COPD Flashcards
what happens in COPD with chronic inflammation
small airways narrowing and lung parechyma destruction
abnormal permanent distal (respiratory bronchioles) airspace enlargement
emphysema
genetic predisposition of COPD:
- increased/decreased macrophage elastase
- increased/decreased alv MMP* (matrix metalloproteinase, collagenase)
- increased/decreased MMP inhibitor (TIMP)
- increased/decreased predisposition to oxidative injury
- increased/decreased anti-oxidant vitamins (C,E)
Increased macrophage elastase
Increased alv MMP* (matrix metalloproteinase, collagenase)
Decreased MMP inhibitor (TIMP)
Increased predisposition to oxidative injury
Decrease anti-oxidant vitamins (C,E)
emphysema due to deficiency
alpha-1-antitrypsin- palnolubar(lower lobe)
how do we treat panlolbular emphysema
replacement therapy
panlobular found in
lower lobe
mechanism of coPD dx,
- chronic inflammation
- imbalance btw elastase and anti-elastase
- oxidant stress
why is there airway collapse in expiration?
loss of radial traction
loss of elastic recoil results in
decreased alveolar driving pressure
hyperinflation on respiratory muscles
altered neuromechanical coupling and decreased neuromuscular capacity
do we see V/Q mismatch in COPD
yasssssssssss
treatment of COPD?
- pulmonary rehab
- improving nutrition to increase strength and immunocompetence
- SABD
Acute exarcebation can lead to
increase in mortality and decrease in lung function
what happens when elastic fibers are destroyed?
resistance increases due to the intra-dependence loss
irreversible airspace enlargement without obvious fibrosis
emphysema
subpleural involvement with formation of blebs and bullae
distal acinar emphysema
irregular emphysema
emphysema adjacent to scars
mucous gland hyperplasia
chronic bronchitis
lymphocytes are a marker for
chronic inflammation
complications of COPD (3)
- PH
- cor pulmonale
- pneumothorax
Chronic inflammatory disorder of airways characterized by recurrent episodes of bronchoconstriction that are at least partially reversible
asthma
asthma histologic changes
goblet cell hyperplasia, thickened basement membrane and submucosal eosinophil-rich inflammation
permanent dilatation of bronchi resulting from or associated with chronic necrotizing infections
bronchiectasis
_____ and _____ are major factors of bronchiectasis
obstruction and infection
how is the cough in bronchiectasis
persistent, foul-smelling and may be bloody
acute inflammation in bronchiectasis is shown with the presence of
neutrophils
distal acinar emphysema has a increased risk fro
pneumothorax
strongest risk factor for asthma
atopy–> increased levels of circulating IgE
prevalence of asthma has
what can account for this?
increased
- hygiene hypothesis
3 hallmarks of asthma
- airway inflammation
- airway hyperresponsiveness
- airflow obstruction
astham: early vs late response
early: bronchospams
late: bronchospasm, edema and inflammation
will asthma show increased resistance
yes
history suggestive of asthma
- nocturnal cough and dyspnes
- cough or wheeze post-exercise
wheezes= asthma
false, it can but there are a lot of other dx. that will also have wheezing
what do we need to be aware of giving supplemental O2 to COPD patients
respiratory rate and minute ventilation to drop due to over-oxygenation
what difference does chronic bronchitis and emphysema have early in its disease course?
chronic bronshitis causes respiratory acidosis and hypoxia
mechanism of SABA
activates adenyl cyclase leading to increase in cAMP and thus smooth muscle relaxation
causes of bronchiectasis
idiopathic or hereditary (CF, kartageners)
most common mutation in CF
delta F508
treatment in CF that can help clear mucous
nebulized DNase
what does inhaled tobramycin do?
supress pseudomonas
