DEVINE Flashcards
(66 cards)
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