respiratory pathology Flashcards
examples of obstructive lung diseases
emphysema , asthma , chronic bronchitis
what are obstructive lung diseases
these are diseases that cause difficulty in air flow during expiration
common term for bronchitis and emphysema
chronic obstructive pulmonary disease
spirometry values for obstructive lung diseases
FEV1 reduced by a large extent
FVC is also reduced that is the final amount of air that is breathed out .
FEV-1 and FVC ratio
FEV1 is usually about 70-80% of FVC
Normal FEV1 is about 3.5 – 4 litres
Normal FVC is about 5 litres
Normal ratio FEV1 : FVC is 0.7 – 0.8
clinical tests for obstructive lung disease
PEFR
spirometry
summary of obstructive lung disease
There is AIRFLOW LIMITATION
Peak Expiratory Flow Rate (PEFR) is reduced
FEV1 is REDUCED
FVC may be reduced
FEV1 is less than 70% of FVC
bronchial asthma
Generally considered to be REVERSIBLE airways obstruction either spontaneously or as a result of medical intervention ( both can be treated by medication )
COPD aetiology
smoking
dust particles from occupation
atmospheric particles in the inhaled air might lead to development of COPD
effect of age
more prevalent in adults
risk factors for development , progression and morbidity in COPD
individual and social factors
general external environment
early life risk factors
noxious exposures
definition of chronic bronchitis clinically
cough productive of sputum most days in at least 3 consecutive months for 2 or more years
morphological changes in chronic bronchitis
both the small and the large airways will be affected .
changes in the small airways in chronic bronchitis
Goblet cells appear
Inflammation and fibrosis in long standing disease
the changes in the small airways are more pathological as the small airways are gaseous exchange sites
morphological changes in the large airways
Mucous gland hyperplasia
Goblet cell hyperplasia (increase in number )
Inflammation and fibrosis is a minor component
emphysema
destruction of the alveoli without fibrosis
which is an increase in the air spaces distal to the terminal bronchiole arising either from dilatation or from destruction of their walls and without obvious fibrosis.
forms of emphysema
centriacinar
panacinar
periacinar
scar
bullous emphysema
centriacinar emphysema
loss of alveoli tissue occurs in the middle bit of the acinus( the most common )
centriacinar emphysema
begins with bronchiolar dilatation then the alveolar tissue is lost
panacinar emphysema
at the base of the alveoli and there is much more destruction
bullous emphysema
has no physiological consequences
scar emphysema ( bullous )
just underneath the pleura
could be present in young people
pathogenesis of emphysema
smoking
lack of alpha -1 -antitrypsin
ageing
smoking and emphysema
there is alot of production of protease and less of antiprotease which is a protective mechanism against inflammatory cells .
therefore there is
alpha -1- antitrypsin deficiency causes emphysema
there is no production of antiproteases so there is destruction of the alveoli by the anti-inflammatory cells
features of COPD that are reversible
smooth muscle tone and inflammation will respond to pharmacological intervention
what happens to the alveoli in emphysema
there is the loss of the radial pull of the terminal alveoli which later on leads to the collapse of the alveoli during expiration
hypoxaemia in COPD
this is the state of leaving with less oxygen and more co2
Airway Obstruction on expiration
Alveolar Hypoventilation - there is less carbon dioxide being taken out
Reduced Respiratory Drive - the chemoreceptors are less sensitive to changes in hydrogen ion concentration
Shunt - Only during severe acute infective exacerbation
changes in the pulmonary vessels
there is physiological vasoconstriction( remember shunt )
all vessels may constrict if there is hypoxaemia.
pulmonary hypertension
normally pulmonary circulation is of low systolic pressure ; in pulmonary hypertension there is :
1.Pulmonary vasoconstriction
2.Pulmonary arterioles
3.muscle hypertrophy and intimal fibrosis
4.Loss of capillary bed
5.Secondary polycythaemia – increased blood viscosity
6.Bronchopulmonary arterial anastamoses
chronic ( hypoxic ) cor pulmonale
this is hypertrophy of the right ventricle which results from disease affecting the function and or the structure of the lung
what is asthma
an obstructive respiratory disease that has no reliable diagnostic test and is mostly symptom based and is reversible
what are the main symptoms of asthma
coughing , wheezing , running out of breath and response to certain asthma medication which makes asthma reversible
causes of asthma
-Host (genes) response to environment
-Physiology abnormal before symptoms (predisposition)
-Host response to exposure important
-It is a syndrome
what are the types of asthma syndromes
infant onset
childhood onset
adult onset
excertional asthma
occupational asthma
main causes of asthma
genetic predisposition which lead to primary epithelial abnormality in the skin /airway /gut while epigenetics alter the disease that is they are a trigger of the disease.
proof of causation in adults
breast -feeding
late weaning
allergens that are released post and ante- natal.
smoking
symptoms to look out for asthma in children
when there is genuine wheezing , cough and shortness of breath .
when there is a problem with the upper respiratory tract
when there is sucking in of ribs
when there is response to corticosteroids ( that is the symptoms are reversed )
guidelines for diagnosis asthma in children
measure the FeNO level in children with a history suggestive of asthma
performing objective tests that may help support a diagnosis of asthma
treatment of suspected asthma for under fives
most likely to have recurrent LRTI
treated with low dose of inhaled corticosteroids and a review is done later on.