, loss of capillary bed, secondary polycythaemia (production of RBC) and bronchopulmonary arterial anastamoses
