COPD pathology Oct10 M1 Flashcards
COPD def (2)
1) Any pulm disorder resulting from increased resistance or decreased lung or chest recoil
2) slowly progressive disorder resulting from emphysema or reduction in caliber of small airways (bronchioles)
5 COPDs
emphysema, bronchiolitis (small airway disease), asthma, COPD, bronchiectasis
2 COPDs that aren’t really obstructive
chronic bronchitis (even if considered true COPD) bronchiectasis
pulmonary acinus def
lung parenchyma distal to terminal bronchiole
pulmonary lobule def
lung tissue surrounded by interlobular septae (group of acini)
pulmonary interstitium def
CT in alveolar and interlobular septae and around vessels and airways
bronchi vs bronchioles
bronchioles = no cartilage
terminal bronchiole def
THE (1) last bronchiole with no alveoli associted with it
major site of injury for many pulmonary diseases
proximal respiratory bronchioles
secondary lobule def + width
region supplied by one terminal bronchiole. Usually 6 acini. surrounded by CT (interlobular septae). 1-2 cm in diameter
secondary lobule (or lobule) blood sup
terminal bronchiole is paralleled by a centrilobular artery.
The veins and lymphatics run in the interlobular septa
emphysema def
abnormal and permanent enlargement of airspaces with destruction of alveolar walls
where elastic tissue found in lung + something important to note
in wall of airways and also in alveoli. Elastic tissue of these two regions is connected
Function of elastic tissue
Stops airways from collapsing when we exhale.
Protein other than elastin found in lung interstitium
some collagen too
Equilibrium between __ and __ is important to maintain elastin and collagen in lung
Proteases (elastase and collagenase) and antiproteases
What causes baseline protease release in the lung
Neutrophils and macrophages in circulation + in alveolar interstitium and septum, everyday, some die and release these enzymes
Mechanisms (one major) to control baseline protease release in the lung (2)
alpha 1 antitrypsin present in the blood (major)
In situ antiproteases in the lung
Cigarette smoke effects on neutrophils (4)
Increases their number
Delays their transit in lung (more chance they release enzymes)
Increase the amount of neutrophil elastase
Increase neutrophil elastase release
Cigarette smoke effect on macrophages
Increases the number of alveolar macrophages
2 antiproteases
1) epithelial cell antiproteases
2) serum alpha 1 antiprotease
3 types of emphysema
centrilobular (proximal acinar)
panlobular (panacinar)
paraseptal (distal acinar)
gross histology of centrilobular emphysema
patchy black holes (black due to cigarette’s carbon).. Foci of coalesced alveoli which can enlarge with time.
centrilobular emphysema affects mostly which parts of the lung
upper zones
location of disease of the lung: different words to characterize it
bilateral vs unilateral
lower vs upper vs middle zones
apexes
what location of disease depends on (what characterizes it)
depends on PP gradient and blood flow
why upper lobe that is affected in centrilobular emphysema (3)
1) underperfusion relative to ventilation (less blood antiprotease)
2) slower transit time of leukocytes (more time for leukocyte elastase release)
3) Less effective clearance of inhaled material from upper lobe
95% of emphysema clinically is _______ (which type) and is related to ___
centrilobular
cigarette smoking
panacinar emphysema affects which regions of the lung
lower zones
cause of panacinar emphysema and when get it
alpha 1 antitrypsin deficiency (normally produced in liver)
get it a young age, can be 40-45 yr old if they smoke
why panacinar emphysema has a predominance in lower zones of the lung
greater blood flow there so more neutrophils
proteases will digest the lung there more
paraseptal (distal acinar) emphysema location
periphery of the lung next to intralobular septae, spaces often next to pleura
physical feature seen in paraseptal emphysema
blebs that form in upper region of the lung
danger of blebs in paraseptal emphysema (name of the disease)
spontaneous pneumothorax. can cause disease when they burst (bc pressure increased inside) bc then continous with pleural space.
bullae def
spaces in the lung larger than a centimeter
bronchiolitis (small airway disease) def
inflammation of the bronchioles
small airway disease 3 characteristics + something in common between patients
mural chronic inflammation
mural fibrosis
epithelial goblet cell hyperplasia and luminal mucus accumulation
Usually cigarette smokers
small airway disease pathophysiology
inflammation, fibrosis and mucous decrease diameter of the lung
goblet cells presence in SAD explanation
not normally in epithelial lining of bronchioles but epithelial cells changed to become goblet cells
chronic bronchitis definition
expectoration (coughing up) of mucous on most days for at least 3 consecutive months for at least two years
SAD: what cigarette smoking causes to bronchioles
irritates them and causes goblet cell metaplasia
chronic bronchitis: what cigarette smoking causes to bronchi
irritates them and causes increase of mucous cells within bronchial glands
chronic bronchitis severity and what it shows
not too bad: mucous won’t obstruct airways and is coughed out
It shows that airways are irritated
chronic bronchitis often seen with ____
bronchiolitis
bronchiectasis def
irreversible dilation of a portion of the bronchial tree
3 adjectives to characterize bronchiectasis and their meaning
cylindrical
varicose (worm like)
saccular (sac like)
3 classifications (location or other) of bronchiectasis
Intraluminal bronchial obstruction
Inherited cellular or molecular defects
Parenchymal fibrosis
intraluminal bronchial obstruction in bronchiectasis caused by what
carcinoma, aspirated foreign body
inherited cellular or molecular defects exemple in bronchiectasis
cystic fibrosis
exemple of parenchymal fibrosis cause in bronchiectasis
sarcoidosis, tuberculosis
