week 5 Flashcards
clinical signs of asthma
a large response to bronchodilators
a large response to 30mg oral prednisolone daily for 2 weeks
serial peak flow measurements showing 20% or greater diurnal or day-to-day variability - reduced but no day-to-day variability with COPD
clinically significant COPD is not present if the FEV1 and FEV1/FVC ratio returns to normal with drug therapy
what will provide evidence of asthma in the diagnosis
eosinophil / IgE / skin prick testing / FeNO (marker of eosinophilic inflammation)
spirometry - airflow obstruction / reversibility / variability
bronchial challenge - airway hyper-responsiveness
imaging - normal / hyperinflated CXR or air trapping HRCT
clinical diagnosis of asthma
>2 of cough, wheeze, SoB, chest tightness nocturnal/AM symptoms triggers/exercise/aspirin/b-blockers allergy family history
how is atopic asthma triggered
triggered by a variety of environmental agents, including dust, pollens, foods and animal danders
nonatopic asthma
isn’t related to an allergy trigger like pollen or dust, and is less common than atopic asthma
can be more severe
measuring FeNO
indicates eosinophilic inflammation in the airway
patient exhales and amount of FeNO in exhaled breath is measured
normal is <25ppb
abnormal >50ppb
only validated in non-smokers - smoking suppresses eosinophilic activity
COPD risk factors
smoking air pollution wood burning occupation nutrition socioeconomic status bacterial colonisation genetics
pathophysiology of COPD
increase in the number of pro-inflammatory cells: neutrophils, CD8+ cells and macrophages
CD8+ cells can release TNF-alpha, perforins and granzymes
neutrophils produce proteases which can cause alveolar destruction, elastase destruction and mucus hypersecretion
macrophages produce proteases and inflammatory mediators
smoke promotes release of pro-inflammatory mediators and inactivates anti-proteases
results in permanent damage to airways, lung parenchyma and vasculature
less elastic recoil in parenchyma will eventually lead to airway collapse creating air trapping and lung expansion as breath cannot be expelled completely
airways become narrowed - increased number of goblet cells, ciliary dysfunction, destruction of alveolar walls, increased size of submucosal glands
protease antiprotease imbalance in COPD
inflammatory cells produce an excess of protease enzymes such as neutrophil elastase over antiproteases such as alpha1-AT
imbalance results in lung tissue damage and subsequent development of COPD
relevance of alpha1-antitrypsin to COPD
strong evidence of a genetic relationship in COPD
deficient release of this molecule results in early development in COPD
ZZ homozygotes produce very low levels of a1-AT
potential factors leading to COPD with recurrent exacerbations
element of asthma bacterial colonisation hypoxia reflux underlying bronchiectasis aspergillus sensitisation
bronchiectasis
purulent daily sputum
50% idiopathic
recurrent infection
crackles on exam
differences between asthma and empysema
asthma - day to day variation, triggers, nocturnal symptoms
empysema - breathlessness, low BMI, O2 requirement
differences and similarities between chronic bronchitis and bronchiectasis
CB - seasonal symptoms, daily sputum especially in winter, recurrent infections
b - daily sputum, crackles, recurrent infection
FEV1/FVC in asthma, chronic bronchitis and emphysema (chronic airways disease)
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