Clinical Phenotypes of airway disease Flashcards
what is the difference between asthma and COPD?
asthma Is a reversible condition whereas COPD is irreversible
what indicators would point to asthma over COPD?
-large (>400ml) response to bronchodilators
-large (>400ml) response to 30mg oral prednisolone daily for 2 weeks
-serial peak Flow measurements showing 20% or greater diurnal or day-to-day variability
-clinically significant COPD is not present if the FEV1 and FEV1/FVC ratio return to normal with drug therapy
what are some clinical diagnosis symptoms of asthma?
->2 of cough, wheeze, SOB, chest tightness
-nocturnal/ AM symptoms
-triggers/ exercise/ aspirin/ b-blockers
-allergy
-family history
what is she objective evidence for diagnosis of asthma?
-eosinophils/ igE/ skin prick testing/ FeNO
-PEFR variability - assuming technique okay
-spirometry - air flow obstruction/ reversibility/ variability
-bronchial challenge - airway hyper responsiveness
-imaging - normal/hyperinflated CXR or air way trapping on HRCT
what does FeNO test tell us?
measures how much nitric oxide in a breath which is directly correlated with eosinophils which are mainly present in asthma
how do measure airway obstruction or inflammation?
measure nitrous oxide in broth
what are some factors on measuring FeNO?
-easy to do at clinic
-asnwer in <5 mins
-normal <25ppb
-abnormal >50ppb
-grey area in between
-only validated in non-smokers
-indicates eosinophilic inflammation in the airway
how do we treat bronchoconstriction in asthma?
-bronchodilators (add LAMA to LABA/steroid inhalers)
-SC bricanyl for true brittle asthma
how do we treat airway inflammation (elevated FeNO) in asthma?
increase/change inhaled steroid
how do we treat allergic drive in asthma?
antihistamines regularly and avoidance of allergen
how do we treat other pathways in asthma?
leukotriene antagonists (children/exercise/polyps)
theophyllines (mixed effacer, little objective evidence for COPD type
macrolides - no evidence
how do we treat IgE total in asthma?
omalizumab monoclonal antibody
what is chronic obstructive pulmonary disease?
-smoking related lung disease
-presents in middle age
-20 pack years
-10% of UK population have FEV1 below predicted value
-6% of UK adult population have symptomatic of this
-worldwide prevalence lower
what is the pathogenesis of COPD?
smoking
air pollution
wood burning
occupation
nutrition
socioeconomic status
bacterial colonisation
genetics
birth and development
where does FEV1 peak usually?
around 25 years
why does smoking cause COPD?
hydrogen peroxide and tars turn to free radicals which results in oxidative stress and inflammation (inflammation causes further damage and lung tissue destruction)
what is the process behind emphysema?
-protease antiprotease imbalance
-inflammatory cells produce an excess of protease enzymes such as neutrophil elastase (NE) over antiproteases such as a1Antitrypsin (a1-AT)
-this protease/antiprotease imbalance results in lung tissue damage and subsequent development of COPD
what happens during emphysema?
airflow obstruction -> peripheral airway disease
hyperinflation
airway compression
loss of elastic support
maldistribution of ventilation (air gets into the lungs but gets trapped so oxygen does not get into blood stream)
effects gas exchange
what Is a1-antitrypsin?
main anti protein in the lung
what is the correlation between a1-antitrypsin?
-strongest evidence of a genetic relationship in COPD
-deficient release of this molecule results in early development of COPD
-ZZ homozygotes produce very low levels of a1-antitrpysin
-OR >30 of developing COPD
-milder forms increased incidence of COPD
-a1At implicated in <1% of patients with COPD
who should get LTOT (long term oxygen therapy)?
-patients whose disease is stable on a full medical regimen with PaO2<7.3 (55mmHg) (corresponding to an SaO2 ,88%)
-patients whose Pa,O2 is 7.3-7.8kPa (55-59mmHg) (Sa,O2 89%) with pulmonary hypertension
-patients who desaturate only during exercise or sleep consider oxygen therapy specifically under those conditions
what is type 2 respiratory failure?
occurs when the respiratory system cannot sufficiently remove carbon dioxide from the body, leading to hypercapnia
what is hypercapnia?
high levels of CO2 in blood
what is non invasive ventilation?
tight fitting mask onto face which is connected to a ventilation machine
uses bi level ventilation
how does bi level ventilation work?
when patients breathe in, it triggers a big push of air into the lungs and when they breath out it leaves a small amount of pressure within the lungs to stop the airways collapsing down
what are the potential factors that COPD would present with recurrent exacerbations?
-element of asthma
-bacterial colonisation
-aspergillus sensitisation
-hypoxia
-reflux
-underlying bronchiectasis
what should not be heard on auscultations during COPD or asthma?
bilateral crackles
what is bronchiectasis?
a long-term condition where the airways of the lungs become widened, leading to a build-up of excess mucus that can make the lungs more vulnerable to infection
what are some presentations of bronchiectasis?
purulent daily sputum
50% IDIOPATHIC
RECURRENT INFECTION
CRACKLES ON EXAM
what are some presentations of empysema?
breathlessness
low BMI
oxygen requirement
what are some clinical presentations of chronic bronchitis?
-seasonal
-daily sputum, esp winter
-recurrent infections
