Airway Pathology Flashcards
5 main non neoplastic airway diseases
BE, asthma, chronic bronchitis, emphysema, BOOP (bronchiolitis obliterans and organizing pneumonia)
pathology of BE
permanent dilation of bronchi, peri bronchial (sub mucosal) inflammation and organization, muco purulent debris in dilated airways
clinical categories of BE
post obstructive, post infectious (includes CF and PCD)
radiology of BE
airway dilation extending into periphery
3 mechanisms for impaired mucus flow
obstruction to outflow, abnormal mucus (CF), dysfn cilia (PCD)
CF patho
defective Cl channels, mucus is not hydrated properly and is difficult to clear
Dx criteria for CF
elevated sweat Cl, loss of fn mutation in both CFTR alleles
describe cilia structure in PCD
normal 9+2 structure (9 outer microtubules surrounding 2 inner) but absent dynein arms connecting them
patho of asthma (not usually done, clinical Dx)
edema, smooth muscle thickening, BM thickening, mucus hyperplasia, more eos, thick intralumen mucus
charcot leyden crystals and curschmann spirals in sputum
clinical dx of chronic bronchitis
productive cough mor than 3 mos a year for 2 or more yrs
patho of chronic bronchitis
mucous cell and glandular hyperplasia, submucosal chronic inflammation, may have bronchiolitis
both goblet cells and mucinous glands in submucosa increased
2 clincal categories of emphysema
cigarrete derived (COPD) and a1AT deficiency
patho of emphysema
etiology is increased elastase activity, dilation of distal airspaces w/ septal destruction
differentiate centrilobular and panlobular emphysema
centrilobular: upper more than lower, cigarette smoking
panlobular: lower more than upper, a1AT deficiency
how does smoking cause emphysema
inhibits a1AT and its antielastase function, also increases PMNs and macrophages which release more elastase
the increased elastase damages alveolar walls
