Lung 1 Flashcards
obstructive atalectasis
blockage prevents new air from coming in
old air resorbed
lung shrinks
compressive atalectasis
pleural fluid pushes part of lung in
contraction atalectasis
lung shrinks all over due to scaring/fibrosis
gross and histo appearance of pulmonary edema
gross- wet, heavy, frothy fluid
histo- eosinophilic proteinaceous fluid
acute respiratory distress syndrome- ARDS
severe ALI- progressive respiratory insufficiency caused by diffuse alveolar damage due to sepsis, trauma, or infection
damaged endothelium with inflammation (not as much as pneumonia)
where does pulmonary edema happen
base of lower lobe
acute interstitial pneumonia (AIP)
pathologic changes consistent with ARDS/DAD but with unknown cause
average age: 50
high mortality rate
acute lung injury
sudden decrease in oxygen and widespread pulmonary infiltrates without heart failure
diffuse alveolar damage (DAD)
histo finding for ARDS
4 major causes of ARDS
sepsis
diffuse pulmonary infections
gastric aspiration
mechanical trauma
key features of ARDS
post insult- trauma, sepsis, infection patchy infiltrate on CXR hypoxemia unresponsive to oxygen ventilation/perfusion abnormalities decreased surfactant --> PEEP ventilation required hyaline membranes uniform temporal appearance
obstructive disease
decreased FEV1
look at flow rate
restrictive disease
decreased FVC and TLC
look at volume
examples of obstructive disease
chronic bronchitis
emphysema
asthma
bronchiectasis
examples of restrictive disease
ARDS
chest wall disorders- polio, obesity
FVC
forced vital capacity
determined by max expiratory effort
FEV1
forced expiratory volume in 1 second
PEF
peak expiratory flow
highest flow measured with peak flow meter
emphysema
irreversible wall destruction with over inflation
obstructive
chronic bronchitis
productive cough with airway inflammation
obstructive
asthma
reversible obstruction
hyperactive airways triggered by allergens, infection, or other
obstructive
COPD
emphysema + chronic bronchitis
common in smokers
centriacinar emphysema
big and small alveoli central with distal sparing upper lobes and apices associated with smoking explained by protease/anti-protease hypothesis
pancinar emphysema
uniformly enlarged acini
from respiratory bronchiole to terminal alveoli
lower lobes
associated with alpha1-AT deficiency (genetic)
gene involved in emphysema
NRF2
PiMM
normal Alpha1-AT enzyme involved with emphysema
PiZZ
abnormal alpha1-AT enzyme involved with emphysema
emphysema is noticed when
1/3 of lung parenchyma is damaged
symptoms of emphysema
dyspnea, cough, wheeze, weight loss cor pulmonale respiratory acidosis pneumothorax RHF
bullous emphysema
end stage for centriacinar
large subpleural blebs
rupture can cause pneumothorax
chronic bronchitis
3 month productive cough with sputum production
goblet cell hyperplasia –> over production of mucos
cigarette smoking
bronchial wall fibrosis
simple chronic bronchitis
productive cough without obstruction
chronic asthmatic bronchitis
hyperactive airways with intermittent bronchospasm and wheezing
obstructive chronic bronchitis
chronic airflow obstruction usually paired with emphysema
pathogenesis of chronic bronchitis
mucos over production with decreased surfactant production in response to chronic inflammation
can become infected
blue bloater
chronic bronchitis- hypercapnia, hypoxemia, cyanosis
barrel chested
pink puffer
emphysema
weight loss, lean forward
breathing through pursed lips
biggest intervention for COPD
smoking cessation
biggest factor of chronic bronchitis
smoking
bronchiectasis
permanent dilation of bronchi/bronchioles due to muscle and elastic tissue destruction from chronic necrotizing infections
mucus gland hyperplasia
chronic bronchitis
airway dilation
bronchiectasis
alveolar wall destruction
emphysema
hyaline membranes
ARDS
