DEVINE Flashcards
ATELECTASIS
collapse of lung w/absorption of air from alveoli
resorptive type
obstruction/block of bronchus by foreign body/mucous/tumor
most common cause of dyspnea
resorptive type - 1st 24hrs postop
compression type
mechanical collapse: pneumothorax, pleural effusion
ARDS
capillaritis = increased permeability»inflammation>widened gap jxn>exudation>neutrophils mediate injury
SARS/influenza
micro=diffuse alveolar damage
permits exudation fr injured vessles into alveoli w/formation of HYALINE MEMBRANES
INCREASED CAP PERMEABILITY
ARDS clinical
rapidly progressive dyspnea w/hypoxemia. poor response to O2 therapy
ARDS causes
local: inhalation smoke/chemicals; near drowning; aspiration of gastric contents, pulm infections, radiation
**SYSTEMIC: systemic inflamm response. septic shock, trauma, narcotics, surgery
spirometry: obstructive
decreased FEV1
spirometry: restrictive
decreased FVC
obstructive disease
block air, destruction of elastic fibers
most common
low O2, normal pH
obstructive disease CAUSES
parenchymal disease of lung (decreased FEV1) asthma emphysema chronic bronchitis/bronchiolitis bronchiectasis
bronchiectasis
bad smelling sputum PERM. dilation and scarring persistent &/or sever infection immotile cilia cystic fibrosis
asthma
smooth muscle hypertrophy
type I: IgE
wheezing
emphysema
acinus (sac)
airspace enlargement - alveolar wall destruction
tobacco smoke (elastase fr neutrophils…LOSS OF ELASTIC RECOIL)
dyspnea
bronchiectasis
bronchiole
inflamm scarring
pulmonary emphysema
dyspnea. barrel chest
“pink puffer” - malnourished, SOB w/o serious hypoxia. pursed lips, hunched over
may die fr resp failure, pneumothorax fr rupture bullae
secondary pulmonary hypertension w/cor pulmonale
bullae
subpleural balloon-like spaces (blebs)
associations w/all forms of pulm emphysema
lung apex
may rupture to produce spontaneous pneumothorax
intersitial emphysema
air w/in connective tissue of the lung
CHRONIC BRONCHITIS
prolonged cough productive of sputum (3mo-2yr)
tobacco smoke
submucosal mucous glands/gob cells increased: hyperplasia/trophy
infiltrates of lymphocytes//mucus plugs, incur mucus glands
ASTHMA
type 1
pollen, allergy
eosinophils, mast cells, IgE
asthma detail
IgE formed in response to exposure to allergen.
IgE antibody attaches to mast cells; mast cells release histamines, proteases; vagal receptors stimulated to produce edema and bronchial constriction.
Eosinophils and neutrophils recruited that damage mucosa; leukotrienes elaborated from arachadonic acid that intensify (2nd phase) bronchoconstriction.
Nonatopic type due to exercise, viral infection or aspirin
Morphology of asthma: Bronchi demonstrate edema, infiltrate of eosinophils, increase in mucous glands and smooth muscle hypertrophy
asthma clin course
first attack = childhood
recurrent eps of sever dyspnea w/wheezing, chron cough last >hours
may progress to COPD
bronchiectasis (ectasis=dilation)
PERMANENT ABNORMAL DILATION OF BRONCHI/BRONCHIOLES due to NECROSIS by INFECTION of WALL
bronchiectasis causes
CF
persistent cough, smells horrible
restrictive lung diseases
decreased FVC (lung vol) ground glass/reticulo (net) nodular appearance on radiographs honeycomb lung of increased interstitial fibrosis on biopsy
restrictive lung disease causes
lung disease in lupus
scleraderma, RA, other type III systemic immune complex diseases
immune complexes
no cough = no FEV1 = no obstructive