Asthma and COPD Flashcards
what is asthma
recurrent episodes of airway obstruction due to chronic inflammatory hypersensitivity and hyperresponsiveness of airways
symptoms of asthma and signs
wheeze (due to turbulent flow) cough SOB atopy family history of asthma, atopy worse at night
kind of inflammation in asthma (cell)
eosinophilic inflammation leadig to bronchospasma and mucosal inflammation
diagnosis of asthma
FEV1/FVC salbutamol test
treatment of acute asthma attack
oxygen, nebulised salbutamol, tiotropium
asthma management
salbutamol (SABA) <3 times per week
otherwise manage with LABA, inhaled steroids/preventers (fluticasone, budesonide)
complications of asthma
acute attack
collagen deposition/fibrosis
smooth muscle cell hyperplasia, goblet cell hyperplasia
salbutamol side effects
tremor
steroid complications in asthma
appettie/weight gain, interrption of sleep
oral thrush, dysphonia (hoarse voice)
prednisolone side effects
weight gain/appetie
mood change
can raise blood sugar
pathology of COPD
chronic bronchial inflammation/obstruction
loss of cilia
mucus hypersecretion
loss of A-C units, gas exchange surface area, loss of elastic support for airways
what is tiotropium
a long acting anticholinergic used in COPD to reduce mucus, reduces exacerbations
treatments available for COPD
anticholinergics (tiotropiums)
SABA
inhaled steroids +- LABA
oxygen if PaO2<55
vaccinations for COPD patients
yearly influenza
5 yearly pneumococcal
what is pneumonia
infection of alveolar units leading to VQ mismatch, diffusion impairment and increased work of breathign
what is the rationale behind empiric antibiotics for community acquired pneumonia?
cover both typical and atypical organisms
outcomes are worse if we wait
usually start with penicillin and doxycyline
antibiotics for TB
INAH, rifampicin, pyrazinamide, ethambutol
findings on examination in asthma attack
tachypnoea anxiety wheeze prolonged expiratory phase cyanosis use of accessory muscles
types of inflammation in COPD
neutrophilic, macrophages
proteinase-antiproteinase imbalance destroying alveolar connective tissue
changes in lung parenchyma in COPD
loss of alveolar-capillary membrane so loss of surface area for gas exchange
loss of elastic support
lose oxygenation capacity
mechanism of emphseama
protease/antiprotease imablance digest elastin and other structureal proteins in alveolar wall
macrophages and t cell inflammation
function of alpha1antitrypsin
degrade proteases in the lung and the liver
why might you use slow vitgal capacity in assessing COPD
forced vital cpacity can cause airway collapse, trapping air and giving an underestimate of vital capacity
what should the forced expiratory ratio be below to indicate obstruction
<0.7